Aims and Scope Current Orthopaedics presents a unique collection of international review articles summarizing the current state of knowledge and research in orthopaedics. Each issue focuses on a specific topic, discussed in depth in a mini-symposium; other articles cover the areas of basic science, medicine, children/adults, trauma, imaging and historical review. There is also an annotation, self-assessment questions and an exam section. In this way, the entire postgraduate syllabus will be covered in a 4-year cycle. The Journal is cited in: Cochrane Center, EMBASE/ Excerpta Medica, Infomed, Reference Update and UMI Microfilms.
Editor Professor R. A. Dickson MA, ChM, FRCS, DSc Leeds General Infirmary, Leeds, UK
Editorial Committee M. A. Farquharson-Roberts (Gosport, UK), I. Leslie (Bristol, UK), D. Limb (Leeds, UK), M. Macnicol (Edinburgh, UK), I. McDermott (Ruislip, UK), J. Rankine (Leeds, UK)
Editorial Advisory Board
Amsterdam
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Boston
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Jena
L. de Almeida (Portugal) G. P. Songcharoen (Thailand) R. W. Bucholz (USA) J. W. Frymoyer (USA) R. W. Gaines (USA) S. L. Weinstein (USA) M. Bumbasirevic (former Yugoslavia)
A. K. Mukherjee (India) A. Kusakabe (Japan) A. Uchida (Japan) M.-S. Moon (Korea) R. Castelein (The Netherlands) R. K. Marti (The Netherlands) G. Hooper (New Zealand) A. Thurston (New Zealand) E. G. Pasion (Philippines)
D. C. Davidson (Australia) J. Harris (Australia) S. Nade (Australia) G. R. Velloso (Brazil) J. H. Wedge (Canada) S. Santavirta (Finland) P. N. Soucacos (Greece) M. Torrens (Greece) J. C. Y. Leong (Hong Kong)
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London
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New York
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Oxford
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Paris
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Philadelphia
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San Diego
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St Louis
Current Orthopaedics (continued 2009 as Orthopaedics and Trauma) Elsevier, ISSN: 0268-0890, http://www.sciencedirect.com/science/journal/02680890 Volume 21, Issue 1, Pages 1-84 (February 2007)
1
Editorial Board, Page i
Mini-Symposium: Frontiers in Spine Surgery 2
(i) Optimizing non-operative care, Charles Pither, Pages 1-8
3
(ii) The role of surgery in low back pain, Eugene J. Carragee, Pages 9-16
4
(iii) Total lumbar disc arthroplasty, H. Michael Mayer, Christoph Siepe, Pages 17-24
5
(iv) Lumbar stabilisation techniques, Steven Lau, Khai S. Lam, Pages 25-39
Shoulder 6
Biomechanical considerations of the normal and rotator cuff deficient shoulders and the reverse shoulder prosthesis, F. Lam, D.N. Bhatia, S.B. Mostofi, K. van Rooyen, J.F. de Beer, Pages 40-46
Children 7
Osteochondritis dissecans of the knee, Oliver S. Schindler, Pages 47-58
Trauma 8
Radial head fractures in adults, J.W.K. Harrison, A. Chitre, K. Lammin, J.G. Warner, S.P. Hodgson, Pages 59-64
Quiz 9
Radiology quiz, Nev Davies, Catherine McCarthy, Pages 65-71
Thrombo-embolic Disease 10
Role of vena cava filters in high-risk trauma and elective orthopaedic procedures, Pages 72-78 Narayan Hulse, Himanshu Sharma, Ashish Mahendra, Bardeep Rana
CME Section 11
CME SECTION, Pages 79-81
12
Answers to CME questions based on the Mini-Symposium on Bullet and Blast Injuries, Page 82
Book Reviews 13
Emerging Spine Surgery Technologies: Evidence and Framework for Evaluating New Technology, T.P. Corbin, P.J. Connolly, H.A. Yuan, Q.-B. Bao, S.D. Boden, Quality Medical Publishing (2005). 611pp., $225, ISBN:0756707641. Page 83, Crispin Wigfield
14
“Who's Who” of North American arthroplasty surgeons, R. Barrack, R. Booth Jr., J.H. Lonner et al. (Eds.). Orthopaedic Knowledge Update. Hip and Knee Reconstruction, Vol. 3. American Academy of Orthopaedic Surgeons (2006). 450pp., £97.95, ISBN: 0-89203-348-7. Pages 83-84, David Macdonald
15
Endoscopic Spine Surgery & Instrumentation—Percutaneous Procedures. Kim D.H., Fessler R.G., Regan J.J., editors. Thieme, New York, Stuttgart (2005). (404pp., $169.95, ISBN: 1-58890-225-0). Page 84, Michael Grevitt
16
Raymond T. Morrissy, Stuart L. Weinstein, Atlas of Pediatric Surgery, Lippincott Williams and Wilkins, ISBN 07817 57894, 2006, (954pp., £215). Page 84, Malcolm Macnicol
Current Orthopaedics (continued 2009 as Orthopaedics and Trauma) Elsevier, ISSN: 0268-0890, http://www.sciencedirect.com/science/journal/02680890 Volume 21, Issue 2, Pages 85-168 (April 2007)
1
Editorial Board, Page i
Mini-Symposium: Children Osteotomies around the Hip 2
(i) The Salter innominate osteotomy, Pages 85-93, M.F. Macnicol
3
(ii) Pelvic osteotomy for the management of hip displacement in neuromuscular disorders, Pages 94-99 Alastair W. Murray, James E. Robb
4
(iii) Bernese periacetabular osteotomy, Pages 100-108 Michael Leunig, Reinhold Ganz
5
(iv) The Chiari medial displacement osteotomy, Pages 109-114 Sanjeev Patil, D.A. Sherlock
6
(v) Proximal femoral osteotomy in childhood, Pages 115-121 Christopher John Dare, N.M.P. Clarke
Spine 7
Spinal deformity in paediatric patients with cerebral palsy, Pages 122-134 Athanasios I. Tsirikos, Patrick Spielmann
Hand 8
Osteoarthritis of the thumb trapeziometacarpal joint, Pages 135-144 Sameer Batra, R. Kanvinde
Trauma 9
Management of lateral humeral condylar mass fractures in children, Pages 145-149 H. Sharma, K. Chirputkar, R.D.D. Duncan
Quiz 10
Radiology quiz, Pages 150-158, Jon Martin, Philip Robinson
Syndrome 11
Cleidocranial dysplasia, Pages 159-162 Verity Currall, Rachel Clancy, Donna Dimond, Rouin Amirfeyz, Chris Kershaw, Martin Gargan
CME Section 12
CME SECTION, Pages 163-165
13
Answers to CME questions based on the Mini-Symposium on Management of Fractures around the Knee Joint, Page 166
14
Erratum to ―The ‗floating knee‘ in adults and children‖ [Curr. Orthop. (2006) 20, 405–410], Page 167 Byron Chalidis, Saurabh S. Mehta, Eleftherios Tsiridis, Peter V. Gioannoudis
15
Richard D. Guyer and Jack E. Zigler, Editors, Spinal Arthroplasty—A New Era in Spine Care, Quality Medical Publishing (2005) ISBN 1-57626-190-5 (343pp., $195). Page 168, Crispin Wigfield
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Nonfusion Techniques for the Spine: Motion Preservation and Balance. Maxwell J.H., Griffith S.L., Welch W.C., editors. Quality Medical Publishing Inc., St. Louis, Missouri (2005), (420pp., $275, ISBN: 1-57626-179-4). Page 168 Michael Grevitt
Current Orthopaedics (continued 2009 as Orthopaedics and Trauma) Elsevier, ISSN: 0268-0890, http://www.sciencedirect.com/science/journal/02680890 Volume 21, Issue 3, Pages 169-248 (June 2007)
1
2
Editorial Board, Page i
Editorial, Page 169. Robert A. Dickson
Mini-Symposium: Computer Aided/Robotic Orthopaedic Surgery 3
(i) Registration techniques for computer navigation, Pages 170-179 Guoyan Zheng, Jens Kowal, Miguel A. González Ballester, Marco Caversaccio, Lutz-Peter Nolte
4
(ii) The accuracy of surgical navigation for orthopaedic surgery, Pages 180-192. R. Phillips
5
(iii) The anterior cruciate ligament and navigation, Pages 193-199. J.C. Panisset, F. Picard
6
(iv) Computer-assisted knee replacement techniques, Pages 200-206. Wolfram H. Kluge
Wrist 7
Management of wrist instability, Pages 207-214. S. Sivananthan, L. Sharp, Y.C. Loh
Children 8
Slipped upper femoral epiphysis, Pages 215-228. Samuel J. Parsons, Cefin Barton, Robin Banerjee, Nigel T. Kiely
Trauma 9
Current management of high-energy tibial plateau fractures, Pages 229-235 Robert D. Zura, James A. Browne, Molly D. Black, Steven A. Olson
Syndromes 10
Osteogenesis imperfecta, Pages 236-241. Clare Michell, Vanisha Patel, Rouin Amirfeyz, Martin Gargan
CME Section 11
CME questions based on the article for this issue—‘‘Management of wrist instability’’, Pages 242-244
12
Answers to CME questions based on the Mini-Symposium on Frontiers in Spine Surgery, Page 245
Book Reviews 13
S.An Howard and L.G. Jenis, Editors, Complications of Spine Surgery. Treatment and Prevention, Lippincott Williams & Wilkins (2005) ISBN 0781757916 (195pp., $139.00). Page 246. Crispin Wigfield
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Michael Suk, Beate Hanson, Daniel Norvell and David Helfet, AO Handbook Musculoskeletal Outcomes Measures and Instruments, Thieme Publishing Group (2006) ISBN 3-13-141061-2 (444 pp. £53.46). Page 246. Roger Hackney
15
Imaging of Soft Tissue Tumors, 2nd ed., Mark J. Kransdorf, Mark D. Murphey, Lippincott Williams & Wilkins, 700pp., $199, ISBN:0781747716. Page 247. James Rankine
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Rockwood and Wilkins Fractures in Children (Sixth Edition), J.H. Beaty, J.R. Kaisser (Eds.). Lippincott Williams & Wilkins, Baltimore, MD (2006). (1120pp, £215), ISBN: 078175769X. Page 247. P.A. Templeton
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Practical Fracture Treatment. R. McRae, M. Esser, fourth ed., Churchill Living Stone (2002). 448pp., £35.07, ISBN:0443070385. Page 248. Robert Metcalf
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Advanced Reconstruction of the Hip. Lieberman Jay, Berry Daniel (Eds.) AAOS (2005). 541pp., £128.95, ISBN: 0892033460. Page 248. Martin Stone
Current Orthopaedics (continued 2009 as Orthopaedics and Trauma) Elsevier, ISSN: 0268-0890, http://www.sciencedirect.com/science/journal/02680890 Volume 21, Issue 4, Pages 249-324 (August 2007)
1
Editorial Board, Page i
Mini-Symposium: Fracture Healing 2
(i) Pathways and signalling molecules, Pages 249-257 V.S. Nikolaou, E. Tsiridis
3
(ii) Factors contributing to non-union of fractures, Pages 258-261 Venkatachalapathy Perumal, Craig S. Roberts
4
(iii) The relevance of mesenchymal stem cells in vivo for future orthopaedic strategies aimed at fracture repair, Pages 262-267 D. McGonagle, A. English, E.A. Jones
5
(iv) The use of bone morphogenetic proteins (BMPs) in long-bone non-unions, Pages 268-279 Haralampos Dinopoulos, Peter V. Giannoudis
6
(V) Which scaffold for which application?, Pages 280-287 Ashley Blom
Hand and Wrist 7
Carpal dislocations, Pages 288-297 D.S. Melsom, I.J. Leslie
Syndromes 8
Duchenne muscular dystrophy, Pages 298-300 Benedict J.A. Lankester, Michael R. Whitehouse, Martin F. Gargan
Children 9
Non-accidental injury, Pages 301-309 Louise Hattingh
General 10
Non-compliance in orthopaedic surgery and its ethical challenges, Pages 310-313 H. Sharma, E. Crane, B. Syme, M. Foxworthy
Knee 11
Management of infected TKR, Pages 314-319 S. Naidu Maripuri, U.K. Debnath, H. Mehtha, R. Thomas, C. Wilson
CME Section 12
CME SECTION. Questions based on the CME designated article for this issue—‘‘Management of Infected TKR’’, Pages 320-322
13
Answers to CME questions based on the Mini-Symposium on Osteotomies around the Hip, Page 323
Current Orthopaedics (continued 2009 as Orthopaedics and Trauma) Elsevier, ISSN: 0268-0890, http://www.sciencedirect.com/science/journal/02680890 Volume 21, Issue 5, Pages 325-404 (October 2007)
Editorial Board, Page i Mini-Symposium: Surgical Rheumatology 2
(i) The surgical management of rheumatoid arthritis of the shoulder and elbow, Pages 325-329 Ziali Sivardeen, David Stanley
3
(ii) Hip and knee reconstruction in the rheumatoid patient, Pages 330-339 J.M. Wilkinson, P. Haslam, C.J.M. Getty
4
(iii) The lower limb in the rheumatoid arthritis patient: Focus on the hind, mid and forefoot and the ankle, Pages 340-343 R.G.H.H. Nelissen
5
(iv) The management of the rheumatoid wrist, Pages 344-357 B.R. Simmen, C. Kolling, D.B. Herren
6
(v) Biological therapy in the management of inflammatory arthritis with particular reference to orthopaedic surgery, Pages 358-363 Deborah Hazlewood, John Winfield
Spine 7
Tuberculosis of spine—Contemporary thoughts on current issues and perspective views, Pages 364-379 Myung-Sang Moon
Inherited Disorders 8
The arthropathy of haemochromatosis and the role of the orthopaedic surgeon, Pages 380-385 L.M. Regan, T. Nissanthan, M.B. Davies
Therapeutics 9
Role of glucosamine in osteoarthritis, Pages 386-389 R. Thakral, U.K. Debnath, C. Dent
Quiz 10
Radiology Quiz, Pages 390-395 Nev Davies, Richard Pennington, Catherine McCarthy
Metabolic Disorders 11
Vitamin D-resistant rickets (X-linked hypophosphataemic rickets), Pages 396-399 Andrew McBride, Matthew Edwards, Fergal Monsell, Martin Gargan
CME Section 12
CME questions based on ‘‘Tuberculosis of the spine—Contemporary thoughts on current issues and perspective views’’, Pages 400-402
13
Answers to CME questions based on the article ‘‘Management of wrist instability’’, Page 403
Book Reviews 14
Manoj Ramachandran, Basic Orthopaedic Sciences—The Stanmore Guide , Hodder Arnold, Paris (2006) ISBN 9780340885024 304pp., £34.99. Page 404, David Limb
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Lovell and Winter's Pediatric Orthopaedics, sixth ed. R.T. Morrissey, S.L. Weinstein, Lippincott (2005). 1632pp., $299.00, ISBN:07817535. Page 404, P. Templeton
Current Orthopaedics (continued 2009 as Orthopaedics and Trauma) Elsevier, ISSN: 0268-0890, http://www.sciencedirect.com/science/journal/02680890 Volume 21, Issue 6, Pages 405-480 (December 2007)
1
Editorial Board, Page i
Mini-Symposium: Shoulder Reconstruction 2
(i) Shoulder arthroplasty for osteoarthritis and rheumatoid arthritis, Pages 405-414
3
(ii) Rotator cuff arthropathy, Pages 415-421
4
(iii) Post-traumatic reconstruction for sequelae of fractures of the proximal humerus, Pages 422-431
5
(iv) Shoulder arthrodesis, Pages 432-437
Joaquin Sanchez-Sotelo
Lennard Funk, John Haines, Ian Trail
R. Hertel, E. Fandridis
David Limb
Syndromes 6
Marble bone disease, Pages 438-441 Sabrina Fudge, Rouin Amirfeyz, Donna Dimond, Martin Gargan
Spine 7
Minimally invasive spinal surgery, Pages 442-450 John K. O’Dowd
Knee 8
Postero-lateral rotatory instability, Pages 451-456 P.G. Haslam, D.R. Bickerstaff
Hip 9
Osteonecrosis of the femoral head: Part 1—Aetiology, pathogenesis, investigation, classification, Pages 457-463 Samuel J. Parsons, Niall Steele
Radiology 10
The diagnosis and percutaneous treatment of osteoid osteomas, Pages 464-470 James J. Rankine
Compression Syndromes 11
Conservative treatment of thoracic outlet syndrome (TOS): Creating an evidence-based strategy through critical research appraisal, Pages 471-476 Konstantine C. Balakatounis, Antonios G. Angoules, Kalomoira A. Panagiotopoulou
CME Section 12
CME questions based on the Mini-Symposium on Shoulder Reconstruction, Pages 477-479
13
Answers to CME questions based on the article—‘‘Management of Infected TKR’’, Page 480
Book Reviews 14
Frank J. Frassica, Paul D. Sponseller and John H. Wilckens, The 5-Minute Orthopaedic Consult , Lippincott Williams & Wilkins, Baltimore, MD (2006) ISBN 0781799716 450pp., price: £28.38. Page 481, P.A. Templeton
15
K. Yamaguchi, G. King, M. McKee and S. O’Driscoll, Advanced Reconstruction—Elbow, American Academy of Orthopaedic Surgeons (2007) 500pp., price: 149.96, ISBN: 0892033916. Page 481, D. Limb
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 1–8
Available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/cuor
MINI-SYMPOSIUM: FRONTIERS IN SPINE SURGERY
(i) Optimizing non-operative care Charles Pither Realhealth Institute, 23-31 Beavor Lane, London W6 9AR, UK
KEYWORDS Low back pain; Non operative care; Yellow flags; Cognitive behavioural therapy; Functional restoration programmes
Summary Surgical treatment of back pain has limited success. It is therefore critical that spinal surgeons (who see most back problems in secondary care) are aware of the results of nonoperative treatments. It is now known that most of the predictors of the development of long term distress and disability following an episode of back pain are psychosocial. Factors such as a tendency to low mood, fear avoidance, passivity, and poor sickness absence record, (known as "yellow flags"), all feed into the pain experience and thus should be included in the work up. Detection of multiple factors can inform the surgeon about why the person is in trouble and enable better decision making about the likelihood of a biological intervention being successful. Of the non-operative treatments available, although there is limited evidence for exercise programmes and back schools, many commonly employed approaches such as passive physiotherapy and facet joint injections are of unproved benefit. The treatments with best evidence of effectiveness are intensive interdisciplinary programmes (also known as functional restoration or pain management programmes). These therapies have been shown to be as effective as spinal fusion surgery and should be offered to persons with persistent difficulties before proceeding to fusion surgery. & 2007 Elsevier Ltd. All rights reserved.
Introduction Most surgeons given the opportunity of providing an introductory lecture to medical students on the broader achievements of surgery would mention the importance of patient selection. Perfect technique is of limited value if, for whatever reason, the patient is unlikely to gain from an operation in the first place. Surgeons operate because they think they can help a patient with a problem, but equally, due to the costs and risks inherent, they soon stop operating if effective alternative non-operative treatments become available. Unfortunately, the results of 0268-0890/$ - see front matter & 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2007.01.006
surgery for back pain are not as convincing as those for, say, hip replacement, and certainly least successful when consigned to the ‘last resort’, when all other treatments have failed. Furthermore, surgery for back pain is performed not on the basis of an objective finding (for example the presence of a colonic malignancy), but for a subjective complaint: pain. The indications are thus always relative not absolute. A person who clutches at the straw of a major operation because they cannot tolerate their symptoms may have eschewed surgery if their pain had been somewhat eased and they had better ways of dealing with it.
ARTICLE IN PRESS 2 I would dare suggest that the surgeon has two duties in this arena: to understand the predictors of success or failure in that particular person and to be aware of the outcome and benefits of non-operative treatments. This paper will attempt to address these two issues by examining the factors that affect pain and the development of disability and looking at the evidence supporting nonoperative treatments.
Concepts and constructs Pain and the pain experience In the field of back pain it is ultimately pain that takes a person to their doctor. Whatever complex definition one uses people visit their doctors, and thus become patients, because they feel ill at ease with their body. Their body hurts and this in effect tells them that something is wrong. For both patient and doctor, a detailed description of the pain is important; the goal is a diagnosis that will allow for fears to be allayed and effective therapy instigated. Arguably the most crucial feature of the pain is its site. The principle, with which both parties align, is that the pain must have its origin in disease, inflammation or irritation in the tissues and this is the source of the problem. But a better understanding of the mechanisms of back pain alloyed with the epidemiology of the condition inescapably leads to the conclusion that this approach has limitations. Back pain correlates poorly with scan and X-ray changes, there are no diagnostic ‘gold standards’, symptoms occur in the majority of the population, etc. Such pain is better thought of as a functional disturbance rather than an anatomical lesion. But even more crucial is the implication that people visit doctors because they hurt not because they have a set level of pathology. Thus, even in straightforward cases pain perception (not just tissue damage) contributes a substantial percentage of the sum of the unpleasant experience. This can be explained pathophysiologically at a number of levels: 1. Spinal cord neurotransmission: this is modified over time with the sensitisation and activation of transmitter systems not contributory in the acute situation. 2. Central pain processing in the limbic system. The unpleasantness of pain is influenced by activity in the cingulate region aside from the sensory processing of noxious information. 3. Higher level influences of mood, fear, etc. Negative thinking and depressed affect inform suffering, which in turn influence motivation, self-worth, etc. Thus back pain is always a pain problem not simply a problem of local tissue pathology.
‘Pain without lesion’ Because it is impossible to prove there is not a lesion it is also impossible to state that a person’s back pain has no local cause. (And, indeed, on the basis that a prime role of a physician is to believe his patient, it is also inappropriate.)
C. Pither However, there are times when it seems that the pathology and physician measured limitation of function (impairment) are so minimal, that it is logical and sensible to focus more on the pain than on any putative pathology. This is still very difficult for most biomedically trained clinicians, who are often only prepared to accept pain without lesion with the appellate ‘mad’ attached to the complainant. However, it must be remembered that those processes that can lead to pain and distress being predominantly centrally generated can occur in persons deemed ‘sane’ even in an insightful orthopaedic psychiatric analysis. Herein lies the rub: such individuals, because they are often intelligent, well educated and psychologically competent, are frequently overinvestigated and treated, with detrimental consequences.
Yellow flags and the development of disability The most singular advance in back pain management over the last decade has been the realisation that psychosocial factors (‘Yellow Flags’) predicate distress and disability.1 As this area has been explored in more detail it has become clear that, in addition to various social influences such as employment record, financial disincentives, etc., there are certain psychological epiphenomena that have consistently been shown to be relevant in predicating an unfavourable outcome. Catastrophising Catastrophising can be thought of as a tendency to fear the worst or focus on potential threat or hazard. Sullivan describes it in three domains: rumination, helplessness and magnification.2 The back pain sufferer who is also a catastrophiser will find that their pain is awful, intense and that they can seemingly do nothing to modify it. This has various negative effects tending to provoke rest and avoidance while priming fear mechanisms and autonomic arousal. An understanding of a propensity to catastrophise can help the surgeon understand how psychological processes feed into behaviour which can foster disability. Depression Persistent pain can cause depression because it is unpleasant to have pain and sufferers’ lives become impoverished in many key ways. However, there is also a link in the other direction; depression has been shown to be a predictor of the development of chronic pain in a number of studies. Thus, persons often become ensnared by a vicious circle of pain, sleeplessness, low mood, inactivity etc, leading to a pattern of helplessness and poor quality of life that is not easily classifiable within a unitary diagnostic construct. It is surprising how common it is to find that the person really in trouble with back pain has a prior past history of depressed symptoms especially in stressful situations. Passivity Persons experiencing musculoskeletal pain have been divided into confronters and avoiders. The former confront their pain by maintaining activity levels and keeping a positive mental attitude. The latter take a passive approach, resting and looking to others to provide treatment and effect a cure.
ARTICLE IN PRESS Optimizing non-operative care Passivity can also be demonstrated in terms of an individual’s belief about whence restitution will be delivered. This ultimately reflects taking responsibility for the illness; is the problem really the doctor’s to solve and sort out or does the patient have a role? Passivity has been shown to be a predictor of poor outcome in various studies of back pain. Anxiety A person attends their doctor not because a biological parameter reaches a certain value but because they experience a symptom. The frequency of primary care attendance can be explained to some extent by health anxiety. A mild cough that one person will tolerate, and whose insignificance they will be able to convince themselves of, will take another to their doctor requesting reassurance and antibiotics. Fear is a crucial component of pain and anxiety can be thought of as a prelude to fear. Persistent pain can provoke fear for a number of reasons, the commonest being fear of the pain itself, fear that an activity will provoke pain, fear as to the cause of the pain and fear as to what the future may hold. Very frequently high levels of trait anxiety underpin the behaviours seen in those persons distressed by persistent pain. Fear avoidance Fear of pain and its consequences leads to avoidance of activity. If the pain settles quickly this need not have longterm consequences as the normal pattern of function can be re-established after a short period of activity. However, the situation changes substantially when pain persists. Not only does the inactivity provoked by the avoidance behaviour have a consequence in terms of secondary deconditioning effects, but patterns of behaviour (and some would say pain experience) can become learned. Probably after 3 months, and certainly after six, the notion of ‘normal’ needs to be revisited: is the old pattern of activity and fitness ‘normal’ or has the new level become the ‘default’? The chronic back sufferer who spends all day resting and eschews any stretching or exercise may have as many consequences of these areas of under-function as from any spinal pathology. Other somatic symptoms In the person characterised by the above constructs (the anxious, passive catastophiser with avoidant behaviours) it is common to find other medical problems not explained by identifiable pathology. There is frequently a history of concomitant problems such as irritable bowel syndrome, headache, fatigue, dysmenorrhoea and other musculoskeletal complaints. Identification of these symptomatic conditions in a detailed medical history is an important part of the work-up as their presence suggests a more generalised sensitivity to pain. This suggests that unless surgery is able to completely remove the source of pain, (which in back pain surgery is not common), symptoms will probably persist at a troublesome level. Yellow Flags Assessment Many of these parameters are embraced by the so-called ‘Yellow Flags’ concept, psychosocial factors predicting pain
3 distress and disability. It is crucial that some form of assessment of these factors is made prior to contemplating any major interventional approach. This can be done informally by an appropriately minded clinician or formally by questionnaires such as the DRAM3 or the OREBRO,4 which provide a pointer to the clinician that distress and somatic focus are prominent. The latter instrument is increasingly being shown to be a useful predictor of the development of chronic incapacity.5
Surgical selection Indications for surgery for back pain are always relative and as such are influenced by a variety of factors both from within and without the medical system. In the USA spinal fusion rates have increased from 0.3 per 1000 enrolees in 1992 to 1.1 per 1000 in 20036 without clear scientific rationale. Surgeons are not only influenced by genuine scientific advances but also by the milieu in which they practice. However, there are major deficits in the scientific evaluation of spinal fusion surgery as highlighted in recent Cochrane reviews.7 The potential for harm from inappropriate surgery has been likened to a loaded gun; in the wrong hands and without suitable constraints, the outcome can be catastrophic. Of course it is not only the surgeon who is influenced by the populist view. Patients expect resolution of their symptoms by means of sophisticated medical technology, especially for something as apparently ‘low tech’ as back pain. As Illich pointed out nearly 30 years ago,8 culture influences society’s tolerance of pain by controlling its necessity. Only pain that is perceived to be unnecessary is intolerable. The surgeon faced with a distressed patient saying they find their symptoms intolerable, on the face of it provides the perfect rationale for heroic intervention. However, such a justification should always be modified by odds of a positive outcome. Medicine that looks only at need and not at outcome smacks of Charlatanism.
Non-operative treatments Two recent systematic reviews have provided helpful synopses of the place of a range of non-surgical treatment options for back pain,.9,10 The commoner modalities will be discussed in more detail.
Physiotherapy and exercise Physiotherapy is probably the first line treatment for back pain that requires anything other than simple analgesics, with about 15% of sufferers receiving a referral following a consultation in primary care10 in the UK. This equates to a million people treated in the NHS per annum. It is clear that the type and quality of treatment provided varies substantially. Gratifyingly there seems to be a move away from passive modalities such as ultrasound and interferential to more active approaches such as core stabilisation exercises (including Pilates) and group-based classes. The crucial issue remains whether physiotherapy treatments are effective for low back pain and what is the best therapy? Without doubt this is a difficult area to investigate, in part because an
ARTICLE IN PRESS 4 aspect of care increasingly being addressed by physiotherapists is education and elements of cognitive behavioural therapy (CBT), which may be having an equal—or even greater effect than the physical component of the treatment provided. A further issue is the duration of the symptoms, with differing outcomes between acute and chronic conditions. This review will focus on studies in chronic populations as this is of most relevance to the title. In a systematic evidence-based review of the available data The European Working party found they could not recommend TENS, heat/cold, traction, laser, ultrasound, short wave, interferential, massage or corsets for the treatment of chronic low back pain.10 They concluded that CBT, exercise therapy, brief educational interventions, and multidisciplinary (bio-psycho-social) treatment should be recommended. They also concluded that back schools and short courses of manipulation could be considered. Given that many medical specialists involved in the treatment of back pain recommend exercise, as do many competent spinal physiotherapists, it is surprising that the evidence for the efficacy of exercise therapy is not compelling. There have been a number of reviews including those of Van Tulder11 who found, in an analysis of 39 studies, that exercise was better than routine GP care but not superior to physiotherapy. They concluded that exercise was helpful as a means of resuming normal activity. It also appears that the exercise does not need to be specific, no particular regimen having been shown to be superior over another.
Back schools The original Back School had its origins in Sweden in the 1980s. These short programmes (typically about 2 h of advice and information delivered over 2 or 3 visits) were effective in changing knowledge but did not gain much support as means of improving patients’ function or reducing pain. However, a recent Cochrane review12 found that they could be of greater efficacy than many other simple therapies especially when delivered in the occupational setting. The concepts of the Back School have been combined with an exercise programme delivered over an 8-week period in the form of a Brief Education Intervention. Although, as yet not formally assessed, this model may have much to recommend it as an early treatment for pain that persists.
Injections and nerve blocks Injections and nerve blocks (such as epidurals and facet joint injections) continue to have a role in the clinical management of patients with persistent back pain in most Western medical cultures in spite of minimal evidence of effectiveness. The notion of an injection having the potential to ‘cure’ low back pain is dependent on a biological model where the source of pain is structural rather than functional, a general view that is losing favour. The use of these techniques is no doubt influenced by the low propensity for harm which easily leads to a ‘well, no harm in giving it a try’ approach. Whilst the risk of adverse complications may be low, this is not the same as implying
C. Pither that the pursuit of such cure-seeking treatment is without harm, the damage stemming from the promotion of the view that passive treatments are the answer to a problem that requires active participation from the sufferer. As with many areas of practice within the field of musculoskeletal medicine, the data available are not only sparse but of poor quality. The place of epidurals in back and leg pain has been subject to a number of critical reviews, the findings generally being that there is no evidence of substantial benefit for chronic back pain. The data for facet joint injections are confounded by outcomes from both neck and back being examined collectively. In particular, the positive outcome in certain selected subjects with post-whiplash pain skews the results. That some pain may emanate from the facet joints is not in doubt (and indeed pain relief following injection therapy is more likely if the joint appears hot on an SPECT bone scan13) but a specific clinical syndrome pointing to the facet as a sole source of pain and enabling prediction of success following injection remains elusive. The overall conclusion is that there is minimal evidence for benefit from facet joint injections. An alternative approach is to use very precise injections to block the medial branch of the dorsal ramus supplying the joints, which can then be permanently ablated using a radiofrequency thermoprobe. This is discussed in the next section. It would be inappropriate for this author to suggest that the implication of the above comments is that there is no place for such techniques, rather that they should be seen as part of a management algorithm with the rationale and likely limitations explained to the patient beforehand, with a clearly delineated route for onward treatment if they are not successful.
Permanent neuroablative techniques The idea of denervating a painful structure in the spine is obviously appealing. This can be achieved by using the thermal energy generated by applying a radiofrequency current through an insulated needle. If the tip of the needle is in close contact with a nerve or nerve root, a neural injury will develop. This technique has been used to ablate the medial branches that supply the facet joint. A similar technique has been used in the disc itself, with a curved electrode inserted percutaneously into the disc (IDET). This latter technique has been evaluated in a number of studies with conflicting outcomes. A further modification involves the use of ‘pulsed’ bursts of current. This reduces the temperature of the needle and thus the extent of the lesion. This may have advantages in terms of reducing the risk of unwanted nerve damage, which does occur with these techniques. The mechanisms of pain relief, given the reduced extent of the neural insult, are unclear. Although there is a substantial industry based around these technologies, there are minimal data to support positive outcomes, and a small risk of painful adverse consequences. A Cochrane review concluded: ‘There is conflicting evidence that radiofrequency denervation is effective for lumbar zygapophysial joint pain. There is
ARTICLE IN PRESS Optimizing non-operative care limited evidence suggesting that intradiscal radiofrequency may not be effective in relieving discogenic low back pain’.14 Although, once again, there is a paucity of high quality data, the inevitable conclusion is that these techniques are not ‘the answer’ to chronic back pain. The tide of disability and pain from chronic back pain will not be reversed by greater provision of facet joint rhizotomy or intradiscal electrotherapy.
Rehabilitation The term rehabilitation can be interpreted in many ways. Implicit in most definitions is the notion of optimisation of function and a return to normal life, given the presence of some ongoing symptoms or impairment, rather than curative treatment.
The development of back-pain rehabilitation In the UK the post-traumatic rehabilitation of injured servicemen commenced with Sir Robert Jones in the First War. The need to rehabilitate the injured to return to functional capacity during the Second War saw stunning successes with only 5% of 20,000 injured servicemen who received intensive rehabilitation between 1941 and 1945 being invalided out of the service and 77% returning to full duty.15 In peace time the imperatives for return to function diminished and lack of funding inevitably reduced provision. There is little record of rehabilitation specific to back pain, albeit that various single units pioneered disparate approaches. In the UK the ‘School for Bravery’ approach was spawned from an injured miners’ rehabilitation clinic. It adopted a vigorous physical reactivation along the lines of no pain, no gain. In the USA the PRIDE programme in Dallas adopted a similar approach without significant concession to psychological contributions either to the conceptual framework or treatment programme. In the 1970s, Wilbert Fordyce, a behavioural psychologist, pursued a vigorous ‘operant conditioning’ paradigm in chronic pain patients arguing that much of the pain was learned. His approach was softened by the introduction of cognitive psychology developing into the cognitive behavioural approach now utilised by many such rehabilitation programmes.
Cognitive behavioural therapy (CBT) CBT has emerged as the most effective and rational psychological therapy for many common mental health problems and physical illness where stress or psychological factors play a part. The cornerstone of CBT is an appreciation of the importance of beliefs, thoughts and fears in their influence over mood and behaviour. The cognitive model posits that people are largely rational in their behaviours but may make unhelpful choices if their information is erroneous. For example, the person who believes that their simple back pain is due to a damaged disc that has ‘worn out’ leaving the bones ‘rubbing together’, will attribute further pain to an extension of that process, implying more
5 physical damage and ultimately a life in a wheelchair. A physical reactivation programme may be the therapy of choice but it is unlikely that the person will make substantial gains without the provision of information aimed at changing the mindset. Whereas in an education model the person is simply given material to read or hear, a CBT model engages with the subject in a more interactive way not only to ascertain their beliefs and fears, but then to develop ways to challenge them and actively explore alternate ways of doing things during the treatment programme. When applied to back rehabilitation the CBT approach attempts to engage the subject in a partnership, with the therapist providing information but also using Socratic dialogue to encourage them to generate ideas. This has the effect of clarifying what the sufferer really believes and enabling the subject to take control by generating challenging statements from within rather than without. Changes to activity schedules are planned and then enacted within the hours of the programme, records are kept and achievements reinforced.
Rehabilitation programmes These are fixed-length group-based programmes. In the UK they are broadly of two types: Pain Management Programmes, generally run by an interdisciplinary team under the auspices of a pain service and Functional Restoration Programmes offering a more intensive physical treatment run by physiotherapists with some psychological input. The feed into the latter is largely from orthopaedic services. The scientific literature often fails to use these terms, using instead the generic term ‘interdisciplinary’ and focussing more on treatment length or intensity. It is important that nomenclature does not confuse the essential components of these programmes. The delivery of hospital care from multiple, separate specialisms has often led to the parallel development of services with little dialogue between their protagonists, albeit that they treat a common group of patients. It is normal to find different departments, or therapists, delivering similar treatment to similar patients but using a slightly different model and different terminology. Disparate specialists see their patients through the gaze of their training, but the large volume of research on chronic back pain indicates that the difficulties experienced by this population are continuous, with considerable overlap between those persons being seen in pain, rheumatology and orthopaedic clinics. It is always important to attempt to match the needs of the patient with the most appropriate programme. The core differences in aims and means and patient characteristics between the two programmes are set out below. Functional restoration programme (FRP) Typically, a functional restoration programme is delivered over a 2–3-week period in an intensive course. The focus of the programme is physical reactivation by an active exercise programme, with education and information provided throughout. Hydrotherapy or time in water is frequently added in. Programmes make a variable concession to include psychological therapy. Many claim they utilise cognitive
ARTICLE IN PRESS 6
C. Pither
behavioural principles, others will have one or two sessions on issues such as stress management, assertiveness training or communication. The aim of the programme is to generate improvements in the understanding of pain, physical function and activity level, fitness and pain. Various centres offering FRPs include additional aspects, which vary with the patient group and the resources available. In particular, vocational aspects are often addressed with an emphasis on ergonomics.
Staff contribution
Aim
Message Pain management programme In the UK, pain management programmes have either been delivered as intensive 3–4-week residential protocols, or as daily outpatient courses offering treatment one day per week for perhaps 8 weeks. The commonalities relate to the prominence of the psychological component within the programme and the interdisciplinary team. This usually comprises psychologist, physiotherapist, nurse and doctor. Whilst exercise and reactivation are still important parts of the package, the level of disability of the patients often limits the vigour with which this can delivered. Equally the higher level of psychological distress mandates a greater emphasis on psychological therapy. The stance is that pain will persist at some level but can be coped with and managed. The differing emphasis of these types of programmes are set out below. Area
PMP
FRP
Work
Probably not working, maybe part-time or sedentary Often more than 2 years Often less than optimal
Likely to be employed, return to full-time work expectation Significant pain less than 2 years ‘normal’ – good social support in place Some limitation of more vigorous activities Not significantly depressed or anxious as assessed at interview and measured by depression inventory Minor limitation in self- reported function and as measured by Oswestryo30, Roland Morriso12
Duration of pain Social situation Leisure pursuits Psychological function
General function
Medications
Aids
Major limitation of pleasurable hobbies and pastimes High levels of distress as assessed at interview and measured by depression inventory Substantial limitation in selfreported function and as measured by Oswestry score 440 or Roland Morris412 Substantial use of medications common Collar, corset, stick, crutches etc common
Modest medication use only Use of aids unusual
Pattern Site of pain
Most sessions ‘taught’, moving towards more selfdirected time Acceptance of some ongoing pain and limitations seen as important part of treatment package ‘You have to learn to manage your own pain and symptoms’ Under-activity and rest common Anywhere
Self-directed time from outset.
Return to normal life is goal, some relief expected
‘You can live a normal life’ Over-activity common Spine
Outcome Outcome research in this area suffers from numerous problems, not least the difficulty of terminology mentioned above. Other issues are the inevitably unique format of programmes (staffing, emphasis, setting) as well as variations in duration and intensity. There are also issues relating to the paradigm predicating the type of journal and thus readership. For example, outcome from pain management programmes, usually run by psychologists, and seen to be delivered from a CBT rubric, will be submitted to a psychological journal, with readership from a similar discipline, whilst an orthopaedic FRP will opt for a surgical journal. Further issues relate to the outcome measures used in the protocol and what constitutes success.
Interdisciplinary programmes This descriptor was that chosen for the Cochrane review16 and encompasses various types of programmes but only those specifically for back pain, thus not including any of the broader chronic pain literature. The view examined ten studies encompassing nearly 2000 patients and concluded that that there was strong evidence that intensive multidisciplinary bio-psycho-social rehabilitation with a functional restoration approach improved function when compared with inpatient and outpatient non-multidisciplinary treatments. There was moderate evidence that the treatment could produce improvements in pain, with equivocal data on return to work. In particular, the authors noted that treatments of shorter duration (o100 h) were less effective and thus could not be recommended. This latter finding has been criticised, however, as the treatment details of the analysed studies often did not include specifics of the treatment timetable other than a total number of hours. However, these conclusions are important as this form of treatment remains the only modality for which there is good evidence for a positive outcome in chronic low back pain. Various studies have compared FRP with surgery. The study by Fairbank17 in a UK setting could find no difference in outcome between surgical stabilisation and an FRP delivered along CBT principles. A similar finding was reported by Brox18 from Denmark. Given the considerable difficulties of planning
ARTICLE IN PRESS Optimizing non-operative care
Table 1
7
Questions to ask to ascertain general levels of pain management skills in a person considering surgery.
Do they have a clear understanding of the cause of their pain? Do they understand the poor correlation between pain and damage? Are they taking excessive medications or seem unduly dependent on them? (unlikely to change with surgery) Can they distract themselves or use relaxation? Are they resting excessively (lying down in the day)? Are they avoidant of activity? Are they dependent on sticks, crutches or aids? Are they as flexible, fit and strong as they can be? Are they prone to negative thinking and depression? Do they have goals other than pain relief? Do they pace and plan their activities?
If the person is not managing their pain effectively before surgery, this will not change unless the pain is totally relieved.
and executing the large-scale surgical studies necessary to clarify the issue more conclusively the current state of knowledge suggests that there is little convincing evidence to suggest that spinal fusion is better than an intensive FRP. The implications of this are clear. Outcome of more psychologically based PMPs has been analysed in a number of reviews which have consistently found benefits for the treatment group. For example, McCracken and Turk19 found that behavioural and cognitive behavioural treatment reduced pain, distress and pain behaviour while improving daily functioning. There is now a consensus that this type of treatment can generate worthwhile improvements in quality of life for persons with persistent pain. The discussion has now moved on to the optimal format of the therapy and how to tailor it more to the individuals needs.
2.
3.
4.
5.
6.
Conclusion
7.
Persistent mechanical back pain has no guaranteed cure and thus the sufferer is at the mercy of their own desperation and the inventiveness of heroic clinicians who will go to any length to try to attempt to eliminate a source of pain. A better understanding of the factors that predicate ongoing pain and distress alloyed with high-quality systematic reviews of the effectiveness of common treatments, has allowed a much more rational approach to the management of such patients. Whilst the evidence for many of the simple treatment modalities (such as physiotherapy, TENS, manipulation) is not sufficiently convincing enough to generate consistent recommendations, this is not true for intensive interdisciplinary treatment programmes which have the best evidence base for any treatment for chronic pain. The result is that it is becoming less and less acceptable that back pain sufferers should be subject to spinal surgery without having undertaken an intensive FRP-type programme (Table 1).
8. 9.
10. 11.
12.
13.
14.
References 15. 1. Kendall NAS, Linton SJ, Main CJ. Guide to assessing psychosocial yellow flags in acute low back pain: predictors of disability and work loss. Accident Rehabilitation and Compensation Insurance
16.
O New Zealand and the National Health Committee. Wellington, New Zealand, 1997. Sullivan MJ, Thorn B, Haythornwhite JA, Keefe F, Martin M. Theoretical perspectives on the relation between catastrophising and pain. Clin J Pain 2001 [Review]. Main CJ, Wood PL, Hollis S, Spanswick CJ, Waddell G. The distress and risk assessment method. A simple patient classification to identify distress and evaluate the risk of poor outcome. Spine 1992;17(1):42–52. Linton SJ, Hallden K. Can we screen for problematic back pain? A screening questionnaire for predicting outcome in acute and subacute back pain. Clin J Pain 1998;14(3):209–15. Linton S Boersma K. Early identification of patients at risk of developing a persistent back problem: the predictive validity of ¨ rebro Musculoskeletal Pain Questionnaire. Clin J Pain The O 2003;19:80–6. Weinstein J, Lurie JD, Olson PR, Bronner KK, Fisher ES. United States’ trends and regional variations in lumbar spine surgery: 1992–2003. SPINE 2006;31:2707–14. Gibson JN, Waddell G. Surgery for degenerative lumbar spondylosis. Cochrane Database Syst Rev 2005;(2): CD001352. Illich I. Limits to medicine: medical nemesis: the expropriation of health. Harmondsworth, NY: Penguin; 1977. Van Tulder M, Koes B, Malmivaara A. Outcome of non invasive treatment modalities on back pain: an evidence based review. Eur Spine J 2006;15:S64–81. European Guidelines cited in Waddell G. The back pain revolution. Edinburgh: Churchill Livingstone; 2004. Van Tulder MW, Malmivaara AE, Koes B. Exercise therapy for low Back pain: a systematic review within the framework of the Cochrane Collaboration Back Review Group. Spine 2000;25(21): 2784–96. Heymans MW, Van Tulder MW, Esmail R, Bombardier C, Koes BW. Back schools for non-specific low back pain. A systematic review within the framework of the Cochrane Collaboration Back Review Group. Spine 2005;30:2153–63. Dolan, et al. The value of SPECT scans in identifying back pain likely to benefit from facet joint injection. Br J Rheumatol 1996;35:1269–73. Niemisto L, Kalso E, Malmivaara A, Seitsalo S, Hurri H. Radiofrequency denervation for neck and back pain: a systematic review within the framework of the Cochrane Collaboration Back Review Group. Spine 2003;28(16): 1877–88. Grahame R. The decline of rehabilitation services and its impact on disability benefits. J R Soc Med 2002;95:114–7. Guzman J, Esmail R, Karjalainen K, Malmivaara A, Irvin E, Bombardier C. Multidisciplinary bio-psycho-social rehabilitation
ARTICLE IN PRESS 8 for chronic low-back pain (Cochrane review). Chichester: Wiley; 2004. 17. Fairbank J, Frost H, Wilson-Macdonald J, Yu L, Barker K, Collins R, for the Spine Stabilisation Trial Group. Randomised control trial to compare surgical stabilisation of the lumbar spine with an intensive rehabilitation programme for patients with chronic low back pain. Br Med J 2005;330:1233–9.
C. Pither 18. Brox J, et al. Randomized clinical trial of lumbar instrumented fusion and cognitive intervention and exercises in patients with chronic low back pain and disc degeneration. Spine 2003;28: 1913–21. 19. McCracken LM, Turk DC. Behavioural and cognitive-behavioural treatment for chronic pain: outcomes, predictors of outcome and treatment process. Spine 2002;27:2564–73.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 9–16
Available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/cuor
MINI-SYMPOSIUM: FRONTIERS IN SPINE SURGERY
(ii) The role of surgery in low back pain Eugene J. Carragee Department of Orthopaedic Surgery, Spinal Surgery Section, Stanford University School of Medicine, Stanford, CA 94305, USA
KEYWORDS Back pain; Lumbar disc degeneration; Discography; Spinal fusion; Artificial disc replacement; Magnetic resonance imaging
Summary Spinal fusion for low back pain (LBP) in the absence of serious underlying disease is controversial. The cause of serious LBP illness is not well understood, there is poor correlation of the presence and degree of degenerative changes with symptoms and nonstructural factors such as central pain intolerance, psychological distress, social and economic issues of compensation and participation, appear to act as co-morbidities to LBP illness. Fusion surgery appears to offer only limited relative benefits over cognitive behavioural therapy and intensive rehabilitation in RCTs of surgical vs. non-operative care. At best, possibly 50% of fusion patients in this setting have high-quality outcomes. Artificial disc replacement has approximately the same outcomes as fusion in short-term studies but the long-term risks of prosthesis placement in relatively young patients is a concern. Future surgical advances may be limited by a lack of clear diagnostic certainty and the high prevalence of serious co-morbidities that impair recovery. & 2007 Elsevier Ltd. All rights reserved.
Introduction Low back pain is common. Most episodes of LBP resolve without medical intervention; acute back pain will usually resolve in short order, but recurrent episodes are very common and persistent low-grade symptoms can be found years after the first episodes. The point prevalence and oneyear prevalence of LBP may be as high as 33%,1 and 73%,2 respectively. In physically active adults such as manual labourers or soldiers undergoing physical training, the experience of LBP may be still higher or nearly universal.3 However, most people with persistent LBP do not report serious or persistent disability. While more than 70% of adults in a large population study reported back pain, only Tel.: +1 650 723 7797; fax: +1 650 723 9805.
E-mail address:
[email protected]. 0268-0890/$ - see front matter & 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2006.01.005
10% had more than minimal functional problems.4 Even in persons with co-morbidities for development of disability, only less than 10% experienced any work loss greater than one week over a five years prospective observation.5 Surgical strategies for low back pain must be considered in the context of the presumed cause and course of the LBP syndrome being treated. The more specific and definitive the pathology, the easier the decision-making and the more predictable the outcome. For example, a patient with persistent LBP may have a relatively straightforward medical history and clear imaging pathology or, at the other extreme, no clear pathologic findings and a complex, chaotic emotional and social situation precluding reliable assessment. In this context, for the surgeon evaluating a patient with back pain the issue is not why someone might have backache, because backache of varying intensities is so common. Rather the real question is why common backache
ARTICLE IN PRESS 10
E.J. Carragee lumbar findings commonly assumed to be associated with a ‘‘disc injury’’ is small, generally less than 20% (Fig. 2).
is such a serious problem for this particular person. The answer may be simple when investigation demonstrates a destructive process such as myeloma, discitis or clear deformity and instability. However, more commonly the cause of the apparently severe LBP illness is obscure.
Special testing Because physical examination and even detailed imaging techniques have not found spinal pathology specific to those patients with serious LBP illness, attempts have been made to identify a hypothetical primary-symptomatic structure (‘‘pain generator’’) using provocative injections and anaesthetic blockade. The validity of these tests is not known as there is no histopathologic ‘gold standard’ against which a positive result could be tested. The issues of regional or central hyperalgesia, placebo or idiosyncratic responses are clearly important but not well quantified. Thus the results of these special diagnostic tests should be carefully considered in their clinical context. This is particularly true of provocative discography which is used to direct most types of invasive treatments (percutaneous disc interventions, fusion and disc arthroplasty). This tests the response of a patient when dye is injected into an intervertebral disc. If an injected, disrupted disc is painful and the pain is similar or exactly like a patient’s usual LBP, proponents have suggested that this result has definitively identified the cause of a patient’s pain. However, it has been shown that disc injection can simulate a quality and location of pain known not to originate from that disc (e.g. pelvic pain, bone tumour).17,18 Furthermore, disc injections are frequently painful (30–80%) in certain asymptomatic subjects, especially in the presence of psychological distress, previous disc surgery, remote chronic pain processes, or disputed compensation19,20 (Fig. 3). As most patients with chronic LBP illness have one or more of these co-morbidities, the risk of false positive results may be high in those individuals. Even in subjects without co-morbidities a positive ‘‘bestcase’’ discography injection (low pressure, annular disruption, negative adjacent discs, and normal psychosocial dimensions) results may still not accurately demonstrate which subject will have a high quality outcome from removing the supposed ‘‘pain generator’’. A study was performed to evaluate diagnostic validity of discography in this best-case situation. Despite these ‘‘ideal’’ subjects achieving a solid fusion after anterior discectomy, less that half of these subjects had high-grade relief of symptoms.
Persistent LBP and lumbar spine degeneration While serious structural diseases of the spine may require complex and invasive treatment strategies, the overwhelming majority of persons with LBP will have non-specific findings rather than serious pathology on imaging studies. In clinical studies of patients with established LBP syndromes structural findings of disc degeneration,6 annular disruption6–8 and endplate changes9,10 are often seen. However, it is impossible to draw conclusions regarding the relationship of these findings to the complaint. In cross-sectional studies of subjects asymptomatic for serious LBP problems, MRI findings of disc degeneration, annular fissures and facet arthrosis have been commonly reported8,11,12 (Fig. 1). From a population point of view, someone with even advanced structural changes, such as disc degeneration or an annular fissure, is much more likely to be doing just fine than having serious LBP illness. Prospective studies of MRI in subjects without serious LBP problems at baseline found that the subsequent development of LBP problems correlated poorly or not at all with baseline MRI findings.5,13–15 Rather future LBP troubles were most strongly predicted by psychological factors, social or occupational factors, or other chronic pain processes. Furthermore, in studies in which MR images are taken at baseline and repeated after 3 or more years, the new MRI findings developing over time were not well correlated with the development of new symptom-type or severity.13,14 In a different study design, subjects with known baseline degenerative changes during a stable and prolonged asymptomatic period, have been re-imaged soon after serious LBP episodes.16 This study design shows that new significant findings were very uncommon (o5%), suggesting that even serious LBP episodes are not due to any gross structural change in vast majority of cases. In fact, when a patient develops a serious disabling LBP episode, the likelihood of finding a de novo development of any of the
Disc Protrusion
High Intensity Zone
Anular Fissures
Disc Degeneration 0%
Figure 1
20%
40%
60%
80%
100%
Prevalence of common changes on lumbar MR in adult subjects without serious LBP illness.
ARTICLE IN PRESS The role of surgery in low back pain
11
New Endplate Signal Changes New Disc Herniation New Disc Degeneration New Anular Fissure 0%
Figure 2
20%
40%
60%
80%
100%
The likelihood of finding specific new changes on MRI after development of serious LBP episode.
80% 70% 60% 50% 40% 30% 20% 10% 0% Healthy young Chronic Non- Compensation men lumbar Pain Claims
Abnormal Psychological Profiles
Multiple Risk Factors
Figure 3 Studies of lumbar provocative discography in subjects without LBP: risk of false-positive testing in different study populations.
The positive predictive value of a single level positive injection in this best-case group appeared to be 50–60% for resolution of LBP illness after removal of suspected pain generator.21 Similarly, facet injections or sacroiliac injections have been advocated to help diagnose specific local causes of serious LBP illness. These tests rely on a subjective assessment of pain relief following the attempted anaesthetic blockade of the suspected painful anatomy. It is interesting that the results of these injections do not appear to correlate with the presence or extent of pathologic changes seen in the facet or sacroiliac joint. To date, these tests have not been validated by the recommended methods for the assessment of diagnostic tests.22–25 Alternatively, without specific test validation (confirming the presence of a specific disease per se), a test may be useful by improving outcomes through patient selection for specific treatment, that is a test may have utility in the absence of confirmed diagnostic validity. There is some suggestion that careful placebo controlled blocks may improve the outcome of neuroablative techniques to the lumbar facet.26 So far,
however, facet and SI joint blocks have not been shown to improve the outcomes of spinal fusion surgery. There is interest in the use of these blocks in patients being considered for disc replacement surgery to exclude serious pain from the facet joints, which may confound the results of disc replacement alone. This theoretical use has yet to be confirmed.
Predictors of poor outcomes While finding a specific structural process that predicts chronic LBP illness has proven elusive, psychosocial factors have been found to strongly predict future disability and health care utilization for LBP in asymptomatic subjects. Patients with high fear-avoidance of pain, psychological distress, compensation claims, personal injury litigation, and job dissatisfaction at initial evaluation for LBP have poorer outcomes and tend more commonly to develop chronic LBP illness than those without these risk factors.5,13,27–29 This effect seems accentuated in persons with
ARTICLE IN PRESS 12 LBP with only degenerative changes found on evaluation, in whom psychological distress and compensation claims are much more common than in patients with definite pathologic or destructive processes.30,31 Specific precipitating activities, unless involving compensation claims, do not appear to be helpful in distinguishing outcomes. When subjects reported LBP episodes arising spontaneously or associated with common activities of daily living, these appeared to have the same risk of evolving into more serious LBP illness as when the LBP episodes followed minor trauma, such as minor falls, lifting injuries, or motorvehicle accidents. Furthermore, if the person had the perception that the minor trauma event was their own fault, or no one’s fault, the recovery potential was actually better. Conversely, subjects perceiving they have been injured through another’s fault, especially if pursing compensation, did much worse.32
Surgical strategies for common degenerative conditions The clinical problem of persistent disabling LBP illness with only non-specific structural findings has proven minimally impacted by most interventions. Non-surgical interventions have been occasionally shown to be more effective than placebo or ‘‘usual care’’ but these effects are most commonly small and often of doubtful clinical relevance.33 While such non-surgical methods are usually of relatively low risk and morbidity, there are some notable exceptions such as the long term non-steroidal anti-inflammatory drugs, chronic poorly monitored and escalating narcotic administration, or repeated corticosteroid administration. Surgical treatment for back pain is still controversial and by its nature is associated with both real risks and sizable costs. Furthermore, there is little consensus in practice on how to apply surgical technology to this problem and enormous geographical variation in practice patterns across the world.34 In general, there are two divergent clinical approaches to the issue of chronic LBP illness in the absence of serious structural disease. The first has focused on the identification and treatment of an occult, local ‘‘pain generator’’. This assumes there is a specific patho-anatomic finding in the spine that accounts for the persisting and disabling symptoms independent of psychological, social or neurophysiological co-morbidities, and this can reasonably be expected to be identified and effectively treated. The opposing view has held that this search for a specific ‘‘pain generator’’ is misplaced. This group has pointed to epidemiologic trends and the poor success in treatments directed at the spine per se. As the local pathology seen on imaging studies is similar in persons doing well with minimal or occasional low back pain as in those with claiming severe pain and disability, the difference in clinical manifestation, by this rationale, is due to other factors, e.g. central pain processes, psychological factors, social disincentives, poor coping strategies, etc. Treatment and prevention according to this approach would be directed at restoring function and supporting adaptive techniques as opposed to medical or surgical treatment of the common spinal changes. In general, before considering specific surgical treatment for LBP and only common degenerative findings, the patient
E.J. Carragee and surgeon should have a relatively high confidence that the intervention is directed at a specific local pathology and has a good chance of real clinical improvement.
Minimally clinical important differences in spinal surgery outcomes The concept of a defined minimally clinically important difference (MCID) in spinal disorders has evolved over the last decade. For surgical techniques, involving much greater patient risks, costs and morbidity, the frequently cited MCID developed for pharmacologic testing (a 1–2 point improvement in the pain scale (0–10) or an improvement of 10–15 on the Oswestry scale), is likely too small a change for the magnitude of intervention contemplated with spinal fusion or disc replacement. Pre-operative evaluation of subjects about to have spinal fusion for spondylolisthesis or presumed ‘‘discogenic pain’’ sources indicate this group perceived that such small changes were inconsistent with their expectations and minimum acceptable outcomes (Table 1). Most patients perceived that a minimum improvement more than 25 points on the Oswestry Disability Index (ODI) would be needed to achieve their minimum functional goals; similarly, an improvement of 4 of 10 on a pain intensity scale was considered a minimum acceptable change.35
Surgical treatments of lumbar disc degenerative, annular disruption or spondylosis Early after the recognition that disc herniation treated with laminectomy and disc removal appeared to be an effective treatment of sciatica, the same decompressive surgery was generally applied to common back pain in the presence of disc degeneration. This approach was remarkable for reported anecdotal successes but much more common failures. By and large laminectomy has been abandoned as a primary treatment of back pain without neurological symptoms due to degenerative changes.36 Currently the three general strategies of surgical treatment used for chronic and severe LBP illness in the absence of serious spinal pathology are commonly considered:
lumbar fusion by a variety of techniques, open surgical methods without fusion (disc arthroplasty, dynamic stabilization),
percutaneous techniques to alter disc mechanics or nociception (nucleoplasty or intradiscal electrothermal annuloplasty).
Lumbar fusion Lumbar fusion for LBP due to serious structural disease is clearly effective. Fusion may be dramatically beneficial in the setting of certain fractures, persistent or complicated spinal infections, progressive deformity, demonstrable radiographic instability with spondylolisthesis, etc. Spinal fusion for unstable isthmic spondylolisthesis can return 70–90% of patients to full occupational function with minimal functional impairment and ceasing all narcotic analgesic medication.21,37
ARTICLE IN PRESS The role of surgery in low back pain
Table 1
13
Minimal acceptable outcomes for fusion surgery in LBP reported prospectively by patients (n ¼ 94). Minimum acceptable outcome
Pain improvement (VAS 0–10)
4 points improvement (median) p2 points improvement acceptable to less than 10% 28 points improvement (median) p14 point improvement acceptable to less than 10% 490% expect to be working full or part-time o10% would accept permanent disability 95% require no narcotic medications o20% would accept daily medications of any kind
Functional score (Oswestry Disability Index) Work status Medications
Table 2
Evidence from RCTs for spine fusion in chronic LBP with degenerative changes.
Study design
Significant exclusion
Effect
Brox et al.39 64 patients with chronic LBP (mean 10 years) RCT: lumbar fusion (1–2 level) vs. ‘‘cognitive intervention’’ and exercise
Serious psychological issues Widespread ‘‘myofascial pain’’ Previous fusion surgery Compensation dispute not an issue (Norway)
One year after treatment begun, no differences in back pain, function, medication usage, work status or satisfaction Approximately 22% of fusion group returned to work, compared to 33% in the non-operative group ‘‘Success’’ rated by independent observer only approximately 20–25% in either group
Fritzell et al.41 294 patients with chronic LBP (mean of 9 years, disabled mean 3 years). RCT: non-standardized physical therapy vs. lumbar fusion (three types of fusion techniques)
Serious psychological issues Previous fusion surgery Compensation dispute not an issue (Sweden)
Back pain improved 33% and function 25% in the fusion group with little change in the physical therapy group 36% of the fusion group returned to work (vs. 13% in non-operative group) 16% of the fusion group were rated as ‘‘Excellent’’ results (vs. 6% in nonoperative group)
Fairbank40 394 patients (age 18–55) with chronic LBP and whose clinician was uncertain if fusion or non-operative treatment would be effective RCT: fusion or Graf stabilization vs. ‘‘cognitive intervention’’ and intensive rehabilitation
Psychiatric disease Previous fusion surgery Strong clinical belief that surgery would be highly effective
Both groups showed clinically significant improvements (20% non-operative vs. 27% surgery decline in ODI, p ¼ 0.04), difference below the MCID for ODI No significant changes in any of the other outcomes measured
The best documented outcomes after lumbar fusion for common degenerative findings without instability or neurological compression is much less impressive.38 There have been three randomized clinical trials comparing non-surgical treatment to spinal fusion published in the last five years (Table 2). Two of these trials (Brox et al.39 from Norway, Fairbank et al.40 from Great Britain), used a cognitivebehavioural model for the non-surgical arms of treatment
which appears to be more effective than ‘‘usual care’’ management. Both of these studies utilizing the cognitive behavioural methods showed only small differences between fusion and non-surgical treatments, with some relative advantages to non-surgical management (fewer complications, better coping strategies, possibly better occupational outcomes) and some relative advantages to fusion (marginally better Oswestry Disability scores in one
ARTICLE IN PRESS 14 study). In the third RCT by Fritzell et al.41 from Sweden, small but statistically significant advantages were seen in the fusion group compared to an unstructured continuance of non-surgical modalities. Nonetheless, high-grade successes were not commonly seen in either group (16% in the fusion group compared to 6% in the non-surgical group) (Table 2). While there have been no RCTs of fusion vs. non-operative care in the United States, data are available from cohort studies comparing various fusion techniques. Many of these studies include fusion for spondylolisthesis and gross instability in heterogeneous cohorts. Nonetheless, in these studies with more concrete pathologic changes lumbar fusion appears to have better outcomes than in the European RCTs performed for non-specific changes. In the three European RCTs, the ODI improvements ranged from 3 to 13 points for non-operative care and 11–15 points for surgery. In a large US trial for FDA approval of different fusion techniques for a heterogeneous diagnostic group with varying severity of pathologies including spondylolisthesis, the mean ODI outcome was approximately 20–25 points.42 A similar range of improvement on the ODI has been seen in other similar FDA studies and prospective cohort studies.43 These ranges begin to approximate the minimum acceptable levels of improvement prospectively identified by patients. However, in the cohort studies which identify only nonspecific DDD or ‘‘internal disc disease’’ as the subject population, the outcomes are much more modest. Slozar et al.44 found that outcomes after lumbar fusion met the patients’ expectations in only 10% of nearly 100 subjects. Similarly, DeBernard et al.45 found satisfactory outcomes were uncommon in subjects having spinal fusion for nonspecific findings in a worker’s compensation setting. McKenna et al. found ODI improvements of only 6–15 points for spinal fusion for non-specific MR changes and discography-positive suspected discogenic pain at one or two levels. Only about 20–30% of these subjects met the minimum acceptable outcomes criteria of 4 points VAS and 28 points ODI improvement. Even in the ‘‘best-case’’ setting of subjects with singlelevel fusion, normal adjacent segments, and no psychosocial co-morbidities, only 40–50% of subjects meet their minimal acceptable goals when fusion is performed for non-specific degenerative changes and a positive discography response.21
Nucleoplasty and intradiscal electrothermal annuloplasty (IDET) Some have attempted to treat back non-specific or suspected ‘‘discogenic pain’’ by altering the annulus or disc nucleus by applying a type of ablative energy to these structures. Despite early enthusiastic application and theoretical conjecture, these techniques have failed to prove effective when tested in a controlled clinical trial. A large RCT of IDET by Freeman et al. failed to show any effect in pain improvement, disability, medication intake or occupational status between subjects treated with the IDET device or a sham intervention. Furthermore, the placement of the catheter, supposed to be critical to achieving the desired effect, did not correlate with outcomes upon close review. An RCT by Pauza et al., in subjects with relatively minor LBP, appeared to show only
E.J. Carragee small differences between IDET and sham treatment, despite methodological problems favouring the IDET group. Another study in Australia testing IDET against a sham control was abandoned when detection of differences between IDET and sham groups were calculated to be highly unlikely based on early data analysis. Finally, radiofrequency thermocoagulation of the nucleus was not shown to be more effective than sham treatment in a small RCT.46 While there may be a role for this strategy in the future, there is insufficient evidence to recommend the current treatments tested so far. Given the widespread application of these apparently ineffective interventions, such as IDET, prior to controlled and rigorous clinical assessment, it is clear that cohort studies alone are insufficient to evaluate efficacy of this technology. Future percutaneous surgeries with similar designs should be viewed with healthy scepticism before true efficacy is confirmed with independent randomized controlled trials.
Artificial disc replacement Treatment of arthritic hip and knee joints with artificial bearing surfaces, that is joint replacement, is a proven orthopaedic intervention. The early history of hip and knee joint replacement surgery was marked by notable and sometimes extraordinary failures. After years of clinical research, relatively stable and durable prostheses have been developed which can be expected to last 15–20 years in a relatively elderly clinical population. Arthrosis of the spine has been recently treated with artificial disc replacement (ADR) using a variety of prostheses. Clearly the facet arthrosis if present will remain untreated by attempts at mechanical disc replacements. Despite this theoretic limitation, short-term trials have proven encouraging in so far as early complications have been infrequent and motion appears to be maintained for several years at least, in many patients. There is a theoretical advantage to continuing motion as it may decrease the rate of disc degeneration at segments adjacent to the surgery compared to fusion. There is obviously a native progression to adjacent segment disease and not all disc degeneration is seriously symptomatic. The advantage, if any, from an ADR over a fusion, on this basis will require a long and carefully controlled clinical assessment. The joint constraint characteristics, mobility, bearing surface composition vary in different designs and thus far no head to head comparison is available to determine whether one type is superior to another. Clinical results comparing the outcome of ADR and fusion for non-specific LBP and degenerative changes have been inconclusive. By most parameters the outcome of these trials have shown little difference in functional outcomes, pain intensity, medication intake or occupation disability.47–49 Approximately 50% of the subjects in both US and UK trials appear to be clinical failures despite rigorous entry criteria.47,49 Long-term follow-up from these trials remains to be examined. A 17-year follow-up from the early European experience with the Charite device has questioned the viability of motion over time and suggested the persistence of motion may not be clinically beneficial so far as pain intensity.50
ARTICLE IN PRESS The role of surgery in low back pain In these early trials the problems of prosthetic loosening, implant wear and reaction to particle debris have not proven to be common. However, since the age of implantation of these devices is only about 40 years, much younger than hip or knee arthroplasty patients, the concern for long term outcomes is real. If after widespread implantation even 10–20% of this group develop aseptic loosening, particle-mediated inflammatory disease, local root-irritation or segmental collapse resistant to primary reconstruction, there may a looming and potentially catastrophic clinical problem in the future. While there are very enthusiastic advocates of this technology, patients need to be advised that the outcomes do not appear clearly better than the marginal results of fusion techniques and the longterm risks remain poorly examined at this stage.
Future directions In the near future, new technologies for surgical treatment of non-specific LBP illness may include biological modification of disc metabolism, alteration of disc genetic expression to change mechanical properties, synthetic nuclear augmentation devices as well as combined facet and disc mechanical replacements. The ability to perform even complex surgical procedures using minimally invasive techniques will undoubtedly continue to evolve. The balance of benefit to risk with many of these newer technologies may not be apparent in early applications. For instance, the use of biological fusion enhancing drugs may have short-term beneficial effects on arthrodesis but the long-term metabolic, immunologic or possibly neoplastic effects are unknown. Similarly drugs designed to enhance disc metabolism may transiently increase the disc hydration or MR signal but may lead to more rapid apoptosis of the activated cells and accelerated disc degeneration. Regardless of the technological advances for intervention, the central question behind any of these strategies however remains. In patients with common degenerative findings alone, why are some doing very well, some are minimally affected with common backache and others severely incapacitated from all common daily activities? The diagnosis of LBP may be a larger problem than choice of intervention. If much of the severe LBP illness associated with only minor changes of the lumbar spine is, in fact, primarily a function of a generalized pain intolerance, or is an expression of psychological illness such as depression or anxiety, or is secondarily driven by compensation issues, dysfunctional social adaptation or poor coping skills, little effect will be seen by intensifying efforts to eradicate local, benign pain processes in that subgroup.
Practice points
There is poor correlation between MR findings of spinal degenerative changes and symptoms in adults
Most people function well despite significant and progressive spinal degenerative changes
The cause of serious LBP illness in the absence of serious spinal diseases such as instability, infection or neoplasm is not well understood and nonstructural factors such as central pain intolerance,
15
psychological distress, social and economic issues of compensation and participation, appear to act as co-morbidities to LBP illness impairing recovery In RCTs of surgical vs. non-operative care, lumbar fusion surgery for common degenerative changes appears to offer only limited relative benefits over intensive rehabilitation. Cohort studies of highly selected subjects have somewhat better outcomes Artificial disc replacement has approximately the same outcomes as fusion in short-term studies but the long-term risks of prostheses placement in relatively young patients remains a concern
References 1. Skovron ML, Szpalski M, Nordin M, Melot C, Cukier D. Sociocultural factors and back pain. A population-based study in Belgian adults. Spine 1994;19:129–37. 2. Cassidy JD. Saskatchewan health and back pain survey. Spine 1998;23:1860–6. 3. Carragee E, Cohen S. Reliability of LBP history in asymptomatic subjects? The prevalence and incidence of reported back pain correlates with surveillance frequency. Proceeding of the North American Spine Society, Chicago, IL, 2004. p. 216. 4. Cassidy JD, Carroll LJ, Cote P. The Saskatchewan health and back pain survey. The prevalence of low back pain and related disability in Saskatchewan adults. Spine 1998;23:1860–6 [discussion 1867]. 5. Carragee E, Alamin T, Miller J, Carragee M. Discographic, MRI and psychosocial determinants of low back pain disability and remission: a prospective study in subjects with benign persistent back pain. Spine J 2005;5(1):24–35. 6. Ito M, Incorvaia KM, Yu SF, Fredrickson BE, Yuan HA, Rosenbaum AE. Predictive signs of discogenic lumbar pain on magnetic resonance imaging with discography correlation. Spine 1998;23:1252–8 [discussion 1259–60]. 7. Aprill C, Bogduk N. High-intensity zone: a diagnostic sign of painful lumbar disc on magnetic resonance imaging. Br J Radiol 1992;65:361–9. 8. Carragee EJ, Paragioudakis SJ, Khurana S. 2000 Volvo Award winner in clinical studies: lumbar high-intensity zone and discography in subjects without low back problems. Spine 2000;25:2987–92. 9. Weishaupt D, Zanetti M, Hodler J, Boos N. MR imaging of the lumbar spine: prevalence of intervertebral disk extrusion and sequestration, nerve root compression, end plate abnormalities, and osteoarthritis of the facet joints in asymptomatic volunteers. Radiology 1998;209:661–6. 10. Salerno SM, Browning R, Jackson JL. The effect of antidepressant treatment on chronic back pain: a meta-analysis. Arch Intern Med 2002;162:19–24. 11. Boden S, Davis D, Dina T, Patronas N, Wiesel S. Abnormal magnetic resonance scans of the lumbar spine in asymptomatic subjects: a prospective investigation. JBJS [Am] 1990; 72-A:403–8. 12. Jensen M, Brant-Zawadzki M, Obuchowski N, Modic M, Malkasian D, Ross J. Magnetic resonance imaging of the lumbar spine in people without back pain. N Engl J Med 1994;331:69–73. 13. Boos N, Semmer N, Elfering A, et al. Natural history of individuals with asymptomatic disc abnormalities in magnetic resonance imaging: predictors of low back pain-related medical consultation and work incapacity. Spine 2000;25:1484–92. 14. Borenstein DG, O’Mara Jr JW, Boden SD, et al. The value of magnetic resonance imaging of the lumbar spine to predict
ARTICLE IN PRESS 16
15.
16.
17.
18.
19.
20.
21.
22.
23.
24. 25.
26.
27.
28.
29.
30.
31. 32.
33. 34.
E.J. Carragee low-back pain in asymptomatic subjects: a seven-year follow-up study. J Bone Jt Surg Am 2001;83-A:1306–11. Jarvik JJM, Hollingworth W, Heagerty P, Haynor DR, Deyo RA. The longitudinal assessment of imaging and disability of the back (LAIDBack) study—baseline data. Spine 2001;26:1158–66. Carragee E, Alamin T, Cheng I, Franklin T, van den Haak E, Hurwitz E. Are first-time episodes of serious LBP associated with new MRI findings? Spine J 2006;6:624–35. Carragee E, Tanner C, Vittum D, Kim D. Positive provocative discography as a misleading finding in the evaluation of low back pain. NASS Procedings, 1997. p. 388. Carragee EJ, Tanner CM, Yang B, Brito JL, Truong T. Falsepositive findings on lumbar discography. Reliability of subjective concordance assessment during provocative disc injection. Spine 1999;24:2542–7. Carragee EJ, Chen Y, Tanner CM, Truong T, Lau E, Brito JL. Provocative discography in patients after limited lumbar discectomy: a controlled, randomized study of pain response in symptomatic and asymptomatic subjects. Spine 2000;25: 3065–71. Carragee EJ, Tanner CM, Khurana S, et al. The rates of falsepositive lumbar discography in select patients without low back symptoms. Spine 2000;25:1373–80 [discussion 1381]. Carragee EJ, Lincoln T, Parmar VS, Alamin T. A gold standard evaluation of the ‘‘discogenic pain’’ diagnosis as determined by provocative discography. Spine 2006;31:2115–23. Reid M, Lachs M, Feinstein A. Use of methodological standards in diagnostic test research: getting better but still not good. 1995 1995;274:645–51. Sackett DL, Rosenberg WM, Gray JA, Haynes RB, Richardson WS. Evidence based medicine: what it is and what it isn’t. Br Med J 1996;312:71–2. Greenhalgh T. Education and debate: papers that report diagnostic or screening tests. Br Med J 1997;315:1–12. Bossuyt P, Reitsma J, Bruns D, et al. Towards complete and accurate reporting of studies of diagnostic accuracy: the STARD initiative. Br Med J 2003;526:41–5. Dreyfuss P, Halbrook B, Pauza K, Joshi A, McLarty J, Bogduk N. Efficacy and validity of radiofrequency neurotomy for chronic lumbar zygapophysial joint pain. Spine 2000;25:1270–7. Burton A, Tillotson K, MAin C, Hollis S. Psychosocial predictors of outcome in acute and subacute low back trouble. Spine 1995;20:722–8. Cassidy JD, Carroll L, Cote P, Berglund A, Nygren A. Low back pain after traffic collisions: a population-based cohort study. Spine 2003;28:1002–9. Hurwitz EL, Morgenstern H, Harber P, et al. A randomized trial of medical care with and without physical therapy and chiropractic care with and without physical modalities for patients with low back pain: 6-month follow-up outcomes from the UCLA low back pain study. Spine 2002;27:2193–204. Cairns MC, Foster NE, Wright CC, Pennington D. Level of distress in a recurrent low back pain population referred for physical therapy. Spine 2003;28:953–9. Carragee EJ. Psychological and functional profiles in select subjects with low back pain. Spine J 2001;1:198–204. Carragee E, Alamin T, Cheng I, Franklin T, Hurwitz E. 2006 ISSLS prize in clinical research: does minor trauma cause serious low back pain illness? Spine 2006;31. Carragee EJ. Clinical practice. Persistent low back pain. N Engl J Med 2005;352:1891–8. Weinstein JN, Lurie JD, Olson PR, Bronner KK, Fisher ES. United States’ trends and regional variations in lumbar spine surgery: 1992–2003. Spine 2006;31:2707–14.
35. Carragee E, Alamin TF. A prospective assessment of patient expectations and satisfaction in spinal fusion surgery. Procedings International Society for the Study of the Lumbar Spine, Vancouver, BC, 2003. p. 74. 36. Allan DB, Waddell G. An historical perspective on low back pain and disability. Acta Orthopaed Scand Suppl 1989;234: 1–23. 37. Swan J, Hurwitz E, Malek F, et al. Surgical treatment for unstable low-grade isthmic spondylolisthesis in adults: a prospective controlled study of posterior instrumented fusion compared with combined anterior-posterior fusion. Spine J 2006;6:606–14. 38. Gibson JN, Waddell G. Surgery for degenerative lumbar spondylosis: updated Cochrane review. Spine 2005;30:2312–20. 39. Ivar Brox J, Sorensen R, Friis A, et al. Randomized clinical trial of lumbar instrumented fusion and cognitive intervention and exercises in patients with chronic low back pain and disc degeneration. Spine 2003;28:1913–21. 40. Fairbank J, Frost H, Wilson-MacDonald J, Yu LM, Barker K, Collins R. Randomised controlled trial to compare surgical stabilisation of the lumbar spine with an intensive rehabilitation programme for patients with chronic low back pain: the MRC spine stabilisation trial. Br Med J 2005;330:1233. 41. Fritzell P, Ha ¨gg O, Wessberg P, Nordwall A, Group SLSS. 2001 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. 42. Dimar JR, Glassman SD, Burkus KJ, Carreon LY. Clinical outcomes and fusion success at 2 years of single-level instrumented posterolateral fusions with recombinant human bone morphogenetic protein-2/compression resistant matrix versus iliac crest bone graft. Spine 2006;31:2534–9 [discussion 2540]. 43. Glassman S, Gornet MF, Branch C, et al. MOS short form 36 and Oswestry Disability Index outcomes in lumbar fusion: a multicenter experience. Spine J 2006;6:21–6. 44. Slosar PJ, Reynolds JB, Schofferman J, Goldthwaite N, White AH, Keaney D. Patient satisfaction after circumferential lumbar fusion. Spine 2000;25:722–6. 45. DeBerard MS, Masters KS, Colledge AL, Schleusener RL, Schlegel JD. Outcomes of posterolateral lumbar fusion in Utah patients receiving workers’ compensation: a retrospective cohort study. Spine 2001;26:738–46 [discussion 747]. 46. 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 C lesion. Spine 2001;26:287–92. 47. Freeman BJ, Davenport J. Total disc replacement in the lumbar spine: a systematic review of the literature. Eur Spine J 2006;15:439–47. 48. Delamarter RB, Bae HW, Pradhan BB. Clinical results of ProDiscII lumbar total disc replacement: report from the United States clinical trial. Orthop Clin North Am 2005;36:301–13. 49. Blumenthal S, McAfee PC, Guyer RD, et al. A prospective, randomized, multicenter Food and Drug Administration investigational device exemptions study of lumbar total disc replacement with the CHARITE artificial disc versus lumbar fusion: part I: evaluation of clinical outcomes. Spine 2005;30:1565–75 [discussion E387–91]. 50. Putzier M, Funk JF, Schneider SV, et al. Charite total disc replacement—clinical and radiographical results after an average follow-up of 17 years. Eur Spine J 2006;15:183–95.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 17–24
Available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/cuor
MINI-SYMPOSIUM: FRONTIERS IN SPINE SURGERY
(iii) Total lumbar disc arthroplasty H. Michael Mayer, Christoph Siepe Spine Centre Munich, Orthozentrum Mu ¨ nchen, Harlachinger Str. 51, D-81547 Mu ¨ nchen, Germany
KEYWORDS Total disc replacement; Disc degeneration; Low back pain
Summary Total disc replacement is a challenge to every spine surgeon. It is a new technology with few mid- and long-term outcomes reported. It is a technique with excellent short-term outcomes at least in uncontrolled clinical trials. It tends to be superior to spinal fusion for selected indications. However, it is also a ‘trendy’ technique for uncritical protagonists, their patients and the media. This increases the pressure on surgeons to adopt the technique, but at the same time one must look very carefully and critically at the empirical outcomes. The fate of a new surgical technique will not only be determined by the results of highly standardized randomized controlled trials. It will also be influenced by ‘experience-based’ data. It is the responsibility of the individual spine surgeon and of the scientific and professional spine organizations to see whether this new technique stands the test of time. & 2007 Elsevier Ltd. All rights reserved.
Introduction Although there is still a significant and controversial debate about its benefit,1–6 spinal fusion for degenerative conditions of the lumbar spine has become a standard surgical procedure.7–12 It is nowadays accepted worldwide as the ultimate treatment option in painful degenerative disc disease (DDD), degenerative spondylolisthesis, degenerative lumbar scoliosis, postdiscectomy syndromes or segmental instability adjacent to a previous fusion for those cases that do not respond to conservative therapy.13–15 The disadvantages of spinal fusion, such as iatrogenic ‘collateral damage’ of different approaches, high complication rates and adverse side-effects have not been emphasized in scientific discussions in the past due to the fact that there was no alternative to these procedures. This is also Corresponding author.
0268-0890/$ - see front matter & 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2007.01.003
true for the potential consequences of immobilizing one or more mobile spinal segments.1,3,4,16–18 In the last few years, total lumbar disc replacement seems to have become a potential alternative treatment.19,20
Implants Seven different types of lumbar total disc implant are currently available worldwide.
The SB Charite ´ III—Disc (Depuy Spine; Raynham, MA, USA) This disc was developed in the former East Germany in the beginning of the 1980s21,22 (Fig. 1). It consists of two metal endplates made out of CoCrMo-alloy.23 The surfaces towards the vertebral endplate are covered with porous
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H.M. Mayer, C. Siepe
Figure 1
SB Charite´ II Disc.
plasma-sprayed titanium and bio-actively coated with calcium phosphate (not available in the US) to promote on-growth of bone from the vertebral endplate. The freefloating biconvex sliding core is made out of ultra-highmolecular-weight polyethylene (UHMWPE), encased between the biconvex endplates and surrounded by a metal wire for radiological marking.23,24 This is, at present, the only non-constrained implant type available.
Figure 2 Prodisc L II Disc.
The Prodisc L Disc (Synthes, Paoli, USA) The Prodisc L was developed in the late 1980s and was used in the early 90s in one single case series in France.25 The second generation of this implant has been available since 1999 (Fig. 2). The implant consists of two flat CoCrMo-alloy endplates. The lordosis angle is given by the design of the superior endplate (61/111). The UHMWPE inlay snaps into the lower endplate during the implantation process.26 It is a semi-constrained implant with a fixed center of rotation (COR) at the level of the endplate of the lower vertebra. The implant does not allow for pure translation movements. The superior vertebra rotates around the fixed center of rotation.26,27
Figure 3 Maverick Disc.
The Maverick Disc (Medtronic, Minneapolis, MN, USA) The Maverick Disc is a metal-on-metal implant (Fig. 3). It consists of two flat metal parts and represents a ball-andsocket joint.28 The center of rotation is fixed and located in the posterior third of the disc space. It is also a semiconstrained device that does not allow for pure translation. Rotation of the upper vertebra around the ball in the lower endplate is determined by the small radius of the ball.
The Flexicore Disc (Stryker, Kalamazoo, MA, USA) This disc is another metal-on-metal captured ball-andsocket joint device29 (Fig. 4). The endplates are domeshaped and thus adapt to the concavity of the vertebral endplates. The surfaces of the endplates are titanium plasma-sprayed to promote bone on-growth fixation. The endplates are linked by the ball-and-socket-joint. Implanta-
Figure 4
Flexicore Disc.
tion is possible through an anterior or antero-lateral approach.
The Mobidisc (LDR me ´dical; Troyes, France) This disc is manufactured in France.30 It consists of three pieces; two flat metal endplates with porous coated
ARTICLE IN PRESS Total lumbar disc arthroplasty
19
surfaces and a keel to provide immediate and long-term stability (Fig. 5). The PE inlay contains a radiological marker inserted in the lower endplate. It is able to perform limited sliding in all directions during movements of the segment and thus adapts to the instantaneous center of rotation, mimicking the physiological movements of a normal nucleus.
Activ L (Aesculap AG Tuttlingen, Germany) This implant resembles the Prodisc, with minor differences. It has a sliding nucleus, which is anchored in the lower endplate (Fig. 6). The endplates are available with spikes and/or keels to allow for different types of primary fixation. This variable design also allows for different approaches (anterior midline or oblique antero-lateral). Figure 7 Kineflex (Centurion) Disc.
Kineflex (Spinal Motion, South Africa)
Results This is another metal-on-metal semi-constrained disc with a flexible center of rotation. Primary fixation is achieved with keels (Fig. 7). Besides these implant models described above, which have made their way into clinical use, there is a great number of other patented devices for total disc replacement (TDR) which might progress to clinical studies in the future.20 However, due to more or less restrictive national and international regulatory and approval processes, these seven implants will most probably be the devices which will dominate the next few years.
Figure 5 Mobidisc.
Figure 6
Activ L Disc.
Charite ´ results This was the first total disc implant, which was used for the first time in the late 1980s. In non-controlled studies, the success rates ranged between 60% and more than 80% in mid- and long-term follow-ups.31–34 The indications in these publications included low back pain in DDD, but also for postdiscectomy segments, spondylolysis/spondylolisthesis cases, as well as in other pathologies. This may explain the heterogeneity of the clinical results. In a randomized controlled trial with a highly selective indication spectrum, results showed a significant improvement in Visual analog Scores (VAS) and Oswestry Disability Scores.35 After 24 months, the overall success, as defined by an improvement of the Oswestry Disability Index of at least 25%, was 63.9% for the TDR as compared to 50.5% for a stand-alonetype of lumbar fusion. The mean improvement in the VAS was 40.6 (TDR) versus 34.1 (Fusion). This difference was statistically significant. There were 3.9% device-related and 9.8% approach-related complications. About 5.4% of the patients required additional surgery at the index level within the first 24 months. The majority of adverse events and complications are approach-related and can reach up to 18%.31,32,36
Prodisc results This implant was used first in the beginning of the 1990s. Marnay reported good and excellent results with the firstgeneration implant after a follow-up of 8–10 years.25 Other authors reported success rates between 80% and more than 90% in non-controlled clinical series.37–39 The complication rates were reported to be o10%. The results from an FDAcontrolled randomized trial comparing TDR with 3601 fusion showed a significant difference in the Oswestry Disability Index favoring TDR.40 Hospital stay was significantly shorter and there was a trend towards higher patient satisfaction rates.
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H.M. Mayer, C. Siepe
Maverick results
Indications for TDR
Preliminary results were reported by Le Huec et al.41 in 2004. In a series of 30 patents with a follow-up of up to 1 year, he reported a clinical success rate of up to 86%. There was only one non-device-related complication (3.3%). A recent publication described the results in 64 patients with an improvement of the ODI in 75% of the patients.42 Since 2003, a prospective FDA-controlled trial has been ongoing in the USA.
There is some consensus about ‘good’ indications for TDR,46 which more or less is oriented on the inclusion criteria of the FDA-controlled randomized controlled trials for the Charite and the Prodisc L.35,47 A very controversial debate is ongoing about so-called ‘borderline indications’ in patients with associated pathologies.
Results for different indications and levels Flexicore results This device is implanted as a single unit. There are no clinical data available at the time of writing. However, patient enrollment for a randomized FDA-controlled IDE study in the USA has begun. The results will be compared with a control group in which a 3601 fusion has been performed. Miz andTheophilos43 reported the 1-year followup of this RCT. There were marked improvements in the VAS as well as the ODI in the TDR and in the fusion group.
Mobidisc results No published results of controlled studies were available at the time of writing. Steib et al.44 reported success rates of 87% and 91% after a follow-up of between 0.5 and 1 year.
Kineflex results Ha ¨hnle et al.45 reported a success rate of 81.3% at the SAS 6 Meeting in Montreal 2006. The follow-up was 2 years. No controlled trials are available yet.
Activ L results As yet, there are no published results for Activ L.
Summary There is a trend for better short-term results with total lumbar disc replacement as compared to spinal fusion (3601 or stand-alone BAK fusion). Randomized controlled trials for the Charite´-type implant show evidence for non-inferiority to BAK cage anterior lumbar interbody fusion. However, it should be noted that this type of fusion is now obsolete in Europe. Randomized controlled trials for the Prodisc L show weak evidence for superiority as compared to 3601 fusion. The analysis of the published data show that although ‘ideal’ indications were present in the RCTs, the results did not reach the level published in uncontrolled studies. Since the indication spectrum in the uncontrolled trials was much less restrictive, including so-called ‘borderline-indications’ (see below), a significant evaluation as well as publication bias can be assumed, ameliorating the clinical results reported.
In a recently published paper with 3-year follow-up in 92 Prodisc L patients, we showed that due to significantly varying outcomes, indications for arthroplasty must be defined precisely.48 Best results were achieved in patients with DDD and concomitant contained soft-disc herniation with predominant low back pain. Better functional outcome was obtained in younger patients under the age of 40. However, subjective outcome evaluation still showed excellent high satisfaction rates in older patients. Therefore, age as a solitary factor does constitute a contraindication for total lumbar disc replacement. This has been supported in a study on patients older than 60 years with TDR.49 Multisegmental disc replacement still belongs to the so-called ‘off-label’ indications for disc replacement, and still lacks evidence in comparison to lumbar fusion procedures in controlled randomized prospective trials. Previously published results from non-controlled clinical studies have reported a wide range of inconsistent and contradictory data regarding postoperative outcome and success rates of mono- versus bi- and multisegmental TDRs. More favorable results have been reported for disc replacement procedures with Charite´ III in patients with isolated disc disease in comparison to patients with DDD at multiple levels, which was attributed to segmental over-distraction due to the biconvex UHMWPE inlay in multisegmental cases.31,50 Bertagnoli and Kumar51 previously published a 98.2% success rate with 134 TDRs implanted in 108 patients. The same author published a similarly high success rate for multisegmental disc replacement procedures of 92–96% (10 bisegmental, 15 trisegmental) and also reported on 4- and 5-level disc replacement procedures previously.52 Tropiano et al.53 reported a 100% success rate in a cohort of 53 patients (40 monosegmental, 9 bisegmental, 2 trisegmental). Carefully selected other studies and results from RCTs could not confirm such high success rates even for highly selected monosegmental cases.31,34,35,47,48,50,54,55 Furthermore, a variety of recently published biomechanical in vitro studies, results from finite-element models and radiological investigations have similarly raised concern in particular with regards to multisegmental disc replacement procedures due to the cumulative increase in rotational instability as well as increased load on the posterior joint structures.56–59 Our own clinical findings closely match those results and have shown significant and distinct differences between mono- and multisegmental disc replacement procedures in favor of monosegmental TDRs.48,60 Significant improvement was seen for both mono- and bisegmental disc replacements. Nevertheless, multilevel disc replacements had significantly higher complication rates and inferior
ARTICLE IN PRESS Total lumbar disc arthroplasty outcome at mid-term follow-up compared to monosegmental interventions. The best results were observed in monosegmental TDRs above the lumbosacral junction. Results, however, deteriorated when TDR included the lumbosacral junction. Significantly inferior results were observed for bisegmental TDRs in comparison to monosegmental disc replacement procedures, and the bisegmental procedures were also associated with a considerably higher complication rate.
Special indications Physical performance and rehabilitation following TDR FDA Investigational Device Exemption (IDE) studies have pointed out that one of the advantages of TDR over lumbar fusion procedures is earlier postoperative mobilization and shorter postoperative recovery times in comparison to lumbar fusion procedures.35,47,54,55 Due to an increasing prevalence of commonly accepted contra-indications with age,61 TDR is predominantly performed in young and active patients with high subjective expectations regarding their postoperative performance. Preoperative patient fitness as well as postoperative rehabilitation and mobilization seem to be key factors for clinical success following lumbar disc replacement procedures. Le Huec et al.62 correlated postoperative outcome to the degree of fatty posterior muscle degeneration and found better outcome for patients with less/little muscle degeneration. Cinotti et al.31 reported greater range of motion at the operated level for patients who began to exercise from an early postoperative stage in comparison to patients who wore a corsett for 3 months. Similarly, other authors adhere to the philosophy of early and active rehabilitation following TDR.36 Siepe et al.63 described highly satisfactory postoperative outcomes in a preselected cohort of athletes with the majority of patients resuming sporting activities within the first 3 (38.5%) to 6 months (another 30.7%). Peak performance was attained on average after 5.2 months up to the level of competitive and professional athletes and patients participating in extreme sports. No specific sport was detected which would have been less suited following total lumbar disc replacement. The authors did not observe any severe implant dislocations as a result of excessive postoperative load increase.
Complications and adverse events Previous studies have described a wide range of complication rates following total lumbar disc replacement from o1%2 to 40%.64 However, previously published complication rates have to be interpreted carefully with regards to ‘exceptionally low complication rates’. In this context, McAfee et al.65 previously commented on authors who described the ‘anecotal incidence of revision and reoperation following TDR’. The majority of all studies have reported complication rates ranging from 10% to 20%.31,33,34,47,48,51 The level of disc replacement also seems to play a significant role in the incidence of peri-/postoperative complications.60 Significantly higher complication rates have been observed in technically demanding disc replacement procedures which included the level of
21 vascular bifurcation in comparison to TDRs performed at the lumbosacral junction.60 However, upon comparing the type of revision surgery, more invasive interventions were required following TDR at the lumbosacral junction with a higher incidence of implant dislocations. Zeegers et al.34 reported a complication rate of 18% and referred 14% of these to the anterior access. About 12 out of 50 patients overall (24%) required secondary surgery. In this context, however, the issue of potentially life threatening anterior revision surgery must be addressed carefully.66 Brau67 reported a 2.6% vascular injury complication rate. However, even this low complication rate is hard to accept in elective spinal surgery. Published data from FDA IDE studies have reported revision surgery rates of 5.4–8.8% at the index level.35,65 Due to the high risk associated with anterior midline exposure, especially in cases of revison surgery, complication-avoiding strategies will gain substantial popularity in the near future. This includes improved preoperative planning and assessment of the vascular anatomy, supplemented with 3D-CT reconstructions of the prevertebral vessels, intraoperative insertion of anti-adhesive membranes to avoid or decrease postoperative scarring or modification of the implants which offer the option of insertion via a lateral access.
Postoperative pain patterns Implant positioning plays a key role in postoperative clinical success. A variety of studies have focused on the influence of implant positioning in anteroposterior and lateral views and computerized image guided systems have been introduced and evaluated.68,69 McAfee et al.70 reported that although it was better to have ideal implant positioning, suboptimal implant placement (o5 mm off ideal placement in either the AP or lateral view) did not detrimentally affect the normal function of the Charite´ disc. However, if implant mal-placement exceeded 5 mm off axis in either the mid-sagittal or coronal planes, the flexion/extension ROM was affected negatively. From clinical experience, however, unsatisfactory postoperative results can be observed in a number of patients even with satisfactory implant positioning. A few issues, therefore, which could potentially impair postoperative outcome remain to be carefully addressed. A variety of studies have reported that the facet joints may be a weak link following TDR. David et al. reported that post-TDR back pain originated from the facet joints in most cases.37 LeHuec et al.62 performed facet infiltrations in 17 out of 64 patients (26.5%) after monosegmental TDR with the Maverick prosthesis, 17.2% of which reacted positively. Biomechanical studies have similarly reported increased load on the posterior structures and altered load patterns with sudden rather than gradual load increase.27,33,56,57 Increased axial rotation and segmental lordosis have similarly been addressed in the literature, all with the potential to impair postoperative outcome. However, it has also been reported that postoperative pain originating from the iliosacral joints may be equally detrimental to clinical outcome and is presently an underestimated source of post-TDR pain.60 The impact on mid- and long-term clinical outcome is presently unknown and will require further investigation.
ARTICLE IN PRESS 22
H.M. Mayer, C. Siepe
Practice points
11.
Total lumbar disc replacement is a good alternative
to spinal fusion in selected cases with predominantly monosegmental discogenic low back pain Patient selection should exclude non-discogenic pain sources There is a trend for better short-term results (clinical improvement, back-to-work; perioperative morbidity) as compared to spinal fusion Early complication and reoperation rates are comparable to spinal fusion The efficacy of multisegmental TDR, TDR in the elderly, in smokers, in levels adjacent to a previous fusion, in postdiscectomy patients and patients with associated pathologies (e.g. fact joint osteoarthritis) is not yet proven
Research directions
12.
13.
14.
15.
16. 17. 18.
Kinematics of TDR at different lumbar levels Effects of TDR on sagittal balance parameters Wear studies (UHMWPE, Metal) MRI-compatible implant materials Oblique and lateral surgical approaches Anatomic press-fit designs for endplates Long-term effects of TDR on adjacent segments and facet joints
19.
20.
21. 22.
References 1. Etebar S, Cahill DW. Risk factors for adjacent segment failure following lumbar fixation with rigid instrumentation for degenerative instability. J Neurosurg 1999;90:163–9. 2. Fritzell P, Ha ¨gg O, et al. Lumbar fusion versus non-surgical treatment for chronic low back pain. Spine 2001;26:2521–34. 3. Frymoyer JW, Hanley EN, Howe J. A comparison of radiographic findings in fusion and non-fusion patients 10 or more years following lumbar disc surgery. Spine 1979;4:435–40. 4. Lee CK. Accelerated degeneration of the segment adjacent to a lumbar fusion. Spine 1988;13:375–7. 5. Mayer HM, Wiechert K. Microsurgical anterior approaches to the lumbar spine for interbody fusion and total disc replacement. Neurosurgery 2002;51/5:159–65. 6. Nachemson A. The evidence base for the treatment of not degenerative disc disease—but back pain. In: Gunzburg R, Szplaski M, Andersson G, editors. Degenerative disc disease. Philadelphia, USA: Lippincott, Williams and Wilkins; 2004. p. 263–71. 7. Blumenthal SL, Baker J, Dossett A. The role of anterior lumbar fusion for internal disc disruption. Spine 1988;13:566–9. 8. Greenough CG, Taylor LJ, Fraser RD. Anterior Lumbar Fusion: results, assessment techniques and prognostic Factors. Eur Spine J 1994;3:225–30. 9. Grob D, Scheier HJG, Dvorak J, Siegrist H, Rubeli M, Joller R. Circumferential fusion of the lumbar and lumbosacral spine. Arch Orthop Trauma Surg 1991;111:20–5. 10. Le Huec JC, Aunoble S, Zdeblick TA. Anterior lumbar interbody fusion versus posterior lumbar interbody fusion for degenerative disc disease. In: Gunzburg R, Szplaski M, Andersson G,
23.
24. 25.
26.
27.
28. 29. 30. 31.
32.
33.
editors. Degenerative disc disease. Philadelphia, USA: Lippincott, Williams and Wilkins; 2004. p. 169–80. O’Brien JP, Dawson MHO, Heard CW. Simultaneous combined anterior and posterior fusion: a surgical solution for failed spinal surgery with a brief review of the first 150 patients. Clin Orthop 1986;203:191–5. Passutti N, Delecrin J, Romih M, Brossard D. Posterolateral fusion. In: Gunzburg R, Szplaski M, Andersson G, editors. Degenerative disc disease. Philadelphia, USA: Lippincott, Williams and Wilkins; 2004. p. 181–7. Kostuik JP, Frymoyer JW. Failures after spinal fusion: causes and surgical treatment. In: Frymoyer JW (Ed. In Chief). The adult spine. New York: Raven Press; 1991. p. 2027–68. Leong JCY, Hoper G, Fang D, Chun SY. Disc excision and anterior spinal fusion for lumbar disc protrusion in the adolescent. Spine 1982;7:623–6. Mayer HM, Korge A. Non-fusion technology in degenerative lumbar spinal disorders: facts, questions, challenges. Eur Spine J 2002;11(Suppl. 2):S85–91. Brodsky AE. Post-laminectomy and post-fusion stenosis of the lumbar spine. Clin Orthop 1976;115:130–5. Gillet P. The fate of the adjacent motion segments after lumbar fusion. Spine 2003;28:338–45. Harris RI, Wiley JJ. Acquired spondylolysis as a sequel to spine fusion. J Bone Joint Surg Am 1963;45:1159–64. Ray CD. The artificial disc: introduction, history and socioeconomics. In: Weinstein JN, editor. Clinical efficacy and outcome in the diagnosis and treatment of low back pain. New York: Raven Press Ltd.; 1992. p. 205–25. Szpalski M, Gunzburg R, Mayer HM. Spine arthroplasty: a historical review. In: Gunzburg R, Mayer HM, Szpalski M, Aebi M, editors. Arthroplasty of the spine. Berlin–Heidelberg– New York: Springer; 2004. p. 3–22. Bu ¨ttner-Janz K. The development of the artificial disc: SB Charite ´. Dallas: Huntley and Associates; 1992. SB Charite ´ Total Disc. US Patents 5 556431; 5 401 269, 4 759766 Link. Link HD. History, design and biomechanics of the Link SB Charite artificial disc. In: Gunzburg R, Mayer HM, Szpalski M, Aebi M, editors. Arthroplasty of the spine. Berlin–Heidelberg–New York: Springer; 2004. p. 36–43. Hallab N, Link HD, McAfee PC. Biomaterial optimization in total disc arthroplasty. Spine 2003;28:S139–52. Marnay T. The ProDisc: clinical analysis of an intervertebral disc implant. In: Kaech DL, Jinkins JR, editors. Spinal restabilization procedures. Amsterdam: Elsevier Science BV; 2002. p. 317–31. Mayer HM, Wiechert K, Korge A. Total disc replacement for low back pain of discogenic origin. In: Gunzburg R, Szpalski M, Andersson G, editors. Degenerative disc disease. Philadelphia: Lippincott, Williams and Wilkins; 2004. p. 249–56. Huang RC, Girardi P, Cammisa Jr FP, Wright TM. The implications of constrain in lumbar total disc replacement. Spine 2003;28: 412–7. Salib 1992; Boyd 1994: European Patent No. 0 754 018; 1 188 423; US Patent Nos. 5 425 773; 5 562 738; 5 258 031. Ralph, et al. US Patents No. 6 648 310 B1, 2002/111681-687 A1, 2003/014111 A1/2003/014112 A1. Beaurain, et al. Patent Nos. WO 02/089701 A2 (LDR); FR 2 824 261 A1. Cinotti G, David T, Postacchini F. Results of disc prosthesis after a minimum follow-up period of 2 years. Spine 1996;21: 995–1000. David TJ. Lumbar disc prosthesis: five year follow-up study on 96 patients. Presented at the annual meeting of the North American Spine Society, New Orleans, October 2000. Lemaire JP, Skalli W, Lavaste F. Intervertebral disc prosthesis. Results and prospects for the year 2000. Clin Orthop 1997; 337:64–76.
ARTICLE IN PRESS Total lumbar disc arthroplasty 34. Zeegers WS, Bohnen LM, Laaper M. Artificial disc replacement with the modular type SB Charite ´ III: 2-years results form 50 prospectively studied patients. Eur Spine J 1999;8:210–7. 35. Blumenthal S, McAfee PC, Guyer RD, Hochschuler SH, Geisler FH, Holt RT, et al. A prospective, randomized, multicenter Food and Drug Administration investigational device exemptions study of lumbar total disc replacement with the CHARITE artificial disc versus lumbar fusion: part I: evaluation of clinical outcomes. Spine 2005;30:1565–75 (discussion E1387-1591). 36. Guyer RD, Ohmeiss DD. Intervertebral disc prostheses. Spine 2003;28:S15–23. 37. Bertagnoli R, Kumar S. Indications for full prosthetic disc arthroplasty: a correlation of clinical outcome against a variety of indications. In: Gunzburg R, Mayer HM, Szpalski M, Aebi M, editors. Arthroplasty of the spine. Berlin–Heidelberg–New York: Springer; 2004. p. 75–80. 38. Mayer HM, Wiechert K, Korge A, Qose I. Minimally invasive total disc replacement: surgical technique and preliminary clinical results. Eur Spine J 2002;11(Suppl. 2):S124–30. 39. Tropiano P, Huang RC, Girardi FP, Marnay T. Lumbar disc replacement: preliminary results with ProDisc II after a minimum follow-up period of 1 year. Spine 2003;28:362–8. 40. Zigler JE, Burd TA, Vialle EN, Sachs BL, Rashbaum RF, Ohmeiss D. Lumbar spine arthroplasty: early results using the prodisc II: a prospective randomized trial of arthroplasty versus fusion. Spine 2003;28:352–61. 41. Le Huec JC, Aunoble S, Friesem T, Mathews H, Zdeblick T. Maverick total lumbar disk prosthesis: biomechanics and preliminary clinical results. In: Gunzburg R, Mayer HM, Szpalski M, Aebi M, editors. Arthroplasty of the spine. Berlin–Heidelberg–New York: Springer; 2004. p. 53–8. 42. Le Huec JC, Mathews H, Basso Y, Aunoble S, Hoste D, Bley B, et al. Clinical results of Maverick lumbar total disc replacement; two-year prospective follow-up. Orthop Clin North Am 2005;36:315–22. 43. Miz G, Theophilos CS. Flexicore metal-on-metal lumbar disc arthroplasty: one-to two-year follow up. SAS proceedings, SAS 6 global symposium on motion preservation technology, Montreal, Canada, May 9–13, 2006. p. 17–8. 44. Steib JP, Aubourg L, Beaurain J, Delecrin J, Allain J, Chataigner H, Bogorin I, Amail M, Dufour T, Stecken J. New lumbar disc prosthesis with mobile nucleus: rationale and report of a multicenter one year follow-up. SAS proceedings, SAS 6 global symposium on motion preservation technology, Montreal Canada, May 9–13 2006. p. 25–26. 45. Ha ¨hnle UR, De Villiers M. Kineflex (Centurion) lumbar disc prosthesis: two-year results. SAS proceedings, SAS 6 global symposium on motion preservation technology, Montreal Canada, May 9–13 2006. p. 24–25. 46. German JW, Foley KT. Disc arthroplasty in the management of the painful lumbar motion segment. Spine 2005;30(16S): S60–7. 47. Zigler JE, Burd TA, Vialle EN, Sachs BL, Rashbaum RF, Ohnmeiss DD. Lumbar spine arthroplasty: early results using the ProDisc II: a prospective randomized trial of arthroplasty versus fusion. J Spinal Disord Tech 2003;16:352–61. 48. Siepe CJ, Mayer HM, Wiechert K, Korge A. Clinical results of total lumbar disc replacement with ProDisc II: three-year results for different indications. Spine 2006;31:1923–32. 49. Bertagnoli R, Yue JJ, Nanieva R, Fenk-Mayer A, Husted DS, Shah RV, et al. Lumbar total disc arthroplasty in patients older than 60 years of age: a prospective study of the Prodisc prosthesis with 2-year minimum follow-up period. J Neurosurg Spine 2006;4:85–90. 50. David T. Lumbar disc prosthesis: surgical technique, indications and clinical results in 22 patients with a minimum of 12 months follow-up. Eur Spine J 1993;1:254–9.
23 51. Bertagnoli R, Kumar S. Indications for full prosthetic disc arthroplasty: a correlation of clinical outcome against a variety of indications. Eur Spine J 2002;11(Suppl. 2):S131–6. 52. Bertagnoli R, Yue JJ, Shah RV, Nanieva R, Pfeiffer F, Fenk-Mayer A, et al. The treatment of disabling multilevel lumbar discogenic low back pain with total disc arthroplasty utilizing the ProDisc prosthesis: a prospective study with 2-year minimum follow-up. Spine 2005;30:2192–9. 53. Tropiano P, Huang RC, Girardi FP, Marnay T. Lumbar disc replacement: preliminary results with ProDisc II after a minimum follow-up period of 1 year. J Spinal Disord Tech 2003; 16:362–8. 54. Delamarter RB, Fribourg DM, Kanim LE, Bae H. ProDisc artificial total lumbar disc replacement: introduction and early results from the United States clinical trial. Spine 2003;28:S167–75. 55. McAfee PC, Fedder IL, Saiedy S, Shucosky EM, Cunningham BW. SB Charite disc replacement: report of 60 prospective randomized cases in a US center. J Spinal Disord Tech 2003;16: 424–33. 56. Denoziere G, Ku DN. Biomechanical comparison between fusion of two vertebrae and implantation of an artificial intervertebral disc. J Biomech 2006;39:766–75. 57. Dooris AP, Goel VK, Grosland NM, Gilbertson LG, Wilder DG. Load-sharing between anterior and posterior elements in a lumbar motion segment implanted with an artificial disc. Spine 2001;26:E122–9. 58. McAfee PC, Cunningham BW, Hayes V, Sidiqi F, Dabbah M, Sefter JC, et al. Biomechanical analysis of rotational motions after disc arthroplasty: implications for patients with adult deformities. Spine 2006;31:S152–60. 59. Sariali el H, Lemaire JP, Pascal-Mousselard H, Carrier H, Skalli W. In vivo study of the kinematics in axial rotation of the lumbar spine after total intervertebral disc replacement: long-term results: a 10–14 years follow up evaluation. Eur Spine J 2006;15:1501–10. 60. Siepe CJ, Mayer HM, Heinz-Leisenheimer M, Korge A. Total lumbar disc replacement: different results for different levels. Spine, 2006, accepted for publication. 61. Huang RC, Lim MR, Girardi FP, Cammisa Jr FP. The prevalence of contraindications to total disc replacement in a cohort of lumbar surgical patients. Spine 2004;29:2538–41. 62. Le Huec JC, Basso Y, Aunoble S, Friesem T, Bruno MB. Influence of facet and posterior muscle degeneration on clinical results of lumbar total disc replacement: two-year follow-up. J Spinal Disord Tech 2005;18:219–23. 63. Siepe CJ, Wiechert K, Khattab MF, Korge A, Mayer HM. Total lumbar disc replacement in athletes: clinical results, return to sport and athletic performance. Eur Spine J, 2007, in press. 64. Griffith SL, Shelokov AP, Buttner-Janz K, LeMaire JP, Zeegers WS. A multicenter retrospective study of the clinical results of the LINK SB Charite intervertebral prosthesis. The initial European experience. Spine 1994;19:1842–9. 65. McAfee PC, Geisler FH, Saiedy SS, Moore SV, Regan JJ, Guyer RD, et al. Revisability of the CHARITE artificial disc replacement: analysis of 688 patients enrolled in the US IDE study of the CHARITE Artificial Disc. Spine 2006;31:1217–26. 66. Nguyen HV, Akbarnia BA, van Dam BE, Raiszadeh K, Bagheri R, Canale S, et al. Anterior exposure of the spine for removal of lumbar interbody devices and implants. Spine 2006;31: 2449–53. 67. Brau SA. Mini-open approach to the spine for anterior lumbar interbody fusion: description of the procedure, results and complications. Spine J 2002;2:216–23. 68. Patel VV, Andrews C, Pradhan BB, Bae HW, Kanim LE, Kropf MA, et al. Computed tomography assessment of the accuracy of in vivo placement of artificial discs in the lumbar spine including radiographic and clinical consequences. Spine 2006;31:948–53.
ARTICLE IN PRESS 24 69. Smith HE, Vaccaro AR, Yuan PS, Papadopoulos S, Sasso R. The use of computerized image guidance in lumbar disk arthroplasty. J Spinal Disord Tech 2006;19:22–7. 70. McAfee PC, Cunningham B, Holsapple G, Adams K, Blumenthal S, Guyer RD, et al. A prospective, randomized, multicenter
H.M. Mayer, C. Siepe Food and Drug Administration investigational device exemption study of lumbar total disc replacement with the CHARITE artificial disc versus lumbar fusion: part II: evaluation of radiographic outcomes and correlation of surgical technique accuracy with clinical outcomes. Spine 2005;30:1576–83.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 25–39
Available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/cuor
MINI-SYMPOSIUM: FRONTIERS IN SPINE SURGERY
(iv) Lumbar stabilisation techniques Steven Lau, Khai S. Lam Department of Trauma and Orthopaedic Surgery, Guy’s and St. Thomas’ Hospital, St. Thomas Street, London SE1 9RT, UK
KEYWORDS Lumbar stabilisation techniques; Lumbar instability; Lumbar spine fusion; Dynamic stabilisation; Lumbar total disc replacement; Nucleus pulposus replacement
Summary Chronic lower back pain due to degeneration of the lumbar spine, commonly referred to as mechanical back pain, is thought to be due to instability of the lumbar motion segment that is secondary to disc degeneration and facet arthrosis. This article concentrates on the various types of stabilisation techniques used to treat such disorders. Traditionally, fusion has been the mainstay of treatment. Many techniques have been developed to maximise fusion rates but a corresponding improvement in clinical outcomes has not been seen. Motion sparing techniques such as dynamic stabilisation, total disc replacement and nucleus pulposus replacement, are alternative forms of treatment. Such new technologies are predicted to have a big impact on the treatment of lumbar instability but as yet require more development and clinical trials. Crown Copyright & 2007 Published by Elsevier Ltd. All rights reserved.
Introduction Chronic lower back pain due to degeneration of the lumbar spine, commonly referred to as mechanical back pain, is thought to be due to instability of the lumbar motion segment that is secondary to disc degeneration and facet arthrosis. The exact definition of lumbar instability is open to much debate and its relation to back pain is poorly understood. Panjabi described the concept of the neutral zone as the range of intervertebral movement within which spinal motion occurs with minimal internal resistance. Instability results from the failure to maintain this neutral zone within normal physiological limits, resulting in pain and disability.1 Most attempts to define radiological instability appear to accept vertebral translation of at least 3.0–3.5 mm or Corresponding author.
E-mail address:
[email protected].
intervertebral angulation greater than 101 on dynamic radiographs with resultant pain or neurological symptoms.2,3 The hypotheses put forward to link instability to pain include excessive translation leading to disc degeneration4 and reduced shear–flexion ratio at the degenerate disc.5 The term ‘‘instability’’ has been used to describe a nonspecific mechanical failure of the spine causing abnormal movement at the joint surface and altered load transmission, resulting in pain. This article will concentrate on the various types of common stabilisation techniques used to treat lower back disorders secondary to degenerative disc disease. Where appropriate a brief history relating to early techniques will be reviewed and this is followed by a description of the current modern fusion techniques used. A brief review of the more novel and controversial motion preserving techniques such as disc arthroplasty, dynamic stabilisation, and nucleus replacement will be discussed. Lumbar stabilisation has traditionally been achieved by fusion, with the aim to prevent abnormal movement in the painful motion segment such that direct load transmission
0268-0890/$ - see front matter Crown Copyright & 2007 Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2006.01.006
ARTICLE IN PRESS 26
S. Lau, K.S. Lam
can occur from ‘bone to bone’ across the fused segment. Spinal fusion was first described in the treatment of Pott’s disease.6,7 Its use was extended for the treatment of other spinal conditions including lower back pain.8 Since then, many techniques have evolved, including posterior, posterolateral, posterior interbody, anterior interbody and circumferential fusion. Fusion aims to eliminate segmental instability, maintain sagittal balance and prevent further degeneration at the level in question. Therefore, pain relief is achieved by eradicating motion across an unstable or degenerate segment.
Fusion techniques Lumbar fusion surgery has improved dramatically over the last two decades. Newer fusion surgery techniques allow for improved fusion rates, shorter hospital stays, and a more active and rapid recovery period. Additionally, better diagnostic tools and improved understanding of indications for a spine fusion are improving outcomes. Lumbar spinal fusion techniques can be divided into posterior, anterior or circumferential fusions.
Figure 1 Antero-posterior plain film X-ray showing a healthy non-instrumented sacral alar-transverse fusion mass.
Posterior fusion techniques
spondylolisthesis, degenerative spondylolisthesis associated with disc space narrowing and patients who will comply with external bracing should they require it.14,17,18 Instrumentation is indicated for other scenarios such as spinal trauma as it provides the initial stability required for fusion to occur.
Uninstrumented posterior fusion There are three specific techniques for uninstrumented fusion via the posterior approach: (i) posterior fusion, (ii) facet joint fusion and (iii) intertransverse process fusion (ITF). Posterior fusion involves placing bone graft onto the decorticated laminae and spinous processes. As the facets joints need not be exposed, there is less soft tissue disruption than for other techniques, and thus posterior fusion has the theoretical advantage of lower infection rates. This technique is not possible if spinal decompression is required. Facet joint fusion requires thorough curettage of the facet joint surfaces followed by insertion of bone graft. Less bone graft is required for this procedure as it bridges the shortest distance between the segments to be fused. Because of the poor early results with uninstrumented posterior onlay and facet joint fusions, ITF became the standard fusion technique prior to the advent of spinal instrumentation (Fig. 1). ITF requires exposure of the tips of the transverse processes and places bone graft across the decorticated transverse processes.9 Exposure can be via a midline approach, which involves extensive muscle stripping as far laterally as the tips of the transverse processes or the muscle splitting Wiltse approach, between the longissimus and multifidus muscles, which has the advantage of less muscle trauma.10 There is still much debate as to the superiority of uninstrumented versus instrumented fusion. Several studies exist, citing no significant differences in clinical or radiological outcomes between instrumented and non-instrumented posterior fusions for the treatment of degenerative disc disease causing lower back pain.11–14 Yet in contrast, other studies have suggested that instrumented fusion had a higher fusion rate and improved clinical outcome when compared to uninstrumented techniques.15,16 Uninstrumented fusion is suitable for patients with sufficient intrinsic stability to allow fusion to occur, those with isthmic
Instrumented posterior fusion Pedicle screw fixation was first used in the treatment of spondylolisthesis19 and its use soon extended to the treatment of various degenerative diseases of the lumbar spine. Pedicle screw fixation with adjoining rods provides initial immobilisation, thus allowing a superior environment for fusion to occur, permits correction of the deformity and aids rehabilitation because immediate post-operative mobilisation is possible. However, disadvantages include a higher rate of vascular and neurological complications, increased soft tissue trauma that is related to screw insertion leading to increased infection rates, and the presence of stainless-steel metalwork which may adversely affect subsequent investigations such as MRI scanning.14 Good surgical experience, a thorough knowledge of spinal anatomy and improved imaging and navigational techniques should help reduce such complications. Instrumented facet joint fusion is an alternative technique, which has been shown to provide similar biomechanical properties to pedicle screw fixation.20 Two techniques exist. The transfacet technique, first described by Boucher in 1959,21 involves inserting a traversing screw across the facet joint from medial to lateral (Fig. 2). The translaminar facet technique was first described by Magerl in 1984.22 This method requires insertion of a screw from a starting point at the base of the spinous process contralateral to the facet to be fused (Figs. 3 and 11). The screw crosses the entire length of the lamina and the facet joint. This latter technique, although technically more challenging and associated with a greater risk of complications,23 allows increased screw purchase and is biomechanically superior to the Boucher technique because the screws cross the facet joint perpendicularly. Compared to pedicle screw fixation, facet screws require less soft tissue dissection, allow more space for bone graft,
ARTICLE IN PRESS Lumbar stabilisation techniques
27
Figure 2 Antero-posterior and lateral plain film X-rays showing Boucher screws inserted at L5/S1.
treatment of discography-proven discogenic pain, showed a 39% good outcome versus 48% poor results.29 Several studies demonstrate superior outcomes with circumferential fusion for the treatment of degenerative disc disease.30,31 Although there is mounting evidence showing the superiority of interbody fusion techniques for the treatment of degenerative disc disease, posterior instrumented fusion is still widely used as it is easier technically, takes less operating time, has lower complication rates and does not destabilise the anterior spinal column.32
Figure 3 Antero-posterior plain film X-rays showing L5/S1 translaminar facet screws fusion.
have a lower neurological complication rate and cost a great deal less.23 Several studies have reported excellent clinical results and fusion rates from 91–95%.23–25 Facet joint screws are indicated for one to two level lumbar degenerative disc disease, where the facet joints are intact, closely apposed, and there is an associated collapsed disc segment which results in reduced biomechanical loading anteriorly. It has been demonstrated that both pedicle and facet screws have similar biomechanical properties.26 Many studies have shown that posterior arthrodesis benefits patients with degenerative or isthmic spondylolisthesis, or those patients with instability due to extensive decompressions.11,13,14,17,18 It is thought to relieve pain due to degenerative disc disease by liminating movement at the painful motion segment. While clinical outcomes have been shown to be comparable to that of interbody procedures for the treatment of degenerative disc disease,27 there is great debate as to whether an isolated posterior arthodesis is as effective as an interbody or circumferential fusion. An isolated posterior fusion may not totally eliminate motion through the painful segment, nor does it remove the disc, which may be a source of inflammatory pain.28 One study, investigating instrumented posterolateral fusion in the
Posterior lumbar interbody fusion (PLIF) PLIF, referring to the placement of implants into the disc space via a posterior approach, was described and popularised by Cloward in 1953 with the aim of obtaining simultaneous nerve decompression and fusion.33 However, it did not gain interest until the introduction of spinal instrumentation and interbody devices. The steps involve laminectomy, discectomy, restoration of disc height space, decortication of the vertebral endplates and insertion of an intervertebral graft. This can be the patient’s own bone (autograft) or an interbody spacer packed with bone (metal or polyetheretherketone (PEEK)), inserted into either side of the cleared disc space. Instrumentation in the form of pedicle screws is then used to provide posterior stability (Fig. 4). The advantages of PLIF include restoration of disc height space, improved maintenance of sagittal balance, allow decompression of the nerve roots and the provision of a superior environment for fusion to occur.34 The risks associated with nerve root retraction make other interbody fusion techniques more appealing. Transforaminal lumbar interbody fusion (TLIF) places the interbody device through a unilateral posterior approach without violating the spinal canal. The unilateral removal of the pars interarticularis and facet complex allows posterolateral access to the disc space. This method reduces the amount of neural retraction and preserves the contralateral facet complex. As with PLIF, posterior instrumentation is used to stabilise the spine
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Figure 4 Antero-posterior and lateral plain film radiographs of PLIF using PEEK cages with pedicle screws and rods. The PEEK cages are visualised as radiolucent markers within the intervertebral space.
Table 1
Indications for PLIF and TLIF.
Indications for PLIF and TLIF
Degenerative disc disease with discogenic pain Post-discectomy collapse with foraminal radiculopathy
Degenerative spondylolisthesis Pseudarthosis Lumbar deformity (when fusion is required beneath the long construct to prevent late pseudarthosis resulting in distal screw pullout)
segment immediately following the insertion of an oblique interbody device. Indications for PLIF and TLIF are outlined in Table 1.
Anterior lumbar interbody fusion (ALIF) Although posterior techniques are more popular, fusion can also be achieved by anterior methods, of which the most frequently used is the ALIF. This was first described by Capener35 in 1932 for the treatment of spondylolisthesis. Interbody fusion combats the disadvantages of uninstrumented posterior fusion, which primarily include the significant rate of fusion failure, possible canal stenosis from the posterior fusion mass and persistent movement across the disc at the fused level36 as well as continued pain emanating from the disc.28 The anterior lumbar spine may be approached through an open transperitoneal or retroperitoneal approach, and via a mini-open or laparoscopic technique. A mini-open exposure minimises the size of the wound and with the aid of a 3601 self-retaining frame-based retractors, e.g. SynFrameTM (Synthes-Stratec, Switzerland), allows a complete discectomy to be performed with direct
Figure 5 Photograph showing the SynFrameTM a frame-based retractor system allowing smaller incisions compared to traditional retractors. This example shows the use of the SynFrame to perform a minimal access lateral approach to the thoracolumbar spine.
placement of interbody devices via a direct anterior approach (Fig. 5). The senior author advocates the use of intra-operative fluoroscopy to ensure safe positioning of the interbody device. Various interbody devices exist for performing an ALIF. Interbody implants may be (autograft or allograft), non-bone materials such as acrylic, or a combination of both. Bone, in the form of tricortical iliac crest or fibula autograft can be harvested and inserted between the endplates. This has the disadvantage of patient donor site morbidity and unreliable bone quality. Allograft is a popular alternative as it eliminates morbidity associated with donor site complications. Pre-contoured, pre-sized femoral ring allograft (FRA) implants and PLIF or TLIF bone spacers are available for use as interbody fusion devices. The FRA implants that are packed with autograft or demineralised bone matrix (DBM) are ideally placed via the anterior approach with
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29
Figure 6 Top: Plain film radiographs of ALIF performed with femoral ring allograft packed with BMP/collagen sponge and supplemented anteriorly using a locking plate or anterior tension band plate (ATBTMSynthes-Stratec, Switzerland). Bottom: CT scan taken at 3 months confirming solid interbody fusion.
instrumentation in the form of a plate or a screw and washer to prevent dislodgement (Figs. 6–8). The pros and cons of different graft types are summarised in Table 2. Metal or PEEK interbody cages packed with harvested bone autograft are also widely used but have the disadvantage of subsidence and difficulty to radiographically assess bone incorporation. Titanium cages are MRI-compatible and are closer to the modulus of bone than stainless steel. Carbon fibre cages have elastic properties closer to those of cortico-cancellous bone compared to metallic cages, and also have the advantage of being radiolucent. However, carbon cages still present concerns associated with foreign bodies. Previous use of carbon fibre in the body, such as cruciate ligament reconstructions, has caused chronic destructive inflamma-
tory reactions and long term follow up of such devices is necessary. Stand-alone threaded cages (Fig. 8), such as the BAK cage (Zimmer), are now no longer favoured in Europe, since the advent of biomechanical papers revealing that stand-alone cages are unstable in extension.37 This instability resulted in pseudarthrosis with poor clinical outcome, and therefore required posterior stabilisation. First generation stand-alone titanium-threaded interbody devices have now been replaced with PEEK or metal cages with locking screws (e.g. Hartshill Horseshoe and SynFixTM [Synthes-Stratec, Switzerland]). More recently newer generation anterior locking screw/plate devices, e.g. ATBTM (Synthes-Stratec, Switzerland) or Pyramid plate (Medtronic Inc., Minneapolis, MN) have gained increased popularity with surgeons trained in the anterior approach, since these devices can be easily
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Figure 7 Photographs of demineralised bone matrix, available in different forms (top left). Femoral ring allograft or FRA (bottom left) and FRA packed with autograft prior to insertion (top right).
of the devices. These devices have been to shown to be biomechanically comparable to circumferential fusion with pedicle screws.
Circumferential fusion
Figure 8 Photographs of various intervertebral cage devices for use in PLIF or ALIF or circumferential fusion.
inserted via a minimal access anterior retroperitoneal route thus obviating posterior surgery and the need to damage the posterior structures (Fig. 6). The locking plates help neutralise the segment following insertion of a load sharing interbody device, thus optimising the occurrence of an interbody fusion. Stand-alone anterior devices are generally indicated for use in end-stage degenerative disc disease, where the facet joints are very rigid, and thus allows the segment to be locked into extension following the insertion
Circumferential fusion, referring to combined interbody and posterior fusion, has resulted in high fusion rates, with some series reporting 100%.38–40 The traditional method of anterior–posterior fusion involves a separate anterior approach for interbody device placement followed by posterior instrumentation (Fig. 9), such as pedicle screws or translaminar screws. The two procedures can be performed under the same anaesthetic or staged over a planned period of time. To that end, the single approach PLIF and TLIF procedures, which are considered by some authors to be 2701 fusions, have gained popularity against a circumferential fusion. Technically, 3601 fusions allow larger single body grafts or cages to be inserted compared to posterior techniques. In addition, device insertion does not require neural retraction and avoids the excessive bone resection that PLIF and TLIF procedures require. However, as 3601 fusions consist of two procedures instead of one, operating times are longer with higher blood loss, cost and hospital stay. Interestingly, fusion rates have been shown to be comparable between the different procedures,40 which questions the justification of circumferential 3601 fusions. New minimal access techniques for ALIF combined with percutaneous pedicle screws, resulting in less invasive surgery, further fuel this debate.
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Table 2
31
Summary of advantages and disadvantages of different graft materials.
Graft type Autograft—bone taken from one anatomical site and transferred to another site in the same individual (no immune reaction) 1. Autograft—cortical
Advantage
Allows immediate load sharing Provides structural support
Disadvantage
Increased donor site morbidity Lower surface area for bone to form Non-viable bone remains, increasing risk of infection
Faster bony incorporation Graft hypertrophies with
Technically demanding with increased
compressive load Less necrotic bone
Increased donor site morbidity
3. Autograft—cancellous
Lower donor site morbidity Good osteoconductivity
Low compressive strength
Allograft—bone transferred from one member of a species to another member (e.g. FRA) (Fig. 7)
no donor site morbidity available in multiple forms osteoconductive, weakly
Risk of infection (o1/106 risk HIV
2. Autograft—vascularised cortical
osteoinductive
operating time
infection)
Immune response (degree related to treatment and storage)
Cost Demineralized bone matrix—processed allograft bone (decalcified cortical bone) (Fig. 7)
Low immunogenicity (due to
Synthetic implants—ceramics (sintered [porous hydroxyapatite or tricalcium phosphate]/replamiform [sea coral])
Not immunogenic No risk of transmitting infectious
Lower fusion rates compared to
disease No donor site morbidity
Difficult to assess healing with X-ray Potential non-immune inflammatory
extensive processing) Available in multiple forms
Lacks structural support Cost
autograft/allograft when used alone
response (eg seroma)
Poor load sharing properties
Figure 9 Plain film radiographs taken 12 months post-circumferential fusion using femoral ring allograft, anterior tension band plate and pedicle screws.
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S. Lau, K.S. Lam
Figure 10 Illustration of Sextant system (left). Plain film radiographs of percutaneous pedicle screws as part of a circumferential fusion. Note the curved rods which allow them to be swung into place to engage with the screw heads. The femoral ring allograft packed with autograft from the L4 vertebral body has been used for the interbody fusion and is held in place with a cancellous screw and washer.
Minimally invasive/access spinal techniques Minimal access spinal procedures have been developed with the aim of reducing approach-related morbidity while obtaining the same clinical outcomes of traditional open procedures. Essential equipment includes an image guidance device, an access portal and modified instruments. The two main methods of guidance are fluoroscopy and frameless spinal stereotaxy. The advantages of fluoroscopy are that it is widely available, simple to use and provides immediate imaging feedback, which may be in multiple planes, while its main disadvantage is radiation exposure. Frameless spinal stereotaxy limits radiation exposure but requires a separate incision for placement of a dynamic reference array.41 The two main techniques for percutaneous spinal fixation are pedicle screws and facet screws. Both have been developed to compliment ALIF procedures in order to perform circumferential fusions with minimal morbidity to the patient. Currently, the most widely used percutaneous pedicle screw system is the Sextant system (Medtronic Inc., Minneapolis, MN). Cannulated, polyaxial screws are placed over guide wires and inserted under fluoroscopic guidance. Screw extenders and rod inserters are attached. A separate incision is made for rod insertion which, after measuring for the right length, is swung into position to engage with the screw heads (Fig. 10). The feasibility of percutaneous facet screw insertion (Fig. 11) was first mentioned by Grob and Humke42 in 1998, but their report contained insufficient details to reproduce the technique.43 Shim et al.43 described a technique for inserting translaminar facet screws under fluoroscopic guidance, without the use of any device. Cannulated lag screws were inserted over carefully placed K-wires. This required careful planning and the surgeon to have good three-dimensional spatial awareness. Minimally invasive techniques are also being practised for ITF, PLIF and TLIF. Tubular retractors (e.g. METRxTM System, Medtronic Inc., Minneapolis, MN) are used for access with
Figure 11
Percutaneous facet screw insertion.
visualisation via microscope, endoscope or loupes. The blunting of sharp instruments allows the surgeon to slip past the nerve root while minimising soft tissue retraction. Such surgery is still evolving; at present there are few outcome studies, and none comparing the outcomes of open versus minimal access techniques, particular in the long term.
Biologics In 1965, Dr. Marshall Urist discovered that bone extracellular matrix is able to induce new bone formation. This osteoinductive agent was later termed bone morphogenic protein (BMP). Over the last 40 years, there have been many advances towards using osteoinductive agents to promote
ARTICLE IN PRESS Lumbar stabilisation techniques spinal fusion. Currently, recombinant human bone morphogenic protein-2 (rhBMP-2 or InductosTM [Medtronic Inc., Minneapolis, MN]) carried on a Type 1 collagen sponge (Fig. 6) is FDA-approved for use in conjunction with a tapered intervertebral cage (LT-cage, Medtronic Inc., Minneapolis, MN) for the treatment of degenerative disc disease. Recombinant human osteogenic protein-1 (rhOP-1), commercially available from Stryker Biotech, has been approved for revision posterolateral lumbar fusions. The superior efficacy of osteoinductive agents, as compared to autologous bone graft, has recently been shown in a few randomised controlled studies. There is no doubt that these osteoinductive agents will have a significant role to play in the future of lumbar fusion surgery. However, the exact role and long-term efficacy are yet to be defined by further case series and randomised clinical trials. Furthermore, the high costs and uncertainty of reimbursement by insurance companies for these biologic agents will affect their use.44
Motion sparing techniques Despite all the advances in fusion techniques over the years, with fusion rates approaching 100%, there has not been a corresponding improvement in clinical outcomes.45,46 Suggested explanations include unrecognised pseudarthrosis, abnormal load transmission through the metal–bone interface with cage fusions and abnormal restoration of sagittal balance. There is also evidence that fusion may increase the biomechanical stresses on adjacent segments47 leading to premature degeneration. This line of thought has led to the
Table 3
33 development of alternative forms of treatment for lumbar instability where motion is preserved.
Dynamic stabilisation Dynamic stabilisation (also known as soft stabilisation) devices attempt to address the matters outlined above by placing the posterior structures under tension, thus increasing lordosis in that area. This aims to shift load transmission favourably and alter movement so as to avoid painful positions with the aim of alleviating both back and leg pain. Many systems have been developed and can be classified into four categories48 (Table 3). A few of the more popular devices are described, but of note, there is yet to be a prospective randomised controlled trial for any dynamic stabilising device. The Graf ligament is a non-elastic braided polyester ligament loop, which is placed around pedicle screws under tension (Fig. 12a). This transfers the load from the anterior to the posterior part of the disc. Several studies have shown clinical outcome comparable to that of fusion49,50; however, there have been documented complications of narrowing of the lateral recess causing undesirable post-operative radiculopathy and late failure due to accelerated posterior disc degeneration. The Dynesys system consists of polycarbonurethane spacers, placed between titanium alloy pedicle screws, which resist compressive forces. Polyester cords, which are connected to the screws, run within the spacer and resist tensile forces. Results have been reported for 83 patients, with the system being concluded by the authors as a safe
Outlining the main categories of dynamic stabilisation devices.
Category
Device name
Free-floating interspinous distraction device
Wallis implant (Abbott) X-stop (St. Francis Medical Technologies Inc.) DIAM—Dynamic Intervertebral Assisted Motion (Medtronic Inc., Minneapolis, MN) (Fig. 12b) Graf ligament (Surgicraft) (Fig. 12a) Dynesys (Zimmer) TOPS-on-Fusion SystemTM (Impliant Inc.)
Interspinous ligaments looped around spinous processes Ligaments placed around pedicle screws Semi-rigid metallic devices placed across pedicle screws
Figure 12 (a) (left)—Image of the global (graf ligament) placed on a spine model; (b) (right)—image of the dynamic intervertebralassisted motion (DIAM) placed on a spine model.
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S. Lau, K.S. Lam
Figure 13 Photograph of X-stop device with plain film lateral X-rays pre (left) and post (right) insertion. Post-operative X-rays clearly show enlargement of the exit foramina.
and effective alternative in the treatment of unstable lumbar conditions.51 However, of the 83 patients, 7 suffered from screw loosening and 12 required revision surgery for same or adjacent segment disease.51 The Wallis implant is a hybrid of an interspinous distraction device and an interspinous ligament which is made of PEEK. It is the second generation of a titanium implant that was held between the spinous processes by Dacron tape, originally described by Senegas et al.52 in 1988. In clinical trials, the original implant was shown to be effective against low-back pain due to degenerative instability and free of serious complications. A randomised clinical trial of the Wallis implant is currently underway. The X-stop device (St. Francis Medical Technologies Inc) (Fig. 13) is a titanium interspinous distraction device, which has completed FDA clinical trials and recently received FDA approval. Results of the multi-center trial conducted in the US indicated that among patients with pain arising from neurogenic claudication secondary to spinal stenosis, the X-STOP provided significantly greater pain relief than the epidural steroid injections.53 A newer PEEK version has been launched recently.
Spinal arthroplasty The aim of any spinal arthroplasty device is to maintain disc height space, allow motion at the affected segment and provide stability. It avoids the problems that fusion procedures encounter with bone graft harvest sites and pseudarthrosis. The posterior structures are left intact as the disc replacements are inserted via an anterior approach, and by maintaining motion at the involved segment, it is thought to reduce accelerated adjacent disc degeneration.54 Two broad groups exist: total disc replacements (TDRs) and partial nucleus pulposus replacements (NPRs). Artifical disc replacement One of the first reports of attempted disc arthroplasty was by Fernstrom who implanted stainless steel balls into the
disc space. Results were published in 1966 for 191 implants in 125 patients. During the 4–7-year follow-up period, there was an 88% subsidence rate. Many years of research into spinal degeneration, biomechanics and biomaterials followed before the development of intervertebral disc prostheses.55 TDR devices are implanted via an anterior retroperitoneal approach, with 3601 retractors allowing mini incisions and simple access to the L5/S1 disc. Gaining access to the discs above this level requires mobilisation of the major retroperitoneal blood vessels, and even in the hands of experienced surgeons, there is a reported 2.8% vascular complication rate.56 The clinical outcome of TDR is highly dependent on patient selection. The inclusion and exclusion criteria used for the FDA controlled, randomised trials for TDR are shown in Table 4. One prospective study reported better outcomes in patients with degenerative disc disease in association with disc herniation and patients under the age of 40.57 Bisegmental disc replacements had a significantly higher rate of complications and inferior outcomes.57 Diagnostic tools used to ascertain suitability for TDR include plain film radiographs, MRI and discography. Facet joint blocks, sacroiliac joint injection and nerve root blocks may also help exclude non-discogenic sources of pain. At present, there are five implants used in the lumbar spine, of which only two, the SB Charite III (Depuy, Johnson and Johnson) and the ProDisc-II (Synthes-Stratec, Switzerland) have been approved in the US by the FDA. The SB Charite III (Fig. 14) consists of two metal endplates made of cobalt–chromium–molybdenum with the bone interface aspect covered with porous plasma-sprayed titanium, coated with calcium phosphate to promote bone on-growth. A free-floating biconvex sliding core made from ultra-high molecular weight polyethylene is inserted and held between the two concave endplates. Over 10,000 implants have been inserted worldwide and a randomised controlled trial for patients with single level L4/5 or L5/S1 degenerative disc disease showed significant improvement in visual pain analogue scores (VPAS) and Oswestry Disability Index (ODI)
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Table 4
35
Showing details of the five main total disc replacement devices.
Device
Materials
No. of components
Articulation
Status
SB Charite-III
CoCrMo on UHMWPE
3
Commercially available
Prodisc-II
CoCrMo on UHMWPE
3
Maverick
CoCrMo metal-onmetal CoCrMo metal-onmetal CoCrMo on UHMWPE
2
Mobile bearing (unconstrained) Ball and socket (semiconstrained) Ball and socket (semiconstrainec) Ball and socket (semiconstrianed) Mobile bearing (semiconstrained)
Flexi-core Mobidisc
Figure 14 ment.
2 3
Photograph of the SB Charite III total disc replace-
scores. Overall success rates at 2 years were 63% for TDR compared to 53% for fusion.58,59 The ProDisc-L (Figs. 15 and 16) and the ProDisc-II, its second-generation counterpart, are also three component devices made from the same materials as the SB Charite III. The main difference is that the UHMWP insert is locked to the lower endplate. Both endplates also have a central keel for immediate stability upon insertion. Success rates between 80% and 98% have been reported in uncontrolled trials.60–63 The FDA-controlled randomised study comparing ProDisc-II with circumferential fusion reported a statistically significant shorter hospital stay, superior ODI success and higher satisfaction rates in favour of the disc replacement.64 Major, but uncommon, complications of total disc arthroplasty include vertebral body fracture, subsidence, malpositioning and radicular pain. Other available devices include the metal-on-metal Maverick device (Medtronic, Minneapolis, MN), the Flexicore disc (Stryker Corp, Kalamazoo, Michigan), and the Mobidisc (LDR Medical, Troyes, France) (see Table 4). There is no doubt that TDR is a new and developing frontier in spinal surgery. Its precise role in the treatment of lumbar instability has yet to be fully defined. More long-
Figure 15
Commercially available Under trial Under trial Under trial
Photograph of ProDisc-L.
term evidence-based data are required to determine its safety, superiority, longevity and ability to prevent adjacent level degeneration as compared to conventional spinal fusion.
Nucleus pulposus replacement Another motion preserving technique is that of NPR, which aims to reconstruct the nucleus pulposus while preserving the biomechanics of the annulus fibrosus and cartilaginous endplates. NPR devices are designed for use in cases in which there is significant nucleus pulposus degeneration but where the annulus is still healthy. Indications presently include lumbar discogenic back pain unresponsive to active conservative treatment for a minimum of 6 months, spondylolisthesis of less than grade 1 at the symptomatic segment, disc height loss of less than 50% (disc height of 45 mm on MRI) and only early stage degenerative changes with absent Schmorl’s nodes.65,66 Presently, there are two categories of NPR devices: Intradiscal implants, which are biomechanically similar to native nucleus pulposus tissue, and in situ curable polymers, which consist of liquid-based compounds that harden after implantation. The curable polymers have the advantage of
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S. Lau, K.S. Lam
Figure 16
Figure 17
AP and lateral plain film X-rays of Prodisc-L inserted into L5/S1.
Photograph showing PDN SOLOs device (left) and Newcleus device (right).
Figure 18
MRI scans of PDN nucleus pulposus replacement in situ at L5/S1 level.
allowing minimally invasive implantation techniques via a small annulotomy and hence a lower risk of extrusion. Clinical results are available only for a few intradiscal implants. By far, the most studied device is the prosthetic disc nucleus (Raymedica Inc., Bloomington, MN) (Figs. 17 and 18), with over 400 patients treated between 1996 and 2002. The device consists of a hydrogel pellet encased in a polyethylene jacket. The hydrogel can absorb up to 80% of its weight in water and swells in size to restore and maintain
disc height. The inelastic jacket limits height gain so as to prevent damage to the vertebral end plates. Two small pellets are commonly inserted, via a posterior approach, although a single larger device has also been used more recently to lower the risk of extrusion. Initial success rates for the PDN were reported at 83%, but fell to 62%, with an increased migration rate, after modification. Re-modification improved the clinical outcome to 79%. This increased to 91% (in 51 patients) after changes in protocol and surgical
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Table 5
37
Showing details of selected nucleus pulposus replacement devices.
Device
Implant type
Biomaterial
Status
Prosthetic disc nucleus (Raymedica)
Intradiscal
Neudisc (Replication Medical Inc.)
Intradiscal
Newcleus (Zimmer, Spine) (Fig. 17)
Intradiscal
Commercially available outside US and Canada Clinical trials planned autumn 2006 Implanted into 10 patients
DASCOR disc arthroplasty device
In situ curing polymer In situ curing polymer
Hydrogel pellet with polyethylene jacket Hydrolyzed polyacrylonitrile polymer reinforced by Dacron mesh Polycarbonate urethane coiled into spiral Injectable polyurethane into expandable balloon Protein hydrogel
BioDisc
instrumentation.61 The main complications are those of device migration, a factor which led to the changes in design and protocol, and end plate fracture with subsidence and extrusion. Other devices are at different preclinical and clinical stages. Some are outlined in Table 5. Most curable polymers are toxic when absorbed in high doses secondary to leaching of the chemical before it sets. Leaching is dependent upon the polymerisation time and the degree of annulus disruption. Two curable polymers are being developed: the DASCOR disc arthroplasty device (Disc Dynamics Inc., Eden Prenrie, MN) and the BioDisc (Cryolife, Kennesaw, GA). The DASCOR disc arthroplasty device is an injectable polyurethane, which is injected into a polyurethane balloon and polymerises within minutes. The BioDisc is a protein hydrogel that is injected directly into the disc space. The minimally invasive insertion prospects and motion sparing nature of NPR has caused widespread interest in this developing field. Issues that will affect success include which materials are used and implant design to help minimise migration.
Conclusion For many years, spinal fusion has been the mainstay of treatment for back pain caused by lumbar instability. A variety of techniques exist, with ever-increasing fusion rates. However, the increase in fusion rates has not been paralleled with an improvement in clinical outcomes. Motion sparing techniques, such as dynamic spacers and spine arthoplasty, have gained widespread popularity as they hold several advantages over spinal fusion, thus increasing the number of techniques available to stabilise the abnormal motion segment. Spinal implants represent the fastest growing sector of the orthopaedic market, with a projected market value of over $7 billion by 2010. Spinal surgeons will face enormous pressure from industry and the public to embrace new technology. Due to the lack of evidence-based data available, it is the author’s opinion that the application of such technology must be approached with caution. Efforts need to be directed towards research, development and clinical trials before motion sparing devices can seriously challenge spinal fusion as the gold standard treatment for lumbar instability. Nonetheless, a new chapter has been
Clinical study in Europe and US Clinical trial in UK, 10 patients
opened and the coming years look set to be a period of exciting change in lumbar stabilisation techniques.
Acknowledgement The authors would like to thank Dr. Isabel Dean of University College London for all her efforts and support.
References 1. Panjabi MM. The stabilizing system of the spine. Part II. Neutral zone and instability hypothesis. J Spinal Disord 1992;5(4):390–6 (discussion 397). 2. Boden SD, Wiesel SW. Lumbosacral segmental motion in normal individuals. Have we been measuring instability properly? Spine 1990;15(6):571–6 (Erratum in: Spine 1991;16(7):855). 3. Iguchi T, et al. Lumbar instability and clinical symptoms: which is the more critical factor for symptoms: sagittal translation or segment angulation? J Spinal Disord Technol 2004;17(4): 284–90. 4. Weiler PJ, King GJ, Gertzbein SD. Analysis of sagittal plane instability of the lumbar spine in vivo. Spine 1990;15(12): 1300–6. 5. Stokes IA, Frymoyer JW. Segmental motion and instability. Spine 1987;12(7):688–91. 6. Hibbs RA. An operation for progressive spinal deformity. NY Med J 1911;21:1013–6. 7. Albee FH. Transplantation of a portion of the tibia into the spine for Potts disease. J Am Med Assoc 1911;57:855–8. 8. Chandler FA. Spinal fusion operations in the treatment of low back and sciatic pain. JAMA 1929;93:1447. 9. Watkins MB. Posterior fusion of the lumbar and lumbosacral spine. JBJS Am 1953;35:1014–8. 10. Wiltse LL, Bateman JG, Hutchinson RH, Nelson WE. The paraspinal sacrospinalis-splitting approach to the lumbar spine. J Bone Joint Surg Am 1968;50(5):919–26. 11. Bernhardt M, et al. Posterolateral lumbar and lumbosacral fusion with and without pedicle screw internal fixation. Clin Orthop Relat Res 1992(284):109–15. 12. Bjarke Christensen F, et al. Long-term functional outcome of pedicle screw instrumentation as a support for posterolateral spinal fusion: randomized clinical study with a 5-year follow-up. Spine 2002;27(12):1269–77. 13. Moller H, Hedlund R. Instrumented and noninstrumented posterolateral fusion in adult spondylolisthesis—a prospective randomized study: Part 2. Spine 2000;25(13):1716–21.
ARTICLE IN PRESS 38 14. Thomsen K, et al. Volvo Award winner in clinical studies. The effect of pedicle screw instrumentation on functional outcome and fusion rates in posterolateral lumbar spinal fusion: a prospective, randomized clinical study. Spine 1997;22(24): 2813–22. 15. Lorenz M, et al. A comparison of single-level fusions with and without hardware. Spine 1991;16(8 Suppl):S455–8. 16. Zdeblick TA. A prospective, randomized study of lumbar fusion. Preliminary results. Spine 1993;18(8):983–91. 17. Fischgrund JS, et al. Volvo Award winner in clinical studies. Degenerative lumbar spondylolisthesis with spinal stenosis: a prospective, randomized study comparing decompressive laminectomy and arthrodesis with and without spinal instrumentation. Spine 1997;22(24):2807–12. 18. France JC, et al. A randomized prospective study of posterolateral lumbar fusion. Outcomes with and without pedicle screw instrumentation. Spine 1999;24(6):553–60. 19. Harrington PR, Tullos HS. Reduction of severe spondylolisthesis in children. South Med J 1969;62(1):1–7. 20. Vanden Berghe L, et al. Stability of the lumbar spine and method of instrumentation. Acta Orthop Belgium 1993;59(2): 175–80. 21. Boucher HH. A method of spinal fusion. J Bone Joint Surg Br 1959;41-B(2):248–59. 22. Magerl FP. Stabilization of the lower thoracic and lumbar spine with external skeletal fixation. Clin Orthop Relat Res 1984(189):125–41. 23. Humke T, et al. Translaminar screw fixation of the lumbar and lumbosacral spine. A 5-year follow-up. Spine 1998;23(10): 1180–4. 24. Jacobs RR, Montesano PX, Jackson RP. Enhancement of lumbar spine fusion by use of translaminar facet joint screws. Spine 1989;14(1):12–5. 25. Grob D, et al. , Translaminar screw fixation of the lumbar spine. Translaminar screw fixation of the lumbar spine. Int Orthop 1992;16(3):223–6. 26. Vanden Berghe L, et al. Stability of the lumbar spine and method of instrumentation. Acta Orthop Belg 1993;59(2): 175–80. 27. Fritzell P, et al. Chronic low back pain and fusion: a comparison of three surgical techniques: a prospective multicenter randomized study from the Swedish lumbar spine study group. Spine 2002;27(11):1131–41. 28. Weatherley CR, Prickett CF, O’Brien JP. Discogenic pain persisting despite solid posterior fusion. J Bone Joint Surg Br 1986;68(1):142–3. 29. Parker LM, et al. The outcome of posterolateral fusion in highly selected patients with discogenic low back pain. Spine 1996;21(16):1909–16. 30. Greenough CG, et al. Instrumented posterolateral lumbar fusion. Results and comparison with anterior interbody fusion. Spine 1998;23(4):479–86. 31. Christensen FB, et al. Circumferential lumbar spinal fusion with Brantigan cage versus posterolateral fusion with titanium Cotrel–Dubousset instrumentation: a prospective, randomized clinical study of 146 patients. Spine 2002;27(23): 2674–83. 32. Christensen FB. Lumbar spinal fusion. Outcome in relation to surgical methods, choice of implant and postoperative rehabilitation. Acta Orthop Scand Suppl 2004;75(313):2–43. 33. Cloward RB. The treatment of ruptured lumbar intervertebral discs; criteria for spinal fusion. Am J Surg 1953;86(2): 145–51. 34. Enker P, Steffee Ad. Interbody fusion and instrumentation. Clin Orthop Relat Res 1994(300):90–101. 35. Capener N. Spondylolisthesis. Br J Surg 1932;19:374–86. 36. Rolander SD. Motion of the lumbar spine with special reference to the stabilizing effect of posterior fusion. An experimental
S. Lau, K.S. Lam
37.
38.
39.
40.
41. 42.
43.
44. 45. 46.
47.
48. 49. 50.
51.
52.
53.
54.
55.
56.
57.
58.
study on autopsy specimens. Acta Orthop Scand 1966(Suppl 90):1–144. Oxland, et al. A comparative biomechanical investigation of anterior lumbar interbody cages: central and bilateral approaches. J Bone Joint Surg Am 2000;82(3):383–93. Grob D, Scheier HJ, Dvorak J, et al. Circumferential fusion of the lumbar and lumbosacral spine. Arch Orthop Trauma Surg 1991;111(1):20–5. Thalgott JS, Giuffre JM, Klezl Z, Timlin M. Anterior lumbar interbody fusion with titanium mesh cages, coralline hydroxyapatite, and demineralized bone matrix as part of a circumferential fusion. Spine J 2002;2(1):63–9. Schofferman J, Slosar P, Reynolds J, et al. A prospective randomized comparison of 270 degrees fusions to 360 degrees fusion (circumferential fusions). Spine 2001;26:E207–12. Holly LT, Foley KT. Intraoperative spinal navigation. Spine 2003;28(15 Suppl):S54–61. Grob D, Humke T. Translaminar screw fixation in the lumbar spine: technique, indications, results. Eur Spine J 1998;7(3): 178–86. Shim CS, et al. Fluoroscopically assisted percutaneous translaminar facet screw fixation following anterior lumbar interbody fusion: technical report. Spine 2005;30(7):838–43. Carlisle E, Fischgrund JS. Bone morphogenetic proteins for spinal fusion. Spine J 2005;5(6 Suppl):240S–9S. Boos N, Webb JK. Pedicle screw fixation in spinal disorders: a European view. Eur Spine J 1997;6(1):2–18. Gibson JN, Grant IC, Waddell G. The Cochrane review of surgery for lumbar disc prolapse and degenerative lumbar spondylosis. Spine 1999;24(17):1820–32. Schlegel JD, Smith JA, Schleusener RL. Lumbar motion segment pathology adjacent to thoracolumbar, lumbar, and lumbosacral fusions. Spine 1996;21(8):970–81. Sengupta DK. Dynamic stabilization devices in the treatment of low back pain. Orthop Clin North Am 2004;35(1):43–56. Gardner A, Pande KC. Graf ligamentoplasty: a 7-year follow-up. Eur Spine J 2002;11(Suppl 2):S157–63 (Epub 2002 July 12). Hadlow SV, Fagan AB, Hillier TM, Fraser RD. The Graf ligamentoplasty procedure. Comparison with posterolateral fusion in the management of low back pain. Spine 1998;23(10): 1172–9. Stoll TM, Dubois G, Schwarzenbach O. The dynamic neutralization system for the spine: a multi-center study of a novel nonfusion system. Eur Spine J 2002;11(Suppl 2):S170–8. Senegas J, et al. Recalibration of the lumbar canal, an alternative to laminectomy in the treatment of lumbar canal stenosis. Rev Chir Orthop Reparatrice Appar Mot 1988;74(1): 15–22. Zuckerman JF, et al. A multicenter, prospective, randomized trial evaluating the X STOP interspinous process decompression system for the treatment of neurogenic intermittent claudication: two-year follow-up results. Spine 2005;30(12): 1351–8. German JW, Foley KT. Disc arthroplasty in the management of the painful lumbar motion segment. Spine 2005;30(16 Suppl):S60–7. Fernstrom U. Arthroplasty with intercorporal endoprothesis in herniated disc and in painful disc. Acta Chir Scand Suppl 1966;357:154–9. Brau SA. Mini-open approach to the spine for anterior lumbar interbody fusion: description of the procedure, results and complications. Spine J 2002;2(3):216–23. Siepe CJ, et al. Clinical results of total lumbar disc replacement with ProDisc II: three-year results for different indications. Spine 2006;31(17):1923–32. Hochschuler SH, et al. Artificial disc: preliminary results of a prospective study in the United States. Eur Spine J 2002; 11(Suppl 2):S106–10.
ARTICLE IN PRESS Lumbar stabilisation techniques 59. Blumenthal S, et al. A prospective, randomized, multicenter Food and Drug Administration investigational device exemptions study of lumbar total disc replacement with the CHARITE artificial disc versus lumbar fusion: part I: evaluation of clinical outcomes. Spine 2005;30(14):1565–75 (discussion E387-91. Erratum in: Spine. 2005;30(20):2356). 60. Bertagnoli R, Kumar S. Indications for full prosthetic disc arthroplasty: a correlation of clinical outcome against a variety of indications. Eur Spine J 2002;11(Suppl 2): S131–6. 61. Mayer HM, Wiechert K, Korge A. Minimally invasive total disc replacement: surgical technique and preliminary clinical results. Eur Spine J 2002;11(Suppl 2):S124–30.
39 62. Tropiano P, et al. Lumbar disc replacement: preliminary results with ProDisc II after a minimum follow-up period of 1 year. J Spinal Disord Technol 2003;16(4):362–8. 63. Siepe CJ, et al. Clinical results of total lumbar disc replacement with ProDisc II: three-year results for different indications. Spine 2006;31(17):1923–32. 64. Delamater R, et al. The results of the prospective randomized multi-centre trial of prodisc L vs circumferential fusion. Montreal, Canada: Spine Arthroplasty Society; 2006. 65. Bao QB, Yuan HA. New technologies in spine: nucleus replacement. Spine 2002;27(11):1245–7. 66. Klara PM, Ray CD. Artificial nucleus replacement: clinical experience. Spine 2002;27(12):1374–7.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 40–46
Available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/cuor
SHOULDER
Biomechanical considerations of the normal and rotator cuff deficient shoulders and the reverse shoulder prosthesis F. Lama,, D.N. Bhatiaa, S.B. Mostofib, K. van Rooyena, J.F. de Beera a
Cape Shoulder Institute, Medgroup Anlin House, Plattekloof, Panorma, Cape Town, South Africa Massachussetts General Hospital, Boston, USA
b
KEYWORDS Cuff tear arthropathy; Reverse shoulder prosthesis; Rotator cuff deficient shoulder; Biomechanics of shoulder
Summary The treatment of combined glenohumeral arthritis and massive rotator cuff deficiency remains a unique challenge. Prosthetic reconstruction is aimed at restoring the normal kinematics of the glenohumeral joint. The reverse shoulder prosthesis medialises the centre of rotation of the glenohumeral joint, thereby lengthening the deltoid lever arm. The centre of rotation is also fixed at the glenoid bone prosthesis interface and this has the effect of reducing the torque on the glenoid component and lessens the risk of glenoid loosening. To further enhance the function of deltoid, the humerus is lowered relative to the glenoid, thereby increasing the deltoid tension. Although the preliminary results have been encouraging, there are still some unresolved issues such as prosthetic joint instability, scapular notching, wear of the polyethylene cup, fixation of the humeral stem and the lack of external rotation following surgery. & 2006 Elsevier Ltd. All rights reserved.
Introduction
Anatomy of the humeral head
The design of a successful shoulder arthroplasty relies on the restoration of the normal anatomical relationship between the humeral head and glenoid so that the normal kinematics of the shoulder joint can be recreated.1 The biomechanical considerations of the normal shoulder joint that are important in prosthetic design will be considered.
The mean humeral head radius is 24 mm (range 19–28) and the mean humeral head thickness is 19 mm (range 15–24).2,3 Both these variables correlate with the humeral head offset, which is the distance between the centre of the humeral head and the longitudinal axis of the humeral shaft. In the coronal plane, the humeral head offset is 7–9 mm medial to the central axis of the humeral shaft. In the axial plane, the humeral head offset is 2–4 mm posterior to the central axis of the humeral shaft. The ratio of the humeral head thickness to humeral head radius is reliably consistent at 0.7–0.9.2,3 This ratio is directly proportional to the amount
Corresponding author.
E-mail address: mrfl
[email protected] (F. Lam). 0268-0890/$ - see front matter & 2006 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2006.10.004
ARTICLE IN PRESS Biomechanical considerations of the normal and rotator cuff deficient shoulders and the reverse shoulder prosthesis
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of humeral head which articulates with the glenoid, irrespective of other variables such as length of the humeral shaft or the size of the patient.3
Anatomy of the glenoid cavity The normal glenoid has a pear shaped appearance with a shorter anteroposterior dimension in the superior half (mean 23 mm) than in the inferior half (mean 29 mm).2 The glenoid offset is the distance between the base of the coracoid and the deepest portion of the glenoid articular surface.2 This measurement determines the location of the glenohumeral joint line and again is not related to the size of the patient. The lateral glenohumeral offset is the distance between the base of the coracoid and the most lateral aspect of the greater tuberosity. This measurement is important as it determines the resting tension of the rotator cuff and the moment arm of the deltoid.
Humeral neck shaft angle The humeral neck shaft angle is defined as the angle between the central intramedullary axis of the humeral shaft and the anatomical neck of the humerus. The mean neck shaft angle is 401 but significant variation does occur between individuals, ranging from 301 to 551.4
Articular geometry of the glenohumeral joint The articular surface of the humeral head has an upwards tilt of 451 and is retroverted 351 with respect to the epicondylar axis of the distal humerus (Fig. 1). The articular surface of the glenoid has a slight upwards tilt of 51 with respect to the medial border of the scapula and retroversion of 71 with respect to the plane of the scapula. The articular surface of the humeral head covers an arc of 1551 but the articular surface of the glenoid covers an arc of only 761. The implication of this difference is that the glenohumeral joint can only allow 791 of true elevation in the scapular plane. Combined with 411 of scapulothoracic motion, the arm can elevate 1201 beyond which an ‘obligatory’ external rotation occurs to achieve maximal elevation.5 This means that the humerus must externally rotate to clear the greater tuberosity from the coracoacromial arch.
Articular congruity of the glenohumeral joint The glenohumeral congruence (conformity) is the relationship between the radius of curvature of the humeral head and the glenoid.6 If the radii of curvature of the humeral head and glenoid are the same, i.e. congruency ratio of 1, then there is maximum contact between the two surfaces. This arrangement occurs in only 9% of individuals.5 The most common configuration (90%) is a smaller radius of curvature for the humeral head relative to the glenoid, such that the congruency ratio is less than 1. This has important biomechanical advantages in terms of increased range of movement but at the expense of decreased stability.
Figure 1 Transverse view of the glenohumeral joint showing the 351 retroversion of the glenoid.
Glenohumeral index This is defined as the maximum transverse diameter of the glenoid divided by the maximum transverse diameter of the humeral head. This ratio is approximately 0.75 in the sagittal plane and 0.6 in the transverse plane.7 A low glenohumeral index is associated with recurrent anterior instability.8
Glenohumeral articular constraint Constraint is the amount of humeral head which is in direct articulation with the glenoid cavity.6 It is related to the depth of the glenoid but is independent of articular congruence. The normal glenoid has a depth of 9 mm in the superoinferior direction and 5 mm in the anteroposterior direction. As a result, the glenoid is more constrained in the superoinferior direction than anteroposterior direction, accounting for the more frequently observed anteroposterior dislocation.
Stability of the glenohumeral joint Unlike the hip joint, the glenohumeral joint is minimally constrained, with little inherent bony stability. The stability of the joint is maintained by an interconnecting network of static and dynamic restraints (Table 1). The static restraints
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Table 1 Static and dynamic stabilizers of the glenohumeral joint. Static Capsuloligamentous 1. Capsule 2. Labrum 3. Glenohumeral ligaments 4. Coracohumeral ligament Articular 1. Humeral head retroversion 2. Scapular inclination 3. Joint conformity 4. Negative intraarticular pressure Dynamic Scapulohumeral 1. Supraspinatus 2. Infraspinatus 3. Subscapularis 4. Teres major 5. Teres minor 6. Long head of biceps 7. Deltoid Axioscapular 1. Trapezius 2. Rhomboids 3. Serratus anterior 4. Levator scapulae Axiohumeral 1. Latissimus dorsi 2. Pectoralis major
may be further divided into soft tissue and articular stabilisers. An important soft tissue restraint is the glenohumeral joint capsule, which originates from the labrum and margin of the glenoid fossa. It is attached laterally to the anatomical neck of the humerus. It forms a continuous fibrous joint lining, except in the biceps groove where the tendon exits the joint. It maintains the negative intraarticular pressure, contributing to the stability of the glenohumeral joint. Cadaveric studies have shown that a simple puncture of the joint capsule can result in 2 cm of distraction of the joint surfaces resulting in significant glenohumeral instability.9 The glenohumeral ligaments are thickenings of the joint capsule and consist of superior, middle and inferior portions. The superior glenohumeral ligament originates from the base of the coracoid process and labrum and inserts into the humerus just above the lesser tuberosity. It functions as the primary restraint to inferior translation of the humeral head. The middle glenohumeral ligament is the most variable and is said to limit external rotation and anterior subluxation of the humeral head when the arm is in mid-abduction. The inferior glenohumeral ligament is the most important ligament in maintaining joint stability.10 It originates from the anterior, inferior and posterior margins of the glenoid labrum and inserts into the neck of the humerus. It consists of an anterior band, axillary pouch and posterior band. The anterior band is maximally taut when the arm is in abduction
and external rotation. Conversely, the posterior band is maximally taut when the arm is in abduction and internal rotation. The coracohumeral ligament originates from the lateral aspect of the base of the coracoid process and runs downwards and laterally to attach to the greater and lesser tuberosities. It acts as the primary restraint to inferior translation of the adducted arm and also functions to limit external rotation of the adducted humerus. The labrum has several important functions. Firstly, it deepens the glenoid by 5 mm in the anteroposterior direction and 9 mm in the superoinferior direction.11 This increases the depth of the glenoid by 50%. Secondly, it provides a site of attachment for the glenohumeral ligaments. Thirdly, it works synergistically with the rotator cuff to compress the humeral head against the glenoid cavity. Finally, it acts as a wedge, preventing translation of the humeral head. It is estimated that removal of the labrum results in a 20% reduction in the translatory force required to dislocate the humeral head over the glenoid rim.12 The articular factors are also important. The mean retroversion of the humeral head is 17.91.13 There is evidence that insufficient humeral retroversion predisposes to anterior instability and Saha7 suggested a corrective humeral osteotomy if the retroversion angle is less than 201. On the glenoid side the version is usually zero, although up to 101 of anteverison or retroversion can be regarded as normal. There is conflicting evidence as to whether hyper-anteversion of the glenoid may be associated with recurrent instability. The dynamic restraints stabilise the joint by several mechanisms: 1. By a passive muscle tensioning effect. 2. By dynamic contraction thereby causing compression of the humeral head into the glenoid and glenoid labrum, sometimes referred to as concavity-compression.14 3. By causing a secondary tightening effect on the static constraints. For example, supraspinatus can simultaneously elevate and externally rotate the arm. The external rotation movement causes tightening of the inferior glenohumeral ligament, limiting upward elevation. 4. By exerting a direct barrier effect. For example, subscapularis acts as a direct anterior stabiliser preventing anteroinferior humeral instability.
Forces acting on the glenohumeral joint5,15 The forces acting on the glenohumeral joint include:
Weight of the arm. Abductor force by deltoid and supraspinatus. Downward pull of arm by subscapularis, infraspinatus and teres minor.
Compressive force on the glenohumeral joint. Shear force of humeral head on glenoid. External forces such as weight held in the hand. The deltoid is the most powerful muscle around the shoulder and can generate a force of up to 6 times the weight of the arm. It has the largest moment arm around
ARTICLE IN PRESS Biomechanical considerations of the normal and rotator cuff deficient shoulders and the reverse shoulder prosthesis the glenohumeral joint and is the most effective muscle in arm elevation, acting superiorly at 631 when the arm is resting at the side of the body (Fig. 2). In the normal shoulder, the deltoid can alone provide 70% of the torque at 301 of abduction and 85% at 901.16 The supraspinatus can generate a force of 2.5 times the weight of the arm and acts 15–201 superiorly. The infraspinatus acts 40–451 inferiorly and the force of the teres minor is also directed inferiorly at 551. Together, the infraspinatus and teres minor can generate a force of 5 times the weight of the arm.17,18 When abduction of the arm is initiated, the shear force on the glenohumeral joint generated by the deltoid is counteracted by the compressive force produced by the rotator cuff. Generally speaking, the compressive force contributes towards joint stability while the shear force induces upward displacement of the humeral head. The combination of shear and compressive forces allows efficient abduction by stabilising the humeral head within the glenoid fossa. The magnitude and direction of the resultant joint reaction force is dependent on the position of the arm. At 901 of abduction, the joint reaction force is at its maximum and equates approximately the weight of the body. Fig. 3 represents a free body diagram of the forces acting on the glenohumeral joint when the arm is abducted 901.
43
Figure 3 Free body diagram of the forces acting on the glenohumeral joint when the arm is abducted 901 (D—Deltoid, SS—Supraspinatus, SB—Subscapularis, IS—Infraspinatus, TM—Teres minor, J—Joint reaction force).
Cuff tear arthropathy The concept of ‘‘cuff-tear arthropathy’’ was first introduced by Neer in 1977 to describe findings of arthritis associated
Figure 4 Cuff tear arthropathy with superior migration of the humeral head.
Figure 2 The direction of the rotator cuff muscle forces when the arm is resting at the side of the body (D—Deltoid, SS—Supraspinatus, IS—Infraspinatus, SB—Subscapularis, TM—Teres Minor).
with massive rotator cuff deficiency.19 He postulated that without the superior stabilising effect of the rotator cuff, the humeral head migrates superiorly, leading to abrasion of the humeral head against the undersurface of the acromion and superior glenoid. Furthermore, as a result of inactivity, there is impaired nutrition of the articular cartilage, leading to osteoporosis and segmental collapse of the humeral head. In 1981, McCarthy et al.20 described similar findings, which they called ‘Milwaukee shoulder’ and postulated that it was a degenerative process caused by hydroxyapatite crystals, neutral proteases and active collagen. The superior migration of the humeral head seen in massive rotator cuff deficiency (Fig. 4) is caused by muscle force imbalance. Normally, the rotator cuff stabilises the humeral head in the glenoid cavity during abduction and the head translates superiorly by 3 mm during the first 301 of motion.21 In massive rotator cuff deficiency, the shear force produced by the intact deltoid is no longer opposed by the
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joint compressive force which is normally produced by the rotator cuff. This results in a superiorly directed resultant vector that occurs with initiation of abduction. Furthermore, the long head of biceps is usually torn in association with large rotator cuff tears, further losing its important role as a humeral head depressor. In advanced cases, as the deltoid contracts the humeral head articulates with the undersurface of the acromion, causing further articular destruction (Fig. 4). The treatment of cuff tear arthropathy remains a difficult challenge. Options vary from hemiarthroplasty, bipolar hemiarthroplasty, massive head hemiarthroplasty, constrained total shoulder replacement, semi-constrained total shoulder replacement and shoulder arthrodesis.22 The use of an unconstrained total shoulder replacement in the treatment of cuff tear arthropathy is now almost obsolete due to the high incidence of glenoid loosening. This is due to the high shear force which loads the superior part of the glenoid eccentrically, a phenomenon described by Matsen23 as the ‘rocking horse phenomenon’. Hemiarthroplasty was also tried. Although it provided good pain relief for some patients, the range of active movement afterwards was still poor.24 There is concern that results deteriorate with time due to erosion of the glenoid and coracroacromial arch. Bipolar hemiarthroplasty was also introduced to add further stability but the functional outcome was no better than hemiarthroplasty.25
Development of the reverse shoulder prosthesis The concept of a constrained total shoulder arthroplasty was first introduced by Scales in 1960 with the Stanmore constrained prosthesis. The rationale for this was to provide a fixed centre of rotation thereby converting the upwardly directed shear force produced by the deltoid into a rotatory movement. In 1972, Kolbel introduced the first reverse ball and socket prosthesis. Since then a number of similar designs have been introduced, including Fenlin, Neer, Liverpool, Gerard and Kessel. Unfortunately, all of these designs had the shortcomings of a lateralized offset of the humeral component, resulting in excessive torque and shear forces at the glenoid prosthetic bone interface, leading to glenoid loosening. Finally, in 1985, Professor Paul Grammont from Dijon, France, developed a semiconstrained reverse ball and socket prosthesis.26 He made a number of key refinements in its design:
found that if the centre of the glenoid hemisphere is medialised by 10 mm, the abduction moment of the deltoid will be increased by 20% when the arm is abducted 601.26,28 Secondly, medialising the centre of rotation helps to recruit more deltoid fibres to act as abductors. Normally, only the middle fibres and part of the anterior fibres of the deltoid act as abductors. When the axis of elevation is medialised, more of the anterior and some of the posterior fibres of the deltoid are additionally recruited for abduction. The humeral neck angle is non-anatomical and has a horizontal inclination of 1551. This lowers the humerus relative to the glenoid and helps to restore deltoid tension. If the centre of the glenoid hemisphere is lowered by 10 mm, the abduction moment of the deltoid will be increased by 30% when the arm is abducted 601.26,28 The humeral component consists of a small cup covering less than half of the glenosphere. This allows a greater range of movement without causing prosthesis bone impingement. The articular geometry of the humeral and the glenoid components are well matched and the deeper socket has increased the articular conformity. Both have contributed to the increased joint stability.
Based on Grammont’s original design, the two most popularly used reverse prostheses are the Delta III (Depuy, Warsaw, Indiana, USA) and the Aequalis Reverse prostheses (Tornier Inc., Houston, TX, USA). The Delta has been in use in Europe since 1992 and the Tornier (Fig. 5) since 1998. When the tension is correct after implantation, pulling the arm downwards should result in only 5 mm of articular
The glenoid component consists of a large hemisphere
with no neck. Compared to a small head, the larger head allows greater excursion of movement yet without compromising stability. The absence of a neck means that the lateral offset will be minimised. The centre of rotation is fixed at the glenoid bone prosthesis interface. This significantly decreases the torsional forces on the component-bone fixation, and thus lessens the risk of glenoid loosening.27 The centre of rotation is also medialised. This has important biomechanical advantages. Firstly, the lever arm of the deltoid is lengthened (Fig. 6), leading to a corresponding increase in the moment force. Grammont
Figure 5 Radiograph of the reverse shoulder prosthesis.
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Figure 6 (A) The normal resting tension of the deltoid. (B) The reverse prosthesis in situ with a medialised centre of rotation and lowering of the humerus, thereby lengthening the deltoid.
surface separation and the joint should remain stable when the arm is adducted.29 The most common indication for the reverse shoulder prosthesis is massive, irreparable cuff tear associated with glenohumeral arthritis. Other indications include revision of a failed hemiarthroplasty or total shoulder arthroplasty associated with irreparable rotator cuff damage, displaced comminuted fracture of the proximal humerus in the elderly, massive irreparable rotator cuff tear without arthritis, failed rotator cuff repair, rheumatoid arthritis and tumour reconstruction. The common denominator in all of these situations is the loss of a stable biomechanical fulcrum for arm elevation (Fig. 6).
Current status of the reverse shoulder prosthesis Several studies have reported favourable results with the reverse shoulder prosthesis in the short to medium term.30,31 In a series of 60 patients with a minimum follow up of 2 years, Frankle et al.30 reported an excellent or good outcome in 41 patients with significant improvement in all parameters of pain and function. There were 13 complications (17%) in 10 patients, 7 of whom required revision surgery to either hemiarthroplasty or another reverse shoulder prosthesis. The most recent published data come from Nice by Boileau et al.31 who reported the results on a consecutive series of 45 patients with a mean follow up of 40 months. There were significant improvements in active elevation (from 551 preoperatively to 1211 postoperatively) and Constant score (from 17 to 58). Fourteen complications in 11 patients were encountered including 3 dislocations, 3 deep infections, 2 periprosthetic humeral fractures, 1 aseptic loosening of the humeral component, 1 intraoperative glenoid fracture, 2 late acromial fractures, 1 wound haematoma and 1 axillary nerve palsy. They found that the
complication rate of the reverse prosthesis carried out for revision surgery was significantly higher than for cuff tear arthropathy (47% and 5% respectively). This experience is shared by Schneeberger and Gerber who reported a similarly high complication rate of 50% in revision cases.32 The long term survival of 80 reverse prostheses was evaluated by a multicentre study with a minimum follow up of 5 years.33 Using replacement of the prosthesis as the end point, the survival rate was 91%. Using glenoid loosening as the end point, the survival rate was 84%. Using an absolute Constant score of less than 30 as the end point, the survival rate was 58% at 120 months. There were two breaks noted in the survival curves. The first break occurred at around 3 years as a result of early loosening of the prosthesis. The second break occurred at around 6 years as a result of progressive functional deterioration of the prosthesis. Clearly, there are still many complicated issues of the Reverse prosthesis that need to be addressed. Firstly, the maintenance of joint stability remains a problem. Instability can be attributed to a variety of factors including insufficient deltoid tension, medial impingement caused by medialisation of the humerus and atrophy of the anterior deltoid. Grammont described the concept of ‘‘global decoaptation’’ which is shown radiographically by a radiolucent gap between the articular surfaces.34 This is thought to be caused by insufficient deltoid tension. Over tensioning of the deltoid, however, can result in fracture of the acromion and can even cause damage to the axillary nerve.29 Scapular notching remains a common complication and was seen in 68% of Boileau’s subjects.31 Its occurrence is a result of impingement of the humeral cup on the scapular neck during shoulder adduction. Concern remains that scapular notching might lead to secondary wear of the polyethylene cup with the potential for inducing osteolysis. Gerber found that by placing the glenosphere 2–4 mm more distally, this significantly improves the abduction and adduction angles thus reducing the risk of inferior glenoid notching.35
ARTICLE IN PRESS 46 The issue of subsidence and loosening of the humeral stem remains a challenge. Boileau29 recommends that the humeral stem should be cemented, as the round cross section of the humeral stem offers little torsional stability. Furthermore, as the host bone in revision cases is often insufficient, a long stem implant should be used. The procedure should be performed in two stages if there is any suspicion of infection. Finally, many patients following successful reverse shoulder arthroplasty still have little or no external rotation. This can be attributed to many factors including lack of compensation of the external rotators by the posterior deltoid, secondary to the medialisation of the centre of rotation, as well as fatty atrophy of the rotator cuff.29 In conclusion, although the short to medium term results of the reverse shoulder prosthesis have been encouraging, the overall complication rate remains high when compared to anatomic implants. Until the long term results are known, the reverse prosthesis should be reserved for the treatment of severely disabling cuff tear arthropathy in patients over 70 years old with low functional demands.
References 1. Mahfouz M, Nicholson G, Komistek R, Hovis D, Kubo M. In vivo determination of the dynamics of normal, rotator cuff deficient, total and reverse replacement shoulders. J Bone Joint Surg Am 2005;87:107–13. 2. Howell SM, Galinat BJ. The glenoid-labral socket: a constrained articular surface. Clin Orthop 1989;243:122–5. 3. O’Connell PW, Nuber GW, Mileski RA, Lautenschlager E. The contribution of the glenohumeral ligaments to anterior stability of the shoulder joint. Am J Sports Med 1990;18:579–84. 4. Williams GR, Iannotti JP. Biomechanics of the glenohumeral joint: influence on shoulder arthroplasty. In: Iannotti JP, Williams GR, editors. Disorders of the shoulder: diagnosis and management. Philadelphia: Lippincott Williams & Wilkins; 1999. p. 471–83. 5. Friedman RJ. Biomechanics and design of shoulder arthroplasties. In: Friedman RJ, editor. Arthropalsty of the shoulder. New York: Thieme Medical Publishers, Inc.; 1994. p. 27–40. 6. Iannotti JP, Williams GR. Total shoulder arthroplasty. Orthop Clin North Am 1998;29(3):377–91. 7. Saha AK. Dynamic stability of the glenohumeral joint. Acta Orthop Scand 1971;42:491–505. 8. Randelli M, Gambrioli PL. Glenohumeral osteometry by computed tomography in normal and unstable shoulders. Clin Orthop 1986;208:151. 9. Clark J, Sidles JA, Matsen III FA. The relationship of the glenohumeral joint capsule to the rotator cuff. Clin Orthop 1990;254:29. 10. O’Brien SJ, Neves MC, Arnoczky SP, et al. The anatomy and histology of the inferior glenohumeral ligament complex of the shoulder. Am J Sports Med 1990;18:449. 11. Howell SM, Galinat BJ. The glenoid-labral socket: a constrained articular surface. Clin Orthop 1989;243:122–5. 12. Lippitt S, Matsen F. Mechanisms of glenohumeral joint stability. Clin Orthop 1993;291:20. 13. Boileau P, Walch G. Adaptabilite et modularite au cours des protheses d’epaule. Acta Orthop Belgica 1995;61(Suppl 1): 49–61. 14. Halder AM, Kuhl SG, Zobitz ME, Larson D, An KN. Effects of the glenoid labrum and glenohumeral abduction on stability of the shoulder joint through concavity-compression: an in vitro study. J Bone Joint Surg Am 2001;83:1062–9.
F. Lam et al. 15. Buechel F, Pappas M, DePalma A. ‘Floating socket’ total shoulder replacement: anatomical, biomechanical and surgical rationale. J Biomed Mater Res 1977;12:89–114. 16. Pollock RG, Deliz ED, Mellveen SJ, Flatow EL, Bigliani LU. Prosthetic replacement in rotator cuff deficient shoulders. J Shoulder Elbow Surg 1992;1:173–86. 17. Inman V, Saunders M, Abbott L. Observations on the function of the shoulder joint. J Bone Joint Surg Am 1944;26:1–30. 18. de Luca, Forrest W. Force analysis of individual muscles acting simultaneously on the shoulder joint during isometric abduction. J Biomech 1973;6:385–93. 19. Neer C, Craig E, Fukuda H. Cuff-tear arthropathy. J Bone Joint Surg Am 1983;65:1232–4. 20. McCarthy DJ, Halverson PB, Carriera CF, et al. Milwaukee shoulder. Association of microspheroids containing hydroxyapatite crystals, active collagens and neutral proteases with rotator cuff defects. J Clin Aspect Arthrit Rheumat 1981;24:464. 21. Poppen NK, Walker PS. Normal and abnormal motion of the shoulder. J Bone Joint Surg 1976;58A:195–201. 22. Yao J, Dines D, Warren R. Surgical arthroplasty options for rotator cuff tear arthropathy. Tech Shoulder Elbow Surg 2003; 4(1):26–34. 23. Franklin J, Barrett W, Jackins S, Matsen F. Glenoid loosening in total shoulder arthroplasty. J Arthroplasty 1988;3:39–46. 24. Favard L, Lautmann S, Sirveaux F, Oudet D, Kerjean Y, Huguet D. Hemiarthroplasty versus reverse arthroplasty in the treatment of osteoarthritis with massive rotator cuff tear. In: Walch G, Boileau P, Mole D, editors. 2000 shoulder prosthesisytwo to ten year follow up. Montpellier France: Sauramps Medical; 2001. p. 261–8. 25. DiGiovanni J, Marra G, Park JY, Bigliani LU. Hemiarthroplasty for glenohumeral arthritis with massive rotator cuff tears. Orthop North Am 1998;29(3):477–89. 26. Grammont PM, Baulot E. Delta shoulder prosthesis for rotator cuff rupture. Orthopaedics 1993;16:65–8. 27. Frankle M, Levy J, Pupello D, Siegal S, Saleem A, Mighell M, et al. The reverse shoulder prosthesis for glenohumeral arthritis associated with severe rotator cuff deficiency. J Bone Joint Surg Am 2006;88:178–90. 28. Grammont PM, Baulot E, Chabernaud D. Resultats des 16 premiers cas d’ arthroplastie totale d’epaule inversee sans ciment pour des omarthroses avec grande rupture de coiffe. Rev Chir Orthop Reparatrice Appar Mot 1996;82(suppl I):169. 29. Boileau P, Watkinson D, Hatzidakis A, Balg F. Grammont reverse prosthesis: design, rationale and biomechanics. J Shoulder Elbow Surg 2005;14:147S–61S. 30. Frankle M, Siegal S, Pupello D, Saleem A, Mighell M, Vasey M. The reverse shoulder prosthesis for glenohumeral arthritis associated with severe rotator cuff deficiency. J Bone Joint Surg Am 2005;87:1697–705. 31. Boileau P, Watkinson D, Hatzidakis A, Hovorka I. Neer Award 2005: The Grammont reverse prosthesis: results in cuff tear arthritis, fracture sequelae, and revision arthroplasty. J Shoulder Elbow Surg 2006;15:527–40. 32. Schneeberger A, Gerber C. Complications with the Delta reversed prosthesis [abstract]. Presented at the ASES Closed Meeting 2004. 33. Guery J, Favard L, Sirveaux F, Oudet D, Mole D, Walch G. Reverse total shoulder arthroplasty. Survivorship analysis of eighty replacements followed for five to ten years. J Bone Joint Surg Am 2006;88(8):1742–7. 34. Grammont PM, Baulot E, Chabernaud D. Resultats des 16 premiers cas d’arthropastie totale d’epaule inverse sans ciment pour des omarthoses avec grande rupture de coiffe. Rev Chir Orthop Reparatrice Appar Mot 1996;82(suppl I):169. 35. Nyffeler RW, Werner CM, Gerber C. Biomechanical relevance of the glenoid component positiong in the reverse Delta III total shoulder prosthesis. J Shoulder Elbow Surg 2005;14:524–8.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 47–58
Available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/cuor
CHILDREN
Osteochondritis dissecans of the knee Oliver S. Schindlera,b, a
Droitwich Knee Clinic, St. Andrew’s Road, Droitwich-Spa, Worcestershire WR9 8YX, UK 21 Wiltons, Wrington, North Somerset BS40 5LS, England, UK
b
KEYWORDS Osteochondritis dissecans; OCD; Osteonecrosis; Avascular necrosis; Loose body; Premature osteoarthritis; Gonarthrosis
Summary Osteochondritis dissecans (OCD) characterises a disease process predominately affecting male teenagers and young adults which, as its end-product, yields the separation of osteochondral fragments from the joint surface. Although OCD may occur in many joints, the knee appears to be by far the most commonly involved. Hence painful locking in a teenage knee should always raise the suspicion of OCD. The cause of the disease remains unclear and many theories have been developed, none of which has received unequivocal agreement. A multifactorial aetiology including elements of repetitive trauma and vascular insufficiency is henceforth considered most likely. The fundamental principle in the treatment of OCD is the timely recognition of the condition as lesions in the early disease process are more likely to be treated successfully. Proper initial assessment and grading of the lesion will allow for the right treatment protocol to be chosen. MRI may help in the staging process and in determining the lesions healing potential. Most cases fair well with conservative measures. In more advanced stages of the disease, surgical intervention ranging from subchondral drilling to fragment refixation may be required. The primary aim of any intervention is to achieve healing of the subchondral bone, and preservation of the articular cartilage as fragment separation may pave the way for subsequent development of osteoarthritis. & 2006 Elsevier Ltd. All rights reserved.
Introduction Osteochondritis dissecans or OCD, is a misnomer in terms of phrase, as it wrongly implies an inflammatory aetiology. It describes an intra-articular pathology affecting subchondral bone and surface cartilage in diarthrodial joints, which most commonly occurs in children and adolescents of male gender. It may result in the partial or total separation of
the osteochondral fragment, thus creating a loose body. If untreated, this may ultimately jeopardise the integrity of the joint and lead to the development of osteoarthritis. The disease may in principle affect any joint and is known to occur in the knee, elbow, ankle and hip. The knee, however, appears to be the site of predilection, with reported figures of 65–75%.
Historical review Corresponding author at: 21 Wiltons, Wrington, North Somerset
BS40 5LS, England, UK. Tel.: +44 1905 793 805; fax: +44 1905 795 916. E-mail address:
[email protected]. 0268-0890/$ - see front matter & 2006 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2006.11.006
The first description of loose bodies in the knee joint dates back to the 17th century and is credited to Ambroise Pare´,
ARTICLE IN PRESS 48 who also appears to be the first surgeon who successfully attempted their surgical removal.1,2 Monroe, in 1726, discovered a pea size loose body originating from the lateral femoral condyle during a cadaver examination, which he believed was caused by trauma.3 Another important historical description dates back to 1817, when the French surgeon Laennec described intra-articular loose bodies as joint mice or arthrophytes.4 By expressing his belief that loose bodies arise from the proliferation of cartilage of the periarticular synovial tissue he may have inadvertently described a condition later known as synovial chondromatosis, rather than OCD. Broca, in 1854, opposed both Monroe’s and Laennec’s opinion by promoting the theory that loose bodies are caused by ‘spontaneous necrosis’ of part of the articulating cartilage.4 Sir James Paget is credited with the classic account of OCD, which he described as ‘quiet necrosis’.5 In 1870 he reported on two children, both of whom suffered loose bodies in their knee. One, a little girl, was known to break thick pieces of wood over her knee whilst the other was an athletic school boy ‘with many blows and strains to his knee from sports’. Paget wrote: ‘How can such pieces of articular cartilage be detached from living bone? They cannot be chipped off—no force can do this. These bodies are sequestra exfoliated after necrosis of injured portions of cartilage without inflammation’. He differentiated OCD from an acute osteochondral fracture and noted that the process involved an avascular sequestrum without evidence of inflammatory change. The phrase ‘Osteochondritis dissecans’ however, was not coined until 1887. Franz Ko ¨nig, Professor of Surgery in Go ¨ttingen, described a series of young and otherwise healthy adults suffering loose cartilaginous fragments in their knee, ankle or elbow.6 Through the lack of trauma in all but one case and the absence of any disease he became intrigued about the aetiology of this condition, which he thought might be caused by a spontaneous process. In Ko ¨nig’s opinion, even severe trauma was unlikely to create osteochondral fragments in the common locations observed without creating significant damage to other structures. However, he did not rule out that in a minority of patients a localised joint surface contusion might induce a process of subchondral necrosis, followed by an inflammatory response and subsequent fragment dissecation. Ko ¨nig deliberately used the suffix ‘–itis’, as he was under the impression that these ‘corpora mobile’ were caused primarily by an inflammatory response to subchondral necrosis, which he based on the finding of giant cells in one of the retrieved specimens. Ko ¨nig was, however, unable to explain what initiated the process of osteochondritis, and hence concluded his article by saying that the true aetiology of OCD remained unknown. Although it is widely thought that the lesion should be more accurately termed ‘osteochondrosis’ or ‘osteochondrolysis’, the term OCD has prevailed.7,8 It is of interest to note that some confusion arose after Ko ¨nig had published his original account on OCD in the late 1880s, through substitution of the word dissecans with desiccans. ‘One author has brought his facts into line with the error in nomenclature by finding that the loose bodies he described were desiccated’, as quoted by Timbrell Fisher in his excellent article on the pathology and aetiology of loose bodies.9
O.S. Schindler
Aetiology A review of the literature reveals the lack of agreement among investigators concerning the aetiology of OCD. The most commonly quoted theories include trauma, followed by ischaemia and abnormal ossification through accessory centres of ossification within the epiphysis. There also appears to be some support for a genetic predisposition. Riedel, in 1896, at the 25th Congress of the German surgical Society, spoke on the subject ‘Contribution to the theory of arthrophytes’ by saying ‘Foreign bodies arise in the joints not only through trauma or as a consequence of arthritis deformans, but also through Ko ¨nig’s OCD. Until now, only the end-products of this disease in the form of completely detached bone-cartilage pieces are known’.10 In many respects little has changed since Riedel’s account some 110 years ago. Although the frequent occurrence of OCD in patients involved in sporting activities would support a repetitive trauma aetiology, on the basis of the currently available knowledge a multifactorial aetiology of OCD appears more likely.
Trauma Most theories on OCD aetiology centre on trauma, described either as an initial macro-trauma followed by repetitive micro-trauma or persistent repetitive micro-trauma alone. Both Paget and Ko ¨nig are often falsely associated as being proponents of the trauma theory, which could not be further from the truth. On reading their original accounts it would appear that both men believed that trauma, when it occurs, should be considered incidental rather than causative in the aetiology of OCD.5,6 Many authors, however, have considered trauma as the predisposing factor in the aetiology of OCD. Their theories are based on anatomical and biomechanical peculiarities of the knee joint. Fick, in 1904, demonstrated the importance of the tibial spines and the inner aspects of the femoral condyles for absorbing compressive forces and for providing guidance under varus, valgus and rotational stress,11 an observation later confirmed by Goodfellow and O’Connor.12 Owing to the central position of the eminence and its antero-posterior course, guidance is most effective in mid flexion and thus at a point where a high degree of rotational freedom is combined with a high axial load. Ludloff, in 1908, was the first to express the view that low-grade trauma slightly above physiological levels may be causative for OCD.13 In 1922, Roesner published a landmark article with the title ‘The development mechanics of OCD of the knee’.14 Based on Adolf Fick’s biomechanical principles of knee motion, Roesner believed that the mechanism of trauma was due to the repetitive impingement of the intercondylar eminence against the lateral aspect of the medial femoral condyle (MFC) during external tibial rotation—a movement pattern known as the ‘screw-homemechanism’. In his cadaver experiments he observed surface cartilage damage in common OCD locations after repeated leg extensions with the tibia held in fixed external rotation. He believed that through this mechanism a ‘dry fracture’ of the subchondral bone is created. He used the term ‘dry fracture’, as he thought that continuing external pressure
ARTICLE IN PRESS Osteochondritis dissecans of the knee through ongoing impingement prevented a subchondral haematoma, leading to a non-union and subsequent fragment dissecation. Fairbanks, in 1933, published his version of an impingement theory which, contrary to Roesner’s ‘screw home mechanism’, was based on a ‘violent rotation inwards of the tibia, driving the anterior tibial spine against the inner condyle’,15 a notion later supported by Wilson16 and Smillie.17 Fairbanks’ theory of anterior tibial spine impingement through internal tibial rotation, however, failed to explain lesions in the most common locations of the posterolateral aspect of the medial femoral condyle. Whilst the impingement theses may explain the development of OCD around the lateral aspect of the medial femoral condyle, they do not account for lesions occurring at other sites such as the lateral femoral condyle and patella. Furthermore, tibial eminence impingement is not seen during normal walking or running and evidence of abnormal tibial eminence morphology or abnormalities in the relationship between tibial eminence to the MFC in OCD cases is missing. Green reported on a number of cases with incomplete separation of the osteo-articular fragment, all of which presented intact surface cartilage in the area closest to the tibial eminence, henceforth questioning the validity of Fairbanks’s and Roesner’s theory of impingement.18 Other theories consider pressure exerted from the patella onto the lateral aspect of the MFC between 901 and 1301 of knee flexion as a potential pathomechanism.19 Bandi based his theory on the observation that during mid-flexion the area of OCD predilection on the MFC becomes trapped between patella and tibia.20 He believed that both tibia and patella work like a pair of pliers, exerting pressure onto the femoral condyle. Through the creation of a perpendicular pressure gradient, which he described as ‘strain waves’, subchondral bone bulges forward and eventually demarcates, thus explaining the often observed chondral prominence of OCD lesions (Fig. 1). A number of experimental studies have given support to the trauma hypothesis. Rehbein performed an experimental study on dogs in which he reproduced OCD like lesions by exposing the anterior aspect of their knees to repetitive
Figure 1 Diagram demonstrating Bandi’s theory of compression. (Reproduced with kind permission and copyright & of the Hans Huber Verlag, Bern.20)
49 micro-trauma. He observed a fibrous demarcation surrounding the surface cartilage and subchondral bone, which was histologically indistinguishable from OCD lesions seen in humans.21 Langenskiold produced lesions, which histologically and radiologically resembled OCD, by cutting a segment of articular cartilage in young rabbits, leaving the cartilage attached to the synovium and replacing the fragment in its bed. He concluded that OCD might be caused by a cartilage fracture in childhood.22 Aichroth conducted a similar study using adult New Zealand White rabbits.7 He was able to show that undisplaced but stable osteochondral fractures resembled OCD in humans both radiologically and histologically. Lesions that were stabilised healed but those with tenuous stability developed into avascular unstable lesions. Clinical and observational studies have also confirmed the association between OCD and trauma. Rosenberg examined osteochondral fractures involving the lateral femoral condyle, which had been caused by endogenous trauma.23 He demonstrated that un-united osteochondral fractures become indistinguishable from OCD both radiologically and microscopically. Kennedy et al.24 found two clinical groups in their study of osteochondral fractures of the femoral condyles. They distinguished between those patients who sustained ‘exogenous’ fractures caused by direct trauma (e.g. direct blow), to patients with ‘endogenous’ fractures caused by rotatory and compressive forces. They were able to reproduce some of these lesions in cadaver knees, although the variety of locations observed in OCD has not been reproduced experimentally. A history of previous knee trauma, usually of moderate degree, is reported in approximately 50% of all patients suffering OCD.7,18,25–29 In light of the clinical and experimental evidence it would appear that direct and indirect trauma, usually related to sports injuries, are implicated in the pathogenesis of OCD, although it is widely agreed that acute macro-trauma when it occurs appears to be incidental rather than causative.
Ischaemia It has been suggested that the interruption of blood-flow to end arteries of the femoral condyle may precipitate ischaemic necrosis with subsequent sequestration of the subchondral bone and articular cartilage.30 Koch, in 1879, performed a series of experiments on bone necrosis and noted that subchondral bone infarction with loose body formation was the result of obstruction of the entire capillary bed of the area concerned.31 Rieger suggested that fat emboli were responsible for blocking the end arteries.32 Watson-Jones, however, believed in a systemic abnormality causing thrombosis or embolism of end arteries, which also helped to explain the large number of cases with multiple site involvement in the absence of antecedent trauma.33 The anatomical microvascularity of the distal femur was first investigated by Rogers and Gladstone in the late 1940s.34 They performed injection studies confirming a rich blood supply with numerous anastomoses in the subchondral bone. The authors concluded that ischaemia would be an unlikely factor in the aetiology of OCD. Enneking, a firm proponent of the ischaemic theory, compared the blood
ARTICLE IN PRESS 50 supply of the subchondral bone to that of the bowel mesentery with its end arterial arcades.30 He found that the terminal branches within the subchondral bone poorly anastomose with their neighbours, hence infarction would result in necrosis of wedge-shaped areas immediately beneath the articular cartilage. Further support to the ischaemia hypothesis was provided by Ficat et al.35 who performed marrow pressure studies on patients suffering OCD and osteonecrosis. All of their patients had abnormal haemodynamics, with increased marrow pressure and circulatory obstruction owing to stasis. Lo ¨hr36 and Lang37 both believed that irregularities in epiphyseal perfusion through changes from capsular to diaphyseal blood supply during epiphyseal closure are a key issue in the development of OCD. Their theory would appear plausible but fails to account for the occurrence of OCD in patients with a wide open physis.
Accessory centres of ossification The development of separate ossific nuclei in the distal femoral epiphysis and their ossification process during maturation has led some researchers to conclude that OCD may simply be a variant of normal growth. Seidenstein38, who considered this process to be a localised disturbance of condylar growth, observed spontaneous healing without active treatment. Ribbing39 reviewed knee radiographs of 291 children for fragmentation of the ossific nucleus and compared those evidencing detached osseous islets within the articular cartilage outside the epiphysis to those with OCD. He found the locations similar in both groups and concluded that the ossification centre was a ‘locus minoris resistentiae’. He henceforth proposed the aetiology of OCD to be based on the separation of an accessory bone nucleus, which at least partially re-attaches during maturation, but which may completely separate if exposed to trauma.
Genetic
O.S. Schindler repetitive loading continues, the healing ability of bone may be impaired leading to avascularity and subsequent bone necrosis. Under ideal circumstances (early detection and treatment), resorption of the avascular bone is initiated by ingrowth of vascular buds and mesenchymal cells, creating a zone of granulation tissue between the viable and necrotic bone. This process of dead bone resorption and its replacement with new bone characterises the repair mechanism known as ‘creeping substitution’, which may, especially in juvenile patients, successfully re-establish the subchondral cancellous bone architecture.26 In most cases, however, the repair is inadequate. The formed callus remains un-calcified, showing an exuberance of cartilaginous elements, which may shield-off the lesion preventing active repair. Expansion of this interstitial callus layer, which Roesner14 described as ‘callus luxurians’, may elevate the osteo-articular fragment beyond the joint level increasing its mechanical vulnerability. This phenomenon is often observed during arthroscopy, when OCD lesions appear slightly protuberant despite intact surface cartilage. The lesion is biomechanically ill-equipped to withstand mechanical forces applied, especially if it is situated in a weight bearing area. Although the necrotic bone is held in place by the macroscopically intact overlying surface cartilage, it is assumed that this process also influences the basilar growth of the articular cartilage and its stress resilience. Once a subchondral non-union is established, the support for the articular cartilage is lost and degenerative changes are likely to occur. Under these circumstances the articular cartilage may fracture, leading to synovial fluid intrusion and inhibition of a potential healing response. Continuing hostile mechanical forces will further compromise fragment stability, eventually creating a loose osteochondral fragment. The fragment may remain in its crater, and through continuing joint movement be eroded. Once discarded into the joint cavity, a loose body is liable to impinge between tibia and femur, leading to third-body wear. The articular cartilage of the detached osteochondral fragment usually remains viable as it receives its nutrition from the synovial
This notion gained some popularity through a number of studies reporting a familial incidence of OCD.40–45 Petrie, however, detected only one OCD case amongst first degree relatives of 34 patients suffering OCD, indicating the rarity of a potential hereditary influence.46 Multiple epiphyseal dysplasia, with its autosomal dominant and recessive hereditary patterns, should always be considered in patients with OCD. Hence, patients who are thought to have a familial form of OCD may, in fact, be suffering a variable expression of multiple epiphyseal dysplasia. Some authors have described an association of OCD with dwarfism, tibia vara and Perthes disease, indicating a possible genetic influence in isolated cases.43,47–49 It would, however, appear that heredity has little if any relationship with OCD other than a possible rare familial form that may exist.
Pathophysiology Precipitating insults at a vulnerable site causes a stress reaction, with locally impaired subchondral bone homoeostasis, which may progress into a stress fracture. If
Figure 2 Anatomical OCD classification. (Reproduced with kind permission and copyright & of the British Editorial Society of Bone and Joint Surgery, London.7)
ARTICLE IN PRESS Osteochondritis dissecans of the knee fluid. The subchondral bone, however, will undergo necrosis and complete resorption.50
Epidemiology OCD has been classified according to the maturation status of the distal femoral physis into three groups: juvenile OCD in patients with wide open physis, adolescent OCD in patients with closing physis and adult OCD with fully closed physis. Juvenile OCD is by far the most common form observed. It has a peak prevalence between the age of 10 and 13 and is rarely seen in patients younger than 10 years of age.26 Boys are more commonly affected than girls, with a ratio of 5:3. Bilateral cases of OCD have been reported in up to 25% of affected individuals, with lesions usually being different in terms of size and symptoms.51,52
51 detaching. Additional prognostic factors are fragment stability, the status of the articular cartilage, and the mechanical environment, especially in view of a potential deviation of the mechanical axis.57
Clinical evaluation
Natural history
The symptoms associated with OCD are often vague and poorly localised. Some patients, however, may be aware of more circumscribed discomfort antero-medial to the patella, owing to the location of the classic OCD lesion on the medial femoral condyle. In the latter patient group a potential differential diagnosis of a medial plica syndrome, a medial meniscal tear or patello-femoral maltracking should be borne in mind.58 The degree of pain described by patients suffering OCD varies greatly, but is usually dull in character. Stiffness and swelling are infrequent and not a general feature in patients with OCD. In more advanced cases, especially those where joint incongruity develops, a sensation of catching, locking or giving-way may be reported. Symptoms are usually intermittent and often related to exertion. Once the lesion detaches and a loose body forms, symptoms become more specific and, more often than not, are unrelated to activities. In these patients a knee effusion and synovitis are sometimes observed. Quadriceps atrophy and weakness may also develop and reflect the chronicity of the condition. A positive Axhausen’s sign describes local tenderness of the involved femoral condyle on direct palpation of the flexed knee.59 Once the osteoarticular fragment has dissecated, the loose body or the defect may be palpable. Movements may be restricted and a mild flexion deformity is often observed (Fig. 3). When examining a child with suspected OCD it is advisable to watch the patient walk, as they may display an antalgic gait. Some patients may walk with an out-toeing gait which, according to Fairbanks15 and Wilson,16 is based on the thesis that impingement of the medial tibial eminence on the
The natural history of OCD is dependant on a multitude of circumstances, with the degree of patient maturity being by far the most important predictive factor. Patients in the juvenile group usually have a high healing potential ranging from 65% to 75%. In principle, the older the individual the less predictable the outcome and the higher the complication rate. In adolescent patients only about 50% achieve complete resolution. In the adult group the chances of healing are low and hence the likelihood of developing premature degenerative joint disease are high.52,55,56 The natural history of OCD in adults has been well documented by Linden,25 who reviewed 40 patients with an average age of 29.4 at diagnosis. All patients were treated conservatively and followed-up for 32.5 years on average. After 20 years, 79% of patients had already developed symptoms of degenerative arthritis, which he estimated to be at least 10 years earlier when compared to the occurrence of primary knee arthritis in an otherwise normal patient group. Other important factors influencing healing and long-term prognosis include the duration of the disorder, size of the lesion and its location. The latter factor is of particular importance as lesions close to or within the weight-bearing surface are at a higher risk of developing non-union and of
Figure 3 Lateral radiograph showing a rare case of OCD affecting the inferior aspect of the retropatellar surface. Within the knee the patella is affected in about 5–10% of OCD cases.
Anatomic location Aichroth developed a classification system based on a survey of 200 patients, defining the various sites of OCD within the knee joint (Fig. 2).7 The lesion most commonly involves the lateral posterior portion of the MFC, where it can be found in about 70% of cases. This is therefore described as the ‘classical’ OCD location.18 A more wide-spread involvement of trochlea and central areas of the MFC is seen in about 15% of cases and is classified as the so-called ‘extended classical’ locations. The lateral femoral condyle is affected in about 10% of cases, where lesions are commonly seen around the central weight-bearing portion, whilst lesions close to the intercondylar notch are rather unusual. Isolated involvement of the femoral trochlea and the patella is seen in less than 5% of cases, with almost all patellar lesions being located in the infero-medial quadrant (Fig. 5).53,54
ARTICLE IN PRESS 52
O.S. Schindler around 301 of knee flexion. External rotation of the tibia immediately relieves this pain.
Investigations
Figure 4 The illustration on the left shows an antero-posterior radiograph of a ‘classic’ OCD lesion on the postero-lateral aspect on the medial femoral condyle. Illustration on the right shows a coronal MRI scanning sequence of the same patient. The OCD lesion shows grade III changes according to the MRI classification in Table 2. The fragment is still in situ but partially surrounded by a fluid layer. Some sclerosis between layers is present.
Figure 5 Lateral radiograph showing an end-stage ‘extended classic’ OCD lesion. Both the defect on the medial femoral condyle (*), and the dissecated osteochondral fragment are visible (**). The patient presented with a 151 fixed flexion deformity and significant pain on full flexion and weight bearing.
lesion causes patients to walk with the leg externally rotated to avoid impingement. The ‘Wilson’s sign’ describes a test in which the knee is flexed to 901, the tibia held in internal rotation and the knee slowly extended.16 The sign is considered positive if the patient experiences pain at
Plain radiographs are usually diagnostic. An antero-posterior tunnel view in 45–601 of knee flexion will place the femoral condyles in greater profile than a standard antero-posterior view and is therefore preferred. Good quality films will reveal a well circumscribed area of subchondral bone demarcated from the surrounding femoral condyle by a crescent-shaped radiolucent line (Fig. 4). On sagittal views the lesion is classically located posterior to the midline.60 The affected subchondral bone may present with slightly increased density when compared to the parent, a finding that is particularly noticeable in sub-acute and chronic cases. Milgram61 showed that the radiodensity is owing to either secondary calcification in degenerating articular cartilage, new bone formation following revascularisation or calcification in new surface layers of cartilage and bone. Subchondral sclerosis alongside the margin of the lesion provides an indication of the chronicity of the disease process and is considered by some authors to be a sign of progressive non-union (Fig. 5). Before the advent of magnetic resonance imaging (MRI), radio-isotope bone scans (Tc99) were considered to be a more sensitive diagnostic investigation for monitoring the clinical course of OCD than radiographs (Table 1).62 Although technetium bone scans are thought to provide information about the biological healing capacity of OCD, they have failed to gain widespread acceptance, most likely owing to the length of the test and the perceived risks associated with the radiotracer. Furthermore, scintigraphy has a poor predictive index, which in part is due to the persistence of nucleotide activity long after lesion resolution. MRI is by far the most sensitive and sophisticated imaging modality allowing for early diagnosis of OCD of the knee (Fig. 4). It may also be helpful in the distinction from osteonecrosis, which often presents a more widespread involvement of the condyle, especially in the adult. Increased signal from fluid at the interface is indicative of delayed union. MRI appears to be the investigation of choice in monitoring the healing process and revascularisation of OCD lesions, by providing the added benefit of assessing the articular cartilage status (Table 2).63,64 Hefti et al.65 described a popular classification system for OCD based on MRI findings, which is in wide usage. Most imaging methods however, carry the disadvantage of failing to provide conclusive evidence on the subchondral fragment stability unless the osteochondral fragment has dissecated. Arthroscopy has become an invaluable tool in the diagnosis and management of OCD in selected cases. Direct visualisation and probing of the lesion allows the surgeon to confirm the diagnosis, accurately stage the lesion, assess fragment stability and to execute treatment. Arthroscopy should, however, be used sparingly and reserved for such cases where surgical intervention is required, especially if a good quality MRI is readily available. Guhl66 developed a classification system based on the arthroscopic assessment of 44 patients with OCD, which has found widespread acceptance (Table 3). It distinguishes four different OCD
ARTICLE IN PRESS Osteochondritis dissecans of the knee
Table 1 Cahill’s classification of OCD based on bone scanning. Stage
Bone scan finding
0
Normal radiographic and scintigraphic appearance Lesion is visible on plain radiographs, but bone scan reveals normal findings Bone scan reveals increased uptake in the area of the lesion Bone scan reveals increased isotopic uptake in the entire femoral condyle Bone scan reveals uptake in the tibial plateau opposite the lesion
1 2 3 4
Table 2 Hefti’s classification system, based on MRI appearances of OCD. Stage
MRI appearances
I
Small change of signal without clear margins of fragment Osteochondral fragment with clear margins, but without fluid between fragment and underlying bone Fluid is visible partially between fragment and underlying bone Fluid is completely surrounding the fragment, but the fragment is still in situ Fragment is completely detached and displaced (loose body)
II
III IV V
Table 3 Guhl’s classification of OCD, based on arthroscopic assessment. Stage
Arthroscopic findings
I II III IV
Intact lesions Lesions showing signs of early separation Partially detached lesions Craters with loose bodies
stages, ranging from stable lesion to those with established loose bodies. Surgeons should be aware that the subchondral bone fragment may be completely separated from its surrounding host bone whilst the covering articular surface cartilage stays in continuity. In this situation, the lesion usually presents ballottment and indentation on probing.
Conservative treatment The treatment of OCD is dependant upon the patient’s age, the anatomical location of the lesion and the degree of
53 involvement. Non-operative management still remains the treatment of choice for skeletally immature children, based on numerous observations of successful healing in this patient group.67–69 Most children with grade I and II lesions can be treated by activity adjustment and observation alone, but symptoms might dictate the need for a temporary regimen of reduced weight bearing.70 Impact and sporting activities, especially those with elements of twisting and turning, should be avoided. It is also important to appraise patients and parents of the 12–18 months time frame for progressive healing. The question of whether or not to immobilise the knee has been the subject of some controversy. Prolonged immobilisation in a position evading contact between the OCD lesion and the tibia has been advocated by many authors, who believe that movement jeopardises healing of subchondral bone. Others have argued that immobilisation has a detrimental effect on cartilage nutrition and emphasised the need for passive mobilisation to promote cartilage health.17,26,71 The failure of the articular cartilage in OCD, however, appears to be secondary to the failure of the subchondral bone. It is therefore plausible to implement a period of rest, if not immobilisation, at least during the acute stages of OCD. Cylinder cast or hinged braces are applied in slight knee flexion and implemented for periods of up to 6 weeks. Braces have the advantage of allowing for passive knee flexion but should only be considered in reliable patients. The use of hinged off-loader braces appears to be an attractive treatment alternative but their efficacy has not yet been evaluated in clinical practice. Flynn et al.72 have recommended a three-phase approach to the non-operative management of OCD. In phase I (week 0–6), the knee is immobilised and patients required to partial weight bear. Patients usually progress to phase II at around 6 weeks, when the acute pain has subsided, and radiographs provide evidence of healing. At this stage, full weight bearing without immobilisation is allowed and a physical therapy programme commenced to improve knee motion and muscle strength. A patient who remains pain-free after 12 weeks and whose radiographs continue to show healing progresses to phase III, in which low level sporting activities are introduced. Activities involving high impact and shear stresses are to be avoided until the child has been pain-free for several months and the lesion shows radiological evidence of resolution. Repeat immobilisation might have to be considered if radiographs show progressive non-union or if symptoms reccur. Treatment compliance poses a problem in this young and active patient group, challenging the physician to emphasise to both parents and patients potential risks and long-term consequences if the protocol is not followed.
Operative treatment Surgical management is dependant on certain characteristics of the lesion but usually reserved for patients who fail to improve with conservative measures or those with lesions of questionable stability and abnormal articular and subchondral status. The main goal is to preserve the
ARTICLE IN PRESS 54
Figure 6 Diagram showing the technique of ‘trans-lesional’ Pridie drilling. (Reproduced with kind permission and copyright & of the Thieme Verlag, Stuttgart, New York.78)
fragment and to maintain joint congruity. Once a lesion has reached Guhl stage II or III, surgical intervention to avoid potential non-union and subsequent detachment of the lesion should be considered. In order to promote healing and successful union between the osteochondral fragment and the subchondral bone, revascularisation of both areas has to be established. In situ drilling is recommended for stable lesions with intact articular cartilage (Fig. 6). The concept, which was first described by Wildey73 for the treatment of un-united fractures in two naval officers, is to create channels for vascular ingress stimulating local revascularisation. Either a trans-articular (antegrade) or a retrograde approach may be used.74 Retrograde drilling using an ACLguide is technically more demanding but avoids violation of the articular surface and may be particularly useful for inaccessible areas on the posterior condyles.75 The procedure is performed using arthroscopic and fluoroscopic control and is aimed to create 3–5 channels by placing a smooth Kirschner wire just below the subchondral articular margin. Post-operatively, patients are encouraged to maintain a full range of motion whilst weight bearing is restricted for 4–6 weeks. Non-weight bearing, however, is to be avoided as it increases articular compressive forces through quadriceps contraction and continuing knee flexion. Results with both techniques have generally been excellent particularly in the immature patient, with healing rates of up to 90%. In skeletally mature patients, the outcome is less predictable with reported healing rates around 50%.74,76,77 In patients with closed, unstable or partially detached lesions (Guhl III), in situ fixation is usually the treatment of choice, with the post-operative rehabilitation regimen being essentially the same as described earlier and based on a prolonged period of limited weight bearing. A variety of bioabsorbable and non-absorbable fixation devices have been
O.S. Schindler promoted which again may be used in antegrade or retrograde fashion.78 In order to provide rotational stability, two such devices are required, which should be placed in divergent directions. Traditionally, Kirschner wires, Herbert screws, and cannulated AO screws have been used successfully, but may require a second procedure for hardware removal.79–81 The use of cannulated screws provides better compression and superior stability than wires or bioabsorbable pins and should be considered for the fixation of very large fragments. Screw heads need to be countersunk to avoid damage to opposing surfaces unless the retrograde technique is utilised. Alternatively, bio-absorbable pins and nails made of polyglycolide or polylactide, which degrade within 6–18 months may be used. Some have surface barbs to improve fixation and to prevent the device from backing-out. Drilling of the bone and the introduction of the device is facilitated through a cannula, allowing for a truly arthroscopic application by causing minimal surface cartilage damage. Some clinical studies have provided encouraging results even in the skeletally mature patient.81,82 Despite the reported success clinicians should be aware of the potential morbidity associated with intraarticular fragment fixation, as a number of complications have been reported. Metallic devices have shown wire migration or screw head prominence, with subsequent damage to adjacent articular surfaces. Bio-absorbable pins and nails may break or loosen and through degradation of the material may create synovitis, foreign body reaction or lytic lesions. Such local reactions are primarily associated with polyglycolide implants with reported figures of up to 40%, and are thought to be due to the speed of material degradation.83 Polylactide implants, which degrade far more slowly, present local reaction in less than 5% of cases (Fig. 7).84,85 Sclerotic margins between the opposing surfaces of subchondral bone sometimes develop in partially detached lesions. These features are well demonstrated on MRI scan or by direct visualisation during arthroscopy. Such lesions require superficial debridement using a burr or a Volkmann spoon, to remove the sclerosis and to expose bleeding bone
Figure 7 Diagram showing the use of biodegradable pins in the fixation of potentially unstable OCD lesions. Introduction of pins in a cross fashion facilitates compression and rotatory stability. (Diagram reproduced with kind permission of ArthroCare Europe, Stockholm).
ARTICLE IN PRESS Osteochondritis dissecans of the knee before stabilisation is attempted, as otherwise healing is less likely to be achieved (Fig. 8).86 Application of additional bone graft is occasionally necessary. This procedure often necessitates an open exposure of the lesion, but in experienced hands an attempt can be made to perform the debridement arthroscopically. Once the lesion has reached Guhl stage IV, arthroscopic assessment is urgently required either to retrieve the loose fragment, to prevent impingement or to attempt fragment re-fixation. The viability and suitability for re-fixation depends on the condition of the surface cartilage and the amount of remaining subchondral bone. If the cartilage appears crenellated or hypertrophic and the subchondral bone stock inadequate to facilitate secure fixation, the
Figure 8 Diagram showing the technique of debridement. This procedure is indicated for detached, unstable or partially unstable lesions where sclerosis at the base of the lesion has developed, hindering vascular ingress despite translesional drilling. (Reproduced with kind permission and copyright & of the Thieme Verlag, Stuttgart, New York.86)
55 fragment should be discarded. The subchondral defect is then debrided of fibrous tissue to evoke a vascular response, which will recruit mesenchymal stem cells that differentiate into fibrocartilage.87 Alternatively, subchondral bleeding can also be facilitated with marrow stimulation techniques such as microfracture and Pridie drilling.7,88 The patient is then required to touch-toe weight-bear for 5 weeks followed by partial weight-bearing for a further 3 weeks. Some surgeons have recommended the use of CPM for 4–6 h daily during the first 4 weeks of treatment89 Although this treatment approach is suitable for patients with defects of less than 10 mm in depth, fibrocartilage is less resilient to mechanical stress, especially shear, compared to hyaline cartilage and deterioration of the repair has been observed over time.90,91 If the defect is deeper than 10 mm and located in a weight-bearing area, grafting procedures may need to be considered. Osteochondral autografts (OATS, Mosaicplasty) have been used with variable success. The technique involves the harvest of cylindrical grafts of at least 10 mm in depth from a non-weight bearing aspect of the joint, usually around the trochlea, and its placement in the defect.92 Graft positioning with matching of surface convexity and graft stability is critical in establishing a normal load bearing surface. Potential disadvantages of this technique are donor site morbidity and graft loosening, especially in uncontained defects and those requiring multiple cylindrical grafts.93 Successful secondary reconstruction with osteochondral block allograft has been described in patients with significant surface defects, but no long-term results in paediatric patients are yet available.94–96 Autologous chondrocyte implantation (ACI) combined with autologous bone grafting, the so-called ‘sandwich technique’, is currently under evaluation and has provided some encouraging preliminary results (Figs. 9 and 10).97,98 Bone graft can be obtained from the proximal tibia, therefore reducing donor site morbidity usually associated with iliac crest graft harvest. The lesion is debrided and freed of fibrous tissue until bleeding subchondral bone is exposed. Loose or damaged cartilage has to be removed and
Figure 9 Debridement (including microfracture), bone grafting and chondrocyte implantation (MACI technique) in a large ‘extended classic’ lesion on the medial femoral condyle in a 19-year-old male. Previous attempts to re-fix two large osteochondral fragments only resulted in healing of the antero-medial portion (dotted line).
ARTICLE IN PRESS 56
O.S. Schindler
Figure 10 Coronal MRI sequences and arthroscopic photographs of the same patient as in Fig. 9. The figures on the left show the extended defect on the medial femoral condyle at the time of the cartilage cell harvest. The figures on the right were obtained 9 months after the MACI procedure, and show reconstitution of the medial femoral condyle.
a firm cartilage rim established. The bone graft is then impacted into the lesion and covered with a periosteal flap or type I collagen membrane. If performed as a two-stage procedure, the patient is then rehabilitated until the bone graft has consolidated, which may take 8–16 weeks. At the second stage a further membrane is placed onto the defect, sutured against the surrounding cartilage rim and sealed with fibrin glue. A suspension of autologous cartilage cells, which are derived from cartilage harvested at least 6 weeks earlier, is then injected under the membrane. Especially in uncontained lesions close to the intercondylar notch, watertight fixation of the type I collagen membrane or periosteal flap is often impossible. In this situation, matrix autologous chondrocyte implantation (MACI) represents an attractive alternative. The membrane, which is impregnated with chondrocytes, is attached to the bone graft using fibrin glue.99 Normal lower extremity alignment is critical for success in ACI, and the clinician should therefore consider performing a corrective osteotomy in mature patients with mechanical axis deviation.57 Post-operative protocol includes limited weight bearing for 6–8 weeks, avoidance of impact and shear forces, with restrictions being placed on sporting activities for up to 18 months. The patient’s commitment to the post-operative rehabilitation programme is of the utmost importance to safeguard success. Although biopsies to-date have not shown true hyaline cartilage regeneration, the durability of these transplants has been well documented in the medium term. In this difficult group of patients, 84% presented good to excellent results, at an average of 3.9 years of follow-up.100
Summary Although OCD has been a known entity for over a century, a definitive cause has yet to be established. The primary aims of treatment are healing of the subchondral bone and preservation of the articular cartilage, with the ultimate goal of preventing arthritis. Surgical intervention has been able to alter the natural history in the more severely affected cases. However, long-term outcome studies to reveal if such interventions will allow the knee to stand up to the various stresses imposed over a lifetime, are still awaited. Timely recognition of the disease is essential as lesions in the early disease process are more likely to be treated successfully. Proper initial assessment and grading of the lesion will allow for the right treatment protocol to be chosen. MRI may help in the staging process and in determining a lesion’s healing potential. The fundamental principle in the treatment of stable lesions is based on shortterm immobilisation, the cessation of repetitive impact loading and a gradual return to normal activity. For stable lesions that fail to improve within 6 months, arthroscopic drilling should be considered. Unstable and partially detached lesions require fixation. If the fragment is unsalvageable and the lesion is small, simple debridement may achieve success through fibrocartilage ingrowth. In larger defects, however, complex reconstructive procedures may be necessary. Patients and parents need to receive realistic appraisal of the long-term prospects and the potential risks and complications, especially if treatment advice is not followed.
ARTICLE IN PRESS Osteochondritis dissecans of the knee
References 1. Pare´ A. Oeuveres Completes, vol. 3. Paris: JB Balliere; p. 1840–18; 32. 2. Pare´ A. The case reports and autopsy records of Ambroise Pare´. In: Hamby WB, editor. Springfield, IL: Charles C. Thomas; 1960. 3. Monroe A. Part of the cartilage of the joint separated and ossified. Med Essays Observations 1738;4:305. 4. Nagura S. The so-called osteochondritis dissecans of Ko ¨nig. Clin Orthop 1960;18:100–22. 5. Paget J. On the production of some of the loose bodies in joints. St Barth Hosp Rep 1870;6:1–4. ¨ ber freie Ko 6. Ko ¨nig F. U ¨rper in den Gelenken. Dtsch Z Chir 1887;27:90–109. 7. Aichroth P. Osteochondritis dissecans of the knee. A clinical survey. JBJS 1971;53-B:440–7. 8. Jonasch E. Das Kniegelenk. Berlin: deGruyter; 1964. p. 231–8. 9. Fisher AGT. A study of loose bodies composed of cartilage or of cartilage and bone occurring in joints. With special reference to their pathology and aetiology. Br J Surg 1920;8:493–526. 10. Riedel. Verhandlungen des 25 Kongress der Deutschen Gesellschaft fu ¨r Chirurgie 1896. 11. Fick A. Handbuch der Anatomie und Mechanik der Gelenke, vol. 1. Anatomie der Gelenke. Jena: Gustav Fischer; 1904. 12. Goodfellow J, O’Connor J. The mechanics of the knee and prosthesis design. JBJS 1978;60-B:358–69. 13. Ludloff R. Zur Frage der Osteochondritis dissecans am Knie. Arch Klin Chir 1908;87:552–70. 14. Roesner E. Die Entstehungsmechanik der sogenannten Osteochondritis dissecans am Kniegelenk. Brun’s Beitr Klin Chir 1922;127:537–61. 15. Fairbanks HAT. Osteochondritis dissecans. Br J Surg 1933;21: 67–82. 16. Wilson JN. A diagnostic sign in osteochondritis dissecans of the knee. JBJS 1967;49-A:477–80. 17. Smillie IS. Osteochindritis dissecans. London: Livingstone; 1960. 18. Green JP. Osteochondritis dissecans of the knee. JBJS [Br] 1966;48-B:82–91. 19. Baumgartl F. Das Kniegelenk. Berlin: Springer; 1964. p. 348–62. 20. Bandi W. Die retropatellaren Kniegelenkscha ¨den. Bern: Huber; 1981. p. 38–41. 21. Rehbein F. Die Entstehung der Osteochondritis Dissecans. Arch Klin Chir 1950;265:69–114. 22. Langenskiold A. Can osteochondritis dissecans arise as a sequel of cartilage fracture in early childhood? Acta Chir Scand 1955;109:206–9. 23. Rosenberg NJ. Osteochondral fractures of the lateral femoral condyle. JBJS 1964;46-A:1013–26. 24. Kennedy JC, Grainger RW, McGraw RW. Osteochondral fractures of the femoral condyles. JBJS 1966;48-B:436–40. 25. Linden B. The incidence of osteochondritis dissecans in the condyles of the femur. Acta Orthop Scand 1976;47:664–7. 26. Green WT, Banks HH. Osteochondritis dissecans in children. JBJS 1953;35-A:26–47. 27. Scott Jr DJ, Stevenson CA. Osteochondritis dissecans of the knee in adults. Clin Orthop 1971;76:82–6. 28. Chiroff RT, Cooke III CP. Osteochondritis dissecans. A histologic and microradiographic analysis of surgically excised lesions. J Trauma 1975;15:689–96. 29. Johnson LL, Uitvlugt G, Austin MD. Osteochondritis dissecans of the knee. Arthroscopic compression screw fixation. Arthroscopy 1990;6:179–89. 30. Enneking WF. Clinical musculoskeletal pathology. Gainsville: Shorter Printing Co.; 1977. p. 147.
57 ¨ ber embolische Knochennekrosen. Arch Klin Chir 31. Koch W. U 1879;23:315. 32. Rieger H. Zur Pathologie von Gelenkma ¨usen. Mu ¨nch Med Wschr 1920;67:719–25. 33. Watson-Jones R. Fractures and joint injuries. 4th ed., vol. 1. London: Livingstone; 1952. p. 97. 34. Rogers WM, Gladstone H. Vascular foramina and arterial supply of the distal end of the femur. JBJS 1950;32-A:867–74. 35. Ficat P, Arlet J, Mazie `res B. Osteochondritis dissecans and osteonecrosis of the lower end of the femur. Value of functional investigation of the bone marrow. Sem Hosp Paris 1975;51:1907–16. 36. Lo ¨hr W. Die Osteochondritis dissecans und das Gelenkmausleiden. Zbl Chir 1929;56:2242. 37. Lang FJ. Die Osteochondritis dissecans. Brun’s Beitr Klin Chir 1941;171:618. 38. Seidenstein H. Osteochondritis dissecans of the knee with spontaneous healing in children. Bull Hosp Jt Dis 1957;28: 123–34. 39. Ribbing S. The hereditary multiple epiphyseal disturbance and its consequences for the aetiogenesis of local malacias—particularly the osteochondrosis dissecans. Acta Orthop Scand 1955;24:286–99. 40. Bernstein MA. Osteochondritis dissecans. JBJS 1925;7:319–29. 41. Gardiner TB. Osteochondritis dissecans in three members of one family. JBJS 1955;37-B:139–41. 42. Pick MP. Familial osteochondritis dissecans. JBJS 1955;37B:142–5. 43. Tobin WJ. Familial osteochondritis dissecans with associated tibia vara. JBJS 1957;39-A:1091–105. 44. Stougaard J. The hereditary factor in osteochondritis dissecans. JBJS 1961;43-B:256–8. 45. Mubarak SJ, Carroll SC. Familial osteochondritis dissecans of the knee. Clin Orthop 1979;140:131–6. 46. Petrie PWR. Aetiology of osteochondritis dissecans. JBJS 1977;59-B:366–7. 47. White J. Osteochondritis dissecans in association with dwarfism. JBJS 1957;39-B:261–7. 48. Wiberg G. Spontaneous healing of osteochondritis dissecans in the knee joint. Acta Orthop Scand 1943;14:270–7. 49. Woodward AH, Decker JS. Osteochondritis dissecans following Legg–Perthes disease. South Med J 1976;69:943–4. 50. Fisher AGT. Internal derangements of the knee-joint. London: HK Lewis & Co; 1933. p. 129–35. 51. Bednarz PA, Paletta Jr GA, Stanitski CL. Bilateral osteochondritis dissecans of the knee and elbow. Orthopedics 1998;21:716–9. 52. Schenk Jr RC, Goodnight JM. Osteochondritis dissecans. JBJS 1996;78-A:439–56. 53. Desai SS, Patel MR, Michelli LS, Silver JW, Lidge RT. Osteochondritis dissecans of the patella. JBJS 1987;69-B: 320–5. 54. Smith JB. Osteochondritis dissecans of the trochlea of the femur. Arthroscopy 1990;6:11–7. 55. Twyman RS, Desai K, Aichroth PM. Osteochondritis dissecans of the knee. A long term study. JBJS 1991;73-B:461–4. 56. Williams Jr JS, Bush-Joseph CA, Bach Jr BR. Osteochondritis dissecans of the knee. Am J Knee Surg 1998;11:221–32. 57. Dolanc B, Burge M, Tabatabai A. Tibia osteotomy in the treatment of osteochondritis dissecans. Orthopa ¨de 1981;10: 80–2 [in German]. 58. Schindler OS. The synovial plicae of the knee. Curr Orthop 2004;18:210–9. ¨tiologie der Ko 59. Axhausen G. Die A ¨hlerschen Erkrankung der Metatarsalko ¨pfchen. Beitr Klin Chir 1922;126:451–76. 60. Harding III WG. Diagnosis of osteochondritis dissecans of the femoral condyles. Clin Orthop 1977;123:25–6.
ARTICLE IN PRESS 58 61. Milgram J. Radiological and pathological manifestations of osteochondritis dissecans of the distal femur. Radiology 1978;126:305–11. 62. Cahill BR, Berg BC. 99m Technetium phosphate compound joint scintigraphy in the management of juvenile osteochondritis dissecans of the femoral condyles. Am J Sports Med 1983;11: 329–35. 63. Mesgarzadeh M, Sapega AA, Bonakdarpour A, Revesz G, Moyer RA, Maurer AH, et al. Osteochondritis dissecans: analysis of mechanical stability with radiography, scintigraphy, and MRI imaging. Radiology 1987;165:775–80. 64. Schneider T, Fink B, Jerosh J, Assheuer J, Ruther W. The value of magnetic resonance imaging as postoperative control after arthroscopic treatment of osteochondritis dissecans. Arch Orthop Trauma Surg 1998;117:235–9. 65. Hefti F, Beguiristain J, Krauspe R, Moller-Madsen B, Ricco V, Tschauner C, et al. Osteochondritis dissecans: a multicenter study of the European Pediatric Orthopedic Society. J Pediatr Orthop 1999;8-B:231–45. 66. Guhl JF. Arthroscopic treatment of osteochondritis dissecans. Clin Orthop 1982;167:65–74. 67. Van Demark RE. Osteochondritis dissecans with spontaneous healing. JBJS 1952;35-A:143–8. 68. Lofgren L. Spontaneous healing of osteochondritis dissecans in children and adolescents. Acta Chir Scand 1953;106:460–78. 69. Edelstein JM. Osteochondritis dissecans with spontaneous resolution. Proceedings of the South African Orthopaedic Association. JBJS 1977;36-B:343. 70. Sales de Gauzy J, Mansat C, Darodes PH, Cahuzac JP. Natural course of osteochondritis dissecans in children. J Pediatr Orthop 1999;8-B:26–8. 71. Helfet AJ. The management of internal derangement of the knee. Philadelphia: JB Lippincott Company; 1963. p. 213–21. 72. Flynn JM, Kocher MS, Ganley TJ. Osteochondritis dissecans of the knee. J Pediatr Orthop 2004;24:434–43. 73. Wildey AG. Un-united fractures treated by long-axial drilling of the fractured bone-ends. Br J Surg 1914;2:423–8. 74. Anderson AF, Richards DB, Pagnani MJ, Hovis WD. Antegrade drilling for osteochondritis dissecans of the knee. Arthroscopy 1997;13:319–24. 75. Matelic TM, Stanitski CL. Operative treatment of osteochondritis dissecans in situ by retrograde pinning. J Orthop Tech 1995;3:17–24. 76. Aglietti P, Buzzi R, Bassi PB, Fioriti M. Arthroscopic drilling in juvenile osteochondritis dissecans of the medial femoral condyle. Arthroscopy 1994;10:286–91. 77. Cahill BR. Osteochondritis dissecans of the knee: treatment of juvenile and adult forms. J Am Acad Orthop Surg 1995;3: 237–47. 78. Blauth W, Schuchardt E. Orthopa ¨disch-chirurgische Operationen am Knie. Stuttgart: Thieme Verlag; 1986 9.11. 79. Cugat R, Garcia M, Cusco X, Monllau JC, Vilaro J, Juan X, et al. Osteochondritis dissecans: a historical review and its treatment with cannulated screws. Arthroscopy 1993;9: 675–84. 80. Rey Zuniga JJ, Sagastibelza J, Lopez Blasco JJ, Martinez Grande M. Arthroscopic use of Herbert screws in osteochondritis dissecans of the knee. Arthroscopy 1993;9:668–70. 81. Dervin GF, Keene GC, Chissell HR. Biodegradable rods in adult osteochondritis dissecans of the knee. Clin Orthop 1998; 356:213–21.
O.S. Schindler 82. Din R, Annear P, Scaddan J. Internal fixation of undisplaced lesions of osteochondritis dissecans in the knee. JBJS 2006;88B:900–4. 83. Hoffmann R, Weller A, Helling HJ, Krettek C, Rhem K. Local foreign body reaction to biodegradable implants: a classification. Unfallchirurg 1997;100:658–66. 84. Prokop A, Jubel A, Helling HJ, Eibach T, Peters C, Baldus SE, et al. Soft tissue reactions of different biodegradable polylactide implants. Biomaterials 2004;25:259–67. 85. Tuompo P, Paritio LK, Patiala H, Jukkala-Partio K, Hirvensalo E, Rokkanen P. Causes of the clinical tissue response to polyglycolide and polilactide implants with an emphasis on the knee. Arch Orthop Trauma Surg 2001;121:261–4. 86. Wirth CJ, Kohn D. Operationen am Kniegelenk. In: Bauer R, Kerschbaumer F, Poisel S, editors. Orthopa ¨dische Operationslehre. Stuttgart: Georg Thieme verlag; 1994 p. 539–45. 87. Aglietti P, Ciardullo A, Giron F, Ponteggia F. Results of arthroscopic excision of the fragment in the treatment of osteochondritis dissecans of the knee. Arthroscopy 2001; 17:741–6. 88. Pridie KW. A method of resurfacing osteoarthritic knee joints. JBJS 1959;41-B:618–9. 89. Steadman JR, Briggs KK, Rodrigo JJ, Kocher MS, Gill TJ, Rodkey WG. Outcomes of microfracture for the traumatic chondral defects of the knee: average 11 year follow-up. Arthroscopy 2003;19:477–84. 90. Anderson AF, Pagnani MJ. Osteochondritis dissecans of the femoral condyles: long-term results of excision of the fragment. Am J Sports Med 1997;25:830–4. 91. Mandelbaum BR, Browne JE, Fu F, Micheli L, Mosely Jr JB, Erggelet C, et al. Articular cartilage lesions of the knee. Am J Sports Med 1998;26:853–61. 92. Bentley G, Biant LC, Carrington RW, Akmal M, Goldberg A, Williams AM, et al. A prospective randomised comparison of autologous chondrocyte implantation versus mosaicplasty for osteochondral defects in the knee. JBJS 2003;85-B:223–30. 93. Kim SJ, Shin SJ. Loose bodies after arthroscopic osteochondral autograft in osteochondritis dissecans of the knee. Arthroscopy 2000;16:E16. 94. Garrett JC. Osteochondritis dissecans. Clin Sports Med 1991;10:569–93. 95. Ghazavi MT, Pritzker KP, Davis AM, Gross AE. Fresh osteochondral allografts for post-traumatic osteochondral defects of the knee. JBJS 1997;79-B:1008–13. 96. Sasha N, Gross AE. Allograft transplantation for articular defects of the knee. In: Jackson DW, editor. Reconstructive knee surgery. 2nd ed. Philadelphia: Lippincott Williams & Williams; 2003. p. 91–404. 97. 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. JBJS 2003;85-B:223–30. 98. Peterson L, Minas T, Brittberg M. Treatment of osteochondritis dissecans of the knee with autologous chondrocyte transplantation: results at 2–10 years. JBJS 2003;85-A(Suppl. 2):17–24. 99. Barlett W, Gooding CR, Carrington RW, Skinner JA, Briggs TWR, Bentley G. Autologous chondrocyte implantation at the knee using a bilayer collagen membrane with bone graft. A preliminary report. JBJS 2005;87-B:330–2. 100. Peterson L, Minas T, Brittberg M. Two to nine year outcome after autologous chondrocyte transplantation of the knee. Clin Orthop 2000;374:212–34.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 59–64
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TRAUMA
Radial head fractures in adults J.W.K. Harrison, A. Chitre, K. Lammin, J.G. Warner, S.P. Hodgson Royal Bolton Hospital, Farnworth, Bolton, BL4 OJR, UK
KEYWORDS Fracture; Fracture-dislocation; Mason classification; Stability; ORIF; Replacement
Summary The radial head is involved in both elbow flexion and extension as well as forearm rotation and is an important stabiliser of the elbow. Fractures account for one-third of elbow fractures in adults and can lead to marked disability. Radial head fractures can be part of a spectrum of injuries to the elbow leading to complex instability. Management of comminuted fractures is controversial, but the present trend is towards stabilisation to allow early mobilization. The majority of radial head fractures are undisplaced and do not require operative treatment. Associated injuries to the elbow potentially leading to instability should be sought. In comminuted fractures with an intact MCL where fixation is not possible excision gives satisfactory long-term results. If instability is present radial length should be restored either by ORIF or replacement and any associated bony or ligamentous injuries repaired to allow early mobilisation to prevent stiffness. & 2006 Elsevier Ltd. All rights reserved.
Anatomy The proximal radius consists of a disc-shaped head and the neck. They set at an angle of approximately 151 to the shaft. The head is elliptical, 2701 of its notch of the ulna forming the proximal radio-ulnar joint. The concave proximal surface articulates with the capitellum and has a slightly larger radius of curvature than the capitellum, forming an incongruent articulation. This allows some translation of the articulating surfaces of the radiocapitellar joint. The annular ligament is an important stabiliser of the proximal radius which permits rotation but prevents proximal migration of the radius with elbow flexion due to the pull of
Corresponding author. NHS, Department of Orthopeadics, 56
Corkland Road, Manchester M21 8XH UK. Tel.: +44 1618 620145. E-mail address:
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biceps. The forearm muscles act to provide a posteriorly directed force to maintain reduction of the radial head. On hand grip and forearm flexion the forces across the elbow are approximately three times body weight due to the long lever arm to the hand, balanced by the short moment arms of the muscles crossing the elbow (biceps, brachialis, triceps, forearm flexors and extensors). This force is shared approximately equally between the trochlea and the capitellum at the distal humerus. At the wrist 80% of the force passes through the distal radius and this is transferred to the ulna via the oblique fibres of the interosseous membrane. After radial head excision load is transferred through the interosseous membrane and the triangular fibrocartilage complex. The central band of the interosseous membrane is important in resisting proximal radial migration following radial head excision; if it stretches with time it can lead to distal radioulnar joint symptoms.1 An EssexLopresti lesion is a tear of the interosseous membrane with an associated comminuted radial head fracture (Fig. 1). If it
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J.W.K. Harrison et al. elbow may dislocate. If there is a tear of the interosseous membrane the axial force will not be transmitted to the ulna and the MCL may not be torn.
Assessment The wrist should be examined for any distal radioulnar joint injury and also the forearm for an interosseous membrane injury. Posterior interosseous nerve palsy and compartment syndrome should be checked for. Radiographic anteroposterior and true lateral views of the elbow should be obtained. If fat-pad sign due to an elbow effusion is seen in the absence of any other obvious injury the radial head and neck should be carefully scrutinised. If an Essex-Lopresti lesion is suspected a standard posteroanterior view of the wrist should be taken to assess for ulnar variance. It is important to check for an associated coronoid fracture, as this is an indicator of a potential for recurrent instability. This is likely to occur with increasing elbow extension as it provides an attachment for the anterior capsule. CT scanning is excellent in assessing the degree of comminution, fracture displacement and any associated injuries, and can provide useful 3-dimensional images (Fig. 3).
Classification Figure 1 Essex-Lopresti lesion showing torn interosseous membrane and proximal migration of radius.
The most commonly used classification for radial head fractures was described by Mason4 in 1954 (Fig. 2). Johnston5 modified this in 1962 to include a Mason–Johnston Type IV.
Type I: marginal fractures with minimal displacement and no mechanical block to movement.
Type II: marginal fractures with displacement. Type III: comminuted fractures. Type IV: associated elbow dislocation. Coronoid fractures have been classified by Regan-Morrey in 1989.6
Figure 2
Mason classification.
is not recognised the radioulnar dissociation can lead to proximal radial migration and ulnar-sided wrist pain.2 The primary stabiliser to valgus forces across the elbow is the anterior band of the medial collateral ligament (MCL). The radial head is a secondary stabilizer and has little role with an intact MCL.3 Thus, it is important to recognise a MCL injury associated with a radial head fracture as this can lead to marked instability.
Mechanism of injury Radial head fractures follow a fall onto the outstretched hand with the elbow extended and the forearm pronated, applying an axial and valgus force to the elbow. The axial load forces the radial head posteriorly and the anterolateral rim of the radial head is loaded. The degree of comminution of the fracture is related to the energy of the fall. Continuing force will lead to tearing of the MCL and the
Type I: Avulsion of the tip. Type II: o50% involved. Type III: 450% involved. Treatment Treatment depends on the amount of head involved, degree of displacement and any associated injuries.
Undisplaced fractures An undisplaced fracture of the radial head (i.e. a step in the articular surface of less than 2 mm) can be managed nonoperatively with a satisfactory outcome. Block to movement can be assessed for by aspiration of the haemarthrosis and instillation of local anaesthetic into the joint. Aspiration can be performed from the radiocapitellar joint or from the olecranon fossa posteriorly which may be easier to palpate. The arm is placed in a collar and cuff at 901 of elbow flexion and active mobilisation commenced as pain allows. As with any elbow injury it should be explained to patients that
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Figure 3 Mason IV injury with CT scan and 3-D reformatted images. Note avulsion of tip of coronoid process (c) and 50% of the radial head involved (d). Treated by internal fixation of radial head and as the elbow was still unstable the coronoid process was fixed using suture anchors through a medial approach.
a loss of extension commonly occurs which is not likely to cause a functional deficit.
Displaced fractures 10% of radial head fractures occur with an elbow dislocation. For it to occur and as the elbow is a congruent joint, it is
likely the collateral ligaments will be damaged. Fixation of the radial head will improve stability and allow earlier mobilisation to prevent stiffness. Displaced fractures should undergo open reduction and internal fixation (Fig. 4). A Kocher approach is most commonly used and develops the interval between extensor carpi ulnaris and anconeus. The forearm is kept in pronation during the dissection to protect the posterior interosseous
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Figure 4
Mason II fracture treated by internal fixation with 2 Herbert screws.
nerve. The annular ligament is normally preserved as it is an important stabiliser and to prevent damage to the nerve which passes around the radial neck just distal to the annular ligament. To improve exposure of the radial head the annular ligament can be divided, and subperiosteal elevation of ECRB, ECRL and capsule off the lateral supracondylar ridge will improve access to structures on the medial side of the joint. Alternatively a posterolateral approach can be used by stripping the anconeus and supinator from the ulna. This allows access to the medial ligament. The patient will need to be in the lateral position with the arm over a support. Headless screws are used for fixation with Herbert screws as these are possibly less bulky. If a plate is required it should be placed in the ‘safe zone’, opposite the sigmoid notch of the ulna with the forearm in neutral rotation.
Comminuted fractures If the radial head is too comminuted to allow fixation a decision has to be made whether to remove the fragments, or excise or replace the head. If greater than a third of the
head is involved there is loss of ‘capture’ of the capitellum. If the radial head is unstable then excision is indicated. The accepted treatment for comminuted fractures of the radial head not amenable to internal fixation with an intact MCL is excision. The reported long-term results are good with one study showing 17 out of 21 as excellent results at 16–30 years follow-up.7 They also suggested the use of indomethacin for 6 weeks post-operatively to prevent heterotopic ossification. Another study with more than 8 years follow-up also showed good results.8 They suggested the MCL and interosseous membrane lengthen with time with ulnar variance having become increasingly positive by an average of approximately 2 mm, and cubitus valgus having increased to an average of 91. This has been suggested by other studies but generally these changes do not seem to cause symptoms. However, the potential for complications such as weakness, cubitus valgus and wrist pain due to proximal radial migration affecting the distal radio-ulnar joint mean reconstruction of the radial head is the ideal. Improved fixation with low profile devices and more extensile exposures may allow fixation of even markedly comminuted fractures. A study of 28 patients with a Mason III fracture
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Figure 5 Comminuted radial head fracture in a 34 year old female treated by radial head replacement as stable fixation could not be achieved at surgery.
who had either ORIF or excision showed improved function and strength in the ORIF group.9 The fixation was a combination of headless screws and low profile T-plates to hold any fragments too small to take a screw. A head replacement will be required if there is valgus instability due to rupture of the MCL to act as a spacer until healing of the MCL occurs (Fig. 5). The MCL is not normally repaired unless instability persists although a cadaveric study has suggested ligament repair alone may be superior to radial head replacement in resisting valgus stress.10 Radial head replacement is indicated in comminuted fractures with a ruptured MCL. Initially silastic replacements were used but have shown poor long-term results. Biomechanical studies have shown Swanson silastic replacements are poor at resisting proximal radial migration and can fracture or lead to synovitis in the longer term.11,12 Metal or ceramic prostheses are now used that maintain the space for valgus stability. Modern designs are short stemmed for ease of insertion and extraction, uncemented and monoblock. The replacement is a hemiarthroplasty and due to the variation in size of radial heads the design of prostheses does not generally provide a congruent articulation. There is little evidence to suggest they transmit physiological loads and therefore do not act as true replacement joints. They have shown reasonable results with some loss of movement’and strength the norm.13 Partly this probably reflects the increased severity of the injury when a prosthetic head is required and also from concern about instability leading to prolonged immobilisation post-operatively resulting in stiffness. Improved results have been seen with early surgery to allow early mobilization.14 The Judet prosthesis was developed to theoretically allow a more congruent articulation with the capitellum. It is a modular design with a ball and socket articulation between the stem and head. Good results have been reported even in chronic situations.15 A radial head replacement can be removed at a later date for lateral elbow pain or if erosion of the capitellum occurs. An extensive soft tissue release is likely to be required to remove a radial head replacement.
Fracture with elbow dislocation Elbow dislocation combined with radial head and coronoid fractures can be markedly unstable and has been named ‘the terrible triad’ by Hotchkiss due to poor results reported.16 There is a high incidence of redislocation whilst in plaster and operative treatment with fixation of even a small coronoid fragment is indicated. The aim is to achieve stability and early mobilisation. Several factors are important to consider when treating these injuries. The coronoid fracture should be fixed (Type II or III) or the anterior capsule repaired if an avulsion of the tip of the coronoid is present (Type I). If a radial head replacement is used it is important not to ‘overstuff’ the radiocapitellar joint as this can lead to instability or reduced movement. The aim is to restore radial length to within 2–3 mm to achieve stability.17 A pre-operative radiograph of the normal side may be helpful to assess radial length. Both medial and lateral collateral ligaments may need to be repaired. They commonly have avulsed from their origins on the distal humeral epicondyles. If the elbow remains unstable after repair a hinged external fixator may be necessary. Mobilisation is commenced at 2 weeks with active movements but avoiding the last 301 of extension for 4 weeks.
Complications Complications include pain, stiffness, decreased strength, posterior interosseous nerve palsy, post-traumatic arthritis, instability, cubitus valgus, mal- and non-union. The functional range of movement of the elbow is from 301 to1301 flexion.11 Patients commonly loose the terminal 151 of extension and, if persisting after 6 months, it should be explained it is unlikely to resolve. An arthroscopic or open release should be considered at this stage if a 351 loss of extension is present.
ARTICLE IN PRESS 64 Pin palsy is likely to be a neuropraxia. Exploration is indicated if it occurs with an open fracture or as a new finding following a closed reduction or open surgery.
Acknowledgements Thanks to Ruth Eaves, Medical Illustration Department, RBH.
References 1. Sowa DT, Hotchkiss RN, Weiland AJ. Symptomatic proximal migration of the radius following radial head resection. Clin Orthop 1995;317:106–13. 2. Essex-Lopresti P. Fractures of the radial head with distal radioulnar dislocation. JBJS 1951;33-B:244–7. 3. Morrey BF, Chao EY, Hui FC. Biomechanical study of the elbow following excision of the radial head. JBJS 1979;61-A:63–8. 4. Mason L. Some observations on fractures of the head of the radius with a review of a hundred cases. Br J Surg 1954;42:123–32. 5. Johnston GW. A follow-up of one hundred cases of fracture of the head of the radius with a review of the literature. Ulster Med J 1962;31:51–6. 6. Regan W, Morrey BF. Fractures of the coronoid process of the ulna. JBJS 1989;71-A:1348–54. 7. Janssen RPA, Vegter J. Resection of the radial head after Mason type-III fractures of the elbow: follow-up at 16 to 30 years. JBJS 1998;80-B:231–3. 8. Coleman DA, Blair WF, Shurr D. Resection of the radial head for fracture of the radial head. Long-term follow-up of seventeen cases. JBJS 1987;69-A:385–92.
J.W.K. Harrison et al. 9. Ikeda M, Sugiyama K, Kang C, Takagaki T, Oka Y. Comminuted fractures of the radial head: comparison of resection and internal fixation. Surgical technique. JBJS 2006;88-A (Suppl 1 Pt 1):11–123. 10. Jensen SL, Deutch SR, Olsen BS, Sojbjerg JO, Sneppen O. Laxity of the elbow after experimental excision of the radial head and division of the medial collateral ligament: efficacy of ligament repair and radial head prosthetic replacement: a cadaver study. JBJS 2003;85-B:1006–10. 11. Morrey BF, Askew LJ, Chao EY. A biomechanical study of normal functional elbow motion. JBJS 1981;63(6):872–7. 12. Worsing Jr RA, Engber WD, Lange TA. Reactive synovitis from particulate silastic. JBJS 1982;64-A:581–5. 13. Moro JK, Werier J, MacDermid JC, Patterson SC, King GJ. Arthroplasty with a metal radial head for unreconstructible fractures of the radial head. JBJS 2001;83-A(8): 1201–11. 14. Chapman CB, Su BW, Sinicropi SM, Bruno R, Strauch RJ, Rosenwasser MP. Vitallium radial head prosthesis for acute and chronic elbow fractures and fracture-dislocations involving the radial head. J Shoulder Elbow Surg 2006;15(4): 463–73. 15. Dotzis A, Cochu G, Mabit C, Charissoux JL, Arnaud JP. Comminuted fractures of the radial head treated by the Judet floating radial head prosthesis. JBJS 2006;88-B:760–4. 16. Ring D, Jupiter JB, Zilberfarb J. Posterior dislocation of the elbow with fractures of the radial head and coronoid. JBJS 2002;84-A(4):547–51. 17. Van Glabbeek F, van Reet RP, Baumfield PG, Neale JA, O’Driscoll SW, Morrey BF, et al. The kinematic importance of radial neck length in radial head replacement. Med Eng Phys 2005;27(4): 336–42.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 65–71
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Radiology quiz Question 1 History A 14-year-old boy complains of dorsolateral foot pain and difficulty when walking on uneven surfaces (Images 1 and 2). (i) What is the diagnosis? (ii) What does the MRI show and why?
Image 1 Lateral radiograph.
Image 2
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MRI (sagittal STIR).
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Radiology quiz
Question 2 History Patient presents with pain in the knee (Images 3 and 4). What is the diagnosis?
Images 3 and 4 Magnetic resonance images (proton density with fat saturation).
Question 3 History This patient had post-operative pain on knee extension (Images 5 and 6). What do the MRI images show?
Images 5 and 6
MRI (sagittal T1).
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Question 4 History An 8-year-old boy presents with pain in the wrist especially at night (Images 7–10). (i) Describe the appearance of the lesion (black arrow). (ii) What would be the differential diagnosis?
Images 7 and 8 AP and lateral radiograph of distal radius/ulna.
Image 9 and 10
Axial CT and coronal reformat CT slices.
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Radiology quiz
Question 5 History A 12-year-old boy presents with an increasing hand deformity (Image 11). Describe the radiograph. What is the diagnosis?
Image 11 Plain AP radiograph.
Question 6 History This elderly patient presented with back pain and haematuria (Images 12 and 13). (i) Can you correlate the pathology in the 2 images? (ii) What is the diagnosis?
Image 12 Plain AP radiograph. Thoraco-lumbar junction.
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Image 13
Axial CT slice (through body of L1).
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Radiology quiz
Answer 1 (i) There is complete fusion of the calcaneo-navicular joint representing osseous calcaneo-navicular coalition. (ii) Increased STIR signal at the site of the coalition represents bone marrow oedema due to stresses secondary to limited joint movement.
Background—tarsal coalition This condition occurs in o1% of the population (bilateral in 50%), and represents failure of segmentation of the tarsal bones. It usually presents in early adolescence as the cartilaginous bar ossifies resulting in the typical rigid flat foot. Symptoms are due to limited motion in the hindfoot, increased stresses elsewhere in the tarsus and often an associated spasm of the peroneal musculature and tendons.
Answer 2 The posterior portion of the medial meniscus is largely absent consistent with a bucket handle meniscal tear (Image 3). The meniscal fragment is displaced beneath the PCL resulting in a ‘double PCL’ sign (Image 4).
Background—menisci on MRI scans A sagittal slice through the body of a normal meniscus creates a ‘bow-tie’ configuration which should be seen on at least two consecutive sagittal MR images. If part of the meniscus is absent (‘absent bow-tie’ sign), the most likely cause, with the exception of previous surgery, is a bucket handle tear and careful inspection is needed to locate the displaced meniscal fragment.
Answer 3 Image 6 shows the ACL graft is intact, seen as a taut low signal structure. Fat returns high signal on T1-weighted images and Hoffa’s fat pad will therefore normally contain high signal material. Image 6 shows a rounded low signal mass (black arrow) within Hoffas fat pad which represents post-operative scar tissue; also known as arthrofibrosis or a ‘Cyclops’ lesion.
Background—approach to looking at ACL reconstruction on MRI 1. Graft integrity: the graft should be seen as taut intact low signal band, there maybe signal up to 2-years post-op (periligamentous revascularisation). 2. Position of the femoral tunnel and hence graft isometry (tension): AP: 11 o’clock right knee and 1 o’clock left knee. Lateral: At intersection of posterior femoral cortex & intercondylar roof. 3. Position of the tibial tunnel and hence signs of impingement: the tibial tunnel should be posterior and parallel to intercondylar roof, if it is too steep, graft will impinge on the femur in extension, if it is too flat, graft may be too lax. 4. Arthrofibrosis: Fibrous tissue seen anterior to the distal graft within notch or Hoffa’s fat pad. 5. Infection: Donor site, tunnels, joint. 6. Hardware: Bone plug failure.
Answer 4 (i) There is a small radiolucent lesion within the medial aspect of the distal radial metaphysis. There is adjacent cortical thickening best appreciated on the lateral view. (ii) The differential diagnosis on the plain radiograph in a child includes osteoid osteoma, Brodie’s abscess and eosinophilic granuloma. The CT scan confirms the diagnosis of an osteoid osteoma by demonstrating a nidus.
ARTICLE IN PRESS Radiology quiz
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Background information—osteoid osteoma The characteristic clinical picture is pain worse at rest and night, which is typically relieved with salicylates. The radiological features are a central nidus (o1 cm) with surrounding sclerosis. The degree of this reactive sclerosis and periosteal new bone formation depends upon the site within bone. It is most marked in a cortical or subperiosteal location.
Answer 5 There are multiple lytic, expansile, radiolucent lesions involving the metacarpals and phalanges, particularly on the ulnar aspect of the hand. These are consistent with multiple enchondromas. The diagnosis is Ollier’s disease.
Background information—Ollier’s disease Ollier’s is a non-hereditary generalized disorder of endochondral bone formation. It is often unilateral, both with respect to the side of the body and location within a bone. The risk of malignant transformation is up to 30%. Its close relation is Maffuci’s syndrome, which combines multiple enchondromas and soft tissue haemangiomas. The presence of haemangiomas in the soft tissues with calcified phleboliths differentiates this from Ollier’s.
Answer 6 (i) The right T12 and L1 pedicles are absent on the plain radiograph. (ii) The computerised tomogram image shows a soft tissue mass destroying the right L1 pedicle and a mass arising from the right kidney. The diagnosis is vertebral metastases from a primary renal cell carcinoma.
Metastases Metastatic lesions predominate in red marrow containing parts of the skeleton i.e. skull, spine, ribs and pelvis. They are rare beyond the knees and elbows. Associated pathological fractures are common. They do not cross-joints or disc spaces.
Nev Davies, Catherine McCarthy Department of Trauma & Orthopaedics, The Great Western Hospital, Swindon & Marlborough NHS Trust, Swindon, Wilts SN3 6BB, UK
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 72–78
Available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/cuor
THROMBO-EMBOLIC DISEASE
Role of vena cava filters in high-risk trauma and elective orthopaedic procedures Narayan Hulsea, Himanshu Sharmab,, Ashish Mahendrac, Bardeep Ranad a
Department of Trauma and Orthopaedic Surgery, Glasgow Royal Infirmary, Castle Street, Glasgow, G4 0SF, UK Department of Trauma and Orthopaedic Surgery, Royal Alexandra Hospital, Corsebar Road, Paisley, PA2 9PN, UK c Department of Trauma and Orthopaedic Surgery, Ayr Hospital, Dalmellington Road, Ayr, KA6 6DX, UK d Department of Trauma and Orthopaedic Surgery, Western Infirmary, Dumbarton Road, Glasgow, G11 6NT, UK b
KEYWORDS Vena cava filters; Thromboembolism; Deep vein thrombosis; Prophylaxis
Summary Pulmonary embolism (PE) is the leading cause of death after trauma and is the most common cause of death in the immediate post-operative period after lower limb reconstructive procedures. Although, systemic anticoagulation is the corner stone of both prophylaxis and treatment of venous thromboembolism, there is increasing awareness and usage of vena caval filters (VCFs) in high-risk patients. Instead of permanent filters, retrievable filters are predominantly used nowadays by interventional radiologists aiming to avoid long-term complications such as inferior vena caval obstruction and post-phlebitic syndrome. It is evident from the available literature that prophylactic filters do protect against fatal PE in high-risk trauma and patients undergoing complex lower limb reconstructive procedures; however, there is uncertainty about the efficacy of different types of filter designs and clear indications of the high-risk group remain controversial. & 2006 Elsevier Ltd. All rights reserved.
Introduction Orthopaedic and trauma patients constitute a major group of hospital patients with an increased risk of venous thromboembolism.1 Incidence of deep vein thrombosis (DVT) has been reported to be as high as 35–65% in trauma patients 2,3 and up to 84% in the patients undergoing total hip and total knee arthroplasties.4 Incidence of pulmonary Corresponding author. 44 Abercorn Road, Newton Mearns,
Glasgow, G77 7NA, UK. Tel.: +44 141 887 9111; fax: +44 141 314 7275. E-mail address:
[email protected] (H. Sharma). 0268-0890/$ - see front matter & 2006 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2006.10.006
embolism (PE) in trauma patients has been reported up to 22% with estimated mortality of 8–35%.5–7 In the United Kingdom, Thromboembolic Risk Factor Consensus Group (THRIFT) and Scottish Intercollegiate Guidelines Network (SIGN) Group have recommended routine thromboprophylaxis to all the patients suffering from major trauma, patients undergoing surgery for a fractured hip, elective total hip and total knee replacement.8,9 However, up to 14% of high-risk trauma patients may not be suitable for routine prophylaxis because of some contraindications to anticoagulation.10,11 In addition, many of the orthopaedic and trauma patients may not be suitable for application of mechanical compression devices because of long bone
ARTICLE IN PRESS Role of vena cava filters in high-risk trauma and elective orthopaedic procedures
a filter via a transvenous catheter under fluoroscopic guidance (Figs. 1 and 2). Femoral, jugular and basilic veins have been used in that order of frequency. Bedside application using a portable ultrasound device has also been reported.17,18
fractures, open wounds, external fixators and plaster casts in situ. In such a scenario, when conventional modalities are contraindicated or have failed, and in patients with a previous history of recurrent DVT or PE, there is a clear indication for the surgical interruption of the emboli propagating from the extremities. Recently, inferior vena cava (IVC) filters are increasingly being used prophylactically in high-risk trauma patients.12–14 Historically, these methods have evolved from ligation or plication of the vena cava to permanent or temporary placement of mechanical filters in the IVC. Indications for the insertion of these filters are expanding. This article is aimed at reviewing the indications, contra-indications, current trends and controversies in the use of vena cava filters in the high thromboembolic risk complex trauma and orthopaedic patients.
Indications VCFs are used when medical treatment is contraindicated, failed or complicated by a serious adverse effect in a patient with proximal DVT or PE.19 The Seventh American College of Chest Physicians (ACCP)19 Consensus Conference on antithrombotic therapy has recommended the following indications: (1) contraindication or complication of anticoagulation in a patient with proximal vein thrombosis of the lower extremity or PE, (2) recurrent thromboembolism despite adequate anticoagulation, (3) chronic PE with pulmonary hypertension, (4) concurrent performance of surgical pulmonary embolectomy or pulmonary endarterectomy and (5) heparin-induced thrombocytopenia.
Types of vena cava filters (VCFs) An ideal filter should effectively protect against PE, be technically easy to insert, mechanically and biologically stable and should have a low incidence of long-term and short-term complications. None of the present filter designs could be labelled as ideal. However, differences in their mechanical properties may influence the selection of a filter specific to some patients. Early implantable endovascular devices for the treatment of venous thromboembolism were the Mobin–Uddin filter15 and Kimray–Greenfield filter.16 Design characteristics of the IVC filters have undergone several changes and many designs are now available for use. Most devices are made up of fatigue resistant stainless steel or titanium alloy. Commonly used filters and their general characteristics are shown in Table 1. There are no studies in the literature that conclusively establish the superiority of one filter design over the others.
In a review by Greenfield and Proctor, indications for IVC filter insertions were contraindications to anticoagulant therapy (45%), complication of anticoagulant therapy (20%) and prophylaxis (13%).20
Prophylaxis in trauma patients In some trauma centres, VCFs have been used prophylactically without a documented PE or DVT.21–24 Table 2 shows the criteria used by the different authors to identify the high-risk trauma patients for the placement of prophylactic IVC filters. Some of the trauma patients may be at a higher risk for bleeding complications after the injury and hence may not be suitable for routine anticoagulation. This includes patients with associated intracranial haemorrhage,
Method of insertion of IVC filters Placement of filters is usually carried out by an interventional radiologist or by a vascular surgeon. Modern filter insertion involves a standard venepuncture and insertion of
Table 1
73
Commonly used filter designs.
Filters
Material
Year
Maximum IVC size (mm)
Insertion site
MR image compatibility
Birds nest Venatech Titanium Green field Simon Nitinol
Stainless steel Phynox Titanium Nickel–titanium
1982 1986 1988 1988
40 28 28 28
Stainless steel Greenfield TrapEase filter
Stainless steel
1973
28
Femoral, jugular Femoral, jugular Femoral, jugular Femoral, jugular anticubital Femoral, jugular
No Yes Yes Yes, but creates minor artefacts No
Nickel–titanium
2000
30
Yes
Venateck—low profile
Phynox
2001
28
Gunther Tulip
Elgiloy
2001
28
Femoral, jugular, anticubital Femoral, jugular, anticubital Femoral, jugular
Yes Yes
ARTICLE IN PRESS 74
N. Hulse et al.
Prophylaxis in patients undergoing hip and knee surgeries
Figure 1
Gunther Tulip vena caval filter.
Patients undergoing revision hip and knee replacements could be the candidates for expanding use of prophylactic VCFs, although there is no supporting evidence in favour of this statement. High-risk patients undergoing primary hip and knee arthroplasties are selected by some authors,27,28 although no worldwide consensus has yet been established. Emerson reported the use of Greenfield filters prophylactically in 47 patients undergoing hip and knee arthroplasties and compared the results with 37 patients receiving only anticoagulation.27 All patients with chronic DVT, prior DVT or PE with major complications of anticoagulation, a major PE or DVT or PE within first 7 post-operative days were considered for a filter insertion. At a follow up of 24–76 months, there was no PE. They encountered two cases of IVC occlusions, one suprarenal placement of filter, one haemothorax and two vagus nerve injuries. Vaughn et al.28 used Greenfield filters prophylactically in 42 patients undergoing hip or knee arthroplasties who had previous thromboembolic complications and therapeutically in 24 patients because of a contraindication to therapeutic anticoagulation or failed prophylaxis with Coumadin. None of the prophylactic group and one in the therapeutic group developed fatal PE.
Prophylaxis in pathological fractures Patients with pathological fractures are at higher risk of thromboembolic events because of a hypercoagulable state29 combined with a fracture and an orthopaedic surgical procedure to stabilise the fracture. Benevenia et al.30 reported the results of prophylactic IVC filters placed preoperatively in 24 patients with metastatic pathological fractures of long bones who were unable to receive pharmacological prophylaxis. They compared 24 patients who received IVC filters plus mechanical prophylaxis (compression stockings and sequential compression boots) and 23 patients who received only the mechanical prophylaxis. At a mean follow up of 11.5 months, all five PE and all two fatal PE occurred in the non-filter group. They reported four complications, which included groin haematoma, insertion thrombosis, distal placement of filter and filter occlusion in one patient each. However, use of filters in such patients has been criticised for high cost and mortality.31
Prophylaxis in spinal cord injuries
Figure 2 Gunther Tulip vena caval filter inserted via transjugular route.
ocular injury with associated haemorrhage, solid intraabdominal organ injury (liver, spleen and kidney), or pelvic or retroperitoneal haematoma requiring transfusion.25,26 Most authors agree that the risk benefit ratio is in favour of VCFs in high-risk trauma patients.21–23
Prophylactic use of VCFs in the spinal injury patients is controversial. Leon et al.32 used VCFs prophylactically in 74 patients undergoing spinal surgeries. Their criteria were (1) history of thromboembolism, (2) diagnosed thrombophilia, (3) malignancy, (4) bed ridden for more than 2 weeks prior to surgery, (5) staged procedures or multiple level surgeries, (6) combined anterior and posterior approaches, (7) expected need for significant iliocaval manipulation during surgical exposure, and (8) single stage anaesthetic time more than 8 h. At a mean follow up of 11 months, one patient developed PE and 27 limbs developed DVT. These authors concluded that despite a high incidence of DVT following high-risk spinal surgeries, prophylactic IVC filters
ARTICLE IN PRESS Role of vena cava filters in high-risk trauma and elective orthopaedic procedures
Table 2
75
Criteria used by different authors to identify the high-risk trauma patients.
Author Rogers et al. (1997)
High risk/indications 23
(1) Complex pelvic fractures (2) Pelvic fractures with long bone fractures or (3) Multiple lower limb fractures or Above injuries with at least one additional risk factor: Age455 Injury Severity Score416 Immobilisation more than 6 weeks
Winchell et al. (1994)49
Head injury, spinal injury, posterior element pelvic fracture, multiple long bone fractures
Langan et al. (1999)13
Prolonged immobilisation with multiple injuries Closed head injuries Pelvic fracture Spine fracture Multiple long bone fracture
Rodriguez et al. (1996)12
Three or more of the following risk factors: Age455 ISS415 Automotive injury score42 on head chest or abdomen Multiple lower limb fracture Pelvic fracture Spinal trauma Subclavian vein cannulation
Khansarinia et al. (1995)21
Injury Severity Score49 Severe head injury with lower extremity fractures or prolonged ventilator dependence Spinal injury with paralysis Major abdominal or pelvic penetrating venous injury
Pasquale and Fabian (1998)25
Patients who cannot receive anticoagulation and 445 years of age or poor cardiopulmonary reserve and Patients having one or more of the following risk factors: Severe closed head injury (Glasgow Coma Scale Score o8) Incomplete spinal cord injury with paraplegia or quadriplegia Complex pelvic fractures with associated long bone fractures Multiple long bone fractures
appear to protect patients from PE. However, in a study of 111 patients with spinal cord injury, patients with paraplegia or tetraplegia, Maxwell et al.33 reported 11.8% and 0.9% incidence of DVT and PE, respectively, which were 9% and 1.8% in general trauma admissions. Incidence of DVT in spinal cord injury patients with long bone fractures was 37.5%. On the basis of low incidence of PE, prophylactic filters in spinal injury patients are only used when it is associated with long bone fractures.
Complications of IVC filters Complications associated with filter placement are uncommon and usually non-fatal. However, both fatal and nonfatal complications have been reported. Becker et al.34 divided non-fatal complications into five groups; technical difficulties during placement of filters, insertion site thrombosis, filter migration, IVC thrombosis and lower extremity DVT. Table 3 shows the reported incidence of
common complications in the studies involving the trauma patients. PE in 0–5% of patients and fatal pulmonary emboli in about 0.7% cases have been reported subsequent to VCF application.7,13,22,23,35 Other complications include insertion site haematoma formation, wound infection, pneumothorax, air embolism, filter malposition and insertion site thrombosis.11–14,21–23,25,34,36–38 Movement of VCFs in both cephalad and caudad directions have been noted.39 In the majority, this migration is minimal and asymptomatic.34 Occlusion of the IVC has been reported in 2–9% of patients.38,39 Post-thrombotic syndrome due to venous insufficiency in the lower limbs seems to be a common problem in studies with long-term follow up (35–44%).7,36,37
Retrievable VCFs Potential long-term risks of permanent VCFs include filter migration, venostasis, infection and vena caval occlusion. However, the true picture in the long-term remains largely
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N. Hulse et al.
Table 3
Results of IVC filter placement in trauma patients.
Author
Indications
Cases
Follow up period (months)
PE
Death
DVT
IVCT
Pathological fractures Prophylactic
24
11.5
0
0
2 (8.3%)
1
1
133
o12
1
1
31 (30%)
0
0
Venous stasis Benevenia et al. (2004)30 Duperier et al. (2003)50 Wojcik et al. (2000)7
105
28.9
0
0
28 (44%)
1 (0.95%)
11 (10.4%)
Langan et al. (1999)13
Prophylactic in 64 and therapeutic in 41 patients Prophylactic
160
19.4
1
0
0
27
Rogers et al. (1998)22
Prophylactic
132
20
1
1
NA
Rogers et al. (1997)23
Prophylactic
35
24
0
2 (5.7%)
0
NA
Khansarinia et al. (1995)21
Prophylactic
108
NA
3 (2.3%) 1 (2.8%) 0
24 (12.8%) 16
0
9%
NA
NA
NA—not available. Refers to 64 patients who had prophylactic filters.
unknown. Many of these patients may have only a temporary contraindication for anticoagulation. It is also an important consideration when a permanent filter needs to be placed in a young trauma patient. Retrievable filters are devised with an intention of preventing PE in the short term while eliminating long-term complications associated with permanent filters. Allen et al.40 placed 53 Gunther Tulip filters in 51 high-risk trauma patients. Retrieval was successful in 24 out of 25 attempts. There were no complications like bleeding, device migration, thrombosis, infection or PE. From the available literature, it appears that the application of retrievable filters is effective in preventing new or severe PE. Most studies investigating the retrieval of the Gutinther Tulip filter have proposed removal within 15 days of implantation, before the filter struts become incorporated into the caval wall.41,42 Retrieval may not be feasible within this time period due to continued contraindication for anticoagulation, recurrent PE or technical difficulties in many patients. However, these filters can be repositioned under angiographic guidance and can be removed within the next 2 weeks.40
Controversies and comments PE is a leading cause of delayed deaths after trauma35 and is the most common cause of death in the immediate postoperative period in patients who underwent reconstructive operations in the lower limbs.43 Ongoing bleeding or increased risk of bleeding often precludes the use of anticoagulants at least in the early period after trauma and most centres would not use the anticoagulants in recent cerebral injury, cerebral haemorrhage, active bleeding, significant thrombocytopenia, cerebral metastasis or a recent large embolic stroke.26
Skeletal injuries in the lower limbs, wounds and immobilisation devices often prevent the use of mechanical compression devices. Although systemic anticoagulation remains as the corner stone for both prophylaxis and treatment of venous thromboembolism, there is a clear indication for the surgical interruption of the emboli when the anticoagulants are contraindicated or failed. It is generally clear from the literature that prophylactic filters protect patients from fatal PE, in high-risk patients and in those patients who have a contraindication for anticoagulation.12,21–24 However, there is no agreement in identifying these high-risk patients. Different authors have used diverse criteria to identify high-risk trauma patients. Increasing age,11,23,35 prolonged immobilisation,2,3,11,35 long bone fractures,2,11,44 increasing injury severity score2,11,44 and pelvic fractures2,11,35,44 are generally agreed as highrisk factors for venous thromboembolism and hence been used by the various authors to guide the patient selection for placement of prophylactic filters. In the absence of well-conducted prospective studies, various groups have arrived at some ‘consensus’ recommendations for their use.8,19,25 Patients undergoing revision hip and knee replacements could be candidates for the expanding use of prophylactic IVC filters because of the high risk of DVT and PE after these procedures and consequences of anticoagulants that may interfere with wound healing.27,28 However, the evidence is slim to support generalised prophylactic use in this group of patients. Concerns have been raised about the increased risk of DVT, IVC thrombosis, and post-phlebitic syndrome after IVC filter insertion. Incidence of subsequent DVT of 35–44% after prophylactic use of IVC filters have been reported in longterm.7,37 Decousus et al.37 in a randomised control study with 8 years of follow up reported similar total number of venous thromboembolic events in patients treated with or
ARTICLE IN PRESS Role of vena cava filters in high-risk trauma and elective orthopaedic procedures without a filter (36.4% vs. 35.45%).36 However, those patients with VCF experienced a greater cumulative incidence of symptomatic DVT (35.7% vs. 27.5%), but significantly fewer symptomatic emboli (6.2% vs. 15%). The authors concluded that at 8 years, VCFs reduced the risk of PE, but increased that of DVT and had no effect on survival. Although their use may be beneficial in patients at high risk of PE, systematic use in the general population with venous thromboembolism is not recommended (PREPIC trial).36 However, other studies in trauma populations have reported no difference in the incidence of DVT in patients with or without VCFs.12,45–47 Attempts to broaden the indications for IVC filter placement have been made since the inception and concerns have been raised about their over use.38,39 Stein et al.38 analysed the National Hospital Discharge Survey Database (NHDS) in the United States and noticed the number of patients who had VCF increased from 2000 in 1979 to 49,000 in 1999. In 1999, 19% were placed prophylactically. McMurtry et al.48 studied the incidence of PE in all the patients admitted to a level-1 trauma centre between 1989 and 1997. They compared the two cohorts corresponding to years of high or low prophylactic filter use. A total of 299 trauma patients received filters which included 248 filters placed prophylactically. Overall the incidence of PE was 0.31% and 0.48% during the year of low and high use of filters respectively. Contrary to the findings of others,23 these authors concluded that increased use of prophylactic filters in trauma patients failed to decrease the overall incidence of PE. Furthermore, indications in spinal injury, joint replacement and pathological fractures remain controversial.27,28,30–33 After reviewing the literature, we found a clear lack of randomised studies assessing the efficacy of the filters for orthopaedic and trauma patients. Placement of VCFs in trauma and orthopaedic patients needs fundamental understanding and further assessment of risk-benefit ratio. Many issues remain unclear and carefully designed randomised controlled studies are needed to establish the expanding clinical indications, efficacy and safety of filters. However, long-term safety of permanent filters is not well established and retrievable filters are currently being evaluated for this purpose. Such studies need to identify the high-risk patients in trauma and complex elective orthopaedic patients. It seems from the literature, even in the absence of wellconducted randomised controlled studies that VCFs do protect against fatal PE in high-risk trauma and complex orthopaedic patients with acceptable early complications.
Practice points
VCFs could be either permanent or retrievable, used
for for the surgical interruption of the emboli propagating from the extremities Used in patients with contraindications to anticoagulation and mechanical compression devices VCFs tend to protect against fatal PE in high-risk trauma and complex orthopaedic patients with acceptable early complications
77
Research directions
To obtain consensus in establishing clear indications
for VCFs in complex trauma and complex reconstructive procedures Long-term efficacy of permanent vs. retrievable filters Outcome in different filter design Role of VCFs in metal-on-metal hip resurfacing
References 1. Gillespie W, Murray D, Gregg PJ, Warwick D. Risks and benefits of prophylaxis against venous thromboembolism in orthopaedic surgery. J Bone Joint Surg Br 2000;82(4):475–9. 2. Geerts WH, Code KI, Jay RM, Chen E, Szalai JP. A prospective study of venous thromboembolism after major trauma. N Engl J Med 1994;331(24):1601–6. 3. Freeark RJ, Boswick J, Fardin R. Posttraumatic venous thrombosis. Arch Surg 1967;95(4):567–75. 4. Clagett GP, Anderson Jr FA, Geerts W, Heit JA, Knudson M, Lieberman JR, et al. Prevention of venous thromboembolism. Chest 1998;114(5 Suppl):531S–60S. 5. Kudsk KA, Fabian TC, Baum S, Gold RE, Mangiante E, Voeller G. Silent deep vein thrombosis in immobilized multiple trauma patients. Am J Surg 1989;158(6):515–9. 6. Cipolle MD, Wojcik R, Seislove E, Wasser TE, Pasquale MD. The role of surveillance duplex scanning in preventing venous thromboembolism in trauma patients. J Trauma 2002;52(3): 453–62. 7. Wojcik R, Cipolle MD, Fearen I, Jaffe J, Newcomb J, Pasquale MD. Long-term follow-up of trauma patients with a vena caval filter. J Trauma 2000;49(5):839–43. 8. Risk of and prophylaxis for venous thromboembolism in hospital patients. Thromboembolic Risk Factors (THRIFT) Consensus Group. BMJ. 1992;305(6853):567–74. 9. Prophylaxis of venous thromoembolism. Edinburgh: Scotish Intercollegiate Guidelines Network; 1995. 10. Leach TA, Pastena JA, Swan KG, Tikellis JI, Blackwood JM, Odom JW. Surgical prophylaxis for pulmonary embolism. Am Surg 1994;60(4):292–5. 11. Shackford SR, Davis JW, Hollingsworth-Fridlund P, Brewer NS, Hoyt DB, Mackersie RC. Venous thromboembolism in patients with major trauma. Am J Surg 1990;159(4):365–9. 12. Rodriguez JL, Lopez JM, Proctor MC, Conley JL, Gerndt SJ, Marx MV, et al. Early placement of prophylactic vena caval filters in injured patients at high risk for pulmonary embolism. J Trauma 1996;40(5):797–802. 13. Langan 3rd EM, Miller RS, Casey 3rd WJ, Carsten 3rd CG, Graham RM, Taylor SM. Prophylactic inferior vena cava filters in trauma patients at high risk: follow-up examination and risk/ benefit assessment. J Vasc Surg 1999;30(3):484–8. 14. Carlin AM, Tyburski JG, Wilson RF, Steffes C. Prophylactic and therapeutic inferior vena cava filters to prevent pulmonary emboli in trauma patients. Arch Surg 2002;137(5):521–5. 15. Mobin-Uddin K, McLean R, Bolooki H, Jude JR. Caval interruption for prevention of pulmonary embolism. Long-term results of a new method. Arch Surg. 1969;99(6):711–5. 16. Greenfield LJ, McCurdy JR, Brown PP, Elkins RC. A new intracaval filter permitting continued flow and resolution of emboli. Surgery 1973;73(4):599–606.
ARTICLE IN PRESS 78 17. Nunn CR, Neuzil D, Naslund T, Bass JG, Jenkins JM, Pierce R, et al. Cost-effective method for bedside insertion of vena caval filters in trauma patients. J Trauma 1997;43(5):752–8. 18. Sing RF, Jacobs DG, Heniford BT. Bedside insertion of inferior vena cava filters in the intensive care unit. J Am Coll Surg 2001;92(5):570–5. 19. Geerts WH, Pineo GF, Heit JA, Bergqvist D, Lassen MR, Colwell CW, et al. Prevention of venous thromboembolism: the seventh ACCP conference on antithrombotic and thrombolytic therapy. Chest 2004;126(3 Suppl):338S–400S. 20. Greenfield LJ, Proctor MC. Current status of inferior vena cava filters. Ann Vasc Surg 2000;14(5):525–8. 21. Khansarinia S, Dennis JW, Veldenz HC, Butcher JL, Hartland L. Prophylactic Greenfield filter placement in selected high-risk trauma patients. J Vasc Surg 1995;22(3):231–5. 22. Rogers FB, Strindberg G, Shackford SR, Osier TM, Morris CS, Ricci MA, et al. Five-year follow-up of prophylactic vena cava filters in high-risk trauma patients. Arch Surg 1998;133(4): 406–11. 23. Rogers FB, Shackford SR, Ricci MA, Huber BM, Atkins T. Prophylactic vena cava filter insertion in selected high-risk orthopaedic trauma patients. J Orthop Trauma 1997;11(4): 267–72. 24. Rogers FB, Shackford SR, Ricci MA, Wilson JT, Parsons S. Routine prophylactic vena cava filter insertion in severely injured trauma patients decreases the incidence of pulmonary embolism. J Am Coll Surg 1995;180(6):641–7. 25. Pasquale M, Fabian TC. Practice management guidelines for trauma from the Eastern Association for the Surgery of Trauma. J Trauma 1998;44(6):941–56. 26. Streiff MB. Vena caval filters: a comprehensive review. Blood 2000;95(12):3669–77. 27. Emerson Jr RH, Cross R, Head WC. Prophylactic and early therapeutic use of the Greenfield filter in hip and knee joint arthroplasty. J Arthroplasty 1991;6(2):129–35. 28. Vaughn BK, Knezevich S, Lombardi Jr. AV, Mallory TH. Use of the Greenfield filter to prevent fatal pulmonary embolism associated with total hip and knee arthroplasty. J Bone Joint Surg Am 1989;71(10):1542–8. 29. Falanga A, Donatti MB. Pathogenesis of thrombosis in patients with malignancy. Int J Hematol 2001;73(2):137–44. 30. Benevenia J, Bibbo C, Patel DV, Grossman MG, Bahramipour PF, Pappas PJ. Inferior vena cava filters prevent pulmonary emboli in patients with metastatic pathologic fractures of the lower extremity. Clin Orthop Relat Res 2004;426:87–91. 31. Rosen MP, Porter DH, Kim D. Reassessment of vena caval filter use in patients with cancer. J Vasc Interv Radiol 1994;5(3): 501–6. 32. Leon L, Rodriguez H, Tawk RG, Ondra SL, Labropoulos N, Morasch MD. Theprophylactic use of inferior vena cava filters in patients undergoing high-risk spinal surgery. Ann Vasc Surg 2005;19(3):442–7. 33. Maxwell RA, Chavarria-Aguilar M, Cockerham WT, Lewis PL, Barker DE, Durham RM, et al. Routine prophylactic vena cava filtration is not indicated after acute spinal cord injury. J Trauma 2002;52(5):902–6. 34. Becker DM, Philbrick JT, Selby JB. Inferior vena cava filters. Indications, safety, effectiveness. Arch Intern Med 1992; 152(10):1985–94.
N. Hulse et al. 35. Davis JW, Hoyt DB, McArdle MS, Mackersie RC, Shackford SR, Eastman AB. The significance of critical care errors in causing preventable death in trauma patients in a trauma system. J Trauma 1991;31(6):813–8. 36. PREPIC Study Group. Eight-year follow-up of patients with permanent vena cava filters in the prevention of pulmonary embolism: the PREPIC (Prevention du Risque d’Embolie Pulmonaire par Interruption Cave) randomized study. Circulation 2005;112(3):416–22. 37. Decousus H, Leizorovicz A, Parent F, Page Y, Tardy B, Girard P, et al. A clinical trial of vena caval filters in the prevention of pulmonary embolism in patients with proximal deep-vein thrombosis. Prevention du Risque d’Embolie Pulmonaire par Interruption Cave Study Group. N Engl J Med 1998;338(7):409–15. 38. Stein PD, Kayali F, Olson RE. Twenty-one-year trends in the use of inferior vena cava filters. Arch Intern Med 2004;164(14): 1541–5. 39. Arnold TE, Karabinis VD, Mehta V, Dupont EL, Matsumoto T, Kerstein MD. Potential of overuse of the inferior vena cava filter. Surg Gynecol Obstet 1993;177(5):463–7. 40. Allen TL, Carter JL, Morris BJ, Harker CP, Stevens MH. Retrievable vena cava filters in trauma patients for high-risk prophylaxis and prevention of pulmonary embolism. Am J Surg 2005;189(6):656–61. 41. Morris CS, Rogers FB, Najarian KE, Bhave AD, Shackford SR. Current trends in vena caval filtration with the introduction of a retrievable filter at a level I trauma center. J Trauma 2004; 57(l):32–6. 42. Millward SF, Oliva VL, Bell SD, Valenti DA, Rasuli P, Asch M, et al. Gunther Tulip retrievable vena cava filter: results from the Registry of the Canadian Interventional Radiology Association. J Vasc Interv Radiol 2001;12(9):1053–8. 43. Hull RD, Raskob GE. Prophylaxis of venous thromboembolic disease following hip and knee surgery. J Bone Joint Surg Am 1986;68(1):146–50. 44. Buerger PM, Peoples JB, Lemmon GW, McCarthy M. Risk of pulmonary emboli in patients with pelvic fractures. Am Surgeon;59:505–8. 45. Greenfield LJ, Proctor MC, Cho KJ, Cutler BS, Ferris EJ, McFarland D, et al. Greenfield extended evaluation of the titanium Greenfield vena caval filter. J Vasc Surg 1994;20(3): 458–64. 46. Greenfield LJ, Proctor MC. Twenty-year clinical experience with the Greenfield filter. Cardiovasc Surg 1995;3(2):199–205. 47. Webb LX, Rush PT, Fuller SB, Meredith JW. Greenfield filter prophylaxis of pulmonary embolism in patients undergoing surgery for acetabular fracture. J Orthop Trauma 1992;6: 139–54. 48. McMurtry AL, Owings JT, Anderson JT, Battistella FD, Gosselin R. Increased use of prophylactic vena cava filters in trauma patients failed to decrease overall incidence of pulmonary embolism. J Am Coll Surg 1999;189(3):314–20. 49. Winchell RJ, Hoyt DB, Walsh JC, Simons RK, Eastman AB. Risk factors associated with pulmonary embolism despite routine prophylaxis: implications for improved protection. J Trauma 1994;37(4):600–6. 50. Duperier T, Mosenthal A, Swan KG, Kaul S. Acute complications associated with Greenfield filter insertion in high-risk trauma patients. J Trauma 2003;54(3):545–9.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 79–81
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CME SECTION Three CME points available The following series of questions are based on the Mini Symposium on Frontiers in Spine Surgery. Please read the articles in the Mini Symposium carefully and then complete the self-assessment questionnaire by filling in the square corresponding to your response to each multiple-choice question. For true or false questions, please fill in one square only. After completing the questionnaire, either post or fax the answer page back to the Current Orthopaedics Editorial Office at the address at the bottom of the RESPONSE sheet. Please photocopy this page if you wish to keep your copy of Current Orthopaedics intact. Replies received before the next issue of Current Orthopaedics is published will be marked and those reaching an adequate standard will qualify for three external CME points. You will be notified of your marks and a CME certificate will be despatched for your records.
Questions 1. Which of the following interventions is amongst those that European Working Party recommend for back pain?
A. B. C. D. E.
Biopsychosocial treatment Interferential Laser therapy TENS Traction
2. Which of the following has the strongest relationship to the development of new back pain symptoms in a population of asymptomatic individuals?
A. Advanced disc degeneration on MRI B. Annular fissures C. Development of new spinal pathology on MRI after an interval of 3 years or more D. Social context E. X-ray evidence of degenerative spinal disease 0268-0890/$ - see front matter & 2007 Published by Elsevier Ltd. doi:10.1016/j.cuor.2007.01.005
3. What did Panjabi define as the range of intervertebral movement within which spinal motion occurs with minimal internal resistance? A. B. C. D. E.
Biomechanically safe zone Neutral axis Neutral zone Physiological range of motion Stable motion segment
4. Spinal fusion first described in the management of which condition? A. B. C. D. E.
Discitis Fracture dislocation Low back pain Scoliosis Tuberculosis
5. Which of the following fusion techniques requires the lowest volume of bone graft? A. B. C. D. E.
Anterior lumbar interbody fusion Facet joint fusion Intertransverse fusion Posterior fusion Posterior lumbar interbody fusion
6. Which of the following is not a perceived advantage conferred by pedicle screw instrumentation on posterior fusion surgery? A. B. C. D. E.
Allows correction of deformity Allows earlier mobilisation Avoids need for external bracing Creates initial environment more conducive to fusion Reduces infection risk
7. Where are dynamic stabilising devices, in general, placed? A. B. C. D. E.
Across the facet joints Flush with anterior longitudinal ligament Flush with posterior longitudinal ligament In posterior column In central axis of vertebral bodies
ARTICLE IN PRESS 80
CME SECTION
8. At approximately what time interval after intervertebral disc replacement was peak sporting performance achieved in a cohort of athletes undergoing surgery?
C. Silicone D. Polyester E. Polyethylene
A. B. C. D. E.
10. Which of the following is currently an indication against nucleus pulposus replacement?
5 weeks 10 weeks 5 months 10 months 2 years
9. Which material is sandwiched between metal endplates in all FDA approved disc replacements? A. Carbon fibre B. Polycarbonurethane
A. Back pain unresponsive to nonoperative treatment for 6 months B. Disc height loss of one-third C. Disc height 8 mm on MRI D. Schmorl’s node at the affected level E. Spondylolisthesis with 10% slip
ARTICLE IN PRESS CME SECTION
81
Please fill in your answers to the CME questionnaire above in the response section provided below. A return address and fax number is given at the bottom of the page. ...............................................................................................
Responses Please shade in the square for the correct answer. 1 2 3 4 5 6 7 8 9 10 11 12
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D D D D D D D D D D D D
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Your details (Print clearly)
NAME. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ADDRESS. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . FAX NO. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . EMAIL. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
RETURN THE COMPLETED RESPONSE FORM by fax to +44-113-392-3290, or by post to CME, Current Orthopaedics, Academic Department of Orthopaedic Surgery, ‘‘A’’ Floor Clarendon Wing, Leeds General Infirmary, Great George Street, Leeds LS1 3EX, UK.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 82
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CME SECTION Answers to CME questions based on the Mini-Symposium on Bullet and Blast Injuries Please find below the answers to the Current Orthopaedics CME questions from Vol. 20, issue 5, which were based on the Mini Symposium on Bullet and Blast Injuries. 1
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0268-0890/$ - see front matter doi:10.1016/j.cuor.2006.05.001
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 83–84
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BOOK REVIEWS Emerging Spine Surgery Technologies: Evidence and Framework for Evaluating New Technology, T.P. Corbin, P.J. Connolly, H.A. Yuan, Q.-B. Bao, S.D. Boden, Quality Medical Publishing (2005). 611pp., $225, ISBN:0756707641 In recent years, there has been an explosion in spinal technologies. The editors of this book recognise the importance of evidence-based medicine and the need for training in the evaluation of that evidence. The book is arranged in four parts with chapters grouped together in related themes. Throughout this book the text is well illustrated and extensively referenced. Part I Basic Considerations looks at basic science, the Food and Drug Administration regulations and the issue of clinician reimbursement from the perspective of the United States. There is a useful insight into the difficulties of getting a product to market and hence the marketing pressure that is generated to promote the use of a device. All surgeons treating low back pain should read chapter 2, by Carragee and Cheng. Part II is focussed on biological and tissue engineering. The biological basis of bone graft fusion is followed logically by the technologies to enhance and stimulate fusion, the use of allograft bone, demineralised bone matrix, growth factors and gene therapy to promote spinal fusion. The chapters have an introduction to each topic that can be understood by a clinician without demanding detailed basic science expertise in each particular field of knowledge. Several chapters cover the basic science of disc degeneration and strategies for repair as well as potential future developments. A slim chapter 13 on spinal cord regeneration and repair outlines several potential treatment regimens
but it rather pulls its punches with respect to the NASCIS trials in view of recent guidelines that have criticised the level of evidence supporting the use of methylprednisolone in acute spinal cord injury. Part III is a short collection of three chapters on the related theme of surgical navigation as applied to the spine. Each chapter is concise and discusses the pitfalls as well as the potential advantages of this technology. The remaining half of the book is contained in Part IV and is dedicated to surgical techniques. Chapters are arranged into sections on minimally invasive and endoscopically assisted techniques, vertebral augmentation and cages, anterior spinal fixation, dynamic neutralisation and ending in seven chapters on disc replacement. Surprisingly, there are no chapters dedicated to open placement of pedicle screw and rod constructs for the treatment of spine trauma and deformity Perhaps this is seen to be no longer an emerging technology but more an established practice. The implant companies still seem to find their own screws to be technologically advanced! Overall, this is an outstanding reference book for the specialist spinal surgeon or even for the non-specialist who wishes to have a deeper understanding of new developments in spinal surgery. General orthopaedic trainees will find useful chapters in the first three parts of this book and dedicated spinal specialists will find educational value from the whole volume. Surgeons will find it helpful to have so many different innovations described in a single text and to have a foundation for understanding the science supporting these developments.
Crispin Wigfield
doi: 10.1016/j.cuor.2006.10.008
‘‘Who’s Who’’ of North American arthroplasty surgeons, R. Barrack, R. Booth Jr., J.H. Lonner et al. (Eds.). Orthopaedic Knowledge Update. Hip and Knee Reconstruction, Vol. 3. American Academy of Orthopaedic Surgeons (2006). 450pp., £97.95, ISBN: 0-89203-348-7 The previous hip and knee edition in 2000, was an ‘‘update’’, whereas this text is a stand alone edition on all
aspects of managing the degenerative hip and knee. This combined with the excellent annotated bibliography at the end of most of the chapters will be very appealing to trainees. Written in 2005, this edition should be all that a trainee needs to know about arthroplasty surgery and joint preserving procedures for the FRCS (orth) or board exams. The UK trainee needs to be aware that this is a North American tome, and should carry a warning when applied to UK practice and exams. Hip resurfacing is covered, but with
ARTICLE IN PRESS 84 only one UK reference, uncemented arthroplasty is given five times the space as cemented arthroplasty and impaction grafting in hip revision surgery is dismissed in a single paragraph. Most of the major differences in practice relate to hip surgery. There seems to be better cross Atlantic concordance in knee surgery, though many will disagree on
Book Reviews their views on venous thromboembolic disease and prophylaxis. Despite these criticisms, I can wholeheartedly recommend this edition to all trainees and departmental libraries.
David Macdonald
doi: 10.1016/j.cuor.2006.06.005
Endoscopic Spine Surgery & Instrumentation—Percutaneous Procedures. Kim D.H., Fessler R.G., Regan J.J., editors. Thieme, New York, Stuttgart (2005). (404pp., $ 169.95, ISBN: 1-58890-225-0). This is a multi-author text with contributors drawn largely from North America. All are acknowledged experts in their respective procedures. It is a technique focused tome with seven chapters arranged according to anatomical region (cervical, thoracic, lumbar), percutaneous procedures (nucleoplasty, kyphoplasty) and image-guided and robotic-assisted surgery. Its aims include ‘yproviding the fundamentals for a complete understanding of the minimally invasive approachy.[and] a useful tool and educational resource for integrating these operative methods into practice’. This book only partially achieves the stated aims. The text is generously illustrated; but in common with previous books on this subject the endoscopic intraoperative figures do not allow the surgical anatomy to be fully appreciated by the surgical tyro.
Several of the procedures are repeated under eponymous titles with the variation based on the type of implant used. I suspect that these techniques will have limited longevity as the technology evolves still further. Furthermore, some of the operations described are based on very limited clinical experience (cf. four patients in the section on microscopic laminoplasty). The broad range of procedures disguises the fact that many have only very limited uptake (laser-based ablative techniques) by the spinal surgical community or even outdated (e.g. stand-alone laparascopic anterior lumbar interbody fusion with cylindrical cages). In conclusion, this book is for the specialist spine surgeon, experienced in the traditional ‘open’ techniques; who is looking to update knowledge of less-invasive approaches. Whilst it does provide a valuable overview of the ‘state of the art’, I suspect the general orthopaedic trainee or resident will not benefit from reading it.
Michael Grevitt
doi:10.1016/j.cuor.2006.10.001
Raymond T. Morrissy, Stuart L. Weinstein, Atlas of Pediatric Surgery, Lippincott Williams and Wilkins, ISBN 07817 57894, 2006, (954pp., £215). Surgical atlases are usually a popular frame of reference for the individual surgeon although it is difficult to ensure that they remain both up-to-date and comprehensive. Ray Morrissy and Stuart Weinstein have now produced a fourth edition of their popular atlas, attempting to cover orthopaedic procedures for all the relevant anatomical regions including the spine. They have brought in four other contributing authors. Much of the text and references is admirable. The black and white illustrations are rendered accurately although colour would enhance the portrayal of the anatomy. The incisions described for certain operations are open to criticism, such as the extensile one for trigger thumb, the obliquity of the Salter osteotomy incision and the inadequate length of the incision to give proper access for a displaced lateral humeral condylar fracture and fixation. The medial approach for the open reduction of the dislocated hip remains contentious. doi:10.1016/j.cuor.2007.01.002
More should have been made of the three-dimensional correction required for supracondylar fracture malunion and during Pauwel’s procedure. Compression screw fixation of the Chiari osteotomy aids more rapid functional recovery and full-threaded screws should be used in operations to secure the slipped upper femoral epiphysis. The periacetabular osteotomy example shown on page 323 appears to have been carried out for minimal acetabular dysplasia with an os acetabuli that has yet to fuse. The radiographs in procedure 4.5 are of poor quality. Mention of the Dunn procedure for SUFE and the Metazieau operation for radial neck angulated fracture would have been welcome and the indication for transiliac lengthening is surely unusual. Overall, this edition of the atlas has succeeded in adding some current orthopaedic procedures. As a general reference book it is commendably wide-ranging. I recommend it to those intent upon a career in orthopaedic surgery, particularly for those who are specialising in paediatric care.
Malcolm Macnicol
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 85–93
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MINI-SYMPOSIUM: CHILDREN—OSTEOTOMIES AROUND THE HIP
(i) The Salter innominate osteotomy M.F. Macnicol Orthopaedic Department, Royal Hospital for Sick Children, Sciennes Road, Edinburgh, EH9 1LF, UK
KEYWORDS Innominate osteotomy; Congruent hip; Acetabular index; Operative details; Alternative procedures
Summary The Salter osteotomy has stood the test of time, proving to be a safe and effective means of improving acetabular cover in the younger child. Alternative procedures are briefly discussed and technical aspects are described. & 2007 Elsevier Ltd. All rights reserved.
Introduction Establishing a stable femoral head is an essential element in treating the dysplastic hip joint after reduction. In the infant up to the age of 18 months an unobstructed replacement of the femoral head deeply within the acetabulum will usually produce satisfactory acetabular growth and deepening. Provided that congruity improves and concentric movement is achieved, further treatment may be unnecessary. Adequate femoral head cover should be demonstrable by 3–4 years of age. The decision-making process is somewhat arbitrary but is based upon (1) the clinical appearances of the hip, since any spasm or limited motion is of concern, particularly if associated with asymmetry of the leg producing the appearance of ‘‘skeletal skew’’ and (2) radiographic improvement including an acetabular index of 301 of more after the age of 312 years; lateralisation of Tel.: +44 131 536 0000; fax: +44 131 536 0852.
E-mail address:
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the femoral head radiographically can be measured using the centre-head distance.1 The latter can only be used in unilateral cases, a distance of more than 6% at the age of 4 or 5 years indicating that supplementary surgery may be necessary. In the toddler older than 18 months full development of the acetabulum after femoral head reduction is less assured. The acetabular response becomes unpredictable and stability of the femoral head after reduction is harder to ensure when both acetabular inclination and deformation of the femoral head may prevent congruent reduction. Nevertheless, it is important that Salter’s prerequisites are met,2 namely that the hip should present with a free range of movement, whether following previous treatment (Fig. 1) or presenting de novo with dysplasia (Fig. 2). He also stated that any reduction achieved after complete dislocation should be reasonably congruent at the time of the osteotomy.
Timing of the osteotomy Deciding when to undertake the Salter osteotomy, in relation to open reduction the hip in the slightly older
ARTICLE IN PRESS 86
Figure 1
M.F. Macnicol
A sequence of radiographs with staged open reduction of the left hip and subsequent Salter innominate osteotomy.
child, is a matter for some debate.3–6 Concurrent innominate osteotomy makes further surgical operations less likely, additionally helping to stabilise the femoral head. It has been suggested that the outcome after simultaneous open reduction and osteotomy may not differ markedly from a staged procedure4 and there is a legitimate concern that both redislocation and avascular necrosis are more likely if the procedures are combined. A more recent paper6 revealed that in a series of 188 Salter osteotomies the best results occurred in children under the age of 30 months, treated by the combined procedure. Staged operations yielded a slightly smaller proportion of satisfactory results (71 per cent versus 89 per cent in the younger child) but the risks of redislocation and avascular necrosis were reduced. Deferring the pelvic osteotomy for some time after the hip has been reduced may of course allow a gradual subluxation of the femoral head before the acetabulum is redirected. Whichever approach is favoured, it is paramount that the capsulorrhaphy in the concurrent procedure is
carefully rendered and that the acetabular inclination is reduced by at least 151 by the osteotomy. Femoral shortening is often required after the age of 212–3 years, especially in the high dislocation. A useful discriminant in the operating theatre is to reduce the femoral head, after an adductor tenotomy, with the knee flexed (to relax the hamstrings) and with the thigh slightly internally rotated. If the femoral head redislocates as the knee is straightened and the thigh returns to a position where the knee is pointing anteriorly, femoral shortening is indicated. When femoral head reduction cannot be achieved without proximal femoral osteotomy and overlapping of the femoral shaft, then clearly a femoral shortening of some 1–2 cm is essential. In bilateral cases the Salter osteotomy should only be undertaken sequentially. Unless one or other femoral head is very unstable after open reduction in these cases, the Salter osteotomy is undertaken some time after closed or open reductions have been achieved. Concurrent, bilateral
ARTICLE IN PRESS The salter innominate osteotomy
Figure 2
87
Combined closed reduction and Salter osteotomy for right hip subluxation.
innominate osteotomies are only indicated in cases of bladder exstrophy as a means of producing adventitial cover anterior to the bladder. If the femoral head lateralises after the Salter innominate osteotomy, or if the acetabular dysplasia is poorly corrected, the outcome will be impaired. Varus and/or derotational proximal femoral osteotomy may be required. Further open reduction and capsulorrhaphy are sometimes indicated but repeating the Salter procedure is not advisable. An augmentation shelf graft, Dega procedure7,8 or a Chiari osteotomy9–11 may help to provide stability. As the Salter osteotomy rotates the acetabulum anterolaterally over the femoral head, a misshapen femoral head or acetabular deformation will adversely affect the result. The Pemberton (or ‘‘Pembersal’’12,13) tends to lateralise the hip joint and increase articular pressure. In the older child and adolescent, it is increasingly difficult to rotate the lower pelvic segment at the symphysis pubis. Therefore, the Ganz,14 Steel15 or
Tonnis16 procedure are indicated, although technically more invasive.
Technique The stages of the Salter osteotomy have been described previously in Current Orthopaedics17 but merit a brief outline. Practical experience of the procedure can only be gained by supervised operating in theatre, repeated regularly. Fuller accounts of the osteotomy are recommended for those with a developing interest in children’s orthopaedics.1,3,18,19
a. Position of the child i. a sandbag is used to tilt the child up on the operation side, but this should be placed under the flank and not the buttock,
ARTICLE IN PRESS 88 ii. the child should be near the side of the table to facilitate access, iii. the C-arm of the image intensifier is draped and positioned transverse to the child on the contralateral side; at lease one operating surgeon should wear a lead apron.
b. Incision i. the transverse (bikini line) ilioinguinal skin incision is centred a finger breadth below the anterior superior spine (13 medial to the spine and 23 lateral to it), ii. the plane between tensor fascia lata and sartorius is developed distally and then dissected proximally, iii. the iliac apophysis is split down to bone by a sharp incision over the anterior 3–4 cm, cracking open and then reflecting the apophysis away from the iliac wing subperiosteally (Fig. 3), iv. the wayward lateral femoral cutaneous nerve should be protected if possible.
c. Soft tissues i. the straight head of rectus and the iliopsoas are tenotomised before any attempt at femoral head reduction, ii. capsule is carefully exposed, particularly anteriorly and medially, iii. capsulotomy is usually undertaken through a T cut, 0.5 cm distal to the rim of the acetabulum, iv. in order to place the femoral head in the acetabulum the ligamentum teres is resected and the limbus
M.F. Macnicol (inverted labrum and capsule, if present) everted after making it more pliant with 4 or 5 radial cuts, v. the pulvinar (fat pad) is not excised and any adhesions or inferior capsular folds should be released, vi. if the head of the femur redislocates after reduction it may be necessary to carry out a proximal femoral shortening, with correction of any significant femoral anteversion, vii. a tight capsulorrhaphy is the most important component of the operation, either by double-breasting the capsule or by excision of the redundant capsule.
d. The innominate osteotomy i. access subperiosteally to the sciatic notch must be careful to avoid sciatic nerve damage or major haemmorage, ii. Watson-Jones bone levers are inserted ‘‘on the side’’ to give posterior space and a curved (901) gall bladder (Moynihan) forceps (Fig. 4) is inserted around the sciatic notch, either medial to lateral or lateral to medial, whichever is easier; suction and a well-directed light are essential, iii. the Gigli saw will pass round the back of the ilium more readily if the loop end of the saw is narrowed and bent to conform around the notch (Fig. 5), iv. the saw is encased in plastic gastric tubing on either side of its cutting, central segment, v. this protects the soft tissues as the saw is moved back and forth; during cutting, the hands should be kept apart and tension maintained evenly (Fig. 6),
Figure 3 The extent of the incision (top left) A ¼ anterior iliac wing, P ¼ proximal thigh, splitting the iliac apophysis (I) (top right), a periosteal elevator (P) allows the iliac wing to be exposed subperiosteally (bottom left), a blunt hook (B) lifts the iliopsoas (I) near the anterior inferior iliac spine (A) (bottom right).
ARTICLE IN PRESS The salter innominate osteotomy vi. anteriorly, the osteotomy can be finished with an oscillating saw if the Gigli saw binds in bone.
f. Displacement of the osteotomy i. when correcting acetabular dysplasia alone, with no need for reduction and capsulorrhaphy, placing the leg in the ‘‘figure 4 position’’ (thigh abducted and externally rotated, knee flexed) will aid in opening the osteotomy anteriorly and directing the lower pelvic fragment laterally,
89 ii. redirection of the lower fragment is better achieved with a towel clip in the anterior inferior iliac spine, an osteotome ‘‘on the flat’’ pressing down on the lower fragment when the capsule has been opened, and the insertion of a Lambotte hook (Fig. 7), iii. triangular metal templates (Fig. 8) allow displacement of the osteotomy to be gauged and the size of the graft to be estimated.
g. Bone graft i. the triangular graft is procured from the anterior iliac wing or further back (Figs. 9 and 10), ii. the graft is carefully trimmed to give squared off edges, inserting it with sequestrum forceps and opening up the anterior osteotomy as fully as possible, iii. bank bone or bone substitutes may be preferred.
Figure 4 Gall bladder forceps (901 curve) with the Gigli saw and leader cord.
Figure 6 The innominate osteotomy is undertaken with the Gigli saw from posteriorly to anteriorly, keeping the lateral hand more distal than the medial hand so that the cut is at right angles to the ilium.
Figure 5 The loop end of the Gigli saw is narrowed and curved, allowing it to be held by the forceps with gastric tubing encasing the saw to prevent soft tissue abrasion.
ARTICLE IN PRESS 90
M.F. Macnicol
Figure 7 The small Lambotte hook (beside the gall bladder forceps) is inserted behind the distal pelvic fragment, pulling it forwards. A gap is developed at the anterior end of the osteotomy with the towel clip and hook in place, allowing a carefully sized template and similarly proportioned bone graft to be readied for insertion.
Figure 8 The metal template has been inserted in the osteotomy gap and can be checked radiographically before inserting the graft and 3 K wires.
h. Graft fixation i. two or three (threaded) K-wires are inserted from above, through the iliac wing, ii. the depth of the wire insertion is checked against a similar K-wire, held parallel to the track of the fixation wire, iii. it is important to check femoral head movement in the acetabulum, or, if the femoral head is out of the socket, to palpate the articular surface for possible protrusion, iv. image intensifier views are helpful at this stage,
v. the wires should be left slightly prominent under the skin for removal at six weeks postoperatively when the hip spica cast is taken off under a general anaesthetic, vi. the use of cannulated screws or Biofix absorbable rods is not recommended.
i. Soft tissue closure i. the apophysis should be accurately apposed, ii. the lateral femoral cutaneous nerve must not be trapped by any suture, iii. after irrigation, skin is closed with a subcuticular sutute.
ARTICLE IN PRESS The salter innominate osteotomy
j. Plaster spica i. an adjustable spica table should be used if possible (Fig. 11), ii. the stockingette is pre-stitched and fits the child accurately (Fig. 12), iii. excessive padding should be avoided if both orthopaedic felt and wool are usually required (Fig. 13),
91 iv. plaster of paris or synthetic materials are used for the spica which should be carefully moulded around the greater trochanter to hold the femoral head secure (Fig. 14).
Figure 11 The adjustable hip spica table with orthopaedic felt in readiness.
Figure 9 The iliac wing is exposed using Watson–Jones levers before obtaining the bone graft with bone cutters or an oscillating saw.
Figure 12 The stockingette is cut and stitched to produce a skin tight fit.
Figure 10 The dimensions of the triangular bone graft are measured out as shown.
ARTICLE IN PRESS 92
M.F. Macnicol ciently strict? And finally, is minimal access surgery a safe advance?
Conclusion The Salter osteotomy offers an effective means of improving acetabular alignment and femoral head stability but should not be considered in the younger child until the acetabulum has shown its ability to improve. Various modifications of the procedure have been described but the essential factor is that the surgeon should be familiar with the osteotomy and that attention to detail must be meticulous. Figure 13
Application of felt and wool for the spica.
References
Figure 14 A well-moulded spica with the legs abducted and semi-flexed.
Complications Complications include general misadventures such as sciatic and femoral nerve injury, entrapment or damage to the lateral femoral cutaneous nerve,20 arterial bleeding, bladder retention, infection and pressure sores. Further specific complications of the procedure include redisplacment of the femoral head, bone graft collapse or absorption, K-wire migration and difficulty in removal, stiffness of the hip (often with an abductor contracture), avascular necrosis of the proximal femoral epiphysis and/or growth plate, and lateralisation of the hip subsequent to capsulorrhaphy. A less recognised but important complication is elongation of the affected leg, both from the stimulus of closed or open reduction and the subsequent Salter innominate osteotomy.21 This is evident in almost 80 per cent of children after late dislocation and can be as much as a centimetre of overgrowth in almost a quarter. Various questions arise in relation to the technique of osteotomy.22 For example, how does one determine congruency and concentric movement of the femoral head within the acetabulum? Arthrography may be useful in this context. Should the pelvic realignment and graft fixation precede or follow femoral head reduction into the acetabulum? Are the guidelines for femoral shortening suffi-
1. Kim HT, Kim JI, Yoo CI. Acetabular cover in congenital dislocation of the hip. Paediatr Orthop 2000;20:701–8. 2. Salter RB. Innominate osteotomy in the treatment of congenital dislocation and subluxation of the hip. J Bone Jt Surg 1961; 43-B:518–39. 3. Salter RB, Dubos JP. The first fifteen years’ personal experience with innominate osteotomy in the treatment of congenital dislocation and subluxation of the hip. Clin Orthop 1974;98:72–103. 4. Barrett WP, Staheli LT, Chew DE. The effectiveness of the Salter innominate osteotomy in the treatment of congenital dislocation of the hip. J Bone Jt Surg 1986;68-A:79–87. 5. Haider RK, Jones RS, Vergroesen DA, Evans GA. Simultaneous open reduction and Salter innominate osteotomy for developmental dysplasia of the hip. J Bone Jt Surg 1996; 78-B:471–6. 6. Macnicol MF, Bertol P. The Salter innominate osteotomy: should it be combined with concurrent open reduction? J Paediatr Orthop B 2005;14:415–21. 7. Dega W, Polakowski L. Surgical treatment of congenital dislocation of the hip in children. A one-stage procedure. J Bone Jt Surg 1959;41-A:920–4. 8. Murray AW, Robb JE. Pelvic osteotomy for the management of hip displacement in neuromuscular disorders. Curr Orthop 2007;21. 9. Chiari K. Ergbnisse mit der Beckenosteotomie als Pfannendasplastik. Z Orthop 1955;87:14–26. 10. Ho+ gh J, Macnicol MF. The Chiari pelvic osteotomy. A long term review of clinical and radiographic results. J Bone Jt Surg 1987;69-B:365–73. 11. Patil S, Sherlock DA. The Chiari medial displacement osteotomy. Currt Orthop 2007;21. 12. Perlik PC, Weston GW, Marafioti RL. Combination pelvic osteotomy for acetabular dysplasia in children. J Bone Jt Surg 1985;67-A:842. 13. Pemberton PA. Pericapsular osteotomy of the ilium for treatment of congenital dislocation of the hip. J Bone Jt Surg 1965;47-A:65–86. 14. Ganz R, Klaue J, Vin TS, Mast JW. A new periacetabular osteotomy for treatment of hip dysplasia. Clin Orthop 1988;222:26–36. 15. Steel HH. Triple osteotomy of the innominate bone. J Bone Jt Surg 1973;55-A:343–50. 16. Tonnis D, Arning A, Bloch M, et al. Triple pelvic osteotomy. J Paediatr Orthop B 1994;3:54–67. 17. Macnicol MF, Al Rawashdeh H, Auld J. Technical aspects of the Salter innominate osteotomy. Curr Orthop 2000;14:209–14. 18. Macnicol MF. Color altas and text of osteotomy of the hip. London: Mosby-Wolfe; 1996. p. 13–22.
ARTICLE IN PRESS The salter innominate osteotomy 19. Morrissy RT, Weinstein SL. Atlas of pediatric orthopaedic surgery, 4th ed. USA: Lippincott Williams and Wilkins; 2006. p. 283–8. 20. Macnicol MF, Thompson WJ. Idiopathic meralgia paraesthetica. Clin Orthop 1990.
93 21. McKinley JC, Macnicol MF. Leg length discrepancy following Salter osteotomy, BOA Annual Meeting Booklet, 2004. p. 37. 22. Macnicol MF. The Salter innominate osteotomy—quirks and questions. J Bone Jt Surg 2005;87-B(Suppl1:71) (BSCOS/GEOP Combined Meeting).
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 94–99
Available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/cuor
MINI-SYMPOSIUM: CHILDREN—OSTEOTOMIES AROUND THE HIP
(ii) Pelvic osteotomy for the management of hip displacement in neuromuscular disorders Alastair W. Murray, James E. Robb Royal Hospital for Sick Children, 9 Sciennes Road, Edinburgh EH9 1LF, UK
KEYWORDS Hip; Pelvic osteotomy; Dega; Pemberton; Chiari; Neuromuscular pathology
Summary Patients with neuromuscular disorders may develop hip displacement and ultimately dislocation as a result of an imbalance of muscle forces acting across the hip joint. Hip displacement can cause pain, mobility and hygiene problems. Management of symptomatic, established hip displacement involves surgical relocation and reconstruction of the abnormal proximal femoral and acetabular anatomy. Several pelvic osteotomies have been described for management of the acetabular abnormalities with the object of preventing recurrent hip displacement. The most common pelvic and periacetabular procedures for management of neuromuscular hip displacement are considered in this article. & 2007 Elsevier Ltd. All rights reserved.
Introduction Subluxation or dislocation of the hip can occur as a consequence of neuromuscular disorder. Muscle spasticity or flaccidity resulting in imbalance of the muscle groups around the hip can result in gradual migration of the femoral head out of the acetabulum. It has also been proposed that pelvic obliquity secondary to neuromuscular scoliosis is a factor. An awareness of the potential for hip displacement in neuromuscular disorders has led to recommendations for clinical and radiological surveillance.
The hip in neuromuscular disorders Hip displacement is seen in about 25% of patients with cerebral palsy (CP) and rises to about 75% in those with more Corresponding author. Tel.: +44 141 201 0275.
E-mail address:
[email protected] (A.W. Murray). 0268-0890/$ - see front matter & 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2007.04.006
severe, total body involvement CP.1 This suggests that the more severe the neurological impairment, the more likely hip displacement occurs. In CP, the increased tone in the adductors and flexors of the hip shifts the centre of rotation from the femoral head towards the lesser trochanter. In the child with CP, the combination of abnormal muscle force, tone and the malleability of skeletally immature bone results in abnormal development of the acetabulum and proximal femur. Physiological values of femoral anteversion in early childhood do not resolve with normal growth and an increased neck-shaft angle may also persist.2,3 Eccentric pressure from the displacing femoral head results in abnormal pressure on the periphery of the developing acetabulum resulting in a predominantly superior acetabular defect. Over a period of some years, therefore, a hip which was normal at birth can dislocate ultimately. Botulinum injections to the adductors, and intrathecal baclofen to reduce abnormal tone or soft tissue surgery to weaken dominant muscle forces may delay eventual dislocation. Once hip subluxation occurs up to 50% of these patients
ARTICLE IN PRESS Pelvic osteotomy for the management of hip displacement develop hip pain. In many, stable seating and access for perineal hygiene are compromised due to the abnormal position of the lower limb on the dislocated side and hip pain.4 Hip relocation and stabilisation can be very effective in managing these symptoms. The hip may also dislocate in lower motor neurone disorders such as spina bifida or spinal cord injury.5,6 Hip pathology in these patients is influenced by the level of the spinal lesion but is not purely due to the resulting muscle imbalance.7 High thoracic lesions result in flail hips and such patients often develop hip flexion contractures and a subsequent dislocation. Muscle imbalance at the hip is maximal in a mid-lumbar lesion as the antagonists of the hip flexors and adductors are weak. This results in a slightly higher risk of hip dislocation than at other neurosegmental levels. Loss of abductor power also results in growth retardation of the greater trochanter and progressive coxa valga, which can exaggerate femoral head uncovering. It remains controversial whether relocation and containment of subluxating hips in spina bifida patients is justifiable.8–10 Hip pain is less of a problem than in CP because of the neurological loss. From a functional point of view, reciprocal movement at the hip is usually still possible when the patient sits or when using assistive devices for walking. Pelvic balance and control of joint contracture appear to be more important factors for these patients. Intact quadriceps function, motivation to walk and reasonable cognition are prerequisites when considering hip relocation in these patients. Children with spina bifida who do not have adequate quadriceps strength are unlikely to maintain independent walking in adulthood. When hip reduction is performed, acetabular cover is most commonly enhanced with a periacetabular or Chiari pelvic osteotomy, although triple osteotomy or even shelf procedures have been used. There is, however, a high rate of redislocation despite efforts to improve cover and patients who have had failed surgery may end up worse off. Hip subluxation is also seen in patients with spinal muscular atrophy and muscular dystrophy but the available evidence suggests that bony surgery is not beneficial for the management of hip subluxation in these patients.11,12 Attention should instead be focussed on maintaining spinal alignment and preventing pelvic obliquity. Despite the controversy surrounding the indications for surgical reduction and containment of the hip in the neuromuscular patient, there is less disagreement about the technical goals once the decision to operate has been taken. Concentric reduction of the hip, soft tissue balancing and correction of both the femoral and acetabular deformities are the objectives. On the femoral side, surgery is aimed at reducing the abnormal neck anteversion to an adult value and often includes femoral shortening and variation to reduce the neck shaft angle to about 1201. A more detailed description of femoral osteotomy is described elsewhere in this symposium. On the acetabular side, the deficiency is usually superior and in many cases postero-superior. The object of acetabular surgery is to improve superior cover and gain increased posterior cover if possible. For this reason, the Salter innominate osteotomy is less suitable for neuromuscular patients as it improves antero-superior cover at the expense of decreasing posterior acetabular cover. The situation is therefore different from
95 that encountered in developmental dysplasia of the hip where the deficiency commonly lies antero-superiorly and is well addressed by Salter’s osteotomy. The osteotomies most commonly used to address acetabular deficiencies will now be considered in more detail.
Pemberton’s periacetabular osteotomy Paul Pemberton from Salt Lake City, Utah, originally described his osteotomy in a personal case series published in 1965 for the management of developmental dysplasia of the hip.13 He described the technique as follows. The patient is placed supine and the hip approached through an anterior, Smith–Peterson approach. The iliac apophysis is split and the glutei and tensor fascia lata are stripped subperiosteally from the outer wall of the ilium to expose the hip capsule and allow visualisation of the greater sciatic notch. Muscle is also stripped from the medial aspect of the ilium back to the greater sciatic notch. Retractors are placed carefully into the sciatic notch and must remain subperiosteal to reduce the risk of damage to the superior gluteal vessels and sciatic nerve. This approach allows open reduction of the hip at this stage if necessary. An osteotomy is then cut in the outer table of the ilium starting just above the anterior inferior iliac spine and progressing posteriorly remaining approximately 1 cm above the attachment of the joint capsule (Fig. 1). This osteotomy is then completed by curving down posterior to the acetabulum to the level of the ilio-ischial limb of the triradiate cartilage. The osteotomy should not enter the sciatic notch. The position of the osteotomy of the inner table of the ilium then dictates the nature of the acetabular cover achieved. By cutting the osteotomy of the inner wall to conform exactly with the outer osteotomy, the acetabular roof will displace to provide enhanced anterior cover. If the posterior part of the inner table osteotomy is placed more anteriorly and inferiorly, more lateral cover will be gained. After joining the two osteotomies by dividing the intervening cancellous bone, the osteotomy is levered open and held by insertion of a cortico-cancellous wedge taken from the iliac crest. As the
Figure 1 Diagram showing the cuts made for the Salter, Pemberton and Pembersal osteotomies (Fig. 1B in Ref.16).
ARTICLE IN PRESS 96 Pemberton osteotomy leaves the posterior column intact, the bone wedge is held firmly in the osteotomy by the natural recoil of the bone. This negates the need for any fixation. The iliac apophysis is then repaired and the wound closed. A plaster spica is often used for a period of 6–8 weeks post-operatively. The Pemberton osteotomy therefore enhances anterior and superior acetabular cover. Potential disadvantages are that posterior cover cannot be improved, although it is not sacrificed, as it would be by a redirectional osteotomy like the Salter. Those who do advocate its use in neuromuscular disorders have reported very satisfactory results in patients with cerebral palsy.14,15 The other theoretical concern is that by using the triradiate cartilage as the fulcrum for displacing the osteotomy, the growth potential of the triradiate may be damaged. There appears to be little evidence to support this concern. A variation of the Pemberton osteotomy was described by Perlik et al.16 and named the Pembersal (Fig. 1). This was because it was thought to combine the apparent advantages of both the Pemberton and Salter osteotomies by allowing reshaping and redirection of the acetabulum. This can be achieved by continuing the posterior part of the osteotomy caudally to cross the ilio-ischial limb of the triradiate cartilage and finish in the body of the ischium. It is admitted that a Pembersal may be the inadvertent result of an attempt to perform a Pemberton as the view posterior to the acetabulum is restricted and the end point of the osteotomy often hard to define. There are no reports of the results of the Pembersal osteotomy in neuromuscular hip disorder but the redirectional element might be considered a disadvantage for the same reason as it is with the Salter. Potential for damage to the triradiate cartilage may also be greater.
Dega’s osteotomies In 1969, Dega reported the results of what he termed a ‘‘transiliac’’ osteotomy for the management of acetabular dysplasia. There has been some confusion surrounding the exact nature of this osteotomy, which has been put down to
A.W. Murray, J.E. Robb the contradictory descriptions originally published by Dega in the Polish and German literature. In effect, he described two different osteotomies.17 One is a supra-acetabular semicircular osteotomy and the other an incomplete transiliac osteotomy with many similarities to the Pemberton. The latter was originally and erroneously described as a complete transiliac osteotomy but the intention is not to divide the ilium completely. The semicircular periacetabular osteotomy is fundamentally different from the Pemberton in that it is unicortical (Fig. 2). The hip capsule and outer wall of the ilium are exposed subperiosteally through an anterior approach but the inner wall of the ilium does not need to be stripped of muscle. A gently curved osteotomy is then cut in the outer wall of the ilium superior to the acetabulum from the anterior inferior iliac spine into the greater sciatic notch. Curved osteotomes are then used to cut down between the walls of the ilium towards the triradiate cartilage. The resulting osteotomy can then be opened, hinging on the triradiate cartilage, and due to the intact inner iliac wall can be held open with cortical bone graft without fixation. A bicortical cut may need to be made at the anterior and posterior aspects of the osteotomy to allow adequate opening. A very similar procedure has been described by others including Mubarak18 who reported a high success rate using this osteotomy in neuromuscular hip disorder. Complications can, however, include inadvertent penetration of the acetabulum and avascular necrosis of the superior acetabular segment, in addition to the other complications common to the other osteotomies described in this article. A modification of the semicircular osteotomy is to bring the posterior part of the cut down behind the acetabulum and not enter the sciatic notch (Fig. 3). It is believed that this allows increased posterior cover. Robb and Brunner19 reported good correction of hip migration in CP patients using this technique even after closure of the triradiate cartilage. This showed that an open triradiate cartilage is not a prerequisite for this variation of the Dega procedure. Grudziak and Ward17 described the incomplete transiliac osteotomy in detail (Fig. 4). It uses the same surgical
Figure 2 Diagram showing the Dega semicircular osteotomy. Blade plate fixation of proximal femoral varus-derotation osteotomy also shown (Fig. 3 from Ref.18).
ARTICLE IN PRESS Pelvic osteotomy for the management of hip displacement approach as the Pemberton with soft tissue and femoral procedures still an integral part of the procedure. A curvilinear osteotomy is cut in the outer wall of the ilium
97 from just above the anterior inferior iliac spine to a point superior to the midpoint of the acetabulum. It is then continued posteriorly to end 1–1.5 cm from the greater sciatic notch, which is where it differs from the Pemberton. The osteotomy is then completed to a varying degree from anterior to posterior through the inner wall of the ilium depending on the desired degree of lateral or anterior cover. It is claimed that, when opened, the osteotomy hinges on the intact pelvic cortex of the sciatic notch, the symphysis pubis and to some extent the triradiate cartilage but carries a lesser risk of physeal damage. Radiographic studies have also shown an alteration in the appearance of the obturator foramen indicating some degree of acetabular redirection as well as reshaping. Jozwiak et al.20 have reported the longterm results of using this osteotomy in neuromuscular hip disorders together with soft tissue and femoral procedures. They found that good short-term results gradually deteriorated with 23% of hips redisplacing between 5 and 25 years post surgery.
Chiari osteotomy
Figure 3 Photograph of hemipelvis showing line of modified Periacetabular Dega osteotomy (Fig. 1 from Ref.19).
Chiari initially described this in 1955 as an alternative to the shelf procedure for the management of hip dysplasia. The osteotomy is transiliac with the intention of improving superior cover by medially displacing the hip with the pubis and ischium (Fig. 5). The resulting increased superior cover is provided by the cancellous bone of the ilium with interposed hip capsule, which then develops a fibrocartilaginous articulation with the femoral head. This is not as desirable as enhancing cover with native hyaline cartilage as achieved with the periacetabular osteotomies
Figure 4 Diagram showing the Dega incomplete transiliac osteotomy (Figs. 3A and B from Ref.17).
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A.W. Murray, J.E. Robb
Figure 5 Diagram and photo showing the Chiari transiliac osteotomy (Figs. 8.16 and 8.17 from: Malcolm F. Macnicol. Colour atlas and text of osteotomy of the hip. Mosby-Wolfe; 1996, p. 75).
and is considered to be a salvage procedure when these other techniques are not possible. This is the case in adolescents and young adults in whom the triradiate cartilage has fused and the pubic symphysis has stiffened. The absolute age when a Chiari should be considered in preference to the periacetabular osteotomies is however not clear. To perform a Chiari osteotomy as originally described21 requires the patient to be semi-supine and uses an anterior/ iliofemoral approach to the hip. As with the Pemberton osteotomy, both tables of the ilium need to be exposed by subperiosteal stripping back to the greater sciatic notch. Care must be taken to ensure that the plane of dissection is subperiosteal at the notch to reduce the risk of inadvertent damage to the sciatic nerve and superior gluteal vessels and allow correct insertion of retractors into the notch. A crucial stage of the procedure is establishment of the correct level for osteotomy of the ilium. Adherent hip capsule should be stripped off the ilium to reveal the true attachment of the capsule and prevent the osteotomy being performed too superiorly where the bone is thin. The groove in the ilium made by the reflected head of rectus femoris is said to be the optimal level for osteotomy. The level should also be checked on image intensifier views. Inadvertent entry into the acetabulum or damage to femoral head by too low a cut must be avoided. The ilium is then divided with osteotomes from lateral to medial with a slight cephalad slope starting at the level of the anterior inferior iliac spine curving over the capsular attachment and exiting into the greater sciatic notch. The osteotomy should not enter the sacroiliac joint. With the ipsilateral leg abducted the lower segment of the pelvis is gently displaced medially but total dissociation of the fragments by excessive displacement should be avoided. Although there is some stability of the ideally displaced fragments derived from interdigitation of the cut surfaces, most authors recommend additional support from a lag screw across the osteotomy. Hip movements need to be checked to ensure that there is no impediment to flexion from a prominent anterior shelf. Postoperative care varies from the use of traction or plaster to immediate mobilisation. As the Chiari is performed in an older age group consideration needs to be given to thromboprophylaxis. The Kawamura variation of the Chiari osteotomy uses a trans-trochanteric approach and elevation of the abduc-
tors.22 The perceived advantage of this is that it allows direct visualisation of the whole lateral wall of the ilium and better control of the contouring of the osteotomy to conform to the shape of the capsular attachment. The Chiari osteotomy mainly provides superior cover and the Kawamura variant has the potential to improve the deficient posterior cover commonly seen in neurological hip dislocation. Stripping of the medial wall of the ilium is not performed and distal trochanteric transfer can be added to compensate for the relative shortening of abductor length and to reduce the risk of trochanteric impingement. The Kawamura osteotomy is also claimed to have a lower risk of sciatic nerve damage, which is one of the main concerns with the Chiari osteotomy. Additional complications common to both procedures include haemorrhage, acetabular damage, fragment dissociation and non-union and narrowing of the pelvic inlet particularly with bilateral procedures. When the Chiari osteotomy is used for the management of neuromuscular hip dislocation, it is commonly combined with soft tissue and femoral procedures. The Chiari osteotomy in CP has been found to produce relatively satisfactory results comparable with other techniques.23 Debnath et al.24 found most patients continued to benefit from relief of pain and better sitting at an average follow-up of 13 years. Sustained improvement in mobility was less clear but influenced by many other factors. Others have shown, however, that between 15% and 30% of hips can redisplace in the longer term following a Chiari osteotomy, which is much more common than when the osteotomy is carried out for management of developmental hip dysplasia.25 This reflects the fact that the pathological processes driving hip displacement remain active in cerebral palsy in the long term. Less satisfactory results have been reported when the Chiari has been used for hip displacement secondary to myelodysplasia with redisplacement in the medium term a common finding.26
Summary Successful management of hip displacement due to neuromuscular disorders requires a thorough understanding of the original pathological processes. Clear and realistic goals
ARTICLE IN PRESS Pelvic osteotomy for the management of hip displacement must be established before embarking on major surgery in patients who commonly have many other health problems. In appropriate circumstances, however, pelvic osteotomy as an integral part of hip reduction and stabilisation can result in very satisfactory relief of symptoms for neuromuscular patients. As is often the case, the choice of osteotomy is less important than its appropriate application and the surgeon’s familiarity with the technique.
References 1. Lonstein J, Beck K. Hip dislocation in spastic cerebral palsy. J Pediatr Orthop 1986;6(5):521–6. 2. Able MF, Wenger DR, Mubarak SJ, Sutherland DH. Quantitative analysis of hip dysplasia in cerebral palsy: a study of radiographs and 3-D formatted images. J Pediatr Orthop 1994;14(3):283–9. 3. Chung CY, Park MS, Choi IH, et al. Morphometric analyis of acetabular dysplasia in cerebral palsy. J Bone Joint Surg [Br] 2006;88B(2):243–7. 4. Bagg MR, Farber J, Miller F. Long-term follow up of hip subluxation in cerebral palsy patients. J Pediatr Orthop 1993; 13(1):32–6. 5. McCarthy JJ, Betz RR. Hip disorders in children who have spinal cord injury. Orthop Clin N Am 2006;37:197–200. 6. Rink P, Miller F. Hip instability in spinal cord patients. J Pediatr Orthop 1990;10(5):583–7. 7. Broughton NS, Menelaus MB, Cole WG, Shurtleff DB. The natural history of hip deformity in myelomeningocele. J Bone Joint Surg [Br] 1993;75B(5):760–3. 8. Heeg M, Broughton NS, Menelaus MB. Bilateral dislocation of the hip in spina bifida: a long-term follow up study. J Pediatr Orthop 1998;18(4):434–6. 9. Feiwell E, Sakai D, Blatt T. The effect of hip reduction on function in patients with myelomeningocele. J Bone Joint Surg [Am] 1978;60A(2):169–73. 10. Alman BJ, Bhandari M, Wright JG. Function of dislocated hips in children with lower level spina bifida. J Bone Joint Surg [Br] 1996;78B(2):294–8. 11. Zenios M, Sampath J, Cole C, et al. Operative treatment management for hip subluxation in spinal muscular atrophy. J Bone Joint Surg [Br] 2005;87B(11):1541–4. 12. Chan KG, Galasko CSB, Delaney C. Hip subluxation and dislocation in Duchenne muscular dystrophy. J Pediatr Orthop Part B 2001;10(3):219–25.
99 13. Pemberton PA. Pericapsular osteotomy of the ilium for treatment of congenital subluxation and dislocation of the hip. J Bone Joint Surg [Am] 1965;47A(1):65–86. 14. Shea KG, Coleman SS, Carroll K, et al. Pemberton pericapsular osteotomy to treat a dysplastic hip in cerebral palsy. J Bone Joint Surg [Am] 1997;79A(9):1342–51. 15. Gordon JE, Capelli AM, Strecker WB, et al. Pemberton pelvic osteotomy and varus rotational osteotomy in the treatment of acetabular dysplasia in patients who have static encephalopathy. J Bone Joint Surg [Am] 2006;78A(12):1863–71. 16. Perlik PC, Westin GW, Marafioti RL. A combination pelvic osteotomy for acetabular dysplasia in children. J Bone Joint Surg [Am] 1985;67A(6):842–50. 17. Grudziak JS, Ward WT. Dega osteotomy for the treatment of congenital dysplasia of the hip. J Bone Joint Surg [Am] 2001; 83A(6):845–54. 18. Mubarak SJ, Valencia FG, Wenger DR. One-stage correction of the spastic dislocated hip. Use of pericapsular acetabuloplasty to improve coverage. J Bone Joint Surg [Am] 1992;74A(9): 1347–57. 19. Robb JE, Brunner R. A Dega-type osteotomy after closure of the triradiate cartilage in non-walking patients with severe cerebral palsy. J Bone Joint Surg [Br] 2006;88B(7): 933–7. 20. Jozwiak M, Marciniak W, Piontek T, Pietrzak S. Dega’s transiliac osteotomy in the treatment of spastic hip subluxation and dislocation in cerebral palsy. J Pediatr Orthop Part B 2000;9:257–64. 21. Chiari K. Medial displacement osteotomy of the pelvis. Clin Orthop 1974;98:55–71. 22. Tachdjian MD. Kawamura’s dome-shaped medial displacement inominate osteotomy through trans-trochanteric approach. In: Tachdjian MD, editor. Paediatric orthopedics. 2nd ed. W.B. Saunders; 1990. p. 506–19. 23. Osterkamp J, Caillouette JT, Hoffer MM. Chiari osteotomy in cerebral palsy. J Pediatr Orthop 1988;8(3):274–7. 24. Debnath UK, Guha AR, Karlakki S, et al. Combined femoral and Chiari osteotomies for reconstruction of the painful subluxation or dislocation of the hip in cerebral palsy. A long-term outcome study. J Bone Joint Surg [Br] 2006;88B(10):1373–8. 25. Dietz FR, Knutson LM. Chiari pelvic osteotomy in cerebral palsy. J Pediatr Orthop 1995;15(3):372–80. 26. Mannor DA, Weinstein SL, Dietz FR. Long-term follow up of Chiari pelvic osteotomy in myelomeningocele. J Pediatr Orthop 1996;16(6):769–73.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 100–108
Available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/cuor
MINI-SYMPOSIUM: CHILDREN—OSTEOTOMIES AROUND THE HIP
(iii) Bernese periacetabular osteotomy Michael Leuniga,, Reinhold Ganzb a
Department of Orthopaedic Surgery, Schulthess Clinic, Lengghalde 2, 8008 Zu ¨ rich, Switzerland Department of Orthopaedic Surgery, Balgrist University Hospital, Forchstrasse 340, CH-8008 Zu ¨ rich, Switzerland
b
KEYWORDS Periacetabular osteotomy; Joint preservation; Residual dysplasia of the acetabulum
Summary The Bernese Periacetabular Osteotomy (PAO) is a reorientation procedure of the dysplastic acetabulum and was first executed in 1984 after extensive feasibility studies in the anatomy lab including injection studies of the blood supply of the periacetabular bone. Dissatisfaction with available techniques led to the new procedure with its power of correction and intracapsular access, avoiding the danger of avascular necrosis. It should not interfere with the natural birth canal. The approach was chosen to produce little morbidity and reduced care in the postoperative period. The resulting procedure using a Smith–Peterson approach evolved to one of the most frequently executed reorientations of today, although the execution is technically rather demanding. Reorientation of the acetabulum became the most successful operation in our armamentarium to preserve the natural joint. Addressing the tendency to produce acetabular retroversion and an eventually insufficient head–neck offset has helped to avoid impingement after reorientation and has further improved the results. Combined pathology of acetabulum and proximal femur is not treatable via a Smith–Peterson approach so a feasibility study on cadavers was undertaken to achieve acetabular and femoral correction using one posterolateral approach. Again, injection studies have shown how interference with the periacetabular bone perfusion can be avoided, even when performing a large capsulotomy with dislocation of the femoral head. The technique has been tested successfully clinically, although the number of cases is still small. & 2007 Elsevier Ltd. All rights reserved.
Introduction Osteoarthritis of the hip is frequently caused by mechanical abnormalities including residual deformity from developCorresponding author. Tel.: +41 44 385 7312;
fax: +41 44 385 7795. E-mail address:
[email protected] (M. Leunig). 0268-0890/$ - see front matter & 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2007.04.005
mental hip disease such as acetabular dysplasia.1 Untreated acetabular dysplasia (Fig. 1) is the most common cause of secondary osteoarthritis2,3 arising from pathological jointloading forces.4 Pelvic osteotomies for residual acetabular dysplasia attempt to increase coverage of the femoral head in order to reduce the joint-loading forces that otherwise exceed the tolerance level of the articular cartilage.5 There are two
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Figure 1 Classic acetabular dysplasia (a) with insufficient anterolateral coverage in an 18-year-old woman. Without treatment OA developed 13 years later (b) and she could only be treated by total hip replacement (c).
Figure 2 Treatment principle in reorientation procedures bringing the insufficient ‘‘roof’’ of the ‘‘head’’ (a) into a better position (b).
ways to achieve this goal, one is by augmentation of the roof, the other is by spatial reorientation of the entire acetabulum. Augmentation procedures are the different types of the shelf procedures6,7 and the Chiari pelvic osteotomy.8 With both operations the intact capsule is interposed, undergoing metaplastic transformation to fibrocartilage. However, fibrocartilage has inferior mechanical characteristics when compared to hyaline cartilage and optimal coverage of the acetabulum is difficult to achieve.9 Moreover, the interposed labrum may continue to create pain when it is avulsed and subjected to shear forces during motion.10 Reorientation procedures provide more physiological coverage by tilting the acetabular hyaline cartilage over the head (Fig. 2a and b). In classic dysplasia there is usually sufficient articular surface available in the postero-inferior area of the socket so that hyaline cartilage supported by subchondral bone offers optimal mechanical properties for load transmission and motion. Reorientation procedures include single, double and triple osteotomies as well as spherical and periacetabular osteotomies. This paper focuses on the Bernese Periacetabular Osteotomy (PAO).
Rationale for the Bernese PAO One of the most frequently performed reorientation procedures is Salter’s single innominate osteotomy.11 Its world-wide acceptance reflects its ease of execution; however, it is a correction hinged at the symphysis pubis,
the weakest structure of the pelvic ring. The supraacetabular bone distal to the osteotomy is pulled anteriorly and laterally, moving the centre of rotation laterally and distally. The desired increase in anterior coverage results in a decrease of posterior coverage producing retroversion.12 Hips after a Salter osteotomy in childhood may fail later from impingement. To overcome the adverse aspects of the Salter osteotomy and to increase the amount of correction, a number of double and triple osteotomies of the pelvis have been proposed. Hopf13 was the first to describe a double osteotomy which was designed for hips with a subluxing femoral head. Besides the innominate osteotomy, he performed a second cut through the empty inferior socket. The technique did not receive wide popularity, mainly because it risked vascular disturbance of the acetabular fragment. In the other double osteotomy, proposed by Sutherland and Greenfield,14 the second cut was near the symphysis. Again, this osteotomy was abandoned because of poor lower fragment correction. LeCoeur was the first to perform a triple osteotomy and he did it long before he published the technique.15 Like the osteotomy later described by Steel16 it was a triple osteotomy distant to the acetabulum, correction being limited by the intact sacro-pelvic ligaments. The power of correction has substantially increased with juxta-articular triple osteotomies. While the proposed operation of Carlioz17 only separates the sacrotuberal ligament from the acetabular fragment, the To ¨nnis osteotomy isolates the fragment from both ligaments allowing a large amount of spatial correction.18 To do this, three incisions and introperative reprinting of the patient is necessary. Both types interrupt the pelvic ring and therefore require careful stabilization. Nishio,19 Eppright,20 Wagner21 and Ninomiya and Tagawa22 described so-called dial or spherical osteotomies very close to the joint. While the Eppright osteotomy has some limitations for anterior correction, the more spherical osteotomies are limited with regard to correction of version and medialization. The Wagner osteotomy in particular may become intraarticular at the level of the tear drop. In addition, spherical osteotomies may produce acetabular avascular necrosis, especially when attempting a simultaneous capsulotomy.
ARTICLE IN PRESS 102 In view of these limitations, the Bernese PAO was developed in 1983 after cadaveric feasibility studies including the vascular supply to the periacetabular bone. The polygonal juxtaarticular osteotomy not only respects the blood supply but also facilitates extensive acetabular reorientation including correction of version and mediolateral displacement. The posterior column remains mechanically intact, protecting the sciatic nerve and enabling minimal internal fixation together with easy postoperative mobilization. The dimensions of the true pelvic cavity remain unchanged with this osteotomy permitting unimpaired vaginal delivery, even when performed bilaterally. This is an important aspect since the majority of patients are female and in their reproductive period.23 All osteotomy cuts are performed through a modified (abductor sparing) Smith–Peterson incision, while the deeper dissections expose the anterior and medial aspects of the periacetabular bone.24 The approach allows a large anterior capsulotomy for the treatment of intra-articular pathology, ensuring impingement-free motion, especially internal rotation in flexion. Since the Bernese PAO crosses the posterior line of the triradiate cartilage, it should not be performed in small children. It may, however, have some advantage over a triple osteotomy shortly before closure of the growth plates.
Indication for the Bernese PAO Acetabular dysplasia in adolescence and early adulthood is the most frequent indication for the Bernese PAO. If there is little cartilage damage on a recent MRI study, with a patient who is in favor of a joint-preserving procedure and a surgeon who has great experience with the osteotomy, the operation may be considered up to the age of 50 years. The upper age limit is also determined by comparing the osteotomy outcome with the prognosis of a total hip arthroplasty. Normally the osteotomy is indicated for a symptomatic hip and not for minor dysplasia, asymptomatic even during provocative clinical testing. However, for a young patient with a substantial but painless dysplasia, it may be advisable to recommend surgery before major cartilage damage further compromises the prognosis of this hip. Contraindications are high subluxations and complete dislocations as well as grade 3 osteoarthritis. Dysplastic hips without improvement of congruency on an abduction radiograph are not appropriate for the PAO and one should be very careful with the Perthes’ hip, which may develop severe functional impingement after correction of the lateral acetabular insufficiency in an apparently congruent hip.
Technical execution of the Bernese PAO The most frequently used approach for the Bernese PAO is a modification of the Smith-Peterson incision.24 In contrast to the original description25 in which the dissection of the deep structures for placement of the mould-arthroplasty was restricted to the outside of the periacetabular bone, the different osteotomy steps of the periacetabular osteotomy have been performed medial to the pelvic ring since 1993, avoiding elevation of the abductors. Access to the pubic
M. Leunig, R. Ganz bone and the anterior approach to the ischium can be achieved medial (direct anterior approach25) or lateral to the rectus muscle as described in the original article.26 With the direct anterior approach the straight head of the rectus muscle does not need to be sectioned but there is a risk of stretching the femoral nerve. The PAO can also be executed via an ilioinguinal approach.27,28 The dissection takes longer but the exposure for the pubic and ischial cuts is easier and the scarring of the skin incision becomes more acceptable compared with the laterally curved Smith-Peterson incision. However, the ilioinguinal approach may produce thrombosis of the femoral vessels. After the curved skin incision over the anterior–superior iliac spine (Fig. 3a) the fascia is incised over the tensor muscle to avoid injury to the lateral femoral cutaneous nerve, running in a layer of fatty tissue between the sartorius and tensor muscles. The anterior–superior iliac spine is then osteotomized and mobilized medially together with the origin of the sartorius muscle and the inguinal ligament (Fig. 3b). Proximally for a distance of about 10 cm, the abdominal obliquus externus and the iliacus muscles are dissected from the iliac crest and inner surface together with the periosteum. This step is facilitated by placing the hip in about 451 flexion to release muscular tension. Deep between the rectus and tensor muscles both heads of the rectus femoris muscle are identified. The reflected head is tenotomized and the direct head is separated from the anterior–inferior iliac spine to allow medial mobilization together with the iliacus muscle covering the anterior surface of the joint capsule (Fig. 3c).29 The next structure medially and distally is the iliopectineal bursa which may be partially obliterated or may represent a large cavity through which the tendon of the psoas muscle takes its course (Fig. 3d). Further distal continuation of the dissection of the iliacus muscle from the capsule allows access to the gap between capsule and psoas tendon and more posteriorly between capsule and the obturator externus muscle (Fig. 3d). This allows access to the infracotyloid groove of the ischial bone. The abductor musculature is elevated from the outside of the ilium only at the level of the horizontal cut of the supra-acetabular osteotomy allowing the insertion of a blunt retractor into this tunnel, reaching the greater sciatic notch with its tip. Medially, the strong periosteum covering the quadrilateral surface of the acetabular bone is elevated allowing a second blunt retractor to be placed on the base of the ischial spine. The obturator neurovascular bundle is protected by two curved retractors around the proximal and distal contours of the base of the pubic bone, which is further exposed by a sharp retractor hooked into the pubic bone about 1.5 cm medial to the iliopectineal eminence. The routine execution of the different osteotomy steps is performed without the assistance of fluoroscopy, depending upon the three-dimensional understanding of this procedure. Nevertheless, fluoroscopy is widely used by those who claim this makes the PAO more accurate and safe. The Bernese PAO consists of five steps. The first step is the incomplete osteotomy of the ischium (Fig. 4a). With the hip in flexion using a leg holder, a specially curved chisel is introduced in the gap between the antero-inferior capsule and the psoas tendon, and at a deeper plane, the obturator externus muscle. After contact with the bone,
Figure 3 Sequence of soft tissue approach to perform the osteotomy cuts. (a) 1, Sarorius muscle; 2, ASIS; and 3, tensor fascia lata muscle. (b) 1, Direct head of rectus femoris muscle; 2, osteotomized ASIS; and 3, rectus femoris muscle. (c) 1, Sartorius muscle; 2, psoas muscle; 3 released rectus femoris muscle; and 4, iliocapsularis muscle. (d) 1, Iliopectineal eminence; 2, released rectus femoris muscle; 3, released iliocapsularis muscle; and 4, joint capsule. (e) 1, Iliopectineal eminence; 2, obturator externus muscle; and 3, joint capsule.
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Figure 4 (a) ‘‘Blind’’ incomplete ischial osteotomy; (b) pubic osteotomy; (c) supraacetabular osteotomy; (d) retroacetabular osteotomy; and (e) controlled fracture of the acetabular fragment.
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104 M. Leunig, R. Ganz
ARTICLE IN PRESS Bernese periacetabular osteotomy the infracotyloid groove (with the postero-inferior acetabular lip as its most proximal extension) is probed. Strong hammer blows are exerted only after good contact of the chisel against the bone is secured by gentle taps. Supported by raising the handle of the chisel, the course of the osteotomy becomes slightly curved and ends at a depth of about 2.5 cm. This depth can be estimated more easily while slowly pulling back the chisel to the starting position than during its forward movement. The quality of the resistance while sideward wiggling of the chisel gives information whether it is in the middle of the bone or overlapping the medial or lateral border. It is important to cut the medial cortex of the ischium. The lateral cortex in close vicinity to the sciatic nerve is thin and can be broken easily during the final manual manoeuvre to free the fragment completely. Care must be taken not to cut distal to the obturator externus muscle where the medial femoral circumflex artery runs parallel to the muscle belly. If performed correctly, bleeding from this area is minimal and only of venous origin. The second step is the complete osteotomy of the pubis (Fig. 4b). It is best performed at its largest diameter close to the joint. Slight adduction in the flexed hip improves the exposure. The two subperiosteal retractors are directed to protect the neurovascular bundle at the level where the tip of the chisel penetrates out of the opposite cortex. With a narrow double osteotomy splintering of the bone during deeper penetration of the chisel can be avoided. The osteotomy starts immediately medial to the iliopectineal eminence and is 451 centrally inclined to avoid penetration into the joint. Completion of the osteotomy is controlled by a spreading manoeuvre with the chisel. The third step is the chevron-shaped supra- and retroacetabular osteotomy (Fig. 4c). Currently the anterior cut is performed more proximally than was described in the original paper.25 It starts at the inferior border of the osteotomized anterior-superior spine and is directed transversely, ending 1–2 cm before it reaches the iliopectineal line. It is performed with an oscillating saw, the abductor musculature being protected by the blunt retractor described earlier. The second cut of the osteotomy is performed with straight and curved chisels. A straight chisel is directed towards the ischial spine at an angle of about 110–1201 to the first leg. However, only the inner cortex is cut to a distance of about 2 cm posterior to the iliopectineal line. A 1-cm bone bridge is controlled with finger palpation between this cut and the border of the sciatic notch. Thereafter a curved chisel is placed into the most proximal part of this cut and directed under visual control towards the lateral cortex superior to the joint. As soon as the lateral cortex of the supra-retroacetabular bone is separated, a distinct warping of the first osteotomy cut becomes visible, indicating that with leverage by a large chisel placed in the corner of both osteotomy segments the cuts will propagate as a controlled fracture further towards the sciatic spine. A 5-mm Schanz screw is inserted into the anterior inferior iliac spine, directed towards the osteotomy corner and parallel to the inner cortex. It provides a good handle for further mobilization of the acetabular fragment, while the retroacetabular osteotomy gap is further opened with a laminar spreader. Occasionally gentle blows on a chisel are necessary to promote this propagation.
105 The fourth step is the distal retroacetabular osteotomy (Fig. 4d) which combines the former cut with the first incomplete ischial osteotomy. It is performed under tension with the spreader to promote a controlled fracture after osteotomizing the inner cortex only. A special chisel is used, allowing the execution of the osteotomy 4 cm posterior to the iliopectineal line at an angle of about 501 towards the quadrilateral surface. Injection studies of the proximal femur and of the periacetabular bone30,31 and also intraoperative laser-Doppler flowmetry32 have shown good perfusion of the acetabular fragment with this arrangement of osteotomies. The acetabular fragment can now be broken completely free by levering it against the surrounding pelvic bone with the simultaneous use of the spreader and the Schanz screw (Fig. 4e). The precise positioning of the mobile acetabular fragment is as demanding as the execution of the osteotomies. The most important correction is anterior rotation of the fragment, which is accompanied by a simultaneous increase of lateral coverage. If there is retroversion the fragment is additionally rotated inwards. After preliminary fixation using K-wires, an anteroposterior radiograph33 of the entire pelvis affords accurate portrayal of the correct spatial orientation of the acetabular fragment. Redirecting the fragment position as frequently as necessary and repeated radiographic control ensure an optimal spatial position of the acetabulum. Fluoroscopy for control of the fragment orientation gives little information on rotation and tilt of the pelvis, while the projected picture also differs by 41 compared with a pelvic radiograph.34 Orientation of the acetabular roof, the position of the head relative to the ilioischial line, the position of the radiographic teardrop, the posterior and the anterior acetabular rims, the inferior border of the acetabulum relative to the inferior border of the femoral head and Shenton’s arc are all evaluated. While radiographs are processed, an anterior capsulotomy allows inspection of the joint for intraarticular pathology and eventual treatment. In particular, labral instability (tears) and an insufficient anterolateral femoral head/neck offset are addressed. After the reorientation is interpreted as radiologically correct, the capsule is closed with a running suture. The acetabular fragment is routinely fixed by means of three, 3.5 mm AO screws, a fixation which is sufficient because of the polygonal shape of the osteotomy and the intact posterior column. The direct head of the rectus is refixed with a non-resorbable suture and the bony fragment of the sartorius origin is fixed back using one 2.7-mm screw. Suction drainage is unnecessary and 80% of the patients do not need blood transfusion; however, a cell saver system is used routinely and autologous blood donation is recommended for young females. Prophylaxis against deep venous thrombosis is routinely ensured for 6 weeks. By the second day after surgery the patient is allowed to walk with crutches. For about 8 weeks, loading of the hip joint is restricted to touch weight bearing. Active flexion of the hip is prohibited for 6 weeks and prophylaxis against heterotopic ossification is only used in patients with a predisposition. At 8 weeks, union of the osteotomies is normally sufficient for full weight bearing and physiotherapy may be started.
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Results with the Bernese PAO The first periacetabular osteotomy was performed in April 1984; almost 1500 hips have been operated since by the senior author. In 1999, the minimum 10-year results of the first 75 osteotomies performed between 1984 and 1987 in 63 patients were published.35 The average age at surgery was 29.3 years and the male:female ratio was 1:3.4; 31% of the operated hips had undergone previous surgery. According to the classification of Severin,36 49% were in group III preoperatively and 44% in group IV, 5% in group V and only 1% in group II. Restriction of walking ability was present in 73%. A total of 71 hips (95%) with adequate documentation were included in the follow-up study at 11.3 years (10–13.8 years). One patient with two PAO hips died 6 years after the second periacetabular osteotomy and two patients (hips) were lost to follow up. In all hips the radiographic parameters were improved significantly and Shenton’s line was restored in 62%. The hip joint was preserved in 58 (82%) of the 71 cases; 13 hips were revised by THR at an average of 6.1 years (1–13.2 years). Clinically, the average Merle d’Aubigne´ score for the 58 hips increased from 14.6 points (7–17 points) to 16.4 points (12–18 points) at the time of the last follow-up. In all, 52 (73%) of the 71 preserved hips had a good or excellent result (Fig. 5a and b). Only 27 hips had no signs of osteoarthritis at the time of surgery (49%). This number increased to 44 hips (80%) at the last follow-up. Six of the 13 non-preserved hips had preoperative, secondary osteoarthritis and five had a primary osteoarthritis (Fig. 6a and b). The two hips with tertiary osteoarthritis were preserved at follow-up. Two non-preserved hips did not have sufficient radiographic documentation. Arthrotomy was not routinely performed. However, in 15 hips a labral lesion was detected at surgery; these hips had a significantly worse outcome. Overall, older age, presence and grade of OA and the presence of a labral lesion were predictors for a negative outcome.
Complications For the first group of 75 hips all major complications occurred in the first 18 hips,35 although the technique was
Figure 5 Good outcome: (a) classic acetabular dysplasia without signs of osteoarthritis with an excellent clinical and radiographic follow-up of over 18 years (b).
Figure 6 Poor outcome: (a) in the presence of significant signs of osteoarthritis (hypersclerosis, joint space loss, osteophytes, calcifications), even after PAO 4 years later the joint was completely destroyed (b).
started clinically only after extensive cadaver work. Hussell et al.28 have collected the complications of 508 consecutive hips including the first 75 osteotomies. Intra-articular osteotomy occurred in 13 hips. Eleven times it was in the inferior intra-articular extension of the ischial osteotomy. All 11 hips had major supero-lateral femoral head migration, leaving an empty inferior capsule. There were no clinical sequelae directly associated with this type of intra-articular osteotomy. In two hips the posterior leg of the supra-acetabular osteotomy extended into the joint, leading to incongruency following correction of the anterosuperior part of the acetabulum. The salvage procedure for both hips was total hip replacement. In four hips substantial undercorrection and in six hips major overcorrection occurred; in three of these patients inadequate intraoperative radiography could be identified to be at least partially responsible for the poor correction. Early reoperation is the best way to treat this type of complication. In three out of four hips, femoral varus osteotomy led to a symptomatic resolution of the subluxation; in the fourth case a shelf graft for a postero-superior subluxation was followed by a full relief of symptoms, now continuing for 22 years. The other possible cause of resubluxation is coxa magna. In the one case in this series the problem was solved with intertrochanteric osteotomy combined with a shelf procedure. Femoral nerve palsies occurred in three patients. One hip had extensive anterior scarring. The other two cases occurred in two of five hips that were exposed through a direct anterior approach.26 All palsies resolved within 3–6 months. Sciatic nerve palsy occurred in five patients; all recovered slowly with no major late deficit. In one case a bone spike was diagnosed using CT and revision surgery with excision of the spike led to a relief of the causalgia. No vascular complication occurred in this series. However, thrombosis of the femoral artery has been reported when using an ilio-inguinal approach. Osteonecrosis of the reoriented acetabulum has been observed in three hips. The first occurred in 1984, when soft
ARTICLE IN PRESS Bernese periacetabular osteotomy tissue stripping was excessive and the inferior cut of the ischium penetrated the inferior acetabulum, interrupting the acetabular artery. Two later cases occurred in patients undergoing revision pelvic osteotomy where the previous surgery had stripped the soft tissue extensively from the bone. All three hips required total hip replacement. Today extensive soft tissue dissection from the external ilium is avoided. Isolated delayed unions of the ilium, ischium or pubis were seen with significant gaps due to large corrections. Only two supra-acetabular non-unions needed revision. Posterior column discontinuity was seen in six patients where the osteotomy line extended into the greater sciatic notch. Prolonged protection from weight bearing led to healing in all cases.
Lessons learned Periacetabular osteotomy is a demanding procedure which needs accurate knowledge of the anatomy, especially the vacular anatomy of the hip. After successful execution of the osteotomies, precise, spatial positioning of the acetabulum is of paramount importance. The acetabular rim may fail with different pathologies before the cartilage itself becomes affected.37 With the routine use of MR arthograms, especially with the technique of radial arthro MR arthography,38,39 an increased number of labral ruptures with acetabular dysplasia were appreciated. Some disruptions occur deep in the substance of the acetabular cartilage, adversely affecting outcome after a reorientation procedure. Since hypertrophy of the labrum seems to be a constant finding in acetabular dysplasia,40 it may be an additional factor indicating surgery for a symptomatic hip with borderline dysplasia. We further learned that acetabular dysplasia is not uniformly an anterolateral insufficiency of femoral head cover. Although the classic anterolateral dysplasia is the most common morphology, one out of six41 or even one out of three42 acetabula is retroverted. All post-traumatic dysplasias and all functional PFFD-hips are retroverted.43,44 Posterior insufficiency of coverage or anterior overcoverage is also very frequent after Salter- and triple-osteotomies in childhood12 and is probably the most frequent reason for ongoing symptoms after surgery. Therefore the orientation of the acetabulum has to be taken into consideration when correcting a dysplastic acetabulum. It is well known that in acetabular dysplasia the proximal femur shows some deformity as well. However, correction for increased anteversion or valgus is rarely necessary. The 10-year follow-up study disclosed that minor deformities of the anterior head–neck junction may lead to an impingement even after correct positioning of the acetabulum. Further studies using radial arthro MR revealed an insufficient junctional ‘‘waist’’ as the cause of impinging.45 As a consequence, impingement tests, especially with internal rotation in flexion, are used intraoperatively and should be confirmed by arthrotomy in seven out of 10 cases. The anterolateral offset of the head–neck junction is then improved by an osteochondroplasty, monitored by showing improved internal rotation. Retroversion of the acetabulum is also frequently seen in non-dysplastic hips and may be the cause of impingement
107 symptoms. Such pathology may be an indication for a periacetabular osteotomy. However, the posterior wall should be clearly medial to the centre of the femoral head. Otherwise the rotatory correction will increase posterior coverage and may lead to posterior impingement.46 A further limitation of the procedure for retroversion is the quality of the acetabular cartilage in the area of the anterior overhang. Preoperative MR arthography should show normal cartilage in this area before considering a reversed periacetabular osteotomy. In summary, the Bernese PAO is potent means of redirecting the acetabulum. For acetabular dysplasia it is a successful but risky operation. The goal of this osteotomy is precise, spatial re-orientation of the acetabulum. Overcorrection is as adverse as undercorrection and false correction. Anteversion or retroversion should be included in the list of corrective details and one has to take into consideration that the orientation of the proximal femur may be pathological as well.
References 1. Aronson J. Osteoarthritis of the young adult hip: etiology and treatment. Instr Course Lect 1986;35:119–28. 2. Solomon L, Schitzler CM. Pathogenetic types of coxarthrosis and implications for treatment. Arch Orthop Trauma Surg 1983;101:259–61. 3. Stulberg SD, Cordell LD, Harris WH, Ramsey PL, MacEwen GD. Unrecognized childhood disease: a major cause of idiopathic osteoarthritis of the hip. Paper presented at Proceedings of the third meeting of the Hip Society, 1975. 4. Hadley NA, Brown TD, Weinstein SL. The effects of contact pressure elevations and aseptic necrosis on the long-term outcome of congenital hip dislocation. J Orthop Res 1990;8: 504–13. 5. Millis MB, Murphy SB, Poss R. Osteotomies about the hip for prevention and treatment of osteoarthrosis. J Bone Joint Surg Am 1995;77:626–77. ¨ ber die Berechtigung fru 6. Ko ¨nig F. U ¨hzeitiger blutiger Eingiffe bei subcutanen Knochenbru ¨chen. Langenbecks Arch Klin Chir 1905;76:23. 7. Lance M. Constitution d’une butre ´e oste´oplastique dans les luxations et subluxations conge ´nitales de la hanche. Presse Med 1925;33:945–8. 8. Chiari K. Beckenosteotomie zur Pfannendachplastik. Wien Med Wochenschr 1953;103:707–14. 9. Klaue K, Sherman M, Perren SM, Wallin A, Looser C, Ganz R. Extra-articular augmentation for residual hip dysplasia. Radiological assessment after Chiari osteotomies and shelf procedures. J Bone Joint Surg Br 1993;75(5): 750–4. 10. Nishina T, Saito S, Ohzono K, Shimizu N, Hosoya T, Ono K. Chiari pelvic osteotomy for osteoarthritis. The influence of the torn and detached acetabular labrum. J Bone Joint Surg Br 1990; 72(5):765–9. 11. Salter RB. Innominate osteotomy in the treatment of congenital dislocation and subluxation of the hip. J Bone Joint Surg Br 1961;43:518–39. 12. Dora C, Mascard E, Mladenov K, Seringe R. Retroversion of the acetabular dome after Salter and triple pelvic osteotomy for congenital dislocation of the hip. J Pediatr Orthop B 2002; 11(1):34–40. 13. Hopf A. Hu ¨ftpfannenverlagerung durch doppelte Beckenosteotomie zur Hu ¨ftgelenksdysplasie und Subluxation bei Jugendlichen und Erwachsenen. Z Orthop 1966;101:559–68.
ARTICLE IN PRESS 108 14. Sutherland DH, Greenfield R. Double innominate osteotomy. J Bone Joint Surg Am 1977;59(8):1082–91. 15. LeCoeur P. Corrections des de´faults d’orientation de l’articulation coxo-femorale par oste ´otomie de l’isthme iliaque. Rev Chir Orthop 1965;51:211–2. 16. Steel HH. Triple osteotomy of the innominate bone. J Bone Joint Surg Am 1973;55(2):343–50. 17. Carlioz H, Khouri N, Hulin P. Oste ´otomie triple juxtacotyloidienne. Rev Chir Orthop Reparatrice Appar Mot 1982;68: 497–501. 18. Tonnis D, Behrens K, Tscharani F. A modified technique of the triple pelvic osteotomy: early results. J Pediatr Orthop 1981; 1(3):241–9. 19. Nishio A. Transposition osteotomy of the acetabulum in the treatment of congenital dislocation of the hip. J Jpn Orthop Assoc 1956;30:483. 20. Eppright RH. Dial osteotomy of the acetabulum in the treatment of dysplasia of the hip. J Bone Joint Surg Am 1975;57:1171. 21. Wagner H. Osteotomies for congenital hip dislocation. Paper presented at Proceedings of the fourth open scientific meeting of the Hip Society, 1976. 22. Ninomiya S, Tagawa H. Rotational acetabular osteotomy for the dysplastic hip. J Bone Joint Surg Am 1984;66:430–6. 23. Fluckiger G, Eggli S, Kosina J, Ganz R. Birth after periacetabular osteotomy. Orthopade 2000;29(1):63–7. 24. Leunig M, Siebenrock KA, Ganz R. Rationale of periacetabular osteotomy and background work. Instr Course Lect 2001;50: 229–38. 25. Murphy SB, Millis MB, Ganz R. The direct anterior approach to the pelvis. Paper presented at: Harvard course on osteotomy of the hip and knee (abstract book), Boston, MA, USA, 1994. 26. Ganz R, Klaue K, Vinh TS, Mast JW. A new periacetabular osteotomy for the treatment of hip dysplasias. Technique and preliminary results. Clin Orthop 1988;232:26–36. 27. Letournel E. The treatment of acetabular fractures through the ilioinguinal approach. Clin Orthop 1993;292:62–76. 28. Hussel G, Mast JW, Howie D, Murphy SD, Ganz R. A comparison of different surgical approaches for the periacetabular osteotomy. Clin Orthop 1999;363:64–72. 29. Ward WT, Fleisch ID, Ganz R. Anatomy of the iliocapsularis muscle. Relevance to surgery of the hip. Clin Orthop 2000;374: 278–85. 30. Beck M, Leunig M, Ellis T, Sledge JB, Ganz R. The acetabular blood supply: implications for periacetabular osteotomies. Surg Radiol Anat Aug 16, 2003. 31. Gautier E, Ganz K, Krugel N, Gill T, Ganz R. Anatomy of the medial femoral circumflex artery and its surgical implications. J Bone Joint Surg Br 2000;82(5):679–83.
M. Leunig, R. Ganz 32. Hempfing A, Leunig M, Notzli HP, Beck M, Ganz R. Acetabular blood flow during Bernese periacetabular osteotomy: an intraoperative study using laser Doppler flowmetry. J Orthop Res 2003;21(6):1145–50. 33. Siebenrock KA, Kalbermatten DF, Ganz R. Effect of pelvic tilt on acetabular retroversion: a study of pelves from cadavers. Clin Orthop 2003;407:241–8. 34. Jamali AA, Mladenov K, Meyer DC, et al. Anteroposterior pelvic radiographs to assess acetabular retroversion: high validity of the ‘‘cross-over-sign’’. J Orthop Res Mar. 7, 2007. 35. Siebenrock KA, Scho ¨ll E, Lottenbach M, Ganz R. Periacetabular osteotomy. A minimal follow-up of 10 years. Clin Orthop 1999;363:9–20. 36. Trousdale RT, Ekkernkamp A, Ganz R, Wallrichs SL. Periacetabular and intertrochanteric osteotomy for the treatment of osteoarthrosis in dysplastic hips. J Bone Joint Surg Am 1995; 77(1):73–85. 37. MacDonald SJ, Garbuz D, Ganz R. Clinical evaluation of the symptomatic young adult hip. Semin Arthroplast 1997;8:3–9. 38. Myers SR, Eijer H, Ganz R. Anterior femoroacetabular impingement after periacetabular osteotomy. Clin Orthop 1999;363:93–9. 39. Siebenrock KA, Schoeniger R, Ganz R. Anterior femoroacetabular impingement due to acetabular retroversion. Treatment with periacetabular osteotomy. J Bone Joint Surg Am 2003;85-A(2):278–86. 40. Leunig M, Rothenfluh D, Beck M, Werlen S, Ganz R. Surgical dislocation and periacetabular osteotomy through a posterolateral approach: a cadaveric feasibility study and initial clinical experience. Oper Tech Orthop 2004;14(2):49–57. 41. Li PL, Ganz R. Morphologic features of congenital acetabular dysplasia: one in six is retroverted. Clin Orthop Relat Res 2003;416:245–53. 42. Mast JW, Brunner RL, Zebrack J. Recognizing acetabular version in the radiographic presentation of hip dysplasia. Clin Orthop Relat Res 2004;418:48–53. 43. Dora C, Buhler M, Stover MD, Mahomed MN, Ganz R. Morphologic characteristics of acetabular dysplasia in proximal femoral focal deficiency. J Pediatr Orthop B 2004;13(2):81–7. 44. Dora C, Zubrach J, Hersche O, Ganz R. Pathomorphologic characteristics of posttraumatic acetabular dysplasia. J Orthop Trauma 2000;14(7):483–9. 45. Ito K, Minka II MA, Leunig M, Werlen S, Ganz R. Femoroacetabular impingement and the cam-effect. A MRI-based quantitative anatomical study of the femoral head–neck offset. J Bone Joing Surg Br 2001;83(2):171–6. 46. Siebenrock KA, Schoeniger R, Ganz R. Anterior femoroacetabular impingement due to acetabular retroversion. Treatment with periacetabular osteotomy. J Bone Joint Surg Am 2003;85-A(2):278–86.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 109–114
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MINI-SYMPOSIUM: CHILDREN—OSTEOTOMIES AROUND THE HIP
(iv) The Chiari medial displacement osteotomy Sanjeev Patil, D.A. Sherlock Young Adult Hip Unit, Department of Orthopaedics, Southern General Hospital, 1345 Govan Road, Glasgow G51 4TF, UK
KEYWORDS Hip dysplasia; Hip joint; Osteotomy; Treatment outcome; Osteoarthritis; Hip
Summary Management of acetabular dysplasia in young adults remains a challenge. A systematic approach is required to assess the nature and degree of the dysplasia in order to plan treatment. This article describes the rationale used to choose surgery appropriate for the dysplasia type and thereby to ensure a satisfactory result. In particular, the indications, surgical technique and the results for the Chiari medial displacement osteotomy and variants are described. & 2007 Elsevier Ltd. All rights reserved.
Introduction Acetabular dysplasia may be idiopathic or a sequel to developmental dysplasia of the hip (DDH), cerebral palsy or Perthes’ disease. Patients frequently complain of increasing pain and disability in adolescence or young adulthood. Whilst it is necessary to exclude other causes of pain such as femoroacetabular impingement, dysplasia is a potent cause of hip pain in this age group as tears or degeneration in the labrum are usually secondary to the mechanical instability. Untreated hip dysplasia inevitably progresses to premature arthritis,1,2 sometimes as early as the second or third decade of life. Advanced arthritis can realistically only be managed by a total joint replacement but the acetabular dysplasia, which caused the premature failure of the native hip also conspires to produce early failure of the replacement because of poor bone stock, the greater demands of a young person and the fact that even a successful hip replacement will not last 40–60 years. In view of this, techniques which normalise or prolong the life of the Corresponding author. Tel.: +44 141 201 1100; fax: +44 141 201 0275.
0268-0890/$ - see front matter & 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2007.04.004
dysplastic joint are indicated until the patient is of an age when a total joint replacement has a reasonable chance of long-term survival become attractive. If the procedure also improves bone stock there is the added bonus that the eventual joint replacement has a better chance of long-term survival.
Anatomy There are varying configurations of acetabular dysplasia. To some extent the morphology of the dysplasia decides the technique available to stabilise the hip. Possible types of dysplasia include: (1) a normal acetabular morphology but with the femoral head larger than the socket with lateral uncovering (Fig. 1), (2) a spherical acetabulum but with reduced lateral cover such that there is no downward tilt to give lateral stability (Fig. 2), (3) a biconcave acetabulum (Fig. 3), and (4) a saucer-shaped acetabulum (Fig. 4).
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Figure 1 Normal acetabulum but over-large femoral head after Perthes’ disease.
Figure 3 Biconcave acetabulum.
Figure 2 Acetabulum with sloping unstable roof.
Types 1 and 2 are congruent hips and can usually be managed by a realignment pelvic osteotomy, such as a Ganz procedure3 or a Wagner spherical acetabular osteotomy.4 These techniques provide the necessary lateral acetabular cover to the femoral head with normal articular cartilage; thereby improving hip anatomy and biomechanics. If performed before the development of obvious arthritic change a realignment pelvic osteotomy might offer a normal life expectancy for the hip.5 The outcome is less successful once degenerative changes are present. Types 3 and 4, however, are incongruent hips which do badly with a realignment pelvic osteotomy because of the considerable discrepancy between the size and shape of the femoral head and acetabulum. These hips are better managed by a salvage acetabular augmentation procedure, which provides extra lateral cover thus preventing subluxation without trying to restore congruency. Such augmentation procedures include the various shelf operations or a Chiari medial displacement osteotomy. Shelf procedures6 augment the anterolateral aspect of the deficient dysplastic acetabulum with corticocancellous
Figure 4 Saucer-shaped acetabula.
graft, thereby buttressing the femoral head and increasing joint stability. The Chiari medial displacement iliac osteotomy7 involves division of the iliac bone from just above the acetabular lip to the inferior part of the sciatic notch with displacement of the distal fragment medially until the femoral head is covered. A variation of the Chiari is the Kawamura dome osteotomy which results in more congruent lateral support for the femoral head than the classical Chiari.8 The Chiari may be combined with a shelf procedure for severe dysplasia. Neither the Chiari nor the shelf procedure place hyaline articular cartilage over the femoral head. Instead
ARTICLE IN PRESS The Chiari medial displacement osteotomy
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they rely upon metaplastic transformation of the hip joint capsule to fibrocartilage.
Diagnosis History and physical examination The diagnosis of acetabular dysplasia is primarily radiological. The features of dysplasia are present on X-ray many years before symptoms develop. The pain of acetabular dysplasia is usually induced initially by overuse, though with time the pain occurs with everyday walking and standing. At first, the pain is commonly due to abductor fatigue and is felt over the buttock, greater trochanter and lateral thigh. Initially, the symptoms are infrequent and short lived, but the high load on the acetabular rim produces progressive degenerative change with more frequent and severe symptoms (acetabular rim syndrome)9 felt in the groin and medial thigh. A description of pops or clicks, shooting pains or catching suggests possible labral pathology. The differential diagnosis includes femoroacetabular impingement10 where the hip pain is usually felt in the medial groin area, and is aggravated by sitting or squatting. Clinical examination reveals good hip motion though some complain of pain with full abduction. Often there is more internal than external rotation due to excessive anteversion of the femoral neck. This is unlike the situation for hip impingement where internal rotation is limited and painful (positive impingement test), particularly with the hip in 901 of flexion. If the internal rotation is decreased and painful this might indicate a labral tear or the onset of early arthritis. Furthermore, patients with hip dysplasia may show anterior instability. This is demonstrated in the supine patient by extending and externally rotating the hip, which produces discomfort and instability when positive (positive apprehension test).11
Imaging An anteroposterior radiograph of the pelvis and both hips remains the most useful view for diagnosis and treatment planning. This view gives a good idea of the type and degree of acetabular dysplasia. The degree of dysplasia can be assessed from measurement of the centre-edge angle and Tonnis angle.12 Acetabular retroversion can be inferred from cross-over of the margins of the anterior and posterior walls of the acetabulum, which is not seen in the normal anteverted acetabulum. (The ‘‘false profile’’ view of Lequesne13 (Fig. 5), taken with the film at 651 to the pelvis in a patient standing with their foot parallel to the film, allows assessment of anterior acetabular cover and of the femoral head–neck offset where impingement is suspected. An MR arthrogram may be helpful in detecting labral tears or degeneration and can also demonstrate abnormal femoral head–neck offset. Three-dimensional CT reconstructions are good for demonstrating the orientation and degree of acetabular and femoral version. However, these studies are not necessary routinely.
Figure 5 ‘‘Faux profil’’ view of hip.
Choice of procedure As noted previously, different types of acetabular dysplasia require different approaches. If the hip is essentially congruent and containable, with the degree of acetabular rotation needed to achieve adequate cover being 301 or less, a pelvic realignment osteotomy has the best chance of achieving long-lasting hip survival. A stiff hip is a contraindication whilst the presence of osteoarthritic change produces poorer results and is a relative contraindication. Where the hip is not congruent or containable or the amount of pelvic tilt required to achieve cover is excessive, acetabular augmentation is the preferred option. Both the shelf procedure and the Chiari osteotomy have been shown to provide useful long-term survival for dysplastic hips though, as for the realignment pelvic osteotomies, the outcome is poorer when degenerative changes are present. A stiff hip is an absolute contraindication. A relative contraindication is a totally uncovered hip with proximal migration preventing the appropriate slope of the osteotomy and inadequate iliac bone cover. Irrespective of the choice of acetabular osteotomy concomitant femoral deformities such as excessive anteversion, varus or valgus may need correction. The Chiari pelvic osteotomy7 was first described in 1953 as a salvage procedure. It appears to work by increasing the area of contact between the femoral head and the acetabulum and by medialisation of the hip, both of which reduce the load per unit area on the hip. Kawamura published his variation in Japanese in 1958 but it was not widely known about till 1982 when he described the dome osteotomy in Tachdjian’s textbook of paediatric orthopaedics.14 Both osteotomies are best delayed until the triradiate physis has closed to avoid iatrogenic dysplasia resulting from damage to this growth plate.
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Technique Chiari pelvic osteotomy With the patient supine on a radiolucent table the hip is displayed via the Smith–Peterson approach. Both the inner and outer subspaces of the ilium are exposed back to the greater sciatic notch. Lateral stripping is minimised to decrease injury to the hip abductor muscles. The curved insertion of the reflected head of rectus femoris provides the marker for the level of the osteotomy. This is established by radiographically using a stout pin to demonstrate both the acetabular lip and the 10–151 angle of osteotomy in the antero-posterior plane. After protecting the sciatic nerve with retractors the ilium is divided with curved osteotomes around the acetabulum (Fig. 6a). A Gigli saw can be used for the most posterior portion of the osteotomy to avoid the risk of injury to the sciatic nerve by the osteotome or by bone splinters or spikes. Abduction of the hip with medial pressure displaces the acetabulum under the ilium (Fig. 7). Displacement of 1–1.5 cm is usually adequate to provide 80–100% lateral coverage of the femoral head. The osteotomy is inherently stable but can be fixed if desired with a screw or threaded pin. Evaluation of femoral head coverage should be performed to identify any remaining anterior or lateral deficiency. If present, further acetabular augmentation should be performed by a shelf procedure. Assessment of the range of motion in the hip is necessary to exclude any anterior block to flexion. Trimming the anterior ilium avoids such femoral neck impingement in flexion and aids wound closure. Postoperative regime Once control of the limb is regained the patient mobilises, touch weightbearing with crutches for 6 weeks. This is progressed to full weight bearing by 12 weeks. Active flexion and abduction should be avoided in the initial postoperative phase.
Dome osteotomy With the patient lying affected side up, a longitudinal incision is made from proximal to the greater trochanter to the iliac crest. Under image intensifier control (with the
Figure 7
Line drawing of medial displacement.
C-arm in the inverted U position to give an antero-posterior view) the greater trochanter is divided in a supero-medial direction. The hip abductors are reflected proximally to expose the outer table of the ilium. A stout wire is inserted and screened to show the level and direction of the osteotomy. A copper or aluminium malleable retractor is inserted from the anterior inferior iliac spine to the sciatic notch to push the sciatic nerve posteriorly and to protect the pelvic contents. The dome osteotomy is made using a narrow-bladed oscillating saw and osteotomes (Fig. 6b). The acetabulum is displaced by medial pressure with the hip abducted. Fixation with threaded pins or screws is usual (Fig. 8). The greater trochanter is reattached, with advancement as needed. Postoperative rehabilitation is similar to that following a Chiari osteotomy.
Complications In addition to the general risks of wound infection and thrombo-embolic disease, damage to the sciatic nerve or lateral cutaneous nerve of thigh are specific risks. Most nerve palsies recover spontaneously. Other complications include iatrogenic arthritis if the cut enters the hip joint or idiopathic chondrolysis. Non-union secondary to complete medial displacement should be avoided by fixation though complete medial displacement with fixation is compatible with a good result (Fig. 9). Narrowing of the pelvic outlet, particularly with bilateral procedures, may require delivery by caesarean section during childbirth.
Outcomes Figure 6 (a) Line drawing of Chiari osteotomy. (b) Line drawing of Dome osteotomy.
Both the Chiari and dome osteotomies rely on remodelling of the ilium and metaplasia of the previously unsupported
ARTICLE IN PRESS The Chiari medial displacement osteotomy capsule and labrum to fibrocartilage. This process can take up to 2 years. Limping is common initially due to longstanding weakness of the hip abductors and the trauma of surgery, but in most patients the limp becomes less marked than pre-operatively due to the improved biomechanics. Good pain relief is produced in 80–90% of patients with 50–60% still doing well 15–20 years from surgery.15–20 The results are poorer if there are obvious degenerative changes prior to surgery. Osteoarthritic change is certainly retarded
Figure 8 Dome osteotomy with supplementary shelf, fixed with 2 threaded pins.
Figure 9
113 but it is likely that in the long-term most patients will require a total hip replacement for degenerative arthritis of the joint. Neither osteotomy prevents conversion to a total hip replacement.
Total hip replacement after Chiari osteotomy This procedure can be difficult due to presence of the scar and the change in local anatomy. It is important to recognise that the antero-posterior diameter of the acetabulum is smaller than the supero-inferior diameter. The anterior and posterior walls should hence be preserved during preparation of the acetabulum. In theory, the projecting shelf of bone anteriorly and laterally may result in dislocation of the hip due to impingement. There is conflicting evidence regarding the results of total hip replacement after Chiari osteotomy. Hashemi-Nejad et al.21 reported results of total hip arthroplasties done in dysplastic hips with and without previous Chiari osteotomy at a mean follow-up of 5 years. Patients with a previous Chiari osteotomy required less bone grafting during the procedure, had better coverage of the cup by host–bone and near anatomic restoration of the centre of motion of the hip. This group also had fewer acetabular augmentation procedures and controlled medialisations, along with a lower mean blood loss and operative time. Minoda et al.22 compared 10 patients undergoing hip replacement after previous Chiari osteotomy with 20 patients undergoing hip replacement for dysplastic hips with no previous surgery. They concluded that the patients with a previous Chiari osteotomy had more blood loss, their surgical time was prolonged and joint forces were more vertical. These two studies reported no significant clinical differences after medium-term follow-up. The authors’ surgical experience of total hip arthroplasty in this subgroup agrees with the observations made by Hashemi-Nejad et al.21 The increased bone stock produced by these procedures assisted the total joint replacement procedure. However, the reconstructive surgeon should observe certain special precautions mentioned above during total hip replacement in this subgroup.
Pre- and post-operation dome osteotomy with complete displacement.
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Conclusion Chiari osteotomy is generally a safe procedure, with good long-term clinical outcomes reported in the literature. It is indicated in patients with symptomatic hip dysplasia in whom redirectional osteotomy is contraindicated due to an incongruous joint. While a stiff hip joint is an absolute contraindication for this procedure, the presence of moderate to severe arthritis remains a relative contraindication. When indicated, patients with previous Chiari osteotomy can expect good short to medium term results after total joint replacement.
References 1. Aronson J. Osteoarthritis of the young adult hip: etiology and treatment. Instruct Course Lectures 1986;35:119–28. 2. Stulberg SD, Harris WH. Acetabular dysplasia and development of osteoarthritis of hip. In: Harris WH, editor. The hip. Proceedings of the second open scientific meeting of the hip society. St. Louis, MO: Mosby; 1974. p. 82–93. 3. Ganz R, Klaue K, Vinh TS, Mast JW. A new periacetabular osteotomy for the treatment of hip dysplasias. Technique and preliminary results. Clin Orthop Relat Res 1988;232:26–36. 4. Wagner H. Osteotomies for congenital hip dislocation. In: The hip. Proceedings of the fourth open scientific meeting of the hip society. St. Louis: CV Mosby; 1976. p. 45–66. 5. Santore RF, Turgeon TR, Phillips Jr WF, Kantor SR. Pelvic and femoral osteotomy in the treatment of hip disease in the young adult. Instruct Course Lectures 2006;55:131–44. 6. Migaud H, Chantelot C, Giraud F, Fontaine C, Duquennoy A. Long-term survivorship of hip shelf arthroplasty and Chiari osteotomy in adults. Clin Orthop Relat Res 2004;418:81–6. 7. Chiari K. Beckenosteotomie zur pfannendachplastik. Wien Med Wochenschr 1953;103:707–10. 8. Kawamura B. Transverse pelvic osteotomy for congenital dislocation of the hip. Nippon Iji Shimpo 1958;1977:109. 9. Klaue K, Durnin CW, Ganz R. The acetabular rim syndrome. A clinical presentation of dysplasia of the hip. J Bone Joint Surg (Br) 1991;B-73:423–9.
S. Patil, D.A. Sherlock 10. Lavigne M, Parvizi J, Beck M, Siebenrock KA, Ganz R, Leunig M. Anterior femoroacetabular impingement: Part I. Techniques of joint preserving surgery. Clin Orthop Relat Res 2004;418:61–6. 11. Garbuz DS, Masri BA, Haddad F, Duncan CP. Clinical and radiographic assessment of the young adult with symptomatic hip dysplasia. Clin Orthop Relat Res 2004;418:18–22. 12. McGrory BJ, Trousdale RT, Cabanela ME, Ganz R. Bernese periacetabular osteotomy: surgical technique. J Orthop Tech 1993;1:179. 13. Lequesne M, de Seze S. Le faux profile du bassin: Nouvelle incidence radiographique pour l’etude de la hanche: son utilite dans les dysplasies et les diffe ´rentes coxopathies. Rev Rhum Mal Osteoartic 1961;28:643–52. 14. Kawamura B, Hosono S, Yokogushi K. Dome osteotomy of the pelvis. In: Tachdjian M O, editor. Congenital dislocation of the hip. New York: Churchill Livingstone; 1982. p. 609–23. 15. Macnicol MF, Lo HK, Yong KF. Pelvic remodeling after the Chiari osteotomy: a long-term review. J Bone Joint Surg 2004;B86:648–54. 16. Windhager R, Pongracz N, Schonecker W, Kotz R. Chiari osteotomy for congenital dislocation and subluxation of the hip: results after 20 to 34 years follow-up. J Bone Joint Surg (Br) 1991;B-73:890–5. 17. Yanagimoto S, Hotta H, Izumida R, Sakamaki T. Long-term results of Chiari pelvic osteotomy in patients with developmental dysplasia of the hip: indications for Chiari pelvic osteotomy according to disease stage and femoral head shape. J Orthop Sci 2005;10:557–63. 18. Rozkydal Z, Kovanda M. Chiari pelvic osteotomy in the management of developmental hip dysplasia: a long term follow-up. Bratislavske Lekarske Listy 2003;104:7–13. 19. Nakata K, Masuhara K, Sugano N, Sakai T, Haraguchi K, Ohzono K. Dome (modified Chiari) pelvic osteotomy. 10 to 18 year followup study. Clin Orthop Relat Res 2001;389:102–12. 20. Anwar MM, Sugano N, Matsui M, Takaoka K, Ono K. Dome osteotomy of the pelvis for osteoarthritis secondary to hip dysplasia. J Bone Joint Surg (Br) 1993;B-75:222–7. 21. Hashemi-Nejad A, Haddad FS, Tong KM, Muirhead-Allwood SK, Catterall A. Does Chiari osteotomy compromise subsequent total hip arthroplasty? J Arthroplasty 2002;17:731–9. 22. Minoda Y, Kadowaki T, Kim M. Total hip arthroplasty of dysplastic hip after previous Chiari pelvic osteotomy. Arch Orthop Trauma Surg 2006;126:394–400.
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MINI-SYMPOSIUM: CHILDREN–OSTEOTOMIES AROUND THE HIP
(v) Proximal femoral osteotomy in childhood Christopher John Darea, N.M.P. Clarkeb, a
Specialist Registrar Trauma and Orthopaedics, Tremona Road, Southampton SO16 6YD, UK University Southampton Universities NHS Trust, Tremona Road, Southampton SO16 6YD, UK
b
KEYWORDS Osteotomy; Femur; Legg–Calve–Perthes disease; Congenital dislocation of the hip; Cerebral palsy; Slipped capital femoral epiphysis; Coxa vara
Summary Abnormalities of the proximal femur in children range from teratologic hip dislocation and congenital coxa vara seen at birth to acquired disorders such as Legg–Calve–Perthes disease and slipped capital femoral epiphysis in later life. Left untreated, these conditions may lead to long-term morbidity in adulthood, ranging from early degenerative joint disease to complete inability to walk. However, treatment itself can be associated with significant complications such as avascular necrosis of the femoral head and chondrolysis, as well as the general risks of surgery. Optimal treatment requires careful consideration and planning and, importantly, involvement of parents in the decision-making process. Many of these conditions can be treated with a readjustment osteotomy of the proximal femur sometimes associated with a pelvic osteotomy. Prompt and timely intervention in the hands of an experienced surgeon can produce excellent results. & 2007 Elsevier Ltd. All rights reserved.
Congenital dislocation of the hip (CDH) CDH is more correctly referred to as developmental dysplasia of the hip (DDH) as few hips are truly dislocated at birth. Hip dislocations in the neonate are thought to be due to teratologic factors. The incidence of late DDH is approximately 2 per 1000 live births, compared to neonatal hip instability of 5–20 per 1000. The majority of these spontaneously stabilise. For 60% of neonates with hip instability no known risk factor(s) can be identified. In 20% of cases both hips are unstable. There are, however, welldocumented risk factors such as a positive family history, female sex, firstborn children, oligohydramnios, high birth Corresponding author. Tel.: +44 2380 796140;
fax: +44 2380 796141. E-mail address:
[email protected] (N.M.P. Clarke). 0268-0890/$ - see front matter & 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2007.04.007
weight and breech presentation. Girls are affected more than boys at a ratio of 5:1. Breech presentation, particularly with extended knees, increases the incidence by a factor of 10. Other congenital anomalies including torticollis, metatarsus adductus, congenital talipes equinovarus (CTEV), congenital vertical talus (CVT) and calcaneovalgus (CV) are associated with DDH. As part of routine post-natal screening, the hips are clinically examined by employing the Ortolani and Barlow tests. These tests become less appropriate in the older infants because secondary signs develop (restriction of abduction, shortening, and thigh crease asymmetry). A toddler with DDH will often be noted to have asymmetric limb lengths and will walk with a limp. Static and dynamic ultrasonography is of value in the assessment and treatment of DDH. Management is dictated by the degree of hip instability, the mainstay of treatment being the abduction harness. Failure to respond to treatment,
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or delay in presentation, results in more invasive treatment, namely an arthrogram, adductor tenotomy, with open or closed reduction of the dislocation.1 Hip dislocation in the older child (Fig. 1) poses a greater challenge. Children presenting beyond the age of 2 years inevitably require an open reduction and are also likely to require a femoral shortening osteotomy to locate the hip without undue femoral head compression. In the infantile hip, femoral neck anteversion and the neck shaft angle are increased. It is also well known that the dysplastic acetabulum is deficient anterosuperiorly. Surgical corrections of these alterations is important.1,2 In the planning stage of surgical correction of the dislocated hip in the older child the parents are counselled about the need not only for an open reduction of the hip but also for a varus derotation, shortening osteotomy. This type of osteotomy is aimed at redirecting the head of the femur both medially and posteriorly, maximising its containment in an otherwise deficient acetabulum. At the time of surgery the hip joint is approached anteriorly through a Smith–Peterson approach. A capsulotomy is performed and the true floor of the acetabulum is identified. Structures blocking reduction are addressed, notably the ligamentum teres, the pulvinar (fat pad) and the limbus. A trial reduction of the hip is then undertaken with the hip in a position of abduction and internal rotation. A second incision is made to approach the lateral femur and a Coventry lag screw is placed in the femoral neck distal to the capital epiphysis. This gives control of the proximal fragment prior to performing subperiosteal subtrochanteric shortening osteotomy sufficient to allow femoral head reduction without tension. The degree of varus is assessed by reducing the hip and the Coventry plate contoured accordingly. The femur is then derotated to bring the foot into a normal anatomical position. The osteotomy is secured with screws through the Coventry plate (Fig. 2). Femoral head stability is improved with a capsulorrhaphy and all wounds are closed. The osteotomy is protected with a spica cast (Fig. 3) for 6 weeks, at which point it is
Figure 2 Intraoperative image intensifier image following varus derotation osteotomy and final placement of metalwork.
Figure 3 Post-operative CT scan scout image demonstrating hip relocation and the one and a half spica.
converted to a broomstick plaster to maintain abduction for a further 6 weeks. The broomstick plaster is exchanged for night splints for 6 weeks. The implants are removed at 4–6 months post-operatively. Residual acetabular dysplasia is addressed by a later pelvic osteotomy.
Cerebral palsy
Figure 1 Late-presenting left-hip dislocation.
Cerebral palsy is a new progressive abnormality of the central nervous system, resulting in an impairment of motor function. The neurological insult occurs before the age of 2 years but the musculoskeletal manifestations may worsen throughout later life. The most common musculoskeletal deformity associated with cerebral palsy is equinus of the foot followed by hip displacement. Neurological subluxation or dislocation of the
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Figure 4 Bilateral neurological hip subluxation in cerebral palsy.
hip in cerebral palsy is more commonly associated with global body involvement such as spastic quadriplegia. Hips are usually located at birth but gradually displace under the influence of abnormal muscle balance and tone. In the normal hip, there is an interaction between the femoral capital epiphysis and the acetabulum stimulating normal development of both the proximal femur and the acetabulum. In the neurological hip, the muscle imbalance results in abnormalities of both the proximal femur and the acetabulum. Excessive femoral anteversion and valgus combine with abnormal acetabular development to produce progressive subluxation and dislocation of the hip (Fig. 4). Treatment of the neurological hip is guided by several factors: whether the child is ambulatory, whether or not the hip is painful and if there are difficulties with sitting balance or perineal hygiene.3 Managing the hip in cerebral palsy requires regular surveillance. When monitoring the neurological hip the most important radiographic parameter is the migration percentage. Since the acetabular index and centre edge angle are unreliable, the migration percentage is calculated from serial radiographs and it measures the percentage of lateral displacement of the hip. Migration of 25–30% (Normal 10%), or an increase of more than 10% in 1 year, is used as the criteron for intervention (early subluxation of 30–50%). Soft tissue procedures are used such as psoas-adductor release. For moderate subluxation of greater than 50% proximal varus derotation shortening osteotomy is recommended, combined with a pelvic osteotomy if acetabular dysplasia is severe enough. For dislocations with a migration percentage greater than 90%, reconstructive or salvage procedures should be considered. Hip subluxation or dislocation occurs in 3–7% of ambulate children with cerebral pulsy. For those with spastic quadriplegia, only 20% will walk.
Figure 5 Varus derotation shortening osteotomy with Coventry lag screw and plate.
Figure 6 Varus derotation shortening osteotomy with DCS.
A seating chisel is used to cut a track for an AO blade plate parallel and distal to the guidewire. Approximately 1–1.5 cm distal to this track the femur is divided parallel to the seating chisel. A second osteotomy is performed at the level of the lesser trochanter and a wedge of bone is removed. The blade plate is inserted into the proximal fragment, parallel to the guidewire, and the shaft of the femur approximated to the plate, thus reducing the cut surfaces. The degree of derotation is then established by ensuring the knee points anteriorly and the implant is stabilised with screws. Alternative methods of fixation are a dynamic condylar screw (DCS), or a Coventry lag screw and plate. Femoral osteotomy often has to be augmented by pelvic osteotomy (Figs. 5 and 6).
Femoral varus derotation shortening osteotomy
Proximal femoral osteotomy as salvage
The patient is placed supine on the operating table with the affected hip supported on a wedge. The proximal femur is approached via the direct lateral approach, elevating rather than splitting vastus lateralis, and exposing the bone subperiostially. The degree of varus correction is estimated from image intensifier images. If 201 of varus is required then a guidewire is passed into the femoral neck under X-ray control at 201 to the transverse plane of the femoral shaft.
Chronically dislocated, painful hips can be dealt with by means of salvage osteotomies. Proximal femoral resection should be performed extraperiosteally to minimise the risk of heterotopic ossification, and this removes bone to 3 cm below the lesser trochanter. Despite resection of the proximal femur proximal migration may still occur, resulting in a painful articulation of the resected proximal femur and acetabulum. This uncommon
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complication can be overcome by a Shanz abduction osteotomy. Lateralisation of the proximal femur abolishes the painful articulation.4,5
Legg–calve–perthes disease (LCPD) The current definition of Perthes’ disease is ‘Osteonecrosis of the proximal femoral epiphysis in a growing child caused by poorly understood non-genetic factors.’ The condition is more common in boys (ratio of 4:1) with an average age of onset of 7 years and a range of 2–12. Some 10–12% are bilateral and that condition is familiar in approximately 10%. There is a predisposition in children with delayed bone age. Symptomatic treatment involves bed rest and skin traction while the hip is irritable followed by partial weight bearing and physiotherapy. Prolonged bed rest and immobilisation does not change the radiological course of the disease. Containment of the femoral head can be achieved by means of an osteotomy of the femur or pelvis. Both require a nearly full range of movement of the hip (no more than 101 loss of motion in any direction). Surgical containment by pelvic osteotomy or by femoral osteotomy has similar results, the latter comprising varus with or without derotation or valgus-extension to relieve hinge abduction. Salter and valgus osteotomies lengthen the leg, whereas femoral varus osteotomy shortens it and may necessitate subsequent distal femoral epiphysiodesis of the contralateral limb.
Treatment of late disease A problematic late sequela of Perthes disease is hinge abduction as described by Grossbard and Catterall.6,7 They described an abnormal movement of the hip which occurs when a deformed femoral head, often with a large
uncovered anterolateral segment, impinges against the lateral lip of the acetabulum (Fig. 7). This most commonly occurs in Perthes’ disease but also in other causes of avascular necrosis (AVN) of the femoral head. Physeal arrest produces a leg length discrepancy with a short femoral neck and a high trochanter resulting in gluteal insufficiency. The valgus-extension osteotomy is designed to increase abduction and bring the more normal medial femoral head into the weight-bearing area. The pre-requisites for this form of osteotomy are (1) an arthrogram confirming hinge abduction and (2) a congruent hip in adduction with a good range of adduction.
The Sugioka valgus osteotomy variant The Sugioka osteotomy is a closing wedge intertrochanteric osteotomy.8 It is performed with the patient in the lateral position. A longitudinal incision is made over the greater trochanter, which is exposed following division of the fascia lata. The flare of the femur at the base of the greater trochanter is exposed and a greater trochanteric osteotomy is performed along the line of the physis. The trochanter and its muscle attachments are reflected cephalad. A closing wedge osteotomy is then performed from the exposed surface of the greater trochanteric osteotomy in a caudal–medial direction, with the apex at the level of the lesser trochanter. The leg is then abducted to close the wedge and the osteotomy secured with two cannulated screws using image intensifier control. The osteotomised greater trochanter is then advanced caudally and secured with wire (Fig. 8). The post-operative regimen requires 6 weeks of nonweight-bearing with crutches followed by partial weightbearing for a further 6 weeks. Metalwork is routinely removed 6–9 months post-operatively.
Figure 7 LCPD of the right hip.
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Figure 9 Severe slipped capital femoral epiphysis of the left hip.
Figure 8 Post-operative radiograph of a Sugioka osteotomy demonstrating increase in the neck shaft angle and advancement of the trochanter.
Slipped capital femoral epiphysis (SUFE) Slipped capital femoral epiphysis usually occurs between the age of 12 and 15 years. It is a disorder characterized by displacement of the femoral capital epiphysis from the metaphysis through the hypertrophic zone of the physis. However, in fact the metaphysis displaces in relationship to the epiphysis. The incidence is reported to be 3/100,000 in whites and 7/100,000 in blacks. It occurs in the left hip more than the right and is bilateral in 25% of cases. Those at risk are often overweight and are undergoing a growth spurt. Endocrinopathies such as hypothyroidism, renal rickets, pituitary deficiency and treated growth hormone deficiency are known risk factors and slippage may cause slippage at a younger age. Radiographs are pathognomic, revealing that Klein’s line does not pass through the lateral edge of the femoral capital epiphysis on the AP and cross-table lateral radiographs of the hip. Other radiological findings include widening and irregularity of the physis and decrease in epiphyseal height. Patients may present with a history of worsening hip or knee pain, for 3 weeks or more, in which case the slip is said to be chronic. For those with prodromal symptoms of less than 3 weeks the slip is said to be acute. The presentation can also be classified into unstable or stable according to whether the child can weight-bear with or without crutches. This distinction is important as the risk of AVN is significantly higher in acute unstable slips. SUFE is also classified depending on the degree of the slip seen on radiographs. Slips of less than 301 are mild whereas those over 601 are severe.
Treatment can be divided into three categories: (1) prevention of further slippage, (2) reduction of the degree of slippage, (3) salvage procedures. Treatment of further slippage is achieved by in situ fixation with pins or a screw. Salvage procedures in the young principally consist of hip arthrodesis. Long-term studies confirm that the outcome following a SUFE depends on the degree of the initial slip and degenerative joint disease commonly follows moderate and severe slips. Osteotomy of the proximal femur is restricted to severe slips (Fig. 9) as surgical intervention is not without risk, particularly avascular necrosis and chondrolysis.9,10 Intracapsular osteotomies are associated with rates of AVN as high as 35% and rates of chondrolysis of 30%. The Southwick osteotomy is extra-capsular with lower rates of complications but provides less correction.11
The Dunn osteotomy Dunn proposed his osteotomy for severe slips in 1964.12 His primary objective was to place the epiphysis on the femoral neck without disruption of the retinacular blood supply. This was achieved through a lateral approach to the hip and a trochanteric osteotomy. The capsulotomy is formed by an incision running around the edge of the acetabulum and a vertical limb along the lateral aspect of the femoral neck to the level of the trochanteric base. The posterior ascending retinacular vessels are carefully preserved. Once the femoral neck has been exposed a trapezoidal osteotomy shortens the femoral neck, allowing the epiphysis to be placed on the cut femoral neck and held with a screw. Weight-bearing is restricted for 6 weeks and the implant removed at 1 year. A contralateral epiphysiodesis may be required.
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C.J. Dare, N.M.P. Clarke The management of moderate to severe SUFE by corrective osteotomy remains controversial because of the risk of significant complications.9
Coxa vara
Figure 10 Reduction and fixation following Fish osteotomy.
Southwick osteotomy Southwick proposed his osteotomy in 1967,13 for slips that were moderate to severe. The anterolateral aspect of the femur is approached subperiosteally and the lesser trochanter identified. The iliopsoas tendon is released. The femur is marked with a vertical line along the lateral edge. Using this orientation mark and templates a technically challenging triplane osteotomy is performed. The hip is then abducted and flexed at the level of the osteotomy achieving the desired correction. In the original description the correction was held with an external fixator but in the modern era a blade plate is used. This osteotomy can be performed at presentation or later if the hip has initially been stabilised with pinning. The advantages of this are that the hip can be monitored for remodeling potential prior to undertaking a Southwick osteotomy, which can be reserved for hips that fail to remodel significantly.
Fish osteotomy Fish reported his series of intracapsular osteotomies in 1984.14 The hip is approached anterolaterally. The capsule is opened longitudinally and transversely both proximally and distally to expose the femoral neck. The capital femoral epiphysis is then identified. A cuneiform osteotomy of the femoral neck distal to the physis is performed. All remaining physeal cartilage is removed using a curette. The epiphysis is seated on the cut femoral neck and held with pins or screws (Fig. 10). Post-operatively the patient is kept touch weight-bearing until healing of the osteotomy is seen radiographically. The pins are removed at a later date.
Coxa vara is a retroverted deformity of the proximal femur where the angle between the neck and the shaft is reduced to less than 1101, and more typically 901 (normal 130–1451). An alternative to this measurement is the Hilgenreinersepiphyseal angle, which is calculated by drawing a line along the physis and through the triradiate cartilages. The natural history of developmental coxa vara is variable, the greater the angle, the more propensity toward shear stress on the physis, and the less chance of spontaneous recovery. Coxa vara has been classified by Beals as developmental, congenital, or traumatic. Infantile or developmental coxa vara is estimated to affect 1:25,000 live births and has a post-natal onset. It is bilateral in about 1/3 of cases. Clinically, there is shortening of the limb of approximately 2 cm, with weakness of the abductors and thigh atrophy. Radiographically, developmental coxa vara is characterized by a triangular metaphyseal fragment of the inferior femoral neck. Associated conditions include spondylometaphyseal dysplasia, spondyloepiphyseal dysplasia, and cleidocranial dysplasia. Other causes of coxa vara are congenital, dysplastic, or traumatic. Congenital coxa vara is the least severe form of proximal focal femoral deficiency and is characteristic of all degrees of severity. The condition is present at birth, usually unilateral and non-progressive. A number of generalised skeletal dysplasias are characterized by dysplastic coxa vara which is often bilateral, progressive and does not remodel. Traumatic coxa vara can obviously result from femoral neck fracture or from proximal femoral physeal arrest with resultant relative overgrowth of the greater trochanter. The latter can follow hip sepsis or avascular necrosis of the femoral head. Coxa vara resulting from relative overgrowth of the greater trochanter is treated by physeal arrest of the greater trochanter or distal transfer of the greater trochanter to improve hip mechanics. Valgus proximal femoral osteotomy at the intertrochanteric or subtrochanteric region is the only effective intervention. Sufficient valgus must be achieved to reduce shear forces along the physis and a valgus osteotomy therefore rotates the proximal femoral physis from a vertical to horizontal position. Pauwels’ Y-shaped osteotomy and Langenskiold’s valgus producing osteotomy are examples of intertrochanteric corrective osteotomies.15 Once the osteotomy has been performed it is held with a variety of internal fixation devices such as a blade plate or screw and plate combination. To minimise the risk of recurrence the Hilgenreiner-epiphyseal angle needs to be reduced to less than 401 and the neck shaft angle increased to greater than 1601. Correct treatment of coxa vara results in a painfree functional hip with a negative Trendelenborg gait. A mild leg length discrepancy may persist post-operatively which can be addressed with a contralateral epiphysiodesis. However, in the majority of cases leg length discrepancy is insignificant.16
ARTICLE IN PRESS Proximal femoral osteotomy in childhood
Conclusion A wide variety of conditions affect the hip in children ranging from the newborn to the adolescent. Osteotomy of the proximal femur may be intracapsular or extracapsular, varus or valgus, and with or without a rotational element. A redirectional osteotomy in some circumstances will need to be augmented with a pelvic osteotomy. Leg length inequality can be a sequela of surgery but can be addressed with a contralateral epiphysiodesis if treated in time. On the whole, there is consensus regarding the management of most hip conditions in the child. However, surgical intervention is far from risk-free and controversy persists around the management of some conditions.
References 1. Clarke NM. Developmental dysplasia of the hip. In: Bulstrode C, Buckwalter J, Carr A, Marsh L, Fairbank J, Wilson-MacDonald J, Bowden G, editors. Oxford textbook of orthopaedics and trauma. Oxford: Oxford University Press; 2002. p. 2543–8. 2. Zionts LE, MacEwen GD. Treatment of congenital dislocation of the hip in children between the ages of one and three years. J Bone Joint Surg Am 1986;68:829. 3. Hoffer MM. Management of the hip in cerebral palsy. J Bone Joint Surg 1986;68:629–31. 4. Hogan KA, Blake M, et al. Subtrochanteric valgus osteotomy for chronically dislocated, painful spastic hips. J Bone Joint Surg 2006;88:2624–31.
121 5. Gaenslen FJ. The Schanz subtrochanteric osteotomy for irreducible dislocation of the hip. J Bone Joint Surg 1935; 17:76–87. 6. Grossbard GD. Hip pain during adolescence after Perthes’ disease. J Bone Joint Surg Br 1981;63:572–4. 7. Catterall A. Adolescent hip pain after Perthes disease. Clin Orthop Relat Res 1986;209:65–9. 8. Sugioka Y. Transtrochanteric anterior rotational osteotomy of the femoral head in the treatment of osteonecrosis affecting the hip: a new osteotomy operation. Clin Orthop Relat Res 1978;130:191–201. 9. Uglow MG, Clarke NMP. The management of slipped capital femoral epiphysis. J Bone Joint Surg Br 2004;86:631–5. 10. Herring JA. The treatment of Legg–Calve–Perthes; disease. A critical review of the literature. J Bone Joint Surg 1994;76: 448–58. 11. Rao J, Francis AM, et al. The treatment of chronic slipped capital femoral epiphysis by biplane osteotomy. J Bone Joint Surg 1984;66:1169–75. 12. Dunn DM. The treatment of adolescent slipping of the upper femoral epiphysis. J Bone Joint Surg Br 1964;46:621–9. 13. Southwick WO. Osteotomy through the lesser trochanter for slipped capital femoral epiphysis. J Bone Joint Surg Am 1967; 49:807–35. 14. Fish JB. Cuneiform osteotomy of the femoral neck in the treatment of slipped capital femoral epiphysis. J Bone Joint Surg 1984;66:1153–68. 15. Cordes S, Dickens DRV, Cole WG. Correction of coxa vara in childhood: the use of the Pauwels’ osteotomy. J Bone Joint Surg Br 1991;73:3–6. 16. Carroll K, Coleman S, Stevens P. Coxa vara: surgical outcomes of valgus osteotomies. J Paediatr Orthop 1997;17:220–4.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 122–134
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SPINE
Spinal deformity in paediatric patients with cerebral palsy Athanasios I. Tsirikos, Patrick Spielmann Scottish National Spine Deformity Centre, Royal Hospital for Sick Children, Edinburgh, UK
KEYWORDS Cerebral palsy; Scoliosis; Spasticity; Pelvic obliquity
Summary Spinal deformity in children with cerebral palsy is common. The incidence is higher with spasticity, inversely proportionate to the level of ambulation. Scoliosis is commonly associated with significant pelvic obliquity, which decreases sitting tolerance, and causes pain from pelvic impingement on the thorax. There may be cardiopulmonary complications. & 2007 Elsevier Ltd. All rights reserved.
Introduction
CP can be also categorized according to the most prominent motor disorder:
Cerebral palsy (CP) is a static encephalopathy affecting the immature brain which leads to permanent motor dysfunction. It is probably the most common neurological condition causing permanent physical disability in childhood. The classification of CP most commonly used by orthopaedic surgeons is based on the anatomic pattern of involvement.
monoplegia: one limb is primarily affected; diplegia: predominantly affecting the lower extremities; hemiplegia: one side of the body is predominantly affected;
triplegia: a hemiplegic pattern exists on one side with diplegia in the lower limbs;
quadriplegia: all four limbs are affected. Whole or total body involvement describes a patient with profound quadriplegic involvement, marked cognitive disability, and severe learning difficulties. Corresponding author. Tel.: +44 131 5360784;
fax: +44 131 6621265. E-mail address:
[email protected] (A.I. Tsirikos). 0268-0890/$ - see front matter & 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2007.01.001
spastic flaccid athetoid mixed types
Spasticity is a velocity-dependent increase in resistance to motion and represents the most common abnormality in motor tone that occurs in children with CP. Spastic and mixed forms account for more than 85% of cases. Spinal deformity is a significant problem in children with CP. It most commonly affects those with spasticity, with an incidence directly proportional to the severity of neurological involvement.1–9 The overall incidence of spine deformity in CP is as high as 20–25%.10 It is considerably higher in non-ambulators and in patients with total body involvement.11,12 The curves usually do not respond to brace treatment, especially during the adolescent growth spurt, are progressive, and lead to both coronal and sagittal imbalance, often associated with pelvic obliquity.5,10,11,13–15
ARTICLE IN PRESS Spinal deformity in cerebral palsy
Pathophysiology It is unclear which component of neurological deficit is more responsible for the development of spine decompensation. Spasticity, muscle weakness, incompetent muscle control, and poor balance are all contributory factors.
Functional deficits The combination of abnormal spinal curvature and neurological impairment can significantly affect function; trunk imbalance and pelvic obliquity may impair walking capacity or sitting tolerance. In ambulators, spinal malalignment and trunk decompensation affect standing balance, limiting walking ability, and cause sitting intolerance in wheelchairbound patients, converting them to hand-dependent sitters.10,12,13 Ambulators may need walking aids or become wheelchair-dependent. In a wheelchair-bound patient, pain may result from impingement of the ribs against the iliac crest on the concavity of the scoliosis. Pressure sores may develop especially if the child has insensate skin. Nonambulators have to rely increasingly on their upper limbs for body support, markedly decreasing their functional abilities and thus an increasing need for nursing care. Additionally, scoliosis in these severely disabled children can cause cardiopulmonary complications, particularly when the curve magnitude is such that the patient can spend little time erect or sitting.15 The symptomatology in children with severe gastro-oesophageal reflux, swallowing disorders, and a history of aspiration may also get aggravated as the spine deformity progresses. The purpose of this systematic review is to investigate the characteristics of spine deformity that develops in children with CP, to give guidelines for treatment, and to increase awareness of the complexity of these deformities and the coexistence of a multitude of associated medical problems that arise in this particular patient population.
Coronal deformity Scoliosis is the most frequently encountered spine deformity in CP and can be associated with a sagittal imbalance ranging from hyperkyphosis to hyperlordosis.
Epidemiology The incidence of scoliosis in patients with spastic diplegia is 5% compared to 65–74% in patients with spastic quadriplegia.10,16 In a review of 272 institutionalized patients with CP, Madigan and Wallace8 found an overall incidence of radiographically confirmed scoliotic curvatures of 64%.
Types of scoliosis Lonstein and Akbarnia7 have defined two distinct scoliotic deformity patterns in patients with CP (Table 1). Group 1 curves are single thoracic or double thoracic and lumbar curves resembling idiopathic scoliotic curvatures with a level pelvis. These are more common in patients with
123 good ambulatory ability and less severe neurological deficits.7,10 Group 2 curves are long thoracolumbar or lumbar Cshaped curves associated with pelvic obliquity, the elevated side of the pelvis being on the concavity of the curve. These curves correspond to the characteristic pattern of spinal malalignment usually seen in non-ambulatory patients. Group 2 curvatures can be further subdivided into 2A with the curve continuing into the sacrum, and 2B when the sacral vertebrae do not form part of the curve.
Sagittal deformity Sagittal spine deformity in CP is rare and usually occurs with scoliosis.22,23 The prevalence has been quoted at 7% in patients with scoliosis.24 Patients with hamstring spasticity or fixed hamstring contracture followed by posterior pelvic inclination and decreased lumbar lordosis develop a compensatory thoracic hyperkyphosis. Children who have undergone dorsal rhizotomy through extensive laminectomies to address persistent lower limb muscle spasticity tend to develop a severe thoracolumbar kyphosis, which gives rise to pain. An additional cause of excessive kyphosis is the presence of generalized trunk hypotonia. As the kyphotic deformity progresses, the patient’s sitting ability and head control in a functional position become affected. Hyperlordosis is seen in ambulatory patients, usually diplegics, with flexion contractures of the hips and anterior pelvic tilt.10 An isolated lumbar lordosis can also be a consequence of multi-level laminectomies performed during a dorsal rhizotomy. In rare cases, a rigid lumbar lordosis may be the result of tethering of the spinal cord. Children with lumbar hyperlordosis often complain of back pain and have an increased risk of developing isthmic spondylolysis and spondylolisthesis.
Clinical Presentation Scoliosis in CP behaves very differently to the idiopathic type. Scoliotic curves may be structural or postural. Young children present, initially, with a flexible postural curve; a structural component develops with further growth. This distinction is important as surgical management can usually be postponed until late childhood or early adolescence. As children with CP enter their adolescent growth spurt, the rate of progression of the scoliotic curve increases dramatically up to 2–4 degrees/month17,18 and a rigid deformity develops rapidly. The rate of curve deterioration and the stiffness of scoliosis also depend on the extent of the patient’s neurological involvement.
Natural history The progression of the scoliotic curve is not confined to the pubertal growth spurt; it is often influenced by muscle imbalance and gravity, and so significant deformity may appear earlier in life and progress beyond skeletal maturity into adulthood.19 It is also important to note that puberty may begin much earlier or later in a person with CP.6,8,20,21 Thometz and Simon21 reported progression of scoliosis beyond the end of skeletal growth, particularly if the curve
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Table 1
A.I. Tsirikos, P. Spielmann The classification of scoliotic curves in cerebral palsy.7
Group 1
Group 2
Single thoracic or double thoracic and lumbar curves resembling idiopathic scoliosis Absent or minimal pelvic obliquity
Large C-shaped lumbar or thoracolumbar curves
was greater than 501 (1.41/year), compared to 0.81/year for curvatures of less than 501 at skeletal maturity. In other reports, scoliotic curvatures of more than 401 progressed at a rate of 41/year,6 or to a mean of 801.18 Even curves as low as 201 may continue to deteriorate into the adult life at a rate of 0.81/year.17
Treatment of spinal deformity The management of spinal deformity in CP is directed at maintaining or improving the functional abilities and quality of life of the child. Thus any treatment must be tailored to the individual patient and consider his/her specific circumstances. Treatment planning must also include a detailed risk–benefit assessment based on the severity of co-existing medical morbidities.
Non-operative treatment Non-operative management of spine deformity in patients with CP includes seating adaptations and the use of orthotics. Unfortunately, none of these measures has a documented effect on curve progression or the final outcome of the spinal curvature. Thus the aim of all non-operative modalities is not to correct the deformity, but to preserve patients’ functional ability as the curve continues to develop. Seating supports These are useful in patients with CP as sitting balance can be improved and an upright posture maintained. They facilitate nursing care and may free the patients’ hands, improving function.9,10,25,26 We believe that appropriate sitting adjustments should be considered the mainstay of managing patients with scoliosis prior to surgical correction. The use
Marked pelvic obliquity
offset chest lateral rests that can be fitted on a wheelchair, which becomes the primary sitting device for those patients over time. Lateral supports need to be revised as the children grow to provide adequate trunk fixation. Shoulder harnesses and straps fitted to the wheelchair can be used for patients with thoracic hyperkyphotic deformities. As the kyphotic curve becomes more rigid, the back of the wheelchair may have to be moulded to accommodate the fixed deformity.
Bracing A moulded thoracolumbosacral orthosis (TLSO) adapted from the treatment of patients with adolescent idiopathic scoliosis has been commonly used in with good initial results.27,28 Miller et al.17 followed 43 children with spastic quadriplegic CP and a neuromuscular scoliosis until spinal fusion. Twenty-one of these patients were managed with and 22 without a TLSO. The authors noticed no statistically significant difference between the rates of curve progression or the age at surgical intervention between the two groups demonstrating that there was no impact of the orthosis on the rate of curve progression, or the natural history of the deformity. While a recent study has supported a possible benefit in certain cases,29 the benefits of bracing are disputed in controlling the curve. However, bracing may be useful in the immature child to slow curve progression until the child can safely undergo spine surgery.30 It must not be forgotten that spinal braces are necessarily tight fitting and may cause considerable skin problems and respiratory compromise. Feeding can also be disturbed, particularly in children with pre-existing disorders and gastro-oesophageal reflux. Poor patient compliance is another frequent problem as the braces are uncomfortable and have to be worn for up to 23 h/day.
ARTICLE IN PRESS Spinal deformity in cerebral palsy We believe that a more reasonable consideration would be the use of a soft underarm brace that can be applied and removed easily, and may improve the children’s sitting balance when they are not using their adapted wheelchair. The combination of seating adaptations built on the wheelchair with a non-rigid bi-valved underarm orthosis when the wheelchair is not used is the authors’ preferred method for young patients with curves that still retain their flexibility.
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Preoperative assessment Patients with CP can have multiple medical co-morbidities which need to be addressed prior to any surgical intervention. The surgeon must be a member of a larger multi-disciplinary team, which includes anaesthetists, neurologists, pulmonologists, gastroenterologists, dieticians, physiotherapists, occupational therapists, and intensive nursing care.
Operative treatment The only management that addresses effectively spine deformity in patients with CP and has a well-documented positive impact in these children’s quality of life is spine fusion using instrumentation. Indications When considering surgical treatment, factors to be included are the size and flexibility of the curve in relation to the patient’s age and general medical condition, as well as the desires expressed by the parents or carers. Surgical correction is indicated when:
there is documented curve progression of greater than 101,
for curves greater than 45–501 in children 10 years of age or older,
if there is considerable deterioration in the child’s level of function.3–5,7,10,26 Surgery can be postponed for a later stage if the patient is still very young and the curvature remains flexible. Patients with extremely severe deformities both in magnitude and stiffness, in whom even a combined anterior–posterior spinal arthrodesis would only achieve minimum correction, who also have a host of associated medical problems, including recurrent respiratory infections and poor feeding status, are at a greater risk of developing serious peri-operative complications. In such patients the risk of intra- or post-operative death outweighs the possible benefits from stabilizing the deformity and they should not be considered as good candidates for surgical intervention. On the other hand, spine surgery would be appropriate for patients with a lesser degree of deformity than set out above at skeletal maturity, due to the well-recognized risk of further deterioration into the adult life. Aims of surgery The objective is to restore trunk alignment, improve respiratory function, alleviate the pain caused by impingement of the ribs against the iliac crest on the concave side of the curve, provide better sitting tolerance in wheel chairbound patients, prevent the development of pressure sores, and retain standing and walking abilities in ambulatory patients, thus maximizing overall level of function.1,4,5,26 A successful outcome would include a balanced spine with his/her shoulders parallel to the pelvis and head and chest centred on top of the pelvis and a normal sagittal balance achieved so that the patient can hold his/her head in an upright position and the body weight is moved forward during sitting.
Respiratory Pulmonary compromise is common in scoliotic patients with CP. Children with CP may have abnormal hypopharyngeal tone or anatomical abnormalities affecting their upper airway. When these anomalies are combined with the effects of a general anaesthetic (muscle relaxation and increased secretions) there is an increased risk of upper airway obstruction or respiratory failure.32 These patients will often have a poor coughing mechanism due to weak chest wall muscles. Respiratory failure and pneumonia occur much more frequently in patients undergoing spine fusion for neuromuscular scoliosis when compared to patients with idiopathic scoliosis.31 This must be considered when an anterior approach to the thoracic or thoracolumbar spine is necessary, as this significantly increases the risk of postoperative pneumonia, particularly if prolonged ventilation is required. Aggressive chest physiotherapy should be routinely used. Gastro-oesophageal reflux should be suspected if the patient presents with a history of coughing bouts during feeding and recurrent chest infections. Such patients are at a higher risk of aspiration pneumonitis particularly if they have a poorly coordinated swallowing mechanism. The aspiration pneumonia can be silent and lead to progressive lung damage and fibrosis without early clinical symptoms.32 Hence preoperative chest radiographs should be routinely obtained to identify evidence of pulmonary fibrosis. While lung function tests would be helpful in detecting respiratory compromise, these are often impossible to perform due to poor patient cooperation. Thoracic spine deformity may critically diminish pulmonary function; a thoracic lordosis will reduce the anteroposterior diameter of the chest, affecting the functional residual capacity and scoliosis may decrease the volume of one lung, impairing gas exchange and expectoration of secretions. Both predispose to recurrent chest infections.9 These problems have obvious implications for the planning of major spine surgery in already compromised children. Close cooperation with paediatric pulmonologists is essential. Postoperative care in the Intensive Care Unit (ICU) is standard but prolonged ventilation post-surgery is rarely required. Preoperative tracheotomy is rarely indicated but may aid the care of children with complex upper airway problems. It may be necessary to aid weaning off the ventilator and aggressive pulmonary toilet can prevent chest infection.
Developmental/nutritional Global developmental delay is common in patients with CP. Growth charts often show the child well below the 25th or
ARTICLE IN PRESS 126 even the 5th percentile for age.10 Feeding is often a significant problem and must be fully evaluated prior to surgical intervention. Attention must be paid to the previous feeding history, the consistency of foods ingested, and the child’s tolerance of oral feeds. As already mentioned, swallowing may be a problem because of uncoordinated muscle contraction or abnormal pharyngeal muscle tone. If the clinical history is suggestive of aspiration it may be necessary to perform swallowing studies. Poor nutritional state predisposes the patient to delayed wound healing and a poor immunological response to infection. As malnutrition is a common finding in these children due to the combination of a poor diet, often deficient in essential vitamins, and a high metabolic demand due to recurrent chest infections or other co-morbidities,32 their nutritional status must be assessed prior to surgery with a detailed history, a thorough clinical examination, supplemented by haematological and biochemical tests. Readily available gross markers of nutrition include serum protein, albumin, and transferrin levels as well as peripheral lymphocyte count. Jevsevar and Karlin33 reported a significantly lower infection rate after spine arthrodesis, a shorter period of endotracheal intubation and less hospitalization time in patients with a preoperative serum albumin of 35 g/L or above and a total blood lymphocyte count of 1.5 cells 109/L or above. Thus, surgical intervention should be postponed in the malnourished patient and preoperative supplemental nutrition may be necessary to optimize a candidate for surgery, preferably administered through the gastrointestinal route using nasogastric or nasojejunal feeding tubes. Night-time feeding by nasogastric tube may also be beneficial. A feeding gastrostomy may be required if tube feedings are not tolerated. In the presence of persistent gastro-oesophageal reflux, a Nissen fundoplication may alleviate the problem. However, if the reflux is not very severe to necessitate immediate treatment it might be better to postpone any surgical repair until after the spine is corrected, because the effect of the spine fusion on the gastro-oesophageal reflux can be totally unpredictable. Gastritis and peptic ulceration are quite common in this group of patients. Gastrointestinal dysmotility is also frequent among children with CP, which again predisposes to severe gastro-oesophageal reflux and constipation. All these factors combined with a long general anaesthetic using opioids increase the risk of developing a postoperative paralytic ileus.32 Parenteral nutrition may be required in the postoperative period if there is prolonged paralytic ileus and malabsorption. The development of chemical pancreatitis with increase of the serum amylase is relatively common after spine fusion in children with CP and is usually asymptomatic. Cholecystitis and cholangitis may also develop in the postoperative period in patients with severe neurological impairment or those with previously undiagnosed gallbladder stones. Vascular compression or obstruction of the third part of the duodenum may occur as it is trapped between the aorta and the superior mesenteric artery. The angle formed between the two arteries narrows considerably after the correction of major scoliotic curves, particularly in the presence of an associated lumbar hyperlordotic component.
A.I. Tsirikos, P. Spielmann
Haematological Intra-operative blood loss is a well-described problem in children with CP. Tsirikos et al.34,35 have previously reported a mean intra-operative blood loss of 2.9 L, corresponding to 1.2 blood volumes in a review of 288 consecutive patients undergoing spine fusion. Patients with CP may also have inherent or acquired disorders of coagulation. This needs to be identified preoperatively as blood loss during spine arthrodesis will be considerable. Anti-seizure agents, such as sodium valproate, have been shown to decrease von Willebrand’s factor36 causing a prolonged bleeding time. Phenobarbital has a similar effect and increases the risk of severe peri-operative bleeding. Liaison with a neurologist is important as these medications may be discontinued and an appropriate alternative commenced prior to surgical intervention. When children are scheduled for surgery there must be at least one blood volume of blood typed and cross-matched. The intra-operative use of a cell saver system may limit the need for transfusion. Controlled hypotensive anaesthesia and meticulous haemostasis during tissue dissection are required to reduce blood loss. Early administration of fresh frozen plasma should be considered in the presence of a gradually increasing intra-operative blood loss, especially in patients with identified coagulopathies, those on anticonvulsant medication and patients with severe neurological involvement. During surgery, transfusion of a significant volume of packed cells and clotting factors may be required. There are, however, many problems associated with large-volume blood transfusions; these include anaphylaxis and lesser febrile reactions, hyperkalaemia, hypocalcaemia, and hypothermia. A consumptive coagulopathy (disseminated intravascular coagulation) may be the result of large volume transfusions and must be avoided with the appropriate administration of clotting products.
Neurological/metabolic/urinary Mental retardation, learning difficulties and behavioural problems are common in children with CP. These may complicate the postoperative care in patients undergoing spine surgery, as good compliance is generally required for chest physiotherapy, mobilization in and out of bed, toileting, and feeding. Considerable effort will be required to nurse these patients effectively and safely. Patients with ventriculo-peritoneal shunts should be assessed before and after spine surgery to confirm adequate function of the shunt. Seizures are another frequent clinical feature of CP. Liaison with a paediatric neurologist is essential to optimize the patient for surgery and prevent uncontrolled seizure activity in the peri-operative period. The side effects of the chronic administration of anti-epileptic medication include the development of osteomalacia. Bone quality is often inherently poor, especially in quadriplegic patients because of disuse osteopenia. Poor bone quality increases the risk of intra-operative blood loss and instrumentation failure during spine fusion. Preoperative management of osteoporosis with the administration of intravenous bisphosphonates might be
ARTICLE IN PRESS Spinal deformity in cerebral palsy a consideration, especially in non-ambulatory quadriplegics with marked osteoporosis, to maximize their bone quality before spine surgery. Intrathecal baclofen therapy has been introduced to control severe spasticity unresponsive to oral anti-seizure agents. A recent study by Shah et al.37 has shown that the administration of botulinum toxin through an intrathecal baclofen pump does not increase the risk of developing progressive scoliosis in this group of patients. Patients with CP have a greater prevalence of recurrent urinary tract infections due to urinary incontinence. The presence of an active urine infection at the time of the spinal fusion may increase the risk of a deep wound infection, with attendant risk to the surgery. Doubly incontinent patients also have a significant risk of developing deep wound infections caused by direct contamination.
Historical The introduction of Harrington instrumentation was a tremendous evolution in the operative management of these complex deformities, but the incidence of pseudarthrosis and consequent curve recurrence remained high.38–40 Harrington instrumentation was used in the surgical management of neuromuscular scoliosis until the late 1970s but the distraction techniques applied through the Harrington system were difficult and often impractical in the soft bone of patients with quadriplegic CP.41 In 1977, Luque38 developed the concept of segmental spinal fixation with the application of translational corrective forces through the use of multiple-level sublaminar wires and two single rods. This achieved a wide distribution of forces over each vertebra, with an increased initial spinal stabilization and a low risk of instrumentation failure.1,42,43 This gave greater correction and decreased risk of implant failure.1,42 However, later reports indicated a rate of pseudarthrosis associated with the Luque system of up to 10%,44 instrumentation-related complications up to 21%,44 and curve progression postoperatively in up to 30% of the cases.13,45 The Galveston technique of intramedullary placement of the rod in the iliac bed was developed by Allen and Ferguson,42 and accomplished a secure pelvic fixation.44 However, it was soon recognized that the two unconnected soft rods introduced by Luque were moving independently, which was the reason why they failed to provide a stable fixation. The use of postoperative immobilization did not prove to resolve the problem.45 The Unit rod, a further development of the Luque–Galveston technique, introduced rigidly connected rods, which allowed improved correction of both spinal curvature and pelvic obliquity, together with restoration of coronal and sagittal trunk balance.46–48
Other techniques More recent instrumentation systems using pedicle screws have been introduced in the management of neuromuscular scoliosis. These are based on the same principle of segmental fixation with pedicle screws or hooks and the alternative of iliac bolds for lumbo-pelvic or sacro-iliac plates for sacropelvic fixation.
127 A common problem in the application of third generation instrumentation that use pedicle hooks or screws in patients with CP and marked associated osteopenia is poor vertebral fixation, which can limit the extent of corrective manoeuvres and may significantly increase the risk of pseudarthrosis. In our experience, in this group of children with considerably poor bone mineral quality, the laminae provide the strongest point of fixation compared to the pedicle or the vertebral body and can withstand segmental translational forces applied through sublaminar wires necessary to achieve correction of the deformity and balancing of the spine in both coronal and sagittal planes. On the other hand, if repeat surgery is required, e.g. to address a non-union, it is technically much easier and safer to revise an instrumentation system that uses pedicle screws with or without hooks as opposed to sublaminar wires. As these modern techniques become common and widely utilized, it is essential to establish benchmarks for degree of deformity correction and complication rate related to the technical aspects of the individual procedure. As third generation spinal instrumentation is being widely utilized, there is also a significant increase in implant cost; this has to be balanced against possible benefits obtained by the use of these latest techniques. We believe that, even in the advent of these more modern instrumentations, the Unit rod still remains the primary system for the treatment of patients with CP because it is simple to use, it is considerably cheaper than most other systems and can achieve good deformity correction with a low loss of correction, as well as a low prevalence of associated complications and a low re-operation rate (Fig. 1).35 In the largest reported series of 288 patients with CP and spine deformity, spinal arthrodesis using the Unit rod instrumentation achieved correction of the scoliosis by 68% and of the pelvic obliquity by 73% with restoration of a normal sagittal alignment in both the thoracic and lumbar spine.35 A very satisfactory correction of spinal curvatures was maintained at a mean follow up of 3.2 years.35 There were no detected pseudarthroses and the overall number of re-operations for technical reasons was very low.35 It is also important to note that the Unit rod instrumentation construct used in this series costs our hospital the equivalent of less than two pedicle screws.
Surgical technique using the unit rod instrumentation General Thorough preoperative assessment (see earlier in this article) of the patients is performed, including evaluation of their respiratory capacity, cardiac function, immune system, coagulation mechanisms, nutritional status, feeding disorders, seizures, urinary system and their overall level of functional impairment. All patients receive prophylactic antibiotic treatment with the administration of a firstgeneration cephalosporin immediately before and for 24 h after surgery. Before anaesthesia induction, arterial and central venous lines are placed, and the central venous line is maintained until the second stage in patients who will have a two-stage procedure. A nasogastric tube is used to
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Figure 1 Preoperative (a) and 2-year follow-up (b) radiographs of the spine on a 10 and a half-year-old patient with quadriplegia who underwent a posterior spinal arthrodesis. The thoracolumbar scoliosis was measuring 801 with associated pelvic obliquity and this was corrected to 151 with a level pelvis following surgery. Note the presence of dextrocardia as well as the insertion of an intrathecal baclofen pump to control severe seizure activity, which did not have a detrimental effect on progression of the scoliosis.
decompress the stomach and a Foley catheter to monitor urinary output. Cell-saver is used intra-operatively, and the patients receive homologous blood transfusions at the discretion of the anaesthesiologist. Spinal cord monitoring with the use of somatosensory or motor-evoked potentials is applied during surgery in the ambulatory patients only. We perform the anterior procedure in the lateral decubitus position, using a thoracic or thoracolumbar retroperitoneal approach, through the bed of a removed rib, depending on the apex of the deformity and the levels of anterior release that are required. The anterior approach allows for an extensive release of the anterior longitudinal ligament, complete annulectomy and discectomy, with the intention to provide angular and rotational mobility of the spinal segments, while at the same time enhancing anterior fusion in the excised disc spaces with the application of morsellized rib graft. No anterior instrumentation is used. Patients who are in a poor medical state and have associated co-morbidities are selected to undergo a twostage procedure under different anaesthetic sessions. In this group, after the anterior stage is completed, the patients are taken to the ICU, where hyperalimentation and aggressive pulmonary care are initiated until the posterior procedure 7–8 days later. The chest drain is removed when the drainage is less than 150 mL/day, usually on the third or fourth day after surgery. Patients whose general medical condition will tolerate the second stage under the same anaesthetic are immediately rolled into the prone position after the anterior procedure is completed, and posterior fusion with the Unit rod instrumentation is performed. The Unit rod instrumentation is used to give segmental posterior fixation, with the spinal
arthrodesis always extending from C7, T1 or T2 to the pelvis using the Galveston technique (Figs. 2–4). Decortication of the transverse processes and lateral laminae with facetectomy is performed and the posterior instrumentation is reinforced with abundant cadaveric bone graft mixed with autogenous graft harvested from the spinous processes. Iliac crest bone cannot be obtained in most of these patients due to various degrees of osteoporosis. Drains are not routinely placed, but meticulous closure of the lumbosacral fascia is essential to obliterate dead space and facilitate wound healing. No postoperative immobilization or external trunk support is used. The patients are mobilized early to an upright position and are engaged to a physical therapy program. Their wheelchair is modified to adapt with the corrected seating posture.
Surgical considerations Levels of fusion The extent of the spinal fusion in patients with CP depends on the type of the scoliotic curve. For group 1 curves, the same fusion-level criteria are used as for idiopathic scoliosis.7,10 In idiopathic scoliosis it is better to fuse the curvature short using instrumentation, in order to achieve satisfactory curve correction and spinal stabilization, but also preserve as many mobile spinal segments as possible.3 Long C-shaped thoracolumbar or lumbar curves that cause severe pelvic obliquity and usually occur in non-ambulators, require extension of the spinal fusion from the upper thoracic spine to the sacrum with pelvic fixation with the
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Figure 2 Preoperative anteroposterior (a) and lateral (b) radiographs of the spine of a 12-year-old patient with total body involvement CP showing a severe collapsing thoracolumbar C-shaped scoliosis measuring 1301 with associated marked pelvic obliquity (black line). The patient had very poor sitting tolerance due to significant spinal pain as well as pain from impingement of the ribs against the left iliac crest on the concavity of the scoliosis.
aim to restore truncal balance.1,4,10,26 The arthrodesis should not stop proximally in the mid-thoracic area, but should extend to T1 or T2 to prevent the development of an add-on kyphotic deformity proximal to the most cephalad instrumented level.10,26,49 Whenever significant pelvic obliquity follows the scoliotic curvature, the instrumented fusion should include the pelvis to provide satisfactory correction of the spinal decompensation and reduce the risk of recurrent deformity.3–5,26 Recurrent distal scoliotic deformity requiring revision surgery and extension of the arthrodesis to include the lumbosacral joint has been previously reported in children with CP who underwent short initial fusions.47 It has been traditionally believed that fusion to the pelvis should be avoided in ambulatory patients in whom the scoliotic deformity is only occasionally associated with pelvic obliquity.1,7,26,50–52 There are no published reports documenting that fusion to the pelvis will decrease the ambulatory capacity of children with CP. This widespread orthopaedic myth probably arose from the early attempts to instrument to the pelvis using straight Harrington rods, which removed all lumbar lordosis and created ‘‘lumbar flatback’’. Additionally, many of the instrumentation systems initially used in the surgical management of neuromuscular scoliosis were not rigid enough to achieve a solid spine fusion without external trunk support and required long periods of bed rest and body casting. A recent study of 24 patients has demonstrated that in ambulatory paediatric patients with spastic CP and neuromuscular scoliosis, spinal fusion with the Unit rod segmental instrumentation provided stable distal fixation to the pelvis,
achieved satisfactory correction of the deformity, and restored trunk balance in both the coronal and sagittal plane, without compromising the patient’s ability to ambulate.53 We believe that with immediate postoperative mobilization and by preserving normal sagittal plane alignment, ambulatory status is not affected by spine fusion extending to the pelvis. Pelvic obliquity Pelvic obliquity is a fundamental difference between an idiopathic and a neuromuscular scoliosis and has to be addressed during the surgical management of the scoliotic curve. It can arise from spinal–femoral, pelvic–femoral or spinal–pelvic muscle contracture.26 It may develop as the result of extension of the scoliotic deformity into the pelvis54 or due to asymmetric contractures of the hip abductors that creates hip imbalance, as part of the hip ‘‘wind-swept’’ deformity. A combination of both factors can occasionally coexist. Previous investigators have postulated that adductor contracture and hip subluxation may lead to pelvic obliquity, which is followed by the development of scoliosis.9 Anterior surgery Anterior release is intended to maximize the flexibility of the curvature and improve the correction using the posterior instrumentation. Thus it is indicated in the presence of severe curve stiffness. The flexibility of the curve can be assessed by obtaining longitudinal traction radiographs with the patient in the supine position or suspension anteroposterior views of the spine. Side-bending radiographs are not
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Figure 3 Anteroposterior (a) and lateral (b) radiographs of the spine of the patient in Fig. 2 following posterior spinal arthrodesis, which has achieved correction of the scoliosis to 251 and balancing of the pelvis (black line). The scoliosis was preoperatively flexible to 501; therefore, an anterior release was not required.
reliably reproduced in this population of patients due to poor compliance. Radiographs with the patient in trunk hyperextension can be obtained to evaluate the flexibility of kyphotic deformities. Estimation of the rigidity of the curve can be also achieved using the physical examination sidebending test introduced by Freeman Miller55 with the patient bent against the examiner’s knee. Combined anterior release/posterior fusion is indicated when curve correction to 40–501 cannot be obtained, when there is a fixed pelvic obliquity of more than 101 or when the thorax cannot be balanced over the pelvis.1,9,10 Recent studies have proved the advantages of combined anterior– posterior procedures to obtain better deformity correction in more severe and rigid curves, through a circumferential spinal arthrodesis, minimizing the risk of pseudarthrosis and curve progression.7,13,21,22,26,39,43,56 Since anterior surgery is intended to increase flexibility of the curve and not to provide a fusion, the use of anterior instrumentation is not recommended, because this will limit the amount of correction than can be achieved through the posterior instrumentation. Crankshaft phenomenon can occur in a very young patient who undergoes a posterior only spinal fusion for scoliosis.
Although the back of the spine is fused, the front of the spine continues to grow causing the twisting characteristic of the fusion mass. The use of the original Luque instrumentation did not prevent the development of crankshaft.13,45 However, Smucker and Miller57 have followed 29 children with open triradiate cartilages who underwent spine fusion with the Unit rod system until the end of their growth and found no progression of the deformity.
One or two-stage procedures There is much debate as to whether the anterior and posterior spinal arthrodesis should be staged. While there have been comparative studies of combined versus staged anterior–posterior spinal surgery in patients with neuromuscular scoliosis which mostly favour the single-stage procedures, they are all of mixed populations with different underlying neurological pathologies.58–63 Tsirikos et al.52 performed the only study on an isolated group of patients with CP. They showed that even though one-stage anterior–posterior spine operations in patients with spastic quadriplegia provided comparable results with the two-stage procedures in correcting spinal malalignment, they were
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Figure 4 Preoperative (a) and postoperative (b) clinical photographs of the patient in Figs. 2 and 3 showing restoration of a good spinal balance in both the coronal and sagittal planes following posterior spinal arthrodesis. The patient could postoperatively sit comfortably on his wheelchair without complaints of rib or spinal pain.
associated with a considerable mortality rate including three immediate postoperative deaths, increased operative morbidity and higher risk of technical complications. We believe that staged spinal procedures on different days is preferable in individuals with very large curves and concomitant medical illness.
Sagittal deformities Lipton et al.64 have recently reported their experience in correcting sagittal plane spinal deformities without concomitant scoliosis in 24 patients. The authors identified deterioration in sitting balance and back pain as the principal indications for surgery. Children with sagittal curves of 701 or greater were more likely to develop severe symptoms; they reported two patients with hyperlordosis presenting with superior mesenteric artery syndrome and one with loss of bowel and bladder function. All of these problems resolved after surgical correction of the deformity. Hyperkyphotic deformities associated with hamstring tightness are considerably improved after hamstring lengthening at an early stage. In the presence of an established kyphotic deformity causing functional problems posterior spine arthrodesis should be considered. This should extend from the cervico-thoracic junction to the pelvis to achieve maximum correction of the kyphotic curvature and prevent risk of proximal recurrent deformity and to control the posterior pelvic tilt. Rigid kyphotic curves need to be treated with anterior release followed by posterior spinal fusion. Excessive kyphosis may affect venous return to the heart and attention must be paid intraoperatively to maintain haemodynamic stability while correcting the deformity. In an earlier previous study, Tsirikos et al.34 have shown that the
presence of severe preoperative thoracic hyperkyphosis was the only deformity factor affecting survival rates and demonstrated statistically significant predictability for a poor life expectancy after spine fusion in children with CP. Lumbar hyperlordosis secondary to hip flexion contractures can be treated initially by muscle lengthening procedures. Fixed lordotic curves require anterior closing wedge osteotomies prior to instrumented fusion. If there is an increased anterior pelvic tilt, the chance of the Unit rod penetrating the inner iliac table is significantly increased, either during insertion of the pelvic leg of the rod or whilst bending the rod in situ to correct the spinal curvature. This can be aggravated by the poor bone quality encountered in these patients. The use of pedicle screws in the lumbar spine may be necessary to allow for a better correction of the increased lordosis or to provide bony fixation in patients who underwent previous laminectomies, but placing pedicle screws if there have been previous dorsal rhizotomies is very demanding, as the posterior vertebral anatomy is distorted due to the multiple laminectomies. In the presence of increased lordosis insertion of the Unit rod into the pelvis can be particularly difficult. To deal with this problem, the rod is cut on one side at the thoracolumbar region and the two pelvic legs inserted to the iliac bones separately. Then when pelvic fixation is achieved bilaterally, the two parts of the Unit rod can be then brought together and secured with rod connectors. When correction of a sagittal deformity is performed, the length of the Unit rod must be adjusted by 1–2 cm to allow for intra-operative lengthening (in hyperlordosis) or shortening (in hyperkyphosis) of the spinal column. In the presence of lumbar hyperlordosis the surgical management of scoliosis becomes significantly more difficult
ARTICLE IN PRESS 132 and the posterior instrumentation is very technically challenging. In a recent study35 excessive lumbar lordosis was associated with a high incidence of technical problems and an increased morbidity; patients with lordosis of more than 601 developed complications involving pelvic fixation of the Unit rod in 15.1% of the cases compared to 3.6% if the preoperative lordosis was less than 601.35 Additionally there was increased blood loss and operative time was prolonged.35 Surgery for hyperlordosis is complicated and is the component of the deformity which is technically most difficult to address using the Unit rod construct.
Postoperative management The patients are managed post-operatively in ICU and may require on assistive ventilation at least for the first night. This is normally necessary for patients with conditions such as tracheomalacia, pharyngeal dysfunction or after a complicated surgical procedure. Attention must be paid to fluid balance, pain management, and pulmonary care and close monitoring of the blood pressure, haemoglobin and electrolyte levels, blood coagulation times, and body temperature are very important. Nutritional support is essential and feedings should be started soon after surgery by central venous hyperalimentation until the patient is ready for gastrointestinal feeding. At that stage, the patients will need to be placed on nasogastric, nasojejunal or gastrostomy feeding depending on individual circumstances. Aggressive physiotherapy is necessary to encourage pulmonary toilet, deep breathing, and expectoration. The patient is mobilized in a newly adapted wheelchair as soon as possible. A reclining wheelchair can be used initially to provide better sitting comfort during the immediate postoperative period. The patient should be ready for discharge when the surgical wound is completely healed, is afebrile, sitting comfortably in a wheelchair, and feeding adequately. This is usually 7–10 days post-operatively. Full recovery should be anticipated by 6 months from surgery.
Postoperative complications The best predictor for the development of postoperative complications is the degree of neurological disability.15 The study by Lipton et al.15 showed that the presence of other disorders such as poor nutrition, gastrostomy feedings, antiseizure medication, tracheal abnormalities or tracheostomy did not constitute additional risk factors. However, other investigators have suggested that inadequate nutritional status increases the risk of urinary infections, prolonged patient intubation and hospital stay.33
A.I. Tsirikos, P. Spielmann involved patients, demonstrating clearly the intensive current medical support provided by the modern health systems. Thus CP should be considered as a disease with which one lives in contrast to the old belief that it should be regarded as a condition from which one dies.68–71 Nonetheless, predicting life expectancy for children and adolescents with CP is difficult. One study has demonstrated a relatively long mean predicted survivorship of 11.2 years for children and adolescents with severe spastic CP and neuromuscular scoliosis who underwent spine surgery.34 The most accurate predictor for survival rates in this group was the number of days spent postoperatively in the ICU. This at least partially reflects general medical status of each patient, particularly related to impaired respiratory function. The positive impact on the child of correcting the scoliotic deformity and maintaining a good coronal and sagittal spinal alignment is shown by a very high satisfaction rate among parents and professional caregivers, who appreciate the impact of spinal realignment surgery on the child’s level of function, sitting ability, physical appearance, comfort, and the ease of nursing care.13,14,72 In two more recent studies, the vast majority of the parents (95.8%) and caregivers (84.3%) who were interviewed considered that the benefits from correcting scoliotic deformity undoubtedly offset the possible risks from surgery, and would have no hesitation in recommending this procedure for children with CP who develop significant scoliosis interfering with their level of function and their overall quality of life.35,73
Summary Spine surgery in paediatric patients with CP who have severe neurological compromise and complex medical problems is technically difficult and there is an increased risk of lifethreatening complications. However, there is a well-documented positive impact on these children by correcting their deformity and maintaining a good coronal and sagittal spinal balance. Spinal arthrodesis is the only surgical procedure that has such a high satisfaction rate among parents and caregivers, especially for quadriplegic patients. With improved medical management and a multidisciplinary approach, life expectancy for this group is higher than previously reported and operative procedures to correct the spine have a definitive effect in improving the patients‘ quality of life.
Key points
Spinal deformity is a frequent orthopaedic problem in children and adolescents with CP.
The risk factors for developing scoliosis in patients with
Life expectancy/outcome after spine surgery While obviously parents should be counselled about prognosis, there is limited information on the predicted survivorship of patients with CP.65,66 Affected individuals were previously assumed to have lower survival rates than the general population,67 but recent studies have shown substantially better survival rates even for the total-body
CP are spastic quadriplegia, absence of ambulatory function, early onset, and thoracolumbar C-shaped curve patterns. The only treatment that addresses effectively spine deformity in these patients and has a well-documented positive impact in their quality of life is spinal arthrodesis using instrumentation. Patients with CP may have a host of medical comorbidities, which will need to be addressed prior to
ARTICLE IN PRESS Spinal deformity in cerebral palsy
scoliosis surgery and will require a well-coordinated multidisciplinary approach. Segmental spinal fixation with the use of the Unit rod instrumentation is simple to use, is considerably cheaper than newer third generation systems, and can provide optimum correction of both scoliosis and the associated pelvic obliquity in this group of patients with a low rate of complications and re-operations for technical problems. Life expectancy in children with CP is higher than previously reported and operative procedures to correct the spine have a definitive impact in improving their quality of life and are associated with a very high satisfaction rate among parents and professional caregivers.
Acknowledgemenrts The authors did not receive grants or outside funding in support of their research or preparation of this manuscript. They did not receive payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, educational institution, or other charitable or non-profit organization with which the authors are affiliated or associated.
References 1. Banta JV, Drummond DS, Ferguson RL. The treatment of neuromuscular scoliosis. AAOS Instruct Course Lect 1999;48: 551–61. 2. Bradford DS. Neuromuscular spinal deformity. In: Bradford D, Lonstein J, Ogilvie J, et al., editors. Moe’s textbook of scoliosis and other spinal deformities. Philadelphia, PA: WB Saunders; 1987. p. 271–305. 3. Herring JA. Disorders of the brain. In: Herring JA, editor. Tachjian’s pediatric orthopaedics. Philadelphia: WB Saunders; 2002. p. 1121–248. 4. Labelle H, Grimard G. Pediatric spine. In: Koval K, editor. Orthopaedic knowledge update 7: Home Study Syllabus. Am Acad Orthop Surg 2002:581–92. 5. Renshaw TS. Cerebral palsy. In: Morrissy RT, Weinstein SL, editors. Lovell and winter’s pediatric orthopaedics. Philadelphia, PA: Lippincott Williams & Wilkins; 2001. p. 563–99. 6. Majd ME, Muldowny DS, Holt RT. Natural history of scoliosis in the institutionalized adult cerebral palsy population. Spine 1997;22(13):1461–6. 7. Lonstein JE, Akbarnia A. Operative treatment of spinal deformities in patients with cerebral palsy or mental retardation. An analysis of one hundred and seven cases. J Bone Joint Surg Am 1983;65A:43–55. 8. Madigan RR, Wallace SL. Scoliosis in the institutionalized cerebral palsy population. Spine 1981;6(6):583–90. 9. Bradford DS, Hu SS. Neuromuscular spinal deformity. In: Lonstein JE, Winter RB, Bradford DS, Ogilvie JW, editors. Moe’s textbook of scoliosis and other spinal deformities. 3rd ed. WB Saunders; 1995. p. 295–322. 10. Lonstein JE. Spine deformities due to cerebral palsy. In: Weinstein SL, editor. The pediatric spine: principles and practice. 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 2001. p. 797–807. 11. Ferguson RL, Allen Jr BL. Considerations in the treatment of cerebral palsy patients with spinal deformities. Orthop Clin North Am 1988;19:419–25.
133 12. Kalen V, Conklin MM, Sherman FC. Untreated scoliosis in severe cerebral palsy. J Pediatric Orthop 1992;12:337–40. 13. Comstock CP, Leach J, Wenger DR. Scoliosis in total-bodyinvolvement cerebral palsy. Analysis of surgical treatment and caregiver satisfaction. Spine 1998;23(12):1412–24 discussion 1424–1425. 14. Cassidy C, Craig C, Perry A, Karlin LI, Goldberg MJ. A reassessment of spinal stabilization in severe cerebral palsy. J Pediatr Orthop 1994;14(6):731–9. 15. Lipton GE, Miller F, Dabney KW, Altiok H, Bachrach SJ. Factors predicting post-operative complications following spinal fusions in children with cerebral palsy. J Spinal Disord 1999;12: 197–205. 16. Edebol-Tysk K. Epidemiology of spastic tetraplegia cerebral palsy in Sweden. I. Impairments and disabilities. Neuropaediatrics 1989;20:41–5. 17. Miller A, Temple T, Miller F. Impact of orthoses on the rate of scoliosis progression in children with cerebral palsy. J Pediatr Orthop 1996;16(3):332–5. 18. Saito N, Ebara S, Ohotsuka K, Kumeta H, Tkaika K. natural history of scoliosis in spastic cerebral palsy. Lancet 1998;351:1687–92. 19. Garrett AL, Perry J, Nickel VL. Paralytic scoliosis. Clin Orthop 1961;21:117–24. 20. Horstman H, Boyer B. Progression of scoliosis in cerebral palsy patients after skeletal maturity. Dev Med Child Neurol 1984;26:261. 21. Thometz JG, Simon SR. Progression of scoliosis after skeletal maturity in institutionalized adults who have cerebral palsy. J Bone Joint Surg (Am) 1988;70A:1290–6. 22. Rinsky LA. Surgery of spinal deformity in cerebral palsy. Twelve years in the evolution of scoliosis management. Clin Orthop 1990;253:100–9. 23. Song EW, Lenke LG, Schoenecker PL. Isolated thoracolumbar and lumbar hyperlordosis in a patient with cerebral palsy. J Spinal Disord 2000;13:455–60. 24. Shook JE, Lubicky JP. Paralytic scoliosis. In: Bridwell KH, Dewald RL, editors. Textbook of spinal surgery. 2nd ed. Philadelphia: Lippincott-Raven; 1977. p. 835–79. 25. Lonstein JE, Renshaw TS. Neuromuscular spine deformities. AAOS Instruct Course Lect 1987;36:285–304. 26. McCarthy RE. Management of Neuromuscular scoliosis. Orthop Clin North Am 1999;30(3):435–49. 27. Bunnel WP, MacEwen GD. Non-operative treatment of scoliosis in cerebral palsy: preliminary report on the use of a plastic jacket. Dev Med Child Neurol 1977;19:45–9. 28. Thometz JG, Simon SR. Progression of scoliosis after skeletal maturity in institutionalized adults who have cerebral palsy. J Bone Joint Surg (Am) 1988;70A:1290–6. 29. Terjesen T, Lange JE, Steen H. Treatment of scoliosis with spinal bracing in quadriplegic cerebral palsy. Dev Med Child Neurol 2000;42:448–54. 30. Bunch WH. The Milwaukee brace in paralytic scoliosis. Clin Orthop 1975;110:63–8. 31. Anderson PR, Puno MR, Lovell SL, Swayze CR. Post-operative respiratory complications in non-idiopathic scoliosis. Acta Anaesth Scand 1985;29(2):186–92. 32. Winter S. Pre-operative assessment of the child with neuromuscular scoliosis. Orthop Clin North Am 1994;25(2):239–45. 33. Jevsevar DS, Karlin LI. The relationship between preoperative nutritional status and complications after an operation for scoliosis in patients who have cerebral palsy. J Bone Joint Surg (Am) 1993;75A:880–4 (published erratum appears in J Bone Joint Surg (Am) 1993;75A:1256). 34. Tsirikos AI, Chang W-N, Dabney KW, Miller F, Glutting J. Life expectancy in paediatric patients with cerebral palsy and neuromuscular scoliosis who underwent spinal fusion. Dev Med Child Neurol 2003;45:677–82.
ARTICLE IN PRESS 134 35. Tsirikos AI, Chang WN, Dabney KW, Miller F. The outcome of spinal fusion using the Unit rod instrumentation in pediatric patients with cerebral palsy and spinal deformity. J Bone Joint Surg (Br) 2004;86B(Supplement II):118. 36. Kreutz W, Linde R, Funk M, Meyer-Schrod R, Foeli E, NowakGoettl U, et al. Induction of von Willebrand disease type I by valproaic acid. Lancet 1990;335(8701):1350–1. 37. Shah SA, Presedo A, Dabney KW, Miller F. The risk of scoliosis progression after intrathecal baclofen therapy in cerebral palsy patients. Abstracts of the 10th annual meeting of the Scoliosis Research Society 2005;109. 38. Luque ER. Segmental spinal instrumentation for correction of scoliosis. Clin Orthop 1982;163:192–8. 39. Bonnett C, Brown JC, Grow T. Thoracolumbar scoliosis in cerebral palsy. J Bone Joint Surg (Am) 1976;58A:328–36. 40. McDonnell MF, Glassman SD, Dimar JR, et al. Perioperative complications of anterior procedures on the spine. J Bone Joint Surg (Am) 1996;78A:839–47. 41. Luque E. The anatomic basis and development of segmental spinal instrumentation. Spine 1982;7(3):256–9. 42. Allen Jr BL, Ferguson RL. L-rod instrumentation for correction of scoliosis in cerebral palsy. J Pediatr Orthop 1982;2:87–96. 43. Swank S, Cohen D, Brown J. Spinal fusion in cerebral palsy with L-rod segmental spinal instrumentation: a comparison of single and two-stage combined approach with Zielke instrumentation. Spine 1989;12:750–9. 44. Gau YL, Lonstein JE, Winter RB, Koop S, Denis F. Luque–Galveston procedure for correction and stabilization of neuromuscular scoliosis and pelvic obliquity: a review of 68 patients. J Spinal Disord 1991;4:399–410. 45. Sussman MD, Little D, Alley RM, McCoig JA. Posterior instrumentation and fusion of the thoracolumbar spine for treatment of neuromuscular scoliosis. J Pediatr Orthop 1996;16:304–13. 46. Boachie-Adjei O, Lonstein JE, Winter RB, Koop S, vanden Brink K, Denis F. Management of neuromuscular deformities with Luque segmental instrumentation. J Bone Joint Surg (Am) 1989;71A:548–62. 47. Dias RC, Miller F, Dabney K, et al. Revision spine surgery in children with cerebral palsy. J Spinal Disord 1997;10:132–44. 48. Bell DF, Moseley CF, Koreska J. Unit rod segmental spinal instrumentation in the management of patients with progressive neuromuscular spinal deformity. Spine 1989;14(12):1301–7. 49. Broom MJ, Banta JV, Renshaw TS. Spinal fusion augmented by Luque-rod segmental instrumentation for neuromuscular scoliosis. J Bone Joint Surg (Am) 1989;71A:32–44. 50. Allen BL, Ferguson RL. The Galveston technique for L-rod instrumentation of the scoliotic spine. Spine 1982;7(3):284–6. 51. Allen BL, Ferguson RL. A 1988 perspective on the Galveston technique of pelvic fixation. Orthop Clin 1988;19(2):409–18. 52. Tsirikos AI, Chang W-N, Dabney KW, Miller F. Comparison of onestage versus two-stage anteroposterior spinal fusion in pediatric patients with cerebral palsy and neuromuscular scoliosis. Spine 2003;28(12):1300–5. 53. Tsirikos AI, Chang W-N, Shah SA, Dabney KW, Miller F. Preserving ambulatory potential in pediatric patients with cerebral palsy who undergo spinal fusion using unit rod instrumentation. Spine 2003;28(5):480–3.
A.I. Tsirikos, P. Spielmann 54. Letts M, Shapiro L, Mulder K, Klassen O. The windblown hip syndrome in total body cerebral palsy. J Pediatr Orthop 1984;4:55–62. 55. Miller F. Spine. In: Miller F, editor. Cerebral palsy. Singapore: Springer; 2005. p. 433–522. 56. Brown JC, Swank S, Specht L. Combined anterior and posterior spine fusion in cerebral palsy. Spine 1982;7(6):570–3. 57. Smucker JD, Miller F. Crankshaft effect after posterior spinal fusion and unit rod instrumentation in children with cerebral palsy. J Pediatr Orthop 2001;21:108–12. 58. Ferguson RL, Hansen MM, Nicholas DA, Allen Jr BA. Same-day versus staged anterior-posterior spinal surgery in a neuromuscular scoliosis population: the evaluation of medical complications. J Pediatr Orthop 1996;16(3):293–303. 59. Hopf GH, Eysel P. One-stage versus two-stage spinal fusion in neuromuscular scoliosis. J Pediatr Orthop B 2000;9:234–43. 60. O’Brien T, Akmakjian J, Ogin G, et al. Comparison of one-stage versus two-stage anterior/posterior spinal fusion for neuromuscular scoliosis. J Pediatr Orthop 1992;12:610–5. 61. Shufflebarger HL, Grimm JO, Bui V, et al. Anterior and posterior spinal fusion: staged versus same-day. Spine 1991;16:930–3. 62. Powell IV ET, Krengel III WF, King HA, et al. Comparison of sameday sequential anterior and posterior spinal fusion with delayed two stage anterior and posterior spinal fusion. Spine 1994;19:1256–9. 63. McDonnell MF, Glassman SD, Dimar JR, et al. Perioperative complications of anterior procedures on the spine. J Bone Joint Surg (Am) 1996;78A:839–47. 64. Lipton GE, Letonoff EJ, Dabney KW, Miller F, McCarthy HC. Correction of sagittal plane spinal deformities with unit rod instrumentation in children with cerebral palsy. J Bone Joint Surg Am 2003;85A:2349–57. 65. Nelson KB, Swaiman KF, Russman BS. Cerebral palsy. Swaiman KF, editor. Pediatric neurology, vol. 1. St Louis: Mosby; 1994. p. 471–88. 66. Strauss DJ, Shavelle RM, Anderson TW. Life expectancy of children with cerebral palsy. Pediatr Neurol 1998;18:143–9. 67. Crichton JU, MacKinnon M, White CP. The life expectancy of persons with cerebral palsy. Dev Med Child Neurol 1995;37:567–76. 68. Evans PM, Evans SJ, Alberman E. Cerebral palsy: why we must plan for survival. Arch Dis Childhood 1990;65:1329–33. 69. Plioplys AV, Kasnicka I, Lewis S, Moller D. Survival rates among children with severe neurologic disabilities. South Med J 1998;91:161–72. 70. Hutton JL, Cooke T, Pharoah PO. Life expectancy in children with cerebral palsy. Br Med J 1994;309:431–5. 71. Hutton JL, Colver AF, Mackie PC. Effect of severity of disability on survival in northeast England cerebral palsy cohort. Arch Dis Childhood 2000;83:468–74. 72. Sponseller PD, Whiffen JR, Drummond DS. Interspinous process segmental spinal instrumentation for scoliosis in cerebral palsy. J Pediatr Orthop 1986;6:559–63. 73. Tsirikos AI, Chang W-N, Dabney KW, Miller F. Comparison of parents’ and caregivers’ satisfaction after spinal fusion in children with cerebral palsy. J Pediatr Orthop 2004;24(1): 54–8.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 135–144
Available at www.sciencedirect.com
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HAND
Osteoarthritis of the thumb trapeziometacarpal joint Sameer Batra, R. Kanvinde Hand Service, Department of Orthopaedics, Gwynedd Hospital, North West Wales NHS Trust, 4, Llys Miaren, Bangor, Gwynedd LL57 2PG, UK
KEYWORDS Osteoarthritis; Thumb; Trapeziometacarpal joint; Surgery
Summary Trapeziometacarpal osteoarthritis is a very common condition, with radiological changes prevalent in 30% of post-menopausal women but a large number being asymptomatic. A lack of bony constraints and laxity of the supporting ligaments, particularly the ‘‘beak’’ ligament is consistently implicated in disease progression. The severity can be staged according to the radiological appearance, which does provides a conceptual framework for rationale of treatment. Fortunately, roles for both conservative and surgical options currently exist to successfully treat joint pain and restore joint stability. The surgical options range from ligament reconstruction or osteotomy for early painful laxity, through to trapeziectomy, arthrodesis and arthroplasty for more severe osteoarthritis. The success of ligament reconstruction tendon interposition arthroplasty in treating trapeziometacarpal arthritis has withstood the test of time. Trapeziometacarpal joint replacement ranges from elastomeric spacers and true total joint replacement to the more current hemiarthroplasty designs with varying results. A better understanding of surgical outcomes for advanced arthritis requires long-term prospective outcome studies while the pursuit for an ideal trapeziometacarpal arthroplasty continues. & 2007 Elsevier Ltd. All rights reserved.
Epidemiology As the humans climbed the evolutionary ladder, the refinement to a dominant prehensile digit to perform myriad functions and movements led to compromise of the stability at the base of thumb. Recession of the palmar metacarpal beak facilitated rotational movements of the thumb ray and the ‘‘residual’’ beak ligament assumed the task of stabilizing the metacarpal in lateral pinch. Ironically these attritional Corresponding author. Tel.: +44 7915053576; fax: +44 1248384935. E-mail addresses:
[email protected] (S. Batra),
[email protected] (R. Kanvinde).
0268-0890/$ - see front matter & 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2007.02.006
changes in the same ligament integral to diverse mobility of thumb appear to be responsible for the pervasive problem of osteoarthritis of the trapeziometacarpal joint (TMJ) in the contemporary hand. Although the thumb TMJ is the second most common hand joint afflicted by osteoarthritis (following the distal interphalangeal joints), it is the most common site for which surgery is sought because of the profound impact on hand function, strength and dexterity and disabling symptoms.1 About 1 in 4 women (in fact, 30% of post-menopausal women) and 1 in 12 men eventually have radiological changes of osteoarthritis at the TMJ, but again the vast majority are asymptomatic.2 The overwhelming female predilection is attributable to anatomic (a smaller less congruous shallow saddle joint, flat trapezial facet),
ARTICLE IN PRESS 136 hereditary (dysplastic joint surfaces) and hormonal factors (increased ligament laxity) all resulting in greater joint contact pressure.3 To date there is no longitudinal natural history study suggesting that TMJ arthritis is caused by certain repetitive work practices. However there is a strong association between excessive joint laxity and the development of premature joint degenerative changes.4
Anatomy and biomechanics The TMJ is a uniquely structured biconcave-convex saddle joint in comparison to the hinge-type joints that dominate the hand. It consists of four articulations: trapeziometacarpal (TM), trapeziotrapezoid (TT), scaphotrapezial (ST) and trapezium-index metacarpal (TIM) articulations. North and Eaton observed that radiographic disease most commonly affects TM and ST joints lying along the longitudinal compression axis of the thumb and typically spares the TT and TIM articulations. The disparate radii of curvature result in large loads being transmitted across small surface areas through much of the range of motion. It has been calculated, using three-dimensional analysis, that during simple pinch of 1 kg force at the finger tips, the joint compression force at the TMJ is 12 kg and increasing to as much as 120 kg during strong grasp. The paucity of bony constraints and intrinsic osseous stability forces the TMJ to rely on static ligamentous constraints to limit metacarpal base translation, which subjects the joint to abnormal pressure loads. The trapezium endures both axial and cantilever stress loads, particularly during lateral pinch and grasp maneuvers.5 Bettinger et al.6 in arthroscopic studies on complex ligamentous anatomy of TMJ described 16 ligaments that stabilize the joint (Fig. 1) (Table 1).
S. Batra, R. Kanvinde Current research, based on biochemical and histologic analysis, continues to describe the ‘‘beak ligament’’ as being the primary restraint to dorso-radial subluxation. The intracapsular ‘‘beak ligament’’ is so named because its obliquely oriented fibers originate just ulnar to the volar styloid process of the first metacarpal base (beak) which may include the anterior oblique ligament (AOL), first intermetacarpal ligament, and ulnar collateral ligament and insert onto the palmar tubercle on the central apex of the trapezium. A predominant palmar pattern of articular surface destruction has been associated with beak ligament attrition (known to occur before cartilaginous destruction) and gross ligament detachment from the native position, which has led to the popularity of ligament reconstruction. Biochemical analysis of the arthritic hyaline cartilage reveals a
Table 1 joint.
Major ligaments of the trapeziometacarpal
Deep anterior oblique Superficial anterior oblique Dorso-radial Ulnar collateral Intermetacarpal Dorsal intermetacarpal
Beak ligament, primary trapeziometacarpal joint stabilizer, pivot point, limits dorsal translation Helps stabilize volar metacarpal subluxation Shortest and thickest ligament in the trapeziometacarpal joint Helps limit volar subluxation Stabilizes metacarpal during radiovolar translation May help restrain metacarpal from collapse after trapezial excision
Figure 1 Anatomy and ligaments of the trapezio-metacarpal joint. (a) Volar and (b) Dorsal views. APL ¼ Abductor pollicis longus, AOL ¼ Anterior oblique (Beak) ligament, UCL ¼ Ulnar collateral ligament, MC ¼ Metacarpal; IML ¼ Intermetacarpal ligament, DRL ¼ Dorso-radial ligament, POL ¼ posterior oblique ligament.
ARTICLE IN PRESS Osteoarthritis of the thumb trapeziometacarpal joint selective loss of glycosaminoglycan from the extracellular matrix and sparing of the collagenous network in the palmar region, where osteoarthritic disease first originates.7 Six other ligaments play contributing roles in TMJ stability. The superficial AOL is longer than the deep AOL and provides the laxity necessary for pronation. The dorsoradial ligament assisted by intermetacarpal ligament; is the shortest and thickest ligament of the TM joint and the first to become taut during dorsoradial subluxation6 however, its significance in providing TM stability has been debated.6 The dorsal intermetacarpal ligament may also help restrain the first metacarpal from collapsing proximally after trapezial excision.
Mechanisms underlying the development of trapeziometacarpal osteoarthritis Articular configuration The articular surface of the trapezium is divided into two slightly concave surfaces, volar and dorsal by an oblique bony ridge. The subtle differences in the curvature of the TMJ surfaces result in there being no position in which they fit together well allowing the joint to sublux during pinch and grasp unless adequately restrained by the surrounding soft tissue structures.
Ligamentous tension The mechanism of ligament laxity was identified in cadaveric studies by Pellegrini7 as one of the key factors underlying the development of TMJ osteoarthritis by allowing excessive shear forces at the joint, altering contact wear patterns.
Muscular activity With incompetence of the volar oblique ligament, dorsal subluxation of the base of the metacarpal progresses unchecked, and two thenar muscles with potential to counter this are abductor pollicis brevis and opponens pollicis. Because the distal aspect of the first metacarpal is dynamically tethered to the second metacarpal by the adductor pollicis muscle, subluxation of its base where the abductor pollicis longus (APL) inserts causes an adducted posture of the first metacarpal. This leads to progressive functional deficit as activities like spreading the hand and palm around jar lids is compromised. Continued efforts to perform these activities lead to the thumb assuming a collapsed deformity of flexion at the TMJ, hyperextension at the metacarpophalangeal (MCP) joint and reciprocal flexion at the interphalangeal (IP) joint.
Changes to contact wear patterns Early work by Pellegrini7 determined that the volar compartment is the major area of joint contact during lateral pinch in the normal joint. Dynamic testing of 20 cadaveric forearm specimens revealed that positioning the TMJ in 301 flexion unloaded the volar compartment, moving
137 the centre of contact pressure dorsally. Thus, suggesting that limiting the amount of joint subluxation, metacarpal pronation, and/or hyperextension will alter the joint contact wear patterns, and may have a role in delaying the development of TMJ osteoarthritis.
Diagnosis Clinical presentation Diagnosis is based on clinical findings such as pain, dropping objects, oedema, instability, limited range of motion, and joint deformities. Typical patients include postmenopausal women with disabling pain at the thumb base, often radiating to the thenar eminence or MCP joint, men with a history of repetitive occupational joint use or trauma and young women with generalized ligamentous laxity and joint hypermobility.8 Carpal tunnel syndrome, De Quervain’s disease, and trigger finger are frequently encountered in patients with TMJ osteoarthritis, as a result of synovial thickening and wrist ganglia attributable to capsular defects. Stiffness is usually not a feature of early disease. Osteophytes may, however, lead to limited motion, eventually resulting in a dorsally fixed and subluxed joint that is adducted, with limited palmar abduction and compensatory MCP joint hyperextension.8 Provocative tests that elicit pain in the TMJ have been described and include the axial compression adduction test, axial compression rotation test (grind test), and the distraction test. The critical determination at the MP joint is the degree of hyperextension during thumb pinch because hyperextension collapse would need to be addressed along with surgical reconstruction of the TMJ.
Diagnostic radiographic assessment and staging Radiographs of the thumb in three planes and the special basal joint stress views are helpful in confirming the diagnosis. Further evidence of painful laxity of the TMJ can be obtained from an Eaton and Littler stress radiograph. This radiograph consists of a PA 301 oblique view centred on both thumbs (the plane of the thumb nails is parallel to the X-ray plate), which is taken when the patient’s thumb tips are touching and being pushed against each other. This stresses the TMJ causing radial subluxation. If the TMJ is lax then, on these radiographs, 50% of the articular surface of the base of the thumb metacarpal lies radial to the trapezial articular surface. An additional view, the pinch lateral, can also be obtained preoperatively to allow later comparison with longitudinal follow up radiographs. The best AP view to show the four trapezial articular facets and often the trapezio-metacarpal osteophyte next to the index metacarpal, is the Robert pronated view (Fig. 2). This is obtained by fully pronating the forearm and internally rotating the shoulder, thus allowing the dorsal surface of the thumb to be placed next to the X-ray plate.9 Historically, several staging systems have been created to correlate radiographic evidence of TM arthritis with clinical symptomatology. Eaton and Glickel’s staging system presented in 198710 (originally described in 1973 by Eaton & Littler) for roentgenographic appearances is extensively used to define the severity of disease into four stages.
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Management Non-surgical treatment The first line of treatment of TMJ osteoarthritis is nonsurgical and includes rest, splinting, anti-inflammatory drugs, steroid injections, physiotherapy, and patient education, usually offered on a 3-month trial. (i) Splintage and hand therapy As heavy stresses are placed on the TMJ, particularly during pinching or grasping, splintage can be useful. A variety of thermoplastic splinting options exist; from a small short opponens splint which supports the TMJ and MCP joint, to a much larger long opponens splint, which includes both the MCP joint and the wrist. Therapists may be able to provide advice on avoiding activities that may lead to thumb metacarpal adduction and on maintaining the first web space and strengthening the thenar muscles.
Figure 2 Robert’s view depicting advanced trapeziometacarpal OA. Subluxation of the first metacarpal bone has occurred. The severity of the malalignment is estimated by the hyperextension at the metacarpophalangeal joint. Osteophytes and sclerosis are present with joint space destruction.
A stage V has recently been suggested to account for pantrapezial arthritis.11 Therapeutically, the real value of this classification is to recognize painful laxity of the TMJ and help to differentiate between patients with isolated ST arthritis and those with TMJ arthritis. Approximately 90% of patients with osteoarthritis at the base of the thumb have isolated TMJ osteoarthritis whereas the remaining 10% have osteoarthritis involving both the TMJ and the articulation between the trapezium, the trapezoid and the scaphoid (STT joint).
Staging of osteoarthritis of the first carpometacarpal joint, as described by Eaton and Glickel
(ii) Intra-articular steroid Injections The beneficial effects of steroids in osteoarthritic joints compared with placebo have been shown to be short-lasting and confined to three weeks only. A recent randomised controlled trial12 showed that no clinical benefit was gained from intra-articular TMJ steroid injection in moderate to severe osteoarthritis compared with placebo injection. Day et al.13 in a prospective analysis of a single intraarticular steroid injection followed by 3 weeks of splinting in 30 thumbs demonstrated 40% substantial relief regardless of radiographic stage. Eighty per cent of Eaton stage I patients experienced pain relief at 18 months; only 25% of stage IV patients and approximately 35% of stages II and III patients had sustained relief. These findings suggest that patients with Eaton stage I disease can be successfully treated with a steroid/splinting regimen, but as osteophytes develop and joint narrowing progresses (stages II and III), results become less predictable. Repeated steroid injections should be avoided, as they can further weaken the joint capsule. Furthermore, due to potential complications including fat necrosis, depigmentation and radial nerve neuritis, steroid injection therapy should be used judiciously in the management of this condition.
Stage Criteria I II
III
IV
Normal articular contours; joint space may be widened due to effusion or ligamentous laxity. Joint space is slightly narrowed but articular contours maintained and there is minimal sclerosis of the subchondral bone. Joint debris and osteophytes o2 mm. ST joint is normal. Markedly narrowed or obliterated joint space with cystic changes, sclerotic bone, and osteophytes 42 mm in size. Varying degrees of subluxation, and the ST joint not affected. Complete obliteration of the joint space with signs of pantrapezial arthritis. Large osteophytes with marked subchondral sclerosis are present along with osteoarthritic changes of the ST joint.
(iii) Adaptations Education about techniques of joint protection can assist in controlling symptoms and delay the need for surgical intervention. These may include use of assistive devices (e.g., tap turners), use of splints or instruction in ways to change their technique for performance of specific tasks (e.g., lifting with two hands).
Surgical management Surgical reconstruction is indicated when non-operative treatment measures have failed to relieve pain and improve thumb function. So although staging can help preoperative planning, patient education and prognostication, the ultimate determinant of accurate diagnosis of the extent of
ARTICLE IN PRESS Osteoarthritis of the thumb trapeziometacarpal joint
Table 2 Treatment options for osteoarthritis of the trapeziometacarpal joint. Conservative NSAIDS Intra-articular steroid injection Splints Operative JLigament reconstructions JTrapezial resection procedures Partial trapezium resection and tendon interposition Complete trapezium resection ’Resection arthroplasty ’Distraction Resection arthroplasty ’Tendon interposition ’Ligament reconstruction and tendon interposition ’Ligament reconstruction JImplant arthroplasty Hemiarthroplasty ’Trapezial stemmed component Ashworth–Blatt ’Metacarpal stemmed component Kessler Swanson titanium Interposition arthroplasty Swanson silicone Eaton Niebauer Proplast Goretex Spherical Interposition arthroplasty Total joint arthroplasty Cafiniere Braun Mayo Steffee Nahigian Ledoux JMetacarpal Osteotomy JArthrodesis
disease and reconstructive procedures is the intraoperative assessment by surgeon. This is because of the poor correlation between radiographic findings and clinical symptomatology and variation in reliability of the Eaton classification system with reported intra-observer and interobserver reliability varying from 0.529 to 0.657 (Table 2). The choice of operative procedure is tailored to the individual patient, with factors being the patient’s age and functional demands, including occupation and activities, and the extent and stage of disease. Currently, the most accepted treatments are variations of the trapezial resection suspension arthroplasty introduced by Eaton and Littler.4 Fundamentally, the specific procedure selected will depend on the presence of cartilage erosion at TMJ and ST joint (i.e. stage I vs. Stage II–IV).
139 (A) Stage I disease There are no clear objective criteria that define the need for surgical intervention at stage I (Painful laxity of TMJ joint) with no radiographic evidence of degenerative disease (‘‘prearthritic stage’’). Extra-articular reconstruction procedures have been described which aim to relieve pain, improve stability and attempt to prevent the progression of osteoarthritis. These include volar ligament reconstruction (Eaton) using flexor carpi radialis (FCR) and others using ECRL and APL. Alternatively, a metacarpal osteotomy may be performed as an effective biomechanical alternative to ligament reconstruction to redistribute TMJ contact area and load. Ligament reconstruction. Stabilization of the TMJ joint by isolated reconstruction of the beak ligament should only be performed in Stage I disease. However, for long-term success, the articular surfaces must be eburnation-free which can be best assessed intraoperatively. The most commonly used is modified technique described by Eaton and Littler4 using 50% of the width of the FCR tendon. Through a palmar approach, half of the FCR tendon is harvested through either a proximal extension of the incision or through a series of short transverse incisions. After capsulotomy, the articular surfaces are inspected and the tendon split longitudinally for 8–10 cm from its insertion proximally detaching the radial half. The strip of FCR tendon is then passed through a tunnel drilled in the base of the thumb metacarpal, from its dorsal surface to its ulnar rim; any subluxation of the TMJ is reduced by abducting the thumb which then is stabilized with a Kirchner wire. The strip is then pulled tight and sutured to the periosteum on the dorsal surface of the thumb metacarpal at the exit site of the intraosseous tunnel. The residual length of the tendon strip is then passed over the palmar surface of the TMJ, around the intact portion of the FCR tendon and back on to the palmar capsule where it is sutured to itself. Metacarpal extension Osteotomy. Pellegrini and others have shown that incompetence of the beak ligament increases the volar shear stresses and lead to cartilage breakdown volarly.9 Extension osteotomy described by Wilson in 1973,14 has been shown to shift contact stresses dorsally and may give symptomatic relief in Stage I or minimal Stage II disease but not in advanced Stage III and IV arthritis. In a review of 41 thumbs at a mean of seven years, Hobby et al.15 found that 80% had achieved good or excellent pain relief. It has been proposed as best suited to high demand young individuals, as it is a more durable procedure than an arthroplasty and less restriction of motion than arthrodesis. However, it is not widely used and its outcome has never been compared with that of other procedures. When there is no laxity at an early stage, denervation has been16 shown to give immediate and satisfactory relief from pain, and can be used as palliative treatment in association with conservative measures. (B) Early stage II Although degenerative changes are clearly present in stage II, there is a spectrum of severity. Some authors feel that cases with no significant joint irregularity are amenable to treatment with volar ligament reconstruction alone.
ARTICLE IN PRESS 140
S. Batra, R. Kanvinde
Figure 3 (a) A lateral view shows the anticipated wedge of bone to be resected to afford an extension osteotomy and (b) completed osteotomy, (c) Trapeziectomy with ligament reconstruction and tendon interposition (LRTI) using flexor carpi radialis (FCR).
If progression of arthritis does occur, revision with interpositional arthroplasty can be added. Others recommend dorsal closing wedge metacarpal osteotomy to unload the volar TM joint (Fig. 3a and b). (C) Late stage II and stage III disease Surgical treatment of established TMJ arthritis has evolved over the last 6 decades since Gervis17 reported trapezial excision in 1949, with the addition of soft-tissue interposition by Froimson18 in 1970 and finally the addition of ligament reconstruction by Burton and Pellegrini in 1986.19 People with Eaton Stage III osteoarthritis show advanced degenerative changes and significantly greater trapezial tilt than people with Eaton Stage I or II. If disease is confined to TMJ, the bulk of the trapezium may be left in place and the joint space resurfaced with autogenous tendon but if the ST joint is also involved, both diseased articulations must be addressed. Procedures include metacarpal osteotomy, trapeziectomy with or without LRTI, interpositional arthroplasty, TMJ replacement or trapeziometacarpal arthrodesis. (a) Trapezial resection procedures (i) Excisional arthroplasty. Gervis first described Trapezial excision in 194917 who was so influenced by it that he underwent the procedure himself. This may be appropriate for cases of advanced Stage II to Stage IV disease or in the low demand older patients. The arthritic articulations are removed, which theoretically treats the source of pain; however, the instability persists, leading to weakness and a significant proximal migration of the first metacarpal with shortening of the thumb. All procedures that involve excision of the trapezium can be performed for patients with isolated TMJ osteoarthritis or combined TMJ and SST joint osteoarthritis. In an assessment of 34 simple trapezial excisions at 5-year follow-up, Varley et al.20 reported only 47% were completely pain-free. (ii) Interpositional arthroplasty. Froimson in 1970 first described Caroll’s concept of using a rolled up piece of FCR (‘anchovy’ spacer) inserted into the cavity left after trapeziectomy without ligament reconstruction.18 This
technique was then adapted using the APL tendon, lyophylized homologous dura mater and fascia lata as interpositional material. Although these procedures initially appeared to considerably decrease thumb shortening, it was subsequently noted that, over time, thumb length was lost due to the metacarpal settling into the interpositional material, and that no significant improvement in function was actually obtained. Swanson, in the mid-1960s, pioneered the use of silicone as an interpositional implant material. Alternative interpositional arthroplasties include procedures which excise either all or part of the trapezium, and interpose the space with materials such as costochondral allograft (Trumble) or expanded polytetrafluoroethylene (Gore-Tex) and polypropylene (Marlex) by Muermans and Coenen.21 (iii) Ligament reconstruction and tendon interposition. For disease limited to TM articulation, the technique used most commonly is the ligament reconstruction and tendon interposition arthroplasty (LRTI) described by Burton and Pellegrini in 1986 using half of the width of the FCR tendon to support the base of the thumb metacarpal after excision of the trapezium.22 The strip of the FCR tendon, with its insertion preserved, is passed through a drill hole in the base of the thumb (articular surface previously resected) and sutured to the periosteum on the dorsal aspect of the base of the thumb metacarpal. The remaining length of the FCR is then rolled up into an ‘anchovy’ and placed into the trapezial void. (Fig. 3c). The ligament reconstruction is protected with a Kirschner wire and a short arm thumb-spica cast for 4 weeks. Thereafter range-of-motion exercises are begun. In its current form, LRTI has yielded favourable results with regard to pain, grip strength and satisfaction in both short and long-term follow-up studies. Although preservation of trapezial height is widely thought to be pertinent for thumb strength, recently studies have failed to show a correlation between thumb key and tip pinch strengths and the height of the pseudarthrosis formed after trapeziectomy alone or with the addition of tendon interposition or LRTI. LRTI has been preferred when compared with silicone implant
ARTICLE IN PRESS Osteoarthritis of the thumb trapeziometacarpal joint replacement arthroplasty and the Ashworth-Blatt interposition implant arthroplasty.22 However, it is not absolutely clear whether these ligament reconstructions produce a stronger thumb than that produced by simple excision of the trapezium without any additional reconstruction procedure, and also whether they shorten the rehabilitation time. Technical variations. Numerous technical variations of LRTI have been described in the literature. Harvesting of the entire FCR versus one-half FCR has not been shown to produce any more morbidity, with respect to wrist strength or endurance. Other variations of LRTI centre on the use of different tendons, variations of tendon configurations, and/ or interposition material. Thompson23 described suspensionplasty: a technical modification using the abductor pollicis longus (APL), rather than the FCR tendon and a different graft configuration. The technique involves detaching half of the APL at its musculotendinous junction, and leaving its dorsal attachment to the thumb metacarpal intact. The APL is then passed retrograde through the dorsal bone hole and out the articular surface hole. The APL tendon is then passed through a second oblique bone tunnel from the trapezial facet of the index metacarpal and heading dorso-ulnarly on the index metacarpal. Next, the APL is woven into the extensor carpi radialis brevis tendon for added stability. Originally, this technique was intended for silicone arthroplasty salvage and only later became a primary procedure. (iv) Partial trapeziectomy. An alternative to the LRTI procedure after trapeziectomy is resection of only part of the trapezium and interposition with autogenous or other tissue. It allows the remaining trapezium to act as a spacer and buttress and to address only the arthritic joint surface. Theoretically, this would improve stability and thumb strength and lead to less proximal migration of the thumb ray. This type of arthroplasty is appropriate for Stage II and III disease Partial trapeziectomy does not allow evaluation of the ST joint, and it makes treatment of ST osteoarthritis technically more demanding. It is important to inspect the scaphotrapezial surfaces at the time of surgery to determine whether single or double interposition is needed as ST joint arthritis has been shown to be more prevalent at operation (62%) than on preoperative radiographs (32%). Nonetheless, with the development and proficiency of arthroscopic procedures, performing a partial trapeziectomy is becoming more prevalent. (b) Prosthetic TMJ arthroplasty. The goal besides eliminating painful articulating joint surfaces is to establish a stable force column during pinch and grip. The force transfer from thumb tip pinch to TMJ is amplified by a factor of 17X. Stability of prosthetic joint articulation must be sufficient to prevent significant metacarpal base subluxation. Competency of innate soft tissue envelope may alone be insufficient and augmentation by local tissues may be necessary for stabilty. Prosthetic joint replacement of the TMJ may be divided simply into three broad categories. (1) Arthroplasties that resurface either trapezium or metacarpal base for strict TMJ arthritis only and (2) trapezium replacement arthroplasties for patients with pantrapezial arthritis, and (3) total joint replacement.
141 (1) Resurfacing arthroplasties. The Swanson convex condylar implant designed for the thumb metacarpal base was one of the first TMJ resurfacing arthroplasties available. Swanson subsequently preferred using these for advanced cases of rheumatoid arthritis. Swanson, in 1984, developed a titanium implant for the TMJ to address the problem of silicone wear particles. However it was reserved for lowdemand patients due to high rates of loosening. A solution to the problem associated with implant instability was reported independently by Kessler and Axer24 and Ashworth et al.25 Kessler devised a prosthesis in the form of a thin silicone disc, which is interposed between the trapezium and metacarpal. The Kessler implant achieved stability by the use of an intramedullary stem, which was Dacron coated and fitted into the metacarpal shaft. The device by Ashworth et al. was a neurosurgical burr hole cover that had been trimmed to fit the surface of the trapezium and had a short stem that was fitted into the body of the trapezium. Both of these were unsuccessful and were abandoned because of problems with synovitis and instability. (2) Interposition arthroplasty. Swanson silicone prosthesis: Swanson pioneered the design of a silicone spacer for the trapezial space and reported excellent results but later reports raised concerns regarding abrasive microparticles producing silicone synovitis, which could cause bone erosion with recurrent pain and swelling, weakness, implant dislocation, fracture of the implant, deformation (cold flow), osteolysis and immunologic alterations. Unfortunately, the silicone prostheses tended to sublux and dislocate. Modifications to the implant, such as a cannulated prosthesis to allow ligament attachment and prosthesis with pegs to slot into the scaphoid and metacarpal, were subsequently developed which effectively overcame the problems of instability. This drew attention to the importance of correct implant seating and to the need for adequate capsular and ligamentous reconstruction. Although good long-term results with silicone implants have been reported, concern regarding silicone synovitis has led most surgeons to abandon this surgical option. Consequently silicone implants tend to be reserved for use in rheumatoid and elderly patients where demands are low. Eaton designed a perforated implant so that a slip of tendon (e.g. a slip of APL) could be passed through the implant and anchored to an adjacent carpal bone for stability and prevent subluxation or dislocation. Another major design change was that the stem is conical in shape, allowing axial rotation of the thumb. Poppen and Niebauer in 1978 introduced a Dacron mesh coated intramedullary stem to promote bony ingrowth, and heavy Dacron ties extended from the prosthesis into either the flexor carpi radialis or the index metacarpal for fixation to prevent subluxation or dislocation of the prosthesis. Sotereanos et al.26 published the longest retrospective follow-up study regarding the Niebauer implant in 1993 citing pain relief in 94%. They also found that 83% of the implants showed subluxation 9 years postoperatively. (3) Total joint replacement arthroplasty. TMJ prostheses most frequently used are ‘‘ball and socket’’ prostheses and may be classified according to their arc of mobility, or according to their mode of primary fixation (cemented,
ARTICLE IN PRESS 142 non-cemented), and to their secondary fixation (hydroxyapatite). De la Caffiniere in 197327 proposed a cemented prosthesis and others were described by Linscheid and Dobyns in 197928, Braun in 198229, and Ferrari and Steffee in 1986.30 Ledoux introduced a cementless prosthesis in 1990 and published his first report in 1994.31 The joint arthroplasty design of de la Caffienierre (Francobal) is very similar to that used in total hip arthroplasty and consists of a polyethylene cup that was fixed into the trapezium and a cobalt–chromium stem that was fixed into the shaft of the first metacarpal. The cemented total joint arthroplasties have presented difficulties, since the constrained, cemented, and articulated implants are all prone to loosening, failure, or dislocation and loss of motion secondary to fibrosis. Another major problem reported is perioperative complications (10%) due to the technically demanding nature of these arthroplasties and difficult revision. The cementless arthroplasty avoids the dislocations, weakness, and synovitis associated with silicone arthroplasties. It also avoids the weakness and instability associated with an interposition arthroplasty. Designs based on a ball-and-socket principle have not been deemed suitable for replacement of the TMJ. The de la Caffiniere prosthesis has the longest follow up, and although some surgeons have reported good long-term results others have recorded high rates of loosening and dislocation, including the designer himself. A study comparing the de la Caffiniere cemented and the Ledoux uncemented joint replacements, both of which are constrained ball-andsocket joints with a fixed centre of rotation of the prosthesis in the axis of the first metacarpal, showed failure rates respectively of 34% at 5 years and 41% at 2 years.32 Both prostheses induce major constraints: their axes do not correspond to the physiological axis, the spherical design does not allow normal translation and the implants are fixed in cancellous bone this is unable to withstand the stress. Currently, prostheses with a less constrained design are being developed. The concerns with implant arthropalsty remain: addressing the pain source(s); tissue compatibility; durability; implant loosening; dislocation; wear; subsidence and revisability. (c) Arthrodesis. Trapeziometacarpal arthrodesis has traditionally been the procedure chosen for younger, active people (often with a post-traumatic cause) who have high joint demands, requiring strong grip and pinch because of their occupation. It is indicated for people with Stage II–III osteoarthritis, i.e., without any ST joint involvement. While it provides stability, strength and pain relief, it does so at the expense of mobility and transfer of joint reaction forces to other joints. The techniques used include crossed Kirschner wires, cerclage wiring, cup-and-cone with a single oblique K-wire, tension band technique and plate and screw fixation has been used as one method of fixation. However, Forseth and Stern33 found that the hardware frequently needed removal (27%) and that patient satisfaction was lower than when Kirschner wires were used. The thumb is fused in a functional position of 201 of radial abduction and 401 of palmar abduction with the thumb tip resting on the middle phalanx of the index finger. Arthrodesis of the TMJ has become less popular because of its many drawbacks. The
S. Batra, R. Kanvinde fixed first–second intermetacarpal abduction angle precludes one from laying the palm flat or from drawing five digits into cone shape to fit narrow openings. Any patient with a stiff MP joint, a zig-zag collapse deformity, an adduction deformity of the metacarpal or a pan-arthritis is not a candidate for this operation. Furthermore, arthrodesis usually requires a prolonged period of immobilization, and is technically demanding with a risk of non-union (5–50%). Even the benefit in terms of strength has been questioned. Despite the significant loss of motion at the base of the thumb, and the inability to flatten the hand, minimal functional deficit has been reported. In a review of 52 thumbs, 85% were pain free at a mean follow-up of 4 years.33 (D) Stage IV osteoarthritis Until recently, the presence of stage IV disease implied that complete trapeziectomy with ligament reconstruction was necessary. Burton LRTI arthroplasty was the most popular technique used to accomplish this. Barron and Eaton described an alternative technique; double interposition arthroplasty. This technique retains much of the trapezium and resurfaces both the TM and ST joints, with the potential advantage of more predictable maintenance of thumb length. Alternatives procedures include trapeziectomy, trapeziectomy with LRTI, interpositional arthroplasties and TM and STT joint replacements. Interpositional arthroplasties for Stage IV osteoarthritis, such as the Swanson silicone implant arthroplasty and the Helal silicone rubber ball spacer remove the entire trapezium. A trapezium sparing double interposition joint replacement34 replaces both the TM and STT joints, and can be performed for Stage IV osteoarthritis.
Associated problems Metacarpophalangeal joint hyperextension: Regardless of the technique chosen for basal joint reconstruction, secondary collapse deformity at the MCP joint should be addressed. Disease at the TMJ can cause dorsal subluxation of the base of the metacarpal leading to metacarpal flexion and adduction and secondary MCP joint hyperextension and can be a distinct source of pain and poor outcome. If the hyperextension deformity is less than 301, and painless, then observation alone or placement of an oblique transarticular Kirschner wire with the joint in 301 of flexion for 4 weeks is appropriate. Alternatively or in conjunction with temporarily fixed flexion, the insertion of extensor pollicis brevis into the base of the proximal phalanx can be moved to metacarpal shaft. If hyperextension is greater than 301, options include palmar capsulodesis or arthrodesis. The latter is especially useful for a very unstable MPJ with degenerative changes and/or ulnar collateral ligament insufficiency as well as for a joint that exhibits little flexion.
Complications Although 80–90% of patients achieve a satisfactory result following a variety of surgical treatments, a minority complain of persistent pain and thumb weakness. The cause
ARTICLE IN PRESS Osteoarthritis of the thumb trapeziometacarpal joint for the persistent pain is a pre-existing condition other than TMJ osteoarthritis (in which case the characteristics of the persistent pain should be similar to the preoperative pain), or due to a complication of surgery. Both the dorsal sensory branch of the radial nerve and palmar cutaneous branch of median nerve are vulnerable to traction injury or laceration when dorsal and volar approaches are used as well as during harvesting of tendons. Damage to these can result in neuroma formation and complex regional pain syndrome.
Practice points
TMJ arthritis is the second most common degenerative
joint disease in the hand with more than 30% of postmenopausal women having characteristic radiological changes but the vast majority of these are asymptomatic. The beak ligament continues to be considered the primary stabilizer and is still implicated in the pathogenesis of TMJ arthritis. Current techniques that restore TMJ stability through ligamentous reconstruction such as the LRTI continue to produce consistently favourable results and have withstood the test of time. In Eaton stages 2–3 disease, the newer hemiarthroplasty designs may be an alternative to the traditional LRTI in patients with good bone stock. Silicone implant arthroplasty is generally reserved for low-demand patients with inflammatory arthritis or collagen vascular disease. Cemented total joint replacement of the TMJ is technically demanding and the results are not encouraging.
Implications for research
Need for further studies to evaluate the long-term
outcomes of the commonly used surgical procedures, in particular volar ligament reconstruction (without trapeziectomy) and LRTI. Randomized studies comparing techniques with common prognostic factors including stage with both objective and subjective outcome assessment and consistent timing of outcome measures. The development of an ideal trapezio-metacarpal joint arthroplasty design.
References 1. Nicholas RM, Calderwood JW. De la Caffiniere arthroplasty for basal thumb joint osteoarthritis. J Bone Joint Surg 1992;74B: 309–12. 2. Armstrong AL, Hunter JB, Davis TRC. The prevalence of degenerative arthritis of the base of the thumb in postmenopausal women. J Hand Surg 1994;19B:340–1. 3. Katarincic JA. Thumb kinematics and their relevance to function. Hand Clin 2001;17:169–74. 4. Eaton RG, Littler JW. Ligament reconstruction for the painful thumb carpometacarpal joint. J Bone Joint Surg 1973;55A: 1655–66.
143 5. Cooney W, Chao E. Biomechanical analysis of statm forces in the thumb during hand function. J Bone Joint Surg 1977;59A: 27–36. 6. Bettinger PC, Linscheid RL, Berger RA, Cooney W P, An KN. An anatomic study of the stabilizing ligaments of the trapezium and trapeziometacarpal joint. J. Hand Surg 1999;24B: 786–90. 7. Pellegrini Jr. VD. Osteoarthritis of the trapeziometacarpal joint: the pathophysiology of articular cartilage degeneration. I. Anatomy and pathology of the aging joint. J Hand Surg 1991;16A:967–74. 8. Poole JU, Pellegrini Jr. VD. Arthritis of the thumb basal joint complex. J Hand Ther 2000;13:91–107. 9. Robeit R. Bulletins et memoires de la Soclete de Radiologie Medicale de France 1936;24:687–94. 10. Eaton RG, Glickel SZ. Trapeziometacarpal osteoarthritis: staging as a rationale for treatment. Hand Clin 1987;3:455–71. 11. Tomaino MM. Thumb basal joint arthritis. In: Green DP, et al., editors. Green’s operative hand surgery. 5th Ed. New York: Churchill Livingstone; 2005. p. 461–85. 12. Meenagh GK, Patton J, Kynes C, Wright GD. A randomised controlled trial of intra-articular corticosteroid injection of the carpometacarpal joint of the thumb in osteoarthritis. Ann Rheum Dis 2004;63:1260–3. 13. Day CS, Gelberman R, Patel AA, Vogt MT, Ditsios K, Boyer MI. Basal joint osteoarthritis of the thumb: a prospective trial of steroid injection and splinting. J Hand Surg 2004;29:247–51. 14. Wilson J. Basal osteotomy of the first metacarpal in treatment of arthritis of the carpometacarpal joint of the thumb. Br J Surg 1973;60:854–8. 15. Hobby JL, Lyall HA, Meggitt BE. First metacarpal osteotomy for trapezlometacarpal osteoarthritis. J Bone Joint Surg 1998;80B: 508–12. 16. Cozzi EP. Denervation des Articulations du Poignet et de la Main. In: Tubiana R, editor. Trait de Chirurgie de la Main. Paris: Masson; 1991. p. 781–7. 17. Gervis WH. Excision of the trapezium for osteoarthritis of the trapeziometacarpal joint. J Bone Joint Surg 1949;42B:537–53. 18. Froimson A. Tendon arthroplasty of the trapeziometacarpal joint. Clin Orthop 1970;70:191–9. 19. Burton RI, Pellegrinl Jr. VD. Surgical management of basal joint arthritis of the thumb. Part II. Ligament reconstruction with tendon interposition arthroplasty. J Hand Surg 1986;11A: 324–32. 20. Varley GW, Calvey J, Hunter JB, Barton NJ, Davis TR. Excision of the trapezium for osteoarthritis at the base of the thumb. J Bone Joint Surg 1994;76B:964–8. 21. Muermans S, Coenen L. Interpositional arthroplasty with GoreTex, Marlex or tendon for osteoarthritis of the trapeziometacarpal joint. A retrospective comparative study. J Hand Surg 1998;23B:64–8. 22. Pellegrini VD, Burton RI. Surgical management of basal joint arthritis of the thumb. Part 1. Long-term results of silicone implant arthroplasty. J Hand Surg 1986;11A:309–24. 23. Thompson JS. Complications and salvage of trapeziometacarpal arthroplasties. Instr Course Lect 1989;38:3–13. 24. Kessler I, Axer A. Arthroplasty of the first carpometacarpal joint with a silicone implant. Plast Reconstr Surg 1971;47:252–7. 25. Ashworth CR, Blatt G, Chuinard RG, Stark HH. Silicone-rubber interposition arthroplasty of the carpometacarpal joint of the thumb. J Hand Surg 1977;2A:345–57. 26. Sotereanos DG, Taras J, Urbaniak JR. Niebauer trapeziometacarpal arthroplasty: a long term follow up. J Hand Surg 1993;18A:560–4. 27. de la Caffiniere JY. Prothese totale trapezo-metacarpienne. Rev Chir Orthop 1973;60:299–308. 28. Linscheid RL, Dobyns JH. Total joint arthroplasty: the hand. Mayo Clin Proc 1979;54:516–26.
ARTICLE IN PRESS 144 29. Braun RM. Total joint replacement at the base of the thumb: preliminary report. J Hand Surg 1982;7:245–51. 30. Ferrari B, Steffee AD. Trapeziometacarpal total joint replacement using the Steffee prosthesis. J Bone Jt Surg [Am] 1986;68A:1177–84. 31. Ledoux P. Cementless total trapezio-metacarpal prosthesis: principle of anchorage. In: Shuind F, editor. Advances in the biomechanics of the hand wrist. New York: Plenum Press; 1994. p. 25–30.
S. Batra, R. Kanvinde 32. Wachtl SW, Guggenheim PR, Sennwald GR. Cemented and noncemented replacements of the trapeziometacarpal joint. J Bone Joint Surg 1998;80B:121–5. 33. Forseth M, Stern P. Complications of trapeziometacarpal arthrodesis using plate and screw fixation. J Hand Surg 2003;28A:342–5. 34. Barron OA, Eaton RG. Save the trapezium: double interposition arthroplasty for the treatment of stage IV disease of the basal joint. J Hand Surg 1998;23A:196–204.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 145–149
Available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/cuor
TRAUMA
Management of lateral humeral condylar mass fractures in children H. Sharma, K. Chirputkar, R.D.D. Duncan Department of Trauma and Orthopaedic Surgery, Royal Hospital for Sick Children, Yorkhill, Glasgow G3 8SJ, UK
KEYWORDS Lateral condylar mass fractures; Elbow; Open reduction internal fixation; Screw; K-Wire
Summary Lateral condylar mass (LCM) fractures of the distal humerus comprise 17% of distal humeral fractures and are the second most common injury around the elbow in the paediatric population, after supracondylar fractures. LCM fractures occur most commonly between five and ten years of age, usually as an isolated injury. Whilst an undisplaced LCM fracture can be treated conservatively with regular radiographic observation, the available evidence recommends open reduction and internal fixation for displaced fractures. Growth plate and articular surface should be aligned and restored during open reduction and internal fixation. Missed, inadequately reduced or improperly fixed lateral humeral condylar fractures can lead to stiffness, non-union, malunion, recurrent dislocation, progressive cubitus valgus deformity and tardy ulnar palsy. & 2007 Elsevier Ltd. All rights reserved.
Introduction Lateral condylar mass (LCM) fractures of the distal humerus comprise 17% of distal humeral fractures and are the second most common injury around the elbow in the paediatric population, after supracondylar fractures.1 LCM fractures occur most commonly between five and ten years of age.2 Most LCM fractures occur as an isolated injury. Whilst an undisplaced LCM fracture can be treated conservatively with close observation, the available evidence recommends open reduction and internal fixation for displaced fractures.
Corresponding author. 44 Abercorn Road, Newton Mearns,
Glasgow G77 7NA, UK. Tel.: +44 141 639 3697; fax: +44 141 314 7275. E-mail addresses:
[email protected] (H. Sharma),
[email protected] (R.D.D. Duncan). 0268-0890/$ - see front matter & 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2007.03.004
There remains little evidence to decide whether pins3,4 or cancellous screws5,6 yield better outcomes. This article provides an overview of the current evidencebased practice in the management of LCM fractures and details of perioperative care, postoperative results and complications.
Mechanism of injury The possible mechanisms7 are (1) ‘push-off’ (blow to palm with elbow flexed when falling); (2) ‘pull-off’/avulsion (adduction of forearm with elbow in extension and forearm in supination during a fall); (3) direct blow to the olecranon.
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There are three main classifications, which are widely used to describe LCM fractures (Table 1). The Milch8 classification is based on the anatomical position of the fracture line (initially described by Stimson). In Type I fractures, the fracture line courses lateral to the trochlea and passes through the capitello-trochlear groove. In the Type II injury, the fracture line extends into the apex of the trochlea. Milch described the more common Type II injury as a fracture-dislocation and the Type I injury as a simple fracture. The Milch type I could be considered as a variant of the Salter-Harris type IV physeal injury, while the Milch type II fracture is equivalent to a Salter-Harris type II physeal fracture.8 Jakob et al.9 described lateral condyle fractures in relation to the degree of displacement and rotation of the fracture fragment. Stage I displaced fractures have less than 2 mm of displacement with an intact articular surface. In Stage II displaced fractures, there is 2–4 mm of displacement with moderate displacement of the articular surface. Stage III displaced fractures demonstrate significant displacement associated with rotation of the fragment.
localised swelling over the lateral aspect of the elbow and tenderness over the lateral condyle. With non-displaced or minimally displaced fractures, these signs may be subtle, leading to delay in detection. Antero-posterior and lateral radiographs of the elbow should be taken and examined for significant soft-tissue swelling of the lateral aspect of the elbow and a ‘fat-pad’ sign if a fracture is not obvious. The location of the fracture line, the degree of displacement and the relationship of the condylar ossification centre to the radial head should be noted. It is important not to miss associated injuries such as fractures of the olecranon, medial condyle, forearm bones, or elbow dislocation. Oblique views may be helpful when there is doubt, as may be arthrograms and MRI or ultrasound scanning.7 The role of the cartilage hinge as a major factor in determining stability of the fracture has been recently stressed.11 An MRI scan may be a better tool in the diagnosis of integrity of this hinge as compared to plain radiographs. Chapman et al.12 described the role of multidetector computerised tomography (MDCT) in accurately detecting the exact degree of displacement and integrity of the lateral soft tissue hinge.
Badelon et al.10 classification
Management strategy
This system of classification describes four different types based upon the degree of displacement of the fracture. This classification helps in fracture management.
For practical purposes, all fractures can be grouped under two categories: undisplaced and displaced (Fig. 1). Most authors agree that fractures with displacements greater than 2 mm need open reduction. Pirker et al.13 suggested that fractures with less than 2 mm displacement can be treated non-operatively but these patients need radiographs out of plaster at 4–6 days to detect further displacement. Progressive loss of position of the fragment in the plaster cast is an indication for open reduction and internal friction and requires surgery.14 Minimally displaced fractures with an intact periosteal hinge can be managed with percutaneous pinning. The available evidence recommends open reduction and internal fixation for displaced fractures.
Classification
Type 1. Undisplaced fracture line seen on single radiograph i.e. projection only. Type 2. Undisplaced fracture line seen on both views. Type 3. Displacement more than 2 mm on both views. Type 4. Complete separation of fragments.
Clinico-radiological assessment Displaced fractures usually produce diffuse swelling that distorts elbow surface anatomy. The key to diagnosis is
Surgical procedure Table 1
LCM fracture classifications.
(A) Postero-lateral approach
8
Milch classification Type I: Fracture line courses lateral to the trochlea and passes through the capitello-trochlear groove Type II: Fracture line extends into the apex of the trochlea Jakob et al.9 classification Stage I: Fractures with less than 2 mm of displacement with intact articular surface Stage II: Displaced fractures with 2–4 mm of displacement with moderate displacement of the articular surface Stage III: Displaced fractures demonstrating a significant displacement associated with rotation of the fragment
This approach is considered a safe approach through the interneural interval (Kocher interval) between anconeus and the exterior carpi ulnaris thus protecting the posterior interosseous nerve.15 This is the senior author’s preferred approach particularly if the child is placed prone when the whole of the posterior surface of the joint can be seen with ease, ensuring an accurate and anatomical fracture reduction. No muscle needs to be released from the distal fragment, thus preserving the blood supply to the physeal fragment.
(B) Lateral approach This approach also uses an interneural interval between extensor digitorum communis and extensor carpi radilois
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Figure 1 Displaced lateral humeral condylar mass fracture.
Figure 2
LCM fracture treated AO Screw (note that no compression is used, opposite cortical purchase is not needed).
brevis but because of its direct lateral nature, risk of injury to posterior interosseous nerve is considered to be high. The displacement and size of the fragment usually are greater than is apparent on the radiograph because of the large cartilaginous portion of the fragment. A single cancellous screw can be used (Fig. 2). It should be inserted proximal to the physis, where possible, to minimise the risk of growth arrest. Hasler and von Laer16 in their study concluded that screw osteosynthesis led to anatomical union, symmetrical carrying angles and full range of move-
ment in all of their operated cases at 10 years average follow-up. None of these patients had any growth disturbances. If K-wiring is preferred two are necessary to prevent rotation of the fragment. The pins may be parallel or crossed, but if crossed pins are used they should not be crossed at the fracture site. Divergent pins (one horizontal and one up the lateral column) also provide a sound fixation (Fig. 3A and B). The pins can be removed at 3 to 4 weeks, while the screw is removed between 3 and 6 months.
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H. Sharma et al. An algorithm for the management of LCM fractures in children is provided in Fig. 4.
Post-operative management The limb is elevated and the neurovascular status is assessed. Patients are usually discharged the following day in a long arm plaster with a broad-arm sling for support. The child is reviewed in the fracture clinic 3 weeks later, at which time the pins are removed without anaesthesia, and a radiograph obtained. A further 3 weeks of immobilisation in plaster is ensured, and active mobilisation is then usually possible without the need for physiotherapy. As full extension is seldom possible on removal of the cast, a further final follow-up is arranged to assess the carrying angle, elbow ROM and return of function. Contact sports and activities likely to result in a fall are not allowed for 12 weeks after the fracture. Follow-up until skeletal maturity is carried out at some centres.
Complications Complications are listed in Table 2.
Figure 3 (A), (B) LCM fracture treated with two K-wires.
(1) Spur formation. Lateral condylar spur formation is the commonest complication. It can be seen in fractures which are treated operatively and non-operatively. It has no functional significance. (2) Cubitus varus. Some overgrowth of the lateral mass is common. Following conservative or operative treatment. The cause is unknown. (3) Cubitus valgus. It is less common than cubitus varus and is more commonly seen with non-unions. It is thought to be due to premature epiphysiodesis on the lateral side.
LCM Fractures
Undisplaced
Displaced Displacement uncertain EUA
Shows displacement
Open reduction internal fixation Either lateral or posterolateral approach Either two K-wires or one cancellous screw
Closed reduction of dislocation and treat LCMF like a displaced fracture
Figure 4
No evidence of cartilage hinge
Evidence of cartilage hinge Closed reduction and percutaneous pinning
Evidence of elbow dislocation
Algorithm for the management of lateral humeral condylar fractures in children.
ARTICLE IN PRESS Management of LCM fractures in children
Table 2 Complications related to LCM fracture and its management. Immediate Infection Neurovascular problems Short term complications Metal related problems Prominence of lateral condyle Scar hypersensitivity Long term complications Non-union Malunion Recurrent dislocation Progressive cubitus valgus deformity Tardy ulnar palsy
(4) Fish tail deformity. There are two types. Firstly, a sharp angled wedge type. There is a gap between the lateral condylar physis ossification centre and medial ossification of the trochlea. The second type is a smooth gentle curve thought to be due to avascular necrosis of the lateral part of medial crista of the trochlea. Rutherford17 suggested that this deformity is caused by inadequate reduction. (5) Delayed union. This is seen mainly in fractures treated non-operatively, even if in satisfactory position. (6) Non-union. Non-union can occur with or without angulation. Flynn et al.14 defined non-union when the fracture had failed to heal by 12 weeks. Non-union with angulation is seen in Badelon type 2 and 3 fractures. Non-union can lead to cubitus valgus deformity and tardy ulnar nerve palsy. Principles of management of non-union are open reduction to achieve apposition of the fracture fragments and then compression across the fracture site. (7) Miscellaneous. Physeal arrest, malunion, myositis ossificans and avascular necrosis (usually iatrogenic secondary to excessive dissection). In summary, closed treatment results in a satisfactory outcome if the initial radiographic displacement does not exceed 2 mm. This requires close follow-up for detection of displacement. Most authors agree that fractures with displacement beyond 2 mm need open reduction.
Practice points 1. Second most common injury around the elbow in the paediatric population, after supracondylar fractures 2. Open reduction and internal fixation are recommended for even minimally displaced fractures 3. Missed, inadequately reduced, or improperly fixed lateral humeral condylar fractures lead to a poor outcome and the place for late fixation or reconstruction is controversial
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Research directions 1. RCT for screw versus K-wire fixation 2. Use of bio-absorbable screw fixation 3. Role of magnetic resonance imaging to assess stability
References 1. Hardacre JA, Nahigian SH, Froimson AI, Brown JE. Fractures of the lateral condyle of the humerus in children. J Bone Joint Surg (Am) 1971;53(6):1083–95. 2. Ippolito E, Tudisco C, Farsetti P, Caterini R. Fracture of the humeral condyles in children: 49 cases evaluated after 18–45 years. Acta Orthop Scand 1996;67(2):173–8. 3. Thomas DP, Howard AW, Cole WG, Hedden DM. Three weeks of Kirschner wire fixation for displaced lateral condylar fractures of the humerus in children. J Pediatr Orthop 2001; 21(5):565–9. 4. Mintzer CM, Waters PM, Brown DJ, Kasser JR. Percutaneous pinning in the treatment of displaced lateral condyle fractures. J Pediatr Orthop 1994;14(4):462–5. 5. Conner AN, Smith MG. Displaced fractures of the lateral humeral condyle in children. J Bone Joint Surg (Br) 1970; 52(3):460–4. 6. Sharma JC, Arora A, Mathur NC, et al. Lateral condylar fractures of the humerus in children: fixation with partially threaded 4.0mm AO cancellous screws. J Trauma 1995;39(6):1129–33. 7. Bulstrode C, et al. Lateral condyle fracture. In: Bulstrode C, Buckwalter J, Carr A, Marsh L, Fairbank J, Wilson-MacDonald J, Bowden G, editors. Oxford textbook of Orthopaedics and Trauma. Oxford: Oxford University Press; 2002. 8. Milch H. Fractures and fracture dislocations of the humeral condyles. J Trauma 1964;4:592–607. 9. Jakob R, Fowles JV, Rank M, Kassab MT. Observations concerning fractures of the lateral humeral condyle in children. J Bone Joint Surg (Br) 1975;57:430–6. 10. Badelon O, Bensahel H, Mazda K, Vie P. Lateral humeral condylar fractures in children: a report of 47 cases. J Pediatr Orthop 1988;8:31–4. 11. Pudas T, Hurme T, Mattila K, Svedstrom E. Magnetic resonance imaging in pediatric elbow fractures. Acta Radiol 2005;46(6):636–44. 12. Chapman VM, Grottkau BE, Albright M, Salamipour H, Jaramillo D. Multidetector computed tomography of pediatric lateral condylar fractures. J Comput Assist Tomogr 2005;29(6): 842–6. 13. Pirker ME, Weinberg AM, Hollwarth ME, Haberlik A. Subsequent displacement of initially nondisplaced and minimally displaced fractures of the lateral humeral condyle in children. J Trauma 2005;58(6):1202–7. 14. Flynn JC. Nonunion of slightly displaced fractures of the lateral humeral condyle in children: an update. J Pediatr Orthop 1989;9:691–6. 15. Mohan N, Hunter JB, Colton CL. The posterolateral approach to the distal humerus for open reduction and internal fixation of fractures of the lateral condyle in children. J Bone Joint Surg (Br) 2000;82(5):643–5. 16. Hasler CC, von Laer L. Prevention of growth disturbances after fractures of the lateral humeral condyle in children. J Pediatr Orthop B 2001;10(2):123–30. 17. Rutherford A. Fractures of the lateral humeral condyle in children. J Bone Joint Surg (Am) 1985;67:851–6.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 150–158
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Radiology quiz QUESTIONS Case 1 A 23-year-old tennis player complaining of shoulder pain. What is the abnormality, and what is the significance of the history?
Figure 1
(a) and (b) Coronal T1W right shoulder arthrogram and (c) axial T1W right shoulder arthrogram.
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Case 2 A 78-year-old man with a history of prostatic carcinoma complaining of right hip pain, and also pain in the distribution of his right sciatic nerve. What examinations are these and what do they show?
Figure 2
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Radiology quiz
Case 3 A 34-year-old female with an enlarging lump on her back. What type of MR images are shown and what is the diagnosis?
Figure 3
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Case 4 A 30-year-old Kurdish farmer recently arrived from Iraq complaining for several weeks of increasing pain in his right hip. There was no history of trauma but he did have a low-grade fever and inflammatory markers were modestly elevated. Plain radiography and ultrasound of the hip were unremarkable but he continued to be unable to weight bear due to pain. What examination is shown in Fig. 4? What are the relevant findings and what is the likely differential diagnosis? What would you do to confirm this?
Figure 4
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Radiology quiz
Case 5 A 57-year-old man complaining of left knee pain. He had been diagnosed with prepatellar bursitis and this had been aspirated to dryness. However, the pain continued and the patient complained of ‘‘locking’’ of the joint. What examination is shown in Fig. 5a and what is the relevant finding? Does this examination show the typical features of this condition? Figure 5b shows a separate abnormality. Apart from the aspiration of the prepatellar bursa recently, there was no history of surgery. What is the relevance of Fig. 5c?
Figure 5
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Case 6 An 84-year-old admitted acutely to hospital after her family discovered her crawling around her flat. She gave a history of being unable to stand for at least 1 week due to leg weakness. There was no loss of sensation and continence had been maintained. She had a long history of back pain but had not had any previous imaging or surgical intervention. The MR scan had been obtained as an emergency. What is shown and is treatment required urgently?
Figure 6 5 level.
From the MR examination: (a) a sagittal T2-weighted image, (b) axial T2-weighted images at L3/4 level, and (c) at the L4/
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Radiology quiz
Case 7 A 22-year-old female who had undergone surgery on her back a few days previously. What operation has been performed? What potentially serious complication is shown? What is the appropriate course of action? (See Fig. 7.)
Figure 7
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ANSWERS Case 1 There is a superior anteroposterior tear of the glenoid labrum (SLAP lesion) with abnormal signal arising from between the insertion of the biceps tendon and the labrum (upper left arrow Fig. 1a) as well as between the glenoid and superior labral cartilage (arrows Figs. 1a–c). These appearances are due to the intra-articular injection of Gadolinium solution extending in to the tears. Using the Snyder classification, this is a type 3 lesion (bucket handle-type tear of the labrum, with an intact biceps tendon). SLAP lesions can arise from a fall on an outstretched hand or can be related to repetitive over arm movements (e.g., tennis serves).
Case 2 Figure 2a is an isotope bone scintigram. The arrow highlights the point of focal uptake within the right sacrum that would be suspicious for a metastasis at this site. However, no sclerotic or lytic lesion is seen in the corresponding area on the CT scan (white ring Fig. 2b). Figure 2c demonstrates high signal inflammatory change affecting right piriformis (arrowed). There is also a subtle insufficiency fracture of the sacrum (not shown). Piriformis is in close association with the sciatic nerve and may explain the patient’s limb symptoms. This highlights the fact that not all areas of increased uptake on a bone scan are necessarily referable to malignant disease.
Case 3 Figure 3a is a T1-weighted axial MR image showing a well-circumscribed lesion arising within the left erector spinae muscle, returning mostly high signal, consistent with fat (lower arrow). It contains a central separate area of low signal within (upper arrow). Figure 3b is a T2 STIR (Short Tau Inversion Recovery) axial image of the same area confirming that the majority of the mass comprises low signal fat (lower arrow). The central area has not fat-suppressed, and returns high signal (upper arrow), implying an oedematous or fluid component. Figure 3c is a T1-weighted post-Gadolinium image showing enhancement of this central area (upper arrow), in keeping with a significant vascular supply, indicating it is oedematous solid tissue and not fluid. These findings in the context of the given history are suggestive of sarcomatous transformation within a lipoma.
Case 4 Figures 4a and b are coronal oblique (a) T1-weighted and (b) T2-weighted fat-suppressed images of the sacroiliac joints showing irregularity of the right sacroiliac joint margins (arrowed) with adjacent high signal oedema of bone and surrounding soft tissues. There is high signal fluid within the SI joint itself. Given the history, the differential diagnosis includes infections such as tuberculosis and brucellosis. Other possibilities might include pyogenic sacroiliitis or sarcoidosis. A bone and sacroiliac joint biopsy was performed under CT guidance to obtain a histological diagnosis. In fact, no organism was isolated, but the patient improved when treated for brucellosis.
Case 5 Figures 5a–c are sagittal proton density-weighted images of the left knee. Figure 5a shows an oblique horizontal tear of the posterior horn of the medial meniscus extending to the inferior articular surface (arrowed). This is a typical finding in knee injury with the medial meniscus injured in approximately 45% of cases, (bilateral in 33% and unilateral in 22%). The posterior horn of the medial meniscus is torn in 60% of cases (body and posterior in 18% and the entire meniscus in 22%). Oblique tears commonly extend to the inferior surface. Figure 5b shows abnormal high signal affecting the mid-portion of the inferior patellar tendon (arrowed). Figure 5c shows a normal-looking anterior cruciate ligament (arrowed). The central portion of the patellar tendon can be used to repair cruciate ligament injuries but there is no history of surgery in this case and the abnormality of the patellar tendon likely relates to the recent attempt at aspiration.
Case 6 At L4/5 there is a grade 1 degenerative spondylolisthesis with moderate-to-severe central canal stenosis (arrowed on Figs. 6a and c) with marked facet joint and ligamentum flavum hypertrophy resulting in virtually complete effacement of the CSF. At L3/4 (arrowed in Fig. 6b) there is moderate-to-severe central canal stenosis with facet joint and ligamentum flavum hypertrophy resulting in almost complete effacement of the CSF. Note the lack of high signal around the nerves that would normally indicate the presence of CSF. These features are not of acute pathology and hence emergency surgery was not performed. Had there been evidence of epidural abscess or a superimposed acute disc protrusion for example, emergency decompression may have been indicated.
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Radiology quiz
Case 7 She has undergone single-stage corrective surgery for scoliosis (in this case, idiopathic structural scoliosis) with intervertebral discectomy and fusion. Idiopathic structural scoliosis is characterised by relative overgrowth of the anterior vertebrae and is treated by fusion to arrest progression. In a skeletally mature patient, the procedure is largely cosmetic. Non-structural scoliosis is the result of another cause of curvature, most commonly due to inequality in leg length with pelvic tilt. In this case, the left T6 pedicular screw tip does not enter the vertebral body, but lies in a paravertebral location (arrow), lying immediately adjacent to the descending thoracic aorta (position suggested by the white circle). The aorta is at risk of injury from the metalwork and she underwent revision of surgery with instrumentation at a superior level.
Jon Martin, Philip Robinson Radiology Department, Clarendon Wing Leeds General Infirmary, Great George Street, Leeds LS1 3EX, UK
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 159–162
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SYNDROME
Cleidocranial dysplasia Verity Curralla, Rachel Clancyb, Donna Dimondc, Rouin Amirfeyzd,, Chris Kershawe, Martin Garganc a
Trauma and Orthopaedics, Cheltenham General Hospital, Cheltenham, UK University of Bristol, Bristol, UK c Bristol Royal Hospital for Sick Children, Bristol, UK d Trauma and Orthopaedics, Frenchay Hospital, Bristol, UK e Orthopaedic Department, University Hospital of Leicester, UK b
Introduction Cleidocranial dysplasia (CCD) (also known as cleidocranial dysostosis or mutational dysostosis) is a rare disorder primarily affecting bones formed by intramembranous ossification (the clavicles, skull and facial bones), but also involving the spine and appendicular skeleton. The syndrome was named by Marie and Sainton in 1898,1 but the first documented case was in 1765.2 It is possible the condition was recognised even earlier, as the character Thersites in Homer’s Iliad has been retrospectively diagnosed with CCD.3
Epidemiology and genetics CCD is an autosomal dominant disorder with complete penetrance, but high variability in expression. It is caused by mutations in the Core Binding Factor Activity 1 (CBFA1) gene on the short arm of chromosome 8. CBFA1 is necessary for osteoblast formation, regulates chondrocyte differentiation and is essential for the vascular invasion of calcified cartilage.4 Despite reports,5 autosomal recessive inheritance is unlikely because mouse models show homozygosity is lethal.6
Corresponding author.
E-mail address:
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There are no gender or racial differences in the prevalence of CCD, which has been estimated as less than one per million,7 although this may be an underestimate as many affected individuals do not seek medical advice.
Clinical presentation Although it is possible to diagnose CCD with prenatal ultrasonography,8 presentation is usually later in life, often due to dental problems, or incidentally, when the patient seeks medical attention for an unrelated condition.9 Patients have normal intelligence and generally short stature, with a head circumference at the upper limit of normal. Conductive deafness may be present and there is a predisposition to otitis media. Characteristic facial features include frontal bossing, hypertelorism (wide-set eyes) and midface hypoplasia, with a depressed nasal bridge and a small maxilla, giving the face a small, flattened appearance. The palate is high arched and dental abnormalities are common. Deciduous teeth are often retained for longer than usual, with delayed eruption of the permanent teeth and a variable number of supernumerary teeth. Different degrees of clavicular hypoplasia give a varying clinical picture, from a minor skin dimple, through easily palpable defects, to steeply sloping shoulders, which can easily be opposed (Fig. 1). The abnormality is usually bilateral; if not, right-sided problems are by far the more common.10 In 10% of cases, the clavicles are entirely absent; in a few patients, they are completely normal. Surprisingly,
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shoulder strength is near-normal, and affected individuals may work at heavy manual jobs with no difficulties. The fingers are short and tapered, except for a long index finger, due to a long second metacarpal, and clinodactyly of the fifth finger has been reported.10 The thorax is narrow and cone-shaped and spinal abnormalities, including scoliosis and kyphosis, are frequently seen.11
There may be a Trendelenburg gait, leg length inequality and reduced range of hip movement if coxa vara is present. A recent series12 has shown that genu valgum and pes planus are the most common skeletal complaints. A tendency to joint laxity is seen, leading to elbow and knee dislocations in particular, but there is no increase in fracture rate. Other occasional findings include neurological and/or vascular signs caused by pressure of the clavicular remnants on the brachial plexus or subclavian artery,13,14 or by syringomyelia, which has an association with CCD.15
Radiological features Skull and face (Fig. 2)
Delayed closure of sagittal and metopic sutures and fontanelles
Underdeveloped or absent paranasal sinuses Shoulder (Fig. 3)
Clavicular defects Flattening of the medial third of the clavicle
Small and deformed scapulae Hands
Shortened middle phalanges Pointed terminal tufts Elongated second metacarpal with an accessory epiphysis
Spine
Cervico-thoracic neural arch defect Posterior wedging of thoracic vertebrae
Lumbar spondylolysis Pelvis (Fig. 4)
Hypoplastic iliac crests Delayed/absent ossification nuclei of pubic symphysis
Widened sacro-iliac joint and Figure 1 A patient with cleidocranial dysplasia.
Figure 2
triradiate cartilage
AP and lateral skull radiographs, showing Wormian bones, frontal bossing and delayed closure of the sagittal suture.
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Figure 3 Absent lateral ends of both clavicles.
Pregnancy—Caesarean section may be necessary if
labour becomes obstructed (more likely if the foetus is also affected, due to cephal-opelvic disproportion). Dental defects—usually most troublesome; multiple procedures often required to extract supernumerary teeth and correctly align the permanent teeth.19 Hearing—a hearing test at diagnosis is recommended.
Acknowledgement The authors would like to acknowledge Mr. Chris Kershaw, Consultant Orthopaedic Surgean for his tremendous help in preparation of the manuscript.
Figure 4 AP pelvis, demonstrating a widened pubic symphysis and triradiate cartilage.
Hips
Abnormal neck-sheft angle (coxa vara more common)
Chef’s hat appearance of the femoral head (elongated) Ankle and feet
Shortened calcaneus Narrowed talus Forefoot deformities similar to those seen in the hands
Treatment
Clavicles—surgical intervention should be restricted to
excision of a clavicular segment causing skin or neurovascular problems.16,17 Coxa vara—a valgus osteotomy is recommended for a neck-shaft angle of 901 or less, a Hilgenreiner-epiphyseal angle of 601 or more or a progressive deformity.18 Other bony deformities—appropriate symptomatic management, either conservative or surgical.
References 1. Mane P, Sainton P. Sur la dysostose cleido-cranienne hereditaire. Rev Neurol 1898;6:835–8. 2. Martin M. Sur un deplacement naturel de la clavicule. J de Med, Chiret de Pharmacol 1765;23:456–61. 3. Beasley AW. Homer and orthopaedics. Clin Orthop Relat Res 1972;89:10–6. 4. Mundlos S. Cleidocranial dysplasia: clinical and molecular genetics. J Med Genet 1999;36:177–82. 5. Goodman RM, Tadmor R, Zaritsky A, Becker SA. Evidence for an autosomal recessive from of cleidocranial dysostosis. Clin Genet 1975;8:20–9. 6. Komori T, Yagi H, Nomura S, et al. Targeted disruption of CBAF1 results on a complete lack of bone formation owing to maturational arrest of osteoblasts. Cell 1997;89:755–64. 7. Wynne-Davies R, Hall CM, Apley AG. Atlas of skeletal dysplasias. Churchill Livingstone; 1985. p. 584–94. 8. Hamner LH, Fabbri EL, Browne PC. Prenatal diagnosis of cleidocranial dysostosis. Obstet Gynecol 1994;83:856–7. 9. Ross DA. Cleidocranial dysostosis—a case report and review of the literature. J Royal Army Med Corps 1998;144:37–9. 10. Jarvis JL, Keats TE. Cleidocranial dysostosis: a review of 40 new cases. Am J Roentgenol Radium Ther NucI Med 1974;121:5–16. 11. Soule AB. Mutational dysostosis (cleidocranial dysostosis). J Bone Jt Surg 1946;28:81–102. 12. Cooper SC, Flaitz CM, Johnston DA, et al. A natural history of cleidocranial dysplasia. Am J Med Genet 2001;104:1–6. 13. Jones HWE. Cleido-cranial dysostosis. St Thomas’s Hosp Gaz 1937;36:193–201.
ARTICLE IN PRESS 162 14. Qureshi KN, Lees TA, Holdsworth J. Acute upper limb ischemia resulting from cleidocranial dysostosis. J Vasc Surg 1997;26:888–90. 15. Dore DD, MacEwen GD, Boulos MI. Cleidocranial dysostosis and syringomyelia: review of the literature and case report. Clin Orthop Relat Res 1987;214:229–34. 16. Aktas S, Wheeler D, Sussman MD. The ‘chefs hat’ appearance of the femoral head in cleidocranial dysplasia. J Bone Jt Surg Br 2000;82:404–8.
V. Currall et al. 17. Wood VE, Marchinski L. Congenital anomalies of the shoulder. In: Rockwood CA, Matsen FA, editors. The shoulder. 2nd ed. WB Saunders Company; 1998. p. 100–2 [Chapter 13]. 18. Richie MF, Johnston CE. Management of developmental coxa vara in cleidocranial dysostosis. Orthopedics 1989;12: 1001–4. 19. Jensen BL, Kreiborg S. Dental treatment strategies in cleidocranial dysplasia. Br Dent J 1992;172:243–7.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 163–165
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CME SECTION Three CME points available The following series of questions are based on the MiniSymposium on Children—Osteotomies around the Hip. Please read the articles in the Mini-Symposium carefully and then complete the self-assessment questionnaire by filling in the square corresponding to your response to each multiple-choice question. After completing the questionnaire, either post or fax the answer page to the Current Orthopaedics Editorial Office at the address at the bottom of the RESPONSE sheet. Please photocopy this page if you wish to keep your copy of Current Orthopaedics intact. Replies received before the next issue of Current Orthopaedics is published will be marked and those reaching an adequate standard will qualify for three external CME points. You will be notified of your marks and a CME certificate will be despatched for your records.
Questions 1. Which of the following procedures places normal hyaline cartilage over the femoral head? A. B. C. D. E.
Chiari osteotomy Kawamura dome procedure Wagner spherical osteotomy Chiari osteotomy with shelf procedure Shelf procedure alone
2. As acetabular dysplasia becomes symptomatic a patient complains of pops and clicks in the hip that are associated with pain. They occur while walking but not when sitting or squatting. What is likely to be responsible for these symptoms? A. B. C. D. E.
Loose bodies Hip subluxation Transverse ligament snapping Labral pathology Rim impingement
3. In which position of the hip can evidence of anterior instability be found in a patient with acetabular dysplasia? A. Extension and internal rotation 0268-0890/$ - see front matter doi:10.1016/j.cuor.2007.05.001
B. C. D. E.
Extension and external rotation Flexion and internal rotation Flexion and external rotation Abduction
4. Which of the following provides the best indication for pelvic realignment osteotomy? A. Acetabular dysplasia with osteoarthritic changes in the hip B. Acetabular dysplasia with a stiff hip C. Congruent and containable hip needing 451 rotation to achieve cover D. Congruent and containable hip needing 151 rotation to achieve cover E. Incongruent hip 5. After a Chiari osteotomy, approximately what proportion of patients would be expected to have continuing good relief of pain 20 years after surgery? A. B. C. D. E.
5% 10% 25% 50% 75%
6. In which of the following groups of patients should the Bernese periacetabular osteotomy not be performed? A. B. C. D.
Young children Females of childbearing age Patients with labral pathology Patients with minimal articular cartilage pathology on MRI E. Patients in which the hip has started to sublux
7. What is the approximate incidence of hip displacement in severe, total body involvement cerebral palsy? A. B. C. D. E.
5% 10% 25% 50% 75%
ARTICLE IN PRESS 164 8. After a Salter osteotomy and adductor tenotomy the patients hip is flexed to 901 whilst the thigh is slightly internally rotated and the knee is held flexed. As the knee is straightened the hip redioslocates. What additional procedure is indicated? A. B. C. D. E.
Capsular reefing Labral repair Femoral shortening Abduction osteotomy Shelf procedure
9. Which musculoskeletal deformity is most commonly associated with cerebral palsy? A. B. C. D. E.
Posterior shoulder dislocation Equinus foot Hip subluxation Hip dislocation Patellar dislocation
10. Which is the most useful parameter for monitoring the hips of patients with cerebral palsy? A. Level of pain B. Acetabular Index
CME SECTION C. Centre edge angle D. Migration percentage E. Passive abduction 11. A patient with cerebral palsy develops 40% lateral migration of the hip. Which of the following procedures is most appropriate to address this? A. B. C. D. E.
Serial casts Psoas adductor release Varus derotation shortening osteotomy Shortening osteotomy combined with shelf procedure Shortening osteotomy combined with Chiari osteotomy
12. Approximately what proportion of walkers with cerebral palsy will develop hip subluxation? A. B. C. D. E.
5% 10% 25% 50% 75%
ARTICLE IN PRESS CME SECTION
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Please fill in your answers to the CME questionnaire above in the response section provided below. A return address and fax number is given at the bottom of the page. ...............................................................................................
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Your details (Print clearly) NAME. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ADDRESS. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . FAX NO. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . EMAIL. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . RETURN THE COMPLETED RESPONSE FORM by fax to +44-113-392-3290, or by post to CME, Current Orthopaedics, Academic Department of Orthopaedic Surgery, ‘‘A’’ Floor Clarendon Wing, Leeds General Infirmary, Great George Street, Leeds LS1 3EX, UK.
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CME SECTION Answers to CME questions based on the Mini-Symposium on Management of Fractures around the Knee Joint Please find below the answers to the Current Orthopaedics CME questions from Vol. 20, issue 6 which were based on the MiniSymposium on Management of Fractures around the Knee Joint.
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0268-0890/$ - see front matter doi:10.1016/j.cuor.2006.12.003
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ERRATUM
Erratum to ‘‘The ‘floating knee’ in adults and children’’ [Curr. Orthop. (2006) 20, 405–410] Byron Chalidis, Saurabh S. Mehta, Eleftherios Tsiridis, Peter V. Gioannoudis The Academic Unit of Orthopaedic Surgery, A Floor, Clarendon Wing, Leeds General Infirmary, Great George Street, Leeds LS1 3EX, UK
The publisher regrets that a spelling error occurred in the name of the 2nd author of the above article. The correct spelling and full list of authors are printed above. Please accept our apologies for any inconvenience caused by this error.
DOI of original article: 10.1016/j.cuor.2006.10.005 Corresponding author. Tel.: +44 113 3922750; fax: +44 113 3923290.
E-mail address:
[email protected] (P.V. Gioannoudis). 0268-0890/$ - see front matter & 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2007.02.008
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BOOK REVIEWS Spinal Arthroplasty—A New Era in Spine Care, Richard D. Guyer, Jack E. Zigler (Eds.), Quality Medical Publishing (2005) (343pp., $195), ISBN: 1-57626-190-5. This book is intended for specialist spinal surgeons to provide a balanced understanding of the importance of motion preservation and stability in the management of degenerative disease especially in the younger patient population. Unfortunately, this book fails to achieve its goal. The text is divided into four sections. Part 1 fundamentals, part 2 biomechanics and development, part 3 techniques and technologies and part 4 future considerations. Part 4 commences in Chapter 17 looking at biological disc repair and introduces the pathogenesis of lumbar disc disease and the biochemistry of the intervertebral disc. Clearly, this information is better placed at the start of the book in part 1. In part 1, the history of the artificial disc and the psychological evaluation of spinal arthroplasty patients make interesting reading but Chapter 3 on indications and contraindications for total disc replacement mainly states the obvious with respect to contraindications but fails to provide convincing objective criteria to identify those
patients who would benefit from spinal arthroplasty. The lack of robust evidence is a notable feature in several chapters. Typically, the conclusions seem excessively enthusiastic and overemphasise the importance of this new technology. There is considerable repetition of information in this book. It is of some interest to contrast the conclusions of Chapter 6 with those of Chapter 12 ‘‘Total disc replacement; implants and clinical results’’. The latter is detailed, extensively referenced and well worth reading if one is considering undertaking spinal arthroplasty. Similarly, Chapters 13 and 14 referring to other disc replacements for the lumbar and cervical spine, respectively, are of value. Chapter 16 on total facet replacement disappoints the reader in that there is no substance to support facet joint replacement in practical terms but instead it relies on extensive comparisons being drawn from experience with hip and knee arthroplasty. Overall, this book does not fill the gap in the literature for a comprehensive, objective text that is of value to either the novice or experienced spinal surgeon.
Crispin Wigfield
10.1016/j.cuor.2006.10.009
Nonfusion Techniques for the Spine: Motion Preservation and Balance. Maxwell J.H., Griffith S.L., Welch W.C., editors. Quality Medical Publishing Inc., St. Louis, Missouri (2005), (420pp., $275, ISBN: 1-57626-179-4). This is a multi-author text, with contributors drawn from clinicians and basic scientists. Its preface entitled ‘Millennium of the motion segment’ claims the book ‘represents a critical mass for the knowledgeable readers who want to ready themselves for a new way of thinking about the spine’. The book is divided into two parts: the first concerns the concept of motion preservation techniques as a surgical strategy for low back pain. The second part then focuses on specific implants for cervical and lumbar disc arthroplasty or nucleus replacement. There is also a section on kyphoplasty.
doi:10.1016/j.cuor.2006.10.002
Much of the data in this book is already superseded by published trials for FDA approval. The brief descriptions of the techniques allow some form of comparison of the different merits of each implant but as argument for the concept itself there are few comparative statistics between the new technology and standard fusion procedures. There is a significant commercial bias in some of the sections with specific surgeon ‘champions’ extolling the virtues of a particular device. This is not a book that should be sought out by the average orthopaedic trainee. If however, the enquiring individual, as part of a spinal surgery attachment, wants a succinct and well-argued treatise on background, plus pros and cons of spinal fusion for back pain; then the first four chapters are well worth the effort.
Michael Grevitt
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EDITORIAL Computer-aided/robotic orthopaedic surgery (CAROS) is a hot and complex subject. Necessarily the mini-symposium includes very technical and complex material. This may be fairly indigestible for many clinical orthopods and if so then I suggest that readers scan through these papers just to get a feel for the subject after taking a liberal quantity of Gaviscon followed by a single malt of your choice.
Robert A. Dickson
0268-0890/$ - see front matter & 2007 Published by Elsevier Ltd. doi:10.1016/j.cuor.2007.06.003
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WRIST
Management of wrist instability S. Sivananthana,, L. Sharpb, Y.C. Lohc a
Trauma and Orthopaedic Surgery, Epsom General Hospital, Dorking Road, Epsom, Surrey KT18 7EG, UK Trauma and Orthopaedic Surgery, Kingston Hospital, Galsworthy Road, London KT2 7QB, UK c Southport and Ormskirk NHS Trust, Wigan Road, Ormskirk L39 2AZ, UK b
KEYWORDS Wrist; Carpal instability; Management
Summary The wrist is a complex structure which has evolved to allow precise and controlled motion in all 3 planes, thus allowing the hand to be positioned perfectly. This paper reviews the normal anatomy of the wrist and how it can go wrong, resulting in static or dynamic instability. A good history, clinical examination, appropriate investigations and the use of classification systems help to localize this instability thus allowing an appropriate management plan to be formulated. Finally, various treatment options are described and explained. & 2007 Elsevier Ltd. All rights reserved.
Introduction The wrist is a complex joint consisting of co-articulation of the carpal bones amongst each other and also with the distal radius and ulna. It permits motion in all 3 planes and allows these complex patterns of motion to take place under considerable strain, for example, when twisting. There are 10 bones involved along with the corresponding ligaments, capsule and tendons. The wrist joint functions is a kinematic linkage system and has evolved in this way to allow the hand to adjust its position in relation to the forearm thus placing it in the best possible position in order to perform a particular function. The way in which the carpal bones are connected to each other and to the distal radius results in certain patterns of carpal bone motion specific to the direction of motion of the hand with respect to the forearm. These unique patterns of motion are a result of carpal bone geometry, ligament Corresponding author.
0268-0890/$ - see front matter & 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2007.03.005
function and muscle activity. Optimal wrist function requires stability of all these carpal components in all joint positions under static and dynamic conditions. Instability is a condition that arises when there is altered joint kinematics whereby one or more carpal bones moves in an abnormal pattern as a result of bony injuries, intrinsic and/or extrinsic ligamentous injuries or joint laxity. Thus the wrist is rendered unstable to external forces of pinch and grasp.
Functional anatomy, classification and aetiology Stability of the wrist is closely linked to its functional anatomy. The shape of the carpal bones and the extrinsic and intrinsic carpal ligaments are important in maintaining stability. The two important ligament support systems are the extrinsic wrist ligaments and the intrinsic or interosseous ligament system.
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S. Sivananthan et al. 2. The distal row of carpal bones acts as a rigid body in which the trapeziums, trapezoid, capitate and hamate are tightly conjoined. 3. The proximal carpal row, which consists of the scaphoid, lunate and triquetrum is a mobile and inherently unstable intercalated segment, which allows the hand to adjust its position relative to the forearm, as its position is relative to the spatial configurations of the radius, TFCC and ulna proximally and the rigid distal carpal row distally. 4. Thus due to the above described bony articulations, ligamentous support is essential for stability of the wrist. The ligament system comprises the short, intrinsic interosseous ligaments, the longer, extrinsic intracapsular ligaments and the extra-articular ligamentous structures. 5. The proximal carpal row flexes in wrist radial deviation and extends in ulnar deviation.
Classification Figure 1 Dorsal view of the wrist joint (Mayfield et al.1).
The extrinsic ligament system includes the proximal and distal volar radiocarpal ligaments that consist of a series of inverted V shaped ligaments with the tip of the V at the capitate and the ligament fibres interconnecting the proximal and distal carpal rows with the distal radius. The radioscaphocapitate ligament (RSCL), which extends from the radial styloid process across a groove at the waist of the scaphoid to the palmar aspect of the capitate, acts as a fulcrum around which the scaphoid rotates. The long radiolunate ligament (LRL), which lies parallel to the RSCL, extends from the palmar rim of the distal part of the radius to the radial margin of the palmar horn of the lunate. The dorsal radiocarpal ligaments (DRCLs) are weaker and are centred on the trapezium (Fig. 1). The intrinsic system consists of the interosseous ligaments of the wrist that connect the individual carpal bones. These interosseous ligaments include the scapholunate (SLL) and the lunotriquetral ligaments (LTLs) that are recognised as the most important stabilizing structures of the proximal carpal row.2,3 The thickest and strongest region of the SLL is located dorsally and that of the LTL is located on the palmar aspect.4 Numerous studies have demonstrated that interosseous ligament injuries alone can give rise to wrist instability. This instability is further increased when the extrinsic ligaments and/or bony injuries are involved.
Kinematics Several theories of wrist stability have been proposed over the years. These include the columnar or vertical carpus theory, the proximal row independence and the oval ring theories. However, the following 5 concepts are widely accepted at present: 1. The distal articular surface of the radius, the triangular fibrocartilage complex (TFCC) and the distal ulna form the base for radiocarpal function.
Classification of carpal Instability has been attempted by numerous authors, most recently by the International Wrist Investigators Workshop (IWIW)5 in order to assist in the diagnosis and treatment of this condition. Unfortunately, there are plethora of confusing classifications that are not helpful in the everyday clinic. Therefore we have summarised the salient points. The carpus is considered unstable if it exhibits symptomatic malalignment, is not able to withstand loads, and does not have normal kinematics during any portion of its arc of motion.6 In order to classify a particular carpal instability, the clinical, radiological and anatomical findings must be taken into consideration. The first two can be obtained in the outpatient setting but the anatomical nature of the instability is best ascertained with MRI or during wrist arthroscopy.2 These newer investigations reveal more subtle degrees of instability. First the instability, once detected, can be classified as static or dynamic. Static instability is defined as carpal malalignment that can be detected on standard posteroanterior and lateral radiographs. Dynamic instability is defined as carpal malalignment that is reproduced with physical examination manoeuvres and/or when stress radiographs are performed. With dynamic instability the carpal bone malalignment is not detected on standard radiographs.7 Secondly, the location of the instability (i.e. joint involved) must be identified. The carpus may be mal aligned between the two rows (intracarpal problem) or remain aligned whilst translating the radiocarpal level to a new position (extracarpal problem). The Mayo Clinic Classification divides the intracarpal instabilities as CID), CIND, CIC or CIA that are described below 1. CID or Carpal Instability Dissociative involves the disruption of an intercarpal ligament within a carpal row. This can result in Dorsal Intercalated Segment Instability (DISI), Volar Intercalated Segment Instability (VISI) or Axial Carpal Instability (Figs. 2–4).
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Figure 3 Gilford et al. (1943) described the wrist as a link joint (A). Instability occurs in compression because of the intercalated segment (B). The scaphoid in (C) links the radius to the distal carpal row and provides stability against compression forces during wrist flexion and extension.9
Figure 2 Volar view of the wrist joint. (A)–(F) Intracapsular ligaments. (G), (H) Capsular collateral ligaments (Mayfield et al.1).
DISI is usually a result of disruption of the SLL or unstable fracture of the scaphoid. Other causes include Kienbock’s disease. Radiographic findings include a scapholunate angle greater than 601 on the lateral radiograph and a scapholunate gap of greater than 3 mm on a PA view with clenched fist (Terry Thomas sign), (Figs. 4a and b). There may also be a break in Gilula’s arc at the scapholunate interval and there may be a cortical ring sign or scaphoid fracture or hump back deformity of the scaphoid. VISI involves the disruption of the LTL. Radiographic findings include a break in Gilula’s arc on the PA view, a radiolunate angle of greater than 151 and a scapholunate angle less than 301 on the lateral radiograph (Figs. 3a and b). Axial Carpal Instability is secondary to violent trauma causing disruption within the proximal and distal carpal rows in a longitudinal fashion, resulting in either a dislocation or a fracture-dislocation, for example, a trans-scaphoid peri-lunate fracture dislocation. These injuries have been further classified by Garcia-Elias into axial-radial, axial-ulnar and combined (Figs. 5–7). 2. CIND or Carpal Instabilily Non-Dissociative is a result of ligamentous disruption leading to instability between rows (radiocarpal or midcarpal). Radiographic examination may reveal translation of the lunate ulnarly (450%) off the lunate fossa of the radius. Mal-union of the distal radius may also result in CIND (Fig. 8).
3. CIC or Carpal Instability Combined, as its name describes is a combination of the above-mentioned instabilities and is a result of ligamentous disruption both within and between rows. The most often quoted example of this is the perilunate dislocation. It is easily missed if one is not cognizant of this injury. Mayfield8 described 4 stages of perilunar instability (Fig. 9) proceeding from radial to ulnar around the lunate and disrupting the following joints: (i) Scapholunate; (ii) Scapholunate and Capitolunate; (iii) Scapholunate, Capitolunate and Lunotriquetral and; (iv) Complete lunate dislocation usually in the volar direction. 4. Extracarpal instabilities are classified as Carpal Injury Adaptive (CIA) which includes secondary changes in the carpus, which results from a non-union or mal-union of the distal radius. Any adaptive carpus, by definition can be treated by an extra carpal intervention that does not require surgery on the carpus but with time, an adaptive carpus may degenerate to a point where the intrinsic ligaments fail and a secondary CID pattern (intracarpal problem) is established.4 Chronic Instability of the wrist may arise as a sequelae Avascular Necrosis (AVN) of one of the carpal bones, most commonly the lunate (Kienbock’s disease) or scaphoid (Preiser’s disease), Scaphoid Non-Union Advanced Collapse (SNAC) or Scapholunate Advanced Collapse (SLAC) (Figs. 10 and 11).
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Figure 5
VISI. Decreased scapholunate angle.
Figure 4 (a) Scapholunate dislocation—Terry Thomas sign, ring sign. (b) Increased scapholunate angle. Figure 6 Diagrammatic representation of VISI.
Therefore, when assessing an unstable wrist, the following factors should be taken into consideration: A. Time since injury: Acute (0–3 weeks), subacute (3–8 weeks) and chronic (over 8 weeks). B. Constancy: Predynamic, dynamic or static. C. Aetiology. D. Anatomic location. E. Direction of instability. F. Pattern for example, CID, CIND, CIC or CIA.
Aetiology Trauma resulting in ligament injury and/or bony fractures is the main cause of wrist instability, However, occasionally, excision of dorsal wrist ganglia, which most often originate from the scapholunate interosseous ligament in young adults, has been shown to be associated with symptoms and signs of dynamic scapholunate instability10 (Table 1). Rheumatoid arthritis, progressive ageing and attenuation of carpal ligaments and extrinsic malalignments can also cause instability and result in an adaptive carpus.
Diagnosis History A good history and clinical examination are the keys to a correct diagnosis. Detailed and directed questions on the symptoms should be asked, for example if the pain is radial, ulnar or central and if it is bilateral or unilateral. Also the presence of aggravating factors should be ascertained. Certain positions or actions, for example dorsiflexion/ palmarflaxion or radial/ulnar deviation may reproduce the pain. The presence of painful clicks or any weakness while performing certain manoeuvres should also be ascertained. If there is a history of injury, the mechanism of injury must be noted; for example, fall on the outstretched hand, hyperpronation or hyperextension injuries, etc.
Examination Examination involves the usual look, feel, move sequence followed by grip and pinch strength assessment and special
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211 Although wrist arthrography is now obsolete, EUA and dynamic wrist fluoroscopy is a useful procedure because movements of all the carpal bones in relation to each other and in relation to the radius and ulna can be evaluated. Diagnostic wrist arthroscopy is now the gold standard in many centres as the definitive diagnostic study for suspected carpal instability due to its increased accuracy. In addition, wrist arthroscopy can be a therapeutic procedure as well. Diagnostic wrist arthroscopy includes an examination of both the radiocarpal and midcarpal joints. In the radiocarpal joint, probing of the scapholunate ligament, the lunotriquetral ligament and the TFCC is carried out. The volar carpal ligaments are assessed in a radial to ulnar direction to determine whether extrinsic ligament injury has occurred. The midcarpal joint is then examined and a diagnosis of partial or complete carpal ligament injury can be established on the basis of the ease of separation of the scaphoid from the lunate and of the lunate from the triquetrum. With wrist arthroscopy specific patterns of injury can be more accurately identified by direct visualisation. The treatment can then be focused on management of the specific ligamentous injury responsible for the pattern of instability visualised. There exist some arthroscopic wrist instability classifications12 which help determine the degree of instability.
Management and treatment
Figure 7
Trans-scaphoid peri-lunate fracture dislocation.
tests (Table 2). It is particularly important to note if any area of clicking is associated with tenderness on palpation. The palpation is always carried out systematically, starting from the non-tender area.
Investigations The Six Shot Series Radiographs are then made for wrists with suspected carpal instability.11 These include posteroanterior (PA) neutral, PA ulnar deviation, PA radial deviation, PA neutral and clenched fist, lateral neutral and lateral clenched fist. The loaded clenched fist view is to rule out scapholunate instability. Then the carpal alignment is evaluated with Gilula’s method where interruption of the normal carpal arcs of either the proximal or distal carpal row indicates an instability pattern. The scapholunate angle is measured from the lateral radiograph. CT scanning being a purely bone investigation has limited usefulness for instability. MRI with gadolinium enhancement can be used to evaluate carpal ligament injuries but the results tend to be inconsistent. MRI is most useful for evaluating suspected osteonecrosis of carpal bones and tumours of bone or soft tissue. In addition, MRI is good for investigation of the ulnocarpal compartment, i.e. the TFCC (Table 3).
The treatment algorithm of wrist instabilities depends on whether the injury is acute or chronic and also on the patient’s occupation and demands on the wrist. Treatment is based on the time since injury, the age of the patient and the severity of injury because this influences prognosis and outcome. Fractures of the scaphoid are best treated by open reduction and internal fixation (ORIF) with or without bone graft in the first instance. Criteria for instability include displacement greater than 1 mm, scapholunate angle greater than 601 and capitolunate angle greater than 151, proximal pole fractures, vertical oblique fractures and comminuted fractures. However, if the fracture is minimally displaced then conservative treatment with a below elbow cast is preferred and has a 95% union rate. For ligament injuries, conservative treatment with the use of static or dynamic wrist splints has a role in certain cases but the failure of conservative treatment, especially for SLL ligament tears is an indication for surgical intervention. Broadly, surgical intervention is performed for 3 main categories of instability. For acute cases, repair7fracture reduction is performed whereas for subacute cases, repair7soft tissue reconstruction is performed. In chronic cases, reconstruction and/or salvage procedures are performed. In acute cases of ligament disruption, for example, SLL dissociation with DISI, closed reduction and percutaneous pinning is the initial treatment of choice. If the position is unsatisfactory, ligamentous repair within 3 weeks of the injury (linkage procedure) is preferred and delayed repair can be performed up to 12 months after the time of injury.
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Figure 8
Malunion of the distal radius resulting in CIND.
However, successful repair depends on the identification of a substantial reparable SLL and a supple scaphoid which can be reduced without extensive dissection. A capsulodesis may be added to a ligament repair, for example if dorsal intercarpal ligament capsulodesis as described by Linschied.13 Dorsal capsulodesis as described by Blatt14 is now of historic interest only although other methods of capsulodesis15 are the treatment of choice for wrists with dynamic scapholunate instability unresponsive to conservative treatment, which is common in adolescents and young adults. Other ligament stabilisation procedures include ligament tenodesis procedures14 or ECU or similar tenodesis procedures.14 If the ligament is not repairable or the deformity is not supple, a stabilisation procedure such as a scaphotrapezialtrapezoid (triscaphe or STT) fusion is advised. Other bony reconstruction procedures designed to stabilise the carpus include four corner fusion, proximal row carpectomy, or for
specific areas, scaphocapitate, scapholunate or triquetrolunate fusions for example. Total wrist fusion is a good salvage operation of last resort. Wrist denervation is used as an adjuvant treatment to relieve pain.
Scaphoid Non-Union Advanced Collapse or SNAC This is a result of non-union of scaphoid fractures and can lead to advanced collapse and progressive arthritis.
Scapholunate Advanced Collapse or SLAC This is the most common form of wrist arthritis and it evolves in a predictable sequence. Causes include Keinbock’s and Preiser’s disease. Injury to the SL ligament and palmar radioscaphoid ligaments leads to a shift of the
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Figure 11 Figure 9
SNAC.
Mayfield’s stages of perilunate instability. Table 1 Causes of wrist instability Trauma Dorsal wrist ganglia excision Rheumatoid arthritis Age Extrinsic malalignments
Table 2 Condition
Name of test
DeQuervain’s Scapho-lunate instability
Finklestein’s Scaphoid shift (Kirk Watson), Scaphoid thrust, Scaphoid lift Midcarpal shift, Pivot shift (Lichtman) Ballotment (Regan), Klieman Shear Test, Compression Ulnocarpal stress Grind Piano key, Radio-ulnar drawer test, Compression, Dimple sign ECU Snap Test
Midcarpal instability Luno-triquetral instability Figure 10
Kienbock’s disease.
pressure centroid of the scaphoid resulting in abnormal intraarticular contact between the scaphoid and the distal radius. Three distinct time-related degenerative changes occur in SLAC. Stage 1: Joint space narrowing between the tip of the styloid process and distal outer aspect of the scaphoid. Stage 2: Degenerative changes along the entire articular surface between the radius and scaphoid. Stage 3: Narrowing of the capitolunate space with arthritis involving the radioscaphoid and capitolunate joints.
Ulnar sided pathology Pisotiquetral arthritis DRUJ instability
ECU subluxation
Initial treatment consists of NSAIDs, wrist splint and modification of activities. For wrists with stage 1 SLAC resistant to nonoperative measures, operative treatment is designed to stabilise the carpus. For wrists with stage 2 and 3 degenerative changes, a motion preserving reconstructive procedure is indicated
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Table 3
S. Sivananthan et al.
Classification of TFCC abnormalities.
most appropriate investigations and management for that particular patient.
Class 1 Traumatic
Class 2 Degenerative
1A: central perforation 1B: Ulnar avulsion7ulnar styloid fracture 1C: Distal avulsion
2A: TFCC wear
References
2B: 2A + lunate7ulnar chondromalacia
1. Mayfield JK, Johnson RP, Kilcoyne RF. The ligaments of the human wrist and their functional significance. Anat Rec 1976;186(3):417–28. 2. Cooney WP, Dobyns JH, Linscheid RL. Arthroscopy of the wrist: anatomy and classification of carpal instability. Arthroscopy 1990;6(2):133–40. 3. Taleisnik J. The ligaments of the wrist. J Hand Surg 1976;1: 110–8. 4. Ritt MJ, Bishop AT, Berger RA, et al. Lunotriquetral ligament properties: a comparison of three anatomic subregions. J Hand Surg 1998;23A:425–31. 5. Gilula LA, et al. Wrist terminology as defined by the International Wrist Investigators’ Workshop (TWIW). JBJS (A) 2002;84: 1–66. 6. The Anatomy and Biomechanics Committee of the International Federation of Societies for Surgery of the Hand: definition of carpal instability. J Hand Surg 1999; 24A: 866–7. 7. Larsen CF, Amadio PC, Gilula LA, Hodge JC. Analysis of carpal instability: I. Description of the scheme. J Hand Surg 1995;20A: 757–64. 8. Mayfield JK, Johnson RP, Kilcoyne RK. Carpal dislocations: pathomechanics and progressive perilunar instability. J Hand Surg 1980;5:226–41. 9. Gilford WW, Bolton RH, Lambrinudi C. The mechanism of the wrist joint. With special reference to fractures of the scaphoid. Guy’s Hosp Rep 1943;92:52–9. 10. Hwang JJ, Goldfarb CA, Gelberman RH, Boyer ML. The effect of dorsal carpal ganglion excision on the scaphoid shift test. J Hand Surg 1999;24-B:106–8. 11. Saffar P. Carpal instability. French Orthop Web J. 12. Berdia S, Shin AY. Carpal ligament instability. EMedicine 2005. 13. Linscheid RL, Dobyns JH, Beabout JW, et al. Traumatic instability of the wrist: diagnosis, classification and pathomechanics. JBJS (A) 1972;54:1612–32. 14. Blatt G. Capsulodesis in reconstructive hand surgery. Dorsal capsulodesis for the unstable scaphoid and volar capsulodesis following excision of the distal ulna. Hand Clin 1987;3:81–102. 15. Wintman BI, Gelberman RH, Katz JN. Dynamic scapholunate instability: results of operative treatment with dorsal capsulodesis. J Hand Surg 1995;20A:971–9.
1D: Radial avulsion
2C: TFCC perforation + lunate7ulnar chrondromalacia 2D: 2C + LT ligament disruption 2E: 2D + ulnocarpal and DRUJ arthritis
Operative treatment can be divided into acute soft tissue treatment, soft tissue augmentation, limited bony fusions or salvage procedures. Soft tissue procedures include the modified Brunelli procedure, ECU tenodesis and wrist denervation. Limited bony fusions include the radial styloidectomy or STT or scaphocapitate arthrodesis. The aim is to maintain the scaphoid in a normal alignment with regard to the longitudinal axis of the wrist thus ensuring that compressive and shear forces are transmitted through a normal radioscapholunate articulation. Salvage procedures include either a four corner fusion with scaphoid excision or a proximal row carpectomy. It is useful to perform an arthroscopic assessment prior to these procedures. Wrist arthrodesis is another option.
Conclusion Wrist instability is a dynamic spectrum ranging from examples like the simple scaphoid fracture or single ligament laxity to the complex trans-scaphoid peri-lunate fracture dislocation or the SLAC wrist. There are various aetiologies for this range of pathologies and the most important clinical concept is to obtain an accurate history and examination in the clinic, which will then lead to the
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MINI-SYMPOSIUM: COMPUTER AIDED/ROBOTIC ORTHOPAEDIC SURGERY
(i) Registration techniques for computer navigation Guoyan Zhenga, Jens Kowala, Miguel A. Gonza ´lez Ballestera, Marco Caversacciob, Lutz-Peter Noltea, a
MEM Research Center for Orthopaedic Surgery, Institute for Surgical Technology and Biomechanics, University of Bern, Stauffacherstrasse 78, CH-3014 Bern, Switzerland b University Hospital, ENT, Head and Neck Surgery Division, Bern, CH-3010, Switzerland
KEYWORDS Computer-assisted surgery; Surgical navigation; Registration; Orthopaedic surgery; Accuracy
Summary Mathematically, registration is a process to determine a geometrical transformation that aligns points in two frames of reference, so that the attributes associated with those points can be viewed and analyzed jointly. Clinically, registration is an important step in computer-assisted surgical navigation to correlate morphological information collected in different surgical stages, before, during and after the operation. This paper gives an overview of registration techniques as applied to computer-assisted surgical navigation for orthopaedic interventions. Challenges in quantifying registration accuracy are discussed, and emerging new registration techniques are presented. & 2007 Elsevier Ltd. All rights reserved.
Introduction With the advent of advanced pre and intraoperative imaging means, the development of sophisticated algorithms for image data processing and visualization, and the accessibility of devices for sub-millimetric, real-time tracking of objects in space, computer navigation systems and robotic devices have been created that aim at enhanced surgical accuracy and reliability, reduced radiation exposure, and ultimately improved clinical outcome. These techniques were initially developed for intracranial interventions, and after further refinement can now cover various procedures in orthopaedics and traumatology. Conceptually, the conCorresponding author. Tel.: +41 31 631 5959;
fax: +41 31 631 5960. E-mail address:
[email protected] (L.-P. Nolte). 0268-0890/$ - see front matter & 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2007.03.002
cept of computerized surgical navigation is analogous to ground-positioning satellite systems as used in cars, constantly displaying the car’s location on a digital map. In order to generate such feedback during surgery three tasks have to be fulfilled by a computer navigation system: (a) a virtual object (VO) generated e.g. from computed tomographic (CT), magnetic resonance (MRI), fluoroscopy (FLC), or ultrasound (US) image data sets, or even from point digitization, has to be provided serving as the ‘‘digital map’’ of the patient, (b) the spatial location of all important instruments has to be measured in real-time by a tracking device, also termed navigator, in three dimensions and in relation to the patient frame of reference established on a therapeutic object (TO), i.e., the part of the patient’s anatomy to be operated on, and (c) the relative instrument position has to be transferred into the space of the virtual object to enable its visualization at the correct location.
ARTICLE IN PRESS Registration techniques for computer navigation The technique used to fulfill this last task is called registration. It is a process to determine the geometrical relationship that aligns points in two frames of reference, i.e., those of virtual and therapeutic objects, so that the attributes associated with those points can be viewed and analyzed jointly. Registration, also known as matching, is an important step in computer navigation to correlate information collected in different surgical stages, before or during the operation. Without registration, a detailed surgical plan and corresponding simulations of the surgical procedure, prepared preoperatively, cannot be optimally implemented in the operating room, thus relying solely on the spatial sense of the surgeon. Motivated by the needs and challenges arising from clinical practice, a wide variety of different medical image registration approaches have been developed and realized following numerous methodologies. The survey articles by Fitzpatrick,1 Lavallee,2 and Maintz3 provide excellent sources for in-depth discussion of medical image registration, associated problems and solution strategies. It should be noted that registration techniques used for image fusion are substantially different from those used for computer navigation. In the former case, all geometric data are matched and their associated attributes are fused within a single, unique coordinate system while in the latter case they also have to be registered with the physical space of the patient. The purpose of this paper is to give an overview of registration techniques used in current systems for surgical navigation.
Theory and terminology From an operational point of view, the inputs of registration are two entities to be registered; the output is a geometrical transformation, which is a mathematical function used to transform points in one entity to points in the second.1 Each entity defines its own local frame of reference and there are attributes associated with points in those entities, e.g., gray values in a CT volume. We define the entity to be transformed the floating entity and the other the reference entity. Mathematically, any registration technique can be described by three main components: (a) a geometrical transformation, which relates the reference and floating entities; (b) a similarity measure which measures similarity between reference and transformed floating entities; and (c) an optimization scheme which determines the optimal geometrical transformation by maximizing the similarity measure. A geometrical transformation can be classified by its complexity into ‘‘rigid transformations’’, where distances between points and angles between lines and planes in the floating entity are preserved, and ‘‘non-rigid or deformable transformations’’, where geometrical relations are stretched or deformed. Mathematically, a rigid transformation can be uniquely described by a rotation and a translation, while the description of a non-rigid transformation is not unique. According to the geometrical transformation used in the registration process, we can categorize the registration techniques for computer navigation into two groups: rigid registration and deformable registration. Most
171 computer navigation systems for orthopaedic surgery only incorporate rigid registration, considering the fact that bone is a rigid, non-deformable tissue. However, deformable registration, specifically statistical model based deformable registration4 or bone morphing,5 has been recently integrated into a few commercially available computer navigation systems. Before we introduce various registration techniques for computer navigation, it is worth explaining an important distinction between registration and another common concept in computer navigation: calibration.2 In general the purpose of calibration and registration is the same. Both aim at determining the geometrical relationship between the frames of reference located in different entities. However, the distinction between registration and calibration is also apparent. According to Lavallee,2 if two frames of reference are rigidly connected to a same object, then their geometrical relation will be estimated through calibration procedures; if associated coordinate systems are totally independent, they are linked through a registration process. For instance, in MRI-based navigation, the geometric distortion induced by the field inhomogeneity is estimated through a calibration procedure using phantom measurements, whereas the relation between a preoperative MRI of a patient and the physical space of this patient is determined through a registration process. Another example of calibration in computer navigation was the introduction of the so-called registration-free systems6 based on a navigated Iso-C3d C-arm (Siemens Medical AG, Erlangen, Germany), in which the challenging and often timeconsuming intraoperative registration process is replaced by an offline and procedure-independent calibration. The principle of such an approach is simple, although its technical implementation is not trivial. In the offline calibration step, the relation between a reference coordinate system rigidly affixed to the Iso-C3d C-arm and the image volume of reconstruction is determined through a paired-points matching process. Intraoperatively, as soon as the CT-like volume data set of the patient is acquired, the navigation system immediately knows its position and orientation in the patient reference coordinate system using the rigid transformation obtained through the offline calibration procedure and the transformation between the patient reference coordinate system and the device reference coordinate system, which is obtained in real time from the tracking device.
Registration techniques for computer navigation As registration is an embedded component in a computer navigation system, the input data to the system, collected at different surgical stages, before or during operation, determine the type of registration technique. Table 1 summarizes the relationship between the type of input data and the type of registration technique. For a more comprehensive classification of different registration techniques, we refer to previously published review papers on this topic.1–3
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Table 1
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The relationship between the type of input data and the type of registration technique for computer navigation.
Types of input data
Types of registration technique
Preoperative
Intraoperative
CT or MRI
Locations of fiducial markers Digitized anatomical points
3D/3D feature-based rigid registration 3D/3D feature-based rigid registration 2D/3D image-based rigid registration 3D/3D image-based rigid registration
Calibrated 2D fluoroscopic images Calibrated 1D (A-Mode), 2D (B-Mode), or 3D ultrasound data set Calibrated CT-like volume data
Image fusion based rigid registration
Knowledge about volumetric imaging device
Volume data
Modality-based rigid registration
Statistical model
Digitized anatomical points/‘‘surgeon–defined anatomy’’ Calibrated 2D fluoroscopic images
3D/3D feature-based deformable registration 2D/3D image-based deformable registration 3D/3D image-based deformable registration
Calibrated 2D/3D ultrasound images
Rigid registration techniques for computer navigation 3D/3D feature-based rigid registration technique Related methods in this category for finding global, rigid transformation to register the virtual and therapeutic objects are paired-points matching and surface matching. They are the registration techniques implemented in the first generation of computer navigation systems for orthopaedic surgery2 and still the most widely used registration techniques in nowadays CT-based navigation systems. This is not surprising, considering that the similar problem to register two sets of geometrical features (e.g., registration of two point sets or registration of points to surface) has been well studied in the fields of robotics and computer vision, which existed long before the introduction of computer navigation. Thus, the existing body of knowledge allows us to establish a rough taxonomy of the different solutions proposed in the literature. Well-known pairedpoints matching algorithms range from iterative solutions to analytic, direct methods using quaternion theory or singular value decomposition while the most well-known surface matching solution is the so-called iterative closest point (ICP) algorithm.1–3 Mathematically, both registration techniques are similar. They both use the geometrical features (points, lines, surface) corresponding to the same anatomical or fiducial structures to derive the registration transformation. However, in paired-points matching, the correspondences are assumed to be known while in surface matching, those correspondences need to be iteratively determined, as shown in Fig. 1 for the specific task of registration for dorsal spinal interventions. The operational procedure for paired-points matching is simple. At least three pairs of distinct points are defined preoperatively in the virtual object and intraoperatively in the therapeutic object. The former set of points is usually
identified using the computer mouse and marking the desired location within the image data. For the intraoperative acquisition, a probe is used. In the case of a navigation system it is tracked by the navigator and for robotic surgery it is mounted onto the robot’s actuator, which the surgeon then guides to the location to be recorded.7 Once both point sets are available, the transformation that links the underlying coordinate systems can be derived using one of the previously mentioned paired-points matching algorithms. Obviously this procedure is highly interactive during both the preoperative definition of registration points and the intraoperative acquisition of their counterparts. Consequently, this step is error-prone, in particular because a good registration result and thus an accurate performance of the navigation system strongly depend on an optimal selection of the registration points and the exact identification of the pairs. To improve the accuracy of this step, alternative and complementing techniques have been proposed. Probably the most obvious was the implantation of artificial objects to create easily and exactly identifiable spots for paired-points registration. Percutaneous markers, pins, or complex marker carriers have been suggested.2 These artificial objects are easily identifiable in the images and intraoperatively on the patient. As a consequence, carrying out an exact matching between the rigid bodies is then very easy or can even be automated. However, these methods require the artificial markers to be represented in the preoperative images, thus necessitating their implantation prior to image acquisition through an additional intervention. For reasons such as costs, infection risk, patient discomfort, etc. none of these methods have gained wide clinical acceptance. Without the use of artificial objects, paired-points matching cannot fulfill the accuracy requirements of most computer-assisted orthopaedic surgical procedures and is thus often complemented with surface matching.8 Surface matching uses the surface of the virtual object as a basis for
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Figure 1 Paired-points matching vs. surface matching. (A) Paired-points matching where the correspondences between homologous anatomical landmarks are known; and (B) surface matching where intraoperatively acquired points are matched to preoperatively segmented surfaces.
registration. With the help of the navigator, points are captured on the therapeutic object’s surface, which are then mapped onto the virtual object’s surface. The technique is based on the fact that a small number of points digitized on the accessible bone surfaces usually describe the surface very precisely. Preoperative image processing allows for the extraction of the exact shape of the bony surface from preoperative CT images. Using this approach, it is not possible to analytically calculate the transformation between the virtual and therapeutic object. The correct transformation must be searched for, usually using a similarity function that measures the degree of correspondence between the points and the surface. A major advantage of surface matching is that it removes the
dependence on the error-prone identification of corresponding anatomical landmarks, as long as the intraoperatively collected points lie on the surface of the anatomy, which has been delineated in the preoperatively acquired medical images.
2D/3D image-based rigid registration techniques The above described feature-based rigid registration is an invasive procedure, which requires either implanting artificial objects or exposing parts of the anatomy to enable contact-based point digitization. As a less invasive alternative, fluoroscopy-based 2D/3D registration (see Fig. 2) has generated a lot of interest.9
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Figure 2 Screenshots of different stages of a CT-Fluoro matching process. (A) Pre-registration for CT-Fluoro matching; (B) final results of CT-Fluoro matching (courtesy of BrainLAB AG, Munich, Germany).
The reported techniques for fluoroscopy-based 2D/3D registration can be split into two main categories: featurebased methods and intensity-based methods. Feature-based methods require an antecedent segmentation stage, which is error-prone and difficult to achieve automatically. Segmentation errors can lead to errors in the final registration. As a consequence, interactive and semiautomatic methods10 have been proposed to extract bone contours from the fluoroscopic images. But in general, this
problem is still unsolved and is a field of very active research. In contrast, intensity-based methods directly compare the calibrated fluoroscopic images with digitally reconstructed radiographs (DRRs), which are obtained by simulating X-ray projections of a preoperative CT volume.11 No segmentation is required. One of the main factors that affects the accuracy of intensity-based methods is the choice of similarity measure, which is a criterion function that is used in the registration procedure for measuring the
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Figure 3 An intraoperative setup for B-mode ultrasound based registration. (A) Intraoperative setup; (B) the final registration results. After registration, ultrasound image information is superimposed onto associated multi-planar reconstructions from the CT data set.
quality of image match. How to design a robust similarity measure so that the registration can be performed successfully in a practical setup is still an active research field.9 Major challenges result from outliers such as interventional instruments present in the projection images. Compared to the feature-based methods, intensity-based methods suffer from higher computation cost, largely due to the process of DRR generation, but demonstrate potentially better accuracy and robustness and are more easily automated. Hybrid 2D/3D registration techniques which avoid the explicit segmentation step in the feature-based methods but require less computation cost have also been proposed recently.12 3D/3D image-based rigid registration techniques The above mentioned 2D/3D rigid registration technique exemplifies how registration between virtual and therapeutic objects can be achieved in a minimally invasive manner. Alternative non-invasive registration techniques, this time employing ultrasound data, shall be discussed next.
Although primarily designed for soft tissue imaging, ultrasonic devices also allow transcutaneous scanning of bone surfaces. Two types of approaches have been explored to use calibrated ultrasonic data for registration: featurebased and intensity-based approaches. Feature-based approaches attempt to acquire bony surface points from calibrated ultrasonic data and then take the acquired surface points as the input to a 3D/3D paired-points or surface matching technique as described in Section 3.1.1 to estimate the registration transformation. Promising results using calibrated or self-calibrating B-mode ultrasound probes have demonstrated their potential for surgical navigation.13,14 In Fig. 3 an experimental intraoperative setup for B-mode ultrasound-based registration is displayed. Currently, technology transfer is hindered by limitations related to automated and accurate localization and identification of the relevant anatomical structures from noisy images and signals.13 In contrast, intensity-based approaches directly make use of the calibrated ultrasound images (a series of sparse 2D images or a 3D volume) to find
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Figure 4 Screenshots of different stages of an intraoperative bone morphing process. (A) Point acquisition; (B) calculation of morphed model; (C) verification of final result (courtesy of BrainLAB AG, Munich, Germany).
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the registration transformation and thus avoid the difficulty of segmenting the bone surface at the US image level.15 However, robustness and accuracy are still challenging issues that need to be improved before these approaches can be transferred from the laboratory into the surgical theatre for routine use.
Deformable registration techniques for computer navigation Preoperative CT imaging is the method of choice for a wide variety of navigated surgical interventions, and it is compulsory for the use of orthopaedic surgical robots. However, the high level of radiation received by patients, the large quantity of data to be acquired and processed, and the high logistic cost involved in acquisition and processing of CT data make them less functional. As alternatives, intraoperative imaging means such as fluoroscopy and ultrasound, or even the so-called ‘‘surgeon-defined anatomy’’,5 which is a technique based on point digitization, have been successfully used to create virtual objects intraoperatively. When compared to CT these techniques suffer from the fact that no complete 3D model structure information is available. The surgeon still needs to mentally fuse data acquired using these techniques. One way to address this dilemma is to do statistical deformable registration (SDR)4 or bone morphing,5 which is a method to reconstruct the geometrical shape of an object from sparse input data using a previously generated statistical shape atlas. In the context of computer navigation for orthopaedic surgery, the shape of the operated bone is predicted based on a statistical shape model (SSM) representing the typical shape of the bone, represented by the statistical mean and the associated morphological variations found in a collection of sample bones of a given population. The SSM is constructed by applying principal component analysis (PCA) to the aligned shape models of these sample bones. In order to create a good estimation of the individual patient’s bone, a rather small number of morphological features (surface points, rotation centers, anatomical axes, etc.) are acquired by the surgeon intraoperatively and enable the underlying algorithms to select parameters that guarantee precise shape prediction. This method therefore differs from the ‘‘surgeon-defined anatomy’’ method, in which abstract bone models are constructed from the acquired data following simple sampling schemes. In contrast, the input data to an SDR algorithm is used to extract the individual deviations of a particular patient from the statistical mean and to deform that mean accordingly. An example for an intraoperative bone morphing process is shown in Fig. 4. This method is heavily employed in so-called ‘‘image-free’’ navigation systems, mainly for knee and hip surgery. However, with the availability of statistical shape atlases of other anatomical regions, the technique could be applied to any part of the skeleton. Such approaches bear significant potential for future developments of computer navigation technology since they are not at all bound to the classical pointer-based acquisition of bony features. In principle, the reconstruction algorithms can be tuned to any type of patient-specific input, such as e.g. intraoperative calibrated
Figure 5 Reconstruction of bone surface from two calibrated fluoroscopic images and a statistical shape model using deformable registration.
fluoroscopic images or tracked ultrasound, thereby potentially enabling new minimally invasive procedures. Fig. 5 shows an example of bone surface reconstruction from calibrated fluoroscopic images and a statistical shape model. Moreover, prediction from statistical atlases is possible not only for the geometric shape of an object. Given a three-dimensional radiological atlas, ‘‘synthetic CT scans’’ could be predicted from intraoperatively recorded data.16
Quantifying registration accuracy Assessing the accuracy of a given registration algorithm in a quantitative manner is a difficult task. The accuracy of a registration transformation cannot be easily summarized by a single number, as it is spatially varying over the image. For paired-point rigid registration using fiducial points, Fitzpatrick et al.1 have presented a theory of error modeling that can predict the expected error distribution based on errors in localizing individual points, and the distribution of points. In this theory, the localization error of the fiducial points is defined as the fiducial localization error (FLE). The residual error in fitting of paired-points is called the fiducial registration error (FRE), which is actually the root mean square (RMS) error between homologous fiducials after registration and is used by most navigation systems in the market to report the registration accuracy. Although helpful to the surgeon to a certain extent, the FRE is less reliable than the target registration error (TRE), which is defined as the error between a measured anatomical target under the registration transformation and its corresponding location in the space of the virtual object. It should be noted that this theory of errors can be used to optimize the design of fiducial markers and the configuration of the fiducial marker distribution. Another approach to quantify the registration accuracy of a given registration algorithm is to use a ‘‘gold standard’’, which is normally derived with high accuracy using fiducial markers. The registration accuracy can now be calculated by comparing the transformation calculated by the given
ARTICLE IN PRESS 178 registration technique with the known, ‘‘gold standard’’ solution. Finally, a more practical approach that can be applied in day to day clinical routine is to perform visual verification. This is usually done by touching anatomical landmarks of the therapeutic object with a tracked pointer and visually checking whether the corresponding location in the virtual object is displayed correctly by the navigation system. This step is mandatory for a safe usage of a navigation system. It is important to note that a point distribution should be chosen, which assures a 3D positional control.
Emerging registration techniques for computer navigation Registration is and will remain an active field of research. New methods and techniques will help to simplify the intraoperative matching procedure with the ultimate goal to fully automate it. In the following, two examples of emerging registration techniques will be presented, which hold potential for improving future computer navigation systems.
Modality-based registration techniques Technical insight into existing and new imaging devices may allow us to design fully automatic registration procedures. An example of such an approach was originally presented by Messmer et al.,17 where the coupling was achieved by obtaining the geometric relation between a CT scanner and acquired images in a one-time offline calibration procedure and the name ‘‘modality-based navigation’’ was coined. This relation could subsequently be used to obtain patient-toimage correspondence for every new acquisition. Another example is the headset-based registration suite.18 In addition to a fully automated patient-to-image registration, it also checks the CT scan quality by detecting patient movement during scanning and by checking for scanner calibration quality. Such a technique provides the user with improved clinical accuracy throughout the surgical volume, while facilitating OR setup and enhancing ease of use. To date, this technique has been applied to skull-base surgery, but in principle it can be applied to any part of the skeleton.
Image fusion based registration techniques Examples of image fusion based registration techniques have been presented above and include both rigid and non-rigid matching of a preoperative CT scan with multiple intraoperatively acquired calibrated image data, e.g. from image intensifiers or ultrasound units. Further research and development effort is necessary before these techniques can be applied in the operating theatre. An image fusion based registration technique with potential for future routine use in trauma cases is described in Rudolph et al.19 It registers calibrated fluoro-CTs from an Iso-C3d to a preoperative CT volume. The used Iso-C3d system is a navigated mobile C-arm that enables the surgeon to acquire CT-like volume data intraoperatively with high
G. Zheng et al. resolution but reduced image quality and smaller field of view when compared to a standard CT scan. An offline calibration procedure (cf. Section 2) allows the surgeon to directly correlate the image volume to the physical space of the patient. By registering such a volume data to a preoperative CT volume, one can enhance the intraoperative visualization of the surgical field. It is well known that CT and MRI data can provide complementary information about bone and soft tissue. Bone structures are better visualized by means of CT while MRI data would for instance let the surgeon assess the quality of joint cartilage. Van de Kraats et al.20 recently presented their non-invasive method for registration of MR images to intraoperatively acquired 3D rotational X-ray images (3DRX). Since the calibrated 3DRX system provides an intrinsic relation between the intraoperatively acquired 3DRX data and the patient, their method indirectly registers the MR with the patient, allowing image-interactive precise navigation in both 3DRX and MR data.
Discussion and conclusion Registration is a key step in every computer navigated orthopaedic intervention. Conceptually it aims at establishing an accurate geometrical relationship that aligns points in two frames of reference, i.e. those of the therapeutic object and its virtual representations, e.g. generated from image data sets. It is a prerequisite for any image-interactive guidance and placement of orthopaedic devices, such as instruments and implants using robotic or navigation technology. Early CT-based orthopaedic navigation systems failed to penetrate the market due to complex, unreliable and often time-consuming matching procedures. Since then different approaches that ultimately provide systems for day to day routine use could be identified among the computer-assisted orthopaedic surgery community. At first navigation technology providers and their clinical partners developed image-free navigation modules using the so-called ‘‘surgeon defined anatomy’’ concept. They successfully made their way into the operating theatre. However, image-free systems supply limited morphological information to the surgeon and thus only cover a few applications, such as knee and hip joint replacement. They do not provide a sound basis for interventions, where imageinteractive surgical actions have to be performed, e.g. in fracture reduction and fixation. The scientific community concentrated on improved design and realization of registration algorithms. They also broke new grounds by introducing statistical shape atlases and bone morphing concepts, initially to expand the potential of image-free systems. Another area of progress was the integration of existing intraoperative imaging means into existing tracking concepts as exemplified by 2D fluoroscopic navigation. These systems for the first time allowed the collection of morphological information and its use for navigation in different stages during the operation. The early success of fluoroscopic navigation stimulated development activities of the image device manufacturers
ARTICLE IN PRESS Registration techniques for computer navigation towards new intraoperative imaging means such as the 3D Carm based fluoro-CT devices. Due to these efforts the computer navigation community can revert to a wide spectrum of potential registration algorithms and techniques. In consequence orthopaedic navigation technology has successfully emerged into fields such as spinal and trauma interventions, which require image interactivity. Still surgeons are confronted with certain complexity of the resulting work flow and need considerable training to be in full control of the registration process. Further research and developments are necessary to achieve the ultimate goal of an accurate, reliable, and fast automated registration. This will require a concerted approach with a close partnership of expert surgeons and technologists.
Acknowledgments This work was supported by the Swiss National Science Foundation under the National Center for Competence in Research CO-ME (www.co-me.ch), BrainLab AG, Munich, Germany, and the AO Foundation, Davos, Switzerland.
References 1. Fitzpatrick JM, Hill DLG, Maurer Jr CR. Image registration. Sonka M, Fitzpatrick JM, editors. Handbook of medical imaging. Medical image processing and analysis, vol. 2. Bellingham, WA: SPIE Press; 2000. p. 447–513. 2. Lavallee S. Registration for computer-integrated surgery: methodology, state of the art. In: Taylor RH, Lavallee S, Burdea GC, editors. Computer integrated surgery: technology and clinical application. Cambridge, MA: The MIT Press; 1996. p. 77–97. 3. Maintz JBA, Viergever MA. A survey of medical image registration. Med Image Anal 1998;2:1–36. 4. Fleute M, Lavallee S. Building a complete surface model from sparse data using statistical shape models: application to computer assisted knee surgery. William III MW, Colchester ACF, Delp S, editors. MICCAI’98, Lecture notes in computer science, vol. 1496. Berlin/Heidelberg: Springer; 1998. p. 878–87. 5. Stindel E, Briard JL, Merloz P, Plaweski S, Dubrana F, Lefevre C, et al. Bone morphing: 3D morphological data for total knee arthroplasty. Comput Aided Surg 2002;7(3):156–68. 6. Ritter D, Mitschke M, Graumann R. Makerless navigation with the intra-operative imaging modality SIREMOBIL Iso-C3D. Electromedica 2002;70:31–6.
179 7. Bargar WL, Bauer A, Boerner M. Primary and revision total hip replacement using the Robodoc system. Clin Orthop 1998;354:82–91. 8. Baechler R, Bunke H, Nolte L-P. Restricted surface matching— numerical optimization and technical evaluation. Comput Aided Surg 2001;6:143–52. 9. Zhang X, Zheng G, Langlotz F, Nolte L-P. Assessment of splinebased 2D-3D registration for image-guided spine surgery. Minim Invasive Ther Allied Technol 2006;15(3):193–9. 10. Gueziec A, Kazanzides P, Williamson B, Taylor RH. Anatomybased registration of CT-scan and intraoperative X-ray images for guiding a surgical robot. IEEE Trans Med Imaging 1998;17(5): 715–28. 11. Penney GP, Weese J, Little JA, Desmedt P, Hill DLG, Hawkes DJ. A comparison of similarity measures for use in 2-D-3-D medical image registration. IEEE Trans Med Imaging 1998;17(4):586–95. 12. Livyatan H, Yaniv Z, Joskowicz L. Gradient-based 2-D/3-D rigid registration of fluoroscopic X-ray to CT. IEEE Trans Med Imaging 2003;22(11):1395–406. 13. Tonetti J, Carrat L, Blendea S, Merloz P, Troccaz J, Lavallee S, et al. Clinical results of percutaneous pelvic surgery—computer assisted surgery using ultrasound compared to standard fluoroscopy. Comput Aided Surg 2001;64:204–11. 14. Barratt DC, Penney GP, Chan CSK, Slomczykowski M, Carter TJ, Edwards PJ, et al. Self-calibrating 3D-ultrasound-based bone registration for minimally invasive orthopaedic surgery. IEEE Trans Med Imaging 2006;25(3):312–23. 15. Amin DV, Kanade T, DiGioia AM, Jaramaz B. Ultrasound registration of the bone surface for surgical navigation. Comput Aided Surg 2003;8:1–16. 16. Yao J, Taylor RH. Non-rigid registration and correspondence finding in medical image analysis using multiple-layer flexible mesh template matching. Int J Pattern Recognition Artif Intell 2003;17(1):1145–65. 17. Messmer P, Gross T, Suhm N, Regazzoni P, Jacob AL, Huegli RW. Modality-based registration. Injury 2004;35(Suppl. 1) SA-24– SA-9. 18. Knott PD, Maurer CR, Gallivan R, Roh H-J, Citardi MJ. The impact of fiducial distribution on headset-based registration in image-guided sinus surgery. Otolaryngol Head Neck Surg 2004;131:666–72. 19. Rudolph T, Ebert L, Kowal J. Noninvasive CT to Iso-C3D registration for improved intraoperative visualization in computer assisted orthopaedic surgery. Cleary KR, Galloway Jr RL, editors. Proceedings of SPIE. Medical Imaging 2006: visualization, image-guided procedures, and display, vol. 6141. SPIE Press; 2006. p. 582–9. 20. Van de Kraats E, van Walsum T, Verlaan J-J, Niessen WJ. Noninvasive MR to 3D rotational X-ray registration of vertebral bodies for image-guided spine surgery. Spine 2004;29(3): 293–7.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 180–192
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journal homepage: www.elsevier.com/locate/cuor
MINI-SYMPOSIUM: COMPUTER AIDED/ROBOTIC ORTHOPAEDIC SURGERY
(ii) The accuracy of surgical navigation for orthopaedic surgery R. Phillips Department of Computer Science, University of Hull, Cottingham Road, Hull, HU6 7RX, UK
KEYWORDS Surgical navigation; Image guided surgery; Accuracy; Validation; Orthopaedics
Summary The ability to place accurately and consistently a tool or implant in orthopaedic surgery is potentially one of the key benefits of using a computer assisted orthopaedic surgery (CAOS) system. To achieve such accuracy CAOS systems are considerably more complex in their design than conventional surgical tools. CAOS systems typically comprise patient data acquisition, computer based planning and a means to help the surgeon carry out the surgical plan. Each of these elements can give rise to inaccuracies which propagate through following workflow elements to contribute to the accuracy of the clinical outcome. This paper discusses the nature of accuracy, where inaccuracies occur in CAOS systems and how a structured approach to validation helps provide CAOS systems that perform reliably. It is clearly important that surgeons are fully aware of all factors at the interfaces between the surgeon and the patient and a CAOS system that might affect the accuracy of the clinical outcome. & 2007 Elsevier Ltd. All rights reserved.
Introduction Computer assisted orthopaedic surgery (CAOS) has been slowly evolving for some 15 years. It has become accepted as commonplace technology for some orthopaedic procedures, for example spinal fixation. Fundamental to CAOS is the basic orthopaedic principle (BOP), which Mohsen defined as the ‘‘placement of an object (guide wire, screw, tube or scope) at a specific site within a region, via a trajectory which is planned from X-ray based two dimensional images or other imaging modalities and governed by three dimensional anatomical constraints’’.1 CAOS can thus be defined Tel.: +44 1482 465680; fax: +44 1482 465823.
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as the application of computer-based technology to assist the surgeon implement the BOP in the operating room (OR). As with all technologies, the user must be aware of the technology’s performance, its limitations and learn how to use it effectively. This is certainly true for CAOS. During an operation confirming the correct position of an implant and/or tool relative to the anatomy at the orthopaedic treatment site is generally achieved by the surgeon checking visually the true reality of the situation. This is achieved by the surgeon checking an actual view of the operating site either directly or via some form of intraoperative imaging such as a fluoroscope, microscope, video camera, etc.; this follows the paradigm of ‘‘what you see is what you have’’. In CAOS this checking of the treatment site is often via a virtual view that has been reconstructed by a computer where the view is close enough
ARTICLE IN PRESS Surgical navigation for orthopaedic surgery to reality and fit for purpose. An example of the latter is the display of the trajectory of a drill bit in a pedicle for a spinal fixation procedure using virtual fluoroscopy. Thus in accepting this virtual view the surgeon must know how accurate this view is and have a good understanding of the factors that influenced the accuracy of this view. Furthermore, the surgeon must be aware of the implications of using CAOS technology so as to obtain surgical results that are acceptable, reliable and repeatable. Accurate placement of a surgical tool or implant is often stated as one of the potential benefits of a CAOS system. However, bone is not a geometric static object. It is a living structure that will adapt to and compensate for less than perfect fracture reduction and placement of a prosthesis. In fact having too good a fit of a prosthesis in the bone can hinder the bone growth around a prosthesis, e.g. for uncemented total hip replacement. This paper starts by defining the terms needed to discuss accuracy issues of CAOS in an unambiguous way. Next it identifies the various sources of imprecision there are in CAOS technology. The paper then considers the notion of the setting of the clinical requirements for accuracy of a CAOS system. It then looks at ways the accuracy of a CAOS system can be determined. This is followed by considering how to design a CAOS system to meet these accuracy requirements. Presented next is a review of some systematic approaches to validate that a CAOS system meets the accuracy requirements. A case study of a CAOS system for distal locking of intramedullary nails is presented along with a discussion of validation experiences.
The terminology of accuracy It is important for the CAOS community and for the users of CAOS that there be a common set of terms with precise meaning relating to accuracy. This helps debate and decision making and if used consistently brings clarity to the interpretation of accuracy results published in research journals and by manufacturers of CAOS systems. This section gives an explanation of various terms related to accuracy. For the purpose of defining accuracy terms, let’s suppose there is a target value T and that an estimate of this target value is given by an actual value A. This actual value could have been produced by a calculation or physically measured. The accuracy of the actual value A is how close that value is to the target value T. The difference between the target value T and the actual value A is termed the error. Note that in this context that ‘error’ does not imply a mistake but rather it is the term for inaccuracy. In practice, if the actual value has been measured there is often an element of uncertainty in the actual value as the measuring tool itself will not be 100% accurate. However, the average size of this measurement error is often at least an order of magnitude smaller than the average error expected between the actual and target values and thus this measurement error can often be ignored for practical purposes. The target value is also often taken as being a ground truth value, i.e. there is no measurement error or it is so small it can be ignored. When an actual value is measured repeatedly in an independent way, the term precision specifies how closely
181 these measured values agree. Thus for repeated measurements the mean value of the measured results are typically given along with the standard deviation of the measured values and often measured values at the extremities of the measured range (i.e. minimum and maximum values for single valued measurements). Results of a CAOS system must be repeatable and reproducible. The metrics for precision (i.e. mean and standard deviation) thus provide a quantitative way of assessing repeatability and reproducibility. The smallest change of an actual value that can be detected by the measurement device is known as the resolution of the measurement. This resolution places a limit on the precision that can be achieved for the measured value. The accuracy of a CAOS system (or component) is normally determined by a set of measured actual values for stated conditions which can be compared with known target values. The error in the system comprises both random errors and systematic errors. Random errors tend to cancel each other out, thus as the number of measured results increases the effect of random errors on the mean actual value decreases and this mean tends towards the target value. On the other hand a CAOS system may have a number of systematic errors. Such errors are always present and contribute to a bias in measured results; this manifests itself as the mean of the actual value being consistently different from the target value. Having the accuracy performance of CAOS systems allows surgeons to compare competitive systems and to judge whether to use CAOS for a surgical procedure by comparing this performance with the accuracy constraints for surgery. To developers of CAOS systems achieving acceptable accuracy results is fundamental to the design and development of such systems. Ideally a CAOS system is designed to have minimal systematic errors and a known behaviour of random errors that together ensure that accuracy of the system meets the clinical accuracy requirements. To verify that a CAOS system performs as designed and to validate that it meets the clinical requirements, extensive accuracy analysis and assessment is normally a major part of the development of a CAOS system.
Sources of inaccuracy errors in CAOS systems The stakeholders who are concerned with the accuracy performance of CAOS systems are the surgeons, the manufacturers and the healthcare providers. This section provides them with insights into the sources of inaccuracy errors in CAOS systems. The surgeon is particularly interested in those aspects of accuracy that influence the surgical outcome for the patient and how accuracy influences the way the surgeon uses CAOS equipment. Thus the surgeon is primarily interested in accuracy at the patient-surgeon interface. Manufacturers of CAOS systems should have a thorough understanding of all accuracy and error issues that contribute to the accuracy performance of the patient-surgeon interface. For this they need to understand all sources of potentially significant errors and understand how they
ARTICLE IN PRESS 182 propagate from their point of origin to affecting the accuracy at the patient-surgeon interface. To construct repeatedly reliable CAOS systems, a manufacturer needs to specify tolerances on the sizes of errors for all potential sources of error in the system, and have appropriate validation and quality assurance procedures to ensure that these tolerances are not exceeded. The final group of stakeholders in accuracy performance are the healthcare providers who must ensure that CAOS systems are fit for purpose and safe. They need to be assured that a CAOS system will consistently perform within its stated limits of accuracy and ensure that appropriate maintenance and quality procedures are in place to ensure the CAOS system keeps working accurately. The accuracy validation process of CAOS equipment must therefore be transparent and ideally be certificated by a trusted authority. The different types of CAOS systems for image guided orthopaedic surgery can be classified on the kind of patient data set used for surgical navigation. The classifications of main interest today are preoperative CT, 2-D fluoroscopy, 3-D fluoroscopy, intraoperative CT and image-free navigation. Nolte and Beutler2 present details of such a classification of CAOS systems. In the majority of these CAOS systems the elements of the work flow specific for an image guided operation are as follows: (1) patient data acquisition, (2) creation of the surgical plan, (3) intraoperative registration of this plan with the patient and (4) navigation of the surgical tool/ implant to implement the surgical plan. These four elements are typically performed in sequence, thus errors from one element propagate through to the following elements. It is often the fact that accuracy is only as good as the weakest link in this sequence. The error in each element is a combination of the errors that are inherent in the equipment used in that element, the errors that arise from the procedural steps associated with that element and errors that have propagated from previous elements in the work flow.
Patient data acquisition There are mainly two types of patient data acquired, namely image-based and image-free. For image-based data there are recording errors which include artifact errors (e.g. motion, metal in CT, etc.), errors from the imaging chain, etc. CT, intraoperative CT and 3D fluoroscopy are all designed to be quantitative imaging devices in that each pixel/voxel corresponds to a known position on the patient. This is not the case for most 2D-fluoroscopy systems. These are essentially qualitative 2D imaging devices which have been retrofitted with a mechanism that provides positional information about an image, for example Medtronic Sofamor Danek’s FluoronavTM and SurgiGATEs (Medivision, Oberdorf, Switzerland). This retrofitting device comprises two parallel grid plates separated by a gap. The device is attached to the X-ray receptor of the C-arm with the device’s position being tracked by an optical camera tracking system. The parallel grid plates are made of X-ray translucent material and contain a grid arrangement of small metallic balls. This plate arrangement has two purposes. Firstly, a fluoroscope
R. Phillips normally displays distorted images due the inherent characteristics of the image intensification tube;3 the grid closest to the X-ray receptor allows the image to be calibrated so that an undistorted and quantified image can be produced. Secondly, using back projection of the balls on the grid offset from the X-ray receptor the position of the X-ray source relative to the X-ray receptor can be determined. The optical tracking system provides the position of the grid arrangement device from which the position of the X-ray receptor and the X-ray source is determined in the coordinate space of the optical camera system. The fluoroscope is only a 2D imaging device, but by knowing the position of the X-ray source and the X-ray image the treatment site can be partially reconstructed from two or more fluoroscopic images. There are a number of error sources in a 2-D fluoroscopy system. The accuracy performance of this imaging system thus depends on the following:
The accuracy of the measured physical position of each ball in the two grids.
The density of balls in each grid. The accuracy of the measured geometric relationship between the two grids.
The distance between the two grids. The image analysis algorithm that calculates the position
in a fluoroscopic image of the centre of each ball in the grid that appears in the image. The algorithm used to calibrate the fluoroscopic image. The algorithm used to calculate the position of the X-ray source. The accuracy of the 6-D position of the grid arrangement provided by the optical position camera system.
The 2-D fluoroscope is a good illustration of the complex nature of achieving the requisite level of accuracy in a COAS system. In fact the above situation is even more complex since the designer of a 2-D fluoroscope for CAOS usage has numerous other design choices associated with the position tracking of the grid. For instance, this includes what level of accuracy is required of the camera system, what is the best arrangement of infrared light emitting diodes (IREDs) on the grid arrangement, how accurately to measure the position of these IREDs on the grid arrangement, etc.
Creation of the surgical plan For the creation of a surgical plan from a volumetric data set, accuracy of this work flow step depends largely on the errors in identifying anatomical features from the volume upon which the plan is based. Such identification might include segmentation of a bone surface, mark up of anatomical features, etc. A surgical planning algorithm then uses these features along with surgeon specified parameters to create a plan. For 2-D fluoroscopic CAOS systems there is only a partial reconstruction of the operating site, thus the surgeon has to be aware or the errors that may arise due to having only this partial volumetric view.
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To be able to implement this computer based surgical plan using image guidance, the plan has to be mapped (i.e. registered) with the patient. For plans created preoperatively, registration can be often point based where a number of fiducials are attached to the patient; the position of these fiducials in the CT are then registered by measuring the position of the fiducials on the patient on the operating table. This measurement is normally done using an optically tracked pointer. To reduce the risk of complications caused by adding fiducials to the patient, many CAOS systems now use anatomic fiducials.4 For these point-based fiducials (both external and anatomical) a rigid body registration algorithm is used. The accuracy of such registration depends on the following:
tracked pointing probe or ultrasound. Yet another approach to registration is to register intraoperative fluoroscopic images with the preoperative CT,6 however, this approach has not yet become mainstream. Where surgical planning is based on intraoperatively acquired image data sets (i.e. 2- and 3-D fluoroscopy), the explicit step of registering the patient to the surgery plan is not required as the patient is in the treatment position when the data sets for planning are required. However, to preserve the registration after initial imaging, any movement of the treatment site should be determined usually by attaching and tracking the position of a DRF that is securely attached to the treatment site. Provided that the treatment site can be treated as a rigid body, then previously acquired registered 2-D fluoroscopic image can be reused in various ways for image guidance; this is known as virtual fluoroscopy.7
The number and spatial configuration of the fiducials,
Navigation of the surgical tool/implant
e.g. errors are reduced by having more fiducials, placing them as far apart as possible, having a suitable noncoplanar configuration. The accuracy of identifying fiducials in the preoperative data set. The accuracy of measuring the position of the fiducials (normally via an optical position tracking system) in the OR. Whether there is any relative movement between the fiducials, this can be either accidental or due to movement at the operating site. The registration algorithm used.
Once a patient has been registered with the surgical plan, it is obviously important that this registration stays correct whilst the plan is implemented. If there is any probability of movement of the operating site, or as an additional safety measure, then there must be some way for detecting this movement. A common approach is to attach a dynamic reference frame (DRF) to a bone in the proximity of the operating site. If movement is detected then the registration can either automatically be dynamically adjusted or a warning can be given and the manual registration then has to be repeated. However, it must be ensured that the DRF is securely attached to the operating site with no possibility of movement as this is yet another source of accuracy error. An alternative approach to the DRF is to check at key points during the surgery that the position of one or more fiducials (external or anatomy) has not moved. The surgeon needs to be fully aware of all such problems that can cause the registration between the surgical plan and the patient to drift in order to use CAOS effectively and thus avoid surgical mistakes and be fully aware of the consequential risks of additional invasive surgical steps (e.g. insertion of fiducials, attachment of DRFs). An alternative to the point to point registration technique described above is to use surface registration.5 Typically in this approach one or more segmented surfaces from the volumetric CT images of the patient are intraoperatively matched with corresponding surfaces on the patient on the operating table. This latter surface information can be gathered by collecting a cloud of points using an optically
The final work flow step is placement of the surgical tool (e.g. drill, guidewire, saw blade, mill, template, etc.) or the implant (e.g. acetabular cup, etc.) at the correct position within the surgical site. This placement can be active, semiactive or passive. Active placement involves the use of a medical robot whose end-effector holds the tool/implant and the robot automatically positions and controls the tool in accordance with the surgical plan (e.g. RoboDoc8 and Caspar). Semi-active placement also involves a robot. Here the surgeon manipulates the end-effector but the robot only applies a constraining force that guides the surgeon to move the tool/implant as required by the plan (e.g. Acrobot9). Passive placement is where the surgeon has full control over the placement of the tool/implant and is given guidance by the computer on where to place the tool/implant normally via some form of targeting display. This is known as freehand navigation. This section will focus on the latter form of navigation for computer assisted drilling. For the freehand navigation task of inserting a drill bit or guidewire, a common approach is to attach a tracked reference frame securely to the surgical drill. This reference frame is tracked by an optical camera system. Computer guidance to the surgeon is often shown graphically by showing the position of the drill bit/tool with respect to the surgical plan. Prior to drilling, an intraoperative registration procedure is usually performed that registers the drilling axis with the coordinate space of the camera system/ patient. Thus errors for navigation arise from errors in the optical tracking system and this registration procedure. A most important error here is operator error, i.e. how well the surgeon can position the drill bit/guidewire in accordance with the computer guidance given. This operator error is likely to be the largest error component of navigation. Drilling is not as straightforward as it might seem as the surgeon must take account of drill slip, whiplash of the drill and bending of the drill whilst holding a vibrating tool, frequently glancing at the computer display (which hampers hand-eye coordination) and maintaining the direct line of sight between the reference frame and the camera system. Langlotz10 provides a good review and discussion of such issues for surgical navigation. Drilling thus becomes
ARTICLE IN PRESS 184 a more intricate surgical task. Ergonomics of freehand navigation is thus a key factor in reducing operator error and making it a repeatable activity of requisite precision. Typically the mean operator error range is between 1 and 2 mm. In image guided orthopaedic surgery this operator error of freehand navigation is a very significant factor that affects the overall accuracy of the surgery and it is therefore important to make this task as precise as possible. Thus surgeons need to be trained appropriately and have a good understanding of all the factors of surgical navigation that affect targeting accuracy. Furthermore manufacturers of free hand navigation should strive to provide systems that are easy to use, ergonomic, foolproof, reduce the fiddle factor and minimize inter- and intra-operator error.
Defining the clinical requirements for accuracy It is obviously desirable to be able to state unambiguously the accuracy in terms of clinical requirements for navigation in image-guided surgery. This involves defining precisely the clinical target for the implant, etc. and a means to define an acceptable level of variation (i.e. precision needed). A precise definition of the clinical target is problematic; the target is often a multiple variable statement that is dependent on the particular operation and patient specific information. Furthermore, there is often no clear consensus on defining the clinical target and there are often various planning heuristics to estimate the target even for the same type of surgery. However, much is known in approximate and broad terms about the effects of accuracy of the surgery and patient outcomes. In hip replacement surgery, a limit of 51 inaccuracy of placement of the acetabular implant is sufficient to ensure that placement accuracy has no significant effect on the positive outcome for a patient.11 Whilst for total knee arthroplasty, a limit of 31 inaccuracy of varus or valgus rotation is sufficient to ensure that placement accuracy has no significant impact on patient outcome.11 A common quoted accuracy statement is that for a surgical navigation system the accuracy of the system, excluding operator error, should be at most 1 mm when the target is a single point and when targeting a straight line trajectory or cutting plane the error should be at most 11. When operator error is then taken into account, the accuracy of CAOS systems is probably most often in the range 2–4 mm for targeting a point and between 11 and 31 for targeting a trajectory. Designers of CAOS systems first need to identify the operations that their systems will be used for. They then need to survey the clinical literature and consult with surgeons issues relating to accuracy requirements. These need then to be carefully analysed to provide a set of accuracy requirements for the system to be developed.
Designing CAOS system to meet accuracy requirements As with engineering of other complex systems, design of a CAOS system is a compromise between performance of meeting and possibly exceeding requirements and costs.
R. Phillips Analysis of accuracy requirements and proposing a solution that meets them is often challenging. There are often a number of design alternatives; a prime consideration is often the accuracy performance of these alternatives. In considering a design option a thorough understanding of all the origins of all inaccuracy errors is required. In designing a component of a CAOS system there are various strategies that can be employed to reduce the effect of inaccuracy errors but often by increasing costs. Within a component errors combine together in a hierarchical manner to produce the error characteristics associated with that component. However, how these errors combine is often non-linear and often difficult to determine analytically. Figure 1 illustrates the combination of errors for intraoperative registration of a surgical drill for freehand surgical navigation which is detailed in Section Sub-system validation. Having a methodological approach is beneficial in analysing errors and estimating accuracy in a CAOS system. A flowchart can be drawn for the whole CAOS system that shows all the sources of errors and the propagation of these errors. This flowchart should include all external sources of errors and include suitable estimates when these errors are not quantifiable, for example patient movement during CT scanning. Another approach is that of Lea diagrams12 which uses nodes, links and groups to provide a diagrammatic notation that is more descriptive for aspects of measurement, calibration and registration which are central to accuracy performance. The links cater for the propagation of errors in a CAOS system and can be used as a basis for simulation to estimate. Viant has combined Lea diagrams with a standard error model13 to provide by simulation an evaluation framework for the estimation of accuracy of a CAOS system. Simulation is particularly advantageous as it allows design options to be modelled and accuracy estimated. Simulation is generally far more cost effective than building physical prototypes and it allows greater exploration of the design space.
Validation of accuracy There are three main kinds of validation of accuracy, namely: clinical validation, end-to-end system validation and sub-system validation.11
Clinical validation Clinical studies provide a good means of assessing the overall postoperative outcome for image-guided surgery. They are generally qualitative in nature but they also can provide quantifiable metrics for undesirable outcomes where there is a clear geometric indicator (e.g. malplacement of screw for an intramedullary nail) or there are accepted heuristics such as pedicle screw placement.14 However, quantitative validation of accuracy at a high precision via clinical studies is problematic. A high precision of clinical assessment of accuracy is desirable so that the accuracy of surgery for each individual patient can be correlated and analysed with all the factors associated with the image guidance system for that patient. Such detailed analysis would allow biases in system error of the CAOS
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Error in calibration of drill
Drill calibration algorithm error
Calibration error between reference frame and calibration block
Operator error in moving drill whilst calibrating
Error from algorithm that computes position of reference frame of block
Error from algorithm that computes position of reference frame of drill
Calibration error of IREDs of calibration block reference frame
Calibration error of IREDs of drill reference frame Error in IRED position from optical tracking system
Figure 1 Graph showing the source of inaccuracy errors and how they propagate through an intraoperative calibration sub-system for the calibration of a drill bit/guidewire when inserted in a surgical drill (see Section Sub-system validation).
system to be identified without having to conduct clinical studies with a very large sample of patients. The various issues that make in-depth accuracy performance assessment problematic in clinical studies, include: there is often no ground truth definition of the clinical target, the quantitative accuracy of CT and radiographic assessment is low, registration with the original patient data set may be required, additional X-ray imaging is undesirable, it is difficult to justify costs of additional imaging, etc. The research literature provides an enormous number of clinical studies on the use of CAOS systems. A recent issue of the Injury journal15 was dedicated to CAOS systems and included clinical validation studies for pedicle screw spine surgery, pelvic screw fixations, total knee replacement and acetabular cup placement in total hip replacement. These are summarized below in Table 1. These results are reported in terms of implant accuracy, operation time, radiation and blood loss. There is also an interesting related debate of testing the CAOS hypothesis that ‘‘the increased accuracy of CAOS is beneficial to patients’’.20 Such testing requires comprehensive outcome studies. However, as much orthopaedic surgery is reasonably low cost and is reasonably successful it becomes difficult to justify the ethics for such studies and the additional healthcare costs. Furthermore, the perceived benefits of increased accuracy for many operations are over the longer term and by the time the results of the outcome studies are complete, which could be over 10 years, the CAOS technology, the implants and procedures will all probably be obsolete. Also when an implant fails there can be numerous other biomechanical and lifestyle reasons that are contributory factors to the failure besides the initial accuracy of positioning the implant. Given the multivariable complexity of patient outcome it is thus difficult
to provide a prima facea case or prove via small-scale outcome studies that for many orthopaedic operations the accuracy has significant patient and and/or healthcare benefits.
End-to-end system validation Thorough end-to-end system in-vitro validation, which tests a complete CAOS system, is obviously an essential prerequisite to its clinical use. This validation helps ensure that a CAOS system is fit for purpose. Part of this validation is an assessment of the accuracy performance of a CAOS system. Ideally, such validation should provide similar conditions to the operating theatre to ensure that all factors that might influence the accuracy performance of the CAOS system are adequately taken into account. For example consideration needs to be given to the following issues where appropriate:
The effect of OR theatre lights, drapes, bright reflections, blood splatter, etc. on optical tracking systems.
The layout of the CAOS equipment in a laboratory should faithfully mimic that in the OR.
Intraoperative imaging in a laboratory provides images of
similar quality to those in the OR (e.g. takes account of real patient anatomy when imaging plastic bone phantoms). Sterilisation (particularly autoclaving) has no adverse effect on CAOS equipment. The surgeon/patient interface is realistic (e.g. in terms of access to the surgical site, tactile responses to the surgeon whilst operating in-vitro, movement of the surgical site due to breath/heart motion, etc.).
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R. Phillips
Table 1 Summary of results from clinical studies presented in Injury, International Journal of the Care of the Injured, Volume 35, Supplement 1, June 2004. Operation
Size of study groups
Navigation at the spine, Gebhard et al.16 Transarticular screw 1.37 cases fixation cl/c2 (Mageri technique) 74 screws 2.78 cases. 156 screws (control group) Clincal applications pelvis, Stockle et al.17 In vivo study of 8 1.36 cases
Navigation: C-CAOS, M-Manual
Evaluation criteria
Results
C; preop CT-based
(a) Malposition of screws (Madawi)
1.(a) Yes—0. No—37
M Anatomy & Intraop fluoro
C: Intraop Fluoro
2.(a) Yes—8. No—70 (b) Lateral deviation of 1.(b) Yes—4. No—33 screws (Madawi) 2.(b) Yes—4. No—33 (c) Surgical time
1.(c) & 2.(c) Times same
(a) Correct screw position (no criteria given)
1.(a) Yes—35. No—1
Percutanous pelvic screw Fixations and 28 (b) Fluoro radiation Transiliosacral screws Joint replacement–total hip replacement with CT-based navigation, Widmer and Grutzner18 Acetabular cup 1. 14 cases C: CT-preop based (a) Manual completion placement for total hip arthroplasty In vivo study (b) Cup position Surgeon (i) (ii) Abduction 451 151 Anteversion 421 261 Cases 9 5 (c) Manual operation time mean: 75 min (d) Manual blood loss mean: 400 ml
1.(b) 0.5 min per case
1.(a) 2 cases
1.(b) Mean Min Max Abduction 41.71 361 481 Anteversion Surgeon (i) 15.81 121 181 Surgeon (ii)24.81 221 281 1.(c) Mean: 121 min Range: 112–150 min Learning curve observed 1.(d) Mean:540 ml
Range: 420–860 ml C-arm based navigation in total hip replacement—background and clinical experience, Grutzner et al.19 Acetabular cup 1.236 cases C: Intraop fluoro (a) Cup position 1.(i) (a) Cup inclination placement measured by comparing position from postop CT with position defined intraoperatively. For total hip (CT-free) Mean Min Max SD arthroplasty. In vivo study Case subsets: Angle 4213613913.61 (i) All cases Error 1.51–51 1.11 (ii) First 50 primary 1.(i) (a) Cup anteversion THA cases (iii) 202 Primary THA Mean Min Max SD cases (iv) 34 revision THA Angle 2111012813.91 cases Error 2.41–611.41 (b) Operation time 1.(b) Mean op time min (i) 96 (iii) 87 (iv) 161 (c) Blood loss 1.(c) Mean Blood loss ml (i) 811 (iii) 712 (iv) 1257
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The surgeons participating in the study should be a representative sample and be trained appropriately in using the CAOS equipment.
Frequently, all the above cannot be adequately covered by a single end-to-end validation study, thus supplementary end-to-end validation studies and complementary subsystem validation studies are conducted. End-to-end system validation studies can be classified into patient phantom, animal and cadaver studies. Using suitable phantoms in an appropriate mock-up of a clinical setting enables many of the potential problems in terms of logistics of using a CAOS system to be identified. However, it will probably not address fully all the issues identified above. Therefore, use of butcher’s specimens, operations on live animals and cadaver studies may be advantageous in providing extra insights into issues at the patient/surgeon interface. There are several aspects to the assessment of accuracy. Firstly, validation needs to ensure that the accuracy performance of the CAOS system is within specified limits and this accuracy performance is repeatable and reproducible. To make this assessment the measurement precision of results required is low (i.e. of the order of 1 mm). Thus placement of tools and implants can be adequately assessed from CT scans, by taking measurements from an optically tracked probe, etc. Secondly, validation needs to verify that the inaccuracy errors in the various CAOS sub-systems and the operator errors that occur during the workflow combine together in a well behaved and predictable manner. For this need it is beneficial to measure the resulting position of a tool/implant in a study with essentially no error of measurement (e.g. by taking measurements with a coordi-
nate measuring machine which has a measurement error of less than 0.01 mm). Given these ground truth measurements one can correlate these accuracy results with values along the error chain within the CAOS system. To do this the CAOS system needs to create a log of all input parameters that affect accuracy and save them in a log file along with all intermediate values that pass between and within the various sub-systems of the CAOS system. With this logged information it is possible to trace resultant inaccuracy errors back down the error chain and identify unexpected inaccuracies, identify whether it is worthwhile improving algorithms and give insights into how to improve the design of components (e.g. add or remove redundancy of function). By maintaining this audit trail of accuracy related information it is then possible to have a CAOS system replay all or a substantial part of an operation (either in vitro or in vivo) with revised software algorithms (e.g. for automatic detection of features in intraoperative images) and observe their effects. This concept of logging key information of an operation and a replay mode for an operation for a CAOS system allows a repository of operations to be maintained, which is very useful for regression testing for new versions of a CAOS system. Another benefit of maintaining an accuracy log is that when unexpected behaviour of a CAOS system occurs, the replay operation facility can be used to diagnose the reason behind this unexpected behaviour. Accuracy results of end-to-end system validation should be reported in absolute terms with appropriate statistics (mean error, standard deviation (SD) of error distribution, root mean square (RMS) error, maximum error, etc.). The research literature provides an enormous number of in vitro end-to-end validation studies on the use of CAOS systems. The recent issue of the Injury journal,15 mentioned
Table 2 Summary of results from end-to-end in-vitro system studies presented in Injury, International Journal of the Care of the Injured, Volume 35, Supplement 1, June 2004. Operation
Size of study groups
Navigation at the spine, Gebhard et al.16 Lumbar transpedicle drill 1.30 lumbar Canals. 2.30 lumbar In vitro artificial spine 3.30 thoracic Study 4.30 thoracic
Navigation: C-CAOS, M-Manual
Evaluation criteria
Results
C: C: C: C:
(a) Position error for planning: target was point anterior to pedicle drill canal
1. 2. 3. 4.
Preop CT-based Intraop fluoro. Preop Ct-based Interop fluoro.
Computer assisted high tibial open wedge osteotomy (HTO) Keppler et al.21 HTO–open wedge, 1.7 cases C: Intraop fluoro. (a) Mechanical axis Fujisawa line of 80% Cadaver study 2.8 cases M: Conventional (Control group) (b) Mean operation time (min) (c) Radiation Gy/cm2
HTO–open wedge,
1.5 case: varus deformities
Preclinical study
6–91
C: intraop fluoro
(a) Intended postop axial alignment. (b) Operation time
(a) (a) (a) (a)
Median Median Median Median
1.8 mm 2.0 mm 1.4 mm 2.6 mm
(a) Mean% range% SD % 1. 80.7 77.5–85.8 3.1 2. 74.2 60.4–83.4 9.7 1. 2. 1. 2. 1.
(b) Op time: 75 min (b) Op time: 58 min (c) Radiation: 41.8 (c) Radiation: 55.2 (a) Mean error: 1.01
Max. error: 2.01 1. (b) Extra 30 min a case
ARTICLE IN PRESS 188 in the previous section, included such studies on pedicle screw spine surgery and high tibial osteotomies. These are summarized below in Table 2.
Sub-system validation In designing and developing a CAOS system, having a structured approach to sub-system validation of accuracy is absolutely essential. Accuracy errors propagate from the various components of a CAOS system through a number of links in an error chain that combines with other error chains until the inaccuracy error appears in the placement of an implant/tool. For key points along the error chain, the designer should have specified the expected inaccuracy error. Thus sub-system tests need to be devised at critical points along each of these error chains. Without this bottom-up validation approach to accuracy, when an inaccuracy error is too big it is exceedingly difficult to trace back down the error chain and locate the cause or, as is often the case, the multiple causes of the error. Let’s consider an example where a CAOS system uses intraoperative calibration of a drill bit using optical tracking. In this situation the drill bit is placed in a surgical drill. Securely attached to this drill is a reference frame of IREDs that will be tracked by an optical tracking camera system. The drill bit is placed in the surgical drill and then calibrated by placing the end of the drill bit in a cone shaped hole in a rectangular calibration block. The calibration block has a reference frame of IREDs securely attached to it so that it can be tracked with the same camera system. Calibration involves moving the drill around whilst keeping the tip of the drill bit in the centre of the calibration hole. From the tracked positions of the drill a computer algorithm automatically computes the axis of the drill bit and the position of drill tip within the coordinate space of the camera system. For this example let’s assume the CAOS developer is using a proprietary optical tracking system but is designing and fabricating the various reference frames and the calibration block. Thus the design of the reference frames will need to consider such issues as how big to make the reference frame, how many IREDs to use and the spatial arrangements of these tracked IREDs. Sub-system validation for this scenario would typically involve the following sequence of validations: 1. Determine the accuracy error of the optical tracking system over its working volume. A common approach here is to have a 0.5 m stick with an IRED placed at either end of the stick. The position of these IREDs is then recorded whilst moving the stick around the camera’s working volume. An analysis of these movements produces statistics on the accuracy within the tracking system’s working volume. 2. After construction and calibration of each of the two tracked reference frames, each needs to be validated for accuracy. This can be achieved by placing a reference frame in a coordinate measuring machine (CMM) and validating its accuracy by comparing the position of the frame as measured by the CMM with the position given by the optical tracking system for the frame. This would be repeated for a large number of different positions and
R. Phillips orientations within the working volume of the optical tracking system. 3. A validation test can then be conducted of the full drill bit calibration system. Note here the CMM will have been used to register both the calibration hole of the calibration block with its attached reference frame and the drill bit with the reference frame attached to the drill; thus both registrations can be taken as ground truths. Here, the validation test comprises conducting the drill bit calibration procedure within the workspace of the CMM. After this calibration, the drill bit can be moved around and its drill tip position and axis checked for accuracy by comparing position measurements of the drill bit taken with the CMM to that given by the CAOS sub-system for tracking the drill bit. The research literature provides results on a large number of sub-system studies on the various position tracking technologies (e.g. optical, electromagnetic, ultrasound) used in CAOS systems, for example Chassat et al. reports on the accuracy of four optical tracking systems.22 Other results on sub-system validation include accuracy assessment of image calibration of the fluoroscope23 and accuracy assessment of intraoperative registration of the patient with computer-based surgical plans.24 Another important aspect of sub-system validation is to determine the accuracy error of a CAOS system due to operator error (e.g. that arises from freehand navigation of surgical tools/implants, manual marking up of anatomical features for the surgical plan) and that due to the technology in the system. The operator error is often a few times larger than the non-operator technology error. This operator error can thus often mask undesirable accuracy behaviour of the technology, such as its systematic bias. Thus sub-system validation is frequently devised to measure just the inaccuracy error of the technology. Malek et al. report on the technology error of a CAOS system for distal locking of intramedullary nails25 whilst Chami et al. report on the operator error associated with free hand navigation.26
Case study of accuracy validation CAOSS—A CAOS system for femoral trauma surgery CAOSS is a virtual fluoroscopy based CAOS system designed for various trauma surgeries of the femur, namely: placement of compression hip screws and cannulated screws for fixation for femoral neck fractures and placement of distal locking screws for intramedullary (IMN) nails for fixation of femoral shaft fractures. This section will focus on the latter intervention. In summary, CAOSS creates a surgical plan for distal locking of the IMN from two intraoperative fluoroscopy images; thus no intraoperative patient registration is required. The surgical plan is created intraoperatively by the surgeon marking a few anatomical features on the images. The surgical plan is implemented using a freehand navigation system aided by a passive arm clamped to the operating table that keeps the surgical drill in a fixed position whilst drilling. An optical camera system based on a two camera array that tracks IREDs is used to track the
ARTICLE IN PRESS Surgical navigation for orthopaedic surgery position of the C-arm of the fluoroscope and to track an endeffector which holds a cannulated guide for drilling. Patient data acquisition for IMN distal locking Computer based planning requires an intraoperative AP and lateral fluoroscopic image of the distal end of a nail showing the two holes. The planning algorithm uses 2D anatomical features from these fluoroscopic images and reconstructs them to produce a 3D surgical plan in the coordinate space of the optical tracking system. This requires, firstly, an accurate 2D calibration of fluoroscopic images and, secondly, accurate registration of the fluoroscopic image space in the coordinate space of the optical tracking system. CAOSS uses a different approach to calibration and registration of the fluoroscope to most other systems which use a twin plated grid of X-ray opaque balls attached to the X-ray receptor screen of the C-arm (e.g. as in the Medtronic Sofamor Danek’s FluoronavTM and SurgiGATEs (Medivision, Oberdorf, Switzerland)). In CAOSS, calibration to correct distortion in the 2D image plane is done preoperatively, whilst registration of the image cone of the C-arm with the optical tracking system is done intraoperatively. A calibration grid containing 64 64 X-ray opaque balls is placed preoperatively on the X-ray receptor cover of the C-arm and imaged with the C-arm in the AP and lateral
189 position. From each image a calibration map is automatically calculated which is then used intraoperatively to calibrate and undistort fluoroscopic images. Registration of the C-arm’s image cone with the tracking system’s coordinate space is achieved by placing a small registration phantom27 in the image space of the C-arm and as close to the patient as possible. The phantom consists of an H arrangement of 21 X-ray opaque metal balls (see Figure 2). The phantom is held in position by an optically tracked end-effector, which is held in position by a lockable passive arm that is attached to the operating table (see Figure 3). Software automatically calibrates the image and then automatically detects the position of the phantom. Knowing the position of the phantom, a computer algorithm calculates the registration between the C-arm and the optical tracking system. CAOSS’s approach in using a small registration phantom rather than a double plated grid is beneficial in that it does not reduce the working volume within the C-arm and the phantom produces less clutter in the image. Creation of a surgical plan for IMN distal locking As mentioned above, creation of the surgical plan requires an AP and lateral fluoroscopic image of the distal end of a nail showing the two holes. A key feature of this surgical
Figure 2 H-shaped phantom for registration of image cone of C-arm fluoroscope with coordinate space of optical tracking system. The three limbs of the H contain 8, 7 and 6 X-ray opaque balls, respectively.
Figure 3 Registration phantom held in the end-effector of a passive arm that is clamped to horizontal bar of operating table. The end-effector’s position is tracked via a reference frame containing seven IREDs.
ARTICLE IN PRESS 190 planning is that a perfect circle projection of the distal screw holes is not required in the lateral view. In the AP view, the IMN and the long bone are each identified by manually marking six points on the image. In the lateral view, the nail is identified by marking six points and each distal hole is identified by dragging a square over the holes. From these the surgical planning algorithm automatically determines the nail axis and recovers the geometry of both the distal holes from these images.28 This creates a surgery plan that includes the drilling axis and position of both holes as well as the length of screw needed for locking. Navigation of the drill bit for IMN distal locking To implement the surgical plan of drilling a hole for a distal screw, the surgeon positions a guiding cannula using guidance displayed on the computer’s monitor. This cannula is mounted in the optically tracked end-effector, which is held by a passive lockable arm. The computer guides the surgeon by a quantitative graphical display of the cannula movements required. When the desired position is achieved, the surgeon rigidly locks the passive arm. A standard orthopaedic drill is then used to drill the hole in the bone along the planned trajectory and through the centre of the nail hole.
The design and validation of accuracy in CAOSS The non-operator accuracy target set for CAOSS was a precision with a standard deviation of 1 mm for position and a standard deviation of 11 for direction. A methodology was developed by Viant13 to identify the propagation of accuracy errors in the system and to provide a means to estimate the accuracy of the complete system using a standard error model. In addition, extensive simulation of various CAOS hardware and software components was conducted to evaluate various design options. Sub-system evaluation and validation of CAOSS There are very little published data on the distortion in quantitative terms that occurs in fluoroscopic images; therefore accuracy validation studies of the calibration sub-system for the fluoroscope are required. The position error of a point in an uncalibrated fluoroscopic image had a mean error of 1.75 mm with a SD of 2.00 mm. This study showed that the approach in Section Patient data acquisition for IMN distal locking that used two calibrating positions had a mean calibration error of 0.13 mm with an SD of 0.11 mm. Furthermore, the study showed that calibrating the C-arm in just one position then the mean calibration error was 0.56 mm with an SD of 0.44 mm thus justifying the need for calibrating preoperatively in two positions. The optical tracking system was a commercial system with a known accuracy error. However, the reference frame attached to end-effector was designed as part of the project. Its design was a trade-off between accuracy, clinical efficacy (e.g. size, line of sight, etc.), design complexity and cost (e.g. number of IREDs). Software simulation using a standard error model was used to estimate the accuracy performance of various design options and to select the preferred design. The accuracy of the reference frame largely determines the accuracy with
R. Phillips which the position of the phantom or the guiding cannula can be measured by the tracking system. A key innovation of CAOSS was its registration phantom. Again, extensive simulations of alternative design options were conducted to evaluate various options within the design space of the phantom. The following are needed to conduct such simulations for the phantom’s design:
an accuracy model for extracting 2D points from fluoroscopic images,
an accuracy model for detecting the centre of X-ray
opaque balls in the phantom, (in fact sub-system validation had showed that such balls could be extracted with an error whose SD was less than 0.1 mm), an accuracy model for determining the position of the phantom in the optical tracker’s coordinate space and an estimate of the movement of the C-arm as it is not an entirely rigid structure.
The design space of the phantom includes: the spatial arrangement of the phantom, clinical efficacy, ease of manufacture, reliability and costs. Sub-system validation studies were first conducted on actual prototypes of the constructed reference frame and then on the registration phantom to check their accuracy performance and appropriate refinements to the design made were necessary. With these sub-systems validated and a level of confidence in how they perform established, they were then used together as the test platform to develop the various algorithms involved in creating the surgical plan. Such algorithms include automatic extraction of the projection of the distal holes from an image and computing the axis of the distal holes. Once developed, these algorithms were validated for accuracy performance as discussed by Malek.25 In fact, this detailed approach to accuracy assessment identified a systematic error bias of just over 1 mm. This was subsequently identified as an oversight in how the tool holding guide of the end-effector was calibrated with its reference frame; it had not taken account of the locking screw which caused a slight misalignment between the axis of the tool and the axis of the tool holding guide.
End-to-end evaluation and validation of CAOSS A number of end-to-end system validation studies were conducted in the laboratory. One such study was distal locking of screws for an IMN inserted in plastic bones with a random set up of the IMN. This demonstrated that CAOSS could insert a drill bit guide through a distal locking hole with a 100% hit rate. Another study varied the various parameters that might influence the accuracy performance of CAOSS for distal locking. This study included varying the rotation in 21 steps of the nail to 151 either side of the perfect circle projection position, varying the position of the projection of the distal part of the nail within the image and varying the location of the registration phantom. The intention of this study was to ensure that CAOSS was reliable for the variations in set up of the C-arm, IMN and the registration phantom that might occur in the OR. Another study used butchers, specimens to ensure the accuracy of
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Figure 4 Images of registration phantom during surgery for insertion of guidewire into femoral neck and head for a compression hip screw. Left: AP fluoroscopic images used for generating the surgical plan; image shows registration phantom and construction of surgery plan for placing guidewire. Right: AP fluoroscopic image after insertion of guidewire; image shows phantom along with the planned trajectory for the guidewire.
CAOSS was still acceptable when drilling into real bones where drill slip, whiplash and bend might occur. Clinical validation of CAOSS CAOSS has been used in clinical studies for drilling a guidewire into the femoral head and neck for the insertion of a compression hip screw for fixation of fractures in the femoral neck region. For this a pilot study was first conducted in the OR to validate the clinical efficacy and reliability of CAOSS. This pilot study identified a number of shortfalls in performance that was largely due to the difference in the OR environment over the laboratory setting, which had not been anticipated. In the OR, recognition of the phantom occasionally failed due to insufficient of the X-ray opaque balls of the phantom being recognised. This was caused by a much wider variation of contrast in the fluoroscopic image (particularly washed out areas) than expected and poor recognition of balls on joint lines, bone edges and regions of deep fat. Furthermore, the ends of callipers were also sometimes being detected as balls. With appropriate refinements to the ball and phantom recognition algorithms, CAOSS was able to recognise the phantom in images from the OR (see Figure 4) with a success rate very close to 100%. Another discovery in the pilot validation study was that repeated autoclaving of the phantom caused it to change shape marginally but it was sufficient to cause the computed position of the C-arm to be incorrect. Recalibration of the phantoms cured this problem. Following the pilot study a small clinical study of 10 patients was conducted by Shah29 where CAOSS was shown to work reliably. A further clinical study of using CAOSS for distal locking of IMN is planned.
Conclusions CAOS systems should be relatively straightforward tools for a surgeon to use. However, internally a CAOS system is a complex engineering system that has to be precisely
constructed and rigorously validated to provide the surgeon with useful surgical tools that are accurate and reliable. The paper has provided numerous insights into where inaccuracies in a CAOS system occur, discussed approaches to validation of CAOS and presented experiences of a CAOS development team via a case study of a CAOS system for distal locking of IMN for the femur. CAOS is not a foolproof technology. There are many aspects at the interface between the patient, the surgeon and the CAOS system that can affect accuracy of the clinical outcome. A surgeon must have a good understanding of such issues and be ever vigilant of accuracy issues during surgery. As the number of CAOS systems increases and there is wider application of CAOS technology, the need is growing to have international standards that define the terminology for accuracy and provide a framework for validation of accuracy of performance and reporting it. This will aid the evaluation and procurement of CAOS systems for healthcare providers and inform surgeons as they seek new and improved ways of applying CAOS technology.
References 1. Mohsen AMMA. Non-invasive intelligent orthopaedic guide: concepts, issues and efficacy assessment. PhD thesis, University of Hull, Hull, UK, 1996. 2. Nolte LP, Beutler T. Basic principles of CAOS. Injury Int J Care Injured 2004;35:S-A6–S-A16. 3. Rudin S, Bednarek DR, Wong R. Accurate characterisation of image intensifier distortion. Med Phys 1991;18:827–33. 4. Papadopoulos E, Girardi F, Sama A, Sandhu H, Cammisa F. Accuracy of single-time, multilevel registration in image-guided spinal surgery. Spine J 2005;5(3):263–7. 5. Lavallee S. Registration for computer-integrated surgery: methodology, state of the art. In: Taylor RH, Lavallee S, Burdea GC, et al., editors. Computer integrated surgery. Cambridge: MIT Press; 1997. p. 77–97. 6. Hamadeh A, Lavallee S, Cinquin P. Automated 3 dimensional computed tomographic and fluoroscopic image registration. J Comput Aided Surg 1998;3:11–9.
ARTICLE IN PRESS 192 7. Hosstetter R, Stomczykowski M, Bourquin Y, et al. Fluoroscopy based surgical navigation concept and clinical applications. Proceedings of the CAR symposium, 1997. p. 956–60. 8. Taylor RH, Joskowicz L, Williamson B, et al. A computerintegrated revision total hip replacement surgery: concept and preliminary results. Med Image Anal 1999;3(3):301–19. 9. Harris SJ, Jakopec M, Cobb J, Davies BL. Intra-operative application of a robotic knee surgery system. In: Proceedings of the MICCAI ‘99, Lecture notes in computer science series, vol. 1679. Berlin: Springer; 1999. p. 1116–24. 10. Langlotz F. Potential pitfalls of computer assisted orthopaedic surgeon. Injury Int J Care Injured 2004;35:S-A17–23. 11. Mor AB, Jaramaz B, DiGioia AM. Accuracy and validation. In: DiGioia AM, Jaramaz B, Picard F, Nolte L-P, editors. Computer and robotic assisted hip and knee surgery. Oxford: Oxford University Press; 2004. p. 307–16. 12. Lea JT, Santos-Munne JJ, Peshkin MA. Diagramming registration connectivity and structure. Proceedings of the medicine meets virtual reality, technology and informatics series, vol. 18. IOS Press; 1995. p. 191–200. 13. Viant WJ. The development of an evaluation framework for the quantitative assessment of computer-assisted surgery and augmented reality accuracy performance. Proceedings of the medicine meets virtual reality, technology and informatics series, vol. 81. IOS Press; 2001. p. 534–40. 14. Madawi AA, Casey AT, Solanki GA. Radiological and anatomical evaluation of the atlantoaxial transarticular screw fixation technique. J Neurosurg 1997;86(6):961–8. 15. Special issue on CAOS and the integrated OR. Injury Int J Care Injured 2004;35 [188pp]. 16. Gebhard F, Weidner A, Liener UC, Stockle U, Arand M. Navigation of the spine. Injury Int J Care Injured 2004;35: S-A35–45. 17. Stockle U, Krettek C, Pohlemann, Messmer P. Clinical applications—pelvis. Injury Int J Care Injured 2004;35:S-A46–56. 18. Widmer KH, Grutzner PA. Joint replacement—total hip replacement with CT-based navigation. Injury Int J Care Injured 2004; 35:S-A84–9. 19. Grutzner PA, Zheng G, Langlotz U, et al. C-arm based navigation in total hip arthroplasty—background and clinical experience. Injury Int J Care Injured 2004;35:S-A90–5.
R. Phillips 20. Mohsen AMMA, Phillips R. Letter of the reviewers. Injury Int J Care Injured 2004;35:2–5. 21. Keppler P, Gebhard F, Grutzner PA, et al. Computer assisted high tibial open wedge osteotomy. Injury Int J Care Injured 2004; 35:S-A68–78. 22. Chassat F, Lavalee S. Experimental protocol of accuracy evaluation of 6-D localizers for computer integrated surgery: application to four optical localizers. In: Proceedings of the medical image computing and computer assisted intervention—MICCAI’98, Lecture notes in computer science series, vol.1496. Berlin: Springer; 1998. p. 277–84. 23. Viant WJ, Phillips R, Bielby MS, et al. A technique for a very high accuracy image intensifier calibration. Proceedings of the medicine meets virtual reality, technology and informatics series. IOS Press; 1999. p. 379–80. 24. Tamura Y, Sugano N, Sasama T, et al. Surface-based registration accuracy of CT-based image-guided spine surgery. J Europ Spine J 2005;14(3):291–7. 25. Malek S, Phillips R, Mohsen A, Viant W, Bielby M, Sherman K. Computer assisted orthopaedic surgical system for insertion of distal locking screws in intra-medullary nails: a valid and reliable navigation system. Int J Med Robotics Comput Assisted Surg 2005;1(4):34–45. 26. Chami G, Ward JW, Phillips R, Mohsen AMMA. Factors affecting targeting using the computer assisted orthopaedic surgery system (CAOSS). Proceedings of the medicine meets virtual reality, technology and informatics series. IOS Press; 2006. p. 90–2. 27. Phillips R, Mohsen A, Viant WJ, et al. A phantom based approach to fluoroscopic navigation for orthopaedic surgery. In: Medical image computing and computer assisted intervention, MICCAI 2004, Lecture notes in computer science series, vol. 3217. Berlin: Springer; 2004. p. 621–8 [part 2]. 28. Zhu Y, Phillips R, Griffiths JG, Viant WJ, Mohsen A, Bielby M. Recovery of distal hole axis in intramedullary nail trajectory planning. Proc Instn Mech Eng Part H: J Eng Med 2002;216(5): 323–32. 29. Shah NH, Malek S, Mohsen AMMA, et al. Clinical results of dynamic hip screw (DHS) insertion using computer assisted orthopaedic surgical system (CAOSS). Proceedings of the computer assisted orthopaedic surgery (CAOS) international, 2004. p. 380–1.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 215–228
Available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/cuor
CHILDREN
Slipped upper femoral epiphysis Samuel J. Parsons, Cefin Barton, Robin Banerjee, Nigel T. Kiely Robert Jones and Agnes Hunt Hospital, Gobowen, Oswestry, Shropshire SY10 7AG, UK
KEYWORDS Slipped upper femoral epiphysis; Paediatric hip disorders
Summary Slipped upper femoral epiphysis is a common adolescent hip disorder. The classic image of the obese hypogonadal male child presenting with a limp is widely known; despite appearances few of these children demonstrate an endocrine disorder. Most are idiopathic, but some are associated with obesity, younger bone age, race and biomechanical factors. Historical treatments, such as spica casts, have been abandoned and in situ pinning is widely held to be the optimum treatment. The more severe slips frequently require osteotomy and may go on to require salvage surgery. This article presents a review of the aetiology, features and treatment options available. & 2007 Elsevier Ltd. All rights reserved.
Introduction Slipped upper femoral epiphysis (SUFE) is a well recognised disorder of adolescent hips. It is characterised by displacement of the capital femoral epiphysis from the metaphysis through the physis. Although the disorder is called SUFE, this term is technically incorrect. The femoral epiphysis maintains its normal relationship within the acetabulum stabilised by the ligamentum teres femoralis and surface tension. It is the femoral neck and shaft that displace relative to the physis and acetabulum. The deformity is one of superior migration, adduction and external rotation of the femoral neck.
Corresponding author. Tel.: +44 1691 404000; fax: +44 1691 404071. E-mail addresses:
[email protected] (S.J. Parsons),
[email protected] (C. Barton),
[email protected] (R. Banerjee),
[email protected] (N.T. Kiely).
0268-0890/$ - see front matter & 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2006.12.001
The epiphysis displaces primarily posterior relative to the femoral neck.1 Most of the children affected by SUFE will not have any demonstrable endocrine abnormality, even when their body habitus suggests otherwise, but some will have an important associated endocrinopathy. Early diagnosis with appropriate management should reduce the morbidity and complications of SUFE that can lead to loss of range of movement, pain, premature arthritis and leg length discrepancy.
Historical perspective Descriptions of SUFE predate X-ray studies for originally SUFE would have just been another cause of a limp. Ambroise Pare—renowned French barber surgeon, is credited with the first description of SUFE in 1564: ‘when the epiphyses and heads of the bones are plucked from the bone whereon they were placed or fastened; which unproperly called kind of luxation, hath place chiefly in the bones of young people. And it is known by the importance of the part
ARTICLE IN PRESS 216 and by the noise and grating together of the crackling bones when they are handled.’ Jean-Louis Petit, in 1723, gave a more sober description and described it thus: ‘decollement—separation of the head from the neck—in the sense that one says a criminal has been beheaded; or else one may understand this word, the separation of the epiphysis from the neck, looking upon the cartilage that is found between them as cement that joins both parts.’ Ernst Muller, in 1888, describes ‘an affection in young individuals from 14 to 18 years; there occurs without special cause or preceding trauma a weariness and gradual shortening of the affected limb. The symptoms develop quite gradually. The patients are in other respects, except for fortuitous affections, healthy specifically without evidence of other joint or bone disease.’ He goes on to comment, from looking at autopsy specimens ‘the femoral neck gives the impression of being molded by pressure from above downward.’ From this he coined the term ‘Schenkelhalsverbiegungen im Jungesalter’ meaning bending of the femoral neck in adolescence.
Demographics and epidemiology The Incidence of SUFE varies by sex, race and geography. The incidence is estimated to be around 2 per 100,000 of the population.2 There is a male predominance, with the left hip affected more than the right. Early in the 20th century 90% of those with the disorder were boys but now this figure is 60%.3 Loder found a male/female ratio of 3:2, and a left/ right ratio of 3:2.2 Of those with unilateral involvement, 60% are left hips.2 Whether this reduction in male prevalence is due to increased participation of girls in sporting activities is not known. The left/right ratio may be due to the sitting posture of right handed subjects whilst writing.4 Average age at diagnosis is 13.5 years for boys and 12.0 years for girls.2 At presentation 80% of the boys were between 12 and 15 years, and 80% of the girls were between 10 and 13 years. Onset before 10 years is unusual for both sexes and after 14 years for girls and 16 years for boys.2 The range of skeletal ages of these children is much narrower than their chronological age.5 Most children with SUFE have an open triradiate cartilage and are Risser 0.6 The youngest reported patient without an identifiable endocrinopathy has been a girl aged 5 years and 9 months.7 Between 51% and 77%, of children with SUFE are obese. With at least 50% being over the 95th percentile for weight according to age.2,8 Age at onset is reduced with increasing weight.2 If a child is over the 95th percentile of weight for age, the mean age at presentation is 12.4 years, and if under the tenth percentile mean age is 14.3 years. Although the chronological age at which slips can occur varies, the physiological age range seems smaller, with a narrow window during which it can occur.5 Obese children with slow maturation appear to be at especially high risk.8 Loder has noted a 40-fold difference in differing races with the highest rates in Polynesian children and the lowest rate in children from the Indo-Mediterranean region.2 The relative racial frequency of SUFE is 1.0 for whites, 4.5 for Pacific Islanders, 2.2 for blacks, 1.05 for American Indians (Hispanic, native Americans), 0.5 for Oriental races
S.J. Parsons et al. (Chinese, Japanese, Thai, Vietnamese) and 0.1 for IndoMediterranean.2 There are two possible explanations for this observation: (1) the mean body weight for the racial group, supporting the idea of obesity being an important factor; (2) a racial variability in acetabular depth and femoral head coverage. We know that the acetabula in adolescent black children are deeper than those in white children.9 However, recently Loder et al.10 felt that these observed racial differences in acetabular size did not correspond with the racial frequencies observed historically in SUFE. The incidence of bilateral involvement is affected by race, method of radiographic measurement and possibly treatment. In most series the prevalence of bilaterality is 18–50%.2 Most studies identify bilateral involvement either on initial presentation or subsequently in around 20–25% of patients while long-term studies have shown radiological evidence of bilateral involvement in the range of 60–80%11–13 of patients. The percentage of bilateral involvement is higher in black children (34%) with White and Hispanic children at 17% and Asian children at 18%.2 Treatment may also affect the incidence of bilaterality since one study has shown a prevalence of 36% in 169 patients treated with in situ pinning and 7% in 30 treated with a spica cast.14 Most children (82%) who go on to develop second hip involvement, having only presented with a unilateral slip, will do so within 18 months.2,11 These patients are younger at presentation than children in whom the disorder is unilateral. This difference is seen in both chronological age and pelvic bone age. There may also be seasonal variation, with increased symptoms in summer and autumn months, but only in races living above 401 north latitude.11 In the same study Hansson also noted an increased tendency for SUFE in rural children compared to urban children.
Aetiology The cause of SUFE is unknown in the majority of patients. Regardless of the aetiology, the final common pathway appears to be a mechanical insufficiency of the proximal femoral growth plate15 occurring because of physiological loads across an abnormally weak physis or abnormally high loads across a normal physis.
Biomechanical factors Shear forces across the epiphyseal plate are least when the plate is perpendicular to the resultant force across the hip joint and the femoral neck is anteverted. Shear strength of the proximal physis varies with age and is dependant on the surrounding perichondrial ring complex, especially in infancy and early childhood. The perichondrial fibrocartilaginous ring complex, is a fibrous band that encircles the physis at the cartilage–bone junction. The perichondrial ring acts as a limiting membrane giving mechanical support to the physis. It contributes significantly to the ability of the epiphysis to resist shear forces. Its shear strength is provided by collagen fibres that run obliquely, vertically and circumferentially. These collagen fibres span the physis, attaching to the ossification groove on the epiphyseal side and powerfully bound to the subperiosteal
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metaphyseal bone. It is strongest in infancy, but decreases in volume and strength especially in adolescence. As children age the mammillary processes (interdigitating reciprocal protrusions of bone and cartilage at the epiphyseal–metaphyseal interface) become more important in providing resistance to shear. Obesity is associated with increased femoral retroversion, anteversion averaging 10.61 in normal weight adolescents, but only 0.401 in obese adolescents.16 This relative femoral neck retroversion increases the shear stress across the physis. Children with SUFE also have a more vertical proximal femoral physis. Patients with a slip had a slope averaging 111 more on the affected side and nearly 51 more on the unaffected side than the controls.17 In laboratory studies shear strength has been shown to vary with physeal inclination. A decrease in the neck shaft angle has been reported in SUFE children when compared to normal non-slip controls; such a decrease results in a more vertical physis, which may increase the shear force across the physis (Figs. 1–8). The combination of mechanical forces resulting from relative retroversion and increased physeal slope may be enough to cause a slip, under physiological conditions. Whereas the mean shear load to failure of the capital physis in normal weight children is four times body weight; the mean shear load to failure in adolescents who are running, who are obese, or who have neutral version (or 101 of retroversion) is five times body weight. Children with greater acetabular depth were felt to be at greater risk for SUFE as this greater coverage yields more stress across the physis. It was also felt that a deeper acetabulum could cause increased shear stress across the femoral epiphysis. However, this difference alone seems not to account for the increased incidence of SUFE in these racial groups. Kordelle et al.18 have not found any differences in the acetabular morphology in the affected and unaffected hips of patients with SUFE. Little potential exists for acetabular remodelling and this may explain the high incidence of bilateral SUFE. Equally, bilateral acetabular symmetry in those with unilateral SUFE suggests that even if increased
Figure 1
acetabular depth is a risk factor there must be other aetiological factors involved. SUFE has also been associated with other lower limb conditions, such as infantile and adolescent Blount’s disease, peroneal spastic flat foot and Perthes disease.
Figure 2 Prepared histological slide of a femoral epiphysis with the Ring of Lacroix circled.
Plain radiograph of a unilateral SUFE.
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Figure 5 Image demonstrating Trethowen’s sign. Klein’s line should transect the lateral capital epiphysis. In SUFE this is lost.
Figure 3 Southwick’s method for the classification of SUFE: (a) AP projection and (b) lateral projection.
Figure 6
CT scan (axial cut) showing the head/neck angle.
Figure 4 MRI axial projection, demonstrating increased signal over the anterior neck, due to stripping of the periosteum, following a slip.
Endocrine factors
Figure 7 Plain AP radiograph showing bilateral SUFE, in a Down’s syndrome patient.
Endocrine abnormalities may account for 5–8% of SUFE cases. SUFE has been estimated to be six times more common in conditions such as hypothyroidism, panhypopituitarism, growth hormone abnormality, hypogonadism, craniopharyngioma, hyperparathyroidism, MEN II-B, Turner’s syndrome and optic glioma. The increased prevalence of hypothyroidism in Down’s children is a likely explanation for the increased risk of SUFE in these children, although hyperlaxity may be contributory. The initial diagnosis of hypothyroidism is often made after the diagnosis of SUFE,
whereas in children with SUFE and growth hormone deficiency the endocrine abnormality is usually known prior to diagnosis. The relative risk of SUFE is increased in children with growth hormone deficiency both prior to and during growth hormone treatment. Blethen and Rundle19 concluded that the risk for development of SUFE in patients receiving growth hormone for idiopathic short stature was the same as that reported in the general population, but was
ARTICLE IN PRESS Slipped upper femoral epiphysis
Figure 8 Same patient as in Fig. 7. Three years have elapsed. The slips were not pinned. Note there is no evidence of AVN and remodelling has occurred.
significantly higher in patients with growth hormone deficiency, Turner’s syndrome or chronic renal insufficiency (91 per 100,000 in their study). When children with hypopitiutarism are treated with growth hormone there is a significant risk of SUFE especially if sex hormones are not given concurrently. A deficiency of sex hormones delays physeal closure and increases the time span during which slip can occur. Sex hormone deficiency is also associated with obesity, thus adding a mechanical factor to the problem. SUFE has been noted to be most common around puberty; it may be that the complex interplay of hormones at this time puts the hips at high risk for SUFE. Decreased physeal strength occurs at puberty, the cause is not clear, but it may be due to increased cartilage width of the zones of hypertrophy and provisional calcification, and thinning of the perichondrial ring. Laboratory studies have also shown that oestrogen narrows the epiphyseal plate and testosterone widens it and clinically girls after the menarche rarely sustain a slipped epiphysis. SUFE associated with chronic renal insufficiency is thought to be as a result of unrestrained secondary hyperparathyroidism. It leads to a 6–8-fold increased risk of SUFE. The highest risk is seen in children on dialysis and on growth hormone therapy. In children with secondary hyperparathyroidism the correct medical management is paramount. If the hyperparathyroidism is controlled slip progression will become rare. These patients differ from classic SUFE in that in up to one-third the slip will be through the metaphysis, and 80–95% are bilateral, usually presenting simultaneously. The results of treatment of this group are worse and this is felt to be due to the fact that the slip is not through the physis.
Other factors Previous radiation therapy to the hip and pelvis increase the risk of SUFE, in a dose-related manner, possibly as high as 10%.20 A genetic basis for SUFE has not been established. In some families there is an autosomal dominant inheritance
219 with incomplete penetrance. Whether this is due simply to a genetic predisposition or due to a tendency to other risk factors (such as obesity) remains unclear. Rennie21 showed that the risk of a SUFE in a second family member was 7.1% and that 14.5% of SUFE patients had a close family member who also had the disorder. There may be an association with HLA markers, such as DL4 or B12 but again this is unclear. There have been mixed results implicating an immunological basis for SUFE. Some studies have shown increased C3 complement and immunoglobulins and possibly higher serum IgA levels. In patients with chondrolysis IgM levels are also elevated. More recent studies have not shown this serum level increase but have shown synovial fluid abnormalities, with immune complexes more likely to be found in the synovial fluid of SUFE joints than non-SUFE joints. The role of these immune complexes or whether they reflect exposed proteoglycan serving as antigenic stimulus is not clear. Hence there is uncertainty if these observed changes are the cause or the effect of SUFE.
Clinical features History The most common findings at presentation of SUFE include pain, limp and decreased range of motion of the hip. Hip or groin pain in an obese, peripubertal child is highly suggestive of SUFE. However hip pain is absent in as many as 50% of the children with SUFE, including up to 8% with a painless limp. Pain is localised to the knee and/or distal thigh in 23–46% of cases. SUFE often presents with only knee pain and not hip pain.22 Previous studies have noted that this can cause significant delay in diagnosis, misdiagnosis, unnecessary radiographs, increased slip severity and sometimes unnecessary knee arthroscopy. These findings indicate the importance of examining the hips in all patients presenting with distal thigh and/or knee pain. Age at diagnosis and symptom duration are very important since older children with longer symptoms do present with more severe slips.23
Examination On examination range of motion and rotational profile of the hips should measured and compared. With SUFE the hip will automatically fall into external rotation (so-called obligate external rotation) as it is progressively flexed. Obligate external rotation is highly suggestive for SUFE. There is also a corresponding loss of internal rotation. Hip rotation is abnormal because of both the abnormal anatomy and synovitis that accompanies the SUFE. In unilateral SUFE comparison with rotation of the other hip clearly demonstrates this change in the arc of motion (it may also be noted that the other normal hip is slightly retroverted). In bilateral SUFE both hips will demonstrate this shift toward external rotation. The ability to flex the hip to 901 is uncommon, and flexion contractures are often seen. Abduction is also limited compared to the contralateral, normal hip. There may be shortening of the affected limb of around 1–2 cm.
ARTICLE IN PRESS 220 If the child can walk there will be a trunk lean to the affected side during stance phase (Trendelenberg gait). If there is marked pain an antalgic gait (decreased stance phase on the affected limb) will be present as well. Chondrolysis produces continuous pain and a greater interference with daily activities due to loss of range of motion. Pain occurs throughout the arc of motion, not just at extremes.
Classification SUFE can be classified by speed of onset of the disorder, by the magnitude of the slip, and by the stability at presentation.
Acute
S.J. Parsons et al. remodelling and further displacement of the capital epiphysis (Figs. 9–17). The complications of AVN and chondrolysis are more common in acute slips. Loder et al.24 reviewed 55 patients presenting with acute SUFE, and separated patients by their ability to weight-bear after the acute clinical event. If the patient’s pain was sufficiently severe to prevent the patient from weight-bearing, even with crutches, these patients were identified as having unstable slips. Those who were able to weight-bear, with or without crutches, were classified as having stable slips. Fourteen (47%) of the thirty patients with unstable slips developed AVN, whereas none of the 25 with stable slips did so.24 SUFE may also be classified by the magnitude of the displacement of the femoral epiphysis relative to the neck. Southwick’s25 method was the femoral head-shaft angle on the frog lateral view. When the hip is in painful
Symptoms are present for less than 3 weeks and X-rays will show no remodelling. AVN frequent complicates acute SUFE with a reported incidence of 17–47% in treated cases.
Chronic Chronic SUFE is more common. Patients present with symptoms over more than 3 weeks. Loder2 reported that 85% of 1630 children with 1993 slips had chronic symptoms and 15% had acute symptoms, as defined by the 3 week’s symptoms. Radiographs of patients with chronic SUFE show a variable amount of posterior migration of the femoral epiphysis and remodelling in the same direction causing bending of the neck.
Acute on chronic Acute on chronic presentation is one in which both ends of the spectrum are present. Prodromal symptoms for more than 3 weeks are followed by a sudden exacerbation of pain with radiographic evidence of both femoral neck Figure 10 Lateral radiograph of anterior screw placement appropriate for the degree of slip.
Figure 9 Image demonstrating the importance of anterior screw placement, to ensure the screw threads enter the epiphysis perpendicular to the growth plate.
Figure 11
The level of suggested femoral neck osteotomies.
ARTICLE IN PRESS Slipped upper femoral epiphysis
221
Figure 12 Plain radiograph showing the epiphysis growing off the screw.
Figure 14 Plain radiograph showing segmental avascular necrosis.
Figure 13 Plain radiograph showing failure of the fixation due to a broken screw.
spasm an accurate portrayal of the frog lateral projection is impossible. Mild: Moderate: Severe:
the head shaft angle differs by less than 301. the angle difference is 30–601. the angle difference is more than 601 in comparison to the contralateral hip, if it is unaffected.
When the other hip is affected or not measured, the femoral head shaft angle of the affected hip is calculated from normal values for this angle. Southwick felt that the normal value was 1451 on the AP and 101 posterior on the frog leg lateral. The degree of slip can also be quantified as a ratio of slip distance to the diameter of the femoral neck at the physis as described by Wilson.30 Using this method the slips are mild (less than 33%), moderate (33–50%) and severe (more than 50%). This method has some flaws due to inconsistent positioning and can change over time due to proximal femoral remodelling.
Imaging modalities
Figure 15 necrosis.
Plain radiograph showing whole head avascular
the patient is able to move their hips. The lateral is important as in 14% displacement may not be visible on the AP alone.26 In mild degrees of slip the lateral projection is more sensitive. Both hips need to be visualised to allow comparison between sides and because of the high incidence of bilateral disease. This also enables Southwick angle measurements to be measured. In unstable cases a lateral film may be omitted if painful and to avoid further displacement. A number of signs are visible on plain films:
Plain films
Trethowan’s sign
Radiologically the plain film is the most important investigation. Good quality AP and frog lateral views are essential, if
Here Klein et al.’s27 line does not transect the capital epiphysis or transects less than on the other hip.
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Ultrasound scan USS can be helpful, though it is rarely used. It can be used to detect early slips by demonstrating a joint effusion and a step between the femoral neck and epiphysis.31
CT scan CT can be helpful in the later management of SUFE by providing additional information if joint penetration has occurred with fixation devices, and the exact position of implants, especially when stiffness of the hip makes plain film evaluation difficult. Scans will show if the growth plates have closed and so may help in deciding about contralateral fixation. 3-D reformatted images are especially useful to assess residual deformity of the upper femur when planning reconstructive osteotomy. Axial CT scan images also enable the head–neck angle measurement. This is similar to the Southwick angle, but is more accurate as it measures the angle from a tangent to the base of the epiphysis and the axis of the femoral neck.32 Figure 16 Distraction arthrolysis of the hip joint, with an external fixator, post-AVN.
Figure 17 Same patient as in Fig. 16 showing advanced degenerative change of the hip joint.
Steel’s28 metaphyseal blanch sign
Bone scan Tc-99m labelled scintigraphy of the hip joints with pin hole collimation is now rarely used. It can be useful to see if AVN is developing. Abnormally decreased uptake in the epiphysis is highly specific for the diagnosis of AVN. When chondrolysis is present there is increased uptake of isotope on both sides of the joint. In a study involving pre-treatment bone scan of 62 patients with 73 SUFEs, 63 of which were stable and 10 unstable, none of the unstable epiphyses become ischaemic, as demonstrated by bone scan, and none developed AVN. Of the 10 unstable SUFEs, six demonstrated ischaemia on bone scanning. Of these, five developed AVN. None of the four unstable slips without ischaemia on bone scan developed AVN. This study suggested that the ischaemia that precedes AVN occurred with the slip and not the treatment.33 Therefore some surgeons feel that scanning may have a role in preoperative assessment of SUFE patients, to document the vascular status of the capital epiphysis, prior to surgery.
MRI
This is a crescent shaped area of increased density that lies over the metaphysis of the femoral neck adjacent to the physis. This increased density is due to the overlapping of the femoral neck and the posteriorly displaced capital epiphysis.
The role of MRI in SUFE is limited. It may have a place in the early detection of AVN but the presence of metallic implants can seriously degrade the images. Some authors have suggested that MRI may be able to detect hips in a ‘preslip’ stage, but there is no convincing evidence that these cases could not have been diagnosed on the plain films.34
Scham’s29 sign
Pathology
Seen on an AP film, in a normal hip the inferomedial femoral neck overlaps the posterior wall of the acetabulum producing a triangular radiographic density. With displacement this dense triangle is lost because this portion of the femoral neck is located lateral to the acetabulum.
With gradual slipping of the capital epiphysis the periosteum is stripped from the posterior and inferior surfaces of the neck. The area between the original femoral neck and posterior periosteum fills with callus, which ossifies and becomes progressively denser. The antero-superior portion
ARTICLE IN PRESS Slipped upper femoral epiphysis of the metaphysis forms a ‘hump’ that can impinge on the rim of the acetabulum. Normally this ridge will remodel with the anterior portion of the neck, contouring into a smoother surface. In an acute slip the anterior periosteum is torn and so a haemarthosis will be present. Classically, the neck migrates anteriorly and rotates externally in relation to the head. With time, changes occur in the superior neck leading to remodelling and, eventually, cyst formation and degeneration. As the slip severity worsens, more external rotation is required in order to be able to flex the hip without impinging. Howorth35 provided a comprehensive review of 169 SUFE hips, treated by open peg epiphyseodesis, open reduction or femoral neck wedge osteotomies. He described a preslip stage characterised by widening of the physis both histologically and radiographically without actual displacement of the capital epiphysis. In this stage the synovial membrane is oedematous, as are the capsule and periosteum to a more limited extent. There is a thickening and irregularity of the growth plate. The failure occurs through the proliferative and hypertrophic zone in an irregular pattern. The resting zone of the physis is usually normal in appearance microscopically, but accounts for a smaller percentage of the total thickness of the physis because of the relative increase in thickness of the proliferative and hypertrophic zones. The hypertrophic zone can account for up to 80% of physeal width, whereas normally it would be around 15–30%. Both the proliferative and hypertrophic zones demonstrate an overall decreased number of chondrocytes with an excess amount of matrix tissue. Collagen fibrils are decreased in number, variable in size, and irregularly organised in these two zones. The columnar alignment of the chondrocytes is disrupted and the cells tend to be organised into clumps. Histology taken before and after fixation demonstrates a return to a more normal architecture following fixation. Such finding suggest that mechanical stabilisation of the physis with removal of abnormal shear across the physis allows at least a partial reversal of the pathology seen in SUFE. Guzzanti et al.36 showed that histological sections of physes in stable and unstable slips after fixation showed an improvement in the cellular architecture and improved columnar organisation of chondrocytes. In addition, Weiss and Sponseller37 found no abnormalities in iliac crest biopsies of patients with SUFE suggesting that the microscopic changes seen in the proximal femoral physis are secondary to the slip rather a manifestation of a generalised disorder.
Natural history Short term natural history of SUFE is one of gradual displacement. With time the physis closes and so stabilises the slip. All slips eventually stop, the timing of which and the degree of slip prior to physeal closure are unpredictable. Most progress slowly, but some do so rapidly. These are the ones which are at the highest risk of significant complications. In the long-term SUFE does appear to put the hip joint at increased risk of developing osteoarthritis, with poorer
223 results following increasing severity of slip. Haggland et al.12 reported radiographic evidence of OA in 27% of SUFE hips at long-term follow (mean follow up 33 years), compared with 9% of controls. Carney and Weinstein38, with a mean follow up of 41 years, reported on 28 patients with 31 untreated slips, they correlated the severity of the slip with radiographic and clinical scores. Patients with mild slips did better with regard to radiographic changes and Iowa hip scores. At longterm follow up Iowa hip scores were at least 80 in all 17 mild slips and in 9 of the 14 hips with moderate or severe slips. There was radiographic evidence of OA in 64% of the mild slips and 100% of the moderate and severe slips. It is thought that SUFE accounts for 2–9% of end stage hip arthritis, and a cadaveric study noted ‘post slip’ morphology in 8% of skeletons and showed that OA was associated with such morphology.39
Treatment The goals of treatment are early detection, prevention of further slippage and avoidance of complications. Attention is focused on the affected hip, though care of the unaffected hip must not be overlooked.
Manipulation Historically this was performed to decrease the proximal femoral deformity and has been described in conjunction with spica casting and internal fixation. Forceful manipulation in cases of SUFE is never safe because of the increased risks of AVN. A serendipitous reduction which may occur with patient positioning on the operating table with the legs extended and gently internally rotated appears not to adversely affect patient outcome.40
Spica casting The goal of spica casting is to prevent progression of SUFE. High rates of complications occur in children treated this way, with increased rates of chondrolysis in both the affected hip and the unaffected hip, progression of slippage and pressure area problems. With the advent of in situ fixation there is little role for spica casting now.
In situ fixation With regard to the more common stable or chronic mild and moderate slips (85%), there is little controversy in the diagnosis and treatment since most surgeons fix the slip in situ on a fracture table with a single cannulated screw after no formal manipulation. Two screw fixation yields only a 33% increase in stiffness compared to single screw fixation and the gain in stiffness with a second screw may not offset the increased risk of complications.41 Clinical studies have repeatedly shown that single screw fixation yields satisfactory, if not superior, results to multiple pin or screw fixation for both stable and unstable slips.42 Blanco et al.43 in a study of 114 hips treated with one two or three screws or pins, found that the
ARTICLE IN PRESS 224 incidence of pin-related complications was directly related the number of pins or screws (4.6% with one screw/pin, 19.6% with two and 36% with three). Carney et al.44 looked at slip progression in stable slips fixed in situ with a single screw. They found those slips that do progress (assessed as a change of greater than 101 from the position achieved at surgery on plain film) had less than five threads engaging the epiphysis. The key points in placement of the screw are as follows: 1. an image intensifier and a radiolucent fracture table; 2. anterior entry site on the neck, appropriate for the degree of slip; 3. no crossing of the physis until bi-planar alignment is achieved; 4. the pin is in the epiphysis and NOT in the joint by multiplanar radiographic evaluation. The operative technique is well described by Morrissy45 who puts the emphasis on pin placement in the central axis of the femoral head and the use of a single screw. For ease in screw placement, the ideal system should be cannulated, fully threaded and easy to remove. Using the image intensifier in the AP position, a smooth Kirschner wire is placed on top of the skin to determine the path of the screw, perpendicular to the physis and into the centre of the head. Mark this line with a marker. Repeat this with the image intensifier in the lateral position. The skin incision is then placed where the two lines on the skin bisect. The most important contribution to the blood supply to the femoral head is from the lateral epiphyseal vessels.46 Brodetti47 demonstrated that these enter the femoral head in the postero-superior quadrant and anastomose with the vessels from the round ligament at the junction of the medial and central thirds of the femoral head. Therefore the ideal position for a screw is in the central area or neutral zone of the femoral head. If a pin is placed in the posterosuperior quadrant the risk of damage to the epiphyseal blood supply is increased. Once the fixation screw is in situ, an arthrogram may be performed via the cannulated screw to ensure that joint penetration has not occurred. Care must be taken not irrigate the joint with debris from surgery if penetration has indeed occurred. This is not something that we routinely perform in our unit. It is better to move the hip through a range of movement and screen under image intensifier. If any doubt persists then a later CT scan of the hip should be performed. The timing of fixation is also very significant. Recent work from the Alder Hey hospital48 has shown an increased rate of AVN in unstable SUFEs if treated between 24 and 72 h, leading to the hypothesis of an ‘unsafe window’ when intervention should be actively avoided. For the severe slips, treatment is controversial. In situ pinning can often be very difficult if not impossible. In these cases primary osteotomy may be indicated. An attempt at in situ fixation can be undertaken, accepting that there will be a functional deficit, and depending on the age at presentation, limited remodelling potential. If the patient is still symptomatic once the physis has closed it may
S.J. Parsons et al. then be possible to undertake a late osteotomy to restore the anatomy.
Femoral osteotomy Proximal femoral osteotomies are classified in terms of their timing (early or late) or anatomically by the level of the femoral neck osteotomy. 1. Early osteotomies are used as part of the acute treatment in an attempt to improve the joint anatomy and prevent further slippage and later complications. They are always accompanied by a pinning of the epiphysis. 2. Late osteotomies are usually performed at least 1 year after initial treatment and only if significant symptoms persist and the deformity is significant. Anatomically, these are (A) subcapital (Dunn49 or Fish50); (B) basal neck (Kramer51 or Barmada et al.52); (C) intertrochanteric (Southwick25 or Imhauser53). The closer to the epiphysis the osteotomy, the greater is the risk of AVN, in Frymoyer’s paper54 reporting 0% AVN using the Southwick procedure compared with up to 30% for subcapital osteotomies. However, the subcapital osteotomy gives the highest degree of correction.
Subcapital osteotomy Slip progression following subcapital osteotomies has not been reported. The Fish50 osteotomy is a cuneiform subcapital osteotomy, where a wedge of bone and accompanying callus is removed from the neck. The head is then reduced onto the neck and pinned in place. Fish reported good to excellent clinical and radiological results in 61 of 66 (92%) patients who had this osteotomy,55 with AVN developing in three hips (4.5%) and chondrolysis in two (3%). The Dunn osteotomy is undertaken more acutely and yields 75% good clinical results.49 Both techniques specify that care needs to be taken in detensioning the blood supply at the posterior neck to minimise the risk of AVN. As with unilateral screw fixation limb length discrepancy is a common problem with these osteotomies, (between 1 and 2 cm, and possibly up to 5 cm55). They are both technically demanding and have a steep learning curve; it is not an operation for the occasional user. Complications can be frequent and severe, leading many authors to recommend caution if you are considering their use.
Neck osteotomy The Kramer et al.51 osteotomy corrects the varus and retroversion of the slip. It is a compensating closing wedge osteotomy at the base of the neck. The osteotomy is fixed classically with 3 threaded Steinmann pins that also cross the epiphysis, but single screw fixation is acceptable.
ARTICLE IN PRESS Slipped upper femoral epiphysis Barmada et al.’s52 osteotomy is identical to Kramer’s apart from it being placed between the insertion of the capsule and the intertrochanteric line making it extra capsular and theoretically preserving the blood supply to the head. Being more distal correction achieved by the osteotomy is limited. Complications again include AVN, chondrolysis and LLD, but the risk of AVN and chondrolysis is less than with subcapital osteotomy.
Intertrochanteric osteotomy Intertrochanteric osteotomies are generally used after closure of the physis. Southwick25 describes a tri-planar osteotomy incorporating valgus, flexion and internal rotation of the distal segment to restore proximal femoral alignment, at the level of the lesser trochanter. Imhauser53 described a bi-planar osteotomy with flexion and internal rotation of the distal portion. Significant internal rotation is required to restore anatomical relations and a functional arc of movement. They are secured using plates or fixed angle devices. Southwick reported good to excellent clinical results with his series in 87% of patients at 18 years. Chondrolysis, delayed union, re-operation, LLD, fracture and late OA have been quoted as complications of the intertrochanteric osteotomy. Being the most distal from the site of the deformity they are limited in the correction they can provide. Despite this there is generally sufficient correction to allow for good clinical outcome, with an acceptably low rate of complications.
Contralateral fixation Prophylactic pinning of the uninvolved hip provokes debate. Proponents of contralateral fixation cite the high risk of bilateral SUFE, the increased risk of OA at long-term follow up, and the decreased risks of prophylactic pinning as technology and technique improve. Opponents of prophylactic pinning cite the complications of prophylactic treatment and the potential risks of pinning a hip that will never slip. With appropriate counselling and close follow up most subsequent slips can be picked up early. The accepted recent frequency for developing a contralateral slip in adolescence following a unilateral slip is 20–25%.56 If you also consider that 5–10% of slips are unstable, then we can conclude that the risk of developing a contralateral, unstable SUFE after a unilateral slip is 1–2%. The procedure of fixing a ‘‘normal’’ hip is not without risk, although more recent studies have shown the complication risk to be negligible.57 Contralateral slips have been reported as late as 5 years following the original but the majority occur by 18 months after the original slip. Age at initial slip seems an important determinant in slippage of a contralateral ‘‘normal’’ hip. The younger the child, the higher the risk especially in boys. Stasikelis et al.58 showed all boys younger than 11 years 7 months at first slip diagnosis went on to develop a contralateral slip, 9 of 22 aged between 11 years 8 months and 14 years 11 months did so, and no male older than 15 years did so. These authors found that a modified Oxford pelvic bone age score59 was highly predictive of a contralateral slip.
225 Puyleart et al.6 looked at pubertal stage and risk of contralateral slip. He showed that the risk was high as long as the triradiate cartilage was open; reducing to 4% once the triradiate cartilage had closed. He concluded that staging puberty is useful to differentiate the risk of contralateral slip. Regular radiographic assessment and parental vigilance are essential. If these be assured, the contralateral hip should be prophylactically fixed. All slips in young children (o10 years) and those due to endocrine disease are routinely fixed bilaterally due to the increased risk of a contralateral slip, 61% of endocrinopathy-related SUFE60 and 95% in chronic renal insufficiency patients61 are bilateral.
Removal of metalwork Our view is that metalwork is best removed, to reduce the stress riser effect of the implant and as there is an increased chance of requiring future arthroplasty. Removal of metalwork can be a difficult and time consuming procedure. It means another anaesthetic, more scarring and risk of infection. Complication rates of 19–53% are reported (implant breakage, extensive bone loss with implant removal, fracture following removal, difficulty in removing titanium screws due to osseo-integration) particularly when the screws/pins have been removed with significant quantities of bone. Provided care is exercised with regard to the choice of hardware and its removal, it is the opinion of the authors that all metalwork should be removed. We routinely use the Richards screw which is fully threaded and has a reverse cutting thread, making removal easier. This should be performed at skeletal maturity or once the physis has closed to prevent the risk of further slippage.
Complications There are many complications of treatment of SUFE. Avascular necrosis of the capital epiphysis and chondrolysis are the two most feared. These can occur spontaneously or may be related to treatment. Other complications can arise such as implant failure, growing off the screw, slip progression, proximal femoral fracture, femoral neck fracture, and leg length discrepancy.
Chondrolysis Chondrolysis is acute necrosis of the articular cartilage. It was first described by Elmslie in 1913. Waldenstro ¨m in 1930 established chondrolysis as a definite pathological entity distinct from AVN. Risk factors for chondrolysis are: 1. 2. 3. 4.
cast immobilisation unrecognised permanent pin penetration severe slip prolonged symptoms before treatment.
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Table 1 of child.
S.J. Parsons et al.
Normal values for cartilage thickness, by age
Age (year)
Normal values (mm)
1–7 8–12 13–17
6 5 4
It usually presents with pain and stiffness, with the hip being held in flexion, external rotation and abduction. X-rays reveal a loss of joint space, the criterion for diagnosis being a loss of more than 50% of the joint space compared to the other hip or an absolute measurement of 3 mm or less. A bone scan may help make the diagnosis but this is seldom necessary (Table 1). The incidence of chondrolysis varies with treatment. It can occur spontaneously without treatment of the slip, but complicates at 0–9% after in situ fixation, rising to over 50% in a series of female patients treated with a spica cast. It is particularly associated with pin penetration of the joint. Rates of chondrolysis by treatment: 1. 2. 3. 4. 5.
spica casting 14–53% subcapital osteotomy 3–18% base of neck osteotomy 2–10% intertrochanteric osteotomy 2–25% in situ fixation and bone peg epiphysiodesis less than 5%.
It affects girls more than boys and black races were thought to be more likely to suffer chondrolysis. This has been disproved but there may be a higher incidence in those of Hawaiian descent. Presentation is usually between 6 weeks and 4 months after treatment of SUFE. Progressive joint space narrowing occurs between 6 and 12 months. Eisenstein and Rothchild,62 in a prospective study of 34 patients with slips, found that all patients had significant elevations in serum immunoglobulins and the C3 component of complement; the nine that developed chondrolysis had a greater elevation in the IgM fraction as well. The authors felt that SUFE could produce an antigen that induces an autoimmune state and that a genetically determined subgroup of people may develop chondrolysis. Walters and Simon63 first implicated joint penetration with metallic implants although some patients with pin penetration did not develop chondrolysis. Transient penetration in experimental models produces less severe cartilage changes than if the pins are left in place. In the rabbit model the severity of the chondrolysis is related to the duration of pin penetration. Multiple fixation devices appear to cause higher rates of chondrolysis because of the risk of unrecognised pin penetration. The risk of chondrolysis is lessened if the penetration occurs in the inferior head or fovea or if penetration is recognised at the time of surgery and the device is removed.64 Pathologically the findings are those of a non-specific inflammatory process, with thickening of the synovium and large villous projections. The synovium then becomes
fibrotic and the capsule thickens. The articular cartilage is initially grossly normal but eventually thins and softens. Both femoral and acetabular cartilage are affected but there is no pannus. With progression, granulation tissue gradually invades the articular surfaces and the fibrous adhesions form between the capsule, the acetabulum and the femoral head. When raw bone is exposed on both sides of the joint, osteoarthritis is inevitable. Treatment of chondrolysis is largely supportive. Firstly infection must be ruled out. Secondly, a CT scan of the hip should be undertaken to ensure that penetration of the joint has not occurred. If penetration has occurred then the screw should be removed, or replaced if the physis has not closed. Patients who do not recover adequate movement or who have severe continued pain may require arthrodesis or arthroplasty.
Avascular necrosis (AVN) Avascular necrosis is a serious complication of SUFE as the prognosis is poor. Most cases of AVN occur in slips that have been treated. The incidence is lowest after open epiphysiodesis or in situ pinning of stable slips where no reduction is attempted. The two main causes are disruption of the blood supply preoperatively by the slip or by the treatment. The condition is unlike Perthes’ disease in that there is a single vascular insult and much less restorative/ remodelling capacity, probably because the children are older. Femoral head necrosis may be total or partial (segmental). Radiographs initially show few changes. Eventually, resorption of necrotic bone becomes apparent. Almost all cases are recognised by 1 year65 with the occasional rare case by 18 months. It is possible to diagnose earlier on bone scan or MRI. However these methods serve only to document the condition, not to help in planning treatment. There is debate as to whether the degree of the slip influences the incidence of AVN. In Tokmakova et al.’s66 paper, none of 204 hips with a stable SUFE developed AVN of the hip, regardless of grade of slip. In addition AVN did not occur in any of the unstable hips that had not undergone reduction. The rate of AVN increased in unstable hips that had been partially or completely reduced (mild, 12.5%; moderate 70%; severe 75%). This supports the view that reduction of the unstable SUFE causes AVN. Timing of the intervention may affect AVN rates, which increase from 0% to 9% before 24 h from symptom-onset to 20% after this time.
Salvage options If chondrolysis and necrosis are avoided then most treated hips will function well into later adult life. Re-directional osteotomies, vascularised fibular grafting and standard bone grafting procedures have been attempted in children, but there are no convincing outcome studies. The results of distribution arthrolysis are variable and difficult to predict so that all that can be offered in the medium and long term is later arthrodesis or arthroplasty.
ARTICLE IN PRESS Slipped upper femoral epiphysis
Acknowledgements We would like to thank Andrew Biggs and Alan Jones, of the Medical Illustration Unit, for their help in producing the images.
References 1. Griffiths MJ. Slipping of the upper femoral epiphysis. Ann R Coll Surg 1976;58:34–42. 2. Loder RT. The demographics of slipped capital femoral epiphysis. An international multicentre study. Clin Orthop 1996;322:8–27. 3. Hansson LI, Haggland G, Ordeberg G. Slipped capital femoral epiphysis in Southern Sweden 1910–1982. Acta Orthop Scand Suppl 1987;226:1–67. 4. Alexander C. The aetiology of femoral epiphyseal slipping. J Bone Jt Surg 1966;48-B:299–311. 5. Loder RT, Farley FA, Herzenberg JE, Hensinger RN, Kuhn JL. Narrow window of bone age in children with slipped capital femoral epiphysis. J Pediatr Orthop 1993;13:290–3. 6. Puylaert D, Dimeglio A, Bentahar T. Staging puberty in slipped capital femoral epiphysis: importance of the triradiate cartilage. J Pediatr Orthop 2004;24:144–7. 7. Keenan WN, Clegg J. Idiopathic bilateral SUFE in a child under six years of age. J Bone Jt Surg 1994;76-B:495–6. 8. Kelsey JL, Acheson RM, Keggi KJ. The body build of patients with slipped capital epiphysis. Am J Dis Child 1972;124: 276–81. 9. Kitadai HK, Milani C, Nery CA, Filho JL. Wiebergs centre-edge angle in patients with slipped capital femoral epiphysis. J Pediatr Orthop 1999;19:97–105. 10. Loder RT, Mehbod AA, Meyer C, et al. Acetabular depth and race in young adults, a potential explanation of the differences in the prevalence of slipped capital femoral epiphysis between different racial groups. J Pediatr Orthop 2003;23:699–702. 11. Hansson LI, Haggland G, Ordeberg G. Epidemiology of slipped capital epiphysis in Southern Sweden. Clin Orthop 1984;191: 82–94. 12. Haggland G, Hansson LI, Ordeberg G. Bilaterality in slipped upper femoral epiphysis. J Bone Jt Surg 1988;70-B:179–81. 13. Billing I, Severin E. Slipping epiphysis of the hip; a Roentgenological and clinical study based on a new Roentgen technique. Acta Radiol 1959;51:1–76. 14. Hurley JM, Betz RR, Loder RT, Davidson RS, Alburger PD, Steel HH. Slipped capital femoral epiphysis. The prevalence of late contralateral slip. J Bone Jt Surg 1996;78-A:226–30. 15. Speer DP. The John Charnley award paper. Experimental epiphysiolysis: aetiological models slipped capital femoral epiphysis. In: Nelson JP, editor. The hip: proceeding of the 10th open scientific meeting of the hip society. St. Louis, MO: CV Mosby Company; 1982. p. 68–88. 16. Galbraith RT, Gelberman RH, Hajek PC, Baker LA, Sartoris DJ, Rab GT, et al. Obesity and decreased femoral anteversion in adolescence. J Orthop Res 1987;5:523–8. 17. Mirkopulos N, Weiner DS, Askew M. The evolving slope of the proximal femoral growth plate, relationship to slipped capital epiphysis. J Pediatr Orthop 1988;8:268–73. 18. Kordelle J, Richolt JA, Millis M, et al. Development of the acetabulum in patients with slipped capital femoral epiphysis: a three-dimensional analysis based on computed tomography. J Pediatr Orthop 2001;21:174–8. 19. Blethen SL, Rundle AC. Slipped capital femoral epiphysis in children treated with growth hormone: a summary of the national cooperative growth study experience. Horm Res 1996; 46:113–6.
227 20. Loder RT, Hensinger RN, Alburger PD, et al. Slipped capital femoral epiphysis associated with radiation therapy. J Pediatr Orthop 1998;18:630–6. 21. Rennie AM. The inheritance of slipped upper femoral epiphysis in young children. J Bone Jt Surg 1982;64-B:180–4. 22. Matava MJ, Patton CM, Luhmann S, Gordon JE, Schoenecker PL. Knee pain as the initial symptom of slipped capital femoral epiphysis: an analysis of initial presentation and treatment. J Pediatr Orthop 1999;19-A:455–60. 23. Loder RT, Starnes T, Dikos G, Aronsson DD. Demographic predictors of severity of stable slipped capital femoral epiphyses. J Bone Jt Surg 2006;88-A:97–105. 24. Loder RT, Richards BS, Shapiro PS, et al. Acute slipped capital femoral epiphysis: the importance of physeal stability. J Bone Jt Surg Am 1993;75-A:1134–40. 25. Southwick WO. Osteotomy through the lesser trochanter for slipped capital epiphysis. J Bone Jt Surg 1967;49-A:807–35. 26. Cowell HR. The significance of early diagnosis and treatment of slipping capital femoral epiphysis. Clin Orthop 1966;48: 89–94. 27. Klein A, Joplin RJ, Reidy JA, et al. Roentgenographic features of slipped capital epiphysis. Am J Roentgenol 1951;66:361–74. 28. Steel HH. The metaphyseal blanch sign of slipped capital femoral epiphysis. J Bone Jt Surg 1986;68-A:920–2. 29. Scham SM. The triangular sign in the early diagnosis of slipped capital femoral epiphysis. Clin Orthop 1974;103:16–7. 30. Wilson PD. The treatment of slipping of the upper femoral epiphysis with minimal displacement. J Bone Jt Surg 1938;20A:379–99. 31. Kallio PE, Lequesue GW, Paterson DC, Foster BK, Jones JR. Ultrasound in slipped capital femoral epiphysis. Diagnosis and assessment of severity. J Bone Jt Surg 1991;73-B(6):884–9. 32. Cohen MS, Gelberman RH, Griffin PP, Kasser JR, Emans JB, Millis MB. Slipped capital femoral epiphysis: assessment of epiphyseal displacement and angulation. J Paediatr Orthop 1986;6: 259–64. 33. Rhoad RC, Davidson RS, Heyman S, Dormans JP, Drummond DS. Pre-treatment bone scan in SCFE: a predictor of ischaemia and avascular necrosis. J Paediatr Orthop 1999;19:164–8. 34. Tins BJ, Cassar-Pullicino VN. Slipped upper femoral epiphysis. In: Davis AM, Johnson K, editors. Imaging of the hip and bony pelvis. Techniques and applications. Berlin: Springer; 2005. p. 173–94 [chapter 12]. 35. Howorth B. Slipping of the capital femoral epiphysis. Clin Orthop 1966;48:11–32. 36. Guzzanti V, Falciglia F, Stanitski C, Stanitski DF. Slipped capital femoral epiphysis, physeal histological features before and after fixation. J Pediatr Orthop 2003;23:571–7. 37. Weiss AP, Sponseller PD. Iliac crest growth plate analysis in slipped capital femoral epiphysis. J Pediatr Orthop 1990;10: 629–32. 38. Carney BT, Weinstein SL. Natural history of untreated chronic slipped capital femoral epiphysis. Clin Orthop 1996; 322:43–7. 39. Goodman DA, Feighan JE, Smith AD, et al. Subclinical slipped capital femoral epiphysis. Relationship to osteoarthrosis of the hip. J Bone Jt Surg 1997;79-A:1489–97. 40. Aronson DD, Loder RT. Treatment of the unstable acute slipped capital femoral epiphysis. Clin Orthop 1996;322:99–110. 41. Karol LA, Doane RM, Cornicelli SF, et al. Single versus double screw fixation for treatment of slipped capital femoral epiphysis: a biomechanical analysis. J Pediatr Orthop 1992;12: 741–5. 42. De Sanctis N, DiGennaro G, Pempinello C, et al. 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 1996;5-B:90–5.
ARTICLE IN PRESS 228 43. Blanco JS, Taylor B, Johnston II CE. Comparison of single pin versus multiple pin fixation in treatment of slipped capital femoral epiphysis. J Pediatr Orthop 1992;12:384. 44. Carney BT, Birnbaum P, Minter C. Slip progression after in situ single screw fixation for stable slipped capital femoral epiphysis. J Pediatr Orthop 2003;23:584–9. 45. Morrissy RT. Slipped capital femoral epiphysis technique of percutaneous in situ fixation. J Paediatr Orthop 1990;10: 347–50. 46. Claffey TJ. Avascular necrosis of the femoral head. An anatomical study. J Bone Jt Surg 1960;42-B(4):802–9. 47. Brodetti A. The blood supply of the femoral neck and head in relation to the damaging effects of screws and nails. J Bone Jt Surg 1960;42-B(4):794–801. 48. Personal communication, from C. Bruce. Alder Hay Children’s Hospital, Liverpool, UK. Paper accepted for publication by JPO. 49. Dunn DM. The treatment of adolescent slipping of the upper femoral epiphysis. J Bone Jt Surg 1964;46-B(4):621–9. 50. Fish JB. Cuneiform osteotomy of the femoral neck in the treatment of Slipped capital femoral epiphysis. J Bone Jt Surg 1984;66-A:1153–68. 51. Kramer WG, Craig WA, Noel S. Compensating osteotomy at the base of the femoral neck for slipped capital femoral epiphysis. J Bone Jt Surg 1976;58-A:796–800. 52. 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 1978;132:98–101. 53. Imhauser G. Pathogenese und therapie der jugendlichen huftenkopflosung. Z Orthop Ihre Grenzgeb 1957;88:3–41. 54. Frymoyer JW. Chondrolysis of the hip following Southwick osteotomy for severe slipped capital femoral epiphysis. Clin Orthop 1974;99:120–4. 55. Fish JB. Cuneiform osteotomy of the femoral neck in the treatment of slipped capital femoral epiphysis. A follow up note. J Bone Jt Surg 1994;76-A:46–59.
S.J. Parsons et al. 56. Jerre R, Billing L, Hansson G, et al. The contralateral hip in patients treated for unilateral slipped upper femoral epiphysis: long term follow up of 61 hips. J Bone Jt Surg 1994;76-B:563–7. 57. Seller K, Raab P, Wild A, et al. Risk benefit analysis of prophylactic pinning in slipped capital femoral epiphysis. J Paediatr Orthop 2001;10:192–6. 58. Stasikelis P, Sullivan C, Philips W, et al. Slipped capital femoral epiphysis: prediction of contralateral involvement. J Bone Jt Surg 1996;78-A:1149–55. 59. Acheson R. The Oxford method of assessing skeletal maturity. Clin Orthop 1957;10:19–39. 60. Loder RT, Wittenberg B, DeSilva G. Slipped capital femoral epiphysis associated with endocrine disorders. J Paediatr Orthop 1995;15:349–56. 61. Loder RT, Hensinger RN. Slipped capital femoral epiphysis associated with chronic renal osteodystrophy. J Paediatr Orthop 1997;17:205–11. 62. Eisenstein A, Rothchild S. Biochemical abnormalities in patients with slipped capital femoral epiphysis and chondrolysis. J Bone Jt Surg 1976;58-A:459–67. 63. Walters R, Simon SR. Joint destruction a sequel of unrecognised pin penetration in patients with slipped capital femoral epiphysis. In: ‘The hip’. Proceedings of the eighth open scientific meeting of the hip society, St. Louis: CV Mosby; 1980. p. 145–64. 64. Vrettos BC, Hoffman EB. Chondrolysis in slipped upper femoral epiphysis. Long term study of the aetiology and natural history. J Bone Jt Surg 1993;75-B:956–61. 65. Krahn TH, Canale ST, Beaty JH, Warner WC, Lourenco P. Long term follow up of patients with avascular necrosis after treatment of slipped capital femoral epiphysis. J Paediatr Orthop 1993;13:154–8. 66. Tokmakova KP, Stanton RP, Mason DE. Factors influencing the development of osteonecrosis in patients treated for slipped capital femoral epiphysis. J Bone Jt Surg 2003;85-A:798–801.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 193–199
Available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/cuor
MINI-SYMPOSIUM: COMPUTER AIDED/ROBOTIC ORTHOPAEDIC SURGERY
(iii) The anterior cruciate ligament and navigation J.C. Panisseta,, F. Picardb a
Clinique des Cedres, 48 avenue de Grugliasco, 38230 Echirolles, France Department of Orthopaedic Surgery, University of Pittsburgh Medical Center, Pittsburgh, PA 15213, USA
b
KEYWORDS Anterior cruciate ligament; Navigation; Graft isometry
Summary Here, we describe the current status of navigation systems used in anterior cruciate ligament surgery. Various systems of navigation are available; we use the Orthopilot system and the Praxim system daily. The goal of navigation is to help the surgeon to place the tibial and femoral tunnels in the correct position before drilling takes place. Thus, the ultimate goal is better positioning and isometry of the ligament graft in order to decrease the risk of adverse outcomes. & 2007 Elsevier Ltd. All rights reserved.
Introduction Surgical navigation has been in clinical use for 10 years now and was pioneered in knee surgery. The first steps were taken with the works of Dessenne,1 Julliard,2 and Cinquin,3 following initial ideas from Julliard, who considered traditional techniques to be too operator dependant and insufficiently adapted to the local anatomy of the knee. Let us first consider some definitions. A new word has appeared in our own language: the ‘surgeries’ of the anterior cruciate ligament. This word expresses the use of computer-assisted navigation on the one hand and robotguided surgery on the other. We will not deal with robotics in this article, since this field is still experimental and is currently prohibitively expensive. We would point out that the robot presently contributes to the surgical process by drilling the tunnels taking into account the three-dimensional data from scans.
Corresponding author.
E-mail address:
[email protected] (J.C. Panisset). 0268-0890/$ - see front matter & 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2007.07.002
Navigation, however, supports the surgeon. It will facilitate correct placement of tunnels. This requires preoperative imaging data (usually CT scan), pre-operative fluroscopy,4,5 or even pre-anatomic data acquisition. This last option is chosen by the users in the majority of cases. The surgeon is still the master of his procedure, but is guided by navigation as a driver is guided by an in-car global positioning system. Of the different systems available today, two have already proven their utility. One is the system developed by Praxim and used by Juliard, Merloz and Plaweski while the other is the Orthopilot system used by Saragaglia and our team.6–8 We will explain the principles of each system with particular emphasis on the Orthopilot system, with which we are most familiar.
Why use navigation? We are aware of the good results of ligament surgery, nevertheless there remains a failure rate of 5–20%.9,10 The causes of failure are multifactorial. The graft type, its quality or its fixation can be the origin of failure. On the
ARTICLE IN PRESS 194 other hand, ligament positioning, and therefore the localization of femoral and tibial tunnels, will directly influence the results.11,12 Elongation of the transplant between the maximum flexion and maximum extension will depend on tunnel positioning. The greater the graft length variation between flexion and extension, the greater the risk of the transplant failure. The goal of the reconstruction is to obtain perfect ligament isometry, i.e. an absence of graft elongation. Staubli and Sati13 have shown that in a series of failures, the tunnel position was poor in 40–60% of cases. Recently, the major factor identified in the analysis of failures was poor positioning of the graft. There are numerous arthroscopic techniques for ACL reconstruction using specific portals and views. Most of the time, these are used independently and their positioning depends on anatomic criteria pre-defined for each method. The goal is to position the femoral or tibial tunnel at the native origin and insertion of the ACL. Gillquist and Odensten14 have shown that only the central fibre of the normal ACL is isometric and that anisometry could vary up to 10 mm according to the position of fibres. However, other authors15 have calculated that there is no perfect isometric position for the ACL and that the length variation of the central fibre is of the order of 6 mm. Friederich16 believes that the most anterior fibre is isometric. If we place our graft at the centre of tibial and femoral insertions, the isometry would be approximately 4 mm.17 In reality, perfect ligament isometry does not exist and we should speak of relative isometry. Isometry is considered acceptable in practical terms if the variation of ligament length between flexion and extension is o2 mm. The goal of surgery is therefore to position a ligament with the utmost isometry. Conventional surgery uses the anatomic insertion sites as the guide to drill the tunnels and experience shows that the results are not so bad! However, if we return to basic ACL anatomy we know that there are two bundles, an antero-medial bundle and a postero-lateral bundle. These are difficult to identify in a normal ACL under arthroscopy, but very real. Over recent years, several teams have been thinking that rebuilding the two bundles is the ideal solution.18,19 In theory, this is a seductive solution but actually increases the complexity of the surgical procedure and consequently the risk of positioning errors. We reserve our interest in this research area to improve our results with those patients who have greater degrees of laxity with major instability and a strongly positive pivot shift test on clinical examination. With traditional surgery we essentially rebuild the anteromedial bundle alone. Increasingly the importance of the postero-lateral bundle is emerging, as it has a very significant influence on anterior translation at 301 flexion, a frequent position of the knee in sports activity. Thus, navigation appears to be more important if we are to manage more and more complex procedures. With navigation we can position the ligament, respecting isometry and avoiding impingement in the intercondylar notch. Completion of the tibial and femoral tunnels is not independent. Navigation takes into account the local anatomy, particularly the intercondylar notch, and also knee kinematics. It is possible to achieve two femoral tunnels and two tibial tunnels, or even two femoral tunnels and one tibial tunnel, depending on the grafts used (patellar
J.C. Panisset, F. Picard tendon or hamstring). With navigation, the surgeon can secure ideal positioning of the tunnels, respecting on one hand, the knee anatomy and on the other hand the ligament isometry before drilling the tunnels.
Reconstruction of the ACL using the Orthopilot system The equipment This technique requires the conventional equipment for this type of surgery plus specific additional materials (Figures 1 and 2):
An optoelectronic infra-red camera. A computer with the proper software. Tibial and femoral specific sights. Palpers. Active or passive sensors directly fixed on the tibia and on the femur via pins, which are linked to the computer system through a wire. Passive sensors, which consist of a retro-reflecting system, alternatively fixed on the palpers, on the sights. This passive system is only visualized via the camera and is not linked to the computer system. It enables better flexibility of use in relation to the active system. Pins of 20/10 mm and their fixation system.
Surgical procedure The operation begins with knee exploration and positioning of the sensors. Conventional arthroscopy is followed by the treatment of meniscal injuries and clearing of the
Figure 1
Instruments necessary for navigation.
ARTICLE IN PRESS (iii) The anterior cruciate ligament and navigation
195
Figure 4
Figure 2
Navigation panel.
Extra-articulation palpation.
We start the procedure by recording several extraarticular points with a passive sensor with 4 reflecting spheres (Figures 3 and 4). Thus, we palpate the anterior tibial tubercule, the tibial crest over the ankle, the centre of the medial tibial space and the lateral tibial space. Then, we record the exact position of the knee at 901 and with full extension. We end with a kinematic acquisition between full extension and 901 of flexion. A measure of anterior tibial translation is possible in extension, with various positions of flexion, or at 901 of flexion, as well as in various positions of rotation. Measurement of the pivot shift is also possible at the end of the intervention after graft fixation, when measurement of rotation can also be made. It is furthermore possible to compare translation and rotation before and after fixation of the graft. Next we complete the intraarticulation palpations. Firstly, we detect the anterior segment of the lateral meniscus, then the anterior tibial edge. Then, we acquire the pattern of the whole anterior edge of the intercondylar notch by recording approximately 15 points. We conclude by recording the femoral attachment site of the ACL. Two points are stored: one at the posterior part of Blumensaat’s line and the other at the back of the notch, at 11 o’clock for a right knee and at 1 o’clock for a left knee. These points are fundamental for the computer to determine the dimensions of the knee and identify possible sites of impingement. The whole procedure can be followed on the computer via the available consecutive displays.
Figure 3 The active sensors on site.
intercondylar notch. We then position the active sensors (rigid body) or passive (Figure 3) directly on the bone with two filleted bicortical pins of 20/10 mm diameter. The sensor is attached to the pins. We position a sensor on the antero-medial side of the tibia, 7 or 8 cm from the joint line, and a further sensor on the antero-medial aspect of the medial tibial condyle. The fixation pins can be replaced by a screw. The fixation of the sensors must be done very thoroughly to avoid any skin alteration on the one hand, and to obtain a sturdy construct on the other hand, which avoids disturbance of sensor position during navigation procedures.
The tibial view The tibial tunnel is located thanks to a specific sight fitted with a passive sensor. This sight is similar to conventional arthroscopic drill guides and has the same stiffness. We place the needle of the sight with the pin at the centre of the intended tibial insertion. The computer then gives us several data. First of all, we see the projection of the intercondylar notch in the pre-spinal area and the conflict zones are marked out in red (Figures 5 and 6). Then, we observe the exact position of the tunnel described in percentage terms compared with the anteroposterior distance on one hand, and also compared to the knee width. At this stage, the surgeon is free to select
ARTICLE IN PRESS 196
J.C. Panisset, F. Picard
Figure 7 Femoral viewing.
Figure 5 Correct tibial viewing, lines are green. No conflict, antero-posterior position and normal frontal position.
Figure 8
Figure 6 Incorrect tibial viewing, too anterior, red line.
the final position according to personally favoured criteria. Once the ideal position is selected it can be drilled with a bit.
Femoral viewing This is also determined using a specific sight (Figure 7). We have two possibilities: either a sight for the inside-out technique, introduced by the arthroscope antero-medially, or a sight for the outside-in technique, which requires a 1 cm external counter incision. The computer guides the surgeon in positioning this by relating to the posterior part of the intercondylar notch via two data: the distance of the tunnel centre compared with the position over the top, and the theoretical isometry of the ligament according to the position of the tibial tunnel and knee kinematics. Finally, the computer gives us information on the tunnel orientation in the frontal plane and of the possibility of conflicts (Figure 8). Once more the surgeon is free to make the final choice and drill the tunnel as soon as a satisfactory position of the pin is found.
Correct femoral viewing.
Anterior tibial translation measurement Once the graft is fixed, we can compare anterior tibial translation to the measurement made at the start of the procedure. This test is carried out manually, under the same conditions as it was at the start of surgery. It remains controversial, since the observer of the test is never impartial. Will we apply the same force to produce anterior translation? But at least this test exists and has an indicative value. We can similarly assess the effect of surgery on rotation.
Discussion We can state that this navigation system has already shown itself to be efficient and very accurate. As with the majority of the current navigation systems, it is in constant development, and the software has regular upgrades. We have recently investigated the accuracy of this system in a survey of 50 cases.20 This survey enabled us to compare the position of the tunnels observed on X-rays with data stored in the computer during surgery. We were able to check tunnel positions against recommendations in the current literature. The results showed the system to be reliable and reproducible. This study also proved that it was difficult to compare data stored by computer with X-ray measurements.
ARTICLE IN PRESS (iii) The anterior cruciate ligament and navigation It is particularly difficult to compare angular data from the computer, as the palpation criteria during surgery are not the values we are able to study on X-rays. Finally, it is obvious that the system is dependent on the number of palpations made to acquire anatomic data and on the way these palpations are performed. That is why we now use ceramic palpation sensors, which are very stiff and which limit the risk of inaccuracy. The system must now evolve to simplify the system of palpation. We must streamline to a system with fewer palpations but all relevant palpations. The Orthopilot system has numerous advantages in our eyes. The setting-up of the system and its use are simple. We have observed that the learning curve is short. After 10 uses, the extra time needed for surgery falls from 20 to 10 min. The computer displays are simple and readable. Securing the sensors to bone by 20/10 pins is easy and does not create secondary problems except for pinpoint scars. This technique does not revolutionise the routine of the surgeon compared with conventional methods. It can be easily learned by a surgeon who is used to anterior cruciate ligament surgery. There are few inconveniences, though it requires considerable attention since the surgeon must remain the master of the procedure and must interpret carefully the predictions made by the computer. The study of Robert6 pinpoints an ideal position for the tibial tunnel, but identifies a femoral positioning which appears a little anterior on the femur. This fact must be considered. Actually, his results on isometry, laxity, and the control of rotation are quite convincing, as are the functional results. Navigation is becoming an essential tool to be adapted to patient morphology. In conventional surgery our methods always position the femoral tunnel at the same point whatever the patient morphology and whatever the tibial tunnel position. This may be the limiting factor for conventional surgery. The advantage of navigation is this relationship between the two tunnels that we do not have with conventional surgery. The Orthopilot system enables us to create an ideal tibial tunnel, avoiding impingement in the notch.21 It enables us to proceed to a femoral tunnel that also has ideal isometry, with control of rotation. For the implementation of two femoral tunnels, navigation is particularly necessary for creating the postero-lateral tunnel. Actually, this does not have a reliable anatomic marker compared with the antero-medial tunnel easily achievable by reading from the posterior edge of the lateral condyle. The study of Ishibashi19 demonstrates the advantages of the Orthopilot system, employing double tunnels to create an anatomic reconstruction of the two ACL bundles.
Other systems Surgigate system This system used by the de Rycke7 team is very similar to the Orthopilot system. It is based on the same principle of fixing the active sensors on the femur and tibia, on the acquisition of the knee kinematics and on the digitization of anatomic markers. The different data are compared with points which are previously stored on simple X-rays.
197 In 2001, de Rycke7 completed 91 ACL reconstructions with this system. He believed the learning curve was long and the procedure was not for everybody. Wiese and Rosenthal,22 recommend the use of navigation in revision surgery. Around 100 cases have been published, with an additional operative time of 15 min per intervention. The authors have not shown any statistically significant differences compared to a control group of patients operated using conventional surgical methods when considering early subjective results and objective measurements of laxity. However, there was a statistically significant difference in the positioning of tunnels estimated by radiographic measures. The position and orientation of tunnels are better with navigation. Nevertheless, we must challenge the results of this study since it is very difficult to get an objective measure of proper radiographic positioning of the tunnels.
Praxim system This method of navigation has been used since 1992 by Julliard.23–26 Like the Orthopilot system, it does not use the pre-operative imaging. The principle of this system is based on the relationship between the tibial insertion and the femoral insertion of the graft. For each dataset, the computer system reveals the ligament anisometry and the possible conflicts with the roof of the notch. The computer permanently computes the isometry of the central fibre of the transplant. Numerous intra-articulation markers are stored during the first stage of surgery: the so called ‘bone morphing’. This step pinpoints the zones of conflict with the notch and will lead the surgeon to reshape the notch or to modify the position of the graft by moving backwards the tibial insertion. The second step is ‘anatomometrics’, which aims to identify the best ligament isometry. Several studies using this computer tool, ‘protocol ACL logics’ have already given interesting results. Plaweski27 has recently observed better results with this technique in terms of laxity and on the rotation stability of the reconstruction using a single bundle of patellar tendon. In a series of 150 cases, he has shown better results in terms of rotational stability, 23% in average, and better results measured by anterior laxity, at 10.1 mm. Therefore, he has used this tool to position the ligament according to local morphology but also used it to measure antero-posterior and rotary laxity. This is an important breakthrough, enabling measurement of these different variables during surgery, facilitating, for example, the decision to use a two-bundle technique or an additional antero-external reconstruction. Robinson and Colombet,28 have also measured per-operatively the axial rotation and coupled antero-posterior translation, before and after reconstruction of two bundles. They have measured axial rotation during the pivot shift and found 291 for one translation of 17 mm in 10 patients. After reconstruction of the antero-medial bundle, the reduction in rotary data was 16.41 for a translation of 6 mm. The addition of a postero-lateral bundle has enabled reduction of axial rotation of 12.61 and decreased anterior tibial translation during the Lachmann test. As we understand more and more about the role of navigation in the per-operative assessment of knee laxity we
ARTICLE IN PRESS 198 are devising interpretations of the best techniques to correct abnormal findings.
Navitrack system This technique of navigation has been used since 1999. The principle is based on the variation in magnetic fields emitted by sensors during position changes. This method employed the recording of markers on a pre-operative scan. Ellermann and Siebold8 have published experience of 16 cases. The difficulties encountered using this system have lead the authors to change to an optoelectronic system since 2001. Nevertheless, the measurements made with the scanner are still essential and the extra average time of the surgery is 20–30 min.
J.C. Panisset, F. Picard define the X-ray criteria to compare the orientation and the position of the tunnels with the computer data. However, the most interesting development is the ability to be able to assess the importance of laxity, rotation and pivot-shift during surgery. Thus, we are able to choose the best surgical method. Navigation is becoming more and more useful in the development of double bundle techniques. Indeed, this complex technique must be simplified by the use of navigation. The positioning of the femoral tunnels is facilitated by navigation, since the absence of a reliable anatomic marker for the postero-lateral tunnel achievement is otherwise a source of error. In conclusion, we can say that navigation in ACL reconstruction has three goals:
to enable the surgeon to place the ligament according to Fluoroscopic systems This system of navigation appeared in 1998, described by Klos.29–31 This technique not only uses a navigation system, similar to those previously described, but also a display intensity amplifier. Klos has completed a study demonstrating the improvement in the positioning of tibial and femoral tunnels with virtual fluoroscopy when compared with conventional fluoroscopy (without any navigation system). This system is interesting but it requires extra equipment and ionizing radiations.
Conclusion Navigation in ACL reconstruction is a modern technique in constant evolution. Our experiences point out that this technique improves graft positioning and limits conflicts with the intercondylar notch. Navigation gives the surgeon an assessment of the central fibre isometry of the proposed graft, even before the tunnel is drilled, according to the positioning of the pins representing the centre of each tunnel. Some studies are starting to show the clinical impact of navigation. What is most important for the surgeon is to achieve a strong graft with reliable longevity. Several studies have pointed out the importance of tunnel positioning for long-term clinical results. If our conventional arthroscopic guides enable precision in tunnel positioning, navigation provides a more relevant positioning adapted to the anatomy of each knee, taking into account its kinematics. However, the nature and the quality of the graft are never taken into account in navigation, though the transplant is of primary importance in the control of anterior laxity. This is why navigation does not remove all failure risks of ligamentoplasty. To be useful in regular practice, the navigation system should not increase the extent of the surgical approach and should not be complex to use. It must not inordinately increase surgical time and above all it should be reproducible. The Orthopilot system and the Praxim system seem to meet these criteria. However, it is necessary to conduct prospective surveys to demonstrate the reliability of the systems in tunnel positioning. These studies should compare post-operative radiographic measures with per-operative computer data. The difficulty with this study will be to
the patient’s individual anatomy,
to enable less experienced surgeons to avoid major mistakes in positioning, and
to enable the experienced surgeon to evolve a more anatomic reconstruction using a two-bundle technique. We must not forget, whatever system is used, that the surgeon must be the master of his acts.
References 1. Dessenne V. Gestes me ´dicaux chirurgicaux assiste ´s par ordinateur: applications `a la ligamentoplastie du genou et `a la chirurgie orthognatique. These de Doctorat en Ge´nie biome ´dical, Grenoble, 1996. 2. Julliard R, Lavallee S, Dessenne V. Computer assisted reconstruction of the anterior cruciate ligament. Clin Orthop 1998; 354:57–64. 3. Julliard R, Plaweski S, Merloz Ph, Cinquin P. La navigation sans imagerie du ligament croise ´ ante ´rieur (NASALCA). Anterior cruciate ligament navigation. In: trocart J, Merloz Ph, editors. Sauramps medical. Grenoble: SURGETICA; 2002. p. 254–62. 4. KLos TVS. Computer assistance in arthroscopic anterior cruciate ligament reconstruction. Clin Orthop 1998;354:65–9. 5. Merloz P, Plaweski S. Navigation chirurgicale fluoroscopique. Rev Chir Orthop 2000;86:637–8. 6. Robert H, Boux de Casson F, Leitner F. Re´sultats anatomiques de 30 plasties du LCA navigue ´es `a 6 mois de recul minimum. Travaux de la Socie ´te ´ franc- aise d’arthroscopie. Rev Chir Orthop 2006;(Suppl au no. 8):92. 7. De Rycke J. Clinical expe ´riences for ACL—repair with the surgigate system. Navigation and robotics in total joint and spine surgery. Berlin: Springer; 2003. 8. Ellermann A, Siebold R. ACL reconstruction with the navitrack system. Critical analysis of navigation in ACL-surgery. Navigation and robotics in total joint and spine surgery. Berlin: Springer; 2003. 9. Almekinders LC, Chiavetta JB, Clarke JP. Radiographic evaluation of anterior cruciate ligament graft failure with special reference to tibial tunnel placement. Arthroscopy 1998;14: 206–11. 10. Amis AA, Jakob RP. Anterior cruciate ligament graft positioning tensioning and twister. Knee Surg Sports Traumatol Arthrosc 1998;6(Suppl 1):2–12. 11. Harner CD, Giffin R, Dunteman RC, Annunziata CC, Friedman MJ. Evaluation and treatment of recurrent instability after anterior cruciate ligament reconstruction. J Bone Joint Surg (Am) 2000;82:1652–64.
ARTICLE IN PRESS (iii) The anterior cruciate ligament and navigation 12. Dejour H, Dejour D, Aı¨t Si Selmi T. Laxite ´s ante´rieures chroniques du genou traite´es par greffe libre du tendon rotulien avec plastie late ´rale extra-articulaire. Rev Chir Orthop 1999; 85:777–89. 13. Sati M, Bourquin Y, Sta ¨ubli H-U, Nolte L-p. Considering anatomic and functional factors in ACL reconstruction: new technology. USA: CAOS; 2000. 14. Gillquist J, Odensten M. Arthoscopic reconstruction of the anterior cruciate ligament. Arthroscopy: J Arthroscopic Rel Surg 1988;4(1):5–9. 15. Sapega AA, Moyer R. Testing for isometry during reconstruction of the anterior cruciate ligament: anatomical and biomechanical considerations. J Bone Joint Surg 1990(A-72):259–67. 16. Friederich NF, Mtiller W. The knee and the cruciate ligaments, chapter functional anatomy of the cruciate ligaments. Berlin: Springer; 1992. p. 78–91. 17. Muneta T, Yamamoto H. Relationship between changes in length and force in in vitro reconstructed anterior cruciate ligament. Am J Sports Med 1993;21(2):299–304. 18. Zantop T, Herbort M, Raschke MJ, Fu F, Petersen W. The role of the anteromedial and posterolateral bundles of the anterior cruciate ligament in anterior tibial translation and internal rotation. Am J Sports Med 2007;35(2):223–7. 19. Ishibashi Y, Tsuda E, Fukuda A, Tsukada H, Toh S. Future of double-bundle anterior cruciate ligament (ACL) reconstruction: incorporation of ACL anatomic data into the navigation system. Orthopedics 2006;29(Suppl 10). 20. Panisset JC, Boux de Casson F. Navigated anterior cruciate ligament reconstruction: correlation between computer data and radiographic measurements. Orthopedics 2006;29(Suppl 10). 21. Picard F, Digioia Am, Moody J. Accuracy in tunnel placement for ACL reconstruction. Comparison of traditional arthroscopic and computer-assisted navigation techniques. Comput Aided Surg 2001;6:279–89. 22. Wiese M, Rosenthal A, Bernsmann K. Clnical experience using the surgigate system. Navigation and robotics in total joint and spine surgery. Berlin: Springer; 2003.
199 23. Julliard R, Plaweski S, Merloz Ph, Cinquin P. La navigation sans imagerie du ligament croise anterieur (NASALCA). Anterior cruciate ligament navigation. In: Trocart J, Merloz Ph, editors. Sauramps me ´dical. Grenoble: SURGETICA; 2002. p. 254–62. 24. Julliard R, Plaweski S, Lavallee S. ACL Surgeries: an efficient computer-assisted technique for ACL reconstruction. Navigation and robotics in total joint and spine surgery. Berlin: Springer; 2003. 25. Julliard R, Merloz P, Plaweski S, Perrier JP. La surge´tique du ligament croise ´ ante ´rieur. Table ronde Chirurgie de la hanche et du genou assiste ´e par ordinateur: robots versus systemes passifs. So.F.C.O.T. 76 e´me Re´union annuelle. Rev Chir Orthop 2002;88(suppl au no. 5). 26. Julliard R, Cinquin P, Lavalle ´e S. la surge ´tique du ligament croise ´ ante ´rieur. La navigation sans imagerie. (NASA). Table ronde Chirurgie de la hanche et du genou assiste´e par ordinateur: robots versus systemes passifs. So.F.C.O.T. 76e´me Re´union annuelle. Rev Chir Orthop 2002;5:88–90. 27. Plaweski S, Dumas, J, Kirshmaier M. Reconstruction du ligament croise ´ ante´rieur `a un faisceau: e´valuation de la laxite ante ´rieure et rotatoire. Travaux de la Socie ´te´ franc- aise d’arthroscopie. Rev Chir Orthop 2006(suppl au no. 8);92. 28. Robinson JR, Colombet Ph, Allard M, Bousquet V, De Lavigne C, Jambou S. Reconstruction du ligament croise ´ ante´rieur: mesures per-ope´ratoires de la cine ´matique utilisant la navigation. Travaux de la Socie ´te ´ franc- aise d’arthroscopie. Rev Chir Orthop 2006;(suppl au no. 8):92. 29. KLos TVS. Computer assistance in arthroscopic anterior cruciate ligament reconstruction. Clin Orthop 1998;354:65–9. 30. Merloz P, Plaweski S. Navigation chirurgicale fluoroscopique. Rev Chir Orthop 2000;86:637–8. 31. Plaweski S, Merloz Ph. Navigation chirurgicale fluoroscopique: application `a la reconstruction du ligament croise ´ ante ´rieur. Table ronde Chirurgie de la hanche et du genou assiste´e par ordinateur: robots versus syste `mes passifs. So.F.C.O.T.76 e `me Re´union annuelle. Rev Chir Orthop 2002;88(suppl au no. 5): 90–1.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 200–206
Available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/cuor
MINI-SYMPOSIUM: COMPUTER-ASSISTED SURGERY IN ORTHOPAEDICS
(iv) Computer-assisted knee replacement techniques Wolfram H. Kluge Bradford Royal Infirmary, Duckworth Lane, Bradford BD9 6RJ, UK
KEYWORDS Computer-assisted knee replacement; Navigation; Implant alignment; Soft tissue balance; Electromagnetic tracking
Summary Implant alignment errors are associated with inferior results after total knee arthroplasty. Computer assistance supplements mechanical instrumentation by the addition of measurements which are used to locate landmarks, direct surgical tools and thereby better align prosthetic components. Modern navigation systems are based on infrared-light tracking or, more recently, on electromagnetic guidance. After initial scepticism a variety of systems have found acceptance and a remarkable number of clinical and laboratory studies have been published. There appears to be a consensus that computer assistance brings about a significant reduction in the number of outliers and improved varus/valgus, rotation and slope alignment of components. Most studies conclude with the prediction that individual and cumulative improvement in component alignment will ultimately lead to better long-term results. The controversies surrounding routine use of computer assistance in knee arthroplasy are discussed. Data analysis founded on navigated dynamic intra-operative investigation will possibly be the key to future implant design and alignment. & 2006 Elsevier Ltd. All rights reserved.
Introduction Knee replacement surgery has gained the reputation of generally being successful. Patients assume that welltrained orthopaedic surgeons consistently operate to produce satisfactory results. The term ‘‘satisfactory’’ embraces a range of good and acceptable outcomes. Nevertheless, outcome studies have made it clear that even experienced surgeons, using conventional knee replacement techniques, are occasionally faced with major post-operative limb malalignment and errors of implant positioning. Such cases are confined to difficult clinical situations such as obese Tel.: +44 1274 382634; fax: +44 1274 366592.
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[email protected]. 0268-0890/$ - see front matter & 2006 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2006.11.005
patients, dysplasia, trauma or metabolic disorders.1 Orthopaedic surgeons are in agreement that the outcome of total knee replacement surgery is sensitive to variations in surgical technique.2,3 Several studies have suggested that coronal leg alignment errors of more than 31 are associated with more rapid failure and inferior functional results after total knee arthroplasty. 4–9 Major clinical problems can be related to poor component positioning, including sagittal plane and rotational mal-alignment.10,11 Exact axial alignment promotes longevity of the implant, mal-positioning can lead to loosening.12,13 Mechanical alignment systems are being improved continuously. However, it has been estimated that errors in tibial and femoral alignment of over 31 occur in at least 10% of total knee arthroplasties, even when carried out by skilled surgeons using up-to-date mechanical alignment
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Figure 1 Current principles of navigation. Electromagnetic system (left): navigation of tibial cutting block via paddle traced within an electromagnetic field. Optical system (right): navigation of cutting block traced via infrared camera.
tools. Conventional systems have elementary drawbacks that limit their ultimate accuracy. Precision of pre-operative X-ray templating is limited by the errors inherent in measuring from radiographs. Intra-operative determination of crucial landmarks, such as the centre of the femoral head and the centre of the ankle, is hard to achieve. Most importantly, traditional alignment and sizing devices assume a standard bone geometry that may not apply to a specific patient. All available mechanical instrumentation systems rely on visual inspection to confirm the accuracy of implant placement and stability at the conclusion of the total knee replacement procedure.14 Computer-assisted systems have been designed to address the limitations associated with mechanical instrumentation for knee replacement surgery.15,16 In principle, computer-assisted alignment for knee replacement can be classified as navigation or robotics. Robotic systems use equipment that takes over part of the surgical procedure. Navigation complements mechanical instrumentation by the addition of measurements used to locate landmarks, direct surgical tools and thereby align prosthetic components. Image-free navigation systems acquire and feed back information during surgery. Image-based navigation systems use pre-operative CTs or intra-operative fluoroscopic images. Modern navigation systems function using infrared-light tracking or, most recently, electromagnetic guidance (Fig. 1).
Operative technique: optical systems Optical navigation systems vary with regard to the method of handling by the surgeon. Some use special pointers connected to a PC, others use foot pedals or sterile touch-screens. The presence of a computer specialist is usually not required. Navigation instruments and an infrared camera communi-
cate, either via active light-emitting diodes (active optical system) or reflective spheres mounted on navigation arrays (passive optical system). Positioning of these trackers in bone is achieved either through an additional surgical incision or within the operative site. Fixation is achieved using mono- or bi-cortical anchorage. Once registration of anatomical landmarks has been performed, rigid fixation of navigation arrays to anatomical structures has to be safeguarded. The centre of the femoral head, as the proximal landmark for the physiological axis of the femur is identified by analysis of the rotational pivoting movement of the femoral tracker. Single-point referencing identifies the epicondylar axis, Whiteside’s line, the distal femoral and proximal tibial centres and the centre of the ankle joint. Some systems also use ankle movement, with trackers fixed to the foot, in order to determine the centre of the talus. Surface registration is carried out to identify abnormalities of the femoral condyles or tibial plateaus in order to allow reconstruction of the joint line. During the registration process information about the soft tissue condition and ligament tension is gained, which in turn allows for controlled release of contracted structures. Initial data collected are used to identify the preoperative status of the knee. Dynamic investigations can be performed in order to document the initial range of movement and soft tissue alignment. These data can be recalled during the operation, allowing for a strictly individual approach. Clinicians using navigation rely on the ability of the computer systems to use arithmetical algorithms, which can compensate for surgeon’s error during registration of landmarks.17 One striking example is the mathematical matching procedure used to identify the individual femoral rotation by taking into account Whiteside’s line, the epicondylar axis and alignment of the posterior condyles. The amount of data analysed simultaneously for these calculations is probably beyond the
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Figure 2 Tibial cut. A passive optical reference array is shown slotted into the tibial cutting block: navigation of coronal alignment, tibial slope and cutting depth. The tibial reference array is placed outside the operative wound. Inlay/screenshot: the blue plane represents the actual slot position being aligned until it overlays the yellow planned plane.
capacity of even the most brilliant human brain. Various attempts were made in the past to navigate power-tools directly via reference arrays attached to the instrument. However, it proved to be more reliable to navigate cutting blocks, anchor these rigidly to bone and perform the saw-cut using a blade that is fitted precisely into the cutting slot (Fig. 2). Computer-assisted surgery seems to have freed the surgeon from mechanistic repetition of standardised operative steps, allowing movement towards an individual approach to knee surgery. Dynamic joint examination and its changes during surgery used to be performed by the unassisted, manual sense of stability within the range of movement. Navigation systems now allow verification of the surgeon’s perception.
Outcome studies Over the last decade orthopaedic surgeons have spectated upon the introduction of computer assistance for total joint arthroplasty with scepticism. Nevertheless, an impressive variety of systems have already been introduced to orthopaedic surgical practice. Equally remarkable is the number of clinical and laboratory studies published on the topic. Opinions regarding computer-assisted knee surgery understandably depend upon personal experience with various systems.18 Ba ¨this et al.19 analysed 80 patients after total knee arthroplasty performed with a passive optical image-free navigation system, comparing the varus/valgus alignment to 80 knees operated using conventional technique. They found
W.H. Kluge that 96% of the navigated knees were within 731 of optimal leg alignment, compared to 78% after conventional surgery. Post-operative assessment was performed on long leg coronal and lateral films. Perlick et al.20 analysed 50 CT-based navigated and 50 conventional knee arthroplasties. They established a significant improvement in prosthesis alignment with computer assistance but also documented considerably higher extra costs for pre-operative CT scans, time-consuming planning and lack of a ligament balancing module within the CT-based software. CT-free navigation was used in a multi-centre study published by Jenny et al.,21 who observed the mechanical leg axis within 731 in 88% of navigated knees, while only 72% of patients reached a comparable leg axis when using the conventional technique. Oberst et al.22 presented the results of a controlled, prospective and randomised trial comparing navigation with conventional surgery. CT analysis revealed that all 12 navigated knees were within the interval of 731 varus/ valgus deviation, in comparison with only 8 of 13 nonnavigated knees. Analysis of femoral component rotation showed no difference between the two groups. Chauhan et al.23 performed a cadaver trial and a controlled randomised clinical trial to establish the benefits of computer navigation in total knee replacement. The authors found varus/valgus alignment of the tibial component, tibial posterior slope, tibial rotation, femoral rotation and standing leg alignment significantly improved when using an imageless optical navigation system compared to the results using a jig-based conventional system. The clinical study, involving 70 knees, is particularly interesting because a specific CT protocol, with outcome measurements from defined mechanical and anatomical axes, has been used to accurately define coronal, sagittal and axial alignment characteristics of the femoral and tibial components. Beaver et al.24 assessed post-operative CT scans (75 patients) in a controlled study, which showed a statistically significant improvement in component alignment when using computer-assisted surgery for femoral varus/valgus, femoral rotation, tibial varus/valgus, tibial posterior slope and tibial rotation. Blood loss was reduced, though navigated surgery was more time consuming (mean increase of 13 min). Haaker et al.25 compared 100 conventionally implanted with 100 navigated knees and measured significantly better tibial and femoral component positioning, with less outliers in the computer-assisted group. The authors did not report any navigation-specific complications. A mean additional 10 min of operating time was considered acceptable. Sparmann et al.1 conducted a prospective randomised and externally evaluated study to investigate 120 hand-guided and 120 navigated total knee arthroplasties. They found a highly significant difference in favour of navigation with regard to the mechanical leg axis, the frontal and sagittal femoral component axis and the frontal tibial component axis. Stulberg26 has shown that mechanical total knee replacement alignment systems have a tendency to leave the knee in slight flexion, to hyperextend the femoral component, to posteriorly tilt the tibial implant and to internally rotate the femoral implant. If implant longevity, pain relief, and function are related to the accuracy of component positioning, the Stulberg study emphasises that current
ARTICLE IN PRESS Computer-assisted knee replacement techniques mechanical instrumentation is associated with decreased accuracy at each step of the procedure. Matsumoto27 analysed 30 CT-free navigated and 30 matched conventional manual implantations, comparing post-operative long-leg radiographs. The results revealed a significant difference in favour of navigation. Matsumoto suggested that surgeons using navigation systems should be aware of possible over-sizing of the femoral component. Victor et al.28 compared 50 fluoroscopy-based computer navigated knee arthroplasties to 50 conventional procedures in a prospective randomised controlled trial. They found variability in the coronal plane was significantly reduced after computer-assisted surgery when compared with conventional techniques. The maximum deviation between the calculated kinematic centre of hip rotation and the fluoroscopically determined anatomic centre of the hip was 5 mm (mean: 1.6 mm). Chin et al.29 studied standardised long leg coronal and sagittal X-rays in 90 patients with knee arthroplasty prospectively, who were randomised into three groups with extra-medullary or intra-medullary tibial guidance and computer-navigated surgery. Results in the coronal view revealed that 93.3% of patients in the computer-assisted group had ideal outcomes compared with 73.4% in the extramedullary group and 60.0% with intra-medullary guidance. Equivalent results were found for the sagittal view. Kim et al.30 prospectively compared 69 total knee arthroplasties using imageless computer-assisted navigation with 78 manually instrumented knees. Coronal alignment in full length standing radiographs revealed a larger variation in alignment in the manual group; 58% within 2 degrees of neutral, compared with 78% of the navigated group. Anderson and colleagues31 evaluated the early outcomes of 116 navigated consecutive knee replacements and 51 conventional operations. The post-operative mechanical axis was within 31 of neutral mechanical alignment in 95% of the navigation cases versus 84% of the conventional cases. The number of outliers decreased with use of navigation. Sikorski32 found computer assistance useful in revision situations in which significant bone deficits were encountered and bone grafting was needed. According to the author the remaining anatomical landmarks along with the old prosthesis, prior to removal, provide sufficient reference points to allow for controlled grafting or/and cementation. The use of imageless navigation, especially for ligament balancing in rheumatoid knee arthritis, appears to be useful because cutting errors can be detected and corrected intraoperatively.33 Fehring et al.34 identified 18 knees believed not to be treatable using traditional instrumentation because of posttraumatic femoral deformity, retained femoral hardware, a history of osteomyelitis, or severe cardiopulmonary disease. Computer-assisted surgery was successfully used in 17 knees. The authors conclude that computer-assisted navigation was helpful in difficult situations where accurate alignment remains crucial, yet traditional instrumentation is not applicable. The performance of integrated robotic systems for accurately machining bone surfaces has been evaluated. This includes cutting trials using plastic bones, followed by clinical trials in which the results of the anatomical registration and bone cutting have been noticed to be of
203 high quality (Acrobot).35 Shi et al.36 presented a hand-eye robotic model for total knee replacement that combines with a movable hand-eye navigation system. Without using CT images and landmark pins in the patient’s bones, it is said to directly measure the mechanical axis with high precision. Siebert et al.37 treated 70 patients suffering from idiopathic gonarthrosis with a robot-assisted technique using a commercial robotic surgical system (CASPAR) to assist in pre-operative planning and intra-operative execution. No major adverse events related to the use of this CT-guided robotic system have been observed. The mean difference between pre-operatively planned and post-operatively achieved tibiofemoral alignment was reported to be 0.81 (0–4.11) in the robotic group vs. 2.61 (0–71) in a manually operated control group of 50 patients. Because of better prosthetic alignment and improved bone-implant fit, implant loosening is anticipated to be diminished, which may be most evident in non-cemented prostheses. Disadvantages such as the need for placement of markers, increased operating times and higher overall costs were discussed.
Discussion Accurate registration of anatomical landmarks is fundamental to the usefulness of computer-assisted orthopaedic alignment systems. The potential causes of registration errors using any given system must be understood by the surgeons who use these devices. The most important cause of registration inaccuracy is thought to be surgical technique.14 Registration errors might possibly be reproduced, and carried on through the navigated intervention up to final implantation of the implants. This is, in principle, true for mechanical as well as for navigated surgery. Navigation systems usually recognise large numbers of landmarks in order to determine one particular parameter. Thereby the initial registration error should be minimised. Coronal alignment of the lower limb is particularly hard to define because of its wide variation among healthy individuals. Jenny et al.38 performed antero-posterior long-leg radiographs on 100 Caucasian patients without known knee abnormality. They found a wider than commonly estimated variation in the lower limb axes and concluded that for knee reconstruction the specific knee axes of the patient to be operated have to be taken into account. Individual re-alignment appears very valuable in unicompartmental knee replacements. It seems rather academic for total knee replacements, because individual (prearthritic) leg axes are unknown for patients with advanced bilateral tri-compartmental osteoarthritis. Post-operative analysis of implant/leg alignment became a matter of debate with the introduction of navigation systems. It has now been accepted that plain radiographs provide a poor indication of overall alignment.39 Even if strictly standardised one-legged stance radiographs are taken, the measured alignment of the implant is not precise. Positioning errors of 2–31 have to be acknowledged with X-ray follow up.1 Therefore CT-based methods appear to provide the only reasonably accurate three-dimensional outcome study capable to assess possible cumulative error concerning mal-alignment of components. Yet again analyses are performed without definitive landmarks, limiting the value of conclusions drawn. Dynamic
ARTICLE IN PRESS 204 intra-operative investigations performed using navigation systems (on-line tracing of component positioning during movement) will probably be the only way to find satisfactory answers concerning component position and to guide future implant design. Jenny and Boeri40 concluded that to define the rotational alignment of a femoral component the trans-epicondylar axis may not be as reproducible as expected. This highlights the on-going debate about rotational alignment of components in knee replacement. The importance of the femoral rotation has been established to influence patello-femoral tracking.41–43 Some studies claim to have shown no patellar complications1 because of appropriate rotational alignment when using navigation. A study by Siston et al.44 highlights the need for kinematic studies using computer-assisted techniques to improve our knowledge regarding perfect femoral component rotation. Also Yau et al.,45 using a cadaveric experiment, emphasise the challenge of achieving accurate femoral rotational alignment and the need for further refinement in navigation technology. Navigation systems were found to be particularly useful for measurement of kinematic joint characteristics before and after surgery. Soft tissue laxity in flexion and extension can be determined using computer tools. Ligament balance and stability are essential to the immediate and long-term clinical success.46 Navigation devices designed for universal implants are widely available but do not seem to offer the precise and user-friendly set-up we appreciate with specific implantrelated systems. Navigation systems combined with individual implants seem to allow for less invasive instrumentation and thereby relatively shorter operating time with less bone and soft tissue damage. This appears to influence the number of thrombembolic events47 and blood loss.24 Chauhan et al.48 reported reduced loss of blood in navigated compared to conventional surgery. They attributed this finding to non-penetration of the femoral medullary canal and less invasive soft tissue management. As with any new surgical tool, the debate regarding the learning curve for surgeons who would like to use navigation is controversial. Orthopaedic trainees are generally open and often enthusiastic about the idea of computer-assisted knee replacement surgery. Established surgeons might argue that they do not need it because they believe that they get sufficiently good results with conventional instruments. The experienced surgeon might also fear prolonged operating time. Research appears to challenge such statements.1 Planning and operating time do not appear to be increased significantly once the surgeon has passed the learning curve and image-free systems are being used.20,49 One study1 reports wound healing problems and early infection with computer-assisted knee surgery. It is suggested that navigation-guided procedures might cause more trauma to soft tissues. This might be the case with methods fixing trackers within the operation site and at the same time attempting to minimise the size of the incision. It is advisable to fix reference arrays far away from the surgical wound using percutaneous fixation and to flex the knee during insertion of the femoral trackers in order to avoid quadriceps damage. The use of computer-assisted tools by orthopaedic surgeons requires individual instruction tailored to the
W.H. Kluge technology used. Learning Centres and clinical input from colleagues experienced in the routine use of computerassisted orthopaedic systems are paramount to success. Although clinical studies are difficult to conduct over a long period because conditions for investigation change frequently (system updates) it is recommended to feed back experiences to colleagues and manufacturers. Electromagnetic tracking is a new key technology allowing miniature implantable trackers and overcoming line-ofsight restrictions of optical tracking. In the future, we should see navigation enabling new classes of less invasive and more functionally appropriate implants. The technologies that will permit this include new measurement systems for soft tissue management and conservative bone preparation tools. According to implant manufacturers automatic pre-operative planning and possibly auto-registration technologies should enable the surgeon to have a custom procedure kit that could greatly improve surgical productivity (Figs. 3 and 4). Electromagnetic tracking technology eliminates line-ofsight issues associated with traditional optical systems. Electromagnetic tracking uses miniaturised computer tracking devices that can be positioned in vivo to facilitate in less invasive procedures. These tracking devices can for example be placed under the muscle during knee arthroplasty, causing no secondary trauma to the patient. Leading joint replacement manufacturers have committed to investment in research aimed at the improvement of navigation systems. Navigation technology should enable reliable minimal access surgery and remove the outliers that mar the accuracy of the surgical procedure. Currently, the cost/benefit ratio of computer-assisted surgery is abstract. If surgery is performed better the patient should benefit in having a better functional outcome and greater implant longevity. This, if realised, will produce material benefits to surgeons, patients and the community at large. There should be fewer revision procedures with all the associated savings.49 Five years ago computer-assisted operations were criticised for additional surgical steps, which were time consuming and required more manpower. Recently systems
Figure 3 Electromagnetic technology (reproduced by kind permission of Zimmers): Tibial Alignment Guide with electromagnetic paddle in the slot of the tibial cut guide.
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Computer-assisted surgery facilitates both less invasive procedures and traditional surgical techniques
Research directions
Data collected in computer-assisted knee arthro Figure 4 Electromagnetic technology (reproduced by kind permission of DePuys): the surgical image shows a local 3D magnetic field generator (square black housing). A sensor is being pushed into a hole drilled into bone. It will pick up the field signals from the generator. Sectional view: layout of three separate coils hidden inside the bone sensor.
and operative skills using the technology have greatly improved. For advanced navigation systems surgical time and instrumentation can be equal or even reduced compared with the conventional approach. Additional imaging should not be necessary for modern systems. Infrared trackers anchored to bone, and the theoretical risks of associated morbidity, will become obsolete with the wider introduction of electromagnetic tracing. The size of navigation machines used to be similar to that of an image intensifier. Modern systems are far smaller and more userfriendly. The graphical user interface and computer workflow is under constant update. Several processes to improve the recognition of tools, including the use of radio frequency identification chips, are being implemented.50 Integration of pre- and intra-operative data acquisition with post-operative verification and clinical outcomes should lead to refinement of surgical techniques. One contentious point remains the financial expenditure. Hard- and software are cost intensive and one system alone usually does not satisfy the needs of a hospital with a substantial orthopaedic productivity. As orthopaedic surgeons we are required to employ cost-effective methods, however advanced technology with scientifically validated outcomes should be the norm in our practice.
Practice points
A navigation system is a basic tool allowing us to understand and to modify individual knee joint biomechanics
Navigation systems complement mechanical instru-
mentation by the addition of measurements used to direct surgical tools and thus better align prosthetic components Computer assistance aims to enhance accuracy in knee replacement surgery and may thereby improve long-term outcomes
plasty will help to design future implants and determine most favourable alignment Computer-assisted procedures should help to improve our knowledge regarding femoral component rotation and patellar tracking Can auto-registration technologies be introduced to further reduce operating time Will electromagnetic tracing become a reliable, user-friendly and cost-effective method replacing optical systems
References 1. Sparmann M, Wolke B, Czupalla H, Banzer D, Zink A. Positioning of total knee arthroplasty with and without navigation support. A prospective randomised study. J Bone Jt Surg 2003;85B:830–5. 2. Dorr LD, Boiardo RA. Technical considerations in total knee arthroplasty. Clin Orthop 1997;205:5–11. 3. Teter KE, Bregman D, Colwell Jr. CW. Accuracy of intramedullary versus extramedullary tibial alignment cutting systems in total knee arthroplasty. Clin Orthop 1995;321:106–10. 4. Feng EL, Stulberg SD, Wixson RL. Progressive subluxation and polyethylene wear in total knee replacements with flat articular surfaces. Clin Orthop 1994;229:60–71. 5. Laskin RS. Total condylar knee replacement in patients who have rheumatoid arthritis. A ten-year follow-up study. J Bone Jt Surg 1990;72-A:529–35. 6. Piazza SJ, Delp SL, Stulberg SD, Stern SH. Posterior tilting of the tibial component decreases femoral rollback in posteriorsubstituting knee replacement: a computer simulation study. J Orthop Res 1998;16:264–70. 7. Ritter MA, Faris PM, Keating EM, Meding JB. Postoperative alignment of total knee replacement. Its effect on survival. Clin Orthop 1994;299:153–6. 8. Garg A, Walker PS. Prediction of total knee motion using a three-dimensional computer-graphics model. J Biomech 1990; 23:45–58. 9. Jeffery RS, Morris RW, Denham RA. Coronal alignment after total knee replacement. J Bone Jt Surg 1991;73-B:709–14. 10. Stockl B, Nogler M, Rosiek R, Fischer M, Krismer M, Kessler O. Navigation improves accuracy of rotational alignment in total knee arthroplasty. Clin Orthop 2004;426:180–6. 11. Bargren JH, Blaha JD, Freeman MAR. Alignment in total knee arthroplasty: correlated biomechanical and clinical investigations. Clin Orthop 1983;173:178–83. 12. Oswald MH, Jakob RP, Schneider E, Hoogewoud HM. Radiological analysis of normal axial alignment of femur and tibia in view of total knee arthroplasty. J Arthroplasty 1993;8:419–26. 13. Wasielewski RC, Galante JO, Leighty R, Natarajan RN, Rosenberg AG. Wear patterns on retrieved polyethylene tibial inserts and their relationship to technical considerations during total knee arthroplasty. Clin Orthop 1994;299:31–43.
ARTICLE IN PRESS 206 14. Stulberg SD, Loan P, Sarin V. Computer assisted navigation in total knee replacement: results of an initial experience in thirty-five patients. J Bone Jt Surg 2002;84-A(Suppl 2):90–8. 15. Matsen 3rd FA, Garbini JL, Sidles JA, Pratt B, Baumgarten D, Kaiura R. Robotic assistance in orthopaedic surgery. A proof of principle using distal femoral arthroplasty. Clin Orthop 1993;296:178–86. 16. Stulberg SD, Picard F, Saragaglia D. Computer assisted total knee replacement arthroplasty. Op Tech Orthop 2000;10:25–39. 17. Jerosch J, Filler T, Peuker E. Ausmaß der interindividuellen Variationsbreite bei der intraopertiven Bestimmung der interepicondyla ¨ren Achse in der Knieendoprothetik. Orthopa ¨dische Praxis 2001;37:293–7. 18. Holt G, Gregori AG. Computer assisted knee arthroplasty is here today. BMJ 2005;330:197. 19. Ba ¨this H, Perlick L, Tingart M, Lu ¨ring C, Zurakowski D, Grifka J. Alignment in total knee arthroplasty: a comparison of computer assisted surgery with the conventional technique. J Bone Jt Surg 2004;86-B:682–7. 20. Perlick L, Ba ¨this H, Tingart M, Perlick C, Grifka J. Navigation in total-knee arthroplasty. CT-based implantation compared with the conventional technique. Acta Orthop Scand 2004;75:464–70. 21. Jenny JY, Mielke RK, Kohler S, Kiefer H, et al. Total knee prosthesis implantation with a non image-based navigation system: a multicentric analysis. In: Proceedings of the 70th annual meeting AAOS, American Academy of Orthopaedic Surgeons, 2003. p. 96. 22. Oberst M, Bertsch C, Wurstlin S, Holz U. CT analysis of leg alignment after conventional vs. navigated knee prosthesis implantation. Initial results of a controlled, prospective and randomized study. Unfallchirurg 2003;106:941–8. 23. Chauhan SK, Scott RG, Breidahl W, Beaver RJ. Computer assisted knee arthroplasty versus a conventional jig-based technique. A randomised, prospective trial. J Bone Jt Surg 2004;86-B:372–7. 24. Beaver RJ, Chauhan SK, Scott RG, Breidahl W, Sikorski JM. A prospective randomized controlled trial of computer assisted versus conventional total knee arthroplasty. J Bone Jt Surg Proc 2004;86-B:475. 25. Haaker RG, Stockheim M, Kamp M, Proff G, Breitenfelder J, Ottersbach A. Computer assisted navigation increases precision of component placement in total knee arthroplasty. Clin Orthop Relat Res 2005;433:152–9. 26. Stulberg DS. How accurate is current TKR instrumentation? Clin Orthop 2003;416:177–84. 27. Matsumoto T, Tsumura N, Kurosaka M, et al. Prosthetic alignment and sizing in computer assisted total knee arthroplasty. Int Orthop 2004;28:282–5. 28. Victor J, Hoste D. Image-based computer assisted total knee arthroplasty leads to lower variability in coronal alignment. Clin Orthop 2004;428:131–9. 29. Chin PL, Yang KY, Yeo SJ, Lo NN. Randomized control trial comparing radiographic total knee arthroplasty implant placement using computer navigation versus conventional technique. J Arthroplasty 2005;20:618–26. 30. Kim SJ, MacDonald M, Hernandez J, Wixson RL. Computer assisted navigation in total knee arthroplasty: improved coronal alignment. J Arthroplasty 2005;20(Suppl):123–31. 31. Anderson KC, Buehler KC, Markel DC. Computer assisted navigation in total knee arthroplasty: comparison with conventional methods. J Arthroplasty 2005;20(Suppl):132–8.
W.H. Kluge 32. Sikorski JM. Computer assisted revision total knee replacement. J Bone Jt Surg 2004;86-B:510–4. 33. Perlick L, Ba ¨this H, Lerch K, Luring C, Tingart M, Grifka J. Navigated implantation of total knee endoprostheses in secondary knee osteoarthritis of rheumatoid arthritis patients as compared to conventional technique. Z Rheumatol 2004;63:140–6. 34. Fehring TK, Mason JB, Moskal J, Pollock DC, Mann J, Williams VJ. When computer assisted knee replacement is the best alternative. Clin Orthop Relat Res 2006; Aug 3: electronic publication ahead of print. 35. Jakopec M, Harris SJ, Rodriguez y Baena F, Gomes P, Cobb J, et al. The first clinical application of a ‘‘hands-on’’ robotic knee surgery system. Comput Aided Surg 2001;6:329–39. 36. Shi F, Zhang J, Liu Y, Zhao Z. A hand-eye robotic model for total knee replacement surgery. Int Conf Med Image Comput Assist Interv 2005;8:122–30. 37. Siebert W, Mai S, Kober R, Heeckt PF. Technique and first clinical results of robot-assisted total knee replacement. Knee 2002;9:173–80. 38. Jenny JY, Boeri C, Ballonzoli L. Coronal alignment of the lower limb. Acta Orthop 2005;76:403–7. 39. Swanson KE, Stocks GW, Warren PD, Hazel MR, Janssen HF. Does axial limb rotation affect the alignment measurements in deformed limbs? Clin Orthop 2000;371:246–52. 40. Jenny JY, Boeri C. Low reproducibility of the intra-operative measurement of the transepicondylar axis during total knee replacement. Acta Orthop Scand 2004;75:74–7. 41. Berger RA, Crossett LS, Jacobs JJ, Rubash HE. Malrotation causing patello-femoral complications after total knee arthroplasty. Clin Orthop Relat Res 1998;356:144–53. 42. Miller MC, Berger RA, Petrella AJ, Karmas A, Rubash HE. Optimizing femoral component rotation in total knee arthroplasty. Clin Orthop Relat Res 2001;392:38–45. 43. Singerman R, Pagan HD, Peyser AB, Goldberg VM. Effect of femoral component rotation and patellar design on patellar forces. Clin Orthop Relat Res 1997;334:345–53. 44. Siston R, Patel JJ, Goodman SB, Delp SL, Giori NJ. The variability of femoral rotational alignment in total knee arthroplasty. J. Bone Jt Surg 2005;87-B:2276–80. 45. Yau WP, Leung A, Chiu KY, Tang WM, Ng TP. Intra-observer errors in identification of visually selected anatomic landmarks in nonimage-based computer navigation total knee replacement system. A J Arthroplasty 2005;20:591–601. 46. Delp SL, Stulberg DS, Davies B, Picard F, Leitner F. Computer assisted knee replacement. Clin Orthop 1998;354:49–56. 47. Kalairajah Y, Cossey AJ, Verrall GM, Ludbrook G, Spriggins AJ. Are systemic emboli reduced in computer assisted knee surgery? A prospective, randomised, clinical trial. J Bone Jt Surg 2006; 88-B:198–202. 48. Chauhan SK, Clark GW, Lloyd S, Scott RG, Breidahl W, Sikorski JM. Computer assisted total knee replacement. A controlled cadaver study using a multi-parameter quantitative CT assessment of alignment (The Perth CT Protocol). J Bone Jt Surg 2004;86-B:818–23. 49. Sikorski JM, Chauhan S. Aspects of current management. Computer assisted orthopaedic surgery: Do we need CAOS? J Bone Jt Surg 2003;85-B:319–23. 50. Swank ML. Orthopaedic navigation solutions. Computer assisted surgery/orthopaedic navigation in total joint reconstruction. US Muscoloskeletal Rev 2006:85–7.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 229–235
Available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/cuor
TRAUMA
Current management of high-energy tibial plateau fractures Robert D. Zuraa, James A. Brownea, Molly D. Blacka, Steven A. Olsonb, a
Division of Orthopaedic Surgery, Duke University Medical Center, DUMC 3389, Durham, NC 27710, USA Orthopaedic Trauma, Duke University Medical Center, USA
b
KEYWORDS Tibial plateau fractures; External fixation; Internal fixation; Biologic osteosynthesis; High energy; Damage control
Summary High-energy tibial plateau fractures present a therapeutic challenge to the orthopaedic trauma surgeon, both in terms of the osseous injury as well as the concomitant soft-tissue insult. Surgical treatment has evolved to address these fractures in a more biologically favourable manner without further compromising the soft tissues. We present a summary of these injuries and outline the contemporary approaches to treatment. Potential complications and their avoidance are also discussed. Outcomes following these injuries are reviewed to assist with determination of treatment goals. & 2007 Published by Elsevier Ltd.
Introduction Tibial plateau fractures associated with high-energy trauma are frequently complex injuries that portend a poor prognosis. The status of the soft-tissue envelope typically mirrors the amount of energy imparted to the bone. Highenergy fractures present a therapeutic challenge to the orthopaedic trauma surgeon due to the high incidence of open fractures, comminution, soft-tissue injury, and neurovascular compromise. Traditionally, internal fixation of these injuries has been fraught with complications, including infections and wound breakdown. Contemporary or biologic surgical treatment emphasises preservation of vascularity and soft-tissue integrity by minimising further insult to the soft tissues. We present a summary of these Corresponding author. Tel.: +1 919 668 3000;
fax: +1 919 668 2933. E-mail address:
[email protected] (S.A. Olson). 0268-0890/$ - see front matter & 2007 Published by Elsevier Ltd. doi:10.1016/j.cuor.2007.02.007
injuries and the currently acceptable approaches to treatment as well as potential complications. We also briefly discuss the determinants of successful outcomes following internal fixation.
Classification Adopted by the Orthopaedic Trauma Association, the AO/ ASIF classification provides a thorough and descriptive catalogue of tibial plateau fracture morphology. This system defines fractures as extraarticular, partial articular, and complete articular, with further subdivision based upon increasing fracture severity and comminution. Its length and organisation makes it useful for research purposes. For ease of communication, many North American surgeons use the Schatzker classification (Table 1).1 Tibial plateau fractures are classified by the presence or absence of a sagittal split, a depressed articular segment, the presence or absence of a medial condylar fragment, and
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Table 1 Schatzker classification of tibial plateau fractures1. Type I Type II Type III Type IV Type V Type VI
Pure split fracture of lateral tibial plateau Split-depression fracture of lateral tibial plateau Pure central depression fracture of lateral tibial plateau Medial tibial plateau fracture Bicondylar tibial plateau fracture Bicondylar tibial plateau fracture with metaphyseal–diaphyseal dissociation
attachment to the tibial shaft. Six fracture patterns are defined and correlate with the energy of injury. For the purposes of this text, we will limit the discussion to Schatzker fracture types IV, V, and VI. A type IV injury involves a medial plateau split from the articular surface that exits out the medial metaphysis. Given the relative bony strength and mechanical axis, medial plateau fractures represent a much higher-energy mechanism of injury than their counterparts in the lateral plateau. In this type of fracture, the medial plateau piece remains in its anatomic position while the lateral fragment and entire lower leg displaces. Some authors describe this type as a ‘‘fracture dislocation’’ of the knee. These fractures have a higher incidence of lateral collateral ligament, anterior cruciate ligament, popliteal artery, and peroneal nerve injury than other subtypes. Type V fractures are bicondylar with varying degrees of comminution. Type VI fractures are bicondylar as well with meta-diaphyseal extension resulting in dissociation of the metaphysis and diaphysis. This subtype also has varying degrees of comminution.
Clinical assessment Patients who have sustained a high-energy injury require a thorough trauma evaluation, typically by a multi-disciplinary team in accordance with established trauma care protocols. Potentially life threatening injuries are addressed initially and once stabilised, the orthopaedic injuries are evaluated. The evaluation of the neurologic status, the vascular status and the soft tissues is the critical first step of fracture care. The skin is inspected circumferentially around the distal thigh, knee, and leg. Openings in the skin are inspected to rule out the presence of communication with the fracture. At our facility, any skin embarrassment is digitally photographed and recorded as part of the patient’s medical chart in our institution’s trauma registry database. The Gustilo and Anderson classification for open fractures, originally used for tibial shaft fractures, is applied to these injuries.2 The classification of the injury is based upon the amount of skin injury, soft-tissue damage, fracture severity, contamination, and vascular status. In simple terms, Grade I injuries have a laceration less than 1 cm; Grade II injuries have increased periosteal stripping and typically a larger laceration (1–10 cm); Grade III injuries are more severe and are further subclassified (III A injuries have a laceration
410 cm, and/or increased comminution, contamination, or stripping, III B injuries require a soft-tissue coverage procedure to cover bone, and III C injuries require vascular repair to achieve salvage). This classification is formally done in the operating room, but an initial assessment using Gustilo’s system is performed in the emergency department to guide early care of open fractures. Closed injuries are also closely assessed. The presence of contusions, blisters, and swelling is noted. Tscherne and Goetzen3 have described a classification system for the soft tissues associated with closed fractures. Grade 0 represents minimal soft-tissue damage done with an indirect force. Grade 1 represents superficial abrasion or contusion via pressure from within. Grade 2 represents deep, contaminated abrasion(s) with localised skin/muscle contusion and impending compartment syndrome. Grade 3 represents extensive skin contusion/crush, subcutaneous avulsion, underlying muscle damage, or compartment syndrome. This classification can help with both written and verbal communication. High-energy injuries are commonly associated with neurovascular injury. Neurologic examination focuses on function of the peroneal nerve, which is most vulnerable in these fractures. The tibial nerve is in close proximity to the zone of injury and must also be evaluated. Vascular examination focuses on the popliteal artery. This examination is especially important in medial plateau injuries, which have a higher risk of arterial embarrassment. It is important to remember that posteriorly displaced fracture fragments can directly impinge on the neurovascular bundle. Ankle-brachial indices are obtained if there is any question of vascular injury. If these are less than 0.9 and other hard physical examination findings point to an arterial injury, an arteriogram and vascular surgical consultation is considered. Thorough and accurate documentation of the examination is crucial. Although often difficult to assess acutely, knee stability should be evaluated. It is important to remember that a knee dislocation can pose as a fracture, heightening the importance of a thorough neurovascular examination in all cases. Stability to varus and valgus stress is tested in full extension. In the conscious patient, this often will require sedation. The knee effusion and haematoma is aspirated and replaced with local anaesthetic under strict aseptic conditions. To minimise the patient’s discomfort, this assessment can be delayed until the operating room in fractures that have an operative indication beyond knee instability. The timely diagnosis and management of compartment syndrome is critical. A high index of suspicion for compartment syndrome should be maintained when dealing with high-energy plateau fractures, and it must be ruled out in every patient with these injuries. Tense, firm compartments are early signs and may be sufficient for diagnosis. Severe pain and pain with passive stretch of muscle groups in the leg are diagnostic of compartment syndrome. Compartment pressures should be measured if the clinical examination is inconclusive or if the patient is obtunded or intubated and sedated. Compartment pressures within 30 mmHg of the diastolic blood pressure are diagnostic. The threshold for compartment measurement and fasciotomy should be low, given the disastrous consequences of a missed or delayed diagnosis. Schatzker V and VI fractures have an especially high incidence of compartment syndrome.4 Serial examinations
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are critical as compartment syndrome may develop several hours or more after the initial injury and post-operatively. Pallor, pulselessness, paresthesiae, and poikliothermia are late signs of compartment syndrome, and ideally patients are treated with fasciotomy prior to developing these ominous signs.
soft tissues appear healthy enough to withstand incisional trauma. Time to definitive fixation will vary from a few days to 3 weeks or more. This treatment algorithm has evolved from the use of temporary external fixation in the treatment of pilon and femoral shaft fractures.6–8 Catastrophic wound consequences following early surgery through compromised soft tissues have been well described. Delayed internal fixation after initial external fixation has enjoyed good outcomes with low complication rates in the treatment of high-energy proximal tibial fractures.9,10 Egol reports 5% deep wound infections in 53 patients with 57 high-energy tibial plateau fractures treated with temporary spanning, external fixation.9 Typically the external fixator spans the knee joint. A common construct is two pins in the femur (above the suprapatellar pouch) and two pins in the tibia (Fig. 1). If possible, the pins in the tibia should be distal to the zone of injury and away from the anticipated internal fixation. The femoral pins can be anterior, lateral, or antero–lateral. Anterior pins may provide a more rigid frame construct, but some have concerns for loss of knee motion due to scarring
Radiological assessment Plain orthogonal radiographs are obtained. A 101 craniocaudal angle on the anteroposterior (AP) view of the knee allows assessment of the joint surface, given the posterior slope of the proximal tibia. This view is improved with traction in displaced fractures. The majority of fractures can be classified from the AP film. The lateral films afford a better assessment of coronal fracture lines and subtle joint depressions. The plateaux can be distinguished on the lateral view, as the medial plateau is lower and concave, whilst the lateral is convex. Fine (2–2.5 mm) cut computed tomography (CT) images further delineate fracture morphology and are important in operative planning. It is usually more useful to obtain the CT after applying traction via an external fixator (see treatment section). With traction CT images, the degree of comminution and joint depression are more thoroughly defined. These images, in addition to plain radiographs, have been shown to change fracture classification, and subsequently the operative plan.5 The role of magnetic resonance imaging (MRI) in acute fracture management is controversial. High-energy tibial plateau fractures are associated with a high incidence of ligamentous and meniscal injuries. Although MRI allows for the assessment and diagnosis of intraarticular soft-tissue pathology, there is scant evidence that its routine use impacts on outcomes. Furthermore, incompatible external fixators often preclude the use of MRI with these injuries. The formal role of MRI in these fractures has yet to be defined.
Treatment Temporising treatment All high-energy tibial plateau fractures have a concomitant soft-tissue injury. It is not unusual for these patients to have massive swelling and fracture blisters encompassing the entire proximal leg. The severity of the initial injury and rate of recovery of the soft tissues drives the timing of definitive fixation. Early stabilisation of the fractured extremity is requisite for timely soft-tissue healing. Temporary spanning external fixation is the initial treatment modality of choice, as it stabilises the soft tissues, provides pain relief, assists with fracture reduction via ligamentotaxis, allows visualisation of the soft-tissues, and permits mobilzation. Not all, but most high-energy tibial plateau fractures require temporary external fixation to stabilise the soft tissues, the fracture fragments or both. CT imaging after application of the external fixator is ideal. Casts, splints, traction, and braces are other options for initial treatment, but none of these modalities offers the same broad range of benefits provided by external fixation. Definitive surgical treatment should be delayed until the
Figure 1 A typical temporary spanning external fixator (a). Note the ligamentotaxis and ability to obtain adequate radiographs of the fracture site with appropriate fixator placement (b).
ARTICLE IN PRESS 232 of the quadriceps. Lateral pins avoid these complications, but are often problematic for patients when they lay in bed. Antero–lateral pins avoid the issues of anterior and lateral pins, but the frame construct may not be as biomechanically strong as frames with anterior pins. Connector clamps between external fixator bars are ideally placed outside of the fracture zone to allow fluoroscopic and radiographic images of the reduced fracture without metallic artifact or interference. Consideration should be given to foot pins, a foot plate connected to the fixator, or an ankle foot orthosis (AFO). This is particularly important in patients with multiple injuries, severe soft-tissue injuries with an anticipated long delay prior to definitive fixation and obtunded patients. Open fractures are urgently irrigated and debrided in the operating room. Repeat debridements are performed as necessary. Antibiotics should be administered intravenously for a minimum of 24 h after each debridement. Typically, a first generation cephalosporin is given and Gram-negative coverage is added for Grade III injuries. Clostridial coverage should be initiated in fractures with soil or faecal contamination. Arterial lesions are evaluated with an arteriogram, but should be done, when feasible, in the operating room to avoid delay. Open fractures and high-energy tibial plateau fractures with associated compartment syndrome represent unique and challenging subsets of these fractures. In both instances, urgent operative intervention is required, which violates the soft tissues at or near the fracture. Thus, delayed treatment until the soft tissues recover is not possible in its truest form. This does, however, present an opportunity to perform early internal fixation. At the time of debridement or fasciotomy, internal fixation could be undertaken with limited additional dissection. Stabilisation of fractures is believed to protect the soft tissues from further damage and decrease sepsis. In fact, Benirschke et al. report no deep infections in 14 open plateau fractures treated with immediate internal fixation and delayed closure.11 Early open reduction and internal fixation may facilitate articular reduction and provide rigid fixation that allows earlier knee range of motion and possible improved outcomes. In fact, the primary caveat of Egol’s protocol was knee stiffness.9 Additionally, spanning external fixation and early joint reduction with limited internal fixation could be undertaken, with further definitive internal fixation delayed until the soft tissues heal.
Definitive treatment Non-operative treatment for these high-energy injuries has a role in the medically decompensated patient only. These injuries have poor outcomes with non-operative treatment.1,12 In extreme circumstances, an external fixator can be applied in the intensive care unit. This ‘‘traveling traction’’ allows for stability and reduced soft-tissue damage. It is used until either the patient and soft-tissue envelope can tolerate surgery or the extremity can be placed into a cast brace. External fixation can be used effectively for definitive fixation. Frames usually do not span the knee joint for a prolonged period, so knee motion can be initiated to minimise stiffness. Hybrid, Ilizarov, and monolateral half-pin frames
R.D. Zura et al. have all been used with success.13–16 Olive wires can be used to compress the joint surface. Typically, however, limited incisions are made to facilitate reduction and internal fixation is achieved with lag screws, the frame being used to support the metaphyseal portion of the fracture.14 External fixators must be maintained until sufficient healing has occurred, which can be problematic when pin or wire site complications occur. Definitive internal fixation of closed, high-energy tibial plateau fractures should be undertaken only after the softtissue envelope has healed enough to allow incision. Often the return of the ability of the skin to wrinkle heralds the recovery of the soft tissues. Conventional techniques of high-energy bicondylar tibial plateau fractures often employed a single midline incision with medial and lateral plates. Absolute anatomic reduction and rigid fixation was performed at the expense of vascularity. Historically, soft-tissue complication and infection rates were as high as 50–80%.17 However, contemporary approaches to these fractures have significantly lowered the rate of adverse outcomes. Modern techniques of dual plating through two separate incisions preserves blood flow and soft-tissue integrity, which has lead to a decreased rate of infection.10 Advances in plate design have also afforded more biological approaches to these fractures.18 The use of fixed-angle locking plates avoids the diminished periosteal blood flow and bone necrosis seen with conventional plates under compression. Furthermore, minimally invasive submuscular, extraperiosteal techniques can be employed with these plates and the screws inserted percutaneously. Lateral plateau fractures, if treated with internal fixation, can be fixed with a variety of techniques. Typically, a lateral approach is made. A direct approach is preferable to avoid excessive dissection and devascularisation of the bone fragments and soft tissues. The joint is visualised through a submeniscal arthrotomy and the joint is reduced under direct vision. Meniscal repair is performed if necessary. The joint surface is supported with either allograft or autograft. It is the authors’ opinion that synthetic graft is superior. Fixation is undertaken after reduction. Locking plates are commonly used for periarticular fractures, but their primary indication is for fixation in osteoporotic bone. The medial plateau fragment is the key to fixation of medial and bicondylar tibial plateau fractures. There are biomechanical data to support the use of a single laterally based locking plate19 and these are commonly used and occasionally a good option (Fig. 2). It is crucial, however, for the surgeon to understand both the location and fracture line orientation of the medial fragment and the particular screw configuration of the implant being employed to achieve a successful outcome.18,20 If the medial plateau fragment is non-displaced, this technique has more chance of success.21 While intraoperative traction may reduce the medial fragment and allow laterally based fixation, it may be preferable to approach the medial fragment through a separate incision. Persistently displaced medial fragments should be reduced through a medial incision. The medial incision should be along the posterior border of the tibia. The pes tendons can be cut and repaired at the end of the procedure or retracted. The fragment is reduced and the fragment is fixed, typically with a buttress plate. The medial side is commonly fixed first, so care should be taken to avoid
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Figure 2 A 45-year-old male involved in a motor vehicle accident presented with pain and soft tissue swelling in the left knee. Anteroposterior (A) and lateral (B) radiographs revealed a Schatzker VI tibia plateau fracture. A CT scan revealed significant medial and lateral comminution with dissociation of the metaphysis and diaphysis (C,D). Following temporary spanning external fixation and improvement in the soft tissues, open reduction and internal fixation was performed with a Synthes LISS plate through a submuscular extraperiostal approach via a limited lateral incision (E,F).
ARTICLE IN PRESS 234 screw placement that may hinder later reduction of the lateral plateau.10 Postoperative protocols should emphasise early motion. Although controversial, it is our practice to begin physical therapy with continuous passive motion (CPM) on postoperative day number one to avoid stiffness. Bracing may be performed on an individual basis. Typically, these patients are kept non-weight bearing on the injured extremity for 10–12 weeks after surgery. Progressive weight-bearing and activities are then initiated. We reviewed our experience with bicondylar tibial plateau fractures to illustrate our current approach to these injuries. Our study population was identified using a prospectively collected trauma registry and operative database. Between January 2002 and June 2004, 25 patients with 26 fractures were treated at our institution using the less invasive stabilisation system (LISS) plate and followed to union. There were 14 males and 11 females with an average age of 46 (range: 28–83). Five (19%) of the fractures were open (1 Type II, 2 Type IIIA, 2 Type IIIB). Nine (34%) of the fractures were complicated by compartment syndrome requiring fasciotomy. According to the OTA classification there were 6 (41C1), 8 (41C2), and 12 (41C3) fractures. A single surgeon performed all operations. CT scan and plain radiographs were used routinely for pre-operative planning for all cases. An anterolateral approach to the proximal tibia was used. The lateral meniscus was elevated to allow direct visualisation of the articular surface. Using fluoroscopy and direct visualisation any depressed articular segments were elevated through a cortical window using tamps. The metaphyseal defects were filled with allograft cancellous bone or Norian SRS (Synthes) material. Independent lag screws were used to obtain articular fixation. Fracture fixation was obtained with a tibial LISS plate (Synthes) inserted submuscularly along the anterolateral tibia. A minimum of 4 locked screws were used in the proximal and distal segments. Clinical follow-up was obtained consisting of physical examination and radiographs. Twenty-five patients with twenty six fractures were followed until union, with total follow-up of an average of 8.5 months (range 6–13). Our complications included one varus malunion, one superficial infection, and three deep infections eventually requiring hardware removal. Interestingly, three of the infections occurred in patients requiring fasciotomies. Therefore, the overall infection rate was 15% and in those patients requiring fasciotomies it was 33%. Of note, only one of five open fractures became infected. The average articular step-off was 1.4 mm. Our average initial post-operative varus/valgus alignment was 1.91 of varus. The average change in tibial alignment at last follow-up was less than one degree. The patient with a varus malunion represented axial malalignment present at the index procedure. Union was defined by the presence of bridging callus seen on at least two cortices on AP and lateral radiographs and weight bearing as tolerated was allowed at that time. Time to union averaged 13.1 weeks (range 72–118 days). One patient required refixation and bone grafting to treat a non-union (63-year-old female with grade IIIA open fracture). On exam, patients had an average flexion to 110 degrees (range 85–130). Twenty-one patients (22 knees) had full extension. Four patients had flexion contractures at
R.D. Zura et al. follow-up measuring 51, 51, 51, and 201. No hardware failure occurred.
Outcomes Several studies suggest articular incongruity after tibial plateau fractures, particularly lateral plateau injuries, is well tolerated and that the amount of articular displacement has little effect in determining management outcomes. The tibial plateau articular surface has a thicker articular cartilage layer than do many other joints, but it is not known whether this accounts for its high tolerance for articular malalignment. Lucht and Pilgaard22 found that patients with persistent joint depression of 3–10 mm had an acceptable functional result a mean of 7 years after injury. In another study, the clinical outcome was similar in patients who had 45 mm of articular incongruity than in those who had p5 mm of incongruity (mean follow-up, 7.3 years).23 When those same patients were reevaluated a mean of 20 years after injury, there were no significant changes in clinical outcomes from the original study.24 All 20 patients with articular incongruity between 5 and 10 mm had good or excellent clinical results (including 9 patients with instability of the knee). In addition, all five patients with 410 mm of articular incongruity and stable knees had a good or excellent result. A poor functional and clinical result occurred only when a combination of factors was present: a central depressed lateral condylar fragment; articular incongruity 410 mm; and instability of the knee at the time of follow-up. Honkonen reported that the incidence of secondary OA was not significantly different in the patients with 0 to 3 mm and those with 43 mm of articular incongruity (99 and 25 patients, respectively).25 Koval et al. reported that clinical results were no different for patients with anatomic and non-anatomic reductions (13 and 5 patients, respectively).26 Weigel and Marsh13 found no correlation between articular surface reduction and knee score at an average of 8 years after injury in a group of 23 patients with 24 high-energy tibial plateau fractures treated with external fixation. Some studies that have reported a strong effect of articular reduction on outcomes have methodological problems that make the significance of their conclusions uncertain. Blokker et al.27 reported that the adequacy of articular reduction was strongly associated with outcome in 60 patients treated for tibial plateau fractures. In this study, no patient with a step-off X5 mm had a satisfactory result. This study has been cited as evidence mandating anatomic reduction of the tibial articular surface; however, a final rating of satisfactory required a satisfactory clinical and radiographic result. An unsatisfactory rating in either area resulted in a final rating of unsatisfactory. The radiographic criteria for a satisfactory result required a residual articular depression p5 mm. Thus, a patient with an articular incongruity 45 mm was automatically assigned an unsatisfactory final result, regardless of the clinical rating, suggesting bias in the conclusions. It is generally accepted that knee stability and restoration of mechanical axis are important determinants in patient outcome. As noted above, Lansinger found good to excellent results in 90% of patients with stable knees, which appeared
ARTICLE IN PRESS Current management of high-energy tibial plateau fractures more important in outcome than the quality of articular reduction.24 However, mild varus or valgus instability is often functionally well-tolerated and good results have been reported.13 Mechanical malalignment greater than 101 has been correlated with poor long-term functional results and may complicate future knee arthroplasty.25
235
9.
10.
Conclusion Historically, high-energy tibial plateau fractures have been associated with high complication rates. Although they remain a challenge for the orthopaedic trauma surgeon, contemporary treatment of high-energy tibial plateau fractures can have satisfactory outcomes. Important aspects of management include assessment of soft-tissue injury, management with temporary spanning fixation in select cases, appropriate imaging of articular injury, and timely, accurate reduction and fixation.
11.
12.
13.
14. 15.
Practice points
All high-energy tibial plateau fractures have a
16.
concomitant soft-tissue injury
Temporary spanning external fixation is often the initial treatment of choice
A biologic approach, mindful of the vascularity of
soft tissue and bone, can prevent many adverse outcomes Definitive treatment is aimed at restoring mechanical alignment and joint congruity
17. 18.
19.
References 1. Schatzker J, McBroom R, Bruce D. The tibial plateau fracture. The Toronto experience 1968–1975. Clin Orthop Relat Res 1979;138:94–104. 2. Gustilo R, Mendoza R, Williams D. Problems in the management of type III (severe) open fractures: a new classification of type III open fractures. J Trauma 1984;24:742. 3. Tscherne H, Gotzen L. Fractures with soft tissue injuries. Berlin: Springer; 1984. 4. Andrews JR, Tedder JL, Godbout BP. Bicondylar tibial plateau fracture complicated by compartment syndrome. Orthop Rev 1992;21(3):317–9. 5. Chan PS, Klimkiewicz JJ, Luchetti WT, et al. Impact of CT scan on treatment plan and fracture classification of tibial plateau fractures. J Orthop Trauma 1997;11(7):484–9. 6. Sirkin M, Sanders R, DiPasquale T, et al. A staged protocol for soft tissue management in the treatment of complex pilon fractures. J Orthop Trauma 1999;13:78–84. 7. Nowotarski PJ, Turen CH, Brumback RJ, et al. Conversion of external fixation to intramedullary nailing for fractures of the shaft of the femur in multiply injured patients. J Bone Joint Surg 2000;A-82:781–8. 8. Scalea TM, Boswell SA, Scott JD. External fixation as a bridge to intramedullary nailing for patients with multiple injuries and
20.
21.
22. 23.
24.
25. 26.
27.
with femur fractures: damage control orthopaedics. J Trauma 2000;48:613–23. Egol KA, Tejwani NC, Capla EL, et al. Staged management of high-energy proximal tibia fractures (OTA TYPES 41): the results of a prospective, standardized protocol. J Orthop Trauma 2005;19(7):448–55. Barei DP, Nork SE, Mills WJ, Henley MB, Benirschke SK. Complications associated with internal fixation of high-energy bicondylar tibial plateau fractures utilizing a two-incision technique. J Orthop Trauma 2004;18(10):649–57. Benirrschke SK, Agnew S, Mayo KA, et al. Immediate internal fixation of open, complex tibial plateau fractures: treatment by a standard protocol. J Orthop Trauma 1992;6(1):78–86. Waddell JP, Johnston DW, Neidre A. Fractures of the tibial plateau: a review of ninety-five patients and comparison of treatment methods. J Trauma 1981;21(5):376–81. Weigel DP, Marsh JL. High-energy fractures of the tibial plateau. Knee function after longer follow-up. J Bone Joint Surg 2002; A-84:1541–51. Berkson EM, Virkus WW. High-energy tibial plateau fractures. J Am Acad Ortho Surg 2006;14:20–31. Watson JT, Ripple S, Hoshaw SJ, et al. Hybrid external fixation for tibial plateau fractures: clinical and biomechanical correlation. Orthop Clin North Am 2002;33:199–209. Katsenis D, Vasilis A, Panayiotis M, Minos T, Lambiris E. Minimal internal fixation augmented by small wire transfixion frames for high-energy tibial plateau fractures. J Orthop Trauma 2005; 19(4):241–8. Young MJ, Barrack RL. Complications of internal fixation of tibial plateau fractures. Orthop Rev 1994;23(2):149–54. Cole PA, Zlowodzki M, Kregor PJ. Less invasive stabilization system (LISS) for fractures of the proximal tibia: Indications, surgical technique and preliminary results of the UMC clinical trial. Injury 2003;34:A16–29. Mueller KL, Karunakar MA, Frankenburg EP, Scott DS. Bicondylar tibial plateau fractures: a biomechanical study. Clin Orthop Relat Res 2003;412:189–95. Bhattacharyya T, McCarty III LP, Harris MB, Morrison SM, Wixted JJ, Vrahas MS, et al. The posterior shearing tibial plateau fracture: treatment and results via a posterior approach. J Orthop Trauma 2005;19(5):305–10. Gosling T, Schandelmaier P, Marti A, Hufner T, Partenheimer A, Krettek C. Less invasive stabilization of complex tibial plateau fractures: a biomechanical evaluation of a unilateral locked screw plate and double plating. J Orthop Trauma 2004; 18(8):546–51. Lucht U, Pilgaard S. Fractures of the tibial condyles. Acta Orthop Scand 1971;42:366–76. Rasmussen PS. Tibial condylar fractures: impairment of knee joint stability as an indication for surgical treatment. J Bone Joint Surg Am 1973;55:1331–50. Lansinger O, Bergman B, Ko ¨rner L, Andersson GBJ. Tibial condylar fractures: a twenty-year follow-up. J Bone Joint Surg Am 1986;68:13–9. Honkonen SE. Indications for surgical treatment of tibial condyle fractures. Clin Orthop 1994;302:199–205. Koval KJ, Sanders R, Borrelli J, Helfet D, DiPasquale T, Mast JW. Indirect reduction and percutaneous screw fixation of displaced tibial plateau fractures. J Orthop Trauma 1992;6: 340–6. Blokker CP, Rorabeck CH, Bourne RB. Tibial plateau fractures: an analysis of the results of treatment in 60 patients. Clin Orthop 1984;182:193–9.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 236–241
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SYNDROMES
Osteogenesis imperfecta Clare Michella, Vanisha Patela, Rouin Amirfeyzb,, Martin Garganc a
Bristol University, Bristol, UK Trauma and Orthopaedics, Frenchay Hospital, Bristol, UK c Trauma and Paediatric Orthopaedics, Bristol Royal Hospital for Children, Bristol, UK b
Introduction
Osteogenesis Imperfecta (OI) is an inherited disorder of
type I collagen characterised by bone fragility and low bone mass. Severity varies widely, ranging from intrauterine fractures and perinatal death to very mild forms without fractures. Typical extra-skeletal manifestations are also associated variably with the disorder, and these include blue sclerae, dentinogenesis imperfecta, hyperlaxity of ligaments and skin, hearing impairment, and presence of wormian bones on skull radiographs (see Tables 1 and 2). This article reviews the clinical manifestations, classification, pathogenesis and management of OI (Figs. 1–3).
90%), this is in one or two of the genes that encode the a-chains of collagen type 1 (COL1A1 and COL1A2). Little is known about the pathogenesis of types V–VII. COL1A1 and COL1A2 are large genes (located on chromosomes 17 and 7, respectively) that have been associated with over 200 mutations in OI patients.3 A collagen type 1 molecule consists of three polypeptide chains (two alpha 1 and one alpha 2 chain) that intertwine via a glycine residue at every 3rd position so forming a triple helical structure.4 The mutations can be divided into two categories:5 (1) Excluded: mutations that result in the exclusion of the product of the mutant allele from the mature collagen molecule, (2) Included: those that permit the incorporation of a structurally abnormal chain.
Clinical features
Radiographic features: Diffuse osteopenia associated with multiple fractures and deformities.
Histopathologic features: Generalised decrease in bone tissue.
Epidemiology and genetics
The incidence of OI is about 1 in 20,000,2 and it occurs
equally among males and females and in all racial and ethnic groups. Most cases of OI (types I–IV) are caused by an autosomal dominant genetic mutation, and in most instances (about Corresponding author.
0268-0890/$ - see front matter & 2007 Published by Elsevier Ltd. doi:10.1016/j.cuor.2007.04.003
Exclusion: Type 1 (nondeforming OI) In most cases this phenotype is caused by a mutation that creates a premature stop codon within COL1A1. This results in a null COL1A1 allele,6 which, as a consequence of nonsensemediated decay, destabilises the mRNA and leads to only half the normal amount of type I pro-collagen being synthesised by the fibroblasts of affected individuals.7
Inclusion: Type II–IV (deforming OI) These mutations generate abnormal type 1 procollagen molecules that are more deleterious than those of null mutations. The most typical sequence abnormality is a point substitution mutation that affects a glycine residue in either COL1A1 or COL1A2,7 the phenotypic consequences of which,
ARTICLE IN PRESS Osteogenesis imperfecta
Table 1
237
Skeletal manifestations of OI.
Skeletal manifestations General Skull
Long bones
Spine deformity (60%) Pelvis Thorax deformity
Short stature (Fig. 1) Broad forehead; flattened posterior cranium, overhanging occiput; bulging calvaria; triangular face shape Anterior bowing of humerus, tibia and fibula; lateral bowing of femur, radius and ulna; bone fragility characterised by multiple pathological fractures with poor healing that results in long-bone deformity Thoracic scoliosis (Figs. 2 and 3)
Trefoil-shaped pelvis with protrusio acetabuli Associated with multiple rib fractures; spinal deformity; moulding of the soft thorax; pectus excavatum or carinatum
Adapted from Kocher & Shapiro (1998).
Table 2
because of paucity of type I collagen, thereby making it plausible that agents that augment collagen production have a beneficial effect.7
(2) the position in the triple
helix at which the substitution arises (3) which amino acid is substituted for glycine The consequence of such mutations is high bone turnover,8 and therefore agents that limit degradation might augment bone formation.
It is likely that the phenotypic variations between affected individuals are attributable to unknown environmental and genetic factors that modify the expression of the mutant collagen allele.
Classification
The most widely used classification of OI is by Sillence
and colleagues,9 which distinguishes four clinical types (OI type I–IV) based on clinical, radiological and genetic data. Recently a new group of patients has been identified at the clinical and molecular level and added to the present classification as OI type V–VII.10–12
Extra-skeletal manifestations of OI.
Extra-skeletal manifestations
Type I
Dentinogenesis imperfecta (30%)
This is the most common form and includes patients with
Soft, translucent, brownish teeth. The enamel wears easily, and the teeth are carious, shortened and susceptible to cracking Blue sclera Due to increased corneal translucency Skin Often thin, translucent and easily distensible Ligamentous laxity Typically causes pes planus, but also subluxating patellae and dysplastic hips Basilar impression Compression of the brain stem and high cervical cord can lead to neurological deficiencies that can be treated surgically1 Vascular fragility Non-progressive aortic root dilatation; mitral-valve prolapse Hearing loss From adolescence and becomes problematic for nearly 50% of affected adults Intelligence Often normal Metabolic Hyper-metabolism; heat intolerance; abnormalities elevated body temperature; increased sweating; resting tachypnoea and tachycardia
mild disease and absence of major bone deformities.
It is sub-classified into:
(i) Type A (without dentinogenesis imperfecta), (ii) Type B (with dentinogenesis imperfecta). The sclerae are blue and most fractures occur before puberty. Vertebral fractures are typical and can lead to mild scoliosis. Hearing loss occurs in about 50% of families and women are twice as often affected as males. Connective tissue malfunction, such as thin skin, hernias and generalised joint hyper-mobility, are present. A delay exists in achieving motor milestones, but children with OI type I do have normal intelligence and life expectancy is normal.
Type II
This is lethal in the perinatal period, usually because of respiratory failure resulting from multiple rib fractures.
Narrow thoraces, short and deformed extremities with
multiple fractures, and a typical frog-like position are the main features.13 Newborns have soft calvarial bones, distinctive triangular faces, bluish sclerae, and beaked noses. Survival beyond a year is very rare.14
Adapted from Kocher & Shapiro (1998).
Type III Therefore in patients expressing this mutation, bone formation is defective
depend on: (1) Which of the two alpha
chains is affected
This occurs in approximately 20% of all patients with OI. It is the most severe form in children surviving the neonatal period.
ARTICLE IN PRESS 238
C. Michell et al.
Figure 1 OI patient, wheelchair bound with short stature in this case.
Figure 2 Thoracic scoliosis.
These patients are of very short stature and have
limb and spine deformities secondary to multiple fractures, which can lead to respiratory difficulties (identified as the leading cause of death in this patient group). The sclerae are frequently normal but a significant number have large and asymmetric heads, while the face is triangular. The maxilla is frequently posteriorly inclined and dental malocclusion occurs in 80%. Muscle strength and muscular imbalance are poor.13
Life expectancy is decreased, but affected individuals live into adulthood.
Type IV
This is usually intermediate in severity between types I and III.
Patients exhibit mild to moderate bone deformities, variable short stature, dentinogenesis imperfecta and greyish sclera.
ARTICLE IN PRESS Osteogenesis imperfecta
239
Figure 3 Typical elbow and knee deformities.
Type V
Differential diagnosis
Heredity seems to follow an autosomal dominant pattern
There are many skeletal dysplasias which resemble OI,14
but there remains no evidence of a collagen type 1 abnormality. Patients have normal sclerae and no dentinogenesis imperfecta. The interroseous membrane at the forearm becomes calcifies early in life, which severely limits movement and can lead to secondary dislocation of the radial head. Importantly, after fractures or surgical interventions, patients are predisposed to develop hyperplastic callus, which can mimic osteosarcoma10.
but the main differential diagnosis in a child presenting with multiple unexplained fractures is child abuse, especially if the family history is negative for the disorder.15
Management Aims of non-surgical management: Reduce fracture rates Prevent long bone and spinal deformities Improve functional outcome
Type VI
This is defined on the basis of bone histological findings, which show a higher amount of osteoid than usual and an abnormal ‘fish scale’ pattern of lamellation suggestive of disordered mineralisation of bone tissue, even though concentrations in serum calcium and phosphorus are normal.11
Type VII
This is a moderately deforming recessive disorder that so
far has only been reported in a community of Native Americans in northern Quebec.12 Apart from bone fragility, rhizomelia is a prominent clinical feature, and coxa vara can be present in infancy. The disease has been localised to chromosome 3p22–24.1, which is outside the loci for collagen type 1 genes.12
Physiotherapy, rehabilitation and occupational therapy This is an important element of the multi-disciplinary approach to the management of OI.16 Medical therapy Bisphosphonates. These anti-resorptive agents interfere with the cholesterol biosynthesis of osteoclasts therefore inhibiting these cells but not leading to apoptosis.17 Pamidronate
This is the most widely used, second generation bisphosphonate.
A study by Glourieux et al.,18 has reported successful treatment with pamidronate; there was a reduction
ARTICLE IN PRESS 240
C. Michell et al.
Figure 4 Multilevel tibial osteotomies+IM nailing to correct the deformities. Immediate post operative (left) compared with 8 weeks (middle) and 3 months (right) after the operation.
in fracture rate, increased bone mineral density and increased vertebral coronal area in the treated patients. Administration of bisphosphonates should be achieved as early as possible and a trial by Sokby et al.,19 found that if pamidronate was used in combination with surgery, the bone mineral density would increase and rate of refracture would decrease. Thus the best form of management is to use pamidronate in combination with surgery, pre and post-operatively. However there remains controversy over who should receive bisphosphonate treatment since the longterm effects have not yet been discovered. The concerns arise because bisphosphonates remain buried in the skeleton where they have a half life of many years.15 They may therefore interfere with bone remodelling during growth and the have a possible adverse effect on future pregnancies when the drug is given to premenopausal girls.16 The drawback to pamidronate treatment is the inconvenience of having the dug intravenously infused every few months and therefore oral bisphosphonate therapy (e.g. alendronate) is now being researched.20
Alendronate
Recent trials have found that oral alendronate (a more
potent bisphosphonate than pamidronate) increases bone mineral density in both children and adults,21,22 but more studies are required to evaluate the effects on fracture rates. Since bone mineral density appears to be an indicator of disease severity and may be predictive of long term functional outcome,23 it seems likely that agents such as bisphosphonates would improve function, decrease rates of fracture and the need for surgery.
Analgesia Fracture and non-fracture pain can pose a significant burden for the children and their families, and therefore adequate pain management is essential.24 Bone marrow transplantation Multipotential stromal cells can be isolated from bone marrow and made to differentiate into a variety of cell types, including osteoprogenitor cells.7 Transplantation from an HLA identical or single-antigen mismatched sibling may ameliorate the course of severe OI.25 Transplanting bone marrow stromal cells from healthy people to OI patients will lead to the cells differentiating into osteoblasts and producing normal bone.17
Surgical therapy Intra-medullary rods These are used to stabilise bone and correct deformities.1 The choice of intra-medullary device is important A retrospective trial by Joseph et al.,26 found dual Rush rods and Sheffield telescoping rods in the femur, to be equally effective and superior to a single Rush rod. In contrast, the preferential choice of rod in the tibia is a single Rush rod (Fig. 4). Correction of scoliosis This may be very difficult because of bone fragility.
Gene transplantation Curing the disease is by elimination of the mutated gene or gene product. Most severe cases are due to the presence of abnormal collagen molecules. Therefore the mutant allele needs to be initially inactivated and substituted for its product. More research still needs to be carried out.17
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241
References 1. Engelbert RHH, Pruijs HEH, Beemer FA, Helders PJM. Osteogenesis Imperfecta in childhood: treatment Strategies. Arch Phys Med Rehabil 1998:1590–4. 2. Camach NP, Raggio CL, Blank RD. Osteogenesis Imperfecta [Metabolic Bone Disease]. Current Opinion in Orthopaedics 2000;1l:341–6. 3. Dalgleish R. The human collagen mutation database 1998. Nucleic Acid Res 1998;26:253–5. 4. Kadler KE, Holmes DF, Trotter JA, Chapman JA. Collagen fibril formation. Biochem J 1996;316:1–11. 5. Sykes B. The molecular genetics of collagen. BioEssays 1985;3: 112–7. 6. Willing MC, Deschenes SP, Scott DA. Osteogenesis imperfecta type 1: molecular heterogeneity for COL1A1 null alleles of type 1 collagen. Am J Hum Genet 1994;55:638–47. 7. Byers PH. Osteogenesis imperfecta: perspectives and opportunities. Curr Opin Pediatr 2000;12:603–9. 8. Lund AM, Hansen M, Kollerup G, et al. Collagen-derived markers of bone metabolism in osteogenesis imperfecta. Acta Paediatr 1998;87:1131–7. 9. Sillence DO, Senn A, Danks DM. Genetic heterogeneity in osteogenesis imperfecta. J Med Genet 1979;16:91–116. 10. Glorieux FH, Rauch F, Plotkin H, Ward L, et al. Type V osteogenesis imperfecta: a new form of brittle bone disease. J Bone Miner Res 2000;15:1650–8. 11. Glorieux FH, Ward LM, Rauch F, Lalic L, et al. Osteogenesis type VI: a form of brittle bone disease with a materialisation defect. J Bone Miner Res 2002;17:30–8. 12. Ward LM, Rauch F, Travers R, et al. Osteogenesis imperfecta type VII: an autosomal recessive form of brittle bone disease. Bone 2002;31:12–8. 13. Primorac D, Rowe DW, Mottes M, Barisˇic` I, Antic ˇevic` D, Mirandola S, et al. Osteogenesis Imperfecta at the beginning of bone and joint decade. Croat Med J 2001;42:393–415. 14. Byers PH, Tsiopouras P, Bonadio JF, Starman BJ, Schwartz RC. Perinatal lethal osteogenesis imperfecta (OI type II): a biochemically heterogeneous disorder usually due to new
15.
16.
17. 18.
19.
20. 21.
22.
23.
24.
25.
26.
mutations in the genes for the type I collagen. Am J Hum Genet 1988;42:237–48. Byers PH, Kraqow D, Nunes ME, Pepin. Genetic evaluation of suspected osteogenesis imperfecta (OI). Genetics Med 2006; 8(6):383–8. Rauch F, Glorieux FH. Osteogenesis Imperfecta, Current and Future Medical Treatment. American J Med Genetics Part C 2005;139C:31–7. Glourieux FH, Rauch F. Osteogenesis Imperfecta. Lancet 2004;363:1377–85. Glourieux FH, Bishop NJ, Plotkin H, et al. Cyclic administration of pamidronate in children with severe osteogenesis imperfecta. N Engl J Med 1998;339:947–52. El Sokby MA, Zaky Hanna AA, Basha NE, Tarraf YN, Said MH. Surgery versus surgery plus pamidronate in the management of osteogenesis imperfecta patients: a comparative study. J Pediatr Orthop B 2006;15(3):222–8. Camacho NP, Raggio CL, Blank RD. Osteogenesis imperfecta. Curr Opin Orthop 2000;11(5):341–6. Chevrel G, Schott AM, Fontagnes E, Charrin JE, Lina-Grande G, Duboeuf F, et al. Effects of oral alendronate on BMD in adult patients with osteogenesis imperfecta: a 3-year randomised placebo-controlled trial. J Bone Miner Res 2006;21(2):300–6. Madenci E, Yilmaz K, Yilmaz M, Coskun Y. Alendronate treatment in osteogenesis imperfecta. J Clin Rheumatol 2006; 12(2):53–6. Huang RP, Ambrose CG, Sullivan E, Haynes RJ. Functional significance of bone density measurements in children with osteogenesis imperfecta. J Bone Joint Surg Am 2006;88(6): 1324–30. Zach P, Franck L, Devile C, Clark C. Fracture and non-fracture pain in children with osteogenesis imperfecta. Acta Paediatr 2005;94:1238–42. Hill C, Hampshire D, Silverwood B, Bishop NJ. Recent advances in the management of osteogenesis imperfecta. Curr Paediatr 2003;13:151–7. Joseph B, Rebello G, Chandra Kent B. The choice of intramedullary device for the femur and the tibia in osteogenesis imperfecta. J Pediatr Orthop B 2005;14(5):311–9.
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CME SECTION D. Scaphoid fracture E. Scapholunate ligament rupture
Three CME points available The following series of questions are based on the CME designated article for this issue—‘‘Management of wrist instability’’ by Sivanathan, Sharpe and Loh. Please read the article carefully and then complete the self assessment questionnaire by filling in the square corresponding to your response to each multiple-choice question. After completing the questionnaire, either post or fax the answer page to the Current Orthopaedics Editorial Office at the address at the bottom of the RESPONSE sheet. Please photocopy this page if you wish to keep your copy of Current Orthopaedics intact. Replies received before the next issue of Current Orthopaedics is published will be marked and those reaching an adequate standard will qualify for three external CME points. You will be notified of your marks and a CME certificate will be despatched for your records.
4. Which form of carpal instability is classically caused by perilunate dislocation? A. B. C. D. E.
Axial carpal instability Carpal injury adaptive Carpal instability combined Carpal instability nondissociative DISI
5. Which of the following is least likely to be associated with chronic instability of the wrist? A. B. C. D. E.
Kienbocks disease Preisers disease SLAC SNAC STT arthritis
Questions 6. What sort of wrist instability can be caused by a ganglion? 1. Which of the following is a member of the instrinsic group of wrist ligaments? A. B. C. D. E.
Distal volar radiocarpal ligament Long radiolunate ligament Lunotriquetral ligament Proximal volar radiocarpal ligament Radioscaphocapitate ligament
2. Which of the following is part of the least stable intercalated segment when considering the carpal rows? A. B. C. D. E.
Capitate Hamate Trapezium Trapezoid Triquetrum
A. Carpal injury adaptive B. Carpal injury adaptive with secondary dissociative pattern C. Carpal instability combined D. Carpal instability dissociative E. Carpal instability nondissociative 7. Which of the following tests is helpful in diagnosing lunotriquetral instability? A. B. C. D. E.
ECU snap test Finkelstein’s test Kirk Watson test Klieman shear test Piano key sign
8. What wrist pathology is indicated by the Dimple sign? 3. Which of the following conditions is most likely to be associated with a VISI deformity of the carpus? A. Colles fracture B. Kienbocks disease C. Lunotriquetral ligament rupture 0268-0890/$ - see front matter & 2007 Published by Elsevier Ltd. doi:10.1016/j.cuor.2007.04.008
A. B. C. D. E.
DeQuervains DRUJ instability Lunotriquetral instability Midcarpal instability Pisotriquetral arthritis
ARTICLE IN PRESS CME SECTION 9. An MRI scan of a painful wrist, with gadolinium enhancement, reveals that there is central perforation of the TFCC with chondromalacia of the lunate. What class of TFCC abnormality does this represent? A. B. C. D. E.
1D 2B 2C 2D 2E
243 10. Which of the following can be prevented, but not effectively treated, by the insertion of a screw? A. B. C. D. E.
Kienbock’s disease Lunotriquetral instability Preiser’s disease SLAC SNAC
ARTICLE IN PRESS 244
CME SECTION
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CME SECTION Answers to CME questions based on the Mini-Symposium on Frontiers in Spine Surgery Please find below the answers to the Current Orthopaedics CME questions from Vol. 21, issue 1 which were based on the MiniSymposium on Frontiers in Spine Surgery 1
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0268-0890/$ - see front matter & 2007 Published by Elsevier Ltd. doi:10.1016/j.cuor.2007.01.004
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 246
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journal homepage: www.elsevier.com/locate/cuor
BOOK REVIEWS Complications of Spine Surgery. Treatment and Prevention, S.An Howard, L.G. Jenis (Eds.), Lippincott Williams & Wilkins (2005) (195pp., $139.00), ISBN: 0781757916. This book is a useful addition to any spine surgeon’s library but will be of particular benefit to those clinicians embarking on a career in spine surgery or to those who are likely to encounter post-surgical spinal patients whether on an occasional or regular basis. At only 195pp. this book is not too intimidating. The 19 chapters are arranged within three sections, cervical spine, thoracolumbar/lumbosacral spine and miscellaneous disorders. Although many of the points in each chapter seem to be repetitive and at times stating the obvious this does emphasise the importance of pre-operative planning, appropriate patient positioning, careful surgical technique and post-operative care. There are no
bullet point lists of ‘‘do’s and don’t’s’’ but the text is clearly written and even the casual reader would have no difficulty constructing their own list. The text is appropriately illustrated. Chapters 11 and 12, complications related to thoracic and lumbar pedicle screw instrumentation could have been condensed into one chapter. Chapter 14 on lumbar pseudarthrosis has some helpful case illustrations and it is perhaps a weakness of the book that this approach was not adopted in more of the chapters. The operative management of pseudomeningoceles is mentioned but the technique is then left to the reader’s imagination. Overall, I would recommend this book to any spinal surgery registrar or resident as one of those texts to read very early on in their careers.
Crispin Wigfield
doi:10.1016/j.cuor.2006.11.001
AO Handbook Musculoskeletal Outcomes Measures and Instruments, Michael Suk, Beate Hanson, Daniel Norvell, David Helfet. Thieme Publishing Group (2006). (444 pp. £53.46), ISBN: 3-13-141061-2. Understanding outcome measures is becoming an increasingly important part of everyday practice, and not just the field of the researcher. This book is a real tour-de-force. The first 6 chapters discuss the rationale and development of outcome instruments and should be require reading for any clinician. The authors have trawled the literature for every major musculoskeletal outcome score written, then searched again for studies which assess the criteria by which a score should be measured. The type of scoring system and scale is provided, then any outcomes the score has been validated against and the references supplied. The authors assess the doi:10.1016/j.cuor.2007.02.002
methodological evaluation of the score with points awarded for validity, reproducibility and reliability. The clinical utility scores awarded reflect patient or clinician friendliness. This allows comparison between scores with marks out of 10. Obviously the better developed and validated scores do better, and the populations tested are provided. The one area where the book could be improved is indicating which studies are best for measuring outcome for a particular problem. For example, some scores are better for assessing instability others joint replacement. This perhaps reflects the magnitude of the task. The authors have provided the tools for making the decision, in a text which should form part of every orthopaedic surgeon’s collection.
Roger Hackney
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BOOK REVIEWS Imaging of Soft Tissue Tumors, 2nd ed., Mark J. Kransdorf, Mark D. Murphey, Lippincott Williams & Wilkins, 700pp., $199, ISBN:0781747716 This is the second edition of what has become the definitive text on imaging of soft tissue tumours. The authors draw on the experience of 31,000 soft tissue tumours seen over a ten-year period in the department of soft tissue pathology in the armed forces institute of pathology. This second edition incorporates the changes in classification brought about by the World Health Organisation in 2002, presenting the tumours with their original classification and the new designations. There are initial chapters on the classification and prevalence of tumours and the general principles of imaging. Subsequent chapters deal with each type of tumour with detailed description of the imaging findings illustrated by images of high quality, mostly MRI. Many American texts tend to ignore the benefits of ultrasound in favour of MRI so
it is gratifying to see that ultrasound rightly gets the recognition it deserves. There is a helpful chapter on masses which can mimic soft tissue tumours. The necessarily detailed text is broken up with frequent ‘‘key concept boxes’’ which put forward the main teaching points. There are extensive references throughout the text with most chapters running up several hundred references. None of these seem unnecessary and reflects the fact that the text is based on strong research rather than conjecture. This then, is the definitive textbook on imaging soft tissue tumours and will prove useful to surgeons, radiologists and pathologists involved in treating soft tissue tumours. Principally aimed at radiologists, this textbook is going to be too detailed for the requirements of most orthopaedic surgeons in training, but should find use as an occasional reference book to justify its inclusion in any good orthopaedic library.
James Rankine
doi:10.1016/j.cuor.2007.02.004
Rockwood and Wilkins Fractures in Children (Sixth Edition), J.H. Beaty, J.R. Kaisser (Eds.). Lippincott Williams & Wilkins, Baltimore, MD (2006). (1120pp, £215), ISBN: 078175769X.P.A. Templeton This is the newest Edition of a very well known text. It has 27 chapters by 41 authors from five different countries. The majority of the authors are American but there are some from India, Mexico, Australia and Canada. The book is divided into four sections, namely Basic Principles, Upper Extremity Injuries, Spinal Injuries and Lower Extremity Injuries. All paediatric skeletal injuries are discussed. Each is well illustrated with radiographs, diagrams, charts and tables. doi:10.1016/j.cuor.2007.02.001
Each chapter is well researched, with lengthy lists of up to date references. As with the last Edition, the text is extremely easy to read. I found the author’s ‘‘Preferred Treatment’’ for each injury particularly useful. This is a comprehensive text on children’s fractures and musculoskeletal injuries and is essential reading for all orthopaedic trainees. It is an outstanding reference book for both consultants and trainees and I would strongly recommend that it be on the shelves of all orthopaedic libraries.
P.A. Templeton
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 248
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BOOK REVIEWS Practical Fracture Treatment. R. McRae, M. Esser, fourth ed., Churchill Living Stone (2002). 448pp., £35.07, ISBN:0443070385 The fourth edition of this well-known and popular text, keeps its original format of two main sections. Firstly a section on General Principles, which is written primarily for medical students, but so well summarised that any orthopaedic trainee would be well served by reading this material and reminding themselves of the basics. The second section of Regional Injuries, using a logical and anatomical based approach, covers all the fractures likely to be encountered in one’s practice. In this edition drawings and X-ray images have been improved, with more emphasis placed on internal fixation. However, I am reassured that the detail of non-operative management of certain fractures is still included.
Although the senior trainee studying for Board (FRCS Orth.) Examinations will probably require more detailed texts. The succinct and logical layout, with the inclusion of AO Classifications and Trauma Scores, means this book could certainly be used as an ‘aide memoire’. On a more practical note, the senior orthopaedic resident would benefit from reading the clearly illustrated descriptions of how to treat certain fractures non-operatively, for example of the ankle or tibia. I would certainly recommend purchasing this book at an early stage in an orthopaedic trainee’s career. As it is so easy to reference one may then find oneself using it for that unusual case throughout the remainder of one’s training.
Robert Metcalf
doi:10.1016/j.cuor.2007.04.010
Advanced Reconstruction of the Hip. Lieberman Jay, Berry Daniel (Eds.) AAOS (2005). 541pp., £128.95, ISBN: 0892033460 As its name suggests ‘Advanced Reconstruction of the Hip’ is not a book for beginners in hip surgery. The book is a collection of individual papers by 98 authors! All the famous names in US hip surgery are present together with many lesser known ones. As a result there is considerable overlap between chapters. An extensive knowledge of the subject is required before reading this book. It is clearly originating from and aiming at the American market with little reference to some major world literature references from UK and Europe. The balance is leaning heavily towards the
doi:10.1016/j.cuor.2007.06.001
North American cementless philosophy. It is expensively produced which makes it unclear why black and white photos often poor quality are included. Many add nothing to the text or included line drawings. Despite these shortfalls there are some world class surgeons with important contributions in this book. It will be of interest to the more advanced trainee or Hip Fellow but is not essential reading prior to the Board Exam. It will be a useful book as a reference source in their departmental library.
Martin Stone
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 249–257
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journal homepage: www.elsevier.com/locate/cuor
MINI-SYMPOSIUM: FRACTURE HEALING
(i) Pathways and signalling molecules V.S. Nikolaou, E. Tsiridis Academic Department of Trauma & Orthopaedic Surgery, A Floor, Clarendon Wing, Leeds General Infirmary, Clarendon Way, Leeds LS2 9NS, UK
KEYWORDS Bone; Fracture; Healing; Enhancement; Molecules
Summary Fracture healing is a complex and well orchestrated regenerative process, initiated in response to injury, resulting in optimal skeletal repair and restoration of skeletal function. Fracture healing remains to a great extent an unknown cascade, and recent developments in molecular biology have helped us to better understand the fracture healing cellular and molecular pathways. In this paper, we summarize the current knowledge of the most important molecules involved in the sequence of events during fracture healing, and we also focus on the latest research findings that will play important roles in the near future in better understanding fracture healing at the molecular level. & 2007 Published by Elsevier Ltd.
Introduction Various signalling molecules, including growth and differentiation factors, hormones, and cytokines, interact with several cell types, including bone and cartilage forming primary cells or even muscle mesenchymal cells, recruited at the fracture-injury site or from the circulation. Even though fracture healing remains to a great extent an unknown cascade that involves intracellular and extracellular molecular signalling for bone induction and conduction, today cellular and molecular biology provides the tools for the investigation and understanding of this complex biological process that results from the recapitulation of events which take place during embryonic bone formation. In this paper, we summarize the current knowledge of the most important molecules involved in the sequence of events during fracture healing. We also outline recent Corresponding author.
E-mail address:
[email protected] (E. Tsiridis). 0268-0890/$ - see front matter & 2007 Published by Elsevier Ltd. doi:10.1016/j.cuor.2007.08.001
research findings that may play an important role in better understanding the molecular pathways of fracture healing.
Classical histological approach In classical histological terms, fracture healing has been divided into direct (primary) and indirect (secondary) fracture healing.
Direct (primary) cortical fracture healing Direct fracture healing occurs when rigid internal fixation anatomically reduces the fracture fragments, thereby reducing inter-fragmentary distances.1 During this process, little or no periosteal response is noted (no callus formation).2 There is a direct attempt by the cortex to reestablish new Haversian systems by forming discrete remodelling units known as ‘‘cutting cones’’, a process aimed at restoring mechanical continuity.1
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Indirect or secondary fracture healing Direct fracture healing is a rare process in nature and is usually present after medical intervention by rigid internal fixation. The majority of fractures heal by indirect fracture healing, which involves callus formation through a combination of intramembranous and endochondral ossification. This process is generally enhanced by micro-motion and inhibited by rigid fixation.2 Intramembranous ossification involves the formation of bone directly, without first forming cartilage, from committed osteoprogenitor and undifferentiated mesenchymal cells that reside in the periosteum, farther from the fracture site. It results in callus formation, described histologically as ‘hard callus’.2 Endochondral ossification involves the recruitment, proliferation and differentiation of undifferentiated mesenchymal cells into cartilage, which becomes calcified and eventually replaced by bone. This type of fracture healing is contributed by the periosteum and the external soft tissues adjacent to the fracture providing an early bridging callus, histologically characterized as ‘soft callus’, which stabilizes the fracture fragments. At least five discrete stages of secondary fracture healing have been identified: (a) initial haematoma formation and inflammation, (b) angiogenesis and cartilage formation, (c) cartilage calcification, (d) cartilage removal and bone formation, and (e) bone remodelling.2 The classification of fracture healing into direct and indirect healing reflects the histological events that occur during the repair process. However, ongoing research into bone regeneration has provided further understanding of the cellular and molecular pathways that govern these events.3
Important agents in the fracture healing process The agents that interfere with the healing process at the molecular level can be separated into two general categories: (1) local molecules, and (2) systemic agents promoting fracture healing. These factors interact with various pathways in order to effectively enhance or inhibit the healing process.
Fracture healing promoting molecules During fracture healing, a number of signalling molecules initiate and progress the chain of events of endochondral and intramembranous bone formation by recruiting undifferentiated mesenchymal stem cells (MSCs) and osteoprogenitors cells, and inducing them to proliferate and differentiate into osteoblasts.4 The signalling molecules can be categorized into three groups: (a) the pro-inflammatory cytokines, (b) the TGF-b superfamily and other growth factors, and (c) the metalloproteinases and angiogenic factors.4 Pro-inflammatory cytokines Cytokines are known to be secreted not only by macrophages and inflammatory cells but also by cells of mesenchymal origin present in the periosteum.5 Interleu-
V.S. Nikolaou, E. Tsiridis kin-1 (IL-1), interleukin-6 (IL-6), and tumour necrosis factora (TNF-a) have been found to participate in the initial phase of the repair process (Table 1).6 They show peak expression within the first 24 h following fracture, and then their levels are seen to reduce during the period of cartilage formation. They increase for a second time during the bone remodelling phase. The important central role of these molecules is their chemotactic effect on other inflammatory cells that
Table 1 The essential signalling molecules during fracture healing; their source and targeted cells, and their major functions and expression patterns. Cytokines (IL-1, IL-6, TNF-a) Source: Macrophages and other inflammatory cells, cells of mesenchymal origin Chemotactic effect on other inflammatory cells, stimulation of extracellular matrix synthesis, angiogenesis, recruitment of endogenous fibrogenic cells to the injury site, and at later stages bone resorption Increased levels from day 1 to day 3 and during bone remodeling TGF-b Source: Degranulating platelets, inflammatory cells, endothelium, extracellular matrix, chondrocytes, osteoblasts Targeted cells: MSCs, osteoprogenitors cells, osteoblasts, chondrocytes Potent mitogenic and chemotactic for bone forming cells, chemotactic for macrophages Expressed from very early stages throughout fracture healing PDGF Source: Degranulating platelets, macrophages, monocytes (during the granulation stage) and endothelial cells, osteoblasts (at later stages) Targeted cells: Mesenchymal and inflammatory cells, osteoblasts Mitogenic for mesenchymal cells and osteoblasts, chemotactic for inflammatory and mesenchymal cells Released at very early stages of fracture healing BMPs Source: Osteoprogenitors and mesenchymal cells, osteoblasts, bone extracellular matrix and chondrocytes Targeted cells: Mesenchymal and osteoprogenitor cells, osteoblasts Differentiation of undifferentiated mesenchymal cells into chondrocytes and osteoblasts and osteoprogenitors into osteoblasts Various temporal expression patterns (Table 2) FGFs Source: Monocytes, macrophages, mesenchymal cells, osteoblasts, chondrocytes Targeted cells: Mesenchymal and epithelial cells, osteoblasts and chondrocytes Angiogenic and mitogenic for mesenchymal and epithelial cells, osteoblasts, chondrocytes
ARTICLE IN PRESS Pathways and signalling molecules Table 1. (continued ) a-FGF mainly effects chondrocyte proliferation, b-FGF (more potent) involved in chondrocyte maturation and bone resorption Expressed from the early stages until osteoblast formation IGFs Source: Bone matrix, endothelial and mesenchymal cells (in granulation stage) and osteoblasts and nonhyperthrophic chondrocytes (in bone and cartilage formation) Targeted cells: MSCs, endothelial cells, osteoblasts, chondrocytes IGF-I: Mesenchymal and osteoprogenitor cells recruitment and proliferation, expressed throughout fracture healing IGF-II: Cell proliferation and protein synthesis during endochondral ossification Metalloproteinases Source: The extracellular matrix Degradation of the cartilage and bone allowing the invasion of blood vessels during the final stages of endochondral ossification and bone remodelling VEGFs Potent stimulators of endothelial cell proliferation Expressed during endochondral formation and bone formation Angiopoietin (1 and 2) Formation of larger vessel structures, development of colateral branches from existing vessels Expressed from the early stages throughout fracture healing
enhances extracellular matrix synthesis, stimulates angiogenesis, and recruits endogenous fibrogenic cells to the injury site.5 Recent studies have demonstrated that TNF-a signalling contributes to the regulation of chondrocyte apoptosis and a lack of TNF-a signalling leads to a persistence of cartilaginous callus and delayed resorption of mineralized cartilage by osteoclasts.7 Similarly, absence of TNF-a has been proven to alter the control of angiogenesis and cartilage turnover.7 IL-1, IL-6, and TNF-a also show increased levels of expression during fracture callus re-shaping later in the process of fracture healing and remodelling.
The transforming growth factor-b (TGF-b) superfamily and other growth factors The TGF-b superfamily is a large family of growth and differentiation factors that includes bone morphogenetic proteins (BMPs), transforming growth factor-beta (TGF-b), growth differentiation factors (GDFs), activins, inhibins, and the Mullerian inhibiting substance. At least 34 members have been identified in the human genome.8 Specific
251 members of this superfamily, including bone morphogenetic proteins (BMPs 1–8), growth and differentiation factors (GDF-1, 5, 8, 10) and transforming factor beta (TGF-b1, b2, b3), promote various stages of intramembranous and endochondral bone ossification during fracture healing.9
The role of BMPs More specifically, BMPs are pleiotropic morphogens and play a critical role in regulating growth, differentiation, and apoptosis of various cell types, including osteoblasts, chondroblasts, neural cells, and epithelial cells.10 BMPs elicit their cellular effects through activating specific combinations of type I and type II serine/threonine kinase receptors and their downstream effector proteins, which are termed Smads.11 Their role in fracture healing has been proved to be crucial as they induce a cascade of events for chondro-osteogenesis, including chemotaxis, mesenchymal and osteoprogenitor cell proliferation and differentiation, angiogenesis, and controlled synthesis of extracellular matrix.10 BMPs are divided into at least four separate subgroups depending on their primary amino acid sequence. Group 1 consists of BMP-2 and BMP-4, and group 2 includes BMP-5, BMP-6, and BMP-7. The third group includes GDF-5 (or BMP-14), GDF-6 (or BMP-13) and GDF-7 (or BMP-12), and finally group 4 includes BMP-3 (or osteogenin) and GDF-10 (or BMP-3b).10 The extracellular matrix comprises the main source of BMPs being produced by osteoprogenitors, mesenchymal cells, osteoblasts and chondrocytes (Table 1). BMPs are closely structurally and functionally related; however, each has a unique role as well a distinct temporal expression pattern during the fracture repair process (Figure 1). Studies of the role of BMPs in fracture healing in the mouse and rat have shown a variety of osteogenic effects, temporal expressions and mitogenic capacities (Tables 2 and 3).3,9,12 Since 1965, when Urist revolutionized the current understanding of fracture healing by hypothesizing the existence of bone morphogenetic proteins (BMPs),13 extensive research has been ongoing to further clarify the role of BMPs in fracture healing. Cheng in 2003,14 analysing the osteogenic activity of 14 types of BMPs in osteoblastic progenitor cells, suggested that an osteogenic hierarchical model exists, in which BMP-2, 6, and 9 may play an important role in inducing osteoblast differentiation of mesenchymal stem cells. In contrast, most BMPs are able to stimulate osteogenesis in mature osteoblasts.14 BMPs may also stimulate the synthesis and secretion of other bone and angiogenic growth factors such as insulin-like growth factor (IGF) and vascular-endothelial growth factor (VEGF).15 Furthermore, it has been shown that BMPs may also stimulate bone formation by directly activating endothelial cells to stimulate angiogenesis.11 Studies investigating the role of BMPs in fracture healing in animals have shown a variety of osteogenic effects, temporal expressions, and mitogenic capacities.9,12,16 In humans, Riedel and ValentinOpran were the first to report preliminary results from the use of BMP-2 to augment the treatment of open tibial fractures.17 Later, the use of recombinant (rh) BMP-2 was investigated in the treatment of open tibial fractures,18 and a faster and higher union rate in the group of patients treated with rhBMP-2 was reported. Another member of the BMP family, BMP-7, has also been introduced in clinical
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IL-1, IL-6 TNF-α PDGF TGF-β1 TGF-β2 TGF-β3 GDF-8 BMP-2 BMP-3,8 *BMP-4 *BMP-7
GDF-10 BMP-5,6 GDF-5 Angiopoietin 1 VEGFs IGF-I IGF-II IGFs Fracture
Day 1
Day 3
Day 7
Day 14
Day 21
Bone Remodelling
Figure 1 Schematic summary of the temporal expression patterns of the signalling molecules during fracture healing (the dashed line represents a difference of opinion amongst scientists in terms of the timing of expression).
practice. In 1999, Greesink et al.19 in a prospective, randomized double-blind study in 24 patients undergoing high tibial osteotomy, evaluating the use of BMP-7 (or human recombinant osteogenic protein [OP-1]) showed the high osteogenic activity of BMP-7 in a validated critically sized human defect. Similarly, Friedlaender et al.20 in a large prospective randomized study, assessed the efficacy of rhBMP-7 over iliac crest bone graft in the treatment of 122 patients with 124 tibial non-unions. The authors concluded that BMP-7 was a safe and effective alternative to bone graft in the treatment of tibial non-unions.
The role of transforming growth factor beta It is well documented that transforming growth factor beta (TGF-b) stimulates the formation of new bone both in vitro and in vivo.21–23 Five isoforms of TGF-b have been isolated.24 Transforming growth factor beta one (TGF-b1) affects osteogenesis and chondrogenesis by stimulating different cell types and plays an important role in repair and remodelling of mesenchymal tissue.25 Recently, it has been suggested that TGF-b2 and possibly TGF-b3 may play more important roles in fracture healing than TGF-b1, as their expression peaks during chondrogenesis.9 It is believed that TGF-b acts as a potent chemotactic stimulator of mesenchymal stem cells (MSCs) and additionally stimulates proliferation of MSCs, pre-osteoblasts, chondrocytes and osteoblasts.26 Its main role is thought to be
during chondrogenesis and endochondral bone formation (Table 2).27,28 Additionally, TGF-b might initiate signalling for synthesis of BMPs, thus indirectly promoting the fracture healing process.16
The role of the platelet-derived growth factor (PDGF) Platelet-derived growth factor is a homo- or hetero-dimeric protein composed of the A- and B-polypeptide chain (PDGFAA, PDGF-BB, and PDGF-AB forms).29 There are two different receptors: the ‘a’ receptor binds all three dimeric forms equipotentially, whereas the ‘b’ receptor binds PDGFBB with the highest affinity.30 PDGF is reported to be an essential factor in bone repair inducing new bone formation in vivo.31 PDGF is released by platelets during the early phases of fracture healing and it is a potent chemotactic stimulator for inflammatory cells and a major proliferative and migratory stimulus for MSCs and osteoblasts (Figure 1).26 Although it is established that bone cells produce and respond to PDGF, its roles in fracture repair have not been fully defined. Nash et al.32 showed an increased callus density and volume in tibial osteotomies in rabbits treated with PDGF. In another animal study, Fujji et al.33 suggested that PDGF contributed in part to the promotion of the chondrogenic and osteogenic changes of mesenchymal cells from the early to the mid-phase of fracture healing. Consequently, recruitment of mesenchymal cells in the initial step and interaction between osteoclasts and
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Table 2 Temporal and functional characteristics of members of the TGF-beta superfamily observed during fracture healing in animal models. Member of Time of expression the TGF-b superfamily
Specific responses in vivo and in vitro
GDF-8
Restricted to day 19
Potential function as a negative regulator of skeletal muscle growth
BMP-2
Day 1 to day 219,12 (the earliest gene to be induced and second elevation during osteogenesis)
Recruitment of mesenchymal cells Chondrogenesis May initiate the fracture healing cascade and regulate the expression of other BMPs BMP-2, 6, 9 may be the most potent to induce osteoblast lineage-specific differentiation of MSCs
BMP-3, 8
Temporal data Day 14 to day 219 (restricted expression suggest a role in the during osteogenesis) regulation of osteogenesis
BMP-4
Transient increased expression in the surrounding soft tissues 6 h to day 516 Day 14 to day 219
Involvement in the formation of callus at a very early stage in the healing process In vitro: BMP-3 and 4 stimulate the migration of human blood monocytes
Through out fracture healing12 BMP-7
Day 14 to day 219
GDF-10
Day 3 to day 219
Regulatory role in both types of ossification BMP-6 may initiate chondrocyte maturation
Day 7 (maximal) to day 149 (restricted expression during chondrogenic phase)
GDF-5 an exclusive involvement in chondrogenesis is suggested
Regulatory role in both types of ossification From the early stages In vitro: Stimulation of fracture healing16 of relative mature osteoblasts
BMP-5, 6
GDF-5, 1
Table 2 (continued ) Member of Time of expression the TGF-b superfamily
Specific responses in vivo and in vitro
GDF-1 at extremely low levels
Stimulation of mesenchymal aggregation and induction of angiogenesis through chemotaxis of endothelial cells and degradation of matrix proteins
GDF-3 GDF-6, 9
No detectable levels within the fracture callus9
TGF-b1
Day 1 to day 219
TGF-b2 TGF-b3
Day 3 to day 149 Day 3 to day 219
GDF-6 may be expressed only in articular cartilage and with GDF-5, 7 more efficiently induce cartilage and tendon-like structures in vivo Potent chemotactic for bone forming cells and macrophages Proliferation of undifferentiated mesenchymal and osteoprogenitor cells, osteoblasts, chondrocytes
osteoblasts in the bone remodelling phase might be stimulated by the mediation of PDGF. Nevertheless, at the present time, the exact therapeutic potential of PDGF remains unclear.
The role of the fibroblast growth factors (FGFs) Fibroblast growth factors are present in significant amounts in bone and several studies have suggested that they may be involved in normal fracture healing.34 The family of FGFs consists of nine structurally related polypeptides. The acidic and basic FGFs are the most abundant FGFs in normal adult tissue.35 Investigators have found that during normal fracture repair bFGF is expressed in the cells of the expanded cambial layer and is associated with a rapid increase in the population of fibroblast-like mesenchymal cells.36 In a rat model, multiple local injections of aFGF to a fractured femur resulted in an increase in the cartilage portion of the forming callus.37 Similarly, in a canine tibial osteotomy model, a single injection of b-FGF was associated with an early increase in callus size.38 When one application of bFGF was delivered in a fibrin gel, it increased the callus size, mineral content, and mechanical strength in fractured fibulae in normal rats and in those with diabetes,39 and similar effects were observed on intraosseous bone formation after a single injection of bFGF into the femurs of
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Table 3 Timing of cellular events and expression of signalling molecules during murine fracture healing.20,33,43
Cytokines: IL-1, IL-6, Day Haematoma 1 formation, TNF-a released by inflammation inflammatory cells Recruitment of PDGF, TFG-beta mesenchymal cells released from Osteogenic degranulating differentiation of MSCs platelets BMP-2 expression and from bone marrow restricted to day 1 expression of GDF-8 Day MSCs proliferation begins 3 Proliferation and differentiation of preosteoblasts and osteoblasts in regions of intramembranous ossification Angiogenesis begins
Decline of cytokines
Day Peak of cell proliferation in 7 intramembranous ossification between day 7 and 10 Chondrogenesis and endochondral ossification begins (day 9–14 maturation of chondrocytes)
Peak of TGF-b2 and
Day Cessation of cell 14 proliferation in intramembranous ossification, but osteoblastic activity continues Mineralization of the soft callus, cartilage resorption, and woven bone formation Neo-angiogenesis which infiltrates along new mesenchymal cells Phase of most active osteogenesis until day 21
Decreased levels of
levels
Expression of TGF-b2, -b3, GDF-10, BMP-5, 6
Angiopoietin-1 is induced
TGF-b3 expression
Expression of GDF-5 and probably GDF-1
expression for TGF-b2, GDF-5, and probably GDF-1 Expression of BMP-3, 4, 7, and 8 VEGFs expression Second increase of IL-1 and TNF-a which continues during bone remodeling
Decreased expression Day Woven bone 21 remodelled and of TGF-b1 and TGF-b3, subsequently replaced GDF-10, and BMPs by lamellar bone (2–8)
normal rabbits and into rabbits that had been ovariectomized.40 The role of the insulin-like growth factors The sources of IGF-I (or somatomedin-C) and IGF-II (or skeletal growth factor) are the bone matrix, endothelial cells, osteoblasts and chondrocytes. IGF-I is a 7.6-kDa polypeptide that produces in conjunction with the type 1 IGF receptor (IGF1R) a potent proliferative signalling system, which stimulates growth in various cell types and blocks apoptosis. In vitro, it mediates stimulatory effects on osteoblast activity and chemotaxis.41,42 IGF-II acts at a later stage of endochondral bone formation and stimulates type I collagen production, cartilage matrix synthesis, and cellular proliferation (Figure 1).43 In vivo results on new bone formation using IGF-I have been quite disparate. The continuous infusion of IGF-I in rats with a femoral osteotomy did not enhance fracture healing, and the callus weight in the IGF-I treated animals was even slightly reduced compared to the untreated controls.44,45 Conversely, new bone was formed upon subcutaneous administration in rats leading to a full bridging of 8-mm calvarial defects within 8 weeks.46,47 The variation of the findings of studies assessing the influence of IGF on skeletal repair indicates the need of further studies regarding this agent.27 The role of growth differentiation factors (GDFs) Bone morphogenic protein-14 (BMP-14), also known as growth and differentiation factor-5 (GDF-5) and cartilage derived morphogenetic protein-1 (CDMP-1), is best known for its role in joint formation and tendon healing but has recently been shown to influence endochondral bone growth.48 Its involvement in fracture repair was shown in GDF-5 deficient mice, which showed a delay in fracture repair. This delay was probably related to impaired cellular recruitment and chondrocyte differentiation during the early stages of the repair process.48 Spiro et al.49 performed spinal fusions in rabbits using GDF-5 in three different collagen matrices. They found no significant difference between autograft and at least two of the formulations of GDF-5 with fusion rates as high as 80% for the mineralized collagen strips containing 1 mg/cm3 of rhGDF-5. These results suggest that this molecule has potential as a supplement in fracture repair but at the moment, there are no human studies supporting its clinical use. Metalloproteinases and angiogenic factors During endochondral bone repair, as with embryonic bone development, there is an intimate coordination between the resolution of chondrogenic events with the programmed death of chondrocytes and the initiation of bone formation. Central to this transition is the removal of the cartilage and its matrix in coordination with the ingrowth of new vasculature to support new bone formation.7 During this remodelling phase, specific matrix metallopoteinases (MMPs) degrade cartilage and bone, allowing the invasion of blood vessels (Table 1).4 Recent studies have demonstrated the requirement specifically for MMP-9 in the embryonic growth plate, as well as in fracture repair. In an animal study, mice with targeted deletions of MMP-9 displayed impaired revascularization and hypertrophic
ARTICLE IN PRESS Pathways and signalling molecules chondrocyte apoptosis. At the fracture site in these mice, there were larger amounts of cartilaginous callus, delayed degradation of cartilage matrix, and non-unions.50 Similarly, Takahara et al.51 showed that MMP-9 positive cells cooperated with vascular endothelial cells in cartilage angiogenesis in an animal model studying the vascular and cellular invasion in endochondral ossification in long bones. A further association between MMP activity and concurrent angiogenic events is demonstrated by the observation that the healing of fractures in MMP-9 deficient mice can be rescued with recombinant vascular-endothelial growth factor (VEGF) treatment.50 VEGF has been demonstrated to be required for both normal bone formation and repair.52 Street et al. showed that fracture repair was enhanced by the exogenous administration of VEGF.53 Additionally, VEGF appears to have direct effects on osteogenic cell differentiation independent of its angiogenic influences and VEGF bioavailability during fracture repair may be dependent on local MMP activity.7 However, VEGF contribution in bone repair has yet to be clarified.
Systematic agents promoting fracture healing Parathyroid hormone (PTH) Parathyroid hormone is involved in regulating serum calcium and in bone remodelling. Continuous exposure of the skeleton to PTH has resulted in increased bone turnover and a decrease in bone mass, mainly due to the catabolic effect of PTH through the direct activation of osteoblasts. Nevertheless, recent studies have found that intermittent exposure to PTH can have anabolic effects.54 Interestingly, PTH administration enhanced bone remodelling in the early stages of fracture healing in parathyroidectomized rats.55 Similarly, in experiments with rats, Andreassen et al. showed that administration of a high dose of PTH increased tibial fracture callus volume and ultimate load strength by 75% and 99%, respectively, after 20 days.56 Other animal studies have also confirmed fracture healing enhancement through the use of recombinant human parathyroid hormone (PTH 1–34).57,58 At the moment, PTH has been approved in several countries for treating postmenopausal osteoporosis, with good results.59 Clinical trials to test the efficacy of PTH for enhancing skeletal repair are currently underway. Growth hormone (GH) As early as 1959, it had been proposed that growth hormone has positive effects in fracture healing.60 Since then several studies have shown conflicting results.61,62 Growth hormone is a systemic hormone and its effect on the skeleton is mediated by IGF-1 (known as somatomedin-C), which promotes bone matrix formation (type I collagen and noncollagenous matrix proteins) by fully differentiated osteoblasts.3 In a recent study, Raschke et al.63 looked at recombinant porcine growth hormone (r-pGH) in the repair of experimentally induced tibial fractures in pigs. The investigators found that the treated animals had a significant increase in bone mineral content while no difference was seen in bone mineral density, in comparison with the control group treated with normal saline. Additionally, the strength of the fracture callus was significantly greater in the animals treated with r-pGH. In another study, in a
255 fracture healing and distraction osteogenesis model in pigs, administration of homologous recombinant porcine GH led to an increase in serum IGF-1, stimulation of fracture healing and acceleration of ossification of bone regenerate in distraction osteogenesis.64 HMG-CoA reductase inhibitors There is evidence that HMG-CoA reductase inhibitors (statins) can affect bone mineral density in humans and reduce the risk of fracture,65,66 HMG-CoA reductase inhibitors are lipid-lowering drugs that inhibit cholesterol synthesis by blocking mevalonic acid production. Skoglund et al. tested Simvastatin in a mouse model of femur fracture.67 This study showed that at day 14, the mechanical strength of the Simvastatin group was 63% greater than in the control mice and the callus was 53% larger. Nevertheless, at day 21, this increase did not continue. It seems that statins enhance osteoblast activity through increased expression of BMP-2, nevertheless there are not enough data at the moment to support the use of this drug category for fracture healing enhancement.
Most recent advances and future directions Gene therapy Gene therapy involves the transfer of genetic material into a targeted cell’s genome, thus allowing the expression of bioactive factors from the cell itself for long periods of time. The gene transfer can be performed using a viral (transfection) or a non-viral (transduction) vector, by either an in vivo or ex vivo gene-transfer strategy.68 Gene therapy has been used to promote fracture repair through the expression of BMP-2 and BMP-4 in animal studies.69,70 For example, Lieberman et al.69 devised a delivery system using BMP-2 and bone marrow cells. They implanted the transfected cells into critical sized defects in rat femora and compared bone regeneration at 2 months with rhBMP-2 or vehicle-treated bone marrow cells. Results showed that each of the defects treated with BMP-2 transfected bone marrow cells and rhBMP had healed radiographically, while control animals had failed to heal. Although promising, issues of its biosafety and efficacy need to be answered before gene therapy application in humans takes place.
Muscle derived stem cells (MDSC) Muscle derived stem cells have the ability to differentiate into multiple lineages, including osteogenic and haematopoietic lines.71 These muscle-based progenitor cells possess a therapeutic potential for tissue repair and regeneration applications in various musculoskeletal as well as cardiac muscle disorders, either as a source of inducible progenitor cells or as gene delivery vehicles. Peng et al.72 used MDSCs to study the effects of VEGF in BMP-4 induced bone regeneration. MDSCs were transfected with either BMP-4 or VEGF. The investigators then impregnated Gelfoam disks with cells expressing BMP-4 alone or cells expressing both BMP-4 and VEGF. The disks were then placed in cortical defects in the parietal bones of mice. The results showed that with the addition of VEGF, there was a significant
ARTICLE IN PRESS 256 increase in the density of the bone formed. In a more recent study the same investigators used MDSCs that were transfected with noggin, a specific BMP antagonist, to regulate the bone formation induced by locally implanted BMP-4. In this way, they were able to control the amount of bone formed reducing thus the heterotropic or overabundant bone formation otherwise seen with unopposed BMP-4 transfection.73
Conclusions Our knowledge regarding fracture healing has significantly improved following increased understanding of the multiple and complex molecular pathways involved, and is expected to improve further in the near future. These advances may potentially facilitate the development of drugs or techniques to accelerate repair, heal non-unions, and prevent delayed unions. Nevertheless, whilst intensive research is conducted in the laboratories, more well designed clinical trials are needed to investigate the efficacy and most importantly the safety of the new treatment methods. The molecular understanding of fracture healing extends beyond fracture repair to organogenesis and differentiation during embryonic development. It is of great importance to identify the molecular signalling of these events in order to predict and potentially to treat musculoskeletal and other related connective disorders at the embryonic stage.
References 1. McKibbin B. The biology of fracture healing in long bones. J Bone Joint Surg Br 1978;60-B(2):150–62. 2. Einhorn TA. The cell and molecular biology of fracture healing. Clin Orthop Relat Res 1998;355(Suppl.):S7–S21. 3. Dimitriou R, Tsiridis E, Giannoudis PV. Current concepts of molecular aspects of bone healing. Injury 2005;36(12): 1392–404. 4. Gerstenfeld LC, et al. Fracture healing as a post-natal developmental process: molecular, spatial, and temporal aspects of its regulation. J Cell Biochem 2003;88(5):873–84. 5. Kon T, et al. Expression of osteoprotegerin, receptor activator of NF-kappaB ligand (osteoprotegerin ligand) and related proinflammatory cytokines during fracture healing. J Bone Miner Res 2001;16(6):1004–14. 6. Einhorn TA, et al. The expression of cytokine activity by fracture callus. J Bone Miner Res 1995;10(8):1272–81. 7. Lehmann W, et al. Tumor necrosis factor alpha (TNF-alpha) coordinately regulates the expression of specific matrix metalloproteinases (MMPS) and angiogenic factors during fracture healing. Bone 2005;36(2):300–10. 8. ten Dijke P, et al. Signal transduction of bone morphogenetic proteins in osteoblast differentiation. J Bone Joint Surg Am 2003;85-A(Suppl. 3):34–8. 9. Cho TJ, Gerstenfeld LC, Einhorn TA. Differential temporal expression of members of the transforming growth factor beta superfamily during murine fracture healing. J Bone Miner Res 2002;17(3):513–20. 10. Sakou T. Bone morphogenetic proteins: from basic studies to clinical approaches. Bone 1998;22(6):591–603. 11. Valdimarsdottir G, et al. Stimulation of Id1 expression by bone morphogenetic protein is sufficient and necessary for bone morphogenetic protein-induced activation of endothelial cells. Circulation 2002;106(17):2263–70.
V.S. Nikolaou, E. Tsiridis 12. Bostrom MP, et al. Immunolocalization and expression of bone morphogenetic proteins 2 and 4 in fracture healing. J Orthop Res 1995;13(3):357–67. 13. Urist MR. Bone: formation by autoinduction. Science 1965; 150(698):893–9. 14. Cheng H, et al. Osteogenic activity of the fourteen types of human bone morphogenetic proteins (BMPs). J Bone Joint Surg Am 2003;85-A(8):1544–52. 15. Deckers MM, et al. Bone morphogenetic proteins stimulate angiogenesis through osteoblast-derived vascular endothelial growth factor A. Endocrinology 2002;143(4):1545–53. 16. Bostrom MP. Expression of bone morphogenetic proteins in fracture healing. Clin Orthop Relat Res 1998;355(Suppl.): S116–23. 17. Riedel GE, Valentin-Opran A. Clinical evaluation of rhBMP-2/ ACS in orthopedic trauma: a progress report. Orthopedics 1999;22(7):663–5. 18. Govender S, et al. Recombinant human bone morphogenetic protein-2 for treatment of open tibial fractures: a prospective, controlled, randomized study of four hundred and fifty patients. J Bone Joint Surg Am 2002;84-A(12):2123–34. 19. Geesink RG, Hoefnagels NH, Bulstra SK. Osteogenic activity of OP-1 bone morphogenetic protein (BMP-7) in a human fibular defect. J Bone Joint Surg Br 1999;81(4):710–8. 20. Friedlaender GE, et al. Osteogenic protein-1 (bone morphogenetic protein-7) in the treatment of tibial nonunions. J Bone Joint Surg Am 2001;83-A(Suppl. 1 (Pt 2)):S151–8. 21. Kekow J, Gross WL. Transforming growth factor beta: its mechanism of action and clinical significance. Dtsch Med Wochenschr 1992;117(6):228–35. 22. Sumner DR, et al. Enhancement of bone ingrowth by transforming growth factor-beta. J Bone Joint Surg Am 1995;77(8): 1135–47. 23. Baylink DJ, Finkelman RD, Mohan S. Growth factors to stimulate bone formation. J Bone Miner Res 1993;8(Suppl. 2):S565–72. 24. Kingsley DM. The TGF-beta superfamily: new members, new receptors, and new genetic tests of function in different organisms. Genes Dev 1994;8(2):133–46. 25. Cornell CN, Lane JM. Newest factors in fracture healing. Clin Orthop Relat Res 1992(277):297–311. 26. Lieberman JR, Daluiski A, Einhorn TA. The role of growth factors in the repair of bone. Biology and clinical applications. J Bone Joint Surg Am 2002;84-A(6):1032–44. 27. Barnes GL, et al. Growth factor regulation of fracture repair. J Bone Miner Res 1999;14(11):1805–15. 28. Joyce ME, Jingushi S, Bolander ME. Transforming growth factorbeta in the regulation of fracture repair. Orthop Clin North Am 1990;21(1):199–209. 29. Heldin CH, Westermark B. PDGF-like growth factors in autocrine stimulation of growth. J Cell Physiol Suppl 1987(Suppl. 5):31–4. 30. Hart CE, Bowen-Pope DF. Platelet-derived growth factor receptor: current views of the two-subunit model. J Invest Dermatol 1990;94(6 Suppl.):53S–7S. 31. Bolander ME. Regulation of fracture repair by growth factors. Proc Soc Exp Biol Med 1992;200(2):165–70. 32. Nash TJ, et al. Effect of platelet-derived growth factor on tibial osteotomies in rabbits. Bone 1994;15(2):203–8. 33. Fujii H, et al. Expression of platelet-derived growth factor proteins and their receptor alpha and beta mRNAs during fracture healing in the normal mouse. Histochem Cell Biol 1999;112(2):131–8. 34. Radomsky ML, et al. Potential role of fibroblast growth factor in enhancement of fracture healing. Clin Orthop Relat Res 1998(355 Suppl.):S283–93. 35. Wang JS. Basic fibroblast growth factor for stimulation of bone formation in osteoinductive or conductive implants. Acta Orthop Scand Suppl 1996;269:1–33.
ARTICLE IN PRESS Pathways and signalling molecules 36. Bourque WT, Gross M, Hall BK. Expression of four growth factors during fracture repair. Int J Dev Biol 1993;37(4):573–9. 37. Jingushi S, et al. Acidic fibroblast growth factor (aFGF) injection stimulates cartilage enlargement and inhibits cartilage gene expression in rat fracture healing. J Orthop Res 1990; 8(3):364–71. 38. Nakamura T, et al. Recombinant human basic fibroblast growth factor accelerates fracture healing by enhancing callus remodeling in experimental dog tibial fracture. J Bone Miner Res 1998;13(6):942–9. 39. Kawaguchi H, et al. Stimulation of fracture repair by recombinant human basic fibroblast growth factor in normal and streptozotocin-diabetic rats. Endocrinology 1994;135(2): 774–81. 40. Nakamura K, et al. Stimulation of bone formation by intraosseous application of recombinant basic fibroblast growth factor in normal and ovariectomized rabbits. J Orthop Res 1997; 15(2):307–13. 41. Ernst M, Froesch ER. Growth hormone dependent stimulation of osteoblast-like cells in serum-free cultures via local synthesis of insulin-like growth factor I. Biochem Biophys Res Commun 1988;151(1):142–7. 42. Panagakos FS. Insulin-like growth factors-I and -II stimulate chemotaxis of osteoblasts isolated from fetal rat calvaria. Biochimie 1993;75(11):991–4. 43. Prisell PT, et al. Expression of insulin-like growth factors during bone induction in rat. Calcif Tissue Int 1993;53(3):201–5. 44. Aspenberg P, Albrektsson T, Thorngren KG. Local application of growth-factor IGF-1 to healing bone. Experiments with a titanium chamber in rabbits. Acta Orthop Scand 1989;60(5): 607–10. 45. Kirkeby OJ, Ekeland A. No effects of local somatomedin C on bone repair. Continuous infusion in rats. Acta Orthop Scand 1992;63(4):447–50. 46. Thaller SR, Dart A, Tesluk H. The effects of insulin-like growth factor-1 on critical-size calvarial defects in Sprague–Dawley rats. Ann Plast Surg 1993;31(5):429–33. 47. Thaller SR, et al. Effect of insulin-like growth factor-1 on zygomatic arch bone regeneration: a preliminary histological and histometric study. Ann Plast Surg 1993;31(5):421–8. 48. Chhabra A, et al. BMP-14 deficiency inhibits long bone fracture healing: a biochemical, histologic, and radiographic assessment. J Orthop Trauma 2005;19(9):629–34. 49. Spiro RC, Thompson AY, Poser JW. Spinal fusion with recombinant human growth and differentiation factor-5 combined with a mineralized collagen matrix. Anat Rec 2001;263(4):388–95. 50. Vu TH, et al. MMP-9/gelatinase B is a key regulator of growth plate angiogenesis and apoptosis of hypertrophic chondrocytes. Cell 1998;93(3):411–22. 51. Takahara M, et al. Matrix metalloproteinase-9 expression, tartrate-resistant acid phosphatase activity, and DNA fragmentation in vascular and cellular invasion into cartilage preceding primary endochondral ossification in long bones. J Orthop Res 2004;22(5):1050–7. 52. Gerber HP, et al. VEGF couples hypertrophic cartilage remodeling, ossification and angiogenesis during endochondral bone formation. Nat Med 1999;5(6):623–8. 53. Street J, et al. Vascular endothelial growth factor stimulates bone repair by promoting angiogenesis and bone turnover. Proc Natl Acad Sci USA 2002;99(15):9656–61.
257 54. Komarova SV. Mathematical model of paracrine interactions between osteoclasts and osteoblasts predicts anabolic action of parathyroid hormone on bone. Endocrinology 2005;146(8): 3589–95. 55. Fukuhara H, Mizuno K. The influence of parathyroid hormone on the process of fracture healing. Nippon Seikeigeka Gakkai Zasshi 1989;63(1):100–15. 56. Andreassen TT, Ejersted C, Oxlund H. Intermittent parathyroid hormone (1–34) treatment increases callus formation and mechanical strength of healing rat fractures. J Bone Miner Res 1999;14(6):960–8. 57. Alkhiary YM, et al. Enhancement of experimental fracturehealing by systemic administration of recombinant human parathyroid hormone (PTH 1–34). J Bone Joint Surg Am 2005; 87(4):731–41. 58. Nakajima A, et al. Mechanisms for the enhancement of fracture healing in rats treated with intermittent low-dose human parathyroid hormone (1–34). J Bone Miner Res 2002;17(11): 2038–47. 59. Neer RM, et al. Effect of parathyroid hormone (1–34) on fractures and bone mineral density in postmenopausal women with osteoporosis. N Engl J Med 2001;344(19):1434–41. 60. Koskinen EV. The repair of experimental fractures under the action of growth hormone, thyrotropin and cortisone. A tissue analytic, roentgenologic and autoradiographic study. Ann Chir Gynaecol Fenn Suppl 1959;48(90):1–48. 61. Bak B, Jorgensen PH, Andreassen TT. Increased mechanical strength of healing rat tibial fractures treated with biosynthetic human growth hormone. Bone 1990;11(4):233–9. 62. Carpenter JE, et al. Failure of growth hormone to alter the biomechanics of fracture-healing in a rabbit model. J Bone Joint Surg Am 1992;74(3):359–67. 63. Raschke M, et al. Homologous growth hormone accelerates healing of segmental bone defects. Bone 2001;29(4):368–73. 64. Bail HJ, et al. Systemic application of growth hormone for enhancement of secondary and intramembranous fracture healing. Horm Res 2002;58(Suppl. 3):39–42. 65. Meier CR, et al. HMG-CoA reductase inhibitors and the risk of fractures. JAMA 2000;283(24):3205–10. 66. Wang PS, et al. HMG-CoA reductase inhibitors and the risk of hip fractures in elderly patients. JAMA 2000;283(24):3211–6. 67. Skoglund B, Forslund C, Aspenberg P. Simvastatin improves fracture healing in mice. J Bone Miner Res 2002;17(11):2004–8. 68. Chen Y. Orthopedic applications of gene therapy. J Orthop Sci 2001;6(2):199–207. 69. Lieberman JR, et al. The effect of regional gene therapy with bone morphogenetic protein-2-producing bone-marrow cells on the repair of segmental femoral defects in rats. J Bone Joint Surg Am 1999;81(7):905–17. 70. Shen HC, et al. Structural and functional healing of critical-size segmental bone defects by transduced muscle-derived cells expressing BMP4. J Gene Med 2004;6(9):984–91. 71. Deasy BM, Li Y, Huard J. Tissue engineering with muscle-derived stem cells. Curr Opin Biotechnol 2004;15(5):419–23. 72. Peng H, et al. Synergistic enhancement of bone formation and healing by stem cell-expressed VEGF and bone morphogenetic protein-4. J Clin Invest 2002;110(6):751–9. 73. Peng H, et al. Noggin improves bone healing elicited by muscle stem cells expressing inducible BMP4. Mol Ther 2005;12(2): 239–46.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 258–261
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MINI-SYMPOSIUM: FRACTURE HEALING
(ii) Factors contributing to non-union of fractures Venkatachalapathy Perumal, Craig S. Roberts Department of Orthopaedic Surgery, University of Louisville School of Medicine, 210 East Gray Street, Suite 1003, Louisville, KY 40202, USA
KEYWORDS Non-union; Local factors; Systemic factors
Summary Non-union of a fracture can be caused by various factors. This review summarizes current concepts of systemic conditions (malnutrition, diabetes, nicotine usage, osteoporosis and non-steroidal anti-inflammatory drugs (NSAIDs) usage) and local factors (infection, vascularity, biomechanical instability, poor bone contact, iatrogenic factors and magnitude of injury) that may be of etiological relevance. Key points for assessing non-unions include checking for malnutrition and peripheral neuropathy, advising smoking cessation, avoiding NSAIDs, and identifying clinical and radiological signs of delayed healing at the earliest possible instance. The prevention of non-union is preferable to the treatment of nonunion. & 2007 Elsevier Ltd. All rights reserved.
Introduction There is no universal definition of fracture non-union. The traditionally generally accepted definition is of an interval of at least 9 months from the time of fracture without fracture healing, during which multiple therapeutic measures have been tried. Waiting the traditional 9 months to diagnose a non-union is unrealistic and is associated with prolonged morbidity, inability to return to work, narcotic dependence and emotional impairment. Non-union of fractures is a multifactorial phenomenon. This review summarises current concepts and understanding of factors which contribute to the non-union of fractures. We review systemic conditions (malnutrition, diabetes, nicotine usage, Corresponding author. Tel.: +1 502 852 6964; fax: +1 502 852 7227. E-mail addresses:
[email protected] (V. Perumal),
[email protected] (C.S. Roberts).
0268-0890/$ - see front matter & 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2007.06.004
osteoporosis and nonsteroidal anti-inflammatory drug (NSAID) usage) and local factors (infection, vascularity, biomechanical instability, poor bone contact, iatrogenic factors and magnitude of injury) (Table 1).
Systemic medical conditions Malnutrition and vitamin deficiency Patients with long bone fractures have increased rates of catabolism and significant urinary protein loss that may lead to negative nitrogen balance. Protein malnutrition affects callus composition rather than size early in the process of fracture healing.1 Histological and mechanical testing shows that malnutrition negatively affects early callus composition.1 Guarniero et al.2 also showed the beneficial effects of protein nutritional support on the healing of long bone fractures. Protein malnutrition affects both membranous and endochondral bone formation. Protein deficiency has
ARTICLE IN PRESS Factors contributing to non-union of fractures
Table 1
Etiology of non-union.
Local causes
Systemic causes
Infection
Malnutrition and vitamin deficiency Systemic medical conditions Smoking Metabolic bone disorders Medications
Mechanical instability Inadequate vascularity Poor bone contact Iatrogenic Magnitude of injury
a negative effect on early proliferation and differentiation events of those cells required for fracture repair. Vitamin B6 deficiency causes changes in bone which causes imbalance in the coupling between osteoblasts and osteoclasts, as a result of marked diminution of Glucose-6 phosphate deficiency (G6PD) activity in the periosteal region of the bone formation and in the developing callus, which significantly delays the maturation of the callus and union.3 This suggests vitamin B6 status may be important in fracture healing deficiency.
Diabetes Perlman and Thordarson4 studied 88 patients with ankle fusions and showed a 28% non-union rate in patients who had diabetes. Sensory neuropathy was implicated as a possible cause of non-union. Morgan et al.5 reported a 95% arthrodesis rate and failed to obtain fusion only in those patients noted preoperatively to have a neuropathy. Frey et al.6 also concluded that diabetes contributed to non-union of ankle fusions.
Cigarette smoking and nicotine usage Although some studies show no clear association between smoking and bone mass, there is overwhelming evidence of an increased incidence of osteoporosis and osteoporotic fractures in patients who smoke cigarettes. There is a 5–10% bone density deficit in patients who smoked compared with patients who were non-smokers. Human studies of the effect of smoking on bone healing focuses on spinal fusion. Brown et al.7 found a 40% pseudarthrosis rate in patients who smoked and an 8% pseudarthrosis rate in those who did not smoke. The difference was attributed to a mean peripheral oxygen saturation of 78.5% in the individuals who smoked versus a mean peripheral oxygen saturation of 92.9% in those who did not smoke. Schmitz et al.,8 in their study with a follow-up of 146 patients with closed and grade I open tibial fractures, showed a 69% delay in radiographic union in the group of individuals who smoked. In a double-blind, prospective randomized study using a rabbit model, Wing et al.9 demonstrated that chronic nicotine exposure was associated with decreased spinal fusion rates. Discontinuing smoking before surgery improved fusion rates. McKee et al.10 showed a higher rate of non-union in smokers who underwent Ilizarov limb reconstruction. Chen et al.11 reported that 30%
259 of patients who smoked had delayed union or non-union after ulnar shortening osteotomy. Nicotine inhibits alkaline phosphatase and collagen production and stimulates deoxyribonucleic acid synthesis, possibly secondary to increased cell death and turn over. Cigarette smoking has been shown to decrease collagen deposition by 30–50%. Feitelson et al.12 showed that 2 weeks of nicotine treatment caused decreased bone blood flow.
Osteoporosis The relationship between fracture healing and osteoporosis is complex, and the available clinical evidence is inconclusive. Animal research on oophorectomized rats has shown significant reductions in bone mass and delay in fracture healing. Available evidence suggests that altered bone metabolism in osteoporosis seems to delay callus maturation and decelerate fracture healing.13
Nonsteroidal anti-inflammatory drugs NSAIDs inhibit osteogenic activity and fracture healing. Glassman et al.,14 in a retrospective review of 228 patients who underwent instrumented spinal fusion, reported an odds ratio with a five-fold increased chance of non-union with NSAIDs. The pathogenesis of NSAID-inhibiting osteogenesis is not clearly understood. Animal studies show reversibility of NSAID effects when prostaglandin E2 levels are gradually restored after short-term treatment.15 Late exposure to NSAIDs, 61–90 days after a humeral shaft fracture, was associated with non-union.16 There is a correlation between the use of NSAIDs and non-union, especially when NSAIDs are used for more than 4 weeks.17 In this series, 70% of patients with non-union had taken NSAIDs. Although all NSAIDs inhibit fracture healing, cyclooxygenase-2 (Cox-2 inhibitors) have been shown to inhibit fracture healing more than the less specific NSAIDs.15 Current evidence suggests that avoidance of NSAIDs in the post-operative and post-injury period may prevent nonunions.
Local factors Infection Although bone infection does not cause non-union per se, it can contribute to fracture non-union through bone death because of pus, the creation of gaps by osteolytic infectious granulation tissue, and motion from loosening of prosthetic implants. The inflammatory response to bacteria at the site of the fracture disrupts callus, increases gaps between fragments, and increases motion between fragments, which cause fracture union to fail. Infection causes decreased bone quality, which can cause fixation devices to loosen, thereby causing non-union.
Inadequate vascularity The extent of vascular damage is directly correlated with failure of skeletal repair. However, the exact mechanisms
ARTICLE IN PRESS 260 underlying ischemia-related effects on bone healing are not well understood. Lu et al.,18 in an animal study, found that ischemia at the fracture site decreased the amount of bone formation. Reed et al.19 demonstrated that the number of blood vessels in atrophic non-unions was significantly fewer than in a normal healing group, and concluded that early diminished vascularity may prevent fractures from uniting. Insufficient vascularity is one of the potential causes of nonunion, and in particular diminished vascularity in the interfragmentary gap in the first 3 weeks after fracture may prevent fracture union. Loss of blood supply occurs in open fractures as a result of the loss of the soft tissue envelope and damage to nutrient vessels. Karladani et al.20 showed that the risk of developing non-union was higher in patients with open fractures than those with closed fractures. The rate of non-union in type III open tibial fractures was 20–30%.
Biomechanical instability The stability of fracture fixation and the resulting mechanical conditions existing at the fracture site influence fracture repair. The size of the fracture callus is a function of both the magnitude and frequency of interfragmentary motion. Differentiation of mesenchymal cells towards either an osteoblast or chondrogenic cell line is dependent on fracture stability. Epari et al.21 showed that less rigid fixation increased the time required for the healing of fractures. Lienau et al.22 also showed initial mechanical stability to the fracture led to increased vascularity and tissue differentiation, early callus formation and faster fracture union.
V. Perumal, C.S. Roberts fractures. Fracture distraction more than 3 mm during stabilization of tibial fractures increases four-fold the odds of developing a non-union.24
Magnitude of injury (high versus low energy) The magnitude of energy causing a fracture is a good predictor of fracture healing.20 In a review of 104 tibial shaft fractures, the positive predictive value of high-energy trauma (grade III open fractures) for non-union was 26%, and it was concluded that fractures caused by high-energy trauma are more likely to develop non-union. Displacement of the fracture fragments noted radiographically is also a good indicator of the degree of soft tissue injury. Displacement of the fracture fragments by more than the diameter of the bone, in distraction or translation, will be associated with excessive periosteal stripping, diminished vascularity and thus non-union risk.
Practice points
Check for malnutrition when treating fractures Check for peripheral neuropathy due to diabetes Advise smoking cessation Avoid NSAIDs following fractures Identify clinical and radiological signs of delayed healing of fractures Inform patients of the risk factors of fracture nonunion Non-union of fractures cannot be prevented in all cases
Poor bone contact Bone-to-bone contact is an important requirement for fracture healing. Poor bone-to-bone contact compromises the mechanical stability and creates a defect that the fracture repair process must bridge. Small defects produce high strain at the fracture site.23 Although osteoblasts do not tolerate high-strain environment, such environments can be good for chondroblasts and fibroblasts. Larger defects have low strain and do not promote osteoblastic activity. The amount of strain over the fracture site to produce osteoblastic activity remains unknown. The maximal bridging of a cortical defect through direct osteonal healing is about 1 mm in animal studies. Poor bone-to-bone contact at the fracture site may result from various factors including soft tissue interposition, malposition or malalignment of fracture fragments, bone loss, and distraction of the fracture fragments. As the defect increases in size, the chances of fracture union decrease.
Iatrogenic factors Excessive stripping of the periosteum and damage to the bone and soft tissue blood supply during implant or fixation device insertion can decrease vascularity at the fracture site and contribute to non-union. Intramedullary nailing in distraction of the fracture site increases the gap between the fracture fragments and contributes to non-union of
References 1. Day SM, DeHeer DH. Reversal of the detrimental effects of chronic protein malnutrition on long bone fracture healing. J Orthop Trauma 2001;15(1):47–53. 2. Guarniero R, de Barros Filho TE, Tannuri U, Rodrigues CJ, Rossi JD. Study of fracture healing in protein malnutrition. Rev Paul Med 1992;110(2):63–8. 3. Dodds RA, Catterall A, Bitensky L, Chayen J. Abnormalities in fracture healing induced by vitamin B6-deficiency in rats. Bone 1986;7(6):489–95. 4. Perlman MH, Thordarson DB. Ankle fusion in a high risk population: an assessment of nonunion risk factors. Foot Ankle Int 1999;20(8):491–6. 5. Morgan CD, Henke JA, Bailey RW, Kaufer H. Long-term results of tibiotalar arthrodesis. J Bone Joint Surg Am 1985;67(4):546–60. 6. Frey C, Halikus NM, Vu-Rose T, Ebramzadeh E. A review of ankle arthrodesis: predisposing factors to nonunion. Foot Ankle Int 1994;15(11):581–4. 7. Brown CW, Orme TJ, Richardson HD. The rate of pseudoarthrosis (surgical nonunion) in patients who are smokers and patients who are nonsmokers: a comparison study. Spine 1986;11(9): 942–3. 8. Schmitz MA, Finnegan M, Natarajan R, Champine J. Effect of smoking on tibial shaft fracture healing. Clin Orthop Relat Res 1999;365:184–200. 9. Wing KJ, Fisher C, O’Connell JX, Wing PC. Stopping nicotine exposure before surgery. The effect on spinal fusion in a rabbit model. Spine 2000;25(1):30–4.
ARTICLE IN PRESS Factors contributing to non-union of fractures 10. McKee MD, DiPasquale D, Wild LM, Stephen DJ, Kreder HJ, Schemitsch EH. The effect of smoking on clinical outcome and complication rates following Ilizarov reconstruction. J Orthop Trauma 2003;17(10):663–7. 11. Chen F, Osterman AL, Mahony K. Smoking and bony union after ulna-shortening osteotomy. Am J Orthop 2001;30(6):486–9. 12. Feitelson JB, Rowell PP, Roberts CS, Fleming JT. Two week nicotine treatment selectively increases bone vascular constriction in response to norepinephrine. J Orthop Res 2003; 21(3):497–502. 13. Giannoudis P, Tzioupis C, Almalki T, Buckley R. Fracture healing in osteoporotic fractures: is it really different? A basic science perspective. Injury 2007;38(Suppl. 1):S90–9. 14. Glassman SD, Rose SM, Dimar JR, Puno RM, Campbell MJ, Johnson JR. The effect of postoperative nonsteroidal antiinflammatory drug administration on spinal fusion. Spine 1998; 23(7):834–8. 15. Gerstenfeld LC, Al-Ghawas M, Alkhiary YM, et al. Selective and nonselective cyclooxygenase-2 inhibitors and experimental fracture-healing. Reversibility of effects after short-term treatment. J Bone Joint Surg Am 2007;89(1):114–25. 16. Bhattacharyya T, Levin R, Vrahas MS, Solomon DH. Nonsteroidal anti-inflammatory drugs and nonunion of humeral shaft fractures. Arthritis Rheum 2005;53(3):364–7. 17. Giannoudis PV, MacDonald D, Matthews SJ, Smith RM, Furlong AJ, De Boer P. Nonunion of the femoral diaphysis. The influence
261
18.
19.
20.
21.
22.
23.
24.
of reaming and non-steroidal anti-inflammatory drugs. J Bone Joint Surg Br 2000;82(5):655–8. Lu C, Miclau T, Hu D, Marcucio RS. Ischemia leads to delayed union during fracture healing: a mouse model. J Orthop Res 2007;25(1):51–61. Reed AA, Joyner CJ, Isefuku S, Brownlow HC, Simpson AH. Vascularity in a new model of atrophic nonunion. J Bone Joint Surg Br 2003;85(4):604–10. Karladani AH, Granhed H, Karrholm J, Styf J. The influence of fracture etiology and type on fracture healing: a review of 104 consecutive tibial shaft fractures. Arch Orthop Trauma Surg 2001;121(6):325–8. Epari DR, Schell H, Bail HJ, Duda GN. Instability prolongs the chondral phase during bone healing in sheep. Bone 2006;38(6): 864–70. Lienau J, Schell H, Duda GN, Seebeck P, Muchow S, Bail HJ. Initial vascularization and tissue differentiation are influenced by fixation stability. J Orthop Res 2005;23(3):639–45. Perren SM, Cordey J. The concepts of interfragmentary strains. In: Uhthoff HK, editor. Current concepts of internal fixation of fractures. New York: Springer; 1980. Gaebler C, Berger U, Schandelmaier P, et al. Rates and odds ratios for complications in closed and open tibial fractures treated with unreamed, small diameter tibial nails: a multicenter analysis of 467 cases. J Orthop Trauma 2001;15(6): 415–23.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 262–267
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MINI-SYMPOSIUM: FRACTURE HEALING
(iii) The relevance of mesenchymal stem cells in vivo for future orthopaedic strategies aimed at fracture repair D. McGonagle, A. English, E.A. Jones The Leeds Institute of Molecular Medicine, University of Leeds, Chapel Allerton Hospital, Leeds LS7 4SA, UK
KEYWORDS Mesenchymal stem cells; Fracture repair
Summary The concept of a stem cell first emerged from studies on haematopoiesis where it was demonstrated that a rare clonogenic highly proliferative bone marrow (BM) cell, the haematopoietic stem cell (HSC), could give rise to all of the blood lineage cells. Hot on the heels of this work was the discovery of a second highly clonogenic and proliferative BM stem cell, later dubbed the mesenchymal stem cell (MSC) that was capable of giving rise to bone and cartilage and other stromal lineages. Whilst HSCs have been successfully utilized in the clinic for over two decades and have transformed the management of advanced haematological malignancy, the situation with MSCs is somewhat different. Despite the ability to generate billions of MSCs in vitro and over 300 proof of concept studies demonstrating in vivo fracture repair in animal models, MSCs have not yet been generally embraced by the orthopaedic community as the preferred agents to promote fracture repair. & 2007 Elsevier Ltd. All rights reserved.
Introduction Why has orthopaedic medicine apparently failed to grasp this opportunity? In our view, there are a number of practical and academic explanations for this apparent shortcoming. Firstly, unlike haematopoietic stem cells (HSCs), which remain the only viable option for transplantation of the haematopoietic system, a number of alternative Corresponding author. Tel.: +44 113 392 4747;
fax: +44 113 392 4991. E-mail address:
[email protected] (D. McGonagle). 0268-0890/$ - see front matter & 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2007.07.004
strategies have been successfully used to augment bone repair. These encompass autologous and allogeneic bone, osteoinductive scaffolds and growth factors (Table 1). Secondly, from an academic perspective, which is the main thrust of this article, the in vivo biology of mesenchymal stem cell (MSCs) in relationship to both bone homeostasis and fracture repair is very poorly understood. This is compounded by the fact that the frequency of MSCs in bone marrow (BM) aspirates is believed to be of the order of 10–100 cells per million marrow cells.1,2 This could certainly dissuade the aspiring academic orthopaedic scientist from investigating a cell that could at least 100-fold less numerous than marrow HSCs. Nevertheless, some of the
ARTICLE IN PRESS The relevance of mesenchymal stem cells in vivo for future orthopaedic strategies
Table 1
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Potential contribution of host MSCs to bone repair in the fracture setting.
Bone repair technique
Factors contributing to bone repair and the proposed role of host MSCs
Bone autograft
Both autologous grafted MSCs and autologous bone matrix containing BMPs. Local MSCs at the graft interface may contribute to osteointegration. Both allogeneic bone matrix containing BMPs and allogeneic MSCs. The latter are likely to initiate the repair cascade, but long-term graft survival may depend on contribution by host MSCs. Direct contribution of injected MSCs.49,50 Attract and enhance osteogenic differentiation of host MSCs.56 Act on MSCs located at fracture site.57,58 Exogenous MSCs proliferate and differentiate on the scaffold. The contribution of host MSCs is unknown.59,60 Exogenous MSCs proliferate and differentiate on the scaffold. The contribution of host MSCs is unknown.61
Bone allograft
Autologous marrow injection Nude scaffolds BMP injection (BMP2, BMP7) Scaffolds pre-seeded with culture expanded MSCs Scaffolds pre-seeded with culture expanded MSCs and encapsulated growth factors
applied methodologies for bone repair use a rudimentary knowledge of in vivo MSCs. This article reviews the emerging knowledge relating to BM MSCs in vivo and points to how this may influence future orthopaedic developments.
The history of MSCs and their identification ex vivo Until recently the study of BM MSCs in vivo or ex vivo was not possible, and was only indirectly feasible following cumbersome and time-consuming in vitro culture. Following aspiration of marrow and subsequent plastic adherence, a rare fibroblastic cell was identified that formed clonogenic colonies (named colony-forming unit-fibroblast or CFU-F).2 These colonies were large enough to be counted so that the frequency of the rare ancestral cell could be established. CFU-Fs can be culture expanded to generate billions of daughter MSCs that retained the ability to form bone and cartilage in vitro and in vivo.1,3–5 The considerable body of studies published in relationship to MSCs has been performed in relationship to this culture-manipulated cell population and it has been assumed that a similar profile would fit the ancestral cell in vivo. However, the CFU-F assay has a number of problems for directly defining MSCs in vivo, which include a lack of knowledge of the identity of the ancestral cell that gives rise to CFU-Fs. Elementary questions, including whether the cell responsible for bone repair was indeed a ‘‘stem cell’’ or whether mature osteoblasts or bone lining cells could dedifferentiate to MSCs, could not be addressed. Indeed, the argument whether the term MSC should represent a mesenchymal stem cell (MSC) or a marrow stromal cell is still ongoing.6,7 To complicate matters further, the historical idea that a MSC was largely confined to the marrow has been challenged by the recent demonstration of MSCs at numerous extraskeletal sites including fat, synovium, synovial fluid, periosteum, artery wall and even in placental tissue.8–13 Lack of knowledge on the in vivo topography and phenotype of BM MSCs has hampered the prospect for clarifying the relationship between these various stem cell populations. In this context, the inability to define MSCs in vivo makes the interpretation of classical orthopaedic
experiments virtually impossible. For example, BMP injection at extraskeletal sites along the lines of the classic experiment by Urist et al. has been shown to lead to ectopic new bone formation,14 but what type of MSCs involved is still unknown. Conversely, knowledge of in vivo MSC biology would allow one to establish whether this was due to osteoinduction of resident tissue MSCs or homing of MSCs from the marrow to ectopic sites, or both.
The recent purification of MSCs without prior culture manipulation To begin to understand MSC biology in vivo, we and other groups have begun by defining surface markers specific for these rare cells. The first marker of MSCs to be described was Stro-1, which could yield a 100-fold enrichment of MSCs.15 However, due to the rarity of MSCs and the antibody’s cross-reactivity with erythrocyte progenitors, complete purification of CFU-Fs could not be achieved. Following this work, but prior to the purification of in vivo BM MSCs, a phenotypic profile of culture-expanded MSCs was discovered.1,16 Specific markers of cultured BM MSC included CD73 (SH3) and CD105 (SH2) and it seemed logical that these markers would also be present in vivo on MSCs not manipulated in culture. Indeed, both of these markers enriched for BM MSCs in immunoselection protocols based on magnetic beads.17,18 In the mid-1990s, it was also reported that BM Stro-1-positive cells expressed nerve growth factor receptor,19 now clustered as CD271. On the other hand, negative depletion methods suggested that MSCs were lacking established leukocyte and endothelial cell markers.20 Based on these and other available data, we developed a novel methodological approach in which we combined immunomagnetic enrichment for an anti-fibroblast antigen D7-FIB with cell sorting for a CD45-negative CD271-positive cell. As a result, we were able to isolate BM MSCs to a high degree of purity.21,22 Other groups have utilized a similar strategy (pre-enrichment followed by cell sorting) but used different antibody cocktails to obtain similarly pure populations of BM MSCs.23,24 Aspirated BM MSCs have a frequency of between 1/10,000 and 1/100,000 cells.2 The basis for this heterogeneity
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Figure 1 Alakaline phosphatase (ALP) staining of freshly purified bone marrow MSCs (top panel), passage 0 and passage 6 cultured MSCs (middle panel) and cultured MSCs grown for 14 days in standard osteoinductiove conditions (bottom panel). Note the disappearance of ALP-positive cells during standard MSC passaging and its restoration during osteogenic differentiation. The understanding of these in vivo and in vitro differences in osteogenic status of BM MSCs is relevant for the uncovering the role of MSCs in the fracture repair setting. The presence of ALP, a perceived marker of mature osteoblasts but not MSCs, on MSCs in vivo but its down-regulation following culture expansion illustrates that much about MSCs in relationship to bone differentiation still awaits elucidation.
remains unclear but MSC numbers appear to be higher prior to skeletal maturity, which usually occurs late in the second decade of life.25 It has also become clear that adult MSCs are distinct from adult HSC as the cells are so different, both morphologically and phenotypically. In general, BM MSCs express markers that are shared with other stromal cells and fibroblasts from different sites. These include CD10, CD13, D7-FIB and CD90 and it is likely that these markers are not best suited for the discrimination between an MSC and a mundane fibroblast. More recently, both CD73 and CD105 were also shown to be expressed on fibroblasts from different tissues.26 Morphological and phenotypical analysis of in vivo MSCs has also revealed that they could be identical to BM stromal supportive cells, also known as adventitial reticular cells (ARCs). Both MSCs and ARCs are CD271 and alkaline
phosphatase positive.6,20,22 The alkaline phosphatase positivity is especially noteworthy, since it is believed to be an osteoblast variably expressed in culture-expanded MSCs20 but has enhanced expression levels in MSC cultures differentiated into osteoblasts.27,28 Our data show that the alkaline phosphatase activity declines following MSC passaging but can be restored in osteoinductive conditions (Figure 1). Therefore, it appears the phenotype of the MSC in the marrow may be more akin to an osteoblast than to a culture expanded MSC. Indeed, we and others have shown the loss of several other markers of in vivo MSCs during culture expansion including Stro-1, CD271 and HLA-DR.21,29 Although these phenotypic changes may not be associated with obvious loss of osteogenesis in an in vitro system, it remains to be determined whether these changes may alter MSC function in vivo.
ARTICLE IN PRESS The relevance of mesenchymal stem cells in vivo for future orthopaedic strategies Initially, there was a perception that MSCs were phenotypically heterogeneous because different groups used a restricted set of unrelated markers to enrich for these cells. However, when assessed with a comprehensive range of markers, it emerged that all groups were isolating the same cell.22 Recently, several other markers, including those of the wnt signalling pathway known to be intimately involved in bone metabolism, have been shown on uncultured MSCs.30 With the ability to characterise MSCs ex vivo, it is then possible to ascertain their location within the marrow. Our studies and work from other laboratories so far suggest that marrow MSCs occupy the ARC niche, as already mentioned, but may also be present on the abluminal surface of marrow endothelium31 and on the bone lining.32 With respect to the location and numbers of MSCs in tissues outside the marrow, data is more limited but some studies have suggested that such cells occupy a pericyte niche.24,33 As already mentioned, the fact that MSCs and tissue resident fibroblasts share some common markers will make this issue difficult to resolve.
Biology of MSCs in fracture repair It is hardly surprising that the rudimentary knowledge of MSCs in the physiology of bone in vivo has also translated into a lack of knowledge of their role in fracture repair. As already stated, culture-expanded MSCs can bridge critical size defects in animal models34,35 but it is less clear whether fracture repair in vivo is exclusively mediated by the BM MSC population. This is because there is evidence that mature osteoblasts and osteocytes may also proliferate and contribute to the osteoprogenitor pool.32 Also, MSCs from the periosteum11 and adjacent tissues9,36 may also play a role. Moreover, the presence of MSCs, utilizing indirect CFU-F assays, has been shown in haematoma fluid.37,38 The origins of such cells or their contribution to fracture repair remain to be defined. An issue that remains highly controversial is the role of circulating MSCs and their potential roles in fracture repair. Several studies have suggested that MSCs circulate and that they can home to sites of injury (reviewed in Ref. 39). However, when these studies are critically appraised, only some experiments have actually demonstrated the functional capacity of circulating cells to form clones and differentiate towards bone, cartilage and fat lineages (reviewed in Ref. 40). Furthermore, the studies that suggested that MSCs circulated used fairly limited immunophenotypic definitions.41,42 When we applied strict immunophenotypic criteria and clonogenic assays we were unable to show the presence of circulating MSCs in health in man.40 However, we believe that there is one instance where MSCs circulate that may be of considerable academic interest to the orthopaedic surgeon, although of less practical value. Following fracture, microscopic fat aggregates are released from the marrow and can occasionally be implicated in the fat embolisation syndrome.43 We and others have previously isolated the BM fat fraction and showed that in this fraction the yield of MSCs was three to four-fold higher compared to their yield in the mononuclear cell fraction.22,44 This indicates that MSCs may have a very close spatial relationship to the BM adipocytes. The
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relevance of these findings for MSC homing to sites of fracture may be debatable but it is conceivable that such aggregates could become deposited at fracture sites via the systemic circulation and thus contribute to tissue repair. In another study, MSCs were shown to form aggregates with megakaryocytes.45 This ‘‘symbiotic’’ relationship is interesting: MSCs may regulate platelet differentiation from megakaryocytes46 whereas platelets may produce PDGF needed for MSC survival and proliferation.19 The understanding of the relationship between MSCs and platelets is even more important in the context of haematoma formation during fracture repair.47
Existing role of culture expanded and in vivo MSCs in fracture repair As already stated, despite the ability to generate billons of culture expanded MSCs,1 the orthopaedic community has thus far shied away from such an approach for fracture treatment3 even though proof of principle experiments exist. The culture expansion of autologous MSCs is timeconsuming and expensive. An alternative view, which is still very much active, is the idea the allogeneic ‘‘off the shelf’’ MSCs could be used for fracture repair. The risk of pathogen transmission and uncertainties about tissue rejection have not been resolved, but a long track record of using allogenic whole bone grafts for fracture repair does exist (reviewed in Ref. 47). The place of host MSCs in an array of potential bone repair therapies has not been sufficiently considered and is summarized in Table 1.
The potential role of in vivo MSCs in future orthopaedic developments We would like to emphasize a pragmatic and quick technique that orthopaedic surgeons have used for bone repair that relies on the direct exploitation of in vivo MSCs—namely autogenous marrow injection into the fracture site. The heterogeneous outcomes following this technique have been recognized. However, recent elegant studies by Hernigou et al. and Ma et al. have addressed this.48,49 When marrow is aspirated and injected into nonunion fracture repair is generally excellent providing 50,000 CFU-Fs are present in the autogenous marrow.50 Without knowing the phenotypic identity of the in vivo MSCs, the authors were able to define their required numbers based on an in vitro CFU-F assay. It is likely that the MSCs in fat aggregates that could have been introduced into fracture sites would have increased total numbers of MSCs by 5–10-fold since the latter cells would have been discarded prior to performing the CFU-F assay. The autogenous marrow procedures that failed were due to very low CFU-F yields but these issues could be redressed in future as discussed below. The application of cytometric assays for MSC enumeration could allow for a marrow sample to be sent to the laboratory and have its MSC content established within 1 h thus allowing injection of exact numbers of MSCs. It is possible that the low yields of CFU-Fs may be due to dilution of the marrow aspirate by blood and that subsequent re-aspiration may increase the
ARTICLE IN PRESS 266 yield of MSCs. Therefore, we propose that rapid determination of the exact number of MSCs in an autogenic cellular preparation is now feasible. Also the recognition that MSCs may be much more common than hitherto recognized (present in the marrow fat and trabecular surfaces) could lead to methods for the robust isolation of numbers of MSCs that would be adequate for direct clinical application within hours. Three molecules directly relevant to the orthopaedic surgeon, namely BMPs 2 and 7 for fracture repair and PTH for osteoporosis, have reached the clinic (reviewed in Ref. 51). The clinical trial data from all of these molecules is impressive (reviewed in Ref. 51) but surprisingly, their mechanism of action on in vivo MSCs is not yet known. However, several studies have explored their action on cultured MSCs.52,53 An improved knowledge of these cells in vivo could have implications for cellular therapy as well as for more traditional approaches based on small molecules.
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11.
12. 13.
14. 15.
16.
Conclusions This article offers a perspective on the biology of MSCs in vivo. Whilst still in its infancy it is clear that this could have significant translational benefits. The ability to utilize cells non-expanded in culture would offset worries about loss of potency or genetic instability of MSCs culture expanded cells in vitro.54,55 The provision of an autologous source of MSCs with cell yields sufficient for fracture repair within hours of requirement may have a considerable impact in the field of orthopaedics.
References 1. Pittenger MF, Mackay AM, Beck SC, Jaiswal RK, Douglas R, Mosca JD, et al. Multilineage potential of adult human mesenchymal stem cells. Science 1999;284:143–7. 2. Castro-Malaspina H, Gay RE, Resnick G, Kapoor N, Maeyers P, Chiarieri D, et al. Characterisation of human bone marrow fibroblast colony-forming cells (CFU-F) and their progeny. Blood 1980;56:289–301. 3. Friedenstein AJ, Latzinik NW, Grosheva AG, Gorskaya UF. Marrow micro-environment transfer by heterotopic transplantation of freshly isolated and cultured-cells in porous sponges. Exp Hematol 1982;10:217–27. 4. Bruder SP, Jaiswal N, Ricalton NS, Mosca JD, Kraus KH, Kadiyala S. Mesenchymal stem cells in osteobiology and applied bone regeneration. Clin Orthop Related Res 1998;S247–S256. 5. Caplan AI. Mesenchymal stem cells: cell-based reconstructive therapy in orthopedics. Tissue Eng 2005;11:1198–211. 6. Bianco P, Riminucci M, Gronthos S, Robey PG. Bone marrow stromal stem cells: nature, biology, and potential applications. Stem Cells 2001;19:180–92. 7. Horwitz EM, Le Blanc K, Dominici M, Mueller I, SlaperCortenbach I, Marini FC, et al. Clarification of the nomenclature for MSC: the international society for cellular therapy position statement. Cytotherapy 2005;7:393–5. 8. Zuk PA, Zhu M, Mizuno H, Huang J, Futrell JW, Katz AJ, et al. Multilineage Cells from human adipose tissue: implications for cell-based therapies. Tissue Eng 2001;7:211–28. 9. De Bari C, Dell’Accio F, Tylzanowski P, Luyten FP. Multipotent mesenchymal stem cells from adult human synovial membrane. Arthritis Rheum 2001;44:1928–42. 10. Jones EA, English A, Henshaw K, Kinsey SE, Markham AF, Emery P, et al. Enumeration and phenotypic characterization of
17.
18.
19.
20.
21.
22.
23.
24.
25.
26.
27.
synovial fluid multipotential mesenchymal progenitor cells in inflammatory and degenerative arthritis. Arthritis Rheum 2004;50:817–27. De Bari C, Dell’Accio F, Vanlauwe J, Eyckmans J, Khan YM, Archer CW, et al. Mesenchymal multipotency of adult human periosteal cells demonstrated by single-cell lineage analysis. Arthritis Rheum 2006;54:1209–21. Abedin M, Tintut Y, Demer LL. Mesenchymal stem cells and the artery wall. Circ Res 2004;95:671–6. Miao ZN, Jin J, Chen L, Zhu JZ, Huang W, Zhao JD, et al. Isolation of mesenchymal stem cells from human placenta: comparison with human bone marrow mesenchymal stem cells. Cell Biol Int 2006;30:681–7. Urist MR, Delange RJ, Finerman GAM. Bone cell-differentiation and growth-factors. Science 1983;220:680–6. Gronthos S, Graves SE, Ohta S, Simmons PJ. The Stro-1(+) fraction of adult human bone-marrow contains the osteogenic precursors. Blood 1994;84:4164–73. Majumdar MK, Thiede MA, Haynesworth SE, Bruder SP, Gerson SL. Human marrow-derived mesenchymal stem cells (MSCs) express hematopoietic cytokines and support long-term hematopoiesis when differentiated toward stromal and osteogenic lineages. J Hematother Stem Cell Res 2000;9:841–8. Boiret N, Rapatel C, Veyrat-Masson R, Guillouard L, Guerin JJ, Pigeon P, et al. Characterization of nonexpanded mesenchymal progenitor cells from normal adult human bone marrow. Exp Hematol 2005;33:219–25. Majumdar MK, Banks V, Peluso DP, Morris EA. Isolation, characterization, and chondrogenic potential of human bone marrow-derived multipotential stromal cells. J Cell Physiol 2000;185:98–106. Gronthos S, Simmons PJ. The growth-factor requirements of Stro-1-positive human bone-marrow stromal precursors under serum-deprived conditions in-vitro. Blood 1995; 85:929–40. Rickard DJ, Kassem M, Hefferan TE, Sarkar G, Spelsberg TC, Riggs BL. Isolation and characterization of osteoblast precursor cells from human bone marrow. J Bone Miner Res 1996;11: 312–24. Jones EA, Kinsey SE, English A, Jones RA, Straszynski L, Meredith DM, et al. Isolation and characterization of bone marrow multipotential mesenchymal progenitor cells. Arthritis Rheum 2002;46:3349–60. Jones EA, English A, Kinsey SE, Straszynski L, Emery P, Ponchel F, et al. Optimization of a flow cytometry-based protocol for detection and phenotypic characterization of multipotent mesenchymal stromal cells from human bone marrow. Cytometry B Clin Cytom 2006:391–9. Gronthos S, Zannettino ACW, Hay SJ, Shi ST, Graves SE, Kortesidis A, et al. Molecular and cellular characterisation of highly purified stromal stem cells derived from human bone marrow. J Cell Sci 2003;116:1827–35. Shi S, Gronthos S. Perivascular niche of postnatal mesenchymal stem cells in human bone marrow and dental pulp. J Bone Miner Res 2003;18:696–704. D’Ippolito G, Schiller PC, Ricordi C, Roos BA, Howard GA. Agerelated osteogenic potential of mesenchymal stromal stem cells from human vertebral bone marrow. J Bone Miner Res 1999;14:1115–22. Ishii M, Koike C, Igarashi A, Yamanaka K, Pan H, Higashi Y, et al. Molecular markers distinguish bone marrow mesenchymal stem cells from fibroblasts. Biochem Biophys Res Commun 2005;332:297–303. Gronthos S, Zannettino ACW, Graves SE, Ohta S, Hay SJ, Simmons PJ. Differential cell surface expression of the STRO-1 and alkaline phosphatase antigens on discrete developmental stages in primary cultures of human bone cells. J Bone Miner Res 1999;14:47–56.
ARTICLE IN PRESS The relevance of mesenchymal stem cells in vivo for future orthopaedic strategies 28. Walsh S, Jefferiss C, Stewart K, Jordan GR, Screen J, Beresford JN. Expression of the developmental markers STRO-1 and alkaline phosphatase in cultures of human marrow stromal cells: regulation by fibroblast growth factor (FGF)-2 and relationship to the expression of FGF receptors 1-4. Bone 2000;27:185–95. 29. Simmons PJ, Torokstorb B. Identification of stromal cell precursors in human bone-marrow by a novel monoclonalantibody, Stro-1. Blood 1991;78:55–62. 30. Buhring H-J, Battula VL, Treml S, Schewe B, Kanz L, Vogel W. Novel markers for the prospective isolation of human MSC, vol. 1392. Annals of New York Academy of Sciences; 2007. p. 1000. 31. Short B, Brouard N, Occhiodoro-Scott T, Ramakrishnan A, Simmons PJ. Mesenchymal stem cells. Arch Med Res 2003; 34:565–71. 32. Tuli R, Tuli S, Nandi S, Wang ML, Alexander PG, Haleem-Smith H, et al. Characterization of multipotential mesenchymal progenitor cells derived from human trabecular bone. Stem Cells 2003;21:681–93. 33. Meirelles LDS, Chagastelles PC, Nardi NB. Mesenchymal stem cells reside in virtually all post-natal organs and tissues. J Cell Sci 2006;119:2204–13. 34. Bruder SP, Kurth AA, Shea M, Hayes WC, Jaiswal N, Kadiyala S. Bone regeneration by implantation of purified, culture-expanded human mesenchymal stem cells. J Orthop Res 1998; 16:155–62. 35. Barry FP, Murphy JM. Mesenchymal stem cells: clinical applications and biological characterization. Int J Biochem Cell Biol 2004;36:568–84. 36. Wickham MQ, Erickson GR, Gimble JM, Vail TP, Guilak F. Multipotent stromal cells derived from the infrapatellar fat pad of the knee. Clin Orthop Related Res 2003:196–212. 37. Mizuno K, Mineo K, Tachibana T, Sumi M, Matsubara T, Hirohata K. The osteogenetic potential of fracture hematoma-subperiosteal and intramuscular transplantation of the hematoma. J Bone Jt Surg—Br Vol 1990;72:822–9. 38. Oe K, Miwa M, Sakai Y, Lee SY, Kuroda R, Kurosaka M. An in vitro study demonstrating that haematomas found at the site of human fractures contain progenitor cells with multilineage capacity. J Bone Jt Surg—Br Vol 2007;89B:133–8. 39. Fox JM, Chamberlain G, Ashton BA, Middleton J. Recent advances into the understanding of mesenchymal stem cell trafficking. Br J Haematol 2007;137:491–502. 40. Jones EA, McGonagle D. Human bone marrow mesenchymal stem cells in vivo. Rheumatology, in press. 41. Zvaifler NJ, Marinova-Mutafchieva L, Adams G, Edwards CJ, Moss J, Burger JA, et al. Mesenchymal precursor cells in the blood of normal individuals. Arthritis Res 2000;2:477–88. 42. Khosla S, Eghbali-Fatourechi GZ. Circulating cells with osteogenic potential. In: Skeletal development and remodeling in health, disease, and aging. vol. 1068. Annals of the New York Academy of Sciences; 2006. p. 489–497. 43. Moylan JA, Evenson MA. Diagnosis and treatment of fatembolism. Annu Rev Med 1977;28:85–90. 44. Blazsek I, Chagraoui J, Peault B. Ontogenic emergence of the hematon, a morphogenetic stromal unit that supports multipotential hematopoietic progenitors in mouse bone marrow. Blood 2000;96:3763–71. 45. Miao D, Murant S, Scutt N, Genever P, Scutt A. Megakaryocytebone marrow stromal cell aggregates demonstrate increased colony formation and alkaline phosphatase expression in vitro. Tissue Eng 2004;10:807–17.
267
46. Nagahisa H, Nagata Y, Ohnuki T, Osada M, Nagasawa T, Abe T, et al. Bone marrow stromal cells produce thrombopoietin and stimulate megakaryocyte growth and maturation but suppress proplatelet formation. Blood 1996;87:1309–16. 47. Meijer GJ, de Bruijn JD, Koole R, van Blitterswijk CA. Cell-based bone tissue engineering. PLoS Med 2007;4:e9. 48. Hernigou P, Poignard A, Manicom O, Mathieu G, Rouard H. The use of percutaneous autologous bone marrow transplantation in nonunion and avascular necrosis of bone. J Bone Jt Surg—Br Vol 2005;87B:896–902. 49. Ma HL, Chen TH, Hung SC. Development of a new method in promoting fracture healing: multiple cryopreserved bone marrow injections using a rabbit model. Arch Orthop Trauma Surg 2004;124:448–54. 50. Hernigou P, Poignard A, Beaujean F, Rouard H. Percutaneous autologous bone-marrow grafting for nonunions—influence of the number and concentration of progenitor cells. J Bone Jt Surg—Am Vol 2005;87A:1430–7. 51. Jones EA, Pountos I, Yang XB, Mcgonagle D. Mesenchymal stem cells and their future in osteoporotic fracture repair. Adv Osteoporotic Fracture Manage 2006;4:11–6. 52. Rickard DJ, Wang F, Votta BJ, Kumar S, Nuttall ME. Intermittent treatment with parathyroid hormone (PTH) inhibits adipocyte differentiation in human bone marrow stromal cells. J Bone Miner Res 2003;18:S344. 53. Rickard DJ, Wang FL, Rodriguez-Rojas AM, Wu ZN, Trice WJ, Hoffman SJ, et al. Intermittent treatment with parathyroid hormone (PTH) as well as a non-peptide small molecule agonist of the PTH1 receptor inhibits adipocyte differentiation in human bone marrow stromal cells. Bone 2006; 39:1361–72. 54. Banfi A, Bianchi G, Notaro R, Luzzatto L, Cancedda R, Quarto R. Replicative aging and gene expression in long-term cultures of human bone marrow stromal cells. Tissue Eng 2002;8: 901–10. 55. Serakinci N, Guldberg P, Burns JS, Abdallah B, Schrodder H, Jensen T, et al. Adult human mesenchymal stem cell as a target for neoplastic transformation. Oncogene 2004;23:5095–8. 56. Lutolf MP, Hubbell JA. Synthetic biomaterials as instructive extracellular microenvironments for morphogenesis in tissue engineering. Nat Biotechnol 2005;23:47–55. 57. Govender S, Csimma C, Genant HK, Valentin-Opran A. Recombinant human bone morphogenetic protein-2 for treatment of open tibial fractures—a prospective, controlled, randomized study of four hundred and fifty patients. J Bone Jt Surg—Am Vol 2002;84A:2123–34. 58. Friedlaender GE, Perry CR, Cole JD, Cook SD, Cierny G, Muschler GF, et al. Osteogenic protein-1 (bone morphogenetic protein-7) in the treatment of tibial nonunions—a prospective, randomized clinical trial comparing rhOP-1 with fresh bone autograft. J Bone Jt Surg—Am Vol 2001;83A:S151–8. 59. Quarto R, Mastrogiacomo M, Cancedda R, Kutepov SM, Mukhachev V, Lavroukov A, et al. Repair of large bone defects with the use of autologous bone marrow stromal cells. N Engl J Med 2001;344:385–6. 60. Warnke PH, Springer ING, Wiltfang J, Acil Y, Eufinger H, Wehmoller M, et al. Growth and transplantation of a custom vascularised bone graft in a man. Lancet 2004;364:766–70. 61. Yang XB, Green DW, Roach HI, Clarke NMP, Anderson HC, Howdle SM, et al. Novel osteoinductive biomimetic scaffolds stimulate human osteoprogenitor activity-Implications for skeletal repair. Connect Tissue Res 2003;44:312–7.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 268–279
Available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/cuor
MINI-SYMPOSIUM: FRACTURE HEALING
(iv) The use of bone morphogenetic proteins (BMPs) in long-bone non-unions Haralampos Dinopoulos, Peter V. Giannoudis Department of Trauma and Orthopaedics, Academic Unit, Clarendon Wing, Floor A, Leeds General Infirmary, Leeds Teaching Hospitals NHS Trust, Great George Street, Leeds LS1 3EX, UK
KEYWORDS Bone morphogenetic proteins (BMPs); Recombinant (rh) BMP-2 and rh-BMP-7; Osteogenic protein-1 (OP-1); Long-bone non-unions
Summary The use of bone morphogenetic proteins (BMPs) in treating the clinical challenge posed by fracture delayed and non-union is still under investigation. When used to supplement basic surgical management clinical trials while few in number have demonstrated that BMPs are effective and safe for human application and have an efficacy comparable with that of autologous bone-grafting and eliminate donor site morbidity and reduces the risk of infection at the recipient site. Level one evidence has shown that recombinant human bone morphogenetic protein-7 (rh-BMP-7 or OP-1) is a reasonable alternative to autologous bone grafting in the treatment of long bone non-unions. & 2007 Elsevier Ltd. All rights reserved.
Introduction Un-united fractures, especially those with large osseous defects resulting from trauma or tumor resection, are complex clinical problems. Despite bone’s regenerative and reparative capacity and progress made in their treatment, approximately 5–10%, of fractures are associated with impaired healing.1 Non-union is a challenging complication for both patient and treating physician, often requiring long term treatment. It is often associated with chronic symptoms such as pain, functional and psychosocial disability, not to underestimate the socio-economic burden as well.2,3
Corresponding author. Tel.: +44 113 3922750;
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[email protected] (P.V. Giannoudis). 0268-0890/$ - see front matter & 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2007.07.007
Treatment of aseptic non-unions depends on an accurate assessment and classification of the non-union,4–7 including the mechanical stability in the fracture area (internal or external fixation), assessment and enhancement of the bone and surrounding tissue biology (biological stimulation). Autologous cancellous bone-grafting (ABG) is the gold standard biological method to promote union by stimulating the local micro-environment at the non-union site. However, clinical studies have demonstrated up to a 30% rate of unsatisfactory results after surgical treatment of segmental bone defects caused by complicated fractures8,9 and its limited availability, donor site morbidity such as pain, neurovascular injury, or infection have driven the search for alternative methods of biological stimulation10–14 used either alone or in combination such as allografting, bone marrow injections, electrical, ultrasound, and shockwave stimulation, and bone graft substitutes, with either osteoconductive or both osteoconductive and osteoinductive properties.15–29
ARTICLE IN PRESS The use of bone morphogenetic proteins (BMPs) in long-bone non-unions Bone morphogenetic proteins (BMPs) and platelet-derived growth factors, also, appear to be safe and efficacious.30–33 After their osteoinductive properties their genetic sequences had been identified, they have been produced by recombinant gene technology.34 Recombinant BMPs (rh-BMPs) are alternatives or adjuncts in the treatment of cases where bone regeneration is not anticipated.
The bone morphogenetic proteins BMPs were first described by Dr. Marshall Urist in 1965 (Table 1).35 They are members of the transformation growth factor-b (TGF-b) superfamily and have great osteoinductive potential.36 Having been isolated from different species, and due to the lack of standardization of these purifications, several of the BMPs have alternate names that are often used interchangeably, e.g. BMP-7 is OP-1, BMP-8 is OP-2, BMP-12 is Growth and Differentiation Factor 7 (GDF-7), and BMP-13 is both GDF-6 and CDMP-2.37 At least 40 different sub-types have been described to date and these have been divided into groups according to their primary amino acid sequence as below38:
BMP 2/4: BMP-2 and BMP-4 (BMP-2b). BMP 7/OP1: BMP-5, -6 (Vgr-1), -7(OP1), -8(OP2), -8b(OP3).
BMP 3: BMP-3 (osteogenin) and BMP-3b (GDF-10). CDMP: BMP-12, -13, -14 (CDMP1-3). Others: Growth/differentiation (GDF) 5, 6 and 7, BMP-15, BMP-16. Their role in inducing differentiation of fibroblasts to convert to osteoblasts thus form bone has been established in vivo.39 Work continues to clearly define the biological activity of each of these molecules38 but BMPs at tiny concentrations strongly induce new bone formation both within osseous lesions and at ectopic sites, such as skeletal muscle.37,40,41 They stimulate chemotaxis, proliferation and differentiation of mesenchymal cells into chondrocytes and osteoblasts.42,43 Meyer et al. in 2001, showed in rats that the expression of BMPs and their receptors peaks at one to two weeks after fracture and then sharply decreases to very low or undetectable levels in young rats, in which fractures heal, and in old rats, in which non-unions develop.44 In particular BMP-2, BMP-4, and BMP receptor type IA (BMPR-IA) mRNA peaked at one to two weeks after fracture and then fell to very low levels at four to six weeks after fracture.44 Kloen Table 1
269
et al. using immuno-histochemical analysis to investigate the expression of BMPs and the activation of BMP-signaling components in human fracture non-unions45 to determine whether BMPs, BMP receptors, or SMAD1 (one of the signaltransducing, receptor-regulated Smad proteins) disappear from the involved tissues during the development of a fracture non-union and whether their disappearance contributes to the development of the non-union. They studied delayed unions or non-unions with an average duration of 22 months in 21 adult patients.45 BMP-2, BMP-4, BMP-7, and their BMP receptors (BMPR-IA, BMPR-1B, and BMPR-II) as well as Smad1 were examined. The site of all of the BMPsignaling components was demonstrated in 81% of the patients, and the staining patterns showed co-localization of the BMPs with their receptors. Thus, the concept that the expression and activation of BMPs and their signaling components are lacking at the sites of delayed unions or non-unions was not supported by this study.45 However, although delayed unions and non-unions of long duration showed persistent expression of BMPs, their receptors and signaling components, the authors accepted that the concentrations of the BMPs and/or their receptors may not be sufficient to obtain normal healing. This raises questions about fundamental differences among critical-sized segmental bone defects, which heal in the presence of exogenous BMPs but do not heal spontaneously, fractures that heal readily in the presence of endogenous BMPs, and fractures with a propensity for non-union, which do not heal despite an initial increase in the levels of BMPs and their receptors44,46 and about the persistent presence of BMPs in the specimens of non-union. BMPs facilitate the repair of critical-sized segmental bone defects in experimental animals by stimulating the migration of mesenchymal stem cells from muscle, periosteum, endosteum, and bone marrow into the defect, by the proliferation and differentiation of the mesenchymal stem cells, and by the formation of bone through endochondral ossification. Recently much has been learned about the cellular and molecular mechanisms by which the BMPs induce bone formation.47 Most of these studies have involved critical-sized segmental osteoperiosteal defects in experimental animals (Table 2).51–54,63,60 In the experimental operative procedure used to create the osteoperiosteal defect, the soft tissues surrounding the defect are generally preserved and there is an abundant source of mesenchymal stem cells, particularly in the surrounding muscle. The experimental defect is stabilized by internal fixation or by an intact radius or tibia when the defect is created in the ulna or fibula, respectively.
Commercially available rh-BMP-2 and rh-BMP-7.
Commercially Composition available product
Commercially available forms
Mechanisms of action Studies
OP-1TM Implant Stryker Biotech
rh-BMP-7 with Type-1 collagen
Resorbable bovine collagen scaffold Osteoinduction
Human and animal studies
InFUSEs bone graft
Genetically engineered human protein (rh-BMP-2)
Lyophilized powder reconstituted with saline to form wet paste The addition of carboxy-methylcellulose forms a putty Absorbable collagen sponge carrier
Osteoinduction
Human and animal studies
ARTICLE IN PRESS 270
Table 2
H. Dinopoulos, P.V. Giannoudis
Segmental bone defects in animal models treated with BMP-preparations.
Implant/carrier
Animal model
Bone
Defect size
Analysis methods
Author
bBMP bBMP bBMP/PLA dBMP/PLA rh-BMP-2/DBM
Rat Dog Dog
Femur Ulna Radius
1.0 cm 2.5 cm 0.3 cm
Ro, histology Ro, histomorphometry Ro, histomorphometry
Tagaki and Urist48 Nilsson et al.49 Heckman et al.50
Rat
Femur
0.5 cm
histology, radio-isotope
Yasko et al.51
Rabbit Dog Green monkey Rabbit Sheep Sheep Dog Dog Rabbit Rabbit Dog Dog Sheep
Ulna Ulna Ulna and tibia Ulna Tibia Tibia Radius Radius Radius Radius Ulna Ulna Femur
1.5 cm 2.5 cm 2.0 cm
Ro, torsion test, boneimaging Ro, torsion test, Ro, torsion test, Ro, torsion test,
histology histology histology
Cook et al.52 Cook et al.53 Cook et al.54
2.0 cm 1.6 cm 1.6 cm 2.5 cm 2.5 cm 2 cm 1.0 cm 2 cm 2.5 cm 2.5 cm
Ro, torsion test, histology Ro, torsion test, histology Ro, torsion test, histology Ro, torsion test, histology Ro, torsion test, histology Ro-morphometry, histomorphometry Ro Ro, histomorphometry Ro, torsion test, histology Ro, histology
Rat
Femur
0.5 cm
Ro, torsion test
Bostro ¨m et al.55 Gao et al.56 Gao et al.57 Sciadini et al.58 Sciadini et al.59 Zegzula et al.60 Zellin and Linde61 Itoh et al.62 Cook et al.63 Kirker-Head et al.64 Lane et al.65
Rabbit
Radius
2.0 cm
Ro
Texeira and Urist66
Rabbit Dog Rat
Radius Radius Femur
2.0 cm 0.3 cm 0.5 cm
Radiomorphometry, torsion test Ro, histomorphometry Ro, histology
Wheeler et al.67 Heckman et al.68 Isobe et al.69
Rat
Femur
0.5 cm
Ro, torsion test
Ohura et al.70
Dog Rat
Radius Femora
2.5 cm 5 mm
Ro, histology, biomechanical Ro-morphometry, histomorphometry
Sciadini–Johnson71 Betz72
rhOP-1/collagen rhOP-1/collagen rhOP-1/collagen rh-BMP-2/PGA sBMP/TCP mBMP/coral bBMP/DBM bBMP/coral rh-BMP-2/PLA rh-BMP-2/PLA rh-BMP-2/PDLLA rhOP-1/collagen rh-BMP-2/PDLLA/ PGA rh-BMP-2/PDLLA/ PGA rh-BMP-2/PLA/ PGA Rh-BMP-2/PLA cBMP/PLA rh-BMP-2/PLA/ PGA rh-BMP-2/TCPMCPM rh-BMP-2/collagen Ad.BMP-2/gene
Human fracture may differ greatly from those in experimental animals in geometry and complexity which may be as important in determining whether a non-union will occur as the concentration of endogenous or exogenous BMPs at the fracture site. Also in response to the chemotactic stimulus of BMPs, mesenchymal stem cells may have too great a distance to migrate from muscle and periosteum to the interstices of the fracture fragments and in open fractures, particularly after debridement with loss of muscle and periosteum, there may be an inadequate supply of mesenchymal stem cells.
BMP manufacture Cadaver bone provides only small quantities purified human BMP (hBMP), limiting commercial production. Thus, industry turned to recombinant gene technology and focussed on those with the greatest potential for bone induction.a a
This technology is viewed by the FDA as being associated with risk, thus recombinant BMPs are classified as Class-III devices.
Recombinant human BMP-2 and BMP-7 (OP-1) have been approved for limited clinical use,41 but their application and efficacy has been reduced by delivery problems. As they have very short biological half-lives and are difficult to retain at sites of local application, large bolus doses are required to induce bone healing.73,74,30 Under these conditions, release of growth factors is not uniform. Instead, there is an initial rapid ‘‘out-flux’’ saturating surrounding tissue with supra-physiological concentrations of growth factor, leading to systemic exposure. Subsequent release, although slower, provides much lower, suboptimal concentrations.75–77 Another disadvantage of using recombinant proteins is their high cost.78 These products have been investigated as an alternative to bone autografting in a variety of clinical situations, including spinal fusions, internal fixation of fractures, treatment of bone defects, and reconstruction of maxillofacial conditions. Rh-BMPs are delivered to the bonegrafting site as part of a surgical procedure. A variety of carrier and delivery systems have been investigated. Carrier systems, absorbed over time, including non-organic material, synthetic polymer, natural polymers and bone
ARTICLE IN PRESS The use of bone morphogenetic proteins (BMPs) in long-bone non-unions allograft, help to maintain the concentration of the rh-BMP at the treatment site, provide temporary scaffolding for osteogenesis and prevent ectopic bone formation. The rh-BMP and carrier may be placed to the recipient area via a delivery system, which may also provide mechanical support e.g. for interbody spinal fusion, delivery systems have included interbody fusion cages. As carrier and delivery systems are important variables, and different clinical applications require different dosages of rh-BMP with different carriers and delivery systems, the results of one clinical application cannot be extrapolated to others.
Preclinical animal studies Numerous preclinical studies have been published on the use of BMPs on large critical-sized diaphyseal segmental defects (i.e., defects that cannot heal without exogenous osteogenic stimulation) in rats, rabbits, dogs, sheep and nonhuman primates to evaluate the osteoinductive properties of BMP48–72 (Table 2). These studies have shown that the implantation of BMPs with carrier matrices in bone defects led to biomechanical and biologically sound bone formation.52–54,58,59,71 In such animal models, BMP was equivalent to or better than autologous bone-grafting, the standard treatment in clinical practice.49,52–54,58,59,63,71,79,80 This demonstrated the potential for BMPs to be used as an alternative to autologous bone-grafting. This has been investigated intensively as bone-graft harvest causes morbidity, such as persistent pain, numbness, or hypersensitivity at the donor site.49 Einhorn et al. studied a single percutaneous injection of rh-BMP81 144 male Sprague— Dawley rats, torsional biochemical testing showed that stiffness of rh-BMP treated fractures was twice that of control groups at 2, 3 and 4 weeks. This showed that a single injection of BMP-2 would accelerate fracture repair and suggested their use in fractures not requiring operative treatment or treatment without direct exposure of the fracture site.81 BMP was also shown to accelerate bone formation and repair in non-critical size defects in closed fracture models with an early return of strength and stiffness. A few preclinical animal studies are set out in Table 2.
Clinical use of BMPs in bone defects and non-unions Delayed and non-unions remain a clinical challenge. While BMPs have been studied, prospective randomized controlled studies are lacking. We review the first clinical studies by anatomical site and various clinical trials are summarized in Table 3.
Tibial non-union Johnson et al. evaluated several small series of resistant non-unions and segmental long-bone defects had been treated with hBMP.31,82,83,90–92 Urist had purified the protein in his laboratory, and Johnson and colleagues used the protein in clinical settings.31,91 These uncontrolled retro-
271
spective series (Level-IV evidence) gave encouraging results and led to further studies. As recombinant BMPs were not yet available, a purified mixture of BMP proteins (hBMP) was used, in combination with insoluble non-collagenous proteins, both derived from human donor bone. At that time the risk of immunogenicity associated with alloimplants was becoming apparent, but it remained unknown which specific proteins were responsible for the osteoinductive activity and how this activity should be managed to develop an applicable clinical product. However, these three small case series were the first studies to assess purified BMPs clinically and they demonstrated that these implants were tolerated and could be useful in the management of difficult nonunions.31,82,83,90–92 Johnson in his small series of six cases attempted to enhance bone regeneration by augmenting autogenic cancellous bone graft with human BMP implants.31,91 The patients had segmental tibial bone loss ranging from 3 to 17 cm and five had a history of infection. Four had had previous treatment with external factors, and three had failed previous autogenic cancellous grafting. The latter three patients had also failed pulsed electromagnetic bone growth stimulation. An rh-BMP strip was placed under the medial periosteal sleeve of the defect while autogeneic cancellous bone filled the intercalary defect between the proximal and distal shaft fragments. They concluded that rh-BMP can be implanted without any adverse effects. Johnson’s second series of four patients distal tibial metaphyseal non-unions with residual anterior cortical bone loss.82 They had open tibial fractures and had significant posterior bowing deformities with fibular malunion with bony overgrowth prevented manual correction of the tibial deformity. They had had an average of 5.8 previous surgical procedures (six plate stabilizations and seven autogeneic cancellous iliac crest bone grafts). They underwent reduction and fixation of the posterior tibial cortex and rh-BMP implants were positioned across the anterior tibial cortical defect in contact with the residual freshened bone of the distal tibial metaphysis. All four non-unions united at an average of 4.4 months.82 In 1992, the United States Food and Drug Administration (FDA) approved a human clinical trial for the evaluation of OP-1 in treatment of tibial non-union. In this large prospective, randomized, controlled, partially blinded, multicenter study, Friedlaender et al.30 assessed the efficacy of the OP-1 Device (3.5 mg of rh-BMP-7 in a bovine bone-derived type-1 collagen-particle delivery vehicle; Stryker Biotech, Hopkinton, Massachusetts) comparing it to autografting in the treatment of 122 patients with a total of 124 tibial non-unions. All non-unions were at least nine months old and had shown no progress toward healing for the three months prior to the patient’s enrollment in the study. All the patients were treated with reamed intramedullary nailing and were then randomized to have either autograft bone or OP-1 implanted at the non-union site. Despite randomization, there were more smokers in the OP1 group. Nine months after the surgery, 81% of the 63 nonunions treated with OP-1 and 85% of the 61 treated with autograft had clinical evidence of union. Radiographic assessments suggested healing of 75% and 84% of these non-unions, respectively. As statistical analysis of these
ARTICLE IN PRESS 272
Table 3
H. Dinopoulos, P.V. Giannoudis
Overview of clinical trials on use of BMP in long-bone non-unions.
Author Johnson et al.
Anatomic Site 31
Tibial bone loss
No.
Type of study
Material
Results
6
Case series (small)
rh-BMP strip Partially purified BMP extract with or without autogenous or an allogenic bone graft rh-BMP strip
Healing without any adverse effects Healing in 11/12 cases after single intervention
Johnson et al.31
Femoral non-union
12
Case series (small)
Johnson et al.82
Distal tibial defect non-union
4
Case series (small)
Johnson et al.83
Femoral non-union
30
Geesink et al.84
Fibular defect of critical size Tibial non-unions
Friedlaender et al.30
McKee et al.85
6 124
Tibial, calvarias humeral, ulnar, femoral non-unions Humeral non-unions
31
Dimitriou et al.87
Tibial non-unions, femoral, humeral, ulnar, patellar, and clavicular non-union
17
Giannoudis and Tzioupis88
Atrophic persistent long-bone nonunions, various anatomic sites
395
Jones et al.89
Tibial diaphyseal fracture with defect
Ronga et al.75
Long-bone nonunion, 46 tibia, 26 femur, 20 humerus, 12 forearm, 2 clavicle
Susarala et al.86
6
Case series
Case series (small)
Partially purified BMP extract7autogenous graft rh-BMP-7
5 out of 6 pts
Prospective, randomized, controlled, partially blinded, multicenter study Case series
OP-1 vs. autograft
Comparable clinical outcome of OP-1 and autograft (81% vs. 85%)
OP-1
Good osteogenesis in all patients
Case series (small)
OP-1
Case series
rh-BMP77autologous graft
Multicenter, retrospective study, non-randomized study
OP-1 alone 74%
Union achieved in 11/12 cases Union in 8/9 cases managed only with rh-BMP-7 and in 16/ 17 cases treated with combination therapy Successful outcome 82%
OP-1+ autograft 23% rh-BMP-2 and autogenous or an allogenic bone graft 106
All 4 non-unions united (aver. 4.4 months) 24 of 30 (80%) healed
An observational, retrospective, nonrandomized study
results showed equivalent efficacy between OP-1 and autograft. The authors concluded that OP-1 was a safe and effective alternative to bone graft in the treatment of tibial non-unions. A limitation of the study was that the investigators could not control for the potential healing effects produced by reamed intramedullary nailing of tibial non-unions but it is noteworthy that half of the non-unions treated in this study were of fractures that had failed to
rh-BMP-7 vs. rh-BMP7+autograft
Better results with rh-BMP-2 [13/15] than with bone graft [11/15] Successful outcome in 88/105 patients (83.8%)
heal following reamed nailing as a primary treatment. Friedlaender et al. did show that the risk of infection at the implantation site was significantly lower in the rh-BMP-7 group than it was in the group treated with autologous bonegrafting (p ¼ 0.002). The authors concluded that BMPs were an effective alternative to autografting if the morbidity associated with harvesting of the graft is taken into consideration.30
ARTICLE IN PRESS The use of bone morphogenetic proteins (BMPs) in long-bone non-unions
BMP for the treatment of femoral non-union Johnson reported a series of 12 patients with intractable non-union of the femoral diaphyseal or metaphyseal–diaphyseal shaft with an average duration of non-union of 31.6 months. All had radiographic discontinuity gaps with abnormal mobility and pain. Eleven patients had previously failed 43 procedures and pulsed electromagnetic field bone growth stimulation. Seven patients were stabilized with plate osteosynthesis and five received intramedullary nailing. The BMP was used to aid in fracture union and was positioned in the peri-non-union area. BMP was thought to have favorably influenced the healing in 11 of 12 patients.31 Johnson in 2000, reported a series of 30 patients average age 47 years with femoral diaphyseal or diaphyseal–metaphyseal reconstructions augmented with rh-BMP and allogeneic, autolyzed antigen-free bone carrier alloimplants.83 The series included 24 shortened atrophic femoral nonunions, four equal length atrophic non-unions, and two longstanding shortened malunions. They had had an average of two previous failed procedures and an average of two failed autogenous cancellous bone-graftings per patient and the average time from initial femoral fracture to rh-BMP implantation was 39 months. Patients with shortened femoral non-unions underwent standard deformity correction and restoration of the mechanical axis. In addition, the non-unions were lengthened with a one-stage distraction creating an intercalary defect at the non-union site. The rh-BMP allograft bridged the medial aspect of larger intercalary defects greater than 2 cm. Autograft material was required to bridge these defects and allow host bone induction and remodeling. Thirteen patients received additional autogenous cancellous bone grafts to the intercalary segmental defect after onestage lengthening. The interface between the implant and the host bone above and below the defect was not in contact with any cancellous graft material. Twenty-four of 30 femora healed with rh-BMP allogeneic implants and plate osteosynthesis with an average time to healing of 6 months. The mean percentage of increased length over the pretreatment shortened femur was 7%. Six patients had fatigue failure of the plate implant of which four patients underwent revision surgery due to persistent distal metaphyseal non-unions. Three patients required additional cancellous grafting to the anterior and posterior aspects of the intercalary defects at an average of 5 months after lengthening.
Osseous defects While there are many preclinical animal studies of BMPs in osseous defects, Geesink et al. were the first to demonstrate clinically the osteoinductive capacity and effectiveness of rh-BMP-7 in humans in inducing healing of cortical bone defects.84 They investigated the osteogenic activity of OP-1 in bridging fibular defects made at the time of tibial osteotomy for varus or valgus deformity of the knee. Radiological and DEXA (dual energy X-ray absorptiometry) evaluation showed that in patients in whom the defect was left untreated no formation of bone occurred, whereas in five of six patients, rh-BMP-7 bound to collagen particles
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was shown to be effective with a critically sized fibular defect.
BMP use in other non-unions Other studies of various anatomic sites have confirmed the above evidence.75,85–89 In a study of 31 patients with 6 tibial, 9 calvarial, 10 humeral, 2 ulnar, and 4 femoral nonunions undergoing standard internal fixation supplemented with OP-1, McKee et al. found abundant new bone formation in all 31 patients and fracture healing at a mean of 13 weeks without any adverse effects.85 A retrospective study of 12 humeral non-unions treated with OP-1 by Susarala et al. showed clinical and radiographic evidence of union in 11 of the 12 patients at an average of 162 days (Table 3).86 Giannoudis et al. in a recent retrospective, non-randomized, multicenter study evaluated the use of recombinant BMP in 653 patients in different clinical scenarios.88 Three hundred and thirty-five patients with atrophic non-unions in various anatomic sites were treated with a single application of 3.5 mg OP-1 with an appropriate surgical procedure. OP-1 was used alone in 74% of the non-unions and combined with autograft in 23%. The overall success rate was up to 82% in terms of clinical and radiological non-union with no systemic complication or adverse effects.88 In another study, conducted by Dimitriou et al., fracture non-unions were treated with rh-BMP-7 including 10 tibial, eight femoral, three humeral, three ulnar, one patellar, and one clavicular non-unions.87 Seventeen had autologous bone graft in addition to rh-BMP-7 and nine cases received only rh-BMP-7. Sixteen cases (94.1%) managed with combination of BMP and bone graft while eight cases (88.9%) treated exclusively with rh-BMP-7 achieved clinical and radiological union (Table 3).87 In a prospective, randomized, controlled trial by Jones et al., 30 adult patients with a tibial diaphyseal fracture and a residual cortical defect received either autogenous bone graft or allograft (rh-BMP-2/cancellous bone chips) for staged reconstruction of the tibial defect.89 Ten patients in the autograft group and 13 patients in the rh-BMP-2/ allograft group had healing without further intervention. In another observational, retrospective, non-randomized study by the BMP-7 Italian Observational Study (BIOS) Group on the use of BMP-7, 105 non-unions in various sites were treated with additional grafts if deemed necessary clinically.75 The mean follow-up was 29.2 months by radiographic and clinical assessment of the two groups, groups: BMP-7 with autograft or BMP-7 alone. There was an 88.8% success rate with an average healing time of 7.9 months. This demonstrated the efficacy of BMP-7 both with and without bone-grafting for the treatment of long bone non-unions.75
Open tibial fractures and rh-BMP-2 There is a growing clinical interest in rh-BMPs in open tibial fractures. Riedel reported a series examining the effect of rh-BMP-2 on extraarticular, open tibial fractures (GustiloAnderson II or higher) in 12 patients.93 Patients underwent surgical procedures that including fracture reduction within 24 h of injury, repeated wound debridement, and fracture coverage within 14 days of the injury. Median time between
ARTICLE IN PRESS 274 injury and rh-BMP-2/ACS implantation was 4 days. Eleven patients completed 9-month follow-up and their fractures healed without further intervention. The remaining three patients required second surgical interventions for delayed union and underwent bone-grafting 16–17 weeks following injury. Two patients had positive antibody titers to rh-BMP2. He concluded that the implantation of rh-BMP-2 with an absorbable collagen sponge is surgically feasible and safe.93 More recently, the BMP-2 Evaluation in Surgery for Tibial Trauma (BESTT) study group reported the results of a large multicenter, prospective, randomized, controlled study of the effects of INFUSE (rh-BMP-2 on an absorbable type-1 collagen sponge; Medtronic Sofamor Danek, Memphis, Tennessee) in open tibial fractures.94 Four hundred and fifty patients were initially managed with irrigation, de´bridement, and intramedullary nail fixation. At the time of definitive wound closure, the patients were randomized to one of three groups: standard closure, standard closure and the addition of 6 mg of rh-BMP-2 to the fracture site, or standard closure and the addition of 12 mg of rh-BMP-2 to the fracture site. The primary outcome measure in this study was the rate of secondary interventions i.e., further operative treatment. The group treated with the higher dose of rh-BMP-2 had fewer secondary interventions. Interestingly, although not used as primary outcome measures, an accelerated time to union, improved woundhealing, and a reduced infection rate were also found in the patients treated with the high dose of rh-BMP-2. This could be in part related to increased vascular supply at the fracture site induced by BMP-2.94 In a similar study to that of the BESTT group, McKee et al. investigated the use of OP-1 in the treatment of open tibial fractures.33 Fractures were treated initially with irrigation, de´bridement, and locked intramedullary nailing. At the time of definitive wound closure, the patient was randomized to be managed with either standard closure or standard closure with 3.4 mg of OP-1 to the fracture site. One hundred and twenty two patients with a total of 124 tibial fractures were enrolled in the study. There was a significant decrease in the rate of secondary interventions for delayed unions and nonunions (the primary outcome measure) in the OP-1-treated group (p ¼ 0.02). There was a corresponding improvement in patient function, with 80% of the OP-1 group having no or mild pain with activity at 12 months post-injury compared with 65% of the control group (p ¼ 0.04).33 Miniscalco et al. conducted a randomized controlled pilot study to examine the effect of OP-1 in fresh tibial fractures.95 Fourteen patients with type A1 or A2 closed tibial shaft fractures treated with a monolateral external fixator were randomized into two groups. One group received OP-1 while the other acted as a control group. Time to bone healing in the OP-1 group was similar to the control group. Hence he did not recommend OP-1 for fresh fractures of the tibia. As most fresh fractures are adequately managed by other conventional techniques, the routine use of BMP may not be justified in such cases.95 These studies suggest that the use of rh-BMP-2 in open tibial fractures accelerates the time to union, lowers the rate of secondary interventions, improves wound-healing and reduces the infection rate. However, McKee and Miniscalco et al. have shown that OP-1 does not accelerate fracture healing of open and fresh tibial fractures, but
H. Dinopoulos, P.V. Giannoudis might decrease the rate of secondary interventions for delayed unions and non-unions and improve the patient’s function.33,95
Discussion While it took almost 40 years from the discovery of BMPs by Urist for them to become available for clinical application,35 they have led to a major step forward in the understanding of bone physiology and the evolution of more advanced surgical techniques. They have the unique potential to induce new bone formation, even at extraskeletal sites. However, the factors such as optimal therapeutic dosage, delivery system, and local conditions for bone repair are still under investigation and basic surgical management to provide adequate environmental conditions of the implantation site, such as soft-tissue coverage, host-bed vitality, and biomechanical stability, remains essential. Clinical trials, although still limited in number compared with preclinical studies, have demonstrated that BMPs are effective and safe for human use and have an efficacy comparable with that of autologous bone-grafting. Growth-factor therapy with BMPs offers a new surgical approach that can augment or even replace bone-grafting procedures. However, despite contrary results in animal studies, treatment of fresh fractures with BMP in humans has not resulted in a significantly higher rate of bone healing compared with that achieved by the current treatment techniques such as autologous bonegrafting and BMPs must be given in much higher doses to accomplish osteoinductive activity in humans. Clinical studies of BMP-2 and 7 have shown that bone formation is not consistent, possibly due to the relative osteoinductivity of the applied BMPs in the presence of responding cells and the time at which the BMPs are presented locally by their carrier. Better understanding of these mechanisms is needed to develop better carrier systems and possible combination therapies with other BMPs or growth factors. Production of individual recombinant human BMPs (rh-BMPs) has led to two important conclusions. Firstly, single BMPs are osteoinductive by themselves and secondly, the osteoinductivity of a single BMP has a dose–response ratio,96,97 unmodified by individual patient characteristics as they act locally. Hence the concentration of BMPs at the site of implantation is more important than the total dose. The dose must overcome a threshold before effective induction of bone formation; if the dose of BMPs is too low there will be inadequate bone formation, and if it is too high there will be more bone formation and more rapid osteoinduction than desired.97 This increased bone formation eventually results in direct (intramembranous) ossification, bypassing the intermediate phase of endochondral ossification that occurs when lower doses are used. However, with high doses of BMPs, initial localized resorption of bone can be seen as a result of increased osteoclastic activity, as BMPs also stimulate osteoclastogenesis and osteoclastic activity.98–100 At this point, a higher dose of BMPs is ineffective, as no further acceleration of bone formation occurs.97,101–103 Local overdoses of BMPs could be expected to lead to heterotopic ossification, but this phenomenon has not been shown to occur under physiological
ARTICLE IN PRESS The use of bone morphogenetic proteins (BMPs) in long-bone non-unions conditions. In a mouse model of BMP-4-induced heterotopic ossification, Glaser et al. demonstrated in vivo that heterotopic ossification in fibrodysplasia ossificans progressiva may not be due to the genetic overexpression of BMP-4 but rather to the underexpression of the extracellular antagonist of BMPs, noggin.104 Excessive ossification in this animal model could be prevented by local delivery of noggin, illustrating the highly regulated negative feedback mechanisms for BMPs that prevent abnormal or heterotopic bone formation even with high doses. In addition, the dose of BMP needed for clinical efficacy must overcome a threshold, and the dose–response curve becomes steeper as one progresses from rodent to non-human primate models. The latter species, most closely related to humans, was used to derive the human therapeutic dosage of 3.5 mg/ 4 mL of sterile saline solution or 0.88 mg/mL of sterile saline solution for rh-BMP-7 and 12 mg/8 mL of sterile water or 1.50 mg/mL of sterile water for rh-BMP-2. Rh-BMPs are expensive and are used in current clinical applications at concentrations that are ten to 1000-fold higher than those of native BMPs.105 These high doses of BMPs are used in an attempt to produce a clinical effect comparable with that shown to be osteoinductive in animal studies. The strongly regulated signaling mechanisms and the rapid local and systemic clearance of BMPs in higher species also necessitate higher doses. It has also been assumed that higher species have fewer responding cells than do lower species which raises important questions regarding combination therapies of BMPs and the development of more efficient and more cost-effective delivery systems.105 Currently two recombinant BMPs, rh-BMP-2 and rh-BMP-7 (also known as osteogenic protein-1 [OP-1]) are available for clinical use. Each has been evaluated in randomized controlled trials involving trauma patients, providing Level-I evidence. BMPs 2 and 7 have been studied in treating non-union of long bones. Several randomized controlled trials have compared BMP to autograft in the treatment of both open and closed tibial fractures.94,95 Patients with closed tibial fractures showed similar outcomes regardless of treatment regimen.94 Tibial non-unions also showed similar outcomes.30 Data from one randomized controlled trial suggested that open tibial fractures benefited from treatment with BMP compared with standard treatment.94 Patients who received the BMP implants tended to have shorter operative times and shorter hospital stays,94 but the differences were not statistically significant. In addition, patients with BMP implants did not experience donor site pain in comparison to autograft patients. Two small series of femoral non-union have been published.31,83 Patients had positive outcomes following BMP treatment, but it is uncertain if BMP had a significant effect on outcomes as there was no comparison group. Randomized controlled trials of BMP in spinal fusions compared to autograft have shown similar outcomes regardless of treatment but patients with BMP implants did not experience donor site pain. Rh-BMP-7 has received FDA approval through the Humanitarian Device Exemption process as an alternative to bone autograft in recalcitrant long-bone non-unions.106 The data presented to the FDA has now been published.102,103
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Osteogenic protein-1 (OP-1) is a growth factor, which is one of the components of the autologous bone graft. It plays an important role in bone formation by stimulating stem cells to differentiate into osteoblasts. The Friedlaender et al. randomized controlled trial of OP-1 on tibial nonunions demonstrated equivalence between autologous bone-grafting and OP-1.30 The rate of clinical and radiological success in tibial non-unions was comparable to the autologous-bone grafting when used in conjunction with intramedullary rod fixation. In addition, the rate of postoperative infection at the recipient site was significantly lower in those treated with OP-1. This study represents the cornerstone for the rh-BMP-7 use. Based on this trial, the FDA issued a Humanitarian Device Exemption to authorize the marketing of OP-1.106 In the Friedlaender et al. study both treatment groups received an intramedullary rod and compared rh-BMP-7 with autologous grafting improved. The authors chose a difficult population of patients with non-union to study; the majority had had prior bone-grafting and intramedullary rod fixation before inclusion in the study and about half of the patients had undergone a prior attempt at fusion with an intramedullary rod and from 30–40% had undergone a prior autograft. The union rate was similar in the two groups, which also did not differ with regard to clinical or radiographic healing characteristics. Although comparative efficacy was demonstrated, the goal of the BMP therapy, a higher healing rate, was not achieved. It is interesting to speculate that the rh-BMP-7 might have been more effective, as the percentage of patients with atrophic non-union was higher in the rh-BMP-7 group (41%) than it was in the group treated with autologous bone-grafting (25%). Unfortunately, the authors did not conduct a power analysis for their study, and the lack of differences between the groups may have been the result of a type-II statistical error. No statistical analysis with adjustment for atrophic non-union was performed. Other methods such as percutaneous injection of autologous bone marrow which contains stem cells, unspecialized cells that can differentiate and produce mature osteoblasts and capable of producing bone, for the treatment of long-bone non-unions have reported success rates ranging from 75% to 95%.18,19,29,107–113 It would be sensible to wait for any randomized control trials to compare it to the gold standard. Non-union and delayed union sites have been shown to possess all the components of the BMP-signaling pathway. However, it still remains unclear as to why union does not occur in some cases despite the presence of the BMPsignaling pathway.45 Some have hypothesized that the levels of the BMPs and/or their receptors at the sites of delayed unions and non-union might be suboptimal while others believe that BMP inhibitors like noggin which bind to the same receptors as BMP might be playing a role.42,44,114 Regardless of the micro-environment, it is well established that exogenous BMPs can drive osteogenesis or chondrogenesis and they will undoubtedly play an instrumental role in bone healing at non-union and delayed union sites. BMP may appear a cost effective tool in the surgeon’s armamentarium since it reduces the number of secondary interventions and sickness payment expenses, however, a sound economic
ARTICLE IN PRESS 276 model is needed to assess the cost-effectiveness and budget impact of rh-BMP.78 At the present time, two rh-BMPs and associated carrier/ delivery systems have received FDA approval are available in the market (Table 1). OP-1 has received FDA approval through the Humanitarian Device Exemption process.115
Conclusion Based on level one evidence, OP-1 is as effective as autologous bone-grafting and offers the advantages of eliminating donor site morbidity and reducing the risk of infection at the recipient site. Therefore, OP-1 is a reasonable alternative to autologous bone-grafting in the treatment of long bone non-unions and the decision to use it should be left to the discretion of treating physicians. Non-unions and delayed unions are one of the most difficult scenarios encountered in orthopaedic practice. Judicious use of BMP in certain clinical scenarios can revolutionize management of non-unions and delayed unions. The major constraints for routine use of BMP are inadequate clinical trials in humans and the need for further evaluation of cost benefit in various clinical situations. The expression and activation of BMPs from the surrounding tissues and their participation in the quite complex mechanisms of healing have just started to be understood. Future preclinical and clinical research must clarify issues regarding the relative effectiveness of BMPs, the interaction between BMP sub-types, on delayed unions, non-unions and bone defects and the characteristics of responding cells in much greater detail. BMPs have great clinical potential, but in the next decades we will have to determine whether there is a single pathway to efficiently treat non-unions or whether different clinical situations require different formats. Other emerging technologies and modalities, like gene therapy and or percutaneous techniques like autologous bone marrow grafting, have to be assessed in the future to individualize non-union scenarios and treatment options.
References 1. Praemer A, Furner S, Rice DP. Musculoskeletal injuries. In: Musculoskeletal conditions in the United States. Park Ridge, IL: American Academy of Orthopaedic Surgeons; 1992. p. 85–124. 2. Heckman JD, Sarasohn-Kahn J. The economics of treating tibia fractures: the cost of delayed unions. Bull Hosp Jt Dis 1997; 56(1):63–72. 3. Saleh K, et al. Socioeconomic burden of traumatic tibial fractures: nonunion or delayed union CME. /http://www. medscape.com/viewprogram/625_pntS. 4. Brinker MR. Nonunions: evaluation and treatment. 3rd ed. Browner BD, Jupiter JB, Levine AM, Trafton PG, editors. Skeletal trauma basic science management and reconstruction, vol. 1. Philadelphia: Saunders; 2003. p. 507–604. 5. Paley D, Catagni MA, Argnani F, et al. Ilizarov treatment of tibial nonunions with bone loss. Clin Orthop 1989;241:146–65. 6. Weber BG, Cech O. Pseudoarthrosis: pathology, biomechanics, therapy, results. Berne, Switzerland: Hans Huber Medical Publisher; 1976.
H. Dinopoulos, P.V. Giannoudis 7. Wiss DA, Stetson WB. Tibial nonunion: treatment alternatives. J Am Acad Orthop Surg 1996;4(5):249–57. 8. Sorger JI, Hornicek FJ, Zavatta M, Menzner JP, Gebhardt MC, Tomford WW, et al. Allograft fractures revisited. Clin Orthop Relat Res 2001;382:66–74. 9. Suedkamp NP, Barbey N, Veuskens A, Tempka A, Haas NP, Hoffmann R, et al. The incidence of osteitis in open fractures: an analysis of 948 open fractures (a review of the Hannover experience). J Orthop Trauma 1993;7:473–82. 10. 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. 11. Banwart JC, Asher MA, Hassanein RS. Iliac crest bone graft harvest donor site morbidity. Spine 1995;20(9):1055–60. 12. Fernyhough JC, Schimandle JJ, Weigel MC, Edwards CC, Levine AA. Chronic donor site pain complicating bone graft harvesting from the posterior iliac crest for spinal fusion. Spine 1992; 17(210):1474–80. 13. Lietman SA, Tomford WW, Gebhardt MC, Springfield DS, Mankin HJ. Complications of irradiated allografts in orthopaedic tumor surgery. Clin Orthop Relat Res 2000;375:214–7. 14. Seiler 3rd JG, Johnson J. Iliac crest autogenous bone grafting: donor site complications. J South Orthop Assoc 2000;9:91–7. 15. Bauer TW, Muschler GF. Bone graft materials. An overview of the basic science. Clin Orthop 2000;371:10–27. 16. Brighton CT. The treatment of non-unions with electricity. J Bone Joint Surg Am 1981;63(5):847–51. 17. Brighton CT, Friedenberg ZB, Zemsky LM, Pollis PR. Direct current stimulation of non-union and congenital pseudarthrosis. Exploration of its clinical application. J Bone Joint Surg Am 1975;57(3):368–77. 18. Connolly JF, Guse R, Tiedeman J, Dehne R. Autologous marrow injection as a substitute for operative grafting of tibial nonunions. Clin Orthop Relat Res 1991;266:259–70. 19. Garg NK, Gaur S, Sharma S. Percutaneous autogenous bone marrow grafting in 20 cases of ununited fracture. Acta Orthop Scand 1993;64(6):671–2. 20. Healey JH, Zimmerman AB, McDonnell JM, Lane JM. Percutaneous bone marrow grafting of delayed union and non-union in cancer patients. Clin Orthop 1990;256:280–5. 21. Mayr E, Frankel V, Ruter A. Ultrasound—an alternative healing method for nonunions? Arch Orthop Trauma Surg 2000; 120(1–2):1–8. 22. Moucha CS, Einhorn TA. Enhancement of skeletal repair. 3rd ed. Browner BD, Jupiter JB, Levine AM, Trafton PG, editors. Skeletal trauma basic science management and reconstruction, vol. 1. Philadelphia: Saunders; 2003. p. 639–60. 23. Nolte PA, van der Krans A, Patka P, et al. Low-intensity pulsed ultrasound in the treatment of non-unions. J Trauma 2001; 51(4):693–702. 24. Paterson DC, Lewis GN, Cass CA. Treatment of delayed union and nonunion with an implanted direct current stimulator. Clin Orthop 1980;148:117–28. 25. Reckling FW, et al. Treatment of non-unions of fractures of the tibial diaphysis by posterolateral cortical cancellous bonegrafting. J Bone Joint Surg 1980;62-A:936–41. 26. Schaden W, Fischer A, Sailler A. Extracorporeal shock wave therapy of nonunion or delayed osseous union. Clin Orthop 2001;387:90–4. 27. Scranton PE. Use of bone graft substitutes in lower extremity reconstructive surgery. Foot Ankle Int 2002;23(8):689–92. 28. Shors EC. Coralline bone graft substitutes. Ortho Clinics North Am 1999;30(4):599–613. 29. Wilkins RM, Chimenti BT, Rifkin RM. Percutaneous treatment of long bone nonunions: the use of autologous bone marrow and allograft bone matrix. Orthopedics 2003;26(Suppl. 5):s549–54. 30. Friedlaender GE, Perry CR, Cole JD, Cook SD, Cierny G, Muschler GF, et al. Osteogenic protein-1 (bone morphogenetic
ARTICLE IN PRESS The use of bone morphogenetic proteins (BMPs) in long-bone non-unions
31.
32.
33.
34.
35. 36.
37. 38. 39.
40.
41.
42. 43.
44.
45.
46.
47.
48.
49.
50.
51.
protein-7) in the treatment of tibial nonunions. J Bone Joint Surg Am 2001;83(Suppl. 1):S151–8. Johnson EE, Urist MR, Finerman GA. Bone morphogenetic protein augmentation grafting of resistant femoral nonunions. A preliminary report. Clin Orthop 1988;230:257–65. Jimenez ML, Anderson TL. The use of allograft, platelet derived growth factors, and internal bone stimulation for treatment of recalcitrant nonunions. In: OTA 19th annual meeting; 2003 [abstract]. McKee MD, Schemitsch EH, Waddell JP, Kreder HJ, Stephen DJG, Leighton RK, the Canadian Orthopaedic Trauma Society, et al. The effect of human recombinant bone morphogenic protein (rh-BMP-7) on the healing of open tibial shaft fractures: results of a multi-center, prospective, randomized clinical trial. In: Proceedings of the 18th annual meeting of the Orthopaedic Trauma Association; Toronto, Ontario, Canada; October 11–13; 2002. p. 157–8. Ozkaynak E, Rueger DC, Drier EA, et al. OP-1 cDNA encodes an osteogenic protein in the TGF-beta family. EMBO J 1990;9(7): 2085–93. Urist M. Bone formation by autoinduction. Science 1965; 12(150(698)):893–9. Harwood PJ, Giannoudis PV. Application of bone morphogenetic proteins in orthopaedic practice: their efficacy and side effects. Expert Opin Drug Saf 2005;4(1):75–89. Chen D, Zhao M, Mundy GR. Bone morphogenetic proteins. Growth Factors 2004;22:233–41. Matthews SJE. Biological activity of bone morphogenetic proteins (BMP’s). Injury, Int J Care Injured 2005;36S:S34–7. Rutheford RB, Gu K, Racenis P, Krebsbach PH. Early events: the in vitro conversion of BMP transduced fibroblasts to chondroblasts. Connect Tissue Res 2003;44(Suppl. 1):117–23. Reddi AH. Bone morphogenetic proteins: from basic science to clinical applications. J Bone Joint Surg Am 2001;83(Suppl. 1 Pt 7):S1–6. Mont MA, Ragland PS, Biggins B, Friedlaender G, Patel T, Cook S, et al. Use of bone morphogenetic proteins for musculoskeletal applications. An overview. J Bone Joint Surg Am 2004; 86(Suppl. 2):41–55. Sakou T. Bone morphogenetic proteins: from basic studies to clinical approaches. Bone 1998;22:591–603. Wozney JM, Rosen V. Bone morphogenetic protein and bone morphogenetic protein gene family in bone formation and repair. Clin Orthop Relat Res 1998;346:26–37. Meyer RA, Meyer MH, Pheiffer LS, Banks DM. Delayed union of femoral fractures in older rats: decreased gene expression. BMC Musculoskelet Disord 2001;2:2. Kloen P, Doty SB, Gordon E, Rubel IF, Goumans MJ, Helfet DL. Expression and activation of the BMP-signaling components in human fracture nonunions. J Bone Joint Surg Am 2002;84: 1909–18. Hollinger JO, Kleinschmidt JC. The critical size defect as an experimental model to test bone repair materials. J Craniofac Surg 1990;1:60–8. In: Proceedings of the international conference on bone morphogenetic proteins; Lake Tahoe, CA. June 7–11; 2000. J Bone Joint Surg Am 2001;83(Suppl. 1) (Pt 1). Takagi K, Urist MR. The role of bone marrow in bone morphogenetic protein-induced repair of femoral massive diaphyseal defects. Clin Orthop 1982;171:224–31. Nilsson OS, Urist MR, Dawson EG, Schmalzried TP, Finerman GA. Bone repair induced by bone morphogenetic protein in ulnar defects in dogs. J Bone Joint Surg Br 1986;68:635–42. Heckman JD, Boyan BD, Aufdemorte TB, Abbott JT. The use of bone morphogenetic protein in the treatment of non-union in a canine model. J Bone Joint Surg 1991;73-A(5):750–64. Yasko AW, Lane JM, Fellinger EJ, Rosen V, Wozney JM, Wang EA. The healing of segmental bone defects, induced by
52.
53.
54.
55.
56.
57.
58.
59.
60.
61.
62.
63.
64.
65.
66.
67.
68.
277
recombinant human bone morphogenetic protein (rhBMP-2). A radiographic, histological, and biomechanical study in rats. J Bone Joint Surg Am 1992;74:659–70. Cook SD, Baffes GC, Wolfe MW, Sampath TK, Rueger DC, Whitecloud TS. The effect of recombinant human osteogenic protein-1 on healing of large segmental bone defects. J Bone Joint Surg 1994;76-A(6):827–38. Cook SD, Baffes GC, Wolfe MW, Sampath TK, Rueger DC. Recombinant human bone morphogenetic protein-7 induces healing in a canine long-bone segmental defect model. Clin Orthop 1994;301:302–12. Cook SD, Wolf MW, Salkeld SL, Rueger DC. Effect of recombinant human osteogenic protein-1 on healing of segmental defects in non-human primates. J Bone Joint Surg Am 1995;77:734–50. Bostro ¨m M, Lane JM, Tomin E, Browne M, Berberian W, Turek T, et al. Use of bone morphogenetic protein-2 in the rabbit ulnar nonunion model. Clin Orthop 1996;327:272–82. Gao TJ, Lindholm TS, Kommonen B, Ragni A, Paronzini A, Lindholm TC, et al. Enhanced healing of segmental tibial defects in sheep by a composite bone substitute composed of tricalcium phosphate cylinder, bone morphogenetic protein, and type IV collagen. J Biomed Mater Res 1996;32:505–12. Gao TJ, Lindholm TS, Kommonen B, Ragni P, Paronzini A, Lindholm TC, et al. The use of coral composite implant containing bone morphogenetic protein to repair a segmental tibial defect in sheep. Int Orthop 1997;21:194–200. Sciadini MF, Dawson JM, Johnson KD. Bovine-derived bone protein as a bone graft substitute in a canine segmental defect model. J Orthop Trauma 1997;11(7):496–508. Sciadini MF, Dawson JM, Johnson KD. Evaluation of bovinederived bone protein with a natural coral carrier as a bonegraft substitute in a canine segmental defect model. J Orthop Res 1997;15:844–57. Zegzula HD, Buck DC, Brekke J, Wozney JM, Hollinger JO. Bone formation with use of rhBMP-2 (recombinant human bone morphogenetic protein-2). J Bone Joint Surg Am 1997;79: 1778–90. Zellin G, Linde A. Treatment of segmental defects in long bones using osteopromotive membranes and recombinant human bone morphogenetic protein-2. An experimental study in rabbits. Scand J Plast Reconstr Hand Surg 1997;31(2): 97–104. Itoh T, Mochizuki M, Nishimura R, Matsunaga S, Kadosawa T, Kokubo S, et al. Repair of ulnar segmental defect by recombinant human bone morphogenetic protein-2 in dogs. J Vet Med Sci 1998;60(4):451–8. Cook SD, Salkeld SL, Brinker MR, Wolfe MW, Rueger DC. Use of an osteoinductive biomaterial (rhOP-1) in healing large segmental bone defects. J Orthop Trauma 1998;12(6):407–12. Kirker-Head CA, Gerhart TN, Armstrong R, Schelling SH, Carmel LA. Healing bone using recombinant human bone morphogenetic protein 2 and copolymer. Clin Orthop 1998; 349:205–17. Lane JM, Yasko AW, Tomin E, Cole BJ, Waller S, Browne M, et al. Bone marrow and recombinant human bone morphogenetic protein-2 in osseous repair. Clin Orthop 1999;361: 216–27. Teixeira JO, Urist MR. Bone morphogenetic protein induced repair of compartmentalized segmental diaphyseal defects. Arch Orthop Trauma Surg 1998;117(2):27–34. Wheeler DL, Chamberland DL, Schmitt JM, Buck DC, Brekke JH, Hollinger JO, et al. Radiomorphometry and biomechanical assessment of recombinant human bone morphogenetic protein 2 and polymer in rabbit radius osteotomy model. J Biomed Mater Res 1998;43(4):365–73. Heckman JD, Ehler W, Brooks BP, Aufdemorte TB, Lohmann CH, Morgan T, et al. Bone morphogenetic protein but not
ARTICLE IN PRESS 278
69.
70.
71.
72.
73.
74.
75.
76.
77.
78.
79.
80.
81.
82.
83.
84.
85.
H. Dinopoulos, P.V. Giannoudis transforming growth factor-beta enhances bone formation in canine diaphyseal non-unions implanted with a biodegradable composite polymer. J Bone Joint Surg 1999;81-A(12): 1717–29. Isobe M, Yamazaki Y, Mori M, Amagasa T. Bone regeneration produced in rat femur by polymer capsules containing recombinant human bone morphogenetic protein-2. J Oral Maxillofac Surg 1999;57:695–8. Ohura K, Hamanishi C, Tanaka S, Matsuda N. Healing of segmental bone defects in rats induced by a beta-TCP-MCPM cement combined with rh-BMP-2. J Biomed Mater Res 1999; 44(2):168–75. Sciadini MF, Johnson KD. Evaluation of recombinant human bone morphogenetic protein-2 as a bone-graft substitute in a canine segmental defect model. J Orthop Res 2000;18: 289–302. Betz OB, Betz VM, Nazarian A, Pilapil CG, Vrahas MS, Bouxsein ML, et al. Direct percutaneous gene delivery to enhance healing of segmental bone defects. J Bone Joint Surg Am 2006;88:355–65. Boden SD, Zdeblick TA, Sandhu HS, Heim SE. The use of rhBMP2 in interbody fusion cages. Definitive evidence of osteoinduction in humans: a preliminary report. Spine 2000;25:376–81. Einhorn TA. Clinical applications of recombinant human BMPs: early experience and future development. J Bone Joint Surg Am 2003;85(Suppl. 3):82–8. Ronga M, Baldo F, Zappala G, Cherubino P. Recombinant human bone morphogenetic protein-7 for treatment of long bone nonunion: an observational, retrospective, non-randomized study of 105 patients. Injury, Int J Care Injured 2006;37S: S51–6. Talwar R, Di Silvio L, Hughes FJ, King GN. Effects of carrier release kinetics on bone morphogenetic protein-2-induced periodontal regeneration in vivo. J Clin Periodontol 2001;28: 340–7. Uludag H, Gao T, Porter TJ, Friess W, Wozney JM. Delivery systems for BMPs: factors contributing to protein retention at an application site. J Bone Joint Surg Am 2001;83(Suppl. 1 Pt 2):S128–35. Alt V, Heissel A. Economic considerations for the use of recombinant human bone morphogenetic protein-2 in open tibial fractures in Europe: the German model. Curr Med Res Opin 2006;22(Suppl. 1):19–22. den Boer FC, Wippermann BW, Blokhuis TJ, Patka P, Bakker FC, Haarman HJ. Healing of segmental bone defects with granular porous hydroxyapatite augmented with recombinant human osteogenic protein-1 or autologous bone marrow. J Orthop Res 2003;21:521–8. Gerhart TN, Kirker-Head CA, Kriz MJ, Holtrop ME, Hennig GE, Hipp J, et al. Healing segmental femoral defects in sheep using recombinant human bone morphogenetic protein. Clin Orthop Relat Res 1993;293:317–26. Einhorn TA, Majeska RJ, Mohaideen A, Kagel EM, Bouxsein ML, Turek TJ, et al. A single percutaneous injection of recombinant human bone morphogenetic protein-2 accelerates fracture repair. J Bone Joint Surg Am 2003;85:1425–35. Johnson EE, Urist MR, Finerman GA. Distal metaphyseal tibial nonunion. Deformity and bone loss treated by open reduction, internal fixation, and human bone morphogenetic protein (hBMP). Clin Orthop 1990;250:234–40. Johnson EE, et al. Human bone morphogenetic protein allografting for reconstruction of femoral nonunion. Clin Orthop Relat Res 2000;371:61–74. Geesink RG, Hoefnagels NH, Bulstra SK. Osteogenic activity of OP-1 bone morphogenetic protein (BMP-7) in a human fibular defect. J Bone Joint Surg Br 1999;81:710–8. McKee MD, Waddell JP, Wild L. The treatment of long bone nonunion with rh BMP: results of a prospective pilot study.
86.
87.
88. 89.
90.
91.
92.
93.
94.
95. 96.
97.
98.
99.
100. 101.
102. 103.
In: Poster presentation #242, 71st AAOS meeting, March 10–14, 2004. Susarla A, Tejwani NC, Koval KJ, Egol KA. OP 1 implant as an adjunct to mechanical fixation in humeral non-union. In: Poster presentation #241, AAOS meeting, March 10–14, 2004. Dimitriou R, Dahabreh Z, Katsoulis E, Matthews J, Branfoot T, Giannoudis PV. Application of recombinant BMP-7 on persistent upper and lower limb non-unions. Injury, Int J Care Injured 2005;36S:S51–9. Giannoudis PV, Tzioupis C. Clinical applications of BMP-7. The UK perspective. Injury, Int J Care Injured 2005;36S:S47–50. Jones AL, et al. Recombinant human BMP-2 and allograft compared with autogenous bone graft for reconstruction of diaphyseal tibial fractures with cortical defects. A randomized, controlled trial. J Bone Joint Surg Am 2006;88(7): 1431–41. Johnsson R, Stromqvist B, Aspenberg P. Randomized radiostereometric study comparing osteogenic progrien-1 (BMP-7) and autograft bone in human noninstrumented posterolateral lumbar fusion. Spine 2002;27:2654–61. Johnson EE, Urist MR, Finerman GA. Repair of segmental defects of the tibia with cancellous bone grafts augmented with human bone morphogenetic protein. A preliminary report. Clin Orthop Relat Res 1988;236:249–57. Johnson EE, et al. Repair of segmental defects of the tibia with cancellous bone grafts augmented with human bone morphogenetic protein. Clin Orthop 1988;236:249–57. Riedel GE, Valentin-Opran A. Clinical evaluation of rh-BMP-2/ ACS in orthopedic trauma: a progress report. Orthopedics 1999;22:663–5. Govender S, Csimma C, Genant HK, Valentin-Opran A, Amirt V, Arbel R, et al. BMP-2 evaluation in surgery for tibial trauma (BESTT) Study Group. Recombinant human bone morphogenetic protein-2 for treatment of open tibial fractures: a prospective, controlled, randomized study of four hundred and fifty patients. J Bone Joint Surg Am 2002;84:2123–34. Miniscalco P, et al. Healing of fresh tibial fractures with OP-1. A preliminary report. Acta Bio-Medica 2002;73(1–2):27–33. Ripamonti U, Van Den Heever B, Sampath TK, Tucker MM, Rueger DC, Reddi AH. Complete regeneration of bone in the baboon by recombinant human osteogenic protein-1 (hOP-1, bone morphogenetic protein-7). Growth Factors 1996;13: 273–89. Valentin-Opran A, Wozney J, Csimma C, Lilly L, Riedel GE. Clinical evaluation of recombinant human bone morphogenetic protein-2. Clin Orthop Relat Res 2002;395:110–20. Canalis E, Economides AN, Gazzerro E. Bone morphogenetic proteins, their antagonists, and the skeleton. Endocr Rev 2003; 24:218–35. Itoh K, Udagawa N, Katagiri T, Iemura S, Ueno N, Yasuda H, et al. Bone morphogenetic protein 2 stimulates osteoclast differentiation and survival supported by receptor activator of nuclear factor-kappaB ligand. Endocrinology 2001;142: 3656–62. Udagawa N. Mechanisms involved in bone resorption. Biogerontology 2002;3:79–83. Sampath TK, Maliakal JC, Hauschka PV, Jones WK, Sasak H, Tucker RF, et al. Recombinant human osteogenic protein-1 (hOP-1) induces new bone formation in vivo with a specific activity comparable with natural bovine osteogenic protein and stimulates osteoblast proliferation and differentiation in vitro. J Biol Chem 1992;267:20352–62. Sandhu HS. Bone morphogenetic proteins and spinal surgery. Spine 2003;28:S64–73. Sandhu HS, Kanim LE, Kabo JM, Toth JM, Zeegen EN, Liu D, et al. Effective doses of recombinant human bone morphogenetic protein-2 in experimental spinal fusion. Spine 1996;21: 2115–22.
ARTICLE IN PRESS The use of bone morphogenetic proteins (BMPs) in long-bone non-unions 104. Glaser DL, Economides AN, Wang L, Liu X, Kimble RD, Fandl JP, et al. In vivo somatic cell gene transfer of an engineered Noggin mutein prevents BMP4-induced heterotopic ossification. J Bone Joint Surg Am 2003;85:2332–42. 105. Termaat MF, Den Boer FC, Bakker FC, Patka P, Haarman HJ. Bone morphogenetic proteins development and clinical efficacy in the treatment of fractures and bone defects. J Bone Joint Surg Am 2005;87:1367–78. 106. New humanitarian device approval, OP-1TM-H010002. Web reference: /http://www.fda.gov/cdrh/mda/docs/h010002. htmlS. 107. Goel A, Sangwan SS, Siwach RC, Ali AM. Percutaneous bone marrow grafting for the treatment of tibial non-union. Injury 2005;36(1):203–6. 108. Jean J-L, Tang H-L, Wang S-J, Chang J-H, Lin S-C, Chen C-J, et al. Efficacy of autologous percutaneous bone marrow graft injection for treatment of nonunion of the tibia. Formosan J Surg 2001;34(6):294–301. 109. Matsuda Y, Sakayama K, Okumura H, Kawatani Y, Mashima N, Shibata T. Percutaneous autologous bone marrow transplan-
110.
111.
112.
113.
114.
115.
279
tation for nonunion of the femur. Nippon Geka Hokan 1998;67(1):10–8. Pan KL, Shukur MH, Ghani MAN, Pan KL. The role of bone marrow grafts in tibial nonunions. J Orthop Surg (Hong Kong) 1996;4(2):47–51. Sim R, Liang TS, Tay BK. Autologous marrow injection in the treatment of delayed and non-union in long bones. Singapore Med J 1993;34(5):412–7. Siwach RC, Sangwan SS, Singh R, Goel A. Role of percutaneous bone marrow grafting in delayed unions, non-unions and poor regenerates. Indian J Med Sci 2001;55(6):326–36. Wang L, Li WS, Zhang QS. Autogenous bone marrow graft for the management of nonunion of tibia. Zhongguo Xiu Fu Chong Jian Wai Ke Za Zhi 2001;15(1):24–5. Schmitt JM, Hwang K, Winn SR, Hollinger JO. Bone morphogenetic proteins: an update on basic biology and clinical relevance. J Orthop Res 1999;17:269–78. Food and Drug Administration (FDA). OP-1 implant. Summary of safety and probable benefit. Available from /http://www. fda.gov/cdrh/pdf/h010002b.pdfS.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 280–287
Available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/cuor
MINI-SYMPOSIUM: FRACTURE HEALING
(v) Which scaffold for which application? Ashley Blom Avon Orthopaedic Centre, Southmead Hospital, University of Bristol, Bristol BS10 5NB, UK
KEYWORDS Bone grafting; Scaffolds; Bone graft substitutes; Ceramics; Osteoconduction; Osteointegration; Orthobiologics
Summary Scaffolds are usually osteoconductive, but rarely osteoinductive and extremely rarely osteogenic. They do however have the potential advantage of providing structural support. The load bearing capability of each type of scaffold needs to be determined prior to clinical use if it is to be used in a load-bearing situation. Some scaffolds are resorbable. These are best used in clinical situations where the biology of the host will promote effective new bone formation. It is preferable to have a scaffold that osteintegrates as this will allow bonding at a molecular level between the scaffold and host bone. Synthetic scaffolds have the lowest risk of infection and antigenicity. At present, there is no scaffold available that is suitable for all bone grafting procedures. & 2007 Elsevier Ltd. All rights reserved.
Introduction Orthobiologics can be divided into scaffolds, growth factors and stem cells. This article is a brief overview of scaffolds. The epidemiology of bone grafting as well as the advantages and disadvantages of autograft and allograft are discussed. A classification system for scaffolds is proposed and then different types of scaffolds are examined with particular reference to their advantages, disadvantages and clinical uses.
Semantics It will be useful to start this chapter with a few definitions. Osteointegration means bonding at a molecular level between a given substance and bone. Examples of substances that osteointegrate are titanium, hydroxyapatite and tricalcium phosphate. Examples of substances that do not osteointegrate are stainless steel and polymethylmethaE-mail address:
[email protected] 0268-0890/$ - see front matter & 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2007.06.005
crylate. When a substance osteointegrates, the bond between it and the bone is incredibly strong, often exceeding the tensile strength of both the substance itself and of bone. Dental studies have shown that when ceramics osteointegrate with bone, the bond between the bone and the ceramic is so strong that attempts to separate the two usually result in fracture of either the ceramic or the bone, but rarely separation at the interface.1 An osteoconductive material provides a scaffold for bone to grow along. This is dependant on the material characteristics as well as the morphology of the material. An osteogenic material forms new bone on its own. For this, it needs to contain both the cellular element as well as the morphogens required to produce bone. An osteoinductive material induces pluripotential stem cells to become osteoblasts.
Orthobiologics Orthobiologics can be divided into three fields: (A) scaffolds, (B) growth factors and (C) stem cells.
ARTICLE IN PRESS Which scaffold for which application
281 Scaffolds are usually osteoconductive, but rarely osteoinductive and extremely rarely osteogenic. They do however have the potential advantage of providing structural support (Figures 1 and 2). Growth factors include the Bone Morphogenic Proteins (BMPs), which are part of the Transforming Growth Factor Beta superfamily of proteins. The term Bone Morphogenic Protein was coined by Marshall Urist in the 1960s, but is probably a misnomer. These proteins do not just promote bone morphogenesis, but are involved in organogenesis in general. It would be more accurate to refer to them as Morphogenic roteins. Currently, BMP’s 2, 4 and 7 are commercially available. BMP 7 is extracted from Chinese hamster ovaries. Under the influence of BMP’s, bone is regenerated by pluripotential stem cells that are converted to osteoblasts.2–5
Bone grafting Bone is the second most transplanted tissue after skin. In the USA in 2001, 643,000 bone grafting procedures were performed. The cost of these procedures has been estimated at approximately $600 million p.a. The current breakdown by type of procedures is as follows:
Figure 1
Pre-op radiograph.
Figure 2 Post-op impaction grafting with ceramic bone graft substitute.
45% autologous bone 45% allogenic bone 10% synthetics. In Europe, 287,300 procedures of bone grafting were carried out in 2000 and 429,660 procedures in 2003. Autografting is still considered to be the gold standard in bone grafting, but there are problems with autografting. These include: bulk limitations, graft donor site morbidity (particularly pain and injury to the lateral cutaneous nerve of thigh) and lengthening of the procedure whilst harvesting occurs. For these reasons, allografting has become more popular. Allografting, however, has introduced new problems, which include cost, availability, antigenicity, infectivity, reproducibility and structural stability. Since the initial reports of morsellised impaction grafting appeared in the literature in the early 1990s, the technique has become extremely popular. Demand for bone has risen without a corresponding increase in supply. For example, in Scotland, the Scottish National Blood Transfusion Service performs Bone Banking. They collect and distribute all the bone that is used in revision total hip arthroplasty in Scotland. In 1993, they collected 1559 femoral heads and issued 1061. In 1995, they collected 1778 heads and issued 1567. This represents a 13% increase in supply, against a 50% increase in demand over a 2-year period. Between 1993 and 1995, the number of primary total hip arthroplasties performed increased by approximately 1.8%, whilst the number of revision arthroplasties increased by approximately 20%. Galea et al. predicted that between 1995 and the year 2000, the number of primary total hip replacements would increase by 12% and the number of revisions would increase by 100%. They predicted that their supply of donor femoral heads would have been outstripped by demand before 2000 and concluded: ‘‘This source cannot
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meet the demand for revision surgery of the hip or for other operations because of the increase in the number of revisions and the use of techniques which require more bone, such as impaction grafting, which may use up to five femoral heads. Other studies have reached similar conclusions.6–9 Allografts have the potential to invoke graft rejection by activating T cell-mediated immune responses in the host. Fresh, untreated allograft bone provokes both humoral and cell-mediated host responses. Bone that has been frozen and stored prior to implantation evokes a much diminished host response, probably due to diminished antigen presentation by the graft. Freeze-drying diminishes this response even further.10 Friedlander et al. have identified donor-specific anti-HLA antibodies in human recipients of freeze-dried allografts.11 Although sensitisation is a potential cause for concern, Musculo et al. did not show a correlation between sensitisation and poor clinical outcome12 and at present most bone banks make no effort at tissue typing between donors and recipients. Although most bone banks screen donors meticulously for potential sources of infection, harvest and store bone under sterile conditions, and in many cases irradiate bone, there is still a problem with both viral and bacterial infection. The literature records a number of cases of transmission of the Human Immunodeficiency Virus (HIV) through bone allograft transplantation despite rigorous precautions. It is imperative to exclude people with high risk factors from donating. According to Huo et al., the first recorded case of HIV transmission via allograft bone was in a woman who developed AIDS 312 years after receiving bone from a frozen femoral head that was used for spinal fusion.13 Simonds et al. reported a tragic case where seven recipients developed AIDS after receiving tissue from a single donor. Four had received organs and three had received bone. The donor was a victim of a homicide who had no known risk factors for HIV infection. Two serum samples taken at the time of harvest tested negative for HIV. Subsequent culture of the donor’s cryopreserved spleen cells grew HIV.14 Buck studied the risks of unknowingly implanting HIV infected bone when utilising bone-banked bone in the United States of America. If all the recommended checks are rigorously adhered to, the risk is slight. When there is failure to take adequate precautions, he estimates the risk to be 1/161.15 The problem with screening for HIV infection is that there is a highly variable window between infection and the presence of detectable antibodies. This window may range
Table 1
from a few months to several years. HIV is usually tested for by means of ELISA and Western blot assay. The sensitivity and specificity of these methods is between 90% and 99%. The incidence of bacterial infection with allograft bone varies considerably, depending on a number of factors including the storage and processing of the bone, the immune status of the recipient and the host site. The postoperative incidence of bacterial infection is twice as high with allograft bone as compared with autograft bone when used in similar surgery.16 Infection rates in total hip arthroplasty with the use of allograft bone vary between authors. Gie et al.17 and Harris et al. reported no infections.18 Jofe et al. reported four infections in 28 cases19 and Mankin et al. reported 13 infections in 91 cases.20 Reconstruction following tumour resection carries a higher risk of infection. Meding et al.21 published a study in the Journal of Bone and Joint Surgery in 1997. They outlined the cost of the disposables used during impaction grafting surgery in their institution. Femoral heads cost $950 each. Often impaction grafting requires up to five femoral heads.9 Highly polished double taper femoral stems cost approximately $2000 each and cortical strut allografts cost $500 each. If the use of allograft from femoral heads can be substituted with a cheaper, but as effective source, then the cost of some operations can be reduced by as much as 4500 US dollars. Allograft bone is not reproducible. The quality of the bone is dependant on both donor factors (age, osteoporosis, and co-morbidities) and processing (sterilisation methods, storage). This is reflected in the variable clinical outcomes. Eldridge et al. reported a 12% early massive subsidence when using allograft bone in impaction grafting of the femur.22
Synthetic scaffolds Due to the problems outlined above, there has recently been a surge in interest in synthetic scaffolds. Bone grafts and bone graft substitutes can be broadly classified as shown in Table 1.
Xenografts Bovine bone has been investigated as a potential substitute for human allograft bone since the 1960s.26 More recently,
Classification of bone graft substitutes.
Biological human
Biological non-human
Synthetic nonabsorbable
Synthetic absorbable
Biological/ synthetic combinations
Autograft
Xenograft
Methylmethacrylate
Calcium sulphate
Collagen matrix (ceramic/fibrillar collagen)
Allograft
Corraline
Glass-ionomers
Ceramic: hydroxyapatite tricalcium phosphate Polyhydroxyacids
Other (such as bamboo23,24 and eggshell25)
ARTICLE IN PRESS Which scaffold for which application Levai et al. reported good results in 27 out of 30 cases using bovine bone in acetabular reconstruction in total hip revision.27 Bovine bone is biocompatible for human osteoblasts.28 Hubble et al. showed that when cyclically loaded, bovine bone exhibited stability similar to human bone when used as a morsellised graft in impaction grafting of the femur.29 Their pilot studies in sheep showed graft incorporation with new bone formation comparable with allograft.30 Other studies have highlighted problems with bovine xenograft. Begley demonstrated that bovine xenograft causes intense inflammatory reactions that are not provoked by coral when used in identical circumstances.31 Charalambides et al. reported very poor results in revision hip surgery using bovine bone, with more than 25% of cases needing rerevision at an average follow-up of 36 months.32 There are also fears with regard to infection and patient acceptability in view of recent scares caused by bovine spongioform encephalopathy.
Coralline-derived hydroxyapatite This biomaterial is derived from reef building coral of the genus Porites. The calcium carbonate exoskeleton is converted to hydroxyapatite by means of a hydrothermal chemical exchange, whilst still maintaining the original microstructure.33 The microstructure of the coral is similar to bone with a porous structure and pore size that facilitates bony ingrowth.34 A pore size of around 500 mm has been demonstrated to be optimal for bony ingrowth.35,36 Coral has a low potential for infectivity37,38 and antigenicity.39 Coralline hydroxyapatite has been shown to osseointegrate well in rabbits,40 rats,41 dogs,42 baboons43 and sheep.44 It has successfully been used in humans as a space filling material in maxillofacial surgery.38,45 However, it is fragile and does not appear to possess the mechanical strength46 to be used in load-bearing bone such as the proximal femur.
Polymethylmethacrylate (bone cement) This is a non-absorbable material widely used to fix prostheses in joint replacement surgery. It is a filling material and not glue. Although it has been used as a bone graft substitute in tumour surgery,47 it has many limitations including low tensile strength, brittleness and a tendency to provoke an aggressive osteolytic response.48 When used to replace lost bone stock in revision total hip arthroplasty the results have invariably been poor. Its application as a bone graft substitute is therefore limited.
Calcium sulphate (plaster of paris) Calcium sulphate was used as long ago as 1892 by Dreesman to fill bony defects caused by tuberculous osteomyelitis.49 Since then it has fallen into disfavour as it is quickly absorbed (within 4–8 weeks) and thus provides poor structural stability.50,51 In addition, it is prone to fracture when shear-loaded. Nevertheless, Coetzee reported excellent results in 110 patients when using calcium sulphate to
283 repair cranial defects. He reported complete substitution of calcium sulphate with bone within 8 weeks.52 There have been no other reports in the literature to support these dramatic results.
Glass-ionomer ceramics These are formed by sintering glass in different proportions of SiO2, Al2O3, CaF2 and AlPO4 with or without hydroxyapatite. Glass-ionomers are not resorbable, as bone cannot eliminate the silicate and aluminium from which they are constructed. They have been demonstrated to have good osseoconductive potential between particles, but not within them, as well as being biocompatible without causing foreign body reactions.53 After bony ingrowth has occurred, the glassionomer remains permanently within the new fibro-osseus matrix.54 It remains unclear whether this enhances structural stability or whether the persistence of unresorbed foreign particles prevents restitution of normal morphology with permanent weakening of the bone. These issues are still to be resolved in long-term studies. An ovine study using a glass-ionomer as a bone graft expander in impaction grafting of the femur performed at the University of Bristol showed good clinical, but poor histological results (with multiple voids within the graft and little graft incorporation) at 6 months.55
Absorbable ceramics Ceramics are manufactured by baking or firing minerals. The ceramics most commonly used as bone graft substitutes are made of tricalcium phosphate (Ca3(PO4)2) (TCP) and hydroxyapatite (Ca10(PO4)6(OH)2) (HA). Ceramic powder is obtained by precipitation from an aqueous solution, for example by adding ammonium phosphate ((NH4)HPO4) to a calcium nitrate solution (Ca(NO3)2) at pH of 11–12.56 This is then cold-pressed to form tablets. These are baked or fired at a high temperature (4800 1C) causing their crystals to fuse. This process is called sintering. This produces a dense material with a porosity by volume of between 1% and 5% (depending on parameters such as sintering temperature, sintering time and grain distribution). High porosity is achieved in the manufacturing process by one of a number of methods including the addition of glucose (which expands when heated and is then combusted), or the addition of hydrogen peroxide (H2O2) or naphthalene.57 Porosity is important as it allows effective ingrowth of bone (osteoconduction within the ceramic particles).40,58,59 Hanft states: ‘‘The principle limitation of calcium phosphate materials as hard-tissue implants has apparently been their mechanical properties.’’ He goes on to say ‘‘Unfortunately, these mechanical weaknesses have prevented this material from being used in cases where they must bear the initial structural load alone’’.60 In rebuttal Jarcho cites compressive strength of porous calcium phosphate as similar to that of cancellous bone while the tensile strength is 72% of the tensile strength of cancellous bone. Non-porous calcium phosphate has a tensile and compressive strength far in excess of both cancellous and cortical bone.61
ARTICLE IN PRESS 284 Bouler et al. studied the influence of five synthesis parameters on compressive strength of porous biphasic calcium phosphate ceramics.62 These parameters were as follows: 1. 2. 3. 4. 5.
Chemical composition Percentage of macropores Mean size of macropores Isostatic compaction pressure Sintering temperature.
Macroporosity and final sintering temperature exerted the major influences on compressive strength. Two ratios of HA:TCP were studied. These were 45% HA, 55% TCP and 75% HA, 25% TCP. The lower ratio of HA provided slightly better compressive strengths. Isostatic compression had comparatively little influence on compressive strength. The more porous the ceramic, the less resistant it was to compressive forces. For a given volume percentage porosity, a few 500 mm pores were better than many 100 mm pores. When the thickness of the bridges between the pores fell below a critical size, the ceramic structure disintegrated when subjected to even low compressive forces. Bouler’s study also showed that compressive strength increased significantly with a rise in sintering temperature. At 900 1C, boundaries between grains of ceramic were formed. Mechanical properties of biphasic ceramics are dependent on the number and size of these grain boundaries. At temperatures between 900 and 1100 1C densification (the elimination of connected and non-connected micropores) occurred. This densification corresponded with further increase in compressive strength. Blom et al. have demonstrated that porous biphasic absorbable ceramics can be manufactured that are both more stable and give more reproducible stability than allograft.63 Tsugura et al. have demonstrated the importance of porosity in allowing osteoconduction.35 They compared the same ceramic with different pore sizes, thus isolating pore size as the only variable. Their studies showed that a porosity of around 500 mm allowed greater bony ingrowth than smaller pores. Guillemin et al. compared the bony ingrowth into two species of coral implanted into both ovine and porcine long bones. Porites coral resorbed twice as fast as Acropora coral and had twice the bony ingrowth. Interestingly, Porites has a mean pore diameter of 250 mm (range 150–400) and Acropora coral has a mean pore diameter of 500 mm (range 200–800).64 It would therefore appear that both pore size and rate of resorption of the ceramic influence osteoconduction. Porosity also allows a greater degree of resorption to occur (by both dissolution and phagocytosis) as the surface area of the ceramic is increased. The body resorbs ceramics at different rates, depending on their chemical composition and structure. Two different biological processes govern resorption. These are dissolution (in physiological solutions) and phagocytosis. Frayssinet et al. observed both these processes causing resorption of calcium phosphate ceramics implanted into sheep bone. Multinucleated giant cells caused localised areas of
A. Blom resorption. In addition, a uniform dissolution was observed around the implant surfaces.65 Guillemin et al. have observed osteoclast resorption of implanted coral-derived ceramic.66 The dissolution of HA and TCP in both buffered acid and buffered basic solutions has been compared. The HA and TCP ceramics studied were prepared with similar structural characteristics, so that any difference in resorption would be due to their chemical compositions. The TCP ceramic dissolved 12.3 times faster in the acid and 22.3 times faster in the basic solution than the HA ceramic.67 Kay compared the dissolution rate of various calcium phosphates in an aqueous solution at 37 1C and pH of 7.3. TCP was 25 times more soluble than HA. Calcium phosphate was 667 times more soluble than HA.68 Shimazaki and Mooney compared both implant resorption and new bone formation between HA and TCP ceramics implanted into rabbit tibiae. At 24 weeks post-implantation, 46.4% of the TCP had resorbed compared with 27.5% of the HA. The HA however allowed 8% more new bone formation than the TCP.69 Ceramics have been used extensively as bone graft substitutes in humans. In a randomised study of spinal fusion in 341 patients, Ransford et al. obtained similar results with autograft and Triosites (a ceramic consisting of 60% hydroxyapatite and 40% tricalcium phosphate).70 As these materials contain no proteins, they do not provoke an antigenic response from host tissue.70,71 Porous hydroxyapatite has been used to repair tibial plateau fractures in a series of 17 patients with fracture union occurring in all cases.72 Oonishi reports excellent results using hydroxyapatite to fill massive acetabular73 and femoral74 defects at the time of revision hip replacement, despite the loads of up to 240% of body weight achieved whilst mobilising with crutches.75 Hydroxyapatite and tricalcium phosphate ceramics have demonstrated marked osteointegration and osteoconduction both radiologically and histologically in a number of studies in humans and animals.70,73,76–79 One of these ceramics has been successfully used in an impaction grafting model in sheep with clinical, radiological and histological changes comparable to allograft.80
Polyhydroxyacids Polyhydroxyacids have been used for the past 30 years to manufacture absorbable sutures such as Dexon, which is made from polyglycolic acid (PGA).81 Glycolic acid is a naturally occurring substance produced during normal human metabolism. It belongs to the same family of acids as lactic acid. PGA is most commonly used to manufacture multifilament yarns, but a variety of substances can be manufactured including screws,82 pins,83 rods84 and mesh.85 These have a wide range of clinical applications ranging from the internal fixation of wrist86 and elbow87 fractures, to the fixation of osteotomies.88 These products have the advantage of obtaining good fracture fixation and then gradually resorbing. PGA and polylactic acid (PLA) multifilament yarns have been synthesised as delivery agents for BMPs. These yarns
ARTICLE IN PRESS Which scaffold for which application have very consistent and predictable rates of bioabsorption and thus produce a controlled delivery of BMPs. In 1995, Robinson et al. described the use of blocks of porous PGA, which structurally mimic cancellous bone, to repair calvarial bone defects.89 Polyhydroxyacids have not been demonstrated to provide the structural support needed in high load bearing bone such as the acetabulum, proximal femur and proximal tibia.
Collagen matrix This are formed by a combination of purified fibrillar collagen (usually bovine) and ceramic composed of hydroxyapatite and tricalcium phosphate. The collagen provides a structure similar to extracellular matrix; however, it potentially has the same problems of bovine bone xenograft with regard to infection and antigenicity. Chapman et al. reported raised antibody titres in 12 patients treated with a bovine collagen—calcium phosphate graft material for long bone fractures. Despite this, the patients showed no ill effects. With regard to fracture healing, those treated with the collagen matrix material did as well as those treated with autograft.90 Collagen matrix substances have also been used experimentally in animals as cranial onlay grafts91 and to heal tibial defects in sheep92 and rabbits.93 Not all reports have been favourable. Muschler compared a collagen matrix substance to autograft when attempting spinal fusion in dogs. The collagen matrix substance performed markedly worse than the autograft.94 At present, these materials are available in a paste form and have FDA approval in the United States of America for fixation of long bone fracture defects, provided they are used in conjunction with internal or external fixation.
References 1. Denissen HW, de Groot K. Immediate dental root implants from synthetic dense calcium hydroxyapatite. J Prosthet Dent 1979; 42:551–6. 2. Bertrand B, Doyen A, Eloy P. Triosite implants and fibrin glue in the treatment of atrophic rhinitis: technique and results. Laryngoscope 1996;106:652–7. 3. Coetzee A. Regeneration of bone in the presence of calcium phosphate. Arch Otolaryngol 1980;106:405–9. 4. Hashimoto-Uoshima M, Ishikawa I, Kinoshita A, Weng H, Oda S. Clinical and histological observation of replacement of biphasic calcium phosphate by bone tissue in monkeys. Int J Periodon Rest Dent 1995;15(2):205–12. 5. Urist M, Strates B. Bone morphogenetic protein. J Dent Res 1971;50:1392–406. 6. Gavin S, Kenicer M, Teo P, Cresswell J, Foster K. Total elective hip and knee joint replacement: a comparative assessment. Scottish Needs Assessment Programme SNAP, 1993. 7. Galea G, Lumley S. SNBTS Strategic Review 1994/1995: tissue banking services. The ‘‘What’’ Phase, 1995. 8. Madhok R, Lewellen DG, Wallrichs SL, et al. Trends in the utilisation of primary total hip arthroplasty, 1969 through 1990: a population-based study in Olmsted County, Minnesota. Mayo Clin Proc 1993;68:11–8. 9. Galea G, Kopman D, Graham BJM. Supply and demand of bone allograft for revision hip surgery in Scotland. J Bone Jt Surg 1998;80-B:595–9.
285 10. Friedlander GE, Strong DM, Sell KW. Studies on the antigenicity of bone. Freeze-dried and deep-frozen bone allografts in rabbits. J Bone Jt Surg 1976;58-A:854–8. 11. Friedlander GE, Strong DM, Sell KW. Studies on the antigenicity of bone. Donor specific anti-HLA antibodies in human recipients of freeze-dried allografts. J Bone Jt Surg 1984;66-A:107–12. 12. Musculo DI, Caletti E, Schajowicz F, et al. Tissue typing in human massive allografts of frozen bone. J Bone Jt Surg 1987; 69-A:583–95. 13. Huo MH, Friedlander GE, Salvati EA. Bone graft and total hip arthroplasty. A review. J Arthroplasty 1992;7:109–20. 14. Simonds RJ, Holmberg SD, Hurwitz RL, et al. Transmission of human immunodeficiency virus type 1 from a seronegative organ and tissue donor. N Engl J Med 1992;326:726–32. 15. Buck B, Malinin T, Brown M. Bone transplantation and human immunodeficiency virus. An estimate of risk of acquired immunodeficiency syndrome (AIDS). Clin Orthop 1989;240: 129–36. 16. Lord CF, Gebhardt MC, Tomford WW, Mankin HJ. Infection in bone allografts. J Bone Jt Surg 1988;70-A:369–76. 17. Gie GA, Linder L, Ling RSM, Simon J-P, Slooff TJ, Timperley AJ. Impacted cancellous allografts and cement for revision total hip arthroplasty. J Bone Jt Surg 1993;75-B:14–21. 18. Harris AI, Sheinkop MB, Gitelis S, Rosenborg AG. Total hip replacement surgery using large proximal femoral allograft– prosthetic composites. New Orleans: AAOS; 1990. 19. Jofe MH, Gebhardt MC, Tomford WW, Mankin HJ. Reconstruction for defects of the proximal part of the femur using allograft arthroplasty. J Bone Jt Surg 1988;70-A:507–16. 20. Mankin HJ, Doppelt SH, Sullivan TR, Tomford WW. Osteoarticular and intercalary allograft transplantation in the management of malignant tumours of bone. Cancer 1982;50:613–30. 21. Meding J, Ritter M, Keating E, Faris P. Impaction bone-grafting before insertion of a femoral stem with cement in revision total hip arthroplasty. A minimum two year follow-up study. J Bone Jt Surg 1997;79-A:1834–41. 22. Eldridge JD, Smith EJ, Hubble MJ, Whitehouse SL, Learmonth ID. Massive early subsidence following femoral impaction grafting. J Arthroplasty 1997;12(5):535–40. 23. Kosuwon W, Laupattarakasem W, Saengnipanthkul S, Manhaisavariya B, Therapongpakdee S. Charcoal bamboo as a bone substitute: an animal study. J Med Assoc Thailand 1994;77(9): 496–500. 24. Li S, Liu Q, De Wijn J, Zhou B, De Groot K. Invitro calcium phosphate formation on a natural composite material, bamboo. Biomaterials 1997;18(5):389–95. 25. Dupoirieux L, Pourquier D, Souyris F. Powdered eggshell: a pilot study on a new bone substitute for use in maxillofacial surgery. J Cran Max Fac Surg 1995;23:187–94. 26. Heiple K, Kendrick R, Herndon C, Chase S. A critical evaluation of processed calf bone. J Bone Jt Surg 1967;49-A:1119–27. 27. Levai J, Boigard S. Acetabular reconstruction in total hip revision using a bone graft substitute. Clin Orthop 1996;330: 108–14. 28. Doherty M, Schlag G, Schwarz M, Mollan R, Nolan P, Wilson D. Bio and compatability of xenogeneic bone, commercially available coral, a bioceramic and tissue sealant for human osteoblasts. Biomaterials 1994;15(8):601–7. 29. Hubble M, Kuiper J, Learmonth I. The initial stability of femoral prostheses in human, bovine and sheep impacted bone graft. Act Orthop Scand 1996;67(Suppl. 272):92. 30. Hubble M, Goodship A, Learmonth I. Xenograft bone for impaction grafting in revision total hip arthroplasty. An in vivo pilot study. J Bone Jt Surg 1997;79-B(Suppl. IV):468. 31. Begley C, Doherty M, Mollan R, Wilson D. Comparative study of the osseoinductive properties of bioceramic, coral and processed bone graft substitutes. Biomaterials 1995;16(15): 1181–5.
ARTICLE IN PRESS 286 32. Charalambides C, Beer M, Cobb AG. Poor results after augmenting autograft with xenograft (Surgibone) in hip revision surgery: a report of 27 cases. Acta Orthop 2005;76(4):544–9. 33. Roy D, Linneham S. Hydroxyapatite formed from coral skeletal carbonate by hydrothermal exchange. Nature 1974;247: 220–2. 34. Cooke F. Ceramics in orthopaedic surgery. Clin Orthop 1992; 276:135–46. 35. Tsugura E, Takita H, Itoh H, Wakisaka Y, Kubokin Y. Pore size of porous hydroxyapatite as the cell-substratum controls BMPinduced osteogenesis. J Biochem 1997;121:317–24. 36. Kuhne J, Bartl R, Frisch B, Hammer C, Jansson V, Zimmer M. Bone formation in coralline hydroxyapatite. Acta Orthop Scand 1994;65(3):246–52. 37. Piecuch J, Fedorka N. Results of soft tissue surgery over replemineform hydroxyapatite. J Oral Maxillofac Surg 1983;41: 801–6. 38. Byrd H, Hobar P, Shewmake K. Augmentation of the craniofacial skeleton with porous hydroxyapatite granules. Plast Recon Surg 1993;91:15–22. 39. Begley C, Doherty M, Mollan R, Wilson D. Comparative study of the osseoinductive properties of bioceramic, coral and processed bone graft substitutes. Biomaterials 1995;16(15): 1181–5. 40. Kuhne J, Bartl R, Frisch B, Hammer C, Jansson V, Zimmer M. Bone formation in coralline hydroxyapatite. Acta Orthop Scand 1994;65(3):246–52. 41. Wang J, Aspenberg P. Basic fibroblast growth factor promotes bone ingrowth in porous hydroxyapatite. Clin Orthop 1996;333: 252–60. 42. Holmes R, Mooney V, Bucholz R, Tencer A. A coralline hydroxyapatite bone graft substitute. Clin Orthop 1984;188: 252–62. 43. Magan A, Ripamonti U. Geometry of porous hydroxyapatite implants influences osteogenesis in baboons. J Craniofac Surg 1996;7(1):71–8. 44. Gao T, Tuominen T, Lindholm S, Kommonen B, Lindholm T. Morphological and biomechanical difference in healing in segmental tibial defects implanted with biocoral or tricalcium phosphate cylinders. Biomaterials 1997;18:219–23. 45. Salyer K, Hall C. Porous hydroxyapatite as an onlay bone graft substitute for maxillofacial surgery. Plast Reconstr Surg 1981; 84:236–44. 46. Hanft J, Sprinkle R, Surprenant M, Werd M. Implantable bone substitute materials. Implant Biomater 1995;12(3):437–55. 47. Porsson B, Ekelund L, Londaal R, et al. Favourable results of acrylic cementation for giant cell tumours. Acta Orthop Scand 1984;55:209–14. 48. Jones L, Hungerford D. Cement disease. Clin Orthop 1987;225: 192–206. 49. Peltier L. The use of plaster of paris to fill defects in bone. Clin Orthop 1961;21:1–31. 50. Bell W. Resorption characteristics of bone and bone substitutes. Oral Surg 1964;17:650–7. 51. Edberg E. Some experiences of filling osseous cavities with plaster. Acta Chir Scand 1930;67:313–9. 52. Coetzee A. Regeneration of bone in the presence of calcium phosphate. Arch Otolaryngol 1980;106:405–9. 53. Suominen E, Aho A, Juhanoja J, Yli-Urpo A. Hydroxyapatite– glass composite as a bone substitute in large metaphyseal cavities in rabbits. Int Orthop 1995;19:167–73. 54. Jonck L, Grobbelaar C. A glass ionomer for reconstructive surgery: ionogran—an ionomeric microimplant. A biological evaluation. Clin Mater 1992;9:85–103. 55. Eldridge J, Cunningham J, Samuels A, Lawes T, Learmonth I, Goodship A. Glass ionomer as a potential osteoconductive expander of allograft in revision arthroplasty of the hip. Key Eng Mater 2001;192–195:951–4.
A. Blom 56. Wintermantel E, Suk-Woo H. Biokompatible Werkstoffe und Bauweisen. Implantate fur Medizin und Umwelt. Gebundene Ausgabe. Berlin: Springer; 1998. 57. Ravaglioli A, Krajewki A. Bioceramics, materials, properties, applications. London: Chapman & Hall; 1992. 58. Klawitter J, Hulbert S. Application of porous ceramics for the attachment of load bearing orthopedic applications. J Biomed Mater Res Symp 1971;2:161–230. 59. Tsugura E, Takita H, Itoh H, Wakisaka Y, Kubokin Y. Pore size of porous hydroxyapatite as the cell-substratum controls BMPinduced osteogenesis. J Biochem 1997;121:317–24. 60. Hanft J, Sprinkle R, Surprenant M, Werd M. Implantable bone substitute materials. Implant Biomater 1995;12(3): 437–55. 61. Jarcho M. Calcium phosphate ceramics as hard tissue prosthetics. Clin Orthop 1981;157:259–78. 62. Bouler J-M, Trecant M, Delecrin J, Royer J, Passuti N, Daculsi G. Macroporous biphasic phosphate ceramics: influence of five synthesis parameters on compressive strength. J Biomed Mater Res 1996;32:603–9. 63. Blom AW, Grimm B, Miles AW, Cunningham J, Learmonth ID. Subsidence in impaction grafting. The effect of adding a ceramic bone graft substitute. Eng Med Proc Inst Mech Eng Part H: J 2002;216:265–70. 64. Guillemin G, Meunier A, Dallant P, Christel P. Comparison of coral resorption and bone apposition with two natural corals of different porosity. J Biomed Mater Res 1989;23:765–79. 65. Frayssinet P, Trouillet JL, Rouquet N, Azimus E, Autefage A. Effects of the chemical composition of calcium phosphate ceramics on their osseointegration. Orthop Int 1993;1(4): 308–13. 66. Guillemin G, Patat J-L, Fournie J, Chetail M. The use of coral as bone graft substitute. J Biomed Mater Res 1987;21:557–67. 67. Jarcho M. Calcium phosphate ceramics as hard tissue prosthetics. Clin Orthop 1981;157:259–78. 68. Kay JF. Bioactive surface coatings for hard tissue biomaterials. In: CRC handbook of bioactive ceramics, vol. 2, 1990. p. 111–22 69. Shimazaki K, Mooney V. Comparative study of porous hydroxyapatite and tricalcium phosphate as bone substitute. J Orthop Res 1985;3(3):301–10. 70. Ransford A, Morley T, Edgar M, et al. Synthetic porous ceramic compared with autograft in scoliosis surgery. J Bone Jt Surg 1998;80-B(1):13–8. 71. Uchida A, Nade S, McCartney E, Ching W. The use of ceramics for bone replacement. J Bone Jt Surg 1984;66-B:269–75. 72. Itokazu M, Matsunaga T, Ishii M, Kusakabe H, Wyni Y. Use of arthroscopy and interporous hydroxyapatite as a bone graft substitute in tibial plateau fractures. Arch Orthop Trauma Surg 1996;115:45–8. 73. Oonishi H. Orthopaedic applications of hydroxyapatite. Biomaterials 1991;12:171–8. 74. Oonishi H, Iwaki Y, Kin N, Kushitani S, Murata N, Wakitani S, et al. Hydroxyapatite in revision of total hip replacements with massive acetabular defects. J Bone Jt Surg 1997;79-B(1): 87–92. 75. Bergmann G, Rohlmann A, Graichen F. Hip joint forces during physical therapy after joint replacement. Orthop Trans 1990; 14:303–4. 76. Frayssinet P, Braye F, Weber G. Analysis of sections of implanted macroporous calcium phosphate bone substitutes by protoninduced X-ray emission method and energy-dispersive spectrometry. Scanning 1997;19:253–7. 77. Hashimoto-Uoshima M, Ishikawa I, Kinoshita A, Weng H, Oda S. Clinical and histological observation of replacement of biphasic calcium phosphate by bone tissue in monkeys. Int J Periodon Rest Dent 1995;15(2):205–12. 78. Uchida A, Nade S, McCartney E, Ching W. The use of ceramics for bone replacement. J Bone Jt Surg 1984;66-B:269–75.
ARTICLE IN PRESS Which scaffold for which application 79. Bertrand B, Doyen A, Eloy P. Triosite implants and fibrin glue in the treatment of atrophic rhinitis: technique and results. Laryngoscope 1996;106:652–7. 80. Blom AW, Cunningham J, Hughes G, Lawes TJ, Smith N, Blunn G, et al. Functional and biological compatibility of ceramic bone graft substitutes as allograft extenders for use in impaction grafting of the femur. J Bone Jt Surg 2005;87-B:421–5. 81. Gilding D, Reed A. Biodegradable polymers for use in surgerypolyglycolic/poly(lactic acid) homo- and polymers. Polymer 1979;20:1459–64. 82. Hirvensalo E, Partio E, Bostman O, et al. Self-reinforced polyglycolide and polylactide rods and screws in the fixation of fractures and osteotomies. Br J Surg 1993;80(Suppl. 71). 83. Hope P, Williamson D, Coates C, Cole W. Biodegradable pin fixation of elbow fractures in children. A randomised trial. J Bone Jt Surg 1991;73-B(6):965–8. 84. Chapman M, Bucholz R, Cornell C. Treatment of acute fractures with a collagen—calcium phosphate graft material. J Bone Jt Surg 1997;79-A(4):495–502. 85. Ylinen P, Raekallio M, Toivonen K, Vanionpaa S. Preliminary study of porous hydroxyapatite particle containment with a curved biodegradable implant in the sheep mandible. J Oral Maxillofac Surg 1991;49(11):1191–7. 86. Casteleyn P, Handelburg F, Haentjens P. Biodegradable rods versus Kirschner wire fixation of wrist fractures. A randomised trial. J Bone Jt Surg 1992;74-B(6):858–61.
287 87. Makela E, Bostman O, Kekomaki M, et al. Biodegradable fixation of distal humeral physeal fractures. Clin Orthop 1992;283: 237–43. 88. Hirvensalo E, Partio E, Bostman O, et al. Self-reinforced polyglycolide and polylactide rods and screws in the fixation of fractures and osteotomies. Br J Surg 1993;80 (Suppl. 71). 89. Robinson B, Hollinger J, Szachowicz E, Brekke J. Calvarial bone repair with porous D,L-polylactide. Otolaryngol Head Neck Surg 1995;112:707–13. 90. Chapman M, Bucholz R, Cornell C. Treatment of acute fractures with a collagen—calcium phosphate graft material. J Bone Jt Surg 1997;79-A(4):495–502. 91. Schendel S, Bresnick S, Cholon A. Preliminary report: a ceramic containing crosslinked collagen as a new cranial onlay and inlay material. Ann Plast Surg 1997;38:158–62. 92. Gao T, Lindholm T, Kommonen B, et al. Enhanced healing of segmental tibial defects in sheep by a composite bone substitute composed of tricalcium phosphate cylinder, bone morphogenetic protein, and type IV collagen. J Biomed Mater Res 1996;32:505–12. 93. Suh H, Lee C. Biodegradable ceramic–collagen composite implanted in rabbit tibiae. ASAIO J 1995;41:M652–6. 94. Muschler G, Negami S, Hyodo A, Gaisser D, Easley K, Kambich. Evaluation of collagen ceramic composite graft materials in a spinal fusion model. Clin Orthop 1996;328:250–60.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 310–313
Available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/cuor
GENERAL
Non-compliance in orthopaedic surgery and its ethical challenges H. Sharma, E. Crane, B. Syme, M. Foxworthy Department of Trauma and Orthopaedic Surgery, Crosshouse Hospital, Kilmarnock, Scotland KA2 0BE, UK
KEYWORDS Ethics; Orthopaedics; Surgery; Patients; Non-compliance; Complications
Summary Non-compliance is described as ‘‘the degree to which patient behaviour (in terms of taking medication, following diets, executing lifestyle changes) is congruent with the recommendations of the health care provider. Non-compliance is a difficult problem, and can take many forms including patients not attending follow-up appointments and not taking prescribed medications. In trauma and orthopaedic surgery, the final outcome can be significantly compromised by poor compliance, resulting in morbidity to the patient as well as substantial financial implications to the health system. Knowing sub-groups of patients who are more likely to be non-compliant should enable us to predict those at risk of non-compliance in order to take necessary steps for improvement. In order to consider refusing treatment to a noncompliant patient there has to be robust ethical justification. All surgeons have a duty of care, which includes taking steps to improve patient compliance. & 2007 Elsevier Ltd. All rights reserved.
Introduction Non-compliance is a difficult problem, and can take many forms including patients not attending follow-up appointments and not taking prescribed medications. In trauma and orthopaedic surgery, the final outcome can be significantly compromised by poor compliance, resulting in morbidity to the patient as well as substantial financial implications to the health system. It is likely that the cases we see are merely the tip of the iceberg.1 Ethical challenges inevitably arise as a result of non-compliance, which affects patients as well as treating surgeons. Directly or indirectly, there Corresponding author. 44 Abercorn Road, Newton Mearns,
Glasgow G77 6NA, UK. Tel.: +44 141 639 3697; fax: +44 1563 577976. E-mail address:
[email protected] (H. Sharma). 0268-0890/$ - see front matter & 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2007.02.005
remains a wide gap between doctor–patient bonding in such situations in spite of offering medical care and formal treatment. We need to explore ways to improve compliance during what often becomes a counter-productive situation.
What is non-compliance? Non-compliance is described as ‘‘the degree to which patient behaviour (in terms of taking medication, following diets, executing lifestyle changes) is congruent with the recommendations of the health-care provider.’’2,3 Noncompliance can take several forms including failing to attend follow-up appointments, not adhering to post-operative instructions, not taking prescribed antibiotics and not complying with physiotherapy regimen. Non-compliance
ARTICLE IN PRESS Non-compliance in orthopaedic surgery does not always result in poorer outcomes4; however, this is a clear example of lack of compliance leading to a compromised outcome, chronic morbidity and disability. It has been suggested that the criticised term ‘non-compliance’ (described as being too authoritarian) be replaced by terms such as ‘‘adherence’’ and ‘‘concordance’’. The proponents of this terminology would argue that it suggests the problem lies in the doctor–patient relationship, not merely with the patient.5 Others would argue that simply changing the word used to describe the concept is a semantic solution that offers no additional meaning.6
Patients’ perception Patients’ priorities are different from their health care providers, therefore the patient places a higher value on something other than the surgeon’s primary objective; some patients do not understand their illness or the importance of following instructions given to them; others may not be in a position to follow these instructions. There are some patients who do not believe or trust their surgeons, whereas other non-compliant patients may simply have difficulty with life organisation. In addition, there are those patients who believe that their health care providers are solely responsible for their health and do not appreciate that they themselves have a crucial role to play. It should be remembered that a small number of patients deliberately do not comply with treatment and seek to prolong their illness.7 Sometimes these patients have deeprooted psychosocial difficulties and subconsciously may not want to get better. Alternatively, there are patients who seek financial or emotional rewards via ill-health. Both these groups of patients are very difficult to manage effectively and challenging them often results in further deterioration in the situation.
Patients at risk There are sub-groups of patients who are more likely to be non-compliant. These include younger patients as well as those living in social isolation.8 Those who misuse drugs or alcohol9,10 are also much more likely to default from treatment programs, as are those with emotional or mental health difficulties.10,11 Some people simply forget to follow advice or find it inconvenient to attend appointments or adhere to physiotherapy programs. To a certain extent, knowing this should enable us to predict those at risk of noncompliance in order to take necessary steps for improvement.
Surgeon’s role in non-compliance The patient alone cannot be blamed for non-compliance. It is the clinician’s responsibility to ensure patient understanding of the disease and the rehabilitation process, in language the patient understands. Non-compliance can occur simply because the patient does not understand the importance of following the surgeon’s instructions. Some patients also do not believe or trust their surgeon and this may be indicative of a poor doctor–patient relationship.7
311 When faced with non-compliance, irritation on the surgeon’s part can result in further deterioration in the relationship with the patient, perpetuating the problem. If a patient is labelled ‘‘non-compliant’’, it can often result in a prejudicial attitude towards the patient,12 especially when different health care professionals are involved in the same patient’s care. The non-compliant label is passed on and can result in preconceived misjudgements about the patient. The patient may be treated by several doctors and by doctors of varying experience, there can be disparity and discrepancy in the treatment advice given and the way urgency of rehabilitation explained. It is easy to overrule on the basis of non-compliance of the patient, nevertheless, one should look into it in more depth and detail.
Non-compliance and health system resources In health-care systems worldwide, it is inevitable that resource scarcity can contribute to non-compliance. Examples would be a significant wait for clinic appointments or surgery, delays in receiving physiotherapy or having to travel large distances for treatment. Another problem is when patients are not given enough support for co-existing medical problems whilst undergoing orthopaedic treatment. A typical example would be failing to provide a detoxification and support programme for those with substance misuse problems.9 A vicious cycle can occur in the form of noncompliance and being neglected in the wards and clinics. Patients who have poor experiences during hospital visits may be less likely to attend for further appointments.13 Lengthy clinic waiting times and a poor clinic environment are areas which could be improved. Financial restrictions on the patient may result in them not being able to travel to treatment centres, or not being able to pay for necessary treatment, depending on the type of healthcare system.
What should we do? As the causes of non-compliance are multi-factorial, so too must the solutions be. Clear communication with regular reinforcement of the therapeutic goals is the mainstay of achieving compliance. All the health care professionals who have contact with the patient must clearly and consistently reinforce the message to the patient. Patient education is vital and could utilise verbal, written and audiovisual materials. One effective strategy, if the patient agrees, is to involve family members, friends, etc. They can be a useful source of encouragement and may help patient compliance. Written or telephone reminders to prompt patients to attend for physiotherapy, clinic appointments or even surgery are useful as some patients simply forget their appointments. An efficient communication infrastructure is needed for this to be successful and is unfortunately not always available. Targeting high risk non-compliant groups should be employed. Those with drug and alcohol problems may be more co-operative if a detoxification programme is provided, which should continue in the out-patient setting. Conservative treatment may be preferable in some situations. Drug treatment tends to have better compliance if long-acting, infrequent dosing preparations are used so
ARTICLE IN PRESS 312 these should be prescribed where possible. Encouraging and achieving lifestyle changes can be very difficult. Weight loss and stopping smoking have positive benefits on the outcomes of orthopaedic surgery. Peer support groups, drug therapy and psychological support may all play a part.11 The clinic is one area where big improvements could be made. If patients’ expectations are modified and they are given realistic information about appointment waiting times and time spent in clinic (including investigations), patients may be more likely to attend.13 A pleasant clinic environment with sufficient, comfortable seating may also help. Although logistically challenging, co-ordinating clinic visits with physiotherapy appointments, imaging investigations and so on would minimise patient inconvenience and perhaps reduce non-attendance rates. Finally, the surgeon has a crucial role to play. He/she must not discharge all responsibility for compliance onto the patient. The surgeon must constantly educate and reinforce the importance of compliance in achieving the desired outcome. The surgeon must not be discouraged from attempting to improve compliance simply because another clinician has labelled the patient non-compliant. A good rapport fosters a healthy doctor–patient relationship which undoubtedly improves compliance. Patient non-compliance can be very frustrating for surgeons. All physicians have a duty of care and cannot refuse to treat patients in need of urgent medical care. Some ethical concepts however suggest that care could be refused in some circumstances; refusing care is a dangerous situation and must be backed up by sound ethical argument.
Patient autonomy in decision making: when does it become unsafe? Patient autonomy has become the most overwhelming principle in medical ethics. The first thing to establish would be, is the patient autonomous. There must be several components present for this to be the case. The patient must be fully informed, making a voluntary decision about their treatment and this decision must be based on reasoning. If any aspect is missing, then the patient may be said to have a lack of decision-making capacity, that is to say may be incompetent to make decisions.14,15 With an incompetent, non-compliant patient, the principle of beneficence can be used to justify treatment, so long as this treatment is recognised as reasonable by an appropriate group of peers. This principle is fairly easy to apply in certain groups of patients such as children, those with mental illness or those with acute confusional states. Here, the concept of paternalism16—which is usually unacceptable in this age of patient autonomy—may be safely applied. The grey area is that non-compliant patients are often deemed competent therefore further ethical principles have to be applied to their subsequent management.
Refusal of treatment to a non-compliant patient: is it ethical? In order to consider refusing treatment to a non-compliant patient there has to be robust ethical justification. The
H. Sharma et al. concept of futility can be helpful in refusal of treatment. Calling a treatment futile seems like a cold statement of fact rather than simple refusal of treatment without reason. The difficulty is that a particular treatment may be aiming to be curative and the surgeon may know that it is unlikely to succeed, yet if a patient (or their family) gain even a small improvement from the treatment, then it is difficult to call the treatment truly futile. Furthermore, how is likelihood of success versus failure quantified? Previous experience is not always applicable to the current situation and a percentage likelihood of treatment success cannot realistically be assigned to each patient. Therefore, with this in mind, treatment cannot be refused on the grounds of futility alone. Non-maleficence comprises a large part of the moral justification for refusing treatment. Doing no further harm is vitally important and it does not just refer to the patient. If treating a patient will do harm to others (family, staff members, other patients) it presents a morally challenging situation. A surgeon’s duty is to his patient, compliant or otherwise. A stronger case may be made for refusing treatment if it harms others but is not in itself justification for treatment refusal. It may be that changing from curative to maintenance treatment may cause less harm and be less futile, in the context of changing therapeutic goals (improvement rather than cure).17 One area that is always difficult to reconcile with sound ethical practice is financial considerations.18 This can be more problematic in a free health care system, where the surgeon is in the unenviable position of allocating scarce resources to the most needy. Decisions of this nature are seldom clear-cut, though refusing expensive, futile treatment in a non-compliant patient can be more easily justified than where the treatment is inexpensive. Surgeons also fear litigation in the difficult circumstance of a non-compliant patient. The possible resultant financial penalties undoubtedly influence decision making about these patients, in spite of ethical considerations.19 Whether it was the patient’s fault or the surgeon’s fault? It can be justified or counterjustified easily, however, without any net gain.
Conclusions With some patients, non-compliance cannot be improved and refusal of care may be contemplated. In such a situation, there must be a sound ethical argument to justify refusing treatment and it must not be simply based on irritation with the patient’s unwillingness to comply. If it is, the clinician will have failed in their duty of care to the patient and may leave themselves open to litigation. All surgeons have a duty of care, which includes taking steps to improve patient compliance.
References 1. Morris LS, Schulz RM. Patient compliance—an overview. J Clin Pharm Ther 1992;17:283–95. 2. Haynes RB. Introduction. In: Haynes RB, Taylor DW, Sackett DL, editors. Compliance in health care. Baltimore, MD: The John Hopkins University Press; 1979. 3. Kardas P. Non-compliance—some myths, some facts. Cas Lek Cesk 2004;143:556–60.
ARTICLE IN PRESS Non-compliance in orthopaedic surgery 4. King PJ, Malin AS, Scott RD, Thornhill TS. The fate of patients not returning for follow-up five years after total knee arthroplasty. J Bone Joint Surg Am 2004;86:897–901. 5. Baines LS, Zawada Jr ET, Jindal RM. Psychosocial profiling: a holistic management tool for non-compliance. Clin Transplant 2005;19:38–44. 6. Friberg F, Scherman MH. Can a teaching and learning perspective deepen understanding of the concept of compliance? A theoretical discussion. Scand J Caring Sci 2005;19:274–9. 7. Spaeth GL. ‘‘Noncompliance’’—not a patient problem, but rather a sign of a sick doctor–patient relationship. Ophthal Surg 1995;26:189–93. 8. Denhaerynck K, Dobbells F, Cleemput I, et al. Prevalance, consequences and determinants of nonadherence in adult renal transplant patients: a literature review. Transplant Int 2005;18: 1121–33. 9. Charalambous CP, Zipitis CS, Kumar R, Hirst P, Paul AS. Case report: managing fractures in non-compliant alcoholic patients—a challenging task. Alcohol Alcoholism 2003;38:357–9. 10. Seaborn Moyse H, Osmun WE. Discharges against medical advice: a community hospital’s experience. Can J Rural Med 2004;9:148–53.
313 11. Jindal RM, Joseph JT, Morris MC, Santella RN, Baines LS. Noncompliance after kidney transplantation: a systematic review. Transplant Proc 2003;35:2868–72. 12. Hill J. Non-compliance. Lancet 2004;363:9425. 13. Levesque J, Bogoch ER, Cooney B, Johnston B, Wright JG. Improving patient satisfaction with time spent in an orthopedic outpatient clinic. Can J Surg 2000;43:431–6. 14. Ganzini L, Volicer L, Nelson WA, Fox E, Derse AR. Ten myths about decision-making capacity. J Am Med Dir Assoc 2005;6: S100–4. 15. Capozzi JD, Rhodes R. Assessing a patient’s capacity to refuse treatment. J Bone Joint Surg Am 2002;84:691–3. 16. Capozzi JD, Rhodes R. Paternalism. J Bone Joint Surg Am 2001; 83:623. 17. Browne A, Dickson B, van der Wal R. The ethical management of the noncompliant patient. Camb Q Health Ethics 2003;12: 289–99. 18. Cleemput I, Kesteloot K, DeGeest S. A review of the literature on the economics of noncompliance. Room for methodological improvement. Health Policy 2002;59:65–94. 19. Crane M. How to cut loose from a troublesome patient. Med Econ 2000;77 54,59,63–6.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 288–297
Available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/cuor
HAND AND WRIST
Carpal dislocations D.S. Melsoma,, I.J. Leslieb a
Hand and Upper Limb Unit, Department of Orthopaedics, Princess Alexandra Hospital, Ipswich Road, Woolloongabba, Brisbane 4102, Australia b 2 Clifton Park, Clifton, Bristol BS8 3BS, UK
KEYWORDS Carpel dislocations; Lunate; Perilunate; Trans-scaphoid; Fixation
Summary Carpal dislocations represent a group of injuries for which an accurate diagnosis, prompt treatment and attention to detail are important to a successful outcome. It is possible to gain a functioning wrist and return patients to heavy manual work despite a severe injury. There is some evidence that the purely ligamentous injuries do less well than those combined with bony injuries perhaps due to the more frequent open reduction and anatomical restoration achieved in the latter. Salvage procedures include partial or total arthrodesis or proximal row carpectomy. Individual carpal bone excision appears to produce a poorer functional outcome. & 2007 Elsevier Ltd. All rights reserved.
Introduction Carpal dislocations are an important group of injuries in terms of their clinical and economic impact on the patient who is generally young. These injuries are easily missed and can be difficult to treat, with potential devastating effects on the patient if mismanaged. This article outlines the important aspects of diagnosis and management of these injuries, and provides an understanding of their classification.
History In 1855, prior to the introduction of radiography, Malgaigne1 and, slightly later, De Quervain,2 were the first to publish a description of perilunate fracture dislocations. The first true series was reported in 1906 by Tavernier in France,3 and in 1918, Destot studied the wrist more carefully and described Corresponding author.
0268-0890/$ - see front matter & 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2007.03.006
these injuries in greater anatomical detail.4 Unfortunately, enthusiasm for the study of wrist dislocations was lost until 1968, when Fisk presented the Royal College of Surgeons Hunterian Lecture on the concept of the intercalated segment. In 1972, Linscheid and Dobyns further modified the intercalated segment concept by introducing the terms volar intercalated segment instability (VISI) and dorsal intercalated segment instability (DISI). In 1980, Mayfield illustrated the mechanism of perilunar wrist instability as a series of four stages, resulting in perilunate dislocations or lunate dislocations.5 Recently much progress has been made in classifying these injuries, and further studies of the kinematics of the wrist have enabled more detailed insights into the mechanisms of injury and the rationale of reconstruction.
Epidemiology The true incidence and prevalence of these injuries are difficult to define precisely, and there are few studies that
ARTICLE IN PRESS Carpal dislocations give a clear picture of the epidemiology. However, there is a belief that perilunate injuries in general are underdiagnosed. The peak incidence is in the third decade with a predominance of males. The perilunate dislocation, the lunate dislocation and the perilunate fracture dislocation variants have been estimated to comprise less than 10% of all wrist injuries. In a study of 166 carpal dislocations by Herzberg in 1993, it was noted that perilunate fracturedislocations were more frequent than the perilunate dislocations at a ratio of two to one. The initial diagnosis was missed in 25% of cases.6
Anatomy Biomechanics The wrist has been thought of functionally in terms of either rows or columns, or even more recently, as a combination of the two. In reality, it is likely that individuals differ depending on anatomical variation in ligamentous laxity and the osseous configuration of the carpus, the distal radius and ulna. The object of carpal kinematics is to maintain joint congruency throughout all ranges of motion. The forces transmitted through the radius and ulna do vary and it has been calculated that the radius transmits 100% of the axial force with an ulna negative wrist but 30% of the force will go through the ulna if there is a ulna positive variance.7 Clearly the position of the wrist will also significantly alter the kinetics and therefore the forces through the wrist at the time of injury which will influence the injury pattern. Johnson8 divided the wrist into arcs which are named the greater and lesser arcs. These give rise to the terminology of greater and lesser arc injuries. The lesser arc injuries are those confined to ligamentous injuries around the lunate and greater arc injuries are fractures involving bones around the lunate. These are not to be confused with Gilula’s lines which are drawn along the borders of the carpal bones (Fig. 1) and are akin to Shentons’ line of the hip. Gilula’s
289 lines guide the eye looking for relational incongruity between the carpal bones.
Kinematics The lunate is the keystone in terms of comprehending the kinematics of the wrist and it is important to identify the factors influencing its position to help understand the various dislocation patterns. A compressive force across the wrist will exert a palmar-flexion force on the scaphoid. The triquetrum, due to its articular relationship to the hamate, will tend to dorsi-flex under compressive load. The triquetrum and scaphoid therefore influence the position of the lunate via their respective ligaments producing equilibrium of forces on the lunate with the default position of the lunate being slight dorsi-flexion. An imbalance in the forces secondary to trauma and disruption to the scapho-lunate or luno-triquetral ligaments will thus cause deformation in the normal relations within the carpus and lead to carpal instability. If the scapho-lunate ligament is ruptured the lunate rotates dorsally due to the reaction of the triquetrum creating the DISI pattern. If the luno-triquetral ligament is ruptured the lunate rotates volarwards with the scaphoid producing the VISI pattern. In terms of total flexion and extension, the midcarpal and radio-carpal joints roughly contribute an equal amount although there is individual variation. The midcarpal joint tends to provide more extension and the radio-carpal joint more flexion. In radial deviation the proximal carpal row moves from extension to flexion and the distal row dorsiflexes to compensate. As alluded to earlier, the more accurate the reduction of the carpus after injury, the better the outcome. It is therefore important to understand the normal carpal relationships and to restore them with appropriate treatment. The scapho-lunate angle, measured on a true lateral radiograph in neutral, normally lies between 301 and 601 and there is said to be scapho-lunate dissociation when this angle exceeds 701. The capitate and lunate should be almost collinear (7151). The carpal height ratio, which is the ratio of the carpus to the third metacarpal, should be approximately 0.54. Fig. 2 shows how to use a lateral radiograph to measure the axes of the various bones. In addition, translocation of the carpus in the ulna direction needs to be recognized. This measurement was made by comparing the distal radial articular width with the distance from radial styloid to the ulnar edge of the lunate. This ratio should be 0.87 þ0:04 (Fig. 3).9 There are other measurements which can be made but these provide a useful minimum set to assess whether a satisfactory reduction has been obtained.
Ligaments
Figure 1 Gilula’s arcs.
The carpal ligaments are pivotal in the stability and kinematics of the wrist joint and an understanding of their anatomy is important for wrist injury reconstruction. The carpal ligaments are divided into extrinsic and intrinsic, dorsal and volar. The intrinsic ligaments attach the carpal bones one to another. The dorsal and volar
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Figure 2 Axes for assessing the scaphoid, lunate, capitate and radius alignment on a lateral radiograph; R: Radius, C: Capitate, L: Lunate, and S: scaphoid. Reprinted from Greens Operative Hand Surgery, fifth edition, Green Hotchkiss, Pederson & Wolfe, Figs. 14-12 from Green: Green’s Operative Hand Surgery, 5/e, & 2005 Elsevier Inc., with permission from Elsevier.
Figure 3 Ulna translocation ratio R/P-Lu (radial articular surface length/styloid to ulna side of lunate, normal 0.87) and carpal height ratio, L2/L1 (0.54). Reprinted from Greens Operative Hand Surgery, fifth edition, Green Hotchkiss, Pederson & Wolfe, Figs. 14-14 from Green: Green’s Operative Hand Surgery, 5/e, & 2005 Elsevier Inc., with permission from Elsevier.
extrinsic ligaments are extra-articular and are often best appreciated from within the joint at arthroscopy. The important intrinsic ligaments include the scapholunate and the lunotriquetral ligaments of the proximal row, and the intrinsic ligaments of the distal row. The distal interosseous ligaments allow almost no movement at the distal row but the scapho-lunate and the luno-triquetral ligaments provide a complex link in proximal carpal interrelationship. The extrinsic ligaments are different histologically from the intrinsic ligaments and have also been shown to fail in a
different way due to their differing yield strengths. The intrinsic ligaments tend to fail at the bone–ligament interface whereas the extrinsic ligaments tend to fail midsubstance.10 This clearly has implications in terms of repair particularly of the scapho-lunate ligament. The main extrinsic dorsal ligament complex comprises the dorsal radio carpal ligament (DRCL) which runs from the radius to the triquetrum (radio-triquetral ligament). The dorsal intercarpal ligament reinforces the intrinsic ligament. There is no extrinsic dorsal ulno-carpal ligament. The deep and superficial volar ligaments form in such a way that creates a theoretical space and an actual area of weakness termed the ‘‘Space of Poirier’’ at the capito-lunate interval—between 4, 3 and 2 (Fig. 4). This is the ‘‘space’’ through which the lunate will dislocate in a lunate dislocation—the path of least resistance. The proximal radio carpal ligament links the radius and the proximal row, and the larger distal inverted ‘‘V’’ links proximal and distal rows while the radioscapho-capitate ligament links all three. The important ligaments are the radioscaphoid, radioscapho–capitate and short and long radio-lunate ligaments. The radioscapho-capitate ligament is a fulcrum for the scaphoid and it flexes and extends around this. Incidentally, the much quoted ligament of Testut is, in actual fact, not a true ligament and although it is termed the radioscapho-lunate ligament, it has no structural integrity and is thought to be a vascular supply for the scapho-lunate ligament and carpus. The palmar side comprises the radio-carpal and ulno-carpal ligaments. In 1980 Mayfield et al. performed a cadaver study which gave an insight into the probable sequence of injury in the perilunate spectrum of injury.4 On impact from a fall on the forward outstretched hand, the force through the wrist produces a supination injury and begins radially then either passes through the body of the scaphoid with a fracture, or through the scapho-lunate interval with ligamentous disruption. The four stages he described provide a spectrum of carpal injuries relating to lunate and perilunate dislocations. These are illustrated in Fig. 5 and are defined as: stage 1, progressive rupture of the scapho-lunate ligament from volar to dorsal, followed by stage 2, dorsal dislocation of the capitate with dissociation
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Figure 4 Carpal ligaments; 1: radio-scaphocapitate lig; 2: ulno-capitate lig; 3: long radio-lunate lig; 4: Scapho-lunate lig; 5: Radiolunate lig; 6: luno-triquetral lig; 7: radio-triquetral lig. Reprinted from Greens Operative Hand Surgery, fifth edition, Green Hotchkiss, Pederson & Wolfe, Figs. 14-2 from Green: Green’s Operative Hand Surgery, 5/e, & 2005 Elsevier Inc., with permission from Elsevier.
at the luno-capitate joint with tearing at the space of Poirier, then stage 3, luno-triquetral ligament disruption, with the rest of the carpus being displaced, usually dorsally, and finally, stage 4 is complete ligament disruption with the lunate forced volarwards by the proximal portion of the capitate resulting in dislocation of the lunate through the space of Poirier. A fall on the hand placed behind the body results in the reactive force through the ulna side of the wrist producing a pronation type injury. The ligament disruption then starts with the luno-triquetral and propagates in the reverse direction—sometimes called a ‘‘reverse Mayfield injury’’.
Diagnosis As noted in the study by Herzberg and Garcia-Elias, carpal dislocations are often missed on initial evaluation.6,11 What is required is a good history of the mechanism of injury, a high index of suspicion and adequate assessment, both clinically and radiographically. A reason for misdiagnosis can be the fact that these injuries are high energy causing multiple injuries, resulting in the less obvious wrist injuries being overlooked. It is also important to remember that a missed chronic dislocation can fool the unwary, as the amount of wrist movement can be deceptively good in some cases. Neurological sequelae are not uncommon and in particular the median nerve is at risk from perilunate dislocations and volar lunate dislocations. In the assessment of acute injuries the following radiological images are mandatory: a postero-anterior (PA) in neutral rotation, a lateral and an oblique view (451 pronated). The lateral view is pivotal and if there is any concern that the radius, lunate and the capitate are not in alignment then a carpal disruption must be suspected. Figs. 6a and b show a volar lunate dislocation on the lateral not seen so well on the PA where there is, however, overlapping of the scaphoid, lunate and capitate. The radiographic sign is the ‘‘spilled teacup’’ sign of the lunate when it rotates anteriorly around the radio-lunate ligament.
This frank dislocation of the lunate is, however, the extreme end of a spectrum of injuries.
Mechanism of injury Most carpal dislocations result from a staged disruption of the ligamentous structures as described by Mayfield. Forces may be directed through the carpal bones themselves resulting in a fracture. Less commonly the forces are transmitted through the ulnar side of the wrist as a result of falling backwards producing a pronation of the carpus. This can result in a trans-triquetral perilunate injury. The capitate–hamate diastasis injury is rather different in that it is caused by an anterior–posterior crush type force which forces the intrinsic ligaments apart and, because this is radiographically quite subtle, is easily missed.
Classification These injuries may be acute or chronic. (i) Perilunate injury (A) Lesser arc 1. Dorsal or volar perilunate dislocation or isolated lunate dislocation (end stage perilunate dislocation). (B) Greater arc 1. Dorsal or volar fracture/dislocations. (ii) Axial dislocations (iii) Isolated carpal dislocations
(I) Perilunate injuries A. Lesser arc injuries Scapho-lunate ligament rupture The lesser arc injures are a spectrum of disorders and this first stage is described by Mayfield as stage 1.
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Figure 6 Palmar lunate dislocation with ‘‘spilled teacup’’ sign on the lateral and crowded carpus on the AP.
Figure 5 (a) Mayfield’s stages of perilunate injury. Sagittal plane; (b) Mayfield’s sequence PA view. Reprinted from Greens Operative Hand Surgery, fifth edition, Green Hotchkiss, Pederson & Wolfe, Figs. 14-6 from Green: Green’s Operative Hand Surgery, 5/e, & 2005 Elsevier Inc., with permission from Elsevier.
Dorsal perilunate dislocations After scapho-lunate injuries these are the most common injuries seen—the lunate remains within the lunate fossa of the radius whilst the remainder of the carpus displaces dorsally (Fig. 7). Lunate dislocations The lunate is most commonly dislocated in a palmar direction leaving the volar and ulno-lunate ligaments intact. Palmar perilunate injuries These are rare injuries being only 3% of all perilunate injuries and are most likely to represent a hyperflexion and supination force at the time of injury. It is not uncommon for the scaphoid to have been fractured and, unlike the trans-
Figure 7 Dorsal perilunate dislocation (with permission from Dr. M. Ross, Brisbane).
scaphoid perilunate injury, the fracture is usually more vertical and unstable. It is characterized by the ‘‘crowded carpus’’ sign similar to Fig. 6 on the PA view, although it is more easily diagnosed on the lateral radiograph. These are extremely unstable injuries. Luno-triquetral ligament rupture These are a variation of the Mayfield injuries and can be thought of as a reverse stage 1 with forces opposite of those producing the scapho-lunate ligament injury.
ARTICLE IN PRESS Carpal dislocations
(B) Greater arc injuries Perilunate fracture dislocations These can occur in a variety of configurations (Fig. 8a and b). By far the most commonly encountered is the transscaphoid perilunate injury which accounts for 60% of carpal dislocations. These usually involve a transverse fracture of the scaphoid waist with the proximal portion remaining with the lunate, although according to Herzberg, 3.6% will also have an SL ligament injury. Trans-scaphoid, trans-capitate perilunate dislocations— described by Fenton—are caused by hyperextension during which the capitate is forced against the dorsal distal radius and result in a transverse fracture of the capitate, the proximal part of which is then forced into a volar tilt by the eventually normally aligned distal fragment.
293 cases a trans-triquetral injury occurs instead of a rupture of the luno-triquetral ligament resulting in a greater arc injury.
(II) Axial fracture/dislocations of the carpus These are caused by crush injuries resulting in splitting of the column of the carpus where there is an axial division leaving the radial carpus aligned normally with the radius, and the ulna side displaced, or the ulna portion normally aligned with the radius and the radial portion of the carpus displaced. The injury may also split the corresponding metacarpals with their respective carpus and clearly this can also result in a severe soft tissue injury and a high level of suspicion should exist for compartment syndrome and neurovascular injury (Fig. 9).
(III) Isolated carpal dislocations Transtriquetral perilunate dislocations This represents a reverse Mayfield’s injury and most commonly this is a ligamentous injury (75%) only. In this case the luno-triquetral ligaments are torn while the distal row pivots around the lunate making it a lesser arc injury. The radio-lunate ligaments, presumably being stronger, keep the lunate in position, while the weaker lunotriquetral ligament ruptures. Only in about a quarter of
All the carpal bones have been reported to dislocate in an isolated fashion and probably represent a localized injury directed over the bone concerned. The scaphoid has been shown to dislocate anteriorly (type 1) or in association with a capitate–hamate injury (type 2). These injuries are too rare for the exact mechanism of injury to be identified but a violent force is presumed to be required with a sudden pronation with the wrist in ulna deviation and extended wrist probable for the type 1 injury.11 The pisiform can be avulsed from its ligamentous attachments by forced and violent contraction of the flexor carpi ulnaris, and may dislocate proximally or distally, if, for example, the tendon itself ruptures.12 The trapezium and the trapezoid have also been reported as isolated dislocations.13,14 Isolated triquetral dislocations have been described only four times in the literature. A crushing injury was described in two, the others being of uncertain aetiology.15 The capitate has been reported to have been dislocated three times with two volar and one dorsal displacement. All were reduced by open reduction apparently successfully.16 The hamate has also reported to have been dislocated by high energy injuries or penetration of the carpus causing direct displacement. Either removal, open reduction or closed reduction appears to have been satisfactory in the few cases.17
Treatment
Figure 8 (a) Trans-styloid perilunate dislocation variation. Note the previous scapho-lunate ligament repair from a previous injury; (b) post-reduction, k-wire and dorsal scapholunate ligament reconstruction.
Carpal dislocations require urgent identification and reduction to avoid a poor outcome. There are three main categories of treatment, namely, closed reduction and cast, closed reduction and percutaneous Kirschner-wire (k-wire) fixation and open reduction with fixation. It is important to reduce the dislocation as soon as possible. This is best achieved in the operating theatre; however, if there is no immediate access to theatre it may be necessary to perform a closed reduction in the emergency room if there is neuro-vascular compromise. Either regional or general anaesthetic is required. Longitudinal traction is applied to the wrist for several minutes
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Peri-trapezoide Peri-trapezium
Trans-hamate Peri-pisiform
Peri-trapezium
Peri-hamate Peri-pisiform
Trans-trapezium
Peri-hamate Trans-triquetrum
Figure 9 Axial carpal injuries. Reprinted from Greens Operative Hand Surgery, fifth edition, Green Hotchkiss, Pederson & Wolfe, Figs. 14-71 from Green: Green’s Operative Hand Surgery, 5/e, & 2005 Elsevier Inc., with permission from Elsevier.
before attempting the reduction manoeuvre. An effective way of achieving traction is to use Chinese finger traps attached to the index and middle fingers. The fingers may be suspended vertically or horizontally with the elbow at right angles. Weights can be added to the arm or fingers to increase the traction which can be left for several minutes to take advantage of the visco-elasticity of the tissues before the reduction is attempted. In order to identify the injury pattern more effectively, it is useful to obtain radiographic images in traction. Closed reduction is then attempted and the manoeuvre for a lunate dislocation is one method which was originally described by Tavernier in the early 1900s.18 This involves applying a counterforce to the volar lunate while simultaneously flexing the wrist (capitate) over the lunate with axial traction. Reduction should be accompanied by a definite click as the capitate engages with the lunate. Although closed reduction is used for initial treatment, further stabilization is usually necessary to maintain an accurate reduction. In particular, a trans-scaphoid injury has a high incidence of non-union without internal fixation of the scaphoid fracture despite a good initial reduction of the fracture.
Closed reduction and percutaneous fixation Closed reduction and percutaneous fixation are acceptable if the reduction can be achieved with accuracy. The temptation to compromise must be avoided. In cases where the acute injury is being managed by a surgeon with less experience it is preferable to perform closed reduction, apply a cast and refer for more specialist management. Inappropriate initial surgery can compromise the definitive repair. The priority in closed reduction is to maintain a satisfactory position of all carpal bones and this can often be achieved using k-wires. Temporary k-wires inserted dorsally into the lunate and scaphoid can be used as joysticks to achieve correct relative orientation. Definitive wires can be placed from the scaphoid into the lunate to maintain reduction. If a satisfactory reduction is achieved on image, a second wire is placed from the scaphoid into the capitate once traction has been relieved and a third wire placed across the luno-triquetral articulation. Generally, the wires are removed after 6–8 weeks and the wrist splinted for a further 6 weeks to allow the ligamentous disruption to heal. If the scaphoid fracture is adequately reduced, it is possible to fix this percutaneously with a cannulated differential pitch screw using the technique described by
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Slade.19 There is, however, a risk of causing fracture displacement if there is instability and this may necessitate open reduction. k-wires fixation for stabilizing the scaphoid fracture may be possible but is not ideal. An image intensifier is generally used to reduce and fix the carpal bones; however, arthroscopy is also useful although comparative studies have not been undertaken to compare the two methods.
Open reduction Studies would suggest that open reduction and internal fixation give the most satisfactory results in terms of anatomical restoration and outcomes. Subtle injuries may be found such as small osteochondral fractures, which were not initially seen on plain films. These may well require reattachment and other ligamentous injuries can be more accurately repaired and intra-articular soft tissue removed. This infers, but does not prove, a better outcome. If a displaced scaphoid fracture is present then open reduction is required. If the injury is a purely ligamentous one then the decision whether to perform an open repair needs to be made according to the type of injury, the degree of instability and the likelihood of anatomical reduction with more conservative techniques. Patient factors such as age and occupation will also influence the decision as to whether open reduction is preferable.
Approach What approach is best to use? Dorsal, volar or a combined approach? The fear has always been that a dorsal approach would lead to lunate and scaphoid avascular necrosis due to interference with their blood supply. This has so far remained a theoretical rather than a real complication. Campbell et al.20 reported on nine patients with a dorsal perilunate dislocation reduced via a dorsal approach with no avascular complications. The lunate or proximal pole of the scaphoid will sometimes exhibit signs of increased radio density in the ensuing post-operative period but this does not generally lead to collapse but resolves as revascularization occurs. The dorsal approach allows greater accuracy in reduction of the scapho-lunate interval and repair of the ligament while, with a volar lunate dislocation a volar approach allows the important volar ligaments to be repaired and the carpal tunnel to be decompressed. The scapho-lunate and luno-triquetral ligaments may avulse from the bone–ligament interface and reattachment of the ligament may require intraosseous sutures or bone anchor fixation to provide adequate reconstruction. The dorsal approach is made via a longitudinal incision over the wrist centered on Lister’s tubercle. The third dorsal compartment is entered and extensor pollicis longus retracted. The fourth compartment is then subperiostealy elevated in an ulna direction to aid exposure of the dorsal capsule. Alternatively the fifth dorsal compartment may be incised and the distal half of the extensor retinaculum reflected to Lister’s tubercle. The capsule may be found to be avulsed from the radius and require repair. The palmar approach is via an extended carpal tunnel incision retracting the median nerve radially. The lunate and
Figure 10 View of the carpal tunnel showing the lunate (arrow) displaced through the volar capsular rent into the space of Poirier (with permission from Dr. M. Ross, Brisbane).
volar capsular rent will be visible in a palmar lunate dislocation and it can be reduced through this and the capsule repaired (Fig. 10). Several authors recommend utilizing a palmar approach in addition to the dorsal one and Sotereanos used combined approaches in 11 perilunate fractures and fracture-dislocations and obtained good clinical results at a mean follow-up of 30 months.21 Ligament repair There is a trend for direct ligamentous repair in carpal dislocations in an attempt to improve long-term stability. Several studies have shown the superiority of this method but it is not clear whether this is due to a greater accuracy of reduction or due to the repair of the ligaments. Adkinson treated cases via a dorsal approach and direct visualization of reduction and percutaneous pinning without repair of the ligaments with good results.22 In the absence of data to answer this question, it is recommended that significant ligamentous injuries should be repaired during open reduction which will most often require a combined dorsal and palmar approach. The dorsal approach will provide access to the scapho-lunate ligament and dorsal luno-triquetral ligament, and the palmar approach will allow repair of the volar luno-triquetral ligament and the extrinsic radioscaphocapitate ligament (Fig. 11). Fracture fixation The greater arc injuries involving a fracture of the scaphoid require fixation even if undisplaced, as non-operative
ARTICLE IN PRESS 296
Figure 11 Dorsal approach to the wrist, demonstrating disruption of the scapho-lunate interosseous ligament and a chronic (8 month) dorsal lunate dislocation.
treatment leads to a non-union rate of about 50%.23 These are extensive injuries and the amount of energy imparted to the tissues is much greater than for an isolated undisplaced scaphoid fracture. In order to fix the scaphoid, various types of screw fixation can be used. There are no direct studies comparing acute fixation methods in such injuries, but a study from Derby (UK) looked at healing rates and adequacy of fixation in scaphoid non-unions.24 Double k-wire fixation, Herbert screw and AO mini fragment screw fixations were compared in terms of union rates and time in the cast. The two screw fixations achieved similar rates of union (85% and 77%, respectively) but the wire fixation resulted in much reduced union rates (55%) with prolonged immobilization. k-wire fixation provides inadequate compression and it may indeed result in distraction at the fracture site. If there is significant comminution of the scaphoid, primary bone grafting may be required to prevent malunion in a ‘‘humpback’’ deformity (Fig. 12).
Treatment of late injuries There are a significant number of injuries which are missed on initial presentation. It is well established that delayed treatment as well as the adequacy of reduction influences the final outcome. Reduction of a perilunate dislocation has been undertaken by the authors at 35 weeks with a good result at one year. Even at this stage attempt at reduction should be made as the results are better than expected. Reduction may be facilitated by external fixator application prior to definitive treatment by open reduction. If good anatomical reduction is not achieved then the results tend to be poor. If reduction is not possible and the patient is symptomatic, then a proximal row carpectomy may be helpful for a lunate dislocation. An arthrodesis, especially for an old perilunate dislocation, is considered a useful salvage procedure. Excision of the lunate or scaphoid in isolation gives a poor result.25
Prognosis Herzberg et al. looked at the outcomes of trans-scaphoid perilunate injuries. Of 14 treated with acute open reduction
D.S. Melsom, I.J. Leslie
Figure 12 Acute fracture of the scaphoid showing flexion with proximal fragment rotation. Reprinted from Greens Operative Hand Surgery, fifth edition, Green Hotchkiss, Pederson & Wolfe, Figs. 14-16 from Green: Green’s Operative Hand Surgery, 5/e, & 2005 Elsevier Inc., with permission from Elsevier.
and internal fixation, the mean Mayo wrist score was 86 for the Mayfield stages ii or iii and 79 for stage iv (normal 100).26 Aspergis et al. looked at 28 cases of perilunate dislocations and fracture/dislocations and eight of these were treated with closed reduction alone and 19 with internal fixation. It was suggested that the poorer outcome in the closed treatment group was related to the instability of the injury with lack of direct anatomical reduction and ligament repair. The scoring system used, however, was not validated and the groups were somewhat heterogeneous.27 Minami et al. treated 13 patients with lunate and perilunate dislocations and correlated the anatomical reduction from post-operative radiographs with the followup clinical outcome at an average of 2 years. They suggested that a scapho-lunate gap of greater than 3 mm leads to a poorer functional outcome. Two of their patients failed to obtain normal carpal architecture and both went on to have wrist arthrodesis and proximal row carpectomy.28 In both greater and lesser arc injuries, the best radiological results were observed after open reduction, internal fixation and direct ligament repair. In the greater arc group, the fixation of the scaphoid alone was not always sufficient and occasionally a scapholunate dissociation, luno-triquetral dissociation, ulnar translation of the carpus or other carpal collapse pattern remained at follow up. The initial appraisal of both the osseous and ligamentous pathology was felt to be very important and best performed at operation. Weir described the outcomes of late perilunate reductions. The radiographic assessment and the range of movement were relatively poor at a mean follow up of two years although the functional results were surprisingly good despite radiographic evidence of arthrosis in 57%.29 In a study by Garcia-Elias, however, delayed treatment of dorsal perilunate dislocations had a significant correlation with poorer outcome. Poorer outcomes were also correlated with accuracy of reduction and maintenance of reduction.30
ARTICLE IN PRESS Carpal dislocations For trans-scaphoid perilunate injuries the average Mayo clinic score at eight years was 79 (normal 100) with recovery of 1101 of movement and 75% grip strength. The poorer results have been associated with poor anatomic restoration e.g., ulna translocation or a higher energy injury with a stage iv Mayfield injury.26 Although traditionally many of these injuries, whether treated by open or closed means, have been treated with prolonged immobilization, there is increasing evidence that earlier mobilization is better and does not seem to compromise the ligamentous repair. Inoue et al. treated 28 trans-scaphoid perilunate injuries with open reduction, ligament repair and Herbert screw fixation of the scaphoid and noted that those treated by 4 weeks of cast immobilization had a significantly better range of movement than those with greater than 5 weeks.31
References 1. The active and exemplary life of J. F. Malgaigne, surgeon of Lorraine (1806–1865). Ann Med Nancy 1965;4:527–49. 2. Thurston AJ. ‘AO’ or Eponyms: the classification of wrist fractures. ANZ J Surg 2005;75:347. 3. Tavernier L. Les de ´placements traumatiques du semilunaire. The ´se. Lyon; 1906. p. 138–9. 4. Destot E. Injuries of the wrist: a radiological study. [Atkinson FRB, Trans.]. New York, NY: Paul B Hoeber; 1926. 5. Mayfield JK, Johnson RP, Kilcoyne RK. J Hand Surg 1980;5: 226–41. 6. Herzberg G, Comtet JJ, Linscheid RL, Amadio PC, Cooney WP, Stalder J. Perilunate dislocations and fracture-dislocations: a multicenter study. J Hand Surg [Am] 1993;18(5):768–79. 7. Palmer AK, Werner FW. Biomechanics of the distal radio-ulna joint. Clin Orthop 1984;187:26–35. 8. Johnson RP. The acutely injured wrist and its residuals. Clin Orthop 1980;149:33–44. 9. Bouman HW, Messer E, Sennwald G. Measurement of ulnar translation and carpal height. J Hand Surg 1994;19B:325–9. 10. Berger RA, Kauer JM, Landsmeer JM. Radioscapholunate ligament: a gross anatomic and histologic study of fetal and adult wrists. J Hand Surg [Am] 1991;16(2):350–5. 11. Garcia-Elias M, Irisarri C, Henriquez A, Abanco J, Fores J, Lluch A, Gilabert A. Perilunar dislocation of the carpus. A diagnosis still often missed. Ann Chir Main 1986;5(4):281–7. 12. Sharara KH, Farrar M. Isolated dislocation of the pisiform bone. J Hand Surg [Br] 1993;18:195–6. 13. Siegel MW, Hertzberg H. Complete dislocation of the greater multangular (trapezium). J Bone Joint Surg Am 1969;51: 769–72.
297 14. Inoue G, Inagaki Y. Isolated palmar dislocation of the trapezoid associated with attritional rupture of the flexor tendon. J Bone Joint Surg Am 1990;72:446–8. 15. Goldberg B, Heller AP. Dorsal dislocation of the triquetrum with rotary subluxation of the scaphoid. J Hand Surg [Am] 1987;12: 119–22. 16. Lowrey DG, Moss SH, Wolff TW. Volar dislocation of the capitate: report of a case. J Bone Joint Surg Am 1984;66:611–3. 17. Gunn RS. Dislocation of the hamate bone. J Hand Surg Br 1985; 10:107–8. 18. Micheloni P. Information and medical curiosities in the Voyages of Jean Baptiste Tavernier (1605–1680). Ann Med Nav (Roma) 1950;55(6):768–82. 19. Slade JF, Jaskwhich D. Percutaneous fixation of scaphoid fractures. Hand Clin 2001;17(4):553–74. 20. Campbell RD, Thompson TC, Lance EM, Adler JB. Indications for open reduction of lunate and perilunate dislocations of the carpal bones. J Bone Joint Surg Am 1965;47:915–37. 21. Sotereanos DG, Mitsionis GJ, Giannakopoulos PN, Tomaino MM, Herndon JH. Perilunate dislocation and fracture dislocation: a critical analysis of the volar-dorsal approach. J Hand Surg [Am] 1997;22(1):49–56. 22. Adkison JW, Chapman MW. Treatment of acute lunate and perilunate dislocations. Clin Orthop Relat Res 1982;164: 199–207. 23. Gelberman RH, Wolock BS, Siegel DB. Fractures and non-unions of the carpal scaphoid. J Bone Joint Surg Am 1989;71:1560–5. 24. Christodoulou LS, Kitsis CK, Chamberlain ST. Internal fixation of scaphoid non-union: a comparative study of three methods. Injury 2001;32(8):625–30. 25. Siegert JJ, Frassica FJ, Amadio PC. Treatment of chronic perilunate dislocations. Hand Surg [Am] 1988;13(2):206–12. 26. Herzberg G, Forissier D. Acute dorsal trans-scaphoid perilunate fracture-dislocations: medium-term results. J Hand Surg [Br] 2002;27:498–502. 27. Apergis E, Maris J, Theodoratos G, Pavlakis D, Antoniou N. Perilunate dislocations and fracture-dislocations. Closed and early open reduction compared in 28 cases. Acta Orthop Scand Suppl 1997;275:55–9. 28. Minami A, et al. Correlation between clinical results and carpal instabilities in patients after reduction of lunate and perilunate dislocations. J Hand Surg 1986;11-B:213–20. 29. Weir IG. The late reduction of carpal dislocations. J Hand Surg [Br] 1992;17(2):137–9. 30. Garcia-Elias M, Irisarri C, Henriquez A, Abanco J, Fores J, Lluch A, et al. Perilunar dislocation of the carpus. A diagnosis still often missed. Ann Chir Main 1986;5(4):281–7. 31. Inoue G, Imaeda T. Management of trans-scaphoid perilunate dislocations. Herbert screw fixation, ligamentous repair and early wrist mobilization. Arch Orthop Trauma Surg 1997; 116(6–7):338–40.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 298–300
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SYNDROMES
Duchenne muscular dystrophy Benedict J.A. Lankestera, Michael R. Whitehouseb, Martin F. Garganc, a
Specialist Registrar in Trauma and Orthopaedics, Avon Orthopaedic Centre, Southmead Hospital, Westbury-on-Trym, Bristol BS10 5NB, UK b SHO in Trauma and Orthopaedics, Bristol Royal Infirmary, Bristol BS2 8HW, UK c Consultant in Trauma and Orthopaedics, Bristol Royal Infirmary and Bristol Hospital for Sick Children, Bristol BS2 8HW, UK
Introduction
Clinical presentation and diagnosis
In 1868, Guillaume Duchenne (1806–1875), working in Paris, described a ‘‘pseudohypertrophic paralysis y which deceives and deludes by giving the limbs the appearance of great muscularity’’.1 Duchenne muscular dystrophy (DMD) is the most common childhood neuromuscular disorder, was the first muscular dystrophy described, is incurable at present and is invariably fatal. The disease involves a progressive degeneration of skeletal muscle without associated abnormality in the central or peripheral nervous system.2
Affected boys are normal at birth and early motor milestones may be appropriate (head control, sitting, etc.). Independent ambulation is usually delayed, with tiptoe walking and delayed speech. Steady progression results in a waddling gait with frequent stumbling and tripping, difficulty standing up and problems with stair climbing. Proximal muscle weakness precedes distal. Early involvement of the gluteal musculature results in Gower’s sign (when rising from the floor, the child ‘‘walks’’ his hands up his thighs due to weakness of hip extension, although widely described as pathognomonic for DMD, this sign can also be present in the early stages of discitis).3 Relative sparing of tibialis posterior function causes tiptoe walking and equinovarus deformity (Fig. 1). Another classic feature is calf pseudohypertrophy due to fibro-fatty infiltration, giving a firm rubbery feel on palpation. By the age of 7, walking becomes increasingly difficult. The knee is hyperextended and the torso tilted back in an attempt to lock out the hip and knee joints. The ability to walk is lost on average at 9 years of age (range 6–12), after which the patient becomes wheelchair bound and may develop severe flexion contractures. Scoliosis affects 90%, with progressive collapse into a C shape, and severe pelvic obliquity leading to loss of sitting balance. Painful hip dislocation may occur. Most die in their early 20s from cardio-respiratory failure. The lack of dystrophin in the cell membrane leads to the release of creatine kinase (CK) from myocytes, allowing the diagnosis to be made by markedly increased serum CK levels (100 normal) before symptoms and signs develop. Carrier
Epidemiology and genetics DMD has an incidence of 2–3 per 100,000, or 1 in 3500 boys. It is an X-linked recessive disorder, and can therefore present in XO females (Turner’s syndrome). The incidence is reducing due to genetic counselling, but 30% of cases involve spontaneous mutations. The gene involved was first mapped in 1987 and is located on the short arm of the X chromosome (Xp21). It codes for dystrophin, a 400 kDa membrane protein involved in membrane stability. Many different mutations and deletions have been described, causing varying phenotypic severity. Corresponding author. Tel.: +44 0117 923 2121;
fax: +44 0117 928 2659. E-mail addresses:
[email protected] (B.J.A. Lankester),
[email protected] (M.R. Whitehouse),
[email protected] (M.F. Gargan). 0268-0890/$ - see front matter & 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2007.07.001
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299
females, although asymptomatic, will also have CK levels 75% greater than normal. Electromyography will demonstrate myopathic signs (short duration action potentials and polyphasic units) and muscle biopsy shows absence of
dystrophin on staining. Genetic testing is available for confirmation in the affected boy, carrier mother or foetus. The pattern of physical findings should allow a clinical diagnosis to be made from the age of 3 years onwards, but it is often missed at first presentation, leading to the potential for further affected pregnancies in uninformed families. A serum CK estimation should be carried out on any boy with a clumsy or abnormal gait or with an unexplained equinus deformity.4 The only way reliably to reduce the age of diagnosis would be to introduce a newborn screening programme,5 but there are no plans for this in the UK. The less common but milder Becker muscular dystrophy, which involves a different type of mutation in the same gene, causes structurally abnormal dystrophin to be produced. There is a later age of onset and slower progression.
Treatment General Figure 1 Equino-varus foot deformity.
Figure 2
Currently, no curative treatment is available for DMD. Affected boys should be kept ambulatory or standing for as
Scoliosis pre and post operatively.
ARTICLE IN PRESS 300 long as possible. Regular stretching and strengthening exercises, night-time splinting, ground-reaction AFOs and a standing frame may all be useful. Corticosteroids (prednisolone and deflazacort) have been shown to delay the loss of muscle strength and function by up to 3 years2 and delay or prevent the onset of scoliosis,6 but have serious potential side effects including weight gain and Cushing’s syndrome.
B.J.A. Lankester et al.
Acknowledgements The authors would like to thank Simon Gatehouse and Mike Gibson, Newcastle General Hospital, for providing the figures.
References Lower limbs Serial hip radiographs are used to screen for subluxation.7 Flexion and abduction contractures of the hip may require percutaneous release. Equinovarus foot deformity is treated with tendo achillis lengthening and tibialis posterior transfer which prolongs the ability to walk.8 Surgical release of soft tissue knee contractures is less effective. Aggressive post-operative rehabilitation is needed to preserve overall function, with an avoidance of prolonged immobilisation.
Spine The spinal deformity is not amenable to non-surgical control.2 Early fusion with segmental instrumentation improves the Cobb angle, delays the deterioration in lung function and improves survival (Fig. 2).9,10 Timing is crucial, with a narrow window of opportunity after the curve starts to develop, but before respiratory and cardiac function are compromised to the point that the risk of surgery is too great.2 An FVC less than 30% of the predicted value does not necessarily preclude surgery.11 A long thoraco-lumbar fusion is performed. In boys with significant shoulder weakness, any kyphosis should be only partially corrected to avoid the loss of ability to raise the hand to the mouth. Blood loss12 and overall complications13 are higher than for idiopathic scoliosis correction. The vital capacity at the age of 10 is a good predictor of the speed of progression14 and is useful in identifying those that require early surgical intervention.
Gene therapy Although the gene defect responsible for DMD was identified nearly 20 years ago, the development of effective therapy has been slow. The large size of the dystrophin gene makes transfer difficult by the standard vector systems, necessitating the development of novel approaches. A minigene has been successfully transferred in a mouse model of DMD, with restoration of normal muscle function.15 Other attempts are being made to target the downstream effects of DMD, such as the implantation of myoblasts into dystrophic muscle to repair a proportion of damaged myofibrils.16 Together these advances in molecular biology suggest a cure for DMD may be available in the near future.
1. Wenger DR, Rang M. The art and practice of children’s orthopaedics. Philadelphia, PA: Lippincott; Baltimore: Williams and Wilkins; 1993. 2. Sussman M. Duchenne muscular dystrophy. J Am Acad Orthop Surg 2002;10:138–51. 3. Miroysky A, Copeliovich L, Halperin N. Gowers’ sign in children with discitis of the lumbar spine. J Paediatr Orthop B 2005; 14:68–70. 4. Read L, Galasko CSB. Delay in diagnosing Duchenne muscular dystrophy in orthopaedic clinics. JBJS [B] 1986;68B:481–2. 5. Parsons EP, Clarke AJ, Bradley DM. Developmental progress in Duchenne muscular dystrophy: lessons for earlier detection. Eur J Paediatr Neurol 2004;8:145–53. 6. Alman BA, Raza SN, Biggar WD. Steroid treatment and the development of scoliosis in males with Duchenne muscular dystrophy. JBJS [A] 2004;86A:519–24. 7. Chan KG, Galasko CSB, Delaney C. Hip subluxation and dislocation in Duchenne muscular dystrophy. J Paediatr Orthop B 2001;10:219–25. 8. Scher DM, Mubarak SJ. Surgical prevention of foot deformity in patients with Duchenne muscular dystrophy. J Paediatr Orthop 2002;22:384–91. 9. Galasko CSB, Delaney C, Morris P. Spinal stabilization in Duchenne muscular dystrophy. JBJS [B] 1992;74B:210–4. 10. Bentley G, Haddad FS, Bull TM, Seingry D. The treatment of scoliosis in muscular dystrophy using modified Luque and Harrington–Luque instrumentation. J Bone Joint Surg Br 2001; 83:22–8. 11. Marsh A, Edge G, Lehovsky J. Spinal fusion in patients with Duchenne’s muscular dystrophy and a low forced vital capacity. Eur Spine J 2003;12:507–12. 12. Fox HJ, Thomas CH, Thompson AG. Spinal instrumentation for Duchenne’s muscular dystrophy: experience of hypotensive anaesthesia to minimise blood loss. J Paediatr Orthop 1997;17: 750–3. 13. Ramirez N, Richards BS, Warren PD, Williams GR. Complications after posterior spinal fusion in Duchenne’s muscular dystrophy. J Paediatr Orthop 1997;17:109–14. 14. Yamashita T, Kanaya K, Kawaguchi S, Murakami T, Yokogushi K. Prediction of the progression of spinal deformity in Duchenne muscular dystrophy: a preliminary report. Spine 2001;26: 223–6. 15. Biggar WD, Klamut HJ, Demacio PC, Stevens DJ, Ray PN. Duchenne muscular dystrophy: current knowledge, treatment, and future prospects. Clin Orthop 2002;401:88–106. 16. Sohn RL, Gussoni E. Stem cell therapy for muscular dystrophy. Expert Opin Biol Ther 2004;4:1–9.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 314–319
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KNEE
Management of infected TKR S. Naidu Maripuri, U.K. Debnath, H. Mehtha, R. Thomas, C. Wilson Department of Trauma and Orthopaedics, University Hospital of Wales, Cardiff CF14 4XW, UK
KEYWORDS Infection; Total knee replacement; Revision arthroplasty
Summary Treatment of infected total knee replacement is complex. A thorough clinical and diagnostic assessment is essential followed by careful planning of treatment. The ultimate goal is eradication of infection, and restoration of a pain-free and functional knee. An algorithm based on a literature review is set out. & 2007 Elsevier Ltd. All rights reserved.
Introduction Infection after total knee replacement (TKR) is a potentially devastating complication and is one of the most common reasons for revision TKR.1 The reported rate of infection following TKR is 1%–2.5%.2 It results in significant patient morbidity and higher treatment expenses and poses a therapeutic challenge to the surgeon. It has been estimated that surgical treatment of infections following TKR requires 3–4 times the resources of the hospital and surgeon compared with a primary TKR and twice the resources of aseptic revision TKR.3 Treatment options are:
long-term antibiotics, open or arthroscopic debridement with retention of prosthesis,
one stage revision, two-stage revision, arthrodesis, Corresponding author. 23, Barons Court Road, Cardiff CF23 9DF,
UK. Tel.: +44 7811165794; fax: +44 2920453745. E-mail address:
[email protected] (U.K. Debnath). 0268-0890/$ - see front matter & 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2007.03.003
resection arthroplasty, and amputation. We reviewed the literature on the management of infected TKR and discuss various management strategies and the rationale for each and present an algorithm based on current evidence (Fig. 1).
Types of infection Infection is classified as superficial or deep. The Centre for Disease Control (CDC) criteria for superficial infection are shown in Table 1. Deep infection may be:
intra-operative positive cultures, early infection, late or chronic infection, and haematogenous infection (Table 2).4
The diagnosis of superficial infection is often unreliable; the reliability of the third criteria (Table 1) for superficial infection has been challenged recently because of low interobserver agreement, arising from the lack of objectivity in judging tenderness, redness, localised swelling and heat.5
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315
Figure 1 Treatment algorithm for infected TKR.
Table 1 Criteria for superficial infection (Centre for Disease Control). Criterion
Definition
1
Purulent drainage from the superficial infection
2
The superficial infection yields organisms from the culture of aseptically aspirated fluid or tissue, or from a swab and pus cells are present
3
At least two of the following symptoms and signs of inflammation: pain or tenderness localised swelling redness heat and (a) the superficial infection is opened by a surgeon to manage the infection, unless the incision is culture-negative or (b) a clinician’s diagnosis of superficial incisional infection
Thus, the surgeon should have a low threshold for proceeding to debridement of the knee.
Diagnosis A high index of suspicion and careful consideration of several factors is essential in diagnosis.
Clinical features These include knee pain, swelling, reduced knee movements, fever, local erythema, local warmth, wound discharge, and wound breakdown, etc.
Pain is the most common presenting symptom of an infection of a knee arthroplasty. Thus onset of pain different from preoperative pain should raise the suspicion of infection. It typically occurs while the patient is at rest or wakes the patient at night. It is usually not aggravated by weight-bearing, although component loosening giving rise to such pain may be a sequel of infection.6 Usually, fever during the first 5 days of the postoperative period is physiological due to the inflammatory process. Thus, pyrexia by itself in the absence of other features of infection does not warrant further investigation during this period.7 Even in the absence of infection, the local temperature around a newly replaced knee can remain elevated for up to 6 months postoperatively.8 Serous discharge in the first few days following surgery should be addressed with caution. Persistent discharge from the wound beyond 7 days is a serious problem as a superficial discharge may often arise from a deep source of infection.
Investigations Clinical suspicion of infection should be confirmed by investigation, which should initially include a full blood count, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and plain radiographs. Wound swabs are discouraged as they complicate the clinical situation by yielding skin contaminants.6 Empirical use of antibiotics is also condemned by many authors as it leads to multi-drugresistant infection and it may mask the clinical features of infection long enough to preclude the option of early debridement and prosthetic salvage.3,9 CRP and ESR are non-specific inflammatory markers. Both may be elevated in inflammatory, infectious and neoplastic processes.10 CRP usually peaks between 5 and 7 days following surgery and then gradually decreases. Any peak after this period should increase the suspicion of infection8 but it must be noted that it remains elevated for as long as 6 weeks in non-rheumatoid patients following the index
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Table 2
S.N. Maripuri et al. Classification of deep infections.4 Type l
Type 2
Type 3
Type 4
Timing
Positive intraoperative culture
Early postoperative infection
Acute haematogenous infection
Late(chronic) infection
Definition
42 positive intraoperative cultures
Infection within one month after surgery
Haematogenous seeding of site of previously well functioning prosthesis
Chronic indolent clinical course; infection present for 41 month
Treatment
Appropriate antibiotics
Debridement and salvage of prosthesis
Debridement with salvage or removal of prosthesis
Removal of prosthesis
surgery. In rheumatoid patients it may take up to 18 weeks to return to preoperative levels. High CRP (410 mg/L) levels after these intervals should raise the suspicion of infection.10 The measurement of ESR and CRP together increases the predictability of periprosthetic infection. Spangehl et al. (1999) have observed that when both the measurements are normal i.e. ESR (o30 mm/h) and CRP (o10 mg/L), the probability of infection is 0.00; when both tests are positive, the probability of infection rises to 0.83.10,11
Joint aspiration When the inflammatory markers are elevated with a clinical suspicion of infection, formal joint aspiration is indicated to establish the diagnosis. Joint aspirate should be sent for Gram staining, and cultured for anaerobic and aerobic bacteriae and fungi. Gram staining has a sensitivity of as low as 12%, but a specificity of 98.8.4 The most common organisms reported are Staphylococcus(s) aureus, coagulase-negative Staphylococcus, methicillin-resistant S. aureus, S. epidermidis and Pseudomonas aeruginosa.12 White cell count with the differential cell count should also be performed on the aspirate. A sensitivity of 75%, specificity of 96% and accuracy of 90% is noted with knee aspirates in diagnosing infection prior to revision.13 Indeed Duff et al. (1996) reported 100% sensitivity, 100% specificity and 100% accuracy!14 That said, a negative first aspirate does not rule out infection. If the suspicion of infection remains following the first aspiration, then any antibiotic therapy should be discontinued for a minimum of 10 days to 2 weeks, and aseptic aspiration should then be repeated13,15 on at least two further occasions.
Radionuclide imaging Radioisotope scans are not particularly useful in the acute postoperative period.6 111In-labelled white blood cells in combination with 99mTc-sulphur colloid marrow imaging is superior to other scans in the assessment of infection in total joint replacement, with a reported sensitivity, specificity and accuracy of 100%, 91% and 95%, respectively.16,18 (F) fluorodeoxyglucose F-FDG imaging is less accurate. Thus, a combination scan of 111In-labelled white blood cells and 99mTc-sulphur colloid marrow is currently the investigation of choice in diagnosing periprosthetic infection.16
Current research in diagnostics Serum Interleukin-6 (IL-6) has been evaluated as a marker of periprosthetic infection. Increased levels have been shown to be positively correlated with the presence of periprosthetic infection.17 It is important to distinguish between a septic and aseptic failures in revision arthroplasty situations.18 Neutrophils at the site of a S. aureus infection express different genes than neutrophils at a site of an aseptic inflammation such as gout. Based on these principle new simple diagnostic tests could be designed to differentiate between a septic and aseptic inflammatory process. This is probably a more sensible and a promising approach towards the diagnosis of periprosthetic infection and may circumvent current problems associated with blood tests and cultures.19 Further studies are necessary before this can be used clinically.
Treatment Superficial infection should be debrided and treated with appropriate antibiotics (Fig. 1). Debridement includes excision of infected soft tissue and scar in an elliptical fashion down to the joint capsule. Great care must be taken to ensure that there is no extension of infection in to the joint.15 If discharge is persistent or deep infection is suspected, it should be treated aggressively. If the patient is being treated empirically with antibiotics, these should immediately be discontinued and the patient closely monitored with a reassessment in a week to 10 days.13,15 Once deep infection is confirmed, treatment involves either prosthetic retention or prosthetic removal. The clinical presentation is usually helpful in determining whether the prosthesis needs removal.4 When feasible, most patients prefer to retain their existing prosthesis or insertion of a new prosthesis rather than one of the nonprosthetic treatment alternatives.9 Prosthetic retention after debridement is indicated in a selected group of patients (Table 3).4,9 Debridement should be open as arthroscopic debridement is less efficacious.20 There are two reasons for this. Firstly, exchange of the polyethylene liner cannot be accomplished arthroscopically and secondly adequate debridement cannot be performed.
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Table 3 Criteria for debridement and retention of prosthesis.9 Indications
Contraindications
An acute infection within 4 weeks after prosthesis implantation Late hematogenous infection in an otherwise wellfunctioning prosthesis A susceptible microorganism that can be treated by oral antibiotics A good soft tissue envelope
Chronic infections (430 days)
A well-fixed prosthesis
Prosthesis loosening
A poor soft tissue envelope Patient has other joint arthroplasties or a heart valve Drug-resistant bacteria
For open debridement, an elliptical incision should be made excising the scar. The deep fascia and capsule should be opened through the previous incision. Then a thorough and careful debridement should be carried out. Sometimes a fibrous membrane may need excision. Multiple tissue samples (at least two) should be collected for microbiology and histological examinations. The glycocalyx membrane around the polyethylene liner should be removed and liner should be exchanged and the knee thoroughly washed with at least 3 L of antiseptic-saline solution.21 Specific antibiotics should be started based on the culture and sensitivity report. Post-operatively, inflammatory markers (ESR & CRP) should be checked twice weekly. Repeat debridement may be needed if infection does not settle. Multiple debridements can be successful in early infections in a healthy host22 but if infection persists two-stage revision will need to be undertaken.
One-stage revision arthroplasty One-stage revision has been reported as being successful when performed within 4 months of the index procedure, in patients with less than 4 weeks of symptoms, antibiotic sensitive gram-positive organisms, well-fixed components with no radiological evidence of osteitis, and in young healthy patients.22 If successful it substantially reduces the treatment cost. However, when treatment by irrigation and debridement is unsuccessful, eradication of the infection seems most likely with a two-stage procedure or an arthrodesis. At operation, intra-operative frozen section is a useful tool in diagnosing infection. At least three samples should be collected from suspected areas such as joint pseudocapsule and interface membrane. Each sample should be sent for frozen section and cultures. If the polymorphonuclear leucocyte count is more than 10 then active infection is likely, if less than 5 then active infection is unlikely.28
Two-stage revision arthroplasty Two-stage revision is the most commonly performed operation for the infected TKR.1,23 It involves removal of implants and debridement followed by re-implantation at a later date once infection is controlled. The knee is approached through the previous scar and multiple samples are collected. Intra-operative collection of the samples into Rosenow’s broth has been shown to improve aero-anaerobe recovery.24 The prosthesis and all the cement should be removed followed by thorough debridement and washout. Many temporary spacers are in use. The antibiotic impregnated cement spacer is favoured as it is associated with a lower incidence of re-infection.1,9,13 Some authors advise use of antibiotic beads in addition to cement spacers.25 Specific antibiotics should be administered and patient be monitored with twice weekly inflammatory markers. Some authors advocate cultures of the knee aspirate 4 weeks after stopping the antibiotics and before second stage re-implantation.26 We believe that this is unnecessary as a routine and should be restricted to those patients with a suspicion of persistent infection and in the presence of elevated inflammatory markers. Once infection control is established the second stage re-implantation is performed and multiple tissue samples should be taken at the second stage procedure. Two-stage re-implantation has been reported as successful in 80.0% of knees with low-virulence organisms (e.g. coagulase-negative Staphylococcus, Streptococcus), 71.4% with polymicrobial organisms, and 66.7% with high-virulence organisms (methicillin-resistant S. aureus). Re-implantation was successful in 82% of patients with a primary diagnosis of osteoarthritis and in 54% of patients with rheumatoid arthritis (p ¼ 0.024). The success rate was 92% if infection occurred after primary arthroplasty but only 41% if after multiple previous knee operations (arthroscopy, osteotomy, or revision total knee arthroplasty).27
Antibiotic therapy Empirical antibiotic treatment for suspected periprosthetic infection should be guided by the class of the infection and the findings of Gram-staining. Until final culture results are available, acute haematogenous infections should be treated initially with a combination of cefazolin and gentamicin. All chronic and acute post-operative infections with Grampositive bacteria and all cases in which a Gram stain fails to identify bacteria should be managed with vancomycin. Infections with Gram-negative bacteria should be managed with a third- or fourth-generation cephalosporin. Infections with mixed Gram-positive and Gram-negative bacteria should be treated with a combination of vancomycin and a third- or fourth-generation cephalosporin. If culture results and other confirmatory tests are not positive by the fourth post-operative day, termination of empirical antibiotic therapy should be considered.31 Duration of antibiotic treatment during one- or two-stage revision is controversial. Most studies suggests antibiotic treatment for 4–6 weeks.5,29 A recent study by Hart et al. (2006) suggested that 14 days of intravenous vancomycin during two-stage revision produced comparable results.25
ARTICLE IN PRESS 318 They used custom-made antibiotic impregnated cement spacers and antibiotic cement beads based on the culture results of preoperative knee aspirates. They concluded that an extended course of antibiotic does not alter the incidence of recurrent or persistent infection. More multicentric studies are required to confirm the efficacy of these protocols. Long-term antibiotic suppression alone is an option in selected patients. This should be considered only in extreme situations, as this strategy will not eliminate deep periprosthetic infection and is generally associated with a very poor prognosis.30 This treatment should be considered only when all of the following criteria are met: 1. it is not feasible to remove the prosthesis, most often because of a medical condition that precludes an operative procedure, 2. the microorganism is of low virulence, 3. the microorganism is susceptible to an oral antibiotic, 4. the antibiotic can be tolerated without serious toxicity, and 5. the prosthesis is not loose.15 The presence of other joint prostheses should be considered a contraindication for this treatment.6,9,31
Salvage procedures Arthrodesis and amputation are the last options in patients who have had several attempts at revision. Currently the most common indication for an arthrodesis of the knee is failed infected total knee prosthesis. Knee arthrodesis can be an effective treatment option for relieving pain and restoring some function after the failure of a total knee arthroplasty as the result of infection.32 Permanent resection arthroplasty or amputation usually results in a poor outcome. Amputation is indicated in lifethreatening infection, persistent infection, irreparable softtissue deficiency, severe bone loss, and the wishes of the patient following multiple failed attempts at reconstruction. Amputation rates following TKR in general are 0.02%–0.18%, but higher rates of up to 6% were also reported. Resection arthroplasty may be best tolerated by patients who are willing to accept loss of ambulation, such as those who are already disabled because of multiple joint involvements.33
References 1. Wang CJ, Hsieh MC, Huang TW, Wang JW, Chen HS, Liu CY. Clinical outcome and patient satisfaction in aseptic and septic revision total knee arthroplasty. Knee 2004;11(1):45–9. 2. Rorabeck CH. Session IV: salvage of the infected total knee replacement. Infection: the problem. Clin Orthop Relat Res 2002;404:113–5. 3. Hebert CK, Williams RE, Levy RS, Barrack RL. Cost of treating an infected total knee replacement. Clin Orthop Relat Res 1996;331:140–5. 4. Segawa H, Tsukayama DT, Kyle RF, Becker DA, Gustilo RB. Infection after total knee arthroplasty. A retrospective study of the treatment of eighty-one infections. J Bone Joint Surg (Am) 1999;81(10):1434–45.
S.N. Maripuri et al. 5. Allami MK, Jamil W, Fourie B, Ashton V, Gregg PJ. Superficial incisional infection in arthroplasty of the lower limb. Interobserver reliability of the current diagnostic criteria. J Bone Joint Surg (Br) 2005;87(9):1267–71. 6. Leone JM, Hanssen AD. Management of infection at the site of a total knee arthroplasty. J Bone Joint Surg (Am) 2005;87(10): 2335–48. 7. Ghosh S, Charity RM, Haidar SG, Singh BK. Pyrexia following total knee replacement. Knee 2006;13(4):324–7. 8. Mehra A, Langkamer VG, Day A, Harris S, Spencer RF. C reactive protein and skin temperature post total knee replacement. Knee 2005;12(4):297–300. 9. Hanssen AD. Managing the infected knee: as good as it gets. J Arthroplasty 2002;17(4 (Suppl. 1):98–101. 10. Spangehl MJ, Masterson E, Masri BA, O’Connell JX, Duncan CP. The role of intraoperative gram stain in the diagnosis of infection during revision total hip arthroplasty. J Arthroplasty 1999;14(8):952–6. 11. Atkins BL, Athanasou N, Deeks JJ, Crook DW, Simpson H, Peto TE, et al. Prospective evaluation of criteria for microbiological diagnosis of prosthetic-joint infection at revision arthroplasty. The OSIRIS Collaborative Study Group. J Clin Microbiol 1998;36(10):2932–9. 12. Parvizi J, Ghanem E, Menashe S, Barrack RL, Bauer TW. Periprosthetic infection: what are the diagnostic challenges? J Bone Joint Surg (Am) 2006;88(Suppl. 4):138–47. 13. Barrack RL, Jennings RW, Wolfe MW, Bertot AJ. The Coventry Award. The value of preoperative aspiration before total knee revision. Clin Orthop Relat Res 1997;345:8–16. 14. Duff GP, Lachiewicz PF, Kelley SS. Aspiration of the knee joint before revision arthroplasty. Clin Orthop Relat Res 1996;331: 132–9. 15. Tsukayama DT, Goldberg VM, Kyle R. Diagnosis and management of infection after total knee arthroplasty. J Bone Joint Surg (Am) 2003;85(Suppl. 1):S75–80. 16. Love C, Marwin SE, Tomas MB, Krauss ES, Tronco GG, Bhargava KK, et al. Diagnosing infection in the failed joint replacement: a comparison of coincidence detection 18F-FDG and 111In-labeled leukocyte/99mTc-sulfur colloid marrow imaging. J Nucl Med 2004;45(11):1864–71. 17. Di Cesare PE, Chang E, Preston CF, Liu CJ. Serum interleukin-6 as a marker of periprosthetic infection following total hip and knee arthroplasty. J Bone Joint Surg (Am) 2005;87(9):1921–7. 18. Bare J, MacDonald SJ, Bourne RB. Preoperative evaluations in revision total knee arthroplasty. Clin Orthop Relat Res 2006;446:40–4. 19. Deirmengian C, Lonner JH, Booth Jr. RE. The Mark Coventry Award: white blood cell gene expression: a new approach toward the study and diagnosis of infection. Clin Orthop Relat Res 2005;440:38–44. 20. Waldman BJ, Hostin E, Mont MA, Hungerford DS. Infected total knee arthroplasty treated by arthroscopic irrigation and debridement. J Arthroplasty 2000;15(4):430–6. 21. Svoboda SJ, Bice TG, Gooden HA, Brooks DE, Thomas DB, Wenke JC. Comparison of bulb syringe and pulsed lavage irrigation with use of a bioluminescent musculoskeletal wound model. J Bone Joint Surg (Am) 2006;88(10):2167–74. 22. Silva M, Tharani R, Schmalzried TP. Results of direct exchange or debridement of the infected total knee arthroplasty. Clin Orthop Relat Res 2002;404:125–31. 23. Insall JN, Thompson FM, Brause BD. Two-stage reimplantation for the salvage of infected total knee arthroplasty. J Bone Joint Surg (Am) 1983;65(8):1087–98. 24. Senneville E, Savage C, Nallet I, Yazdanpanah Y, Giraud F, Migaud H, et al. Improved aero-anaerobe recovery from infected prosthetic joint samples taken from 72 patients and collected intraoperatively in Rosenow’s broth. Acta Orthop 2006;77(1):120–4.
ARTICLE IN PRESS Management of infected TKR 25. Hart WJ, Jones RS. Two-stage revision of infected total knee replacements using articulating cement spacers and short-term antibiotic therapy. J Bone Joint Surg (Br) 2006;88(8):1011–5. 26. Mont MA, Waldman BJ, Hungerford DS. Evaluation of preoperative cultures before second-stage reimplantation of a total knee prosthesis complicated by infection. A comparison-group study. J Bone Joint Surg (Am) 2000;82(11):1552–7. 27. Hirakawa K, Stulberg BN, Wilde AH, Bauer TW, Secic M. Results of 2-stage reimplantation for infected total knee arthroplasty. J Arthroplasty 1998;13(1):22–8. 28. Wong YC, Lee QJ, Wai YL, Ng WF. Intraoperative frozen section for detecting active infection in failed hip and knee arthroplasties. J Arthroplasty 2005;20(8):1015–20. 29. Goldman RT, Scuderi GR, Insall JN. 2-stage reimplantation for infected total knee replacement. Clin Orthop Relat Res 1996;331:118–24.
319 30. Bengston S, Knutson K, Lidgren L. Treatment of infected knee arthroplasty. Clin Orthop Relat Res 1989;245:173–8. 31. Fulkerson E, Valle CJ, Wise B, Walsh M, Preston C, Di Cesare PE. Antibiotic susceptibility of bacteria infecting total joint arthroplasty sites. J Bone Joint Surg (Am) 2006;88(6): 1231–7. 32. Bargiotas K, Wohlrab D, Sewecke JJ, Lavinge G, Demeo PJ, Sotereanos NG. Arthrodesis of the knee with a long intramedullary nail following the failure of a total knee arthroplasty as the result of infection. J Bone Joint Surg (Am) 2006;88(3): 553–8. 33. Christie MJ, DeBoer DK, McQueen DA, Cooke FW, Hahn DL. Salvage procedures for failed total knee arthroplasty. J Bone Joint Surg (Am) 2003;85(Suppl. 1):S58–62.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 301–309
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CHILDREN
Non-accidental injury Louise Hattingh Department of Radiology, Bradford Royal Infirmary, Bradford Teaching Hospitals NHS Foundation Trust, Bradford BD9 6RJ, UK
KEYWORDS Child abuse; Diagnostic imaging; Battered child syndrome
Summary Orthopaedic surgeons dealing with children in their practice are likely to be faced with the problem of non-accidental injury (NAI). Clues in the history may point to the possibility of child abuse. The range and radiographic appearances of skeletal injuries, some more specific to abuse than others, are discussed. Recognition of the classical metaphyseal lesion is paramount. Further investigation and differential diagnosis of NAI is considered, with emphasis on the use of follow-up radiographs in difficult cases. Imaging should be directed by experienced radiologists privy to all clinical information. Controversies surrounding the use of other imaging modalities are mentioned. A brief description of the legal issues and multidisciplinary approach to NAI is included. & 2007 Published by Elsevier Ltd.
Introduction The phrase ‘‘non-accidental injury’’ (NAI) is often coined when referring to suspected physical abuse in children. Other forms of abuse such as neglect, psychological and sexual abuse should not be overlooked, but it is the physical injury to an infant or small child that can provide the tangible evidence of inflicted injury. The presence of child abuse in our society is now generally accepted and the responsibility to recognise abuse lies with all those involved in the care of children. An orthopaedic surgeon or radiologist may be the first to suspect abuse following skeletal injury. This must lead to the initiation of appropriate child protection procedures. The paediatric radiologist John Caffey was the first to describe long bone fractures associated with subdural haematomas in young children.1 His later description of the metaphyseal fracture, followed by the extensive work of Tel.: +44 1274 364123; fax: +44 1274 366895.
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Paul Kleinman and colleagues, have contributed to the understanding of injury mechanisms in abused infants.2,3 When a young child with a skeletal injury is referred to an orthopaedic surgeon for further management, several clues may raise the suspicion of NAI. These will be discussed in further detail. This article concentrates mainly on the range of skeletal injuries to physically abused children, but both visceral and head injuries will be mentioned as these may at first be overlooked with dire consequences. Controversies around radiological investigation of NAI will be discussed. Virtually any bone in the body may be involved in NAI. Certain injury patterns are highly specific to abuse. In infants, metaphyseal, rib and skull fractures are seen more frequently. In older children, skull and long bone diaphyseal fractures are more common.4
The classic metaphyseal lesion (CML) The CML is regarded as the most specific finding to suggest that injury was inflicted (Fig. 1). The radiographic appearance
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Figure 1 (a) Lateral view of the knee in an abused infant. Metaphyseal lesions of the distal femur and proximal tibia appear as corner fractures, (b) CML of the proximal humerus. Note the lucency in the subphyseal region of the metaphysis. (c) Healing CMLs in an abused infant. There is a corner fracture of the distal femoral metaphysis and bucket-handle fractures of the proximal tibia and fibula. Note the pathologic periosteal reaction along the shafts of the long bones.
is frequently that of subtle lucency in the subphyseal region of the metaphysis. Appearances will also depend on the angle at which the radiograph was taken, as well as the stage of healing. It may not be visible on all radiographic projections. On some views, a small fragment at the periphery will be seen as a typical corner fracture. On other views, a classical bucket-handle appearance is attributed to the fracture disrupting the primary spongiosa of the metaphysis and producing a disk-like fragment. The peripheral margins, or corners, of the fragment are thicker as they encompass the subperiosteal bone collar. It is important to note that although often the only radiographic abnormality is a corner fragment, the plane of injury is typically transmetaphyseal.5 Forces required to produce such an injury are shearing, as occurs when an infant is shaken with the limbs unsupported or with the child held and shaken by the arms or legs. This explains the prevalence of the CML almost entirely in children under the age of 2 years.6 Forces leading to the CML do not occur during falls or normal handling of an infant.
Radiologically, the CML is difficult to date and these injuries are typically asymptomatic. Subperiosteal new bone formation (SPNBF) may be absent. Early healing may appear similar to the acute injury. If present, hypertrophic cartilage growth into the metaphysis, seen as lucent extension of the growth plate into the metaphysis, is indicative of healing. However, the assessment of healing is best performed by an experienced radiologist.
Subperiosteal new bone formation Most typically seen as part of the healing process following a fracture (Fig. 2), SPNBF also may occur in isolation. When a force leads to subperiosteal haemorrhage, the periosteum is lifted from the bony cortex. After 5–15 days, a thin layer of subperiosteal new bone is evident on radiographs. It may be difficult to differentiate from ‘‘physiologic’’ periosteal reaction in infants (Fig. 3). When innocent, it usually is bilateral, seldom greater than 2 mm in thickness, preferentially occurring in the femur, tibia and less likely the
ARTICLE IN PRESS Non-accidental injury
Figure 2 Subperiosteal new bone formation accompanying a spiral fracture of the shaft of the right tibia. Note also the presence of a distal tibial CML.
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Figure 4 Bone scintigram. The increased uptake along the left femoral shaft confirmed the presence of traumatic SPNBF in this abused infant.
Rib fractures
Figure 3 Physiological subperiosteal new bone formation along the shaft of the proximal right femur.
humerus and forearm. If there is uncertainty, follow-up radiographs are very helpful in demonstrating an interval change in traumatic SPNBF.7 Bone scintigraphy (BS) is a powerful adjunct to demonstrate injury (Fig. 4). SPNBF is a non-specific finding seen in a wide range of other conditions, including infectious, metabolic and idiopathic causes.
Fractures may occur anywhere along the rib arc, but particularly the posterior fractures carry high specificity for abuse. The mechanism of injury has been shown to be due to manual compression, the child held by the rib cage and forcefully squeezed. Posterior fractures occur because the rib acts as a lever, the vertebral transverse process being the fulcrum. This mechanism does not occur during cardiopulmonary resuscitation (CPR). Indeed, research has demonstrated that rib fractures are extremely rare, even in prolonged CPR. When present, such fractures do not involve the posterior rib arcs.8 In a cohort of 467 children suspected of suffering abuse, Carty and Pierce9 found that 408 children had a total of 1689 fractures. Rib fractures occurred in 154 (38%). Interestingly, in 11 children (2.4%) a single rib fracture was the only fracture found, but there were other clinical signs of abuse. This demonstrates that even a single rib fracture found on a young child’s X-ray should raise concern and initiate a thorough clinical examination. Radiological appearances vary considerably. Acute posterior fractures are frequently undetectable on initial anteroposterior radiographs. Healing becomes evident as subtle widening of the rib neck, faint sclerosis along the fracture margins or obvious callus formation and SPNBF. The conspicuity of findings is very variable. A further clue may be the presence of pleural fluid or extrapleural soft tissue density. Detection of occult rib fractures is improved by the inclusion of oblique rib views in the skeletal survey (SS). Some institutions also advocate the use of BS. Follow-up
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L. Hattingh five instances of spinal fractures. Vertebral body compression fractures (Fig. 6) are most frequently encountered following a hyperflexion force or axial loading. In some instances the vertebral body height is maintained, but a fracture through the superior end plate may be seen. Radiologically, the appearances may be of irregularity at the anterosuperior margin of the vertebral body or a discrete bony fragment at this margin. Unlike vertebral body fractures, which are moderately specific, spinous process fractures are highly specific of inflicted injury. Forceful hyperflexion may avulse the tips of the spinous processes at the insertion of the interspinous ligament. If the avulsed fragment is cartilage, it may only become obvious on delayed imaging when calcification and ossification is apparent. Due to the nature of the applied force, associated vertebral fractures are common.10 Stating the obvious, the spine serves as protection to the spinal cord. Sadly, severe spinal fractures and dislocations may present with paralysis. Hyperflexion spinal injuries may also direct the clinician to visceral injury. The lifethreatening injuries require appropriate management, but should not be to the detriment of documenting all other injuries. An MRI may demonstrate spinal cord and ligamentous injury well, but the SS should not be forgotten once the patient is stabilised in a safe environment.
Figure 5 (a) Presenting chest X-ray in an abused child. The fractures of the posterior shafts of the left second and third ribs are difficult to identify. (b) A radiograph taken 2 weeks later. Callus formation now makes the rib fractures (arrows) much more conspicuous.
radiographs, usually 2 weeks after the presenting X-rays, are valuable (Fig. 5).
Scapular and sternal fractures Sternal and scapular fractures are thought to be rare, but carry high specificity for abuse. Detection of sternal fractures rely on a lateral view and therefore Kleinman advocates the use of a lateral film of the thorax as part of the SS in cases of suspected abuse. Fractures of the acromion, coracoid and rarely the scapular body may be detected by meticulous radiographic scrutiny.8
Vertebral injuries Spinal injuries are infrequently seen in abused children. In the British cohort studied by Carty and Pierce,9 there were
Figure 6 Lateral view of the thoraco-lumbar region demonstrates a wedge compression fracture of one of the lower thoracic vertebrae in an abused child.
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Skull fractures These fractures may occur following a direct blow with an object or as part of shaking injury ending in an impact. Shaken infants do not always have skull fractures, hence the need for head computed tomography (CT) when such an injury is suspected. The excellent review by Lonergan et al.11 includes a detailed description of the radiological and pathological appearances of intracranial injury seen in child abuse. Simple skull fractures are seen in NAI and have no differentiating features from accidental injuries. Complex fractures are more worrying. They may cross sutures, have more than one fracture line or have a stellate pattern. Depressed fractures, multiple, compound and comminuted fractures are further concerning features (Fig. 7). Diastasis of fracture margins is sometimes seen, usually in association with underlying dural injury. Traumatic sutural diastasis must be differentiated from the more symmetrical diastasis seen with chronically raised intracranial pressure. Skull fractures may be difficult to appreciate on CT scans and BS, hence the inclusion of skull radiographs in the SS.
Long bone fractures Fractures to the shaft of long bones occur both in accidental and non-accidental incidents. When assessing an infant or young child presenting with a fracture, it is important to take the child’s age and developmental capabilities into consideration. The proposed mechanism of accidental injury and time of presentation may provide significant clues.
Figure 8 Healing fracture of the right femoral neck as well as a spiral fracture of the shaft of the femur without evidence of periosteal reaction. Multiple fractures of differing ages is suspicious for NAI.
Spiral fractures of the femur and humerus are uncommon in young children and should raise concern12 (Fig. 8). ‘‘Acute’’ fractures showing evidence of healing on the presenting radiographs must also be viewed with suspicion. Sometimes there is a delayed presentation without adequate explanation. In pre-mobile children, fractures of the bones in the fingers and toes should be regarded with suspicion: they may be the victims of beating or forceful squeezing of the hands or feet (Fig. 9).
Soft tissue and visceral injury
Figure 7 Frontal skull X-ray in a child suffering NAI. Note the bilateral parietal fractures and diastasis of the right parietal fracture.
The wide range of other injuries found in abused children is beyond the scope of this article, but it is important to remember that these are often the injuries that cause death. In the clinical setting of a child presenting with skeletal injury, a thorough clinical examination is required to search for evidence of soft tissue, brain or visceral trauma. Injury to the central nervous system is a leading cause of mortality and long-term morbidity in NAI. Visceral injuries, although less common, occur in a higher age group, and carry a mortality of up to 50% (Fig. 10). Delayed presentation and delay in diagnosis are thought to contribute to this high rate of death. Pancreatitis and pancreatic pseudocyst formation warrant special consideration. In adults, this is commonly secondary to alcohol abuse, but in children blunt abdominal trauma is the most common cause of pancreatic pseudocysts. A rare complication may be the presence of multiple, painful lytic lesions in the bone secondary to medullary fat necrosis following systemic release of pancreatic enzymes. The lesions may raise the suspicion of disseminated malignancy, but elevated amylase levels may point to the correct diagnosis.13
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Differential diagnosis As already discussed, accidents are often offered as explanations for NAI. It is the duty of the court to decide whether this was the case. The role of investigating clinicians and radiologists is to provide the information required by the court to make its decision. A knowledge and understanding of the forces required to produce specific fractures in young children cannot be overemphasised. There are many conditions which may mimic NAI. Included in this list are normal variants, obstetric injuries, osteogenesis imperfecta, other inherited bone dysplasias, infections, malignant and metabolic disorders. The rare condition of congenital indifference to pain, also known as asymbolia, deserves special mention, as the radiological appearances can be identical to NAI (Fig. 11). A careful examination should provide the correct diagnosis.14 Sometimes the presence of an underlying generalised bone disorder can be difficult to prove and specialist expertise should be sought in these cases. A controversial entity called ‘‘temporary brittle bone disease’’ (TBBD) has been suggested as a cause of fractures in suspected abuse. However, in a joint statement by the Society for Pediatric Radiology and the European Society of Paediatric Radiology, the scientific grounds for such an entity are strongly questioned. In the field of paediatric radiology, TBBD is not generally accepted as a diagnosis.15
Investigation Once the possibility of NAI has been raised, appropriate steps are taken to protect the child from further harm. Further investigation is aimed at confirming or refuting the Figure 9 There is a fracture of the proximal aspect of the big toe metatarsal bone. Skeletal survey detected many other fractures in this abused child.
Figure 10 Axial CT scan of the abdomen in a fatally abused child. Note the small aorta and brightly enhancing adrenal glands as signs of acute shock. There is a large amount of peritoneal blood.
Figure 11 Congenital indifference to pain. The ulnar fracture is non-united and there is considerable periosteal new bone formation. The child continued to use the arm despite the presence of a fracture.
ARTICLE IN PRESS Non-accidental injury diagnosis of NAI. This is the stage at which other possibilities in the differential diagnosis should be considered. A diagnosis of NAI, if made incorrectly, can be catastrophic for a family. However, if NAI is overlooked, it may have fatal consequences for the abused child.9 A multidisciplinary approach is imperative. Protocols and management may vary within countries. In the United Kingdom (UK), many hospitals will have a ‘‘lead clinician’’ who is experienced in dealing with suspected NAI. Early involvement by appropriate clinical and social services specialists is important. Meticulous and legible documentation of the social history, clinical examination and radiological findings are often later required in court. This may include photographic evidence of inflicted injuries. The radiologist can provide advice on the most appropriate further investigations. Both the British Society of Paediatric Radiology and the American Academy of Pediatrics have issued guidelines for imaging suspected NAI.16,17 In children under the age of three, a full SS is performed by staff experienced in paediatric radiography, during normal working hours (Table 1). A so-called ‘‘babygram’’, in which the entire infant is imaged on a single projection, is no longer an acceptable practice. In the UK, the paediatrician caring for the child has the responsibility of explaining the need for further imaging to the next of kin. The SS images are reviewed by a radiologist, who may request further views if there are areas of concern. Follow-up films of such areas may also be arranged at this time and in many institutions it is normal practice to perform a follow-up chest X-ray (CXR) in 1–2 weeks. Delayed films can be valuable in dating injuries. Controversy still surrounds the routine use of other imaging modalities in the initial radiological investigation of NAI. In the UK, many believe that all pre-mobile infants suspected of being victims of NAI should be considered for a CT scan of the brain.16 Even when CT has been performed,
Table 1
The skeletal survey.16
Skull:
AP and lateral Towne’s view if suspected occipital injury
Chest:
AP thorax Left and right oblique rib views
307 the skull X-ray must not be omitted from the SS. If the CT is equivocal or if intracranial haemorrhage requires more accurate dating, an MRI may be indicated. The role of BS is a further source of debate. Some advocate the use of routine BS in suspected NAI. A recently published comprehensive review of the literature on this subject18 suggests that both the SS and BS may miss injuries: the SS most often misses rib fractures (but the routine use of oblique rib views should reduce the number of missed rib fractures), whereas the BS can miss skull, metaphyseal and epiphyseal injuries. Both studies are more sensitive when combined. There is evidence that a repeat SS after 2 weeks can yield significant information and that this should be considered in cases where physical abuse is strongly suspected.19 Most of our knowledge of NAI is based on research using high-detail film–screen combinations. Worldwide, use of digital radiography is increasing. These imaging systems used in general radiography do not perform at the same high spatial resolution achievable with film–screen combinations. Further research is required to ensure that the high standards of imaging in suspected NAI are not compromised.20
Dating fractures Fracture dating is frequently a difficult task and exact timing of injury based purely on radiological appearances is impossible. O’Connor and Cohen provide valuable guidelines in the radiographic dating of fractures: SPNBF can be seen as early as 4 days following injury and by 20 days fractures will almost always have SPNBF. Soft callus formation can be seen from 10 days onwards, peaking at 2–3 weeks. Remodelling occurs as early as 3 months and peaks at 1 year, but can continue well beyond this time.21 The radiologist should always be provided with as much clinical history as possible. As an example, if the history suggests an injury less than 1 day old and the fracture shows evidence of SPNBF, the radiologist can report the discrepancy with certainty. A well-informed report will also be of greater value as evidence in a court of law.
Legal issues
Abdomen: AP, including pelvis and hips Spine:
Lateral cervical, thoracic and lumbar
Upper limbs:
AP both humeri AP both forearms DP both hands
Lower limbs:
AP both femora AP both tibiae and fibulae AP both feet
Additional: Lateral view of any fracture Coned views of suspicious areas, as directed by supervising radiologist
Laws governing the welfare of children will vary between countries. In the UK, Section 47 of the Children Act 1989 stipulates that councils with social services responsibilities must conduct enquiries when they receive information that a child is suffering or likely to suffer significant harm. It is the duty of all other agencies, including the National Health Service, to assist in these enquiries. Central to the act is the belief that children are best cared for within their family, with both parents playing a full role and without the need to resort to legal proceedings. This is the ideal situation to which society should strive. In England, during the year ending March 2002, councils conducted 69 900 enquiries under section 47 of the Children Act. This led to 34 800 initial child protection
ARTICLE IN PRESS 308
L. Hattingh
conferences.22 Such conferences are multiagency meetings convened to decide whether a child is at risk and whether the child’s name should be placed on the child protection register. Some cases can be resolved without legal involvement, but in other cases, proceedings under civil law may be instigated to decide whether NAI occurred and to make arrangements to protect the child from harm. The court will appoint a guardian (usually a senior social worker) to represent the interests of the child during proceedings. In cases of serious assault, the police may commence a criminal investigation, which is then dealt with under criminal law. There are important differences between civil and criminal law, which are beyond the scope of this article. Medical professionals may be asked to provide legal statements outlining their involvement in the management and investigation of a case. Those experienced in dealing with NAI can be asked to act as expert witnesses. Good record keeping in all cases of child abuse will be rewarding when the time comes to provide a medical report. Medical witnesses should also be aware of their own limitations and should not attempt to provide opinions outside their area of expertise.
Practice points
Clues in the history and radiographic appearances of
a fracture may alert the surgeon or radiologist to the possibility of abuse Failure to recognise non-accidental injuries may expose the infant or child to life-threatening danger The classical metaphyseal lesion is highly specific to abuse under the age of 2 A single rib fracture found incidentally on a young child’s CXR should raise alarm bells Spiral fractures of the femur and humerus are uncommon in young children Visceral injuries carry a high mortality as they may at first be overlooked The SS is paramount in the investigation of suspected child abuse Follow-up radiographs often detect fractures initially missed A multiagency approach aims to ensure the child’s physical protection as well as protecting the legal rights of the child
Research directions
Assessing the diagnostic performance of digital radiography in the investigation of NAI
Investigating the feasibility of fracture dating by MRI
Investigating whether fracture detection is significantly increased by routine follow-up SS in all cases of suspected NAI
Conclusion All children have the right to humane treatment. Society must not turn a blind eye to the abuse of children. Where physical abuse has led to fractures, the orthopaedic surgeon or radiologist may be the first to raise the alarm. Failure to do so can result in serious harm to the child. A working knowledge of the features suggestive of abuse is essential. An understanding of further investigations, including their limitations, will aid the clinician in arriving at the correct diagnosis in individual cases.
Acknowledgements The author wishes to thank Dr. R.J. Arthur for kindly providing the cases used for illustration.
References 1. Caffey J. Multiple fractures in the long bones of infants suffering from chronic subdural hematoma. Am J Roentgenol 1946;56:163–73. 2. Caffey J. Some traumatic lesions in growing bones other than fractures and dislocations: clinical and radiological features. Br J Radiol 1957;30:225–38. 3. Kleinman PK, editor. Diagnostic imaging of child abuse, 2nd ed. St. Louis, MO: Mosby; 1998. 4. Kleinman PK. Skeletal trauma: general considerations. In: Kleinman PK, editor. Diagnostic imaging of child abuse. 2nd ed. St. Louis, MO: Mosby; 1998. 5. Kleinman PK, Marks SC, Blackbourne B. The metaphyseal lesion in abused infants: a radiologic–histopathologic study. Am J Roentgenol 1986;146:895–905. 6. Merten DF, Radkowski MA, Leonidas JC. The abused child: a radiological reappraisal. Radiology 1983;146:377–91. 7. Chapman S. Non-accidental injury. Imaging 2004;16:161–73. 8. Kleinman PK. Bony thoracic trauma. In: Kleinman PK, editor. Diagnostic imaging of child abuse. 2nd ed. St. Louis, MO: Mosby; 1998. 9. Carty H, Pierce A. Non-accidental injury: a retrospective analysis of a large cohort. Eur Radiol 2002;12:2919–25. 10. Kleinman PK. Spinal trauma. In: Kleinman PK, editor. Diagnostic imaging of child abuse. 2nd ed. St. Louis, MO: Mosby; 1998. 11. Lonergan GJ, Baker AM, Morey MK, Boos SC. From the archives of the AFIP: child abuse: radiologic–pathologic correlation. RadioGraphics 2003;23:811–45. 12. Kleinman PK. Differential diagnosis III: accidental and obstetric trauma. In: Kleinman PK, editor. Diagnostic imaging of child abuse. 2nd ed. St. Louis, MO: Mosby; 1998. 13. Kleinman PK. Visceral trauma. In: Kleinman PK, editor. Diagnostic imaging of child abuse. 2nd ed. St. Louis, MO: Mosby; 1998. 14. Brill PW, Winchester P, Kleinman PK. Differential diagnosis I: disease simulating abuse. In: Kleinman PK, editor. Diagnostic imaging of child abuse. 2nd ed. St. Louis, MO: Mosby; 1998. 15. Mendelson KL. Critical review of ‘‘temporary brittle bone disease’’. Pediatr Radiol 2005;35:1036–40. 16. BSPR NAI standard for skeletal surveys. /http://www.bspr.org. uk/S. Accessed September 2006. 17. ACR Practice guidelines for skeletal surveys in children. Revised 2006 /http://www.acr.org/s_acr/bin.asp?TrackID=&SID=1&DID= 12286&CID=543&VID=2&DOC=File.PDFS. Accessed September 2006. 18. Kemp AM, Butler A, Morris S, et al. Which radiological investigations should be performed to identify fractures in suspected child abuse? Clin Radiol 2006;61:723–36.
ARTICLE IN PRESS Non-accidental injury 19. Kleinman PK, Nimkin K, Spevak MR, et al. Follow-up skeletal surveys in suspected child abuse. Am J Roentgenol 1996;167: 893–6. 20. Kleinman PL, Kleinman PK, Savageau JA. Suspected infant abuse: radiographic skeletal survey practices in pediatric health care facilities. Radiology 2004;233(2):477–85.
309 21. O’Connor JF, Cohen JC. Dating fractures. In: Kleinman PK, editor. Diagnostic imaging of child abuse. 2nd ed. St. Louis, MO: Mosby; 1998. 22. Department for Education and Skills. The Children Act Report 2002 /www.dfes.gov.uk/publications/childrenactreport/docs/ DfES-Childrens%20Act.pdfS. Accessed September 2006.
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Questions 1. What is the approximate infection rate after primary TKR? A. Less than 1 in 1000 B. 0.2% C. 0.5% D. 2% E. 5% 2. What is the most common symptom or sign of infection in a replaced knee? A. Local warmth B. Erythema around the wound C. Pain not aggravated by weight bearing D. Pain aggravated by weight bearing E. Fever within 5 days of surgery 3. For how long after knee arthroplasty does local warmth to palpation persist? A. 24 h B. 2–3 days C. 2–3 weeks D. 2–3 months E. 6 months 0268-0890/$ - see front matter doi:10.1016/j.cuor.2007.08.003
4. Which of the following investigations is least helpful in a patient who develops symptoms suspicious of infection after knee replacement? A. FBC B. CRP C. ESR D. X-ray E. Wound swabs 5. For how long after knee replacement in non-rheumatoid patients does the CRP remain elevated? A. 24 h B. 1 week C. 6 weeks D. 6 months E. 1 year 6. What is the approximate probability of infection being present in a replaced knee if the CRP and ESR are normal (o10 mg/l and 30 mm/h, respectively)? A. Zero B. 0.1 C. 0.2 D. 0.3 E. 0.5
7. What is the approximate sensitivity of gram staining of knee aspirate in the diagnosis of infection? A. o5% B. 10% C. 30% D. 66% E. 90%
8. What is the approximate success rate of 2-stage revision knee replacement in the presence of a high virulence organism such as MRSA? A. 10% B. 25% C. 33% D. 66% E. 90%
ARTICLE IN PRESS CME SECTION 9. Which of the following is not a criterion for the assumption of a strategy of antibiotic suppression in a chronically infected knee replacement? A. unfeasibility of prosthesis removal B. organism is sensitive to oral antibiotics C. antibiotics can be tolerated in the longer term D. high virulence organism E. prosthesis remains well fixed
321 10. What is the reported amputation rate after knee replacement according to most studies? A. 0.01% B. 0.1% C. 1% D. 2% E. 5%
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MINI-SYMPOSIUM: SURGICAL RHEUMATOLOGY
(i) The surgical management of rheumatoid arthritis of the shoulder and elbow Ziali Sivardeen, David Stanley Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK
KEYWORDS Management; Rheumatoid arthritis; Shoulder; Elbow
Summary The management of the rheumatoid shoulder and elbow is a challenging problem. In this review we aim to summarise the main management options for shoulder and elbow disease placing particular emphasis on surgical treatment. We believe that by using the techniques available and with good patient selection excellent results can be achieved, reducing the patients pain and also providing independence for activities of daily living. & 2007 Published by Elsevier Ltd.
Introduction Rheumatoid arthritis (RA) is a systemic debilitating disease characterised by progressive joint destruction. It affects 1–3% of the population with a peak age of onset between 35 and 45 years. Small joints are usually affected early in the disease but involvement of the elbow and shoulder are not uncommon. In this review, we aim to summarise the main management options for shoulder and elbow disease placing particular emphasis on surgical treatment. Before doing this however it is important to stress the role of medical management in the overall care of the rheumatoid patient.
achieve this aim the patient requires the care of a multidisciplinary team which as a minimum should include a rheumatologist, orthopaedic surgeon, physiotherapist and occupational therapist. In addition, further specialist input may be required to deal with particular problems. Medical treatment of the disease process is important because it will minimise synovitis, reduce joint destruction and enable the surgeon to perform more limited procedures when surgical interventions are required. The specific medical therapy is dictated by the individual needs of the patient and may involve combinations of drugs from simple analgesics through to the newer disease modifying agents.
Shoulder Medical management The objective of treatment is to induce disease remission allowing the patient to lead as normal a life as possible. To Corresponding author.
E-mail address:
[email protected] (D. Stanley). 0268-0890/$ - see front matter & 2007 Published by Elsevier Ltd. doi:10.1016/j.cuor.2007.07.006
Shoulder symptomatology is a common finding in patients with long-standing RA. Studies have shown that more than 90% of patients who have had the disease for more than 5 years develop shoulder problems.1 Patients often present with symptoms that are indicative of the articular and periarticular nature of the condition, namely pain, swelling and a decreased range of motion. Rotator cuff insufficiency is
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common affecting more than 70% with approximately 30% developing full thickness tears.2
Classification RA of the shoulder has been classified by Laine et al.,3 and later by Neer4 into three stages that reflect the severity of the condition with respect to clinical and radiological findings. Neer’s dry, wet and resorptive stages approximately correlate with Laine’s stages.
Stage 1 Stage 2 Stage 3
ROM
Pain
Radiology
Slight decrease Moderate decrease Severe decrease
Mild
Generalised osteopenia Erosive bony changes, joint space narrowing Advanced erosive changes of humeral head and glenoid
Moderate Severe
Non-surgical management In Stage 1 there are no significant osseous changes, and this is the ideal time for non-operative treatment. The mainstay of treatment is medical, and involves the use of NSAIDs, disease modifying drugs, antimetabolics and oral steroids. Activity modification, intra-articular or subacromial steroid injections may also be helpful. Patients who have not had significant benefit form oral medication often improve with steroid injections. However, the improvement may only be temporary and must be weighed against the potential harmful effects injections have on rotator cuff healing and articular cartilage.5 Physiotherapy is useful in maintaining and regaining range of motion depending on the stage of the disease.
Surgical management Surgical management is indicated when non-surgical treatment has failed to control pain and maintain function. The type of procedure performed is determined by the severity of the disease, taking into consideration the level of involvement of articular cartilage, bone and the periarticular soft tissues. If there is significant articular cartilage preservation, procedures such as synovectomy and debridement may be useful in relieving the patients’ symptoms. However, once articular cartilage loss has occurred prosthetic replacement using either a hemiarthroplasty or total joint replacement is usually necessary. Order of surgical procedures RA is a disease that often affects multiple joints simultaneously. It is therefore useful to have a general strategy to deal with these patients. The majority of surgeons agree that the most symptomatic joint should be treated first. If however the symptoms are similar, in the upper and lower limb, then the lower limb surgery will normally take precedence. Upper limb surgery should be deferred until the use of ambulatory aids is no longer required.
The elbow takes precedence over the shoulder. In one study, a superior functional result and a longer interval between arthroplasties was gained when the elbow was operated on before the shoulder.6 The exception to this is if the shoulder is ankylosed. In this situation the shoulder is addressed first to minimise increased rotational stresses that might be put on the elbow due to absent shoulder motion. Joint preserving procedures Synovectomy produces the best results in patients with Stage 1 disease. The procedure can be performed open or arthroscopically with up to 80%7 gaining a painless range of movement. Often the procedure involves a glenohumeral joint synovectomy with a subacromial bursectomy. In the presence of rotator cuff insufficiency, an acromioplasty and/ or release of the coracoacromial ligament is contraindicated as this may lead to antero-superior instability. Joint debridement may result in symptomatic relief; however, this is often transitory and is not usually related to a significantly increased range of motion.8 Joint sacrificing procedures When non-surgical and joint preserving procedures have failed, joint replacement is indicated. This can be in the form of a hemiarthroplasty or a total shoulder replacement, with both procedures resulting in significant pain relief, increased range of movement and function.9 The two types of prosthesis in common use are either surface replacements (Figs. 1A and B) or traditional stemmed implants. Although, this improvement is maintained over time10 the overall results are not as good as in patients with osteoarthritis.9 In general, the results of total shoulder replacement are superior to hemiarthroplasty with better functional results and less pain.11 However, in situations associated with an increased risk of glenoid failure such as an irreparable rotator cuff tear or deficient glenoid bone preventing adequate implant fixation, it is better to perform a hemiarthroplasty. Up to 35% of patients who require a shoulder arthroplasty have rotator cuff tears. These should be repaired at the same time as the arthroplasty to achieve the best results.12 If this is not possible consideration should be given as to whether a reverse polarity shoulder arthroplasty is indicated (Figs. 2A and B). This device alters the biomechanics of the shoulder allowing the deltoid to partly compensate for the deficient rotator cuff.
Elbow Elbow rheumatoid disease occurs more commonly than at the shoulder with 50% of patients experiencing elbow symptoms within 5 years.13 It is often associated with shoulder or wrist involvement (around 90%). Patients often present with pain and restricted range of motion due to synovitis in the joint. Ten percent spontaneously resolve.13 However, if the synovitis continues fixed flexion deformities, instability, compression neuropathies and joint destruction may occur. Fixed deformities are often due to the patient holding the arm in a flexed position to minimise pain. Instability of the radial head occurs after destruction of the annular ligament and the subsequent anterior pull of the biceps. Instability of the elbow results
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327
Figure 1 (A and B) Patient with glenohumeral arthritis treated with a Copeland resurfacing arthroplasty.
from destruction of the medial and lateral collateral ligament complexes. If the synovitis extends beyond the joint, compression of the ulnar or posterior interosseous nerve will produce neurological symptoms.14 Long-standing synovitis leads to articular cartilage destruction and degenerative changes.
Classification Morrey has described four stages in the Mayo Clinic Classification of the rheumatoid elbow.15
Figure 2 (A and B) Patient with cuff tear arthropathy treated with a reverse polarity arthroplasty.
Non-surgical management Early rheumatoid disease of the elbow should be managed non-operatively by a rheumatologist. As the disease progresses, the use of activity modification physiotherapy, steroid injections, and elbow braces may help alleviate symptoms.
Surgical management Stage I
Stage II Stage IIIA Stage IIIB Stage IV
Radiology
Synovitis
Minimal, except soft tissue swelling and peri-articular osteopenia Joint space narrowing bony architecture preserved Moderate bony architecture changes Severe bony architecture changes Gross destruction of the joint gross instability
Mild
Persistent synovitis Synovitis variable Synovitis variable Minimal synovitis
Satisfactory management of the rheumatoid elbow is sometimes not possible with non-surgical treatment. Synovectomy and total joint replacement are the main surgical options, however resection arthroplasty and interposition arthroplasty may occasionally have a role. Joint preserving procedures Synovectomy can be performed open or arthroscopically, and is normally indicated after 6 months of painful synovitis that has not resolved after appropriate medical treatment. Open synovectomy with or without radial head excision has been shown to produce satisfactory results in patients
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with Stages II, III and IV disease; however, the results are best in those with Stage II disease.16 A satisfactory outcome is achieved in 70–90%.16 When performed early the results can last over 10 years in 80% of patients.17 Radial head excision is controversial, with no clear distinction in the literature between the results reported with or without excision.18 Removing the radial head will improve forearm rotation and decrease impingement; however, the loss of its role in stability in the rheumatoid elbow may lead to instability and ulnar nerve irritation. Arthroscopic synovectomy, although demanding technically and associated with an increased risk to the neurovascular structures, has various theoretical advantages over the open procedure. It can be performed as a day-case, is associated with a rapid return to normal motion, and a more complete synovectomy is technically possible.19 The early results have been promising, but longer term studies are required. Lee and Morrey19 reported a 93% success rate at 6 months, but only 57% were rated as good or excellent using the Mayo Elbow Index at 3.5 years. Horiuchi et al.20 reported an increase in the Mayo Elbow Index from 48.3 to 77.5 at a mean follow-up of 97 months, but only patients with mild radiographic changes had good long-term results. The most common complication after synovectomy is recurrence of pain. Although some authors have advocated a repeat procedure, the results have been less predictable with 55% still having pain following the second procedure.21 The best results occur if there has been a favourable response to the first procedure.22 Other complications are instability (15%) and nerve damage.23 Although synovectomy may give good results it should be borne in mind that patients who subsequently undergo total elbow arthroplasty have technically more difficult operations and poorer clinical results at 2 years follow-up.23
Joint sacrificing procedures Interposition arthroplasty has been shown to produce satisfactory results in young patients with Stage II or IIIA disease. The procedure involves limited bone resection in order to preserve normal architecture and stability. The graft (fascia, skin or synthetic material) is then placed and secured over the distal humerus. An external fixator is used to distract the joint surfaces and allow elbow movement whilst the soft tissues heal. Around 75–80% benefit from surgery24 and pain relief can be maintained for up to 20 years. Conversion to a total elbow replacement is possible but the results are inferior to a primary total joint arthroplasty.8 Excision arthroplasty is now normally used as a salvage procedure mainly for infection. Pain relief is often gained in 80%,25 but extensor weakness and instability can be a problem. Total joint arthroplasty is the treatment of choice for patients with Stages III and IV disease. Historically, early designs of elbow replacement were rigid hinged devices, which suffered from an unacceptable rate of loosening. The most common types of replacements used today are either unlinked or linked implants. These are associated with decreased rates of loosening due to reduced stress transfer to the prosthesis–bone interface compared to the rigid hinged devices. Linked arthroplasties (Figs. 3A and B) have a sloppy-hinge design that allows 5–10 degrees of motion in varus/valgus
Figure 3 (A and B) Patient with severe elbow arthritis treated with the linked Kudo total elbow arthroplasty 14 years after surgery.
and axial rotation. This allows the soft tissues to absorb some of the stresses that would normally transfer to the prosthesis–bone interface. Excellent results have been obtained, with Morrey reporting 85% good or excellent results and overall survivorship of 92% at 10–15-year followup using the Coonrad–Morrey elbow replacement9 (Fig. 4). Unlinked implants rely on bone and ligamentous structures for their stability; they have less stress transfer to the prosthesis–bone interface but have increased instability26 compared with linked implants. In general, most studies show that superior results are achieved when a linked device is used rather than an unlinked device in the rheumatoid elbow.
Conclusions The management of the rheumatoid upper limb is a challenging problem, with various techniques available to the surgeon. Using these techniques and with good patient
ARTICLE IN PRESS Surgical management of rheumatoid arthritis
Figure 4
The Coonrad–Morrey total elbow arthroplasty.
selection excellent results can be achieved, reducing the patients, pain and also providing independence for activities of daily living.
References 1. Cuomo F, Griller MJ, Zuckerman JD. The rheumatoid shoulder. Rheum Dis Clin North Am 1998;24:67–82. 2. Curran JF, Ellman MH, Brown NL. Rheumatologic aspects of painful conditions affecting the shoulder. Clin Orthop 1983; 173:27–37. 3. Laine VAI, Vainio KJ, Pekanmaki K. Shoulder affections in rheumatoid arthritis. Ann Rheum Dis 1954;13:157–60. 4. Neer CS. The rheumatoid shoulder. In: Crubbs RL, Mitchell NS, editors. The surgical management of rheumatoid arthritis. Philadelphia, PA: JB Lippencott; 1971. p. 117–27. 5. Rozental TD, Sculco TP. Intra-articular corticosteroids: an updated overview. Am J Orthop 2000;29:18–23. 6. Friedman RJ, Ewald FC. Arthroplasty of the ipsilateral shoulder and elbow in patients who have rheumatoid arthritis. J Bone Jt Surg Br 1987;69A:661–6. 7. Petersson CJ. Shoulder surgery in rheumatoid arthritis. Acta Orthop Scand 1986;57:222–6. 8. Hess EV. Rheumatoid arthritis: treatment. In: Schumacher Jr. HR, editor. Primer on the rheumatic diseases. 9th ed. Atlanta, GA: Arthritis Foundation; 1988. p. 93–6. 9. McCoy SR, Warren RF, Bade III HA, et al. Total shoulder arthroplasty in rheumatoid arthritis. J Arthroplasty 1989;4: 105–13.
329 10. Sneppen O, Fruensgaard S, Johannsen HV, et al. Total shoulder replacement in rheumatoid arthritis: proximal migration and loosening. J Shoulder Elbow Surg 1996;5:47–52. 11. Cofield RH, Frankle MA, Zuckerman JD. Humeral head replacement for glenohumeral arthritis. Semin Arthroplasty 1995;6: 214–21. 12. Rozing PM, Brand R. Rotator cuff repair during shoulder arthroplasty in rheumatoid arthritis. J Arthroplasty 1998;13: 311–9. 13. Inglis AE, Figgie MP. Septic and non-traumatic conditions of the elbow: rheumatoid arthritis. In: Morrey BF, editor. The elbow and its disorders. 2nd ed. Philadelphia, PA: WB Saunders; 1993. p. 751–66. 14. Westkaemper JG, Varitimidis SE, Sotereanos DG. Posterior interosseous nerve palsy in a patient with with rheumatoid synovitis of the elbow: a case report and review of the literature. J Hand Surg 1999;24A:727–31. 15. Morrey BF, Adams RA. Semi-constrained arthroplasty for the treatment of rheumatoid arthritis of the elbow. J Bone Jt Surg Am 1992;74:479–90. 16. Tulp NJ, Winia WP. Synovectomy of the elbow in rheumatoid arthritis: long-term results. J Bone Jt Surg Br 1989;71:664–6. 17. Alexeides MM, Scott TS, Figgie MP, Inglis AE. Minimum 10 year follow-up for elbow synovectomy for rheumatoid arthritis. Orthop Trans 1990;14:255. 18. Copeland SA, Taylor JG. Synovectomy of the elbow in rheumatoid arthritis: the place of excision of the head of the radius. J Bone Jt Surg Br 1979;61B:69–73. 19. Lee BPH, Morrey BF. Arthroscopic synovectomy of the elbow. A prospective study. J Bone Jt Surg Am 1997;79B:770–2. 20. Horiuchi K, Momohara S, Tomatsu T, et al. Arthroscopic synovectomy of the elbow in rheumatoid arthritis. J Bone Jt Surg Am 2002;84:342–72. 21. Rymaszewski LA, Mackay I, Amis AA, et al. Long-term effects of excision of the radial head in rheumatoid arthritis. J Bone Jt Surg Br 1984;661B:109–13. 22. Ferlic DC, Patchett CE, Clayton ML, Freeman AC. Elbow synovectomy in rheumatoid arthritis. Clin Orthop 1987;220: 119–25. 23. Schemitsch EH, Ewald FC, Thornhill TS. Results of total elbow arthroplasty after excision of the radial head and synovectomy in patients who had rheumatoid arthritis. J Bone Jt Surg Br 1996;78A:1541–7. 24. Morrey BF. Interposiitonal arthroplasty. In: Morrey BF, editor. Reconstructive surgery of the joints. 2nd ed. Ville: Churchill Livingstone; 1996. p. 493–637. 25. Figgie MP, Inglis AE, Mow CS, et al. Results of reconstruction for failed total elbow arthroplasty. Clin Orthop 1990;253: 123–323. 26. Kudo H, Iwano K. Total elbow arthroplasty with a nonconstrained surface replacement prosthesis in patients who have rheumatoid arthritis. J Bone Jt Surg Br 1990;72A:355–623.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 330–339
Available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/cuor
MINI-SYMPOSIUM: SURGICAL RHEUMATOLOGY
(ii) Hip and knee reconstruction in the rheumatoid patient J.M. Wilkinsona,, P. Haslamb, C.J.M. Gettyc a
Academic Unit of Bone Metabolism, University of Sheffield, Sorby Wing, Northern General Hospital, Harries Road, Sheffield S5 7AU, UK b Department of Orthopaedics, Doncaster Royal Infirmary, Doncaster, UK c Department of Orthopaedics, Northern General Hospital, Sheffield, UK
KEYWORDS Rheumatoid arthritis; Hip; Knee; Arthroplasty; Treatment
Summary Surgical management of the rheumatoid patient requires a multidisciplinary approach. A successful outcome necessitates appropriate management not only of the joint disease but also of the soft tissues, polyarthropathy, co-morbidities, and polypharmacy. At the hip standard implants give good long-term function and implant survivorship, with a complication rate that is similar to other patient groups. At the knee it is important to appreciate the pan-articular nature of the joint involvement and use appropriate implants. Severe ligamentous laxity and fixed deformity may require the use of constrained implants. Complication rates and implant survivorship after hip and knee arthroplasty in patients with rheumatoid arthritis are broadly similar to patients with osteoarthritis. Late functional outcome is dictated, in part, by polyarthritis, rather than the diagnosis of rheumatoid arthritis in itself. Patient satisfaction after hip and knee arthroplasty for rheumatoid arthritis is high. & 2007 Elsevier Ltd. All rights reserved.
Background Rheumatoid arthritis (RA) is a systemic inflammatory disorder that affects approximately 1% of the adult population worldwide and is twice as prevalent in women versus men. The aetiology of RA remains unclear, but is thought to comprise both heritable and environmental factors. Twin Corresponding author. Tel.: +44 114 2714705;
fax: +44 114 2618775. E-mail address:
[email protected] 0268-0890/$ - see front matter & 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2007.08.002
and family studies suggest that the overall heritable contribution to RA is approximately 60%.1 Smoking is associated with an increased incidence of RA, and low socio-economic status is associated with a poorer prognosis. Remission of RA is well-documented in pregnancy and oral contraceptive use may postpone disease onset. The natural history of RA is chronic, progressive polyarticular joint destruction, such that by 3 years 20–30% of patients may become permanently work-disabled.2 By 20 years following diagnosis up to 80% of patients have functional disability.3 Extra-articular manifestations affecting the cardiovascular, respiratory, and neurological systems
ARTICLE IN PRESS (ii) Hip and knee reconstruction in the rheumatoid patient also contribute to functional impairment and reduce life expectancy by 5–10 years compared to populations without RA.4 The clinical course of RA varies between individuals. Ten percent of patients present with an acute and rapidly progressive pattern of disease, and 70% of patients have a polycyclic course characterised by periodic flares in inflammatory activity.5 Twenty percent of patients experience a single episode of inflammation that is not followed by progressive joint destruction. Where active disease is present for greater than 3 months, this usually progresses to chronic disease. The musculoskeletal manifestations of RA are characterised by symmetrical inflammatory polyarthritis that affects both small and large joints.6 Patients with RA may be referred for a surgical opinion for a variety of reasons including joint destruction and deformity, ligamentous instability, tendon rupture or dislocation, bone fracture, and the neurological sequelae of spinal involvement. In a previous article we reviewed the surgical management of the rheumatoid patient with reference to general clinical assessment, decision-making regarding surgical priorities, pre-operative assessment, and peri-operative management in relation to medical co-morbidities commonly present in this population.7 This article focuses on the role of hip and knee arthroplasty, including the changing incidence and pattern of disease progression, clinical presentation and radiological features, indications for surgery, choice of prosthesis and surgical challenges, functional outcomes, complications, and implant survivorship.
Changing incidence and disease progression The proportion of patients presenting for hip and knee reconstruction with a diagnosis of RA relative to other diagnoses is decreasing in Western societies. Data from the Norwegian Arthroplasty Register demonstrates a decrease in RA as the primary diagnosis for total hip arthroplasty (THA) surgery from 3.7% in 1987–1990 to 2.4% in 2004,8 although the absolute number of patients undergoing THA for RA remained static during this period. During the period 1975–2003 the yearly number of arthroplasties for RA reported to the Swedish Knee Arthroplasty Register decreased marginally.9 A recent retrospective populationbased analysis by Sokka et al.10 examined the incidence of THA and total knee arthroplasty (TKA) in RA versus non-RA for the period 1987–2003. Whilst they found that the ageadjusted incidence of THA and TKA in non-RA patients increased by 2- and 9.8-fold, respectively, the incidences of THA and TKA in RA patients had not changed significantly. Part of this observed change in epidemiology can be explained by an increase in the number of patients with osteoarthritis presenting for surgery. However, evidence also suggests that the prevalence and pattern of disease progression of RA is also changing. Studies in the UK indicate that the prevalence of RA in women aged 45–64 years has decreased by approximately 50% to 1.2% over the 30 years up to 1992, and secular decreases in both the incidence and prevalence of RA in North American, European and Asian populations have also been reported.11,12 Recent years have seen major developments in the role and efficacy of disease modifying drugs (DMARDs) used to treat RA, particularly with
331 the emergence of a new class of ‘biological’ DMARD therapies that target specific cytokine pathways. The results from clinical trials and observational studies suggest that these agents slow disease progression.13 In a cohort study of 482 patients with RA, Verstappen et al.14 found that treatment with DMARDs immediately after diagnosis resulted in less joint surgery when compared with a delayed start.
Clinical assessment Destruction of the hip joint occurs late in the course of RA and affects 50% of patients. The knee is affected earlier in the course of RA (usually within 10 years of onset) and affects approximately 80% of patients. Bilateral joint involvement is common at both sites.6 The typical presentation of a patient with hip or knee involvement includes chronic and progressive pain, with deterioration in mobility and ability to perform activities of daily living. Presentation with an acute episode of hip pain and impaired function may indicate acute conditions such as femoral head collapse secondary to avascular necrosis, femoral neck fracture, or rarely, septic arthritis. Patients with RA affecting the knee may present with symptoms of instability, deformity secondary to collateral ligament insufficiency or avascular necrosis of the femoral or tibial condyles, or occasionally with knee stiffness due to fibrous ankylosis. Clinical assessment of the patient presenting with hip or knee involvement includes a full medical and social history, and appropriate local and systemic examination (Table 1). At the hip the patients’ gait and posture, leg lengths, and range of joint motion should be assessed. Deformities and limitations in the functional range of motion at the neck, back, knee, ankle and foot should also be assessed. A screening examination of the cervical spine, and upper and lower limb neurological function should also be made to exclude a neurogenic cause (such as cervical myelopathy) for deterioration in walking ability. An assessment of the skin condition over the hip and the leg is made, with particular reference to the sole of the foot, together with an examination of the vascular tree of the leg and foot. In general, significant involvement of the forefoot should be addressed surgically before management of the hip, as skin loss and secondary infection may put a hip prosthesis ‘atrisk’ of infection (Fig. 1). Involvement of the shoulders and elbows is common in RA, and an assessment of the upper limbs with respect to the potential for mobilisation with crutches post-operatively is also made.
Radiological features The plain radiographic features of RA include global joint space narrowing and periarticular osteoporosis that commonly involves joints symmetrically (Table 2). The former is due to enzymes from the inflammatory pannus that cause dissolution of articular cartilage, the latter is thought to be due to synovial hyperaemia. At the hip protrusio acetabuli is common due to axial or superior migration of the femoral head with reactive bone remodelling in the pelvis (Fig. 2). Occasionally, large rheumatoid cysts in the pelvis or femoral
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Table 1 patient.
Pre-operative assessment of the rheumatoid
History Disease onset Pattern and temporal sequence of joints involved Presence and persistence of joint swelling Pain—site, severity and radiation Morning stiffness and duration Functional difficulties Presence of non-articular features (e.g. nodules) Systemic features (e.g. anorexia, fatigue, weight loss) Psychological effects Full review of systems Previous anaesthetic and surgical history Drugs and allergies Examination
Complete medical Evidence of joint inflammation Joint damage, range of motion, and previous surgical scars
Tendon and ligamentous damage Presence of extra-articular features (e.g.
seen on the anteroposterior view, and suprapatellar pouch distension seen on the lateral view are features of a large effusion. Erosion of the anterior femoral cortex at the level of the suprapatallar pouch secondary to pannus erosion also occurs (Fig. 4). Valgus malalignment of the joint arises as a result of bone loss in the lateral femoral condyle and to a lesser extent the lateral tibial condyle, and is exacerbated by laxity of the medial collateral ligament. An external rotatory deformity of the tibia on the femur occurs, with contracture of the ilio-tibial band.
Indications for arthroplasty The primary indications for arthroplasty are progressive pain that is inadequately controlled with conservative measures, loss of function, difficulty with activities of daily living, and progressive deformity. The aims of surgery are to provide a sterile, pain-free, stable, mobile, and long-lasting joint replacement. Contra-indications to arthroplasty include uncontrolled medical co-morbidity, skeletal immaturity, and active infection. Relative contraindications include neurological deficits that limit mobility (myelopathy: Ranawat stage 3 or 4), peripheral vascular disease, and poor skin condition that increases the potential for infection (e.g. active vasculitic lesions),
splenomegaly, leg ulcers, vasculitis)
Grip strength General health, anaemia, muscle atrophy Dental inspection, assessment of mouth opening ability, dysphonia Neurological assessment for cervical myelopathy and peripheral neuropathy Investigations
Full blood count, urea, creatinine, electrolytes, and liver function tests
Chest radiograph, lateral cervical spine flexion and extension radiographs
Electrocardiogram Urine dipstick7culture to exclude occult infection Pulmonary function tests in patients with limiting lung disease
Echocardiogram in patients with limiting cardiac involvement
Choice of prosthesis and surgical challenges In the setting where the hip and knee are symptomatic and warrant joint reconstruction, the hip is usually addressed prior to the knee. THA restores correct femoral alignment and length, facilitating correct implant alignment at subsequent TKA. In practice however, hip disease typically presents later in the natural history of RA than knee involvement. A more common scenario is presentation with symptomatic bilateral hip or knee involvement that requires bilateral total joint arthroplasty. Parvizi et al.15 found no difference in 90-day mortality rates between age and sex matched patients undergoing unilateral versus bilateral simultaneous THA. At the knee bilateral TKA my also be performed successfully as a single procedure, or staged, depending upon the individual patients co-morbidities.16–18 However, these studies were conducted in non-RA populations, and should be extrapolated to the patient with RA with caution.
Hip reconstruction head, termed geodes, may also be present (Fig. 3). Marginal erosions at the junction of the femoral head and neck may also be seen. Segmental avascular necrosis of the femoral head may be present due to primary disease, or as a complication of steroid therapy. Reactive bone formation in the form of subchondral sclerosis and osteophytes is absent in pure RA, but commonly seen where secondary osteoarthritis follows joint destruction. Fibrous ankylosis may be seen occasionally. Magnetic resonance imaging features include effusion, erosion, diffuse cartilage loss, bone marrow oedema, and pannus formation. At the knee, in addition to the typical radiological features (Table 2), lateral bulging of the normal fat lines
Prosthesis selection Either cemented or cementless THA components may be used in the patient with RA. For implants using a metal-onconventional polyethylene bearing, current data favour cementless or cemented femoral components in combination with a cemented acetabular component. Eskelinen et al.19 have reported the results of THA surgery in 2557 patients with RA under the age of 55 years from the Finnish Arthroplasty register. They reported a 15-year survival rate for cementless proximally circumferentially porous-coated stems of 87%. The 15-year survivorship for cemented stems was 81% (relative risk for failure cemented versus cementless stems 2.0, p ¼ 0.01). In contrast, cementless
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Figure 1 Soles of the feet in a patient with rheumatoid arthritis. There is distal subluxation of the forefoot fad pad with exposure of subluxed metatarsal heads and resultant callosity formation.
Table 2 Common radiographic features in rheumatoid arthritis. Soft tissues overlying the joint Swelling Effusion Rheumatoid nodules Intra-articular changes
Global joint space narrowing Marginal erosions Secondary osteoarthritic change (osteophytes, sclerosis, cysts)
Condylar bone collapse Peri-articular changes
Juxta-articular osteoporosis Metaphyseal cysts (geodes) Periostitis (common at the digits, rare at large joints) Joint mal-alignment (alignment abnormaities due to ligament incompetence, joint subluxation, joint dislocation)
with RA (63 patients, 100 hips) versus osteoarthritis (54 patients, 66 hips). Survivorship of the femoral component was 85% in patients with RA versus 74% in patients with OA, survivorship of the acetabular component was 79% versus 59%, respectively. The role of resurfacing arthroplasty in RA remains unclear. Although there are short-term data on the efficacy of this intervention in juvenile idiopathic arthritis,22 there are no intermediate or longterm data on clinical outcome or survivorship in RA. Surgical challenges The local surgical considerations at THA are the management of local bone defects such as found in protrusio acetabuli, and osteoporosis, which carries an increased risk of intra- or perioperative periprosthetic fracture. One of the goals in the management of protrusio is to restore the centre of hip rotation to its anatomic position. This may be achieved using cemented or cementless acetabular components in combination with impacted morsellised bone allograft (Fig. 2).23,24 In the elderly patient, or where the severity of protrusio is mild, the defect may be filled using a conventional cemented acetabular component without the use of bone graft. Large geodes (Fig. 4), where present, should be managed using impaction grafting of the femoral head or using allograft.
Knee reconstruction cup 15-year survivorship was poorer than for cemented cups, 67% versus 80%, respectively (relative risk for failure 1.4, p ¼ 0.001). Odent et al.20 in a long-term follow-up study of 62 cementless Zweymuller THAs in 34 patients with juvenile chronic arthritis report 13-year survivorship of the femoral component of 100% and 90% for the acetabular component. Sochart and Porter21 reported the 25-year survivorship of cemented Charnley THA in young patients
Prosthesis selection At the knee the gold standard implant is the cemented TKA. The cumulative 10-year revision rate of cemented TKA between 1993 and 2002 in RA patients reported to the Swedish Knee Arthroplasty Register (n ¼ 4417 implants) was 5%.9 Good early clinical outcomes are also reported for cementless implants,25 although large-scale and long-term
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Figure 2 Plain radiograph of the pelvis in a patient with rheumatoid arthritis. On the right side there is protrusio acetabuli, on the left this has been treated with cemented total hip arthroplasty plus impaction of morsellised allograft to the protrusio defect.
Figure 3
Plain radiograph of the pelvis in a patient with rheumatoid arthritis showing bilateral large iliac geodes.
follow-up outcome data in rheumatoid patients are limited. Sharma et al.26 reported the 16-year survivorship of the cementless ‘Low Contact Stress’ TKA in 47 patients with RA as 94%. In contrast to osteoarthritis, where degeneration may be limited to a single compartment, in RA the degenerative change is pan-articular necessitating replacement of the entire tibio-femoral articulation. The merits of including patellar resurfacing remain less clear. In a review of 4381 TKAs for RA in the Swedish Knee Arthroplasty Register, Robertsson et al.27 found a 10-year cumulative revision rate
for unicompartmental prostheses of 25%, versus 5% for TKA. However, there was no significant difference in revision rates between patellar resurfaced versus non-resurfaced TKAs. Kawakubo et al.28 in a retrospective review of 60 TKA patients, found that thickness of the non-resurfaced patella decreases with time, particularly in the RA patient. The incidence of anterior knee pain following TKA was 12% in OA patients versus 28% in RA patients. A recent meta-analysis of patellar resurfacing in TKA has also demonstrated that resurfacing reduces the risk of anterior knee pain and re-operation after TKA.29 However, patients with RA were
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Figure 4 (a) and (b) Plain anteroposterior (a) and lateral (b) radiographs of the knee in a patient with rheumatoid arthritis. Degenerative changes are present in all 3 joint compartments. There is collapse of the lateral compartment with resultant valgus deformity. Erosion of the anterior aspect of the distal femoral metaphysis due to pannus is also seen.
included in only 2 out of the 12 trials studied and clear conclusions cannot be drawn in this patient group. The relative benefits of the use of a mobile-bearing versus a fixed-bearing TKA in the patient with RA also remain unresolved for similar reasons.30
Surgical challenges The reconstructive challenges faced in TKA in the setting of RA include ligamentous instability, focal bone loss, and periarticular osteoporosis. In general, knee deformity is associated with ligament incompetence rather than contracture, with the exception of severe fixed flexion deformities that result from wheelchair dependence, rather than local disease at the knee. Valgus deformities are associated with a variable degree of hyperextension, more commonly than fixed flexion. Varus deformities are seen where secondary OA change occurs and may be associated with a variable degree of fixed flexion. Fixed valgus deformity is due to loss of height within the lateral compartment, mainly due to femoral condylar bone loss, with contracture of the iliotibial band (that also causes fixed external rotatory deformity), lateral collateral ligament, popliteus muscle, postero-lateral capsule, and biceps femoris muscle (Fig. 4). There is secondary laxity within the medial collateral ligament. Lateral maltracking of the patella is associated with fixed valgus deformity due to secondary contracture of the lateral patello-femoral ligament and capsule. Fixed varus deformity arises as a result of loss of height within the medial compartment, mainly due to tibial condylar bone loss with shortening of the medial collateral ligament, postero-medial capsule, pes anserinus,
and semimembranosus muscle. Secondary laxity within the lateral collateral ligament occurs late. Symmetrically balanced collateral ligaments are important for satisfactory outcomes in TKA. Incorrect soft tissue balance leads to unequal loading, asymmetric stresses on the implant, and eventual implant loosening. Ligament balancing requires a stepwise approach to the release of the contracted tissues.31–33 Those causing fixed valgus may be accessed through a medial parapatellar approach using techniques described by Insall et al. and others.34,35 Alternatively, a lateral approach to the knee has the advantage of allowing direct access to the contracted structures and allowing a complete lateral capsular release that helps correct patellar tracking, whilst maintaining the medial blood supply to the patella.36,37 The necessary releases for fixed varus deformities are readily accessed through a medial parapatellar approach. Severe coronal plane deformities are commonly associated with significant loss of condylar bone that may be corrected by use of a thick tibial condyle bone resection and a polyethylene insert of appropriate thickness to restore the level of the tibial joint line. Structural bone graft or prosthetic augmentation blocks may be required to restore large bone defects. Where large cysts are present in the metaphyseal region, these should be managed using impaction bone grafting, and may require the use of a stemmed prosthesis to bypass the defect and protect the graft during its incorporation. The severity of the ligamentous incompetence and associated bone loss dictates the choice of implant that can be used for the joint reconstruction. In mild deformities of less than 151 a cruciate-retaining or sacrificing implant
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Patients with RA had SF-12 physical scores that were 15% poorer than patients with OA (Fig. 5, p ¼ 0.004). There was no difference in the SF-12 mental score between groups (p40.05). The SF-12 summary score (physical score+mental score) was 8% poorer in patients with RA versus those with OA (p ¼ 0.01). There was no difference between RA and OA patient groups for the Oxford hip score or Harris hip score (Fig. 1, p40.05 both comparisons). Within the individual P=0.004
60 40 20
ta To
To R
A-
AO
l
l ta
l ta
A-
M
M R
O
A-
Ph
en
en
ic
ta
al
al ic
ys
ys Ph R
A-
AO
l
0
Data from patients with OA of the hip or knee suggest timing of surgery has a significant impact on clinical function after surgery. Patients with poorer pre-operative function scores do not achieve the same post-operative scores as those with better pre-operative function, although their improvement relative to their pre-operative function is similar.40,41
P>0.05 60
Oxford Hip Score
50 40 30 20 10 0 OA
RA P>0.05
100
Harris Hip Score
The post-operative improvement in function after THA for RA is good. Katsimihas et al.42 reported an improvement in Harris hip score from 22 pre-operatively to 82 at a mean of 9 years later in 50 patients. Tang and Chiu43 reported an improvement in Harris hip score from 25 pre-operatively to 89 at 11 years in 20 patients. Espehaug et al.44 in a case matched study, found that patients with RA had similar postoperative improvements in modified Merle d’Aubigne scores for pain and walking ability as patients undergoing THA for OA at a mean of 5 years post-operatively. Creighton et al.45 have suggested that the functional outcome is poorer in RA compared to patients undergoing THA for other diagnoses. In contrast, Bischoff-Ferrari et al.46 in a study designed to examine the effects of a number of variables on function after THA, found that RA was not a significant independent predictor of poor function (poor function was defined as a WOMAC score of o50). We have reviewed and compared the late functional outcome of THA in patients with RA versus OA. Sixty-one patients (92 hips) were reviewed at a mean of 12 years postoperatively. The underlying diagnosis was RA in 26 patients (45 hips) and OA in 35 patients (47 hips). The mean age of subjects in the RA group was 67711 years versus 7778 years in the OA group (po0.001), and a greater proportion of rheumatoid patients had received bilateral THA (po0.001). The number of medical co-morbidities was similar between patient groups (p40.05), however, a greater proportion of patients with RA were of Charnley grade C (po0.001).
P=0.01
80
Functional outcome
The hip
P>0.05
100
SF-12 Score (%)
may be used. A recent Cochrane meta-analysis of 8 clinical trials of retention versus sacrifice of the posterior cruciate ligament (PCL) in TKA found no clear evidence to support a difference in surgical outcomes between the two approaches.38 However, data were not stratified for effect of underlying disease, so a potential effect in RA has not been excluded by this analysis. Where deformity is 15–301, resection of the PCL is often required in order to achieve appropriate collateral ligament balance. In such cases reconstruction is made using a posterior-stabilised implant. Where deformity is greater than 30–401, collateral ligament incompetence necessitates use of a constrained prosthesis in most cases.39 A stepwise approach is also taken to management of patellar maltracking. An adequate lateral capsular release is combined with medialisation of the patellar button, lateralisation of the femoral component on the femoral condyle and external rotation of the tibial component, in order to achieve correct patellar tracking on the femoral trochlea.
J.M. Wilkinson et al.
75
50
25
0 OA
RA
Figure 5 Late clinical outcome scores after total hip arthroplasty in subjects with rheumatoid arthritis versus osteoarthritis. Top panel shows short-form 12 results, middle panel shows Oxford hip score results, bottom panel shows Harris hip score results. Between group comparisons made using the Mann–Whitney test.
ARTICLE IN PRESS (ii) Hip and knee reconstruction in the rheumatoid patient domains of the Harris hip score patients with RA had poorer function scores versus patients with OA for walking distance (p ¼ 0.003), stair climbing (po0.001), putting on of socks and shoes (po0.001), and the ability to use public transport (po0.001). Pain relief, limp, sitting comfort, use of walking aids, absence of deformity and range of movement were similar between groups (p40.05 all comparisons). Our results agree with the findings of Creighton et al.45 that functional outcome is poorer in subjects with RA than in subjects with non-inflammatory arthritis, although with the caveat that this is more apparent for some activities only, and that this association with RA is likely a function of polyarthropathy rather than the disease itself. BischoffFerrari et al.46 have also highlighted the role of multiple joint involvement in influencing functional outcome after THA. They also found that poor mental health, obesity, presence of 2 or more chronic diseases, and less than college education are risk factors for poor functional outcome. Roder et al.47 in a long-term study of the results of THA also found Charnley grade to be an important determinant of functional outcome.
The knee Patient satisfaction after TKA is generally high in the RA population, and correlates better with pain relief than with restoration of clinical function. Bullens et al.48 found that satisfaction after TKA was higher in patients with RA versus those with OA, despite similar improvement in Knee Society Scores. Ritter et al.49 found that patients with OA had greater pre-operative to post-operative improvement in knee society score versus patients with RA in 207 subjects younger than 55 years of age undergoing cruciate-retaining TKA, although implant survivorship was similar. Patients with RA can also expect good long-term functional outcomes after TKA. Crowder et al.50 reported the long-term results of 47 cemented condylar TKAs in 32 patients under the age of 55 years at surgery with a minimum follow-up of 15 years. They reported an improvement in knee society score from 41 pre-operatively to 86 at late review. The 20-year implant survival was 94%. Ito et al.51 have reported the 15-year functional results of condylar TKA in 25 Japanese patients (36 TKAs) with RA. 78% of knees were classified as good or excellent using the Hospital for Special Surgery (HSS) knee scoring system, and mean range of flexion was 991. Implant survivorship was 94% at 15 years. Kristensen et al.52 have reported similar improvement in HSS knee scores from 99% poor or fair pre-operatively to 77% good or excellent at follow-up in 46 European patients (71 knees) with RA and a mean age at surgery of 52 years.
Complications Life expectancy is decreased by 5–10 years in patients with RA versus the general population, which is accounted for mainly by excess cardiovascular deaths.53 However, risk of early post-operative death after THA or TKA is not increased in patients with RA versus those with OA, but is greater than the background population. In the Norwegian arthroplasty register death in the first 60 days after primary THA was
337 compared in RA versus general, non-operated, age-matched Norwegian population.54 The standardised mortality ratio (SMR) was 1.48. Parvizi et al. examined 30-day mortality rates after THA in 30,714 patients, and after TKA in 22,540 patients operated at the Mayo Clinic (Rochester, MN, USA) in the period 1969–1997.55,56 Age over 70 years, pre-existing cardiovascular disease, and male sex were associated with a higher 30-day mortality. Patients with RA had a similar mortality rate to those with OA. There is little contemporary information examining the risk of venous thromboembolic events (VTE) after surgery in the patient with RA. Buchanan and Kraag57 compared the rates of deep venous thrombosis in patients with OA versus RA in patients undergoing THA and TKA. OA was associated with a 2.3 times higher risk of DVT versus RA. This decreased risk of VTE in patients with RA may be explained by greater use of non-steroidal anti-inflammatory agents in the rheumatoid population.58 The incidence of heterotopic ossification is also reported to be lower in patients with RA versus those with OA,59 which might also be accounted for by non-steroidal anti-inflammatory agent use. Recent data from 14,314 patients reported to the Scottish Arthroplasty Register suggests that the rate of dislocation after THA in patients with RA is similar to other patient groups.60 However, van Stralen et al.61 have previously reported a dislocation rate of 3.8% in patients with RA versus 1.4% overall in a study of 884 THAs inserted using a posterior approach to the hip.
Infection, aseptic loosening, and implant survivorship Although historical data sets have suggested a higher rate of infection and aseptic loosening after THA in RA patients versus other patient groups, this has not been supported in subsequent studies. Poss et al.62 reported a higher infection rate after 138 THAs in 98 subjects with RA versus that found in OA. However, data from the Norwegian arthroplasty register in 53,698 THAs showed no difference in the rate of revision for infection or aseptic loosening in subjects with RA versus those with OA.63 A study by Nercessian et al.64 in 633 Charnley THAs inserted from 1970 to 1984 (16% for RA) found no increased risk of osteolysis associated with RA. Sochart and Porter21 reported higher 25-year survivorship for both implant components for the Charnley prosthesis in subjects with RA versus those with OA. In an analysis of patient-related factors associated with Charnley implant failure Kobayashi et al.65 although associating poor bone quality with implant failure, found no association of RA with aseptic loosening. Himanen66 reported the 10-year survivorship of the AGC knee implant in 6306 subjects with OA versus 2161 with RA from the Finnish Arthroplasty Register. They identified male sex and young age as risk factors for revision. The survival rates for OA and RA were similar at 94% and 96%, respectively. The 10-year cumulative all-causes revision rate for TKA in the Swedish Knee Arthroplasty Register in patients with RA versus OA is also similar at 5%,9 however the revision rate for infection was higher in RA, particularly in men. In a review of 9200 TKA’s from the Mayo Clinic, Rand and Ilstrup67 reported 10-year implant survivorship of 83% in patients with RA versus 80% in patients with OA (po0.01).
ARTICLE IN PRESS 338
Summary Total joint arthroplasty at the hip and knee are effective treatments for RA both in terms of functional improvement and implant survivorship. Patients with RA have a greater number of co-morbidities compared to the general arthroplasty population, and polyarticular involvement is the norm rather than the exception. Optimal care of this patient group requires a co-ordinated multidisciplinary approach involving physician, anaesthetist, surgeon and rehabilitation specialists in order to achieve optimum results. Bone loss, osteoporosis, deformity, ligamentous laxity, and delicate soft tissues may present challenges in joint reconstruction. Implant selection choices are broadly similar to those made for the osteoarthritis patient with the exception that at the knee unicompartmental joint replacement is not recommended. Early mortality after joint replacement in RA is similar to other groups. The rate of VTE and heterotopic ossification may be slightly lower due to a higher prevalence of NSAID use. Rates of dislocation, infection, and aseptic loosening are broadly similar to those in patients with OA. Late functional outcomes in RA are limited by polyarticular disease, rather than local factors at the replaced joint. However, patient reported satisfaction scores are high.
References 1. MacGregor AJ, Snieder H, Rigby AS, Koskenvuo M, Kaprio J, Aho K, et al. Characterizing the quantitative genetic contribution to rheumatoid arthritis using data from twins. Arthritis Rheum 2000;43:30–7. 2. Sokka T. Work disability in early rheumatoid arthritis. Clin Exp Rheumatol 2003;21:S71–4. 3. Scott DL, Symmons DP, Coulton BL, Popert AJ. Long-term outcome of treating rheumatoid arthritis: results after 20 years. Lancet 1987;1:1108–11. 4. Kvien TK. Epidemiology and burden of illness of rheumatoid arthritis. Pharmacoeconomics 2004;22:1–12. 5. Fleming A, Crown JM, Corbett M. Early rheumatoid disease. I. Onset. Ann Rheum Dis 1976;35:357–60. 6. Fleming A, Benn RT, Corbett M, Wood PH. Early rheumatoid disease. II. Patterns of joint involvement. Ann Rheum Dis 1976; 35:361–4. 7. Wilkinson JM, Stanley D, Getty CJ. Surgical management of the rheumatoid patient. Curr Orthop 2004;18:357–70. 8. The Norwegian Arthroplasty Register. /http://www.haukeland.no/nrlS. 9. Swedish knee arthroplasty register annual report 2004. /www. ort.lu.se/kneeS. 10. Sokka T, Kautiainen H, Hannonen P. Stable occurrence of knee and hip total joint replacement in Central Finland between 1986 and 2003: an indication of improved long-term outcomes of rheumatoid arthritis. Ann Rheum Dis 2007;66:341–4. 11. Abdel-Nasser AM, Rasker JJ, Valkenburg HA. Epidemiological and clinical aspects relating to the variability of rheumatoid arthritis. Semin Arthritis Rheum 1997;27:123–40. 12. Alamanos Y, Voulgari PV, Drosos AA. Incidence and prevalence of rheumatoid arthritis, based on the 1987 American College of Rheumatology criteria: a systematic review. Semin Arthritis Rheum 2006;36:182–8. 13. Pincus T, Ferraccioli G, Sokka T, Larsen A, Rau R, Kushner I, et al. Evidence from clinical trials and long-term observational studies that disease-modifying anti-rheumatic drugs slow radiographic progression in rheumatoid arthritis: updating a 1983 review. Rheumatology 2002;41:1346–56.
J.M. Wilkinson et al. 14. Verstappen SM, Hoes JN, Ter Borg EJ, Bijlsma JW, Blaauw AA, Albada-Kuipers GA, et al. Joint surgery in the Utrecht Rheumatoid Arthritis Cohort: the effect of treatment strategy. Ann Rheum Dis 2006;65:1506–11. 15. Tarity TD, Herz AL, Parvizi J, Rothman RH. Ninety-day mortality after hip arthroplasty: a comparison between unilateral and simultaneous bilateral procedures. J Arthroplasty 2006;21: 60–4. 16. Barrett J, Baron JA, Losina E, Wright J, Mahomed NN, Katz JN. Bilateral total knee replacement: staging and pulmonary embolism. J Bone Jt Surg 2006;88-A:2146–51. 17. Forster MC, Bauze AJ, Bailie AG, Falworth MS, Oakeshott RD. A retrospective comparative study of bilateral total knee replacement staged at a one-week interval. J Bone Jt Surg 2006;88-B:1006–10. 18. Stanley D, Stockley I, Getty CJ. Simultaneous or staged bilateral total knee replacements in rheumatoid arthritis. A prospective study. J Bone Jt Surg 1990;72-B:772–4. 19. Eskelinen A, Paavolainen P, Helenius I, Pulkkinen P, Remes V. Total hip arthroplasty for rheumatoid arthritis in younger patients: 2,557 replacements in the Finnish Arthroplasty Register followed for 0–24 years. Acta Orthop 2006;77: 853–65. 20. Odent T, Journeau P, Prieur AM, Touzet P, Pouliquen JC, Glorion C. Cementless hip arthroplasty in juvenile idiopathic arthritis. J Pediatr Orthop 2005;25:465–70. 21. Sochart DH, Porter ML. The long-term results of Charnley lowfriction arthroplasty in young patients who have congenital dislocation, degenerative osteoarthrosis, or rheumatoid arthritis. J Bone Jt Surg Am 1997;79:1599–617. 22. Mogensen B, Svantesson H, Lidgren L. Surface replacement of the hip in juvenile chronic arthritis. Scand J Rheumatol 1981; 10:269–72. 23. Hansen E, Ries MD. Revision total hip arthroplasty for large medial (protrusio) defects with a rim-fit cementless acetabular component. J Arthroplasty 2006;21:72–9. 24. Rosenberg WW, Schreurs BW, Waal Malefijt MC, Veth RP, Slooff TJ. Impacted morsellized bone grafting and cemented primary total hip arthroplasty for acetabular protrusion in patients with rheumatoid arthritis: an 8- to 18-year follow-up study of 36 hips. Acta Orthop Scand 2000;71:143–6. 25. Armstrong RA, Whiteside LA. Results of cementless total knee arthroplasty in an older rheumatoid arthritis population. J Arthroplasty 1991;6:357–62. 26. Sharma S, Nicol F, Hullin MG, McCreath SW. Long-term results of the uncemented low contact stress total knee replacement in patients with rheumatoid arthritis. J Bone Jt Surg 2005;87-B: 1077–80. 27. Robertsson O, Knutson K, Lewold S, Goodman S, Lidgren L. Knee arthroplasty in rheumatoid arthritis. A report from the Swedish Knee Arthroplasty Register on 4,381 primary operations 1985–1995. Acta Orthop Scand 1997;68:545–53. 28. Kawakubo M, Matsumoto H, Otani T, Fujikawa K. Radiographic changes in the patella after total knee arthroplasty without resurfacing the patella. Comparison of osteoarthrosis and rheumatoid arthritis. Bull Hosp Jt Dis 1997;56:237–44. 29. Pakos EE, Ntzani EE, Trikalinos TA. Patellar resurfacing in total knee arthroplasty. A meta-analysis. J Bone Jt Surg Am 2005;87: 1438–45. 30. Jacobs W, Anderson P, Limbeek J, Wymenga A. Mobile bearing vs. fixed bearing prostheses for total knee arthroplasty for postoperative functional status in patients with osteoarthritis and rheumatoid arthritis. Cochrane Database Syst Rev 2004;2: CD003130. 31. Kanamiya T, Whiteside LA, Nakamura T, Mihalko WM, Steiger J, Naito M. Ranawat Award paper. Effect of selective lateral ligament release on stability in knee arthroplasty. Clin Orthop 2002;404:24–31.
ARTICLE IN PRESS (ii) Hip and knee reconstruction in the rheumatoid patient 32. Peters CL, Mohr RA, Bachus KN. Primary total knee arthroplasty in the valgus knee: creating a balanced soft tissue envelope. J Arthroplasty 2001;16:721–9. 33. Whiteside LA. Soft tissue balancing: the knee. J Arthroplasty 2002;17:23–7. 34. Clarke HD, Fuchs R, Scuderi GR, Scott WN, Insall JN. Clinical results in valgus total knee arthroplasty with the ‘‘pie crust’’ technique of lateral soft tissue releases. J Arthroplasty 2005; 20:1010–4. 35. Ranawat AS, Ranawat CS, Elkus M, Rasquinha VJ, Rossi R, Babhulkar S. Total knee arthroplasty for severe valgus deformity. J Bone Jt Surg 2005;87-B(Suppl. 10):271–84. 36. Buechel FF. A sequential three-step lateral release for correcting fixed valgus knee deformities during total knee arthroplasty. Clin Orthop 1990;260:170–5. 37. Keblish PA. The lateral approach to the valgus knee. Surgical technique and analysis of 53 cases with over two-year follow-up evaluation. Clin Orthop 1991;271:52–62. 38. Jacobs WC, Clement DJ, Wymenga AB. Retention versus sacrifice of the posterior cruciate ligament in total knee replacement for treatment of osteoarthritis and rheumatoid arthritis. Cochrane Database Syst Rev 2005:CD004803. 39. Sculco TP. The role of constraint in total knee arthoplasty. J Arthroplasty 2006;21:54–6. 40. Fortin PR, Penrod JR, Clarke AE, St Pierre Y, Joseph L, Belisle P, et al. Timing of total joint replacement affects clinical outcomes among patients with osteoarthritis of the hip or knee. Arthritis Rheum 2002;46:3327–30. 41. Lingard EA, Katz JN, Wright EA, Sledge CB. Predicting the outcome of total knee arthroplasty. J Bone Jt Surg 2004; 86-A:2179–86. 42. Katsimihas M, Taylor AH, Lee MB, Sarangi PP, Learmonth ID. Cementless acetabular replacement in patients with rheumatoid arthritis: a 6- to 14-year prospective study. J Arthroplasty 2003;18:16–22. 43. Tang WM, Chiu KY. Primary total hip arthroplasty in patients with rheumatoid arthritis. Int Orthop 2001;25:13–6. 44. Espehaug B, Havelin LI, Engesaeter LB, Langeland N, Vollset SE. Patient satisfaction and function after primary and revision total hip replacement. Clin Orthop 1998;351:135–48. 45. Creighton MG, Callaghan JJ, Olejniczak JP, Johnston RC. Total hip arthroplasty with cement in patients who have rheumatoid arthritis. A minimum ten-year follow-up study. J Bone Jt Surg 1998;80-A:1439–46. 46. Bischoff-Ferrari HA, Lingard EA, Losina E, Baron JA, Roos EM, Phillips CB, et al. Psychosocial and geriatric correlates of functional status after total hip replacement. Arthritis Rheum 2004;51:829–35. 47. Roder C, Parvizi J, Eggli S, Berry DJ, Muller ME, Busato A. Demographic factors affecting long-term outcome of total hip arthroplasty. Clin Orthop 2003;417:62–73. 48. Bullens PH, van Loon CJ, Waal Malefijt MC, Laan RF, Veth RP. Patient satisfaction after total knee arthroplasty: a comparison between subjective and objective outcome assessments. J Arthroplasty 2001;16:740–7. 49. Ritter MA, Lutgring JD, Davis KE, Faris PM, Berend ME. Total knee arthroplasty effectiveness in patients 55 years old and younger: osteoarthritis vs. rheumatoid arthritis. Knee 2007;14:9–11. 50. Crowder AR, Duffy GP, Trousdale RT. Long-term results of total knee arthroplasty in young patients with rheumatoid arthritis. J Arthroplasty 2005;20:12–6.
339 51. Ito J, Koshino T, Okamoto R, Saito T. 15-year follow-up study of total knee arthroplasty in patients with rheumatoid arthritis. J Arthroplasty 2003;18:984–92. 52. Kristensen O, Nafei A, Kjaersgaard-Andersen P, Hvid I, Jensen J. Long-term results of total condylar knee arthroplasty in rheumatoid arthritis. J Bone Jt Surg 1992;74-B: 803–6. 53. Goodson N, Marks J, Lunt M, Symmons D. Cardiovascular admissions and mortality in an inception cohort of patients with rheumatoid arthritis with onset in the 1980s and 1990s. Ann Rheum Dis 2005;64:1595–601. 54. Lie SA, Engesaeter LB, Havelin LI, Gjessing HK, Vollset SE. Mortality after total hip replacement: 0–10-year follow-up of 39,543 patients in the Norwegian Arthroplasty Register. Acta Orthop Scand 2000;71:19–27. 55. Parvizi J, Johnson BG, Rowland C, Ereth MH, Lewallen DG. Thirty-day mortality after elective total hip arthroplasty. J Bone Jt Surg 2001;83-A:1524–8. 56. Parvizi J, Sullivan TA, Trousdale RT, Lewallen DG. Thirty-day mortality after total knee arthroplasty. J Bone Jt Surg 2001; 83-A:1157–61. 57. Buchanan RR, Kraag G. Is there a lower incidence of deep venous thrombosis after joint replacement in rheumatoid arthritis? J Rheumatol 1980;7:551–4. 58. van Heereveld HA, Laan RF, van den Hoogen FH, Malefijt MC, Novakova IR, van de Putte LB. Prevention of symptomatic thrombosis with short term (low molecular weight) heparin in patients with rheumatoid arthritis after hip or knee replacement. Ann Rheum Dis 2001;60:974–6. 59. Eggli S, Woo A. Risk factors for heterotopic ossification in total hip arthroplasty. Arch Orthop Traum S 2001;121:531–5. 60. Meek RM, Allan DB, McPhillips G, Kerr L, Howie CR. Epidemiology of dislocation after total hip arthroplasty. Clin Orthop 2006; 447:9–18. 61. van Stralen GM, Struben PJ, van Loon CJ. The incidence of dislocation after primary total hip arthroplasty using posterior approach with posterior soft-tissue repair. Arch Orthop Trauma Surg 2003;123:219–22. 62. Poss R, Maloney JP, Ewald FC, Thomas WH, Batte NJ, Hartness C, et al. Six- to 11-year results of total hip arthroplasty in rheumatoid arthritis. Clin Orthop 1984;182:109–16. 63. Furnes O, Lie SA, Espehaug B, Vollset SE, Engesaeter LB, Havelin LI. Hip disease and the prognosis of total hip replacements. A review of 53,698 primary total hip replacements reported to the Norwegian Arthroplasty Register 1987–99. J Bone Jt Surg 2001;83-B:579–86. 64. Nercessian OA, Joshi RP, Martin G, Su BW, Eftekhar NS. Influence of demographic and technical variables on the incidence of osteolysis in Charnley primary low-friction hip arthroplasty. J Arthroplasty 2003;18:631–7. 65. Kobayashi S, Saito N, Horiuchi H, Iorio R, Takaoka K. Poor bone quality or hip structure as risk factors affecting survival of totalhip arthroplasty. Lancet 2000;355:1499–504. 66. Himanen AK, Belt E, Nevalainen J, Hamalainen M, Lehto MU. Survival of the AGC total knee arthroplasty is similar for arthrosis and rheumatoid arthritis. Finnish Arthroplasty Register report on 8,467 operations carried out between 1985 and 1999. Acta Orthop 2005;76:85–8. 67. Rand JA, Ilstrup DM. Survivorship analysis of total knee arthroplasty. Cumulative rates of survival of 9200 total knee arthroplasties. J Bone Jt Surg 1991;73-A:397–409.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 340–343
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MINI-SYMPOSIUM: SURGICAL RHEUMATOLOGY
(iii) The lower limb in the rheumatoid arthritis patient. Focus on the hind, mid and forefoot and the ankle R.G.H.H. Nelissen Department of Orthopaedic Surgery, Leiden University Medical Centre, P.O. Box 9600, 2300 RC Leiden, The Netherlands
KEYWORDS Rheumatoid disease; Forefoot; Hindfoot; Synovectomy; Arthroplasty
Abstract Rheumatoid arthritis (RA) is a systemic disease which involves multiple joints. The primary target of RA is the synovial membrane. In 90% of RA patients symptoms related to the foot or ankle will eventually develop. Usually, symptoms appear in the toes and forefeet first, then in the hindfeet or the back of the feet, and finally in the ankles. The goal of any intervention on a RA patient is to improve functional ability and thus self-support of the patient, objective evaluation of the surgical procedure and its impact on the patient can be difficult. The potential chronic course of RA makes evaluation of a specific surgical procedure and its effect on the patient difficult to interpret. But it also implies that correct planning of the sequence of these procedures is important. The management of the RA patient requires a multidisciplinary approach. An overview of the different options at the forefoot, mid- and hindfoot and ankle joint are given. & 2007 Elsevier Ltd. All rights reserved.
Introduction Rheumatoid arthritis (RA) is the most common inflammatory joint disease, affecting about 1% of the population. It is more common in women than men. Treatments options are focussed on reduction of pain and improvement in mobility. The goal of any intervention on a RA patient is to improve functional ability and thus self-support of the patient. The potential chronic course of RA makes evaluation of a specific surgical procedure and its effect on the patient difficult to interpret. The management of the RA patient requires a multidisciplinary approach; the role of the surgeon is to
Corresponding author. Tel.: +31 71 526 3606.
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improve functional ability for the patient by reconstructing a deteriorated joint by total joint arthroplasty (TJA). For the lower extremity, besides joint destruction treatment, correction of malalignment is also used either in conjunction with arthroplasties or in order to postpone TJA or even prevent it. This implies that weight bearing radiographs of the knee, ankle, hindfoot and forefoot are essential for the planning of the different treatment options.
Indications for surgery In the rheumatoid patient total hip and total knee arthroplasty are established procedures with excellent long-term results with respect to pain relief, quality of life
ARTICLE IN PRESS The lower limb in the rheumatoid arthritis patient and cost effectiveness.1 Although this paper will focus on ankle, hindfoot and forefoot surgery in the rheumatoid patient, the systemic character of the disease needs a broad approach, which has to include assessment of the hips and knees. Changes in any of the lower extremity joints will affect gait. The main goal of treatment is a stable comfortable weight-bearing foot. In general, if multiple joints are affected and if they all affect functionality, which is rare, the surgical preference list would be hindfoot, forefoot, ankle, hip, and then knee. A common combination is the valgus hindfoot, forefoot problems and valgus in the knee: correcting the first two might postpone knee prothesis surgery. Pain location can be used as a basis for treatment options, especially in the less involved joints (i.e. Larsen I and II): A simple guide for pain location and pathology at the ankle and midfoot level is:
Anterior: ankle joint. Medial: tibialis posterior tendon synovitis and talonavicular joint.
Lateral: subtalar joint. Hindfoot pathology The subtalar joint is affected in 60% of RA patients, with the midfoot involved in 40–60%.2–4 Tibialis posterior synovitis and subsequent rupture will cause a cascade of deformities: valgus deformity of the hindfoot, instability of tarsometatarsal joint, external rotation in the first metatarsal, and pronation of the hallux. Finally, a progressive abduction moment in the knee will result in a progressive valgus
Figure 1
341 deformity in this joint. Treatment options are focussed on prevention of this cascade of events:
Synovectomy of the tibialis posterior tendon. Talonavicular arthrodesis, if local arthritis and destruc-
tion of this joint predominates and a neutral to slight valgus alignment of the hindfoot. Due to this local arthrodesis, the subtalar movements are blocked as well (‘‘the key that locks the door’’), although this local arthrodesis is known for its high rate of non-union. Triple arthrodesis (subtalar, talonavicular and cuboidcalcaneal joint), in the presence of valgus X101, and fixed rotational deformities in the midfoot (Fig. 1).
Forefoot pathology The hand and foot are known to show the first symptoms of RA. The forefoot is affected in up to 90% of RA patients, and usually both feet are involved in different ways.4,5 The variation is due to differences in synovitis between various joints, as well as differences in weight bearing. The common picture (Fig. 2) involves dislocation of metatarsalphalangeal (MTP) joints, a hallux valgus, a compensatory varus position of the fifth toe. The plantar fatpad is dislocated distally (underneath the toes) due to the dorsally and proximally dislocated proximal phalanges at the MTP level (Fig. 3). Consequently, the lesser toes claw, resulting in difficulties wearing shoes. The latter is usually the reason for patients seeking medical attention. However, by this time the disease process in the foot is well advanced, and few preventive measures are possible. Treatment options should aim to restore the contact of the toes (especially the plantar
Hindfoot and midfoot pathology and postoperative Triple arthrodesis.
Figure 2 Rheumatoid foot: claw toes; pronation of right hallux.
ARTICLE IN PRESS 342
R.G.H.H. Nelissen
side of the hallux) with the ground. Such treatments include:
J
Oblique metatarsal osteotomies and MTP I relocations (prerequisite: radiographic normal joints or only subluxated).
Shoe adaptations, such as insoles with retrocapital support for the metatarsal heads.
Surgical correction of forefoot deformities J
J
Hallux valgus correction, by arthrodesis of the MTP-I joint or minimal resection of the proximal phalanx (e.g. Mayo procedure).6 A resection arthroplasty (i.e. Keller–Brandes procedure) is considered inferior in the RA forefoot. Resection arthroplasty (i.e. oblique subcapital resection of the metatarsal heads). In the presence of plantar foot ulcers: debridement with resection and systemic antibiotics depending on culture.
Figure 3
Rheumatoid foot: subluxated MTP joints.
Ankle pathology The standard surgical treatment for a severely painful and diseased ankle joint is arthrodesis. In general, an arthrodesis produces a painless and stable ankle at the expense of loss of motion. With longer follow-up there is an increased risk of the development of osteoarthritis in the joints of the ipsilateral foot and possible injury to the knee due to an increased extension movement at this joint. For a comfortable gait with an ankylosed ankle an altered motion of the ipsilateral knee and midtarsal joints is required. Total ankle replacement using a mobile-bearing prosthesis is a valid treatment option for the severely affected joint and an alternative to arthrodesis, with near normal kinematics of the ankle prosthesis,7–9 thus reducing the risk of secondary arthritic changes to the adjacent joints in the foot. The long-term results (10–16 years results) of a mobile ankle prosthesis show a mean survival of 88% with revision being the endpoint. Bone fixation of the tibial component can be improved (Figs. 4 and 5), as is suggested by a recent roentgen stereophotogrammetric analysis (RSA) study on micromotion of the tibial component.10 Although ankle prostheses show promising clinical results they cannot compete (yet) with the excellent long-term results of total hip and total knee prostheses.
Figure 4 Mobile-bearing ankle prosthesis (Buechel Pappas) preoperative and postoperative.
Figure 5 Mobile-bearing ankle prosthesis (improved tibial fixation, CCI).
ARTICLE IN PRESS The lower limb in the rheumatoid arthritis patient Treatment options for ankle pathology:
Ankle prosthesis, if ankle deformity is less than 101 valgus
or varus. If the hindfoot deformity exceeds this, the valgus deformity should be corrected first (triple arthrodesis). The varus might be corrected in the same procedure with a medial malleolar osteotomy (Doets 2007). Ankle arthrodesis J For failed prosthesis. J Severe osteonecrosis of the talar dome. J Severe deformities of the hind and midfoot, without corrective possibilities.
Discussion The goal of any intervention in an RA patient is to improve functional ability and thus self-support of the patient. Objective evaluation of the surgical procedure and its impact on the patient can be difficult. The potential chronic course of RA makes evaluation of a specific surgical procedure and its effect on the patient difficult to interpret. The management of the RA patient requires a multidisciplinary approach; the role of the surgeon is to improve the functional ability of the patient by planning preventive conservative but also surgical procedures. The goal is to keep the RA patient mobile with a minimum of surgical procedures with nevertheless a maximum effect on functionality. In the end, reconstruction of a deteriorated joint by TJA may be necessary. Even more so, the preoperative state of the joint/extremity determines the extent of
343 postoperative functional gain. Thus, postponing TJA too long will give less functional benefit.
References 1. Nelissen RGHH. The impact of total joint replacement in rheumatoid arthritis. Best Pract Res Clin Rheumatol 2003; 17(5):831–46 Review. 2. Dounis E. Hindfoot problems in rheumatoid arthritis. In: Proceedings of the EFORT 2007, Florence. 3. Stockley I, Betts RP, Rowley DI, Getty CJ, Duckworth T. The importance of the valgus hindfoot in forefoot surgery in rheumatoid arthritis. J Bone Joint Surg Br 1990;72:705–8. 4. Nassar J, Cracchiolo A. Complications in surgery of the foot and ankle in patients with rheumatoid arthritis. Clin Orthop Relat Res 2001;391:140–52. 5. Fuhrmann R. The forefoot in rheumatoid arthritis. In: Proceedings of the EFORT 2007, Florence. 6. Grondal L, Brostro ¨m E, Wretenberg P, Stark A. Arthrodesis versus Mayo resection: the management of the first metatarsophalangeal joint in reconstruction of the rheumatoid forefoot. J Bone Joint Surg Br 2006;88:914–9. 7. Anderson T, Montgomery F, Carlsson A. Uncemented STAR total ankle prostheses. Three to eight-year follow-up of fifty-one consecutive ankles. J Bone Joint Surg Am 2003;85A:1321–9. 8. Doets HC, Brand R, Nelissen RG. Total ankle arthroplasty in inflammatory joint disease with use of two mobile-bearing designs. J Bone Joint Surg Am 2006;88(6):1272–84. 9. Doets HC, van Middelkoop M, Houdijk H, Nelissen RG, et al. Gait analysis after successful mobile bearing total ankle replacement. Foot Ankle Int 2007;28(3):313–22. 10. Nelissen RGHH, Doets HC, Valstar ER. Early migration of the tibial component of the buechel-pappas total ankle prosthesis. Clin Orthop Relat Res 2006;448:146–51.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 344–357
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MINI-SYMPOSIUM: SURGICAL RHEUMATOLOGY
(iv) The management of the rheumatoid wrist B.R. Simmen, C. Kolling, D.B. Herren Schulthess Clinic, Lengghalde 2, 8008 Zurich, Switzerland
KEYWORDS Rheumatoid Disease; Synovitis; Arthrodesis; Arthroplasty; Inflammatory wrist arthropathy; Surgical management; Classification systems
Summary The wrist joint is often involved early in Rheumatoid arthritis (RA) and is regarded as one of the main targets of the disease. As the wrist plays a key role in the chain of the articulations in the upper extremity, treatment of this joint preserves the patient’s ability to work and to remain independent. When surgical therapy is considered, evaluation of the stage of the disease is as important as the type of rheumatoid involvement. This can be achieved by an extensive clinical and functional assessment of the whole extremity. Moreover, adequate understanding of the radiological findings helps to recognize the type of rheumatoid destruction, possible further development of the disease and its direct consequences on surgical decisions. Several classifications exist that describe the rheumatoid wrist involvement and present possible treatment algorithms. The success of surgical management depends on a well-considered strategy in timing the different procedures. Prophylactic surgery may prevent further destruction and deformation. This includes synovectomy of the tendons in order to prevent attrition rupture, to avoid challenging tendon reconstruction. Together with synovectomy of the wrist, including the distal radio-ulnar joint, long-lasting pain relief can be observed. In later stages of the disease, it is the extent of destruction at the radiocarpal level which has great implications in reconstructive surgery. Possible options are partial joint fusion, combined with an ulnar head resection, total wrist fusion or wrist arthroplasty. In cases of severe destruction, however, definitive stabilization by total wrist fusion is indicated. A pain-free, stable wrist joint often outweighs the disadvantage of the lack of mobility. & 2007 Elsevier Ltd. All rights reserved.
Introduction Rheumatoid arthritis (RA) is a life-long condition, and the disease activity might change over time. Therefore, an understanding of the pathomechanics and the possible Corresponding author. Tel.: +41 44 385 75 83;
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course of the disease is important to provide an individualized management for every patient. Usually, the wrist joint is involved early in the course of the disease and it is regarded as one of the main targets in RA. As the wrist plays a key role in the chain of articulations in the upper extremity, treatment of this joint preserves the patient’s ability to work and to remain independent. When surgical therapy is considered, evaluation of the stage of the disease is equally as important as the type of rheumatoid involvement.
ARTICLE IN PRESS The management of the rheumatoid wrist
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Figure 1 Patient with severe dislocation of both wrists.
Figure 2
Clinical picture of caput ulnae syndrome with ruptures of the extensor tendons to the small and ring fingers.
Natural course of the rheumatoid wrist Wrist deformation Three main factors play an important role in the pathologic process of wrist deformation: cartilage destruction, synovial proliferation and ligamentous laxity. The cartilaginous thinning is caused by cytochemical effects, with degradation and inhibition of new cartilage synthesis.1 The synovial expansion may cause bony erosion, particularly at the sites of vascular penetration of bone. These erosions cause sharp bony edges, which might lead to tendon rupture.2 In addition, synovial expansion causes stretching of the retaining extrinsic and intrinsic ligaments of the wrist, thus causing carpal supination and ulnar translation.3 Stretching of the scapholunate ligament results in scapholunate dissociation, whereas more global laxity and instability are responsible for ulnar translation.
Force application across the wrist is predominantly caused by muscles which act in palmar and ulnar directions. With ongoing destruction of the rheumatoid wrist, they lose their physiologic moment arms in relation to the centre of rotation and become a deforming force3 (Fig. 1). Parallelling the processes at the radiocarpal and midcarpal joints, the distal radioulnar joint undergoes pathologic changes, which were described by Backdahl4 and subsequently were called the caput ulnae syndrome (Fig. 2). The ulnar side of the wrist is often the first place of significant synovitis in the rheumatoid wrist. The long-term prognosis, however, is determined by progression of the disease at the radiocarpal level. Together with progressive ligamentous laxity, palmar subluxation of the carpus occurs. An associated supination of the carpus causes a luxation of the extensor carpi ulnaris (ECU), a major stabilizer of the ulnar side of the wrist and the distal ulna.
ARTICLE IN PRESS 346 The wrist deformity pattern has an influence on the development of deformities of the distal aspects of the hand. Shapiro3 associated radial carpal supination together with palmar subluxation with ulnar phalangeal drift, ulnar carpal translocation with radial phalangeal deviation, and loss of carpal height with swan neck deformity of the fingers.
Involvement of the soft tissues around the wrist Soft tissue involvement around the wrist is common. However, tenosynovitis and, as an end stage, impending tendon rupture, may be the most important indication for surgery. Since reconstruction of ruptured tendons is usually very challenging, it is of prime importance to prevent attrition rupture by early surgical intervention. Flexor tendons Tenosynovitis of the flexor tendons at wrist level may cause locking, limitation of motion, nerve compression and, in the worst case, rupture of tendons. Early clinical signs include localized pain, morning stiffness, triggering of single digits, and nocturnal paresthesia due to carpal tunnel syndrome (CTS). In rheumatoid patients, flexor tendon involvement seems to correlate with higher disease activity. Gray and Gottlieb5 observed a significantly higher prevalence of rheumatoid nodules, CTS, wrist extensor synovitis, and elbow epicondylitis in patients with active flexor tendon inflammation. Rupture of the flexor tendons is significantly less frequent than of the extensor tendon in RA.6 The main mechanisms of tendon destruction are invasion of the tendon by the inflammatory synovial mass, attrition on prominent bony
B.R. Simmen et al. spurs, or a combination of both.7 Owing to its anatomic localization near the scaphoid, the flexor pollicis longus (FPL) tendon, followed by the profundus to the index finger, is the most common flexor tendon to rupture.8 It is not only contact with a bony spur but also the carpal instability in advanced wrist destruction that might cause tendon attrition.7 Although FPL and also index profundus ruptures often cause little disability in rheumatoid patients, surgery is warranted to prevent further tendon ruptures. The incidence of compression neuropathy in patients who have RA is high. CTS in association with flexor tenosynovitis is observed in as many as 60% of the patients.9
Extensor tendons Extensor tenosynovitis often presents as a painless soft tissue mass at the dorsum of the wrist in the region of the retinaculum or, more frequently, distal to it. Pain related to pathology of extensor tendons, unlike the flexor tendons, is unusual; in these cases, underlying wrist pathologies must be excluded. The extent of synovial mass in the extensor compartments does not correlate with the degree of tendon damage, and prediction of possible ruptures is difficult, even when magnetic resonance imaging (MRI) is used.10 Rupture of an extensor tendon might be the end of a process of synovial infiltration, attrition on bony prominences, and ischemia (Fig. 3). Dorsal dislocation of the ulna and persistent tenosynovitis of more than 6 months are additional risk factors.11 Owing to its anatomical course, the tendon of the extensor digiti minimi ruptures first. This rupture might be clinically silent, because the extensor digitorum communis extends all four fingers. Therefore, patients must be checked for independent little finger extension.12
Figure 3 Intraoperative finding of multiple extensor ruptures. The appearance of the tendon ends suggest an attrition mechanism.
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Evaluation of the rheumatoid wrist
Table 1 Simmen classification of the rheumatoid wrist involvement.13
Clinical examination Physical examination should always include the whole chain of articulations within the limb to be treated. Bad function of the elbow and the shoulder joint might endanger the result of interventions at the level of the hand. When assessing the function of the upper extremity, the following parameters should be checked:
Ranking
Operation
Type 1 Type 2
Spontaneous tendency for ankylosis Osteoarthritic destruction pattern relatively stable over time Disintegration with progressive destruction and loss of alignment Ligamentous destabilization Bony destabilization
Type 3 3A 3B
Localized swelling and tenderness; the extent and the exact anatomic localization should be noted.
The degree and location of any deformity should be
checked; the degree to which the deformity is actively or passively correctable should be distinguished. The range of motion, using a goniometer, should be recorded according to the neutral-zero method; at the level of the hand, all joints should be measured, regardless of the planned site of intervention. The examination of the wrist differentiates between the radiocarpal, midcarpal, and distal radioulnar joints. Often due to marked deformity or pain, or both, the classic instability signs in the wrist might be difficult to check; do not hurt the patient more than necessary during the examination. Check for tendon continuity; especially important tendons at wrist level are the radial-sided extensors. Independent function of the superficial and deep flexors must be controlled as well as independent function of the two extensors in the second and fifth digits. Compression neuropathy, especially carpal and cubital tunnel syndrome, should be looked for. If applicable, strength measurement should be performed; grip strength and key pinch are recorded, using a Jamar dynamometer or a vigorimeter.
Computed tomography and magnetic resonance imaging Computed tomography (CT) and MRI are rarely indicated in the evaluation of a rheumatoid wrist. There is limited additional information that these examinations could provide. For the following conditions, CT or MRI examination might be considered:
Staging of synovitis (MRI) Identifying of tendon ruptures (MRI) Monitoring disease activity (MRI) Evaluation of the distal radioulnar joint (CT)
Sonography High-resolution sonography is becoming a more and more popular diagnostic tool as experienced examiners achieve precise detection of erosions and synovitis with a high intraand interobserver reliability.14
Functional assessment of the rheumatoid wrist and hand Radiological examination The type and extent of destruction in the wrist are best seen in conventional radiographs, which should always be taken in at least two different planes, preferably anteroposterior and true lateral views. Radiographs repeated at fixed intervals show the evolution of destruction over time and help to optimize the surgical treatment strategy. When considering surgical therapy of the rheumatoid wrist, it is mandatory to know the type of rheumatoid destruction. Especially in early disease, recognizing the type of disease, will facilitate the choice of procedure for the individual patient. In order to address the possible future evolution of the disease and its direct consequences on surgical decisions, Simmen and Huber,13 proposed a classification of rheumatoid wrist involvement based on a radiologic long-term analysis (Table 1 and Figs. 4–7). The Schulthess classification of rheumatoid wrist involvement is integrated into the universal wrist classification of Stanley, Lluch, Simmen and Herren (Table 3).
To evaluate the pre-therapeutic state of the hand, disease progression, and outcome of treatment, specific assessment tools of wrist and hand function are needed. In patients with RA, not only improvement of single function parameters but also general improvement of health status and quality of life should be measured in a standardized manner. Three different approaches to assess the extent to which the hand is affected might be differentiated: 1. Description of the anatomic deviation and disorders. This can be done by measuring with a goniometer, using photographic documentation or video-based image analysis. 2. Measurement of functional deterioration. Several tests have been described15,16 to evaluate hand function in complex deformity patterns. 3. Assessment of disability. Different tools, usually selfadministered questionnaires, exist to measure disability related to the wrist (patient-rated wrist evaluation questionnaire),17 to the hand (Michigan hand outcomes
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Figure 4
Type 1 (ankylosing) rheumatoid wrist with spontaneous fusion of the radiolunate joint.
questionnaire)18 or to the whole upper extremity (disabilities of the arm, shoulder, and hand questionnaire).19
Surgical management of the rheumatoid wrist Timing of the surgery The success of surgical reconstruction depends on a wellconsidered strategy in timing the different procedures. Souter20 defined general rules when choosing priorities in the surgical sequence of rheumatoid patients:
lower limb before upper limb; from proximal to distal; painful joints first; prophylaxis versus reconstruction versus salvage; consider combinations: hand and foot, elbow and wrist, wrist and metacarpophalangeal joints; and start with a winner operation.
In addition, Souter also established a ranking system of operations20: based on the parameters of elimination of
pain, improvement of function, preventive value, cosmetic improvement, and hazard of complications, the possible operations are ranked according to their order. Table 2 lists the corresponding procedures at the level of the hand and wrist. However, indications for surgical procedure might be influenced by multiple factors: concomitant musculoskeletal involvement, the general health condition, disease activity, patient’s needs and desires, compliance, social and medical environment. Therefore, a careful analysis of the needs during rehabilitation is important before a surgical procedure is proposed.
Classification and treatment algorithm of the rheumatoid wrist A treatment algorithm will always generate controversy. A disease, such as RA, with so many different faces, may profit from classification. Besides typing and staging wrist involvement in RA, the distribution of certain categories should describe surgical consequences. The classifications that are presented in Tables 3 and 4 are based on the observations of experienced RA surgeons and summarize the ideas of Stanley, Lucht, and Simmen.
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Figure 5 Type 2 (arthritic-arthrosis) rheumatoid wrist with a destruction pattern that is similar to osteoarthritic change. The carpus is still well centered, with destruction of the radiocarpal and the midcarpal joints.
Prophylactic surgery Two main goals can be achieved when undertaking prophylactic surgery. Firstly, it may stop or, at least, retard the disease process. Secondly, and even more importantly prophylactic surgery may prevent complications that could have otherwise occurred.
In general, the indications for carpal synovectomy include:
persistent synovitis that does not respond to adequate medication for more than 6 months;
persistent pain and local tenderness without major bone deformity; and
treatment in combination with dorsal tenosynovectomy Synovectomy of the wrist joint Wrist synovectomy may not be indicated in every situation. Rheumatoid wrists classified as type 1 (ankylosis) and type 2 (arthritic) may qualify for this procedure, whereas in type 3 wrists (destabilization) bony stabilization is needed in addition to the synovectomy. The removal of synovitis decreases the pressure in the joint and may have some sort of prophylactic effect before the synovial mass has stretched the retaining structures. In addition, some denervation effect is supposed. The main effect of synovectomy is pain relief but often at the expense of some wrist motion, especially in flexion.21 To diminish this problem, arthroscopic synovectomy might be considered in selected cases of localized synovitis if no extensor tendon or distal ulna treatment is needed.
or treatment of the distal ulna, or both. Synovectomy of the extensor and flexor tendons Indications for extensor tendon synovectomy are similar to those for wrist synovectomy: persistent, even painless, swelling in the extensor compartment after adequate medical treatment is an indication for surgical intervention. There are two main indications for isolated flexor tendon synovectomy. First is CTS, often combined with excision of bony spurs and synovectomy. Secondly, in a case of tendon rupture, excision of bony spurs is almost mandatory to prevent further tendon damage. A combination of dorsal wrist surgery and decompression of the carpal tunnel is possible, because there are no special rehabilitation requirements after flexor synovectomy.
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Figure 6 Type 3A (ligamentous unstable) rheumatoid wrist that shows complete dislocation of the carpus to the palmar-ulnar side, with preserved bone stock.
Treatment of the distal radioulnar joint The treatment of the distal radioulnar joint has, besides functional and therefore reconstructive aspects, a significant prophylactic importance. It is a frequent target of RA destruction. According to Resnick,22 synovial proliferation is observed in three areas of the distal radioulnar joint: distal to the ulnar head, in the prestyloid recess, and in the recess of the ECU tendon. This is important to recognize when a synovectomy of the radioulnar joint is performed. The damage of synovitis is related to the duration and degree of inflammation, as well as the mechanical stress imposed on the anatomical structure.23 The synovitis invades the triangular fibrocartilage complex and the palmar and dorsal radioulnar ligaments, resulting in destabilization of the distal radioulnar joint. Synovial infiltration of the ECU tendon provokes a palmar subluxation of the tendon with further instability. Parallel processes at the dorsal lip of the sigmoid notch enhance this situation. The classic caput ulnae syndrome, as described by Backdahl,4 is an end stage of this
destructive process and presents with a characteristic dorsal prominence of the distal ulna in combination with the local bulge of the synovia and even signs of tendon rupture. Forearm rotation is markedly reduced and painful. Instability of the distal radioulnar joint may produce a painful clicking in supination/ pronation. Deformaty alone is not necessarily an indication for surgery. Often, a combination of pain and functional impairment, together with the need to prevent further damage, provide the indication for a surgical procedure. A more aggressive approach is required in cases of tendon rupture to prevent further damage. The basic principle of the surgical correction of the distal radioulnar joint in RA includes:
Joint and tendon synovectomy Partial or total resection of the ulnar head
ARTICLE IN PRESS The management of the rheumatoid wrist
Figure 7 carpus.
351
Type 3B (bony unstable) rheumatoid wrist with complete bony destruction, loss of bone stock, and dislocation of the
Stabilization of the ulnar stump Stabilization of the radiocarpal joint if needed In early cases, and most often in younger patients, with limited destruction, there may be an indication for joint and tendon synovectomy only. In the majority of cases, the distal ulna has to be addressed by complete or partial resection or by fusion of the distal radioulnar joint. General results of the combined approach with synovectomy and ulnar head resection are consistent with good to excellent pain relief and a minimal incidence of recurrent synovitis and symptomatic distal ulnar stump instability.24 However, critical analysis, especially of higher-demand patients, shows a significant rate of failures and unsatisfactory results, such as instability of the distal ulnar stump and a significant increase in ulnar wrist translocation.25 To overcome these problems, different variations of ulnar head resection, such as the Bower’s hemiresection-interposition arthroplasty26 or the matched ulnar resection according to Watson et al.,27
were also proposed for the rheumatoid wrist. These techniques have the advantage of leaving some of the stabilizing structures of the ulnar side of the wrist, although a correction of the carpal subluxation and a complete stabilization of the distal radioulnar joint are difficult to achieve. Greater popularity, especially among European surgeons, has been noted for the Sauve–Kapandji procedure in which the distal ulnar sturnp is fused more proximally to the radius with an ulnar pseudarthrosis. This procedure preserves the stabilizing elements on the ulnar aspects of the wrist. Several series reported good results for rheumatoid conditions, although unstable distal ulnar stumps are also reported.28 Different procedures were proposed to prevent or to correct this ulnar stump instability. The most popular are stabilization slings from the ECU or the flexor carpi ulnaris26 or pronator quadratus interposition transfer.29 Because most distal ulnar stumps tend to be dorsally dislocated, it makes more sense to use a flexor carpi ulnaris tenodesis. In addition, once ulnar translation starts,
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Table 2 Ranking of operations according to the effect that can be expected; adapted from Souter.20 Ranking
Operation
First order
Caput ulnae resection Dorsal tenosynovectomy Arthrodesis of first MCP joint Synovectomy of flexor tendons
Second order
Arthroplasty of MCP joints Arthrodesis of the proximal interphalangeal joints Correction of swan-neck deformity Carpal synovectomy Carpal arthrodesis
Third order
Synovectomy of MCP joints Correction of boutonnie `re deformity Proximal interphalangeal arthroplasty (carpal arthroplasty)
Table 3 Universal classification of typing and staging of inflammatory wrist arthropathy. Universal wrist classification in inflammatory polyarthropathy Type of disease Slow progressive type without significant OA (destructive type) Slow progressive type with marked OA (reactive type) Progressive soft tissue distruption (ligamentous type) Progressive bony destruction (mutilans type) Spontaneous intercarpal ankylosis (Juvenile type) Stage of disease Early, erosions with or without early reducible translation (LDE stages I and II) Translation, translaction, volar subluxation, nonreducible, with or without radiocarpal OA (LDE stages III and IV) Some or all of the previous characteristics with midcarpal joint loss Disorganized wrist, with or without significant bone substance loss Intercarpal ankylosis LDE, Larsen, Dahle, and Eck classification; OA, osteoarthritis. Adapted from Stanley JK, Lluch A, Simmen BR, Herren DB. Universal wrist classification in inflammatory polyarthropathy [in preparation].
it is unlikely that this process can be stopped by a Sauve–Kapandji operation. These cases need stabilization on the level of the radiocarpal joint. Another method of treating a destroyed distal radioulnar joint is ulnar head replacement. It was first described by Swanson,30 who used a silicone cap for better stabilization of the ulnar side of the wrist. Several studies proved unsatisfactory results in the long-term31 with these implants
and, therefore, this technique is no longer recommended. Subsequently, different implants have been developed as a more constrained articulation with two components28,32 or as a simpler replacement of the distal ulna with a ceramic head.33 These implants were primarily developed as salvage for recurrent instability after failed surgery at the distal ulna. Their long-term results will determine if more generous indications can be justified. It is important to keep in mind that it is not possible to stabilize the radiocarpal joint by reconstruction of the ulnar aspect of the wrist. Furthermore, the long-term prognosis of the wrist is depends on radiocarpal integrity.
Reconstructive surgery Partial fusion The expected natural course of disease at radiocarpal level has great implications for the decision regarding which surgical procedure should be performed. Type 1 and 2 wrists, according to the Simmen classification, have low probability of undergoing radiocarpal dislocation. Therefore surgical treatment, including the aforementioned wrist and tendon synovectomy and usually ulnar head resection, gives satisfactory long-term results.25,34 In contrast, type 3 wrists, because of ligamentous or bony destruction, or both, require a procedure that provides realignment and stability. In the later stages of the disease, an original type 2 wrist, which is considered stable, might undergo significant carpal collapse and may begin to mimic type 3 (unstable) evolution. Partial fusion of the rheumatoid wrist in the early stages, is a prophylactic procedure. In an established deformation pattern, reconstruction may be necessary. The concept of partial fusion in rheumatoid wrists was first described by Chamay et al.35 and later by Linscheid and Dobyns.36 It includes the realignment of the subluxed carpus by reduction of the proximal carpal row combined with longterm stability. In cases of excessive radiocarpal damage, the concept of limited wrist fusion might be expanded to a radioscapholunate fusion. A review of the literature shows good clinical results and high patient satisfaction for limited wrist fusion in rheumatoid patients. The range of motion varies postoperatively but, on average, is reported to be in the functional range.35,37 It should be noted, however, that most series observed deterioration over time with ongoing destruction of the wrist.36,37 Advanced disease stages and already destabilized wrists should therefore be treated by total wrist fusion.37 Because radiolunate fusion provides stability on the ulnar side of the wrist, it is usually combined with an ulnar head resection. It is possible to perform radiolunate fusion together with a Sauve–Kapandji procedure (Fig. 8). Although there may be a theoretical advantage to that approach, no series has shown superior results so far. However, this combined procedure preserves the contour of the ulnar head and therefore might benefit in a cosmetic sense. Total wrist fusion There is an ongoing debate on whether to fuse a destroyed rheumatoid wrist or perform a radiocarpal arthroplasty.38 Despite the good clinical results of complex wrist arthroplasty,39 the complication rate remains high. In addition,
ARTICLE IN PRESS The management of the rheumatoid wrist
Table 4
353
Treatment options according to the type and the stage of the disease in the wrist.
Disease type
Stage of disease I
II
III
IV
V
A. Destructive
Synovectomy, soft tissue balancing7ulnar head surgery
R(S)L fusion; ulnar head surgery
TWR or panarthrodesis
TWR or panarthrodesis
B. Reactive
Synovectomy, soft tissue balancing7ulnar head surgery
R(S)L fusion; ulnar head surgery R(S)L fusion7ulnar head surgery Panarthrodesis
Capitate head replacement+R(S)L fusion; 7ulnar head surgery TWR Capitate head replacement +R(S)L fusion; TWR Panarthrodesis
TWR or panarthrodesis
TWR or panarthrodesis
Panarthrodesis
Panarthrodesis
Panarthrodesis
Panarthrodesis
Panarthrodesis
Panarthrodesis
C. Ligamentous D. Mutilans E. Juvenile
R(S)L fusion 7ulnar head surgery Synovectomy, soft tissue balancing7ulnar head surgery
Panarthrodesis
R(S)L, radio(scapho)lunate fusion; TWR, total wrist replacement.
Figure 8 Combined radiolunate fusion and Sauve–Kapandji procedure.
wrist arthroplasty requires good bone stock and a reasonable, or reconstructible, tendon balance, two conditions that are rarely present in advanced rheumatoid destruction.
Silicon wrist spacers offer an alternative, although they are only recommended by most investigators in low-demand patients.40 Most wrists with advanced rheumatoid disease require definitive stabilization by total wrist fusion. The advantage of a pain-free, fusion of the wrist joint often out-weighs the disadvantage of lack of mobility.38,41,42 Bilateral wrist fusion is still a subject of controversy,38 and most patients would personally prefer to have at least one mobile wrist. However, personal experience and the publication of Rayan43 show patients with a high degree of acceptance even for bilateral fusion. Two main concerns dominate the discussion that surrounds wrist arthrodesis: the position of fusion and the surgical technique to obtain secure and stable fixation. For most activities of daily living a functional range of motion requires 101 of flexion and 351 of extension.44 By analyzing different tasks, activities concerning personal care and hygiene were found to be performed in slightly flexed wrist positions. However, besides overall function, wrist position seems to affect grip strength. Flexed wrist posture is associated with decrease of grip strength, whereas there is no difference in strength between neutral (01) and an extended fusion position.45 In patients who have RA, associated elbow and shoulder disease, as well as bilateral hand involvement have to be taken into consideration when choosing the ideal arthrodesis position. Lateral deviation affects the position and the function of the fingers, especially with coexisting ulnar drift at the metacarpophalangeal (MCP) joint level. Five to ten degrees of ulnar deviation are needed to counterbalance an ulnar drift of the fingers.3,23 Most investigators prefer a neutral flexion–extension position with mild ulnar deviation for wrist fusion in rheumatoid patients.43 In most cases, a neutral or slightly flexed position for the dominant hand, to facilitate personal care, and a slightly extended position for the nondominant hand combined with 5–101 of ulnar deviation are chosen.
ARTICLE IN PRESS 354 Different fixation methods for wrist fusion have been described in the literature. Since the first description by Clayton46 in 1965, which was later popularized by Mannerfelt and Malmsten,47 different investigators have favoured the Rush or Steinmann pin technique in the original method or with slight modifications41,48 (Fig. 9). There are some reports of radiocarpal fusion using bone grafts with or without absorbable internal fixation.42,49 Bone grafting alone had a longer time to fusion than a combination of bone grafting and internal fixation. As an alternative to the pin technique, plate fixation for wrist fusion is popular,
B.R. Simmen et al. especially in posttraumatic conditions (Fig. 10). A comparison between plate and pin fusion techniques in rheumatoid patients showed no significant difference in the clinical results or in the complication rate.50 However, pin fixation has some significant advantages over the plate fixation in RA. RA is more frequent in women, who, with small wrist sizes, cannot always accommodate the plate, which is often too bulky to be applied. In addition, the soft tissue and skin condition may not be ideal to cover a plate adequately and, most often, secondary removal of the implant is needed. In severe RA, bone quality might be so poor that no screw
Figure 9 (A) Complete dislocation of a rheumatoid wrist type 3. (B) Final radiograph after completed Rush pin and staple augmentation total wrist fusion.
Figure 10 Radiolunate fusion with a 2 mm condylar plate. Despite good initial reposition, there was redislocation of the carpus back to initial deformity. Subjectively, there was no pain, and no revision was needed.
ARTICLE IN PRESS The management of the rheumatoid wrist fixation is possible. Rheumatoid patients also have a high fusion rate that tends to require less rigid fixation than osteoarthritic patients. Lastly, pin osteosynthesis is clearly less costly. Tendon reconstruction Extensor tendon reconstruction: As outlined above, rupture of extensor tendons is the final stage of a complex pathomechanical process. The best treatment of tendon rupture is prevention by early aggressive treatment of the distal radioulnar joint and the accompanying tenosynovitis. It is mandatory, when planning extensor tendon reconstruction, to assess wrist and MCP joint function. Any wrist correction or treatment of MCP joint dysfunction, or both, should be best performed together with tendon reconstruction. No tendon reconstruction can mobilize a subluxed MCP joint, and a secondary procedure that consists of MCP joint reconstruction and extensor tenolysis may not give satisfactory results. If there is any doubt about MCP joint function, traction on the distal ends of the tendons for reconstruction demonstrates the quality of MCP joint extension ability. If needed, subluxed extensor tendons should be recentered over the MCP joints at the same time that the extensor reconstruction is performed. Direct end-to-end repair of ruptured tendon in rheumatoid patients is almost never feasible. The long-standing process of tendon attrition creates a wide zone of destruction within the tendon. Therefore, the most frequently used techniques for extensor tendon repair are tendon transfer and, in selected cases, tendon reconstruction with a free tendon graft.51 With two sites of suture lines, the free tendon graft has the disadvantage of greater possibility of adherence, although Bora et al.51 reported no differences between free tendon grafts and tendon transfers. As free tendon grafts, the palmaris longus tendon or, in cases of wrist fusion, a graft from the radial wrist extensors might be used. The use of toe extensor tendons in RA must be carefully undertaken to avoid secondary morbidity. Tendon transfers might be performed as end-to-side transfers or an end-to-end reconstruction. Table 5 gives an
355 overview of possible transfers for the different rupture scenarios. The best tendon for transfer is the extensor indicis proprius (EIP) tendon, followed by the flexor superficialis of the ring or middle fingers. The use of wrist extensor tendons is not advised because the excursion of the wrist motors is significantly less than that of the finger extensor tendons, thus producing incomplete motion. The prognosis of tendon reconstruction is best in single or double tendon rupture, whereas the treatment of multiple ruptures is considered as a salvage procedure. The rupture of the extensor tendons to the thumb is often an isolated event, which is best treated with a transfer of the EIP to the extensor pollicis longus tendon. Flexor tendon reconstruction: As outlined before, the flexor tendon that ruptures most commonly in RA is the FPL, followed by the profundus tendon of the index finger. Rupture of flexor tendons in the region of the finger pulleys is rare, and most flexor tendons rupture in the carpal canal. Principally, this is a good zone for safe flexor tendon reconstruction with minimal danger of postoperative adhesions. In cases of flexor tendon rupture, an excision of bony spurs is mandatory to prevent further ruptures. Before surgery and possible tendon reconstruction, the following points should be clarified:
How much functional loss does the patient have with the ruptures?
What is the general condition of the wrist and finger joints?
Is the patient suitable for what might be a long rehabilitation process with an unpredictable result? As an alternative to tendon reconstruction, interphalangeal joint fusion, especially in arthritic joints, may be indicated as there are far fewer rehabilitation difficulties. If there is an indication for flexor tendon reconstruction, the following principles are important2,6,8:
Isolated FPL ruptures are reconstructed with a transfer of
Table 5 Possible tendon transfer sets in the different clinical scenarios.
Ruptured tendons
Transfer
Alternatives
EDM EDM, EDC V
EDM to EDC V EDV V to EDC IV
No treatment EDC V to EDC IV EIP to EDM
EDM, EDC V, EDC IV
EIP to EDM (+EDC V) EDC IV to EDC III
EDM, EDC V, EDC IV,
EIP to EDC IV and V
Flexor digitorum
EDC III
EDC III to EDC II
Superficialis IV to EDC IV and V EIP to EDC III
a superficialis tendon, preferably from the ring finger, depending on the conditions of the other tendons. Ruptures of profundus tendons are best treated by an end-to-side tenodesis with an intact adjacent profundus tendon. In cases of rupture of the profundus and superficialis tendons in one finger, a tendon transfer from an intact superficialis is performed. Some investigators have recommended bridge grafts2,6; others prefer tendon transfers.8 Isolated superficialis tendon ruptures, which are rare, need no reconstruction.
Salvage procedures
EDC, extensor digitorum communis; EDM, extensor digiti minimi; EIP, extensor inidicis proprius.
The definition of wrist salvage procedures in RA is quite difficult. Some authors might believe that wrist fusion is already considered as salvage, because it implies a definitive end in the treatment ladder. However, in the disease course of RA patients, a multitude of interventions is to be
ARTICLE IN PRESS 356 expected, and there is no space for experimental procedures. In the wrist, resection interposition arthroplasty might be considered a salvage procedure together with silicone wrist replacement.
Conclusion Knowing the natural course of rheumatoid wrist involvement is mandatory if one is to provide RA patients with the best possible surgical treatment. Treatment of soft tissue involvement is as important as bony reconstruction. Early surgical intervention may prevent tendon rupture. Although the indications for surgery arise more often from ulnar wrist involvement, the long-term prognosis depends on the course of the radiocarpal joint. For the treatment of the distal ulnar joint, ulnar head resection combined with dorsal tenosynovectomy may be advised for elderly and lessdemanding patients. The Sauve–Kapandji procedure, perhaps combined with a flexor carpi ulnaris tenodesis or a pronator transposition, may be preferred in the younger, more demanding RA patient. Depending on the type of rheumatoid wrist involvement, a destabilized wrist needs additional fixation of the radiocarpal joint in the early stages. In patients with unsalvageable, functionally unacceptable, recurrent instability of the distal ulna, an ulnar head prosthesis may be considered.
Acknowledgements This work was partially funded by Georg and Bertha Schwyzer-Winiker Foundation.
References 1. Cush JJ, Lipsky PE. Cellular basis for rheumatoid inflammation. Clin Orthop Relat Res 1991;265:9–22. 2. Ertel AN. Flexor tendon ruptures in rheumatoid arthritis. Hand Clin 1989;5(2):177–90. 3. Shapiro JS. The wrist in rheumatoid arthritis. Hand Clin 1996;12(3):477–98. 4. Backdahl M. The caput ulnae syndrome in rheumatoid arthritis. A study of the morphology, abnormal anatomv and clinical picture. Acta Rheumatol Scand Suppl 1963;5:1–75. 5. Gray RG, Gottlieb NL. Hand flexor tenosynovitis in rheumatoid arthritis. Prevalence, distribution, and associated rheumatic features. Arthritis Rheum 1977;20(4):1003–8. 6. Ertel AN, Millender LH, Nalebuff E, McKay D, Leslie B. Flexor tendon ruptures in patients with rheumatoid arthritis. J Hand Surg [Am] 1988;13(6):860–6. 7. Baer W, Dumont CE. Mechanical wearing down of flexor tendons in rheumatoid arthritis as a result of extreme volar-flexed intercalated segment instability. Scand J Plast Reconstr Surg Hand Surg 2002;36(3):189–91. 8. Ferlic DC. Rheumatoid flexor tenosynovitis and rupture. Hand Clin 1996;12(3):561–72. 9. Barnes CG, Currey HL. Carpal tunnel syndrome in rheumatoid arthritis. A clinical and electrodiagnostic survey. Ann Rheum Dis 1967;26(3):226–33. 10. Rubens DJ, Blebea JS, Totterman SM, Hooper MM. Rheumatoid arthritis: evaluation of wrist extensor tendons with clinical examination versus MR imaging—a preliminary report. Radiology 1993;187(3):831–8.
B.R. Simmen et al. 11. Ryu J, Saito S, Honda T, Yamamoto K. Risk factors and prophylactic tenosynovectomy for extensor tendon ruptures in the rheumatoid hand. J Hand Surg [Br] 1998;23(5):658–61. 12. Williamson L, Mowat A, Burge P. Screening for extensor tendon rupture in rheumatoid arthritis. Rheumatology (Oxford) 2001;40(4):420–3. 13. Simmen BR, Huber H. The wrist joint in chronic polyarthritis—a new classification based on the type of destruction in relation to the natural course and the consequences for surgical therapy. Handchir Mikrochir Plast Chir 1994;26(4):182–9. 14. Wakefield RJ, Gibbon WW, Conaghan PG, O’Connor P, McGonagle D, Pease C, et al. The value of sonography in the detection of bone erosions in patients with rheumatoid arthritis: a comparison with conventional radiography. Arthritis Rheum 2000;43(12):2762–70. 15. Backman C, Mackie H. Arthritis hand function test: inter-rater reliability among self-trained raters. Arthritis Care Res 1995;8(1):10–5. 16. Evans DM, Lawton DS. Assessment of hand function. Clin Rheum Dis 1984;10(3):697–725. 17. Labi ML, Gresham GE, Rathey UK. Hand function in osteoarthritis. Arch Phys Med Rehabil 1982;63(9):438–40. 18. Chung KC, Pillsbury MS, Walters MR, Hayward RA. Reliability and validity testing of the Michigan Hand Outcomes Questionnaire. J Hand Surg [Am] 1998;23(4):575–87. 19. 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. 20. Souter WA. Planning treatment of the rheumatoid hand. Hand 1979;11(1):3–16. 21. Shott S. Effect of early synovectomy on the course of rheumatoid arthritis. J Rheumatol 1993;20(1):199. 22. Resnick D. Rheumatoid arthritis of the wrist: why the ulnar styloid? Radiology 1974;112(1):29–35. 23. Linscheid RL, Dobyns JH. Rheumatoid arthritis of the wrist. Orthop Clin North Am 1971;2(3):649–65. 24. Thirupathi RG, Ferlic DC, Clayton ML. Dorsal wrist synovectomy in rheumatoid arthritis—a long-term study. J Hand Surg [Am] 1983;8(6):848–56. 25. Ishikawa H, Hanyu T, Tajima T. Rheumatoid wrists treated with synovectomy of the extensor tendons and the wrist joint combined with a Darrach procedure. J Hand Surg [Am] 1992;17(6):1109–17. 26. Bowers WH. Distal radioulnar joint arthroplasty: the hemiresection-interposition technique. J Hand Surg [Am] 1985;10(2): 169–78. 27. Watson HK, Ryu JY, Burgess RC. Matched distal ulnar resection. J Hand Surg [Am] 1986;11(6):812–7. 28. Vincent KA, Szabo RM, Agee JM. The Sauve–Kapandji procedure for reconstruction of the rheumatoid distal radioulnar joint. J Hand Surg [Am] 1993;18(6):978–83. 29. Ruby LK, Ferenz CC, Dell PC. The pronator quadratus interposition transfer: an adjunct to resection arthroplasty of the distal radioulnar joint. J Hand Surg [Am] 1996;21(1):60–5. 30. Swanson AB. Implant arthroplasty for disabilities of the distal radioulnar joint. Use of a silicone rubber capping implant following resection of the ulnar head. Orthop Clin North Am 1973;4(2):373–82. 31. McMurtry RY, Paley D, Marks P, Axelrod T. A critical analysis of Swanson ulnar head replacement arthroplasty: rheumatoid versus nonrheumatoid. J Hand Surg [Am] 1990;15(2):224–31. 32. Scheker LR, Babb BA, Killion PE. Distal ulnar prosthetic replacement. Orthop Clin North Am 2001;32(2):365–76. 33. van Schoonhoven J, Fernandez DL, Bowers WH, Herbert TJ. Salvage of failed resection arthroplasties of the distal radioulnar joint using a new ulnar head prosthesis. J Hand Surg [Am] 2000;25(3):438–46.
ARTICLE IN PRESS The management of the rheumatoid wrist 34. Alnot JY, Leroux D. Realignment stabilization synovectomy in the rheumatoid wrist. A study of twenty-five cases. Ann Chir Main 1985;4(4):294–305. 35. Chamay A, Della Santa D, Vilaseca A. Radiolunate arthrodesis. Factor of stability for the rheumatoid wrist. Ann Chir Main 1983;2(1):5–17. 36. Linscheid RL, Dobyns JH. Radiolunate arthrodesis. J Hand Surg [Am] 1985;10(6, Pt. 1):821–9. 37. Della Santa D, Chamay A. Radiological evolution of the rheumatoid wrist after radio-lunate arthrodesis. J Hand Surg [Br] 1995;20(2):146–54. 38. Vicar AJ, Burton RI. Surgical management of the rheumatoid wrist—fusion or arthroplasty. J Hand Surg [Am] 1986;11(6): 790–7. 39. Cobb TK, Beckenbaugh RD. Biaxial total-wrist arthroplasty. J Hand Surg [Am] 1996;21(6):1011–21. 40. Kistler U, Weiss AP, Simmen BR, Herren DB. Long-term results of silicone wrist arthroplasty in patients with rheumatoid arthritis. J Hand Surg [Am] 2005;30(6):1282–7. 41. Barbier O, Saels P, Rombouts JJ, Thonnard JL. Long-term functional results of wrist arthrodesis in rheumatoid arthritis. J Hand Surg [Br] 1999;24(1):27–31. 42. Pech J, Sosna A, Rybka V, Pokorny D. Wrist arthrodesis in rheumatoid arthritis. A new technique using internal fixation. J Bone Joint Surg Br 1996;78(5):783–6.
357 43. Rayan GM. Wrist arthrodesis. J Hand Surg [Am] 1986;11(3): 356–64. 44. Brumfield RH, Champoux JA. A biomechanical study of normal functional wrist motion. Clin Orthop Relat Res 1984;187:23–5. 45. Pryce JC. The wrist position between neutral and ulnar deviation that facilitates the maximum power grip strength. J Biomech 1980;13(6):505–11. 46. Clayton ML. Surgical treatment at the wrist in rheumatoid arthritis: a review of thirty-seven patients. J Bone Joint Surg Am 1965;47:741–50. 47. Mannerfelt L, Malmsten M. Arthrodesis of the wrist in rheumatoid arthritis. A technique without external fixation. Scand J Plast Reconstr Surg 1971;5(2):124–30. 48. Stanley JK, Hullin MG. Wrist arthrodesis as part of composite surgery of the hand. J Hand Surg [Br] 1986;11(2):243–4. 49. Juutilainen T, Patiala H. Arthrodesis in rheumatoid arthritis using absorbable screws and rods. Scand J Rheumatol 1995;24(4):228–33. 50. Rehak DC, Kasper P, Baratz ME, Hagberg WC, McClain E, Imbriglia JE. A comparison of plate and pin fixation for arthrodesis of the rheumatoid wrist. Orthopedics 2000;23(1):43–8. 51. Bora Jr. FW, Osterman AL, Thomas VJ, Maitin EC, Polineni S. The treatment of ruptures of multiple extensor tendons at wrist level by a free tendon graft in the rheumatoid patient. J Hand Surg [Am] 1987;12(6):1038–40.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 358–363
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MINI-SYMPOSIUM: SURGICAL RHEUMATOLOGY
(v) Biological therapy in the management of inflammatory arthritis with particular reference to orthopaedic surgery Deborah Hazlewood, John Winfield Department of Rheumatology, The Royal Hallamshire Hospital, Glossop Rd, Sheffield S10 2JF, UK
KEYWORDS Inflammatory arthritis; Biological therapy; Orthopaedic surgery
Summary Research over the past 20 years has identified that tumour necrosis factor-a is one of the key cytokines in the pathogenesis of rheumatoid arthritis, psoriatic arthritis and ankylosing spondylitis. This has led to targeted disease modifying therapies, the ‘‘biological agents’’ which have revolutionised modern rheumatology practice. This article outlines the currently available biological therapies, their indications, modes of action, benefits and potential side effects together with the current advice on their use at times of general and orthopaedic surgery. & 2007 Published by Elsevier Ltd.
Introduction Tumour necrosis factor-a (TNF-a) is a pro-inflammatory cytokine, a type of cell messenger, which has a key role in perpetuating the inflammatory response in various rheumatic disorders, particularly rheumatoid arthritis, psoriatic arthropathy and the spondylo arthropathies. TNF-a is also pivotal in maintaining host resistance by mediating an acute and chronic inflammatory response against infection and in promoting tissue healing. Thus blocking the actions of TNF-a with specific antagonists suppresses the body’s inflammatory response, thereby improving the symptoms and signs of an inflammatory arthropathy but, at the same time, may Corresponding author. Tel.: +44 11 42711943; fax: +44 11 42711844. E-mail addresses:
[email protected] (D. Hazlewood),
[email protected] (J. Winfield).
0268-0890/$ - see front matter & 2007 Published by Elsevier Ltd. doi:10.1016/j.cuor.2007.07.005
interfere with host resistance and healing. This led to TNF-a being identified as an attractive therapeutic target in rheumatological management whilst recognising the potential complications of its inhibition. TNF-a blocking drugs, commonly called ‘‘biological therapies’’ have been shown to be very effective in the control of refractory inflammatory arthritis, particularly rheumatoid arthritis (RA).
Clinical assessment of rheumatoid disease activity Rheumatoid disease activity is assessed by the Disease Activity Score using 28 target joint sites (the DAS 28). This is a computerised score of the number of swollen, tender joints out of 28 combined with the patient’s own global assessment of their disease activity on a visual analogue scale of 100 mm combined with an ESR. Patients with a DAS
ARTICLE IN PRESS (v) Biological therapy in the management of inflammatory arthritis score of greater than 5.1 are judged to have active rheumatoid disease. Those with a DAS 28 score of less than 1.2 are judged to be in a relative remission. Serial DAS measurements over time, typically one month apart, will identify those patients with persistent inflammatory joint disease, and will assess the patient’s response to initial therapy. Patients with a low disease activity score, i.e. less than 5.1, are deemed to have insufficient activity of their joint disease to justify going onto anti-TNF therapy, and hence will fail to meet the BSR and NICE criteria. However, low DAS scores are not synonymous with cure of rheumatoid synovitis, only a relative remission of active disease.
Current non ‘biological’ therapeutic approaches Disease modifying anti-rheumatic drugs (DMARDs) such as Methotrexate—now the ‘gold standard’ therapy—leflunomide or sulphasalazine1,2 used either singly or in combination(s) remain the cornerstone of treatment for inflammatory arthritis, but they rarely induce complete and sustained remission. Thus rheumatic patients usually continue to suffer joint pain and stiffness with signs of ongoing joint inflammation and variable radiographic cumulative joint damage. It is now generally agreed that rheumatoid disease can be diagnosed in patients with symptoms of less than three months duration and that patients should be referred early for specialist advice. Patients waiting for more than one year between symptom onset and specialist referral have a greater risk (73% compared with 34% of patients seen within one year) of developing erosive damage prior to treatment being initiated.3 DMARDs are now increasingly used very early in an attempt to suppress joint inflammation and reduce joint damage,4,5 but it has proved difficult to accurately predict which patients with very early inflammatory synovitis, i.e. ofor less than six weeks, will go on to develop progressive joint damage, but any patient with persistent synovitis with an inflammatory response, i.e. a raised ESR and/or CRP, are most at risk.6 There is also evidence that rheumatoid arthritis may be more responsive to both DMARD and anti-TNF-a therapy early in the course of the disease, possibly as short as 3–4 months from onset. This may lead to better suppression of the disease and an improved functional outcome.1,4
The inflammatory response and the mechanism of action of the biological therapies In the inflammatory cascade activated T cells release a range of cytokines including interleukin 2, interferon gamma, lymphocytotoxin, interleukin 3 and TNF-a. Monocytes and fibroblasts are also capable of producing TNF-a. In turn, via TNF-a receptors on the cell surface TNF-a stimulates macrophages which produce more TNF-a and interleukin 1 and 6. The cumulative effect of these various cytokines is to produce an acute phase response characterised by fever, leucocytosis and a raised C reactive protein. TNF-a is also powerfully chemotactic for neutrophils, can release prostaglandin E2 and promotes phagocy-
359
tosis. It also promotes the release of the matrix metalloproteinases, MMP1 and 3 and leukotrienes from chondrocytes, osteoclasts and fibroblasts which have been shown to be responsible for the erosion of cartilage and bone in inflammatory arthritis.7 Both TNF-a and TNF-a receptors possess important cellular regulatory functions which include activation of immune cells and regulation of apoptosis, the programmed cell death of immune cells. Hence, targeting TNF-a or the TNF-a receptor, to potentially block the effect of TNF-a, is theoretically an attractive therapeutic target and this has proved to be the case in clinical practice.8 Currently three TNF-a antagonists are now widely available in rheumatology practice in the UK. They work by either neutralising TNF-a by binding directly with it or by blocking the TNF-a receptor. Infliximab and Adalimumab are specifically designed monoclonal antibodies engineered to bind with high affinity to both the soluble and transmembrane forms of TNF-a preventing its action with the receptor. Infliximab is a chimeric (25% mouse, 75% human) monoclonal TNF-a antibody produced by a recombinant cell line cultured by continuous perfusion. Adalimumab is a fully humanised monoclonal antibody with a 100% human peptide sequence and structure produced by recombinant DNA technology in a mammalian cell expression system. The third agent, Etanercept, is a fusion protein made up of two recombinant p75 soluble receptors fused to the Fc fragment of human IgG 1. It is produced by recombinant DNA technology in a Chinese hamster ovary mammalian cell expression system and works by binding directly to the TNF-a molecule thus preventing TNF from binding to or activating the TNF-a receptor. All are expensive e.g. Infliximab costs £7500 for drug costs alone per year, and Etanercept and Adalimumab £9295. As they are not curative, treatment is ongoing year on year with cumulative costs. They are administered by intravenous infusion (Infliximab) or by subcutaneous injection (Etanercept and Adalimumab). The biological agents should only be used with specialist advice from rheumatologists and administration supervised by specialist nurses with particular knowledge and expertise in the use of these drugs. Patients can be taught how to administer the subcutaneous injection themselves at home although patients requiring intravenous infusions of Infliximab are currently admitted as day cases to hospital. For the one third of rheumatic patients who may be unresponsive to anti-TNF-a drugs rituximab, a monoclonal antibody which depletes B cells, may be an alternative approach. The biological agents are usually co-administered with methotrexate even though the previous response to methotrexate may have been incomplete. There are two reasons for this, firstly methotrexate is continued to prevent the gradual rejection of the monoclonal antibody through the body’s immune response against the biological agent, notably in the use of Infliximab which contains a mouse antigen and secondly the co-administration of methotrexate has been shown to be more beneficial than the biological agent alone in suppressing joint inflammation and reducing erosive damage.9 Current drug treatment for newly diagnosed RA still includes a DMARD such as methotrexate. Patients with a
ARTICLE IN PRESS 360 poor response to such therapy are either changed to an alternative DMARD, or are commenced on a combination of DMARD therapies. There are some patients who respond suboptimally to all the currently available DMARD therapies, and some patients are intolerant of DMARD therapy and are forced to withdraw from treatment. The British Society for Rheumatology (BSR) guidance states that all patients should have a formal assessment of treatment response or lack of it to justify continuing on therapy or changing drugs.10 It is at this stage that the anti-TNF therapies are now being considered when there has been an incomplete response to DMARD therapy. The current BSR and NICE guidance on the use of biological therapies states that patients with rheumatoid arthritis should have tried at least two DMARDs, one of which should be methotrexate, at maximum dosage for six months, and have also demonstrated a sub-optimal response, i.e. persistent joint inflammation, before biological agents are considered. At present in the UK the use of the biological agents before DMARD therapy is not felt to be justified in those patients who might respond equally well to much cheaper DMARD therapy but there is now good evidence that the biological agents are more effective than standard DMARD therapy. Trials assessing the addition of anti TNF therapy to methotrexate have shown evidence of a substantial additional response by combining the biological therapies with methotrexate, even in patients who have been previously been poorly responsive to methotrexate. Similar clinical responses have been documented with all three biological agents.11–13
Funding issues In the UK application for appropriate funding for these drugs has to be made through the patients’ Primary Care Trust using the clinical guidance provided by the BSR and the National Institute of Clinical Excellence (NICE).14,15 The current NICE guidance in the UK has been criticised for limiting patients’ access to biological therapy due to the huge cost implications for Primary Care Trusts. There are no reliable predictors of future responsiveness to DMARD therapies but there is increasing evidence suggesting that early aggressive DMARD treatment markedly improves outcome.16 However if patients fail to respond to DMARD therapies, over months or possibly years whilst they are trialling these drugs, either singly or in combination, their disease will be progressing and irreversible joint damage will occur. As clinical experience builds, it is likely that biological agents will be increasingly used at an earlier stage in the management of inflammatory arthritis, possibly at onset of disease, in an attempt to induce a complete remission at the earliest possible opportunity preventing morbidity and progressive joint damage. The cost/benefit of early aggressive DMARD and/or biological therapy awaits detailed financial analysis.
Selection of patients suitable for anti TNF therapy It is now possible to identify patients with inflammatory joint disease for whom biological therapy is appropriate but it is not suitable for all of them as there are certain
D. Hazlewood, J. Winfield contraindications. Thus it is important that they are carefully screened for suitability before treatment. In particular the biological agents should not be prescribed for patients who have active viral or bacterial infections. Serious infections including fatalities have been reported whilst on anti-TNF therapy. Of particular relevance are pneumonia, pyelonephritis, septic arthritis and septicaemia.17,18 Therefore patients with a history of recurrent chest, urinary or joint infections may be unsuitable for biological therapy. It should be remembered that before the TNF-a era the incidence rate of infection in the rheumatoid population was nearly twice as high as in matched non-rheumatoid controls, due to rheumatoid disease itself which alters immunological function, decreases mobility and causes skin sepsis and also due to the use of immuno-suppressive drugs, particularly steroids.19,20 In the early placebo controlled trials evaluating the three anti-TNF agents the rate of infection did not exceed the rate in the placebo group but, as the early studies had strict inclusion criteria and were relatively short studies, infection was not thought to be a specific risk. Indeed two post-marketing studies from Sweden and the UK suggested that the risk of developing serious infections was not increased in patients receiving TNF-a therapy for rheumatic diseases with around five infection events per 100 patient years for all three anti-TNF drugs.21,22 Since then numerous case reports or small series of patients with serious infections, including tuberculosis (TB) and opportunistic infections, have been reported worldwide. TB was the most frequently reported granulomatous infection and has been reported with the use of all three anti-TNF-a blockers,23–25 particularly relevant for Infliximab. Latent TB can be reactivated and present in a disseminated, miliary form or develop at extra pulmonary sites with most cases occurring in patients with a known past history of tuberculosis. A pre-treatment chest X-ray looking specifically for TB is mandatory. Skin testing for the presence of TB with the tuberculin reaction or Heaf test may be unreliable. The Elispot test has shown promise in identifying patients with a latent TB infection. When the presence of TB is uncertain advice from respiratory or infectious diseases physicians is advisable and anti-tuberculous therapy may be necessary prior to commencing anti-TNF therapy if there is a high index of suspicion. Other invasive opportunistic infections also occur with the three TNF-a blocking drugs including pneumocystis carinii pneumonia, disseminated histoplasmosis, listeriosis and aspergillosis.25,26 Even after these have been excluded prior to commencing anti-TNF-a treatment, patients must be regularly monitored during treatment for the possible emergence of infection and should carry an ‘‘infection alert card’’ and be advised to report any symptoms suggestive of infection. Patients are also asked to report to their clinical nurse specialist if they have been started on antibiotics by their general practitioner for incidental infections during the course of treatment to assess the severity of the infection, its duration, the response to antibiotic treatment and the possible need for temporary withdrawal from anti-TNF-a therapy. Further specific contra-indications to biological therapy include moderate to severe heart failure (New York Heart Association grade 3 or 4), patients with a history of demyelinating disease, women who are pregnant or breast
ARTICLE IN PRESS (v) Biological therapy in the management of inflammatory arthritis feeding and patients who have had a current or past history of malignancy except for certain cases of skin malignancy. This is relevant because patients with rheumatoid arthritis have an increased risk of developing a malignancy over time, particularly lymphoma. So far the theoretical increased risk of developing solid tumours in rheumatoid patients taking anti-TNF therapy, due to the therapy itself, has not been realised but ongoing surveillance is necessary.
Other indications for anti TNF therapy Anti-TNF drugs have been shown to be effective in the management of poorly controlled psoriatic arthritis and ankylosing spondylitis. The use of anti-TNF drugs has provided a new line of treatment opportunity for patients with both these conditions based on the early work in rheumatoid arthritis.25–29
Issues for orthopaedic management The increasing use of the biological agents has implications for the orthopaedic surgeon as there has been much debate about the risks associated with their use around the time of surgery. The main concern is the risk of peri/post operative infection if patients remain on anti-TNF therapy during the surgical period due to the immunosuppressive nature of their mode of action, but also the concomitant risk of losing control of inflammatory joint disease and inducing a ‘flare’ if therapy is stopped, particularly in patients with severe disease. It has been estimated that 25% of patients with RA will require surgery within 20 years of the disease onset, a figure which may be declining.30 Hopefully the majority will now be patients whose overall disease is controlled on their current therapy, but who already have irreversible joint damage requiring joint replacement. These cases require careful assessment. Rheumatoid disease commonly causes atrophy of the skin and subcutaneous tissue over time, exacerbated by steroid therapy. Careful handling of the patient’s limbs and tissues before, during and after a surgical procedure to minimise soft tissue bruising and shearing stresses across the skin and meticulous skin closure at surgery are imperative. Even so it is common to observe small sections of a surgical wound breaking down after major orthopaedic surgery in rheumatoid patients. Fortunately most of these will heal without any further complications. The most important complication in elective orthopaedic surgery is surgical site infection (SSI).31,32 Patients with RA are already at increased risk of infection which has been demonstrated in several high quality randomised trials and there is a further increased risk of infection with the biological agents.19 The calculated odds ratio for infection from pooled high quality randomised trials of patients on biological therapy between 1998 and 2004 revealed a figure greater than 1.5 for sepsis. Infections were found to be more likely to occur in the presence of increased age, extraarticular features of rheumatoid arthritis, leukopenia, and other co-morbidities. Strong predictors for the development of serious systemic infection were previous orthopaedic surgery and high cumulative steroid dose.19,20
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Several studies assessing the infection risk peri-operatively in RA have identified various poor prognostic factors. These include the type of surgery especially foot operations, previous SSIs, co-morbidities particularly diabetes mellitus and pulmonary disease, active RA and steroid use.2 There is no convincing evidence that disease modifying agents such as methotrexate, sulphasalazine, hydroxychloroquine, leflunomide and Myocrisin increase this risk,33 but many surgeons still express concern about their effect on initial wound healing, subsequent wound dehiscence and the risk of surgical wound infection. There is little objective evidence of a relationship between anti TNF agents and infection risk at the time of orthopaedic surgery, but preliminary reports have suggested higher rates of infection in these patients.34,35 However several small studies have since failed to identify an increased incidence of SSIs.36 Wendling et al. reported a retrospective study of 50 surgical procedures in 30 rheumatoid patients. In 18 cases TNF was stopped prior to surgery, the remainder had surgery between their two sequential anti TNF injections. Minor post operative complications were recorded in 6%, principally delays in wound healing of 1–2 weeks, and a moderate, short lasting rheumatoid disease flare was reported in 12% of those who had their anti TNF drugs withdrawn. The study did not demonstrate an increased frequency of adverse events related to uninterrupted use of anti TNF, but did raise an important consideration about planning surgery between anti-TNF-a treatments.36 Bibbo et al. analysed the risk of healing/infectious complications in a small number of rheumatoid patients undergoing elective foot and ankle surgery.37 All patients continued their anti-rheumatic medications, with 16 patients on non TNF disease modifying treatments and 15 on anti TNF therapies. The study demonstrated no difference in complication rates for both groups including an analysis of sepsis rates. Giles et al. however reported adverse findings. Their study identified 91 patients from the Johns Hopkins Arthritis Centre who had undergone orthopaedic surgery38 who had an increased risk of infection, with an odds ratio of 5:3, for patients receiving anti TNF therapy. Unfortunately due to patient record ambiguities there was some uncertainty regarding the timing of their last preoperative administration of anti TNF, which may have affected interpretation of data. Den Broeder et al. performed a large retrospective study to assess the effect of withholding vs maintaining anti TNF therapy on the incidence of SSI, and secondarily looked at the effect of discontinuation of anti TNF therapy on other complications.32 A total of 1219 procedures were performed on 768 patients. Factors which led to an increased risk of SSI included foot, ankle or elbow surgery, but a history of previous SSI was by far the strongest predictor of future sepsis. Continued peri-operative use of biological agents was not a strong factor associated with the risk of SSI. However wound dehiscence and bleeding occurred significantly more frequently in patients who continued on anti-TNF-a therapy. Limitations of this study included the overall low infection rates. A study with much larger numbers to assess such risks is required. There was also a lack of data on rheumatoid disease activity which could affect the risk and incidence of sepsis.
ARTICLE IN PRESS 362 In Sheffield it has been our practice not to stop or reduce any of the conventional DMARD therapies over the operative period. We have not observed any particular orthopaedic complications by continuing DMARDs. We have found that withdrawing disease modifying drugs over the operative period usually results in a flare of rheumatic disease activity which can take weeks or months to re-stabilise, during which time the patient is trying to mobilise and rehabilitate following their operation. Withdrawing anti-TNF-a treatments pose a similar issue. In a small retrospective study in Sheffield reported at the meeting of the European Rheumatoid Arthritis Surgical Society in Zurich in 2006 we reviewed 49 of our rheumatoid arthritis patients on biological therapies who underwent various major and minor orthopaedic operations under different orthopaedic surgeons and some non-orthopaedic surgery (13 total knee replacements and four total hip replacements). In all patients the biological agents were withdrawn for two weeks prior to surgery and recommenced once the sutures had been removed and the wound had healed. No peri-operative infections or wound complications were identified but patients experienced flare ups of their rheumatoid arthritis on temporary withdrawal of their antiTNF therapy. This was also seen in patients undergoing other orthopaedic operations such as metacarpophalangeal joint replacements, soft tissue corrections, forefoot arthroplasties, ankle and wrist fusions and a cervical decompression. Eleven patients underwent non-orthopaedic operations including mastectomy, coronary artery bypass surgery, cochlear implant and dental extractions. They also had flares of their rheumatoid disease activity but no problems with wound infections or systemic sepsis on withdrawal of anti-TNF-a therapy. Rheumatoid disease control was reestablished when patients were re-started on their biological agent in 46 of the 49 patients who had surgery but the remaining three patients required a switch to an alternative anti-TNF agent. Notably several patients experienced delayed wound healing despite being off anti TNF therapies, leading to significant delays in recommencing anti-TNF-a treatment and hence suffered marked prolonged flares of their disease. A confounding difficulty was regular examination of the wound for healing in patients with a plaster cast for a joint fusion. In this study we also reviewed 14 patients with rheumatoid arthritis who had undergone mini-arthroscopy of the knee under local anaesthesia. In these patients the anti-TNF drugs were not stopped before, during or after the procedures. No complications were identified apart from one case of minor knee swelling postoperatively but no infection was identified.
Should biological therapy be continued or withdrawn at the time of surgery? Due to the lack of firm evidence current guidelines vary. Our current policy in Sheffield, supported by knowledge of the half life of the various biological agents used, is to withdraw the biological agent two weeks prior to the planned date of surgery to ensure a ‘‘washout period’’ and then to only restart the biological therapy two weeks after sutures have been removed and the wound has been shown to be fully healed. This view is supported by the manufacturers of the biological agents.
D. Hazlewood, J. Winfield The Dutch guideline recommends cessation of anti TNF treatments four drug half-life times prior to an operation, which varies for the different treatments (Infliximab 39 days, Etanercept 12 days, Adalimumab 56 days).32,37 Most centres in the UK consider that it is prudent to stop antiTNF-a treatments prior to surgery and a common timescale is cessation 2 weeks prior to surgery with reintroduction when wound healing is complete.
Summary The available data do not give any clear evidence based recommendations regarding the continued use or discontinuation of anti TNF therapies peri-operatively. Higher patient numbers on anti-TNF-a therapy are required in controlled trials to assess the risks of continuing on antiTNF-a therapy at the time of surgery. Given the lack of available data current guidance errs on the side of caution and recommends the withdrawal of the biological agents over the operative period. The length of time needed for withdrawal either side of surgery is still not clear but current practice in the UK is to withdraw the biologicals two weeks prior to a procedure and restarting when the wound has healed, accepting a loss of rheumatoid disease control which can be prolonged, particularly in the presence of delayed wound healing. Practice points:
Early diagnosis, early referral and aggressive suppressive
DMARD therapy is necessary for most patients with inflammatory arthritis to minimise joint damage and maintain function. Disease modifying drugs, notably Methotrexate, still remain the cornerstone of suppressive treatment for the majority. Patients with an incomplete response to DMARDs including Methotrexate should be considered for anti-TNF-a therapy using the BSR and NICE Guidance. Biological therapy carries an increased risk of infections during treatment, including activation of latent TB and opportunistic infection and there are specific contraindications to anti-TNF-a therapy. Currently biological therapy should be temporarily withdrawn over the operative period to obviate sepsis but flares of inflammatory joint disease active are common on withdrawal. Research directions:
Controlled trials of patients undergoing orthopaedic
operations who continue or discontinue their anti-TNF-a therapy over the surgical period should be carried out to compare and document whether there is an increased risk of sepsis over the surgical period if the drug is continued and/or whether disease flares can be avoided by continuing on therapy. Such a study should include an analysis of other risk factors for sepsis. Earlier use of anti-TNF-a therapies in the course of an inflammatory arthritis may result in excellent remissions possibly reducing the future requirement for orthopaedic intervention.
ARTICLE IN PRESS (v) Biological therapy in the management of inflammatory arthritis
References 1. Boers M, et al. Randomised comparison of combined step down Prednisolone, Methotrexate and sulfasalazine with sulfasalazine alone in early rheumatoid arthritis. Lancet 1997;350(9074):309–18. 2. Choy EHS, Smith C, Dore ´ CJ, Scott DL. A meta analysis of the efficacy and toxicity of combining disease modifying antirheumatic drugs based on patient withdrawal. Rheumatology 2005;44:1414–21. 3. Irvine S, et al. Early referral, diagnosis, and treatment of rheumatoid arthritis: evidence for changing medical practice. Ann Rheum Dis 1999;58(8):510–3. 4. Nell VP, et al. Benefit of very early referral and very early therapy with disease modifying anti-rheumatic drugs in patients with early rheumatoid arthritis. Rheumatology (Oxford) 2004; 43(7):906–14. 5. Fuchs HA, et al. Evidence of significant radiographic damage in rheumatoid arthritis within the first 2 years of disease. J Rheumatol 1989;16(5):585–91. 6. Mottonen TT. Prediction of erosiveness and rate of development of new erosions in early rheumatoid arthritis. Ann Rheum Dis 1988;47(8):648–53. 7. Jenkins JK, et al. The pathogenesis of rheumatoid arthritis: a guide to therapy. Am J Med Sci 2002;323(4):171–80. 8. Feldmann M, Brennan FM, Elliott MJ, Williams RO, Maini RN. TNF alpha is an effective therapeutic target for rheumatoid arthritis. Ann NY Acad Sci 1995;766:272–8. 9. Quinn MA, Conaghan PG, O’Connor PJ, et al. Very early treatment with Infliximab in addition to Methotrexate in early, poor-prognosis rheumatoid arthritis reduces magnetic resonance imaging evidence of synovitis and damage, with sustained benefit after Infliximab withdrawal: results from a twelvemonth randomised, double-blind, placebo-controlled trial. Arthritis Rheum 2005;52:27–35. 10. Luqmani R, et al. British Society for Rheumatology and British Health Professionals in Rheumatology Guideline for the management of rheumatoid arthritis (the first two years). Rheumatology (Oxford) 2006;45(9):1167–9. 11. Weinblatt ME, Kremer JM, Bankhurst AD, et al. A trial of Etanercept, a recombinant tumour necrosis factor receptor: Fc fusion protein, in patients with rheumatoid arthritis receiving methotrexate. N Eng J Med 1999;340:253–9. 12. Barrera P, Van der Maas A, Van Ede AE, et al. Drug surviva, efficacy and toxicity of monotherapy with a fully human antitumour necrosis factor—a antibody compared with methotrexate in long-standing rheumatoid arthritis. Rheumatology 2002; 41:430–9. 13. Maini RN, Breedveld FC, Kalden KR, et al. Therapeutic efficacy of multiple intravenous infusions of anti tumour necrosis factor—a monoclonal antibody combined with low dose weekly methotrexate in rheumatoid arthritis. Arthritis Rheum 1998;41:1552–63. 14. Report of a working party of the British Society for Rheumatology. Guidelines for prescribing TNF blockers in adults with RA. BSR, available from /www.rheumatology.org.ukS April 2001. 15. National Institute for Clinical Excellence. Guidance on the use of Etanercept and Infliximab for the treatment of rheumatoid arthritis. Technology Appraisal Guidance No 36. London: NICE, 2002. /http://www.nice.org.uk/pdf/RA-PDF.pdfS. 16. Quinn MA, Conaghan PG, Emery P. The therapeutic approach of early intervention for rheumatoid arthritis: what is the evidence? Rheumatology 2001;40:1211–20. 17. Kroesen S, Widmer AF, Tyndall A, et al. Serious bacterial infections in patients with rheumatoid arthritis under ANTITNF-a therapy. Rheumatology 2003;42:617–21. 18. Malloy E, Ramakrishnan S, Murphy E, et al. Morbidity and Mortality in rheumatoid arthritis patients during treatment with adalimumab and infliximab. Rheumatology 2004;43:522–3.
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19. Doran MF, Crowson CS, Pond GR, et al. Frequency of infection in patients with rheumatoid arthritis compared with controls: a population based study. Arthritis Rheum 2002;46(9):2287–93. 20. Singh G, Ramey DR, Rausch PL, et al. Serious infections in rheumatoid arthritis: relationship to immunosuppressive use. Arthritis Rheum 1999;42(Suppl.):S71–4. 21. Dixon WG, Hyrich KL, Watson K, et al. Serious infection rates in patients receiving biologics therapy in the United Kingdom: results from the BSR biologics register EULAR Congress 2002. OP0094. 22. Jacobsson LTH, Turesson C, Gu ¨lfe A, et al. No increase in severe infections in rheumatoid arthritis patients treated with TNF blockers. EULAR Congress 2005. SAT0164. 23. Keane J, Gershon S, Wise RF, et al. Tuberculosis associated with Infliximab; a tumour necrosis factor alpha—neutralising agent. N Engl J Med 2001;345:1098–104. 24. Mohan AK, Cote TR, Block JA, et al. Tuberculosis following the use of Etanercept: a tumour necrosis factor inhibitor. Clinic Infect Dis 2004;39:295–9. 25. Keystone EC. Safety of biologic therapies—an update. J Rheumatol Suppl 2005;74:8–12. 26. Culm NF, Lederman ER, Wallace MR. Infections associated with tumour necrosis factor—alpha antagonists. Medicine 2005;84: 291–302. 27. Mease PJ, et al. Adalimumab for the treatment of patients with moderately to severely active psoriatic arthritis: results of a double blind randomised placebo controlled trial. Arthritis Rheum 2005;52(10):3279–89. 28. Mease PJ, et al. Adalimumab is effective against skin and joint disease in psoriatic arthritis patients. 48 week results of ADEPT trial. Adalimumab Effectiveness in Psoriatic Arthritis Trial. Poster presented at BSR 2006. 29. Lambert RGW, et al. Adalimumab reduces spinal and sacroiliac joint inflammation in patients with ankylosing spondylitis (AS)—52 week magnetic resonance imaging (MRI) results from the Canadian AS study. Ann Rheum Dis 2006; 65 (Suppl. 11, abstract OP38). 30. Da Silva E, et al. Declining use of orthopaedic surgery in patients with rheumatoid arthritis? Results of a long term population based assessment. Arthritis Rheum 2003;49:216–20. 31. Grennan DM, et al. Methotrexate and early post operative complications in patients with rheumatoid arthritis undergoing elective orthopaedic surgery. Ann Rheum Dis 2001;60:214–7. 32. den Broeder A, et al. Risk factors for surgical site infections and other complications in elective surgery in patients with RA with special attention for anti tumor necrosis factor: a large retrospective study. J Rheumatol 2007;34:689–95. 33. Lacaille D, et al. Are DMARDs associated with increased risk of infection in RA? Highlights from the American College of Rheumatology Scientific meeting 2004. Abstract 1805. 34. Halligan CR, et al. Perioperative management of disease modifying antirheumatic agents and postoperative prosthesis infection in patients with rheumatoid arthritis undergoing total joint arthroplasty. Arthritis Rheum 2005;52(Suppl.):840. 35. Giles JT, Gelber AC, Nander S, et al. TNF-a inhibitor treatment increases the risk of post-operative orthopaedic infection in patients with rheumatoid arthritis. Arthritis Rheum 2004; 50(Suppl.):S660. 36. Wendling, et al. Surgery in patients receiving anti-tumour necrosis factor a treatment in rheumatoid arthritis: an observational study on 50 surgical procedures. Ann Rheum Dis 2005;64:1378–9. 37. Bibbo, et al. Infectious and healing complications after elective orthopaedic foot and ankle srgery during tumour necrosis factor— alpha inhibition therapy. Foot Ankle International 2004;25(5). 38. Giles J, et al. TNF inhibitor therapy and risk of serious post operative orthopaedic infection in rheumatoid arthritis. Arthritis Rheum 2006;55(2):333–7.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 364–379
Available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/cuor
SPINE
Tuberculosis of spine—Contemporary thoughts on current issues and perspective views Myung-Sang Moona,b, a
Spine Center, Sun General Hospital, Daejeon, Republic of Korea Moon-Kim’s Institute of Orthopedic Research, Shi-Bum Apt. 14-105, Yoe-Ee-Do-Dong, Youngdeungpo-Ku, Seoul, Republic of Korea b
KEYWORDS Tuberculosis; Dormant; Spine; Diagnosis; Paralysis; Deformity; Management
Summary Despite the belief that spinal tuberculosis is controlled, some issues of diagnosis and management have been neglected. This paper based on the author’s large experience looks at the behaviour of tubercle bacilli and new diagnostic and therapeutic methods including medical and surgical procedures. & 2007 Elsevier Ltd. All rights reserved.
Introduction While tuberculosis remains a major killer1–11 particularly in developing countries1,4,5,7,9,10, in the last 2 decades in developed countries it had been thought that tuberculosis of spine was a curable medical disease without sequelae. About 95% of tuberculosis patients are in the developing world1,4,5,9,10; China has 1.4 million new cases every year.12 Tuberculous spondylitis, although less common, is the most dangerous form of skeletal tuberculosis, and the World Health Organization estimates that there are 1.81 million deaths from tuberculosis in Asia each year. The US center for disease control (CDC) predicted that the number of new Moon-Kim’s Institute of Orthopedic Research, Shi-Bum Apt.
14–105, Yoe-Ee-Do-Dong, Youngdeungpo-Ku, Seoul, Republic of Korea. Tel.: +82 2 785 6065; fax: +82 42 603 7387. E-mail addresses:
[email protected],
[email protected] (M.-S. Moon). 0268-0890/$ - see front matter & 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2007.09.006
diagnoses of active tuberculosis worldwide will increase from 7.5 to 11.8 million per year. The incidence of the disease will rise from 143 to 173 per 100,000 and deaths due to tuberculosis will climb from 2.5 to 3.5 millions or more per year.9,10
HIV/AIDS In 2006 there were 42 million HIV-infected, and yearly deaths from AIDS of 25 millions.13,14 HIV disables and destroys the thymic lymphocytes and tissue macrophages that are the body’s main defense against tuberculosis making those who are HIV-positive extremely susceptible to the disease. The risk of acquiring an opportunistic infection is proportional to the extent and duration of immunosuppression17,19,20 and tuberculosis is the most common and most virulent opportunistic infection associated with HIV disease. In some African countries, the number of reported tuberculosis cases has doubled or even
ARTICLE IN PRESS Tuberculosis of spine tripled from 2001 to 2003 because of the spread of HIV/ AIDS.10,13,15,16 Indeed tuberculosis coupled with HIV disease is ‘‘the cursed duet’’. Tuberculosis behaves differently in HIV patients; in HIVnegative patients, only 3–5% of tuberculosis is skeletal but in HIV-positive patients about 60% of the cases involve bone.10,13 Concomitantly there has also been a significant increase in the incidence of disseminated Mycobacterium aviumintracellulare complex (MAIC) infection, which occurs almost exclusively in patients with a more severely decreased CD4+lymphocyte count below 100 cells/mm3 (50–200 cells/ mm3)10,17 which, taken with the recent resurgence of chemoresistant Mycobacterium tuberculosis variants, has raised concerns worldwide2,3,18 and suggests the need to prepare for the re-emergence of spinal tuberculosis. This has not occurred so far as there are very potent chemotherapeutic agents effective in HIV-positive patients and the surgical techniques to manage, aided by the fact that tuberculosis infectivity in HIV-positive patients is less than that of the HIV-negative patients (although Mantoux skin test positivity rate in diagnosis is lower in HIV positive patients than that of the HIV-negative patients).9–11,13–17 The high prevalence of tuberculosis in those with a low CD4 count emphasizes the importance of screening for active tuberculosis before commencing tuberculosis preventive and antiretroviral therapy. Active tuberculosis should be excluded before isoniazid (INH) preventive therapy and continued surveillance for INH resistance is essential.9,10,18
Management of spinal tuberculosis Management has changed significantly in the second half of the 20th century.1,9,10,21,22 Even as late as 1970s the primary goal of the management was to save the patient’s life by curing the disease rather than prevention and/or correction of spinal deformity and there were no surgical techniques to treat what were seen as patients’ aesthetic demands which became more marked since the early 1980s.9,10,21,23 Antituberculous drugs changed everything. Specific chemotherapeutic agents alone could cure not only active tuberculosis, but also helped in the recovery from paralysis.6,8–10,23–25 Antituberculous drugs made surgery safer9,10,21,23,25–27 but operative treatment was reserved for:
failure of drug therapy; recrudescence of the disease; Pott’s paraplegia that did not resolve after 4–6 weeks of chemotherapy;
involvement of the spinal cord; other complications. However, there remain a significant number of issues in the management of spinal tuberculosis that up to now have not received much attention in spite of their significant clinical importance.
365 This paper seeks to address these issues in diagnosis and management in particular
newer diagnostic techniques including non-culture laboratory methods;
new chemotherapeutic protocols with regard to the latent tuberculosis;
hyperbaric oxygen therapy; surgical options for the spinal deformity and associated neural involvement;
instrumentation; implant removal time; the fate of the instrument-immobilized joints. Staging of the disease Disease staging must be of practical use in management. There is no universally accepted staging system. Kumar’s7 did not satisfy clinicians’ requirements. Thus terms such as early and late, early and advanced, and kyphotic and nonkyphotic are used in staging the disease, as is vertebral body loss expressed as a percentage and severity of the deformity (Table 1). A satisfactory system is still awaited.
Diagnostic issues The insidious onset, the lack of early constitutional symptoms and local signs of spinal tuberculosis militate against early diagnosis10,25 and there is no single diagnostic test which can detect all cases of tuberculosis. With the increasing incidence of tuberculosis of all types throughout the world, physicians and surgeons must exercise a high index of suspicion to achieve early diagnosis.32 Thus clinicians typically rely on a battery of methods and diagnosis can take from several days to many weeks and involve expensive, invasive and complex procedures.10,25,29 The diagnostic techniques include observation and investigation of clinical signs and symptoms, the use of various imaging techniques, and laboratory methods.
Tuberculin skin test (TST) The TST has inherent limitations of sensitivity and specificity. Even in high tuberculosis-burden areas about 20% of Table 1
Staging of spinal tuberculosis (Moon, 1992).
Disease progress
Size of lesion
Deformity
Disease advancement (stages) Stage I: minimally (very early) Stage II: early Stage III: relatively (moderately) Stage IV: far advanced
Degree of body destructive loss o20% (2/10)
Degree of kyphosis p12.21
26–50% 51–100%
12.2–22.251 22.26–39.01
101–200%
39.1–72.51
Note: percentage and degree of kyphosis in cases of conservative treatment is calculated by Rajasekaran’s formula (Y ¼ 5.51+30.51 degree of body destruction).28
ARTICLE IN PRESS 366 individuals are negative to TST throughout life, despite repeated exposure to the tubercle bacilli. Additionally the sensitivity decreases in immuno-compromised patients for whom accurate diagnosis of latent tuberculosis infection is essential. In terms of specificity, TST is influenced by BCG vaccination and non-tuberculous mycobacterial infection.
Imaging Imaging techniques such as simple radiographs, bone scan, CT and MRI are useful but not diagnostic; e.g. when disc and/or end-plate destruction with surrounding soft tissue swelling is observed on simple radiographs spine infection should be suspected. Diffusion-weighted MRI has been found to have limited usefulness for differentiating spinal infection and malignancy.30
Laboratory Laboratory aids to diagnosis include:
complete blood counts including total lymphocyte and
CD4 lymphocyte (helper-inducer T-cell) counts, ESR and CRP; smear and/or culture; histology; detection of specific antigen; metabolic products; patient’s antibody response and detection of antibody to M. tuberculosis; DNA sequence polymerase-chain reaction (PCR) of M. tuberculosis.
The diagnostic gold standard has traditionally been the isolation of M. tuberculosis by smear and/or culture from clinical samples e.g. aspirates and tissue specimens, and the typical histology.9,10,15 However, the tubercle bacilli is difficult to culture due to its fastidious growth requirements and slow rate of growth. Hence the need for the development of various laboratory methods. There are three diagnostic non-culture laboratory tests:
M.-S. Moon reports that T-SPOT is more sensitive than TST in immunocompromised subjects. These assays detect tuberculosis infection, but they cannot differentiate between latent tuberculosis infection and active tuberculosis. Therefore, when the TST and IFN-g assay results are positive, differentiation of latent infection and active tuberculosis should be carried out on the basis of the clinical history, chest and skeletal imaging studies and tissue studies. The other major non-culture test is the molecular diagnostic test, PCR, which amplifies the DNA of M. tuberculosis. A primer pair targeting a 123 base pair (bp) segment of the repetitive sequence IS6110 of the M. tuberculosis complex is used, which covers M. tuberculosis, M. africanum, M. bovis, M. canetti and M. microti.9 This technique represents an exciting development. It has been used as a marker to monitor response to treatment9,10,27,31 and has been shown to provide rapid information on drug resistance and clonality in epidemiological investigation of outbreaks.
Histology The histological lesions caused by M. tuberculosis in AIDs and anti-TNF-a treatment patients range from the classical caseating granulomas, to more frequently a non-specific chronic inflammatory reaction without necrosis. Thus it is important to use acid-fast staining in non-specific inflammatory lesions to rule out M. tuberculosis infection.9,10,15 PCR techniques utilizing microdissection of the tissue specimen is another diagnostic option and is one of the most advanced diagnostic techniques.31 To summarize, despite recent advances, there is yet no 100% accurate diagnostic technique. The author’s preference, in cases of diagnostic delay, is for image-guided needle bone biopsy. This is a simple and safe procedure allowing bacteriological and histological assessment of aspirates and bone specimens.
Management Chemotherapy
immunological tests; antigen and antibody; metabolic product detection such as extracorporeal
interferon-g test, and amplification of DNA of M. tuberculosis by PCR.31
Lymphocytes secrete interferon-g when T-lymphocytes are exposed to tubercle bacilli making extracorporeal interferon g test for latent tuberculosis particularly noteworthy. Two ex-vivo interferon-g (IFN-g) assay kits have been marketed recently; Quanti-FERON* TB Gold [Cellestis limited, Carnegie Victoria, Australia, QFT-G] and T-SPOT, TB [Oxford Immunotec, Oxford, UK, T-SPOT]. The former uses the ELISA technique and T-SPOT uses enzyme-linked immunoserbent spot (ELISPOT) technique. Both use M. tuberculosis-specific antigens, ESAT-6 and CFP10 as stimulants. As BCG does not contain ESAT-6 and CFP10, these assays are more specific than TST in the diagnosis of tuberculosis infection. They have variable sensitivity, dependent on host factors and methods used. There are
Chemotherapy is the mainstay of treatment of spinal tuberculosis.1,4,12 There are six main anti-tuberculous drugs (see below). With the increasing incidence of drug-resistant tuberculosis worldwide, it is very important to know the bacterial sensitivities before commencing chemotherapy. By culture of aspirate or tissue specimens, sensitivity tests of the cultured tubercle bacilli against each drug can be ascertained. Non-culture laboratory techniques are also utilized. Pyrazinamide Pyrazinamidase activity is assessed by either
rapid detection of mutation in Pnc A gene by PCR-CSCP in one to 2 days, or
flowcytometric array with BACTEC TB 460 or BACTEC MGIT 960. Data are available 2 h after the initiation of testing procedures.
ARTICLE IN PRESS Tuberculosis of spine
Table 2
367
First and second line antituberculous drugs.
First-line agents
Second-line agents
Isoniazid (H) Rifampicin (rifampin) (R) Pyrazinamide (Z) Ethambutol (E)
Amikacin (AMK) Capreomycin (CPM) Ciprofloxacin Cycloserine (CS) Ethionamide Kanamycin (K) Ofloxacin P-Aminosalicylic acid (PAS) Streptomycin (S)
Table 3
Antituberculous ‘‘standard regimens’’.
Three drug regimen: (nos. ¼ months)
Davies PC (1996): 2HRZ 10HR (12 months) * Drug resistance case: 2S(E) HRZ 10HR (12 months) Moon et al. (1987, 1995, 1997, 2004): 12RHE(Z) (12 months)
Upadhyay et al. (1999): AIF 3HPaS, 3HPa (6 months) 3HPaS 6HPa (9 months) Four drug regimens: Yilmaz c et al. (1999): 2SRHZ 7RH (9 months) Metha IS et al. (2001): 2RHEZ 4RHE 6RH (12 months) Govender and Kumor (2003): 12 RHZE (12 months) Hassan (2003): 12 RHE (at least) (12 months) Sundaranaj et al. (2003): 4RHEZ, 14RHE (18 months)
Streptomycin Resistance is assessed by detection of 16S-RNA with ribosomal S12 protein and mutation in regions surrounding the nucleotides 530–912 in 16s-RNA, or by PCR, gyrase A (Gyr A) and ribosomal protein SR (rPSL) mutation. Isoniazid (INH) As this drug is a prodrug, being active only in the presence of an enzyme, Kat G gene mutation is studied. Rifampicin, ethambutol and ciprofloxacin The localized mutation in a RNA polymerase (rPOB) gene for rifampicin, mutation in embB codon 306 for ethambutol, and gyrase A and rPSL mutation for ciprofloxacin are shown.3,9,10 While the ideal antituberculous chemotherapeutic regimen is based on drug sensitivity of cultured M. tuberculosis, as already discussed, it is not always possible clinically to discover M. tuberculosis by the direct smear and/or on tissue slide. Furthermore, it is difficult to culture tuberculosis bacilli successfully from abscess and tissue aspirate at all. Hence the development of non-culture diagnostic and drug sensitivity techniques.9,10,31 To date, chemotherapy with currently available agents remains highly effective in extrapulmonary tuberculosis in children and adults, even in patients with concomitant HIV infection (Table 2)2,6,8–10,12,16,18 but, as with all chemotherapy, compliance with therapy is of the utmost importance. Measures, including directly observed therapy (DOT) to maximize compliance are essential as inadequate treatment and/or patient non-compliance are the most common causes of drug-resistant strains. Controversial issues regarding chemotherapy are:
drug combination formulae; duration of drug administration in surgical and nonsurgical management;
when to reassess drug efficacy i.e. slow , inadequate and non-responder, and
when to change the initial chemotherapy. Because patients differ and each has varying disease severity, and is infected with different bacterial strains,
Table 4
Suggested regimens for the drug-resistant cases.
Resistant drug
Suggested regimen
Duration of Therapy
Comments
INH, SM, PZA
RMP, PZA, EMB, AMK
6–9 months
INH, EMB (7SM)
RMP, PZA, OFL/CIP, AMK PZA, EMB, OFL/CIP, AMK PZA, OFL/CIP, AMK, Plus 2 EMB, OFL/CIP, AMK, Plus 2 OFL/CIP, AMK, plus 3
6–9 months
Estimated 100% response rate and o5% relapse rate Efficacy should be comparable to the above regimen Consider surgery
INH, RMP (7SM) INH, RMP, EMB (7SM) INH, RMP, PZA (7SM) INH, RMP, PZA, EMB (7SM)
18–24 months 24 months after Conversion 24 months after Conversion 24 months after Conversion
Consider surgery Consider surgery Surgery, if possible
INH ¼ isoniazid; SM ¼ streptomycin; PZA ¼ pyrazinamide; EMB ¼ ethambutol; RMP ¼ rifampin; AMK ¼ amikacin; OFL ¼ ofloxacin; CIP ¼ ciprofloxacin.
ARTICLE IN PRESS 368 they respond differently to treatment. Thus a standard ‘‘accepted regimen’’ is not applicable to every patient. Table 3 sets out the regimens adopted as standard by most physicians.2,3,6,7,15,26 It appears that short course chemotherapy (9 months)33,34 and intermittent chemotherapy for non-skeletal tuberculosis is as effective as old long course regimens of 12–18 months (Table 3).8–10,21,22,27,35 However, chemotherapy should be changed for non-responders i.e. in cases of serious clinical deterioration, notably the onset of paraparesis, untoward change in existing paraparesis or clear-cut radiographic extension of the spinal disease. In such cases misdiagnosis, drug resistance or improper combination of drugs has to be considered. For non-responders, initially the dose is increased for 3–4weeks. If this fails, therapy should be changed from a 3 drug to 4–5 drug regimen. Multi-drug resistant tuberculosis is defined on the basis of resistance to both INH and rifampicin. As the management for resistant tuberculosis is very complex, the best available expertise should be sought. However, it is best never to add
M.-S. Moon a single drug to failing regimen, because it creates an ideal condition for the development of resistance to the new medication. The WHO warned in 2004 that the super-strain tuberculosis bacilli which had emerged in Eastern Europe and middle Asia had 10 times higher rates of drug resistance compared to other areas. Around 80% of these ‘‘super strains’’ are resistant to 3–4 drugs. Hence consistent use of 2 or more effective agents at the time of initial chemotherapy is therefore essential.9,10,21,27 Drug resistance usually reflects the failure to choose an appropriate regimen and dosage or to ensure adherence to therapy (Table 4). Thus treatment should be initiated with at least two effective drugs to which the patient has never previously been exposed. For those who had received incomplete treatment with multiple drugs in the past, initial therapy with as many as 9 drugs has been used until sensitivity results became available. Surgery has a role in the treatment of multidrug resistant tuberculosis if the infection is sufficiently localized to be amenable to resection.
Figure 1 (A) Preoperative radiographs of L2-3 tuberculosis in a 38-year-old male showing markedly narrowed disc space with mild left lateral tilt of L2 body on L3. (B) Post-anterior fusion of L2-3 showing iliac bone graft and incomplete correction of the tilted L2. (C) Nine months post-operative radiographs showing re-tilting of L2 body over L3 despite the good consolidation of fused L2–3 bodies. (D) Twelve months post-operative radiographs showing further consolidation of the fused L2–3 bodies, but no further tilting of L2. This is an example of under-correction of the scoliotic spine at the time of anterior fusion. Some over-correction with bone graft for tuberculous scoliosis is preferably recommended to prevent retilting.
ARTICLE IN PRESS Tuberculosis of spine The author’s experience is that chemotherapy cannot be shortened by anterior radical surgery.10,15 For latent tuberculosis, combined anti-TNF-a therapy, hyperbaric oxygen and vasodilator drug therapy (PGE2: Opalmon) are recommended by the author to awake the dormant bacilli, because dormant bacilli do not respond even to sensitive drugs10,15 (Fig. 1), (pyrazinamide has been reported to kill a population of semidormant tubercle bacilli not affected by other antituberculous drugs).
Concomitant rheumatoid arthritis It must not be forgotten that immune suppressors e.g. steroids and TNF-a blocker [(TNF-a inhibitors) etanercept (infliximab, adulimumab)] can activate latent tuberculosis by inhibiting lymphocytic and macrophage activity. Thus for rheumatoid arthritis and related disease patients with latent tuberculous infection, anti-TNF-a treatment should be started at least after 3 weeks of anti-tuberculous chemotherapy, and for rheumatoid patients with active tuberculosis TNF-a agent therapy should be started at least after 2 months of anti-tuberculous chemotherapy (Fig. 1). As most cases of tuberculosis after biologic therapy represent reactivation rather than new onset disease,
369 screening before TNF-a blocker therapy is critical to prevent such relapse. However during anti-TNF-a therapy, postoperative rigor or fever other bacterial infection must be excluded.14,16 Extra- or intra-dural extra-medullary or intra-medullary tuberculoma There has been debate as to whether cord tuberculoma is a medical or surgical condition, because of the grave sequelae of surgical removal. The author recommends combined medical treatment after diagnostic biopsy; anti-tuberculous chemotherapy and anti-TNF-a blocker treatment (subcutaneous injection of etanercept, 25 mg twice weekly up to 6–8 weeks) that has degranulating effect. This can obviate the need for total excisional surgery for tuberculoma.
HIV and spinal tuberculosis Two key points to remember are that the chemotherapeutic effect is the same for HIV positive and negative patients nor does host immuno-competence influence the neural outcome in Pott’s paralytic patients. However, HIV infected patients appear to be more prone to adverse reactions to antituberculosis agents than HIV negative individuals.15
Figure 2 (A) Preoperative radiographs of active tuberculosis of L2–3 in a 32 year old female, managed with anterior radical surgery and triple chemotherapy. (B) Immediate postoperative radiographs showing regained disc height with two iliac bone grafts and restored lumbar lordosis. (C) Two month post-operative radiographs showing the re-collapsed disc space and absorbed bone graft. (D) Four months post-operatively with further corporeal destruction with graft collapse. (E) Radiographs 2 years and 10 months postoperatively showing solid fusion of L2–3 with mild kyphosis.
ARTICLE IN PRESS 370 The new HIV protease inhibitors14 have great potential for HIV patients with spinal tuberculosis. The author’s view is that primary prophylactic use of INH (300 mg/day for 12 months) for the HIV patients is more cost-effective in preventing tuberculosis recurrence than triple chemotherapy after tuberculosis infection. HIV positive patients with tuberculosis must be treated initially with at least three agents, the ultimate regimen being chosen according to culture and sensitivity testing. However, long-term suppressive therapy is not recommended.
Other drug therapies The use of the immunopotentiators such as oral levamisole and vaccines (BCG and DPT) is recommended as is combined use of NSAIDs with antituberculous agents, despite their gastrointestional side effects because they are effective in alleviation of back pain and might prevent bony destruction attributable to non-specific synovial membrane inflammation and inhibit or minimize the bone resorption by
M.-S. Moon prostaglandin E2 in the early course of disease (4–6 weeks).9,10,15,27
Surgery Chemotherapy alone cannot treat bone and joint destruction. Thus despite effective conservative treatment, surgery still has an important role in the management of spinal tuberculosis,9,10,23,25,29,36 but it cannot solve every problem! Surgery can have a place in the management of cold abscess, paraplegia and spinal deformity. In most cases, small and even medium-size cold abscesses rapidly resolve spontaneously with chemotherapy alone. In the author’s series, evacuation of abscesses did not alter patients’ general condition, and very often resulted in a persistent draining sinus.9,10,27 Routine drainage even for large abscesses is not recommended. A further factor to be considered is the patient’s aesthetic demand regarding spinal deformity that surgeons have to
Figure 3 (A) Preoperative radiographs of tuberculosis of T12-L-1 in a 2-year-old girl showing destruction of disc and vertebral bodies of T12 and L1 with relatively good bony contact. (B) Immediate postoperative radiographs showing the interspinous fixation wire between T12-L1. (C) Radiographs at 25 weeks post-operatively showing no further body destruction. (D) Radiographs at 1 year and 6 months post-operatively showing the consolidated T12-L1.
ARTICLE IN PRESS Tuberculosis of spine
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take into account. Hence the need to prevent or minimize spinal deformity. Hyperalimentation may be necessary to restore patients from a preoperatively physically debilitated state to their pre-morbid nutritional status. The goal should be to achieve a serum albumin level 43g/dl, an absolute lymphocyte count 4800/mm,3 and a 24-h urine creatinine excretion 410.5 mg in men and 45.8 mg in women. Predicting the final kyphotic angle A formula to predict the final kyphotic angle in the ambulant chemotherapy group, proposed by Rajasekaran and Shanmugasundaram in 1987 has been widely used.37 Accuracy has been reported to be as high as 90%, but Jain et al.36–38 in 2004 reported 77.64% accuracy. The author’s view is that the discrepancy was due to inaccurate estimation of initial vertebral body loss.32 Because accurate estimation of the pre-treatment vertebral body loss is impossible discrepancy of the final kyphosis reaches 6.11(30.5 0.2). Additionally the formula is only applicable to adult patients.
Spinal fusion Hong Kong surgeons stress that surgical fusion is essential to heal spinal tuberculosis, and if fusion has not been achieved, some of those cases are untreatable.9,10,33,34,39 My view is that bony and mixed replacement of the intervertebral space are not always synonymous with clinical healing, and that anterior radical surgery in adults to obtain cure through intercorporeal fusion is not justified in every case, because spontaneous fusion can be obtained by modern chemotherapy alone, and that cure can be also obtained without fusion.6,8,21,27,30,39 Fusion is desirable, but is not essential for every patient.22,35 In particular ‘block spine’ after anterior fusion in children is not desirable, as it accelerates the tuberculous kyphosis during growth.40,41 It has become clear that the only advantage of anterior radical surgery is a degree of deformity correction, a reduced tendency for deformity progression and stabilization of the diseased unstable segment. The author’s experience suggests that because of graft failure the procedure was not always successful in preventing kyphosis progression and/or correcting pre-existing kyphosis (Figs. 1 and 2) and that it is unwise to rely solely on the anterior radical surgery to correct the spinal deformity and to maintain correction. Because of this, the author uses posterior instrumentation surgery in addition to the anterior surgery.9,10,23,25 Huang et al. reported that video-assisted thoracoscopic surgery for tuberculosis of the dorsal spine was effective and safe.42 The current author’s view is that the procedure has significant practical limitations Figs. 3 and 4.
Stabilizing instrumentation surgery Timing of surgery has been an issue. Patients’ demands differ, even with the same severity of the disease at the same level at presentation. Some are more concerned about spinal deformity than others who choose the conservative treatment despite being well informed regarding disease prognosis.
Figure 4 (A) Preoperative AP and lateral radiographs of tuberculosis of L1-2 in a 7 year-old girl showing the completely destroyed L1-2 disc and bony contact of the remaining bodies of the destroyed L1 and L2 vertebrae. (B) Radiograph after interspinous wiring between L1 and L2.
Posterior spinal stabilization instrumentation surgery for the tuberculous spine has been controversial since its introduction by Moon et al.23,25 in 1981, particularly with regard to stage of disease or for what condition the spinal fixation should be carried out. Issues remain as to whether spinal instrumentation is essential to prevent the progress of kyphosis and to minimize the residual deformity, to prevent and/or treat the paralysis, and to allow early mobilization. Is it applicable to any spinal level? Because of the variability of the disease these questions are very difficult to confidently answer. Moon et al. found that posterior instrumentation surgery with or without anterior radical surgery was helpful in arresting the disease early, providing early fusion, preventing progression of and correcting kyphosis, and satisfying the cosmetic and aesthetic demands of patient with kyphosis. They therefore suggested that if progression of the kyphosis was thought likely, or the kyphosis was severe, posterior instrumentation should be performed as a first-stage procedure to correct or prevent progression of tuberculous kyphosis. Posterior instrumentation provided stability to the
ARTICLE IN PRESS 372 anterior graft, prevented graft collapse, and speeded graft incorporation.9,23 They utilized the British Medical Research Council (MRC) grading (mild, moderate and severe) of dorsolumbar kyphosis. Since 1990, they have recommended posterior instrumentation, using Rajasekaran and Shanmugasundaram’s residual kyphosis predicting formula37 e.g. the patient with 470% destructive vertebral body loss in the dorsolumbar spine will heal with 4301 residual kyphosis. According to Rajasekaran a vertebral body loss of 0.75 in the dorsal and dorsolumbar region and 1.0 in the lumbar region is an indication for surgery.37,43 Between 1997 and 2002, Moon27 recommended posterior instrumentation surgery to restore the sagittal alignment when there was vertebral body loss 440% and final residual kyphosis 4201. By doing so the author attempted to prevent development of the compensatory lumbar hyperlordosis and adjacent segment disease in cases of the conservative treatment. More recently, he has aimed to surgically restore the normal spinal alignment. The types of vertebral body collapse and development of kyphosis in the tuberculous spine differ at the various levels
M.-S. Moon of the spine; cervical, dorsal, dorsolumbar and lumbar. In the dorsal and dorsolumbar spines the pattern of vertebral collapse is kyphotic, whereas that in cervical and lumbar spines is rather vertical (telescoping).27,43 It follows that the indications for posterior instrumentation in the cervical and lumbar spines are different from the dorsal and dorsolumbar spines. On theoretical grounds posterior instrumentation surgery is recommended for very early disease, but latterly patients’ high aesthetic demands have tended to drive decision making rather than pure surgical indications. Sadly surgeons are gradually becoming cosmetic surgeons of the musculoskeletal system. Informed consent is essential!
Surgery for dorsolumbar tuberculosis with non-rigid kyphosis Jain et al.38 recommended operative stabilization of the kyphosis in the active stage of the disease when the patients had an initial vertebral body loss of two without giving a
Figure 5 (A,B) A 6-year-old boy with tuberculosis of T12–L2. (C) Lateral radiograph immediately after posterior segmental stabilization with two Rush nails and segmental wiring showing some correction of kyphosis. (D) Radiograph after anterior interbody fusion. (E) One year 9 month post-operative radiograph showing the fused block spine (T12–L2). (F) Two years 3 months after removal of the instrument showing the fused block.
ARTICLE IN PRESS Tuberculosis of spine reason, which would give a 66.51 final kyphosis (Y ¼ 5.51+30.51 2). The author’s view is that their recommendation was related to the late development of neurological compromise, rather than directly to the kyphosis. He does not agree, particularly in relation to aesthetic and neurological problems. Posterior stabilizing/corrective spinal surgery is most effective in the management of the active progressive kyphosis and established residual non-rigid kyphosis (Figs. 5–8), but kyphosis correction when there is the destructive body loss, will produce a bony gap in the anterior column. This gap should be reconstructed by an anterior strut graft,23,25 otherwise the posterior instrumentation will ultimately fail secondary to anterior column re-collapse.
Corrective spine surgery for severe rigid kyphosis Non-paralytic young patients tend to have very high aesthetic demands.23,25 This has led to the development of safe and effective corrective surgical procedures for the unsightly kyphosis,38,40,44,45 but each patient must be considered individually.
373 In healed severe tuberculous kyphosis at cord level, the bony anatomy is severely deformed and the cord in this area is ischemic, deformed and less mobile. It is often trapped in the deformed, narrow, hypoplastic canal and is adherent to the dura.29,36 There are several possible surgical procedures, ranging from single-stage to multistage procedures for rigid tuberculous kyphosis (Figs. 9–11)23,25,45,46 including posterior closing wedge osteotomy, decancellation procedure, and hemi- or total spondylectomy as a single stage operative procedure.15 While correction is possible, surgery is high risk, technically challenging and dangerous with high complication rates. Any decision to operate must weigh the high complication and reoperation rates against anticipated improvement. Therefore, an informed consent discussion should include the patient and his or her support group. Risks and complications must be fully understood, and the patient will ultimately choose between those risks and his/her quality of life. The surgeon should offer options and probability, but it is the patient who must bear the consequences of that decision.
Spinal column shortening The ideal size of the longitudinal spondylectomy—en-bloc hemi- or total spondylectomy—in the correction of the
Figure 6 (A,B) A 25-year-old female with severely damaged T11 body due to tuberculosis of T10–T12 with moderate kyphosis. (C,D) Radiographs after H-instrumentation (T9–L2) showing complete correction of kyphosis with huge anterior corporeal gap between T10–T12 (phantom vertebra phenomenon). (E) Post-anterior interbody fusion showing large bone graft between T10–T12. (F) Radiograph 2 years after anterior fusion showing solidly fused block vertebrae. No loss of correction of kyphosis is seen.
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Figure 7 (A,B) Preoperative radiographs of a 29-year-old female with tuberculosis of T10–T12 and wedge shaped destroyed T11 body and narrowed discs. (C,D) Radiographs after Harrington rodding between T9–L1 and anterior fusion showing the two iliac grafts between T10–T12 and good correction of kyphosis. (E,F) Three month post-operatively radiographs showing good consolidation of the grafts with minimal increase in kyphosis. (G,H) Two years after initial surgery and removal of Harrington rods showing complete consolidation of the grafts.
spinal deformity in relation with the cord function has rarely been discussed, and there is no consensus view. In the normal spine, cord length, spinal canal and anterior spinal column length are equal, while in the idiopathic adolescent scoliosis the anterior column length is longer than the canal length. Therefore, if the scoliotic spinal column is corrected by longitudinal distraction alone, the cord will be stretched, which may result in paralysis. When en-bloc total spondylectomy is performed for a spine tumour, the preoperative relationship of the cord and spinal column length should be maintained. Sometimes the spinal column can be lengthened or shortened at the time of anterior column reconstruction and instrumented stabilization; in the former the cord will be stretched and in the latter the cord will be axially compressed which results in cord ischemia leading to paralysis. Kawahara et al.47 reported that the dural kinking was not observed in any patients undergoing a column shortening procedure; 22.2% (7 mm74–10 mm) of the corpectomy defect in the 40 patients. In none was neurological
degradation observed postoperatively. However, 2 of the 3 preoperative Frankel B paraparetics did not recover, while one recovered to Frankel E. Seven out of 13 preoperative Frankel C paraparetics improved to E, 5 improved to D, and in one there was no improvement. Six Frankel D paraparetics improved to E in all. They concluded that 20% column shortening in spinal tumours might be safe. Kobayashi et al.24 reported the results in dogs of longitudinal column shortening surgery. Up to 7.2 mm shortening produced no morphological change in the dura mater or spinal cord. If the shortening was between 7.2 and 12.5 mm the cord remained straight in spite of ‘ruffling’ of the dura mater. Above 12.5 mm of shortening, the cord became kinked. Abnormal evoked potentials were recorded with column shortening of 15 and 20 mm, causing incomplete paralysis of the hind limbs in 1 of 3 and 3 of 4 dogs, respectively. With column shortening of 5, 10, 15 and 20 mm cord blood flow changed to 146%, 160%, 102% and 93% of the preoperative blood flow, respectively. Column shortening less than 15 mm significantly increased the diameter of the anterior spinal artery,
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Figure 8 (A) A 30-year-old paraparetic female with tuberculous kyphosis of 431 at L1–2. (B) After H-distraction instrumentation, kyphosis decreased to 201. (C) Four weeks later AIF was performed. (D) Two years post-operatively following removal of Harrington instrumentation.
Figure 9 A 26-year-old female with T12–L3 tuberculous kyphosis (981): Pre (A) and post-op (B) lateral radiographs with H-distraction rods (961 kyphosis-331).
while shortening over 15 mm decreased the anterior flow. They concluded that the safety limit for column shortening was 12.5 mm (62.5%).
Tanaka et al.48 reported their results of the cranial half shortening spondylectomy (14–23 mm, mean 20 mm) of the L1 body for adult patients with tethered cord syndrome;
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Figure 10 (A) Preoperative severe tuberculous kyphosis of 1121. (B) Radiograph taken 1 month after application of halo-pelvic traction, anterior release and anterior multiple rib grafts showing the well-corrected kyphosis down to 761. (C) Radiograph 12 months post-operatively showing well-maintained correction of the sagittal curve.
there were symptomatic improvements after spinal column shortening. The procedure was found safe and effective, but they did not discuss spondylectomy size.
Thus in children, posterior instrumentation is thought to be the best procedure with or without posterolateral fusion, utilizing several tether devices.
Tuberculous kyphosis in children
Quadriplegia or paraplegia with or without kyphosis
In children spontaneous intercorporeal fusion rarely occurs during chemotherapy. I occurs later after the cure of the tuberculosis at lower rates than in adults. This has not been satisfactorily explained. Study of BMP and anti-BMP factors in the tissue around the tuberculous lesion may clarify the cause. In most children there was a gradual increase of spinal deformity in spite of disease cure, when the growth plates were destroyed in either unfused and fused vertebrae. When the unfused segment was unstable, the deformity progressed more rapidly than that of the fused block vertebrae. The unsightly hunchback residual kyphosis can be distressing to patients, their parents and surgeons alike. Initially in the early 1970s the author used posterior interspinous wiring and fusion. This was followed by interspinous wiring and cementation to stabilize the involved segment and to arrest the posterior spinal element growth. Both techniques failed because of loosening of wires and cement (Figs. 3 and 4),15 and they were succeeded by posterior instrumentation (Fig. 5).23,25 Posterior instrumentation in the management of the pediatric tuberculous kyphosis can contribute to growth correction of the kyphosis by growth arrest of the posterior column when applied before age 10–11 years.12,15
There are three main causes of paralysis
cord compression by abscess and granulation tissue; cord compression by sequestrum and the posterior bony edge of the vertebral body at the level of the kyphosis;
bony canal stenosis of the deformed spine above the level of the kyphosis. The management of Pott’s paralysis and mild, moderate or severe kyphosis is still controversial. This author made treating the paralysis the priority, and did not aim to correct the kyphosis simultaneously. There are two approaches to manage paralysis, conservative medical or surgical. The timing, whether immediate or delayed, for decompression surgery under chemotherapeutic cover is still debated. Slowly progressive paralysis due to abscess and granulation tissue and in the early stage can be effectively managed by chemotherapy alone38,42,45 which cannot only cure the disease but also the neural deficit without surgical decompression regardless of the severity of kyphosis. However, if the paralysis does not improve within
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Figure 11 (A) Severe tuberculous kyphoscoliosis at T10–T12 in a 14-year-old boy with Frankel C paralysis. (B) Corrected kyphosis after bilateral costo-transversectomy and posterior segmental instrumentation with Rush nail and segmental wiring. (C) Three rib grafts were inserted between T10–L1 to fill the anterior column defect. (D) Corrected deformity was well maintained up to 7 months with no graft failure.
maximum of 4–6 weeks after commencement of chemotherapy, decompression surgery should be undertaken. When there is acute onset paraplegia with rapidly worsening neurology by bony cord compression and fibrosis, and chronic cord compression within the narrow canal surgical decompression is indicated. In the author’s experience, posterior instrumentation surgery alone regardless of the disease stage and/or severity of deformity can hasten the neurological recovery without direct decompression surgery by stabilizing the unstable diseased segment (Fig. 12).
Extent of stabilization and timing of implant removal Long rodding immobilizes normally mobile segments and may later cause these segments to stiffen and degenerate (Figs. 5,6,8,11). Therefore the author normally removes the rods after solid intercorporeal fusion about 9 months postoperatively to remobilize these instrumented segments38,45 and over the last 15 years has carried out short rather than long segment posterior instrumented stabilization before anterior fusion.
In children with unacceptable tuberculous kyphosis, posterior instruments should be left until maturity to maximize gradual growth correction of the deformity due to the tethering effect of the implants.
Bacterial response to implant and chemotherapy Until implants such as titanium cages, screws and rods, P.V.P and ceramic cups in the tuberculous focus were found to be harmless, there was concern that the use of such materials would hinder the healing of the tuberculosis, or cause arrested or quiescent infection to flare up. This has been shown not to be a concern.7,10,18 M. tuberculosis has biologically very specific behavioral characteristics which differ from pyogenic bacteria. A good understanding of these characteristics is vital as is knowledge of bacterial response to implanted material and chemotherapy.9,10,18 M. tuberculosis lesions represent a planktonic form which reproduces slowly, producing minimal adhesion molecules and slime, and occasionally becomes dormant. Thus, M. tuberculosis has little tendency to adhere to implants that can be safely used in tuberculous lesions, but they do form a nidus to perpetuate tuberculous infection. However,
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Figure 12 (A) Preoperative plain AP and lateral radiographs in a 67-year-old type B Pott’s paraplegic patient with a tuberculous lesion at T10–T11 and wedged T12 vertebral body. Triple chemotherapy was started immediately. (B) AP and lateral radiographs after posterior instrumentation between T8–L1 showing some improvement in sagittal curve and well placed pedicle screws. 24 h after instrumentation there was complete neurological recovery without additional surgical decompression. (C) Six month post-operative radiographs showing consolidated vertebral bodies of T10–11. (D) Pre-operative MRI showing destroyed disc between T10–11 and partially destroyed vertebral bodies of T10 and T11 and pre-vertebral and epidural abscesses compressing the cord anteriorly. (E) MRI taken 1 month after instrumentation showing the resolved epidural abscess.
in HIV positive patients the use of biomaterials in the infected foci is inappropriate, because they are susceptible to a variety of other opportunistic infections.13,16,17,23,45 Additionally bacteria adhere less to titanium than stainless steel,18–20,28,44,49,50–52 because titanium has a less electrochemically active oxide surface compared to stainless steel, which has a higher surface free energy (440 m N/ m) and hence more available ligands for binding with cells both bacterial and tissue competing for the biomaterial surface. It follows that stainless steel implants should not be used for spinal stabilization.
Conclusions Spinal tuberculosis is treatable with the presently available therapeutic agents and surgical techniques. Chemothera-
peutic agents are the mainstay of curative treatment with surgery supplementary, i.e. spinal tuberculosis is essentially a medical condition. Surgery has a place in those patients with structural and/or neurological complications.
References 1. Adis Internat Editors; Stop the tuberculosis epidemic. Med Prog 15–21, 1994. 2. Bellin E. Failure of tuberculosis control—a prescription for change. J Am Med Assoc Kor 1994:10–1. 3. Bloch AB, Cauthen GM, Onorato IM, Dansbury KG, Kelly GD, Driver CR, et al. Nationwide survey of drug-resistant tuberculosis in the United Sates. J Am Med Assoc—Kor 1994: 27–33. 4. Davies PDP. Tuberculosis in the elderly–epidemiology and optimal management. Med Prog 1996:25–8.
ARTICLE IN PRESS Tuberculosis of spine 5. KenYan/British Medical Research Councils. Tuberculosis in Kenya 1984:a third national survey and a comparison with earlier surveys in 1964 and 1974. Tubercle 1989;70:5–20. 6. Konstam PG, Blesovsky A, The ambulant treatment of spinal tuberculosis. Brit J Surg. 50:26–38. 7. Kumar K. Tuberculosis of spine (natural history of disease and its judicious management). J. Western Pacif Orthop Assoc 1988; XXV-1:1–8. 8. Moon MS, Yoo CI. Ambulatory treatment of the tuberculosis spine in children J. Kor Orthop Assoc 1970;5(3):155–62. 9. Moon MS. Tuberculosis of the spine; controversies and new challenges—spine update. Spine 1997;22(15):1791–7. 10. Moon MS. Managing tuberculosis of the spine. Med Prog 2004;31(12):593–602. 11. Weyer K, Fourice PB. Die epidemiologic van tuberculose in Suider-Afrika. Contin Med Educ 1989;7:239–47. 12. China Tuberculosis Control Collaboration. The effect of tuberculosis control in China. Lancet 2004;364:417–22. 13. Klepser MZ, Klepser TB. Opportunistic infections in HIV. Med Prog 1997;1:17–23. 14. Nelson MH, HIV-Protease inhibitors; Viral resistance, pharmacokinetic boosting, and medication adherence, US Pharmacist. HS 2006;1:5–12 15. Moon MS. Development in the management of tuberculosis of the spine. Curr Orthop 2006;20:132–40. 16. Von Roenn JH. Management of HIV-related body weight loss. Med Prog 1995:31–7. 17. Weinstein MA, Esmont FJ. Infections of the spine in patients with human immunodeficiency virus. J Bone Joint Surg 2005; 87A:604–9. 18. Yew WW, Chau CH. New antitubercular drugs. Med Prog 1997: 13–5. 19. Arens S, Schlegel U, Printzen G, et al. Influence of materials for fixation implants on local infection. An experiment of steel versus titanium DCP in rabbits. J Bone Joint Surg 1996;78B: 647–51. 20. Cunliffe D, Smart CA, Alexander C, Vulfson EN. Bacterial adhesion at synthetic surfaces. Appl Environ Microbiol 1996; 65(11):1995–5002. 21. Moon MS, Kim I, Woo YK, Park YO. Conservative treatment of tuberculosis of the thoracic and lumbar spine in adults and children. Int Orthop (SICOT). 1987;11:315–22. 22. Tuli S. Tuberculosis of the skeletal system (bones, joints, spine and bursal sheaths), 3rd ed. New Delhi: Jaypee Brothers Medical Publishers Pvt Ltd.; 2004. 23. Moon MS. Combined posterior instrumentation and anterior interbody fusion of the thoraco-lumbar spine. Curr Orthop 1991;5:177–9. 24. Kobayashi T, Kawahara N, Murakami H, et al. An experimental study on the influence of spinal shortening on the spinal cord. Japan Orthop Assoc Congress Book, 2005; 3A-P9-1. 25. Moon MS, Woo YK, Lee KS, Ha KY, Kim SS, Sun DH. Posterior instrumentation and anterior interbody fusion for tuberculosis kyphosis of dorsal and lumbar spine. Spine 1995;20:1910–6. 26. Moon MS, Lee MK. A study on the change of the kyphosis of the tuberculous spine in children following ambulatory treatment. J Kor Orthop Assoc 1971;6(3):203–8. 27. Moon MS, Moon YW, Moon JL, Kim SS, Sun DH. Conservative treatment of tuberculosis of the lumbar and lumbosacral spine. Clin Orthop 2002;398:40–9. 28. Oga M, Arizono T, Takasita M, et al. Evaluation of the risk of instrumentation as a foreign body in spinal tuberculosis clinical and biological study. Spine 1993;18:1890–4. 29. Moon MS, Ha KY, Sun DH, Moon JL, Moon YW, Chung JW. Pott’s paraplegia-67 cases. Clin Orthop 1996;323:122–8. 30. Pui NH, Mitha A, Rae WID, Corr P. Diffusion-weighted magnetic resonance imaging of spinal infection and malignancy. J Neuroimag 2005;15(2):164–70.
379 31. Jambhekar NA, Kulkarni SP, Madur BD, Agarwal S, Rajan MGR. Application of the polymerase chain reaction on formalin-flixed, paraffin-embedded tissue in the recognition of tuberculous osteomyelitis. J Bone Joint Surg 2006;88B:1097–101. 32. Jutte PC, Van Altena R, Pras E, Thijn CJ. Cause of misdiagnosis and mistreatment of spinal tuberculosis with radiotherapy in nonendemic area: a pitfall in diagnosis and treatment: hazards of radiotherapy on the tuberculous lesion. Spine 2005;30(11): E300–4. 33. Upadhyay S, Saji M, Sell P, et al. The effect of age on the change in deformity after anterior debridement surgery for tuberculosis of the spine. Spine 1996;21:2356. 34. Upadhyay S, Saji M, Sell P, et al. Spinal deformity after childhood surgery for tuberculosis of the spine: a comparison of radical surgery and debridement. J Bone Joint Surg 1994;76B:91. 35. Tuli S. Results of treatment of spinal tuberculosis by ‘‘middle path’’ regime. J Bone Joint Surg 1975;57B:13. 36. Moon MS, Moon JL, Moon YW, et al. Pott’s paraplegia in patients with severely deformed dorsal or dorsolumbar spines: treatment and prognosis. Spinal Cord 2003;41:167–71. 37. Rajasekaran S, Shanmugasundaram TK. Prediction of the angle of gibbus deformity in tuberculosis of the spine. J Bone Joint Surg (Am) 1987;69:503–9. 38. Jain AK, Aggarwal PK, Arora A, Singh S. Behaviors of the kyphotic angle in spinal tuberculosis. Int Orthop 2004;28(2): 110–4. 39. Puig Guri J. The formation and significance of vertebral ankylosis in tuberculous spine. J Bone Joint Surg 1947;29: 136–47. 40. Fountain S, Shu L, Yau A, Hodgson A. Progressive kyphosis following solid anterior spine fusion in children with tuberculosis of the spine. J Bone Joint Surg 1975;57A:1104. 41. Schulitz K, Kothe R, Leong J, Wehling P. Growth changes of solidly fused kyphotic bloc after surgery for tuberculosis:comparison of four procedures. Spine 1997;22:1150. 42. Huang T-J, Hsu RW-W, Chen S-H, Liu H-P. Video-assisted thoracoscopic surgery in managing tuberculous spondylitis. Clin Orthop 2000;379:143–53. 43. Rajasekaran S. The problem of deformity in spinal tuberculosis. Clin Orthop 2002;398:85–92. 44. Ha KY, Chung YG, Ryoo SJ. Adherence and biofilm formation of Staphylococcus epidermis and mycobacterium tuberculosis on various spinal infections. Spine 2004;29(24):1–6. 45. Kalra KP, Dhar SB, Shetty G, Dhariwal Q. Pedicle subtraction osteotomy for rigid posttuberculous kyphosis. J Bone Joint Surg 2006;88B:925–7. 46. Yau A, Hsu L, O’Brien J, Hodgson A. Tuberculosis kyphosis; correction with spinal osteotomy, Halo pelvic distraction, and anterior and posterior fusion. J Bone Joint Surg 1974;56A:1419. 47. Kawahara N, Tomita K, Murakami H, Akameru M, Hata T, Spinal shortening in total enbloc spondylectomy. Japan Orthop Assoc Congress Book, 2005; 3-A-P9-4. 48. Tanaka Y, Kokubun S, Ozawa K, et al. Shortening spinal osteotomy for tethered cord syndrome. Japan Orthop Assoc Congress Book, 2005. 3A-P9-2. 49. An YH, Stuart GW, McDowell CJ, McDaniel SE, Kang O, Friedman RJ. Prevention of bacterial adherence to implant surfaces with a crosslinked albumin coating in vitro. J Orthop Res 1996;14: 846–9. 50. Kim YY, Yoon YS. Replacement arthroplasty using the Charnley prosthesis in old tuberculosis of the hip. Internet Orthop (SICOT) 1979;3:81. 51. Sanzen L, Linder L. Infection adjacent to titanium and bone cement implants: an experimental study in rabbits. Biomaterials 1995;16:1273. 52. Sheehan E, McKenna J, Mulhall KJ, Marks P, McCormack D. Adhesion of staphylococcus to orthopedic metals, an in vivo study. J Orthop Res 2004;22:39–43.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 380–385
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INHERITED DISORDERS
The arthropathy of haemochromatosis and the role of the orthopaedic surgeon L.M. Regan, T. Nissanthan, M.B. Davies Sheffield Department of Orthopaedic Surgery, Northern General Hospital, Herries Road, Sheffield S5 7AU, UK
KEYWORDS Haemochromatosis; Arthropathy
Summary Haemochromatosis is thought to be an uncommon condition which may present as a disabling symmetrical polyarthropathy. Early diagnosis can prolong life by preventing the development of co-morbidities. & 2007 Elsevier Ltd. All rights reserved.
Introduction
Iron homeostasis—physiology
Haemochromatosis was first described in 1865 by Tousseau in a diabetic patient with the characteristic bronzed skin pigmentation and the stigmata of liver cirrhosis. It is characterised by abnormal deposition of iron in tissue parenchyma throughout the body. Despite affecting 1 in 250 people within Northern Europe,1,2 haemochromatosis is still erroneously considered to be a rare condition. It can be divided into two broad categories: primary which predominantly occurs in the Caucasian population and is caused by a genetic mutation and secondary to a haematological disorder such as sideroblastic anaemia, myelofibrosis, excess blood transfusion therapy and porphyria cutanea tarda. Schumacher first described an associated arthropathy in 1964.3 This had been regarded as a rheumatological problem for a number of years, but the need for orthopaedic intervention was identified. This article describes the typical features of the arthropathy and the management of primary haemochromatosis.
Approximately, 20 mg/day of iron is needed by the bone marrow to maintain erythrocyte production. The main source is from the destruction of mature erythrocytes and it is transported to the marrow by binding to plasma transferrin. Up to 2 mg/day of iron is ingested and transferred to the plasma component or stored as ferritin in the liver. This iron store is only depleted when erythrocytes come to the end of their life span. This slow consumption of iron stores is the reason that excess iron in the body may easily accumulate (Fig. 1).
Corresponding author. Tel.: +44 114 2714956;
fax: +44 114 2266371. E-mail address:
[email protected] (M.B. Davies). 0268-0890/$ - see front matter & 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2007.09.002
Iron homeostasis—pathophysiology Iron only causes tissue damage when supply exceeds demand. The mechanism of tissue injury leading to arthropathy is unclear, but there have been many proposed theories including stimulation of collagen production by excess iron, and lipid peroxidation of organelles. There may be even be an inflammatory component as in one study, finely granular iron deposition was seen in macrophages located within synovium.4 The end result of tissue injury is the deposition of iron within organ parenchyma.
ARTICLE IN PRESS The arthropathy of haemochromatosis and the role of the orthopaedic surgeon
Figure 1
Iron homeostasis.
Genetics Primary haemochromatosis is an autosomal recessive condition due to different mutations in the HFE gene on chromosome 6; C282Y (tyrosine is substituted for cysteine at amino acid position 282) and H63D (aspartic acid is substituted for histidine in position 63). The more significant is C282Y which leads to an increased absorption of iron from the gut resulting in progressive iron overload in parenchymal organs such as the joints, liver, pancreas, pituitary gland, heart and skin. The lesser mutation, H63D, also leads to an increase in iron absorption but is not as destructive. Although the genetic defect is present at birth, it rarely manifests until late adulthood, and even then predominantly in homozygotes. Men are nine times more at risk than women, probably due to the protective effect of menstrual loss of iron.
Figure 2
381
The structure of articular cartilage.
tends to be most prominent on sun-exposed skin, particularly on the face. Due to earlier diagnosis, only 8% of patients display the distinctive triad on presentation.6 The most common presentation (84%) is with features of chronic liver disorder.6 Thus, a typical patient may present with abdominal pain and moderate hepatomegaly. Joint pain is the next most frequent presenting complaint (11% of patients)6 (Table 1). Those diagnosed late are more likely to present with diabetes (due to destruction of the endocrine pancreas), a multitude of cardiac presentations due to iron deposition in the Bundles of His and Purkinje fibres such as congestive cardiomyopathy, conduction defects and arrhythmias or hepatocellular carcinoma. Other endocrine effects include decreased gonadotrophin production and resultant secondary infertility due to pituitary impairment, which can lead to diffuse osteoporosis.
Histopathology of arthropathy
Arthropathy
Sheldon was the first to note that haemosiderin deposits were present in the articular cartilage and synovium of patients with haemochromatosis.5 Initially the underlying biochemical pathology was not understood, but it is now clear that the chronic excess of unbound circulating iron has a toxic effect on chondrocytes. This leads to the characteristic features of the arthropathy, narrowing of the zone of calcified cartilage, splitting and avulsion of articular cartilage at the level of the tidemark (Fig. 2), calcium pyrophosphate deposition and eventually osteonecrosis.4
Arthropathy associated with primary haemochromatosis occurs in approximately 50% of patients. The symptoms are usually chronic,7 but the arthropathy may present acutely with a hot, swollen joint that can mimic gout or acute rheumatoid arthritis. In up to 72% of cases of acute joint symptoms, there may be radiographic features of chrondrocalcinosis with calcium pyrophosphate crystals in aspirated joint fluid accounting for this presentation and thus, refuting the diagnosis of gout.7,8 The arthropathy is usually non-inflammatory and degenerative, affecting the small joints (hands) first and the larger joints (hips, knees, ankles) years later. The characteristic presentation is of a symmetrical polyarthropathy, which may lead to the erroneous diagnosis of rheumatoid disease. However, the characteristics of rheumatoid disease such as synovial thickening, ulnar deviation of the fingers and rheumatoid nodules are not present, and the rheumatoid factor test is negative and a synovial biopsy usually does not show inflammatory changes.
Clinical features When haemochromatosis was first described, the typical clinical features included the triad of cirrhosis, diabetes mellitus and hyperpigmentation of the skin. The distinctive hyperpigmentation of haemochromatosis is a result of iron deposition in the skin causing an increased production of melanocytes. This brown, bronze or slate grey appearance
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Table 1
L.M. Regan et al.
Clinical features of haemochromatosis.
Symptoms and signs of haemochromatosis
Findings at investigation
Symptoms (frequency %)
Signs
Abdominal pain (16%) Joint pain (11%) Weakness (9%) Symptoms of diabetes (2%) Frequent infections Impotence Loss of libido Infertility Breathlessness on exertion Increased skin pigmentation Loss of body hair Menstrual irregularity
Hepatomegaly Hand/wrist arthritis Skin pigmentation Testicular atrophy
Abnormal liver function tests HFE gene testing Excess stainable iron on liver biopsy Increased liver density on CT Chondrocalcinosis Increased transferrin
capacity measures how well iron is transported around the body. Serum ferritin levels can indicate the amount of iron in the liver. Liver function tests may confirm chronic liver disease and in times past, in conjunction with increased liver density on CT, would have led to a liver biopsy to look for excess stainable iron. However, the discovery of the HFE mutation has altered the way the condition is diagnosed. Genetic tests for the C282Y and H63D mutations can confirm the diagnosis and identify asymptomatic patients.
Radiographic features
Figure 3 Plain radiographs demonstrating joint space narrowing and claw osteophyte formation typical of the arthropathy of haemochromatosis involving the index and middle metacarpophalangeal joints.
Classically the arthropathy of haemochromatosis causes a decreased range of motion at the index and middle metacarpophalangeal joints (Fig. 3). In a study of 31 patients with haemochromatosis, 30 patients showed this distribution of arthropathy. Nine patients also displayed a comprehensive arthropathy affecting the larger joints.7 In many cases, joint pain may be the only noticeable symptom suggestive of the disorder. Sixteen out of 25 patients in another study8 had reported symptoms of arthralgia up to 3 years before haemochromatosis was diagnosed.
Investigations A comprehensive haematinics profile may suggest the diagnosis of haemochromatosis. In primary haemochromatosis, the serum iron concentration is usually greater than 150 mcg/dl. The transferrin saturation test can detect how much iron is bound to transferrin and total iron binding
In general, the arthropathy follows a degenerative rather than inflammatory pattern and the radiographic features are similar to osteoarthrosis, i.e. joint space narrowing, subarticular cyst formation, sclerosis and osteophyte formation. In contrast to osteoarthrosis, these changes follow a symmetrical pattern. Moreover, chondrocalcinosis is known to affect up to two-thirds of patients with haemochromatosis-associated arthropathy7 and there may be radiographic features of this inflammatory process in menisci of the knee, the triangular fibrocartilaginous complex, intervertebral discs of the lumbar spine and in the symphysis pubis.9 Involvement of the index and middle metacarpal heads is characteristic. Early features in the hand include subarticular cysts in the metacarpal head surrounded by a sclerotic border. These cysts can progress and extend into the joint space causing narrowing of the joint space and claw osteophyte formation (Fig. 3). In addition, there may be enlargement of the metacarpal heads and the proximal carpal row and the distal radio-ulnar joint may also be affected with cyst formation. In the foot and ankle, radiograph changes degenerative joint disease of the ankle, naviculocuneiform and metatarsophalangeal joints.2,10 Larger joints such as the shoulder and elbow are less frequently affected, and they typically demonstrate less dramatic sclerosis and cyst formation.7 In the hip, a wedgeshaped subchondral radiolucency deep to the articular surface of the femoral head is thought to be pathognomonic
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predominantly male, in the fourth or fifth decade of life exhibiting a bilateral, symmetrical joint disease, which has implications when considering primary arthroplasty surgery especially with symmetrical joint involvement. As the early diagnosis of haemochromatosis leads to a normal lifespan, patients require revision arthroplasty surgery. Such literature as there is tends to focus on total hip arthroplasty (THA). One paper reported that 10 out of the 28 patients with an average age of 60.6 years required THA.16 In a series of five patients with hip arthropathy of haemochromatosis, three of these patients went on to THA.15 The success of these arthroplasties is unclear. There is only one series looking at the outcome of THA for haemochromatosis.4 Over a 10-year period, 19 total hip
Figure 4 Plain AP pelvic and lateral hip radiographs demonstrating the arthropathy and how the appearances could be mistaken for early rheumatoid disease.
of primary haemochromatosis.11 Another prominent feature in the hip was the dense calcification of the fibrocartilage of the articular labrum7 (Fig. 4).
Practice points
Affects 1 in 250 Northern Europeans Predominantly male Presents in middle age Index and middle MCPJ commonly affected Symmetrical polyarthropathy
Medical management Venesection continues to be the mainstay of treatment. A unit of blood of 450 ml contains 220 mg of iron. Blood is taken weekly until ferritin concentration is less than 20 mcg/l and the target transferrin saturation level is below 50%. This may take years to achieve. Once achieved, maintenance therapy of venesection every 4 months is needed to maintain normal levels. At this stage, patients may then have a normal life expectancy provided that they have not developed other chronic complications such as diabetes, cirrhosis or cardiac involvement.12 Interestingly, venesection does not appear to affect the symptoms of arthralgia and these symptoms may even manifest after therapy has been commenced.8,13
Orthopaedic management Aside from the holistic approach to patient management and establishing the diagnosis of haemochromatosis, the orthopaedic management of diseased joints is poorly documented,2,4,10,13–15 but seems to reflect current practice for the surgical management of other arthropathies. The key difference lies in the age and activity levels of the patient population that suffer from haemochromatosis. They are
Figure 5 Plain radiographs demonstrating the ankle arthropathy.
ARTICLE IN PRESS 384 arthroplasties were performed on 15 patients with hip arthropathy. The average patient age was 59 years. Patients were assessed using the Hospital for Special Surgery hip score (maximum score 40 points). Patients experienced an average improvement in function from 15 to 30 points after surgery. One patient had to undergo a revision due to acetabular loosening; the focus of a more recent study. Lunn et al.17 compared a group of primary THA with a group of revision hip arthroplasties and found that patients who are homozygous for the C282Y mutation of the HFE gene appear to have an increased risk of developing aseptic loosening. Total knee arthroplasty (TKA) for haemochromatosis arthropathy has not been specifically studied. Two papers reviewed TKA with a variety of prostheses and fixation techniques in patients under the age of 50 years14,18 including small numbers with haemochromatosis (2–10%). No comment was made as to whether the disease process was associated with poor results or early failure. Similarly, the management of haemochromatosis ankle arthropathy has been briefly discussed in the literature. Conventional wisdom has very narrow indications for total ankle arthroplasty (TAA) especially in younger, more active patients, and generally, foot and ankle surgeons try and avoid bilateral ankle fusions, particularly if there are
L.M. Regan et al. degenerative changes within the midfoot. Two papers address TAA for this condition. Hintermann performed TAA on two patients with haemochromatosis out of a total of 48 patients19 and while the results were good, no specific mention was made of the two cases. Another paper specifically addressed TAA in haemochromatosis. Four male patients (average age 60 years) underwent five total ankle arthroplasties.2 All patients had bilateral, symmetrical ankle arthropathy with radiographic uniform loss of tibiotalar joint space with other degenerative changes (Fig. 4). Interestingly, three of the four patients in this latter series had undergone other large joint arthroplasties: hip, knee and elbow (Figs. 5 and 6). There is even less in the literature regarding the upper limb. While involvement of the shoulder, elbow and wrist, is well documented, the orthopaedic management is not clear. There is a case report using Swanson’s arthroplasty for metacarpophalangeal joint arthropathy.13
Discussion Haemochromatosis has long been considered a general medical condition. While this remains true, not infrequently, it may present as an arthropathy. Given that early diagnosis of the condition leads to an improved patient prognosis, any middle-aged patient with a symmetrical arthropathy should be investigated for haemochromatosis by the orthopaedic surgeon. There is a range of surgical options available for managing diseased joints including arthroplasty, although some evidence may show that the disease predisposition to aseptic loosening.17 Therefore, it is clear that further research and audit of the outcome of surgery for this arthropathy is essential.
References
Figure 6 The radiographic appearances of the arthropathy of haemochromatosis affecting the elbow.
1. McCurdie J, Perry JD. Haemochromatosis and exercise related joint pains. Br Med J 1999;318:449–51. 2. Davies MB, Saxby T. Ankle arthropathy of hemochromatosis: a case series and review of the literature. Foot Ankle Int 2006;27(11):902–5. 3. Schumacher HR. Hemochromatosis and arthritis. Arthritis Rheum 1964;7:41–50. 4. Montgomery KD, Williams JR, Sculco TP, Dicarlo E. Clinical and pathological findings in hemochromatosis hip arthropathy. Clin Orthop 1998;347:179–87. 5. Sheldon JH. Haemochromatosis. London: Oxford University Press; 1935. 6. Adams PC, Kertesz AE, Valberg LS. Clinical presentation of hemochromatosis: a changing scene. Am J Med 1991;90:445–9. 7. Dymock IW, Hamilton EBD, Laws JW, Williams R. Arthopathy of hemochromatosis: clinical and radiological analysis of 63 patients with iron overload. Ann Rheum Dis 1970;29:469–76. 8. Faraawi R, Harth M, Kertesz A, Bell D. Arthritis in hemochromatosis. J Rheumatol 1993;20:448–52. 9. Wardle EN, Patton JT. Bone and joint changes in haemochromatosis. Ann Rheumatol Dis 1969;28:15. 10. Baker ND, Jahss MH, Leventhal GH. Unusual involvement of the feet in hemochromatosis. Foot Ankle 1984;4(4):212–5. 11. Axford JS, Bomford AB, Revell P, Watt I, Hamilton EDB. A case of haemochromatosis arthritis. Br J Rheumatol 1992;31:547–53.
ARTICLE IN PRESS The arthropathy of haemochromatosis and the role of the orthopaedic surgeon 12. The Haemochromatosis Society UK. An iron overload disorder—what is the treatment? [Online] Available: /http://www. ghsoc.org/home.htmlS; 2005 [accessed 20.12.2006]. 13. Monroe Laborde J, Green DL, Askari AD, Muir A. Arthritis in hemochromatosis: a case report. J Bone Joint Surg Am 1977; 59-A:1103–7. 14. Dalury DF, Ewald FC, Christie MJ, Scott RD. Total knee arthroplasty in a group of patients less than 45 years of age. J Arthroplasty 1995;10(5):598–602. 15. Lecoules S, el Maghraoui A, Damiano J, Lechevalier D, Magnin J, Eulry F. Hip arthroplasty in genetic hemochromatosis. Report of 5 cases. Rev Med Int 2002;23(5):454–9.
385
16. Axford JS, Bomford A, Revell P, Watt I, Williams R, Hamilton EBD. Hip arthropathy in genetic haemochromatosis. Arthritis Rheum 1991;34:357–61. 17. Lunn JV, Gallagher PM, Hegarty S, Kaliszer M, Crowe J, Murray P, et al. The role of hereditary hemochromatosis in aseptic loosening following primary total hip arthroplasty. J Orthop Res 2005;23(3):542–8. 18. Hungerford DS, Krackow KA, Kenna RV. Cementless total knee replacement in patients 50 years old and under. Orthop Clin North Am 1989;20(2):131–45. 19. Hintermann B. Short and mid-term results with the STAR total ankle prosthesis. Orthopade 1999;28(9):792–803.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 386–389
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THERAPEUTICS
Role of glucosamine in osteoarthritis R. Thakrala, U.K. Debnathb,, C. Dentc a
Department of Trauma and Orthopaedics, Adelaide and Meath Hospital Incorporating National Children’s Hospital, Tallaght, Dublin-24, Ireland b Department of Trauma and Orthopaedics, University Hospital Cardiff, Cardiff CF14 4XW Wales, UK c Department of Orthopaedics, University Hospital Cardiff, Cardiff CF14 4XW Wales, UK
KEYWORDS Glucosamine; Action; Cartilage; Arthritis
Summary Long-term follow-up studies on the effects of glucosamine preparations are still awaited. At present, only short-term results are available. They are known to relieve pain and decrease the rate of joint space narrowing clinically in osteoarthritis of knee, whilst the side effects are less when compared to the anti-inflammatory drugs and even placebos. It is probably safe – but there is no good evidence that it works. It would be ideal to have a medication that is a normal constituent of the human cartilage, which modifies the natural history of the disease. It is possible that long-term clinical studies with glucosamine may result in modifications to the indications for joint surgery or the time patients can live with osteoarthritis before developing substantial disability. & 2007 Published by Elsevier Ltd.
Introduction Glucosamine sulphate is a normal constituent of the extracellular matrix of mammalian articular cartilage and synovial fluid, which is required for synthesis of glycosaminoglycans (GAGSs).1 It also helps in synthesising mucin or mucous secretions, which act as lubricant or protective agents in human joints. In 1956, Lennart Roden from Stockholm first showed glucosamine HCL-stimulated production of chondroitin sulphate in cartilage matrix by at least three times its control value. It was not until the 1980s that clinical trials of
glucosamine as a therapeutic drug for osteoarthritis (OA) of knee began. Now, it is readily available for purchase from health/food shops and pharmacies in the UK, USA and throughout Europe, for the relief of musculoskeletal symptoms.2,3 The range of products that includes chondroitin sulphate, vitamins C, D and E, minerals and herbs, as well the oligoelements (such as zinc, selenium, manganese and copper) are together called nutripharmaceuticals.4 Glucosamine has gained popularity in the last two decades for the treatment of OA.5
Glucosamine and its properties Corresponding author. Present address: 23, Barons Court Road,
Cardiff CF23 9DF, UK. Tel.: +078 1116 5794. E-mail address:
[email protected] (U.K. Debnath). 0268-0890/$ - see front matter & 2007 Published by Elsevier Ltd. doi:10.1016/j.cuor.2007.04.002
Glucosamine is an amino monosaccharide found in chitin, glycoproteins and in GAGSs (formerly known as mucopolysaccharides), such as hyaluronic acid and heparan sulphate.
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CH:CH O H
H H CH
H
H
NH3+
HO
OH
2 Figure 1 Chemical structure of glucosamine.
It is the basic building block of the amino sugars and hence is an important constituent of the cell wall and interstitial proteins.6 The chemical structure of glucosamine is shown in Fig. 1. Glucosamine (2-amino-2-deoxyalpha-D-glucose) is one of the two hexosamine sugars (six carbon amino sugars) common in human cells. Structurally, glucosamine is modified glucose, with an –NH3 group replacing the –OH group found on carbon two (C-2). G6-P is an amino monosaccharide (amino sugar) produced in the body by the combination of glutamine with fructose, through the enzymatic action of glucosamine synthetase.6 Glucosamine is available commercially as a nutritional supplement in three forms: glucosamine HCl, glucosamine sulphate and N-acetyl-glucosamine. All three forms are water soluble, the salt acting as a delivery vehicle. At neutral and physiological pH, the amino group in glucosamine is protonated, resulting in a positive charge. Salt forms of glucosamine contain negative anions to neutralise the charge. In the case of glucosamine hydrochloride, the anion is chloride, and in glucosamine sulphate the anion is sulphate. N-acetylglucosamine is a delivery form of glucosamine in which the amino group is acetylated, thus neutralising its charge. To date, most of the clinical studies examining the effect of glucosamine on OA have been performed with either the sulphate or the chloride salts of glucosamine. The glucosamine used in supplements is typically derived from marine exoskeletons.7 Synthetic glucosamine is also available.
Pharmacokinetics About 90% of glucosamine administered orally as a glucosamine salt gets absorbed from the small intestine and from there it is transported, via the portal circulation, to the liver. It appears that a significant fraction of the ingested glucosamine is catabolized by first-pass metabolism in the liver.8 Healthy men have serum glucosamine concentrations of 0.04 mmol/L when they are not consuming supplemental glucosamine.9,10 Ingestion of recommended oral doses of glucosamine in humans achieves serum levels of approximately 0.06 mmol/L.11 It is not presently known how much of an ingested dose is taken up in the joints in humans. Most relevant clinical trials have used patented crystalline glucosamine sulphate in 1500 mg, once a day, soluble powder form.12,13 This is a prescription drug in most European and
non-European countries. However, the Dietary Supplement Health and Education Act of 1994 favoured the appearance of several undocumented glucosamine salts (e.g. hydrochloride), derivatives (e.g., N-acetyl-glucosamine) on the dietary supplement market in the USA and other countries, and various other dosage forms and regimens.14 Persiani et al.14 studied the pharmacokinetics of glucosamine and found that it is bioavailable after oral administration of crystalline glucosamine sulphate. This persists in circulation, and its pharmacokinetics support once-daily dosage. Steady-state peak concentrations after a therapeutic oral dose of 1500 mg show bioavailability at concentrations that are in line with those found to be effective in selected in vitro models, which may explain the favourable clinical results in OA.
Mechanism of action of glucosamine in human tissues Glucosamine is preferentially incorporated by chondrocytes into the components of the GAG chains in intact cartilage and stimulates the synthesis of physiological proteolglycans. It also decreases the activity of catabolic enzymes, including matrix metalloproteases (MMP).15-17 In certain tissues, glucosamine has a higher affinity for glucose transporters than glucose itself and is incorporated into glycoproteins faster than glucose.18 It also inhibits the degradation of equine articular cartilage induced by interleukin 1 and lipopolysaccaharides.19 This supports the suggestion that exogenous glucosamine acts mainly as a substrate for biosynthesis of mucopolysaccharides and biopolymers of joints and bones and, thus, contributes to restoration of damaged cartilage.8,20
Articular cartilage in OA of the knee The degenerative disease OA is a manifestation of an imbalanced synthesis of articular cartilage (AC) matrix and the associated growth factors.21 Knee cartilage defects, for example, may result in an increased rate of cartilage breakdown, leading to decreased cartilage volume and joint space narrowing. OA represents loss of homeostasis in the normal maintenance of articular cartilage by the degradation and synthesis of the matrix components. The inciting mechanisms are not fully understood, although the aetiology seems multifactorial.22 The end pathway is an imbalance between proteinases, which break down the matrix constituents, and proteinase inhibitors.
The role of glucosamine in OA of the knee The long-term combined structure-modifying and symptommodifying effects of gluosamine sulphate suggest that it could be a disease modifying agent in OA.12 Besides synthesis of GAGs, it also exerts an anti-catabolic effect on AC by inhibiting the anti-inflammatory responses.23 The theory of synthesis of GAGs does not, however, explain the observed glucosamine mediated increase in collagen type II. The literature shows a positive effect of
ARTICLE IN PRESS 388 glucosamine on GAG production in human chondrocytes in cell culture, and the same anabolic effect is found in bovine and rat explants.16–18 TGF-b is considered to be a multifaceted cytokine that plays key roles in many downstream effects, such as mesenchymal differentiation, matrix production, stimulation of chondrocytes and controlled differentiation of stem cells.24,25 In adults, TGF-b’s are also believed to maintain a critical balance between the various anabolic and catabolic functions of chondrocytes for proper functioning of the cartilage. Varghese et al.26 provide evidence that glucosamine mediated increase in the production of specific matrix components involves TGF-b1 up-regulation, possibly through the hexosamine pathway in optimal concentrations of glucosamine. The effect of glucosamine on chondrocytes was found to be dependent upon the culture conditions. Is there an effect on gene expression, in both anabolic and catabolic activities of chondrocytes, in response to glucosamine treatment in the human OA explant model? Another study added a pre-culture experimental agent to human cartilage harvested during knee arthroplasty procedures. To this model, they added different concentration of glucosamine. They found that glucosamine (5 mM) addition to a human OA explant reduced the enzymatic breakdown of the cellular matrix.27 The authors of this study also suggested that chondroprotective properties of the glucosamine in vivo may be based on inhibiting further degradation due to catabolic activities, rather than on the ability to rebuild cartilage.28
Glucosamine in clinical practise Three rigorous meta-analyses show that individuals with OA of the knee or spine have significantly less symptoms while taking glucosamine than those taking placebo.29–31 McAlindon et al.28 conclude that glucosamine is moderately efficacious for the relief of symptoms of OA. Richy et al. conclude that glucosamine has highly significant effects on all aspects of knee OA.32 A recent randomized clinical trial included 414 post menopausal women followed for 3 years. The authors documented no decrease in joint space with glucosamine treatment whilst there was a decrease in the placebo group; the differences were significant (Po0.001).20 Reviewing the literature it appears that authors have looked at the knee, focussing on medial compartment arthritis, as a clinical substrate to analyse the effects of glucosamine treatment.12,31 Natural joint space narrowing in knee OA is slow (o0.1 mm/yr in average), but can be prevented by glucosamine sulphate, which concurrently induces a significant symptom improvement.31 When individual joint-space changes were analysed, twice as many patients receiving placebo had striking joint space narrowing, than those receiving glucosamine sulphate.11 Reginster et al.12 did a randomised , placebo-controlled clinical trial on 212 patients and found that joint space narrowing was significantly less when compared to the placebo group. They reported 20–25% improvement in symptoms. The joint space narrowing difference between the placebo and the glucosamine group was found to be 0.46 mm after 3 years. Pavelka et al.13 did a similar double
R. Thakral et al. blind study on 202 patients in Czech Republic. They also found a significant difference between the two groups (P ¼ 000.1) when they analysed the joint space narrowing at 3 years follow up. Cochrane reviews have concluded that glucosamine reduces the pain caused by OA but has not shown any effects on stiffness and improvements in function. High-quality preparations of glucosamine probably reduce pain in OA. A review on the efficacy of glucosamine in alleviating pain showed a significantly larger reduction in pain in patients who received glucosamine than in those who received placebo (15 RCTs, standardised mean difference 0.61%, 95% CI 0.95–0.28).32
Side effects Oral administration of glucosamine at very large doses (5000–15,000 mg/kg body weight) is well tolerated without documented toxicity.11 The most common symptoms reported with placebo and oral glucosamine are: mild gastrointestinal symptoms including constipation, diarrhoea, nausea, dyspepsia, excessive gas, abdominal distension and abdominal cramps. Headache and skin rash or pruritis are also known to occur. Some studies have also shown side effects such as increased musculoskeletal pain, urinary tract infection, vertigo, blood pressure fluctuation and depression.12,33 Although side effects occur with the use of glucosamine, it appears to be a generally safe compound when used in patients with OA. It favourably compares with the adverse effect profiles of other drugs used in the treatment of OA, such as analgesics and NSAIDs.12,31
Conclusion Long-term follow-up studies on the effects of glucosamine preparations are still awaited. At present, only short-term results are available. They are known to relieve pain and decrease the rate of joint space narrowing clinically in osteoarthritis of knee, whilst the side effects are less when compared to the anti-inflammatory drugs and even placebos. It is probably safe – but there is no good evidence that it works.31 It would be ideal to have a medication that is a normal constituent of the human cartilage, which modifies the natural history of the disease. It is possible that long-term clinical studies with glucosamine may result in modifications to the indications for joint surgery or the time patients can live with osteoarthritis before developing substantial disability.
References 1. Hamerman D. The biology of osteoarthritis. N Engl J Med 1989; 320:1322–30. 2. Briffa J. A critical review of the use of glucosamine sulphate in the treatment of osteoarthritis. Int J Alt Comp Med 1997;15: 15–6. 3. Baker CL, Ferguson CM. Future treatment of osteoarthritis. Orthopaedics 2005;28(Supp 2):227–34.
ARTICLE IN PRESS Role of glucosamine in OA 4. Hauselmann HJ. Nutripharmaceuticals for osteoarthritis, best practice and research. Clin Rhematol 2001;15(4):595–607. 5. Phoon S, Manolios N. Glucosamine A nutraceutical in osteoarthritis. Aus Fam Physician 2002;31(6):539–41. 6. Kelly GK. The role of glucosamine sulfate and chondroitin sulfates in the treatment of degenerative joint disease. Alternative Med Rev 1998;3(1):27–39. 7. Lahiji A, Sohrabi A, Hungerford DS, Frondoza CG. Chitosan supports the expression of extracellular matrix proteins in human osteoblasts and chondrocytes. J Biomed Mater Res 2000; 51(4):586–95. 8. Setnikar I, Rovati LC. Absorption, distribution, metabolism and excretion of glucosamine sulfate. Rev Arzneimittelforschung 2001;51(9):699–725. 9. Monauni T, Zenti MG, Cretti A, Daniels MC, Targher G, Caruso B, Caputo M, McClain D, Del Prato S, Giaccari A, Muggeo RC, Bonora E, Bonadonna RC. Effects of glucosamine infusion on insulin secretion and insulin action in humans. Diabetes 2000;49(6):926–35. 10. Pouwels M, Jacobs JR, Span PN, Lutterman JA, Smits P, Tack CJ. Short-term glucosamine infusion does not affect insulin sensitivity in humans. J Clin Endocrinol Metab. 2001;86(5):2099–103. 11. Anderson JW, Nicolosi RJ, Borzelleca JF. Glucosamine effects in humans: a review of effects on glucose metabolism, side effects, safety considerations and efficacy. Food Chem Toxicol 2005;43:187–201. 12. Regnister JY, Deroisy R, Rovati LC, Lee RL, Lejeune E, Bruyere O, Giacovelli G, Henrotin Y, Dacre JE, Gossett C. Long term effects of glucosamine sulphate on osteoarthritis progression : a randomised, placebo-controlled clinical trial. Lancet 2001;357:251–6. 13. Pavelka K, Gatterova J, Olejarova M, Machacek S, Giacovelli G, Rovati LC. Glucosamine sulphate use and delay of progression of knee osteoarthritis: a 3-year, randomized, placebo-controlled, double-blind study. Arch Intern Med 2002;162(18):2113–23. 14. Persiani S, Roda E, Rovati LC, Locatelli M, Giacovelli GP, Roda A. Glucosamine oral bioavailability and plasma pharmacokinetics after increasing doses of crystalline glucosamine sulfate in man. Osteoarthr Cartilage 2005;13:1041–9. 15. Noyszewski EA, Wroblewski K, Dodge GR, Kudchodkar S, Beers J, Sarma AV, Reddy R. Preferential incorporation of glucosamine into the galactosamine moieties of chondroitin sulfate in articular cartilage explants. Arthr Rheum 2001;44:1089–95. 16. Bassleer C, Rovati LC, Franchimont P. Stimulation of proteoglycans production by glucosamine sulphate in chondrocytes isolated from human osteoarthritic articular cartilage in vitro. Osteoarthr Cartilage 1998;6(6):427–34. 17. Dodge GR, Jimenez SA. Glucosamine sulfate modulates the levels of aggrecan and matrix metalloproteinase- 3 synthesized by cultured human osteoarthritis articular chondrocytes. Osteoarthr Cartilage 2003;11(6):424–32. 18. Uldry M, Ibberson M, Hosokawa M, Thorens B. GLUT2 is a high affinity glucosamine transporter. FEBS Lett 2002;524(1–3): 199–203.
389 19. Takamiya Y, Friedlander RM, Brem H, Malick A, Martuza RL. Inhibition of angiogenesis and growth of human nervesheath tumors by AGM-1470. J Neurosurg 1993;78(3):470–6. 20. Bruyere O, Pavelka K, Rovati LC, Deroisy R, Olejarova M, Gatterova J, Giacovelli G, Reginster JY. Glucosamine sulfate reduces osteoarthritis progression in postmenopausal women with knee osteoarthritis: evidence from two 3-year studies. Menopause 2004;11(2):134–5. 21. Sokoloff L. Osteoarthritis as a remodeling process. J Rheumatol 1987;14:7–10. 22. Owens S, Wagner P, Vangsness Jr. CT. Recent advance in glucosamine and chondritin supplementation. J Knee Surg 2004; 17(4):185–93. 23. Chan PS, Charon JP, Orth MW. Short-term gene expression changes in cartilage explants stimulated with interleukin beta plus glucosamine and chondroitin sulfate. J Rheumatol 2006; 33(7):1329–40. 24. Lippeillo L. Glucosamine and chondritin sulphate: biological response modifier of chondrocytes under simulated conditions of joint stress. Osteoarthr Cartilage 2003;11(5):335–42. 25. Qiao B, Padilla SR, Benya PD. Transforming growth factor (TGF)beta-activated kinase 1 mimics and mediates TGF-beta-induced stimulation of type II collagen synthesis in chondrocytes independent of Col2a1 transcription and Smad3 signaling. J Biol Chem 2005;280(17):17562–71. 26. Varghese S, Theprungsirikul P, Sahani S, Hwang N, Yarema KJ, Elisseeff JH. Glucosamine modulates chondrocyte proliferation, matrix synthesis, and gene expression. Osteoarthritis Cartilage 2006; July 15 (Epub ahead of print). 27. Uitterlinden EJ, Jahr H, Koevoet JA, Jemmiskens YM, BiermaZeinstra SM, Degroot J, Verhaar JA, Weinans H, van Osch GJ. Glucosamine decreases expression of anabolic and catabolic genes in human osteoarthritic cartilage explants. Osteoarthr Cartilage 2006;14(3):250–7. 28. McAlindon TE, LaValley MP, Gulin JP, Felson DT. Glucosamine and chondroitin for treatment of osteoarthritis: a systematic quality assessment and meta-analysis. J Am Med Associat 2000; 283(11):1469–75. 29. Richy F, Bruyere O, Ethgen O, Cucherat M, Henrotin Y, Reginster JY. Structural and symptomatic efficacy of glucosamine and chondroitin in knee osteoarthritis: a comprehensivemeta-analysis. Arch Intern Med 2003;163(13):1514–22. 30. Towheed TE, Maxwell L, Anastassiaides TP, Shea B, Houpt J, Robinson V, Hochberg MC, Wells G. Glucosamine therapy for treating osteoarthritis. Cochrane Database Syst Rev 2005;18(2): CD002946. 31. Chard J, Dippe P. Glucosamine for osteoarthritis: magic, hype, or confusion? Bri Med J 2001;322:1439–40. 32. Bazian Ltd. Glucosamine for osteoarthritis. Evidence-based Healthcare Pub Health 2005;9:322–31. 33. Hughes R, Carr A. A randomised, double-blind, placebo controlled trial of glucosamine sulphate as an analgesic in osteoarthritis of the knee. Rheumatomlogy 2002;41:279–84.
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QUIZ
Radiology Quiz Patients 1 and 2 History: Two different patients present with back pain and fever.
Question 1 (1) What are the main imaging features and the diagnoses?
Images A and B: Two sagittal T2-weighted MR images of the spine in two different patients.
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Patient 3 Questions 2 (1) What do the images show? (2) Can you link the pathology?
Image (A) A control (plain) radiograph of the kidneys. (B) A full-length abdominal radiograph after injection of intravenous contrast obtained during an intravenous urogram (IVU).
Patient 4 History: Eighteen-year-old man involved in high speed road traffic accident, head on collision, wearing seatbelt.
Question 3 (1) What is the diagnosis?
Images A and B: Lateral radiograph and AP radiograph of the cervical spine.
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Radiology Quiz
Further imaging
Image C and D: CT sagittal reformats of another patient with a similar injury at the C6/7 level. Image D shows the inferior articular facet of C6 (black arrow) is dislocated anterior to the superior articular facet of C7 and lies within the neural exit foramen.
Patient 5 History: Middle aged man with low back pain and right-sided anterior thigh pain.
Question 4 (1) What do the MR images show?
Image A: Right parasagittal, Image B midline sagittal and Image C left parasagittal T2-weighted MR images of the lumbar spine.
ARTICLE IN PRESS Radiology Quiz
Patient 6 History: 15-year-old girl presents with knee pain and swelling.
Question 5 (1) Describe the lesion on the plain radiographs and suggest a diagnosis.
Image A: AP and Image B lateral radiographs of the proximal tibia and fibula.
Patient 7 History: 19-year-old man presents with atypical knee pain.
Question 6 (1) What do the images show and what is the likely diagnosis?
Image A: Coronal STIR and Image B sagittal T2* gradient echo MR images through the knee.
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Radiology Quiz
Answers 1 Image A: The L2–S1 vertebral marrow returns patchy high T2 signal and there is an abscess tracking beneath the anterior longitudinal ligament at these levels. The discs and end plates are preserved. The diagnosis is tuberculous (TB) spondylodiscitis. Image B: There is destruction of the L1/2 disc and adjacent end plates. The disc space contains high T2 signal material which has an epidural component which displaces the conus. The diagnosis is pyogenic spondylodiscitis.
AP radiograph:
The spinous processes at and above the level of dislocation are rotated off the midline. They point to the side of the dislocation. Lateral radiograph:
The dislocated upper vertebra is anteriorly displaced by
Discussion: Comparison of TB and pyogenic spondylodiscitis. TB: 1. Gradual insidious onset. 2. Previous or current pulmonary TB in 50% on chest radiograph. 3. Contiguous vertebral involvement with subligamentous spread. 4. Initial preservation of discs and end plates. 5. Gibbus deformity. 6. Large paraspinal masses which may be calcified. Pyogenic: 1. Acute onset and sepsis. 2. Commonly involves two vertebral bodies centred on the disc. 3. Early rapidly progressive disc and vertebral end plate destruction. 4. Inflammatory masses are more ill defined and not as large as seen with TB, often appearing as a cuff around the involved vertebra and disc.
Answers 2
approximately 25% of the antero-posterior diameter of the vertebra below. The vertebrae below the dislocation are in a true lateral profile and the articular pillars are superimposed. Above the level of dislocation, the articular pillar on the side of rotation projects anterior to the opposite unrotated articular pillar. This double set of articular pillars for each vertebra creates the characteristic ‘bow-tie’ or ‘butterfly’ appearance. The distance between the posterior surface of the articular pillars and the spinolaminar line of the vertebrae below the dislocation is preserved whereas this space is narrowed above the level of dislocation.
Answer 4 Far lateral disc protrusion at L3/4 on the right. Discussion: Lateral disc protrusion. A lateral disc protrusion is often not evident on the midline sagittal images and inspection of the parasagittal images is important. The exiting nerve roots are normally seen in the neural exit foramina on parasagittal images as low signal round structures surrounded by high signal fat on both T1- and T2-weighted images (see normal appearances on the left). A lateral disc protrusion is seen as low signal material obliterating the high signal fat and compressing the nerve root in the exit foramen (white arrow). This can be confirmed on axial images (see image D, black arrow).
Image A: There is medullary nephrocalcinosis on the control radiograph of which the three most common causes are medullary sponge kidney, renal tubular acidosis and hyperparathyroidism. Image B: There is a lytic expansile lesion within the medial head and neck of the left femur which represents a Brown tumour of hyperparathyroidism. (The pelvicalyceal systems, ureters and bladder are normal.) Discussion: Brown tumours. A brown tumour results from parathyroid hormone stimulating osteoclastic activity. This results in bone resorption and replacement by fibrous tissue containing osteoclasts and giant cells. Typical subperiosteal bone resorption of hyperparathyroidism may accompany Brown tumours.
Answer 3 Unilateral C3 on C4 facet dislocation. Discussion: Plain radiographic features of unilateral facet dislocation.
Image D: Axial T1-weighted image at L3/4 level confirming right lateral disc protrusion (black arrow).
ARTICLE IN PRESS Radiology Quiz
Answer 5 There is an expansile radiolucent lesion with a thinned ‘egg shell’ cortex in the proximal fibular metaphysis of an unfused skeleton. These features are in keeping with an aneurysmal bone cyst. Discussion: Aneurysmal bone cyst (ABC). Aneurysmal bone cysts are most common in the 2nd decade affecting males more than females (2:1). They can be found in any bone but are most common in the metaphysis of lower limb long bones. The exact cause is unknown, but most widely thought to be a reactive process secondary to trauma or vascular disturbance. Internal fluid–fluid levels are a typical finding on MRI but are not specific for an ABC. They confirm the non-homogeneity of the lesion (see image C).
395
Answer 6 A well-defined lesion with a low signal sclerotic margin is present in the epiphysis of an unfused skeleton. Internal low signal foci on all sequences is in keeping with internal calcification. This lesion has a benign appearance which in this age group and location is most likely a chondroblastoma. Discussion: Chondroblastoma. This rare, benign tumour derived from chondroblasts usually arises in the epiphysis of long bones of the lower limb. It behaves unusually for a benign tumour as cases of local bone and soft tissue invasion, as well as pulmonary metastases have been reported.
Nev Davies, Richard Pennington, Catherine McCarthy Department of Orthopaedics and Radiology, Great Western Hospital, Swindon, UK E-mail address:
[email protected] (N. Davies)
Image C: Coronal STIR MR image of the ABC showing multiple cystic spaces and a few fluid-fluid levels.
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METABOLIC DISORDERS
Vitamin D-resistant rickets (X-linked hypophosphataemic rickets) Andrew McBridea,, Matthew Edwardsa, Fergal Monsellb, Martin Garganb,1 a
Department of Trauma & Orthopaedic Surgery, Bristol Royal Infirmary, Bristol BS2 8HW, UK Department of Trauma & Orthopaedic Surgery, Bristol Royal Hospital for Sick Children, Bristol BS2 8HW, UK
b
KEYWORDS Vitamin D-resistant rickets; X-linked hypophosphataemic rickets
Summary Rickets is a condition affecting the growing skeleton, causing demineralisation of bone, growth disturbance and deformity. Most forms of the disease are due to alterations in vitamin D homeostasis. Vitamin D-resistant rickets, however, is due to a disorder of renal phosphate reabsorption. X-linked hypophosphataemic rickets (XLHR) is the commonest inherited form of these disorders and this article will concentrate on this variant of the disease, summarising its clinical features and pathophysiology and outlining the goals and methods of treatment & 2007 Elsevier Ltd. All rights reserved.
Introduction The term rickets broadly covers a variety of disease states with differing aetiology but a common pathophysiological mechanism. This leads to a relative decrease in calcium or phosphate or both, the scale of which produces a failure of normal mineralisation of bone and epiphyseal cartilage causing skeletal deformity. Rickets occurs in the growing skeleton; its equivalent in the mature skeleton is osteomalacia. Historically, rickets was one of the earliest syndromes to be defined. In 1645, Daniel Whistler described the ‘‘English disease, commonly known as rickets’’. The first classic medical text on the subject is attributed to Francis Glisson Corresponding author. Tel.: +44 117 928 2828.
E-mail addresses:
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in 1650. Pommer in 1885 fully described and defined the histological changes occurring within the epiphyseal plate and cortical and medullary bone. The links to diet and environment were made at the beginning of the 20th century. During the 1920s the first of the vitamin Ds were isolated and by the end this decade rickets and osteomalacia were considered to be deficiency diseases curable by the addition of vitamin D to the diet. In the 1930s it became apparent that some individuals with rickets or osteomalacia were resistant to even massive doses of supplemental vitamin D. Three such patients were described by Albright et al. in 1937 as a clinical entity. They named the condition ‘‘rickets resistant to vitamin D,’’ and postulated the cause was a chemical lesion in the renal tubule.1 Further types of renal tubular syndromes and hypophosphataemic rickets were described following this, and in 1958 Winters et al. first described a hereditary cause of vitamin D-resistant rickets with a sex-linked-dominant inheritance.2 This X-linked hypophosphataemic rickets
ARTICLE IN PRESS Vitamin D-resistant rickets (XLHR) is the commonest form of inherited rickets affecting 1 in 20,000 of newborns.3
397 (hot-cross-bun skull), cranial synostosis, delayed dentition, enamel hypoplasia and severe dental caries. Sensorineural hearing loss can also occur in the adult.
Clinical features Spine and torso The clinical features of XLHR vary with the age on onset. Presentation is usually in the second year of life; occasionally, it may be much later, such as early adulthood. Generally there is an impairment of growth, although weight may be normal or even higher than age-matched normals. Growth disturbance can be variable and affect the upper body as much as the lower limbs. Although major milestones may be delayed, muscle weakness, tetany and convulsions are unusual, as the serum calcium is usually normal. A degree of hypotonia may affect gait or the onset of walking. The child may be clumsy, inattentive and irritable; the wrists and ankles may be thickened and the tibias bowed. Fractures are uncommon. In the child with florid disease the findings are more striking and males are more severely affected. It is unclear whether XLHR compromises life expectancy.3
The chest may demonstrate enlargement of the costal cartilages (rachitic rosary), indentation of the lower ribs where the diaphragm inserts (Harrison’s groove) and pectus carinatum. The spine may become kyphotic and adults can develop spinal stenosis.
Limbs Distal femoral and tibial bowing causes genu valgum or varum. Ankles, knees and wrists are typically thickened. Bone and large joint pains are common and often disabling. The risk of a slipped upper femoral epiphysis is increased in the young adolescent.4 Ectopic ossification of tendinous
Facial features The effects of rickets on the facial skeleton include flattening of the skull, frontal bossing (due to the delay in closure of the anterior fontanelle), caput quadratum
Figure 1
Figure 2
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A. McBride et al.
insertions and in periarticular regions have been reported in adults.5 Thigh pain in adults can be caused by incomplete femoral stress fractures (Looser’s zones).
Investigations Biochemical tests The biochemical traits of XLHR are hypophosphataemia (with an increased renal phosphate leakage) and high alkaline phosphatase. Serum calcium and 25-OH-vitamin D are normal. The diagnosis is thus made on these findings, with the clinical features of rickets and a positive family history if relevant. Diagnosis in the newborn can be difficult because phosphate levels can remain normal for up to 9 months. Alkaline phosphatase levels begin to rise from 4 months of age, confirming the diagnosis in those with a family history of the disorder and radiographic changes.
Radiology The characteristic skeletal changes seen in rickets occur early with widening of the physeal plates and cupping and fraying of the adjacent metaphysis. The bones most commenly affected are the proximal and distal tibia, the distal femur and the distal radius and ulna (Figs. 1 and 2). Although changes around the knee become more pronounced as the child grows, the wrist changes tend to be minimal with thickening and slight loss of movement. Looser’s zones are common and represent incomplete stress fractures which heal with demineralised callus. Affected sites include the humerus, femur, pubic ramus and scapula. Rickets due to disturbances of vitamin D homeostasis produce secondary hyperparathyroidism, leading to osteopenia and subperiosteal bone resorption. This does not occur in XLHR where thickened cortices and more dense trabecular bone are sometimes seen.
Aetiology and histopathology The pathogenesis of XLHR is not fully understood. Transport of phosphate is defective across renal proximal tubule cells. The disorder is inherited as an X-linked-dominant trait. Recently, mutations in the PHEX gene on chromosome
Figure 3
Figure 4
ARTICLE IN PRESS Vitamin D-resistant rickets Xp22.1 have been isolated.6 This gene encodes for an endopeptidase that has been postulated to be important in the breakdown of FGF23, a fibroblast growth factor protein, known to inhibit renal phosphate reabsorption. Histologically the condition is characterised by the presence of demineralised osteoid and in the growing child proliferation of chondroid hypertrophic cells at the sites of endochondral bone growth.
Treatment The treatment of XLHR requires a multidisciplinary approach involving both medical and orthopaedic specialists, preferably in centres with the necessary experience in the timing and type of treatment best suited to the individual. It is widely agreed that a key to maximising success of treatment is the early recognition of the condition. Early treatment leads to the best chance of reducing the likelihood of significant deformity and short stature. Indeed the diagnosis should be considered in any child presenting with angular deformity of the limbs and delayed growth.7 Without a correct diagnosis, early and perhaps inappropriate major surgery is doomed to failure. The goals of treatment are to prevent or correct limb deformity before skeletal maturity and to achieve optimal height.3
399 Treatment ideally begins in infancy with oral 1, 25dihydroxyvitamin D3 and phosphate supplementation. Radiological resolution of the defects in skeletal growth and improvement of the histological abnormalities can be observed in complaint patients. Whether final height can be influenced using medical therapies remains controversial.8 Complications of supplementary treatment include hypercalciuria, leading potentially to nephrocalcinosis, and hypercalcaemia due to increased calcium absorption. Following corrective surgery or fracture patients who are non-weight bearing immobilisation hypercalciuria and hypercalcaemia may develop unless supplementation is stopped temporarily. Orthopaedic evaluation should occur at least yearly in childhood and twice yearly during the adolescent growth spurt. Limb bracing, epiphysiodesis and osteotomies may have to be considered if deformity is progressive or symptomatic, ideally delayed until adolescence.9,10 Osteotomies are usually bilateral and are fixed with no plates or external fixation (Figs. 3–5). Newer treatments remain controversial and experimental. Recombinant Growth hormone (rhGH) is known to enhance renal phosphate reabsorption and has been shown to increase plasma phosphate concentration and height scores but also exacerbates upper to lower segment ratios.11
References 1. Albright F, Butler AM, Bloomberg E. Rickets resistant to vitamin D therapy. Am J Dis Child 1937;54:529–47. 2. Winters RW, Graham JB, Williams TF, McFalls VW, Burnett CH. A genetic study of familial hypophosphatemia and vitamin D resistant rickets with a review of the literature. Medicine (Baltimore) 1958;37:97–142. 3. Whyte MP. Rickets and osteomalacia (acquired and heritable forms). In: Wass JAH, Shalet SM, editors. Oxford textbook of endocrinology and diabetes. Oxford: Oxford University Press; 2002. p. 707–10. 4. Nixon JR, Douglas JF. Bilateral slipping of the upper femoral epiphysis in end-stage renal failure. J Bone Jt Surg 1980;62B: 18–21. 5. Polisson RP, Martinez S, Khoury M, Harrell RM, Lyles KW, Friedman N, et al. , Calcification of entheses associated with X-linked hypophosphatemic osteomalacia. N Engl J Med 1985; 313:1–6. 6. The HYP Consortium. A gene (PEX) with homologies to endopeptidases is mutated in patients with X-liked hypophosphataemic rickets. Nat Genet 1995;11:130–6. 7. Evans GA, Arulanantham K, Gage JR. Primary hypophosphatemic rickets. J Bone Jt Surg 1980;62A:1130–8. 8. Stickler GB, Morgenstern BZ. Hypophosphataemic rickets: final height and clinical symptoms in adults. Lancet 1989;11:902–5. 9. Rubinovitch M, Said SE, Glorieux FH, Cruess RL, Rogala E. Principles and results of corrective lower limb osteotomies for patients with vitamin D resistant hypophosphataemic rickets. Clin Orthop 1988:264–70. 10. Ferris B, Walker C, Jackson A, Kirwan E. The orthopaedic management of hypophosphataemic rickets. J Pediatr Orthop 1991;11:367–73. 11. Haffner D, Nissel R, Wuhl E, Mehls O. Effects of growth hormone treatment on body proportions and final height among small children with X-linked hypophosphatemic rickets. Pediatrics 2004;113:593–6.
Figure 5
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CME SECTION CME questions based on ‘‘Tuberculosis of the spine—Contemporary thoughts on current issues and perspective views’’ The following series of questions are based on the CME designated article for this issue—‘‘Tuberculosis of the spine—Contemporary thoughts on current issues and perspective views’’ by Myung-Sang Moon. Please read the article carefully and then complete the self-assessment questionnaire by filling in the square corresponding to your response to each multiple-choice question. After completing the questionnaire, either post or fax the answer page to the Current Orthopaedics Editorial Office at the address at the bottom of the RESPONSE sheet. Please photocopy this page if you wish to keep your copy of Current Orthopaedics intact. Replies received before the next issue of Current Orthopaedics is published will be marked and those reaching an adequate standard will qualify for three external CME points. You will be notified of your marks and a CME certificate will be dispatched for your records.
Questions 1. Which of the following was not a remaining indication for surgery after the introduction of effective antitubercular drugs? a. Failure of drug therapy b. Recrudescence of the disease c. Paraspinal abscesses d. Paraplegia persistent after 6 weeks of drug treatment e. Spinal cord involvement 2. According to Moon (1992), which of the following would be classified as stage II disease? a. 30% loss of body with 151 of kyphosis b. 40% loss of body with 251 of kyphosis c. 50% loss of body with 351 of kyphosis d. 60% loss of body with 401 of kyphosis e. 70% loss of body with 451 of kyphosis 3. Which of the following is not a diagnostic non-culture test for Mycobacterium tuberculosis infection? a. Quantiferon*TB Gold b. Detection of specific antigen 0268-0890/$ - see front matter doi:10.1016/j.cuor.2007.10.001
c. T-SPOT d. PCR e. CD4 count 4. Which of the following is a pro-drug used in the treatment of tuberculosis? a. Isoniazid b. Ethambutol c. Rifampicin d. Streptomycin e. Pyrazinamide 5. Which of the following is a second line drug used in the management of tuberculosis? a. Isoniazid b. Ethambutol c. Rifampicin d. Streptomycin e. Pyrazinamide 6. Resistance to which of the following pairs of antibiotics defines multi drug resistant tuberculosis? a. Isoniazid and Ethambutol b. Isoniazid and Rifampicin c. Ethambutol and Rifampicin d. Rifampicin and Streptomycin e. Streptomycin and Pyrazinamide 7. According to experimental data from dogs, what is the safe limit for spinal cord shortening? a. 10 mm b. 12.5 mm c. 15 mm d. 17.5 mm e. 20 mm 8. Which of the following is least commonly responsible for paraplegia in cases of spinal tuberculosis? a. Abscess b. Granulation tissue c. Spinal artery compromise d. Sequestrum e. Bony canal stenosis above the level of kyphosis
ARTICLE IN PRESS CME SECTION 9. In children with unacceptable tuberculous kyphosis, when should posterior instrumentation be removed? a. After 9 months of antituberculous therapy b. When the ESR falls to normal c. When there is radiological evidence of fusion d. After cessation of spinal growth e. Never, but anterior fusion is added after disease healing
401 10. Which of the following statements is untrue? a. M. Tuberculosis produces fewer adhesion molecules than pyogenic bacteriae b. Bacteria adhere more avidly to stainless steel than to titanium c. M. Tuberculosis reproduce relatively slowly d. Titanium implants are preferred for spinal stabilisation of infected bone e. Titanium implants can be used effectively in infected foci in patients with HIV
ARTICLE IN PRESS 402
CME SECTION
Please fill in your answers to the CME questionnaire above in the response section provided below. A return address and fax number is given at the bottom of the page. ........................................................................................................
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Your details (Print clearly) NAME. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ADDRESS. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . FAX NO. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . EMAIL. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
RETURN THE COMPLETED RESPONSE FORM by fax to +44-113-392-3290, or by post to CME, Current Orthopaedics, Academic Department of Orthopaedic Surgery, ‘‘A’’ Floor Clarendon Wing, Leeds General Infirmary, Great George Street, Leeds LS1 3EX, UK.
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CME SECTION Answers to CME questions based on the article ‘‘Management of wrist instability’’ Please find below the answers to the Current Orthopaedics CME questions from vol. 21, issue 3, which were based on the article ‘‘Management of wrist instability’’ by Sivananthan, Sharp and Loh. 1
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BOOK REVIEWS Basic Orthopaedic Sciences—The Stanmore Guide, Manoj Ramachandran. Hodder Arnold, Paris (2006). 304pp., £34.99, ISBN: 9780340885024 This book is based on the successful Stanmore Basic Sciences course, which is a preparatory course for the Intercollegiate FRCS(Tr&Orth) examination in the UK. The course content has been developed over a number of years and this book has benefited from the evolution of topic coverage to closely correlate with what is expected of candidates in postgraduate orthopaedic examinations. A number of basic science revision aids have been produced in the past and most are beginning to show their age. Some focus on a narrow field, such as biomechanics, but this handy volume has concise chapters covering the range of subject matter that comes under the umbrella title of basic science. There are 29 chapters and the general pattern is that each is written by a trainee and a consultant or other expert in the field. Contributors have done a uniformly good job of condensing their subject matter into a few pages that, unlike some competing works, remain easy to read. The first chapter on statistics, for example, conveys more useful
information in 14pp. than some ‘basic’ books on the subject. Diagrams throughout are in 2 tone only, but are clear and well produced. Black and white plates of X-rays are sufficiently clear to demonstrate relevant radiological findings. At the end of each chapter is a box labelled ‘viva questions’. These questions might be useful for the reader who wants to test their own knowledge but care must be taken in drawing any conclusions about the sort of questions that might be asked in an actual exam. While many of the questions are typical opening questions that might be used in a viva, the development of the question to test for competence and for advanced knowledge does not occur. Overall this is a useful and relatively inexpensive book. It is already a common sight in the clutches of candidates for higher examinations in orthopaedics. For UK candidates, its content can be compared with the syllabus for higher surgical training to reveal a good match, which probably explains this observation.
David Limb
doi:10.1016/j.cuor.2007.08.005
Lovell and Winter’s Pediatric Orthopaedics, sixth ed. R.T. Morrissey, S.L. Weinstein, Lippincott (2005). 1632pp., $299.00, ISBN:07817535 The sixth edition of Lovell and Winters’: Pediatric Orthopaedics replaces the last edition of 2001. Fifty authors, all from North America except one from France, have written 34 chapters, spread over two volumes. The authors are mostly children’s orthopaedic surgeons but also include neurosurgeons, neurologists, prosthetics experts, physical therapists, radiologists and paediatricians. The chapters are not grouped into sections but cover all basic science subjects and disease processes relevant to the child’s musculoskeletal system. There is only one large chapter on children’s fractures and a smaller one on child abuse. A new chapter on the evaluation of medical literature has been included in this edition, in order to emphasize the need to provide evidence-based medicine in our day-to-day practice. All the chapters have been
doi:10.1016/j.cuor.2007.06.002
thoroughly researched and each chapter includes an extensive reference list at the end. An outline of the content is present at the beginning of each chapter. The editors have tried to focus on ‘‘the decision-making processes’’ that lead up to the selection of a surgical technique. The details of these techniques are found in a separate, and equally excellent, Atlas of Pediatric Orthopaedic Surgery by Morrissey and Weinstein. Each chapter is well written and illustrated with radiographs, photographs, charts, tables and drawings. Both volumes include all information for both training and consultant orthopaedic surgeons. Although there is only one European author, I believe that the North American viewpoints are still relevant to us. I would strongly recommend this excellent text as an essential addition to any orthopaedic postgraduate library.
P. Templeton
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 405–414
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MINI-SYMPOSIUM: SHOULDER RECONSTRUCTION
(i) Shoulder arthroplasty for osteoarthritis and rheumatoid arthritis Joaquin Sanchez-Sotelo Department of Orthopedic Surgery, Mayo Clinic Rochester, 200 First Street SW, Rochester MN 55905, USA
KEYWORDS Shoulder; Arthroplasty; Osteoarthritis; Rheumatoid arthritis
Summary Replacement arthroplasty represents the treatment of choice for most patients with endstage glenohumeral osteoarthritis or rheumatoid arthritis. Multiple studies have documented reliable improvements in pain, range of motion, function and quality of life after this procedure. Total shoulder arthroplasty seems to be associated with more reliable pain relief and improvements in elevation when compared to hemiarthroplasty. The main surgical principles of shoulder arthroplasty apply equally to patients with osteoarthritis and rheumatoid arthritis; however, the different underlying pathology associated with these two conditions needs to be understood in order to modify the surgical technique accordingly. Most patients with osteoarthritis have an intact rotator cuff and enough glenoid bone stock to allow implantation of a glenoid component. Asymmetric posterior glenoid erosion often needs to be corrected and capsular releases are needed to restore elevation and external rotation. In rheumatoid arthritis, implantation of a glenoid component may not be possible in the presence of severe glenoid bone loss or a massive irreparable cuff tear; in addition, rheumatoid involvement of other joints needs to be taken into consideration. Infection, instability, periprosthetic fractures, and glenoid loosening or erosion are the main failure mechanisms of shoulder arthroplasty. Careful surgical technique and a well-executed physical therapy program translate into successful outcomes in most patients with osteoarthritis and rheumatoid arthritis. & 2007 Elsevier Ltd. All rights reserved.
Introduction Replacement arthroplasty of the glenohumeral joint is indicated most commonly in patients with end-stage osteoarthritis and rheumatoid arthritis of the shoulder.1,2 The general principles of shoulder arthroplasty apply to both osteoarthritis (OA) and rheumatoid arthritis (RA), but there are some fundamental differences in the underlying E-mail address:
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pathology of these conditions with clinically relevant implications for both the surgical technique and the anticipated outcomes of the procedure.
Pathology of shoulder osteoarthritis and rheumatoid arthritis Osteoarthritis and rheumatoid arthritis are two of the most common conditions affecting the glenohumeral joint.
ARTICLE IN PRESS 406
J. Sanchez-Sotelo
Table 1 Surgical pathology of osteoarthritis and rheumatoid arthritis. Primary osteoarthritis
Rheumatoid arthritis
Cartilage loss
Humeral
Humeral head Glenoid (central)
Glenoid bone loss
Posterior
head Glenoid (posterior)
Central Superior (cuff pathology)
Associated osteopenia (glenoid, humerus) Capsule
Anterior
Attenuated
shortening Posterior lengthening Inferior shortening Rotator cuff
Usually
Other
AC joint
intact
may be affected
Attenuated Torn in some Other joints may be involved (AC, sternoclavicular, cervical spine, elbow, wrist, hand)
Both are characterized by various degrees of articular cartilage loss, but they behave differently in terms of the patterns of bone loss and the involvement of the rotator cuff tendons and other soft-tissues (Table 1).
Osteoarthritis Primary osteoarthritis is characterized by cartilage loss, which usually affects both the humeral head and the glenoid. Prominent osteophytes are commonly present at the humeral head–neck junction and at the glenoid rim. The joint remains well centered in some patients, but many shoulders develop posterior subluxation, which is associated with posterior glenoid erosion and posterior capsular elongation (Fig. 1). These abnormalities need to be taken into consideration at the time of arthroplasty to correct abnormal glenoid version and posterior subluxation. The inferior capsule is contracted, especially in patients with loss of passive elevation; release of the inferior capsule is needed to restore elevation reliably. The rotator cuff tendons are usually intact; associated rotator cuff tendon tears, when present, tend to be small or medium in size and should be repaired at the time of arthroplasty. Radiographic findings of acromioclavicular joint osteoarthritis are very common; however, this joint needs to be addressed
Figure 1 Anteroposterior (A) and axillary (B) radiographs of a shoulder with primary osteoarthritis. Note the decreased joint line space, the prominent osteophytes at the humeral head– neck junction, and the posterior subluxation and posterior glenoid erosion.
surgically at the time of arthroplasty only when found to be symptomatic in the preoperative evaluation.
Rheumatoid arthritis Cartilage degradation is usually present both at the humeral head and glenoid. Many patients with rheumatoid disease present with decreased bone mineral density, which increases the risk of intraoperative fractures and may compromise component fixation, especially when cement is not used. Bone loss tends to be central (Fig. 2); superior bone loss is seen
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Figure 2 Anteroposterior (A) and axillary (B) radiographs of a shoulder with rheumatoid arthritis. Note the loss of articular cartilage, the central glenoid erosion and the decreased bone mineral density. The proximal aspect of the humeral component of a total elbow arthroplasty may be appreciated on the axillary view. Table 2 Spectrum of shoulder pathology in rheumatoid arthritis.
Glenohumeral joint o o o o
Synovitis Arthritis Sepsis Steroid-induced osteonecrosis
Subacromial bursitis Rotator cuff tears Acromioclavicular joint synovitis and arthritis Sternoclavicular joint synovitis and arthritis Scapulothoracic fibrosis Referred pain (cervical spine)
mostly in patients with associated rotator cuff tears. When central or superior bone loss is severe, secure implantation of a glenoid component may not be possible. The joint capsule is often attenuated; extensive releases are less commonly needed. In addition to rheumatoid synovitis and arthritis, some patients with rheumatoid arthritis may present with superimposed steroid-induced osteonecrosis or deep infection. A substantial number of rheumatoid patients have associated rotator cuff tears; in some, the size of the tendon tear precludes surgical repair, which affects surgical decision-making in terms of implantation of a glenoid component or consideration of a reverse prosthesis. Rheumatoid arthritis may affect other joints in the shoulder region (acromioclavicular, sternoclavicular), may be associated with scapulothoracic fibrosis, and oftentimes will affect the cervical spine, elbow, wrist and hand (Table 2).
Preoperative evaluation The evaluation of patients with osteoarthritis or rheumatoid arthritis being considered for shoulder arthroplasty
should start with a clear assessment of the pain severity and functional limitations experienced. Most patients complain of moderate to severe pain, both during the day and at night, aggravated by the use of the shoulder, and associated with various degrees of decreased motion.
Physical examination Examination of the shoulder usually reveals pain with glenohumeral range of motion, which is associated with crepitus in many patients with osteoarthritis. It is important to document passive and active range of motion. Limitation of passive external rotation is more typical of osteoarthritis, and may require elongation of the anterior capsule and subscapularis at the time of the arthroplasty. A large difference between active and passive motion is more common in rheumatoid arthritis, and usually indicates associated rotator cuff dysfunction. Strength in abduction, external rotation and internal rotation should also be tested; strength is usually normal in osteoarthritis, but may be decreased in patients with rheumatoid arthritis, again indicating associated rotator cuff dysfunction. The physical examination of patients with rheumatoid arthritis should be completed by evaluation of the cervical spine, acromioclavicular and sternoclavicular joints, elbow, wrist and hand. Some patients may benefit from elbow, wrist or hand surgery before or after shoulder arthroplasty, depending on the degree of pain and limitations imposed by these other joints. In general, the most affected joint should be addressed first, and it is important to formulate a comprehensive surgical plan for the whole upper extremity. A limited number of patients with osteoarthritis will also have pain secondary to acromioclavicular joint osteoarthritis; failure to recognize and address these symptoms at the time of shoulder arthroplasty may result in incomplete pain relief and satisfaction.
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Figure 3 Computed tomography of a shoulder with primary osteoarthritis. Note the posterior glenoid erosion, abnormal glenoid version, prominent glenoid osteophytes and decreased glenoid bone stock: (A) axial cut and (B) coronal reconstruction.
Imaging studies Radiographs The radiographic features of osteoarthritis and rheumatoid arthritis of the shoulder are quite typical (Figs. 1 and 2) and help establish the diagnosis and plan the surgical procedure. Our usual radiographic projections include two anteroposterior radiographs in the plane of the scapula in internal and external rotation of the shoulder and one true axillary radiograph. If the joint line space is well preserved in all three views in a patient with rheumatoid arthritis, the patient should be evaluated for symptomatic synovitis, infection or rotator cuff disease. The axillary view is very helpful to identify posterior subluxation and posterior glenoid erosion in patients with osteoarthritis. Attention should be paid to the remaining glenoid bone stock. Secure implantation of a glenoid component may not be possible when glenoid bone loss results in medialization of the glenoid face to the base of the coracoid or severe asymmetric glenoid bone loss superiorly or posteriorly. The acromioclavicular and sternoclavicular joints should be evaluated for degenerative changes, especially in patients with rheumatoid arthritis. Radiographs of the cervical spine should also be obtained in rheumatoid patients to identify atlantoaxial instability in preparation for anesthesia.
Computed tomography Computed tomography is obtained by many surgeons routinely in every patient scheduled to undergo shoulder arthroplasty. This is due in part to difficulties obtaining a satisfactory axillary radiograph in some institutions. Computed tomography allows accurate estimation of glenoid version and the amount of bone stock remaining for glenoid component implantation (Fig. 3). In addition, it helps understand the location and size of glenoid osteophytes, which when unrecognized may mislead the surgeon at the time of preparation of the glenoid. Associated atrophy
and fatty infiltration of the rotator cuff muscles may also be evaluated.
Magnetic resonance imaging This imaging technique plays a minor role in the evaluation of patients with osteoarthritis but can be very helpful in patients with rheumatoid arthritis. It is indicated mainly when associated rotator cuff tears are suspected as well as in patients with minor radiographic changes and other possible explanations for their pain, such as synovitis, infection, rotator cuff disease or steroid-induced avascular necrosis.
Surgical technique Total shoulder arthroplasty is the most reliable surgical procedure for patients with end-stage osteoarthritis or rheumatoid arthritis of the shoulder.1,2 Hemiarthroplasty has been shown to provide incomplete pain relief in some patients and is associated with lesser improvements in motion. However, severe glenoid bone loss may preclude the secure implantation of a glenoid component, and in those cases shoulder hemiarthroplasty is the only viable option. In patients with rheumatoid disease and a large irreparable rotator cuff tear, the risks and benefits of shoulder hemiarthroplasty and a reverse total shoulder arthroplasty should be discussed with the patient. Shoulder hemiarthroplasty in this patient population will not reliably restore motion and may be associated with persistent pain, but has a very low rate of mechanical failure. Reverse total shoulder arthroplasty is likely to result in better pain relief and active motion, but the mid- and long-term survival of this design is a concern in rheumatoid patients with bone loss and osteopenia.3 Tables 3 and 4 summarize some specific technical considerations to take into account for shoulder arthroplasty in osteoarthritis and rheumatoid arthritis.
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Table 3 Shoulder arthroplasty in osteoarthritis: technical considerations.
Table 4 Shoulder arthroplasty in rheumatoid arthritis: technical considerations.
Careful assessment of passive external rotation (ER)
Early rather than late surgery may improve outcome High risk intraoperative fractures
under anesthesia J In passive ERo301 consider subscapularis release off bone for elongation
J
Consider anteromedial approach
High incidence of rotator cuff attenuation and tears Extensive inferior capsular release required in most patients J mm active elevation J Improves exposure
J J
Glenoid bone loss J
Careful assessment of posterior glenoid erosion/ abnormal glenoid version J Asymmetric glenoid reaming for defectso1 cm J Larger defects a. Hemiarthroplasty b. Bone grafting c. Custom-made components
Preserve coracoacromial arch Repair associated rotator cuff tears if possible
J J
J
Preoperative CT scan Intraoperative assessment Better outcome when glenoid component implanted Consider hemiarthroplasty if a. Insufficient glenoid bone stock b. Irreparable cuff tear
Humeral stem Stable cementless fixation of the humeral stem is
J
possible in most cases Correct soft-tissue imbalances o Internal rotation contracture o Posterior subluxation
J
The acromioclavicular joint rarely needs to be addressed
Selective uncemented fixation Beware of current or future elbow replacement a. Cement restrictor b. Shorter stems c. Consider resurfacing (bone stock permitting)
Humeral head size based more on soft-tissue tension than humerus size
Address associated acromioclavicular/sternoclavicular pathology
Postoperative rehabilitation J
Surgical approach The long deltopectoral approach is the standard surgical exposure for shoulder arthroplasty in osteoarthritis and rheumatoid arthritis. Although this exposure is well described in the orthopedic literature and well known to most orthopedic surgeons, a few technical pearls may help in the performance of shoulder arthroplasty. At our institution, we tend to place the skin incision lateral to the anatomic location of the deltopectoral interval. This requires elevation of a larger medial and superior skin flap to reach the deltopectoral interval, but centers the surgical field in the more difficult part of the procedure, the glenoid preparation and implantation. It is important to develop the whole length of the deltopectoral interval, from the clavicle to the humeral shaft. Preservation of the cephalic vein seems to be associated with decreased postoperative hand swelling; the vein is displaced medially with the pectoralis, which requires coagulation of its multiple deltoid branches. Release of the adhesions between the rotator cuff group and the deltoid and conjoined tendon helps increase exposure and motion. The joint is accessed by incision of the subscapularis tendon and capsule in a single layer and minimal extension of the arthrotomy along the inferior aspect of the rotator cuff interval. In patients with passive external rotation inferior to 301 (typical of osteoarthritis), the incision is performed at the lesser tuberosity to allow a more medial reattachment at the end of the procedure in order to achieve greater postoperative external rotation.
J
Standard vs limited-goals program Scapulothoracic fibrosis may limit range of motion
Most of the times the incision is performed about 1 cm medial to the lesser tuberosity, as tendon to tendon repair seems to be more secure in the shoulder. The so-called anteromedial approach may be useful in some circumstances.4 It involves extending the deltopectoral approach by detaching the deltoid off the clavicle, acromion and spine of the scapula. This approach is well tolerated as long as a meticulous transosseous reattachment is performed. It is mainly indicated in rheumatoid patients with severe osteopenia and stiffness in order to prevent intraoperative fractures. It may also be helpful in patients with osteoarthritis and severe posterior glenoid bone loss requiring structural bone grafting.
Glenoid preparation and implantation Adequate glenoid exposure is critical for proper glenoid preparation and implantation (Fig. 4A). Glenoid exposure is improved full development of the deltopectoral interval, selective release of the pectoralis tendon, inferior capsular release, complete removal of humeral osteophytes after resection of the humeral head, use of adequate glenoid retractors, and complete excision of the labrum.
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Figure 4 (A) Adequate exposure is paramount for adequate glenoid preparation and implantation. (B) Structural bone grafting may be required in patients with osteoarthritis and severe posterior bone loss.
Figure 6 The humeral head should be implanted approximately 1 cm above the highest point of the greater tuberosity.
Figure 5 Anteroposterior radiograph of a modern shoulder arthroplasty design using a cementless humeral stem, anatomic humeral head and cemented pegged all-polyethylene glenoid component. Note the appropriate positioning of the humeral head relative to the tuberosity and the absence of postoperative glenoid radiolucent lines.
Loss of glenoid bone stock should be recognized on preoperative radiographs and computed tomography and confirmed intraoperatively (Fig. 3). When central glenoid bone loss may compromise secure glenoid implantation, a pilot hole may be drilled at the center of the glenoid to determine how much bone remains to provide fixation. A minimum of 2–3 cm is required for safe implantation of a glenoid component. Posterior glenoid defects typical of osteoarthritis may be corrected by asymmetric glenoid
reaming, structural bone grafting or custom-made components (Fig. 4B). Asymmetric glenoid reaming may be used for defects up to 1 cm in depth. When a glenoid component cannot be implanted, consideration should be given to reaming the glenoid to improve its congruency with the humeral head and bone grafting of large defects to improve bone stock should further reconstruction be needed in the future. Currently, most glenoid components in anatomic total shoulder arthroplasty are all-polyethylene cemented components. The quality of cement fixation seems to be associated with radiolucent lines and loosening. Better cement fixation is obtained with careful bone preparation, a dry surgical field with minimal blood at the bone–cement and cement–implant interface, pulsatile lavage, and pressurization of the cement (Fig. 5). The rate of early radiolucent lines seems to be less with pegged as compared to keeled components. Radiolucent lines are also less prevalent when there is a slight mismatch between the radius of curvature of the glenoid and the humeral head.5 Reverse arthroplasty is very controversial in rheumatoid shoulders with irreparable cuff tears.3 Reverse glenoid components are cementless and fixed with screws. Ideally, these components should be implanted with their inferior edge flush with the inferior aspect of the glenoid to decrease the risk of glenoid notching. There are substantial
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arthritis (Fig. 7). Most reverse humeral components are fixed with bone cement. In patients with rheumatoid arthritis, attention should be paid to the length of the humeral stem. Patients may have or need an elbow arthroplasty and the humeral stem needs to leave room in the canal for the stem of the elbow arthroplasty component. Use of a resurfacing humeral component is quite popular in some countries. The benefits of a resurfacing humeral component include preservation of bone stock and ease of implantation in patients with humeral deformity, elbow stems or previous hardware. Their disadvantages include a more difficult glenoid exposure, limited ability to modify offset and soft-tissue tension by use of modular humeral heads, and potential failure of fixation in patients with compromised proximal humerus bone stock. We have limited experience with the use of resurfacing components, but good results have been published by some authors.8,9
Soft tissue balance
Figure 7 Anteroposterior radiograph after total shoulder arthroplasty in a patient with rheumatoid arthritis. Both components are fixed with cement.
differences amongst the different reverse designs in terms of their initial fixation and biomechanical features.
Humeral preparation and implantation Some variation exists in the two most important anatomic parameters to be reproduced by replacement of the humeral head, namely version and head-greater tuberosity relationship. Some surgeons recommend performing the humeral head osteotomy in the plane of the anatomic humeral neck in order to individualize version and inclination for each patient.6 However, performing the osteotomy in about 301 of retroversion allows a successful reconstruction for most patients. Less retroversion may be indicated in patients with preoperative posterior subluxation. The prosthetic humeral head is usually positioned approximately 1 cm higher than the greater tuberosity (Fig. 6), in order to restore the so-called ‘‘gothic arch’’ of the shoulder (line connecting the inferior edge of the scapular body with the medial aspect of the humeral shaft). However, different prosthetic head designs may require different heights. Most current systems also allow adjustments in the position of the humeral head relative to the stem.6 We favor cementless fixation of the humeral component whenever possible in order to avoid complications related to cement removal if revision surgery is ever needed (Fig. 5).7 However, cement is used whenever primary implant stability cannot be achieved with a cementless stem, which is more commonly the case in patients with rheumatoid arthritis. Impaction of bone from the resected humeral head into the humeral metaphysis at the time of component implantation increases the number of components which can be securely fixed without cement. When cement is used, consideration should be given to antibiotic-impregnated polymethylmethacrylate, especially in patients with rheumatoid
The soft tissues around the shoulder should be tensioned to achieve joint stability and restore as much motion as possible. Soft tissue tensioning is affected by component positioning, humeral head size, and selective shortening or lengthening of the capsule and rotator cuff. Ideally, the prosthetic humeral head should translate in all directions to the rim of the glenoid component and spontaneously return to a centered position, and the reconstruction should allow passive elevation to approximately 1601 and passive internal and external rotation to approximately 851 without dislocation. Excessive joint stuffing results in decreased range of motion and may place excessive tension on the subscapularis and interval repair; failure of this repair may result in anterior instability, decreased active range of motion, weakness and pain, and the results of a later repair or reconstruction are somewhat unpredictable.10 For these reasons, the subscapularis repair cannot be overemphasized.
Primary osteoarthritis In primary osteoarthritis, the two most common patterns of joint imbalance are internal rotation contracture and posterior shoulder subluxation. As mentioned above, lengthening of the anterior soft tissue structures should be planned when passive external rotation under anesthesia is less than 301. Although z-plasty of the subscapularis and capsule has been reported as a method for anterior elongation, it compromises the thickness of the anterior structures. We prefer to detach the subscapularis and capsule off the lesser tuberosity and repair them in a more medial position into the humeral neck. In addition, the anterior capsule may be divided at its junction with the anterior labrum to mobilize the capsule and subscapularis; in cases of severe capsular shortening and thickening, a subtotal anterior capsulectomy may be performed. Posterior shoulder subluxation can usually be corrected by insertion of the glenoid component in the proper version, selective decreased retroversion of the humeral component, and adequate humeral head sizing. When posterior instability persists despite all these efforts, consideration should be
ARTICLE IN PRESS 412 given to plication of the posterior capsule and rotator cuff to decrease the volume of the posterior joint space. Three to six nonabsorbable sutures may be placed into the posterior capsule and the posterior cuff in a horizontal mattress fashion before implantation of the humeral component. Sutures are then tied after all of them have been placed.
J. Sanchez-Sotelo Currently, the author uses a more aggressive rehabilitation protocol after reverse prostheses unless the fixation of the glenoid component is suboptimal. Patients are usually immobilized for 2 or 3 weeks, and then start a program of active-assisted range of motion exercises. Strengthening exercises for the deltoid are started 6 weeks postoperatively and continued for 3–6 months.
Rheumatoid arthritis
Outcome In rheumatoid arthritis, the two most common patterns of joint imbalance are multidirectional joint laxity and anterosuperior instability in patients with an associated massive irreparable cuff tear. Capsule and tendon attenuation with rheumatoid disease usually results in elongated soft-tissue structures. Use of a humeral head size relatively larger than anticipated for the patient size usually helps correct this problem; some systems provide heads with increased thickness for the same diameter, which may be especially useful in these circumstances. In the second category of patients with a massive irreparable cuff tear, if anterosuperior instability is noted at the time of hemiarthroplasty, consideration may be given to conversion to a reverse prosthesis, although reverse arthroplasty is controversial in rheumatoid arthritis as mentioned above. Physical therapy An adequate physiotherapy program is a key element for a successful outcome after shoulder arthroplasty. The goals of the physical therapy program are to restore motion, protect any soft-tissue repairs, improve the overall strength of the different shoulder muscle groups, and maintain stability. Physiotherapy in our unit is advanced according to the following protocol:
For the first 6 weeks, the shoulder is placed in a shoulder
immobilizer and patients perform passive range of motion exercises three to four times a day. The limits for elevation and external rotation are based on intraoperative assessment of stability and the soft tissues. The shoulder immobilizer is removed at 6 weeks and patients are advanced to active-assisted range of motion exercises with no limits unless the physical examination at the time recommends differently. Isometric strengthening exercises are added at 10 weeks. Active-resisted strengthening exercises with elastic rubber bands are added at 12 weeks.
Physiotherapy is continued for 4–6 months, and many patients continue to improve their motion and strength up to 1 or 2 years after surgery. A home-based program similar to the one described above has been shown to maintain the range of motion achieved at the time of shoulder arthroplasty.11 In rheumatoid patients with a deficient rotator cuff and compromised soft tissues at risk for instability after shoulder hemiarthroplasty, the so-called limited-goals rehabilitation may be used. This program sacrifices mobility in the interest of stability. Motion is limited to no more than 901 or 1001 for elevation and no more than 201 of external rotation for the first 3 postoperative months.
Many studies have documented a high rate of satisfactory outcomes after shoulder arthroplasty for osteoarthritis than rheumatoid arthritis. Pain improves in most patients. Motion and function are usually improved as well. Total shoulder arthroplasty seems to be associated with a better outcome than hemiarthroplasty in both primary osteoarthritis and rheumatoid arthritis.1,12,13
Primary osteoarthritis Shoulder arthroplasty is associated with improved pain, motion, strength, function and patient-perceived outcome in patients with primary osteoarthritis. Several investigators have reported good results using hemiarthroplasty in patients with osteoarthritis. Wirth et al.14 and Lynch et al.15 reported significant improvements in pain and function in 50 and 35 shoulder hemiarthroplasties, respectively, followed a minimum of 2 years. However, a recent metaanalysis of four prospective randomized studies consistently demonstrated significantly better results in terms of pain, active elevation and motion when total shoulder arthroplasty is compared to hemiarthroplasty in patients with osteoarthritis.1 In our experience, most patients who receive a total shoulder arthroplasty for primary osteoarthritis experience complete pain relief and achieve more than 1301 of active elevation and more than 601 of active external rotation, although final motion largely depends on preoperative motion.16 Data from our institution has also shown better long-term survivorship with total shoulder arthroplasty as compared to hemiarthroplasty in patients younger than 50 years.17
Rheumatoid arthritis Shoulder arthroplasty is associated with pain relief in most rheumatoid patients; functional improvements have not been consistently reported in the literature. When a glenoid component can be safely implanted, total shoulder arthroplasty is associated with a better outcome than humeral head replacement. Likewise, when an associated cuff tear is found, concomitant cuff repair significantly improves postoperative clinical shoulder scores compared with patients in whom tears are not repaired. The results of a multicenter prospective study were recently published.2 Thirty-six hemiarthroplasties and 25 total shoulder arthroplasties were followed for a mean on 3 years. The underlying diagnosis was rheumatoid arthritis in 53 shoulders and other inflammatory conditions in the remaining shoulders. Shoulder arthroplasty was associated with a significant improvement in pain and quality of life. Motion was also improved, to a mean of 901 with
ARTICLE IN PRESS (i) Shoulder arthroplasty for osteoarthritis and rheumatoid arthritis hemiarthroplasty and 1151 with total shoulder arthroplasty. Complications included four periprosthetic fractures (two intraoperative), glenoid loosening in two shoulders, and progressive glenoid erosion in four hemiarthroplasties. Other authors have reported a high incidence of rotator cuff tears occurring after shoulder arthroplasty in RA, as well as higher rates of glenoid loosening with longer follow-up. The Mayo Clinic experience with shoulder arthroplasty for rheumatoid arthritis was recently updated.2 Three hundred and three shoulder arthroplasties (95 hemiarthroplasties and 187 total shoulder arthroplasties) were reviewed at a mean follow-up of 11 years. Shoulder arthroplasty was associated with significant improvements in pain and motion. Total shoulder arthroplasty was associated with better pain relief, more motion and a lower risk of revision than hemiarthroplasty only in rheumatoid shoulders with an intact rotator cuff tear. However, the rate of glenoid radiolucent lines was approximately 70%. As mentioned above, reverse shoulder arthroplasty may be considered for patients with rheumatoid arthritis, an associated irreparable cuff tear, and pseudoparalysis. In a small series of eight rheumatoid shoulders treated with a reverse arthroplasty, the average constant score improved from 17 to 63 points; there were two cases of glenoid loosening and three failed acromion osteosynthesis.3 These findings emphasize the functional improvement that can be expected after reverse arthroplasty as well as the high rate of mechanical failure and other complications.
also occur in osteoarthritis with some long press-fit stems. When recognized intraoperatively, every effort should be made to achieve stable fixation of the fracture so that the physical therapy program does not need to be altered. As in other locations, the treatment of postoperative fractures is selected based on the location of the fracture and the fixation of the humeral components.19 Fractures distal to a well-fixed humeral stem may be treated nonoperatively; however, many displaced fractures require internal fixation if the humeral component is well-fixed or revision of loose humeral components with or without associated internal fixation. Aseptic failure of the humeral component is rare and seldom symptomatic. On the contrary, several studies have documented various rates of radiographic radiolucent lines at the glenoid component interface. Some will progress to symptomatic aseptic loosening, which is the main mode of long-term failure in total shoulder arthroplasty. Interestingly, revision for painful glenoid erosion after hemiarthroplasty seems to be more prevalent than revision for glenoid loosening after total shoulder arthroplasty.17 The long-term outcomes of reverse shoulder arthroplasty in rheumatoid arthritis are largely unknown; mechanical failure of the glenoid component is expected to be the main failure mode of reverse shoulder arthroplasty.
Research directions
Develop reliable surgical techniques to allow secure
Complications and failures The main complications of shoulder arthroplasty include infection, instability and periprosthetic fractures. Infection after shoulder arthroplasty is difficult to diagnose preoperatively; many patients with deep infection have normal radiographs and laboratory parameters. Cultures from joint aspirates should be observed for a minimum of 7–10 days to allow identification of Propionibacterium acnes, a slow-growing microorganism commonly responsible for shoulder infections. Two-stage reimplantation is associated with a low rate of reinfection but is technically challenging and not always associated with a good clinical outcome.18 Dislocation or subluxation is another relatively common complication of shoulder arthroplasty. Instability is usually related to inadequate soft-tissue balance and/or component malpositioning. Anterior instability is almost invariably associated with disruption of the subscapularis tendon repair. Posterior instability usually reflects excessive redundancy of the posterior soft-tissues and/or excessive combined glenohumeral retroversion. The outcome of revision surgery for instability after shoulder arthroplasty is very unpredictable.10 Subscapularis failure is best treated when identified early and addressed with prompt surgical repair. In the presence of an irreparable cuff tear or marked posterior soft-tissue redundancy, consideration should be given to revision to a reverse prosthesis. Periprosthetic fractures may occur intraoperatively or postoperatively. Intraoperative fractures are more common in rheumatoid patients secondary to osteopenia, but may
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implantation of a glenoid component in most patients with severe glenoid bone loss by using structural bone graft, graft substitutes or custom-made implants. Define the role of reverse shoulder arthroplasty for patients with end-stage rheumatoid arthritis and a massive irreparable cuff tear.
References 1. Bryant D, Litchfield R, Sandow M, Gartsman GM, Guyatt G, Kirkley A. A comparison of pain, strength, range of motion, and functional outcomes after hemiarthroplasty and total shoulder arthroplasty in patients with osteoarthritis of the shoulder. A systematic review and meta-analysis. J Bone Joint Surg Am 2005;87(9):1947–56. 2. Sperling JW, Cofield RH, Schleck C. Total shoulder arthroplasty versus hemiarthroplasty for rheumatoid arthritis: results of 303 consecutive cases. In: 2007 annual meeting of the American Academy of Orthopaedic Surgeons. San Diego, CA, USA; 2007. 3. Rittmeister M, Kerschbaumer F. Grammont reverse total shoulder arthroplasty in patients with rheumatoid arthritis and nonreconstructible rotator cuff lesions. J Shoulder Elbow Surg 2001;10(1):17–22. 4. Gill DR, Cofield RH, Rowland C. The anteromedial approach for shoulder arthroplasty: the importance of the anterior deltoid. J Shoulder Elbow Surg 2004;13(5):532–7. 5. Walch G, Edwards TB, Boulahia A, Boileau P, Mole D, Adeleine P. The influence of glenohumeral prosthetic mismatch on glenoid radiolucent lines: results of a multicenter study. J Bone Joint Surg Am 2002;84-A(12):2186–91. 6. Walch G, Boileau P. Prosthetic adaptability: a new concept for shoulder arthroplasty. J Shoulder Elbow Surg 1999;8(5): 443–51.
ARTICLE IN PRESS 414 7. Sperling JW, Cofield RH, O’Driscoll SW, Torchia ME, Rowland CM. Radiographic assessment of in growth total shoulder arthroplasty. J Shoulder Elbow Surg 2000;9(6): 507–13. 8. Levy O, Copeland SA. Cementless surface replacement arthroplasty (Copeland CSRA) for osteoarthritis of the shoulder. J Shoulder Elbow Surg 2004;13(3):266–71. 9. Levy O, Funk L, Sforza G, Copeland SA. Copeland surface replacement arthroplasty of the shoulder in rheumatoid arthritis. J Bone Joint Surg Am 2004;86-A(3):512–8. 10. Sanchez-Sotelo J, Sperling JW, Rowland CM, Cofield RH. Instability after shoulder arthroplasty: results of surgical treatment. J Bone Joint Surg Am 2003;85-A(4):622–31. 11. Boardman III ND, Cofield RH, Bengtson KA, Little R, Jones MC, Rowland CM. Rehabilitation after total shoulder arthroplasty. J Arthroplasty 2001;16(4):483–6. 12. Gartsman GM, Roddey TS, Hammerman SM. Shoulder arthroplasty with or without resurfacing of the glenoid in patients who have osteoarthritis. J Bone Joint Surg Am 2000;82(1): 26–34. 13. Lo IK, Litchfield RB, Griffin S, Faber K, Patterson SD, Kirkley A. Quality-of-life outcome following hemiarthroplasty or total shoulder arthroplasty in patients with osteoarthritis.
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14.
15.
16.
17.
18.
19.
A prospective, randomized trial. J Bone Joint Surg Am 2005; 87(10):2178–85. Wirth MA, Tapscott RS, Southworth C, Rockwood Jr CA. Treatment of glenohumeral arthritis with a hemiarthroplasty: a minimum five-year follow-up outcome study. J Bone Joint Surg Am 2006;88(5):964–73. Lynch JR, Franta AK, Montgomery Jr WH, Lenters TR, Mounce D, Matsen III FA. Self-assessed outcome at two to four years after shoulder hemiarthroplasty with concentric glenoid reaming. J Bone Joint Surg Am 2007;89(6):1284–92. Torchia ME, Cofield RH, Settergren CR. Total shoulder arthroplasty with the Neer prosthesis: long-term results. J Shoulder Elbow Surg 1997;6(6):495–505. Sperling JW, Cofield RH, Rowland CM. Minimum fifteen-year follow-up of Neer hemiarthroplasty and total shoulder arthroplasty in patients aged fifty years or younger. J Shoulder Elbow Surg 2004;13(6):604–13. Mileti J, Sperling JW, Cofield RH. Reimplantation of a shoulder arthroplasty after a previous infected arthroplasty. J Shoulder Elbow Surg 2004;13(5):528–31. Kumar S, Sperling JW, Haidukewych GH, Cofield RH. Periprosthetic humeral fractures after shoulder arthroplasty. J Bone Joint Surg Am 2004;86-A(4):680–9.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 415–421
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MINI-SYMPOSIUM: SHOULDER RECONSTRUCTION
(ii) Rotator cuff arthropathy Lennard Funk, John Haines, Ian Trail Wrightington Upper Limb Unit, Wrightington Hospital, Hall Lane, Apley Bridge, Wigan, UK
KEYWORDS Rotator cuff arthropathy; Shoulder; Deltoid rehabilitation; Hyaluronan injections; Arthroscopic shoulder surgery; Biceps tenotomy; Biceps tenodesis; Surface replacement; Reverse geometry arthroplasty
Summary Rotator cuff arthropathy is a specific and uncommon disease entity. It affects mainly elderly, but often active people. The exact causes are not known, but there is evidence of genetic predisposition, crystal disease and mechanical factors. There are numerous treatment options for both the pain and dysfunction. Generally, non-operative measures are successful, if used appropriately and timely. Arthroscopic debridement and washout alone has only short-term benefit, but arthroscopic biceps tenotomy or tenodesis is effective in eliminating pain caused by long head of biceps tendon pathology. Anatomical hemi-arthroplasty, whether stemmed or surface replacement, primarily improves pain. However, modern designs specifically for cuff tear arthropathy have shown improved functional results. Surface replacement implants also confer the benefits of being less invasive and of preserving bone. Reverse total shoulder arthroplasty is a powerful tool for the elderly patient with unresponsive painful pseudoparalysis. However, it has a high complication rate and should be used with care. & 2007 Elsevier Ltd. All rights reserved.
Introduction Rotator cuff arthropathy is characterised by rotator cuff insufficiency, diminished acromiohumeral distance and arthritic changes of the glenohumeral joint. The first descriptions of rotator cuff arthropathy date back to 1853, when Professor Adams at the University of Dublin described chronic rotator cuff tears leading to localised destructive arthritis.1 The term Milwaukee shoulder was introduced in 1981 to describe the condition in four elderly women who had recurrent bilateral shoulder effusions, severe radiographic destructive changes of the glenohumeral joints and massive tears of the rotator cuff. Corresponding author.
E-mail address:
[email protected] (L. Funk). 0268-0890/$ - see front matter & 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2007.11.003
Charles Neer coined the term ‘‘cuff tear arthropathy’’ in 1977 and published his classic article in 1983.2 Neer described the pathoanatomical changes associated with massive, chronic full-thickness rotator cuff tears, which include erosions of the osseous structures, humeral osteopaenia, and restricted shoulder motion. The massive tears allow superior displacement of the humerus resulting in ‘‘femoralisation’’ of the humeral head (erosion of the greater tuberosity) and ‘‘acetabularisation’’ of the coracoacromial arch (reshaping of the arch so that it creates a socket for the proximal aspect of the humerus).2
Pathomechanics The exact cause of cuff arthropathy is not known. Although the progression of rotator cuff tears seems to play a role in
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the development of cuff tear arthropathy, it appears to be a separate pathological entity and not simply the end stage of chronic cuff tears. Neer and co-workers estimated that cuff tear arthropathy would develop in only 4% of patients with a complete rotator cuff tear. Rotator cuff arthropathy differs from other causes of glenohumeral arthritis and should be recognised as a distinct clinical entity. In glenohumeral osteoarthritis, all the usual sequelae of osteoarthritis are present and the rotator cuff is typically intact. Any associated rotator cuff tear is usually traumatic or attritional in nature and repair is typically possible. Rheumatoid arthritis, when associated with massive cuff deficiency, can present in a similar fashion to rotator cuff arthropathy. However, in rheumatoid arthritis there is the added presence of destructive pannus, multiple joints are often involved and patients typically have systemic symptoms at some point in the disease process. Three main theories have been proposed for the development of cuff arthropathy.
Crystal Mediated Theory Halverson, in 1981,3 proposed that the calcium-phosphate crystals in synovial fluid induce an immunologic cascade and the release of collagenase. These activated products cause destruction of the periarticular and articular structures. In response to calcium-containing crystals in the synovial tissue, a low-grade inflammatory response initiates cellular and fibroblast proliferation. Human fibroblasts may then secrete proteolytic enzymes that are responsible for the rapid degradation of cartilage matrix components, as seen in cuff tear arthropathy. There may be a genetic predisposition to crystal mediated cuff arthropathy. Peach et al.4 showed that cuff tear arthropathy is associated with variants in ANKH and TNAP that alter extracellular inorganic pyrophosphate concentrations causing calcium crystal deposition. This supports a theory that genetic variants predispose patients to primary crystal deposition which, when combined with a massive rotator cuff tear, leads to the development of arthritis.
Figure 1 Mechanical and nutritional theories for the development of cuff arthropathy. (Adapted from: Neer et al.2)
associated with the loss of primary and secondary stabilisers of the glenohumeral joint. The wear on the glenoid is often eccentric, involving the anterior superior part. This leads to an accelerated process of further cuff destruction and arthropathy. Nutritional factors The nutritional factors associated with massive full-thickness tears are related to loss of motion and periarticular damage due to loss of a normal joint milieu. The loss of fluid pressure and the accompanying reduction in the quality of the chemical content of synovial fluid leads to cartilage and bone atrophy. Recurrent bloody effusions and loss of glycosaminoglycan content of the cartilage further accelerate the destruction of both bone and soft tissue
Force Couple Theory Cuff Tear Theory In 1983, Neer et al. postulated that massive rotator cuff tears lead to degeneration of the shoulder joint in a percentage of shoulders.2 Two mechanisms contribute to the destruction of shoulder joint and articular cartilage: mechanical and nutritional pathways. Neer et al. based this concept on clinicopathological observations made at the time of surgery and upon a review of histological samples (Fig. 1). Mechanical factors The mechanical factors associated with massive rotator cuff tears lead to unbalanced muscle forces. These factors are anteroposterior instability of the humeral head, resulting from a massive tear of the rotator cuff and rupture or dislocation of the long head of the biceps, leading to proximal migration of the humeral head and acromial impingement. Glenohumeral articular wear occurs as a result of repetitive trauma from the altered biomechanics
Burkhart5 analysed fluoroscopic comparisons of the kinematic patterns of functional and non-functional rotator cuff tears. He showed that the loss of the coronal and sagittal force couples lead to accelerated wear and further disruption of transverse and coronal plane force couples (Fig. 2).
Diagnosis Rotator cuff arthropathy usually presents in the seventh decade. Patients are typically elderly females with longstanding symptoms. Bilateral involvement is present in 60% of cases. The presenting symptoms include: 1. Pain—can range from mild ache, sharp pains with movement to constant and night pain 2. Weakness—with overhead activities, mainly 3. Pseudoparalysis—complete inability to actively move the shoulder, due to cuff deficiency
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Figure 2 Transverse and coronal force couples. The loss of balance between each force couple leads to cuff tear arthropathy. (Blue circle indicates the centre of rotation of the glenohumeral joint.) (Adapted from: Burkhart.5)
Figure 3 Anterior synovial swelling of the left shoulder.
4. Recurrent swellings—as a result of large synovial effusions 5. Instability—deficient cuff leads to anterosuperior escape of the humeral head with attempted elevation of the arm.
A patient may present with some or all of the above symptoms, which can be extremely disabling. Clinical examination usually reveals swelling of the glenohumeral and subacromial joint (which is one articulation) (Fig. 3) and atrophy of supraspinatus and infraspinatus muscles. Active and passive range of motion can be limited because of fixed glenohumeral subluxation. Active glenohumeral motion may be accompanied by palpable or audible crepitus and usually is painful. Weakness of the external rotators may be profound. If the long head of biceps tendon is ruptured, a ‘‘popeye’’ biceps sign will be present, with a bunched up and flaccid biceps muscle. If the long head is intact, it is usually subluxed medially and a source of pain. It is essential to assess the function of the deltoid muscle, as this is the only remaining elevator of the arm in a cuff deficient shoulder. Anterosuperior subluxation (known as ‘‘escape’’) may be seen with resisted attempted active abduction, due to loss of the anterosuperior cuff and biceps tendon (Fig. 4). Acromioclavicular joint arthritis may also be present.
Figure 4 Pseudoparalysis with anterosuperior subluxation of the humeral head with attempted abduction.
Investigations Plain radiography is the most useful investigation for diagnosing and assessing the severity of rotator cuff arthropathy. The typical and characteristic findings are: 1. Superior migration of the humeral head, articulating with the overlying acromion 2. Narrowing of the glenohumeral joint space 3. Osteophytes 4. Rounding off of the greater tuberosity 5. Periarticular soft-tissue calcifications Occasionally, in severely affected shoulders, erosive changes are seen both in the glenohumeral joint and in adjacent structures such as the base of the coracoid process, the lateral end of the clavicle and the anterior aspect of the acromion. Advanced superior migration and medialisation can become marked, producing ‘‘acetabularisation’’ of the coracoacromial arch and ‘‘femoralisation’’ of the humeral head.6 However, if the arm is relaxed and
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L. Funk et al. necessary. They have been shown to be of benefit for early and late osteoarthritis of the shoulder, but have not been investigated for cuff arthropathy yet.9,10 Hyaluronans act by blocking pain receptors, stimulating endogenous hyaluronan production and have a direct anti-inflammatory effect by inhibiting leukocyte action. Deltoid Rehabilitation Program In the absence of a rotator cuff overhead movements are almost impossible without ‘‘trick’’ movements and assistance from the opposite arm. A well-structured program of retraining the anterior and middle deltoid muscles has been shown to be effective in restoring active arm elevation.11 This is mainly effective where pain is not a predominant feature or can be controlled adequately.
Figure 5 Characteristic radiographic features of rotator cuff arthropathy, with femoralisation and acetabularisation (see text).
dependent during radiographic examination the true extent of subacromial narrowing may not be appreciated. Any anterior or posterior instability of the glenohumeral joint is usually apparent from the axillary radiographs. This instability may become fixed and in these cases computerised tomography can be helpful to determine the degree of glenoid erosion (Fig. 5).
Treatment Patients presenting with a cuff arthropathy, present with pain, disability or both. Numerous treatment options are available. The choice of treatment varies according to the patient’s circumstances, surgeon’s preferences and resources. ‘‘No operation’’ does not mean ‘‘no treatment’’.
Treatment options for pain relief 1. 2. 3. 4.
Anti-inflammatory and analgesic drugs Intra-articular injections of steroid Intra-articular injections of hyaluronans Physiotherapy techniques, including local therapy and acupuncture 5. Re-education and limitation of use 6. Modifying lifestyle 7. Surgical options
Arthroscopic surgical procedures Arthroscopic irrigation to remove activated enzymes and crystals offers only limited, short-term relief. Arthroscopic acromioplasty and tendon debridement is commonly used for cuff arthropathy, but there is little supportive data.12 Release of the coracoacromial ligament and excessive bone should be avoided, as it could lead to anterosuperior escape of the humeral head. Tuberoplasty or reversed acromioplasty, arthroscopic debridement of the greater tuberosity, has been shown to be effective in some situations if the tuberosity is not already smoothed down.21 The biceps tendon, if intact, has been thought to be the main source of shoulder pain in patients with large cuff tears and cuff arthropathy. This has been recently published.13 Arthroscopic biceps tenotomy and arthroscopic biceps tenodesis have been shown to treat the severe pain or dysfunction caused by an irreparable rotator cuff tear associated with a biceps lesion. However, the presence of pseudoparalysis is a contraindication to this procedure.14
Shoulder arthroplasty The main indication for arthroplasty in cuff arthropathy is uncontrolled pain affecting the patient’s quality of life. It is contraindicated in the absence of confirmed arthritis of the glenohumeral joint. The current replacement options include (in order of increasing complexity): 1. Anatomical prostheses: Surface replacement Stemmed hemi-arthroplasty 2. Reverse geometry prosthesis
Treatment options for disability 1. Physiotherapy—Deltoid Rehabilitation Programs 2. Occupational therapy—use of aids (and home modifications) 3. Surgical options
Intra-articular injections Repeated intra-articular injections of corticosteroids are discouraged, as they have been shown to be largely ineffective.7,8 They also only have short-term benefit. Hyaluronan injections are safer and may be repeated as
Surface replacement arthroplasty Surface replacement has the advantages of being a less invasive and quicker procedure, for the typically elderly and frail group of patients with cuff arthropathy. It also preserves bone, thus simplifying future possible revision procedures. The modern surface replacement prosthesis has been popularised by Copeland, who has reported good results in pain relief, but not in range of motion.15 The recent
ARTICLE IN PRESS Rotator cuff arthropathy Copeland Extended Articular Surface (EAS) prosthesis offers theoretical advantages in improving the lever arm of the deltoid and therefore allowing for some improvement of active function post-operatively. It is not indicated when there is dislocation or escape as this could lead to a painful escaped prosthesis.
Stemmed hemi-arthroplasty Hemi-arthroplasty is preferred to total shoulder replacement for cuff arthropathy at the moment, as glenoid loosening is much more common.17 This is due to the loss of normal shoulder kinematics and abnormal glenoid forces causing a ‘rocking-horse’ glenoid loosening. The humeral component articulates on the edges of the glenoid component, causing it to rock loose. Numerous stemmed prostheses have been used for cuff arthropathy. It has been common practice to oversize the humeral head in order to avoid further superomedial erosion and improve the lever arm of the deltoid. Bipolar designs have been developed, which have good functional results in the short term.16 However, later revision is difficult and radiographs of the shoulder in varying degrees of abduction revealed no motion at the glenoid–prosthesis interface or at the bipolar polyethylene liner-humeral head articulation. Concerns that have been raised regarding the modified bipolar prosthesis include potential overstuffing of the shoulder joint, rupture of the subscapularis tendon due to the vertical orientation of the component, and the effect of polyethylene wear. More recent head designs have been developed specifically for cuff arthropathy (Fig. 6). These designs, such as the CTA Head (DePuy), have the same theoretical advantages as the Copeland EAS. Early 2-year results seem promising in terms of range of motion and pain relief, with an average doubling of active flexion post-operatively.18 As with the surface replacement, it is not indicated when there is dislocation or anterosuperior escape.
Reverse geometry arthroplasty Interest in the reverse geometry arthroplasty (RGA) has increased in Europe over the past 12 years, popularised by
419 Grammont in France.19 He established the basic principle for the modern prosthesis, which includes medialisation and lowering of the centre of rotation of the joint, thereby increasing the lever arm and improving deltoid muscle efficiency. The semiconstrained design of the prosthesis ensures stability, even in the presence of anterosuperior escape. Until Grammont’s device, all reverse designs had a lateral offset of the glenoid component relative to the glenoid surface. This attachment site proved to be the site of failure, as the lateral offset increased the moment arm of the resultant joint reactive force, which further stressed the glenoid–prosthetic bone attachment. On the other hand, the medialisation of the Grammont design diminishes the moment arm on the joint reactive force (Fig. 7a and b). The RGA has been used successfully for over 10 years now with excellent medium term results in the elderly cuff arthropathy patient and for complex revision surgery, where the cuff is deficient. It has been shown to both significantly improve pain, as well as improve motion and function of the shoulder.20 It has been able to restore useful function to extremely disabled patients (Figs. 8 and 9). However, complication rates are significantly higher than anatomical prostheses and further revision options are difficult, therefore less invasive options must be exhausted first. The main indication for the RGA is a pseudoparalytic cuff arthropathy in an elderly patient. It is also indicated where there is escape and revision situations with dislocation. A functional deltoid must be present in all cases. As mentioned above, RGA is considered when rehabilitation has failed, and conventional surgical reconstruction methods cannot satisfactorily manage shoulder pain and loss of function. Because of the magnitude of the intervention and potential risks of RGA, non-operative means of improving the patient’s quality of life merit a dedicated trial prior to surgery. The RGA is contraindicated in patients with
1. 2. 3. 4.
Nonfunctional deltoid muscle Active infection Insufficient bone to seat the implant components Muscular, neurologic, or vascular deficiencies that compromise the affected extremity 5. High levels of physical activity (e.g., competitive sports, manual labour)
Figure 6 Anatomical arthroplasty designs for cuff tear arthropathy. From left to right: Copeland surface replacement (Biomet), Copeland EAS (Biomet), bipolar hemi-arthroplasty (Biomet), CTA Head (DePuy).
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Figure 7 (a) Grammont principles of medialising the centre of rotation with the reverse geometry prosthesis and increasing the deltoid lever arm. (b) The deltoid is detensioned and shortened, due to superior subluxation of cuff arthropathy (left). The RGA increases the lever arm of deltoid, with lowering and tensioning of deltoid (right). (Adapted from: Matsen et al.20)
Figure 9 Treatment algorithm for managing cuff arthropathy.
Figure 8 Post-operative radiograph of a reverse geometry arthroplasty.
As one would expect with a prosthesis that is large and complex inserted into more challenging elderly and revision cases the complication rates are higher than with other implants. These are more frequent still when RGA is used to revise a failed prior arthroplasty.
ARTICLE IN PRESS Rotator cuff arthropathy Intra-operative complications include humeral cortical perforations, shaft fractures or glenoid fractures. Prevention requires respect for the osteopaenic bone of older patients and gentle reaming by hand. Pre-operative planning is essential to ensure that there is sufficient glenoid bone to accept the glenoid component. CT scans are often required to assess the glenoid bone stock pre-operatively. Post-operative haematomas are common, facilitated by the large dead space that occurs after surgery with an absent cuff. Humeral shaft fracture is another relatively common post-operative complication. These fractures usually are due to a fall or to abrupt passive elevation or rotation of the arm. They often occur at the tip of the prosthesis. Loosening of the humeral component is uncommon and usually is associated with a fracture or infection. Infection is more common with RGA. Contributing causes include haematoma formation, revision of a previous arthroplasty, the magnitude of the surgery, and the compromised general health of some patients. Other complications include unscrewing of the junction between the metaphyseal and diaphyseal portions of the humeral component and loosening of the glenoid component. Glenoid erosion by impingement of humeral component on the inferior glenoid is often seen. It usually is not progressive but needs to be observed and revised if severe. These complications are lessening due to improvements in prosthetic design. Dislocation is a relatively common complication, especially after the revision of a previous arthroplasty, when the osseous and soft-tissue anatomy has been distorted by prior trauma, when components are malpositioned, or when the humeral component levers against glenoid bone. Fractures of the acromion occur commonly as a result of a pre-existing acromial lesion, overtensioning of the deltoid, or osseous fatigue from loading of an osteopenic acromion. Neurological injuries include axillary nerve damage from surgical dissection or traction injuries from excessive tension resulting from lengthening of the arm. These injuries are most common in revisions with difficult surgical exposures.
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2. 3.
4.
5.
6.
7. 8.
9.
10. 11.
12. 13.
14.
15. 16.
Conclusions Rotator cuff arthropathy is an uncommon, challenging disease. Elderly people are, in general, more active nowadays and have an increasing demand for continued useful function into old age. Increased understanding of cuff arthropathy and improving technology gives us more knowledge and tools to skilfully manage this condition (Fig. 9).
17. 18.
19. 20.
References 21. 1. Adams R. Illustrations of the effects of rheumatic gout or chronic rheumatic arthritis on all the articulations: with
descriptive and explanatory statements. London: J Churchill; 1857. p. 1–31. Neer II CS, Craig EV, Fukuda H. Cuff-tear arthropathy. J Bone Joint Surg Am 1983;65:1232–44. Halverson PB, Cheung HS, McCarty DJ, Garancis J, Mandel N. ‘‘Milwaukee shoulder’’—association of microspheroids containing hydroxyapatite crystals, active collagenase, and neutral protease with rotator cuff defects. II. Synovial fluid studies. Arthritis Rheum 1981;24:474–83. Peach CA, Zhang Y, Dunford JE, Brown MA, Carr AJ. Cuff tear arthropathy: evidence of functional variation in pyrophosphate metabolism genes. Clin Orthop Relat Res 2007;462:67–72. Burkhart SS. Fluroscopic comparision of kinematics patterns in massive rotator cuff tears. A suspension bridge model. Clin Orthop 1992;284:146. Hamada K, Fukuda H, Mikasa M, et al. Roentgenographic findings in massive rotator cuff tears: a long-term observation. Clin Orthop 1990;254:92–6. Williams Jr. GR, Rockwood Jr. CA. Hemiarthroplasty in rotator cuff-deficient shoulders. J Shoulder Elbow Surg 1996;5:362–7. Koester MC, et al. The efficacy of subacromial corticosteroid injection in the treatment of rotator cuff disease: a systematic review. J Am Acad Orthop Surg 2007;15(1):3–11. Valiveti M, Reginato AJ, Falasca GF. Viscosupplementation for degenerative joint disease of shoulder and ankle. J Clin Rheumatol 2006;12(3):162–3. Funk L. Ostenil hyaluronan for inoperable osteoarthritis of the shoulder. Osteoarthritis Cartilage 2004;12(Suppl. B). Ainsworth R. Physiotherapy rehabilitation in patients with massive, irreparable rotator cuff tears. Musculoskeletal Care 2006;4(3):140–51. Jensen KL, Williams GR, Russell IJ, Rockwood CA. Rotator cuff tear arthropathy. J Bone Joint Surg Am 1999;81:1312–24. Kontakis GM. The long biceps tendon as the main cause of shoulder pain in rotator cuff tears. Orthopedics 2007;30(3): 185. Boileau P, Baque F, Valerio L, Ahrens P, Chuinard C, Trojani C. Isolated arthroscopic biceps tenotomy or tenodesis improves symptoms in patients with massive irreparable rotator cuff tears. J Bone Joint Surg Am 2007;89(4):747–57. Levy O, Copeland SA. Cementless surface replacement arthroplasty of the shoulder. J Bone Joint Surg (Br) 2001;83-B:213–21. Sarris IK, Papadimitriou NG, Sotereanos DG. Bipolar hemiarthroplasty for chronic rotator cuff tear arthropathy. J Arthroplasty 2003;18(2):169–73. Ball CM. Arthroplasty for the treatment of rotator cuff arthropathy. Oper Tech Orthop 2003;13(4):290–300. Visotsky JK, Basamania C, Seebauer L, Rockwood CA, Jensen KL. Cuff tear arthropathy: pathogenesis, classification, and algorithm for treatment. J Bone Joint Surg Am 2004;86:35–40. Grammont PM, Baulot E. Delta shoulder prosthesis for rotator cuff rupture. Orthopedics 1993;16:65–8. Matsen FA, Boileau P, Walch G, Gerber C, Bicknell RT. The reverse total shoulder arthroplasty. J Bone Joint Surg (Am) 2007;89:660–7. Scheibel MT, Lichtenberg S, Habermeyer P. Reversed arthroscopic subacromial decompression for massive rotator cuff tears. J Shoulder Elbow Surg 2004;13:272–8.
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MINI-SYMPOSIUM: SHOULDER RECONSTRUCTION
(iii) Post-traumatic reconstruction for sequelae of fractures of the proximal humerus R. Hertel, E. Fandridis Lindenhofspital, Bremgartenstrasse 117, 3012 Bern, Switzerland
KEYWORDS Proximal humerus; Fractures; Complications; Treatment
Summary In spite of the development of new techniques and implants, undesirable early and late sequelae may occur after both nonoperative and operative treatment of fractures of the proximal humerus. In this review, we aim to give some clear directions on how to manage these often complex post-traumatic conditions, in an area where there is a little consensus on treatment in the literature. & 2007 Elsevier Ltd. All rights reserved.
Introduction
Shoulder stiffness
Ageing and osteoporosis lead to an increased incidence of fractures of the proximal humerus.1 Kannus et al.2 have predicted a three-fold increase in the incidence of these fractures over the next three decades. The majority of them are minimally displaced and treated nonoperatively. Approximately, one-fifth of these fractures require operative treatment.3 Late sequelae may occur after either nonoperative or operative treatment. The purpose of this paper is to discuss late sequelae that significantly affect the patient’s outcome, such as shoulder stiffness, heterotopic ossification (HO), avascular necrosis (AVN), malunion, nonunion and post-traumatic arthritis.
Shoulder stiffness is a common complication after osseous injuries, such as fractures and/or fracture-dislocations of the proximal humerus; it may occur after both closed and open treatment. Motion loss in isolated directions may progress to global limitation of movement. Factors that contribute to this complication include the severity of the initial injury, inadequate operative technique (including non-anatomic reduction) and inadequate rehabilitation. Post-traumatic shoulder stiffness can be categorized according to Fig. 1. Shoulder stiffness after minimally displaced fractures may be related to soft tissue contractures4 and/or glenohumeral cartilage erosion. The soft tissue contractures can be subdivided into intra- and periarticular variants, accepting that intra- and periarticular adhesions frequently coexist.5 Malunions and nonunions can also result in shoulder stiffness, while associated soft tissue adhesions often contribute. Infection, especially low-grade infection, can be an additional cause of painful stiffness, and this should always be ruled out prior to the implementation of any treatment.
Corresponding author. Tel.: +41 31 300 8070 ;
fax: +41 31 318 8181. E-mail address:
[email protected] (R. Hertel). 0268-0890/$ - see front matter & 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2007.11.005
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Posttraumatic Shoulder Stiffness
Non-distorted anatomy
soft tissue abnormalities
intraarticular
cartilage damage
Distorted anatomy
infection
malunion
nonunion
periarticular
Figure 1 Possible causes of post-traumatic shoulder stiffness. The stiffness can be related to more than one cause. For example, malunion may coexist with cartilage erosion, soft tissue contractures or infection, and so on.
Figure 2 Arthroscopic release of post-traumatic shoulder stiffness in the presence of a humeral head arthroplasty. Right shoulder, sitting position.
The choice of treatment depends on the cause of the stiffness. In patients with mild limitation of shoulder motion or endurable pain due to soft tissue contractures, the treatment will include exercises, pain medications or intraarticular corticosteroids. Patients with severely limited range of motion due to soft tissue scarring and contractures, as well as patients who did not improve with nonoperative care, are to be considered for operative treatment.
Arthroscopic techniques are effective for intra- and periarticular arthrolysis (Fig. 2). Where hardware removal is required due to pain or impingement, we recommend a combined arthroscopic and open procedure. Arthroscopically, the intra-articular release can be performed and with the open procedure periarticular release can be completed. Regions of the capsule that require release are determined by physical examination. Loss of external rotation requires
ARTICLE IN PRESS 424 a release of the superior and middle glenohumeral ligaments, the rotator interval and the coracohumeral ligament extra-articularly. Loss of elevation requires release of the antero-inferior capsule including the anterior band of the inferior glenohumeral ligament, while loss of internal rotation requires postero-superior and postero-inferior capsular release.6 The treatment of post-traumatic stiffness caused by cartilage erosion depends on the severity of damage. Arthrolysis can be performed in the presence of mild arthritic changes, while shoulder replacement is an option in advanced arthrosis. Biceps tenotomy should always be considered when the biceps tendon is adherent to the bicipital groove. Stiffness after malunion with minimally distorted anatomy requires soft tissue release, while in the case of severely distorted anatomy, corrective osteotomy and soft tissue release may be necessary. Stiffness associated with nonunion can be managed by soft tissue release, internal fixation, and supervised rehabilitation according to the stability of the fixation. Stiffness associated with infection requires immediate treatment with irrigation, open and/or arthroscopic debridement combined with intravenous culture-based antibiotics.
Heterotopic Ossification HO has been reported by several authors, especially after fracture–dislocations of the proximal humerus.7 Neer reported HO in 12% of patients with three- and four-part fractures including fracture–dislocations that were treated with closed reduction, ORIF or hemiarthroplasty. It is unusual for HO to occur after uncomplicated fractures, but it is seen not infrequently in patients with neglected fracture–dislocations.8 Pre-disposing factors to HO are: head9 and spinal cord10 injury, ankylosing spondylitis, diffuse idiopathic skeletal hyperostosis, history of HO formation11 and extensive local soft tissue damage or dissection. Boehm et al.12 reviewed 121 patients who were treated with total shoulder replacements or hemiarthroplasties; 48 of 121 patients had sustained a fracture and/or fracture-dislocation of the proximal humerus. There was no statistical difference in the HO between total and hemiarthroplasty, and the proximal humerus trauma patient group did not present increased risk for HO formation. Interestingly, HO has little clinical relevance to the patient’s functional outcome.7 True bony bridging of the glenohumeral space is rare. Anatomically, we observed limiting HO in the substance of the subscapular muscle, the metaphyseal calcar region and the subacromial bursa. Surgical resection is possible, when HO is the reason for limitation. Excision should be attempted only after the ossification has matured; that means when the osseous trabecular structure has been well formed and the cortical line has been clearly defined. For most patients, this requires a period of 6–9 months after the initial surgery.11 Standard radiographs and computed tomography (CT), especially three-dimensional (3-D) reconstruction images, are necessary for full evaluation of the ossification. Scintigraphy and biological markers are not so important for the assessment of maturation.13,14 Bone excision from the glenohumeral joint requires meticulous dissection due to the proximity of the axillary nerve and branches
R. Hertel, E. Fandridis of the brachial plexus. In our practice, we aim at wide excision of the HO i.e. epineoperiosteal dissection. Additionally, we use indomethacin 25 mg three times daily for 3 weeks.15
Avascular Necrosis AVN may occur as a late complication of fractures of the proximal humerus and its development is strongly related to the blood supply of the humeral head. Although studies have emphasized the importance of the anterior circumflex vessels and the arcuate artery,16 this has not been confirmed by anatomical and clinical studies in the fractured humerus. The arcuate artery is generally interrupted even in the most simple fracture patterns. The main perfusion to the humeral head is most likely derived from the posterior circumflex vessels.17–19 Lee and Hansen20 reported that revascularization through creeping substitution may also occur. In patients with a fracture of the proximal humerus and constitutionally high dominant anterior vessels, only a postero-inferior part of the head remains perfused initially. This ischaemic cranial part can be revascularized when adequate contact with bleeding cancellous bone and a stable mechanical environment is provided.19 Humeral head ischaemia is associated with fracture lines at the anatomical neck level, small length of the dorsomedial metaphyseal extension and disruption of the medial hinge. Head angulation, tuberosities displacement and glenohumeral dislocation are relatively poor predictors of head ischaemia.19 Hagg and Lundberg21 reported AVN rate of 3–14% after closed reduction of displaced three-part fractures and a rate of 13–34% after four-part fractures, while Sturzenegger et al.22 reported 34% incidence of AVN in a series of 17 patients treated with a T-plate. The extensive soft tissue exposure needed for internal fixation with bulky implants, was thought to be a factor for AVN in this series. However, AVN may be associated with satisfactory function if anatomic reconstruction was obtained.23 The treatment of post-traumatic AVN depends on the patient’s disability and the radiological stage.24 In the early stages of AVN, in patients with no pain or limited joint motion, nonoperative treatment can be an option, while in patients present with pain or impaired function, humeral resurfacing arthroplasty can be a suitable solution (Fig. 3). In end stages of AVN with collapse of the subchondral bone and destroyed articular cartilage, shoulder arthroplasty with glenoid replacement is the primary option (Fig. 4). The application of stemless humeral resurfacing arthroplasty has several advantages over a stemmed prosthesis, such as the minimal bone removal, the uncomplicated revision surgery if necessary, the avoidance of stress risers, thus eliminating the risk of periprosthetic fractures, and the accurate recreation of proximal humeral anatomy. In our practice, most of the patients that we treat with post-traumatic AVN have already a Ficat stage III or IV. These patients are preferably treated with surface replacement arthroplasty.
Nonunion Nonunion may result as a consequence of the initial injury or more frequently as a consequence of its treatment.
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Figure 3 Four-part fracture of the proximal humerus-type H-G-L-S that was initially treated with ORIF. AVN of the humeral head developed over a 4-year period. Successful treatment using a humeral resurfacing arthroplasty.
Figure 4 Four-part fracture-type H-G-L-S. ORIF with k-wires. End stage AVN with associated arthritis. Successful treatment with a hybrid shoulder arthroplasty.
We define nonunion of the proximal humerus as the failure of the fracture to heal 6 months after the initial injury. The presence of rounded sclerotic fracture ends and the absence of bridging callus are generally considered criteria for nonunion. Both displaced and minimally displaced fractures of the proximal humerus may result in nonunion.25,26 We still do not know the incidence of post-traumatic nonunion. Factors contributing to nonunion include open fractures,
interposition of soft tissues, inadequate fixation, devascularization, metabolic diseases, hematologic disorders, alcoholism, and poor patient compliance.27–29 Patients with nonunion of the proximal humerus experience pain and loss of function of a variable degree. Nonunion often is associated with soft tissue stiffness, and it is very difficult to assess the true glenohumeral motion due to the pathologic instability at the nonunion site. In our clinical
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Table 1 Nonunion patterns in analogy to the HGLS fracture classification. Two-part nonunions
Three-part nonunions
Four-part nonunion
Type Type Type Type Type Type Type
Type Type Type Type Type Type
Type 14: H-G-L-S
1: 2: 3: 4: 5: 6: 7:
HGL-S H-GLS HSL-G HGS-L HG-LS HL-GS HS-GL
8: HL-G-S 9: HG-L-S 10: H-G-LS 11: H-L-GS 12: H-GL-S 13: HS-G-L
H: humeral head; G: greater tuberosity; L: lesser tuberosity; S: shaft. The short line between the letters represents the nonunion level.
assessment, we palpate with one hand on both tuberosities and perform an assisted, active external rotation of the arm. If the tuberosities do not rotate, then the observed motion is due to instability at the nonunion site. We also observed that many of the patients present with a false positive external rotation lag sign due to the instability at the nonunion site, and not to a torn rotator cuff. Basic radiological assessment such as anteroposterior, axillary and lateral scapular views may not be sufficient to assess the degree of displacement, thus a CT scan is often valuable. We suggest using a classification of humeral nonunions of the proximal humerus that is analogous to the binary fracture description.30,31 There are 14 possible nonunion patterns. They can be described with a sequence of four letters: H (humeral head), G (greater tuberosity), L (lesser tuberosity) and S (shaft). The letters can be used in any sequence and a short line between them, represents a nonunion plane. A surgical neck nonunion will be abbreviated like HGL-S. A three-part nonunion is an HL-G-S if the lesser tuberosity is attached to the humeral head or an H-G-LS if the lesser tuberosity is attached to the shaft, and so on. With this description, 14 basic nonunion patterns can be defined (Table 1). It is out of the scope of this paper to analyze every nonunion pattern. We will focus on the most frequent patterns.
Greater tuberosity nonunion (HLS-G) Closed treatment of greater tuberosity fractures may result in posterior and superior migration of the tuberosity due to the action of the supraspinatus, the infraspinatus and the teres minor muscles.32 Displacement of more than 5–10 mm may result in subacromial impingement and rotator cuff dysfunction.33 In patients with pain and rotator cuff insufficiency, reconstruction should be considered. After debridement and decortication of the nonunion, mobilization and release of the rotator cuff is the most important step. Splitting of the rotator interval, dissection of the coracohumeral ligament and posterior capsulotomy or capsulectomy are mandatory in order to mobilize the retracted rotator cuff. Anatomic reduction of the greater tuberosity assures that proper tension of the rotator cuff is restored. In our practice, we perform debridement,
decortication and rotator cuff release, followed by fixation of the greater tuberosity with transosseous sutures, plus in the case of larger fragments, augmentation with 2.7 or 3.5 mm cortical screws. We believe that especially small tuberosity fragments should not be removed, in order to allow better healing.
Surgical neck nonunion (HGL-S) Nonunion of the surgical neck usually requires operative treatment. The viability of the humeral head and the quality of the cartilage will define the choice of treatment. Preoperative work up may include conventional radiographs, CT scans and magnetic resonance imaging (MRI). In the presence of hardware a metal suppression CT scan can be used. Alternatively, the hardware can be removed, in order to have an MRI analysis. The intraoperative assessment of the head’s viability is an additional diagnostic tool. Clear backflow after the head is drilled in its central part and the use of Doppler laser, if available, may give a positive proof of head perfusion. Treatment options are either head preserving or rarely replacement arthroplasty. Head preserving techniques are based on decortication, recanalization and stable fixation. For fixation there are several options, such as plates, nails, rods and tension bands.34–39 Additionally, bone grafts can be used either to enhance stability, to enhance healing or both. The use of intramedulary rods with or without tension bands, has not been satisfactory in reported papers, mainly due to the impinging metal.40 Several studies34,41 reported poor results after replacement arthroplasty and the reason was failure of healing of the tuberosities to the humeral shaft. We agree that indications for arthroplasty should be examined cautiously. In cases with a short proximal segment, fixation might be insecure, and large autologous bone grafts may be inadequate in elderly patients due to poor mechanical properties of the graft. Donor site morbidity, including fractures of the iliac wing, especially in the elderly patients, may also affect patient outcome. Although, there are several problems with internal fixation in surgical neck nonunions, most studies do support the use of plates.34–38,42 Blade plates, T-plates and angular stable plates can be considered as methods of stabilization. In most cases, healing is achieved and hardware removal is usually not required. Despite generally good results, complications do occur after ORIF, such as hardware impingement if placed too superiorly, AVN due to extensive medial soft tissue stripping, and infection.7,25,43 In our practice, the mechanical stability of the construct and preserving the biological potential remain the main goals to foster union. The mechanical stability can be enhanced by impaction of the humeral shaft with the head, and slight valgus overreduction (Fig. 5). We use an AO 1/3 tubular plate or a 3.5 blade plate in patients with good bone quality. We also use autologous bone graft in bone defects, but not routinely, in order to enhance the healing process.
Malunion Malunion may occur along the five basic fracture planes and therefore can be complex to understand.19 It is helpful to
ARTICLE IN PRESS Post-traumatic reconstruction for sequelae of fractures
427 malrotation of the proximal humerus, and thus not to a soft tissue abnormality. X-rays in different degrees of rotation can also give valuable information on the deformity pattern. Most malunions are 3-D deformities, which can be precisely visualized by CT scan, including 2-D and 3-D reconstructions. Also, we should not ignore the importance of the initial trauma films, which will furnish information on the type of injury, and very likely on the cause of the malunion. The treatment depends on the degree of the anatomical distortion, the type of soft tissue abnormalities, and the patient’s needs and expectations.
Malunion of the surgical neck
Figure 5 Three-part fracture-type HL-G-S (perfused head) treated with ORIF. Nonunion of the surgical neck with varus deformity and malrotation. Correction with decortication, recanalization, impaction and double bend blade plate osteosynthesis.
analyze the malunion pattern in analogy to the HGLS system, as described above. The most frequent malunion patterns are greater tuberosity malunion, varus malunion of the humeral head, extension malunion of the humeral head, and lesser tuberosity malunion. We also agree that various soft tissue abnormalities have to be considered in preoperative planning.44 Soft tissue abnormalities include stiffness, scarring, rotator cuff deficiencies and deltoid muscle lesions. We believe that any further categorization does not offer further help in choosing treatment directions, in consideration of the individual personality of any given malunion case. For instance, a patient with 401 varus malposition of the humeral head may function well, while another patient with the same deformity may be functionally impaired. In our opinion, soft tissue contribution to the poor function of any malunion is always a question, and scrutiny is mandatory to find the real cause of the patient’s problems. Rodosky et al.45 reported that soft tissue scarring and adhesions are the main causes of limited shoulder range of motion and presented good results after open release and trimming of any prominent spikes. A carefully combined clinical and radilological evaluation will probably reveal the cause of functional impairment. For instance, a shifted arc of motion with a normal range, is probably due to
Malunion of the surgical neck may result in extension, varus or valgus deformity. Varus and extension malunions are more frequent, and in severe deformities may cause limited flexion or abduction.44 Varus angulation can also limit external rotation due to impingement of the greater tuberosity against the glenoid. Several authors have reported that osteotomy, such as valgus corrective wedge osteotomy, can improve shoulder function.8,46,47 In our practice, corrective osteotomies combined with focused soft tissue procedures produce reliable results (Fig. 6). Nevertheless, we would like to draw the reader’s attention to the fact that a medially hinged closing wedge osteotomy may not result in the desired anatomical correction as it may lead to lateralization of the center of rotation. Translation of the shaft with respect to the epiphyseal fragment is often necessary to restore the mechanical axis of the proximal humerus, i.e. to restore normal offset. An important element in planning the osteotomy, is to retain at least a 10 mm long medial metaphyseal extension, in order to preserve head perfusion. For fixation, anatomically contoured plates are not useful, because correction leads to shortening and shortening leads to a right-angled step in the lateral cortex. Therefore, a custom contoured plate with a double bend is required.
Malunion of the tuberosities The greater tuberosity may be displaced posteriorly and superiorly various degrees, which may lead to a loss of abduction and external rotation.48 For marked displacement, corrective osteotomy of the greater tuberosity after mobilization of the rotator cuff should be considered. Arthroscopic acromioplasty is an option only for minimally displaced malunions of the greater tuberosity. In cases where the greater tuberosity lies far posteriorly, the anterior deltopectoral approach may be insufficient and a more extensive deltoid-off approach could be necessary. The methods of fixation may include sutures, screws and wires. In our practice, we mobilize the osteotomized greater tuberosity via a juxtalabral postero-superior capsulotomy. We have observed that in acute lesions the supraspinatus tendon is torn in the line of its fibers approximately 5 mm posterior to its leading edge. Since the tuberosity fragment is displaced, this results in a v-shaped opening of the supraspinatus. In chronic lesions, such as malunions, this opening is filled and obliterated with reparative scar
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R. Hertel, E. Fandridis
Figure 6 Surgical neck fracture fixed in 501 of internal malrotation. Corrective osteotomy and fixation with double bend blade plate was performed.
tissue. In order to obtain anatomic reduction this v-shaped scar tissue needs to be excised. We usually stabilize the greater tuberosity with transosseous sutures and we augment the fixation with 2.7 or 3.5 mm cortical screws (Fig. 7). Malunion of the lesser tuberosity is a common but underdiagnosed deformity. The functional impairment is related to a mechanical block of internal rotation (intraarticular impingement) or to impingement to the coracoid process (extra-articular impingement). Intra-articular impingement can be treated arthroscopically. The intraarticular step is due to the prominent rim of humeral head that usually remains attached to the lesser tuberosity. This prominent cartilage-covered rim can be trimmed in order to allow impingement-free internal rotation. If extra-articular impingement exists, osteotomy of the lesser tuberosity, mobilization of the subscapular muscle and secure fixation of the lesser tuberosity in the anatomical position may be necessary.
Post-traumatic arthritis Post-traumatic arthritis is infrequent after minimally displaced fractures of the proximal humerus, but its incidence is higher after more complex injuries. Zyto et al.49 reported a 64% post-traumatic arthritis rate after three and four-part displaced fractures that were treated nonoperatively or
with internal fixation. Possible causes of post-traumatic arthritis are malunion and nonunion with joint incongruity, including splitting injuries of the humeral head and malunions of the tuberosities, neglected unreduced dislocations, recurrent subluxations or dislocations and late stages of AVN. In the management of post-traumatic arthritis, bone and soft tissue injuries should be carefully considered. Associated malunion or nonunion, stiffness and rotator cuff tear make the treatment of post-traumatic arthritis a real challenge. Infection and nerve lesions should be carefully assessed. Several authors have reported inferior results for shoulder arthroplasties undertaken for the sequelae of fractures than for hemiarthroplasties in acute fractures.50,51 They also reported less favorable results when posttraumatic arthritis was associated with malunion, nonunion or humeral head defects.52 Patients with insignificant symptoms and mild shoulder arthritic changes can be managed with nonoperative care, while patients with considerable pain and impaired function may be considered for operative treatment. Hemiarthroplasty, total shoulder arthroplasty, reverse arthroplasty, shoulder arthrodesis and resection arthroplasty are the operative options in the surgeon’s armory. Extensive glenoid cartilage erosion remains the main indication for glenoid replacement, though many authors prefer to perform a hemiarthroplasty in young, active patients with intact glenoid cartilage. For others, the potential complications
ARTICLE IN PRESS Post-traumatic reconstruction for sequelae of fractures
Figure 7 Malunion of the greater tuberosity with posterosuperior displacement. Anatomic reduction and secure fixation with transosseous sutures and screws.
associated with the glenoid component are additional reasons for the choice of hemiarthroplasty.53 However, Boileau et al.41 reported the advantages of total shoulder arthroplasty over hemiarthroplasty, in terms of relief of pain and improvement in function. Copeland54 recommended drilling of the articular surface of the glenoid in order to promote formation of fibrocartilage, while biological resurfacing with various autogenic or allogenic materials (achilles tendon, fascia lata, dermis and anterior capsule) has also been reported.55 Future studies with long-term follow-up will determine the potential of biological techniques. Resurfacing humeral arthroplasty with or without glenoid replacement is a surgical option for the treatment of posttraumatic arthritis. In our practice, the anterior deltopectoral approach is a standard, reproducible, simple approach that provides adequate exposure. The identification of the humeral neck and the removal of the superior and inferior osteophytes of the head, are the key points in anatomic component insertion. The humeral head resurfacing prosthesis also provides the option to accept some variation in proximal humeral anatomy (Fig. 8). Preservation of bone stock for future revisions, no stress risers for the shaft of the humerus, and the avoidance of intramedullary reaming, are other advantages of resurfacing arthroplasty. In our hands, hybrid shoulder arthroplasty, with a resurfacing humeral head and a polyethylene glenoid component, provided satisfactory medium term results. Some authors56,57 have pointed out that greater tuberosity osteotomy is related to poor results after shoulder arthroplasty and that one should avoid it. We believe that
429
Figure 8 Post-traumatic arthritis with associated moderate malunion. Intact glenoid. Delibrate implantation of humeral resurfacing arthroplasty in extra-anatomic position.
post-traumatic reconstruction should replicate the proximal humerus as anatomically as possible, and that severe malposition of the tuberosities results in impaired function. Nonanatomic tuberosities reconstruction may lead to significant functional impairment and increase of the torque requirements.58 In our practice, tuberosity osteotomy followed by fixation with wire-cerclages provided a high rate of healing, and can therefore be considered for selected cases. Shoulder fusion (arthrodesis) is a well-established procedure that is significantly less frequently indicated since the advent of shoulder arthroplasty. We agree that there are indications related to post-traumatic sequelae, such as chronic infection, post-traumatic brachial plexus injury, severe deltoid muscle insufficiency and failed shoulder arthroplasties in selected patients, which can be treated with shoulder fusion.59 Fusion is generally less well tolerated in elderly patients with poor scapulothoracic muscles. Resection arthroplasty may also have a therapeutic role in post-traumatic salvage procedures. Resection arthroplasty may be indicated in infected shoulder arthroplasties, especially in patients with significant comorbidities or in those with severe soft tissue deficiencies, which may not be amenable to a further implantation.60
Conclusion Surgeons will be facing an increasing number of posttraumatic conditions, which may be due to the demographic
ARTICLE IN PRESS 430 changes and our limited capabilities in treating complex and osteoporotic fractures. The spectrum of post-traumatic conditions is wide. Treatment plans should be customized and adapted to the particular situation. Directions for treatment can be derived, by analyzing the soft tissue abnormalities and the osseous deformities, with reference to the HGLS system of fracture classification.
References 1. Bengner U, Jonhell O, Redlund-Johnell I. Changes in the incidence of fracture of the upper end of the humerus during a 30-year period. A study of 2125 fractures. Clin Orthop Relat Res 1988;231:179–82. 2. Kannus P, Palvanen M, Niemi S, Parkkari J, Jarvinen M, Vuori I. Osteoporotic fractures of the proximal humerus in elderly Finnish persons: sharp increase in 1970–1998 and alarming projections for the new millennium. Acta Orthop Scand 2000; 71(5):465–70. 3. Bigliani LU. Fractures of the proximal humerus. In: Rockwood CA, Matsen FA, editors. The shoulder. Philadelphia: WB Saunders; 1990. p. 278. 4. Cotta H, Correll J. The post-traumatic frozen shoulder. Unfallchirurgie 1982;8(5):294–306. 5. Goldman RT, Koval KJ, Cuomo F, Gallagher MA, Zuckerman JD. Functional outcome after humeral head replacement for acute three- and four-part proximal humeral fractures. J Shoulder Elbow Surg 1995;4(2):81–6. 6. Bowen MK, Warren RF. Ligamentous control of shoulder stability based on selective cutting and static translation experiments. Clin Sports Med 1991;10(4):757–82. 7. Neer II CS. Displaced proximal humeral fractures. II. Treatment of three-part and four-part displacement. J Bone Surg Am 1970; 52:1090–103. 8. Rockwood CA, Matsen FA, Wirth MA, Lippit SB. The shoulder, 3rd ed. Philadelphia: WB Saunders; 2004. 9. Sazbon L, Najenson T, Tartakovsky M, Becker E, Grosswasser Z. Widespread periarticular new-bone formation in long term comatose patients. J Bone Joint Surg 1981;63B:120–5. 10. Stover SL, Hahn HR, Miller III JM. Disodium etidronate in the prevention of heterotopic ossification following spinal cord injury. Paraplegia 1976;14(2):146–56. 11. Iorio R, Healy WL. Heterotopic ossification after hip and knee arthroplasty: risk factors, prevention and treatment. J Am Acad Orthop Surg 2002;10(6):409–16. 12. Boehm TD, Wallace WA, Neumann L. Heterotopic ossification after primary shoulder arthroplasty. J Shoulder Elbow Surg 2005;14(1):6–10. 13. Garland DE, Hanscom DA, Keenan MA, Smith C, Moore T. Resection of heterotopic ossification in the adult with head trauma. J Bone Joint Surg Am 1985;67(8):1261–9. 14. Orzel JA, Rudd TG. Heterotopic bone formation: clinical, laboratory, and imaging correlation. J Nucl Med 1985;26(2): 125–32. 15. Ritter MA, Gioe TJ. The effect of indomethacin on paraarticular ectopic ossification following total hip arthroplasty. Clin Orthop Relat Res 1982;167:113–7. 16. Gerber C, Schneeberger AG, Vinh TS. The arterial vascularization of the humeral head. An anatomical study. J Bone Joint Surg Am 1990;72(10):1486–94. 17. Brooks CH, Revell WJ, Heatley FW. Vascularity of the humeral head after proximal humeral fractures. An anatomical cadaver study. J Bone Joint Surg Br 1993;75(1):132–6. 18. Duparc F, Muller JM, Freger P. Arterial blood supply of the proximal humeral epiphysis. Surg Radiol Anat 2001;23(3): 185–90.
R. Hertel, E. Fandridis 19. Hertel R, Hempfing A, Stiehler M, Leuniq M. Predictors of humeral head ischemia after intracapsular fracture of the proximal humerus. J Shoulder Elbow Surg 2004;13(4): 427–33. 20. Lee CK, Hansen HR. Posttraumatic avascular necrosis of the humeral head in displaced proximal humeral fractures. J Trauma 1981;21(9):788–91. 21. Hagg O, Lundberg B. Aspects of prognostic factors in comminuted and dislocated proximal humeral fractures. In: Baterman JE, Weksh RP, editors. Surgery of the shoulder. Philadelphia: BC Decker; 1984. p. 51–9. 22. Sturzenegger M, Fornaro E, Jakob RP. Results of surgical treatment of multifragmented fractures of the humeral head. Arch Orthop Trauma Surg 1982;100(4):249–59. 23. Gerber C, Hersche O, Berberat C. The clinical relevance of posttraumatic avascular necrosis of humeral head. J Shoulder Elbow Surg 1998;7(6):586–90. 24. Ficat RP, Arlet J. Necrosis of the femoral head. In: Hungerford DS, editor. Ischemia and necrosis of bone. Baltimore, MD: Williams & Wilkins; 1980. p. 171–82. 25. Neer II CS. Displaced proximal humeral fractures. I. Classification and evaluation. J Bone Joint Surg Am 1970;52(6):1077–89. 26. Schweiger G, Ludolph E. Fractures of the shoulder joint. Unfallchi 1980;6:225. 27. Gristina AG. Management of displaced fractures of the proximal humerus. Contemp Orthop 1987;15:61–93. 28. Covenrty MB, Laurnen EL. Ununited fractures of the middle and upper humerus: special problems in treatment. Clin Orthop Relat Res 1970;69:192–8. 29. Rooney PJ, Cockshott WP. Pseudarthrosis following proximal humeral fractures: a possible mechanism. Skeletal Radiol 1986;15(1):21–4. 30. Hertel R, Mees C, Scholl E, Ballmer FT, Siebenrock K. Morphologic classification of fractures of the proximal humerus. A validated, teachable and practicable alternative. In: Presented at the Eighth international conference on shoulder surgery (ICSS), 2001. 31. Codman EA. Fractures in relation to the subacromial bursa. In: Codman EA, editor. The shoulder, rupture of the supraspinatus tendon and other lesions in or about the subacromial bursa. Malabar, FL: Krieger; 1934. p. 313–31. 32. Craig EV. Open reduction and internal fixation of greater tuberosity fractures, malunion, and nonunion. In: Craig EV, editor. The shoulder. Master techniques in orthopaedic surgery. New York, NY: Raven; 1995. p. 289–307. 33. Pugh DM, Mckee MD. Advances in the management of humeral nonunion. J Am Acad Orthop Surg 2003;11(1):48–59. 34. Healy WL, Jupiter JB, Kristiansen TK, White RR. Nonunion of the proximal humerus. A review of 25 cases. J Orthop Trauma 1990;4(4):424–31. 35. Jupiter JB, Mullaji AB. Blade plate fixation of the proximal humeral nonunions. Injury 1994;25(5):301–3. 36. Norris TR, Green A, McGuigan FX. Late prosthetic shoulder arthroplasty for displaced proximal humerus fractures. J Shoulder Elbow Surg 1995;4(4):271–80. 37. Ring D, McKee M, Perey BH, Jupiter JB. The use of a blade plate and autogenous cancellous bone graft in the treatment of ununited fractures of the proximal humerus. J Shoulder Elbow Surg 2001;10(6):501–7. 38. Scheck M. Surgical treatment of nonunions of the surgical neck of the humerus. Clin Orthop Relat Res 1982;167:255–9. 39. Walch G, Badet R, Nove-Josserand L, Levigne G. Nonunions of the surgical neck of the humerus: surgical treatment with an intramedullary bone peg, internal fixation and cancellous bone grafting. J Shoulder Elbow Surg 1996;5(3):161–8. 40. Nayak NK, Schickendantz MS, Regan WD, Hawkins RJ. Operative treatment of nonunion of surgical neck fractures of the humerus. Clin Orthop Relat Res 1995;313:200–5.
ARTICLE IN PRESS Post-traumatic reconstruction for sequelae of fractures 41. Boileau P, Coste JS, Ahrens PM, Staccini P. Prosthetic shoulder replacement for fracture: results of the multicentre study. In: Walch G, Boileau P, Mole ´ D, editors. 2000 Shoulder prostheses: two to ten years follow-up. Montpellier: Sauramps Me ´dical; 2001. p. 561–78. 42. Galatz LM, Williams GR, Fenlin JM, Ramsey ML, Iannotti JP. Outcome of open reduction and internal fixation of surgical neck nonunions of the humerus. J Orthop Trauma 2004;18(2): 64–7. 43. Kristiansen B, Christensen SW. Proximal humeral fractures. Late results in relation to classification and treatment. Acta Orthop Scand 1987;58(2):124–7. 44. Beredjiklian PK, Iannotti JP, Norris TR, Williams GR. Operative treatment of malunion of a fracture of the proximal aspect of the humerus. J Bone Joint Surg Am 1998;80(10):1484–97. 45. Rodosky MW, Duralde XA, Pollock RG, et al. Operative treatment of proximal humerus fractures. In: Tenth open meeting of the American shoulder and elbow surgeons, New Orleans, February 1994. 46. Solonen KA, Vastamaki M. Osteotomy of the neck of the humerus for traumatic varus deformity. Acta Orthop Scand 1985;56(1):79–80. 47. Benegas E, Zoppi Filho A, Ferreira Filho AA, Ferreira Neto AA, Negri JH, Prada FS, et al. Surgical treatment of varus malunion of the proximal humerus with valgus osteotomy. J Shoulder Elbow Surg 2007;16(1):55–9. 48. Thompson FR, Winant EM. Unusual fracture-subluxations of the shoulder joint. J Bone Joint Surg Am 1950;32:575–82. 49. Zyto K, Kronberg M, Brostom LA. Shoulder function after displaced fractures of the proximal humerus. J Shoulder Elbow Surg 1995;4(5):331–6. 50. Cofield RH. Total shoulder arthroplasty with the Neer prosthesis. J Bone Joint Surg Am 1984;66(6):899–906. 51. Bosch U, Skutek M, Fremerey RW, Tscherne H. Outcome after primary and secondary hemiarthroplasty in elderly patients
431
52.
53. 54.
55.
56.
57.
58.
59.
60.
with fractures of the proximal humerus. J Shoulder Elbow Surg 1998;7(5):479–84. Mansat P, Guity MR, Bellumore Y, Mansat M. Shoulder arthroplasty for late sequelae of proximal humeral fractures. J Shoulder Elbow Surg 2004;13(3):305–12. Boileau P, Sinnerton RJ, Chuinard C, Walch G. Arthroplasty of the shoulder. J Bone Joint Surg Br 2006;88(5):562–75. Copeland SA. Cementless total shoulder replacement. In: Post M, Morrey BF, Hawkins RJ, editors. Surgery of the shoulder. St. Louis, MO: Mosby Year Book; 1990. p. 289–93. Krishnan SG, Nowinski RJ, Harrison D, Burkhead WZ. Glenohumeral arthritis. Two to fifteen-year outcomes humeral hemiarthroplasty with biologic resurfacing of the glenoid for glenohumeral arthritis. Two to fifteen-year outcomes. J Bone Joint Surg Am 2007;89:727–34. 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(5): 401–12. Boileau P, Chuinard C, Le Huec J, Walch G, Trojani C. Proximal humerus fracture sequelae. Impact of a new radiographic classification on arthroplasty. Clin Orthop Relat Res 2006; 442:121–30. Frankle MA, Greenwald DP, Markee BA, Ondrovic LE, Lee WE. Biomechanical effects of malposition of tuberosity fragments on the humeral prosthetic reconstruction for fourpart proximal humerus fractures. J Shoulder Elbow Surg 2001; 10(4):321–6. Clare DJ, Wirth MA, Groh GI, Rockwood CA. Current concepts review. Shoulder arthrodesis. J Bone Joint Surg Am 2001;83(4): 593–600. Rispoli DM, Sperling JW, Athwal GS, Schleck CD, Cofield RH. Pain relief and functional results after resection arthroplasty of the shoulder. Bone Joint Surg Br 2007;89(9):1184–7.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 432–437
Available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/cuor
MINI-SYMPOSIUM: SHOULDER RECONSTRUCTION
(iv) Shoulder arthrodesis David Limb Chapel Allerton Hospital, Leeds LS7 4SA, UK
KEYWORDS Arthrodesis; Arthroplasty; Infection
Summary Shoulder arthrodesis is rarely performed, but is a valuable reconstructive option for difficult shoulder problems. The success of shoulder arthroplasty has significantly diminished the frequency with which this operation is carried out. However, the durable results of arthrodesis have stood the test of time and it remains the operation of choice for highly selected patients with various forms of paralytic and destructive pathology about the shoulder, particularly problems that are not suitable for shoulder replacement. & 2007 Elsevier Ltd. All rights reserved.
Indications The main indications for shoulder arthrodesis are listed in Table 1. If the technical skill has been mastered then arthrodesis can be considered in the range of ‘one off’ difficult reconstructive cases that present to the specialist shoulder surgeon with tumour, trauma or infection, or indeed a combination of these aetiological factors. It is contraindicated if there is no scapular control, if there is a progressive underlying neurological problem, in the face of active sepsis and if the patient would not be able to cope with the rehabilitation demands afterwards. It should also be considered as contraindicated if the underlying pathology can be treated in any other way that preserves shoulder function, particularly shoulder arthroplasty, except in exceptional circumstances. Infection was the major indication for shoulder arthrodesis in the era before antibiotics, particularly in cases of tuberculosis. As was the case in other joints, such as the hip, attempts were made to avoid entering the infected joint. Tel.: +44 113 392 4779; fax: +44 113 392 4585.
E-mail address:
[email protected] 0268-0890/$ - see front matter & 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2007.11.009
Extra-articular arthrodesis was therefore developed, as exemplified by the arthrodesis between the greater tuberosity and acromion described by Watson Jones.1 After bringing the decorticated surfaces into contact a plaster spica was applied and had to be worn continuously for 4 months. Brittan2 described a technique using a tibial cortical strut graft between the medial shaft of the humerus and the lateral column of the scapula—a truly extraarticular arthrodesis, but with the potential for significant complications, including donor site morbidity. An inevitable consequence of the techniques that were developed to bring the articular surfaces together was that the tendon of the long head of the biceps had to be sacrificed. Moseley described biceps tenodesis in its humeral groove3 specifically to facilitate bone-to-bone contact in the shoulder whilst minimising the cosmetic effect of biceps division and the loss of supination power that can accompany this.
Modern techniques As intra-articular arthrodesis between the humeral head, glenoid and acromion became more common, with removal of the cortical layer from the three surfaces to be fused, so
ARTICLE IN PRESS Shoulder arthrodesis
Table 1
Indications for shoulder arthrodesis.
Flail shoulder with functional hand/arm (e.g. brachial plexus injury) Some cases of axillary nerve palsy End stage septic arthritis Failed shoulder arthroplasty Some cases of shoulder instability After tumour resection Occasionally osteo- or rheumatoid arthritis, cuff tears and malunion
433 require long unthreaded shafts to glide through the humeral head and short threaded sections at the tip to gain purchase in the relatively limited bone available in the glenoid. The best scapular fixation is in the glenoid and although a significant length of plate can be contoured to run along the scapular spine, the bone of the spine is very thin and often only short screws will be accepted. It is still therefore common to brace the arm afterwards, though this can be removed to facilitate the rehabilitation programme that is required.
Surgical technique Planning Ensure that there is sufficient bone for compression arthrodesis. This is particularly important if there have been shoulder arthroplasty implants in situ or in cases of tumour resection. The arm can be shortened by a few centimetres without any diminution of function, but consideration can be given to autologous bone grafting or even allograft if there is significant bone loss. In very difficult cases free tissue transfer may be required, such as free fibular transfer, and cooperation should be sought from a plastic surgeon. If an adjustable brace is to be used after surgery then this can be fitted before surgery. The patient can even wear it for a few days to accommodate to the level of inconvenience that they are likely to face after surgery. It is much easier to fit and adjust the brace when the patient is mobile and can stand upright than when they are recovering consciousness on an operating table.
Patient positioning
Figure 1 plate.
Shoulder arthrodesis using a single-compression
methods of compression fixation were explored to bring the denuded bone surfaces into contact. Perhaps not surprisingly, Charnley has described compression arthrodesis at the shoulder,4 an extension of his successful development of the techniques using Steinman pin external fixation that he popularised in other joints, particularly the knee and ankle. In 1970 the ASIF described compression plate fixation and this has been the standard method since. The main modification to this has been to gravitate towards using a single plate rather than the double plate technique originally described (Figure 1). The technique of plate fixation follows straightforward AO principles—after denuding the surfaces of the humeral head, glenoid and acromion, the humeral head is compressed into the two scapular surfaces using the lag screw principle. This fixation is then protected by using a neutralisation plate across the joint. The lag screw(s) can, with proper planning, be inserted through the precontoured plate if required. It is important to note that the lag screws
Access is required to the spine of the scapula, acromion, deltoid and anterolateral humerus. Furthermore it should be possible to accurately assess the position of the arm in relation to the body during surgery, as it will be extremely difficult to change the position after arthrodesis. The beach chair position fulfils these requirements, preferably on a table designed for shoulder arthroscopy, which allows good access to the back of the shoulder. If free tissue transfer is required then the patient position may have to be modified, or provision made for a change of position during the procedure. Similarly access for structural grafts should be considered if substantial bone is to be excised, such as in cases of failed arthroplasty or tumour.
Approach The incision extends along the lateral 10 cm or so of the scapular spine to the tip of the acromion, turning smoothly to run over the acromion onto the anterolateral aspect of the humerus, splitting the deltoid (Figure 2). Often there is no deltoid function when arthrodesis is being carried out, so there is no need to worry about axillary nerve injury. If arthrodesis is being carried out in the presence of an innervated deltoid then it is desirable to keep the axillary nerve intact to reduce the speed and extent of deltoid
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D. Limb compressed through the plate, though care has to be taken to ensure the plate is long enough to obtain purchase in the spine medial to the osteotomy. Bone loss can be accommodated by humeral shortening if not severe, or with cancellous grafting if the bone quality is impaired, as might be the case after removal of a prosthesis. In cases of tumour resection or failed shoulder replacement with bone loss, consideration should have been given to using a vascularised bone graft.
Position of arthrodesis
Figure 2 shoulder.
The skin incision for plate arthrodesis of the
wasting and preserve skin sensation in the regimental badge area. Detachment of the deltoid from the lateral and anterior acromion is required to gain access to the shoulder. Thereafter excision of the rotator cuff and biceps tendons has to take place, counterintuitive as it is, to allow decortication and compression. If the biceps remains innervated then tenodesis at this stage will prevent distal migration.
Preparation of the joint surfaces The minimum requirement is that the articular cartilage and subchondral cortical layer is removed from the entire surface of the glenoid, the corresponding area of the humeral head when the arm is positioned in the attitude of intended fusion and from the undersurface of the acromion that will articulate with the humeral head in this position. Although the aim is to preserve as much bone as possible, in practice the majority of the humeral head is decorticated to dispense with the need to accurately predict the final position of arthrodesis at this stage. In order to preserve bone stock it is helpful to use instruments for decortication that can shave off matching concave and convex surfaces. This can be completed carefully with a high-speed burr. Another alternative is to use reamers designed for surface shoulder replacement. If shoulder resurfacing instruments are not available then acetabular reamers of a similar size to the humeral head can be used to shape the glenoid and undersurface of the acromion simultaneously, whilst curved osteotomes can be used to prepare the convex humeral head. Occasionally the glenohumeral component of the fusion has excellent bone stock but the contact area with the glenoid is diminished by pushing the humeral head upwards to obtain simultaneous ‘extra articular’ arthrodesis with the undersurface of the acromion. It is acceptable if this occurs to osteotomise the spine of the scapula to allow the acromion, with its attached deltoid, to flap down into contact with the humeral head whilst the head itself makes secure contact with the glenoid. In this position it can be
At the end of the day a position is required that permits maximum function. Although there have been many opinions expressed as to the ideal position, any increase in one particular angle results in a diminution of range in the opposite direction and the ideal position may vary from patient to patient, as it depends on desired functions. However, once the arthrodesis has been performed the range of available movement will depend entirely on scapulothoracic movement, so the fusion must be positioned to take full advantage of this. A working party reported on the ideal position for arthrodesis in 19425 and there was immediate controversy not only on the recommendations made, but also on the methods of measurement used (abduction angle was measured between the lateral border of the scapula and the humerus, with a recommended angle of 45–501, whereas many refer to the angle between the humerus and the vertical axis when the patient is standing). A surprising range of movement is possible after fusion, accompanied by inevitable scapular winging at the end range, though in this case the winging is brought about by muscle activity pulling the scapula away from the chest wall to increase range and not usually by muscle weakness. It is pointless, therefore, to fuse the shoulder with the arm by the side. Abduction would still be possible by rotating the scapula; a greater range is possible if the arm is fused in a position of abduction to begin with. Every 101 of increased fusion angle results in a further 101 of available abduction range. However the position of abduction must leave sufficient scapulothoracic range for the arm to be returned to the side. Fixed abduction is painful, as the scapulothoracic articulation is strained and fatigues, and should be avoided. Likewise, care has to be taken in choosing a position of internal/external rotation. Scapular protraction and retraction allows apparent internal and external rotation of the arm after arthrodesis. If the fusion is established with the arm in too much internal rotation, elbow flexion brings the forearm into contact with the abdomen and retraction of the scapula brings about limited apparent external rotation. On the other hand, if fused in excessive external rotation the hand is in a useful position for work but even with full scapular protraction the hand cannot be brought to the mouth. Although the final position can be discussed with the patient it is useful to offer advice on what has been tried and trusted in the past. The authors preference is the ‘30/30/30’ position, that is with the humerus in 301 of abduction in the coronal plane, 301 of flexion in the sagittal
ARTICLE IN PRESS Shoulder arthrodesis plane and 301 of internal rotation, allowing the hand to reach the pocket and the mouth.
Fixation The principle of fixation, as indicated above, is to compress the surfaces that are to be fused. Before the plate arthrodesis methods popularised by the AO group, screw arthrodesis was favoured. This was supported by external bracing until bony union. The duration and extent of external bracing required was reduced by neutralising external forces across the lag screw fixation using dynamic compression plates. Assuming a single plate is to be used, this should be sufficiently strong for the forces it will encounter, and small fragment plates are simply not up to the task. Large fragment plates are needed and although reconstruction plates are more easily contoured, for many patients the additional strength of a standard plate is required. Careful contouring is needed so that, when the arm is held in the intended position of fusion, the plate sits perfectly along the scapular spine, acromion then curves smoothly onto the humerus. Since the humerus is in a position of flexion the plate usually has to be twisted in order that it can lie on the anterolateral surface. A small channel can be cut into the lateral edge of the acromion so that the plate can be sunk into the edge as it crosses this bony prominence. This reduces the significant prominence of the plate that can result in this location, particularly in thin individuals and those with deltoid wasting. A small amount of overcontouring can be performed such that the last turn of the lag screw compresses the plate onto bone. More should be avoided so as not to influence the position of arthrodesis by reducing the intended abduction angle. Once the plate is accurately bent the fixation can be achieved. The arm is held in the intended position and humeroglenoid fixation is achieved using a large, partly threaded cancellous screw inserted through an appropriate hole in the plate if possible. Further lag screws can then be inserted through the acromion into the humeral head and neutralisation screws in the glenoid neck, scapular spine and humeral shaft.
435 resurgence of interest, as this method is more amenable to minimally invasive and arthroscopic techniques. The nonunion rate has been reported to be higher after screw techniques,6 with inferior mechanical strength associated with screw fixation.7 Recent mechanical studies have suggested that alternative patterns of screw insertion, with up to six lag screws, may give mechanical conditions at the shoulder joint similar to plate arthrodesis, raising the possibility that similar union rates might be achievable.8 Decortication of the surfaces is still required, however, and although this can be carried out through a limited incision, arthroscopy allows complete decortication using a power shaver through only two or three portals. Although arthroscopic arthrodesis has been described9 there are only few, small series available with limited follow up, so the place of this technique has yet to be established.
Results If complications do not ensue, shoulder arthrodesis leads to high levels of shoulder function and improved function.10 It has to be remembered, however, that the procedure is usually being carried out because of severe neurological or destructive pathology, so routine outcome measures such as the constant score should be interpreted in terms of the improvement that occurs after surgery. The absolute score achieved will be low compared to what is observed after virtually any other shoulder procedure. The constant score includes 40 points for range of movement along with 25 more points for power measured in a position of the arm that is usually impossible to achieve after shoulder arthrodesis. After appropriate scapulothoracic mobilisations and training a very useful range of ‘shoulder’ movement can be achieved. Clearly the range depends on the position of fusion and therefore the range reported in the literature is wide. As a guide, most patients will achieve flexion and abduction up to the horizontal level, with sufficient ‘rotation’ (scapulothoracic protraction and retraction) to each the front pocket and, to a lesser extent, the back pocket. Functions that do not involve overhead positioning or significant rotation are usually well within the capabilities of the patient, including tasks that require the lifting of heavy weights.11
Postoperative management A period of brace support is conventional after shoulder arthrodesis. Six weeks allows significant progress towards union and load sharing with the uniting arthrodesis. Longterm function depends on rehabilitation of the scapulothoracic joint, however, so scapulothoracic mobility and strength can be worked upon as soon as postoperative pain settles. Physiotherapists can also help preserve joint mobility in the elbow and hand, particularly if the neurological status before surgery demands. During the period of bracing it is permissible for the brace to be removed and the arm supported manually to allow for bathing.
Alternative methods Although screw fixation was largely abandoned after the introduction of plate techniques, there has been a
Complications The major complications occurring after attempted shoulder arthrodesis are non-union (Figure 3), fracture and persisting pain. Furthermore the procedure can be complicated by infection, poor positioning and rarer complications such as pneumothorax. In the largest series reported to date, 35 patients (25 of 71) required reoperation for complications.12 Non-union rates vary, but Cofield and Briggs12 described three non-unions in 71 arthrodeses. A recent study including both screw and plate arthrodeses reported a rate of three non-unions in 30 cases, though the authors had carried out arthrodesis for challenging indications, such as infection and for reconstruction after removal of a shoulder prosthesis.13 In general non-union can be successfully managed by grafting and compression plating, replacing the original fixation if necessary.
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D. Limb
Figure 3 Non-union of arthrodesis—in this case the arthrodesis had been carried out for infected fracture non-union. Arthrodesis was secured by revision compression plating and autogenous bone grafts.
Humeral shaft fracture occurs much more frequently after shoulder arthrodesis than, for example, after plating of proximal humeral fractures (Figure 4). Without the mobility of the glenohumeral articulation, forces transmitted from the arm traverse the vulnerable junction at the tip of the plate. After disuse the humeral shaft is weakened by mineral loss and fracture at this site is reported in approximately 10%; prophylactic grafting has even been recommended.14 Non-operative management with humeral bracing is satisfactory for the majority of cases, though if the fracture occurs after union of the arthrodesis then consideration can be given to removing the arthrodesis plate and treating the new fracture by internal fixation. Persisting pain is not at all unusual after arthrodesis; in cases of arthrodesis for end stage instability persistence of the sensation of dislocation can even continue after fusion occurs. Overall, substantial relief of pain is reported, though unfortunately any neurogenic pain associated with brachial plexus injury is unlikely to be improved.
Summary and Conclusion Shoulder arthrodesis is primarily indicated in cases of brachial plexus trauma where scapular control remains intact, but there is irrecoverable loss of rotator cuff and deltoid function. The flail arm regains an active range of motion derived from the scapulothoracic joint that restores
Figure 4 Fracture beyond the arthrodesis plate, in this case through the site of a fracture that had occurred when the patient sustained the original brachial plexus injury.
useful shoulder function and restores the ability to exert some control over hand positioning. A fusion position of approximately 301 each of abduction, forward flexion and internal rotation is preferred. Substantial scapulothoracic conditioning is required during rehabilitation, and it is not uncommon for some discomfort to persist. For most indications other than paralysis arthrodesis should be avoided if alternative methods, such as joint replacement, are feasible. However, it remains a very valuable technique for difficult and revision reconstructive problems about the shoulder.
References 1. Watson-Jones R. Extra-articular arthrodesis of the shoulder. J Bone Joint Surg 15:862–71. 2. Brittain HA. Architectural principles in arthrodesis, 3rd ed. Edinburgh: E&L Livingstone; 1952. 3. Mosely HF. Arthrodesis of the shoulder in the adult. Clin Orthop 1961;20:156–62. 4. Charnley J, Houston JK. Compression arthrodesis of the shoulder. J Bone Joint Surg Br 1964;46:614–20.
ARTICLE IN PRESS Shoulder arthrodesis 5. Barr J, Freiberg JA, Colonna PC, Pemberton PA. A survey of end results on stabilisation of the paralysed shoulder. J Bone Joint Surg 24: 699–707. 6. Cofield RH, Briggs BT. Glenohumeral arthrodesis. Operative and long term functional results. J Bone Joint Surg Am 1979;61: 668–77. 7. Miller BS, Harper WP, Gillies RM, Sonnabend DH, Walsh WR. ANZ J Surg 2003;73(12):1015–7. 8. Ruhmann O, Kirsch L, Buch S, Kirschner S, Bonsack M, Wirth C. Primary stability of shoulder arthrodesis using cannulated screws. J Shoulder Elbow Surg 2005;14(1):51–9. 9. Syal A, Macdonald P. Arthroscopic arthrodesis of the shoulder. J Shoulder Elbow Surg 2007 [e-pub ahead of print].
437 10. Richards RR, Beaton DE, Hudson AR. Shoulder arthrodesis with plate fixation: a functional outcome analysis. J Shoulder Elbow Surg 1993;2:225–39. 11. Nagy L, Koch P, Gerber C. Functional analysis of shoulder arthrodesis. J Shoulder Elbow Surg 2004;13(4):386–95. 12. Cofield RH, Briggs BT. Glenohumeral arthrodesis. Operative and long term functional results. J Bone Joint Surg Am 1979;61: 668–77. 13. Ruhmann O, Schmolke S, Bonsack M, Flamme C, Wirth C. Shoulder arthrodesis—indications, technique, results and complications. J Shoulder Elbow Surg 2005;14(1):38–50. 14. Muller ME, Allgower AM, Willenegger H. Manual of internal fixation, 2nd ed. Berlin: Springer; 1979.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 438–441
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SYNDROMES
Marble bone disease Sabrina Fudgea, Rouin Amirfeyzb, Donna Dimondc, Martin Gargand, a
University of Bristol, Bristol, UK Trauma and Orthopaedics, Gloucestershire Royal Hospital, Gloucester, UK c Bristol Royal Hospital for Sick Children, Bristol, UK d Trauma and Paediatric Orthopaedics, Bristol Royal Hospital for Sick Children, Bristol, UK b
Introduction
Epidemiology and genetics
Albers-Scho ¨nberg first reported osteopetrosis in 1904 in an adult patient with generalized bone sclerosis and multiple fractures.1 Osteopetrosis is a heterogeneous group of inherited bone remodeling disorders in which there is a defect in bone resorption by osteoclasts. The disease is associated with an increase in skeletal mass due to abnormally dense bone. The decrease in osteoclastic activity also affects the shape and structure of the bone. Abnormal remodeling of primary woven bone to lamellar bone results in brittle bone that is prone to fracture. The clinical manifestations and prognosis vary depending on the classification and genetic features. In severely affected patients, the medullary cavity is filled with new bone leaving little space remaining for haematopoietic cells, leading to a number of haematological and metabolic abnormalities. Neurological sequelae are common in osteopetrosis, particularity auditory and optic nerve dysfunction.2 Canal stenosis can lead to blindness and deafness. In addition facial nerve paralysis, developmental delay, and mental retardation can occur. Orthopaedic problems relevant to all clinical variants include pathological fractures, coxa vara, long-bone bowing, back pain, arthritis and osteomyelitis.3
The human variants of osteopetrosis can be categorized as:
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(1) Infantile autosomal recessive. (2) Intermediate autosomal recessive. (3) Autosomal dominant (further divided into autosomal dominant I and II). The condition is rare; incidences have been reported at 1 in 20,000–500,000 for the dominant form4 and 1 in 200,000 for the recessive forms.5 The infantile autosomal recessive form of osteopetrosis is most commonly diagnosed soon after birth or within the first few years of life, with symptoms of infection, haemorrhage, or profound anaemia. The condition worsens rapidly and in the absence of effective medical intervention, leads invariably to death in the first few years. Balemans et al. report that 75% of untreated patients die by the age of 4 years as a consequence of associated complications.6 Intermediate autosomal recessive osteopetrosis is a milder form of the condition; more commonly diagnosed towards the end of the first decade of life, and not following the malignant course. Often fracture brings about diagnosis due to the characteristic radiograph features of increased density and decreased metaphyseal remodeling.7 Other associated findings include:
Mild disproportionate short stature. Macrocephaly. Recurrent fractures. Osteomyelitis. Mild anaemia.
ARTICLE IN PRESS Marble bone disease
439
The autosomal dominant form is the most benign variant of osteopetrosis and is not associated with shortened lifespan. Almost half of patients diagnosed with this condition are asymptomatic. The major symptom is pathological fractures, found in approximately 40% of patients. Such fractures are often transverse. Bone pain, especially in the lumbar area, is reported in 25% of patients (Table 1).8
Radiological appearance The diagnosis of osteopetrosis is radiological, supported by computerized tomography if necessary. Global features are of a generalized symmetrical sclerosis and metaphyseal widening. The clinical manifestations as diagnosed by radiograph in infantile autosomal recessive osteopetrosis are a significant increase in skeletal bone mass resulting in total or near-total obliteration of the bone marrow cavity (Fig. 1A and B). Bones can appear short and broad or long and thin. The entire skull is usually involved in infantile osteopetrosis, with the base of the cranium being the most severely affected.9 Pathological fractures are the main presenting feature of intermediate autosomal recessive osteopetrosis. Radiologically patients may have a disproportionately short stature, dental abnormalities, and evidence of a chronic osteomyelitis.10 The metaphyses are wider and failure of remodeling is seen especially in the distal femora as the ‘‘Ehrlenmeyer flask’’ deformity. In some patients the endobones can be seen. In 1987, Anderson and Bollerslev divided the autosomal dominant form radiologically into two distinct types. In type I, sclerosis of the skull mainly affects the vault and was associated with marked calvarial thickening (Fig. 1C). In contrast Type II, sclerosis was found in the base of the skull. Thickening and sclerosis of veretebral endplates (rugger jersey spine, Fig. 1D) is always present.11 Table 1
Other bony defects have been reported such as frontal bossing and genu valgum. The appearance of ‘‘bone within bone’’ is most characteristic of adult osteopetrosis, and is an unusual finding in the infantile form.10
Biochemical markers Early diagnosis of the condition is important for the subsequent management of the affected patients. A recent study investigated the correlation of serum creatine kinase (CK) isoenzyme patterns, specific biochemical markers of bone metabolism and cytokines in correlation with the pathophysiology of osteopetrosis.12 Serum CK-BB of the patient was found to be elevated to 18.0% (normal 1.67–7.6%) and biochemical markers of bone resorption were decreased. These markers may be used to differentiate osteopetrotic patients from other sclerosing bone diseases. If used for prenatal diagnosis early bone marrow transplantation can be planned ahead and possibly result in a better chance of survival.
Orthopaedic manifestations Fractures Fractures are common and are one of the classical features of osteopetrosis. The long bones are most frequently affected and fractures tend to occur only after moderate trauma. Two types of fracture are seen in children with infantile osteopetrosis. These are either diaphyseal or metaphyseal fractures that are generally transverse and minimally displaced. There is a high incidence of hip and proximal femoral fractures in the autosomal dominant group. These can undergo successful internal fixation, although extreme hardness of the bone makes intervention difficult.13 Fractures heal, although the time to healing is often prolonged. Chhabra et al. report drill flutes being immediately filled by
Key features of osteopetrosis. Infantile autosomal recessive
Intermediate autosomal recessive
Autosomal dominant
Diagnosis
First year
First decade
Adulthood
Presentation
Failure to thrive Infection Bleeding Hepatosplenomegaly Fractures
Anaemia Hepatosplenomegaly Osteomyelitis
Asymptomatic Fracture Back pain
Radiological features
Metaphyseal widening Bone-within-bone appearance Medullary obliteration
Sclerosis Medullary obliteration
Generalized sclerosis Vault thickening Rugger jersey spine Bone-in-bone appearance
Musculoskeletal features
Pathological fracture
Pathological fracture Coxa vara Mild short stature
Pathological fracture Back pain Bone pain Coxa vara Femoral bowing Hip and knee osteoarthritis
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S. Fudge et al.
Figure 1 (A) Distal femur showing bone within bone appearance; (B) upper arm showing sclerotic bones and loss of cortiomedullary differentiation; (C) marked calvarial thickening; and (D) rugger jersey spine.
bone and hence rendering the drill ineffective, and generation of significant frictional heat resulting in breakage of the drill, hence highlighting the importance of preoperative planning, patience and caution required.14
involving the femur, or more rarely the tibia, humerus, radius and ulna. This deformity may be secondary to malunion after diaphyseal and metaphseal fractures.9
Osteomyelitis Coxa vara Many patients develop coxa vara deformity, some in the first few years of life. This deformity is seen in the intermediate and autosomal dominant forms and is the most common deformity in these specific groups.9 The coxa vara deformity appears to be caused by stress fractures in the femoral neck, with gradual deformity ensuing. The deformity can be treated by osteotomy, but can be complicated by difficulty with fixation, delayed healing, non-union and recurrent deformity.7
Long bone deformity Other long bone deformity is occasionally seen in autosomal dominant oteopetrosis. There is lateral bowing, usually
Due to diminished vascularity of the bones and impaired white cell function, osteomyelitis is frequently seen with osteopetrosis. The most common site of involvement is the mandible.15 The teeth are generally impaired and are prone to become carious.9 Long bone infections also occur and once established in patients are difficult to eradicate.
Back pain Back pain is most frequently reported in cases of benign autosomal dominant osteopetrosis. This rarely requires surgical intervention, but can be persistent requiring bracing and medication regimens. Associated spondylolysis or scoliosis has been described, but the majority of cases present with no structural abnormality.10
ARTICLE IN PRESS Marble bone disease
Osteoarthritis Degenerative arthritis of the hip and knee is seen with increased frequency in mid-adult life in patients with the autosomal dominant form. It is theorized that increased stiffness of the dense subchondral bone predisposes to premature cartilage degeneration.10 Total hip and knee arthoplasties have been performed with good results, but technical difficulties can be encountered during reaming, cementing and implanting due to the extremely hard bone and narrow or absent intramedularry canals. The use of instruments made from tungsten carbide has allowed successful treatment for demanding cases, such that it has been recommended that in elective surgery it is mandatory that specialist equipment is available.16 The technical difficulty during total hip arthroplasty due to the absence of the femoral canal can be avoided by resurfacing arthroplasty. However special equipment (and screws) might be needed.17
Acknowledgement The authors wish to thank Dr. Colin Steward for the support in the preparation of this manuscript.
References 1. Albers-Scho ¨nberg HE. Ro ¨ntgenbilder einer seltenen Knockenerkrankung. Munch Med Wochenschr 1904;51:365–8. 2. Steward CG. Neurological aspects of osteopetrosis. Neuropathol Appl Neurobiol 2003;29(2):87–97. 3. Shapiro F. Osteopetrosis. Current clinical considerations. Clin Orthop Relat Res 1993;294:34–44. 4. Dahl N, Holmgren G, Holmberg S, Ersmark H. Fracture patterns in malignant osteopetrosis (Albers-Schonberg disease). Arch Orthop Trauma Surg 1992;111(2):121–3.
441 5. Tolar J, Teitelbaum SL, Orchard PJ. Osteopetrosis. N Engl J Med 2004;351(27):2839–49. 6. Balemans W, Van Wesenbeeck L, Van Hul W. A clinical and molecular overview of the human osteopetroses. Calcif Tissue Int 2005;77(5):263–74. 7. Stoker DJ. Osteopetrosis. Semin Musculoskelet Radiol 2002; 6(4):299–305. 8. Armstrong DG, Newfield JT, Gillespie R. Orthopedic management of osteopetrosis: results of a survey and review of the literature. J Pediatr Orthop 1999;19(1):122–32. 9. Kocher MS, Kasser JR. Osteopetrosis. Am J Orthop 2003;32(5): 222–8. 10. Shapiro F. Osteopetrosis. Current clinical considerations. Clin Orthop Relat Res 1993(294):34–44. 11. Bollerslev J, Andersen Jr. PE. Radiological, biochemical and hereditary evidence of two types of autosomal dominant osteopetrosis. Bone 1988;9(1):7–13. 12. Chan MH, Wong K, Chan IH, Luo YF, Tam S. Specific biochemical markers of bone metabolism and cytokine study confirm the diagnosis of malignant infantile osteopetrosis at birth using cord blood sample. Pathology 2005;37(1):51–5. 13. Breck LW, Cornell RC, Emmett JE. Intramedullary fixation of fractures of the femur in a case of osteopetrosis. J Bone Joint Surg Am 1957;39-A(6):1389–94. 14. Chhabra A, Westerlund LE, Kline AJ, McLaughlin R. Management of proximal femoral shaft fractures in osteopetrosis: a case series using internal fixation. Orthopaedics 2005; 28(6):587–92. 15. Bakeman RJ, Abdelsayed RA, Sutley SH, Newhouse RF. Osteopetrosis: a review of the literature and report of a case complicated by osteomyelitis of the mandible. J Oral Maxillofac Surg 1998;56(10):1209–13. 16. Ramiah RD, Baker RP, Bannister GC. Conversion of failed proximal femoral internal fixation to total hip arthroplasty in osteopetrotic bone. J Arthroplasty 2006;21(8):1200–2. 17. Girard J, Vendittoli PA, Lavigne M, Roy AG. Resurfacing arthroplasty of the hip in osteopetrosis. J Bone Joint Surg Br 2006;88(6):818–21.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 442–450
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SPINE
Minimally invasive spinal surgery John K. O’Dowd The RealHealth Institute, 23-31 Beavor Lane, London W6 9AR, UK
KEYWORDS Spine; Surgery; Minimally invasive; Endoscopic
Summary Recent advances in endoscopy, imaging and retractor technology have led to major developments in minimal access surgery of the spine. Their place in practice probably awaits the results of prospective trials. & 2007 Elsevier Ltd. All rights reserved.
Introduction
Mini open Posterior – Lumbar – Cervical J Anterior – Lumbar – Thoracic – Thoracolumbar junction Image guided surgery Vertebroplasty J Vertebroplasty J Lordoplasty J Kyphoplasty J
Minimally invasive spinal surgery can be defined as the performance of procedures on the spinal column using either a percutaneous image guided, endoscopic or minimally open procedure all aimed at minimising soft tissue trauma and optimising patient recovery and rehabilitation. A suggested classification is
Percutaneous Chymopapain Percutaneous lumbar discectomy J Intradiscal electrothermal annuloplasty J Percutaneous instrumentation Endoscopic J Posterior – Lumbar – Cervical J Anterior – Lumbar – Thoracic – Thoracolumbar J J
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Background The main area of debate is related to the comparison between endoscopic and mini open spinal procedures. The endoscopic approach is best suited to open cavities such as the thorax or an insufflated peritoneal cavity. Mini open approaches are modified standard surgical approaches utilising recently developed sophisticated retractors that have allowed the development of specialist portals and approaches to the spine. While these are technically open procedures, and sometimes endoscopically assisted, they
ARTICLE IN PRESS Minimally invasive spinal surgery use very small skin incisions and consequently minimise soft tissue trauma. However, they require a very comprehensive knowledge of spinal anatomy, often acquired in training for performing traditional wider approaches, before progressing to a small portal with specialist retractor systems. Many structures are difficult to identify, and particularly vascular and extra spinal neurological structures are at significant risk. These approaches are for fully trained and experienced spinal surgeons, not beginners. The development of minimally invasive spinal surgery was driven by the desire to minimise surgical trauma, while avoiding complications, allowing rapid rehabilitation and mobilisation and giving long-term clinical results as good as the fully open approaches. As this mindset is applied both to the approaches to the spine and the procedure itself, percutaneous techniques such as chemonucleolysis are included in this review, which looks at each technique in turn. However increasingly there is hybrid usage of minimal access techniques, e.g. the combination of endoscopic visualisation in a mini open procedure using a specialised retractor and simultaneous image guidance.
Complications Of course minimally invasive surgery does not mean minimal complications. The potential for major vascular or neurological injuries during endoscopic and minimal access techniques exists just as with open approaches to the spine. Thus a surgeon must be very aware of the minimal access anatomy and there is probably no substitute for cadaveric training and proctoring during initial clinical experience. The list of complications reflects those seen in open procedures but there are some specific complications that will be covered under the individual techniques.
Percutaneous spinal procedures Percutaneous procedures on the spine are performed with radiological guidance. While typically the intervertebral disc is penetrated under fluoroscopy control, increasingly frequently real time CT guidance is used and some have persisted with MRI-guided percutaneous procedures. The classical portal into the intervertebral disc postero-laterally uses the gap between the exiting nerve root and the isthmus and facet joint. On an oblique radiograph there is a triangular portal into the disc that allows insertion of the needles and dilators. Using cannulas, various instruments can be inserted down through the portal into the disc.
Chemonucleolysis Chymopapain is an enzyme originally derived from papaya fruit. It was first used clinically in 1964 by instillation into the disc where it literally dissolves the nucleus pulposus in humans. When the procedure was popular its use was predominantly limited to contained disc herniation. Technique A needle is inserted into the intervertebral disc by the classic posterolateral technique. Discography is used to confirm needle placement in the centre of the disc,
443 following which the chymopapain is instilled. The procedure is performed under local anaesthesia and patients can be discharged home shortly after the procedure. Results Initial reported results were excellent. A randomised trial against saline in 1992 with a 10-year follow-up in 60 patients showed a success rate of 80% for relief of leg pain in a contained disc protrusion compared to 34% with the saline. The ultimate surgery rate was 20% in the chymopapain group compared to 47% in the saline group. In the same year a prospective randomised trial of chemonucleolysis versus open discectomy1 in 92 patients showed an overall better outcome with open surgery at 6 weeks and 3 months but no significant difference at 1 year. This may well relate to the long-term natural history of non-surgically treated disc herniation. The reported severe anaphylactic reaction rate is between 0.2% and 0.7% of cases, but otherwise there are few significant complications and the overall complication rate is 2.3% that compares favourably with an open complication rate of 11–12%. A large reported series had less than a 0.5% neurological injury rate. Current status While chemonucleolysis continues to be used by a small number of enthusiasts, suboptimal early results mean that most surgeons treating acute disc herniation use microdiscectomy which remains the gold standard treatment.
Automated percutaneous lumbar discectomy (APLD) Percutaneous discectomy has been performed by a variety of percutaneous and endoscopic methods. Percutaneous discectomy and (APLD or the Onik method) was popularised in the 1980s. This uses a posterolateral approach inserting instruments with a rotating cutting end through a cannula under radiology control into the disc and in combination with suction, removing fragments of nuclear material. Initially this was thought to offer higher success rates. Results Early results from the originators of the technique suggested a 70–85% success rate but a 1995 randomised controlled trial from Liverpool2 was halted just after half of the patients had been recruited because the results of APLD were so poor. Microdiscectomy patients had an 80% excellent or a good outcome compared to the APLD patients with a 30% excellent or good outcome. The patients who required subsequent microdiscectomy following APLD had a lower success rate than those that had microdiscectomy performed primarily. Current status More recently a refinement called ‘‘disc nucleoplasty’’ introduced in 2000 uses a combination of suction catheter and plasma energy system used to remove the disc tissues. No long-term data is available but early results suggest 50–60% level of pain reduction in acute sciatica.
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Intradiscal electrothermal annuloplasty (IDET) This was introduced in 1997 and was widely used in the US. Technique Patients are intra venously sedated on the X-ray table as the procedure can be uncomfortable. A standard needle is used to instrument the centre of the disc and discography performed to confirm the diagnosis and positioning. An electrothermal catheter is then passed through the needle and circled around the inside of the annulus to position metallic wires near the posterior annulus. The wire is then heated up to 90 1C for approximately 15 min. Theoretically the heat denatures protein promoting healing and destroying the local nerve endings that may be generating the pain. Results Randomised studies have demonstrated 50–60% of patients experiencing good or excellent pain relief from either discogenic lower back pain with or without a radicular component to the pain. Success rates appear to relate to patient selection and catheter placement. A randomised double-blind placebo-controlled trial from 2005,3 compared the outcomes in patients in whom the IDET wire was inserted into the region of the annular tear with the electrothermal therapy applied with those where the wire was inserted but no energy delivered. It was concluded that the procedure was safe with no permanent complications, but shows no significant change in outcome measures in either group at 6 month follow-up and they could demonstrate no benefit of IDET over placebo. Current status A small number of enthusiasts continue to offer patients IDET as a treatment for discogenic pain for underlying annular tear although realistically the benefits are limited to a few patients and are probably relatively short term.
Percutaneous pedicle screws and rod systems Magerl in Switzerland first described and popularised the use of percutaneous Schantz screws inserted into the pedicles with an external spinal fixation system. This was partly to give provisional stabilisation of the injured spine and for testing whether stabilisation had an effect on a particular patient in terms of managing axial back pain. However the screws were left piercing the skin and gave rise to significant infection problems. The use of image guidance systems has facilitated percutaneous pedicle screw placement and indeed instrumentation of any spine either open or percutaneously. Initial image guidance systems used CT data to produce virtual models of the spine and then reference markers to demonstrate where the patient’s spine was in space and to correlate this with the position of a marked instrument. More recently the technology has been extended to use imaging data acquired from a series of fluoroscopic shots taken before the procedure starts and from MRI data. The use of these techniques and in some hands the use of fluoroscopy allows percutaneous placement of pedicle screws with a safety margin that is similar to pedicle screws
J.K. O’Dowd inserted in an open fashion. Development of percutaneous insertion jigs that allow insertion of rods into the back of the pedicle screws, inserted percutaneously has now made it possible to insert instrumentation virtually percutaneously and achieve pedicle screw stabilisation posteriorly.4 Some lumbar anterior interbody fusion devices are adequately stabilised using trans-laminar screws posteriorly (also described by Magerl) rather than a full pedicle screw system. Most surgeons insert translaminar screws using a semi-percutaneous technique by making a small midline incision to visualise the spinous process and lamina and inserting the screws percutaneously from more laterally. The surface projection of the desired track for screw insertion is about a hand’s breadth from the midline. The technology exists to insert these screws percutaneously without the small midline incision. The size of the drill bit and screw introducer needs to be quite narrow because of the size of the lamina but the offset from the spinous process to the skin entry point makes for instability of the drill and insertion screwdriver. This is a technique that may be improved with real time imaging techniques but has not yet achieved widespread popularity.
Endoscopic spinal surgery Introduction Significant advances in video endoscopic technology led to the use of this technology to approach the spine, both anteriorly and/or posteriorly. In the early 1990s laparoscopic surgery for anterior lumbar procedures and transthoracic thoracoscopic thoracic procedures led to significant changes in spine care. Endoscopes through cannulae with working channels for irrigation and laser that were initially used for posterolateral approaches to the lumbar inter vertebral discs have subsequently been adapted for use in the cervical spine both anteriorly and posteriorly. The whole spinal column with some exceptions at junctional areas can now be approached percutaneously and endoscopically from the front or the back. As with minimally invasive spinal surgery in general, in experienced hands, there is no question that such approaches minimise trauma to soft tissues and often provide excellent visualisation of the spine and pathology. There is evidence that in some cases the degree of surgery to the spinal column is restricted by using narrow endoscopic portals and these restrictions have helped identify the indications for each technique. There are significant potential complications to viscera, vessels and nerves as with other minimally invasive techniques and there are specific complications related to the technology including breakage of instruments which are often very fine, to allow introduction through very narrow portals. However these endoscopic procedures have probably contributed most to opening up the possibility of ambulatory day case surgery of the spinal column.
Posterior The addition of video-endoscopy was a natural progression from the percutaneous lumbar disc techniques described
ARTICLE IN PRESS Minimally invasive spinal surgery above. With some saline irrigation and using the posterolateral working portal a scope can be introduced into the foraminal area, the disc itself and into the spinal canal. Excellent visualisation of the traversing and exiting nerve roots and particularly degenerative pathology is achieved. Initial percutaneous discoscopy and nucleotomy techniques described in 1992 used a series of dilators introduced over an initial needle, then replaced with the working portal for the endoscope. The same group also popularised the use of laser through the working channel of the endoscope and increasingly sophisticated instruments allowed enhanced surgical capability through this portal. The arthroscopic microdiscectomy technique described initially in Philadelphia included a 701 side viewing scope with backbiting forceps allowing both central nucleotomy and also a selective fragmentectomy for contained but herniated discs. Progressive improvements in manufacturing technology and use of a more lateral insertion point, make it possible to introduce endoscopes with good optical resolution and working channels (including the option to use laser) into the intervertebral foramen past the exiting nerve root and pathology and also the lateral aspects of the central spinal canal.
Results This technology is initially expensive and the learning curve is very steep particularly for surgeons without a background in general orthopaedic arthroscopy. The predominant use of the technique has been for disc herniations producing radicular pain with appropriate clinical indications for intervention. Results approaching those of open disc surgery have been achieved. A 2002 study5 looked at long-term results, albeit retrospectively, with a percutaneous transforaminal approach and 88% of patients had an excellent or good result; this reflects the results reported in other retrospective studies. This is an area of spinal surgery where high quality randomised controlled trial data were not available.
Current status In the hands of very experienced enthusiasts a lot can be achieved endoscopically, but these techniques have not achieved widespread acceptance by the generality of orthopaedic and neurosurgeons. Experts in the technique can decompress, stabilise and fuse the spine and undoubtedly in their hands the degree of soft tissue trauma is less than more conventional open procedures. The gold standard open approach however for disc herniation in any location remains microdiscectomy which inflicts fairly minimal trauma to the non-diseased spinal column and can readily be performed on a day case basis. The advantages of the endoscopic techniques then are marginal although the latter have the specific advantage of allowing visualisation of the intervertebral foramen. It may be that degenerative pathology here ultimately is better treated using these methods, but good quality scientific data are required which must include cost utility and cost effectiveness analysis.
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Cervical The use of posterolateral endoscopic approaches in the lumbar spine has led on to their use in the cervical spine. Technique Posterior endoscopic cervical foraminotomy is often performed with the patient in a semi-upright position. The surgeon uses the needle and dilators to progressively enlarge a portal down to the region of the cervical lamina and then a tubular retractor system is used to permit the insertion of a scope with a working channel. The use of high-speed drills allows the completion of a posterior localised transfacetal foraminotomy using a very similar technique to that used during open surgery. Protagonists report a surgical procedure lasting 45 min to 1 h and discharge within a few hours of the procedure without a supporting collar. Patients can return to work within a few days. Reports suggest above 80% success rate for relief of radicular symptoms particularly in patients with a pathology more easily accessed using a posterior foraminotomy approach. The posterior endoscopic approach to the cervical spine undoubtedly significantly reduces the otherwise often extensive soft tissue stripping required to access the facet and foraminal area with a posterior approach. As with the open techniques it is inadvisable to consider this approach for more significant anterior pathology such as disc spondylophytes and herniations anterior to the nerve root. As the surgical technique on the spine itself is similar to the open technique it seems likely that in experienced hands equivalent results can be achieved.
Anterior The same advantages in video technology had led to the general and thoracic surgeons using endoscopic transthoracic thoracoscopic and intraperitoneal laparoscopic procedures to manage pulmonary and abdominal visceral problems. In the background in both of these surgical fields is the spine and it was only a short time before these techniques became popular to address spinal pathology.
Lumbar History The first laparoscopic discectomy was described in 1991 and by 1993 two groups had reported early experiences with anterior lumbar interbody fusion using a transperitoneal endoscopic or laparoscopic approach. The laparoscopic approach took orthopaedic surgeons into unfamiliar anatomical territory and in the US it was considered mandatory to have a general surgeon to perform the surgical approach. There was a significant albeit small problem with retrograde ejaculation in male patients undergoing this technique and for this reason by 1996 the first description of a balloon assisted endoscopic retroperitoneal approach to the lumbar spine was described. The main problem using either approach was the great vessels and the emerging technology highlighted the variability in the anatomy of the bifurcation of the aorta and the inferior vena cava. In most hands the anterior
ARTICLE IN PRESS 446 transperitoneal approach to the lumbosacral disc was straightforward and safe. However the endoscopic approach to the L4/5 level was significantly more challenging and anterior endoscopic access to levels above this was only routinely achieved by very few experienced surgeons. Technique A standard laparoscopic approach is used with carbon dioxide insufflation of the peritoneal cavity. Multiple abdominal wall cannulas are inserted with channels for the scope, spinal approach instruments, retractors and ultimately the system for introducing the spinal implant. The pioneers of this technique used one or two cylindrical anterior cages introduced either in an anterior–posterior direction or obliquely. Results Reported results indicated that there was a significant learning curve both in terms of difficulty and operative time. Experienced surgeons achieved access to L4/5 and L5/S1 in most cases with an acceptable complication rate, but most series include one significant vascular injury but with no fatalities. A randomised control led trial showed significant advantages of one level endoscopic BAK cage insertion over open BAK cage insertion with a significantly higher return to work rate and a much more rapid return to work. In many cases the surgery could be performed on a day case basis but postoperative nursing and physiotherapy care in the United States is of a very high quality. Taking into account the economic impact of earlier return to work, this trial established the overall direct and indirect costs as being significantly less using laparoscopic surgery on an ambulatory or day case basis. The Nottingham (UK) study6 established a shorter time to sitting postoperatively, mobilisation and discharge home for one level laparoscopic than one and two level open surgery with a low complication rate. The average hospital stay was 4.6 days and day case surgery was not achieved. Current status Many surgeons have changed from endoscopic techniques for anterior lumbar surgery to the mini open approaches described below. A small number of surgeons still routinely perform endoscopic anterior lumbar surgery despite the widespread acceptance that stand-alone intervertebral body fusion techniques are not adequate to achieve good clinical results.6 Such endoscopic anterior procedures should be augmented with some form of posterior stabilisation such as percutaneous translaminar screws or percutaneous pedicle screws.
Thoracic/thoracolumbar With the advent of advanced antimicrobial therapy particularly for tuberculosis the use of thoracoscopy as an adjunct to management of respiratory disease had gradually declined until the arrival of modern video assisted technology in 1990. The first description of thoracoscopic surgery in 1993 looked at 10 cases with for a variety of diagnoses. Since then the indications for thoracoscopic treatment have
J.K. O’Dowd widened to include most diseases of the thoracic spine and the thoracolumbar junction. There is an emerging group managing mild scoliosis entirely endoscopically. Additionally it has found a role in the management of degenerative disc disease in the thoracic spine and for biopsy and definitive treatment of anterior column conditions including tumour, fracture and infection throughout the thoracic and thoracolumbar spine. It has found significant use in managing difficult junctional zones particularly the upper three thoracic spinal levels and the thoracolumbar junction without taking down the diaphragm.
Technique Unlike laparoscopic spinal surgery where insufflation is required the endoscopic portals can be inserted through the chest wall and no pressurisation is required. Typically forwards looking or 301 offset 10 mm thoracoscopes are ideal for performing a spinal procedure. By gentle blunt dissection it is possible routinely to expose the body of L1 using a transthoracic endoscopic technique, allowing instrumentation and procedures to be performed down to L1 and effectively across the diaphragm. Soft tissue procedures including pleurotomy, segmental vessel ligation and discectomy are performed with standard soft tissue thoracic surgical and spinal surgical instruments. Indeed one of the advantages of the non-pressurised portals is that standard spinal instruments can be used through the portals without any particular adaptations as long as they are small enough to fit through. With good illumination and suction, the use of high-speed burs through the endoscopic portals allows resection of diseased or normal vertebral body. After corpectomy or vertebrectomy the anterior spinal column can be reconstructed with strut bone grafts, cages packed with bone graft or intervertebral body replacement devices using the endoscopic assisted approach.7 Many surgeons trained in the use of the operating microscope continue to prefer to use the microscope through a small open portal and this will be discussed below. The use of thoracoscopy in scoliosis surgery started with discectomies, anterior releases and anterior growth arrests, including anterior convex hemiepiphysiodesis in early onset scoliosis in which posterior growing instrumentation was being used at the same procedure. Some units employ two surgical teams to undertake simultaneous posterior instrumentation and thoracoscopic growth arrest and release with a prone patient. Inevitably instrumentation has been developed that can be used endoscopically and in some parts of the US endoscopic anterior correction of scoliosis surgery has become a routine for mild early idiopathic curves.8 In general terms curves with a Cobb angle greater than 501 or which are very stiff are too difficult to treat endoscopically. Again there is a very significant learning curve but experienced surgeons report operating times of similar duration as open surgery. Complications are similar to those seen in open surgery. Visualisation of fine structures such as the sympathetic chain or thoracic duct is probably better with endoscopic techniques than with open techniques although there is no evidence to support a reduced complication rate with the endoscopic techniques.
ARTICLE IN PRESS Minimally invasive spinal surgery Results There are no prospective or high quality randomised controlled trials in this area. The recent study from San Diego8 showed equivalent corrections of the preoperative Cobb angles (60%) and significantly less marked change in forced vital capacity following endoscopic surgery as opposed to open surgery for scoliosis in the thoracic cavity. This study however demonstrated a 50% longer operating time for the endoscopic scoliosis surgery.
Cervical Anterior cervical endoscopic surgery is probably the least recognised of the innovative methods of approaching the spine. Conventional anterior cervical spine approaches are relatively atraumatic and at most levels no muscular structures except platysma need to be cut. However, as the technology for posterior endoscopic treatment in the lumbar spine has developed a small number of interested surgeons have adapted these techniques, for anterior cervical surgery, although no body cavity exists. Technique The current technique involves an open incision through the skin and then dissection through the superficial and deep fascia medial to the carotid artery and lateral to the oesophagus using the finger. A posterior lumbar type endoscopic portal is then docked with the anterior cervical spine and with the use of an endoscope, special endoscopic retractors and a high speed burr using a transdiscal approach allows access to the spine for an anterior cervical decompression and fusion as in the open technique. At this stage no significant results are available and it seems unlikely that this is a technique that will achieve
447 much popularity as it is only a variation on the open approach to the anterior cervical spine.
Mini open spinal surgery (minimal invasive spinal surgery (MISS)/least invasive spinal surgery (LISS)) Mini open spinal surgery, MISS or LISS are used synonymously by various groups. They represent a natural evolution from various attempts to minimise surgical trauma and which led to the development of the endoscopic techniques above. The technology that allowed this was the development of specialist retractors, often table mounted. The first of these emerged at the same time as the laparoscopic and thoracoscopic surgical techniques. The basic principle is to use a more conventional surgical approach pathway that has the great benefit of familiarity to the spinal surgeon which obviates the need for an approach surgeon experienced with endoscopic transperitoneal and transthoracic techniques. In the thoracic spine the use of the small retractor system allows an operating microscope to be used and access to single levels within the thoracic spine can be achieved without rib resection or a wide thoracotomy. So-called smart instruments were developed, e.g. a combination of retractor with illumination or retractor with suction to minimise the clutter at the base of the often very small operative field. Mayer in Germany developed the oblique approach to the anterior lumbar spine. X-ray control was used to identify the location on the lateral body wall that directly overlay the lumbar intervertebral disc and this was planned anatomically to coincide with the lateral margin of the anterior longitudinal ligament. Having made a small skin incision it was a matter of simple muscle splitting to come
Figure 1 Anterior lumbar approach using ‘‘smart retractor system.’’
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Figure 2
Anterior exposure of lumbo-sacral disc using Synframe retractor.
Figure 3 Anterior column reconstruction following mini thoracotomy in osteoporotic post traumatic kyphosis.
straight down on to the spine but disadvantages of the oblique approach soon became apparent, especially in relation to device insertion. The wide-open approaches to the anterior lumbar spine popularised by the Hong Kong school used an anterior incision either midline or paramedian, then diverting around the peritoneum and retracting the peritoneal contents to one side so making an extraperitoneal approach. The advent of the new retractor systems allows this to be performed through either a small skin crease incision low down on the abdominal wall or an equally small longitudinal midline or paramedian insertion. The rectus sheath is opened anteriorly, and the rectus muscle mobilised laterally to avoid injuring its nerve supply. Then distal to the arcuate line the extraperitoneal dissection is performed with a finger until the psoas muscle and external iliac vessels are identified. Then specialised retractor blades with blunt vascular tips or fine Hohmann retractors that can be attached to the retractor frame are inserted and excellent visualisation is achieved at the L4/5 and L5/S1 disc. The technique is more easily adaptable to access higher lumbar discs than the endoscopic approaches that essentially had to use an approach between the aorta and the vena cava (Fig. 1). Using the mini open approach to the anterior lumbar spine segmental vessels can be ligated and the aorta and vena
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Figure 4
Mini thoracotomy showing scoliosis correction.
cava mobilised across to the right side to allow clear visualisation of the midline of the spine. It was a fortunate coincidence that the advent of the small open approaches, achievable by most orthopaedic and neurosurgeons, occurred simultaneously with the two emerging technologies which now dominate anterior spinal surgery. The first of these was the use of anterior intervertebral body cage devices to enhance or achieve fusion and the second is the emergence of total disc replacement or lumbar disc arthroplasty as an alternative treatment for managing the painful degenerative lumbar spine (Fig. 2). The critical analysis of these two techniques is beyond the scope of this article but in general terms both types of devices can now be inserted using a 3–5 cm cosmetically very acceptable anterior body wall incision well below the umbilicus. There does seem to be a correlation with more rapid mobilisation much as was seen with the endoscopic techniques as described above.
Thoracolumbar junction The same small open approaches are ideal for managing disease in spinal conditions of the thoracolumbar junction. A transthoracic approach can be used and using X-ray control the incision is placed directly over the T12/L1 disc. The chest cavity is opened and then the diaphragm is retracted with the abdominal contents beneath it. Then as with the endoscopic technique, blunt dissection is used to elevate the diaphragm from T12 and L1. Access can routinely be achieved to the T12/L1 level. The scope with the small open approaches is very similar to that of the endoscopic approaches and the majority of reconstructive spinal units in Europe now use the small open
approach to manage single level disease at any level in the thoracolumbar spine from T3 to the sacrum (Fig. 3). For multilevel conditions, particularly scoliosis, the technology now allows completion of five, six or seven level scoliosis surgery in the chest using a 10 cm incision, sometimes without rib resection. Some surgeons prefer to use two small incisions but since both are between the anterior and posterior axillary lines, they are essentially invisible with the patient’s arm by their side. The implant may need to be inserted percutaneously but excellent correction can be achieved and currently the majority of scoliosis surgeons having adopted a minimal access technique use them in preference to endoscopic approaches (Fig. 4).
References 1. Muralikuttan KP, Hamilton A, Kernohan WG, Mollan RA, Adair IV. A prospective randomized trial of chemonucleolysis and conventional disc surgery in single level lumbar disc herniation. Spine 1992;17:381–7. 2. Chatterjee S, Foy PM, Findlay GF. Report of a controlled clinical trial comparing automated percutaneous lumbar discectomy and microdiscectomy in the treatment of contained lumbar disc herniation. Spine 1995;20:734–8. 3. Freeman BJ, Fraser RD, Cain CM, Hall DJ, Chapple DC. A randomized, double-blind, controlled trial: intradiscal electrothermal therapy versus placebo for the treatment of chronic discogenic low back pain. Spine 2005;30(21): 2369–77. 4. Foley KT, Gupta SK, Justis JR, Sherman MC. Percutaneous pedicle screw fixation of the lumbar spine. Neurosurg Focus 2001; 10(4):E10.
ARTICLE IN PRESS 450 5. Yeung AT, Tsou PM. Posterolateral endoscopic excision for lumbar disc herniation: Surgical technique, outcome, and complications in 307 consecutive cases. Spine 2002;27(7): 722–31. 6. O’Dowd JK. Laparoscopic lumbar spine surgery. Eur Spine J 2000; 9(Suppl 1):S3–7.
J.K. O’Dowd 7. Khoo LT, Beisse R, Potulski M. Thoracoscopic-assisted treatment of thoracic and lumbar fractures: a series of 371 consecutive cases. Neurosurgery 2002;51(Suppl 5):S104–17. 8. Newton PO, Marks M, Faro F, Betz R, Clements D, Haher T, Lenke L, et al. Use of video-assisted thoracoscopic surgery to reduce perioperative morbidity in scoliosis surgery. Spine 2003;28:249–54.
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Available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/cuor
KNEE
Postero-lateral rotatory instability P.G. Haslama,, D.R. Bickerstaffb a
Doncaster Royal Infirmary, Thorne Road, Doncaster DN2 5LT, UK The One Health Group-Sheffield Limited, 131 Psalter Lane, Sheffield S10 8UX, UK
b
KEYWORDS Postero-lateral corner; Postero-lateral rotatory instability; Popliteo-fibular ligament; Knee ligament injury; Dial test
Summary The three key components of the postero-lateral corner are the lateral collateral, the popliteal muscle-tendon unit and the popliteo-fibular ligament. Injuries to these structures are becoming increasingly recognized either in isolation or more commonly as part of a combined ligament injury. Careful assessment will avoid missing such injuries and MRI scanning is an aid to diagnosis. Treatment options range from conservative for mild isolated injuries, to surgical repair and/or reconstruction for combined and chronic injuries. & 2007 Elsevier Ltd. All rights reserved.
Introduction Injuries to the postero-lateral corner of the knee are relatively rare, accounting for less than 2% of acute knee injuries. Despite this, knowledge of injuries to the postero-lateral corner of the knee has expanded considerably over the last 10 years, so much so that even FRCS (Tr and Orth) examiners expect candidates to have some grasp of Postero-Lateral Rotatory Instability (PLRI). Anatomical structures and function are now more clearly defined, and treatment options have expanded accordingly. Despite recent advances, PLRI is still frequently missed and left untreated. Presentation can be isolated or more commonly as a part of a multi-ligamentous injury.
Surgical anatomy Numerous cadaveric studies1–3 have clarified our understanding of the postero-lateral structures. However, some Corresponding author.
E-mail address:
[email protected] (P.G. Haslam). 0268-0890/$ - see front matter & 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2007.07.008
structures may be absent. The lateral side of the knee was divided into three layers by Seebacher et al.4 from superficial to deep (see Fig. 1):
ilio-tibial band and biceps tendon; patellar retinaculum and patello-femoral ligament; capsule, lateral collateral ligament (LCL), arcuate ligament, fabello-femoral ligament, popliteo-fibular ligament, popliteus muscle tendon unit. It is the third, deepest layer which causes confusion regarding both nomenclature and variability of anatomical structures. The three key components of the postero-lateral corner are the LCL, popliteo-fibular ligament and popliteus muscle tendon unit. These form an inverted ‘Y’ inserting onto the lateral aspect of the femur (Fig. 2). The lateral collateral ligament runs from just proximal and posterior to the lateral epicondyle and inserts just anterior to the midpoint of the head of the fibula. The popliteo-fibular ligament runs posterior to the lateral collateral ligament from the styloid process of the fibula
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Figure 1 Anatomical dissection of the postero-lateral corner of the knee.
proximally to the musculo-tendinous junction of the popliteal tendon. The popliteus muscle tendon unit is a complex structure with three popliteo-meniscal fascicles, viz.; the popliteofibular ligament (described above), the arcuate ligament and the muscle and tendon of popliteus itself. The tendon attaches to the lateral aspect of the femur approximately 2 cm distal and anterior to the LCL,5 passing intra-articularly into the popliteal hiatus which is formed by the three popliteo-meniscal ligaments. These anchor the popliteal tendon to the lateral meniscus. The arcuate ligament is a broad sheet of tissue that runs from the popliteus muscle belly to the posterior capsule and lateral meniscus. The fabello-fibular ligament6 is a variable structure running parallel to the LCL from fibula to fabella.
Biomechanics of the postero-lateral corner The biomechanics of the postero-lateral corner has been largely defined by sequential cadaveric sectioning studies.1–4,7–9 After the application of a load, motion is measured following division of structures first individually and then combined to determine the contribution that each structure makes to the stability of the knee. From these studies, it is clear that the LCL is the primary restraint to varus translation and the popliteo-fibular ligament and popliteal muscle tendon unit are important
Figure 2 Simple diagram showing the 3 key structures of the postero-lateral corner of the knee.
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secondary stabilizers. If the LCL and deep structures are absent, the ACL and PCL have a secondary restraining role. The LCL, popliteo-fibular ligament and popliteal muscle tendon unit are all primary restrainers of tibial external rotation, maximal at 301 of flexion, whereas at 901 of flexion, the ACL and PCL are important secondary stabilizers. These biomechanical data form the basis for the dial test. Finally, the postero-lateral corner structures are secondary restraints to posterior translation.
Mechanism of injury A combined varus and hyperextension force10 are thought to produce PLRI and it may also occur with forced external rotation. Isolated injuries are rare, usually the injury is combined most commonly with a PCL, ACL or both as in an acute knee dislocation. In such severe injury, the biceps may be avulsed and the common peroneal nerve is at risk.11 There is disagreement in the literature as to the most common site of postero-lateral corner injury with Ross et al.15 stating that the majority occur distally, whilst Stannard et al.16 stated they occurred from the femoral side. The difference of opinion regarding the site of rupture may be due to the magnitude of trauma and pattern of associated injuries. The former series were all sports injuries with ACL ruptures, whilst the latter were highenergy injuries resulting in a multi-ligamentous knee injury.
Clinical features In the acute setting, the presentation depends on the degree of trauma. In a severely traumatized patient with an acute dislocation, having first stabilized the patient’s general condition, a careful vascular and peripheral nerve examination must be carried out as injuries to one or both are common. However, patients with lesser degrees of trauma may present as outpatients, and a high index of suspicion is essential to avoid missing such pathology. Patients presenting late usually complain of pain and instability. The pain is typically postero-lateral and there is instability in extension. On examination, there may be a varus deformity with hyperextension and lateral thrust in the stance phase of gait. Lateral collateral instability is detected by applying a varus stress with the knee flexed to 301. If the joint also opens in full extension, this suggests a concomitant cruciate ligament injury. Three tests have been described to look specifically for PRLI and its most common associated ligament injury, the PCL:
The reverse Lachman test This is performed as one would for a Lachman to identify ACL laxity. On performing the test, there is the impression of AP laxity but with a definite end point. One should always suspect PL corner laxity in this situation. The PL corner controls posterior translation towards extension. If one looks carefully, there is an impression of posterior movement rather than anterior with coupled external rotation, i.e. the tibial tubercle appears to externally rotate.
Figure 3
X-ray showing fibula avulsion fracture.
Dial test13 With the patient prone, the degree of external rotation is compared with the normal side at 301 and 901 of flexion. If the knee has an increase of 101 external rotation at 301 flexion then PRLI is suspected. If there is an increase at 901 then associated posterior cruciate ligament injury is suspected. This should be part of a routine knee examination.
Hughston test12 With the patient supine, both lower limbs are elevated by lifting the great toes. On the effected side, the leg drops into hyperextension and varus, if positive injuries to both the PCL and PLRI are suspected.
Imaging Plain X-rays may show a Segond fracture, avulsion from the fibula or Gerdy’s tubercle any of which should alert the physician for the possibility of PLRI (Fig. 3). MRI is used to demonstrate the extent of injury and particularly whether the cruciates have been injured. The larger structures of the postero-lateral corner such as the biceps tendon, lateral collateral ligament and popliteal muscle tendon unit are readily identified on MRI. Smaller structures such as the popliteo-fibular ligament, arcuate ligament and the fabello-fibular ligament are less easily seen and dependent on image quality and interpretation.14 Secondary MRI features of PLRI include bone bruising typically on the medial femoral condyle.15 It is important to try and determine the level of injury, i.e. whether structures are avulsed from the femur or tibia/fibula or injured in mid substance, as this influences treatment.
Treatment: Acute injuries Conservative Mild to moderate isolated PLRI does well if treated conservatively particularly in older age group low demand patients.
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Acute repair with or without augmentation Acute injuries (within 2–3 weeks) may be amenable to surgical repair. The aim of surgery is to restore the three key structures of the postero-lateral corner: the LCL, PFL and popliteal muscle tendon unit. Concomitant cruciate ligament injury should be addressed at the same time. The lateral structures are exposed through a hockey shaped incision based over Gerdy’s tubercle. From superficial to deep, the postero-lateral corner structures are explored, taking care to protect and assess the common peroneal nerve. Any tendon avulsion from bone can be repaired directly with suture anchors but usually the popliteal muscle ruptures at the musculo-tendinous interval and is difficult to repair. We prefer augmentation with a Larsontype procedure if midsubstance rupture occurs. There is evidence now16 that acute augmentation is better than repair alone.
Treatment: Chronic injuries The majority of patients present with chronic injuries are commonly associated with a PCL injury. Treatment must therefore address both injuries. The type of graft material used (allograft or autograft) must be chosen. If autograft is used should both hamstrings be harvested or ipsilateral hamstring and patella tendon?
Osteotomy Valgus osteotomy should be considered in all patients, either as a staged procedure or combined with ligament reconstruction. Patients with varus alignment of the lower limbs and obvious lateral thrust clinically are more suitable for osteotomy and osteotomy alone may be sufficient to reduce symptoms to an acceptable level in low demand patients.
PLRI reconstruction Whichever of the many techniques have been described over the years for reconstruction of the postero-lateral corner, there are some basic principles17: - restoration of the three key structures of the posterolateral corner; - a graft of sufficient strength to support the posterolateral corner; - an isometric graft through all ranges of flexion and extension. A variety of techniques have been described. Hughston and Jacobsen18 used a lateral gastrocnemius, capsular, LCL and popliteus advancement procedure. This technique has fallen out of favour as it relies on the integrity of postero-lateral structures and did not offer a strong enough repair for more severe injuries. Clancy19 diverted the biceps tendon into a trough formed in the lateral epicondyle and fixed there with a screw and washer. The theoretical advantage of this procedure is that it reduces the external rotation effect of the biceps
Figure 4
Clancy technique.
tendon. Exponents of this technique claim excellent results (Fig. 4). Muller20 used a strip of the ilotibial band along the line of the popliteus tendon as a popliteal bypass procedure. The Larson21 technique, currently commonly used, utilizes a free semitendinosis graft as a figure of eight through a fibula tunnel and around a screw and washer in the lateral femoral condyle. The tunnel technique22 is similar but simplified in that the semitendinosis loop forms a triangle and is secured in the lateral epicondyle using an interference screw. Recently, the two-tailed technique16 has been described which although being more complex gives a more anatomical reconstruction by adding a tibial tunnel to the construct.
Authors’preferred surgical technique After induction of anaesthesia with the patient supine, a full examination of the knee ligaments is repeated and compared with the opposite side. The tourniquet is then inflated and the patient is prepared and draped. The semitendinosis and gracilis tendons are harvested, trimmed to the required length and whipstitched with No. 5 Ethibond. With the knee flexed to 60–701, a lateral curved skin incision is centred distally between Gerdy’s tubercle on the tibia and the anterior aspect of the fibular head. The skin and subcutaneous tissue are reflected from the fascia as a posteriorly based flap. The iliotibial band is then split in the line of its fibres at the level of the lateral femoral condyle and along the length of the skin incision. The common peroneal nerve is exposed at the inferior portion of the
ARTICLE IN PRESS Postero-lateral rotatory instability
455 Surgery is aimed to restore the three key structures of the postero-lateral corner: the lateral collateral ligament, popliteo-fibular ligament and the popliteus muscle tendon unit. A variety of techniques have been described to reconstruct the postero-lateral corner.
References
Figure 5 (a) Tunnel technique coronal view; (b) tunnel technique sagittal view.
biceps tendon and is dissected free of its fascial attachments and protected. The fibular head is exposed and a transverse tunnel is made using a cannulated reamer (usually 7 or 8 mm). The lateral epicondyle is dissected and a guide wire is inserted from lateral to medial at the site of insertion of the popliteus tendon and lateral collateral ligament. A blind ending 40 mm tunnel is made (8 or 9 mm diameter depending on graft size) and the edges rasped to prevent damage to the tendon. The graft is pulled through the fibular tunnel and then the posterior limb is passed under the iliotibial band. The anterior limb is used to reconstruct the lateral collateral ligament and the posterior limb to reconstruct the popliteo-fibular ligament. The No. 5 Ethibond suture ends are threaded through the guide wire which is then pulled through the medial side of the knee. Whilst maintaining tension on the suture, the graft is positioned so that the posterior limb lies anteriorly and the posterior limb posteriorly within the tunnel. The graft is tensioned and cycled to ensure isometry. A Bio fix interference screw of size 1 mm larger than the reamer size is inserted. The iliotibial band is closed with No. 0 vicryl and a subcuticular 3/0 moncryl used for skin. Post-operatively if combined with PCL reconstruction, a PCL brace is used for 2 weeks in full extension followed by 4 weeks weight bearing. If combined with an ACL reconstruction, they are braced for 6 weeks with weight bearing as tolerated (Fig. 5a and b).
Conclusion Injury to the postero-lateral corner, although rare in isolation, is increasingly recognized in association with cruciate ligament injuries. Careful examination will avoid missed injuries.
1. Shahane SA, Ibbotson C, Strachan R, Bickerstaff DR. The popliteofibular ligament. An anatomical study of the posterolateral corner of the knee. J Bone Jt Surg Br 1999;81(4): 636–42. 2. Goolehon DL, Torzilli PA, Warren RF. The role of the posterolateral and cruciate ligaments in the stability of the human knee. A biomechanical study. J Bone Jt Surg Am 1987;69(2): 233–42. 3. Grood ES, Stowers SF, Noyes FR. Limits of movement in the human knee. Effect of sectioning the posterior cruciate ligament and postero-lateral structures. J Bone Jt Surg Am 1988;70(1):88–97. 4. Seebacher JR, Inglis AE, Marshall JL, Warren RF. The structure of the postero-lateral corner of the knee. J Bone Jt Surg Am 1982; 64(4):536–41. 5. Brinkman JM, Schwering PJA, Blankeworth L, et al. The insertion geometry of the postero-lateral corner of the knee. J Bone Jt Surg Br 2005;87B(10):1364–8. 6. Minowa T, Murami G, Kura H, et al. Does the fabella contribute to the reinforcement of the postero-lateral corner of the knee by inducing development of associated ligaments? J Orthop Sci 2004;9(1):59–65. 7. Nielsen S, Helmig P. The static stabilizing function of the popliteal tendon in the knee. An experimental study. Arch Orthop Trauma Surg 1986;104(6):357–62. 8. Neilsen S, Oversen J, Rasmussen O. The posterior cruciate ligament and rotatory knee instability. An experimental study. Arch Orthop Trauma Surg 1985;104(1):53–6. 9. Neilsen S, Rasmussen O, Ovesen J, Anderson K. Rotatory instability of cadaver knees after transection of collateral ligaments and capsule. Arch Orthop Trauma Surg 1984;103(3): 165–9. 10. Fanelli GC. Surgical reconstruction for acute postero-lateral injury of the knee. J Knee Surg 2005;18(2):157–62. 11. Montgomery AS, Birch R, Malone A. Entrapment of a displaced common peroneal nerve following knee ligament reconstruction. J Bone Jt Surg Br 2005;87(6):861–2. 12. Hughston JC, Norwood Jr. LA. The postero-lateral drawer test and external rotational recurvatum test for postero-lateral rotatory instability of the knee. Clin Orthop 1980;147:82–7. 13. Cooper DE. Tests for postero-lateral instability of the knee in normal subjects. Results of examination under anaesthesia. J Bone Jt Surg Am 1991;73(1):30–6. 14. LaPrade RF, Gilbert TJ, Bollom TS, Wentorf F, Chaljub G. The magnetic resonance imaging appearance of individual structures of the postero-lateral knee. A prospective study of normal knees and knees with surgically verified grade III injuries. Am J Sports Med 2000;28(2):191–9. 15. Ross G, Deconciliis GP, Choi K, Scheller AD. Evaluation and treatment of acute postero-lateral corner/anterior cruciate ligament injuries of the knee. J Bone Jt Surg Am 2004;86A (Suppl. 2):2–7. 16. Stannard JP, Brown SL, Farris RC, et al. The postero-lateral corner of the knee. Repair versus reconstruction. Am J Sports Med 2005;33:881–9. 17. Davies H, Unwin A, Aichroth P. The postero-lateral corner of the knee: anatomy, biomechanics and management of injuries. Injury 2004;35:68–75.
ARTICLE IN PRESS 456 18. Hughston JC, Jacobsen KE. Chronic postero-lateral rotatory instability of the knee. J Bone Jt Surg 1985;67A:351. 19. Clancy WG, Meister K, Craythorne CB. Postero-lateral corner collateral ligament reconstruction. Master techniques in orthopaedic surgery. Reconstructive knee surgery. Raven Press; 1995. p. 143–56. 20. Muller W. Form, function, and ligament reconstruction. The knee. Berlin: Springer; 1983.
P.G. Haslam, D.R. Bickerstaff 21. Larson RV, Sidles J, Beals T. Isometry of the lateral collateral and popliteofibular ligaments and a technique for reconstruction. In: International teaching meeting. The Wellington Hospital, London, 21–22 March 1996, p. 92–6. 22. Kumar A, Jones S, Bickerstaff DR. Postero-lateral reconstruction of the knee: a tunnel technique for proximal fixation. Knee 1999;6:257–60.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 457–463
Available at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/cuor
HIP
Osteonecrosis of the femoral head: Part 1—Aetiology, pathogenesis, investigation, classification Samuel J. Parsonsa,, Niall Steeleb a
Robert Jones and Agnes Hunt Hospital, Gobowen, Oswestry, Shropshire SY10 7AG, UK Department of Arthroplasty, Robert Jones and Agnes Hunt Hospital, Gobowen, Oswestry, Shropshire SY10 7AG, UK
b
KEYWORDS Osteonecrosis; Hip; Classification; Pathogenesis
Summary Changing understanding of the pathology and aetiology of osteonecrosis of the femoral head is leading to a greater insight into potential treatments. This review of idiopathic osteonecrosis looks at causes, classification and treatments options, including more novel approaches. & 2007 Elsevier Ltd. All rights reserved.
Introduction
Epidemiology
Osteonecrosis is a disease arising from impaired osseous blood flow which can follow traumatic or non-traumatic conditions. Originally it was thought to be secondary to infection, but negative bacteriological studies led to the use of the term aseptic necrosis. Further studies showed that the necrotic bone was not only sterile but also avascular, hence the terms ischaemic necrosis, avascular necrosis, and bone infarction. The cessation of blood flow may arise in any part of the vascular network: arterial, capillary, sinusoidal, or venous. If secondary to a mechanical interruption it is termed ‘traumatic osteonecrosis’, whereas atraumatic osteonecrosis results from a range of direct and indirect insults.
It is most common in the second to fifth decades of life. The typical patient is a male, in his mid 30s. As such patients have a longer life span, and are economically active, this can be costly to society; while joint replacement is the definitive treatment, it has a much higher failure rate in this group of patients, possibly reflecting continued steroid use and younger age. Without treatment more than 70% of femoral heads with osteonecrosis will proceed to collapse, requiring prosthetic joint replacement within 3–4 years of diagnosis.1 Merle d’Aubigne’ et al. showed 20% collapse at 1 year, and 75% by 3 years.2 Osteonecrosis accounts for 5–12% of all primary total hip replacements varying geographically from around 10% in the US, up to 45% in Taiwan.
Corresponding author. Tel.: +44 169 140 4000; fax: +44 169 140 4071. E-mail addresses:
[email protected] (S.J. Parsons),
[email protected] (N. Steele).
Aetiology/risk factors
0268-0890/$ - see front matter & 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2007.11.004
Causation of atraumatic osteonecrosis of the femoral head is believed to be multifactorial, in some cases associated with
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Steroids
Table 1 Indirect cause
Direct cause
Steroids Alcohol Coagulation disorders Smoking Hyperlipidaemia Connective tissue disorders/ SLE Sarcoidosis
Trauma Radiation Sickle cell disease/trait Caissons disease Gaucher’s disease Chemotherapy/cytotoxics Myeloproliferative disorders
Cushing disease Other endocrine disorders Gout Pregnancy OCP use Pancreatitis Inflammatory bowel disease Shwartzmann reaction HIV (virus/drugs) Haemophilia Renal failure Organ transplant Thermal injuries Thalassaemia
both a genetic predisposition and exposure to certain risk factors. There are many factors associated with osteonecrosis of the hip. There are anatomical factors. In a study of the vascular anatomy of 99 hips undergoing vascularised fibular grafting, 93 had abnormal vascular patterns. In contrast, in a control group only 31% had abnormal vascular patterns. Absence or hypoplasia of the superior capsular artery was the most common abnormality.3 These findings suggest that there is a population of patients at risk for osteonecrosis as a result of anomalies of the microvascular circulation of the femoral head. The lateral epiphyseal vessels supply the superolateral aspect of the femoral head with little collateral circulation. Therefore, this region is sensitive to circulatory impairment and is in fact the most frequent site for osteonecrosis. Additional factors give rise to direct impairment of the circulation, e.g. trauma, radiation, caisson disease, myeloproliferative disorders, etc. For most the pathophysiology is uncertain, with no direct correlation between risk factors and development of the condition. The majority are idiopathic, but alcohol and steroids account for the majority of cases with an identifiable cause (Table 1). While a minimal dose and duration of either steroid and alcohol is necessary to cause osteonecrosis, the amount has not been determined and there is marked patient variability. Fewer than 5% of those with heavy alcohol consumption and between 5% and 10% of those receiving high dose steroids go on to develop osteonecrosis of the hip. What distinguishes those patients that do develop osteonecrosis from those that do not, has yet to be determined.
Conditions such as systemic lupus erythematosus, organ transplant, etc. are regularly treated with significant doses of steroids, often for prolonged periods, and there is a clear association with osteonecrosis. In particular, the risk of steroid associated osteonecrosis is especially high in patients undergoing renal transplant, possibly due to underlying mineralisation defects and structural weakening of the cancellous bone. Hence, the difficulty in determining whether the osteonecrosis is related to the disease process or its treatment. Multivariate analysis has suggested that high dose steroid use is an independent variable despite such confounding factors. The dose of steroid necessary to cause osteonecrosis is not known, but the mean daily or peak dose rather than cumulative or duration of therapy appears has been implicated; higher doses, even of short duration, present greater risks. Specifically doses of 420 mg/day appear to be associated with a higher risk of osteonecrosis or total doses of 42 g of prednisolone within 2–3 months. Lower doses seem not to be typically related to osteonecrosis of the femoral head. A meta-analysis of 22 studies of steroid associated osteonecrosis revealed a 4.6-fold increase in the rate of osteonecrosis for every 10 mg/day increase in mean daily dose.4 The level of activity and the number of mesenchymal cells in both the haemopoietic and the stromal compartments of the bone marrow have been shown to be depressed in patients with steroid related osteonecrosis of the femoral head. Steroid treatment produces a hyperlipidaemic state that often leads to osteoporosis but not usually osteonecrosis and it is not possible to predict which patients of the many treated with steroids will develop osteonecrosis. Prolonged steroid treatment also stimulates the differentiation of pluripotent bone marrow stromal cells into adipocytes.5 Steroid induced adipogenesis in bone stem cells and the systemic changes in lipid metabolism are major contributors to steroid induced osteoporosis and osteonecrosis5,6 and fat cell hypertrophy can result in elevated intraosseous pressure producing an intraosseous compartment syndrome that may result in ischaemia and osteonecrosis.7 As well as enhancing the expression of adipocytes specific genes, steroids decrease the expression of type 1 collagen and osteocalcin mRNA.6,7 The marrow becomes lipid infiltrated with less collagen and osteocalcin and there are fewer osteoprogenitor cells available to repair damage. MRI based studies on patients on steroids have shown that the risk period is more easily defined. The initial necrotic changes, seen as well demarcated bands on MRI, appear between 3 and 5 months after starting steroid treatment, with virtually all appearing before 12 months.
Alcohol There is a higher risk of osteonecrosis in occasional and regular drinkers when compared to non-drinking controls, both in the volume of alcohol consumed and the duration of consumption. Although the true incidence of osteonecrosis is low, in alcoholics figures of 5–12% have been reported.
ARTICLE IN PRESS Osteonecrosis of the femoral head Matsuo et al. found an elevated risk in regular drinkers (48 ml alcohol daily) compared to non-drinking controls, relative risk of 7.8. They also demonstrated a significant dose response relationship, with relative risks of 3.3, 9.8, and 17.9, for current drinkers imbibing o400, 400–1000, and 41000 ml/wk of alcohol, respectively.8 The relative risk increased from 2.7 for o4000 drink years to 9.0 for 10,000 drink years. (Drink years defined as weekly alcohol consumption multiplied by the number of years of drinking.)
Coagulation/embolic abnormalities The most likely common pathophysiologic event in nontraumatic osteonecrosis is intravascular coagulation and microcirculatory thrombosis. Thrombotic emboli have been found in both arterioles and venules in specimens of osteonecrotic tissue and have been associated with osteocyte necrosis in some animal models. Those with an inherited coagulation disorder may be at risk for the development of osteonecrosis of the femoral head, indeed thrombotic occlusion of the microcirculation in the femoral head has been associated with hypofibrinolysis (a reduced ability to lyse intravascular thrombi) and thrombophilia often caused by reduced levels of the liver derived anticoagulants:
Protein C Protein S (protein S potentiates the effect of APC) Antithrombin III Hypofibrinolysis may be due to elevated levels of plasminogen activator inhibitor 1 (PAI-1), and/or decreases in tissue plasminogen activator (tPA). The presence of lipoprotein associated antigen Lp(a) also leads to impaired fibrinolysis. Hypofibrinolysis can also occur be due to a resistance to activated protein C (RAP-C). Activated protein-C is a serine protease that degrades factor Va and VIIIa. It also promotes fibrinolysis by inactivating PAI-I. Factor V leiden results from arginine to glutamine substitution in the factor V peptide chain; as this occurs at the point of cleavage of factor V by its regulatory protein (protein C) it makes factor V resistant to inactivation. This is measured clinically as resistance to activated protein C. Altered anti-phospholipid antibody levels, such as lupus anticoagulant, and anticardiolipin antibodies, cause hypercoagulability. They react against a b-2 glycoprotein in endothelial cell membranes and promote the activation of soluble clotting factors. Jones and Hungerford9 looking at nine different coagulation factors found at least one clotting factor abnormality in 82% of patients with osteonecrosis compared to 30% of controls, two or more were found in 47% of patients compared with 2.5% of controls. Hypercoagulability associated with any one of these conditions represent an underlying predisposition for microvascular thrombosis and osteonecrosis. Some of these disorders have a known inheritance pattern so it may be possible to screen people at risk.
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Smoking Smoking has been shown to inhibit osteogenesis and fracture healing, so it is not surprising that it is risk factor for osteonecrosis. There is an increased risk for current smokers (relative odds 4.7), and a cumulative effect of smoking was evident only in association with twenty pack years or more. The exact pathophysiology is uncertain, but vascular compromise and decreased marrow activity have been proposed as possible mechanisms.
Other factors Dysbaric osteonecrosis or Caisson disease is associated with working in pressurised environments (as in tunnelling) using compressed air or diving with poorly controlled decompression. The risk of osteonecrosis under dysbaric conditions appears to be related directly to the depth and number of dives, uncontrolled decompression, and low partial pressures of oxygen. The circulatory nitrogen bubbles formed cause osteonecrosis directly via cryogenic insults resulting in cell death. Additionally, the bubbles act as space occupying lesions that kill osteocytes. In certain Asian populations (Taiwan, etc.), while steroid use may explain the increased rates, recent genetic linkage studies have identified mutations in the type II collagen gene (COL2A1 gene) on chromosome 12q13 in a Taiwanese pedigree that strongly predisposes to osteonecrosis.10 Radiation causes a direct injury leading to osteocyte death and the development of osteonecrosis. The dead cells cause further damage by acting as a space-occupying lesion. Radiation may also compromise the microvasculature and disturb bone repair. Lipid disorders such as Gaucher’s disease cause external vascular occlusion of the affected bone due to abnormal cell mass. Pregnancy can be complicated by osteonecrosis. Such patients typically have no other risk factors. In a series of 13 pregnancies11 patients became symptomatic in the last 4 months of pregnancy, and 11 of the 13 were pregnant for the first time and had small body frames and large weight gains during the pregnancy. Many were initially misdiagnosed as having transient osteoporosis.
Pathogenesis/pathology While the vascular insult that leads to osteonecrosis may be a single event, it must be remembered that the development of osteonecrosis is a multifactorial process. Failure of perfusion occurs by three mechanisms:
Vascular interruption Vascular occlusion Extravascular compression Any of these leads to a decreased blood supply/ischaemia to the femoral head. Cell death from anoxia is not immediate, but rather occurs in progressive stages of ischaemic injury. After about 2–3 h of ischaemia, osteocyte necrosis occurs, though histological evidence of osteocyte death is only
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apparent after 24–72 h, when they are seen to be absent from their lacunae. Adipocyte and haemopoietic marrow necrosis occur before osteocyte necrosis. There then follows a sequence of reactions to the injury and variable attempts at repair. There will be adjacent areas of bone with an intact blood supply and viable cells, and the remodelling cycle continues there, but unfortunately bone resorption predominates, causing further weakening of the subchondral bone, and ultimately progressive collapse of the subchondral trabeculae. This gives rise to the radiolucent ‘crescent sign’, before flattening of the articular surface. Eventually this process involves the cartilage and subchondral endplate causing gross collapse of the articular surface of the femoral head. Once established, these changes are irreversible and lead to progressive joint damage with increasing symptoms. Local oedema develops and, seen on MRI, may extend a considerable distance beyond the necrotic lesion. Areas
without circulation may remain stable for some time, but with mechanical stress transmitted to subchondral trabeculae, microfractures occur that now cannot be repaired weakening the subchondral bone. Osteoclasts resorb necrotic bone, which weakens the structure of the cancellous bone between viable and necrotic areas leading to multiple microfractures and eventual collapse. A unifying concept has been suggested by Aaron12 which emphasises the central role of vascular occlusion and ischaemia leading to both marrow cell and osteocyte necrosis (Fig. 1).
Presentation and investigation Prompt diagnosis allows earlier treatment ideally before femoral head collapse and should alter prognosis. Risk factors should be sought.
Figure 1 Possible pathogenesis of osteonecrosis.
ARTICLE IN PRESS Osteonecrosis of the femoral head The commonest presenting symptom is deep groin pain. Physical examination can be unremarkable, or demonstrate pain on internal rotation, a reduced range of movement, and an antalgic gait. Due to the high risk of bilateral disease, both hips should be thoroughly examined. Radiographic studies are essential. Plain radiographs are still the first investigation necessary, good quality AP and lateral films are mandatory, and enable measurement of the combined necrotic angle. Prior to the advent of MRI, lesion size was estimated with the use of outlines of the lesion on AP and lateral radiographs as described by Kerboul et al.13 where the arc of the surface involved by the necrotic process is measured. These two angles are added together to give the combined necrotic angle. Kerboul reported that when the combined angle is greater than 2001 it is predictive of a poorer clinical outcome. Bone scans which rely on the uptake of a labelled tracer onto the surface of hydroxyapatite crystals during osteogenesis can detect osteonecrosis before radiographic evaluation. Bone scans were formerly used for high risk patients who had normal plain films, but recent studies have shown they can mislead, due to a 25–45% false negative rate when compared with cases subsequently diagnosed by MRI or histology. Additionally, bone scanning is also less sensitive in the presence of bilateral disease as interpretation of scans is often based on asymmetric findings. MRI has become the standard for diagnosing osteonecrosis. It is 99% specific and sensitive. A single density line on T1-weighted images demarcates the normal/ischaemic bone interface and double density lines (‘double line sign’) on the T2-weighted images represents the hyper-vascular granulation tissue. Using MRI it is also possible to differentiate between transient osteoporosis and osteonecrosis, as MRI shows oedema into the femoral neck and metaphysis in transient osteoporosis, which is not common with osteonecrosis. CT and tomograms can identify collapse, but are rarely used due the dose of radiation involved, and the accuracy of MRI. Functional evaluation of bone, an invasive procedure, in which marrow pressure was measured directly, intramedullary venography, and biopsy are now rarely undertaken since the advent of MRI.
461 system described three stages.14 A fourth stage was added later15: Stage I Stage II Stage III Stage IV
Normal X-ray Diffuse sclerosis of femoral head Normal joint space Subchondral fracture, ‘crescent sign’ +/ Head collapse Femoral head collapse Acetabular involvement Joint destruction (OA)
In 198516 stage 0 was added, giving the current five stage classification: Stage 0 Stage I Stage II Stage III Stage IV
Preclinical Pre-radiographic (+ve MRI/bone scan) Pre-collapse (reparative stage before flattening occurs) Collapse Osteoarthritis
Steinberg/University of Pennsylvania The Ficat and Arlet system predated the routine use of MRI and has a number of drawbacks; it depended upon invasive techniques, such as core decompression and functional exploration of bone and did not quantify the size of the osteonecrotic segment, so restricting the measurement of progression. This failing was addressed by the Steinberg classification which uses MRI to define seven distinct stages.17 Whilst similar to Ficat and Arlet it has the addition of stages V and VI. For each stage from I to V, there is further subdivision depending on the size of lesion, or degree of collapse. No attempt is made to quantify the extent of involvement in stage 0 or VI. Steinberg suggested that once the stage was determined then the extent of involvement should be measured as lesion size is directly related the probability of collapse. Clinically this was determined visually as mild moderate or severe. More precise measurement for research purposes calculated the percentage of head involvement and the collapse in millimetres, then placing in group A, B, or C (Table 2).
Staging/classification The classification of osteonecrosis has undergone many changes. A disease classification should guide treatment and prognosis. Not all classifications enable this but may be better suited to allow comparisons of treatments. Of the many classifications, the most widely used are Ficat and Arlet, Steinberg, Association Research classification Osseous (ARCO), and the Ohzono classification.
Stage 0 Stage I Stage II Stage III Stage IV
Ficat and Arlet The Ficat and Arlet classification system for osteonecrosis of the femoral head is still the most widely used. Their original
Stage V Stage VI
Normal or non-diagnostic imaging. FEB positive Normal X-ray, abnormal bone scan and/ or MRI Abnormal X-ray showing cysts and sclerotic change in femoral head Subchondral collapse without flattening ‘Crescent sign’ Flattening of the femoral head (normal acetabulum) Joint narrowing with or without acetabular involvement Advanced degenerative changes
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Table 2 Stage
Grade
I and II
A, mild B, moderate C, severe
o15% of head involved as seen on MR or X-ray 15–30% 430%
III
A, mild B, moderate C, severe
Subchondral collapse beneath (crescent) o15% of articular surface Crescent beneath 15–30% Crescent beneath 430%
IV
A, mild B, moderate C, severe
o15% of surface has collapsed and depression is o2 mm 15–30% collapsed or 2–4 mm depression 430% collapsed or 44 mm depression
V
A, mild B, moderate C, severe
Average of femoral head involvement, as in Stage IV and estimated acetabular involvement
Figure 2
Ohzono classification.
ARCO
Stage II Stage III
This is a five stage system based on the Steinberg system proposed by Association Research classification Osseous (ARCO).18
Stage 0 Stage I
Normal radiography, histology only Normal X-ray/CT. Positive bone scan/MRI (subclassified)
Stage IV
Sclerosis, osteolysis (sub-classified) Crescent sign, +/ flattening of articular surface (sub-classified) Osteoarthritis, acetabular changes, joint destruction
Stages I, II, and III are subclassified, as minimal (A), moderate (B), and extensive (C), depending on extent of involvement as previously described in the Steinberg system (see Table 2).
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Ohzono Developed in 1991, Ohzono19 described a classification based on the radiographic characteristics of the necrotic lesion in the femoral head and was able to show that this could be used to predict the fate of the hip. Type 1 is characterised by the presence of a demarcation line in the femoral head and is divided into three subtypes, by its relationship to weight bearing area (1 A, B, and C). Type 2, shows early flattening of the weight-bearing surface but has no demarcation line around the necrotic area. Type 3, demonstrate cystic lesions and is divided into two subtypes according to their site within the femoral head (3A medial, 3B lateral). They showed that types 1A, 1B, and 3A had little tendency to collapse whereas types 1C, 2, and 3B had a high incidence of collapse and hence a poor prognosis (Fig. 2). Collapse by stage/percentage: 1A/0% 1B/19% 1C/94%
2/100% 3A/12% 3B/100%
References 1. Steinberg ME. Recent advances in the management of osteonecrosis of the hip. Introduction. Semin Arthroplasty 1998;9: 181–3. 2. Merle d’Aubigne R, Postel M, Mazabraud A, Massias P, Gueguen J. Idiopathic necrosis of the femoral head in adults. J Bone Joint Surg 1965;47-B:612–33. 3. Wheeless CR, Lins RE, Knelson MH, Urbaniak JR. Digital subtraction angiography in patients with osteonecrosis of the femoral head. In: Osteonecrosis: aetiology, diagnosis and treatment. Rosemont, IL: American Academy of Orthopedic Surgeons; 1997. p. 241–5. 4. Felson DT, Anderson JJ. A cross study evaluation of association between steroid dose and bolus steroids and avascular necrosis of bone. Lancet 1987;1:902–6.
5. Cui Q, Wang GJ, Balain G. Steroid induced adipogenesis in a pluripotential cell line from bone marrow. J Bone Joint Surg 1997;79-A:1054–63. 6. Cui Q, Wang GJ, Su CC, et al. The Otto Aufranc Award: Lovastatin prevents steroid induced adipogenesis and osteonecrosis. Clin Orthop 1997;344:8–19. 7. Wang GJ, Cui Q, Balain G. The Nicolas Andry Award: the pathogenesis and prevention of steroid induced osteonecrosis. Clin Orthop 2000;370:295–310. 8. Matsuo K, HIrohata T, Sugioka Y, Ikeda M, Fukuda A. influence of alcohol intake, cigarette smoking and occupational status on idiopathic osteonecrosis of the femoral head. Clin Orthop 1988;234:115–23. 9. Jones LC, Hungerford DS. Osteonecrosis: etiology, diagnosis and treatment. Curr Opin Rheumatol 2004;16:443–9. 10. Liu YF, et al. Type-II collagen variants and inherited osteonecrosis of the femoral head. N Eng J Med 2005;352: 2294–301. 11. Montella BJ, Nunley JA, Urbaniak JR. Osteonecrosis of the femoral head associated with pregnancy. A preliminary report. J Bone Joint Surg 1999;81-A:790–8. 12. Aaron RK. Osteonecrosis: etiology, pathophysiology and diagnosis. In: Callaghan JJ, Rosenberg AG, Rubash HE, editors. The adult hip. Philadelphia: Lippincott-Ravin; 1998. p. 451–66. 13. Kerboul M, Thomine J, Postel M, Merle D’Aubigne ´ R. The conservative surgical treatment of idiopathic aseptic necrosis of the femoral head. J Bone Joint Surg 1974;56-B:291–6. 14. Arlet J, Ficat RP. Forage-biopsie de la tete femorale dans l0 osteonecrose primative. Observations histo-pathologiques portant sur huit forages. Rev Rhumat 1964;31:257–64. 15. Ficat RP, Arlet J. In: Hungerford DS, editor. Ischaemia and necrosis of bone. Baltimore: Williams and Wilkins; 1980. 16. Ficat RP. Idiopathic bone necrosis of the femoral head. Early diagnosis and treatment. J Bone Joint Surg 1985;67-B:3–9. 17. Steinberg ME, Hayken GD, Steinberg DR. A quantitative system for staging avascular necrosis. J Bone Joint Surg 1995;77-B: 34–41. 18. Gardeniers JWM. Report of the committee of staging and nomenclature. ARCO News Lett 1993;5:79–82. 19. Ohzono K, Saito M, Takaoka K, Ono K, Saito S, Nishina T, et al. Natural history of non-traumatic avascular necrosis of the femoral head. J Bone Joint Surg 1991;73-B:68–72.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 464–470
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RADIOLOGY
The diagnosis and percutaneous treatment of osteoid osteomas James J. Rankine Department of Radiology, Leeds General Infirmary, Leeds LS1 3EX, UK
KEYWORDS Osteoid osteomas; Diagnosis; Treatment
Summary Osteoid osteomas are the commonest benign bone tumours. There is frequently a delay in diagnosis, in some cases of many months or years. The plain film appearances are not always immediately recognised and the characteristic bone sclerosis may be absent in subperiosteal intra-articular lesions. Computed tomography (CT) is the most specific investigation, and in most cases pathological confirmation is not required. Open surgical removal of the lesion has now been replaced by CT guided percutaneous radiofrequency thermal ablation. & 2007 Elsevier Ltd. All rights reserved.
Introduction Osteoid osteomas are the commonest benign bone tumours. They most frequently occur in the lower extremities of children and young adults with a male to female predominance of 3–1. About 10% of osteoid osteomas occur in the spine where they usually involve the posterior elements. Osteoid osteomas are usually small lesions less than 1 cm in diameter. They have a central radiolucent nidus with a variable amount of surrounding reactive bone sclerosis. Osteoblastomas are pathologically similar lesions that traditionally have been distinguished from osteoid osteomas by having a diameter greater than 1.5 cm. In fact osteoblastomas have distinct radiological features other than their size which distinguishes them from osteoid osteomas.1 They less frequently produce reactive bone sclerosis can extend from the bone to involve the adjacent soft
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tissues and frequently involve the posterior elements of the spine.
Clinical and radiological features The classical presentation of osteoid osteoma is a child or young adult with constant pain worse at night relieved by aspirin or other non-steroidal anti-inflammatory drugs (NSAIDs). Response to NSAIDs can be a useful diagnostic test whilst the patient waits for appropriate radiological investigations. The response to NSAIDs is due to the high levels of prostaglandins found within the nidus of the lesion which is also thought to account for the surrounding reactive sclerosis. Intra-articular osteoid osteomas may cause synovitis and present with a non-specific arthropathy that frequently results in a delay in the diagnosis (Fig. 1). These lesions are usually sub-periosteal and may have little if any sclerosis. Osteoid osteomas in the spine may present with a painful scoliosis (Fig. 2).
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Figure 1 Axial T2-weighted sequence of an intra-articular osteoid osteoma. There is a nidus in the femoral neck (large arrow). There is considerable synovitis (small arrows). Gadolinium has been injected into the joint (an MR arthrogram) as the osteoid osteoma was mis-diagnosed clinically as labral pathology.
Plain radiographs are the initial investigation of choice and can be characteristic in long bones when the central radiolucent nidus is identified (Fig. 3). When the osteoid osteoma occurs within the diaphysis of a long bone it usually lies intra-cortically and the surrounding sclerosis results in thickening of the cortex. Unfortunately the nidus is frequently not identified on radiographs and the appearances can be mistaken for a stress fracture (Figs. 4 and 5). When the osteoid osteoma occurs in flat bones or intraarticularly there may not be any surrounding sclerosis (Figs. 6 and 7). Radioisotope bone scans are almost invariably positive and the characteristic appearance is an intense area of uptake representing the nidus surrounded by a less intense halo that is the hyperostosis. With intra-articular lesions the appearances may be non-specific and suggest an arthropathy. A positive isotope bone scan helps to target a CT examination that in most cases shows such specific appearances that pathological confirmation is not required. As the nidus can be very small thin 1.0 mm sections are required so the CT has to be targeted to a specific area guided either by the plain radiograph or isotope bone scan. A thin section CT of a whole long bone would result in several hundred images and a significant radiation dose. With the increasing availability of magnetic resonance imaging (MRI) many patients with bone and joint pains are having MRI as the first line investigation. MRI shows intense oedema that can involve the adjacent soft tissues (Fig. 8). Whilst a nidus is frequently seen on MRI it may not always be apparent depending on the thickness of the slices the obliquity of the sections through the nidus and partial volume effects. The bone and soft tissue oedema can be non-specific and suggest infection or stress reaction and the
radiologist must always consider the diagnosis of an osteoid osteoma and perform a CT when necessary.
Treatment The natural history of osteoid osteoma is for spontaneous resolution so medical management with NSAIDs is an option for some patients. Spontaneous resolution however can take many years and surgical intervention is frequently performed. In the past this involved an open surgical procedure with en bloc resection or a burr down technique with curetting of the nidus. The procedure could result in a relatively large amount of bone being removed requiring post-operative immobilisation. Furthermore as an intraarticular location in the hip is a frequent site many osteoid osteomas are relatively inaccessible. In 1998 Rosenthal et al.2 reported their series of CT guided radiofrequency thermal ablation with equivalent success rates to the open surgical procedure. In 2004, the national institute for health and clinical excellence (NICE) approved the procedure for use in the UK.3 An information sheet for patients can be downloaded from the NICE website which explains the procedure and indicates the success rate of 90%. Laser photocoagulation has also been described with comparable results to radiofrequency ablation. However radiofrequency equipment is commonly found in many hospitals where it is used for ablation of neural tissue by neurosurgeons and pain clinicians so this is the more common technique. The procedure is performed as a day case under a general anaesthetic. A hand held drill bit with an outer diameter of just 1.7 mm is used. This is an eccentric drill that drills a
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Figure 2 Mild sclerosis of the left T8 pedicle within the concavity of a thoracic scoliosis. Strongly positive radioisotope bone scan confirms the presence of an osteoid osteoma.
Figure 3 Periosteal thickening (white arrows) and a radiolucent nidus (black arrow).
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Figure 4 There is cortical thickening of the mid tibia without an apparent nidus.
Figure 5 Tibial stress fracture. There is cortical thickening of the anterior cortex with a central lucent area (black arrow). The lucent area extends from the surface of the anterior cortex and is linear.
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Figure 6
There is enlargement of the lesser trochanter on the left without cortical sclerosis.
Figure 7 Sagittal reformat CT scan of the ankle. There is a thin sclerotic line surrounding the central nidus. The nidus shows central calcification that is an occasional feature of osteoid osteomas.
Figure 8 Coronal STIR (8a) and coronal T1-weighted (8b) MRI (same patient as Fig. 6). There is intense oedema within the lesser trochanter with oedema of the adjacent soft tissues. The nidus (white arrow) is seen as an area of high signal within the low signal cortex.
ARTICLE IN PRESS The diagnosis and percutaneous treatment of osteoid osteomas hole slightly larger than its own diameter allowing a 1.8 mm diameter guide to follow the drill through the cortex. CT guidance is used to locate the nidus and plan the safest route. This may be through the opposite cortex but since the hole is so small there is no risk of subsequent fracture (Fig. 9). It is possible to biopsy the nidus with a Jamshidi type biopsy needle passed down the guide. The imaging features are so characteristic usually more so than the histology and the author has abandoned the biopsy stage opting instead to simply drill out the nidus and then pass the radiofrequency probe through the guide into the centre of the nidus (Fig. 10). This is heated to 90 1C for 4 min. The outer guide can be withdrawn slightly from the tip of the probe to prevent heat conduction to the skin. Mild skin burns
Figure 9 Axial CT showing the radio frequency probe within the nidus (same case as Figs. 6 and 8). The safest approach is to drill through the lateral cortex into the lesser trochanter avoiding the neurovascular structures anteriorly which are in the line of an antero-medial approach and the sciatic nerve in line of the postero medial approach.
Figure 10
469 are the only relatively frequent complication of the procedure. The ablation necroses a 1.0 cm diameter volume of tissue so if the nidus is greater than 1.0 cm in diameter the probe will need to be positioned in several sites to cover the whole nidus. Very occasionally an osteoid osteoma is multifocal
Figure 11 Coronal reformat CT of the femur demonstrating a multifocal nidus which was successfully ablated by three separate ablations. Surgical treatment would have involved removal of a large amount of the femoral cortex.
The radiofrequency probe is passed down the guide into the nidus.
ARTICLE IN PRESS 470 and each separate nidus can be ablated (Fig. 11). Soft tissue structures that fall within the 1.0 cm diameter field of the ablation will also be necrosed. For this reason there has been reluctance to perform the procedure in the spine because of the close proximity to neural tissue; however it can be performed provided a safe margin is present.4 Following the procedure the patient can immediately weight-bear without risk of fracture. Post-procedural pain can be controlled with simple analgesics and most patients are entirely pain-free with resolution of their osteoid osteoma pain within 24 h. In approximately 10% of cases recurrence of pain may occur over the next few months if the nidus has not been completely ablated but the procedure can be repeated.
J.J. Rankine
References 1. Nemoto O, Moser Jr RP, Van Dam BE, Aoki J, Gilkey FW. Osteoblastoma of the spine. A review of 75 cases. Spine 1990; 15(12):1272–80. 2. Rosenthal DI, Hornicek FJ, Wolfe MW, Jennings LC, Gebhardt MC, Mankin HJ. Percutaneous radiofrequency coagulation of osteoid osteoma compared with operative treatment. J Bone Joint Surg Am 1998;80(6):815–21. 3. /http://guidance.nice.org.uk/IPG53S. 4. Hadjipavlou AG, Lander PH, Marchesi D, Katonis PG, Gaitanis IN. Minimally invasive surgery for ablation of osteoid osteoma of the spine. Spine 2003;28(22):E472–7.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 471–476
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COMPRESSION SYNDROMES
Conservative treatment of thoracic outlet syndrome (TOS): Creating an evidence-based strategy through critical research appraisal Konstantine C. Balakatounisa,b,, Antonios G. Angoulesc, Kalomoira A. Panagiotopouloua a
Filoktitis Medical Center, Center of Excellence in Physical Medicine and Rehabilitation, Athens, Greece School of Health and Social Care, Oxford Brookes University, Oxfordshire, UK c Academic Department of Trauma & Orthopaedics, Leeds Teaching Hospitals, University of Leeds, Leeds, UK b
KEYWORDS Thoracic outlet syndrome; Conservative treatment; Rehabilitation; Compression Syndromes
Summary Thoracic outlet syndrome (TOS) is initially treated non-operatively. Upon failure or unsatisfactory improvement surgical treatment is contemplated. The purpose of this review is to critically appraise available primary research on non-operative treatment of TOS, explore the effectiveness of non-operative treatment approaches and propose an evidence-based treatment strategy. & 2007 Elsevier Ltd. All rights reserved.
Introduction Thoracic outlet syndrome (TOS) is a syndrome attributed to the narrowing of the spaces in the thoracic outlet, through which major nerves and vessels pass, resulting in compression of the brachial plexus or vessels.1 Common symptoms include pain on the side of the neck radiating to the ear and face (upper plexus TOS), or anterior/posterior shoulder pain radiating to the medial aspect of the upper extremity and ulnar nerve distribution paresthesia.1 Multiple or double crush syndromes may also occur as a result of compression in
more than one site, such as the thoracic outlet, the cubital or carpal tunnel.2,3 Treatment may be either operative or non-operative. The first non-operative treatment protocol for TOS was described by Peet et al.4 in 1956. Treatment consisted of massage, application of moist heat, strengthening of the shoulder elevators, pectoralis stretching, ergonomics and posture correction. 71 per cent of 55 patients improved. Twelve years later, Urschel et al.5 added active range of motion (ROM) exercises and cervical traction to the ‘Peet et al.’ protocol but only half of the 120 patients experienced symptomatic relief.
Surgery and conservative treatment Corresponding author at: Orfeos 3, P.O. Box 16672, Vari, Athens,
Greece. Tel.: +30 210 9654809. E-mail address:
[email protected] (K.C. Balakatounis). 0268-0890/$ - see front matter & 2007 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2007.11.006
Surgery for TOS consists of decompression of the anterior shoulder region usually with resection of the first rib.
ARTICLE IN PRESS 472 The approach can be either transaxillary or supraclavicular.6 The outcome of TOS is dependent on appropriate patient selection for surgery and identification of patients that can benefit from TOS surgery and lead to satisfactory results.7–10 Current consensus suggests that surgery should follow after conservative treatment failure or/and vascular complications; therefore, it is underlined that conservative treatment is the first option in the treatment of TOS.8,9,11,12
Methodology The keywords used were ‘Thoracic outlet syndrome’ and ‘Conservative treatment’, or ‘Physiotherapy’ or ‘Physical Therapy’, or ‘Rehabilitation’ and the search was limited to clinical studies in the English and French languages published in the last 20 years. Case studies were not included. The databases used for the search strategy were Medline, CINAHL and EMBASE.
Results Treatment administered in studies consisted of either multidisciplinary care,13 orthosis application plus exercise,14 exercise15,16 or a combination of exercise physical modalities and/or other interventions17–19 as presented in Table 1. Outcome criteria and measures ranged from subjective, such as satisfaction, to objectives such as ROM restoration and grip strength. Table 2 presents the outcome criteria used. The results of the studies were favorable for nonoperative treatment compared with control groups or surgery groups. Table 3 presents results and follow-ups of these studies.
Discussion Considerations regarding primary research studies on the conservative treatment of TOS In the studies retrieved, various methodological issues were traced mainly related to sample selection and differential diagnosis for inclusion of patients in the study. Lindgren et al.13 report that in those patients that were satisfied with symptom relief (88%), there existed patients whose real cause of symptoms identified was other than TOS. Thus, the sample had been contaminated by patients presenting with other pathologic conditions. The effectiveness of treatment for TOS may have been different (less or more effective), had the patients presenting with other pathologies been excluded. In that case, the results would better reflect the population of patients presenting with TOS. Twenty-six patients (81%) received psychologic assessment upon admission in the study by Maillis et al.18 but no exclusion of patients took place when psychological issues were identified. Psycho-emotional disturbances were noted in all patients in the non-surgical group with modest or no pain reduction. This finding might have undermined the validity of the study, since pain might be experienced whether psychological issues are present or not, but the
K.C. Balakatounis et al. severity of pain experienced and the ability to cope are closely linked with the patient’s subjective perception of pain, which is affected by psychological status. Therefore the study might have investigated the effect of conservative treatment on patients with TOS presenting with or without associated psychological issues. All patients in the study by Kenny et al.15 presented with osteoarthritic changes in the cervical spine. It is supported in the study that osteoarthritis was an underlying cause for loss of tone of the shoulder muscles which resulted in the development of TOS. Still, this proposition is not supported by other research in this study, and is not generally a widely accepted cause leading to TOS. This criterion might have specified the results to a portion of the population presenting with underlying osteoarthritic changes, and might not reflect the usual patients with TOS. It should be mentioned that in the sample of the study of Maillis et al.18 all patients were unemployed with the possibility of litigation pending. These elements could have influenced the outcome of the study and might have led to malingering in the pre- and post-study period, resulting in poor results. A significant issue not addressed by Ghoussoub et al.16 is the effect of drop-outs on sample homogeneity. Immediately following completion of therapy sessions there were 56 participants, whereas after 6 months there were 17 less, after 1 year 32 and after 2 years only 15 participated. Drop-outs can potentially disrupt the homogeneity of the sample.20 In that way, the sample might not reflect the population intended. The statistical significance of the results is not provided and therefore it is unclear whether the results were significant despite the drop-outs. The results by Maillis et al.18 proved that surgery or conservative treatment were both beneficial for approximately half of the patients. The results may imply that the treatment protocol used is not effective, since this study provided the most discouraging results for both treatment options of all the studies found. The results could be attributed to the length of follow-up, amounting to up to 12–33 months, which is a lot longer than the follow-ups in the other studies. The longest follow-up was that of Maillis et al.18 which is the only study that was clearly more positive for patients than the control surgery group. Therefore the results could be attributed to the length of follow-up. Another consideration is that benefits of treatment might also have disappeared and it is also possible that compliance with exercise and general guidelines after discharge might have been significantly reduced in the sample.
Constructing an evidence-based rehabilitation strategy Nakatsuchi et al.14 produced positive results regarding more objective outcome criteria than subjective satisfaction, such as pain and numbness. Still, the application of an orthosis for 2–3 years is probably not comfortable for patients and may severely restrict mobility, functional activities or even quality of life. Furthermore, no followup took place, thus results reflected maximum treatment effect and not long-term effectiveness. Nevertheless,
Types of study, sample characteristics and treatment details of clinical studies on the conservative treatment of thoracic outlet syndrome. Landry et al.19
Lindgren13
Novak et al.17
Nakatsuchi et al.14
Maillis et al.18
Kenny et al.15
Study
Retrospective study
Prospective clinical trial
Cohort/prospective study
Prospective study
Prospective study
Prospective study
Sample
n ¼ 58.
n ¼ 79 Allocation: treatment proposed by physician. Surgical treatment group n ¼ 15, conservative treatment group, n ¼ 64 Conservative treatment (no further details)
n ¼ 119 (28 men, 91 women)
Cohort/ prospective study n ¼ 42, mean age was 38 years (20–67) and mean symptom duration time 38 months (range 4–240, SD: 39)
n ¼ 86 (74 females), 50 for follow-up, 43 women, 31.7-yearold mean age
n ¼ 32 (16 in each group. Female/male ratio 2.6/1, surgery/ conservative treatment mean age 37.5 y.o./ 37 y.o. Allocation: treatment proposed by physician (or refusal for surgery)
n¼8
Physiotherapy and patient education for 3 months (SD: 2 months), mean number of treatments was 4 (SD ¼ 2), and exercises were performed daily twice per day at home
Treatment lasted a mean of 2 years and 3 months. Application of orthosis lasted until improvement took place. Exercise was also instructed according to Britt’s method. Orthosis was worn at all times except when bathing or sleeping
Conservative treatment comprised physical modalities, stretching, exercise, trigger point injections, and application of a shoulder retraction harness versus surgical treatment
Physiotherapy program which lasted 3 weeks. The physiotherapy program included progressive resisted shoulder elevation exercises
88% of the sample were female
Treatment
The treatment protocol comprised stretching and strengthening of appropriate muscles, massage and respiratory exercise (15 sessions)
Physiotherapy and services from the rest of the rehabilitation team including a psychologist, nurse and occupational therapist. Therapy was initiated in an inpatient rehabilitation ward for a mean of 11.4 days (range 4–24 days) and continued at home with home exercises
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Table 1
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Subjective symptom/ pain relief Pain, numbness, sensory, motor disturbance, grip strength and ability to perform activities of daily living Work and recreational activities, symptom relief Days off from work, symptom reduction, symptoms leading to at least a temporary inability to work, was an inclusion criterion Satisfaction with results, compliance with exercise, recurrence of symptoms
Subjective satisfaction, frequency of return to work, range of motion restoration, grip strength
Maillis et al.18 Nakatsuchi et al.14 Novak et al.17 13
Lindgren 19
Landry et al. Ghoussoub et al.16
Outcome criteria of clinical studies on the conservative treatment of thoracic outlet syndrome. Table 2
Pain reduction (hands, arms, neck), pins/needles sensation, weakness in hands and/or arms. Cervical neck and shoulder movements, blood pressure measurements. Visual analogue scale of symptom severity (pain), muscle test (weakness), sphygmomanometer (blood pressure)
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should the orthosis not affect functional activities or quality of life (e.g. use of a reasonably comfortable orthosis), then the orthosis could be applied along with an exercise program, at the physician’s and therapist’s discretion. It should be stated though that the use of an orthosis is supported by only one clinical trial, thus its use is not particularly evidence based. In the remaining studies, protocols where similar and comprised exercises including shoulder elevation, stretching of muscles in the shoulder girdle, trigger point injections and patient education. Patient education can be considered essential, since the patient should be aware that part of the rehabilitation process includes decision making.21–23 The patient in that way is motivated to follow treatment and take control of his/her progress.21 The interventions mentioned above can be implemented in the multidisciplinary approach as the physiotherapy component and thus result in a comprehensive treatment approach. Lindgren,13 presented results showing general improvement (subjective satisfaction reached 88%, return to work 73%, ROM restoration in 8/10 patients over a mean of 11.4 days). Although the study is not an RCT, well-defined and rigorous inclusion criteria were used and no significant methodological issues were found. The sample size was larger than other studies on TOS, and although the power of the study is not mentioned, it is likely that positive results were not due to chance. Furthermore, the follow-up was 24.6 months, and so insight on long-term effectiveness is provided. Thus the multidisciplinary approach that was used in the study appears to be a promising option for treating TOS conservatively, since it has been found to provide subjectively significant results to patients. The positive results of multidisciplinary rehabilitation are considered due to the fact that through multidisciplinary care the patient receives attention and services from a number of healthcare professionals (who could include an occupational therapist, nurse and psychologist) instead of a limited number or only one professional. Therefore, treatment should also include rehabilitation strategies that have been proven to be effective using objective outcome criteria. It is stressed that a direct comparison of the results across studies can be misleading since numerous variables and confounding factors may influence results.
Conclusion and recommendations for future research All studies produced positive results following conservative treatment, to a significant extent. Exercise, the combination of the use of an orthosis and exercise (active and passive approach) produced positive results as well as exercise included in a multidisciplinary team approach with patient education. A multidisciplinary approach including exercise as the main component appears to be the most effective strategy. Future research should be randomly selected, allocated and homogeneous. Confounding variables such as occupational status, pending litigation and age could be controlled by matching or alternative methods.
Follow-ups and results of clinical studies on the conservative treatment of thoracic outlet syndrome. Landry et al.19
Lindgren13
Novak et al.17
Nakatsuchi et al.14
Maillis et al.18
Kenny et al.15
Follow up
Follow up was obtained right after treatment (completion of 15 sessions), 6 months, 1 and 2 years
Mean follow-up was 4, 2 years (range 2–7, 5 years) after the initial evaluation
24, 6 months
Mean follow-up period after treatment was 1 year
Follow-up ranged from 6 months to 5 years and 9 months. Mean follow-up was 2 years and 3 months
Mean follow-up lasted 33 months (12–66 months) for operated patients, 25 months after second surgery, 3 years for conservatively treated patients
There was no follow-up. Treatment lasted 3 weeks and patients were evaluated at the end of the 3 weeks
Results
Results on completion of 15 sessions. 70% reported improvement and 71% satisfaction with results. After 6 months, 66% reported that they were still compliant with exercise, and 84% were satisfied and there was one recurrence of symptoms. After 1 year, 15% were still compliant and 81% were satisfied. After 2 years only 15 patients responded and 12 were satisfied (80%)
Most patients (59 out of 79) returned to work after either treatment. Conservative treatment resulted in fewer days away from work (po.04). Most patients demonstrated a reduction in the intensity of symptoms in the long term, but the level of symptoms was not significantly reduced in either group. It was concluded that surgery did not significantly improve functional outcome
Subjective satisfaction reached 88%, frequency of return to work amounted to 73% and range of motion restoration was successful in 8 out of 10. Improvement in grip strength and Tinel’s sign was associated with patient satisfaction (po.001) and return to work (po.001). As a conclusion, treatment provided symptom relief
38 patients reported reduced neck and shoulder symptoms, improvement was significantly better when distal nerve compression was not present (po.006). Twenty-five patients reported improvement, 10 no improvement and 7 increase of the intensity symptoms. Twenty-four out of 42, provided feedback on work and recreational activities. 16/24 reported full activities while the remaining 8/24 reported restrictions. Poor outcomes were associated with obesity (po.04), worker’s compensation (po.04), associated carpal or cubital tunnel syndrome (po.04)
In the follow-up, the orthosis was more effective for distal symptoms. Pain disappeared or improved in 67% of patients, numbness in 85%, sensory in 84%, and motor disturbance in 80%. Proximal symptoms relieved in 65%. Half of the patients with weak grip benefited from the orthosis. Ability to perform activities of daily living was excellent in 33%, good in 44%, fair in 12% and poor in 9%. There were no drop-outs, but for the follow-up only 50 out of 86 patients were sent a questionnaire
Only 47% of the operated patients reported very good pain relief and 20% of the conservatively treated patients. Improvement in conservatively treated patients was supported to be due to the use of the harness. Re-operation was deemed necessary for six patients
All patients improved, with a significant decrease (p40.01) in pain (hands, arms, neck), pins/ needles, weakness in hands and/or arms. Cervical neck and shoulder movements were normal in all patients after treatment and blood pressure measurements were not significantly different. There were no dropouts
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Table 3
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ARTICLE IN PRESS 476 Research could also focus on which therapeutic methods in conservative treatment are more effective so as to minimize treatment duration as much as possible, and researchers could also investigate which therapeutic strategies provide more long-term relief.
References 1. Brantigan CO, Roos DB. Etiology of neurogenic thoracic outlet syndrome. Hand Clin 2004;20(1):17–22. 2. Novak CB. Thoracic outlet syndrome. Clin Plastic Surg 2003; 30(2):175–88. 3. Upton AR, McComas AJ. The double crush in nerve entrapment syndromes. Lancet 1973;2(7825):359–62. 4. Peet RM, Henriksen JD, Anderson TP, Martin GM. Thoracic-outlet syndrome: evaluation of a therapeutic exercise program. Mayo Clin Proc 1956;31(9):281–7. 5. Urschel Jr. HC, Paulson DL, McNamara JJ. Thoracic outlet syndrome. Ann Thorac Surg 1968;6(1):1–10. 6. Tender GC, Kline DG. Posterior subscapular approach to the brachial plexus. Neurosurgery 2005;57(4 Suppl):377–81 [Discussion 377–81]. 7. Athanassiadi K, Kalavrouziotis G, Karydakis K. Bellenis I. Treatment of thoracic outlet syndrome: long-term results. World J Surg 2001;25(5):553–7. 8. Degeorges R, Reynaud C, Becquemin JP. Thoracic outlet syndrome surgery: long-term functional results. Ann Vasc Surg 2004;18(5):558–65. 9. Nannapaneni R, Marks SM. Neurogenic thoracic outlet syndrome. Br J Neurosurg 2003;17(2):144–8. 10. Poole GV, Thomae KR. Thoracic outlet syndrome reconsidered. Am Surg 1996;62(4):287–91. 11. Huang JH, Zager EL. Thoracic outlet syndrome. Neurosurgery 2004;55(4):897–902 [Discussion 902–3].
K.C. Balakatounis et al. 12. Urschel Jr. HC, Razzuk MA. Neurovascular compression in the thoracic outlet: changing management over 50 years. Ann Surg 1998;228(4):609–17. 13. Lindgren KA. Conservative treatment of thoracic outlet syndrome: a 2-year follow-up. Arch Phys Med Rehabil 1997; 78(4):373–8. 14. Nakatsuchi Y, Saitoh S, Hosaka M, Matsuda S. Conservative treatment of thoracic outlet syndrome using an orthosis. J Hand Surg 1995;20(1):34–9 [British]. 15. Kenny RA, Traynor GB, Withington D, Keegan DJ. Thoracic outlet syndrome: a useful exercise treatment option. Am J Surg 1993; 165(2):282–4. 16. Ghoussoub K, Tabet G, Zoghby Z, Jebara V. Rehabilitation of thoracic outlet syndrome: about 60 patients. Le J Med Libanais 2002;50(5–6):192–6. 17. Novak CB, Collins ED, Mackinnon SE. Outcome following conservative management of thoracic outlet syndrome. J Hand Surg 1995;20(4):542–8 [America]. 18. Mailis A, Papagapiou M, Vanderlinden RG, et al. Thoracic outlet syndrome after motor vehicle accidents in a Canadian pain clinic population. Clin J Pain 1995;11(4):316–24. 19. Landry GJ, Moneta GL, Taylor Jr. LM, et al. Long-term functional outcome of neurogenic thoracic outlet syndrome in surgically and conservatively treated patients. J Vasc Surg 2001;33(2): 312–7 [Discussion 317–9]. 20. Portney LG, Watkins MP. Foundations of clinical research. Applications to practice, 2nd ed. New Jersey: Prentice-Hall; 2000. 21. Frischenschlager O, Pucher I. Psychological management of pain. Disabil Rehabil 2002;24(8):416–22. 22. Kielhofner G, Barrett L. Meaning and misunderstanding in occupational forms: a study of therapeutic goal setting. Am J Occup Ther 1998;52(5):345–53. 23. Wressle E, Oberg B, Henriksson C. The rehabilitation process for the geriatric stroke patient—an exploratory study of goal setting and interventions. Disabil Rehabil 1999;21(2):80–7.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 477–479
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CME SECTION CME questions based on the Mini-Symposium on Shoulder Reconstruction The following series of questions are based on the MiniSymposium on Shoulder Reconstruction. Please read the articles in the Mini-Symposium carefully and then complete the self-assessment questionnaire by filling in the square corresponding to your response to each multiplechoice question. After completing the questionnaire, either post or fax the answer page to the Current Orthopaedics Editorial Office at the address at the bottom of the RESPONSE sheet. Please photocopy this page if you wish to keep your copy of Current Orthopaedics intact. Replies received before the next issue of Current Orthopaedics is published will be marked and those reaching an adequate standard will qualify for three external CME points. You will be notified of your marks and a CME certificate will be despatched for your records.
Questions 1. A patient has limited external rotation after sustaining a minimally displaced fracture of the proximal humerus. Which of the following releases would be most appropriate to restore this movement? A. Posterosuperior and posteroinferior capsule B. Posterior band of inferior glenohumeral ligament and inferior capsule C. Anterior band of inferior glenohumeral ligament and anteroinferior capsule D. Anterior capsule including middle glenohumeral ligament and subscapularis E. Superior glenohumeral ligament, coracohumeral ligament and rotator interval 2. What is the main source of perfusion to the humeral head? A. B. C. D. E.
Anterior circumflex vessels Arcuate artery Intratendinous vessels supplying the rotator cuff Posterior circumflex vessels Subscapular artery
0268-0890/$ - see front matter & 2007 Published by Elsevier Ltd. doi:10.1016/j.cuor.2007.11.008
3. Which of the following is least useful as a predictor of humeral head ischaemia after shoulder fractures? A. B. C. D. E.
Disrupted medial hinge Fracture lines at the anatomical neck Glenohumeral dislocation Short posteromedial metaphyseal extension Varus tilt of head whilst shaft and tuberosities remain relatively undisplaced
4. Where is the bony glenoid erosion most commonly situated in patients with osteoarthritis? A. B. C. D. E.
Superior Anterior Inferior Posterior Central
5. Where is the bony glenoid erosion most commonly situated in patients with rheumatoid arthritis? A. B. C. D. E.
Superior Anterior Inferior Posterior Central
6. Which of the following is not clinically useful in improving glenoid exposure when carrying out total shoulder replacement? A. Coracoid osteotomy B. Excision of all humeral osteophytes after resection of the head C. Excision of the whole glenoid labrum D. Inferior capsular release E. Selective release of the upper part of pectoralis major tendon 7. For how long after shoulder replacement can motion and strength improve with appropriate rehabilitation? A. More than five years B. One to two years
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CME Section C. Six months D. Three months E. Six weeks
8. What is the most significant determinant of postoperative range of movement after shoulder replacement? A. B. C. D.
Age of the patient Extent of osteophytes before surgery Preoperative range of motion Whether or not subscapularis lengthening was carried out E. Whether total joint replacement or hemiarthroplasty was carried out
9. According to Neers estimates, what is the likelihood of a patient with a full thickness tear of the whole rotator cuff developing rotator cuff arthropathy? A. B. C. D. E.
Less than 1 in 100 About 1 in 25 About 1 in 10 About 1 in 5 More likely than not
10. What is the mechanism for the proposed genetic predisposition to rotator cuff arthropathy? A. Enzyme variants increasing the extracellular inorganic pyrophosphate concentrations
11. Which of the following potential complications of reverse shoulder arthroplasty would be considered 11. unusual? A. B. C. D. E.
Acromial fracture Humeral component aseptic loosening Humeral shaft fracture Perioperative glenoid fracture Postoperative haematoma
12. Which of the following is not an indication for shoulder arthrodesis? A. Brachial plexus injury B. End stage recurrent instability with bone loss in a light manual worker C. Failed shoulder arthroplasty D. Joint destruction by past septic arthritis E. Progressive myopathic weakness of the rotator cuff with preserved hand function Please fill in your answers to the CME questionnaire above in the response section provided below. A return address and fax number is given at the bottom of the page. .......................................................................................................................................................
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Your details (Print clearly) NAME............................................................................................ ADDRESS....................................................................................... FAX NO.......................................................................................... EMAIL............................................................................................
RETURN THE COMPLETED RESPONSE FORM by fax to +44-113-392-3290, or by post to CME, Current Orthopaedics, Academic Department of Orthopaedic Surgery, ‘‘A’’ Floor Clarendon Wing, Leeds General Infirmary, Great George Street, Leeds LS1 3EX, UK.
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 480
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CME SECTION Answers to CME questions based on the article—‘‘Management of Infected TKR’’ Please find below the answers to the Current Orthopaedics CME questions from Vol. 21, issue 4 which were based on the article—‘‘Management of Infected TKR’’ by Naidu Maripuri et al. 1
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0268-0890/$ - see front matter doi:10.1016/j.cuor.2007.08.004
ARTICLE IN PRESS Current Orthopaedics (2007) 21, 481
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BOOK REVIEWS The 5-Minute Orthopaedic Consult, Frank J. Frassica, Paul D. Sponseller, John H. Wilckens. Lippincott Williams & Wilkins, Baltimore, MD (2006). 450pp., price: £28.38, ISBN: 0781799716 This is a hard-backed book of 496 pages in length. There are over 60 contributors, all of whom had been residents at The Johns Hopkins University School of Medicine in the Department of Orthopaedics. It is intended that this book be left in the clinic, to be used as a quick reference. The content includes all common orthopaedic conditions and common fractures, which are listed alphabetically, for ease of reference. For each topic the information is spread out over two facing pages and includes basic background to
the condition, diagnosis, treatment and follow-up, additional information on further reading and ICD 9-cm codes. The text is mostly illustrated with line drawings; however, there are some photographs and X-rays. Paediatric and adult topics are mixed together. This book is well written, with a standard format applied to each topic. It includes all common problems that will be encountered in an orthopaedic clinic. It is aimed at trainees passing through orthopaedics or those in their first few years of an orthopaedic programme. This book will benefit any budding orthopaedic surgeon early on in their career and I would recommend that every department have one copy in the clinic.
P.A. Templeton
doi:10.1016/j.cuor.2007.11.011
Advanced Reconstruction—Elbow, K. Yamaguchi, G. King, M. McKee, S. O’Driscoll. American Academy of Orthopaedic Surgeons (2007). 500pp., price: 149.96, ISBN: 0892033916 This is not a huge tome, with 470 pages, yet 54 chapters are packed in from no less than 70 contributors. Despite the chapters being very concise, sometimes only two or three pages long, there is not any excess of detail and the book remains remarkably readable. The quality of illustrations is, on the whole, excellent and there is liberal use of colour diagrams and photographs. I personally do not like the three-column format, which results in most lines ending in a split word, but this is a minor gripe. The title would suggest that this is a book perhaps only for those with a special interest in elbow surgery and I hope this does not put off potential readers. In fact, it is a pretty comprehensive text on elbow surgery with good tabular summaries of relevant literature. The first section on elbow arthroscopy is perhaps the clearest introduction to this branch of elbow surgery available for trainees. The open procedures described range from tennis elbow surgery and ulnar nerve release upwards in complexity. doi:10.1016/j.cuor.2007.11.012
One possible perceived disadvantage is that the subject is covered in a procedure-based fashion. One method of open surgery for treatment of tennis elbow, for example, is discussed. Although each chapter has a subheading ‘alternative treatments’ this tends to focus on treatments other than surgery. In this way, the reader comes away with views shaped by a single opinion in each case, albeit an opinion from a leading expert. Where there is a clear range of options the editors have chosen to select multiple chapters on the same procedure, nowhere more obvious than in the field of elbow arthroplasty, where six separate chapters describe the same procedure using different implants. In fact, this is a very useful technical overview, but does lead to repetition in the sections on ‘indications’, ‘contra indications’ and ‘alternative treatments’. Overall, I would highly commend this book and would suggest it is not just a text for those wanting to focus on advanced elbow surgery in detail. It is an excellent book for reading up even basic procedures and would justify a place in any departmental library.
D. Limb
