Orthopaedics and Trauma. Volume 23 (2009)

Orthopaedics and Trauma Orthopaedics and Trauma 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 minisymposium; 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-in-Chief D Limb BSc FRCS Ed (Orth) Leeds General Infirmary, Leeds, UK

Editorial Committee M A Farquharson-Roberts (Gosport, UK), I Leslie (Bristol, UK) M Macnicol (Edinburgh, UK), I McDermott (Ruislip, UK), J Rankine (Leeds, UK)

Editorial Advisory Board R Crawford (Australia) D C Davidson (Australia) J Harris (Australia) G R Velloso (Brazil) P N Soucacos (Greece) A K Mukherjee (India) A Kusakabe (Japan) M-S Moon (Korea) R Castelein (The Netherlands) R K Marti (The Netherlands)

Founding Editor Professor R A Dickson MA ChM FRCS DSc Leeds General Infirmary, Leeds, UK

G Hooper (New Zealand) A Thurston (New Zealand) E G Pasion (Philippines) L de Almeida (Portugal) G P Songcharoen (Thailand) R W Bucholz (USA) R W Gaines (USA) S L Weinstein (USA) M Bumbasirevic (former Yugoslavia)

Orthopaedics and Trauma Elsevier, ISSN: 1877-1327, http://www.sciencedirect.com/science/journal/18771327 Volume 23, Issue 1, Pages 1-76 (February 2009) 1

Editorial Board, Page i

2

Editorial, Page 1 David Limb

Mini-Symposium: What’s new in hip replacement—Basic principles 3

(i) Alternative bearing surfaces for hip arthroplasty, Pages 2-7 Timothy Guy McWilliams, James R. Parker

4

(ii) The prevention of infection in total hip arthroplasty, Pages 8-16 Nemandra A. Sandiford, John Skinner

5

(iii) Patient selection and consent, Pages 17-26 C.R. Gooding, F.S. Haddad

6

(iv) Surgical approaches in primary total hip arthroplasty – pros and cons, Pages 27-34 C.M. van Dijk, R. Bimmel, Fares S. Haddad

7

(v) Prevention of dislocation in hip arthroplasty, Pages 35-39 S.W. Veitch, S.A. Jones

8

(vi) Hip outcome measures, Pages 40-45 Miss E. Ashby, M.P.W. Grocott, F.S. Haddad

9

(vii) Current developments in short stem femoral implants for hip replacement surgery, Pages 46-51 Wolfram H. Kluge

Trauma 10

Radiology of fracture complications, Pages 52-60 Emma Rowbotham, Dominic Barron

Foot and Ankle 11

The diabetic foot and ankle, Pages 61-68 James C. Stanley, Andrew M. Collier

Syndromes 12

Thoracic outlet syndrome, Pages 69-73 Hani Abdul-Jabar, Abbas Rashid, Francis Lam

CME Section 13

CME questions based on the Mini-Symposium on ―What’s new in hip replacement — basic principles‖, Pages 7475

14

Answers to CME questions based on the Mini-Symposium on ―Essential biomechanics of hip replacement‖, Page 76

Orthopaedics and Trauma Elsevier, ISSN: 1877-1327, http://www.sciencedirect.com/science/journal/18771327 Volume 23, Issue 2, Pages 77-152 (April 2009) 1

Editorial Board, Page i

Mini-symposium: Imaging for joint replacement 2

(i) Radionuclide imaging of joint prostheses: established & emerging applications, Pages 77-87 Richard J. Robinson, Andrew F. Scarsbrook

3

(ii) Diagnostic plain film radiology of the failing hip replacement, Pages 88-100 Andoni P. Toms, Rajesh Botchu, John F. Nolan

4

(iii) CT and MRI of hip replacements, Pages 101-108 John G. Cahir, Andoni P. Toms

Spine 5

Lumbar pars injury or spondylolysis – diagnosis and management, Pages 109-116 Ujjwal K. Debnath, N. Harshavardhana, Brigitte E. Scammell, Brian J.C. Freeman

Arthroplasty 6

Is infection inevitable in some arthroplasty patients?, Pages 117-121 R.J. Langley, D.I. Rowley

Quiz 7

Radiology quiz, Pages 122-127 Asha Ramakrishnan, Philip Robinson

Adult Hip 8

Hip pain in young adults and the role of hip arthroscopy, Pages 128-136 Ernest Schilders, Alexandra Dimitrakopoulou, J. Charles Talbot, Quamar Bismil

Trauma 9

Stress fractures, Pages 137-143 Mark R. Philipson, Paul J. Parker

Knee 10

Patello-femoral arthrosis, Pages 144-148 F. Rayan, F.S. Haddad

CME Section 11

CME questions based on the Mini-Symposium on “Imaging for Joint Replacement”, Pages 149-150

12

Answers to CME questions based on the Mini-Symposium on “Osteoporosis”, Page 151

Orthopaedics and Trauma Elsevier, ISSN: 1877-1327, http://www.sciencedirect.com/science/journal/18771327 Volume 23, Issue 3, Pages 153-222 (June 2009) 1

Editorial Board, Page i

Mini-symposium: Children's Hip Problems 2

(i) Irritable hip and septic arthritis of the hip , Pages 153-157 M. Padman, B.W. Scott

3

(ii) Surgical approaches to the hip in children, Pages 158-161 M.F. Macnicol

4

(iii) Developmental dysplasia of the hip, Pages 162-168 Benjamin Holroyd, John Wedge

5

(iv) Slipped upper femoral epiphysis, Pages 169-174 Richard J. Montgomery

Basic Science 6

Biofilm and orthopaedic practice: the world of microbes in a world of implants, Pages 175-179 Spyridon P. Galanakos, Stamatios A. Papadakis, Konstantinos Kateros, Ioannis Papakostas, George Macheras

Syndrome 7

Facioscapulohumeral muscular dystrophy assessment and treatment, Pages 180-185 Samuel J. Parsons, Andrew McMurtrie, Stephen Cooke, Birender Balain, David Jaffray

Wrist 8

Ætiology of extraosseous wrist ganglia; the published evidence, Pages 186-188 A.J. Thurston

Musculoskeletal Tissues 9

Current concepts in articular cartilage repair, Pages 189-200 A. Getgood, T.P.S. Bhullar, N. Rushton

Children 10

The management of spastic equinus in cerebral palsy, Pages 201-209 Goran Cobeljic, Marko Bumbasirevic, Aleksandar Lesic, Zoran Bajin

Hip Arthroplasty 11

Computer assisted hip resurfacing, Pages 210-215 Wolfram H. Kluge

Science and Symptoms 12

Why do joints swell?, Pages 216-218 Les Grujic, Sydney Nade

CME Sections 13

CME questions based on the Mini-Symposium on “Children's Hip Problems”, Pages 219-220

14

Answers to CME questions based on the Mini-Symposium on “What’s new in hip replacement — basic principles”, Page 221

Orthopaedics and Trauma Elsevier, ISSN: 1877-1327, http://www.sciencedirect.com/science/journal/18771327 Volume 23, Issue 4, Pages 223-300 (August 2009) 1

Editorial Board, Page i

Mini-symposium: Orthopaedic Oncology 2

(i) Epidemiology of bone and soft-tissue sarcomas, Pages 223-230 Benjamin J.F. Dean, Duncan Whitwell

3

(ii) Investigation of musculoskeletal malignancy, Pages 231-239 Robert U. Ashford, K. Julia Fairbairn

4

(iii) The management of soft-tissue sarcomas, Pages 240-247 Thomas B. Beckingsale, Craig H. Gerrand

5

(iv) Management of benign bone tumours, Pages 248-257 Rob Pollock

6

(v) The non-surgical management of musculoskeletal malignancy, Pages 258-265 Claire Esler

Basic Science 7

Management of articular cartilage defects, Pages 266-273 Ehab Kheir, David Shaw

Adult Pathology 8

Charcot Marie Tooth Disease, Pages 274-277 D.W.J. Howcroft, S. Kumar, N. Makwana

Syndrome 9

Ollier’s disease and Maffucci syndrome, Pages 278-280 Sean Fang, Donna Dimond, Rouin Amirfeyz, Martin Gargan

Trauma 10

The use and abuse of locking plates, Pages 281-290 Paul Szypryt, Daren Forward

Shoulder 11

Shoulder arthroscopy, anatomy and variants - part 1, Pages 291-296 Simon Boyle, Manuel Haag, David Limb, Laurent Lafosse

CME Section 12

CME questions based on the Mini-Symposium “Orthopaedic Oncology”, Pages 297-298

13

Answers to CME questions based on the Mini-Symposium on “Imaging for Joint Replacement”, Page 299

Orthopaedics and Trauma Elsevier, ISSN: 1877-1327, http://www.sciencedirect.com/science/journal/18771327 Volume 23, Issue 5, Pages 301-384 (October 2009) 1

Editorial Board, Page i

Mini-Symposium: Revision Hip Surgery 2

(i) Evaluation of a painful total hip replacement, Pages 301-306 Ardeshir Y. Bonshahi, Anil K. Gambhir

3

(ii) Implant removal in revision hip surgery, Pages 307-321 Andrew R.J. Manktelow

4

(iii) Reconstruction/revision of acetabular failure in revision hip replacement, Pages 322-326 Peter W. Howard

5

(iv) Reconstruction and revision of femoral failure in revision hip arthroplasty, Pages 327-334 Alexander Acornley, Robin Banerjee, Robert Kerry

6

(v) The management of dislocation in hip arthroplasty, Pages 335-341 R. Yarlagadda, S.A. Jones

7

(vi) Management of periprosthetic infection in total hip arthroplasty, Pages 342-349 M.T.S. Sukeik, F.S. Haddad

8

(vii) Management of periprosthetic fractures in the lower limb, Pages 350-356 Panos Makrides, Harpal Singh Uppal, Steve Krikler

Basic Science 9

Arthroscopic powered instruments: a review of shavers and burrs, Pages 357-361 S. Singh, A. Tavakkolizadeh, A. Arya, J. Compson

Syndrome 10

Nail-patella syndrome, Pages 362-364 Charlotte Jones, Donna Diamond, Rouin Amirfeyz, Martin Gargan

Shoulder 11

Shoulder arthroscopy, anatomy and variants – part 2, Pages 365-376 Simon Boyle, Manuel Haag, David Limb, Laurent Lafosse

Principles 12

Safer surgery: how a checklist can make orthopaedic surgery safer, Pages 377-380 Mark Emerton, Sukhmeet S. Panesar, Kirsty Forrest

CME Section 13

CME questions based on the Mini-Symposium “Revision Hip Surgery”, Pages 381-382

14

Answers to CME questions based on the Mini-Symposium on “Children’s Hip Disorders”, Page 383

Orthopaedics and Trauma Elsevier, ISSN: 1877-1327, http://www.sciencedirect.com/science/journal/18771327 Volume 23, Issue 6, Pages 385-462 (December 2009) 1

Editorial Board, Page i

Mini-Symposium: Foot and Ankle 2

(i) The principles of foot and ankle arthrodesis, Pages 385-394 Lee Parker, Dishan Singh

3

(ii) Flatfoot deformity: an overview, Pages 395-403 Kurt Thomas Haendlmayer, Nick John Harris

4

(iii) Entrapment neuropathies of the foot and ankle, Pages 404-411 Timothy H.D. Williams, Andrew H.N. Robinson

5

(iv) Imaging of foot and ankle disorders, Pages 412-419 James J. Rankine

Peripheral Nerve 6

The anatomy, investigations and management of adult brachial plexus injuries, Pages 420-432 Jonathan Gregory, Alex Cowey, Matthew Jones, Simon Pickard, David Ford

Trauma 7

Acute compartment syndrome of the lower extremity: an update, Pages 433-440 Christopher Tzioupis, George Cox, Peter V. Giannoudis

Anaesthesia 8

Regional analgesia and orthopaedic surgery, Pages 441-449 Andy Wilson

Basic Science 9

Hyaline articular cartilage, Pages 450-455 Ehab Kheir, David Shaw

Syndrome 10

Multiple hereditary exostoses, Pages 456-459 Payam Tarassoli, Rouin Amirfeyz, Martin Gargan

CME Section 11

CME questions based on the Mini-Symposium on “Foot and Ankle Problems”, Pages 460-461

12

Answers to CME questions based on the Mini-Symposium on “Orthopaedic Oncology”, Page 462

Editorial

Editorial

required for specialist certification and those who are already trained to keep at this level. In short, quality has not and will not be sacrificed. Indeed we now have an opportunity to calibrate our content with the needs of our intended audience. In the UK we have a curriculum for training in trauma and orthopaedics that sets the standard for specialist certification (www.ocap.org. uk/curriculum) and soon, established consultants will need to recertify and prove that they have maintained these standards in the areas in which they practice. We therefore have a template to follow and will try to cover the important and changing areas of the curriculum at least once in each training cycle. Articles will be commissioned that help with specialist training but also, and equally importantly, update the surgeon in those areas in which they practice that are not their prime subspecialty interest. We hope that our readers approve of the changes that have occurred and we commit to further improvements as the worlds of both orthopaedics and publishing move on.

David Limb The first issue of 2009 heralds changes to the journal formerly known as Current Orthopaedics. The most obvious is that its name has changed, and with it the design and format. There have also been changes in the Editorial team, but I am especially pleased that Bob Dickson, one of the founders of Current Orthopaedics, has stayed on as Emeritus Editor to lend his wisdom and skills to the task of attracting high quality articles to this respected organ. Some things remain unchanged however. The core values of the journal hold strong and our prime function remains to educate and inform both trainees and established practitioners. Our articles should reflect the state of the art of thinking and practice, helping those in training reach the level

David Limb BSc FRCSEd(Orth) is a Consultant Orthopaedic Surgeon within the Leeds Teaching Hospitals Trust, UK. He is also Editor-in-chief of Orthopaedics and Trauma.

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© 2009 Elsevier Ltd. All rights reserved.

Mini-symposium: What’s new in hip replacement — Basic principles

(i) Alternative bearing surfaces for hip arthroplasty Timothy Guy McWilliams James R Parker

Abstract Over 50,000 hip replacements are performed per year in NHS hospitals, independent sector hospitals and treatment centres. Since the concept of low frictional arthroplasty was first introduced, aspirations and lifestyles have changed dramatically. Expectations of outcomes have risen, yet more patients with severe co-morbidity of affluent lifestyle (obesity, diabetes and hypertensive cardiac disease) undergo surgery. Implant survival will be aided by reduced wear rates, either through design and material changes to the bearing on polyethylene or in the use of hard on hard bearings. Surgeons have a responsibility to assess the risk-benefit ratio of the bearing used. This article provides a review of the choices available.

Keywords ceramic on ceramic; highly cross linked polyethylene; metal on metal; osteolysis; wear

Figure 1 Balloon osteolysis and aseptic loosening associated with polyethylene wear.

Introduction Wear, caused by adhesion, abrasion and fatigue should be distinguished from damage, though the latter can influence the former. Damage occurs through deficiencies in manufacturing and surgical technique. This should be borne in mind when outlying results of increased wear are presented. It is estimated that 70% of revision surgery is for implant failure secondary to wear and aseptic loosening1 (Figure 1). The majority of such wear-related particulate debris originates from motion between the two bearing surfaces (Mode 1) but combinations of modes of wear may occur (Modes 1–4, Table 1).2 Polyethylene particles in periprosthetic debris are implicated in the biologic response leading to periprosthetic osteolysis and loosening.3 They are phagocytosed by macrophages, stimulating the release of soluble pro-inflammatory mediators and cytokines. Particle size may vary but those of sub-micron size exert more biological activity. Osteolysis is self-sustaining: as bone resorption and prosthetic loosening progress, abrasion and fretting at the interface produce increased wear. The revision burden is rising (>10%) and the choice of different prostheses remains high (155 acetabular cups and 176 femoral stems).4 Each bearing

couple introduced has its own material properties and possible consequences.

Metal on polyethylene Metals used in conjunction with polyethylene(PE)have principally been stainless steel and cobalt-chromium-molybdenum (Co-CrMo) alloy, but also titanium alloy. The latter has a high coefficient of friction compared with cobalt-chrome and its ­ vulnerability

Mechanisms of wear in Orthopaedic joints Mode

Type of articulation

Example

1

Between intended bearing surfaces Between a bearing and non-bearing surface

Femoral head and acetabular cup Femoral head through worn acetabular liner to metal shell Cement, metal or bone debris between femoral head and acetabular cup Backside wear

2

3 Timothy Guy McWilliams MBBS BSc FRCS FRCS(Tr/Orth), is Consultant Orthopaedic Surgeon at Calderdale and Huddersfield NHS Foundation Trust, UK.

4

James R Parker MBChB(hons) MRCS MRCS(Glasg) is a Specialist Registrar in Trauma and Orthopaedics.

ORTHOPAEDICS AND TRAUMA 23:1

Between 2 intended bearing surfaces and interposed 3rd body Between 2 non-bearing surfaces

Table 1



© 2008 Published by Elsevier Ltd.

Mini-symposium: What’s new in hip replacement — Basic principles

to abrasion by entrapped third body particles increases wear and makes titanium a poor bearing choice.5 The wear rate of polyethylene against stainless steel has been comparable to Co-Cr-Mo both in simulator studies and in vivo measurement (typically reported to be 0.05–0.2 mm per year). This is the standard of wear against which other bearings are judged.6,7 It should be noted these historic data are strengthened by the fact they include implants which have accelerated wear rates due to third body damage and radiation-induced oxidative degradation of the ­polyethylene. Traditional acetabular cups over a decade ago were fabricated from ultra-high molecular weight polyethylene (UHMWPE) by extrusion, bulk compression moulding or net-shape moulding followed by gamma irradiation sterilisation in air. Irradiation in air results in oxidative degradation during post-irradiation ageing (polyethylene embrittlement through reduction of crosslinks). This results in delamination, pitting and fracture. In addition to inducing cross-linking, irradiation causes scission of molecular chains and creates uncombined electrons – free radicals. These react with oxygen causing additional chain scission, increasing crystallinity and decreasing fatigue strength, fracture ­toughness and wear resistance. Several manufacturers perform gamma sterilization with the UHMWPE component sealed in a suitable oxygen-free atmosphere, including vacuum or inert gas (argon or neon), where free radicals will recombine. Other manufacturers have chosen to sterilise without irradiation, using ethylene oxide or gas plasma to decrease the production of reactive free ­radicals.

manufacture of head/stem tapers as well as increasing ceramic quality and strength have reduced the potential for fracture. In clinical application, care must be taken to use only stem and head assemblies from the same manufacturer. A ceramic taper should not be used on a damaged femoral neck (eg. retained stem at revision) or fracture may ensue. To counter this ceramic heads with metal reinforcement sleeves have been introduced but no long-term clinical results on their use are available.

Developments in polyethylene bearings Concerns regarding polyethylene wear and osteolysis have stimulated the development of highly cross-linked polyethylene. The method of increasing cross-linking polyethylene varies between manufacturers. Important steps are radiation cross-linking, thermal treatment and terminal sterilisation.10 Irradiation breaks down the carbon-hydrogen chains within the polymer, creating free radicals in the process. The free radicals combine with adjacent molecules to forms cross-links. As the dose of radiation increases (usual range from 2.5 to 10 Mrad) so does the amount of cross-linking. Cross-linking increases the wear resistance but as the amount of cross-linking increases, there is a corresponding decrease in some mechanical properties including ultimate tensile strength and resistance to fatigue crack propagation.11,12 This is increased with implant malalignment and/or neck liner impingement, emphasising the importance of surgical technique. The reduced mechanical properties of highly cross-linked polyethylene have the potential to be a limiting factor in device performance. Hylamer was introduced in 1987 and promoted as more wear resistant UHMWPE. Bar stock was produced using high temperatures and re-melting under high pressure with the aim of increasing crystallinity and strength. However, the process produced a chain extended structure with higher stiffness but relatively fewer tie molecules. The material was susceptible to oxidation, breaking the low number of tie molecules and weakening it. Components exhibited inferior clinical wear and delamination when compared to virgin UHMWPE. Hylamer was withdrawn from the market in 2001. Thermally treating the UHMWPE reduces the quantities of free radicals and subsequent oxidative damage. Thermal processing varies with different polyethylenes. Heating above the melting point (melting) allows further cross-linking and results in reduced crystallinity in the polyethylene. Annealing (heating below the melting point) avoids the reduction in crystallinity but fails to extinguish the free radicals which in an oxygen rich environment will result in oxidative degradation of the polymer.13 Following the thermal treatment, terminal sterilisation is performed either as a surface treatment in the form of gas plasma, ethylene oxide or as a sterilising dose of gamma irradiation in an inert ­atmosphere.11 Traditional UHMWPE acetabular components exhibit increasing volumetric wear as a function of larger femoral head diameter. In contrast simulator studies suggest wear in modern highly crosslinked UHWMPE is so reduced14 that it is almost independent of femoral head diameter.15,16 Using larger femoral heads reduces dislocation (greater jump distance required) and depending on the head/neck ratio may also give an increased arc of motion at the joint (Figure 2). No long-term clinical results are yet available for highly cross-linked polyethylene, but several prospective

Ceramic on polyethylene Alumina ceramic femoral head components were introduced as low-friction metallic substitutes reducing wear against polyethylene cups. Some studies report little radiographic difference in wear whilst some early types of ceramic documented unacceptably high wear.8 Zirconia femoral heads were introduced in the mid 1980’s to address concerns with ceramic component fractures and allow use of smaller diameter (22 and 26 mm) femoral heads. They were only used in conjunction with polyethylene. The finer grain size of zirconia gave improved fracture toughness and bending strength as compared to alumina. The material could undergo phase transformation at high temperatures and in wet environments, weakening it and increasing surface roughness. In 2001, zirconia femoral heads were recalled from circulation by the Medical Devices Agency because of an observed high rate of fracture. Use of a ceramic head in a modular hip system requires no difference in operative technique. These materials are highly biocompatible, smoother, harder, and more scratch-resistant than their metallic counterparts. Laboratory studies have documented reductions in wear volume (up to twenty times less wear compared with that of metal on polyethylene). Most in vivo studies have demonstrated lower wear rates (0.03 mm/yr after bedding in, compared to 0.07 mm/yr with standard metal on polyethylene), offering the prospect of increased polyethylene longevity and a decreased potential for osteolytic response. Ceramic components enjoy substantial use in younger populations despite the concerns of added cost and a small reported incidence of brittle fracture (four in 100,000).9 Improvements in the

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© 2008 Published by Elsevier Ltd.

Mini-symposium: What’s new in hip replacement — Basic principles

of 45°) in 65% of the squeaking hips. In contrast, only 6% of the non-squeaking hips were outside this range. Revised hips had evidence of articulation damage due to impingement or edge-loading as a result of suboptimal component positioning. The exact mechanism causing squeaking has not been defined but micro-separation may be an important mechanism leading to the generation of noise. Whilst COC bearings are increasing in popularity, fracture of the ceramic bearing remains a complication in some designs. The resultant debris predisposes to third body wear thereafter. One report of third generation alumina-on-alumina implants noted fracture prevalence up to 1.4%. All fractures in this series occurred during normal physical activities and all occurred in hips with a short neck. The fractures involved a circular crack along the circumference of the thinnest portion of the head, extending radially along the longitudinal axis. This rate of component fracture may be specific to this particular design,26 highlighting the need for published long-term results for each implant.

Figure 2 Head size, head/neck ratio and arc of motion till rim impingement.

Metal on metal bearings Cobalt chromium alloy has been used in Orthopaedics for many years. The first generation of metal-on-metal (MOM) bearings, such as the Mueller, McKee-Farrar and Ring designs had imperfect manufacturing tolerances and fell out of favour with respect to the Charnley stainless steel on polyethylene low frictional arthroplasty (LFA). The awareness of the osteolytic effects of polyethylene wear debris and the long-term results of McKeeFarrar implants as compared to Charnley LFA was an impetus for the development of modern hip resurfacing and renewed interest in MOM implants in conventional total hips.27 Larger implant diameters may be used, so increasing the jump distance needed for dislocation. Close control of component dimensions, sphericity, and surface finish are also critical, but they add to manufacturing costs. Currently, both cast and wrought cobaltchromium-molybdenum alloys of differing carbon content are in use. High carbide content hardens the material reducing adhesive wear. This hardness gives a capacity to “self-heal” by polishing out third-body scratches in contact areas. Hip-simulator studies demonstrate the importance of specific diametrical clearances (90–200μm) to facilitate polar bearing and access for serum lubrication, resulting in a 20–100 fold reduction in the amount of particle generation in comparison with that demonstrated in similar evaluations of metal-ultra-high molecular weight polyethylene articulations.28,29 Despite the lower total volume of debris with MOM bearings (smaller size), the total number of metal particles generated annually are anywhere from 13–500 times the number of polyethylene particles from a metal-on-polyethylene bearing.30 As hip resurfacing has expanded, the importance of surgical technique has become apparent. At present one-year revision rates for hip resurfacing in the UK are higher than for cemented hip replacement.4 Patient selection and implant positioning is of vital importance.31 Similar to wear rate, MOM bearings produce ion levels that are high initially during the 1–2 year run-in phase and then may decrease.32,33 Present data preclude the use of MOM in patients with chronic renal failure (as they are excreted in urine) or fertile women (where they cross the placenta).

randomised studies show significant wear reduction with differing diameter femoral heads at up to 5 years follow up.17–22 The multiple options available with modern polyethylenes such as lipped, anteverted and lateralised liners in differing head sizes offer the surgeon increased flexibility in restoring stable biomechanics to the hip. Surgeons should be aware of the manufacture of the polyethylene they implant in relation to the possible effects on microstructure, crystallinity and mechanical properties.

Ceramic-on-Ceramic (COC) bearings The advantages of COC as a bearing relates to its hardness, wettability, inertness and high level of oxidation, which provide resistance to major scratches, increased implant longevity and high biocompatibility. Implants require careful positioning due to the reduced liner lip and neck length options available. Results of first generation alumina-on-alumina bearings included early fracture, impingement, pain that limited activities and implant loosening secondary to excessive wear rates.23 Compared to the results achieved with metal-on-polyethylene implants, such alumina-on-alumina implants held a minority market share. The quality of today’s ceramic is much improved, with minimization of impurities, which are potential stress­risers. Reduction of grain boundaries (by hot isostatic pressing) increases material strength and toughness. Along with improved quality control through proof-testing the prevalence of component fracture has substantially reduced. Tribological properties of wear, lubrication, and friction are excellent. Simulator studies have demonstrated that COC articulations have lower wear than all other currently available bearing couples (linear wear rates of 0.03 μm/year, or up to 5000 times less wear volume than metalon-polyethylene have been reported in hip simulators.24) Audible squeaking in a small number of patients has received much attention recently. The incidence has been reported as 0.7% of 2397 hip arthroplasties over an eight-year period.25 The mean time to the onset of squeaking symptoms was fourteen months. Cup positioning was found to be outside of the ideal range (anteversion in excess of 25° and abduction in excess

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© 2008 Published by Elsevier Ltd.

Mini-symposium: What’s new in hip replacement — Basic principles

and sub-group them to identify different types. Revision surgery will be identified in relation to surgeon and unit. With present knowledge limitations, surgeons are asked to report cases of ­tissue reaction to the MHRA or submit patient samples and data to the Imperial College implant retrieval centre.

Metal wear particles are small (50–500 nm) in comparison with those that activate macrophages but concerns have been raised in relation to their possible teratogenic, cytotoxic and ­biological effects. Metal ions are raised in blood and urine in patients with MOM articulations. Research is ongoing investigating variation in metal ion levels in relation to component position, wear rates and clinical outcome. A hypersensitivity response with an aseptic lymphocyte-dominated vasculitis-associated lesion (ALVAL) has been described, but it is yet incompletely understood.34 The clinical presentation is of painful sterile effusions or pseudotumours and histological analysis reveals perivascular lymphocytes, often with plasma cells, fibrin deposition and oedema. The incidence with differing MOM articulations is yet to be accurately ­determined. Despite the concerns regarding chromosomal aberrations and translocations,35,36 changes in the proportions of peripheral blood lymphocytes37,38,39 and the risk of cancer, all of which have been raised in the literature, the International Agency for Research on Cancer concluded in two different reports40,41 that there is inadequate evidence in humans regarding the carcinogenicity of orthopaedic implants. Two earlier epidemiologic studies assessed the risk of neoplasia following MOM hip replacement compared to the general population.42,43 Although there were variations in the incidences of certain cancers between the two groups the conclusion was MOM hip replacement had no effect on cancer risk. In the UK, the Medicines and Healthcare products Regulatory Authority (MHRA) and Committee on Mutagenicity of Chemicals in Food (COM) published statements in 2006 concluding that there was no clinical evidence to suggest MOM hip replacement posed a significant health risk, but neither was that possibility excluded. The National Joint Registry will identify MOM patients

Ceramic on metal Ceramic-on-metal (COM) couples have been postulated over the last decade in an attempt to retain the wear properties of each hard bearing, whilst limiting rim cracking and metal ion release. Whilst the subject of presentations at meetings, the little published evidence for this bearing is only on simulator studies: in comparison to MOM these bearings have shown no bedding in and even further reduction in wear rates44 even under harsh microseparation conditions. Metal ion levels measured in serum samples were comparable to COC and again much lower than MOM.45 Although these data are encouraging there are no medium to long term clinical studies to support the use of COM bearings outside of a clinical trial.

Conclusion The potential advantages and disadvantages of bearing couples are summarised in Table 2. New technologies such as alternative bearings offer the potential to reduce wear and osteolysis, prolong implant survival, and lower revision rates following total hip arthroplasty. Nevertheless, in an era of limited health-care resources, the benefits of new, more costly technology intended to replace conventional bearings, must be reviewed with respect to additional clinical risks and economic costs associated with its use.

Advantages/disadvantages of differing bearing couples Bearing combination

Potential advantages

Potential disadvantages

Metal on PE sterilised in ethylene oxide or gas plasma

No long term oxidation Maximum strength, elongation and fracture toughness Some cross-linking Some wear reduction Minimal PE wear No long term oxidation

No cross-linking thus does not minimise wear

Metal on PE sterilised with γ-irradiation in low oxygen Metal on Cross-linked thermally stabilised PE Ceramic on PE Ceramic on ceramic

Lower wear of PE than with conventional metal on PE Low wear High biocompatibility

Metal on metal

Low wear Can self polish

Metal on ceramic

Low wear Reduced metal ions

Residual free radicals, possible long term oxidation PE wear not minimised Little in vivo clinical data Debate re optimum method of thermal stabilisation Higher cost Difficulty of revision if Morse taper damaged Higher cost Component fracture No lipped liners Higher cost Reaction long term to metal ions ALVAL Higher cost Little/no in vivo clinical data Patients should be part of a trial Higher cost

Table 2

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Mini-symposium: What’s new in hip replacement — Basic principles

Using an analytic model46 for a population of fifty-year-old patients, use of an alternative bearing with an incremental cost of $2000 would be cost-saving over the individual’s lifetime if it were associated with at least a 19% reduction in the twentyyear implant failure rate when compared with the failure rate for a conventional bearing. In patients over the age of sixty-three years, the same implant would be associated with higher lifetime costs than would a conventional bearing, regardless of the presumed reduction in the revision rate. Conversely, an alternative bearing that adds only $500 to the cost of a conventional total hip arthroplasty could be cost-saving in a population of patients over the age of sixty-five years, even if it were associated with only a modest reduction in the revision rate. In patients over the age of seventy-five years, no alternative bearing would be associated with lifetime cost-savings, regardless of the cost or the presumed reduction in the revision rate. In an attempt to reduce historic wear rates and prolong the implant survival of metal-on-polyethylene, changes in material and alternate bearing couples are marketed. It is the responsibility of the surgeon to assess the risk-benefit ratio of the bearing to be used. The challenge lies not only in producing technologically advanced solutions but perhaps more importantly using them wisely with correct surgical technique. ◆

13 Ries MD, Pruitt L. Effects of cross-linking on the microstructure and mechanical properties of ultra-high molecular weight polyethylene. Clin Orth Rel Res 2005; 440: 149–56. 14 Bragdon CR, O’Connor DO, Muratoglu OK. A new polyethylene with undetectable wear at 12 million cycles. Trans 24th Soc Biomaterials 1998; 21: 2. 15 Muratogolu OK, Bragdon CR, O’Connor DO, Jasty M, Harrris WH. A novel method of cross-linking ultra-high-molecular-weight polyethylene to improve wear, reduce oxidation and retain mechanical properties. J Arthroplasty 2001; 16: 149–160. 16 Hermida JC, Bergula A, Chen P, et al. Comparison of the wear rates of twenty-eight and thirty-two millimetre femoral heads on crosslinked polyethylene acetabular cups in a wear simulator. J Bone Joint Surg Am 2003; 85: 2325–2331. 17 Digas G, Karrholm J, Thanner J, et al. Highly cross-linked polyethylene in cemented THA: Randomised study of 61 hips. Clin Othop Relat Res 2003; 417: 126–138. 18 Digas G, Karrholm J, Thanner J, et al. Highly cross-linked polyethylene in total hip arthroplasty: Randomised evaluation of penetration rate in cemented and uncemented sockets using radiostereometric analysis. Clin Othop Rel Res 2004; 429: 6–16. 19 Bragdon CR, Greene ME, Freiberg AA, et al. Radiostereometric analysis comparison of wear of highly cross-linked polyethylene against 36 vs 28mm femoral heads. J Arthroplasty 2007; 22(6): 125–129. 20 Engh CA, Stepniewski AS, Ginn SD, et al. A randomised prospective evaluation of outcomes after total hip arthroplasty using crosslinked Marathon and non cross-linked Eduron polyethylene liners. J Arthroplasty 2006; 21(2): 17–25. 21 Triclot P, Grosjean G, El Masri F, et al. A comparison of the penetration rate of two polyethylene acetabular liners of different levels of cross-linking. J Bone Joint Surg Br 2007; 89: 1439–1445. 22 Dorr LD, Wan Z, Shahrdar C, et al. Clinical performance of a Durasul highly cross-linked polyethylene liner for total hip arthroplasty at five years. J Bone Joint Surg Am 2005; 87: 1816–1821. 23 Mahoney OM, Dimron III JH. Unsatisfactory results with ceramic total hip prosthesis. J Bone Joint Surg Am 1990; 72A: 663–671. 24 Clarke IC, Good V, Williams P. Ultra low wear rates for rigid on rigid bearings in total hip replacements. Proc Inst Mech Eng (H) 2000; 214: 331–347. 25 Walter WL, O’Toole GC, Walter WK, Ellis A, Zicat BA. Squeaking in ceramic-on-ceramic hips: the importance of acetabular component orientation. J Arthroplasty 2007; 22: 496–503. 26 Koo KH, Ha YC, Jung WH, Kim SR, Yoo JJ, Kim HJ. Isolated fracture of the ceramic head after third-generation alumina-on-alumina total hip arthroplasty. J Bone Joint Surg Am 2008; 90: 329–36. 27 Sliva M, Heisel C, Schmalzried TP. Metal on metal total hip replacements. Clin Orthop 2005; 430: 53–61. 28 McKellop H, Park SH, Chiesa R. In vivo wear of three types of metal on metal hip prosthesis during two decades of use. Clin Orthop 1996; 329(Suppl): S128–S140. 29 Jacbsson SA, Djerf K, Wahlstrom O. Twenty year results of McKeeFarrar versus Charnley prosthesis. Clin Orthop 1996; 329(Suppl): S60–S68. 30 Doom PF, Campbell PA, Worrall J. Metal wear particle characterization from metal on metal total hip replacements: transmission electron microscopy study of periprosthetic tissues and isolated particles. J Biomed Mater Res 1998; 42: 103–111.

References 1 Harris WH. The problem is osteolysis. Clin Orthop 1995; 311: 46–53. 2 McKellop HA, Campbell P, Park SH. The origin of submicron polyethylene wear debris in total hip arthroplasty. Clin Orth Rel Res 1995; 311: 3–20. 3 Archibeck MJ, Jacobs JJ, Roebuck KA, Glant TT. The basic science of periprosthetic Osteolysis. Instr Couse Lect 2001; 50: 185–195. 4 National Joint Registry for England and Wales, 4th Annual Report 2007. ISSN 1753–9382. www.njrcentre.org.uk 5 Lombardi Jr. AV, Mallory TH, Vaughn BK, Drouillard P. Asceptic loosening in total hip arthroplasty secondary to osteolysis induced by wear debris from titanium-alloy modular femoral heads. J Bone Joint Surg Am 1989; 71A: 1337–42. 6 Ilchmann T, Markovic L, Joshi A, Hardinge K, Murphy J, Wingstrand H. Migration and wear of long term successful Charnley total hip replacements. J Bone Joint Surg Br 1998; 80-B: 377–81. 7 Wroblewski BM, Fleming PA, Siney PD. Charnley low frictional torque arthroplasty of the hip, 20-30 year resuls. J Bone Joint Surg Br 1999; 81-B: 427–30. 8 Allain J, Le Mouel S, Goutaillier D, Voison McAllain J. Poor eight year survival of cemented zirconia-polyethylene total hip replacements. J Bone Joint Surg Br 1999; 81B: 835–42. 9 Greenwald A, Garino JP. Alternative bearing surfaces: the good, the bad and the ugly. J Bone Joint Surg Am 2001; 83-A: 68–72. 10 Gordon AC, D’Lima DD, Colwell Jr. CW. Highly cross-linked polyethylene in total hip arthroplasty. J Am Acad Orthop 2006; 14(9): 511–23. 11 Bradford L, Baker D, Ries MD, et al. Fatigue crack propagation resistance of highly cross- linked polyethylene. Clin Orthop Relat Res 2004; 429: 68–72. 12 Tower SS, Currier JH, Currier BH, Lyford KA, van Citters DW, Mayor MB. Rim cracking of the Cross-linked Longevity acetabular liner after total hip arthroplasty. J Bone Joint Surg Am 2007; 89: 2212–2217.

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risks to humans. Cobalt in hard metals and cobalt sulfate, gallium arsenide, indium phosphide and vanadium pentoxide; Vol 86. Lyon, France: IARC, 2003. 42 Visuri T, Koskenvuo M. Cancer risk after McKee-Farrar total hip replacement. Orthopedics 1991; 14: 137–142. 43 Visuri T, Pukkala E, Paavolainen P, Pulkkinen P, Riska EB. Cancer risk after metal on metal and polyethylene on metal total hip arthroplasty. Clin Orthop 1996; 329(Suppl): S280–S289. 44 Firkins PJ, Tipper JL, Ingham E, et al. A novel low wearing differential hardness ceramic-on-metal hip joint prosthesis. J Biomech 2001; 34: 1291–1298. 45 Williams S, Ingham E, Isaac G, et al. Ceramic on metal hip replacements: Part 1 in vitro testing. (extended abstractat the London hip meeting. London 2007). 46 Bozic KJ, Morshed S, Silverstein MD, Rubash HE, Kahn JG. Use of cost effectiveness analysis to evaluate new technologies in Orthopaedics: The case of alternative bearing surfaces in total hip arthroplasty. J Bone Joint Surg Am 2006; 88: 706–14.

31 Brodner W, Grübl A, Jankovsky R, Meisinger V, Lehr S, GottsaunerWolf F. Cup inclination and serum concentration of cobalt and chromium after metal-on-metal total hip arthroplasty. J Arthroplasty 2004; 19(Suppl 3): 66–70. 32 Brodner W, Bitzan P, Meisinger V, Kaider A, Gottsauner-Wolf F, Kotz R. Elevated serum cobalt with metal on metal articulating surfaces. J Bone Joint Surg B 1997; 79: 316–32 activity and ions in patients with metal on metal bearing hip prostheses. J Bone Joint Surg A 2005; 87: 781–787. 33 Heisel C, Silva M, Skipor AK, Jacobs JJ, Schmalzreid TP. The relationship between activity and ions in patients with metal on metal bearing hip prostheses. J Bone Joint Surg Am 2005; 87: 781–787. 34 Willert HG, Buchhorn GH, Fayyazi A. Metal on metal bearings and hypersensitivity in patients with artificial hip joints. A clinical and histomorphological study. J Bone Joint Surg Am 2005; 87: 28–36. 35 Case CP. Chromosomal changes after surgery for joint replacement. J Bone Joint Surg Br 2001; 83: 1093–5. 36 Tharani R, Dorey FJ, Schmalzried TP. The risk of cancer following total hip or knee arthroplasty. J Bone Joint Surg Am 2001; 83: 774–80. 37 Savarino L, Granchi D, Ciapetti G, et al. Effects of metal ions on white blood cells of patients with failed total joint arthroplasties. J Biomed Mater Res 1999; 47: 543–50. 38 Case CP, Langkamer VG, Lock RJ, Perry MJ, Palmer MR, Kemp AJ. Changes in the proportions of peripheral blood lymphocytes in patients with worn implants. J Bone Joint Surg Br 2000; 82: 748–54. 39 Granchi D, Savarino L, Ciapetti G, et al. Immunological changes in patients with primary osteoarthritis of the hip after total joint replacement. J Bone Joint Surg Br 2003; 85: 758–64. 40 International Agency for Research on Cancer, World Health Organization. IARC monographs on the evaluation of carcinogenic risks to humans. Surgical implants and other foreign bodies; Vol 74. Lyon, France: IARC, 1999. 41 International Agency for Research on Cancer, World Health Organization. IARC monographs on the evaluation of carcinogenic

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Research Directions • The biological response to the wear debris generated from highly cross-linked polyethylene (particles of biologically active size). • Longer follow-up of wear rates of highly cross linked UHMWPE and correlation with a reduced osteolysis and implant failure. • Long term results of larger diameter third generation ceramic on ceramic bearings. • Identification of biologic response to cobalt and chromium ions and bearing couples to reduce this. • Patient categorisation and implant selection with a cost benefit analysis.



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(ii) The prevention of infection in total hip arthroplasty

60000 50000 40000

Nemandra A Sandiford

30000

John Skinner

20000 10000 0 2003

Abstract Infection after total hip arthroplasty (THA) can lead to pain, decreased function, dislocation and lengthy revision operations over a protracted period of time. We must also consider the psychological impact on the patient and the consequent dissatisfaction with the operation. Modern surgical techniques and technology have contributed significantly to ­reductions in infection rates, using principles that are firmly based on the observations of pioneers such as Pasteur and Lister from the mid nineteenth century. This paper presents an evidence based review of techniques used to reduce the risk of infection during total hip arthroplasty. Early and contemporary methods are discussed along with the basis for their use.

2005

2006

Figure 1 Number of primary Total Hip Arthroplasties performed annually in the UK (UK National Joint Registry).

Predisposing factors These are numerous and relate to the patient, the operating theatre infrastructure and operating theatre personnel, including the surgeon. Patient factors Gillespie2 noted that general measures, such as stopping smoking, and control of comorbid diseases, such as diabetes, are important in decreasing the risk of infection. The temporary cessation of drugs such as methotrexate also decreases this risk.3 As with diabetes, sickle cell disease and rheumatoid arthritis are associated with an increased risk of infection and disease control needs to be optimised pre operatively.4,5 Periodontal and urinary tract sepsis must be eradicated. Of these two, urogenital foci of infection are the most important sources for the haematogenous spread of sepsis.6 Jenkins et al.7 found that patients with a BMI above 35.5 had an infection rate of 18.8%, which is well above the 6.9% overall infection rate for the entire group. These authors also found that there was a four-fold increase in infection rate among patients who had a perioperative complication compared to those who did not. Factors local to the surgical site include skin quality and the presence of previous sepsis or scars at the planned incision site. These predispose to surgical site infection.8,9 Pre operative lymphocyte counts of less than 1500/mm3 and serum albumin ­levels of less than 3.5 g/dl also increase the risk of post operative ­infection.10,11

Keywords infection; prevention; total hip arthroplasty

Introduction Infection of a total hip replacement (THR) is a challenging problem for the surgeon and has a great effect on the well being of the patient. The surgeon has to face performing multiple, often technically demanding, procedures. The patient may face longer inpatient stays, repeated episodes of general anaesthesia, lengthy surgical procedures and a protracted period of rehabilitation and disability. Along with the physical complications of prolonged hospital, stay such as decubitus ulcers and nosocomial infections, there are also the unseen but equally important psychiatric issues such as depression and overall dissatisfaction with an unsuccessful operation. Added to this is the drain on hospital resources that is incurred. It is estimated that the cost of managing an infected THR is four times that of a primary procedure without infection.1 This issue is particularly relevant, as the number of primary total hip replacements performed in the United Kingdom (UK), as in many other countries, has been increasing over the last 4 years (Figure 1).

Burden of infection The UK National Joint Registry reported that for the period 2003 to 2006, infection accounted for 19% of all failures leading to revision. This was only surpassed by aseptic loosening (22%) and dislocation (20%) and accounts for 81% of two-stage revision procedures. Charnley reported infection rates of 9.5% for his series of primary total hip replacements.12 Using a combination of clean air systems and as occlusive operating gowns, this figure decreased to 0.5%.13 Current rates of 0.3% in Sweden14 and 1.4% in the UK15 are now accepted as the true risk of infection associated with this operation.

Nemandra A Sandiford MRCS MRCS Ed MFSEM is a Clinical Research Fellow at Queen Mary’s Hospital, Sidcup, Kent, UK. John Skinner FRCS FRCS(Trauma/Orth) is a Consultant Orthopaedic Surgeon and Senior Lecturer at The Royal National Orthopaedic Hospital, Stanmore, Middlesex, UK.

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Kurtz et al. reported an overall incidence of infection after THR of 0.88% in the USA, with urban non-teaching hospitals accounting for the majority of these.16 They noted that this incidence was apparently increasing. The infection rate for revision THR’s is more than double that for primary procedures.

The natural history of infection Available evidence justifies the long term follow-up of patients with THR. The Medical Research Council (MRC) trial on the effects of ultra clean air found that the rate of revision for infection doubles between 2 and 7–8 years post-operatively.18 Hamilton and Jamieson24 found that clinically apparent infection rates doubled between 2 and 20 years. Both authors felt that these ‘late onset’ infections were not due to haematogenous spread but to direct seeding of the joint, usually at the time of surgery.

Historical perspective As early as 400 BC Hippocrates suggested that clean air might prevent the spread of disease.17 Much later, in 1964, Charnley reported deep infection rates of 9.5% in his early series, which he thought was due mainly to poor ventilation of his operating theatres.12 He was able to reduce his infection rate almost 20 fold (9.5% to 0.5%) by employing cleaner air techniques and by using occlusive clothing for operating theatre staff. These findings were supported by subsequent results of the Medical Research Council study,18 which found that deep infection rates were reduced by 75% in clean air theatres compared to those with standard ventilation.

Bacteriology The main sources of contaminants in THA surgery are the skin of the patient25 and organisms present in particles circulating in the air of the theatre. These particles arise from persons present in the operating theatre.26 Davis et al.23 found contamination rates of 11.4% for sucker tips, 9.4% for skin (outside) blades, 3.2% for inside blades, 28.7% for outside gloves used for preparation and draping the patient and 14.5% for light handles within the laminar flow zone. Coagulase negative staphylococci accounted for 81.2% of all infections in this series (Table 2). More recently Walls et al.27 described a 1% infection rate with Methicillin Resistant Staphylococcus aureus (MRSA). Deep infection rates after revision THR are more than twice those for primary procedures. This is similar for infection rates in primary total hip arthroplasty after previous surgical intervention.19 Technological advancements have contributed significantly to our understanding of organisms as well as the aetiology and management of infected total hip arthroplasties. Duguid, using ultrasonic lavage during cases of aseptic loosening found bacterial growth in 22% of cases. Bacterial DNA was found in 72% of the sample population.28 Studies using polymerase chain reaction (PCR) techniques have revealed that most implants carry evidence of associated bacteria. Multiple surgical procedures result in multiple contaminating species.19

Pathophysiology of deep prosthetic infection The risk of deep infection is increased by the presence of a foreign body within the hip joint.19 Many studies have verified that a foreign body significantly reduces the inoculum needed to start an infection. Elek and Cohen20 showed that skin infections can be caused by 10 fold fewer organisms in the presence of a suture than in intact skin. In the presence of a cemented THR comparable results have been much more worrying. Southwood et al.21 have shown that while 10,000 organisms are needed to infect a normal marrow cavity, only 50 organisms produced this result in the presence of a cemented THR. Petty et al.22 examined the effect of various types of material on infection rates (Table 1). They found that of the materials they studied, the greatest risk of infection occurred with the use of polymethylmethacrylate (PMMA) polymerised in vivo. This was closely followed by PMMA polymerised ex vivo. Charnley thought that only 10 organisms were needed to produce infection in a total hip arthroplasty. Though his figure was not derived by strict scientific methods it does highlight the potential for infection, particularly when one considers that even in laminar flow, ultra clean air theatres 29% of gloves, 14.5% of light handles and 18% of gowns are contaminated by the end of the procedure.24

Prevention of infection Charnley realised, as noted above, that one of the main routes for infection was the air in the operating theatre. By addressing this issue and employing occlusive garments for theatre personnel he was able to reduce his infection rates by almost 20 times.12,13

Common contaminants in the found operating room (From Davis et al.23)

Relationship between material implanted and infection risk (From Petty et al.22) Implant

Staphylococcus epidermidis ID50

Polymerised PMMA in vivo Polymerised PMMA HDP and stainless steel Cobalt Chrome Control

104 106 108 109 109

PMMA– polymethyl methacrylate. HDP– high density polyethylene. ID50 – Number of bacteria necessary to produce infection in 50% of cases.

Frequency (%)

Coagulase negative staphylocci Viridans type streptococci Micrococcus spp. Pseudomonads spp. Diptheroids Bacillus spp. Anaerobic diptheroids Staphylococcus aureus Pasteurella haemolyticum

81.2 4.7 3.8 3.8 1.9 1.9 0.9 0.9 0.9

Table 2

Table 1

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wearer.29 They have been proven to be 95% effective as barriers but once they become damp bacteria can translocate through them via a wick effect. Masks should be changed between cases. While each member of the operating team should wear a mask, there is no evidence that personnel outside the operating field need to wear them in order to decrease infection.32

Blowers’ produced a report for the Medical Research Council in 196829 which highlighted the main risk factors for deep infection in orthopaedic surgery. These factors are as relevant today as they were at the time they were written. They include:

Theatre personnel These should be kept to a minimum. The MRC trial found that wound contamination was much higher in cases where there were 15 persons in the operating room compared to cases where there were 6 persons. Up to 40% of the population are nasal carriers of coagulase positive S. Aureus and 12% carry it on their perineum. The hands, hair and ears are also heavily contaminated with multiple species in healthy subjects.19 These organisms are scattered into the air in many ways. Sneezing disperses 39,000 organisms while 710 are released by coughing. Thirty six organisms are dispersed by speaking at 100 words per minute.18 These numbers all increase proportionately with the number of persons in the operating theatre.

Gloves and hand washing Davis et al.23 showed that 29% of gloves are contaminated after draping the patient. Also, 50–67% of outer gloves are perforated during arthroplasty procedures.33 Double gloving and the use of cotton over-gloves have been shown to reduce this incidence between 3–9 times.34,35 The wearing of rings is associated with a higher rate of glove perforation, but not directly with increased bacterial loads or rates of wound infection. This information has led not only to the routine practice of double gloving for major procedures by most surgeons but also frequent changes of the outer glove. It is universally accepted that infection can be spread by direct contact. Handwashing with povidone iodine and/or 4% chlorhexidine is practiced throughout the UK. O’Shaugnessy et al. showed that 2 minutes is the optimal time for handwashing and no benefits are gained after this.36 They also found that washing with 4% chlorhexidine reduces hand contamination by as much as 80%. This effect was cumulative with progressive washes.

Movement Quite apart from the number of persons in the operating theatre, movement of each person has been identified as a risk factor for infection.30 Increased movement (i.e. running versus walking) increases the number of skin squames shed. Without any movement 109 squames are shed from the skin of each person daily. These originate mainly from the perineal region and are caused by the friction of clothing on skin below the waist. Each squame breaks into smaller particles, 10% of which are less than or equal to 10μm, the majority being 12–14 μm. Each squame is capable of transporting up to 4 bacteria.19 Large numbers of personnel within the operating room therefore increase the number of squames and the risk of an infection. Unnecessary movements should therefore be discouraged.

Operating theatre air quality Pasteur realised the important infection risks posed by contaminated air. Lister, in 186737 revealed that he had adopted Pasteur’s views. He used carbolic spray to disinfect the air. This measure alone led to a 31% decrease in the mortality rate after lower limb amputations. Improvements in aseptic surgical techniques and ventilation have since made carbolic spray redundant, but the principles of antisepsis remain the same. One of the major advances in air decontamination was the use of ultraviolet (UV) light, pioneered in the USA. Infection rates at Duke University were 11.3% and mortality rates 1.4% due mainly to staphylococci and streptococci. These rates fell to 0.24% with the use of UV light.38 Lowell39 found that the use of UV light at intensities of 25–30 μwatts/cm2 led to a 5 and 30 fold decrease in infection rates for total hip and total knee arthroplasties respectively. While the above levels of UV radiation have been chosen for health and safety reasons, more recent authors have used intensities of up to 300 μwatts/cm2 without noticing any side effects.40 Lidwell has also reported that in clean theatres a similar level of decontamination can be achieved with either ultra clean air ventilation or UV light at 300 μwatts/cm2. Berg et al.’s results were even better – they showed that colony counts in air treated with UV light at 290 μwatts/cm2 were less than those in theatres with Charnley-Howarth vertical laminar flow enclosures.41 Taylor et al.42 performed a similar study in a plenum ventilated theatre using UV light at 300 μwatts/cm2. They looked at colony counts on the wound edges and in theatre air during THR surgery. The UV light was left off for the first 15 minutes of the procedure then turned on. They found high levels of air and

Theatre clothing Traditionally this has been the same for all personnel and included cotton shirts and trousers, hats, masks and shoes. Balloon cotton, from which the garments are manufactured, has an average pore size of 80 μm and therefore provides no barrier to skin squames. Modern garments made from woven synthetic fibres offer far superior protection. Gore-Tex has an average pore size of 0.2 μm and polyester is almost as good. This computes to a 1000 fold improvement in their efficiency as barriers to bacteria.28 The recommended number of cycles of cleaning for polyester garments is 70 after which they should be discarded. Theatre hats are mandatory for all personnel. These are particularly important in laminar flow environments where they decrease contamination of downstream air up to 15 fold.19 Bannister thought that these might have little value outside laminar flow theatres but Hughes and Anderson31 thought that it was necessary not only to wear a hat, but a hood which covered all hair, including facial hair.

Face masks Face masks have been shown to reduce infection rates by up to 7 fold. These deflect bacteria from the respiratory tract of the

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wound contamination without UV light but after 15 minutes of UV light exposure these areas were sterile. These benefits are augmented by the fact that UV light is relatively cheap and easy to install and run when compared to laminar flow systems. It does have downsides however. The National Research Council of North America, in a controlled trial, found little benefit using UV light in clean cases and no benefit when using on previously contaminated wounds.19 The efficacy of UV light is also decreased in the presence of blood.42 There are also Health and Safety implications, as all exposed skin of theatre staff must be protected. The operating team need to wear 2 caps and all theatre personnel must wear visors. This method is currently being used in some European and North American centres but has not gained widespread popularity in the UK. Its cost benefit is mainly experienced in centres performing less than 200 arthroplasties annually.42 Data from the United Kingdom National Joint registry show that 98% of all hip arthroplasty procedures are carried out in operating theatres equipped with laminar flow technology.

120 100 80 60

Infection rate (%)

40 20 0 2003

2004

2005

2006

Figure 2 Relationship between laminar flow and infection rates in the UK (UK National Joint Registry).

in the broken air stream below his head. This is a situation that is likely to happen throughout surgery. Salvati recorded an increase in infection rates from 1.4 to 3.9%, though he used a horizontal laminar flow system.47 Laminar flow systems are also expensive to install and maintain. Charnley found that ultra clean air systems were most effective when combined with occlusive clothing. This prompted the development of body exhaust suits. These two measures further reduced his infection rates from 1% to 0.6%.13 Lidwell et al. found similar results in the MRC trial with infection rates of 0.75% when the same combination was used.44 Hubble et al.48 found that occlusive clothing alone reduced infection rates to 1%. The disadvantages of body exhaust suits are that they are noisy and are reported to be uncomfortable. Whyte et al.49 found that gowns made of closely woven elasticated polyester fibres and balaclava-type hats, which were much more comfortable and easier to use, produced similar reductions in theatre air counts when compared to exhaust suits. Bannister19 noted that ultra clean air systems are most efficient if used in combination with occlusive garments and other methods, including antibiotics. Klenerman et al.50 confirmed this observation with their findings of a 1.1% early infection rate using a combination of ultra clean air and pre operative intravenous cefuroxime in an elderly, susceptible population. Antibiotic prophylaxis is now commonly used throughout the UK in two ways. Pre operative antibiotics are given prior to the initial incision and antibiotic impregnated bone cement is used for cemented components, and in two-stage revision procedures, with the sole purpose of reducing the incidence of deep infection. Burke’s classic study51 revealed that antibiotics were most effective if used prior to bacterial colonisation. His results suggested that there was no benefit from this method beyond 3 hours. Tachdijan and Compere52 found that infection rates were higher in cases in which post operative antibiotics were used. This supported Burke’s findings. Al Buhairan et al.53 found that antibiotic prophylaxis reduced the absolute risk of infection by 8% and the relative risk by 81% compared to not using any antibiotics. Rosenberg et al.54 clearly showed that devoting a specified time to administration of intravenous antibiotics – which in their case was included in the ‘time out’ period during which checks were done to prevent wrong site surgery – significantly improved compliance with antibiotic administration from 65% to 97%.

Air filtration techniques This is the most widely employed method of cleaning theatre air in the UK. In the initial years operating theatre air was replenished with air from adjacent theatre corridors. This proved unacceptable in patients undergoing hip arthroplasty and in other vulnerable groups such as burns patients.5,43 Plenum ventilated theatres formed the benchmark and, using this design, there are 20 air changes per hour. The current standardised method of assessing the efficiency of operating theatres however is by looking at the colony forming units (CFU) of contaminating organisms per cubic metre of theatre air.19 There is an inverse relationship between the numbers of colony forming units and air cycling rates up to 20 air changes per hour – hence the choice of this rate for plenum theatres. Using current techniques plenum theatres are considered efficient if the colony count is 35 CFU/m3 or less.19 Lidwell et al.18 reported an infection rate of 3.4% using plenum ventilation. This figure was similar to Charnley’s own experience in his plenum ventilated unit.13,44 Improvements in air filtration technology led to the introduction of vertical laminar flow enclosures within operating theatres. These systems enable up to 300 air changes per hour and are considered to produce ultra clean air if there are less than 10 CFU/m3 inside the laminar flow zone. This technology led to a further reduction in infection rates to 1% in Charnley’s series and to 1.6% in the series reported in the MRC trial – both significantly down from 3.4%.44 The number of revisions for infected primary total hip replacements in the UK has decreased proportionately with the increased use of laminar flow systems (Figure 2). While these results have been very positive, laminar flow systems can potentially direct contaminants into the wound from operating theatre personnel. Several authors have reported findings to support this possibility. Marotte et al.45 found that laminar flow was only beneficial in preventing infection in cemented THA. There was no benefit in uncemented THA. Taylor and Bannister46 performed an interesting experiment during which a surgeon placed his head in a laminar flow stream. Colony forming units in the air above and below his head were measured and found to be 27 times higher

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Laminar Flow (%)

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trial in the mid 1970’s 30% of isolates yielded this organism and 18% consisted of coagulase negative organisms. By 1981 this relationship started to change, a finding mainly attributed to specific targeting of the coagulase positive organism. By the mid 1980’s there was a full reversal with only 17% of infections being caused by coagulase positive staphylococci.65 By the late 1980’s 77% of cemented THA’s were infected by resistant species. James et al.66 found that the number of multiply resistant strains of Staphylococcus epidermidis was increasing. Methicillin Resistant Staphylococcus aureus (MRSA) has had a significant impact on surgical patients in the UK has been well documented. Up to 40% of S.Aureus strains are methicillin resistant while the prevalence of vancomycin resistant enterococci (VRE) is 23%. It is estimated that such resistant species will be more frequently isolated from cultures taken from infected arthroplasty prostheses.67

Experiments with specific antibiotics started in the early 1970’s. Ericson managed to eliminate surgical site infections using cloxacillin pre operatively and for 2 weeks post operatively in patients undergoing total hip arthroplasty.55 Hill et al.56 had similar results using cefazolin pre operatively and for 5 days post operatively. It is common practice in many units across the UK to use 3 intravenous doses of cefuroxime, one dose pre operatively and 2 further doses at 8 and 16 hours post operatively. The minimum number of doses investigated in high level studies has been 5. Bannister also notes that one dose is inadequate for bone penetration.19 Wymenga’s findings support this. He compared one versus three doses of cefuroxime and found that infection was almost twice as prevalent in the one dose group.57 Results from the MRC trial showed that infection rates in the cohort treated with cephalosporins was 0.3% versus 0.75% in the cloxacillin treated group.19 This popularised the use of cephalosporins – a practice which is still widely practiced. Antibiotics are also mixed into bone cement for the purpose of reducing infection in cemented THA. Joseffson et al.58 reported a 4 fold reduction in deep infection rates from 1.6% to 0.4% with the prophylactic use of gentamicin impregnated bone cement. Joseffson and Kolmert59 also showed that gentamicin impregnated cement lost its effectiveness by 10 years. Block and Stubbs60 found that antibiotic impregnated bone cement was consistently more effective at reducing deep infection when compared to plain cement based on results from 22 studies. Bone cement provides an economical medium for introducing antibiotics directly to where they are needed. Along with gentamicin, both oxacillin and cefazolin are released from cement in biologically active forms. This is dependent on the type of cement used however, as antibiotics elute for longer periods and at higher doses from Palacos cement (Zimmer, Warsaw, Indiana) than from Simplex P, Sulifix (Zimmer, Warsaw, Indiana) or Simplex (Stryker, Kalamazoo, Michigan) cements.61,62 Hanssen and Spengehl62 advise that cement should be prepared specifically according to its intended use. Low dose cement (1 to 2 g of antibiotics/40 g cement) should be used for prophylaxis and more than 2 g of antibiotics/40 g cement for therapeutic beads and spacers. In keeping with the findings of Dunne et al. they note that adding greater than 4.5 g of antibiotics/40 g cement weakens the cement structure and should not be used for fixation. Their results strongly supported the use of antibiotic impregnated cement as a means of reducing deep infection in primary THA. Dunne et al.63 impregnated a 40 gm block of Palacos R bone cement with 1, 2, 3 and 4 grams of gentamicin sulphate and found that, as expected, the amount of gentamicin released over 72 hours increased with amount of antibiotic added. There was, however, a significant decrease in the compressive and four part bonding strength of the cement as the amount of antibiotic increased in vitro. Similar studies have also shown that lyophilised vancomycin also significantly reduces the number of cycles to failure of cement.64 The beneficial effect of preventing formation of the bacterial biofilm was not apparent after 3 days. Possibly the most important side effect of generalised use of antibiotics has been the emergence of resistant organisms. Coagulase positive streptococci comprise the major group of infecting organisms. This organism was responsible for 50% of infection in Charnley & Eftekhar’s series in 1969.5 In the MRC

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Pulse lavage Hope et al.68 reported that pulsatile lavage removes up to 87% of all organisms from wounds. Taylor et al.,69 using animal tissue models, found that 79% and 57% of organisms were removed from fat and muscle respectively by pulsed lavage. When combined with 0.05% chlorhexidine its efficacy increased to 98%. This was responsible for a 0.45% infection rate in patients undergoing THA at the Bristol Unit.70 Some studies have found chlorhexidine based aqueous scrubs71 to be more effective than povidone iodine based solutions in reducing the numbers of colony forming units (CFU’s) on the hands, but the evidence is not conclusive in this area. It must be remembered, however, that chlorhexidine is harmful to exposed cartilage and meninges and therefore needs to be used with due care.

Skin decontamination and preparation High bacterial skin counts are a source of wound contamination.19 Deacon et al.72 also noted that skin infections and decubitus ulcers can be a source of early haematogenous seeding of infection. O’Shaugnessy et al.36 found that sending patients for two showers with antiseptic solution correlated with a decrease in wound infections. There was no difference in wound infection rates between the control patients (surgical site infection rate 11.7%), those using chlorhexidine (9%) and those using soap (12.8%) however. Webster and Osborne73 reviewed the results of over 10,000 patients, all of which had pre operative showers with 4% chlorhexidine. There was no significant difference between this and placebo or soap and only one study found it to be better than no bathing at all. Hair removal pre operatively is also a potential source of infection. Wet shaving, clipping and depilatory creams all produce less skin excoriation and correspondingly fewer infections than dry shaving. Dry shaving the night prior to surgery is associated with the highest risk of infection (GB). Neither Cruse and Foord74 nor Edwards et al.75 found any reduction in infection with the use of plastic skin drapes or iodophor impregnated plastic drapes respectively. Fairclough et al.76 found that application of ioban drapes to the incision site 24 hours prior to surgery reduced infection rates from 15% to 1.6%. 12

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Mini-symposium: What’s new in hip replacement — Basic principles

surgery. In many cases revision is a two stage procedure, each stage being a major invasive procedure. None of these, however, compare to the human cost of risks to the patient, dissatisfaction and depression.19 The most expensive measures for prophylaxis include vertical laminar flow systems, exhaust body suits, antibiotic impregnated bone cement and intravenous antibiotics.19 Other, more inexpensive but effective measures include ultraviolet light, 4% chlorhexidine for skin and hand preparation and a syringe and broken needle for lavage. This has the same effect as expensive pulse lavage systems. The actual cost of an infected primary THR cannot be fully estimated due to its far reaching impact. Prevention of infection is economically favourable to all possible interventions. While all measures have their own merits, it is a combination of prophylactic measures which is most effective for prevention of infection in THA.

Patient transfer This is an easily overlooked route for introduction of contaminants. Patients are usually transferred to a clean trolley with clean linen to avoid contamination of the air in the anaesthetic room from the patient’s blankets, clothes and bed.77 This is particularly important when instruments are exposed in the operating theatre or the theatre is poorly ventilated.

Surgeon related factors The contribution of surgeon factors to surgical site infections has been widely studied. Infection rates vary with the duration of surgery, with rates of 2.6% for procedures lasting up to one hour, 4.9% for those 1–2 hours long, and 8.5% for those lasting more than 3 hours.78 This correlates with the observation that skin preparation is only effective for 3 hours, increasing the risk of infection after this period. While it is known that shorter operating times are a function of experience, Bannister suggested methods more junior surgeons can employ in order to expedite their procedures including planning the procedure, being familiar with the instruments and making sure that the nursing staff are likewise familiar with them.19 Infection rates also vary among experienced surgeons. In a single large unit with equal case mix, Taylor70 found more than a six fold difference among consultants. Bannister et al.19 also found correlation of infection rates with specific surgeons.

Guidelines In the UK recommendations have been made by the British Orthopaedic Association (BOA) and the National Institute of Health and Clinical Excellence (NICE) on the measures that can be taken to avoid surgical site infections. The BOA84 views the availability of well maintained clean air theatres as being vital for units performing arthroplasty procedures. Hair must be covered at all times and masks worn at all times while in theatre and the number of persons in the theatre must be kept to a minimum. Persons must enter and leave the theatre via clearly marked doors and traffic to and from dirty areas must be strictly controlled. They specify that all drapes and gowns must be manufactured from impervious material. The NICE guidelines,85 published a decade later (2008) advise that patients should have a bath on the day of, or before, their procedure and warn against routine hair removal and nasal decontamination of MRSA in order to minimize the emergence of resistant organisms. Electric clippers should be used to remove hair on the day of surgery when necessary. Antibiotic prophylaxis should be given to all patients having arthroplasty procedures. They also advise minimal staff movement within the operating room and advise members of the operating team to remove all hand jewellery, artificial nails and nail polish prior to starting the procedure. Despite the time difference between these publications it is clear to see that their focus is similar. This reflects that the principles of prevention of surgical site infection have remained unchanged and simple measures can make a huge difference to the lives of the surgeon and the patient.

Methicillin resistant Staphlococcus aureus (MRSA) This organism has gained more recent media attention than most other types of infection. Walls et al. reported a 1% incidence at 5 years. There was an 11 fold increase in hospital stay and only 3 of their 16 cases attained a pain free joint. Engemann et al.79 found that patients with MRSA infections had longer and more costly inpatient stays than Methicillin Sensitive Staphylococcus aureus (MSSA). Methicillin resistance is also independently linked to increased mortality.80 Hospital acquired MRSA mainly affects patients with indwelling devices81 which includes the group of elderly and trauma patients requiring orthopaedic surgery. The organisms reach the surface of the implant and form a protective biofilm, allowing colonies to proliferate. Practices including strict screening protocols, barrier precautions and cohort nursing have been adopted in Finland and Denmark, two developed nations with MRSA prevalence rates of only 1%, in order to combat these problems. Hacek et al.82 found that nasal screening and decolonisation with mupirocin reduced the incidence of SSI from 1.7% to 0.77%. Separation of MRSA negative patients and those at low risk from high risk patients significantly reduces the incidence of new MRSA ­infections.83

Summary Infection after total hip arthroplasty (THA) is a complication feared by the patient and surgeon alike. Sequelae of infection include pain, decreased function, dislocation and lengthy revision operations over a protracted period of time. Added to this is the psychological impact on the patient and their generalised dissatisfaction with the operation. While modern surgical techniques and technology have contributed significantly to reductions in infection rates, the principles used today to prevent infection are

Economic aspects of prophylaxis against infection in total hip arthroplasty Infection leads to increased hospital stay and increased use of multiple resources including laboratory personnel, microbiologists, nurses and doctors. The cost of revision surgery and of the prostheses themselves can be up to four times that of primary

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firmly based on the observations of pioneers such as Pasteur and Lister from the mid nineteenth century. ◆

20 Elek SD, Conen PE. The virulence of Staphylococcus pyogenes for man; a study of the problems of wound infection. Br J Exp Pathol 1957 Dec; 38(6): 573–86. 21 Southwood RT, Rice JL, McDonald PJ, Hakendorf PH, Rozenbilds MA. Infection in experimental hip arthroplasties. J Bone Joint Surg Br 1985 Mar; 67(2): 229–31. 22 Petty W, Spanier S, Shuster JJ, Silverthorne C. The influence of skeletal implants on incidence of infection. Experiments in a canine model. J Bone Joint Surg Am 1985 Oct; 67(8): 1236–44. 23 Davis N, Curry A, Gambhir AK, et al. Intraoperative bacterial contamination in operations for joint replacement. J Bone Joint Surg Br 1999 Sep; 81(5): 886–9. 24 Hamilton H, Jamieson J. Deep infection in total hip arthroplasty. Can J Surg 2008 Apr; 51(2): 111–7. 25 Ha’eri GB, Wiley AM. Total hip replacement in a laminar flow environment with special reference to deep infections. Clin Orthop Relat Res 1980 May; 148: 163–8. 26 Howorth FH. Prevention of airborne infection during surgery. Lancet 1985 Feb 16; 1(8425): 386–8. 27 Walls RJ, Roche SJ, O’Rourke A, McCabe JP. Surgical site infection with methicillin-resistant Staphylococcus aureus after primary total hip replacement. J Bone Joint Surg Br 2008 Mar; 90(3): 292–8. 28 Duguid JP. The size and duration of air carriage of respiratory droplets and droplet nuclei. Hygiene Camb 1946; 44: 471–79. 29 Aseptic methods in the operating theatre. A report to the MRC. Lancet 1968; 20: 705–837. 30 Duguid JP, Wallace AT. Air infection with dust liberated from clothing. Lancet 1948 Nov 27; 2(22): 845–9. 31 Hughes SP, Anderson FM. Infection in the operating room. J Bone Joint Surg Br 1999 Sep; 81(5): 754–5. 32 Mitchell NJ, Hunt S. Surgical face masks in modern operating rooms – a costly and unnecessary ritual? J Hosp Infect 1991 Jul; 18(3): 239–42. 33 Lankester BJ, Bartlett GE, Garneti N, Blom AW, Bowker KE, Bannister GC. Direct measurement of bacterial penetration through surgical gowns: a new method. J Hosp Infect 2002 Apr; 50(4): 281–5. 34 Sebold EJ, Jordan LR. Intraoperative glove perforation. A comparative analysis. Clin Orthop Relat Res 1993 Dec; 297: 242–4. 35 Doyle PM, Alvi S, Johanson R. The effectiveness of double-gloving in obstetrics and gynaecology. Br J Obstet Gynaecol 1992 Jan; 99(1): 83–4. 36 O’Shaughnessy M, O’Malley VP, Corbett G, Given HF. Optimum duration of surgical scrub-time. Br J Surg 1991 Jun; 78(6): 685–6. 37 Lister J. On the antiseptic principle in the practice of surgery. Br Med J 1867; ii: 246. 38 Hart D. Bactericidal ultraviolet radiation in the operating room. Twenty-nine-year study for control of infections. J Am Med Assoc 1960 Mar 5; 172: 1019–28. 39 Lowell JD, Kundsin RB, Schwartz CM, Pozin D. Ultraviolet radiation and reduction of deep wound infection following hip and knee arthroplasty. Ann N Y Acad Sci 1980; 353: 285–93. 40 Lidwell OM. Ultraviolet radiation and the control of airborne contamination in the operating room. J Hosp Infect 1994 Dec; 28(4): 245–8. 41 Berg M, Bergman BR, Hoborn J. Ultraviolet radiation compared to an ultra-clean air enclosure. Comparison of air bacteria counts in operating rooms. J Bone Joint Surg Br 1991 Sep; 73(5): 811–5. 42 Taylor GJ, Bannister GC, Leeming JP. Wound disinfection with ultraviolet radiation. J Hosp Infect 1995 Jun; 30(2): 85–93.

References 1 Dreghorn CR, Hamblen DL. Revision arthroplasty: a high price to pay. BMJ 1989 Mar 11; 298(6674): 648–9. 2 Gillespie WJ. Prevention and management of infection after total joint replacement. Clin Infect Dis 1997 Dec; 25(6): 1310–7. 3 Bridges Jr. SL, López-Méndez A, Han KH, Tracy IC, Alarcón GS. Should methotrexate be discontinued before elective orthopedic surgery in patients with rheumatoid arthritis? J Rheumatol 1991 Jul; 18(7): 984–8. 4 Acurio MT, Friedman RJ. Hip arthroplasty in patients with sickle-cell haemoglobinopathy. J Bone Joint Surg Br 1992 May; 74(3): 367–71. 5 Charnley J, Eftekhar N. Postoperative infection in total prosthetic replacement arthroplasty of the hip-joint. With special reference to the bacterial content of the air of the operating room. Br J Surg 1969 Sep; 56(9): 641–9. 6 Schmalzried TP, Amstutz HC, Au MK, Dorey FJ. Etiology of deep sepsis in total hip arthroplasty. The significance of hematogenous and recurrent infections. Clin Orthop Relat Res 1992 Jul; 280: 200–7. 7 Jenkins PJ, Simons TA, Ng CY, Ballantyne JA. Surgical site infection after total hip replacement. J Bone Joint Surg Br 2008; 90-B(Suppl III):533. 8 Canner GC, Steinberg ME, Heppenstall RB, Balderston R. The infected hip after total hip arthroplasty. J Bone Joint Surg Am 1984 Dec; 66(9): 1393–9. 9 Jupiter JB, Karchmer AW, Lowell JD, Harris WH. Total hip arthroplasty in the treatment of adult hips with current or quiescent sepsis. J Bone Joint Surg Am 1981 Feb; 63(2): 194–200. 10 Coventry MB. Treatment of infections occurring in total hip surgery. Orthop Clin North Am 1975 Oct; 6(4): 991–1003. 11 Greene KA, Wilde AH, Stulberg BN. Preoperative nutritional status of total joint patients. Relationship to postoperative wound complications. J Arthroplasty 1991 Dec; 6(4): 321–5. 12 Charnley J. A clean-air operating enclosure. Br J Surg 1964 Mar; 51: 202–5. 13 Charnley J. Low friction arthroplasty of the hip – theory and practice, Berlin/Herdleberg: Springer-Verlag, 1979. 14 Lidgren L. Joint prosthetic infections: a success story. Acta Orthop Scand 2001 Dec; 72(6): 553–6. 15 Fender D, Harper WM, Gregg PJ. Outcome of Charnley total hip replacement across a single health region in England: the results at five years from a regional hip register. J Bone Joint Surg Br 1999 Jul; 81(4): 577–81. 16 Kurtz SM, Lau E, Schmier J, Ong KL, Zhao K, Parvizi J. Infection burden for hip and knee arthroplasty in the United States. J Arthroplasty 2008 Oct; 23(7): 984–91. 17 Phillips GB, Runkle RS. Biomechanical applications of laminar airflow, 1st edn. Cleveland, Ohio: CRC Press, 1973. 18 Lidwell OM, Lowbury EJ, Whyte W, Blowers R, Stanley SJ, Lowe D. Effect of ultraclean air in operating rooms on deep sepsis in the joint after total hip or knee replacement: a randomised study. Br Med J (Clin Res Ed) 1982 Jul 3; 285(6334): 10–14. 19 Bannister G. Prevention of infection in joint replacement. Curr Orthop Dec 2002; 16(6): 426–433.

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43 Bourdillon RB, Colebrook L. Air hygiene in dressing roomsfor burns after major wounds. Lancet 1946; 1: 601–605. 44 Lidwell OM. Air, antibiotics and sepsis in replacement joints. J Hosp Infect 1988 May; 11(Suppl C): 18–40. 45 Marotte JH, Lord GA, Blanchard JP, et al. Infection rate in total hip arthroplasty as a function of air cleanliness and antibiotic prophylaxis. 10-year experience with 2,384 cementless Lord madreporic prostheses. J Arthroplasty 1987; 2(1): 77–82. 46 Taylor GJ, Bannister GC. Infection and interposition between ultraclean air source and wound. J Bone Joint Surg Br 1993 May; 75(3): 503–4. 47 Salvati EA, Robinson RP, Zeno SM, Koslin BL, Brause BD, Wilson Jr. PD. Infection rates after 3175 total hip and total knee replacements performed with and without a horizontal unidirectional filtered airflow system. J Bone Joint Surg Am 1982 Apr; 64(4): 525–35. 48 Hubble MJ, Weale AE, Perez JV, Bowker KE, MacGowan AP, Bannister GC. Clothing in laminar-flow operating theatres. J Hosp Infect 1996 Jan; 32(1): 1–7. 49 Whyte W, Bailey PV. Reduction of microbial dispersion by clothing. J Parenter Sci Technol 1985 Jan-Feb; 39(1): 51–61. 50 Klenerman L, Seal D, Sullens K. Combined prophylactic effect of ultraclean air and cefuroxime for reducing infection in prosthetic surgery. Acta Orthop Belg 1991; 57(1): 19–24. 51 Burke JF. The effective period of preventive antibiotic action in experimental incisions and dermal lesions. Surgery 1961 Jul; 50: 161–8. 52 Tachdjian MO, Compere EL. Postoperative wound infections in orthopedic surgery; evaluation of prophylactic antibiotics. J Int Coll Surg 1957 Dec; 28(6, Part 1): 797–805. 53 AlBuhairan B, Hind D, Hutchinson A. Antibiotic prophylaxis for wound infections in total joint arthroplasty: a systematic review. J Bone Joint Surg Br 2008; 90-B: 915–919. 54 Rosenberg AD, Wambold D, Kraemer L, et al. Ensuring appropriate timing of antimicrobial prophylaxis. J Bone Joint Surg Am 2008 Feb; 90(2): 226–32. 55 Ericson C, Lidgren L, Lindberg L. Cloxacillin in the prophylaxis of postoperative infections of the hip. J Bone Joint Surg Am 1973 Jun; 55(4): 808–13, 843. 56 Hill C, Flamant R, Mazas F, Evrard J. Prophylactic cefazolin versus placebo in total hip replacement. Report of a multicentre doubleblind randomised trial. Lancet 1981 Apr 11; 1(8224): 795–6. 57 Wymenga A, van Horn J, Theeuwes A, Muytjens H, Slooff T. Cefuroxime for prevention of postoperative coxitis. One versus three doses tested in a randomized multicenter study of 2,651 arthroplasties. Acta Orthop Scand 1992 Feb; 63(1): 19–24. 58 Josefsson G, Lindberg L, Wiklander B. Systemic antibiotics and gentamicin-containing bone cement in the prophylaxis of postoperative infections in total hip arthroplasty. Clin Orthop Relat Res 1981 Sep; 159: 194–200. 59 Josefsson G, Kolmert L. Prophylaxis with systematic antibiotics versus gentamicin bone cement in total hip arthroplasty. A ten-year survey of 1,688 hips. Clin Orthop Relat Res 1993 Jul; 292: 210–4. 60 Block JE, Stubbs HA. Reducing the risk of deep wound infection in primary joint arthroplasty with antibiotic bone cement. Orthopedics 2005 Nov; 28(11): 1334–45. 61 Marks KE, Nelson CL, Lautenschlager EP. Antibiotic-impregnated acrylic bone cement. J Bone Joint Surg Am 1976 Apr; 58(3): 358–64. 62 Hanssen AD, Spangehl MJ. Practical applications of antibiotic-loaded bone cement for treatment of infected joint replacements. Clin Orthop Relat Res 2004 Oct; 427: 79–85.

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63 Dunne NJ, Hill J, McAfee P, Kirkpatrick R, Patrick S, Tunney M. Incorporation of large amounts of gentamicin sulphate into acrylic bone cement: effect on handling and mechanical properties, antibiotic release, and biofilm formation. Proc Inst Mech Eng [H] 2008 Apr; 222(3): 355–65. 64 Klekamp J, Dawson JM, Haas DW, DeBoer D, Christie M. The use of vancomycin and tobramycin in acrylic bone cement: biomechanical effects and elution kinetics for use in joint arthroplasty. J Arthroplasty 1999 Apr; 14(3): 339–46. 65 Carlsson AK, Lidgren L, Lindberg L. Prophylactic antibiotics against early and late deep infections after total hip replacements. Acta Orthop Scand 1977; 48(4): 405–10. 66 James PJ, Butcher IA, Gardner ER, Hamblen DL. Methicillin-resistant Staphylococcus epidermidis in infection of hip arthroplasties. J Bone Joint Surg Br 1994 Sep; 76(5): 725–7. 67 Garvin KL, Hinrichs SH, Urban JA. Emerging antibiotic-resistant bacteria. Their treatment in total joint arthroplasty. Clin Orthop Relat Res 1999 Dec; 369: 110–23. 68 Hope PG, Kristinsson KG, Norman P, Elson RA. Deep infection of cemented total hip arthroplasties caused by coagulase-negative staphylococci. J Bone Joint Surg Br 1989 Nov; 71(5): 851–5. 69 Taylor GJ, Leeming JP, Bannister GC. Effect of antiseptics, ultraviolet light and lavage on airborne bacteria in a model wound. J Bone Joint Surg Br 1993 Sep; 75(5): 724–30. 70 Taylor GJ, Bannister GC, Calder S. Perioperative wound infection in elective orthopaedic surgery. J Hosp Infect 1990 Oct; 16(3): 241–7. Erratum in: J Hosp Infect 1991 Feb;17(2):155. 71 Tanner J, Swarbrook S, Stuart J. Surgical hand antisepsis to reduce surgical site infection. Cochrane Database Syst Rev 2008 Jan 23(1): CD004288. 72 Deacon JM, Pagliaro AJ, Zelicof SB, Horowitz HW. Prophylactic use of antibiotics for procedures after total joint replacement. J Bone Joint Surg Am 1996 Nov; 78(11): 1755–70. 73 Webster J, Osborne S. Preoperative bathing or showering with skin antiseptics to prevent surgical site infection. Cochrane Database Syst Rev 2007 Apr 18(2): CD004985. 74 Cruse PJ, Foord R. The epidemiology of wound infection. A 10-year prospective study of 62,939 wounds. Surg Clin North Am 1980 Feb; 60(1): 27–40. 75 Edwards PS, Lipp A, Holmes A. Preoperative skin antiseptics for preventing surgical wound infections after clean surgery. Cochrane Database Syst Rev 2004; (3): CD003949. 76 Fairclough JA, Johnson D, Mackie I. The prevention of wound contamination by skin organisms by the pre-operative application of an iodophor impregnated plastic adhesive drape. J Int Med Res 1986; 14(2): 105–9. 77 Bourdillon RB, Colebrook L. Lancet 1946; 1: 561–601. 78 Pavel A, Smith RL, Ballard A, Larsen IJ. Prophylactic antibiotics in clean orthopaedic surgery. J Bone Joint Surg Am 1974 Jun; 56(4): 777–82. 79 Engemann JJ, Carmeli Y, Cosgrove SE, et al. Adverse clinical and economic outcomes attributable to methicillin resistance among patients with Staphylococcus aureus surgical site infection. Clin Infect Dis 2003 Mar 1; 36(5): 592–8. Epub 2003 Feb 7. 80 Patel A, Calfee RP, Plante M, Fischer SA, Arcand N, Born C. Methicillin-resistant Staphylococcus aureus in orthopaedic surgery. J Bone Joint Surg Br 2008 Nov; 90(11): 1401–6. 81 Wertheim HF, Vos MC, Ott A, et al. Risk and outcome of nosocomial Staphylococcus aureus bacteraemia in nasal carriers versus noncarriers. Lancet 2004 Aug 21–27; 364(9435): 703–5.

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83 Biant LC, Teare EL, Williams WW, Tuite JD. Eradication of methicillin resistant Staphylococcus aureus by “ring fencing” of elective orthopaedic beds. BMJ 2004 Jul 17; 329(7458): 149–51. 84 www.boa.ac.uk 85 www.nice.org.uk

82 Hacek DM, Robb WJ, Paule SM, Kudrna JC, Stamos VP, Peterson LR. Staphylococcus aureus nasal decolonization in joint replacement surgery reduces infection. Clin Orthop Relat Res 2008 Jun; 466(6): 1349–55. Epub 2008 Mar 18.

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(iii) Patient selection and consent

not a life saving operation, but an operation to improve quality of life. There are no short cuts in the assessment of a patient and a full history and examination are necessary before considering management options. In most cases, patients will have already tried non-operative means of managing their symptoms before presenting to a surgeon.

CR Gooding FS Haddad

Patient assessment History Patient selection starts with the patient’s history. In most cases the main indication for hip arthroplasty is pain, specifically groin pain, although other symptoms such as reduced hip flexion can make dressing and performing pedicure difficult. From the history it is possible to characterize the pain in terms of severity, site and precipitating, exacerbating and relieving factors. Pain that is particularly severe often wakes the patient from sleep at night. Constant pain, particularly at night, is exhausting and often persuades the most unwilling patient into a hip operation. It can be unclear whether the patient’s pain is coming from the hip or from elsewhere. Hip pain is usually felt in the groin, but it may radiate to the buttock and down to the knee. Very occasionally a degenerate hip may present as a painful knee alone, which can ‘catch out’ the unwary. Often patients complain of ‘hip pain’ but on close questioning may point to the lateral aspect of their hip and recall that the pain radiates down the back of their leg. This is classically nerve root pain, which may result from a posterolateral disc prolapse or facet joint degeneration. An L3-4 disc tends to cause anterior thigh pain whereas an L4-5 or L5-S1 disc results in pain that radiates below the knee with associated numbness and tingling. Pain secondary to a degenerate disc is often in the lower back, buttock and posterior aspect of the thigh. Pain from spinal stenosis is often associated with thigh weakness and pain, heaviness or weakness on walking (spinal claudication), which starts proximal to distal unlike vascular claudication which is distal to proximal. Some patients with bilateral hip disease present with back pain secondary to hip stiffness and a compensatory lumbar lordosis. There are other mimics of hip joint pain, although they are less common (Table 1). Meralgia paraesthetica from lateral femoral cutaneous nerve compression may result in anterolateral thigh pain; this is always associated with numbness and can be confused with L3-4 disc herniation. The piriformis syndrome is rare and is often associated with patients with spasticity. These patients complain of buttock pain associated with some local tenderness, with their symptoms exacerbated by hip abduction in extension and internal rotation. Pain from trochanteric bursitis is usually located just behind the greater trochanter without any associated muscle weakness or loss of movement. There may be other causes for pain over the lateral aspect of the hip. Persistent pain and weakness in this region may be due to deficiencies in the tendon attachments of the gluteus medius or minimus. Tears of the gluteus medius and minimus tendons share similarities to tears of the rotator cuff tendons in the shoulder. As with cuff tears in the shoulder, it has been suggested that these “rotator cuff tears” of the hip are attritional

Abstract Appropriate patient selection and consent for a total hip replacement or hip resurfacing is a serious undertaking and one that should not be taken lightly. From the patients’ first presentation, we cover the common pitfalls that can be encountered in the patients’ history and examination as well as specific indications and contraindications to hip resurfacing and hip replacement. Possible alternatives to arthroplasty are discussed ranging from simple analgesia to the more controversial treatments such as hyaluronic acid injections. The different options available for a total hip replacement are considered including the choice of a cemented or uncemented implant, the bearing surface and the reasons for making those choices. Unfortunately hip arthroplasty is not without risk and these potential complications are discussed. The incidence of a lower extremity thrombosis has been quoted as high as 70% but this can be mitigated with thromboembolic prophylaxis. The risk of infection varies from approximately 0.4 to 1.5%.The risk of dislocation between 0 and 2% and fracture less than 1%. Nerve injury can be as high as 3% but is commonly quoted nearer to 1%, and is higher in revision operations at up to 4 %. As well as possible complications, patients should also be made aware of the normal post-operative course from what to expect when they wake up to the type of tests they will have in their immediate postoperative recovery. With the pressures of clinic and operating lists it can be all to easy to rush through these important issues, however, time invested at this stage of the proceedings is well spent.

Keywords arthroplasty; complications; consent; examination; history; indications; patient selection; total hip replacement

Introduction When considering any surgical intervention, there must be a consensus between the patient and surgeon that there is a significant chance for improvement in the patient’s symptoms if the ­procedure is performed. This is particularly important when ­considering an operation such as a hip arthroplasty, which is

CR Gooding BSc MD FRCS (Tr & Orth) is a Specialist Registrar at University College London Hospital, UK. FS Haddad BSc MCh(Orth) FRCS Ed FRCS(Tr & Orth) is a Consultant Orthopaedic Surgeon, University College London Hospital, UK.

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Mini-symposium: What’s new in hip replacement — basic principles

Another helpful indicator as to how patients’ symptoms affect their quality of life is their level of activity. Patients who are house bound because of their pain tend to be at the more severe end of the spectrum compared to those who get some discomfort after a day’s work or after sport. There are specific questions to ask if the patient is of working age. The type of work they do is important, whether they plan early retirement because of their hip problem or if they are considering a change of career so that they can work around their symptoms, helps with the planning process. Some patients are self-employed and can ill afford to take time off to recuperate from a hip operation and would prefer to explore non-operative means to ‘tide them over’ until they either retire or can make provision for taking time off work. With this line of inquiry, one is able to guide the patient as to the timing of surgery, the type of hip arthroplasty and possible job modification. As well as the history of the presenting complaint, the past medical history must be elucidated, to uncover any possible risks posed by an anaesthetic, or previous history of a thromboembolic disorder, for example. A note should also be made of any relevant childhood disorders such as congenital dislocation of the hip (usually noted at birth), septic arthritis (characteristically presents at 0 to 5 years of age), tuberculosis of the hip, Perthes’ disease (aged 5 to 10 years), slipped capital femoral epiphysis (aged 10 to 15 years) as well as protrusio acetabuli (if it affects both sides, it is called Otto pelvis). A detailed family history should be taken. Patients with congenital dislocation of the hip have a 12 to 33% positive family history1,2 and 6% of patients with Perthes’ disease have a positive family history.3 Metal allergy has been correlated with osteolysis and aseptic loosening of implanted metal hardware.4–7 However, statistical reviews of cases involving adverse reactions after implantation of metal hardware have shown that metal sensitivity is the cause in less than 0.1% of cases in which sensitivity reactions exist.5,8,9 Therefore, the clinical significance of metal sensitization remains a question. Nonetheless, it is important to be aware of the potential problem, and when other more common causes of implant failure have been excluded, the possibility of an allergic reaction to the metal must be considered, evaluated, and treated.

Possible causes for hip pain Differential diagnosis of hip pain In the young adult Labral tear Femoroacetabular impingement Psoas impingement Snapping hip Piriformis syndrome Enthesopathy of Obturator Internus Loose Bodies Avascular necrosis (eg secondary to alcohol excess, steroids, blood disorders such as sickle cell anaemia) Gluteus medius or minimus tears Trochanteric bursitis Meralgia paraesthetica Inflammatory arthritis Infective (eg Staphylococcus aureus) Non-infective (seropostive eg rheumatoid arthritis; seronegative eg ankylosing spondylitis, psoriatic arthritis, reactive arthritis; crystal arthropathies eg gout and pseudogout) Osteoarthritis Primary Secondary (eg trauma) Osteoporosis (insufficiency fractures) Pelvic and Abdominal pathology Aortic aneurysm Pelvic inflammatory disease Kidney stones Swollen lymph nodes Hernia (eg femoral, inguinal) Pain radiating to the hip Nerve root impingement (eg secondary to degenerative arthritis of the spine, intervertebral disc pathology) Sacro-iliac joint inflammation Knee pathology Tumours Benign (eg pigmented villonodular synovitis) Malignant (eg metastases)

Examination From the physical examination the type and degree of deformity, the gait, the presence of weak abductors, fixed flexion deformity, range of movement, leg length as well as the condition of the skin should be documented. A neurovascular examination should also be made as well as an assessment of the spine, the opposite hip and ipsilateral knee. The first sign of hip pain is pain on internal rotation with the hip flexed at 90 degrees. With disease progression, rotation in flexion is lost, associated with leg shortening, fixed flexion deformity and the affected limb fixed in external rotation.

Table 1

injuries associated with increasing age. Physical examination may reveal a mild Trendelenberg gait, pain, and weakness with resisted abduction of the hip when compared to the other side. The combination of abductor weakness, persistence of symptoms after non-­operative management and magnetic resonance imaging findings of a high signal within the tendon, confirms the diagnosis of an abductor tear. One must not forget the more sinister causes of hip pain. The femoral neck and proximal femur are common sites for metastatic deposits. Neoplastic pain is non-mechanical, patients complain of pain at rest unless of course there is an impending pathological fracture, in which case they will have pain on weight-bearing.

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Investigations One of the key investigations is an antero-posterior plain radiograph of the pelvis and a lateral of the affected hip. The view of the femur should include the upper half of the femur and well beyond the proposed area where the femoral stem of the hip 18

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Mini-symposium: What’s new in hip replacement — basic principles

arthroplasty will finish; this is best gauged using templates. In the recent literature some authors have suggested that an anteroposterior pelvic radiograph with the patient supine and with both legs internally rotated by 15 degrees in order to maximise the length of the femoral neck is the best view.10 However, the obvious benefits of taking an antero-posterior pelvic radiograph with the patient standing is that the surgeon is able to see the hip joint with the hip in its functional role, which gives a better representation of the degree of joint space narrowing. A cross table lateral radiograph with the patient supine and with the contralateral hip and knee flexed beyond 80 degrees and the symptomatic hip internally rotated 15 degrees to expose the antero-lateral surface of the head-neck junction is helpful since this part of the femoral head is not seen on the antero-posterior radiograph. As the magnification of antero-posterior radiographs of the pelvis is variable, placing a marker ball of known diameter in the plane of interest between the patient’s thighs will help correct for this. As most radiographs are now digital, the surgeon can accurately scale these images and then template using commercially available software.11 If more information is needed regarding the bony architecture then a CT scan can be useful. Features to identify from the radiograph include the loss of joint space, femoral head migration, acetabular dysplasia, presence of a medial osteophyte, cysts, as well as general bone quality. The Singh’s index can be used to make an objective assessment of bone density and possible osteoporosis.12 Dorr’s classification13 can also be helpful, which may alter the choice of femoral implant or the method chosen for securing it. With regards to femoral head migration, there are 4 directions: superiorly and laterally, superiorly, medially and medially and inferiorly. The cause of the latter is difficult to attribute. Symptomatically, patients complain of significant pain much earlier than would be expected. Concentric arthritis tends to be seen with an inflammatory arthropathy, such as rheumatoid arthritis. An adequate history and examination together with appropriate radiographs are sufficient in the majority of patients who present with hip pain. However, questions may remain if the patient’s symptoms appear out of proportion to their examination and radiographic findings, and further investigations or referral to another specialty may be necessary. If there is any doubt then bone scans, CT and MRI scans can be helpful and the MR-arthrogram should not be overlooked in the patient with normal radiographic findings with severe hip pain, especially on flexion, adduction and internal rotation, suggestive of a labral tear. Other more invasive procedures can also be helpful. Patients who have co-existing back pain as well as complaining of hip pain can pose a problem. To put a patient through a hip replacement and only then discover that their symptoms originate from their back is clearly a disaster to be avoided. To resolve this problem, patients can have an image guided injection of steroid and local anaesthetic into the hip joint. Patients are asked to record what, if any, pain relief they get from the procedure and how long it lasts. Alternatively, a hip arthroscopy can also be useful in the determining the cause of hip pain. This can be performed as a day case procedure enabling a comprehensive assessment of the hip articular surface. As well as the diagnostic benefits of this procedure, certain therapeutic manoeuvres are also possible, such as resection of labral tears and/or ­ debridement of

ORTHOPAEDICS AND TRAUMA 23:1

cam lesions or osteophytes in the mild to moderately osteoarthritic hip.

Non-operative management Once the surgeon is clear in his/her own mind as to the diagnosis, the next step is to construct a management plan. One should determine whether there has been an adequate trial of nonoperative measures such as the use of anti-inflammatories, weight-loss, use of walking aids and activity modification. Patients often ask about glucosamine and chondroitin sulphate. It is hypothesized that glucosamine stimulates the production of cartilage extra-cellular matrix and that chondroitin inhibits the production of cartilage proteolytic enzymes as well as reducing inflammation. So far it has not been determined whether glucosamine offers any advantages over established drugs such as acetaminophen, traditional NSAIDS, or selective Cox-2 inhibitors.14 One of the largest clinical trials, the Glucosamine/chondroitin Arthritis Intervention Trial (GAIT), has produced two sets of negative results. In 2006, the researchers reported on a 24-week study that involved 1583 patients who were randomly assigned to receive 500 mg of glucosamine hydrochloride three times daily, 400 mg of sodium chondroitin sulfate three times daily, 500 mg of glucosamine plus 400 mg of chondroitin sulfate three times daily, 200 mg of celecoxib (Celebrex) daily, or a placebo. The study found that glucosamine and chondroitin, alone or together, did not reduce osteoarthritis knee pain more effectively than a placebo whereas the celecoxib group did about 17% better than the placebo group.15 Regarding the efficacy of hyaluronic acid injections, the majority of studies have been performed on the knee and one of the best studies is a meta-analysis performed by Lo et al. In this paper they concluded that intra-articular hyaluronic acid has a small effect when compared with an intra-articular placebo. Although they did add that the presence of publication bias may suggest that even this effect may be an overestimation.16 However, the results from studies looking at intra-articular injections of hyaluronic acid into the hip seem to have shown better results. Fufulas et al compared two groups: the first group were given Nimesulide (an NSAID) and the other group were given 5 injections of hyaluronic acid. They concluded that the patients given the hyaluronic acid had a better amelioration of their pain and their relief lasted longer.17

Surgical management Pre-operative considerations If non-operative measures have failed, then it is important to determine whether the patient is realistic regarding the risks, benefits and possible limitations associated with hip arthroplasty. A labourer with a degenerate hip who lifts heavy objects on a regular basis and who needs to run and jump should be advised that these activities are not advisable post hip replacement. It is also useful to assess at this stage whether a patient will comply with precautions to reduce the risk of hip dislocation and to avoid high impact activities to reduce the risk of polyethylene wear and loosening. Patients should be adequately pre-assessed to ensure that they are medically fit. Patients should be evaluated to ensure that conditions such as hypertension, ­pulmonary 19

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Mini-symposium: What’s new in hip replacement — basic principles

disease and cardiac disease are optimally controlled. Careful assessment of the patient’s extremities for skin lesions such as venous ulcers, areas of psoriasis and infected toenails should be made. These conditions should be treated before considering hip arthroplasty. Other infective conditions such as UTI and dental caries should also be treated before considering an elective hip arthroplasty. Any condition which may predispose the patient to an increased risk of infection such as rheumatoid arthritis18 and other autoimmune conditions should be noted. Historically, diabetes was thought to be a risk factor for deep infection but Chan et al found that this was not the case, although these patients were at increased risk of a prolonged hospital stay.19 Additionally, a comprehensive drug history must include details of any anticoagulants including clopidogrel, which should be stopped 14 days before elective surgery in discussion with the patient’s cardiologist. Immunosuppressants can be an issue, although those patients taking disease modifying drugs for rheumatoid arthritis are at risk of greater morbidity from stopping them and a resultant rheumatoid flare, rather than deep infection. Also, patients who have been on long-term steroids may require additional steroid support peri-operatively due to their impaired stress response. It is best to liaise with the patient’s rheumatologists as well as the anaesthetist well in advance before considering altering their medical management. Procedure selection Once the surgeon is happy that the patient is an appropriate surgical candidate, then the next step is to determine which surgical intervention is appropriate for the patient. Some patients with early degenerative changes affecting only part of the articular surface and who also have mechanical abnormalities may benefit from pelvic or femoral osteotomies. The young patient with unilateral hip disease and complete loss of articular cartilage, who has a physical job may benefit from an arthrodesis. At the other end of the scale, patients with poor ambulation who are not very fit may be candidates for a resection arthroplasty. However this is more of a salvage procedure and is rarely performed nowadays. Once the decision has been made to proceed with a hip arthroplasty, the surgeon is faced with a number of options. Broadly speaking, those choices fall between hip resurfacing (Figures 1a and b) and total hip arthroplasty (Figure. 2a and b). Resurfacing represents 10% of all total hip replacements in England and Wales.20 Men who are younger than 65 years of age have similar survival curves after resurfacing than they do after THR, 98% at a mean follow up of 5 years.21 However, a higher risk of shortterm failure has been demonstrated in men older than 65 years and in all women (this appears to be particularly linked to small femoral head sizes). In the Australian hip registry, hips that had evidence of developmental dysplasia, inflammatory arthritis or osteonecrosis did not do as well as those that underwent resurfacing for osteoarthritis. The main cause for failure is femoral neck fracture, with the Australians reporting a rate of 1% in men and 2% in women.22,23 Recent studies have suggested that it is not whether the patients are male or female that predisposes to fracture but femoral neck diameter or head size used.24 There have been a number of studies looking at the selection criteria for resurfacing.25–29 Exclusions should include patients with known metal allergies or altered renal function. Inflammatory arthritis,

ORTHOPAEDICS AND TRAUMA 23:1

60-year-old male with osteoarthritis of his right hip. Post-operative radiographs show a right hip resurfacing (Birmingham hip resurfacing). Figure 1

developmental hip dysplasia in women, women of child bearing age and limb length discrepancy of more than 2 cm are relative contraindications for the procedure. Radiographic factors that can make resurfacing more of a challenge include a short femoral neck, a high riding greater trochanter or a decreased head-neck ratio (large neck relative to head, increasing the chance of notching).30 Areas of controversy include those patients with osteonecrosis. In most patients with osteonecrosis of the femoral head, the osteonecrosis does not involve the entire head. Several studies have reported favourable results in this patient group.31–33 Beaule et al went further and developed a Surface Arthroplasty Risk Index (SARI) based on a 6 point scoring system: femoral head cyst >1 cm = 2 points; weight ≤82 kg = 2 points; previous hip surgery = 1 point and the University of California (UCLA) activity score >6 = 1 point. A SARI score >3 represented a 12 times increased risk in early failure or adverse radiologic changes in patients of 40 years of age or less.27 20

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Mini-symposium: What’s new in hip replacement — basic principles

of metal ions could be minimised with optimal orientation of the acetabular ­component.35 Implant selection When it comes to deciding what type of total hip arthroplasty to offer a patient the choices are between an uncemented, cemented or hybrid replacement. On the acetabular side there have been a number of prospectively randomised studies comparing cemented and cementless sockets. However, most studies in this area have been carried out over the short term and show little difference between the two techniques.36 However, a report from the Norwegain Hip register of 73,000 arthroplasties revealed that uncemented sockets with more than 6 years follow-up, have an overall increased revision rate compared to cemented cups due to wear and osteolysis; this observation was particularly prevalent in young patients.37 This last study was published in 2000; more recently, with the advent of highly cross-linked polyethylene liners with better wear characteristics, the uncemented socket has gained in popularity. When it comes to the femoral stem however, the choices are not so cut and dry. Cemented stems have evolved considerably since the 1970’s, and with improved cementing techniques this has proven to be a very durable option. However, cemented fixation was found to be less successful in young, active patients and in heavier patients. Most surgeons use the cemented option in the smaller, less active, elderly patient, especially when the femoral canal is capacious (stove pipe) and osteopenic. Cemented femoral fixation is also used in cases of previous infection with the advantage that antibiotics can be added to the cement. Cemented fixation is best avoided in heavy, young active patients, especially if they have good bone stock. Initial experiences with an uncemented stem were not favourable, with reports of femoral fractures, subsidence, thigh pain, osteolysis and stress shielding. Newer designs with a tapered femoral stem plus proximal hydroxyapatite coating to prevent stress shielding have addressed many of these problems. Femora of Dorr types A and B are ideally suited to a tapered stem. Initial stable fixation is essential for bone ingrowth to take place. Those patients with Dorr type C femurs (stove pipe) and with rheumatoid arthritis, however, are at greater risk of intra-operative fracture and often a larger implant is required to produce primary stability for bone ingrowth at a later date. This results in a stiffer implant with greater stress shielding, resulting in proximal bone loss. Patients may also complain of thigh pain. For this reason some have advocated the use of titanium stems in these patients, which are less stiff than cobalt chrome. However, many would use a cemented component in this scenario. When it comes to deciding what bearing surface to use the options include highly cross-linked polyethylene on cobalt chrome or ceramic, ceramic-on-ceramic or metal-on-metal. There is some controversy regarding highly cross linked polyethylene (HXLPE). Compared to standard polyethylene, HXLPE has lower volumetric wear but generates an increased number of particles in the biologically active range (of approximately 1 micron in diameter) according to Marrs et al.38 Overall, however, HXLPE has improved resistance to wear and allows a larger head, thus providing the benefit of greater mobility and enhanced stability without causing unacceptably high levels of volumetric wear. Digas et al concluded from their 5 year results that highly

61-year-old female with severe osteoarthritis of both hips. Right hip more symptomatic. Proceeded to a right uncemented total hip replacement (Synergy/Reflection). Figure 2

There has also been some discussion in the literature regarding the influence of malpositioning of components and subsequent failure of resurfacing. De Haan et al showed that malpositioning of the acetabular component resulted in a higher number of revisions, due to excessive abduction (mean 69.9 degrees, range 56-98 degrees) or insufficient or excessive anteversion.34 They also showed that malpositioning of the components was associated with metallosis and a high level of serum ions. Sometimes, to achieve a good press fit the acetabular component alignment is compromised. De Haan’s study showed that such a compromise is likely to result in early failure and so should be avoided. Hart et al made a similar conclusion from their work. They showed that an acetabular inclination angle of greater than 50 degrees significantly increased the wear rates as shown by increased whole blood chromium and cobalt ions in metal-on-metal hip resurfacings. They suggested that the level

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Mini-symposium: What’s new in hip replacement — basic principles

crosslinked PE instead of conventional PE reduced wear by more than 95% and advocated this bearing surface particularly in the young, active group.39 Ceramic-on-ceramic articulations have many advantages; they are hydrophilic, which contributes to enhanced lubrication with a very low coefficient of friction and a low wear rate. Ceramics are hard and relatively scratch resistant. In addition, tissues readily cover its surface following ­implantation. Although these characteristics seem ideal, when ceramic-on-ceramic bearings were first used there was an unacceptably high fracture rate of up to 13% and additional difficulties of obtaining a stable fixation of the ceramic cup to the surrounding bone did not provide an auspicious start.40 However, with the advent of alumina metal-backed cups this problem was solved. An improvement in manufacturing to achieve a higher density with small grains has also reduced the fracture rate considerably. However, there have been some reports of problems with this bearing surface including squeaking. Squeaking, defined as a reproducible sound of squeaking, clicking, or grating, was found in up to 20% of cases in the series reported by Keurentjes et al.41 Walters et al looked into the reasons why a ceramic bearing should squeak and they found that edge-loading was the dominant causative factor in their patients.42 They also postulated that incorrect seating of the liner into the acetabular shell may also be a cause for this phenomenon. Compared with other bearing surfaces it also is not as versatile, although it remains an attractive option in the young active patient because of its extremely low wear rates43 and low prevalence of osteolysis.44 Metal-on-metal articulations initially were not a success and it is only relatively recently that they have become more popular. High carbon cobalt-chromium-molybdenum alloy with a carbon content of 0.2% is currently used for metal-on-metal bearings. This provides a hard surface that is very resistant to wear. In addition to the material itself, other factors influencing the lubrication such as head size, sphericity, radial clearance and surface roughness are also important factors. It is the thickness of the fluid film that determines the friction at the metal-on-metal interface and resultant wear. With fluid film lubrication there is very low friction and low volumetric wear as a result. However, there are concerns regarding this bearing surface. It has been shown that particulate and ionic metallic debris is systemically disseminated and this has been associated with delayed type-IV hypersensivity,45 toxicity46 and mutagenesis.47 Research is ongoing regarding the significance of this ‘metallic debris’ but for the time being this articulation is not recommended in women of child-bearing age. In the increasingly litigious world we live in, informed consent has taken on a whole new meaning. The majority of surgeons and lawyers alike would understand that informed consent means, in essence ‘what a reasonable person would do under the circumstances knowing the facts’. The facts refer to the type of surgery proposed, possible alternatives and a discussion of the important risks and complications. It is important during this part of the consultation that one remembers that the procedure proposed is not about saving the patients’ lives but improving the quality of their life; as a result, the surgeon, cannot recommend but offer surgery. At the end of the day, it is the patient who makes the decision to proceed with an elective operation and it is the surgeon’s responsibility to ensure that they are provided with the facts on which they can base their decision.

ORTHOPAEDICS AND TRAUMA 23:1

Potential complications Anaesthesia It must be explained to all patients that a hip operation is major surgery performed under a general or spinal anaesthetic, which may take several hours, and necessitates a hospital stay of between 5 to 7 days depending on how quickly they rehabilitate post-operatively. All operations, however routine, carry the potential for developing complications - some minor and some major. Although there is a possibility of death or permanent ­disability from a CVA for example, the majority of surgeons would only mention this in particularly high-risk patients and would not deem it appropriate in all cases. Patients should understand that there is a risk of complications from the anaesthetic plus those specifically related to hip surgery. Sufficient information should be provided to the patient so that they understand that there is a small chance of a complication which might prolong their hospital stay or necessitate specific treatment or even re-operation. These include infection, deep vein thrombosis, pulmonary embolism as well as hip dislocation. Patients should be reassured, however, that the majority of complications can be treated and totally resolved, although a small minority cannot. Patients that are not a suitable candidate for general anaesthesia because of other co-morbidities, such as chronic obstructive airways disease and end-stage heart failure, may be offered spinal regional anaethesia as an alternative. Some patients may prefer regional anaesthesia as this presents a lower overall risk compared to a general anaesthetic, plus they may wish to remain awake during the procedure. It also holds advantages in terms of reducing the risk of thromboembolic complications. That is not to say that it is without possible complications. Trauma to the local tissues at the site of puncture can lead to back pain in some patients and can result in a localised haematoma. A localised haematoma can be something relatively trivial, which is localised within the skin and fat, or it can be more significant as can occur with a large tear of the epidural veins that fails to clot, leading to a large spinal haematoma that can compromise the spinal cord. The local anaesthetic can be injected into the wrong place; intravenous administration may lead to dangerous arrhythmias and central nervous system toxicity. Alternatively, injection outside the desired location will obviously lead to a failed block. Puncture of the meninges and leakage of cerebrospinal fluid can act as a pathway for infection, with the risk of meningitis. A post-dural puncture headache is a well described complication of spinal anaesthetics. This occurs from a leak of cerebrospinal fluid so that when the patient is sitting up it is thought that the brain shifts slightly and places extra tension on meningeal structures, causing pain; this tends to be alleviated in the supine position. Of course, there is also a risk in any epidural anaesthetic that the dura may be breached, but at least there is no intention to do so as part of the procedure. In those epidural procedures that breach the dura, the headaches are often more severe because the needles used tend to have wider bores. Other structures that can be damaged include the spinal nerves. The risk of neurological injury by direct needle trauma is very low (0.01-0.8% for permanent injury and 0.02-0.07% for transient neurological deficits48); however, the risk is increased with very fine bore needles. 22

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Mini-symposium: What’s new in hip replacement — basic principles

­ orbidity and shorten hospitalization. The use of antibioticm loaded cement reduces deep joint sepsis by a factor of 11, systemic antibiotics by a factor of 4.8, ultra-clean air theatres by 2.6 and exhaust suits by 2.2 (Prophylactic measures identified by the Medical Research Council (MRC) trial, 1982).

A total spinal occurs when the anaesthetic spreads to involve the entire spinal cord, which can cause haemodynamic compromise. Loss of vascular sympathetic tone in capacitance vessels leads to hypotension. Under normal circumstances the body corrects this by increased activity in the sympathetic ­cardioaccelerator fibres to the sinoatrial node, but these are paralysed by the anaesthetic. The combination of hypotension and bradycardia causes the cardiac output to drop leading to poor organ perfusion. Total spinals may also impair the function of intercostal nerves, resulting in dyspnoea, and an abnormally high blockade (above C4) may cause phrenic nerve paralysis, necessitating urgent ventilatory support. Unopposed activity of the parasympathetic gut fibres can also result in excessive gastrointestinal motility and cause nausea and vomiting. This is fortunately very rare.

Dislocation The incidence of dislocation ranges from 0 to 2%.52 Hip stability depends on component design (head-neck ratio, femoral head size), component alignment (acetabular anteversion of 10-20 degrees, acetabular coronal tilt of 35-45 degrees, femoral component anteversion of 10-15 degrees), soft tissue tensioning (head offset and neck length) and finally soft tissue function. It is perfectly reasonable for a patient to ask how the risk of dislocation can be reduced and to be able to break the possible causes down is both helpful for the patient and surgeon.

Venous thromboembolism (VTE) The incidence of lower extremity deep vein thrombosis has been quoted from 8% to as high as 70%, with the risk of fatal pulmonary embolism ranging from 0.1 to 3%.49 However, it should be explained to patients that this incidence can be reduced by up to 70 to 80% with thromboembolic prophylaxis. Current NICE guidelines advise that all patients post hip arthroplasty who are ≥40 years or <40 years with one or more patient related risk factors for a thromboembolic event (Table 2) should be on a low molecular weight heparin (eg Dalteparin) for 4 weeks post-op. It is also advisable that they wear thromboembolic deterrent stockings. Trials of new oral anti-thrombin agents have been very promising.

Fracture The incidence of peri-prosthetic fracture is less than 1%.53 Leg length Minor leg length discrepancies of no more than 1 cm are common after total hip arthroplasty and are usually well tolerated.54 However, in some patients, even these small discrepancies are cause for considerable dissatisfaction. With more significant discrepancies there is an increased risk of nerve injury, low back pain and an abnormal gait. Careful preoperative measurement and assessment of true and apparent leg length, as well as preoperative and postoperative patient education, are important factors in achieving a satisfactory result. Patients should be warned that equal leg lengths cannot be guaranteed and they should be given a realistic assessment of what they can expect post operatively. As well as physical cues from the examination, radiographic evaluation to assess leg length and to preoperatively template the surgical procedure is vital for a successful outcome.

Infection The risk of infection varies from 0.4 to 1.5%.50,51 Prophylactic administration of antibiotics can decrease post-operative

Risk factors for thromboembolism Age ≥40 years

Central venous catheter in situ

Personal or family history of VTE Obesity (BMI ≥ 30  kg/m2) or weight >100  kg Varicose veins with associated phlebitis Immobility (e.g. paralysis or limb in plaster) Combined oral contraceptive or HRT Pregnancy or puerperium Recent MI or stroke Active cancer/cancer treatment

Active heart or respiratory failure Acute medical illness

Inflammatory bowel disease Continuous travel of more than 6 hours approx 4 weeks before or after surgery

Aseptic loosening Chambers et al looked into the radiological features predictive of aseptic loosening in cemented Charnley stems.55 They concluded that a defective or incomplete cement mantle, radiolucency of over 50% at the cement-bone interface or a failure to cover the tip of the stem with cement increased the risk of loosening and failure. Barrack et al56 have shown that with improved cementing techniques (2nd generation, Table 3) the risk of aseptic loosening diminished (2%). They graded the radiographic appearance of the initial cementing into 4 grades: Grade A corresponded to complete filling of the medullary cavity (white out); Grade B, slight radiolucency of the cement-bone interface; Grade C, radiolucency involving 50-99% of the cement-bone interface or a defective or incomplete cement mantle; Grade D, radiolucency of the cement-bone interface of 100% in any projection or failure of the tip of the prosthesis to be covered with cement. Chambers et al showed that a cement mantle corresponding to grades C or D resulted in an increased risk of failure secondary to aseptic loosening.55

Paraproteinaemia Myeloproliferative disease Severe infection Nephrotic syndrome Bechet’s disease Antiphospholipid syndrome Sickle cell/Thalassaemia syndrome Inherited thrombophilias Paroxysmal nocturnal haemoglobinuria

Nerve injury The reported incidence of sciatic or femoral nerve palsy after total hip arthroplasty ranges from 1 to 3 %.57–59 After a primary total

Table 2

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Mini-symposium: What’s new in hip replacement — basic principles

uncemented implants (99% survival at 13 years67), but to qualify this with the fact that no surgeon can guarantee how long an implant will last in a particular patient. In this vane it would be appropriate to mention to the patient that should the hip replacement fail then it can be revised, although the results may not be as good as the primary procedure and may not last as long. All patients should have clearly explained to them the normal post-operative course, including what they should expect when they wake up, for example presence of a drain, where the wound will be, type of dressing and their weight-bearing status. They should be told that on day 1 they will have some blood tests performed and there will be further radiographs 2 to 3 days postoperatively. Some patients are surprised when they have radiographs performed at this stage and assume that something has gone wrong, so it is worth mentioning this point before they have their operation. The timing of when patients can return to work is clearly dependent on what line of work they are in, with the majority of patients who do a desk job returning at the 6 week mark. The majority of patients can drive by 6 weeks or when they can safely perform an emergency stop. Patients should also be given the opportunity to ask questions. Some will be overwhelmed from all the information given to them and would benefit from having all the information presented in an information leaflet that summarises the procedure, preoperative and postoperative care, the expected outcome as well as possible complications. This allows the patient the opportunity to discuss their options with their family, and ideally they should be given the opportunity to return to the outpatient department so that any additional queries can be addressed. These issues are not best addressed on the day of surgery but several weeks beforehand. At all times leading up to surgery, it is important that the patient does not feel pressured into proceeding with the operation. If the patient is unsure then it is perfectly reasonable to continue with conservative means of managing their symptoms. Delaying surgery may raise other issues, but with modern anaesthesia the age of the patient is not a significant factor, although bone loss can prove problematic with advancing osteoarthritis. The rapport between surgeon and patient is as important as the operation itself and it is worth the time involved to establish this before embarking on any elective procedure.

The evolution (generations) of cementing techniques

Distal femoral plug Proximal femoral seal Acetabular pressurization Hand mixing cement Vacuum mixing cement Brushing Pulsatile lavage

1st generation

2nd generation

3rd generation

No

Yes

Yes

No

No

Yes

No

No

Yes

Yes

Yes

No

No

No

Yes

No No

Yes No

Yes Yes

Table 3

hip replacement the incidence is 1-2%, 3-4% after revision, and 5-6% in THR for congenitally dislocated hips.60 Female patients seem to be at significantly higher risk and this is ­probably due to their anatomy as the sciatic nerve lies a lot closer to the posterior aspect of the greater trochanter than male patients. A mild injury that consists of a transient conduction block may recover in days to weeks, however, an injury severe enough to cause axonal damage may take several years or not recover at all. If there is any question of the degree of injury an electromyogram and nerve conduction study should be requested. Management of these injuries can be difficult; a transient conduction block should be managed expectantly whereas if the limb has been lengthened and there is no other cause of injury the knee should be flexed to relieve stretch of the sciatic nerve. If there is transection of the nerve then the local peripheral nerve injury unit should be involved; these injuries carry a very poor prognosis. Residual pain This is thankfully a rare problem, although there have been a number of cases reported in the literature of residual pain following a total hip replacement. The more esoteric causes include pubic rami fracture,61 extrusion of methylmethacrylate following a cemented total hip replacement causing an obturator nerve palsy62 or sciatic nerve palsy63 and pain attributed to the psoas muscle.64 However, the most common causes of residual pain are low back pain and sciatica, aseptic loosening and infection, and these causes should be excluded before more detailed investigations as to the cause of the patient’s symptoms are undertaken. There is clearly a balance to be achieved in providing the patients with sufficient facts for them to be able to make an informed decision without frightening them unnecessarily. It is also important to give some indication to the patient of how long their prosthesis should survive. Each patient is unique and will have different variables that may influence how long their prosthesis will survive, such as their activity levels. However, it would be appropriate to quote the results for the Exeter prosthesis for cemented implants (100% survival at 10 years65) and excellent long term results at 33 years66 and the Furlong results for

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Conclusion In summary, there are many things to consider regarding patient selection and consent. The patient should be at the centre of all decision making and careful assessment of their symptoms and signs are crucial for appropriate orthopaedic management. ◆

References 1 Bjerkreim I, Arseth PH. Congenital dislocation of the hip in Norway. Late diagnosis CDH in the years 1970 to 1974. Acta Paediatr Scand 1978; 67: 329–32 5. 2 Haasbeek JF, Wright JG, Hedden DM. Is there a difference between the epidemiologic characteristics of hip dislocation diagnosed early and late? Can J Surg 1995; 38: 437–8. 3 Poul J. Diagnosis of Legg-Calvé-Perthes disease. Ortop Traumatol Rehabil Oct 30 2004; 6(5): 604–6.

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4 Merritt K, Brown SA. Metal sensitivity reactions to orthopedic implants. Int J Dermatol Mar 1981; 20(2): 89–94. 5 Merritt K, Rodrigo JJ. Immune response to synthetic materials. Sensitization of patients receiving orthopaedic implants. Clin Orthop May 1996; 326: 71–9. 6 Waterman AH, Schrik JJ. Allergy in hip arthroplasty. Contact Dermatitis Nov 1985; 13(5): 294–301. 7 Goldring SR, Clark CR, Wright TM. The problem in total joint arthroplasty: aseptic loosening. J Bone Joint Surg Am Jun 1993; 75(6): 799–801. 8 Panigutti MA, Merritt K, Bruner RJ, et al. Correlation of allergy, metal levels, implant alloy, and implant damage in patients undergoing revision joint arthroplasties. Trans Soc Biomaterials 1992; 15: 7. 9 Szliska C, Raskoski J. Sensitization to nickel, cobalt and chromium in surgical patients. Contact Dermatitis Nov 1990; 23(5): 378–9. 10 Clohisy JC, Carlisle JC, Beaule PE, et al. A systematic approach to the plain radiographic evaluation of the young adult hip. J Bone Joint Surg Am 2008; 90: 47–66. 11 Wimsey S, Pickard R, Shaw G. Accurate scaling of digital radiographs of the pelvis. J Bone Joint Surg Br 2006; 88-B;(11): 1508–1512. 12 Singh M, Nagrath AR, Maini PS. Changes in trabecular pattern of the upper end of the femur as an index of osteoporosis. J Bone Joint Surg Am 1970; 52A: 457–67. 13 Dorr LD. Optimizing results of total joint arthroplasty. AAOS Instr Course Lect 1985; 34: 401–404. 14 Update on glucosamine for osteoarthritis. Med Lett Drugs Ther 2001; 43: 111–112. 15 Clegg and others DO. Glucosamine, chondroitin sulfate, and the two in combination for painful knee osteoarthritis. N Engl J Med 2006; 354: 795–808. 16 Lo Grace H, LaValley Michael, McAlindon Timothy, Felson David T. Intra-articular hyaluronic acid in treatment of knee osteoarthritis: a meta-analysis. JAMA 2003; 290: 3115–3121. 17 Fufulas EL, Tsintzas D, Gabriilidis B. Treatment of hip osteoarthritis with intraarticular injections of hyaluronic acid. J Bone Joint Surg Br 2003; 85-B;SUPP(III): 216–217. 18 Poss R, Maloney JP, Ewald FC, et al. Six- to 11-year results of total hip arthroplasty in rheumatoid arthritis. Clin Orthop 1984; 182: 109–116. 19 Chan PK, Brenkel IJ. Aderinto J. The outcome of total hip arthroplasty in diabetes mellitus. Br J Diabetes Vascular Diseases 2005; 5(3): 146–149. 20 National Joint Registry for England and Wales, 4th Annual Report. 21 Buergi ML, Walter WL. Hip resurfacing arthroplasty: the Australian experience. J Arthroplasty 2007; 22(7); (Suppl 3): 61–5. 22 Shimmin AJ, Back D. Femoral neck fractures following Birmingham hip resurfacing: a national review of 50 cases. J Bone Joint Surg Br 2005; 87B: 463–4. 23 Shimmin AJ, Back D. Complications associated with hip resurfacing arthroplasty. Orthop Clin North Am 2005; 36: 187–93 ix. 24 Shimmin AJ. Gender does not increase risk for femoral neck fracture when correlated with femoral neck size. Unpublished data. 25 Amstutz HC, Campbell PA, Le Duff MJ. Fracture of the neck of the femur after surface arthroplasty of the hip. J Bone Joint Surg Am 2004; 86A: 1874–7. 26 Beaule PE, Dorey FJ, LeDuff M, Gruen T, Amstutz HC. Risk factors affecting outcome of metal-on-metal surface arthroplasty of the hip. Clin Orthop Relat Res 2004; 418: 87–93. 27 Boyd HS, Ulrich SD, Seyler TM, Marulanda GA, Mont MA. Resurfacing for Perthes disease; an alternative to standard hip arthroplasty. Clin Orthop Relat Res 2007; 465: 80–5.

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28 Amstutz HC, Ball ST, LeDuff MJ, Dorey FJ. Resurfacing THA for patients younger than 50 years :results of 2 to 9 year follow up. Clin Orthop Relat Res 2007; 460: 159–64. 29 McMinn D, Daniel J. History and modern concepts in surface replacement. Proc Inst Mech Eng [H] 2006; 220: 239–51. 30 Schmalzried TP, Silva M, de la Rosa MA, Choi ES, Fowble VA. Optimizing patient selection and outcomes with total hip resurfacing. Clin Orthop Relat Res 2005; 441: 200–4. 31 Revell MP, McBryde CW, Bhatnagar S, Pynsent PB, Treacy RB. Metal on metal hip resurfacing in osteonecrosis of the femoral head. J Bone Joint Surg Am 2006; 88A(Suppl 3): 98–103. 32 Mont MA, Seyler TM, Marker DR, Marulanda GA, Delanois RE. Use of metal on metal total hip resurfacing for the treatment of osteonecrosis of the femoral head. J Bone Joint Surg Am 2006; 88A(Suppl 3): 90–7. 33 Fitts SM, Zadzilka JD, Trier K, Stulberg BN. Resurfacing arthroplasty for patients with osteonecrosis (abstract). In: Proceedings of the 75th Annual Meeting of the American Academy of Orthopaedic Surgeons; 2008 Mar 5–9. Rosemont, IL: American Academy of Orthopaedic Surgeons, 2008; p. 409–10. 34 De Haan R, Campbell PA, Su EP, De Smet KA. Revision of metalon-metal resurfacing arthroplasty of the hip: the influence of malpositioning of the components. J Bone Joint Surg Br 2008; 90-B: 1158–63. 35 Hart AJ, Buddhdev P, Winship P, Faria N, Powell JJ, Skinner JA. Cup inclination angle of greater than 50 degrees increases whole blood concentrations of cobalt and chromium ions after metal-on-metal hip resurfacing. Hip Int 2008 Jul-Sep; 18(3): 212–9. 36 Hozack WJ, Rothman RH, Booth Jr. RE, Balderston RA. Cemented versus cementless total hip arthroplasty. A comparative study of equivalent patient populations. Department of Orthoapedics, Thomas Jefferson University, Clin-Orthop. 1993 Apr. (289). P 161–5. 37 Havelin LI, Engesaeter LB, Espehaug B, Furnes O, Lie SA, Vollset SE. The Norwegian Arthroplasty register’ 11 years and 73000 arthroplasties. Acta Orthop Scand 2000; 71(4): 337–353. 38 Marrs H, Barton DC, Ward IM, Doyle C, Fisher J. Comparative wear under three different tribological conditions of acetylene crosslinked ultra high molecular weight polyethylene. Trans Orthop Res Soc 1998; 23: 100. 39 Digas G, Kärrholm J, Thanner J, Herberts P. 5-year experience of highly cross-linked polyethylene in cemented and uncemented sockets: two randomized studies using radiostereometric analysis. Acta Orthop 2007 Dec; 78(6): 746–54. 40 Learmonth ID. Total hip replacement and the law of diminishing returns. J Bone Joint Surg Am 2006; 88-A(7): 1664–1673. 41 Keurentjes JC, Kuipers RM, Wever DJ, Schreurs BW. High incidence of squeaking in THAs with alumina ceramic-on-ceramic bearings. Clin Orthop Relat Res 2008 Jun; 466(6): 1438–1443. 42 Walter William L, Waters Tim S, Gillies Mark, et al. Squeaking hips. J Bone Joint Surg Am Nov 2008; 90: 102–111. 43 Lusty PJ, Watson A, Tuke MA, Walter WL, Walter WK, Zicat B. Orientation and wear of the acetabular component in 3rd generation alumina-on-alumina ceramic bearings. An analysis of 33 retrievals. J Bone Joint Surg Br 2007; 89: 1158–64. 44 Lusty PJ, Tai CC, Sew-Hoy RP, Walter WL, Walter WK, Zicat BA. 3rd generation alumina-on-alumina ceramic bearings in cementless total hip arthroplasty. J Bone Joint Surg Am 2007; 89: 2676–83. 45 Davies AP, Willert HG, Campbell PA, Learmonth ID, Case CP. An unusual lymphocytic perivascular infiltration in tissues around

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with hip arthroplasty. A 12-year radiographic review. J Bone Joint Surg Br May 1992; 74-B: 385–389. 57 Isiklar ZU, Lindsey RW, Tullos HS. Sciatic neuropathy secondary to intrapelvic migration of an acetabular cup. J Bone Joint Surg Am Sep 1997; vol. 79-A(No 9): p1395. 58 Wasielewski RC, Crossett LS, Rubash HE. Neural and vascular injury in total hip arthroplasty. Orthop Clinics of North America 1992; vol. 23: 219–35. 59 Weber ER. Peripheral neuropathies associated with total hip arthroplasty. J Bone Joint Surg Am 1976; vol. 58-A: 66–69. 60 Schmalzried- TP, Amstutz- HC, Dorey- FJ. Nerve palsy associated with total hip replacement. Risk factors and prognosis. J Bone Joint Surg Am 1991 Aug; 73(7): 1074–80. 61 Marmour L. Stress fracture of the pubic ramus stimulating a loose total hip replacement. Clin Orthop 1976; 121: 103–4. 62 Obturator nerve palsy resulting from intrapelvic extrusion of cement during total hip replacement: report of 4 cases. J Bone Joint Surg Am 1985; 67-A: 1225–8. 63 Compression of the sciatic nerve by methylmethacrylate cement after total hip replacement. J Bone Joint Surg Br 1992; 74-B: 729–30. 64 Jasani, et al. Pain related to psoas muscle after total hip replacement. J Bone Joint Surg Br 2002; 84-B: 991–3. 65 Williams HD, Browne G, Gie GA, Ling RS, Timperley AJ. Wendover NA. The Exeter universal cemented femoral component at 8 to 12 years. A study of the first 325 hips. J Bone Joint Surg Br 2002; 84-B: 324–334. 66 2004 Domestic meeting of the European Hip Society:2004 June 23- 26:Innsbruck:Austria. 67 Shetty AA, Slack R, Tindall A, James KD, Rand C. Results of a hydroxyapatite coated (Furlong) total hip replacement: a 13- to 15year follow up. J Bone Joint Surg Br 2005; 87-B(8): 1050–54.

contempory metal on metal joint replacements. J Bone Joint Surg Am 2005; 87A: 18–27. 46 Schins RP. Mechanisms of genotoxicity of particles and fibres. Inhal Toxicol 2002; 14: 57–78. 47 Doherty AT, Howell RT, Ellis LA, et al. Increased chromosome translocations and aneuploidy in peripheral blood lymphocytes of patients having revision arthroplasty of the hip. J Bone Joint Surg Br 2001; 83-B: 1075–78. 48 Faccenda KA, Finucane BT. Complications of regional anaesthesia: incidence and prevention. Drug Saf 2001; 24: 413–42. 49 Paiement GD. Prevention and treatment of venous thromboembolic disease complications in primary hip arthroplasty patients. Instr Course Lect 1998; 47: 331–5. 50 Widmer AF. New developments in diagnosis and treatment of infection in orthopaedic implants. Clin Infect Dis 2001; 33(suppl 2): s94–106. 51 Berbari EF, Hanssen AD, Duffy MC, Steckelberg JM, llstrup DM, Harmsen WS, Osmon DR. Risk factors for prosthetic joint infection: case-control study. Clin Infect Dis 1998; 27(5): 1247–54. 52 Morrey BF. Difficult complications after hip replacement. Dislocation. Clin Orthop Relat Res 1997; 344: 179–187. 53 Duncan CP, Masri BA. Fractures of the femur after hip replacement. Instr Course Lect 1995; 44: 293–304. 54 Maloney WJ, Keeney JA. Leg length discrepancy after total hip arthroplasty. J Arthroplasty 2004 Jun; 19(4 Suppl. 1): 108–10. 55 Chambers IR, Fender D, McCaskie AW. Radiological features predictive of aseptic loosening in cemented Charnley stems. J Bone Joint Surg Br 2001; 83B: 838–42. 56 Barrack RL, Mulroy Jr. RD, Harris WH. Improved cementing techniques and femoral component loosening in young patients

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(iv) Surgical approaches in primary total hip arthroplasty – pros and cons CM van Dijk R Bimmel Fares S Haddad

Abstract Primary total hip arthroplasty has been one of the most successful ­orthopaedic procedures of the last century. Several classical surgical ­approaches to the hip have been described. Each approach has advantages and disadvantages. Recently, minimally invasive techniques have been developed with incisions less than 10cm. The goals of minimally invasive surgery are minimal soft tissue damage and a shorter hospital stay, faster recovery and return to work, less pain, and improved cosme­ tic results. The disadvantages are less visibility, longer operation time, nerve injuries, higher incidence of femoral fractures, malposition of the components and a long learning curve. The originator results with these techniques were promising. Subsequently, more controversial results have been published. Further follow-up and development is necessary to compare the results with the classical proven approaches.

Figure 1 Approaches to the hip and surrounding nerves: Sciatic Nerve (1), Femoral Nerve (2), Lateral Femoral Cutaneous Nerve (3), and Obturator Nerve (4).

surgical approaches to the hip, their complications, advantages and disadvantages.

The posterior approach The posterior approach is the most commonly used operative pathway to expose the hip, and is considered to be technically the easiest to perform, requiring only one assistant. It gives the surgeon easy and quick access to the joint and allows excellent visualisation of the femur. This approach was initially popularised by Moore, with subsequent modifications by Gibson and Marcy and Fletcher. It is also the most commonly used approach for hip resurfacing procedures. Recently, less invasive procedures have been developed from this to decrease soft tissue damage, blood loss, operative time, length of hospital stay and to improve cosmetic appeal. The patient is positioned in the lateral decubitus position between vertical padded rests at the sacrum and pubis. The pelvis is orientated in a neutral position, in line with the spine. An 8 to 15 cm incision is made, centered over the posterior aspect of the greater trochanter, curved posteriorly across the buttock. The subcutaneous tissue is incised down to the tensor fascia lata, which envelopes the lateral aspect of the thigh muscles. The fascial incision is lengthened superiorly in line with the skin incision, and the fibers of the gluteus maximus are gently split. The sciatic nerve is identified posteriorly and deep within the wound as it lies over the external rotators of the hip. The posterior border of the gluteus medius is identified and the piriformis and conjoined tendons are divided at their insertion onto the greater trochanter. Stay sutures may be inserted into the piriformis, obturator internus and gemelli ­tendons. These tendons are retracted posteriorly, thereby protecting the sciatic nerve during the procedure. With this maneuver, the entire posterior capsule of the hip is exposed and can be incised with a T-shaped or longitudinal incision. The femoral head is dislocated by internal rotation and flexion of the hip after the capsulotomy.

Keywords approach; hip; minimally invasive; surgical technique

Introduction Primary total hip arthroplasty (THA) is one of the most common surgical procedures in orthopaedic surgery. Various surgical approaches have been described to perform this operation and multiple minimally invasive procedures have recently been developed (Figure 1). There is no consensus among hip surgeons about the ideal surgical approach and the debate continues. The ideal approach should provide the surgeon with optimal visualisation, be reproducible by most hip surgeons, be less invasive with respect to the surrounding soft tissues without complications, and allow the patient a rapid postoperative recovery, rehabilitation and return to work. This article reviews the most common

CM van Dijk MD is Orthopaedic Registrar in University College Hospital London, UK. R Bimmel MD is Orthopaedic Registrar in Nij Smellinghe, Drachten, The Netherlands. Fares S Haddad BSc MCh (Orth), FRCS (Orth), is Consultant Orthopaedic Surgeon in University College Hospital London, UK.

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hematocrit, blood transfusion requirements, pain scores, or analgesic use. They found no difference in early walking ability or length of hospital stay and no difference in component placement, cement-mantle quality, or functional outcome scores at six weeks, between the two groups (WOMAC, Oxford and Harris hip scores). No significant differences were demonstrated in average stride length, cadence, or walking speed based on incision length. They concluded that minimally invasive THA performed through a single-incision approach by a high-volume surgeon with extensive experience in less invasive approaches to the hip is safe and reproducible. However, it offers no significant benefit in the early post-operative period compared with a standard ­incision. Dorr et al compared the mini-incision technique with the conventional posterior approach.5 They concluded that conventional total hip arthroplasty performed through a posterior minimally invasive approach resulted in better early pain control, earlier discharge home, and less use of assistive devices. Subsequent evaluations at six weeks and three months showed equivalency between the clinical results in the two groups. Khan et al. compared the standard posterior approach with the minimally invasive, piriformis-sparing approach in 200 patients, equally divided in the two groups.1 The average blood loss, mean hospital stay and dislocation rate were significantly less in the minimally invasive surgical (MIS) group. There was a statistically significant improvement in WOMAC score at 3, 12 and 24 months in both groups. The relative improvement in WOMAC scores was greater in the piriformis-sparing approach for up to 1 year. No difference in component positioning was identified between the two groups. The authors concluded that division of the piriformis tendon is unnecessary and does not compromise visualisation of the acetabulum or femur. Because of the stabilising function of piriformis on the hip joint they felt that it should be spared during the posterior approach to the hip.

The mini-incision variations of this exposure involve an approach anatomically identical to that described above but through a smaller skin incision (<10 cm), forming a mobile window that allows intermittent exposure of the acetabular and femoral sides of the hip joint. A mini-incision posterior approach, without division of the piriformis tendon, was described in 2006 by Khan et al.1 A standard mini-incision is performed, centered over the posterior border of the greater trochanter. The gluteus medius is retracted anteriorly to expose the posterior structures. The posterior capsule and tendons of the gemelli and obturator internus are detached as one from their insertion along the inferior border of piriformis, from the edge of the acetabulum to the posterior border of the femur. The quadratus femoris muscle may be partially detached to visualise the inferior part of the neck. If necessary, the inferior capsule is released from the neck. With correct placement of retractors and pins, and correct location of the incision, the view of the acetabulum and femur should be good. The advantage of the posterior approach is that it allows easy access to the hip and avoids disruption of the abductor muscles, which reduces the incidence of postoperative limp and the need for walking aids. This approach is also characterised by less bleeding and more rapid postoperative recovery of function when compared to the anterior or anterolateral approach.2,3 The sciatic nerve and inferior gluteal artery are at risk during the posterior approach. The sciatic nerve can be damaged if it is compressed by a retractor or dissected during the procedure. The inferior gluteal artery leaves the pelvis beneath the piriformis and it turns superiorly to supply the deeper parts of the gluteus maximus muscle. When the muscle is split gently, the vessels must be picked up and coagulated before they are avulsed and retract into the muscle.The biggest concern with the posterior approach remains the high rate of postoperative dislocation. However, an enhanced repair of the soft tissues can reduce the rate of dislocation to less than 1% (Table 1). The advantages of the mini-incision variation are questioned by many authors. Ogonda et al, reported on 219 prospectively randomised THAs performed by a single, experienced surgeon.4 All patients were randomised to undergo total hip replacement through a mini-incision (<10 cm) or standard incision (16 cm). The two groups were matched for age, grade according to the system of the American Society of Anaesthesiologists, and body mass index. No difference was detected with respect to ­postoperative

The anterolateral approach The anterolateral approach to the hip exploits the plane between the tensor fascia lata and the gluteus medius muscle. This approach was popularised by Watson-Jones in 1936. It involves detachment of the abductor mechanism. It can be performed in a supine position or in the lateral position. Advocates of the supine position suggest that leg length discrepancy is best evaluated in that position. The patient is positioned supine on the operating table. A skin incision is made just anterior to the centre of the greater trochanter and it is curved into the posterior aspect of the buttock. The length of incision recommended used to be 20 to 30 cm. Two thirds of the incision is proximal and one third distal to the tip of the greater trochanter. The fascia is incised centrally or slightly posterior to the tip of the greater trochanter. A more posterior fascial incision proximally gives better access to the femoral canal. Release of the abductor mechanism is necessary to expose the anterior capsule of the hip. This release can be done either by a trochanteric osteotomy or a release of the gluteus medius and vastus lateralis tendons. The trochanteric osteotomy was first done and described by Ollier in 1881 and Brakett in 1912. Sir John Charley popularised this approach further. An osteotomy should be at the base of the vastus lateralis ridge.

Rate of dislocation after soft tissue repair in the posterior approach Study

Rate of dislocation after soft tissue repair (%)

Hedley et al, 1990 Pellici et al, 1998 Dixon et al, 2003 Suh et al, 2004 Osmani et al, 2004 Tsai et al, 2008

0.8 0.8 0.4 1.0 1.1 0.0

Table 1

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the posterior approach. The lateral approach preserves the gluteus medius insertion, but does not create as wide a view as the anterolateral approach does. The anterolateral approach has recently been introduced in hip resurfacing procedures. In 2008, Jacobs et al reported on 57 hip resurfacing procedures performed by an anterolateral approach.7 The complication rate was 5,2% (3 cases), and the mean Harris hip score at 38 months was 99 points. They concluded that the anterolateral approach is a reliable and safe approach for hip resurfacing. It offers the surgeon an excellent view, with the advantage of increased hip stability and potentially better preservation of the vascular supply of the femoral head.

The complete gluteus medius is retracted in a proximal direction with the greater trochanter. A release of the tendon of the gluteus medius is made just above its anterior insertion, together with the underlying gluteus minimus. An anterior release leaves a good tendinous cuff to reattach at the end of the procedure. The anterior surface of the capsule is incised and the hip is dislocated by externally rotating the hip after capsule release. The minimally invasive variation of this exposure involves an approach that is identical to a standard exposure but through a smaller skin incision (<10 cm), forming a mobile window. The direct lateral approach described by Kocher in 1903, avoids the need for trochanteric osteotomy and the gluteus medius muscle is preserved. The lateral approach was adjusted by many authors, such as McLaughlin in 1984, and Dall in 1986. This approach was most popularised by Hardinge. He first described his lateral approach in 1982. The gluteus medius and the vastus lateralis tendons are here detached from their posterior borders with a flake of bone. This is thought to afford easier reattachment. In 1993, Frndak was the first to describe the approach without taking a flake of bone of the trochanter. It is supposed to create less bursitis but equally good healing of the gluteus medius. This approach necessitates placing the patient in the lateral position. A longitudinal incision passes over the center of the greater trochanter; two thirds of the incision is proximal and one third distal to the tip of the greater trochanter. After splitting the fascia in line with the skin incision, the gluteus medius muscle is gently split in the direction of its fibres until 3 cm. above the tip of the trochanter. Higher dissection may damage branches of the superior gluteal nerve. The vastus lateralis muscle is split in a distal direction. An anterior flap onto the femoral neck is created by detaching the two muscles from the greater trochanter with a flake of bone and detaching the gluteus minimus tendon. The anterior capsule of the hip joint is fully exposed and a standard capsulotomy is followed by external rotation of the hip to dislocate the hip. At risk in any lateral approach, when dividing the gluteus medius muscle, is the superior gluteal nerve. The nerve innervates the gluteus medius and minimus muscles and the tensor fascia lata. A modification to minimise the risk of superior gluteal nerve damage was proposed by Learmonth and Allen in 1996. They make an ‘Omega incision’ of the tendons to stay further from the nerve. The muscle is not split by this technique and the risk of nerve damage is reduced. Another complication of the lateral approach is the occurrence of heterotopic ossification. In 2.8% severe heterotopic ossification was found by Bourne.6 Heterotopic ossification was mild in 25,7% and moderate in 5,3%. Abductor weakness or lurch only seems to be of importance in the early post-operative period. One year post-operatively there is no difference in comparison with the posterior approach. The disadvantage of an osteotomy is the difficult repositioning and fixation of the greater trochanter. Breakage of wires, non-union, pseudarthrosis and bursitis lead to a high rate of ­reoperations. The anterolateral approach with trochanteric osteotomy creates a wide view of the hip joint. This approach can be especially helpful with badly distorted anatomy. Another advantage of the anterolateral approach is the low dislocation rate compared to

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The anterior approach The classical anterior approach, known as the Smith-Petersen approach, exploits the plane between the sartorius muscle and the tensor fascia lata. This approach was first performed in Paris by Robert Judet in 1947 and has been performed consistently by a small group of surgeons ever since. Access to the hip can be safely achieved with the help of one or two assistants. The advantages of the anterior approach for hip arthroplasty are several. First, the hip is closer to the skin anterior than posterior. Second, the approach follows the anatomic interval between the zones of innervations of the superior and inferior gluteal nerves laterally and the femoral nerve medially. Third, the approach exposes the hip without detachment of muscle from bone. The patient is positioned supine. An incision is made following the anterior half of the iliac crest to the anterior superior iliac spine. From there, the incision must be extended vertically downwards for 8 to 10 cm, directed towards the fibular head. The subcutaneous tissue is incised down to the anatomical plane between the tensor fascia lata and sartorius. External rotation of the leg will make the sartorius muscle more prominent and this assists identification. Care must be taken to avoid cutting the lateral femoral cutaneous nerve, which runs over the fascia of the sartorius. Prevention of this error is achieved by incising the deep fascia on the medial side of the tensor fascia lata and staying within the fascial sheath of this muscle. The sartorius and the nerve are retracted medially and upwards and the tensor fascia lata downwards and laterally. It is sometimes necessary to detach the origin of the tensor fascia lata from the iliac crest. The large ascending branch of the lateral femoral circumflex artery, which lies between the two muscles, must be ligated or coagulated. The rectus femoris is detached from both its origins: the direct head, from the anterior inferior iliac spine, and the reflected head from the superior lip of the acetabulum and anterior capsule of the hip. Retracting the gluteus medius laterally and the iliopsoas medially will expose the anterior capsule of the hip. The capsule can be incised with a T-shaped or longitudinal incision. The femoral head is dislocated by external rotation of the hip. The MIS variation of this exposure was developed by Joel Matta in 1996, who had observed anterior hip replacement in Paris. He rethought his approach to hip replacement and, by abandoning the posterior approach and adopting the anterior approach, his goals were: lower risk of dislocation, enhanced recovery rate, and increased accuracy of hip prosthesis placement and leg length. In his mini-incision approach, the patient is positioned supine on a specially designed orthopaedic traction 29

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Mini-symposium: What’s new in hip replacement — basic principles

A disadvantage of this approach is the fact that a special operating table with traction is required. Potential complications include intra-operative femoral and ankle fractures. These can be avoided through careful manipulation of the limb. If a femoral fracture occurs, the incision can be extended distally by lengthening the skin incision downward along the anterolateral aspect of the thigh, and splitting the interval between the rectus femoris and the vastus lateralis. This extension gives an excellent view of the femoral shaft for application of cerclage wires or other necessary procedures. In obese or muscular patients, where visualisation of the femur is in doubt, an increase in incision length will give the surgeon the required view. Kennon et al,9 reported on a modified anterior, MIS approach developed by Kristaps Keggi, and used for more than 30 years. The anterior skin incision is similar to the distal Smith-Petersen incision and exposes the underlying tensor fascia lata muscle. Splitting the fibers of the tensor fascia lata, retracting the sartorius and rectus femoris muscles medially and the tensor fascia lata and gluteus medius muscles laterally, exposes the anterior hip capsule. The anterior hip capsule is incised to expose the hip joint. An accessory distal lateral stab incision is often necessary to introduce a reamer. This reduces lengthening of the main skin incision and extensive muscle retraction while reaming the acetabulum. Preparation of the femur can be difficult with this technique and a posterior superior stab incision reduces the need for extensive medial or posterior capsule releases to improve femoral exposure and to insert a broach. There are several other techniques to improve preparation of the femur, including placing the hip in hyperextension while lowering the leg, placing a rigid retractor under the greater trochanter to elevate the femur and releasing the tensor fascia lata from the anterior iliac crest. In their survey, they reported on 2132 patients who had a primary total hip arthroplasty done through this minimally-­invasive anterior approach (1–3 incisions technique). They found 5 injuries to the lateral femoral cutaneous nerve (0,23%) and four patients with a foot drop. At six months follow-up, the dislocation rate was 1,3% (28 patients). The authors concluded that this MIS approach is a safe approach to the hip with low rates of intraoperative and early postoperative complications, short operative times and low blood loss.

table (OSI PROfx/HANA tables). This table facilitates surgery through a smaller, less invasive approach, and accommodates external and internal rotation of the operated leg during the procedure. The incision is limited to 5 cm to 10 cm and starts 2–3 cm posterior and 1–2 cm distal to the anterior superior iliac spine. This straight incision extends in a distal and slightly posterior direction to a point 1–3 cm anterior to the greater trochanter. The tensor fascia lata is incised in line with the skin incision where it is translucent, and anterior to the denser tissue of the iliotibial tract. The incision ends slightly distal and proximal to the skin incision. Next, retract the tensor and gluteus minimus muscles laterally and the sartorius and rectus femoris muscles medially. Caution must be taken to identify the lateral femoral circumflex vessels. These vessels are clamped, cauterised and transected. The reflected head of the rectus femoris muscle and the iliopsoas muscle are retracted from the anterior capsule with a periosteal elevator. With appropriate placement of retractors, a view of the anterior circumference of the hip capsule is obtained. The capsule can be incised with a T-shaped or longitudinal incision. The femoral head is dislocated by external rotation of the hip. Visualisation of the acetabulum is easy. The traction table is necessary to expose the femur. This approach preserves posterior structures that are important for preventing dislocation whilst also preserving important muscle attachments to the greater trochanter. The lack of disturbance of the gluteus minimus and gluteus medius insertions facilitates gait recovery and rehabilitation, whilst the posterior rotators and capsule provide active and passive stability and account for immediate stability of the hip and the low risk of dislocation associated with this approach. It is normal for patients undergoing a posterior or lateral approach to follow a strict protocol that limits hip mobility for the first two or three months. This protocol, which limits hip flexion above 90 degrees, has implications for the patient’s daily activities and early rehabilitation. Using the anterior approach, patients are allowed to mobilise their hip freely. The gluteus maximus and tensor fascia lata muscles insert onto the iliotibial band, which joins them and forms a ´hip deltoid´. Lack of disturbance of these abductors and pelvic stabilisers is another benefit of the anterior approach which accelerates gait recovery. Matta et al,8 reported on 437 consecutive, unselected patients who had 494 primary total hip arthroplasty surgeries done through a mini-incision anterior approach from September 1996 to September 2004 (57 bilateral). The mean hospital stay was 3 days, and three patients sustained dislocations of their hip, giving an overall dislocation rate of 0,61% and zero revision surgery. The post-operative leg length discrepancy averaged 3 mm. They concluded that the anterior approach is an accurate and reproducible procedure, applicable to all primary hip patients. The same results are reported by other authors, with dislocation rates below 1%, reduced blood loss, less postoperative pain, shorter length of hospital stay and quicker overall rehabilitation compared to a standard incision. The lateral femoral cutaneous nerve is at risk when the fascia is incised between the tensor fascia lata and the sartorius muscle. Damaging it may lead to diminished sensation on the lateral aspect of the thigh and in the formation of a neuroma. Matta et al. reported only one temporary nerve injury.

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Two-incision MIS technique In 2000, a two incision MIS approach to the hip was described by Berry et al.10 The goal of this technique, which was developed in an anatomy laboratory, was to approach the hip without violating the surrounding nerves, vessels and ­muscles. The patient is set up in a supine position. A 4 to 6 cm skin incision is made obliquely from the intertrochanteric line to the centre of the femoral head, confirmed by intraoperative fluoroscopy. The anterior surgical approach is used to reach the hip joint. Dislocation of the hip is not necessary. The femoral neck is cut in situ, with two osteotomies, one in the subcapital region and one along the preoperatively planned level of the femoral neck. The femoral neck segment is removed with a threaded Steinman pin, followed by the femoral head. The completed femoral cut is checked under fluoroscopy to check if an accurate osteotomy has been achieved. A second, posterior, incision that is 3 to 4 cm in length is made in line with the femoral canal and 30

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Mini-symposium: What’s new in hip replacement — basic principles

The greater trochanter is an important landmark and preoperative templating provides information regarding the femoral and acetabular component size and position (Figure 2). The depth of femoral component insertion is referenced from the tip of the greater trochanter instead of the lesser trochanter, which is used in traditional techniques. The patient is positioned in a lateral decubitus position, as far anterior on the table as possible. This allows maximum adduction of the operated limb, reducing trauma to the gluteus maximus muscle and posterior skin edge. The incision is made in line with the femoral shaft along the posterior proximal edge of the greater trochanter, with the hip flexed 30° and maximally internally rotated. The tip of the greater trochanter should be located 1 cm proximal to the distal edge of the skin incision. The length of the skin incision will vary, depending on patient size and surgeon experience. The muscle fibres of the gluteus maximus are teased apart over 2.5 to 5 cm. proximal and posterior to the greater trochanter, without disturbing the iliotibial band and tensor fascia lata. With external rotation of the hip, the piriformis tendon or conjoined tendon can be ­differentiated from the surrounding tissue. The gluteus minimus is gently retracted cephalad and the complete piriformis tendon is released, as close to its insertion onto the greater trochanter as possible. The remaining short external rotators are not released. A capsulotomy is performed in a hockey-stick fashion and the hip is dislocated with adduction, flexion and internal rotation. After resection of the femoral head, the acetabulum is prepared. An accessory portal is necessary just behind the posterior border of the femur, anterior and lateral to the sciatic nerve, and oriented towards the centre of the acetabulum. A specially designed acetabular guide is used to facilitate portal placement. This portal is necessary to ream the acetabulum and for impaction of the acetabular component. Using this portal avoids crowding of the cup holder and facilitates visualisation of the entire acetabular component in relation to the osseous rim during impaction, which reduces the risk of malposition. The femur is prepared without accessory portals but with a calibrated in-line impactor handle to indicate the distance from the shoulder of the broach to the tip of the greater trochanter. This provides insertion of the stem corresponding to the templated depth. A pre-operative

is confirmed under fluoroscopy. The gluteus maximus fascia is split superficially, and a deep direct pathway to the medullary canal is developed with blunt dissection between the gluteus medius (posterior) and piriformis tendon (anterior). This posterior approach is similar to that described for the insertion of an intramedullary nail. Because of the small incisions, implantation of components is done under intraoperative fluoroscopy to check correct positioning. In the same study, they reported on early results of 375 selected patients treated by a total hip replacement performed with the two-incision technique, under the care of four different surgeons. The average operation time was 85 minutes. The risk of complications in this survey was acceptable and included six proximal femur fractures, two partial, temporary femoral nerve palsies, 16 lateral femoral cutaneous nerve (LFCN) injuries (nine temporary and seven partial), one late infection in a rheumatoid patient, two posterior dislocations (which were treated by closed reduction without redislocation), and one deep vein thrombosis. Over 80% of the patients were discharged within the first 24 hours and 75 patients were treated in an outpatient setting. There were no readmissions or medical complications. The authors concluded that this 2 incision MIS approach is more difficult than either the mini-anterior or mini-posterior approach. In their experience, the early postoperative complication rate has been acceptable but additional experience and long-term evaluation will be needed. The suggestion that the 2-incision approach allows total hip arthroplasty to be done without cutting or damaging any muscle or tendon was studied by Mardones et al.11 Twenty cadaver hips were studied. Ten total hip arthroplasties were done by the 2- incision approach and ten hips by a mini-posterior approach. Damage to the muscle of the gluteus medius and minimus was substantially greater with the 2-incision approach. Every twoincision hip replacement was done with severe muscle damage of the gluteus medius, minimus or external rotators. The authors of this study do not support the suggestion that a 2-incision THA prevents cutting or damaging any muscle or ­tendon. In 2005, Pagnano et al compared 80 consecutive 2-incision hips in unselected patients with 160 consecutive traditional open THAs.12 Significant early complications occurred in 14% of the 2-incision MIS hips. The prevalence of complications in the 160 traditional open THAs was 3%. The authors concluded that the early complication rate of 14% compared with 3% for traditional approaches was a reason to temper enthusiasm for this 2-incision approach. Because of the high complication rates in the wider orthopaedic community, this approach is no longer commonly used in the UK.

Percutaneously assisted total hip arthroplasty (PATHA) In 2008, Penenberg et al described a new soft tissue-sparing approach to the hip.13 The goal in developing this new, minimally invasive technique was twofold. The first goal was to preserve the soft tissues and to improve rehabilitation, accelerating return to normal function. The second goal was to develop an MIS technique without compromising visibility and access during surgery, minimising the early complications seen in other MIS techniques.

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Figure 2 Acetabular guide with accesory portal.

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Mini-symposium: What’s new in hip replacement — basic principles

pelvic radiograph is made with the trial components in place to check offset, component alignment and limb length differences. In their survey, they reported on 250 THAs performed with this PATHA technique. The average incision length was 8.3 cm, the average operation time was 65 minutes, and the estimated blood loss averaged 200 ml. Acetabular and femoral component positioning were within the recommended parameters in 96% of the patients. The mean hospital stay was three days. The mean Harris hip score was 95.6 within three to six months postoperatively. There were no early complications in this study group. The authors concluded that this PATHA technique is an improvement from previously reported studies of MIS techniques for THAs. It is an easy, user-friendly technique with a short learning curve. It does not decrease pre-operative visualisation and component positioning is safe and reliable. Early recovery and shorter hospital stay are other advantages and are safe for patients.

Overview of pros and cons in approaches to the hip in primary total hip arthroplasty

Posterior

Contra

Easy approach Short learning curve

Sciatic nerve at risk Inferior gluteal artery at risk Postoperative dislocation rate* Early postoperative restrictions Disruption femoral head blood supply in resurfacing

Avoids abductor muscles Less bleeding Rapid recovery

Anterior

Easy lengthening of incision Better component positioning Anatomical

Anterolateral

Preserves posterior structures Preserves abductor muscles Low dislocation rate Quick recovery without restrictions Easy lengthening of incision Easy approach

Review of published evidence MIS is increasing in popularity. There is a strong drive from patients, industry, surgeon marketing campaigns, and the media to perform THA through a small incision. The advantage of the minimally invasive approach is the lack of disturbance of the soft tissues surrounding the hip joint, less pain, faster recovery and the potential for earlier return to work, shorter hospital stay and improved cosmetic results. The potential disadvantages of MIS in THA are poorer intraoperative visualisation of the anatomy, longer operation times, nerve injuries, femoral fractures, malpositioning and the learning curve effect that has to be surmounted by the ­surgeon. Each approach has its own advantages and disadvantages and it is the preference of the surgeon as to which approach is used (Table 2). A comparison between all possible different approaches is difficult. Some approaches are recently introduced and not in widespread use, with limited clinical data. Other approaches are not commonly used because of the long ­learning curve. Most recent studies compare the MIS approach to the traditional approach. Meneghini et al,2 reported on a randomised, prospective study of three MIS approaches in THA. The patients underwent preoperative and post-operative gait analysis. They randomised 24 hips to one of three approaches (2-incision, mini-posterior, and mini anterolateral). All groups showed improvements in gait parameters in the early post-operative period. The anterolateral group demonstrated a decrease in the vertical ground reaction force at mid-stance, whereas the other 2 groups showed no significant change. There was no significant benefit of the 2 incision approach over the posterior approach. Despite the MIS approach, the anterolateral group showed a Trendelenburg gait pattern in the early recovery period. Furthermore, of the 8 patients in the two-incision group, 5 patients sustained (temporary) lateral femoral cutaneous nerve palsy. In a retrospective matched-pair controlled study Duwelius et al performed a comparison of the two-incision MIS technique and the mini-posterior approach for total hip arthroplasty.14 They evaluated the Harris Hip score, the Medical Outcomes Study 36-Item Short-Form Health survey, the Medical outcomes Study Sleep Scale, and the WOMAC scores. Mean operation time

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Pro

Short learning curve

2-incision

Easy lengthening of incision Wide view Low dislocation rate Anatomical Preserves posterior structures Preserves abductor muscles Quick recovery Easy lengthening of incision

Special traction table required LFCN at risk Long learning curve

Disturbance of abductor muscles Superior gluteal nerve at risk Heterotopic calcification

LFCN at high risk High rate of femoral fractures Difficult Long learning curve

*Without meticulous closure of the posterior structures.

Table 2

and blood loss was less in the mini-posterior approach. Patients treated with a two incision operation had, overall, better function and there were no more complications in the two-incision group than in the mini-posterior group. There was no significant difference in pain experience between the two groups. Radiographic analysis of both THA components showed a significant difference in acetabular positioning, with better results in the ­posterior 32

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Mini-symposium: What’s new in hip replacement — basic principles

hospital stay, implant positioning, limb length differences, pain scales, WOMAC scores, Harris hip scores and other functional scores were comparable between these two groups. The authors concluded that the mini-invasive anterolateral approach to the hip is an approach with a long learning curve. But once the learning curve is passed results must improve, with a decrease in complications and in pre-operative blood loss. The learning curve for MIS in THA was reviewed by Archibeck and White.17 They reviewed the results of the first ten MIS procedures performed by surgeons who followed and completed the MIS two-incision course. They observed 851 minimally invasive THAs performed by 159 surgeons. The incision length varied between 1.5 to 19 cm for the anterior incision and 1 to 21 cm for the posterior incision. The average operation time of all cases was 148 minutes. The average operation time by the surgeon’s tenth case had decreased to 130 minutes. The estimated blood loss averaged for all cases was 496 ml. The average blood loss at the surgeon’s tenth case was 427 ml. Only 47% of cases were performed without complications. Early complications were fractures of the femur (6,5%), nerve injuries (3,2%), infections (0,9%), dislocations (0,9%), and early revisions (0,9%). Surgeons performing 25 to 50 THAs per year, had a complication rate of 26,5%. This complication rate is significantly higher than in surgeons performing 50 to 100 (7,1%), 100 to 150 (8,6%), or more than 150 (7,1%) THAs per year. The complication rate was not significantly decreased by the surgeon’s tenth case. This study confirms that MIS has a long learning curve (more than 10 cases) and it is best performed by an experienced, specially trained surgeon with a high volume of these MIS cases. There are concerns about the reliability and reproducibility of component placement in MIS. Williams et al reviewed component positioning in total hip arthroplasty performed by one surgeon with a two-incision, minimally invasive approach compared to a standard lateral approach.18 A postoperative radiographic assessment of both components revealed no significant differences. There was also no significant difference in complication or reoperation rate between both groups. They concluded that component positioning is not compromised by either approach. THA can be achieved in a reliable and reproducible fashion using minimally invasive hip surgery. The advantage of the anterolateral approach is supposed to be a lower dislocation rate. In a large review article by Khan et al. in 1981 the dislocation rate was 1.9 percent in the anterior approach.19 The posterior approach had a dislocation rate of 2.1 percent. As mentioned earlier, an enhanced repair of the soft tissues can reduce the rate of dislocation to less than 1%. Other factors, such as femoral head size, orientation of the cup and stem have more impact on dislocation rate than does the approach. Patient selection is of eminent importance. Negative factors are uncontrolled epileptic patients, alcohol addiction, mental disturbance, neurological disorders with abductor weakness and reoperations on the hip. Patients with ASA scores of 1–2 have a lower dislocation rate. Rheumatoid arthritis patients have a higher risk for dislocation. The surgeon’s case volume seems also to be of importance, though this is contradicted by some. The improved cosmetic appeal of the mini-incision variations is questioned by Woolsen and Mow.20 Excluding the persistent wound drainage in two patients in the standard incision group who were on haemodialysis for chronic renal failure, the

approach. There were no differences in stem positioning. Both approaches decreased the average hospital length of stay compared to the traditional THA approach. Mean discharge was for the 2-incision approach 30 hours and for the mini-­posterior approach 45 hours. A clinical, comparative study of the mini-anterior and the mini-posterior approach was undertaken by Nakata et al.15 They classified 182 consecutive patients into two groups by surgical approach. They performed 99 THAs with a mini-anterior approach, and 96 total hip replacements with a mini-posterior approach. The goal of this study was to compare and clarify the short-term clinical and radiographic outcomes of minimally invasive THA performed by the mini-posterior and the mini-anterior approach. There was no difference in operation time and blood loss was less in the mini-posterior group. There was a significant difference in Lewinnek´s safe-zone cup positioning between the two groups in favour of the mini-anterior approach. No difference in positioning of the femoral stem was found. There were no differences in presence of Trendelenburg´s sign pre-­operatively or at 5 days after surgery. At three weeks post-operation there were significant differences in presence of Trendelenburg´s sign, and walking velocity, and in the use of assistive walking aids, in favour of the mini-anterior approach. Single leg stance recovered faster in the mini-anterior group, and there was a significant difference in the ability to walk at 2 months. There were no significant differences in total hip functional score pre-operatively, or at 2 and 6 months after operation between the two groups. The results of this survey suggest a quicker recovery of gait and hip function after minimally invasive THA performed through a mini-anterior approach when compared to a mini-posterior approach. Chen et al compared the anterolateral transgluteal approach to the two-incision minimally invasive approach in terms of clinical outcome in 166 patients treated with primary THA.16 They performed 83 THAs with a two-incision technique and 83 with an anterolateral approach. The 2-incision MIS technique had a longer operation time, increased blood loss and a higher complication rate. Complications included temporary lateral femoral cutaneous nerve palsy in 27 patients, 6 proximal femoral fractures and 1 superficial wound infection. The anterolateral approach was complicated by 4 proximal femoral fractures, 1 superficial wound infection and 1 dislocation (the latter ­occurring in a traffic ­accident 2 months after surgery). There was no significant difference in hospital stay. A functional analysis at 3 and 6 months using the Harris Hip score and WOMAC score showed significantly better hip function in the 2 incision MIS technique. However, subsequent follow-up at 1 and 2 years postoperatively revealed no significant persisting difference between the two approaches. There was a significant difference in NSAID use postoperatively in favour of the two-incision MIS approach. Positioning of the stem was not significantly different between the two groups. There was significantly better positioning of the acetabular component in the anterolateral approach group. In a prospective, comparative study, Laffosse et al compared 35 anterolateral mini-invasive THAs to 43 minimally invasive posterior approached hips.3 The anterolateral technique had a significantly longer operation time and intra-operative complication rate compared to the posterior approach. Blood loss was less in the posterior approach, but not statistically so. Length of

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Mini-symposium: What’s new in hip replacement — basic principles

­ revalence of wound complications was higher in the minip incision group than in the standard incision group. They also concluded that there was no evidence that the mini-incision technique resulted in less bleeding or less trauma to the soft tissues of the hip, factors that would have produced a quicker recovery and a shorter hospital stay, than did the standard technique. Their study failed to confirm the positive clinical outcomes reported by previous uncontrolled cohort studies, and the findings suggest that further analysis of this new technique is needed before it can be recommended for general use. Goldstein et al also questioned the cosmetic appeal of miniincision hip surgery.21 Their survey shows a higher percentage of wound complications, particularly wound edges curling into the scar. Scar length and cosmetic appeal was not as important as pain relief or implant longevity in 98% of the patients.

6 Mulliken BD, Rorabeck CH, Bourne RB, Nayak N. The surgical approach to total hip arthroplasty: complications and utility of a modified direct lateral approach. Iowa Orthop J; 15: 48–61. 7 Jacobs MA, Goytia RN, Bhargava T. Hip resurfacing through an anterolateral approach surgical description and early review. J Bone Joint Surg Am 2008; 90: 38–44. 8 Matta JM, Shahrdar C, Ferguson T. Single-incision anterior approach for total hip arthroplasty on an orthopaedic table. Clin Orthop Relat Res 2005; 441: 115–124. 9 Kennon RE, Keggi JM, Wetmore RS, Zatorski LE, Huo MH, Keggi KJ. Total hip arthroplasty through a minimally invasive anterior surgical approach. J Bone Joint Surgery Am 2003; 85: 39–48. 10 Berry DJ, Berger RA, Callaghan JJ, et al. Symposium: minimally invasive total hip arthroplasty. Development, early results, and a critical analysis. J Bone Joint Surg Am 2003; 85: 2235–2246. 11 Mardones R, Pagnano MW, Nemanich JP. Muscle damage after total hip arthroplasty done with the two-incision and mini-posterior techniques. Clin Orthop Relat Res 2005; 441: 63–67. 12 Pagnano M, Lewallen D, Hanssen A. Two-incision THA in 80 consecutive unselected patients: prevalence of complications. Program and abstracts of the American Academy of Orthopaedic Surgeons 72nd Annual Meeting; February 23–27, 2005; Washington, DC. Course Number 144. 13 Penenberg Brad L, Bolling W Seth, Riley Michelle. Percutaneously assisted total hip arthroplasty (PATH): a preliminary report. J Bone Joint Surg Am 2008; 90: 209–220. 14 Duwelius PJ, Burkhart RL, Hayhurst JO, Moller H, Butler JBV. Comparison of the 2-incision and mini-incision posterior total hip arthroplasty technique, a Retrospective Match-Pair Controlled Study. J Arthroplasty 2007; 22(1): 48–56. 15 Nakata K, Nishikawa M, Yamamoto K, Hirota S, Yoshikawa H. A clinical comparative study of the direct anterior with mini-posterior approach; two consecutive series. J Arthroplasty 2008: [Epub ahead of print]. 16 Chen DW, Hu CC, Chang YH, Yang WE, Lee MS. Comparison of clinical outcome in primary total hip arthroplasty by conventional anterolateral transgluteal or 2-incision approach. A retrospective, case-controlled investigation with 2-year follow-up. J Arthroplasty 2008: [Epub ahead of print]. 17 Archibeck MJ, White Jr. RE. Learning curve for the two-incision total hip replacement. Clin Orthop Relat Res 2004; 429: 232–238. 18 Williams SL, Bachison C, Michelson JD, Manner PA. Component position in 2-incision minimally invasive total hip arthroplasty compared to standard total hip arthroplasty. J Arthroplasty 2008; 23(2): 197–202. 19 Ali Khan MA, Brakenbury PH, Reynolds IS. Dislocation following total hip replacement. J Bone Joint Surg Br 1981; 63: 214–218. 20 Woolson ST, Mow CS, Syquia JF, Lannin JV, Schurman DJ. Comparison of primary total hip replacements performed with a standard incision or a mini-incision. J Bone Joint Surgery Am 2004; 86: 1353–1358. 21 Goldstein WM, Ali R, Murphy SI, et al. Patient priorities and importance of cosmesis after THA: standard versus minimal incision. Presented at the American Academy of Orthopaedic Surgeons 72nd Annual Meeting, Washington, DC, February 23–27, 2005.

Conclusion The choice of approach used to perform a primary remains controversial. The primary goal of hip replacement is to achieve pain relief, functional recovery and implant longevity through a safe and reproducible approach without complications. Mini-incision and minimally invasive approaches are promising in terms of hospital stay and functional recovery. Although recent studies are confirming that component placement in minimally invasive surgery is safe and reliable, no long-term results have yet been published to support this view. Early enthusiasm has been tempered by high observed complication rates. Further follow-up and development is necessary to compare the results with classical, more extensive approaches. ◆

References 1 Khan RJK, Fick D, Khoo P, et al. Less invasive total hip arthroplasty. Description of a new technique. J Arthroplasty 2006; 21(7): 1038–1046. 2 Meneghini RM, Smits SA, Swinford RR, Bahamonde RE. A randomized, prospective study of 3 minimally invasive surgical approaches in total hip arthroplasty comprehensive gait analysis. J Arthroplasty 2008; 23(6 Suppl. 1): 68–73. 3 Laffosse JM, Chiron P, Molinier F, Bensafi H, Puget J. Prospective and comparative study of the anterolateral mini-invasive approach versus minimally invasive posterior approach for primary total hip replacement; early results. Int Orthopaedics 2007; 31: 597–603. 4 Ogonda L, Wilson R, Archbold P, et al. A minimal-incision technique in total hip arthroplasty does not improve postoperative outcomes: a prospective randomized controlled trial. J Bone Joint Surg Am 2005; 87: 701–710. 5 Dorr LD, Maheshwari AV, Long WT, Wan Z, Sirianni LE. Early pain relief and function after posterior minimally invasive and conventional total hip arthroplasty: a prospective, randomized, blinded study. J Bone Joint Surgery Am 2007; 89: 1153–1160.

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Mini-symposium: what’s new in hip replacement — BASIC PRINCIPLES

(v) Prevention of dislocation in hip arthroplasty SW Veitch SA Jones

Abstract Dislocation following primary and revision hip surgery is a common complication. The cause is often multi-factorial including patient factors, surgeon factors, implant design, implant orientation, and soft tissue factors. This article looks at ways of reducing the rate of hip dislocation. Figure 1 Secondary Osteoarthritis following previous acetabular fracture.

Keywords component position; dislocation; hip replacement; stability

(Figure 5). A second revision involved acetabular ­ component exchange with a constrained liner (Figure 6) but this too failed (Figure 7). At a third revision the liner was removed, a metal shell cemented into the existing cup (Figure 8) and an even larger head was inserted to maximise the head neck ratio but this too dislocated (Figure 9). In this case each revision operation addressed only a single aspect in the hip arthroplasty that could potentially prevent further instability. The final revision (Figure 10) addressed multiple issues; component position by revising both cup and stem, the head/neck ratio was maximised, a constrained liner and a trochanteric advancement osteotomy to address soft tissue deficiency. Thereafter there was no further instability. The same principles form the cornerstones of prevention of ­dislocation.

Introduction Dislocation occurs between 0.3% and 10% after primary total hip replacements and up to 28% after revision hip replacement.1 It is most likely to occur in the first three months after surgery, but the cumulative risk increases over the years following implant insertion. While half of those patients who dislocate do so only once, the remainder suffer recurrent instability and often require further surgical intervention.2 The morbidity and cost of revision surgery for instability is considerable and clinical outcome scores and global outcome assessments in patients who have suffered dislocation of their hip are significantly worse than those without3 and do not improve despite successful revision surgery. The cause of dislocation is most often multi-factorial. Every hip replacement has the potential to dislocate and through careful pre-operative assessment, implant choice, component positioning, and surgical technique the risk of dislocation can be reduced. Therefore assessment of patients, risk is an important part of pre-operative planning. This article reviews the risk factors and mechanisms leading to hip dislocation, intra-operative techniques, and the available implants that can improve the stability of a hip replacement.

Mechanism of dislocation The general underlying mechanism of dislocation is impingement at the maximum extent of the primary arc of movement

An illustrative case of recurrent dislocation This case highlights the challenges posed when treating patients with recurrent dislocation. A 72-year-old man with a previous history of acetabular fracture underwent a left total hip replacement (Figures 1 and 2). He subsequently had several episodes of posterior hip dislocation (Figure 3). Even after revision surgery using a larger ­ diameter head and increased head length (Figure 4), he continued to ­ dislocate

SW Veitch MD FRCS(Tr & Orth) is a Lower Limb Arthroplasty Fellow at the University Hospital Llandough, Cardiff, UK. SA Jones MSc FRCS(Tr & Orth) is a Consultant Orthopaedic Surgeon at the University Hospital Llandough, Cardiff CF16, UK.

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Figure 2 Primary Hybrid Total Hip Replacement (THR).

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Mini-symposium: what’s new in hip replacement — BASIC PRINCIPLES

Figure 3 Dislocated Primary THR.

Figure 5 Dislocated revision THR.

Pre-operative planning

at the articulation interface (Figure 11). Levering-out of the joint ­follows and when this exceeds the “excursion distance” or “jump-distance” of the bearing then dislocation occurs. Jump distance is typically half the diameter of the femoral head and it follows that by using a larger diameter femoral head the primary arc of movement before impingement is increased and also the jump distance, thus increasing stability (Figures 12 and 13). Femoral neck geometry also affects impingement; a more slender femoral neck allows a greater primary arc of movement. Therefore by maximising the head neck ratio there is a significant increase in the stability of the articulation. When considering using larger diameter bearings the materials selected and effect on wear must also be taken into account as use of hard-on-soft bearings (metal-on-UHMWPE – Ultra High Molecular Weight Poly-Ethylene) an increase in head size results in increased volumetric wear, but this can be reduced by using highly cross-linked UHMWPE. In hard-on-hard bearings fluid film lubrication is enhanced by larger diameter bearings and wear is not adversely affected by femoral head size.

Comprehensive pre-operative planning must utilize information gained from both patient history and clinical examination. The aim is to restore the joint biomechanics to provide a stable reconstruction and achieve soft tissue balancing of the hip. Preoperative templating guides the surgeon to the type and size of implant and the component position that will optimize the ­biomechanics of the hip joint helping to prevent dislocation, by assessing leg length discrepancy, hip centre, femoral offset and femoral neck cut. Often valuable information can be gained from templating the normal side along with the affected hip joint. Choice of implant that provides a sufficient range of sizes in order to restore hip biomechanics is obviously crucial. Instability is usually multi-factorial, and these fall into five major sub-groups: • Patient Factors • Surgeon Factors • Implant Design

Figure 4 Revision THR with increased head size and offset.

Figure 6 2nd revision THR with acetabular.

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Figure 7 Dislocated constrained component.

Figure 9 Further instability following 3rd revision surgery.

• Implant Orientation • Soft Tissue Factors

Surgeon factors There is evidence from joint registers and insurance company data that higher volume hip surgeons have a lower dislocation risk. Those surgeons working in specialist centres have also demonstrated lower rates of dislocation compared to others. A very significant surgeon factor is the selection of surgical approach. 80% of dislocations after hip replacement occur in the direction of the approach to the joint emphasising the effect that both surgeon and technique have on outcome. The posterior approach has been associated with a higher dislocation rate compared to the direct lateral approaches. However by preserving the short external rotators and capsule and then repairing them with trans-osseous sutures, the dislocation rate following the posterior approach is reduced to a similar incidence to that of lateral approaches.2 Similarly trochanteric

Patient factors Patient factors increasing the risk of instability are assessed mainly from the history. Patients over 80 years old are at significantly greater risk of dislocation reported as up to 15% 4 possibly due to both impaired cognitive and muscle function. Other significant factors include alcoholism, neurological conditions (e.g. epilepsy, stroke, Parkinson’s disease), previous hip surgery, hip trauma, and revision hip surgery, for example elderly patients who undergo hip arthroplasty for failure of fixation of a hip fracture. Patient compliance is also a significant factor; patients suffering from dementia and/or psychiatric disorders are at increased risk. Whist often there is nothing that can be done to improve these patient factors, they must be taken into account both with regards to the implant choice and pre-operative patient counselling regarding the risk of instability.

Figure 10 Successful 4th revision surgery with exchange of both acetabular and femoral components, a large diameter constrained bearing and an advancement trochanteric osteotomy to tension soft tissues.

Figure 8 3rd revision THR with large diameter metal-on-metal bearing.

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Figure 13 Increasing the head diameter increases the jump distance before dislocation occurs.

Acetabular component design also has a significant effect on the primary arc and hence stability, particularly liner design and elevated acetabular rims. Use of an elevated rim liner reduces the primary arc of movement and such liners should not be routinely used to compensate for inappropriate implant positioning. There are systems which have face-changing acetabular liners available that alter the angle of the socket bore without compromising the primary arc. Constrained acetabular liners capture the femoral head thereby increasing the force needed to “lever-out” (Figure 14). There are a variety of designs available and several have reported ­successful medium term results in primary cases and revision surgery for instability. The nature of the bearing constraint results in a reduced primary arc of movement and therefore poorly positioned implants will cause even greater impingement if a constrained liner is inserted. The use of constrained liners is not a substitute for correct implant positioning. Constrained liners also increase the interface stress and can lead to liner failure and cup loosening. They should principally be used in cases of soft tissue deficiency either secondary to neurological cause or mechanical integrity.

Figure 11 Key steps in dislocation are impingement at the limit of the primary arc of movement followed by levering out and once jump distance exceed dislocation.

non-union following a trans-trochanteric approach increases hip instability, so surgical technique when utilising lateral approaches is important when repairing the abductor mechanism to reduce the risk of abductor detachment, anterior hip dislocation and a post-operative Trendelenberg limp. Which ever surgical approach is preferred meticulous repair of the soft tissues violated is vital.

Implant orientation One of the greatest variables in hip arthroplasty surgery is component orientation. Lewnineck et al described the recommended “safe-zone” for cup orientation as 40 +/− 10 degrees abduction or coronal tilt and 15 +/− 10 degrees of cup anteversion. An increase in the dislocation rate from 1.5% to 6.1% was seen if these values were exceeded.5 Many factors affect accurate cup placement. Patient positioning on the operating table and maintaining the pelvis in a fixed position can have a significant effect on implant positioning. To minimize the effect of change of the patient’s position during surgery and the consequent component mal-position, a useful local landmark when positioning the cup is the transverse acetabular ligament (Beverland et al).6 Placing the cup parallel to this ligament will prevent excessive anteversion or retroversion of the cup and assessment of the socket relationship to the transverse ligament after insertion acts as a secondary check on component orientation. Many socket introducers have an attachable reference rod to measure the abduction angle. The femoral component should be anteverted 10–25 degrees. Ranawat7 described an intra-operative method to measure the combined anteversion of both acetabular and femoral components; with the hip flexed to approximately 30 degrees the femur is internally rotated until the profile of the femoral prosthesis is parallel to the face of the acetabular cup and the cup appears to provide equal coverage of the head in all directions. The degree

Implant design As already discussed using an implant with slender neck geometry and larger head size can increase the primary arc which has a significant effect on stability. The effect of longer femoral heads is to increase both the vertical height and leg length and offset of the centre of hip rotation. However when longer modular head sizes are used, they often have a skirt to increase the length of the bore to ensure safe engagement onto the femoral component trunion. Such skirted femoral heads reduce the primary arc and increase risk of impingement and thus should not be used with caution. It is recommended that they should not used in conjunction with constrained liners. In general it is a safer method if possible to use a high-offset femoral component rather than skirted femoral head.

Figure 12 Increasing the head diameter increases the primary arc of movement before impingement occurs.

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s­ tability, a minimum of 45 degrees is recommended. If hip instability is evident then both the femoral and acetabular orientation particularly anteversion should be checked, and any soft tissue or bony cause for impingement such as thickened capsule and osteophytes should be sought.

Key principles in preventing dislocation • Identify the at risk patient • Avoid component malposition • Restore biomechanics of the hip by balancing soft tissues and ensuring adequate femoral offset • Maximise head to neck ratio • Consider constrained acetabular component in high risk ­patients.

Conclusion The aim of hip replacement surgery is to provide the patient with a pain free, stable hip. Dislocation following primary and revision hip surgery is a common complication and the cause is usually multifactorial. Patients who are at increased risk of dislocation should to be identified pre-operatively and surgery planned to maximise joint stability. Templating of radiographs helps the surgeon to select implants to restore the biomechanics of the hip. Close attention to component position is crucial step to prevent dislocation. Intra-operative assessment of stability is vital and if the hip is less stable than desirable, identification and removal of impinging tissue or correction of component position is essential. ◆

Figure 14 A constrained acetabular component.

of internal rotation of the leg is then measured. Ideally with the components parallel, the femur should be internally rotated about 45 degrees to the coronal plane of the patient, making the combined anteversion of the two components 45 degrees. Soft tissue factors Failure to balance the soft tissues around the hip can result in instability either due to inadequate soft tissue tension in the abductors or from restriction of the primary arc and consequent levering out due to failure to correct soft tissue contracture. Stem mal-position in varus or valgus can affect the offset and thus alter the abductor tension. Soft tissue and bony impingement at the extremes of hip motion can cause the femoral head to lever out of the socket. In flexion and adduction, a thickened anterior hip capsule, anterior osteophytes on the femur or acetabulum, or anterior heterotopic bone can cause anterior impingement, resulting in posterior dislocation. Detachment of the greater trochanter either through avulsion or non-union increases the risk of dislocation from 2.8% when the trochanter healed without displacement to 17.6% with a displaced trochanteric non-union.8

References 1 Parvizi J, Picinic E, Sharkey PF. Revision total hip arthroplasty for instability: surgical techniques and principles. J Bone Joint Surg Am 2008; 90: 1134–42. 2 Blom AW, Rogers M, Taylor AH, Pattison G, Whitehouse S, Bannister GC. Dislocation following total hip replacement: the Avon Orthopaedic Centre experience. Ann R Coll Surg Engl 2008; 90: 658–62. 3 Kotwal RS, Ganapathi M, John A, Maheson M, Jones S. Outcome of closed reduction for dislocation following primary total hip arthroplasty. JBJS British Edition, in-press. 4 Newington DP, Bannister GC, Fordyce M. Primary total hip replacement in patients over 80 years of age. J Bone Joint Surg Br. 72-B(3): 450–452. 5 Lewinnek GE, Lewis JL, Tarr R, Compere CL, Zimmerman JR. Dislocations after total hip replacement arthoplasties. J Bone Joint Surg Am 1978; 60: 217–20. 6 Archbold HA, Mockford B, Molloy D, McConway J, Ogonda L, Beverland D. The transverse acetabular ligament: an aid to orientation of the acetabular component. J Bone Joint Surg Br 2006; 88-B: 883–886. 7 Ranawat CS, Rao RR, Rodriguez JA, Bhende HS. Correction of limblength inequality during total hip arthroplasty. J Arthroplasty 2001; 16: 717–20. 8 Woo RY, Morrey BF. Dislocations after total hip arthroplasty. J Bone Joint Surg Am 1982; 64: 1295–306.

Intra-operative assessment of stability Trial reduction prior to insertion of the definitive femoral implant is a vital intra-operative step to permit leg length assessment and offset and stability of the hip. Accurate pre-operative measurement and patient positioning is key to measurement of leg length irrespective of the method used.9 The offset and jump distance can be assessed by the shuck test; with the hip in both flexion and extension, the index and middle finger are placed around the neck of the stem and force is applied in the direction away from the socket. Excessive motion is indicative of poor soft tissue balance and that more offset is required. The primary arc of motion and stability must also be tested. Firstly, with the hip and knee extended, external rotation is applied looking for anterior instability. Secondly, flexing the hip to 90 degrees and internally rotating the leg assess posterior instability. The angle formed between the coronal plane and the tibia at the point that the hip dislocates is a good guide of

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(vi) Hip outcome measures

s­ urgery and even admission to the intensive care unit. As a patient with a SSI spends on average twice the length of time in hospital, SSI is not only distressing for the patient, it is an economic burden for the health care provider. It is proposed that from 2010, all UK hospital SSI data will be available on the “NHS Choices” website. Historically, the success or failure of an orthopaedic intervention was assessed and reported by the operating surgeon. This is changing, now more emphasis is placed on patient-centered assessments and patient-reported quality of life. There are several quality of life assessments available, which fall into three broad categories: generic, disease-specific and joint-specific. Generic surveys aim to investigate all aspects of quality of life and can be used to assess any medical or surgical intervention. Disease specific tools concentrate on disability relating to a particular condition or single disease entity. Joint specific tools are used to assess the impact of disease in one particular joint. Analysis of quality of life outcome data has previously been at group level. However, many recent studies have focused on individual patient outcomes, either by responder criteria or by stateattainment criteria. In the former case, each patient is classified as a responder or a non-responder to treatment based on whether the change in health status exceeds a pre-defined threshold. With state-attainment criteria, a patient is classified not on the basis of change, but on whether a certain level of low symptom severity is attained. Research in both areas is experimental but may provide more relevant results than group level studies. Patient co-morbidity can affect the results of outcome studies. The Physiological and Operative Severity Score for enUmeration of Mortality and morbidity (POSSUM)1 was developed to overcome this problem. Each patient is given a score according to physiological status and the severity of the surgery they are to undergo. In clinical trials, the mean POSSUM scores of all patient groups must be similar to ensure that results are not skewed by patient co-morbidity. A validated orthopaedic version of ­POSSUM is now available.

Miss E Ashby MPW Grocott FS Haddad

Abstract In the UK the Department of Health published a report earlier this year entitled ‘High Quality Care For All’ which requires that all hospitals must collect and publish surgical outcome data by 2010, including post­operative complication rates, surgical site infection rates and patientcentered quality-of-life assessments. This paper gives an overview of the outcome measures used to assess interventions on the hip.

Keywords outcome measures; quality of life; questionnaires

Introduction Outcome measures and scores are used to assess the impact of orthopaedic interventions for many purposes such as clinical trials, comparing different interventions, alternative prostheses, different methods of fixation and surgical techniques. They are used to assess elements of peri-operative care such as the use of prophylactic antibiotics, increased physiotherapy input and different regimens of post-operative analgesia, as well as for audit purposes comparing individuals, departments, hospitals and regions. This enables good practice to be highlighted and propagated, and for remedial action to be instituted where practice is sub-standard. Orthopaedic surgical outcomes can be assessed in several ways, eg. generic clinical outcomes, radiological outcomes, postoperative complication rates, re-operation rates, length of inpatient stay and health-related quality-of-life. Generic clinical outcome measures assess overall mortality and morbidity following surgery. This includes mortality at various time-points after surgery, length of post-operative in-patient stay, and incidence of specific complications (e.g. hip dislocation and periprosthetic fracture). Surgical Site Infection (SSI) is a major risk, giving rise not only to patient pain and discomfort, but also to wound ­ dehiscence, deep infection and generalized sepsis, necessitating ­ further

What makes a good outcome measure? If they are to be good descriptors of clinical or quality-of-life phenomena, outcome measures must fulfill certain psychometric criteria. They must be reliable, validated and sensitive to change and questionnaires should be acceptable to patients, simple, easy to use and score, and preferably short! Reliability is a term used inconsistently in the literature. It is a measure of the degree to which subjects can be distinguished from each other. It can be defined as the ratio of variance between subjects to the total variance. A reliability value of zero indicates a completely unreliable measure, where as a reliability value of one indicates a perfectly reliable measure. Reliability is dependent on the relationship between the measurement error and the variability between subjects. Therefore, internal consistency and reproducibility are both components of reliability. Internal consistency determines whether a survey measures a single variable. The test for internal consistency is Cronbach’s alpha. This summarizes the internal correlation of all questions in a survey onto a single scale. The higher the alpha coefficient, the greater the likelihood the questionnaire is tapping into a single variable and is free from random error.

Miss E Ashby BA MB BChir MA(Cantab) MRCS is Orthopaedic Registrar at Chase Farm Hospital, Middlesex, UK. MPW Grocott BSc MBBS MRCP FRCA is Senior Lecturer in Critical Care Medicine at Surgical Outcome Research Centre, Joint UCLH/UCL Comprehensive Biomedical Research Centre, London, UK. FS Haddad BSc MCh(Orth) FRCS Ed FRCS(Tr & Orth) Consultant Orthopaedic Surgeon, University College London Hospital, UK.

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acceptable to patients. It was designed to identify morbidity of a type and severity that could delay discharge from hospital using a simple data collection process to allow the routine screening of large numbers of patients and concentrates on indicators of clinically important dysfunction in key organ systems (e.g. inability to tolerate enteral diet) rather than traditional diagnostic categories (e.g. DVT). The survey assesses nine domains of morbidity (Table 1) using readily available data and requires no additional investigations; all data are obtained from observation charts, medication charts, patient notes, routine blood test results and direct questioning and observation of the patient. The relationship between short-term generic clinical outcome and long-term quality of life outcome is not yet clearly defined. One significant problem with all quality of life outcome measures is the length of time taken to collect the data. If short-term outcome measures could predict longer-term quality of life, they could be used as early surrogate markers for longer term function and patient satisfaction. While POMS provides early post­operative information, it is as yet unknown whether there is any correlation between POMS data and long-term quality of life data. Hence both short-term and long-term outcome measures are needed to assess the success of any intervention. As well as being a scale to measure and compare post­operative morbidity, POMS can also be used as a tool to assess when patients are ready for discharge. When the POMS score is

Reproducibility investigates if a questionnaire produces the same results if repeated under the same conditions. Interobserver reliability (agreement between two or more observers on the same occasion), intra-observer reliability (same observer on separate occasions), and test-retest reliability (stability of the measure over time in the same subject) are all aspects of reproducibility. Paired sets of data can be compared using the kappa coefficient or the coefficient of reliability according to the method of Bland & Altmann. A higher coefficient indicates a more reproducible questionnaire. Validity examines whether a questionnaire measures what it is proposed to measure. Several types of validity exist: content and face validity, criterion (convergent/concurrent) validity and construct validity. Face and content validity assess whether a survey fully investigates the intended topic of interest. Content validity can be increased by conducting exploratory interviews with patients prior to writing the questionnaire. This will elucidate the priorities and concerns of patients rather than imposing clinical assumptions. Face and content validity are subjective measures with no statistical method to assess them. Criterion validity assesses how a new questionnaire compares to an established questionnaire on the same subject i.e. the current ‘gold standard’. This approach is only tenable when such a ‘gold standard’ is available and begs the question of why a new measure is being developed. For measures where no “gold standard” exists, construct validity examines the extent to which the results from the questionnaire support predefined hypotheses. It can be measured using Pearson correlation coefficients between the total score for the questionnaire and other measures considered to be associated with the underlying construct being investigated. Construct validity investigates if a single concept is being measured by the questionnaire. If construct validity is proven, scores can be combined to produce one overall score. Construct validity is tested by calculating the correlation between scale scores. Tests of sensitivity or responsiveness investigate if a survey is capable of detecting clinically significant changes. The definition of sensitivity is the difference in the mean pre-operative and post-operative scores, divided by the standard deviation of the pre-operative scores. An effect size of one is equal to a change of one standard deviation in the sample.

Criteria for a positive POMS score Variable

Criteria for positive result

Pulmonary

Requires supplementary oxygen or ventilatory support Currently on antibiotics or temperature >38 °C in the last 24 hours Oliguria (<500 ml/day), elevated creatinine (>30% pre-op level), catheter in-situ (for non-surgical reason) Unable to tolerate enteral diet for any reason Diagnostic tests or treatment within the last 24 hours for: myocardial infarction, hypotension (requiring pharmacological therapy or fluids >200 ml/hour), atrial/ ventricular arrhythmia or cardiogenic pulmonary oedema Presence of new focal deficit, coma, confusion, delirium Wound dehiscence requiring surgical exploration or drainage of pus from operative wound with or without isolation of organisms Requirement of blood transfusion, platelets, fresh frozen plasma or cryoprecipitate within the last 24 hours Wound pain requiring parenteral opioids or regional anaesthesia

Infection Renal

Gastrointestinal Cardiovascular

Short-term clinical outcome measures There are a variety of ways to describe the overall clinical impact of operative interventions and the associated physiological disturbance of undergoing major surgery, all of which have their limitations. Mortality is now so infrequent for most types of orthopaedic surgery that it is not a useful comparative index. The event rate is so low that very large numbers of operations would have to be compared to demonstrate a meaningful difference in outcome. Length of hospital stay is sometimes used as a surrogate for clinical outcome but this is well known to be influenced by many factors other than the health status of the patient. It is well known that post-operative complications and morbidity following surgery are poorly recorded, which led to the development of the Post-Operative Morbidity Survey2 (POMS). It has been used in post-operative morbidity, outcomes and effectiveness research and has been shown to be reliable, valid and

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Central nervous system Wound complications

Haematological

Pain

Table 1

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erythema, serous and purulent exudates, and the clinical consequences of infection such as prolonged hospital stay and readmission. A score of over 10 indicates an increasing probability and severity of infection (Table 2). The original ASEPSIS scoring method was psychometrically tested and found to be objective and repeatable but the most recent revised version has not undergone the same evaluation. Scoring methods provide more detailed and objective information regarding SSI than CDC and NINSS but they are more costly, complicated and time-consuming to perform, the average time taken to collect the data and calculate an overall ASEPSIS score is 59 minutes.

zero, a patient is likely to be fit for discharge. Therefore, as well as providing useful clinical research and audit data, POMS may be useful to assess the efficiency of a hospital’s discharge processes.

Surgical site infection Wound surveillance in orthopaedic surgery became mandatory in the NHS in England in 2004. Patient follow-up is essential in any wound surveillance program, as half of Surgical Site Infections (SSI)s present after hospital discharge. Reported SSI rates depend on the diagnostic criterias, case mix, the thoroughness of surveillance and documentation, and the length of patient ­follow-up. A reliable and repeatable method for diagnosing SSI is essential for audit and treatment purposes. There is a misconception that SSIs are simple to define and diagnose. However, several definitions of SSI exist and the criteria used vary between surgeons. If SSI rates are to be published, as suggested in ‘High Quality Care For All’ published by the Department of Health,3 the same validated method for diagnosing SSIs must be used by all institutions. Traditionally SSIs were diagnosed by the clinical features of pain (dolor), redness (rubror), heat (calor), swelling (tumor) and impairment of function but the increasing emphasis on clinical governance and accountability in the NHS, more practical, reproducible and reliable methods of diagnosing SSI are necessary. Three common SSI definitions in use today are those of the US Center for Disease Control (CDC) definition, the English Nosocomial Infection National Surveillance Scheme (NINSS) definition and the English ASEPSIS definition. The CDC definition is used worldwide to classify wound infections. It includes any wound infection within 20 days of surgery or one year if an implant is present. Infection is classified as ‘none’, ‘superficial’ or ‘deep’. The CDC definition comprises 4 criteria, only one of which must be fulfilled to diagnose infection. They are: 1) Purulent discharge from the incision (incisional infection) or from a drain below the fascia (deep infection). 2) Surgeon’s diagnosis of infection. 3) For incisional infections, an organism isolated from fluid culture or a surgeon opening the wound, unless cultures are negative. 4) For deep infections, a spontaneous dehiscence or surgeon opening the wound in the presence of fever or local pain, unless cultures are negative or an abscess is present on direct examination. Although widely used, the CDC definition is weak since 3 out of the 4 criteria are subjective. On psychometric evaluation CDC has been shown to be unreliable. The UK NINSS definition of SSI is a modified version of CDC. It requires the presence pus cells for a wound culture to be classified as positive and excludes a surgeon’s diagnosis of infection as a sufficient criterion. These changes were intended to make the CDC definition more objective, but interpretation of NINSS has still been shown to vary both between hospitals and regions. ASEPSIS is a quantitative wound scoring method developed in 1986.4 It provides a numerical score which indicates the severity of wound infection. The score is calculated using objective criteria based on the physical appearance of the wound such as

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Generic quality of life outcome measures Generic outcome measures are used by all medical and surgical specialties. They assess overall health-related quality of life and are not specific to age, disease or treatment group. They can be used to compare the relative burden of disease in general and specific populations and can be used to quantify the overall health benefits from different treatments. The World Health Organisation Quality of Life Group recommended that generic surveys should explore five areas • physical health • psychological health • social relationship perceptions • function • well-being5 Commonly used generic outcome measures are: • Medical Outcomes Study 36-Item Short Form Health ­Survey (SF-36) • Medical Outcomes Study 12-Item Short Form Health ­Survey (SF-12) • European quality-of-life 5 dimension questionnaire (­EuroQol/EQ-5D). The medical outcomes study 36-item short form health survey (SF-36) SF-36 is a multi-purpose questionnaire used to measure general health status.6 It was originally developed in American English but a United Kingdom English version is now available. It refers to health over the previous four weeks but a more acute version, referring to health over the previous week, is available. The questionnaire contains 36 questions, each of which has between 2 and 6 answers. Each is scored between 0 (poor health) and 100 (good health). The questions are grouped into one of eight

ASEPSIS scores ASEPSIS score

Meaning

0–10 11–20 21–30 31–40 Over 40

No infection. Normal healing. Disturbance of healing. Minor infection Moderate infection Severe infection

Table 2

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health domains: bodily pain (BP), physical functioning (PF), role ­limitations due to physical health (RP), general health (GH), mental health (MH), vitality (VT), social functioning (SF) and role limitations due to emotional health (RE). There is also a health transition question that does not contribute to any of the eight domains. The domains can be amalgamated into two higher order groups, known as the Physical Component Summary (PCS) and the Mental Component Summary (MCS). The PCS is calculated from the BP, PF, RP and GH scores and is most responsive to treatments that alter physical symptoms such as hip arthroplasty. MCS is calculated from the MH, VT, SF and RE scores and is most responsive to drugs and therapies that target psychiatric disorders. Three of the scales (VT, GH and SF) have a significant correlation with both the physical and mental summary measures. SF-36 takes approximately ten minutes to complete. It is proven to be suitable for self-administration, computerised administration or administration by an interviewer either in person or by telephone. Scores are calculated by summated ratings and standardised SF-36 algorithms. Individual question scores are summated without standardisation or weighting. Standardisation is avoided by using questions with roughly similar means and standard deviations, and weighting is avoided by selecting equally representative questions. SF-36 has been evaluated in several studies. It is proven to be valid, reliable, sensitive and acceptable to patients. It has been used in over 4,000 publications assessing over 200 different diseases and has been specifically investigated in patients undergoing hip arthroplasty. It was shown to be both valid and reliable. However, these studies also showed that SF-36 has minor ‘floor’ and ‘ceiling’ effects. ‘Floor’ effect refers to the situation where a questionnaire is unable to measure a negative value that is lower than the range provided in the choice of answers. In this situation, if a patient reports the lowest value for a question, and then deteriorates further, the deterioration will not be detected by the questionnaire. ‘Ceiling’ effect refers to the opposite situation where a questionnaire is unable to measure a positive value that is higher than the range provided in the choice of answers. In this situation, if a patient reports the highest value for a question, and then improves, the improvement will not be detected by the questionnaire.

studies since the confidence intervals are largely determined by sample size but could result in insignificant findings in smaller studies. The European quality of life 5 dimension questionnaire (­EuroQol/EQ-5D) The EuroQol (EQ-5D)8 questionnaire comprises two pages. There are 15 questions on the first page regarding five aspects of general health: mobility, self care, usual activities, pain and depression. Each question has three possible answers: ‘no problem’, ‘moderate problem’ or ‘extreme problem’. The second page aims to eludidate how the patient regards their overall health using a visual analogue scale with 0 indicating the worst possible health and 100 indicating the best possible health. Euroqol was designed to be self-administered and takes five minutes to complete and has been shown in studies to be both valid and reliable. However, it suffers from ‘ceiling’ effects due to the restricted response format. This is partially overcome by the use of the visual analogue scale on the second page. There is limited psychometric analysis of the questionnaire for use in patients undergoing lower limb arthroplasty and some evidence of construct validity, test-retest reliability and sensitivity.

Disease-specific quality of life outcome measures Disease-specific outcome measures assess the impact of a disease on a patient’s quality of life. They are used in both research and clinical practice to assess and compare alternate surgical and medical treatments for the same disease entity. There are two commonly used disease specific questionnaires used to assess hip arthritis, the Western Ontario and MacMaster Universities (WOMAC) Osteoarthritis Index and the Arthritis Impact Measurement Scales (AIMS). These can be used to assess arthritis in any joint and are not restricted to assessment of the hip. The Western Ontario and MacMaster universities (womac) osteoarthritis index The WOMAC Index was developed for patients with osteoarthritis.9 The original version contained 5 subscales (WOMAC 5.0) but only three were retained for further development (WOMAC 3.0). Globalisation of WOMAC resulted in several refinements leading to WOMAC 3.1 which is now the standard. It was developed in Canadian English and designed to be self-administered. It comprises 24 questions covering three topics: joint pain, joint stiffness and physical function. Other versions are available with ­differing numbers of questions and dimensions to meet different measurement needs. The standard version uses a 48-hour timeframe but it is sufficiently robust to tolerate variations from 24 hours to 1 month and is available in a 5-point Likert, 100 mm visual analogue and 11-point numerical rating format. Most clinical research uses the Likert and visual analogue versions of WOMAC 3.1. The WOMAC Index has been extensively evaluated and shown to be valid, reliable and sensitive. It has been used in several hundred publications and has been translated and linguistically validated in over 65 languages. It’s validity has been specifically tested in patients undergoing hip arthroplasty where it has been shown to be sensitive, have high internal consistency and acceptable test/retest reliability. However, it does show post-operative

The medical outcomes study 12-item short form health survey (SF-12) SF-127 is an abridged version of SF-36 with 12 out of the 36 questions. SF-12 questions can be amalgamated to produce profiles of the eight SF-36 health concepts but only if the sample size is sufficiently large. If the sample size is too small, there is insufficient data to calculate scores for the eight health profiles. SF-12 scores are calculated using weighted algorithms (i.e. the questions in SF-12 contribute different values to the overall score, unlike SF- 36) for which a computer program is available. The main advantage of SF-12 over SF-36 is that it is shorter and therefore quicker for patients to complete and quicker for research personnel to record and analyse data. One disadvantage is that a computer program is necessary for scoring each survey. A further disadvantage is that SF-12 has less construct validity and sensitivity than SF-36 producing less precise scores for the 8- scale health profile. This is less important in large group

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8 questions and a physical examination. The questions cover 3 dimensions, pain (with a maximum score of 44), function (with a maximum score of 33) and level of activity (with a maximum score of 14). The physical examination assesses hip range of motion and a maximum of 9 points can be awarded. The number of points in each section are added together to make a maximum possible score of 100. The score is rated:

ceiling effects for the pain and stiffness subscales in patients undergoing hip arthroplasty, as with SF-36 and Euroqol. One study showed WOMAC to have superior sensitivity to generic outcome measures. However, disease-specific and generic outcome measures are generally used for different purposes and the use of both instruments together often provides more information than using either individually. It has been hypothesised that WOMAC could be used to predict future health status and health resource utilization but this remains unproven.

90–100 80–89 70–79 60–69 <60

The Arthritis Impact Measurement Scale (AIMS) The Arthritis Impact Measurement Scale (AIMS) was originally developed to measure outcome in patients with rheumatic ­disease but has subsequently been evaluated in patients with osteoarthritis and shown to be sensitive to clinical improvement. AIMS 210 is a modified version of the original AIMS, developed in American English. It was designed to be self-administered and takes 20 minutes to complete. The questionnaire comprises 78 questions exploring 12 concepts: mobility, walking and bending, hand and finger function, arm function, self-care tasks, household tasks, social activity, support from family and friends, arthritis pain, work, level of tension and mood. The range of scores for each concept depends upon the number of questions it contains. Each score within a health concept are simply added. In order to express each scale in the same units, a normalization procedure is performed so that each concept is expressed as a value from 0 to 10 with 0 representing good health status and 10 representing poor health. The AIMS scales can be combined into 3 or 5 component models of health status. The 3 component model groups the scales into general categories of physical function, psychological status and pain. The 5 component model combines the scales into measures of lower limb function, upper limb function, affect, symptoms and social interaction. AIMS2 has been psychometrically evaluated and been shown to be both valid and reliable. A modified version of AIMS is available specifically for patients undergoing hip arthroplasty. This has 57 questions which can be grouped into four higher order profiles: physiologic function, self concept, role function and interdependence. Evaluation of this version proved the questionnaire to be sensitive and valid, but reliability remains unproven.

The original version of the assessment was performed entirely by the surgeon. This has been modified to create a patient reported measure, of 7 questions regarding hip pain, walking aids, limping, walking distance, climbing stairs, putting on shoes and socks and sitting. Each question has between 3 and 7 answers which are expressed on a Likert type scale. The scores are added to give a total score of between 0 and 100, where 0 is the best result. On psychometric evaluation the Harris Hip Score was found to be reliable but other forms of validity remain unproven in the literature. Charnley Score The Charnley Score12 was developed in UK English and is another example of a surgeon assessed outcome. Hip pain, mobility and walking are graded on a 6 point scale. Walking is only assessed in patients who have no other condition that may undermine their walking ability. Higher scores indicate better outcome. Scores for different treatment groups can either be averaged or state attainment criteria can be used where the number of patients scoring 5 or 6 in each group can be compared. There are no studies in the literature validating use of the Charnley Score in hip arthroplasty patients. Oxford Hip Score The Oxford Hip Score (OHS)13 is a joint-specific outcome measure designed to assess outcome in patients undergoing hip arthroplasty. It was developed in UK English and takes five minutes to complete. It contains 12 questions to assess hip pain and functional ability over the preceding four weeks. Each question has five possible answers, scored from 0 to 4 giving an overall score range of 0–48. A score of 0 is the best possible outcome, with higher scores indicating increasing problems. The OHS has been used extensively in orthopaedic literature and its psychometric properties have been rigorously examined. It is internally consistent, reproducible and valid. It is proven to be sensitive in patients undergoing both primary and revision hip arthroplasty. Some studies have found the OHS to be more sensitive than generic measures such as SF-36 and disease-specific measures such as WOMAC.

Hip-specific outcome measures Historically the outcome after hip arthroplasty was assessed by the operating surgeon using tools such as the Harris Hip Score and the Charnley Score. These were derived from clinical and radiological data and ultimately depended on the judgment of the surgeon. Patients, and surgeons, opinions often differ and it became apparent that methods were needed to elicit the patient’s perception of their hip surgery. This led to the design of patient centered hip specific quality of life surveys such as the Oxford Hip Score (OHS), the Hip disability and Osteoarthritis Outcome Score (HOOS) and University of California at Los Angeles (UCLA) hip score.

The Hip Disability and Osteoarthritis Outcome Score The Hip disability and Osteoarthritis Outcome Score (HOOS)14 is a joint-specific survey that evolved from the Knee disability and Osteoarthritis Outcome Score (KOOS). It was designed to be

Harris Hip Score The Harris Hip Score11 was developed in American English to assess patients following hip arthroplasty. It is made up of

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Excellent Good Fair Poor Fail

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self-administered and takes 10 minutes to complete. HOOS has 40 questions, each of which has five possible answers (scored 0– 4). The questions can be grouped into 5 higher order dimensions: pain, other symptoms, activities of daily living, sport and hip-related quality of life. The scores from each dimension are added together and then transformed onto a scale of 0–100 where 100 represents the best outcome. HOOS has been evaluated and proven to be both valid and responsive. HOOS contains all the WOMAC Likert 3.0 questions and thus can be used to calculate WOMAC scores indeed two of the subscales (pain and other symptoms) have been shown to be more responsive than WOMAC.

References 1 Copeland GP, Jones D, Walters M. POSSUM: a scoring system for surgical audit. Br J Surg 1991; 78: 355–60. 2 Bennett Guerrero E, Welsby I, Dunn TJ, et al. The use of a postoperative morbidity survey to evaluate patients with prolonged hospitalization after routine, moderate-risk, elective surgery. Anesth Analg 1999; 89: 514–19. 3 Darzi A. High quality care for all. Next stage NHS review. Final report. DOH June 30th 2008. 4 Wilson AP, Treasure T, Sturridge MF, Gruneberg RN. A scoring method (ASEPSIS) for post-operative wound infections for use in clinical trials of antibiotic prophylaxis. Lancet 1986; i: 311–313. 5 Study Protocol of the World Health Organisation project to develop a quality of life instrument (WHOQOL). Qual Life Res 1993; 2: 153–9. 6 Ware Jr. JE, Donald Sherbourne C. The MOS 36-item Short-Form Health Survey (SF-36). Med Care 1992; 30: 473–483. 7 Ware JR, Konsinski M, Keller SD. A 12-item short-form health survey: construction of scales and preliminary tests of reliability and validity. Med Care 1996; 34: 220–33. 8 Brooks R. Euroqol: the current stage of play. Health Policy 1996; 37: 53–72. 9 Bellamy N. Osteoarthritis - an evaluative index for clinical trials (MSc thesis). Hamilton, Ontario. Canada: McMaster University; 1982. 10 Meena RF, Mason JH, Anderson JJ, Gucione AA, Kazis LE. AIMS2: the content and properties of a revised and expanded arthritis impact measurement scales health status questionnaire. Arthritis Rheum 1992; 35: 1–10. 11 Harris WH. Traumatic arthritis of the hip after dislocation and acetabular fractures: treatment by mold arthroplasty. An end-result study using a new method of result evaluation. J Bone Joint Surg Am 1969; 51: 737–755. 12 Charnley J. The long-term results of low-friction arthroplasty of the hip performed as a primary intervention. J Bone Joint Surg Br 1972; 54: 61–76. 13 Dawson J, Fitzpatrick R, Carr A, Murray D. Questionnaire on the perceptions of patients about total hip replacement. J Bone Joint Surg Br 1996; 78: 185–190. 14 Nilsdotter AK, Lohmander LS, Klassbo M, Roos EM. Hip disability and osteoarthritis outcome score (HOOS) - validity and responsiveness in total hip replacement. BMC Musculoskelet Disord 2003; 4: 10. 15 Amstutz HC, Thomas BJ, Jinnah R, Kim W, Yale C. Treatment of primary osteoarthritis of the hip. A comparison of total joint and surface replacement arthroplasty. J Bone Joint Surg Am 1984; 66: 228–41.

The University of California at Los Angeles hip scale The University of California at Los Angeles (UCLA) hip scale15 is often used to assess post-operative outcome in arthroplasty patients. More recently it has also been used to assess hip arthroscopy outcomes. The scale explores four dimensions: pain, walking, function and activity. There are 10 points on the scale with 10 indicating the best outcome and 1 indicating the worst. While there is no published psychometric evidence validating the UCLA hip scale, many studies still use it as a measure of outcome.

Conclusions To assess orthopaedic interventions knowledge of outcome measures is becoming increasingly important for both research and audit purposes. When outcome data are made available to the general public in 2010, it will be imperative that each institution uses the same validated method for collecting the data. If different outcome measures are used by different institutions, like-for-like will not be compared, and any comparisons will be invalid and misleading. Thus guidelines will have to be given to health-care providers as to which method they should use to collect each data set. Short-term post-operative complications can be recorded using the POMS. Longer-term patient satisfaction can be assessed using generic, disease-specific or joint-specific patient-centered quality of life questionnaires. Of the several published quality of life questionnaires, the most evaluated generic measure is SF- 36, the most evaluated disease-specific measure is WOMAC and the most evaluated hip-specific measure is the Oxford Hip Score. There are also several methods of measuring SSI, none of which has been shown to be definitively superior to the others. ◆

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(vii) Current developments in short stem femoral implants for hip replacement surgery

Implant design Currently a number of metaphyseal implants have a straight stem extending into the upper diaphysis. The question whether these stems guide forces into the metaphysis or switch load distribution towards the upper diaphyseal area has recently been discussed in studies using dual-energy x-ray absorptiometry. Bone mineral density was used as a parameter to evaluate bone redistribution around the prosthesis.6,7 Condensation of bone at the distal part of the proximal metaphysis and the proximal diaphysis indicates that implants achieve early stability and durable biological fixation. However, radiological analysis implies that bone loading might not be as physiological as expected. Kim et al. published a report, which revealed 87% grade 2 stress shielding, and 13% grade 3 loss at the calcar in a distal metaphyseal load bearing stem at mean follow up of 8.8 years (Figure 1).8 Decking et al. confirmed that a decrease in proximal femoral strain seen with conventional hip prostheses corresponds well to the reduction of bone density noted in clinical follow-up studies.9 These radiological findings might not indicate impairment of clinical outcome in the intermediate term, nevertheless they demonstrate that there is room for improvement in stem design.10 Proximal load transfer and the absence of distal stem fixation are essential prerequisites for the best performance of the femoral bone after primary total hip replacement. A stem-less prosthesis which loads both medial and lateral proximal femoral

Wolfram H Kluge

Abstract Bone-saving hip arthroplasty using metaphyseal stems is gaining importance because the number of young patients is on the increase and hip resurfacing is not always indicated. This article outlines the recent developments in short stem hip replacement following the concept of conservative hip implants. The individual decision for use of a particular type of implant remains crucial because a stem for all indications does not exist. Every patient requires thorough pre-operative planning. Short metaphyseal stems attempt to bridge the gap between straight stem implant design and hip resurfacing. A modern femoral implant should spare healthy femoral bone during implantation, load the neck and metaphysis in a near physiological way, construct a biomechanically favourable offset without unduly lengthening the leg and favour less invasive soft tissue handling during implantation.

Keywords bone sparing; conservative implant; less invasive; metaphyseal stem; physiological load

Introduction This article outlines the recent developments in short stem hip replacement which fulfil the concept of conservative hip implants.1 Diaphyseal cancellous bone-saving hip arthroplasty using metaphyseal stems is gaining importance because the number of young patients requiring hip surgery is on the increase and hip resurfacing is not always indicated. Active bone growth into structured bio-inert stem surfaces lined with or without hydroxyapatite/calciumphosphate generates safe long-term fixation even in less favourable bone quality.2–4 Surgical technique and implant characteristics are of paramount importance for superior results in hip replacement surgery.5 Products new to the market take time to find general acceptance. New biomechanical concepts usually require a training period prior to first time use, otherwise future confidence in an implant may be compromised. On the other hand, implants with problematic technology may well make it impossible to achieve good and reproducible results. Short stem hip implants are usually uncemented prosthetic devices. It is important to realize that metaphyseal stems load in defined proximal femoral structures thereby ensuring long-term fixation.

Wolfram H Kluge MD is Consultant Orthopaedic Surgeon, Hon. Senior Lecturer at the University of Leeds, UK.

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Figure 1 Intermediate term follow up radiograph of a proximally coated cementless femoral component. Note: calcar atrophy.

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implantation guide aligning itself in the proximal diaphyseal cavity. The Mayo Conservative Hip has shown good results in longterm studies.14 Small variations in positioning of this short stem within the metaphysis can greatly influence the hip joint mechanism. The implant may be unsuitable when there is critically poor cancellous bone quality and/or adverse cortical anatomy. On the other hand, the Mayo Hip offers a medullary bone-sparing solution in complex femoral deformity (Figure 3). The surgeon should pay particular attention to appropriate individual offset reconstruction.

flares not only requires less intramedullary bone to be removed intraoperatively but also preserves proximal bone stock in the longer term.11,12 Biomechanic assessment of cyclic motion in a short stem prosthesis like the Proxima™ implant (Figure 2) can produce similar results to clinically successful shaft implants. The same is true for fracture occuring when load tested on cadaver bone. The reduced system stiffness of a short stemmed implant suggests better physiological load transfer. Sufficiently good bone stock is required when implanting a short stem because higher cyclic motion and migration were observed for femora with poorer bone quality. Santori et al. reported on clinical and radiological results of a custom made ultra-short stem prothesis with proximal load transfer. 1131 hips were followed up at five-years.13 The stem design was based on a fully coated implant with pronounced lateral flare. The implant provided effective initial stability which remained over time and appeared to imitate the loading pattern in the normal proximal femur.

The Thrust Plate prosesthis The Thrust Plate prosthesis utilizes metaphyseal fixation to transmit load forces of the hip directly onto the femoral neck. Early follow up studies have demonstrated favourable outcomes; larger studies have recently become available.15 Karatosun et al. retrospectively evaluated 71 hips (follow up 28–87 months, patient age over 65 years) after Thrust Plate arthroplasty.16 The overall revision rate was 8.4%. After a history of trauma was excluded, the rate for loosening and technical errors decreased to 4.2%. Karatosun et al. put no age limit on the indication for use of the prothesis. Buergi et al. reported radiological and clinical outcomes of 102 third generation Thrust Plate prostheses with a mean follow-up period of 58 months (implant survival according to Kaplan-Meier 98% after 6 years) Figure 4.17 Fink et al. followed up the survival of 214 implants over a period of at least five years.18 Failure rate was 7.0% (nine aseptic and six septic loosening). The authors concluded that a Thrust Plate implant should not be considered as an alternative to a stemmed endoprosthesis. Jacob et al. implanted 102 Thrust Plates. They state that through the implant’s ability to load the medial cortex of the proximal femur, cortical bone in this region can be preserved (survival rate 98%, mean follow up 144 months).19 According to Angin et al. a comparative gait analysis in patients with intramedullary stemmed prostheses and Thrust Plate prostheses did not produce any remarkable differences.20

Mayo Conservative Hip Concepts for primary fixation offered by current metaphyseal implants are based on a diversity of biomechanical theories. Multi-point cortical fixation supported by cancellous bone compression is typically represented by the Mayo Conservative Hip (Zimmer®). The straight double taper leans on the calcar but does not follow an individual calcarcurve. The implant tip acts like an

Metha® prothesis A recent report published by Lazovic provided data about the short stemmed Metha® prosthesis (Aesculap®) in 150 cases.21 The author pointed out that the shape of the proximal femur limits the flexibility of implant positioning in short stems. Therefore, he employed navigation in order to reconstruct a biomechanically correct offset and stem antetorsion with use of a modular neck implant. The Cut prothesis The Cut prosthesis (ESKA IMPLANTS) can provide good clinical and radiological results, but has shown a higher loosening rate compared with cementless standard stems. Ender et al. reported on 123 Cut femoral neck prostheses (average patient age 53 years) after a mean follow-up of five years.22 Thirteen of the implants had been revised, seven because of aseptic loosening, three because of persisting thigh pain, one because of immediate vertical migration, and two because of septic loosening. The authors concluded that the medium-term survival is unsatisfactory although the surviving implants had a good clinical outcome.

Figure 2 Proxima™ reproduced by kind permission of DePuy®.

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Figure 3 Mayo Conservative Hip (Zimmer®). Reconstruction of a dysplastic right hip.

developed for patients with osteonecrosis involving a large volume of the femoral head. McMinn described improved physiologic proximal loading for the implant compared to earlier designs of neckconserving implants. One-year radio-stereometric analysis showed negligible migration and preservation of femoral neck density.26 The development of new implants, which address bone conservation, is often based on experience with clinically proven implants.27 Some of the newer implants however use entirely new concepts. The Silent Hip (DePuy International) for example is a tapered press-fit implant fixed within the femoral neck without contact to the lateral cortex. The implant is currently in the precommercial clinical phase. The developers report that it allows for nearly physiological proximal femoral loading (Figure 5). A pilot clinical and radiological investigation including 41 patients revealed that distal migration of the Silent stem was within a 1–2 mm limit at 2 years, suggesting good stability of the prosthesis.

Stress analysis of various femoral neck implants revealed that the Cigar prosthesis caused the most pronounced changes in stress distribution at the lateral thrust plate around the bored out hole.23–25 Strain increase in the region of the osteotomy of up to 1440 μm/m could be detected for the Cigar and up to 1000 μm/m for the Rip prosthesis. The stress pattern after implantation of the Cut prosthesis remained similar to the pre-interventional femoral stress distribution. The Birmingham Mid Head Resection prosthesis The Birmingham Mid Head Resection prosthesis (Smith and Nephew Orthopaedics Ltd) is an uncemented short stem ­prothesis

Leg length and offset Wilson remarked in his Report for the Committee for the Study of Femoral-Head Replacement in 1954 that hip prostheses represent a new method of substituting a metallic or plastic counterpart for a portion of skeleton.28 He stated that prosthetic replacement, no matter what kind, has been used too often without attention to the principles and requirements for success in hip arthroplasty. Wilson discussed one of the reasons for implant instability: shortness of the femoral implant neck, which resulted in a relaxed unstable joint. His recommendation to solve this problem was to place the stem in valgus and thereby lengthen the neck. Hip surgeons have since discovered the vital importance to not only adapt the implant neck length but also reconstruct the hip offset. Leg length concerns following hip replacement have become a major medico-legal problem. Individual reconstruction of a biomechanically favourable offset is limited because many implants simply increase the offset along with stem size. It is not recommended to ream the isthmus of the femur in order to fit a bigger implant required by offset considerations. On the other hand, a stem adequately sized to create the appropriate offset might not descend far enough during implantation because of its bulky distal aspect. The latter implant inevitably leads to leg lengthening.

Figure 4 Thrust Plate prosthesis.

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Figure 5 Silent Hip. Reproduced by kind permission of DePuy International. Figure 6 Fitmore™ Hip (Zimmer®).

There is not necessarily an association between the metaphyseal femoral anatomy and neck offset. A large neck offset might present with a very narrow proximal femoral canal (Champagne glass). One could argue that these patients are candidates for hip resurfacing. Indeed this often appears to be the most appropriate treatment option. However, indications for hip resurfacing are limited. Despite promising reports, femoral head vascularity and risks like femoral neck fracture/resorption should be considered individually.29–31 It appears a logical step to remove the defective femoral head and replace it by an implant, which utilises the healthy femoral neck and proximal metaphyseal area for fixation. On-growth to the implant and strengthening of bone should be facilitated by predictable tension/pressure distribution during weight-bearing. The implant must allow for individual offsetreconstruction more or less independent of the stem size avoiding damage to the proximal femoral diaphysis. Implant philosophy has evolved from considering stem alignment in the direction of the diaphyseal axis. Today developers regard it to be safe to fix the stem along the metaphyseal curve. One major advantage of this concept is preservation of the greater trochanter by implantation through the femoral neck. Recently a further metaphyseal stem concept has been introduced. The Fitmore™ Hip (Zimmer®) focuses on reconstruction of individual anatomy as accurately as possible. This anatomical stem follows the metaphyseal curve along the calcar and facilitates less invasive surgery. The implant offers the widest range of offsets independent of stem size. Promising initial results on short-term follow up have been reported (Figure 6). 32

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Practical considerations Survival rates of metaphyseal prostheses currently appear to be lower than for cementless standard stems. Nevertheless, metaphyseal implants have the advantage of preserving proximal femoral medullary bone without the need to disrupt the diaphyseal marrow cavity. Should a change of endoprosthesis become unavoidable, a standard stem anchored in the proximal femur can be utilized.33 In vitro studies of short-stemmed femoral implants have shown more initial migration than for conventional stems. The short implants stabilised when cortical contact was achieved or cancellous bone was compacted sufficiently.34 Lower cyclic motion of the short stems indicate better physiological loading of the bone. Not only intra-operative destruction of the proximal femur is comparatively small but also secondary bone remodelling around the ingrown implant appears closer to physiological conditions. Rasp alignment in short stems can be difficult, because guidance provided by the proximal diaphyseal cavity as in longer stems, is missing. For implants with a shoulder, the surgeon might have to open a gully into the cancellous greater trochanter. Otherwise, the implant deviates into varus position during impaction with increased risk of a calcar crack or intra-operative lateral femoral perforation. Pre-operative analysis of a lateral hip film can be very helpful in order to anticipate potential difficulties in stem ­implantation, 49

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particularly if the surgeon intends to do a high femoral neck resection. Anteversion of the neck and the physiological proximal femoral bend with its apex towards the posterior metaphysis complicate the initial orientation of the implant within the cancellous bone. The experienced surgeon will find the correct entry point far enough posteriorly within the femoral neck osteotomy in order to avoid mal-position, mainly when using a limited soft tissue approach. The decision about an individual indication for use of a particular type of implant remains crucial. A stem for all indications does not exist and surgeons are asked to study the anatomy in every case. Every patient requires thorough pre-operative planning. Medico-legal proceedings in relation to hip replacement surgery are a constant reminder of our responsibilities about implant choice and operative technique. As with any implant, metaphyseal prostheses require special training for the first time user in order to avoid potential pitfalls.

9 Decking R, Puhl W, Simon U, Claes LE. Changes in strain distribution of loaded proximal femora caused by different types of cementless femoral stems. Clin Biomech 2006; 21: 495–501. 10 Karachalios T, Tsatsaronis C, Efraimis G, Papadelis P, Lyritis G, Diakoumopoulos G. The long-term clinical relevance of calcar atrophy caused by stress shielding in total hip arthroplasty: a 10-year, prospective, randomized study. J Arthroplasty 2004; 19: 469–475. 11 Santori N, Albanese CV, Learmonth ID, Santori FS. Bone preservation with a conservative metaphyseal loading implant. Hip Int 2006; 16: 16–21. 12 Westphal FM, Bishop N, Pueschel K, Morlock MM. Biomechanics of a new short-stemmed uncemented hip prosthesis: an in-vitro study in human bone. Hip Int 2006; 16: 22–30. 13 Santori FS, Manili M, Fredella N, Tonci Ottieri, Santori N. Ultra-short stem with proximal load transfer: clinical and radiographic results at five-year follow-up. Hip Int 2006; 16: 31–39. 14 Morrey BF, Adams RA, Kessler M. A conservative femoral replacement for total hip arthroplasty. A prospective study. J Bone Joint Surg 2000; 82-B: 952–958. 15 Steens W, Rosenbaum D, Goetze C, Gosheger G, van den Daele R, Steinbeck J. Clinical and functional outcome of the thrust plate prosthesis: short- and medium-term results. Clin Biomech 2003; 18: 647–654. 16 Karatosun V, Unver B, Gunal I. Hip arthroplasty with the thrust plate prosthesis in patients of 65 years of age or older: 67 patients followed 2–7 years. Arch Orthop Trauma Surg. 2007 Nov 6 [Epub ahead of print]. 17 Buergi ML, Stoffel KK, Jacob HA, Bereiter HH. Radiological findings and clinical results of 102 thrust-plate femoral hip prostheses: a follow-up of 2 to 8 years. J Arthroplasty 2005; 20: 108–117. 18 Fink B, Wessel S, Deuretzbacher G, Protzen M, Ruther W. Midterm results of “thrust plate” prosthesis. J Arthroplasty 2007; 22: 703–710. 19 Jacob HA, Bereiter HH, Buergi ML. Design aspects and clinical performance of the thrust plate hip prosthesis. Proc Inst Mech Eng 2007; 221: 29–37. 20 Angin S, Karatosun V, Unver B, Gunal I. Gait assessment in patients with thrust plate prosthesis and intramedullary stemmed prosthesis implanted to each hip. Arch Orthop Trauma Surg 2007; 127: 91–96. 21 Rapp SM. Surgeon finds navigation enhances his accuracy placing short, modular hip stems. Orthopaedics Today International 2008; 11: 8. 22 Ender SA, Machner A, Pap G, Hubbe J, Grasshoff H, Neumann HW. Cementless CUT femoral neck prosthesis: increased rate of aseptic loosening after 5 years. Acta Orthop 2007; 78(5): 616–621. 23 Wieners G, Pech M, Streitparth F, Jansson V, Plitz W. Photoelastic stress analysis of human femurs before and after implantation of different models of femur neck prostheses. Z Orthop Unfall 2007; 145: 81–87. 24 Steinhauser E, Ellenrieder M, Gruber G, Busch R, Gradinger R, Mittelmeier W. Influence on load transfer of different femoral neck endoprostheses. Z Orthop Ihre Grenzgeb 2006; 144: 386–393. 25 Hofmann D, Ecke H, Nietert M, Langhans M. Experimental study supported by the German Research Society: stress at the proximal femur after implantation of different cementless hip prostheses. Langenbeck’s archives of surgery; Springer Berlin/Heidelberg: 1987 vol. 372, pp. 849. 26 McMinn DJW, Daniel J, Pradhan C. A vascular necrosis in the young patient: a trilogy of arthroplasty options. Orthopedics 2005; 28: 945.

Conclusion Short metaphyseal stems attempt to bridge the gap between straight stem implant design and hip resurfacing. Technically a modern femoral implant should: (A) spare healthy femoral bone during implantation, (B) load the neck and metaphysis in a near physiological way, (C) construct a biomechanically favourable offset without unduly lengthening the leg and (D) favour less invasive soft tissue handling during implantation. ◆

References 1 Learmonth ID. Conservative hip implants. Current Orthopaedics 2005; 19: 255–262. 2 Teloken MA, Bissett G, Hozack WJ, Sharkey PF, Rothman RH. Ten to fifteen-year follow-up after total hip arthroplasty with a tapered cobalt-chromium femoral component (Tri-Lock) inserted without cement. J Bone Joint Surg Am 2002; 84: 2140–2144. 3 Kim KI, Klein GR, Sleeper J, Dicker AP, Rothman RH, Parvizi J. Uncemented total hip arthroplasty in patients with a history of pelvic irradiation for prostate cancer. J Bone Joint Surg Am 2007; 89: 798–805. 4 Parvizi J, Sharkey PF, Hozack WJ, Orzoco F, Bissett GA, Rothman RH. Prospective matched-pair analysis of hydroxyapatite-coated and uncoated femoral stems in total hip arthroplasty. A concise followup of a previous report. J Bone Joint Surg Am 2004; 86: 783–786. 5 Hallan G, Lie SA, Furnes O, Engesaeter LB, Vollset SE, Havelin LI. Medium- and long-term performance of 11 516 uncemented primary femoral stems from the Norwegian arthroplasty register. J Bone Joint Surg 2007; 89-B: 1574–1580. 6 Albanese CV, Rendine M, De Palma F, et al. Bone remodelling in THA: a comparative DXA scan study between conventional implants and a new stemless femoral component. a preliminary report. Hip Int 2006; 16: 9–15. 7 Kulkarni M, Wylde V, Aspros D, Learmonth ID. Early clinical experience with a metaphyseal loading implant: why have a stem? Hip Int 2006; 16: 3–8. 8 Kim YH. The results of a proximally coated cementless femoral component in total hip replacement: a five to 12 year follow-up. J Bone Joint Surg 2008; 90-B: 299–305.

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34 Westphal FM, Bishopa N, Honlb M, Hillec E, Püscheld K, Morlocka MM. Migration and cyclic motion of a new short-stemmed hip prosthesis – a biomechanical in vitro study. Clin Biomech 2006; 8: 834–840.

27 Biomet launches hip technologies to address demand for minimally invasive bone-conserving implants. Biomet, Inc. Warsaw, Indiana. Also available at: http://www.biomet.com. 28 Wilson PD. Report of the Committee for the Study of Femoral-Head Replacement. Symposium on Femoral-Head Replacement Prostheses: based on the Prostheses as Printed in the October (1954) Issue of the Bulletin. J Bone Joint Surg Am 1956; 38: 407–420. 29 Amstutz HC, Beaulé PE, Dorey FJ, Le Duff MJ, Campbell PA, Gruen TA. Metal-on-metal hybrid surface arthroplasty: two to six-year follow-up study. J Bone Joint Surg Am 2004; 86: 28–39. 30 Steffen RT, Pandit HP, Palan J, et al. The five-year results of the Birmingham hip resurfacing arthroplasty. J Bone Joint Surg 2008; 90-B: 436–441. 31 Mont MA, Seyler TM, Plate JF, Delanois RE, Parvizi J. Uncemented total hip arthroplasty in young adults with osteonecrosis of the femoral head: a comparative study. J Bone Joint Surg Am 2006; 88: 104–109. 32 Fitmore™ Hip Stem. A new stem for primary THA. Masterclass. Berne Switzerland 21–22 February 2008. 33 Stukenborg-Colsman C. Femoral neck prostheses. Orthopade 2007; 36: 347–352.

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Practice points • Pre-operative planning is essential in order to avoid malposition of the metaphyseal implant • The surgeon should find the correct entry point far enough posteriorly within the femoral neck osteotomy mainly when using a limited soft tissue approach • Short implants achieve best primary stability when cortical contact is achieved and cancellous bone is compacted sufficiently • Should exchange of the metaphyseal stem become necessary, a standard stem anchored in the proximal femur can be utilized

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TRAUMA

Radiology of fracture complications

The diagnostic imaging of osteomyelitis may require the confluence of multiple imaging modalities; however conventional radiography still remains the primary investigation.5 This is due to its availability, relative ease of interpretation and the invaluable temporal information which it provides. Radiographic evidence of osteomyelitis is first suggested by overlying soft tissue oedema at 3–5 days following infection. Bony changes may not be evident for 14–21 days and this period may be prolonged with the administration of antibiotics. The first bony change is the development of a periosteal reaction. Cortical or medullary lucencies will develop next, although approximately 40–50% bone loss is necessary before there is a detectable lucency on plain radiographs. Bone loss may be either a direct local result of infection or alternatively a more diffuse pattern may be seen where there is a regional increase in blood flow as a result of more generalised infection (Figure 1). Metalwork may serve as a nidus for infection particularly following trauma where the initial wound infection rate is significantly higher (Figure 2). Chronic infection can lead to additional radiographic features. Areas of devitalised bone known as sequestra are frequently present in chronic infection (Figure 3). Sequestra are by definition sclerotic separated bone fragments which serve as nutrient foci for the organisms. Where there is a focus of chronic infection this can promote overgrowth of new bone around the nidus known as an involucrum (Figure 4). In addition breaks in the cortex (cloaca) may develop to allow infected material to escape (Figure 4). The diagnosis of osteomyelitis can often be difficult as an isolated finding; however, in conjunction with an underlying fracture this diagnosis may be made even more complicated due to the presence of soft tissue swelling and obliteration of the usual soft tissue and fat planes.

Emma Rowbotham Dominic Barron

Abstract The overall annual bone fracture rate in England has been estimated at 3.6% of the population. Trauma accounts for the majority of these fractures with the remainder being considered as pathological fractures. Complications of fracture healing cause a significant degree of morbidity and increasingly various imaging modalities are being utilised in order to aid diagnosis and management of these complications. Knowledge of the available and appropriate ­radiology is essential in ensuring accurate assessment of both the fracture, and any associated complications. In the initial assessment of a fracture, plain film radiography will almost certainly be the primary method of imaging. In the majority of cases, this modality alone may provide sufficient information regarding fracture type, position and healing. However, CT, MRI, ultrasound and bone scintigraphy all have a role in the assessment and ongoing management of complications, and often play an invaluable role in guiding treatment both in the acute and chronic setting.

Keywords avascular necrosis; fracture; infection; union problems

Infection Infection, in either the acute or chronic form, is one of the most common complications following a fracture. Open fractures are most likely to become infected, with incidence rates as high as 5% reported in proximal femoral fractures.1,2 Post-traumatic wound infection is the most common cause of chronic osteomyelitis. Due to their blood supply the tibia, femur, humerus, vertebra, maxilla and mandible are the most susceptible.3 Contamination of the wound, delayed treatment and ­surrounding tissue necrosis are all contributory factors. Alternatively osteomyelitis following a fracture may be as a result of surgical intervention. The most common causative organism isolated is staphlococcus aureus which is present in over 50% of cases; other common organisms include streptococci, gram-negative enteric organisms and anaerobic bacteria. A significant degree of morbidity may be associated with ­osteomyelitis and early identification is crucial in order to maximise treatment efficacy. Most cases manifest themselves within a month of the fracture although less commonly infection may not appear for several months.4 Figure 1 a This is a plain radiograph from a young diabetic patient who had a previous open calcaneal fracture. There is now extensive osteopaenia in the midfoot consistent with regional hyperaemia. b This is a sagittal T1 Weighted Fat Saturated Post Gadolinium enhanced image of the foot. This shows extensive bony enhancement consistent with acute osteomyelitis which responded well to IV antibiotics.

Emma Rowbotham MRCS is Specialist Registrar at MRI Department, Leeds General Infirmary, Leeds, UK. Dominic Barron FRCR is Consultant Musculoskeletal Radiologist at MRI Department, Leeds General Infirmary, Leeds, UK.

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Figure 2 Infected tibia after previous screw fixation. There is extensive gas within the subcutaneous fat layers tracking to the skin and the screw tract. Figure 4 Young patient 6 months post fixation for distal tibia and fibula fractures. a AP plain radiograph which shows fracture of some of the distal screws, a large soft tissue swelling medially and osteopaenia. b Axial CT image shows 2 cloacae (arrows) with separation of an anterior fragment. Open exploration of this showed widespread infection.

MRI is effective and sensitive in detecting and localising early osteomyelitis. Sensitivity in the region of 90–100% has been reported due to the fact that MRI is exquisitely sensitive in ­detecting soft tissue oedema which is one of the earliest changes seen. Studies have shown its superiority in defining anatomical location when compared with radiography, CT and radionuclide scanning. The standard examination would include a T1

Weighted sequence to show the anatomy and bone oedema, a STIR (Short Tau Inversion Recovery) sequence to map out the overall oedema pattern and T1FS (Fat Suppressed) post ­gadolinium enhanced sequence to define pockets of pus and devitalised tissue (Figure 1b). The recent exponential improvements in CT technology mean that volumetric data can be assimilated from the area of interest and then reformatted into any plane desired. This is not restricted to straight lines and both curved and 3D reformats are possible for detailed bony anatomy and accurate anatomical localisation. Previously the presence of metalwork used to cause such significant artefact to render CT useless; however, this is no longer the case (Figure 5). CT is often used in combination with MRI as their findings are complementary. It is far superior to MRI for its depiction of bony changes and identification of sequestra, foreign bodies or gas formation. In areas with complex osseous anatomy CT may be particularly helpful to gain a full understanding of the spatial relationships e.g. pelvis, calcaneus and sternum. In these cases 3D reformats may be particularly helpful to plan further ­interventions. Ultrasound is a non-invasive, inexpensive method which may be used in the assessment of infection and may be particularly useful in children. Its primary use is for soft tissue involvement and is the first line for soft tissue abscess, fluid collection and effusions (Figure 6). In addition some information about the bones may be obtained with cortical defects and periosteal reactions often being demonstrated. Without doubt though, its most useful attribute is to guide aspiration / biopsy of infected tissues. Radionuclide imaging may be employed where there is difficulty distinguishing between cellulitis and osteomyelitis; the triple phase technetium bone scan clearly distinguishing these two

Figure 3 20 year old female 7 years after screw fixation for a midhumeral fracture with recent increase in pain at the fracture site. a AP radiograph of the humerus showing the retained screws as well as an area of apparent lucency between the arrows. b Sagittal reformatted CT which highlights the central lucency as well as demonstrating a sclerotic piece of separate bone in the medullary cavity (arrow) which was proven at surgery to be a sequestrum.

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at about 10–14 days and consists of widening of the fracture line with blurring of the opposing fracture fragment margins secondary to resorption of the dead / damaged bone in the initial inflammatory response. Callus formation then occurs as a secondary event. The amount of callus formation associated with a normal healing process will vary depending on the bone involved and on the position of the fracture within the bone. The extent of callus formation should be roughly proportional to the gap between the fracture fragments. Therefore, excess callus formation should raise the suspicion for complications such as inadequate immobilisation or infection around the site of healing. Removal of the cast is important in obtaining accurate information regarding the amount of callus formation around the fracture site. In the majority of cases, plain radiographs are all that is required to adequately depict the degree of fracture healing, in combination with the clinical findings. However it is essential for accurate evaluation of the healing process to review all the radiographs together. This gives excellent temporal documentation of the patient’s progress. Additional modalities may need to be employed when the plain radiographs are inconclusive. This may be because the fracture is in a plane that is not easily imaged by plain radiographs, is comminuted, or spiral in which case CT may be helpful. Regions where CT is most often employed include the carpal bones, tarsals, metacarpals and metatarsals, some elbow fractures, and fractures involving articular surfaces e.g. tibial plateau, ankle pilon and calcaneal fractures. Multi-slice CT scanning allows for volume data to be acquired and reconstructed in any plane ­necessary. The role of MRI in evaluation of fracture healing is limited but may be used in order to assess bone bruising, bone contusions and occult fractures or stress fractures which may otherwise not be appreciated on plain films.

Figure 5 Acute tibial fracture in a 20 year old farmer who crashed his car on a moor-land road, trapping his ankle under the pedals. a Axial CT of the ankle showing severe fragmentation of the bones as well as the external fixator clearly visible on the right of the image. b Sagittal reformat of the same injury showing almost complete loss of the talus with the tibia now articulating with the calcaneus.

Malunion This is union in an altered anatomical position following a fracture (Figure 7). It is most likely to occur where correct anatomical alignment at the fracture site has been inadequate or when the initial injury has involved either loss or deformity of sections of the bone concerned. Symptoms include pain, deformity, swelling and sometimes difficulty in weight bearing depending upon the site which has been affected. In the long term the resultant altered biomechanics may well predispose to early osteoarthritis of adjacent joints. Angular malunions are usually clearly apparent both clinically and radiographically, however, rotational deformities may be more difficult to detect. Angulation in a long bone of more than 15° or a marked rotational deformity may require correction with osteotomy and internal fixation.6 These may well require careful evaluation with axial CT and rotational measurements prior to any intervention.

pathologies. Nuclear studies tend to be forgotten in the diagnostic work-up but they are unique in providing a global ­overview of the patient. This is invaluable in multi-focal infection where it will show up previously unsuspected foci; this condition is particularly seen in children. In the evaluation of acute osteomyelitis it is important not to forget other possible diagnoses such as cellulitis, acute leukaemia and malignant bone tumours all of which may present with similar features.

Union Fracture union is a gradual, continuous process dependent on various parameters including patient age, fracture site and type, blood supply and degree of immobility achieved at the site. The time taken to normal union will vary and therefore quantitative measures are the most useful; the process may be delayed, may be arrested altogether (non-union) or may be complete but in an incorrect anatomical position (malunion). Assessment of bone healing following a fracture will primarily be a clinical decision aided by radiographic findings. The earliest radiographic ­ manifestation of fracture repair occurs

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Non-union Non-union is described as cessation of the fracture healing process completely; this problem occurs chiefly in adults, and is rare in children. Usually a history of persistent pain following a fracture and an abnormal degree of movement at the fracture site are both present in order for a confident diagnosis to be made. 54

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Figure 6 70 year old patient with increasingly swollen and sore right shoulder 1 year post right shoulder hemi-arthroplasty for highly comminuted humeral head fracture. a AP and lateral b shoulder radiographs showing bone lysis around the proximal shoulder implant with further bone resorption around the joint. c Ultrasound demonstrates extensive fluid and granulation tissue arising from the shoulder joint (arrows). d A needle was placed using ultrasound guidance into the centre of the fluid and frank pus was aspirated.

There are two distinct types of non-union: hypertrophic and atrophic. The hypertrophic form is more common and the ­margins of the fracture fragments become well-defined, smooth and sclerotic; under these circumstances no callus crosses the fracture line (­Figure 8). The atrophic form is rare; findings include osteopenia at the fracture site, limited sclerosis and absence of ­callus. In these cases bone grafting and enhanced fixation may be ­necessary. Causes of non-union include bone or soft tissue loss, interposed soft tissue, fracture distraction, poor splintage, infection, poor or interrupted blood supply. Plain radiographs will show a persisting or expanding radiolucent fracture line. There may be little or no callus formation /periosteal reaction. There will be no bridging callus across the fracture site with rounding of the fracture ends and sclerosis. The fracture gap itself fills with fibrous tissue leading to a ­pseudoarthrosis. Unfortunately not all non-unions are so clear cut and it is possible to have a hypertrophic non-union which on the plain radiographs gives the appearance of a full union but in reality has a pencil-in-cup configuration (Figure 8b). Suspicion for a non-union will be raised by clinical concern and in these cases CT is essential to confirm or refute this possibility.

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Delayed union The healing period of fractures at different anatomical sites can be highly variable. The main influencing factors are the age of the patient and the severity of the injury. Other factors include infection, poor blood supply and inadequate immobilisation of the fracture. Failure of a fracture to heal within the given limits for any particular site constitutes a delayed union. The diagnosis of delayed union is made on a combination of both clinical and radiological grounds. Radiographic signs are of persistence of the fracture line and a scarcity or absence of callus formation (Figure 9). Healing may still progress under these circumstances, if adequate immobilisation is continued, but at a slower rate than would usually be expected.

Myositis Ossificans This is a benign condition where there is heterotopic ossification within a muscle, usually secondary to trauma but it may occur without injury in the unconscious or paraplegic patient. This is usually as a result of a soft tissue injury without an associated fracture. Stiffness and reduced range of movement 55

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Figure 7 Lateral radiograph of distal tibia showing both incomplete union at the fracture site as well as marked anterior angulation of the tibia distal to the fracture site.

Figure 8 20 year old motorcyclist 1 year post tibial nail insertion. a Plain radiograph gives the impression of bony union. b CT reformat shows that there is no evidence of bony union.

Figure 9 a AP radiograph which shows multi-segmental fracture of the tibia and fibula after motorcycle RTA. b The 6 month follow-up radiograph demonstrates the intra-medullary nail and the persistent clearly visible fracture line. c CT was performed to more clearly delineate the state of healing and although the fracture line is still clearly visible callus is slowly starting to develop and this is likely to go on to full union.

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intermittent locking of the joint, pain and swelling and chronic stiffness. Ossified loose bodies are usually visible on plain radiographs although additional views may be necessary such as a tunnel view in the knee. When they are not calcified, however, this can create diagnostic difficulties with McCarthy showing that up to 67% of loose bodies may not be evident on conventional ­radiographic studies.7 In difficult cases where there is a high index of clinical concern for a radio-lucent loose body then either a CT or MRI arthrogram would be indicated (Figure 11). These are much more sensitive and will provide additional information about the joint but are more expensive and invasive than the standard radiographic studies.

are delayed symptoms. The site most commonly affected is the thigh, but a similar phenomenon may occur around a joint in association with a dislocation or a fracture-dislocation; this occurs most commonly in the elbow, and less commonly in the hip. It is essential to consider this entity within the differential diagnosis as the predisposing trauma may be sufficiently trivial for the patient not to recall it. If further investigations such as an MRI scan are then performed the imaging findings can be very concerning. Biopsy is not indicated as the findings are of new bone formation and therefore can be suspicious for ­osteosarcoma. Initial plain radiographs may be unremarkable. Between 2 and 6 weeks floccular calcified densities are seen within the soft tissues. By 6–8 weeks the calcifications become well circumscribed and tend to adhere to the underlying periosteum (­Figure 10). Over a period of several months there is resorption of the calcification which in some cases may be complete. Where there is concern ultrasound may be of help to confirm the lack of an associated soft tissue mass.

Loose bodies Loose bodies following a fracture are most commonly found in the knee joint, although the hip, shoulder and elbow joints can also be affected relatively commonly. Symptoms include

Figure 10 a Plain radiograph showing typical eggshell calcification in an area of myositis ossificans. In addition as this is abutting the bone the adjacent periosteal reaction is demonstrated. b Longitudinal ultrasound image showing the clear cut calcified rim with no additional soft tissue element.

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Figure 11 a AP pelvic radiograph which shows the left acetabular fracture. b Axial CT section which shows the large intra-articular bone fragment (arrow) which would prevent accurate relocation of the femoral head into the joint.

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Avascular necrosis Avascular necrosis (AVN) is defined as the cellular death of bone components due to interruption of the blood supply. AVN has a myriad of causes; however, it occurs most commonly secondary to trauma with long term steroid use increasingly recognised. Early identification and treatment is essential in order to preserve the affected area of bone. This includes recognising fractures which have a high association with this entity. The most common of these are subcapital femoral neck, scaphoid and talar neck fractures. These all have a distal to proximal blood supply and therefore fractures of these regions typically endanger this. Typically, pain in the affected region is the presenting symptom. For all causes it is more common in men than women with a ratio of 8:1. Plain radiographic findings may be unremarkable in early presentation with preservation of joint space. Mild to moderate disease may show evidence of sclerosis and changes in bone ­density. In advanced disease there may be subchondral radiolucent lines, deformity of the bone and collapse, particularly when considering the femoral head. In severe (stage 4) disease there will be destruction of cartilage and reduction in joint space. MRI has an overall sensitivity of more than 90%. Indeed this has become the investigation of choice where there is concern for avascular necrosis particularly in the early stages (Figure 12). For non trauma patients this is now a very common rheumatological request in long-term steroid users. The Mitchell classification describes the progressive changes seen on MRI.8 Class A lesions show high signal on T1 and intermediate signal on T2 weighted sequences consistent with fat. Class B lesions show high signal on both T1 and T2 weighted sequences consistent with blood products. Class C lesions show low signal on T1 and high signal on T2 weighted sequences consistent with fluid. Class D lesions show low signal on both T1 and T2 weighted sequences consistent with fibrous tissue. There is a low signal line which defines the margins of the lesions corresponding to sclerotic bone. In classical cases there is an additional high signal band inside this which corresponds to vascularised granulation tissue and/or chondroid metaplasia.9 Gadolinium may be helpful in very early cases where there is non-enhancement of the affected area (Figure 13). In advanced AVN there is cortical breakdown which leads to deformity of the articular surface and sclerosis. In these cases a combination of plain radiographs and CT are often more useful as they are better at delineating bony change. Radionuclide imaging is still often utilised where there is a concern regarding AVN. In early disease, osteoblastic activity and blood flow are increased thus radionuclide scanning at this stage is more accurate than plain film radiography. In more established cases, there is an area of decreased uptake surrounded by an area of increased uptake indicating a reactive area surrounding the necrotic bone; this is known as the doughnut sign. Findings may however be nonspecific and are most helpful in conjunction with other imaging.

Figure 12 This patient had an undisplaced talar neck fracture 3 months previously. a Lateral ankle radiograph which shows a sclerotic proximal half of the talus which is highly suspicious for avascular necrosis. b Coronal T1 Weighted image of the talus showing a clear line of demarcation between the vascular and avascular parts of the talus (arrowheads). c Sagittal STIR sequence showing the oedematous distal talus, the line of demarcation (arrow) and the low signal avascular talar dome.

Metalwork Where fracture management has required either internal or external fixation, subsequent imaging of the affected area may become

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Figure 13 a Plain radiograph of the scaphoid which clearly shows the scaphoid fracture. In addition the proximal pole is very sclerotic and therefore consistent with avascular necrosis. b T1 Weighted image clearly shows the fracture line (arrow). c STIR (Short Tau Inversion Recovery) sequence which shows marked oedema to the scaphoid but surprisingly also to the lunate, capitate and triquetral consistent with bone bruising. d T1 Fat Saturated Post Gadolinium shows that there is enhancement to the proximal pole of the scaphoid so despite the plain radiographic findings the proximal pole has retained its blood supply.

in delineating bony architecture, callus formation/non-unions /sequestra and cloaca formation. MR imaging unfortunately still suffers with the presence of metalwork in several ways. Firstly even with new techniques the artefact is still often so bad as to render the scan useless although it is often worth trying. Secondly Ilizarov frames act as radioantennae and can completely obliterate the MR signal. Finally the magnet can have a significant pull on the metalwork particularly with frames which can be very painful for the patient. Where possible MRI should therefore be carried out either before the metalwork is placed or after it is removed.

problematic. This is because the metal can seriously degrade image quality or obscure relevant findings. Plain ­ radiographs remain the primary imaging modality of choice. This is because they are easily available, are diagnostic in the majority of cases and most importantly provide an excellent temporal record of the fracture progression/healing. In addition these are least affected by any metalwork (Figure 14). Until recently the use of any metalwork rendered CT useless. Recent developments in multi-slice technology however mean that the image quality is now very good. It is primarily of use

Complications These are the same as previously described however there are two additional problems specific to the use of metalwork: Internal fixation results in less peripheral callus formation and it can therefore be very difficult to ascertain whether healing is indeed progressing. Healing is manifest by obliteration of the fracture line rather than florid callus formation (Figure 9). Indeed where there is a significant degree of callus formation either inadequate immobilisation or underlying osteomyelitis should be considered. The Ilizarov external fixator was developed in the 1950’s in Siberia and was introduced to the West in the 1980’s. This has become a popular treatment option for fractures, leg length discrepancies, non-union and osteomyelitis.10 Although this is an excellent treatment the very nature of the fixator means that imaging is very awkward although plain radiographs remain the mainstay. Where leg lengthening is being carried out in addition to the fracture management one of the unique problems associated is performing the lengthening at an appropriate speed. Too fast and the new bone develops cysts and is inadequate, too slow and premature union across the lengthening site occurs. Plain radiographs usually show faint ossification across the regeneration site, however if there is ongoing clinical concern then ultrasound has a unique role (Figure 15). This can show in exquisite detail the appearances of the regenerate bone which should resemble

Figure 14 22 year old with an Ilizarov frame in situ due to an initial open fracture site. a AP plain radiograph demonstrating the complex nature of the fixation. Serial radiographs were suspicious for hypertrophic non-union. b Coronal reformatted CT image confirming the hypertrophic non-union. This shows how CT has developed in that images of this type were not possible only a few years ago.

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Figure 15 a AP Radiograph demonstrating the in situ Ilizarov frame with the intervening area of regenerate bone. Fine ossification is seen across this region. b Longitudinal ultrasound image showing good quality uniform regenerate bone between the arrowheads.

a starry sky. The presence of cysts implies that lengthening is progressing too fast. ◆

5 Santiago Restrepo C, Gimenez CR, McCarthy K. Imaging of osteomyelitis and musculoskeletal soft tissue infections: current concepts. Rheum Dis Clin North Am 2003 Feb; 29(1): 89–109. 6 Apley GA, Solomon L. Complications of fractures P260. In: Apley GA, Solomon L, eds. Concise system of orthopaedics and fractures. Oxford: Butterworth Heinemann Ltd, 1995. 7 McCarthy JC, Busconi B. The role of hip arthroscopy in the diagnosis and treatment of hip disease. Orthopedics 1995; 18(8): 753–6. 8 Mitchell DG, Rao VM, Dalinka MK. Femoral head avascular necrosis: correlation of MR imaging, radiographic staging, radionuclide staging and clinical findings. Radiology 1987; 162: 709–715. 9 Saini A, Saifuddin A. MRI of osteonecrosis. Clin Radiol 2004; 59(12): 1079–1093. 10 Hosny G, Fadel M. Ilizarov external fixator for open fractures of the tibial shaft. Int Orthop 2003; 27: 303–6.

References 1 Donaldson LJ, Reckless IP, Scholes S, Mindell JS, Shelton NJ. The epidemiology of fractures in England. J Epidemiol Community Health 2008; 62: 174–80. 2 Dellinger EP, MIller SD, Wertz. Risk of infection after open fracture of the arm or leg. Arch Surg 1988; 123: 1320. 3 King MD, Randall W, David Johnson. Osteomyelitis 2006-07-13 eMedicine. WebMD. 4 Waldvogel FA, Medoff G, Swartz MN. Osteomyelitis: A review of clinical features, therapeutic considerations and unusual aspects. N Engl J Med 1970; 282: 260.

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The diabetic foot and ankle

­ redicted to be around 750,000 higher for those with undiagp nosed disease. The ratio of type I : type II diabetes is around 1:10, with type II becoming more prevalent due to Britain having the fastest growing rate of obesity in the developed world (the risk of developing type II diabetes is around 10x greater with a body mass index of >30) and an ever aging population. The Department of Health states that the current cost of treating diabetes and its complications is around 5% of the NHS budget, or around £10 million a day, with this figure set to rise 10% by 2011.1 Around half of this figure is spent on the complications of diabetes, with diabetic foot disease being responsible for around 10 to 20% of all diabetic admissions to hospital. Although foot and ankle pathology is common in the non­diabetic population, the orthopaedic surgeon should remain vigilant for patients with undiagnosed diabetes. A high index of suspicion should be used when reviewing patients in the outpatients and emergency departments for apparently simple pathology such as paronychia, slow healing wounds or similar conditions. Simple urine glucose and serum tests will provide early diagnosis of diabetes and may crucially influence decisions on patients requiring surgery.

James C Stanley Andrew M Collier

Abstract Diabetes mellitus is a common malady of our time with ever increasing numbers of patients presenting with diabetic foot and ankle pathology. Diabetes requires treatment by a multidisciplinary team and vascular disease requires management involving vascular surgeons. There is, however, an increasing burden on the orthopaedic surgeon with ulceration, foot deformity, osteomyelitis and Charcot osteo-arthropathy being direct complications of diabetes. Potential severe complications following fracture and elective surgery require an understanding of diabetes and its effects on soft tissue and bone. The key topics are: Pathophysiology effects of hyperglycaemia on vascular, neuronal and immune systems, Assessment - examination of diabetic foot pathology and how to spot the ‘at risk foot’, Ulceration - management of foot and ankle ulceration and indications for intervention, Charcot osteo-arthropathy - brief overview of Charcot-type foot and ankle disease, and Management of ankle fractures - overview of current trends in options for conservative and surgical intervention.

The effects of hyperglycaemia on the foot and ankle Hyperglycaemia promotes changes in the microvasculature secondary to thickening of the basement membrane, sorbitol accumulation and loss of nitric oxide auto-regulation. This ultimately leads to reduced nutrient and oxygen exchange. In the foot this is commonly seen with fat pad atrophy, inability to form skin callus, nerve ischaemia, tissue necrosis, muscle atrophy, and poor healing potential. The ischaemic injury alone is insufficient to fully explain the tissue dysfunction seen in the diabetic foot and ankle. Nerve ischaemic injury is also compounded by cellular structural changes secondary to non-enzymic glycation and damage to essential signal pathways, the degree of which is proportional to the magnitude of hyperglycaemia. All types of peripheral nerve are affected including sensory, motor and autonomic, with each leading to specific changes seen in the diabetic foot and ankle. Sensory nerve damage leads to a typical glove and stocking distribution of sensory loss, resulting in a loss of protective sensation to pressure/traumatic injury. Motor loss causes small muscle atrophy and forefoot deformity with toe deformity and increased prominence of the metatarsal heads. Non-enzymic cross-linking of collagen in the presence of hyperglycaemia makes soft tissues inflexible causing stiff joints and a tight Achilles tendon, worsening the forefoot pressure related to motor dysfunction. Autonomic dysfunction reduces sweating, leading to dry cracked skin and producing potential access for pathological organisms to deeper structures. Autonomic loss also causes arterial dilatation of diseased vessels with a paradoxical hyperaemia, resulting in the deceptive appearance of a well perfused foot. The hyperaemia leads to increased osseous blood flow, ultimately causing a demineralization of the bone matrix (one of the processes thought to be involved in the development of Charcot-type destruction).2 Loss of autonomic control over the venous system also causes venous congestion and further ulceration complications. Innate immunity, essential for initiation of healing and fighting infection, is impaired due to changes in neutrophil activity. The high tissue concentrations of glucose are also an ideal culture

Keywords diabetic ankle fractures; diabetic foot; diabetic ulceration

Introduction Diabetic care requires a multidisciplinary team approach with general practitioners, podiatrists and endocrinologists mediating the majority of care. Vascular disease is common and requires vascular surgical assessment; however, there is an increasing burden on the orthopaedic surgeon in the management of neuropathic ulceration and deformity. While the term ‘diabetic foot and ankle’ often refers to ulceration, gangrene and Charcot osteo-arthropathy, diabetes also has a significant influence on the management of foot and ankle fractures/soft tissue injury. The management of foot and ankle pathology in diabetics requires an understanding of hyperglycaemic tissue injury to predict, prevent and treat complications of soft tissue ulceration, deformity and traumatic injury. The number of people in the UK diagnosed with diabetes mellitus in 1996 was 1.4 million; it has now exceeded 2.3 million (equivalent to ∼3% of the population) with the true figure

James C Stanley MBBS MRCS is Specialist Registrar at the Department of Orthopaedics, Harrogate District Hospital, North Yorkshire, UK. Andrew M Collier MB ChB FRCS(Tr & Orth) is Consultant Orthopaedic Surgeon at the Department of Orthopaedics, Harrogate District Hospital, North Yorkshire, UK.

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general malaise may be the overriding feature of sepsis and standard observations (BP, HR and temp) are required. Surveillance within the community of diabetic patients reduces significant complications by identifying the ‘at risk foot’ and is the cornerstone of a diabetic foot management program. Examination of the skin quality, bony deformity or tight Achilles tendon, sensation and vascularity can identify the ‘at risk foot’ and instigate early referral. Inspection of the diabetic foot will often illustrate common findings. Thin, shiny, dry skin which is hairless and often discoloured due to dependant rubor will require moisturizers, surgical shoes with total contact insoles and regular review. Hypertrophic nails are often misshapen and require chiropody to reduce paronychia and spreading infection. Individual inspection of the web spaces may reveal pathology easily missed by the more casual examiner. Pulses and blood pressure measurements (ankle brachial pressure index or ABPI) are taken, with absent pulses and/or low ABPIs being indicative of poor arterial supply, prompting referral to a vascular surgeon for further assessment. Normal or high ABPI measurements may, however, not reflect the true patency of the vessels as Monckeberg’s sclerosis may occur, with calcification of the tunica media leading to incompressible vessels. Colour Doppler imaging is useful and should be requested via a vascular surgical team. Neurological assessment using Semmes-Weinstein monofilament hairs (size 5.07) is still considered to be the most reliable and reproducible test for protective sensation.3 The filament is pressed against the skin and allowed to bend, which roughly equates to 10 g pressure. It is then repeated in three places. Positive response to 2 out of 3 is considered sufficient to indicate protective sensation is present. This is tested over specific weight bearing areas on the sole of the foot and is easily documented using a simple diagram (Figure 1), with sensation under the 1st metatarsal head being the single most predictive site. It must be noted that any skin callus should be removed before documenting a loss of protective sensation. Further testing with a 75 g filament can then be used to describe profound sensory loss. Specific documentation then needs to be made regarding any deformity, ‘at risk areas’ or ulcerations and signs of infection, with an appreciation of areas requiring surgical intervention. Table 2 summarizes the necessary documentation in the assessment of the diabetic foot (Figure 2).

medium for bacterial colonization. Thus, even in the presence of an apparently adequate blood supply ulceration, infection and poor healing may prevail, leading to the high complication rates seen following traumatic injury and surgical intervention in the diabetic foot and ankle. Table 1 summarizes the various tissue injuries caused by hyperglycaemia and the potential associated pathologies. Delayed fracture healing in diabetics is well described. Although the exact mechanism is unclear, it is likely to be multifactorial involving insulin effects on callus formation, alterations in neutrophil activity and osseous blood flow and glycation of enzymic pathways. Wound healing is similarly affected resulting in high complication rates for open wounds and surgical incisions around the foot and ankle.

Assessment of the foot and ankle in diabetics General assessment of the patient’s condition by the multidisciplinary team includes looking for evidence of retinal and cerebro-vascular pathology, which is relevant to foot and ankle pathology as these contribute to falls, traumatic injury and poor foot hygiene. Renal and cardiac disease may also contribute to poor healing potential and should be optimised as part of the management of diabetic foot pathology. Pyrexia, tachycardia and

Summary of hyperglycaemic tissue injury and potential associated pathology Hyperglycaemic Injury

Potential foot pathology

Arterial wall thickening

• Poor O2/nutrient delivery • Fat pad atrophy • Vessel infarct/tissue necrosis • Poor healing potential • Loss of sensory protection • Unrecognised traumatic/ pressure injury • Small muscle wasting of the foot • Claw toes/prominent metatarsal heads • Loss of sweating with atrophic, dry, cracked skin Arterial • Increased osseous blood flow/demineralization • Paradoxical apparent satisfactory blood flow Venous • Congestion/swelling/ dependant ulceration • Poor tissue perfusion/ nutrient exchange • Neutrophil dysfunction • Infection risk/poor healing potential

Sensory nerve

Motor nerve

Autonomic

Innate immunity

Diabetic foot ulceration Diabetic foot ulceration is not in itself a diagnosis but is a manifestation of a spectrum of co-morbidities. During normal stance there is approximately 3000 mmHg pressure under the metatarsal heads, increasing 2- to 3-fold in the presence of fat pad ­necrosis. Tightening of the tendoAchillis is also a common finding in diabetics, which further increases pressure under the metatarsal heads. It is understandable therefore that foot pathology associated with diabetes is common, with 15% of all diabetics having a foot ulcer or deep infection in their lifetime (Figure 3).4 Around the world approximately half of ulceration and amputation cases are thought to be preventable5 and thus a high index of suspicion, monitoring and prevention by a multi-­disciplinary team for all diagnosed diabetics is vital. The importance of

Table 1

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Summary of necessary documentation in the assessment of the diabetic foot General assessment Lab tests

Blood pressure (BP) Heart Rate (HR) Temperature (Temp) Full blood count/CRP Blood and urine glucose Blood HbA1c

Indicators of sepsis

Vascular assessment

Pulses & capillary refill Swelling and varicosities Doppler

Neurological

Atrophic, dry skin Semmes-Weinstein monofilament testing (10  g in 2 out of 3 areas)

Indictors of infection Indication of current diabetes control Indication of longer term diabetes control Indicators of arterial insufficiency Indicators of venous insufficiency Ankle-brachial pressure index (ABPI) may have to used with caution but is valid if low Indicates risk of barrier breakdown Indicates loss of protective sensation

Table 2 Figure 1 a simple method for illustrating protective sensation is to place a tick in the circle if protective sensation is present (10 g), a dot if it is not and a dot with a circle around it if profound sensory loss (75 g) is noted. Ulceration may also be annotated on the same diagram if necessary.

Management of diabetic foot ulceration Appropriate multidisciplinary team input is always advised to optimise the medical management of the patient’s diabetes. The diabetic foot should be monitored regularly as early treatment of at risk areas can prevent many ulcerations. The simplest treatments include basic foot hygiene and regular moisturising to prevent fissuring secondary to autonomic sweat dysfunction. Toe nails should be regularly trimmed to prevent pressure on the surrounding soft tissues resulting in tissue barrier failure. Dietician input should also be utilized as often diabetic patients require zinc, magnesium and protein supplements to aid the healing process. Close attention to shoe wear is also essential. A loss of protective sensation leads to inadvertent shearing injury from shoe wear. Motor dysfunction often leads to bunions, cavus, claw toes and hammer toe deformities, which produce prominent areas more susceptible to injury, often worsened by fat pad atrophy and venous insufficiency. This further exacerbates poorly fitting shoes due to swelling and skin thinning due to stretching. The majority of patients who develop ulceration will require colour Doppler imaging for evidence of vascular insufficiency, and vascular surgical input. With modern techniques distal revascularization is possible and although often prone to poor long term results, it may provide sufficient support to allow adequate healing and save a potentially threatened limb. Offloading the affected area should redistribute pressure to larger areas, prevent shear and protect from inadvertent trauma and is best achieved with either the current gold standard of total contact casting (TCC) or with a walker boot/modified footwear along with partial weight bearing. Traditionally non-weight

­ iagnosis and correct management cannot be over emphasised as d over 1 in 10 foot ulcerations ultimately results in amputation. In the UK this approximately equates to 100 diabetic patients undergoing minor and major lower limb amputations every week. 40% of ulcers are neuropathic in nature, 25% arterial and 35% mixed, with around 1/3 being deep and 5% having osteomyelitis. Foot ulceration in diabetics is multi-factorial but is often described as being mainly arterial (approx. 25%), neuropathic (approx 40%) or mixed (approx 35%) in origin. Foot ulcers usually occur in prominent areas caused by deformity where the overlying skin is subjected to high or prolonged pressure. The resultant shear stresses lead to a detachment of the skin from the underlying tissue and superficial lacerations. The skin often has a bed with a necrotic cap or ulcer. Ulcers with a mainly neuropathic aetiology will have a healthy granulating bed whilst those with a significant arterial component will have a necrotic bed. The Wagner classification (modified by Brodsky)6 is the most commonly used descriptive classification of diabetic foot ulcerations (Table 3), providing useful guidance to the management of each class of ulcer. A more comprehensive scale has been developed at the University of Texas, which includes risk stratification and expresses tissue breakdown, infection and gangrene separately and this may become more commonly utilized in the future.

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Figure 2 Sensation being testing under the metatarsal heads. The Semmes-Weinstein monofilament is pressed against the skin until the filament bends. Various thicknesses of filaments are available each of which bends with a predetermined pressure documented in grams.

bearing was considered helpful, however, walking may actually improve vascular flow and improve healing provided the ulcer itself is protected from pressure. TCC provides an excellent environment for healing as it prevents point pressure and minimizes shearing of the skin. However, walker boots and modified footwear are also often used as TCC is a specialized technique not available in all centres and is time consuming to apply. The TCC should be changed every 5 to 14 days to allow dressing changes and accommodate any swelling problems and has a reported mean healing time of around 39 days.7,8 TCC is not advised in patients with active infection, significant arterial occlusion, extremely thin skin, swollen skin or in patients with poor compliance (Figure 4). Superficial ulcerations without significant infection should be identified early and treated with ulcer preparation and off-­loading. Normal saline dressings, or absorbent dressings (Alignate, Hydrofibre etc) are often all that is required. Occlusive hydrocolloids, hydrogels or hypertonic saline gels can help remove necrotic tissue, with the Cochrane systematic review suggesting that available trials favour the use of hydrogel dressings for the removal of slough and callus.9 Foams and calcium alginate are also useful for ulcers producing moderate volumes of exudates. Iodine and silver impregnated dressings have also been used. More recently, biologically active dressings that encourage wound healing have been used with some success, including Promogran (cellulose

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Figure 3 Photograph illustrating a typical plantar ulceration seen in diabetic feet. The pressure area has become necrotic exposing granulation tissue without significant infection or tendon/bone exposure (Wagner 1). This is best treated by orthotics and offloading.

and collagen matrix), hyaluronic acid ester (Hyalofill), platelet derived growth factor impregnated dressings (Regranex) and those that apply living foetal foreskin cells (Dermagraft, Apligraft). Ulcer debridement can often be performed in the outpatients due to sensory neuropathy diminishing any discomfort. Simple debridement of necrotic skin edges and necrotic caps will expose tissue capable of healing. In cases where operative intervention is required for extensive infection a long incision is recommended, with Brunner incisions and minimal undermining to reduce iatrogenic soft tissue traction/injury. Tendon sheaths should be opened and washed to clear tracking pus. Vacuum assisted dressings have also been used to aid healing but are usually reserved for patients with ulcers resistant to more simple measures or for large areas. Laval or maggot therapy has been suggested by some authors, however, review articles suggest this to be no more beneficial than hydrocolloid dressings and surgical debridement when indicated.9 Surgical management of ulceration is required for deep infections, osteomyelitis and recalcitrant ulcers. Following debridement 64

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The Wagner classification of diabetic foot ulceration, modified by Brodsky. The original Wagner classification is in italics after the relevant modified classification category Depth Classification 0

At risk with no ulceration

1

Superficial ulceration Not infected (Wagner 1)

2

Deep Ulceration exposing bone or tendon (Wagner 2)

3

Extensive ulceration or abscess (Wagner 3)

Ischaemia Classification A Not ischaemic B Ischaemia without gangrene

C

Partial (forefoot) gangrene (Wagner 4)

D

Complete foot gangrene (Wagner 5)

Education and footwear Regular review Offloading with total contact casting (TCC), Walking brace or footwear modification Surgical debridement and wound care Offloading Culture specific antibiotics Debridement +/− partial amputation Offloading Culture specific antibiotics Regular review Non-invasive vascular testing (Doppler) vascular consultation if symptomatic Vascular consultation for possible re-vascularisation Debridement as above Amputation and vascular consultation

Table 3 Figure 4 Aircast diabetic walker boot. The air bladders inside the boot are inflated to reduce shear stresses on the skin. The rigid outer shell and rocker bottom sole and duel density insole help eliminate pressure points, aid mobility and reduce stresses further.

correction of deformity may be indicated to relieve pressure areas and allow ulcers to heal. Percutanous Achilles lengthening, metatarsal osteotomies, Keller’s arthroplasty, interphalangeal arthroplasty and hammer toe correction may be appropriate. Using this strategy the majority of ulcers will heal within 2 to 3 months. A chronic ulcer recalcitrant to standard treatment should be biopsied to rule out Marjolin’s ulcer (squamous cell carcinoma of a chronic wound) and may require plastic surgical input for local rotational flaps and skin cover. Split skin grafts should be avoided in load bearing areas or those susceptible to shear stress. The presence of an ulcer does not per-se require antibiotics, even with a positive microbiology swab, as colonization by a multitude of different bacteria is common. More important signs of significant infection include spreading cellulitis/lymphangitis, pus/abscess or if systemic illness and pyrexial. Infected ulcers will require surgical debridement down to healthy, viable tissue and broad spectrum intravenous antibiotics should be administered to treat both anaerobic and aerobic organisms. These are often continued as oral medication for approximately 12 weeks, but this should be discussed with the microbiology team. Soft tissue gas in diabetes is most commonly caused by aerobic organisms or by mixed gram-negative rods (rather than Clostridium perfringens), but necrotizing fasciitis must be ruled out as between

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20 to 40% of all cases of necrotising fasciitis are in patients with known diabetes mellitus. Necrotising fasciitis is a progressive, rapidly spreading infection of the deep fascial layers that affects both the overlying skin and underlying muscle. It may be secondary to many types of bacteria, often in synergism, but the commonest isolated organism is Group A Streptococcus. Initial presentation is often itching or pain which progresses to anaesthesia as the overlying skin vessels infarct. Cellulitis may be present initially, although this usually gives way to purplish skin and gangrene over only a couple of hours. Tissue necrosis, putrid discharge, severe pain and general systemic signs (pyrexia, malaise, diarrhoea, vomiting) then become apparent. Soft tissue gas may be felt clinically as crepitus but is often easiest to identify on plain X-ray. Ultimately, the mortality rate of necrotising fasciitis is 80 to 90%, thus early identification and treatment are vital. Following resuscitation early, aggressive surgical debridement and opening of the fascial planes is required. Biospies should be taken from the spreading periphery as within the central gangrenous 65

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area there will be organisms present which neither cause nor add to necrotising fasciitis. The antibiotic of choice would be ­intravenous penicillin, or clindamycin as an alternative, to treat Group A Streptococcus, but this may need to be altered subsequently according to microbiology test results. Hyperbaric oxygen therapy may also be considered but is not available in most centres. The diagnosis of deeper purulent infections and osteomyelitis is based on both clinical and radiographic grounds. Although the exposure of bone at the base of an ulcer does not automatically lead to the diagnosis of osteomyelitis, its presence is highly suggestive and plain X-ray (looking for bone destruction) is indicated. Some care should be made with the diagnosis of osteomyelitis not associated with ulceration because any radiographic changes may be due to Charcot osteo-arthropathy, which requires very different treatment. MRI and white cell labelled scans may aid diagnosis but should be used with caution as many imaging findings are common to both conditions.10 If any doubt remains a biopsy and culture will be required. Septic arthritis may mimic a number of conditions which are similar to those found with other inflammatory or neoplastic conditions, or with Charcot osteo-arthropathy, and when the area is painless due to neuropathy the definitive diagnosis is notoriously difficult.10 However, there should be a high index of suspicion and again biopsy/aspiration will often be required. Amputation will ultimately be required for uncontrolled infection and sepsis, recalcitrant osteomyelitis or unreconstructable vascular insufficiency with gangrene. Amputation of the 1st ray or 4th/5th rays are well tolerated in the diabetic population. Amputations of the 3rd ray are less well tolerated and usually require more proximal amputations, either through the Lisfranc, mid-tarsal (Chopart) or hindfoot (Symes) if there is sufficient soft tissue cover. Otherwise, a transtibial amputation is performed. In mid-tarsal amputations insertion of the dorsi-flexion tendons into the neck of the talus is required to prevent significant equinus from the pull of the tendoAchillis. Hindfoot amputations have the advantage of improving ambulation over short distances without a prosthesis (eg to the toilet), however, prosthetic fitting is more difficult and close collaboration with the patient and orthotist is required in choosing a hindfoot amputation over a transtibial amputation. Previously, below knee re-vascularisation was thought to be futile as microangiopathic occlusive disease was thought to be responsible for tissue necrosis in the diabetic foot. It is now considered that tissue necrosis results more from narrowing and occlusion of larger vessels with the practical implication that infections and ulceration are amenable to treatment and potentially cure through revascularization of below knee ­vessels.

mediated vascular reflex ultimately resulting in a hyperaemia. Thus, in addition to repetitive unrecognized trauma it is thought that the hyperaemia causes an osteopenia (secondary to a mismatch in bone destruction and synthesis2) which weakens bone making it more susceptible to the repeated minor trauma. The commonest joints to be affected by Charcot osteo-arthropathy are those in the foot due to an increase in inadvertent trauma from walking, greater forces through the joints of the lower limb and a greater degree of sensory loss. Charcot osteo-arthropathy occurs in stages, as described by Sidney N Eichenholtz in 1966, resulting in fragmentation, coalescence and consolidation12 which typically occur over a 6-month period . The details of Charcot osteo-arthropathy diagnosis and management are discussed in a separate article, however, in general Charcot osteo-arthropathy causes mid-foot (Rocker bottom foot) and ankle deformity and is usually seen only in a neuropathic which is well perfused with good pulses.

Diabetic foot and ankle fractures The treatment of ankle fractures in diabetes is a notorious challenge due to high complication rates, particularly of surgical and soft tissue wounds. Historically surgical intervention lead to high amputation rates, with more recent reports continuing to highlight significant complication rates of around 45%.13,14 The patient with significant co-morbidities is particularly at risk and a multidisciplinary approach is essential to optimise the patient’s condition. However, in the absence of neuropathy, vascular insufficiency or co-morbidities diabetic patients appear to have an overall risk of complication similar to that for a matched population.14,15 Non-operative management may also lead to significant infective wound complications16 and close attention to ill-fitting casts and patient compliance is essential with regular review. Non-operative treatment is also associated with a higher rate of Charcot osteo-arthropathy17 and hence debate still continues as to the best form of management. There are some principles which must however be followed. In general there should be a low tolerance for any displacement as incongruity of the ankle can cause rapidly progressing post-traumatic arthritis or Charcot osteo-arthropathy. Even if neuropathy is not seen at presentation it cannot be assumed that it will not develop in the future. With loss of sensory protection to the ankle joint a mal-union may cause more significant long term problems and arise in a shorter timeframe. Closed reduction and casting of displaced fractures generally leads to displacement and merely delays surgical intervention, and better results are usually obtained with open reduction and internal fixation.18 If a fracture presents with pre-existing Charcot osteo-arthropathy or significant osteoarthritis then primary fusion is often ­indicated. Of the other fractures of the foot and ankle the general principle should be “do no harm”. Minimally displaced fractures are thus often treated conservatively. Calcaneal fractures are ­ generally best treated conservatively except in the severely displaced as there can be potentially catastrophic wound ­ complications. Talar fractures will require operative intervention if displaced or ­associated with significant collapse from avascular necrosis. Metatarsal fractures generally do well if treated conservatively and although mid-tarsal injuries are rare they often require

Charcot osteo-arthropathy Although tertiary syphilis was one of the leading causes of Charcot joints in the late 1800s, the commonest cause in ­modern society is diabetes mellitus. It is thought that the loss of proprioception and deep sensation ultimately leads to progressive joint degeneration, destruction, and disorganization secondary to repetitive unrecognized trauma. Using scintigraphy, it has been shown that in patients with diagnosed neuropathy there is increased blood flow within bone,11 thought to be due to an autonomic, neurally

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t­reatment for displacement and collapse and should be treated using similar protocols as to those for Charcot osteo-arthropathy in this region. Osteoporosis19,20 and delayed fracture healing21 are potential complications of diabetes. The exact aetiology is poorly understood but is likely to be multi-factorial, and can lead to spinal and hip fractures as well as those in the foot and ankle. It has, however, been shown that fasting hypoglycaemia may be the overriding risk factor for fracture development, and that a well controlled blood sugar level is important.22 The exact increase in fracture healing time in humans is difficult to assess and again is multi-factorial. The type and severity of diabetes is implicated as are associated co-morbidities including vascular insufficiency, renal disease and hyper-lipidaemia. Smoking, diet and age are all also likely to influence the rate of fracture healing. A young fit type II diabetic may well heal at a normal rate whilst an elderly smoker with insulin dependence and co-morbidities may require immobilisation 2 to 3 times longer. The presence of a neuropathy is often used as an appropriate marker in deciding on doubling immobilization time.15,21 Weight bearing status (or not) should follow similar protocols as for those patients without diabetes as excessive non-weight bearing may predispose the patient to developing disuse osteopenia and potentially provoke Charcot osteo-arthropathy. In the presence of significant vascular insufficiency any orthopaedic intervention to treat a fracture will be compromised and a vascular surgical assessment should be requested. Although re-cannulation of distal vessels often produces only short term success, the improved blood supply may be sufficient to promote healing and prevent infection.

References 1 Sue Roberts (National Director for Diabetes). Working together for better diabetes care, clinical case for change. Department of Health, 16 May 2007, p. 1–16. 2 Brower AC, Allman RM. The neuropathic joint: a neurovascular bone disorder. Radiol Clin North Am 1981; 19(4): 571–580. 3 Jerosch-Herold C. Assessment of sensibility after nerve injury and repair: a systematic review of evidence for validity, reliability and responsiveness of tests. J Hand Surg [Br ] 2005; 30(3): 252–264. 4 Pham H, Armstrong DG, Harvey C, Harkless LB, Giurini JM, Veves A. Screening techniques to identify people at high risk for diabetic foot ulceration: a prospective multicenter trial. Diabetes Care 2000; 23(5): 606–611. 5 National Diabetes Support Team. Diabetic foot guide. NHS Clinical Governance Support Team. 2006, p. 1–12. 6 Brodsky JW. The diabetic foot. In: Coughlin MJ, Mann RA, eds. Surgery of the foot and ankle. Mosby, 1999, p. 895–969. 7 Trepman E, Pinzur MS, Shields NN. Application of the total contact cast. Foot Ankle Int 2005; 26(1): 108–112. 8 Myerson M, Papa J, Eaton K, Wilson K. The total-contact cast for management of neuropathic plantar ulceration of the foot. J Bone Joint Surg Am 1992; 74(2): 261–269. 9 Edwards J. Debridement of diabetic foot ulcers. Issue 4. Art. No.: CD003556. Cochrane Database Syst Rev 2002. 10 Jones EA, Manaster BJ, May DA, Disler DG. Neuropathic osteoarthropathy: diagnostic dilemmas and differential diagnosis. Radiographics 2000(20 Spec No): S279–S293. 11 Edmonds ME, Clarke MB, Newton S, Barrett J, Watkins PJ. Increased uptake of bone radiopharmaceutical in diabetic neuropathy. Q J Med 1985; 57(224): 843–855. 12 Eichenholtz Sidney N. Charcot joints. Springfield, Ill., C.C. Thomas, 1966. 13 McCormack RG, Leith JM. Ankle fractures in diabetics. Complications of surgical management. J Bone Joint Surg Br 1998; 80(4): 689–692. 14 Jones KB, Maiers-Yelden KA, Marsh JL, Zimmerman MB, Estin M, Saltzman CL. Ankle fractures in patients with diabetes mellitus. J Bone Joint Surg Br 2005; 87(4): 489–495. 15 Costigan W, Thordarson DB, Debnath UK. Operative management of ankle fractures in patients with diabetes mellitus. Foot Ankle Int 2007; 28(1): 32–37. 16 Flynn JM, Rodriguez-del RF, Piza PA. Closed ankle fractures in the diabetic patient. Foot Ankle Int 2000; 21(4): 311–319. 17 Holmes Jr. GB, Hill N. Fractures and dislocations of the foot and ankle in diabetics associated with Charcot joint changes. Foot Ankle Int 1994; 15(4): 182–185. 18 Schon LC, Easley ME, Weinfeld SB. Charcot neuroarthropathy of the foot and ankle. Clin Orthop Relat Res 1998; 349: 116–131. 19 Levin ME, Boisseau VC, Avioli LV. Effects of diabetes mellitus on bone mass in juvenile and adult-onset diabetes. N Engl J Med 1976; 294(5): 241–245. 20 Krakauer JC, McKenna MJ, Buderer NF, Rao DS, Whitehouse FW, Parfitt AM. Bone loss and bone turnover in diabetes. Diabetes 1995; 44(7): 775–782. 21 Marks RM. Complications of foot and ankle surgery in patients with diabetes. Clin Orthop Relat Res 2001; 391: 153–161. 22 Holmberg AH, Nilsson PM, Nilsson JA, Akesson K. The association between hyperglycemia and fracture risk in middle age. A Prospective, Population-Based Study of 22,444 men and 10,902 women. J Clin Endocrinol Metab 2008; 93(3): 815–822.

Summary • The diabetic foot and ankle is a complex problem requiring a multidisciplinary approach. • Diabetes reduces oxygen and nutrient delivery through chan­ ges in the vascular system. • Neuropathy causes loss of protective sensation, deformity and swelling. • Arteriopathy and changes in innate immunity reduce healing potential. • Ulcerations mainly due to vascular insufficiency, rather than neuropathy, should be treated by the vascular surgeons. • Superficial ulcerations often only require off loading with total contact casting and regular review. • Infected, extensive or deep ulcerations may require surgical debridement +/− antibiotics. • Necrotising fasciitis should be suspected in diabetics with ­rapidly worsening infection and treated expectantly. • Prominent areas secondary to deformity often require surgical correction or excision to aid ulcer healing. • Fractures of the foot and ankle require anatomical reduction and in high risk patients a doubling of immobilisation time. • Distal vascular reconstruction is becoming increasingly ­available to improve soft tissue and bony healing. • Operative intervention is associated with high complication rates, however, poor reduction leads to post-traumatic arthropathy or Charcot osteo-arthropathy and thus further surgical intervention with again high complication rates. ◆ ORTHOPAEDICS AND TRAUMA 23:1

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Learning points

Necrotising fasciitis is most commonly due to Group A Streptococcus. Treatment includes fluid resuscitation, intravenous penicillin or clindamycin, wide surgical debridement of necrotic tissue and incision of fascial planes into healthy tissue. Second review in theatres is required at 24 hours with further debridement if necessary. Delayed primary closure may be possible following successful treatment.

An ABPI >0.7 and <1.3 may be used to determine adequate blood flow. A transcutaneous oxygen pressure of >40 mmHg also suggests adequate arterial flow. Whilst neuropathic ulcers may be tackled by the orthopaedic surgeon, ischaemic ulcers require vascular surgical input as arterial reconstruction may be required for the resolution of ulceration and limb salvage.

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Thoracic outlet syndrome

ago, after the concepts underlying each of its subgroups were either modified or discarded. In contrast the current classification proposed in 1984, is based on the structure(s) injured.2

Hani Abdul-Jabar

True neurologic TOS This is a rare unilateral disorder that occurs predominantly in women in their late teens to mid 50s. It is almost invariably associated with a bony anomaly, such as a small cervical rib or an elongated C7 transverse process. A very taut fibrous band extends from the tip of the bony anomaly to the first thoracic rib which results in stretching of the proximal portion of the lower trunk of the brachial plexus or the distal portion of the T1 anterior primary ramus around the band. Symptoms are predominantly motor, i.e. weakness of hand and forearm muscles with substantial atrophy of the lateral thenar muscles (innervated by the median nerve). While patients admit to having experienced intermittent aching in the median arm, forearm, and the last two digits for many years, the symptoms are typically not severe enough to seek medical attention. In a study by Ozcakar et al 3 using isokinetic muscle testing to assess weakness (muscle strength) and fatigue (endurance), these patients were found to have muscular strength similar to controls but their upper extremities fatigued more quickly than controls.

Abbas Rashid Francis Lam

Abstract Thoracic Outlet Syndrome (TOS) is the constellation of symptoms caused by compression of neurovascular structures at the superior aperture of the thorax, properly the thoracic inlet! The diagnosis and treatment is contentious and some even question its existence. Symptoms are often confused with distal compression neuropathies or cervical ­radiculopathies.

Keywords first rib; scalene muscles; thoracic outlet

Introduction

Arterial vascular TOS This is a rare, unilateral disorder affecting young adults either sex. It is caused by a large bony anomaly, usually a fully formed cervical rib or, less often, a deformed first thoracic rib, which compresses the subclavian artery at the base of the neck. Distal to the point of compression, the turbulent blood flow leads to an aneurysm in which thrombus can form. This may propagate distally, occluding smaller vessels resulting in ischemia, which can in turn cause necrosis, and amputation of fingers or even a hand. Symptoms are similar to those seen in ‘Neurologic TOS’ although they are caused by ischaemia of the nerves distally rather than direct compression of the brachial plexus itself.

Thoracic Outlet Syndrome (TOS) involves compression resulting in injury or irritation of neurovascular structures as they course through three narrow passageways from the base of the neck into the arm via the axilla (Figure 1). The most important of these is the interscalene triangle. Its boundaries are the anterior scalene muscle anteriorly, the middle scalene muscle posteriorly and the medial surface of the first rib inferiorly. The triangle is small at rest but can become even smaller with certain provocative manoeuvres. It can be further constricted by other structures such as fibrous bands, cervical ribs and anomalous muscles. The second passageway is the costoclavicular triangle. Its boundaries are the clavicle anteriorly, the first rib posteromedially and the upper border of the scapula posterolaterally. The third passageway is the subcoracoid space which lies beneath the coracoid process deep to the pectoralis minor tendon.

Venous vascular TOS This is also known as “effort thrombosis syndrome” and “Pagetvon Schroetter disease,”.2 It is a rare unilateral disorder that affects adults of both sexes and is caused by spontaneous thrombosis of the subclavian and/or axillary vein. The onset of symptoms is very sudden and follows prolonged limb exertion. The entire upper extremity becomes swollen, cyanotic and somewhat painful. Again although symptoms are similar to those of Neurologic TOS, the mechanism is vascular compromise of the peripheral nerves.

Classification and Subtypes TOS was first described by Peet et al 1 in 1956. Their original classification focused principally on the mechanism of injury to the neurovascular structures, but was abandoned almost 30 years

Traumatic neurovascular TOS This is a rare, unilateral disorder which usually affects adult males. It is caused by a focal clavicular abnormality, most often a mid-shaft fracture. The proximal portions of the axillary artery, the axillary vein, and the cords of the brachial plexus (usually the medial cord) are injured either singly or in any combination. Mechanisms of injury include: • compression or laceration by bone spicules of either or both blood vessels and nerve fibres at the time of fracture • primary injury of the blood vessels causing an expanding haematoma compressing the brachial plexus elements

Hani Abdul-Jabar MBBS BSc(Hons) MRCS(Eng) is a ST2 in Trauma and Orthopaedics at Department of Orthopaedic Surgery, Hillingdon Hospital, Uxbridge, UK. Abbas Rashid MBBS BSc(Hons) MRCS(Eng) is a ST2 in Trauma and Orthopaedics at Department of Orthopaedic Surgery, Hillingdon Hospital, Uxbridge, UK. Francis Lam MBBS MSc MRCS(Ed) FRCS(Orth) is Consultant in Trauma and Orthopaedics at Department of Orthopaedic Surgery, Hillingdon Hospital, Uxbridge, UK.

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SYNDROMES

Middle Scalene Muscle Anterior Scalene Muscle Intrascalene Triangle Brachial Plexus Clavicle

First Rib

Subcoracoid Space Subclavian Artery

Costaclavicular Triangle Subclavian Vein Figure 1 The thoracic outlet.

diagnosis, and tailor investigation and subsequent management. They also help the clinician to confidently exclude other pathologies which can produce similar symptoms.

• delayed damage to blood vessels and/or, nerve fibres or both caused by the formation of a large callus or by excessive clavicular motion due to non-union. Symptoms and signs are present both locally at the fracture site, and in the distal part of the effected limb. Local findings include tenderness, a bony deformity (e.g., large callus), a mass beneath the damaged portion of the clavicle (e.g., haematoma), or bruit (e.g., pseudo aneurysm).

Adson’s test The patient’s radial pulse is palpated (Figure 2a), then the arm is externally rotated, extended and slightly abducted. The patient is asked to look towards the side being examined and to take a deep breath in (Figure 2b). Abolition or a reduction in the radial pulse is a positive test.

‘Disputed’ TOS This is a disorder with a number of names, including ‘non-specific’, ‘symptomatic’ and ‘assumed’. It first came to notice in the late 1960’s after the publication of the description of a procedure (trans-axillary 1st rib resection) designed to treat it.2 It is a rare bilateral disorder, which affects predominantly adult females. The most common causes are either acute trauma (e.g. whiplash injury) or repetitive use trauma (common in manual factory or office workers). The exact mechanism of injury is still unclear, although it is thought to be secondary to compression of neurovascular structures between the normal 1st rib and congenital bands damaged at either the time of injury or fibrosis of the scalene muscles due to postural abnormalities caused by imbalance of muscle actions.

Diagnosis Symptomatic overlap with other conditions makes it very difficult to confidently diagnose TOS. A variety of provocation tests which reproduce TOS symptoms have been devised to aid

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Figure 2 a Adson’s Test.

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Figure 4 Military Brace Test.

Figure 2 b Adson’s Test.

Investigations

Wright’s test (the hyper-abduction test) The patient’s arm is abducted to 90 degrees in external rotation whilst palpating the radial pulse. Again abolition of the pulse suggests a positive test but there is a high false positive rate.

X-ray and MRI Chest x-rays with apical lordotic views and cervical spine views are mandatory to demonstrate the presence of a cervical rib (Figure 5), an elevated 1st rib caused by tight anterior or middle scalene muscles and clavicle fractures with the associated nonunion and excessive callus. Angiography can demonstrate thromboembolic vessel blockage and aneurysms that may be compressing the plexus. The

Roos’ test The patient’s shoulder is abducted and the elbow flexed to 90 degrees. In this position the patient is asked to open and close their hands for three minutes (Figure 3). Inability to complete this exercise pain free or reproduction of presenting symptoms constitutes a positive result. The Military Brace test With both arms at the side, the patient moves the shoulder downward and backward to draw the clavicle closer to the first rib (Figure 4). Diminution or obliteration of the radial pulse constitutes a positive test.

Figure 5 Cervical rib.

Figure 3 Roos’ Test.

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SYNDROMES

latest techniques give an easy and unequivocal insight into the vascular and non-vascular (indirect) nature of the condition thus aiding clinical management decision making.7 Computed Tomography (CT) may show abnormal fibrous bands in the thoracic outlet 4 and, coupled with MRI, distinguish cervical root injury from degenerative spurs or herniated discs. MRI of the cervical spine and supra-clavicular or brachial plexus area is useful to exclude other pathologies.

Supraclavicular approach The operation is performed with the patient supine and intubated under general anaesthetic, through a lazy “S” incision parallel to the clavicle and extending from the midpoint of the clavicular attachment of the sternomastoid muscle to the anterior edge of the trapezius. Platysma is identified for later careful approximation, then the external jugular vein is ligated and omohyoid divided at its mid-point. The phrenic nerve should be identified on the surface of the anterior scalene muscle as it proceeds distally and protected. Then scalenus anterior is divided from its insertion into the first rib allowing it to retract, carefully dissecting the subclavian artery and vein from its belly. Scalenus medius is then divided from its insertion into the 1st rib, thus fully exposing the 1st rib. The 1st rib is divided anteriorly first with a rib cutter and the entire posterior portion is then removed in a twisting motion ensuring there is no residual first rib left which may otherwise produce new bone and cause recurrence of symptoms.

Ultra-sound Doppler ultra-sound studies will show impeded blood flow in vascular TOS. A near cut-off of flow during the stress manoeuvre with reproduction of symptoms would be most suggestive, but given the high prevalence of abnormal Doppler ultrasound findings in asymptomatic population, duplex may only have a limited role in the investigation of TOS.5 Full occlusion of blood flow can occur in normal subjects but is unusual and is not related to age.6 Electro-physiological testing There are clearly established diagnostic criteria for electro­diagnostic testing, particularly in true Neurologic TOS,8 viz; altered ulnar sensory conduction (low amplitude sensory nerve action potentials) and motor median conduction (low amplitude compound muscle action potential). Routine electro-diagnostic studies can sometimes yield normal results but when there is strong clinical suspicion of a neurogenic TOS and the classical electro-diagnostic abnormalities are not found, F waves may be used at rest and in provocative positions to help support the ­diagnosis.9,10

Transaxillary approach This approach was originally described by Roos in 1982.16 Under general anaesthetic with a double lumen endotracheal tube in the lateral decubitus position the ipsilateral lung is collapsed. Draping the patient should be such as to permit free movement of the arm as well as access to upper hemithorax, axilla, shoulder area and neck. A transverse incision is made below the hairline between the pectoralis major muscle anteriorly and the latissimus dorsi muscle posteriorly. The underlying fascia is incised longitudinally and the tissues are bluntly dissected digitally. The incision is then deepened directly towards the chest wall without angling up towards the 1st rib. When the chest wall is reached the dissection is carried superiorly to the 1st rib. Blunt dissection by touch is continued until the face of the 1st rib can be palpated. Then the dissection is continued subperiosteally along the 1st rib until scalenus anterior is identified. This is then divided near its insertion on the 1st rib and the subperiosteal dissection of the rib continued to separate it from the pleura. A triangular piece of the 1st rib is excised from the avascular area allowing the anterior part of the rib to be removed by dividing the costo-clavicular ligament. Then the posterior part is dissected subperiosteally to the transverse process at which point it is divided and excised.

Anterior scalene block This can sometimes be diagnostic, but the test is difficult and not without risk (e.g. direct damage to the plexus by the needle). If positive, there is usually a good chance of successful surgical decompression.

Treatment Management can either be non-operative or surgical depending on the underlying cause. If surgical intervention is not warranted, the use of heat, physical therapy, analgesics and muscle relaxants coupled with shoulder strengthening exercises, and modification of daily activities and sleeping habits will give relief from symptoms.11 Surgery should be considered in cases where symptoms persist over 3–4 months, if there is intractable pain, vascular loss or neurologic deficit. Depending on the underlying cause, a multi­disciplinary approach to management with both vascular and orthopaedic surgeons will result in a good to excellent surgical outcomes.13

Vascular surgery In cases of venous TOS, subclavian venous thrombectomy can usually be carried out through the supraclavicular approach. In arterial TOS, subclavian endarterectomy can be possible in those patients whose only arterial lesion is occlusion of the subclavian artery secondary to compression.4 If required, arterial reconstruction is best achieved with vein grafts rather than synthetic grafts as low flow through the prosthesis into the high resistance areas distally arising from previous embolisation may predispose to early failure.15

Operative surgical approaches

Surgery for recurrence Complete scalenectomy in redo procedures can offer an improved outcome,12 i.e. scalenus anterior should be removed and not simply sectioned. If part of the brachial plexus penetrates the scalenus medius muscle as an anatomical variant, then the muscle should also be resected, as well as any fibrous bands that may lie behind these muscles.

Surgical decompression can be achieved by scalenectomy with or without resection of the 1st rib using either a supraclavicular or a transaxillary approach. Scalenectomy combined with 1st rib resection gives better results than 1st rib resection alone, whilst simple excision only appears to be sufficient in patients in whom symptoms are caused purely by the presence of a cervical rib.

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Whilst the cause of recurrence remains controversial, it is thought to be due to adhesions of scar tissue to the vessels and nerves in the axilla. As a result, surgical intervention should be carefully planned and performed by surgeons experienced in this area. In recurrent cases, where scalenectomy alone was performed primarily, the 1st rib is better resected via the trans-­axillary approach. This is thought to improve symptoms in almost 80%.14

2 Wilbourn AJ. 10 most commonly asked questions about thoracic outlet syndrome. Neurologist 2001; 7(5): 309–312. 3 Ozcakar L, Inanici F, Kaymak B, Abali G, Cetin A, Hascelik Z. Quantification of the weakness and fatigue in thoracic outlet syndrome with isokinetic measurements. Br J Sports Med 2005; 39(3): 178–181. 4 Rideel DH, Smith BM. Thoracic and vascular aspects of thoracic outlet syndrome. Clin Orthop Relat Res 1986; 207: 31–36. 5 Byrne PG, Coughlin PA, Weston MJ, Kester RC, Kent PJ. Doppler ultrasound in the investigation of thoracic outlet syndrome. Br J Surg 2002; 1(89): 21–24. 6 Colon E, Westdrop R. Vascular compression in the thoracic outlet. Age dependant normative values in non-invasive testing. J Cardiovasc Surg 1988; 29(2): 166–171. 7 Fraschini GF, Ciampi P. Angiographic study in the diagnosis and treatment of thoracic outlet syndrome. J Bone Joint Surg Br 2005; 87-B(II): 177–179. 8 Cuevas-Trisan RL, Cruz-Jimenez M. Provocative F waves may help in the diagnosis of thoracic outlet syndrome: a report of three cases. Am J Phys Med Rehabil 2003; 82(9): 712–715. 9 Jarret SA, Cuzzone LJ, Pasternak BM. Thoracic outlet syndrome: electrophysiologic reappraisal. Arch Neurol 1964; 41: 960–963. 10 Urschel HC, Razzuk MA. Management of thoracic outlet syndrome. N Engl J Med 1972; 286: 1140–1143. 11 Hawkes CD. Neurosurgical considerations in thoracic outlet syndrome. Clin Orthop Relat Res 1986; 207: 24–28. 12 Chan CW, Smith SR. Anterior scalenectomy is beneficial in first but not cervical rib resections for thoracic outlet syndrome. Br J Surg 2004; 91(8): 1088–1091. 13 Lam KS, Sharan D, Moulton A, et al. Outcome of Two Surgeons Approach for Thoracic Outlet Syndrome. J Bone Joint Surg Br 2003; 85-B(I): 48–49. 14 Efstathopoulos D, Mihos P, Gakidis V, Seitaridis S, Kokkalis Z, Kaldis P. Thoracic outlet syndrome. Our experience from resection of the first rib through transaxillary approach. J Bone Joint Surg Br 2004; 86-B(II): 189–190. 15 Judy KL, Heymann RL. Vascular complications of thoracic outlet syndrome. Am J Surg 1972; 123: 521–523. 16 Roos DB. The place for scalenectomy and first rib resections in thoracic outlet syndrome. Surgery 1982; 92: 1077–1085.

Complications of surgery Pneumothorax is common, occurring in up to 30% of cases, arising during resection of the 1st rib due to the proximity to the apical pleura. Vascular damage, particularly to the subclavian artery, where it passes posterior to the scalenus anterior muscle is at risk. Neurological damage can occur to the long thoracic nerve (which will cause scapular winging) to the intercosto-brachial nerve (causing paraesthesia along the posterior aspect of the arm and the lower trunk of the brachial plexus is at risk when the rib is divided posteriorly.

Conclusion The prognosis is generally good with most patients obtaining relief of paresthesiae and numbness and return of strength or activity tolerance. However recurrence is common and to prevent it accurate clinical evaluation, careful preoperative planning and meticulous dissection are essential. Surgery comprising anterior and middle scalenectomy combined with 1st rib resection should be considered in all chronically symptomatic patients, but should be undertaken by surgeons experienced and comfortable with the anatomy and management of potential complications and best by a combined team approach. ◆

References 1 Peet RM, Henriksen JD, Anderson TP, Martin GM. Thoracic outlet syndrome. Evaluation of therapeutic exercise programme. Mayo Clin Proc 1956; 31: 281–283.

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CME section

CME questions based on the Mini-Symposium on “What’s new in hip replacement — basic principles” a 10 b 50 c 100 d 500 e 1000

The following series of questions are based on the Mini­Symposium on “What’s new in hip replacement – basic principles”. 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 Orthopaedics and Trauma Editorial Office at the address at the bottom of the RESPONSE sheet. Please photocopy this page if you wish to keep your copy of Orthopaedics and Trauma Replies received before the next issue of the journal 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.

5 W  hich of the following has the greatest observed bacterial contamination rate by the end of a total hip replacement procedure a Inside knife blade b Light handle within the laminar flow zone c Outside (skin) knife blade d Sucker tip e Surgeons gown

Questions

6 W  hat position of the hip exacerbates symptoms of piriformis syndrome a Abduction in extension with external rotation b Abduction in extension with internal rotation c Abduction in flexion with internal rotation d Adduction in extension with internal rotation e Adduction in flexion with external rotation

1 W  hich of the following is not true when Zirconia is compared to Alumina A Alumina has a coarser grain size B Alumina has greater bending strength C Zirconia has greater fracture toughness D Zirconia femoral heads were withdrawn by the Medical Devices agency because of high fracture rates E Zirconia can undergo phase transformation in wet environments, increasing surface roughness

7 A  fter resurfacing arthroplasty of the hip, which of the following patient groups has the best prognosis a Males under 65 b Males over 65 c Females under 65 d Females over 65 e Patients with osteonecrosis

2 Which of the following is the smallest a The annual linear wear rate of a ceramic on ceramic hip

bearing b The annual linear wear rate of a ceramic on polyethylene

hip bearing after bedding in c The ideal diametrical clearance of a metal on metal bearing

to facilitate polar bearing

8 W  hich of the following is the weakest risk factor for thromboembolic complications of surgery a Antiphospholipid syndrome b Bechets disease c Nephrotic syndrome d Paraproteinaemia e Thrombasthenia

d The typical size of a metal wear particle e The typical size of a skin squame shed by the surgeon

during an operation 3 What is the commonest cause of failure of primary total hip replacements documented in the UK National Joint Registry a Aseptic loosening b Cup fracture c Dislocation d Infection e Stem fracture

9 I n the posterior approach to the hip, which structure leaves the pelvis below piriformis and turns superiorly to supply the deep parts of gluteus maximus a Inferior gluteal artery b Inferior gluteal nerve c Sciatic nerve d Superior gluteal artery e Superior gluteal nerve

4 I f 10000 organisms are needed to initiate infection in a normal marrow cavity, what innoculum has the same effect in the presence of a cemented total hip replacement stem

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CME section

10 I f the deep fascia is incised on the medial side of tensor fascia lata during the anterior approach to the hip and the dissection is continued in this fascial sheath, which structure is thereby protected a Anterior circumflex femoral artery b Femoral artery c Femoral nerve d Lateral cutaneous femoral nerve e Ilioinguinal nerve

Responses Please shade in the square for the correct answer.

11 W  hich of the following has been described as the safe zone for acetabular cup orientation that is associated with the lowest dislocation rates a 30+/− 10 degrees of abduction, 10 +/− 10 degrees anteversion b 30+/− 10 degrees of abduction, 15 +/− 10 degrees anteversion c 40+/− 10 degrees of abduction, 15 +/− 10 degrees anteversion d 40+/− 10 degrees of abduction, 25 +/− 10 degrees anteversion e 45+/− 10 degrees of abduction, 20 +/− 10 degrees anteversion

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Your details (Print clearly) NAME……………………………………………………………… ADDRESS………………………………………………………… ………………………………………………………………………

12 W  hich of the following scores used to assess hip arthritis contains the fewest questions a Arthritis impact assessment scale b EuroQol (EQ-5D) c Hip disability and osteoarthritis outcome score d Oxford hip score e WOMAC score

……………………………………………………………………… ……………………………………………………………………… FAX NO…………………………………………………………… EMAIL……………………………………………………………… RETURN THE COMPLETED RESPONSE FORM by fax to +44113-392-3290, or by post to CME, Orthopaedics and Trauma, Academic Department of Orthopaedic Surgery, “A” Floor Clarendon Wing, Leeds General Infirmary, Great George Street, Leeds LS1 3EX, UK.

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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CME SECTION

Answers to CME questions based on the Mini-Symposium on “Essential biomechanics of hip replacement” Please find below the answers to the Current Orthopaedics CME questions from Vol. 22, issue 5 which were based on the MiniSymposium on “Essential biomechanics of hip replacement”

1 A

B

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E

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B

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Mini-symposium: Imaging for joint replacement

(i) Radionuclide imaging of joint prostheses: established & emerging applications

Plain radiography is not sensitive or specific because both infection and aseptic loosening can manifest as peri-­prosthetic lucency or migration. Alternatively infected prostheses may appear radiographically normal.4,5 Review of sequential plain radiographs increases the accuracy as there is more rapid progression of lucency or migration in infection.6 Computed Tomography (CT) and Magnetic Resonance Imaging (MRI) can be limited due to artefacts caused by the implanted metallic prosthesis. However, newer cross-sectional imaging algorithms have led to a reduction in artefact and an increased role of CT and MRI in imaging the prosthetic joint, particuarly of the peri-articular soft tissues.7,8 Radionuclide imaging reflects functional rather than anatomical changes and is not hampered by the presence of a metallic prosthesis. As a result scintigraphy is currently the modality of choice in the investigation of suspected prosthetic joint infection.2 A number of different techniques have been used in the past including radionuclide arthrography and Gallium-67 scintigraphy but these have largely fallen by the wayside for one reason or another. The most widely utilised investigations are bone scintigraphy and radiolabelled white blood cell imaging which will be discussed in detail below. Immunoscintigraphy using more specific agents is less widely available and generally more expensive but shows promise. The emergence of dual modality imaging using integrated single photon emission computed tomography – computed (SPECT-CT) and positron emission tomography – computed tomography (PET-CT) may also have a valuable role for more accurate accurate assessment of joint replacement complications.

Richard J Robinson Andrew F Scarsbrook

Abstract Bone and radiolabelled white blood cell scintigraphy are widely used in the evaluation of symptomatic joint prostheses. Emerging techniques including dual tracer scintigraphy, positron emission tomography ­computed tomography (PET-CT) and immunoscintigraphy show promise as more specific tools for use in the assessment of prosthetic joint complications. This article will review the current and future role of radio­ nuclide imaging in establishing the presence, and determining the cause of prosthetic joint complications.

Keywords infection; joint replacement; PET-CT; prosthetic loosening; scintigraphy

Bone scintigraphy Bone scintigraphy involves the use of a radiolabelled bone seeking agent (Technetium 99m methyl diphosphonate (MDP)). In the evaluation of prosthetic joint complications planar images are usually acquired in 2 phases. Approximately 10 minutes after injection of the radiopharmaceutical “blood flow” images are obtained. Subsequently “bone phase” images are obtained approximately 3 hours after tracer injection. Static images of the relevant areas are obtained using a gamma camera and tomographic (SPECT) images can be obtained as necessary to provide greater spatial resolution. The normal distribution of this tracer in the body includes the skeleton, genitourinary tract and soft tissues.2,9 The effective dose received by an adult patient with normal renal function is 6 mSv (equivalent to 300 chest X-rays).10 Tracer uptake around the prosthesis greater than the background level can occur as a physiological response for several months following joint replacement. Persistent uptake more than 12 months after surgery is usually abnormal. This is particularly pertinent when reviewing the delayed imaging. MDP uptake depends on blood flow and the rate of new bone formation, therefore any cause of new bone formation around the prosthesis may result in increased tracer uptake or a “hot spot” on the images. Bone scintigraphy is highly sensitive but not very specific as it cannot differentiate between infection and aseptic loosening (Fig. 1). Sensitivities of up to 100% have been reported in the detection of infection, however the specificity in one study was 0%.11 In aseptic loosening of hip prostheses the sensitivity of bone ­scintigraphy is between 70–90% and the specificity is 50–75%,

Introduction By the year 2010 it is estimated that over 100,000 primary hip and knee replacement operations and nearly 25,000 hip and knee revision procedures will be performed annually in the NHS.1 Whilst these operations are generally very successful complications can occur including aseptic loosening, dislocation, peri-prosthetic fracture, and infection. A number of these complications are easily diagnosed with plain radiography however differentiation between aseptic loosening and infection can be more challenging as there is a significant clinical and radiographic overlap between the two conditions. The considerable difference in treatment between the two mandates accurate imaging evaluation in order to ensure appropriate management and minimise unnecessary surgery.2,3 Serum markers of inflammation such as C- reactive protein (CRP) and plasma viscosity (PV) are non-specific and joint aspiration can be unreliable with a sizeable incidence of both false negative and false positive results reported in the literature.2

Richard J Robinson MBChB MRCP FRCR is a Specialist Registrar Department of Radiology at St James’s University Hospital, Leeds Teaching Hospitals NHS Trust, West Yorkshire, UK. Andrew F Scarsbrook BMedSci BMBS FRCR is a Consultant Radiologist & Nuclear Medicine Physician and Head of Department of Nuclear Medicine at St James’s University Hospital, Leeds Teaching Hospitals NHS Trust, West Yorkshire, UK.

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Anterior planar images from a Tc 99m bone scintigram in a 68-year-old women with bilateral knee replacements and knee pain a blood pool phase and b bone phase image. Increased tracer activity is seen around the right femoral component of the total knee prosthesis (arrows) and the tibial component of the left TKR. This indicates a high probability of loosening but cannot differentiate between a septic and aseptic cause. Aseptic loosening was confirmed at surgery. Figure 1

cause is often unclear and further more specific imaging may be necessary (Table 2).

the sensitivity is lower when assessing the acetabular component.12,13 The major utility of the test is its exclusion value as it has a very high negative predictive value (95%) for ruling out significant complications in hip and knee prostheses.14 No specific data are available in the literature regarding the utility of the technique in shoulder, elbow and ankle prostheses (see Table 1). The negative predictive value of the technique is much lower in patients imaged less than 1 year following surgery. Approximately two thirds of prosthetic infection develops in this time 3 but approximately one third of patients with a normal cemented hip prosthesis can have persistently increased tracer uptake at 12 months.15 Tracer uptake is known to persist for an even longer period of time and with more variability in cementless porus coated prostheses and around knee prostheses.2 The advantages of bone scintigraphy are that it is widely available, non-invasive and cheap. In patients with positive scans the

67 Gallium citrate scintigraphy 67 Gallium Citrate is a radiopharmaceutical that can be used for imaging of suspected joint replacement infection. Imaging is performed 18–72 hours after injection of the tracer. Sequential Gallium and bone scintigraphy improves the specificity in differentiating between infection and aseptic loosening.16 Images are interpreted by established criteria comparing congruity of the spatial distribution and intensity of the two different scans. Images are considered positive for infection if gallium and technetium uptake is spatially incongruent or if gallium uptake is congruent and more intense than technetium. Images are interpreted as negative if gallium uptake is congruent and less intense than that of technetium. In instances where gallium and technetium uptake are congruent and of similar intensity, the result

Sensitivity and specificity of bone scintigraphy for aseptic loosening

Bone Scintigraphy Summary

Joint

Sensitivity (%)

Advantages

Disadvantages

Hip Acetabular Femoral Knee Shoulder, Elbow & Ankle

67 88 92 No specific data

Sensitive High negative predictive value

Low specificity Reduced accuracy <1  yr post operation

Specificity (%)

Reference

12 75 13 50 14 76 found in the literature

Cost effective Easily accessible Straightforward methodology Table 2

Table 1

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Mini-symposium: Imaging for joint replacement

is recorded as equivocal. Using this method of imaging gives an overall accuracy rate of approximately 70–80%.17 Whilst the combination of sequential Gallium and bone scintigraphy improves specificity there are a number of drawbacks to its use as a diagnostic test (Table 3). Imaging is performed a long time following injection of the radioisotope which is inconvenient for the patient and Gallium scintigraphy imparts an additional 18mSv of radiation dose when compared to a bone scan alone (equivalent to 900 chest x rays).10 In view of these limitations Gallium scintigraphy has generally been superseded by other techniques but it still may have a role in neutropaenic patients as its mechanism of uptake does not wholly rely on the presence of functioning neutrophils.18

White Blood Cell Scintigraphy

High additional radiation dose

Invasive in vitro methodology Not useful in neutropaenic patients

Radionuclide arthrography is a combined scintigraphic and radiographic technique that has been used for the detection of prosthetic loosening but is not widely practiced. The technique involves a number of different steps which require a well organized protocol. The patient is firstly injected with 99m-Tc MDP as in normal bone scintigraphy. Approximately 1 hour later a solution of ionic contrast material and 111-indium colloid is injected into the joint space using fluoroscopic guidance. The joint is filled with contrast and images are evaluated for the leakage of contrast around the prosthesis to indicate loosening as per a normal radiographic arthrogram. Following radiographic imaging the patient walks around (if possible) to promote an increase in intra-articular pressure. At around 3 hours following injection scintigraphic images are obtained of the joint with the detector configured to record tracer activity of the different radionuclides separately. This allows assessment of any leakage around the prosthesis from the

Not widely performed Unfavorable methodology

Table 3

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High additional radiation dose

Radionuclide arthrography

67 Gallium Citrate Scintigraphy Summary

Improved specificity vs. bone scintigraphy Use in neutropaenic patients

Highly sensitive and specific when combined with sulphur colloid imaging Relatively easy access in the UK

bone marrow to that seen on the white cell scan. Areas which show increased uptake on the white cell scan with an absence of uptake on the bone marrow scan are considered positive for infection (Fig. 3). The dual isotope method is currently considered the gold standard in the investigation of prosthetic joint infection and a suggested algorithm for investigation of symptomatic joint replacements is presented in Fig. 4. However it does have limitations. Radiolabelling of white blood cells is a highly involved process which is relatively inconvenient to the patient. Combined imaging involves a second examination performed up to 72 hours after the initial injection (when using Tc 99m HMPAO).19 This increases the cost of the examination and patients are also subjected to an additional radiation dose. The effective dose of combined indium labelled white cell and sulphur colloid scintigraphy is approximately 12 mSV (600 chest X rays) compared to 8 mSv (400 chest X rays) for stand alone WBC scintigraphy using Tc 99m HMPAO.10 Currently white cell scintigraphy remains the investigation of choice in prosthetic joint infection its limitations, however, necessitate the search for an investigation with similar accuracies but improved methodology. Due to the expense and technical complexity of the technique it is usually rationed and bone scintigraphy is used as the first line test and only those with abnormal bone scans progressing on to a WBC scan.

White blood cell scintigraphy involves labeling of patients’ white blood cells with a radioactive tracer and is widely used in the evaluation of suspected infection and inflammation. Commonly used tracers include Indium-111 oxine and Technetium- 99m Hydroxymethylpropyleneamine oxime (99m Tc HMPAO). The cell labeling technique is labour-intensive and requires appropriately trained staff. Approximately 60 ml of blood is taken from the patient, left to sediment and centrifuged to separate leucocytes from other blood components. The leucocytes are then mixed with the radiotracer and re-injected into the patient. Imaging using 99m Tc HMPAO is performed at 1 and 3 hours following injection (Table 4). Leucocytes circulate peripherally for a short period of time and unless chemotaxis occurs, reside in the bone marrow (90%), spleen, liver and lung. Normal tracer activity is therefore seen at these sites.18 In the setting of prosthetic joint infection increased tracer uptake occurs around the prosthesis indicating the ­accumulation of white blood cells (Fig. 2). One would expect that this would accurately determine the presence of infections however varying degrees of sensitivity and specificity have been reported. This is due to reduced sensitivity in chronic infection, detection of nonspecific inflammation, variable distribution of haematopoeitic marrow in different patients and localised expansion of haematopoetically active marrow caused by the prosthesis itself. These factors make image interpretation more challenging. Sensitivities vary from 65–100% and specificities from 23% to 65%.19 The diagnostic utility of functional imaging has been shown to be significantly improved by performing combined white cell (using Indium 111-WBCs) and bone marrow scintigraphy (using Technetium labeled colloid) increasing the accuracy up to 98%.19 This enables comparison of the normal distribution of

Disadvantages

Disadvantages

Table 4

White blood cell scintigraphy

Advantages

Advantages

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a anterior planar image from a Tc 99m bone scan in a 70-year-old man with bilateral total knee replacements. This reveals abnormal uptake around the left knee prosthesis indicating increased bone turnover suggestive of loosening (arrows). Normal uptake is seen around the right knee prosthesis. b Corresponding anterior planar image from a WBC scan. This reveals focal uptake on the medial side of the tibial prosthesis (arrows) suggestive of septic loosening. Infection was diagnosed at microbiologic evaluation of a surgical specimen. Figure 2

l­oosening. Sensitivities and specificities greater than 80% have been reported around the femoral component with slightly reduced specificity around the acetabular component.12,13,20 The sensitivity (88%) and specificity (88%) of the technique for evaluation of loosening of knee replacements is ­encouraging 21 but there are very little data available in the literature in this area.

intra-articular radionuclide to be estimated using the 99m TC MDP images as a landmark for the location of the prosthesis and bony structures 20 (Fig. 5). Radionuclide arthrography is reported to be more sensitive and specific than bone scintigraphy and radiographic arthrography performed separately for the detection of hip prosthesis

a Anterior planar image from a Tc 99m bone scintigram in a 73-year-old man revealing abnormal increased tracer uptake around the distal aspect of the femoral portion of a long stem hip prosthesis (arrow). This could represent aseptic or septic loosening. b Anterior planar image from a WBC scan in the same patient showing increased uptake at the distal end of the femoral stem (arrow) suggesting infection. c Corresponding anterior planar image from a Tc99m labelled nano-colloid scan revealing a matching area of increased uptake at the distal aspect of the femoral prosthesis (arrow) indicating the presence of ectopic haematopoietic marrow at this point and not infection. This is an example of false positive WBC scintigraphy and highlights the increased specificity of parallel WBC and colloid imaging. Note the normal haematopoietic marrow seen in the right femur (block arrow). Figure 3

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Images from a 55-year-old man with loosening of both components of a cemented prosthesis 8 years after primary joint replacement. a-c Nuclear arthrographic images showing loosening of both. a Anterior bone scan showing moderately increased uptake around the acetabulum, in the inter-trochanteric region and at the tip of the prosthesis. b lndium-111 colloid image with region of interest shown. c lndium-111 region projected on the bone scan: leakage to the tip of the femoral component (arrow) and around the acetabular component. Note leakage in the pelvic soft tissues. d Radiographic arthrographic image after 10 ml of contrast agent showing leakage around the acetabular component (open arrow) and in the lateral, distal segment of the femoral component (solid arrow), indicating loosening of both components. (Reprinted by permission of the Society of Nuclear Medicine from: Wim J.G., Oyen, J.,Albert M., Lemmens, Roland A.M.J. Claessens, James R. van Horn, Tom J.J.H. Slooff, and Frans H.M. Corstens. Nuclear Arthrography: Combined Scintigraphic and Radiographic Procedure for Diagnosis of Total Hip Prosthesis Loosening. J Nucl Med. 1996 37(1): 62–70.) Figure 4

Radionuclide arthrography appears superior to bone scintigraphy alone in the detection of loosening, however, it has major drawbacks (Table 5). It is an invasive investigation carrying with it the potential of significant morbidity including the introduction of sepsis to a previously aseptic joint. It provides additional patient radiation dose and as with bone scintigraphy infection and aseptic loosening are indistinguishable. Its role may lie in difficult cases where there is only minimal loosening especially on the femoral aspect of a hip ­prosthesis22

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and in patients where non-invasive imaging techniques are ­inconclusive.

Positron emission tomography Positron emission tomography (PET) and the more recent hybrid imaging technique of positron emission tomography – computed tomography (PET-CT) utilise a short lived radiotracer which decays emitting a positron. This travels a short distance 81

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Mini-symposium: Imaging for joint replacement

Figure 5 a suggested imaging algorthim for patients with symptomatic joint replacements.

the one most commonly used is 18 Fluorine ­fluorodeoxyglucose (FDG). FDG is an analogue of glucose which concentrates in areas of high glycolytic activity such as rapidly dividing cells. It is widely used in oncology but also has an emerging role in the evaluation of patients with infection or inflammation. Neutrophils and macrophages have increased FDG uptake allowing localization of infection and inflammation.23 The provision of PET-CT cameras in the United Kingdom currently compares unfavorably with Europe and the rest of the world. It is therefore mainly used and funded for cancer-related imaging in the UK 24 (Fig. 6). FDG PET has a number of advantages over single photon imaging. There is improved spatial resolution and imaging is completed within 2–3 hours of radiopharmaceutical injection. In addition PET-CT combines PET with a low or conventional dose CT scan and provides excellent anatomical correlation of any areas of increased activity which increases the accuracy compared to PET alone 25 (Fig. 7). The technique may be more convenient for the patient and also facilitates a more rapid result to the surgeon.

(∼1 mm) through the body before colliding with an oppositely charged electron. Both particles annihilate releasing energy in the form of 2 gamma photons which travel in opposite directions. These ­ photons are detected by a ring of detectors surrounding the patient. The time difference recorded between the detection of the separate photons enable more accurate positioning of an abnormality within the body. This gives greater spatial resolution compared to other nuclear medicine techniques. A number of positron emitting radioisotopes are available for clinical use but

Radionuclide Arthrography Advantages

Disadvantages

Improved accuracy vs. Bone scintigraphy alone

Not widely practiced Invasive examination

Table 5

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Images obtained in 76-year-old woman 26 months after left total hip replacement. Infection was diagnosed at microbiologic evaluation of a surgical specimen. Results of PET, serial conventional radiography, and bone scintigraphy were true-positive. a, attenuation corrected (AC) and, b, non attenuation corrected (NAC) coronal FDG PET images show diffusely increased FDG uptake (arrowheads) around the head and shaft of the left total hip replacement. The NAC image shows additional increased uptake in the soft tissues (arrow) laterally adjacent to the prosthesis. c, d, Conventional anteroposterior radiographs of the left hip show rapid development of osteolysis (arrows) at the boneprosthesis and cement-bone interfaces. d was obtained 6 months after c. e, f, Anterior bone scintigrams obtained during, e, the blood pool phase and, f, the late phase show diffusely increased radionuclide uptake (arrows) around the entire total left hip replacement. All images except c were obtained within 5 days of each other. (Reprinted by permission from Stumpe, K. D., Nötzli, H. P., Zanetti, M., Kamel, E. M., Hany, T. F., Görres, G. W., et al. (2004). FDG PET for differentiation of infection and aseptic loosening in total hip replacements: Comparison with conventional radiography and three-phase bone scintigraphy. Radiology, 231(2), 333–341.) Figure 6

to its increased sensitivity, however limited access may prove problematic in the UK for some time (Table 6).

The patient dose is comparable to other nuclear medicine studies approximately 7mSv (350 chest x rays). ­ Disadvantages include limited access to the modality for the investigation of infection and inflammation and cost. Radiotracers used in PET have short half lives (F-18 FDG half life is 110 minutes) and require access to an expensive cyclotron for production. The limited number of cyclotrons and PET-CT scanners in the UK mean that many centres may not have access to PET-CT for this indication in the immediate future.26 The utility of FDG PET-CT for assessment of joint prosthesis problems has not yet been firmly established. The available literature suggests a universally high sensitivity for the detection of peri-prosthetic infection with figures ranging from 85% to 100%. However, there is much more variability in ­specificity ranging from 9% to 95% depending on the criteria used to interpret the study.23,27–32 Specificity is reduced when imaging knee prostheses.23,29 Some researchers feel there is no added value over combined white cell imaging due to the lower accuracy of FDG PET.29,32 Consensual interpretation techniques have yet to be established which probably accounts for the varying specificity but universally high sensitivity suggests whilst a positive result could represent either septic or aseptic loosening, a negative result offers extremely strong evidence against infection. FDG PET offers definite advantages over bone scintigraphy due

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Future applications of PET FDG is not the only tracer used in PET imaging. A recent small study 33 showed a 100% sensitivity for the detection of early aseptic loosening in total knee prostheses using the bone seeking tracer Fluoride 18. This suggests a role in a number of orthopaedic applications but this result will have to be replicated in future studies. A recent editorial suggests Gallium 68 (68 Ga) labeled peptides may offer fiscal advantages over other agents in the investigation of infection, as it is a positron emitting isotope that can be produced from a generator rather than relying on a more expensive cyclotron. This may be especially pertinent in developing countries but the efficacy of the technique will need to be established in the literature. 34 The labeling of white blood cells with 18F-FDG has also been investigated in a variety of infections throughout the body with high sensitivity and specificity.35 Similar accuracies to white cell scintigraphy have been reported in the detection of prosthetic infection using this technique.36 The improved imaging characteristics of PET-CT are likely to offer advantages over traditional white cell scans but again further correlative work is required before becoming clinically accepted. 83

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Half body PET CT scan performed in a 65 year old patient with potentially operable primary lung carcinoma for staging. a Coronal reformatted image from the low dose CT component b Attenuation corrected coronal image of the FDG PET component. c Fused PET-CT image. There is an FDG positive primary lung carcinoma at the left hilum (arrow). An incidental finding of avid tracer uptake within the right hip joint (block arrow) was seen. Septic arthritis was later proven. This shows the potential FDG PET CT may have in imaging orthopaedic infection and inflammation due to its high sensitivity and specificity. Its role in imaging joint prostheses has yet to be firmly established. Figure 7

localising infection. The technique involves injection of a pre­prepared agent into the patient relying on in vivo tagging of white cells or bacteria. Images are obtained from 1–8 hours following injection with delayed imaging performed at 24 hours to improve accuracy in cases which are equivocal on early imaging.37,38 These techniques have a number of advantages over traditional white cell imaging. The use of a pre-prepared radiopharmaceutical is preferable to the convoluted in vitro labeling technique currently used. This saves time, reduces workload and risk to staff as no blood products are handled. Imaging is generally performed on the day of injection although patients with equivocal results may have to undergo delayed imaging. The ­ciprofloxacin agent is not taken up by bone marrow and does not depend on the white cell status of the patient thereby offering potential benefit when imaging areas containing red marrow or in neutropaenic patients.39 Disadvantages include the possibility of allergic reaction to the cloned murine antibodies utilised although this risk is reduced when using antibody fragments.40 A number of small studies have been performed to try and establish the efficacy of 99m Technetium anti-granulocyte Fab’ fragment (Leukoscan) imaging. A recent meta-analysis of over

Immunoscintigraphy Immunoscintigraphy is a functional imaging technique involving the use of radiolabeled monoclonal antibodies, antibody ­fragments or antibiotics (e.g. ciprofloxacin). Antibody derived tracers directly target surface antigens on granulocytes whilst the ciprofloxacin labeled agent binds directly to bacteria thereby

Positron Emission Tomography Advantages

Disadvantages

High Sensitivity

Limited availability for inflammatory indications Role in prosthetic joint imaging not yet fully established

Improved spatial resolution especially when combined with PET CT Favorable imaging methodology Table 6

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a Images from a Tc-99m WBC scintigram show focal tracer accumulation adjacent to the distal tip of the femoral component of a left hip replacement.but no abnormal findings in the right femur, where a fixation nail is present, in a 77-y-old man who underwent orthopedic surgery 1 y previously. b Tc-99m Ciprofloxacin (Infecton) scintigraphy confirms abnormality in the distal end of the left hip prosthesis and also shows pronounced focal accumulation of tracer in the area of the right femoral fixation nail. Biopsy results confirmed osteomyelitis at both sides. (Reprinted by permission of the Society of Nuclear Medicine from: Kerim Sonmezoglu, Meral Sonmezoglu, Metin Halac, Isik Akgün, Cüneyt Türkmen, Cetin Önsel, Bedii Kanmaz, Kirsor Solanki, Keith E. Britton, and Ilhami Uslu. Usefulness of 99mTc-Ciprofloxacin (Infecton) Scan in Diagnosis of Chronic Orthopedic Infections: Comparative Study with 99mTc- HMPAO Leukocyte Scintigraphy. J Nucl Med. 2001 42(4): 567–574. Figure 3.) Figure 8

than white cell scanning and bone scintigraphy along with comparable results to sequential bone scintigraphy/galllium imaging. Sensitivities of 85–100% and specificities of 78–95% along with improved imaging characteristics suggest Infecton imaging may offer a viable alternative to white cell imaging 39,41–44 (Fig. 8). However, further work is necessary in this area before becoming accepted. One of the limitations of these immunoscintigraphic agents is the high cost which prohibits use in all but very specialised centres at present (Table 7).

500 patients suggested an overall sensitivity of 84% and specificity of 80% in detecting prosthetic infection.41 This is comparable to white cell imaging but its main value lies with a negative test virtually excluding infection rather than a positive test proving it. Early work with 99m Tc ciprofloxacin (Infecton) has shown promising results with a higher reported sensitivity and specificity

Immunoscintigraphy Advantages

Disadvantages

High sensitivity and specificity In vivo imaging methodology

Expensive Possibility of allergic reaction with murine antibody agents Not widely practiced at present in the UK Role in prosthetic joint imaging not yet fully established

Conclusion Bone scintigraphy remains a valuable first line test in patients with symptomatic joint replacements due to its accessibility, cost effectiveness and high negative predictive value. In positive studies or those in which there is significant clinical concern of infection combined white blood cell/bone marrow imaging is currently the gold standard in determining the presence of infection. The use of other agents and techniques including radionuclide arthography and FDG PET-CT may be of value in equivical cases but these are highly dependent on local availability and expertise. The search for an ideal “one stop shop” ­radiopharmaceutical for

Table 7

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use in prosthetic joint imaging remains elusive. Newer agents such as white blood cell labelled PET and immunoscintigraphy are challenging traditional radiopharmaceuticals, however further good quality research is required to confirm their efficacy. ◆

17 Merkel KD, Brown ML, Fitzgerald RH. Jr. Sequential technetium-99m HMDP-gallium-67 citrate imaging for the evaluation of infection in the painful prosthesis. J Nucl Med 1986; 27: 1413–7. 18 Zeissman Harvey A., O’Malley Janis P, Thrall James H. Nuclear medicine: the requisites, third edition (Requisites in Radiology). Mosby. Ref Type: Generic 19 Palestro CJ, Love C, Tronco GG, Tomas MB, Rini JN. Combined labeled leukocyte and technetium 99m sulfur colloid bone marrow imaging for diagnosing musculoskeletal infection. Radiographics 2006; 26: 859–70. 20 Oyen WJ, Lemmens JA, Claessens RA, van Jr. H, Slooff TJ, Corstens FH. Nuclear arthrography: combined scintigraphic and radiographic procedure for diagnosis of total hip prosthesis loosening. J Nucl Med 1996; 37: 62–70. 21 Kitchener MI, Coats E, Keene G, Paterson R. Assessment of radionuclide arthrography in the evaluation of loosening of knee prostheses. Knee 2006; 13: 220–5. 22 Miniaci A, Bailey WH, Bourne RB, McLaren AC, Rorabeck CH. Analysis of radionuclide arthrograms, radiographic arthrograms, and sequential plain radiographs in the assessment of painful hip arthroplasty. J Arthroplasty 1990; 5: 143–9. 23 Zhuang H, Duarte PS, Pourdehnad M, Maes A, Van AF, Shnier D, Garino JP, Fitzgerald RH, Alavi A. The promising role of 18F-FDG PET in detecting infected lower limb prosthesis implants. J Nucl Med 2001; 42: 44–8. 24 Department of Health (UK). A framework for the development of Positron Emission Tomography (PET) services in England. 2005. Ref Type: Generic 25 Strobel K, Stumpe KD. PET/CT in musculoskeletal infection 1. Semin Musculoskelet Radiol 2007; 11: 353–64. 26 Royal College of Radiologists. PET-CT in the UK. A strategy for development and integration of a leading edge technology within routine clinical practice. 2008. Ref Type: Generic 27 Delank KS, Schmidt M, Michael JW, Dietlein M, Schicha H, Eysel P. The implications of 18F-FDG PET for the diagnosis of endoprosthetic loosening and infection in hip and knee arthroplasty: results from a prospective, blinded study. BMC Musculoskelet Disord 2006; 7: 20. 28 Vanquickenborne B, Maes A, Nuyts J, Van AF, Stuyck J, Mulier M, Verbruggen A, Mortelmans L. The value of (18)FDG-PET for the detection of infected hip prosthesis. Eur J Nucl Med Mol Imaging 2003; 30: 705–15. 29 Van AF, Nuyts J, Maes A, Vanquickenborne B, Stuyck J, Bellemans J, Vleugels S, Bormans G, Mortelmans L. FDG-PET, 99mtc-HMPAO white blood cell SPET and bone scintigraphy in the evaluation of painful total knee arthroplasties. Eur J Nucl Med 2001; 28: 1496–504. 30 Reinartz P, Mumme T, Hermanns B, Cremerius U, Wirtz DC, Schaefer WM, Niethard FU, Buell U. Radionuclide imaging of the painful hip arthroplasty: positron-emission tomography versus triple-phase bone scanning. J Bone Joint Surg Br 2005; 87: 465–70. 31 Chryssikos T, Parvizi J, Ghanem E, Newberg A, Zhuang H, Alavi A. FDG-PET imaging can diagnose periprosthetic infection of the hip. Clin Orthop Relat Res 2008; 466: 1338–42. 32 Love C, Marwin SE, Tomas MB, Krauss ES, Tronco GG, Bhargava KK, Nichols KJ, Palestro CJ. 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: 1864–71. 33 Sterner T, Pink R, Freudenberg L, Jentzen T, Quitmann H, Bockisch A, Loer F. The role of [18F]fluoride positron emission tomography in

References 1 Dixon T, Shaw M, Ebrahim S, Dieppe P. Trends in hip and knee joint replacement: socioeconomic inequalities and projections of need. Ann Rheum Dis 2004; 63: 825–30. 2 Love C, Tomas MB, Marwin SE, Pugliese PV, Palestro CJ. Role of nuclear medicine in diagnosis of the infected joint replacement. Radiographics 2001; 21: 1229–38. 3 Palestro CJ. Nuclear medicine, the painful prosthetic joint, and orthopedic infection. J Nucl Med 2003; 44: 927–9. 4 Tigges S, Stiles RG, Roberson JR. Complications of hip arthroplasty causing periprosthetic radiolucency on plain radiographs. AJR Am J Roentgenol 1994; 162: 1387–91. 5 Tigges S, Stiles RG, Roberson JR. Appearance of septic hip prostheses on plain radiographs. AJR Am J Roentgenol 1994; 163: 377–80. 6 Stumpe KD, Notzli HP, Zanetti M, Kamel EM, Hany TF, Gorres GW, von Schulthess GK, Hodler J. FDG PET for differentiation of infection and aseptic loosening in total hip replacements: comparison with conventional radiography and three-phase bone scintigraphy. Radiology 2004; 231: 333–41. 7 Cahir JG, Toms AP, Marshall TJ, Wimhurst J, Nolan J. CT and MRI of hip arthroplasty. Clin Radiol 2007; 62: 1163–71. 8 Naraghi AM, White LM. Magnetic resonance imaging of joint replacements. Semin Musculoskelet Radiol 2006; 10: 98–106. 9 Love C, Palestro CJ. Radionuclide imaging of infection. J Nucl Med Technol 2004; 32: 47–57. 10 International Commission on Radiological Protection. Radiation dose to patients from radiopharmaceuticals. ICRP Publication 53. London, UK: ICRP; 1988; p. 232. Ref Type: Generic. 11 Segura AB, Munoz A, Brulles YR, Hernandez Hermoso JA, Diaz MC, Bajen Lazaro MT, Martin-Comin J. What is the role of bone scintigraphy in the diagnosis of infected joint prostheses? Nucl Med Commun 2004; 25: 527–32. 12 Temmerman OP, Raijmakers PG, Deville WL, Berkhof J, Hooft L, Heyligers IC. The use of plain radiography, subtraction arthrography, nuclear arthrography, and bone scintigraphy in the diagnosis of a loose acetabular component of a total hip prosthesis: a systematic review. J Arthroplasty 2007; 22: 818–27. 13 Temmerman OP, Raijmakers PG, Berkhof J, Hoekstra OS, Teule GJ, Heyligers IC. Accuracy of diagnostic imaging techniques in the diagnosis of aseptic loosening of the femoral component of a hip prosthesis: a meta-analysis. J Bone Joint Surg Br 2005; 87: 781–5. 14 Smith SL, Wastie ML, Forster I. Radionuclide bone scintigraphy in the detection of significant complications after total knee joint replacement. Clin Radiol 2001; 56: 221–4. 15 Kim HS, Suh JS, Han CD, Kim YH, Lee JD. Sequential Tc-99m MDP bone scans after cementless total hip arthroplasty in asymptomatic patients. Clin Nucl Med 1997; 22: 6–12. 16 Horoszowski H, Ganel A, Kamhin M, Zaltzman S, Farine I. Sequential use of technetium 99m MDP and gallium 67 citrate imaging in the evaluation of painful total hip replacement. Br J Radiol 1980; 53: 1169–73.

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the early detection of aseptic loosening of total knee arthroplasty. Int J Surg 2007; 5: 99–104. 34 Sathekge M. The potential role of 68Ga-labeled peptides in PET imaging of infection. Nucl Med Commun 2008; 29(8): 663–5. Ref Type: Generic. 35 Dumarey N, Egrise D, Blocklet D, Stallenberg B, Remmelink M, del MV, Van SG, Jacobs F, Goldman S. Imaging infection with 18FFDG-labeled leukocyte PET/CT: initial experience in 21 patients. J Nucl Med 2006; 47: 625–32. 36 Rini JN, Bhargava KK, Tronco GG, Singer C, Caprioli R, Marwin SE, Richardson HL, Nichols KJ, Pugliese PV, Palestro CJ. PET with FDGlabeled leukocytes versus scintigraphy with 111In-oxine-labeled leukocytes for detection of infection. Radiology 2006; 238: 978–87. 37 Larikka MJ, Ahonen AK, Junila JA, Niemela O, Hamalainen MM, Syrjala HP. Extended combined 99mTc-white blood cell and bone imaging improves the diagnostic accuracy in the detection of hip replacement infections. Eur J Nucl Med 2001; 28: 288–93. 38 Rubello D, Casara D, Maran A, Avogaro A, Tiengo A, Muzzio PC. Role of anti-granulocyte Fab’ fragment antibody scintigraphy (LeukoScan) in evaluating bone infection: acquisition protocol, interpretation criteria and clinical results. Nucl Med Commun 2004; 25: 39–47. 39 Sonmezoglu K, Sonmezoglu M, Halac M, Akgun I, Turkmen C, Onsel C, Kanmaz B, Solanki K, Britton KE, Uslu I. Usefulness

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of 99mTc-ciprofloxacin (infecton) scan in diagnosis of chronic orthopedic infections: comparative study with 99mTc-HMPAO leukocyte scintigraphy. J Nucl Med 2001; 42: 567–74. 40 Iyengar K.P. et al. Functional imaging in orthopaedic infections Update on immunoscintigraphy. 20[1]. 2008. Ref Type: Generic 41 Pakos EE, Trikalinos TA, Fotopoulos AD, Ioannidis JP. Prosthesis infection: diagnosis after total joint arthroplasty with antigranulocyte scintigraphy with 99mTc-labeled monoclonal antibodies–a meta-analysis. Radiology 2007; 242: 101–8. 42 Larikka MJ, Ahonen AK, Niemela O, Junila JA, Hamalainen MM, Britton K, Syrjala HP. Comparison of 99mTc ciprofloxacin, 99mTc white blood cell and three-phase bone imaging in the diagnosis of hip prosthesis infections: improved diagnostic accuracy with extended imaging time. Nucl Med Commun 2002; 23: 655–61. 43 Larikka MJ, Ahonen AK, Niemela O, Puronto O, Junila JA, Hamalainen MM, Britton K, Syrjala HP. 99m Tc-ciprofloxacin (Infecton) imaging in the diagnosis of knee prosthesis infections. Nucl Med Commun 2002; 23: 167–70. 44 Yapar Z, Kibar M, Yapar AF, Togrul E, Kayaselcuk U, Sarpel Y. The efficacy of technetium-99m ciprofloxacin (Infecton) imaging in suspected orthopaedic infection: a comparison with sequential bone/gallium imaging. Eur J Nucl Med 2001; 28: 822–30.

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(ii) Diagnostic plain film radiology of the failing hip replacement

Radiographic technique Standard post-operative radiographs should include an AP of the pelvis and a lateral of the THR. The first post-operative radiograph acts as a baseline investigation with which all subsequent radiographs can be compared. The timing of these first post­operative radiographs varies between surgeons but it is probably best to perform them at the first outpatient visit following surgery. Radiographs that conform to accepted standards5 can be most reliably produced using a radiographic table with patients who are relatively mobile and pain-free, as opposed to patients who are in hospital beds, with abduction wedges, in the first day or two after surgery. An iliac-oblique view (distally centred Judet) of the THR may be a useful adjunct to, or replacement of, the standard lateral projection.6 The iliac-oblique view appears to be the optimal for assessing the cement bone interface of the acetabular component.7 The timing of subsequent follow-up radiographs varies but there seems to be little to be gained by repeating the investigation in the early post-operative course.8

Andoni P Toms Rajesh Botchu John F Nolan

Abstract Conventional radiographs are the main imaging tool for investigating the failing total hip replacement (THR). THRs most commonly fail because of aseptic loosening. The aetiology of aseptic loosening lies in a number of mechanical and biological processes which can result in a variety of different radiological features. These may be used to support or confirm a diagnosis of a loose or failing THR. The reliability and accuracy of some, but not all, of these radiographic signs have been evaluated in the scientific literature. This paper reviews and illustrates these radiographic signs. The pathophysiology for each sign is explained and the evidence supporting the accuracy and reliability is discussed.

Bone loss/osteolysis There are a number of different causes of loss of bone stock around a THR. These include infection, small particle disease and tumour but the most common causes are benign and are associated with aseptic loosening. Normal Preparation of the proximal femur and the exothermic process of setting methylmethacrylate cement causes thermal, chemical and traumatic necrosis of bone adjacent to the cement mantle. It is not uncommon for this layer of dead bone to be resorped and replaced with an investing layer of fibrous tissue which creates a thin lucency (<2 mm thick) at the cement–bone interface on conventional radiographs. This lucency appears within 3 months of operation, is uniform in thickness and is demarcated by a thin sclerotic margin (Figures 1a and b).

Keywords arthroplasty; failure; hip; loosening; radiograph

Introduction Over 66,000 total hip replacements (THRs) were performed in the UK in 2008.1 After ten years approximately one third of components will have become loose2 and 10% will have been revised,3,4 usually for aseptic loosening. Therefore by 2018 approximately 20,000 loose THRs may require radiographic evaluation. Plain radiographs have been the mainstay of follow up for THR for 40 years. The aim of this paper is to review the diagnostic features on conventional radiography that indicate a failing THR. Each radiographic feature will be considered separately. The aetiology of each feature will be described and, where available, the diagnostic accuracy of each radiographic sign will be considered.

Stress shielding Stress shielding is the result of local osteopaenia, usually in the proximal femur, following THR particularly with long stemmed uncemented femoral prostheses (Figures 2a and b). Stress from loading through the joint is transmitted to the cortex of the femoral diaphysis through the femoral prosthesis and the cement mantle bypassing the trochanteric trabeculae, and therefore stress shielding is associated with cortical hypertrophy at the point of distal fixation. With a reduction in stress loading comes a net increase in resorption,9 particularly in the greater trochanter,10 which manifests as decreased mineralisation of the trabeculae and cortex on conventional radiographs. Bone mineralisation reaches a nadir at about two years after surgery and then increases to near normal levels by ten years after surgery. While initially considered a complication of THR,11 particularly associated with wide and stiff femoral prostheses, there appears to be no association with adverse long term outcomes.12,13 Inter-rater reliability for identifying stress shielding on conventional radiographs is excellent only if bone mineral loss is greater than 70%.14 For less severe loss of bone stock CT osteodensitometry is required in order to achieve satisfactory measures of ­reliability.15

Andoni P Toms FRCR is a Consultant Radiologist within the Radiology Department, Norfolk and Norwich University Hospital, Norwich, UK. Rajesh Botchu MBBS MS(Orth) MRCSEd MRCSI is a Radiology StR within the Radiology Department, Norfolk and Norwich University Hospital, Norwich, UK. John F Nolan FRCS(orth) is a Consultant Orthopaedic Surgeon, Orthopaedic Department, Norfolk and Norwich University Hospital, Norwich, UK.

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An immediate post-operative AP radiograph of a left THR a demonstrates a contiguous bone cement interface. b 6 months later there is a well defined linear lucency surrounding the cement mantle with a thin sclerotic margin (arrowhead) at the interface with bone. These appearances remained stable at follow up to 5 years consistent with a fibrous bone-cement interface. c In comparison thick irregular lucency (arrow) surrounding the cement mantle indicates osteolysis. Figure 1

the femoral neck (­Figure 3). Compromised vascularity has also been suggested as a cause for this resorption but has not been substantiated. Proximal femoral osteoporosis can occur in the medulla interposed between the cement mantle and endosteum and should be differentiated from osteolysis. Osteoporosis presents as ­progressively reduced medullary attenuation surrounding the cement mantle but with preservation of secondary ­trabeculae and an absence of a demarcating line of sclerosis (Figure 4). ­Proximal

Narrowing of the femoral neck has been reported as a normal finding in hip resurfacing, both cemented and uncemented, which stabilises within 6 years of operation.16 The authors suggest that this is also a result of osteolysis and cortical remodeling resulting from stress shielding. However this is not a universally held belief. Severe narrowing of the femoral neck is also a recognised feature of resurfacing prostheses which some argue is the result of metal ionosis. The resorption can be severe enough to compromise the mechanical integrity of

AP radiographs of the right and left hips of a 69 year old patient with a left distally fixed uncemented bipolar hemiarthroplasty (Bateman) demonstrating demineralisation of the trabecula and thinning of the cortex (arrow) of the left greater trochanter caused by stress shielding. Figure 2

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AP a and lateral b projections of the right hip in a patient with a Birmingham resurfacing total hip arthroplasty demonstrating narrowing of the femoral neck (arrow) which is much more apparent on the lateral view where the cortical resorption is so severe (arrowhead) that the femoral neck is at risk of fracture. Figure 3

femoral peri-prosthetic osteoporosis is not known to be associated with symptoms or failure of the prosthesis.

Aseptic loosening Several overlapping processes that lead to aseptic loosening (principally mechanical and biological) are responsible for the most common radiographic appearances. Most commonly osteolysis is associated with polyethylene small particle disease, which typically forms foreign body granulomas,17 in combination with elevated hydrodynamic pressures within the effective joint space that can dissect a plane along the prosthesis-cement interface.18 This can result in linear, geographic or erosive patterns of osteolysis17 which typically appear 7 to 8 years after surgery.19 Linear osteolysis can be differentiated from a fibrous bone-cement interface if it is more than 2 mm thick, if its thickness is uneven or if it has progressed with time (Figure 1c). Geographic osteolysis, caused by small particle disease, is well defined with a thin sclerotic margin indicating the slow non-aggressive enlargement of the underlying granuloma. The description of geographic osteolysis suggests that the lesion is contained within bone, although this may often be expanded and thin. Contained osteolysis is amenable to treatment with morcelised bone graft at revision surgery (Figures 5a and b). Erosive osteolysis describes osteolysis that is not contained by bone and typically occurs at the margins of the joint such as the medial calcar and usually requires repair with a mesh to contain the bone graft (Figure 6). The presence of osteolysis alone on conventional radiographs does not necessarily indicate aseptic loosening. However sensitivity for loosening is proportional to the extent of lysis around the cement mantle. If there is no lucency around the cement mantle of an acetabular component (including an iliac-oblique ­projection)

Figure 4 Lateral radiograph of a right bipolar hemiarthroplasty demonstrating asymptomatic osteoporosis (arrows) adjacent to a normal cement mantle which should not be misinterpreted as osteolysis.

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a AP radiograph of a femoral prosthesis demonstrating well defined lucencies with thin sclerotic margins scalloping the endosteum (arrow) caused by small particle granulomas. b A focal area of aggressive osteolysis indicated by ill defined margins and periosteal new bone (arrowheads). In this case the appearances are due to osteomyelitis but could be due to metastases. Figure 5

sensitivities of between 50% and 75%. Ballooning of both these lines in combination is also a reasonably useful sign of medial wall disruption with a specificity of over 80%24 (Figure 8). Resorption of the medial femoral calcar may be due either to stress shielding or small particle disease but is usually not progressive and is not commonly associated with loosening.25 The detection of osteolysis with conventional radiographs has a high specificity, over 90%, but sensitivity is variable. The tendency is to overestimate the degree of osteolysis on the femoral side of the prosthesis26 and underestimate the loss on the iliac side of the joint.27 It is easier to a detect lytic lesion in the ilium

then it is well fixed. If there is a lucency that ­surrounds the whole of cement mantle then there is a 94% incidence of the acetabular cup being loose.20 In between these extremes the severity of lysis is proportionately associated with loosening. The rate of change of lysis is also important. Rapid progression of lysis, particularly early on in the post-operative course, appears to be a predictor for early aseptic loosening.21 Specific osteolysis of the teardrop shadow22 indicates disruption of the quadrilateral plate, or medial wall, of the acetabulum23 (Figure 7). Similarly interruption of the iliopubic or ilioischial (Kohler’s) lines, or a combination of the two, is a specific indicator of medial wall disruption with specificities of over 90% but

Figure 7 AP radiograph of a failing revision THR demonstrating uncontained osteolysis and an absent tear drop (arrow). At operation an osteolytic cavity extended through the medial wall and extended along the medullary canal of the superior pubic ramus.

Figure 6 A cemented THR demonstrating resorption of the medial calcar (arrow) by small particle disease.

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Figure 8 Extensive osteolysis around a cemented (barium free) THR demonstrating ballooning of the ilioischial and iliopubic lines (arrow) caused by extensive periacetabular small particle disease.

than in the ischium and acetabular rim on a single view particularly when lesions are smaller than 10 cm3   28 but detection rates can be increased to 94% by using four different radiographic views (including a Judet iliac-oblique).27 Inter-observer ­reliability for the detection of osteolysis from a single radiograph is poor, although intra-observer reliability can be good or excellent. However, inter-observer reliability can be improved by reviewing a series of radiographs rather than single examinations.29 Advanced acetabular osteolysis can, uncommonly, cause pelvic discontinuity where the ilium becomes separated from the ischium and pubis (Figure 9). This prevalence of pelvic discontinuity is associated with gender, being more common in women, patients with rheumatoid arthritis and significant complication rates following revision surgery.30 Radiographic signs of pelvic discontinuity include fracture lines through the anterior and posterior columns and evidence of movement of the inferior ­hemipelvis, either medial translation or rotation.30 There is no published evidence of the sensitivity or specificity of conventional radiographs in detecting pelvic discontinuity, probably because numbers of patients in any one centre are likely to be small. This is not important because CT is likely to replace conventional radiographs for the assessment of pelvic ­discontinuity. Aggressive osteolysis is defined as focal bone loss with a poorly defined margin and may be accompanied by permeative changes (poorly defined small lucencies) in the adjacent marrow (Figure 5b). The most common causes for this relatively uncommon finding are osteomyelitis and metastases. When infection presents with permeative changes and periosteal new bone there is often accompanying infection in the extra-osseous soft tissues. Most patients with an infected THR will not have specific radiographic features of osteomyelitis and the appearances are often indistinguishable from aseptic loosening.31,32 The periprosthetic infection in these cases is low grade and chronic being confined to a glycocalyx which occupies the areas

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Figure 9 Antero-posterior radiograph of a right THR demonstrating pelvic discontinuity with a sagittal fracture line through the roof of the acetabulum (arrowhead: required CT for confirmation). There is also an eccentrically placed femoral head indicating polyethylene wear and medial calcar resorption (arrow).

of osteolysis. Normal radiographs certainly do not exclude the presence of infection.

Migration The only definite radiographic sign of loosening is the change in position of a prosthesis from one radiograph to another.33–37 For most patients this is assessed using standard interval radiography which can demonstrate movement but is probably inadequate for detecting early mechanical loosening.35,38 Roentgen stereophotogrammatic analysis allows subtle differences in patient and radiographic positioning to be compensated for and is therefore more sensitive to early movement.39,40 Other definitions of loosening, for instance radiolucency demarcating the whole of the margin of the acetabular component,41 are highly effective statistical predictors but not direct evidence of loosening. Early osteolysis adjacent to the superolateral actebulum (zone 1) is strongly associated with progression to acetabular loosening42,43 (Figure 10). The acetabular cup is the more common of the two components to migrate and become loose. Movement can be identified by measuring the acetabular inclination from a transverse 92

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a There is a small focal lucency projected superolateral to the cement mantle (note poor cement interdigitation) 1 year after surgery. b 3 years after surgery the lucency has extended around the cement mantle (arrowheads), an indirect sign of loosening, and there has been a small rotational movement of the cup confirming that it is loose. c Within 1 year the acetabular cup rotates significantly. Figure 10

baseline,44 which is usually a line drawn between the ischial tuberosities45 or the inferior margins of the tear drop opacities 46,47 and demonstrating a difference in position between two radiographs. The absolute position of an acetabular cup does not indicate loosening nor, in isolation, is it associated with complications.48 Although there are criteria for position and orientation of the pelvis for the optimal post-operative radiograph5 in practice if pelvic tilt or rotation are less than 10° this does not have a significant effect on the projected angle of acetabular inclination.49,50 Inter-observer reliability for measuring acetabular inclination has generally been reported as good 33,51,52 but the ability of observers to detect differences between radiographs is less encouraging. Inter-observer correlation coefficients for reporting loosening of the acetabular cup have been reported as only moderate (0.49–0.63)53 and there is no clear evidence of what the minimal amount of detectable change in position on serial radiographs is required for reliable observations. What does appear to be clear is that the reliability of planar imaging to assess changes in anteversion is even less reliable and should probably only be attempted with CT or other three-dimensional imaging techniques.51 Wear of the polyethylene liner of the acetabular cup by the femoral head will eventually lead to a loose articulation (Figure 11). The amount of polyethylene wear can be measured by choosing the shortest radius from the centre of the femoral head, on an AP radiograph, to the outer margin of the acetabular cup. This seems to be considered a reliable technique but it is not clear how much polyethylene wear is significantly associated with loosening or symptoms.54 As well as the acetabular cup rotating within the acetabulum the prosthesis can also migrate proximally or medially, or capsize (Figure 12). This occurs most frequently in patients with inflammatory arthritis compared to those with osteoarthritis.55 Proximal migration, associated with a valgus stem position, appears to be the more common of the two directions with measurements taken from the inter-tear drop line. Medial migration (protrusio acetabuli prosthetica), associated with a varus stem position, is usually defined as migration medial to the ilio-ischial line.56,57 It

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Figure 11 Marked superior migration of the head of a Charnley femoral prosthesis. The polyethylene erosion (arrow) has compromised the structural viability of the cup which has fractured (arrowhead).

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a AP radiograph of a Bateman bipolar hemiarthroplasty demonstrating predominantly cranial migration of the prosthetic head which has eroded through the roof of the acetabulum. b Protrusio acetabuli prosthetica; a Stanmore THR has migrated medial to the ilioischial line. Cement in the pelvis indicates that there was a defect in the medial wall at the time of surgery. There is also loosening, osteolysis and cortical hypertrophy around the femoral stem.

Figure 12

is not certain how reliable this sign is but some have found defining the centre of rotation, using horizontal (x) and vertical (y) coordinates from the teardrop, to be useful for follow up studies of cup migration.58 The femoral stem angle can be measured on either the AP or the lateral views and requires a line to be drawn along the long axis of the stem and compared with the long axis of the proximal femoral diaphysis. Alternatively the position of the tip of the stem within the femoral medullary canal can be measured relative to either the cortex or endosteum. Although the identification of femoral loosening appears to be reliable with good correlation coefficients (0.74–0.8) between observers53 the reliability of femoral stem angle measurements is not known. Whether or not these angles are particularly relevant is another question. Valgus stem migration is a recognised normal finding in certain prostheses. Mechanical loosening of the femoral prosthesis appears to be predominantly due to torque applied to the neck which results in rotational instability of the stem.59 Measures of varus or valgus migration are unlikely to detect rotational loosening until it is quite advanced.

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Cement mantle The cement mantle has failed when loss of integrity allows movement of the prosthesis. This is more common in the femoral than the acetabular component. The femoral cement mantle can be classified according to the number and extent of the defects in the mantle present after surgery. Mantles that lack cement over at least 50% of the margin or fail to cover the tip of the femoral prosthesis (Barrack C and D60) are strongly associated with early failure of the THR61 but do not in themselves indicate a loose prosthesis. The THR can fail from either circumferential or longitudinal defects in the cement mantle. A circumferential defect leads to separation of the proximal and distal segments of the cement which allows the femoral prosthesis to subside. The distal segment of cement mantle is then displaced distally leaving a clear fracture line (Figure 13). Proximally the shoulder of the prosthesis may leave an empty impression in the adjacent cement as it migrates distally (Figure 14). This last sign, on its own, is not diagnostic of a loose prosthesis because some femoral components, such as those with collarless polished tapered stems, are designed to subside at 94

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Figure 14 Migration of the femoral component distally or medially leaves a characteristic bare area of cement (arrow). Similar appearances in some polished collarless tapered stems are normal as 1–2 mm of settling of the prosthesis is allowed.

Figure 13 Circumferential fracture of the femoral cement mantle (arrow) with distal displacement of the distal cement fragment indicating distal migration of the femoral component, resulting in apposition of the proximal femur and acetabulum.

­predictable rates for several years following surgery.62 Longitudinal defects in the mantle will allow the femoral component to rock in flexion and extension, or abduction and adduction, exacerbating osteolysis and eventually causing a fracture, typically of the medial calcar or around the tip of the prosthesis.

Heterotopic ossification Heterotopic ossification (HO) has a reported prevalence of between 26% and 34%.63–65 While the prevalence does not appear to be related to the type of THR 66 there is some evidence to suggest that the prevalence may be higher in ­resurfacing ­prostheses.67 There is also evidence that the position of HO is related to the surgical approach.65 The diagnostic radiographic description of HO is of soft tissue opacities with a discrete cortex and a medulla that often contains slightly disorganised trabeculae. Without identifiable corticomedullary differentiation heterotopic bone cannot be differentiated from other causes of soft tissue calcification. The severity of HO varies; mild disease, with a few scattered small foci of bone, is the most common and is not clinically significant.64 More extensive disease is less common but is associated with reduced functional outcomes68,67 (Figure 15). The extent of HO can be reasonably reliably graded

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Figure 15 Extensive (Brooker grade 4) heterotopic ossification that traverses the joint bridging the ilium and femur and was the cause of decreased range of movement in the patient.

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using one of several systems, which have evolved from and since Brooker’s original description.63 Inter-observer reliability for the original Brooker grading system has been reported with kappa values as low as 0.43,69 which is satisfactory, with more recent ­modifications producing good inter-observer reliability measures of between r = 0.69 and 0.8 70,71 Another cause for periprosthetic soft tissue opacification is metallosis. This was a common complication of first generation metal-on-metal articulations but is uncommon with polyethylene-on-metal THR where it occurs after failure of the polyethylene cup so that the femoral head articulates with the metal liner of the acetabular component releasing large amounts of metal debris in to the joint. This can settle on the deep surface of the joint capsule producing cloud-like opacities which can be mistaken for HO (Figure 16).72

Cortical remodelling and failure Cortical remodelling is a normal response to THR. Within the first four years after surgery it is normal to see an increase in cortical thickness as periosteal new bone is laid down around the cement mantle in response to loading forces that are redistributed from the cement to the cortex.73 On the other hand asymmetrical or focal cortical thickening is abnormal. It most commonly occurs around the tip of the femoral prosthesis (Figure 17). As a result of work in animal models it has been claimed that cortical remodeling is the result of loosening of the prosthesis particularly where the femoral component is fixed distally74 although stem alignment may also influence abnormal focal cortical loading. Cortical remodeling may progress to form a pedestal that bridges the endosteum distal to the tip of the prosthesis.75 Focal cortical thickening acts as a stress riser; a

a AP radiograph of the distal femoral component of an asymptomatic THR demonstrating abnormal asymmetrical cortical thickening (arrow). Asymmetrical remodelling caused by abnormal focal loading through the misaligned tip of the prosthesis. b Alignment of this stem appears to be normal on the AP radiograph but on the lateral view was displaced anteriorly. a & b Endosteal bridging new bone (arrowheads) at the tip of loose prostheses. Figure 17

short transition between areas of cortex with different tensile strengths and therefore provides a point of weakness through which fractures propagate. A neocortex is a feature of a loose uncemented stem. It is characterized by a thin sclerotic line that surrounds the femoral prosthesis from which it is separated by a lucency that is typically several millimeters thick76,77 (Figure 18). Delayed periprosthetic fractures in primary THR are uncommon but after revision THR the incidence rises to between 3.6% and 20.9%.78,79,80 They occur most commonly at the tip of the femoral component81 and appear to be associated with a patient age of over 7081 with a loose, usually uncemented, femoral prosthesis.78 Delayed fractures through the greater trochanter are rare but again are more common after revision surgery.82 They can occur through areas of focal lysis caused by small particle disease.83 They can also occur without obvious lysis when heat from a particularly thick cement mantle lateral to the shoulder of the prosthesis has been postulated as a cause for osteonecrosis of the greater trochanter (Figure 19). However the majority of patients with a periprosthetic fracture have a loose femoral stem and there are usually other radiographic features of loosening.79 Figure 16 AP radiograph of a cemented THR in which the polyethylene cup has fractured allowing the head of the femoral component to articulate with the metal backing. Large amounts of metallic debris were shed in to the joint to lie deep to the joint capsule and produce characteristic cloud-like opacities (arrowhead).

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Prosthetic fracture The femoral prosthesis can fail because the stem suffers a fatigue fracture. This typically occurs in prostheses that are well fixed 96

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Neocortex formation in a patient with a loose distally fixed uncemented THR. A thin line of sclerotic bone (arrowheads, in expanded images to left and right) surrounds the femoral prosthesis. Between this line and the prosthesis is a lucent area filled with a fibrous membrane. Figure 18

Figure 19 AP radiograph of a cemented Charnley EliteTHR demonstrating a delayed fracture of the greater trochanter. Note the shell like cortex of the trochanter and the thick lateral cement mantle (arrow).

distally but are mobile proximally and result in fractures through the middle or proximal third of the stem84 (Figure 20). Fracture of the acetabular cup usually occurs after severe focal wear of the polyethylene liner and can be demonstrated by discontinuity of the circumferential wire marker and medial migration of the head through the defect in the liner or cup (Figure 11).

Figure 20 Fractured femoral prosthesis (arrowhead) in a distally fixed stem with proximal loosening (arrow).

worldwide. As patients survive longer the proportion presenting with symptoms of a failing THR may also increase. Conventional radiographs are likely to remain the imaging ­investigation of choice for the near future. Many of the strengths and limitations of conventional radiography, for diagnosing the ­ failing THR, have now been identified. These have been discussed in this review. ◆

Conclusion With a projected increasingly elderly population there will be a predictable continued increase in the number of hip arthroplasties

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arthrography, scintigraphy and roentgen stereophotogrammetry in prosthetic hips. Acta Orthop Scand 1985; 56: 469–473. 39 Alfaro-Adrian J, Gill HS, Murray DW. Cement migration after THR. A comparison of charnley elite and exeter femoral stems using RSA. J Bone Joint Surg Br 1999; 81: 130–134. 40 Kiss J, Murray DW, Turner-Smith AR, Bithell J, Bulstrode CJ. Migration of cemented femoral components after THR. Roentgen stereophotogrammetric analysis. J Bone Joint Surg Br 1996; 78: 796–801. 41 Mulroy RDJ, Harris WH. The effect of improved cementing techniques on component loosening in total hip replacement. An 11-year radiographic review. J Bone Joint Surg Br 1990; 72: 757–760. 42 DeLee JG, Charnley J. Radiological demarcation of cemented sockets in total hip replacement. Clin Orthop Relat Res 1976; 20–32. 43 Eftekhar NS, Nercessian O. Incidence and mechanism of failure of cemented acetabular component in total hip arthroplasty. Orthop Clin North Am 1988; 19: 557–566. 44 Murray DW. The definition and measurement of acetabular orientation. J Bone Joint Surg Br 1993; 75: 228–32. 45 Herrlin K, Pettersson H, Selvik G. Comparison of two- and threedimensional methods for assessment of orientation of the total hip prosthesis. Acta Radiol 1988; 29: 357–361. 46 Hirakawa K, Mitsugi N, Koshino T, Saito T, Hirasawa Y, Kubo T. Effect of acetabular cup position and orientation in cemented total hip arthroplasty. Clin Orthop Relat Res 2001; 135–42. 47 Massin P, Schmidt L, Engh CA. Evaluation of cementless acetabular component migration. An experimental study. J Arthroplasty 1989; 4: 245–251. 48 Rittmeister M, Callitsis C. Factors influencing cup orientation in 500 consecutive total hip replacements. Clin Orthop Relat Res 2006; 445: 192–196. 49 Thoren B, Sahlstedt B. Influence of pelvic position on radiographic measurements of the prosthetic acetabular component. An experimental study on a pelvic model. Acta Radiol 1990; 31: 133–136. 50 Anda S, Svenningsen S, Grontvedt T, Benum P. Pelvic inclination and spatial orientation of the acetabulum. A radiographic, computed tomographic and clinical investigation. Acta Radiol 1990; 31: 389–394. 51 Kalteis T, Handel M, Herold T, Perlick L, Paetzel C, Grifka J. Position of the acetabular cup – accuracy of radiographic calculation compared to CT-based measurement. Eur J Radiol 2006; 58: 294–300. 52 Olivecrona H, Weidenhielm L, Olivecrona L, et al. A new CT method for measuring cup orientation after total hip arthroplasty: a study of 10 patients. Acta Orthop Scand 2004; 75: 252–260. 53 Kramhoft M, Gehrchen PM, Bodtker S, Wagner A, Jensen F. Inter- and intraobserver study of radiographic assessment of cemented total hip arthroplasties. J Arthroplasty 1996; 11: 272–276. 54 Del Schutte HJ, Lipman AJ, Bannar SM, Livermore JT, Ilstrup D, Morrey BF. Effects of acetabular abduction on cup wear rates in total hip arthroplasty. J Arthroplasty 1998; 13: 621–626. 55 Onsten I, Bengner U, Besjakov J. Socket migration after Charnley arthroplasty in rheumatoid arthritis and osteoarthritis. A roentgen stereophotogrammetric study. J Bone Joint Surg Br 1993; 75: 677–680. 56 McBride MT, Muldoon MP, Santore RF, Trousdale RT, Wenger DR. Protrusio acetabuli: diagnosis and treatment. J Am Acad Orthop Surg 2001; 9: 79–88.

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57 Morley DCJ, Schmidt RH. Protrusio acetabuli prosthetica. Orthop Rev 1986; 15: 135–141. 58 Gates HSr, Poletti SC, Callaghan JJ, McCollum DE. Radiographic measurements in protrusio acetabuli. J Arthroplasty 1989; 4: 347–351. 59 Effenbger H, Heiland A, Ramsauer T, Plitz W, Dorn U. A model for assessing the rotational stability of uncemented femoral implants. Arch Orthop Trauma Surg 2001; 121: 60–4. 60 Barrack RL, Mulroy RDJ, Harris WH. Improved cementing techniques and femoral component loosening in young patients with hip arthroplasty. A 12-year radiographic review. J Bone Joint Surg Br 1992; 74: 385–389. 61 Chambers IR, Fender D, McCaskie AW, Reeves BC, Gregg PJ. Radiological features predictive of aseptic loosening in cemented Charnley femoral stems. J Bone Joint Surg Br 2001; 83: 838–842. 62 Yates PJ, Burston BJ, Whitley E, Bannister GC. Collarless polished tapered stem: clinical and radiological results at a minimum of ten years’ follow-up. J Bone Joint Surg Br 2008; 90: 16–22. 63 Brooker AF, Bowerman JW, Robinson RA, Riley LHJ. Ectopic ossification following total hip replacement. Incidence and a method of classification. J Bone Joint Surg Am 1973; 55: 1629–1632. 64 Nayak KN, Mulliken B, Rorabeck CH, Bourne RB, Woolfrey MR. Prevalence of heterotopic ossification in cemented versus noncemented total hip joint replacement in patients with osteoarthrosis: a randomized clinical trial. Can J Surg 1997; 40: 368–374. 65 Harwin SF. Trochanteric heterotopic ossification after total hip arthroplasty performed using a direct lateral approach. J Arthroplasty 2005; 20: 467–472. 66 Purtill JJ, Eng K, Rothman RH, Hozack WJ. Heterotopic ossification. Incidence in cemented versus cementless total hip arthroplasty. J Arthroplasty 1996; 11: 58–63. 67 Rama KR, Vendittoli PA, Ganapathi M, Borgmann R, Roy A, Lavigne M. Incidence and Severity of Heterotopic Ossification After Surface Replacement Arthroplasty and Total Hip Arthroplasty A Randomized Study. J Arthroplasty 2008. 68 Pohl F, Seufert J, Tauscher A, et al. The influence of heterotopic ossification on functional status of hip joint following total hip arthroplasty. Strahlenther Onkol 2005; 181: 529–533. 69 Della VAG, Ruzo PS, Pavone V, Tolo E, Mintz DN, Salvati EA. Heterotopic ossification after total hip arthroplasty: a critical analysis of the Brooker classification and proposal of a simplified rating system. J Arthroplasty 2002; 17: 870–875. 70 Wright JG, Moran E, Bogoch E. Reliability and validity of the grading of heterotopic ossification. J Arthroplasty 1994; 9: 549–553. 71 Toom A, Fischer K, Martson A, Rips L, Haviko T. Inter-observer reliability in the assessment of heterotopic ossification: proposal of a combined classification. Int Orthop 2005; 29: 156–159. 72 Khan RJ, Wimhurst J, Foroughi S, Toms A. The Natural History of Metallosis From Catastrophic Failure of a Polyethylene Liner in a Total Hip. J Arthroplasty 2008. 73 Adolphson P. Femoral cortical remodeling after uncemented total hip arthroplasty. A prospective radiologic study of 26 hips followed for 2 to 4 years. J Arthroplasty 1997; 12: 99–105. 74 Bergh MS, Muir P, Markel MD, Manley PA. Femoral bone adaptation to unstable long-term cemented total hip arthroplasty in dogs. Vet Surg 2004; 33: 238–245. 75 Manaster BJ. From the RSNA refresher courses. Total hip arthroplasty: radiographic evaluation. Radiographics 1996; 16: 645–660.

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83 Hsieh PH, Chang YH, Lee PC, Shih CH. Periprosthetic fractures of the greater trochanter through osteolytic cysts with uncemented MicroStructured Omnifit prosthesis: retrospective analyses pf 23 fractures in 887 hips after 5-14 years. Acta Orthop 2005; 76: 538–543. 84 Wilson LF, Nolan JF, Heywood-Waddington MB. Fracture of the femoral stem of the Ring TCH hip prosthesis. J Bone Joint Surg Br 1992; 74: 725–728.

76 Harris WH. Will stress shielding limit the longevity of cemented femoral components of total hip replacement? Clin Orthop Relat Res 1992: 120–123. 77 Nelissen RG, Bauer TW, Weidenhielm LR, LeGolvan DP, Mikhail WE. Revision hip arthroplasty with the use of cement and impaction grafting. Histological analysis of four cases. J Bone Joint Surg Am 1995; 77: 412–422. 78 Lindahl H. Epidemiology of periprosthetic femur fracture around a total hip arthroplasty. Injury 2007; 38: 651–654. 79 Lindahl H, Malchau H, Herberts P, Garellick G. Periprosthetic femoral fractures classification and demographics of 1049 periprosthetic femoral fractures from the Swedish National Hip Arthroplasty Register. J Arthroplasty 2005; 20: 857–865. 80 Farfalli GL, Buttaro MA, Piccaluga F. Femoral fractures in revision hip surgeries with impacted bone allograft. Clin Orthop Relat Res 2007; 462: 130–136. 81 Cook RE, Jenkins PJ, Walmsley PJ, Patton JT, Robinson CM. Risk factors for periprosthetic fractures of the hip: a survivorship analysis. Clin Orthop Relat Res 2008; 466: 1652–1656. 82 Ornstein E, Atroshi I, Franzen H, Johnsson R, Sandquist P, Sundberg M. Early complications after one hundred and forty-four consecutive hip revisions with impacted morselized allograft bone and cement. J Bone Joint Surg Am 2002; 84-A: 1323–1328.

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Practice points • Consider iliac-oblique Judet view to supplement or replace standard lateral view • Standard radiography limited for early mechanical loosening • Movement on interval radiographs is the only absolute feature of a loose prosthesis • Other features have lesser sensitivities and specificities and may not be related to symptoms

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(iii) CT and MRI of hip replacements

initial modality of evaluation they do have limitations due to the complex three dimensional geometry of the pelvis.7 Additional useful information can be obtained with both CT and MRI as the previous limiting factors of beam hardening in CT and susceptibility artefact in MRI can now be reduced considerably. CT is particularly useful in the evaluation of bone stock and the integrity of the medial acetabular wall and the anterior and posterior columns. MRI can now accurately evaluate the periprosthetic soft tissues, which is useful in the evaluation of infection or any other associated soft tissue abnormality. MRI has been shown to be a useful problem solving tool in unexplained failed total hip replacement. In one study it resulted in an unsuspected diagnosis in over 50% of cases.8

John G Cahir Andoni P Toms

Abstract Computed tomography (CT) and magnetic resonance imaging (MRI) are now useful imaging techniques in the evaluation of hip arthroplasty. The recognised problems of beam hardening in CT and magnetic susceptibility artefact in MRI have been significantly reduced. MRI is useful for assessing the peri-prosthetic soft tissues and in evaluation of the painful replacement with normal plain films. CT is better than plain films in evaluating bone stock around a hip replacement.

Technical considerations MRI MRI when first introduced had limited scope in the imaging of metallic implants. This was due to magnetic susceptibilty artefact produced by orthopaedic hardware. Magnetization of implants distorts the local field gradients causing proton dephasing which gives rise to signal voids and spatial distortion. The introduction of higher field strengths unfortunately results in even greater distortion. Technical alterations however can now largely overcome these problems. Artefact secondary to metallic implants can be reduced by increasing frequency encoding gradients, using fast spin echo techniques, reducing the volume of voxels and using short tau inversion recovery (STIR) sequences rather than using spectral fat suppression. The frequency encoding direction of the image is more susceptible to artefact. Selective orientation of the frequency and phase encoding directions of the acquisition can result in reduction of artefact in the regions of specific interest.4,9

Keywords arthroplasty; CT; hip; MR

Introduction There are approximately 1.5 million hip arthroplasties performed world wide each year.1 In 2000 it was reported that the NHS in England was performing over 30 000 hip replacements at a cost of £140 million.2 Even though complication rates following arthroplasty are low the large number of arthroplasties performed means that complications are encountered frequently. All prostheses are likely to fail eventually given enough time as a result of infection, mechanical failure or flaws in surgical technique or prosthesis manufacture. Most patients have a satisfactory long-term outcome however an annual revision burden (derived by calculating the percentage of revision arthroplasties relative to the total number of primary and revision arthroplasties) of up to 17% has been described.3 Complications following hip arthroplasty include mechanical aseptic loosening, osteolysis secondary to granulomatous disease, heterotopic new bone formation, infection both superficial and deep, peri-prosthetic and prosthetic fracture and infrequently local nerve damage. Some of these complications are a source of morbidity and may require revision surgery.4,5 When revision surgery is performed it includes both the acetabular and femoral component in 37% of cases, the acetabular component only in 40% of cases and the femoral stem in approximately 22% of cases.6 Plain films are the first line investigation in evaluation of the painful total hip replacement. While plain radiographs are the

John G Cahir MRCP FRCR is a Consultant Musculoskeletal Radiologist at the Department of Radiology, Norfolk and Norwich University Hospital, Colney Lane, Norwich, UK. Figure 1 Coronal T1 MRI (left) and plain radiograph (right) of a titanium stem with a ceramic bearing. Metal artefact reduction allows differentiation of the cortex, marrow and even the ridges on the edge of the prosthesis (arrows).

Andoni P Toms FRCS FRCR is a Consultant Musculoskeletal Radiologist at the Department of Radiology, Norfolk and Norwich University Hospital, Colney Lane, Norwich, UK.

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Figure 2 Infection at the tip of a femoral prosthesis. There is cortical destruction and also a periosteal reaction (arrow).

The exact imaging parameters necessary to optimize sequences vary depending on manufacturer and the available software and may require some trial and error in order to optimize imaging.The manipulation of these technical factors using metal artefact reduction sequences (MARS) enables visualisation of the cortex, cement and marrow around the femoral stem (Figure 1). It is more difficult to reduce artefact arising from the acetabular cup due to the oblique orientation in relation to the direction of the magnetic field. CT The most significant problem encountered when imaging orthopaedic hardware with CT is beam hardening. Beam hardening is

a Axial STIR image of an infected collection (arrow) of the posterior aspect of the hip. There is oedema of the overlying soft tissues. b Axial T1 post gadolinium imaging demonstrates rim enhancement of the collection (arrowheads). Figure 4

seen as alternating high and low attenuation lines which appear to radiate from implants. This problem can be overcome by increasing the output from the tube (mA and kVp). Technical factors mean that modern multislice CT scanners have a lower baseline artefact than older equipment. The data set obtained with multi slice CT can be reformatted in any plane with a soft tissue and smooth reconstruction filters with overlapping sections which also reduces artefact.10

Complications Infection In the early stages of infection plain radiographs will be normal in appearance. When infection is suspected ultrasound has an

Figure 3 A normal post-operative finding of a small seroma in the line of the post surgical scar.

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Figure 5 Axial T2 weighted image of a sinus tract (arrowheads) communicating with the posterior aspect of the joint.

important role in the assessment of the hip prosthesis as it can demonstrate the presence of periprosthetic collections and joint effusions. Ultrasound or fluoroscopy can guide aspiration of the joint. CT has been shown to be a useful diagnostic tool in the assessment of infection. Soft tissue changes are a more significant finding than periprosthetic bone abnormalities. Periprosthetic bone abnormalities do not allow differentiation of infection from complications not related to sepsis apart from periostitis which has a 100% specificity but only a 16% sensitivity (Figure 2). In cases of proven infection the bone may appear normal on CT in 25% of cases. Soft tissue abnormalities such as joint distension, fluid filled bursae and fluid collections in

Figure 7 Coronal CT showing extensive cortical destruction of the proximal femur secondary to osteolysis. The arrow heads depict the original outline of the lateral cortex. The lesser trochanter is fractured (arrow).

muscles and perimuscular fat result in a 83% sensitivity, 96% specificity and 94% accuracy for infection when evaluating a painful prosthesis.5 MRI is a better imaging modality than CT for demonstrating periprosthetic soft tissues. MRI is better at depicting soft tissues around the femoral stem than in the region of the acetabulum. It is not uncommon to see a small seroma in the line of

Figure 8 Axial CT image of a soft tissue mass and cortical destruction due to small particle disease(arrow). The osteolysis is of similar density to muscle (arrowhead).

Figure 6 Coronal T1 weighted image of an infected prosthesis which shows osteomyelitis of the medial calcar (arrowhead) and also infection tracking through a defect in the iliotibial tract (arrow).

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Figure 9 Coronal T1 image (left) of osteolysis (arrow) of the acetabulum. The small particle disease is of low signal. There is a breach of the medial wall (arrowheads) Coronal STIR imaging (right), where the osteolysis is of intermediate signal.

surgical approach (Figure 3). Infection on MRI has a signal intensity similar to that of fluid and will usually have an illdefined margin (Figures 4a and 4b). MRI can depict bony involvement and assess the extent and route of sinus tracts. (Figures 5 and 6)

components over time and cement fracture are indicative. It is not known if CT or MRI offer any benefit over plain films in the assessment of mechanical loosening (Figure 10). Fractures and pelvic discontinuity Periprosthetic fractures occur for a variety of reasons such as osteolysis, loosening, stress risers and unfavourable biomechanics.15 Periprosthetic fractures involving the bone adjacent to the tip of the femoral stem or the greater trochanter are usually diagnosed without difficulty with plain radiographs. Cross sectional imaging is useful in the evaluation of hip pain which may be due to occult fracture.16,8 Some fractures may be difficult to detect on plain radiographs. Subtle insufficiency fractures, stress fractures and fractures through areas of osteolysis may not be appreciated with plain radiographs. Both MRI and CT can demonstrate fractures immediately adjacent to metalwork however CT is better at evaluating the bone near the acetabulum (Figure 11). Pelvic discontinuity is a separation of the cephalad aspect of the pelvis from the caudal aspect as a result of fracture or bone loss, wherein the anterior and posterior columns are non-supportive. Bone loss may be due to infection, osteolysis or mechanical abrasion (Figure 12).17 Pelvic discontinuity is more common in women and patients with rheumatoid arthritis. Pelvis radiotherapy is also a risk factor.18 The integrity of the medial wall of the acetabulum and the anterior and posterior columns are important factors which determine surgical planning, technique and theatre time. Pelvic discontinuity may require reconstruction with a plate and anti-protrusio acetabular cage before insertion of bulk allograft and a cemented cup or a custom built acetabular component.17,19

Osteolysis Polyethylene wear particles are phagocytosed by macrophages which accumulate to create foreign body granulomas. The subsequent inducement of osteoclastic activity is a significant cause of periprosthetic osteolysis. Patients may remain asymptomatic until extensive bone loss has occurred.11e13 Plain radiographs are the first line investigation in evaluation of osteolysis but are limited in their ability to assess the complex anatomy of the hip particularly around the acetabulum. CT has been shown to be more accurate at identifying periacetabular osteolysis than plain radiographs and will show medial wall perforations not detectable on a plain film.7 The presence of well demarcated lucencies adjacent to the socket or screws with absence of osseous trabeculae with CT are characteristic of osteolysis.14 Osteolysis may cause extensive cortical destruction (Figure 7). Soft tissue masses due to granulomatous disease have a similar density on CT to that of muscle (Figure 8). The typical signal characteristics of osteolysis on MRI are low signal on T1 imaging and low to intermediate high signal on T2 weighted imaging (Figure 9) there may be a surrounding low signal rim. Peripheral enhancement may be demonstrated on post gadolinium studies.4 The main indication for imaging of patients with osteolysis is to provide an accurate assessment of bone loss which is then helpful to the surgeon in planning revision surgery. Important areas which may be affected by osteolysis are the medial wall, the roof of the acetabulum and the anterior and posterior columns. Extensive osteolysis may result in pelvic discontinuity.15

Metal-on-metal soft tissue reaction Technical advances with improvements in machine tolerances have result in the development of second and third generation metal on metal prostheses. These prostheses have the potential advantage of avoiding the problems of small particle disease and osteolysis which are recognized complications associated with conventional metal on polyethylene prostheses.20 An unusual

Loosening Mechanical loosening of the prosthesis is the most common cause of pain following hip arthroplasty. The plain radiograph findings of prosthesis movement, progressive lucency around

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Figure 11 Coronal CT in a patient with bilateral THRs, there is an insufficiency fracture (arrow) of the posterior column on the right side.

The plain radiographs are typically normal and may therefore be falsely reassuring. The imaging findings suggestive of a metal on metal soft tissue reaction are a fluid collection which has a thick irregular wall surrounding the neck of the prosthesis, bone marrow oedema in the proximal femoral diaphysis, and oedema of the surrounding musculature. The associated collection may sometimes extend a considerable distance from the joint (Figure 13). The associated soft tissue reaction and necrosis may damage important adjacent structures (Figure 14).20,23 The exact cause of this specific soft tissue reaction, which has not been described with other implants, has not been established.

a STIR image with cortical thickening and periosteal reaction (arrow) several cms distal to the tip of the femoral stem. Oedema is also present in the bone marrow. b Axial STIR image of the same patient with a florid periosteal stress reaction (arrow) surrounding the femur. Figure 10

reaction associated with metal on metal (cobalt chromium alloy) prostheses, both total and resurfacing has been described. A perivascular infiltration of lymphocytes and an accumulation of plasma cells in association with macrophages containing metallic wear debris particles have been demonstrated.21e23 These histological appearances have been termed aseptic lymphocytic vasculitis-associated lesions. The clinical presentation is typically early recurrence of pain or discomfort after the initial surgery which may be initially induced with exercise.24

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Figure 12 Coronal CT image showing pelvic discontinuity (arrow). There is also extensive wear of the acetabular component of this right THR with an eccentric position of the head of the femoral component in relation to the cup.

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Figure 13 Coronal STIR image which showing large non-infective collections (arrows) associated with bilateral resurfacing prostheses. There is a low signal lymph node (arrowhead) which contained metallic particles. The patient required revision surgery of both hips.

Figure 15 The psoas bursa (arrow) is visible even in close proximity to the acetabular cup. The acetabular cup usually produces more artefact than the femoral stem on MRI.

Theories include a hypersensitivity reaction with a type IV immune response to the metal alloy components.24

The short external rotators are best imaged with axial T1W imaging. Coronal imaging is useful in evaluation of the gluteus minimus and medius attachments.25 A transgluteal approach may predispose to greater trochanteric bursitis. In the presence of clinical uncertainty of the diagnosis then MRI will demonstrate fluid like signal deep to the gluteus maximus tendon. There may be also associated gluteus minimus or minimus tendinopathy. It is however common to visualise some fluid signal on fat saturated T2 weighted imaging in the region of the greater trochanter in asymptomatic patients.28 Ilio-psoas bursitis may be a cause of hip pain following arthroplasty. This can be seen on MRI even though it is immediately adjacent to the acetabular cup. (Figure 15)

Tendon attachments Avulsion of the gluteal tendons is a recognized complication following hip arthroplasty. Patients may have weakness of hip abduction however many cases appear to be asymptomatic. Short external rotator avulsion is also a recognized complication following THR typically when a posterior approach has been used.25 Muscle atrophy and tendon avulsion may also be related to severe osteoarthrosis and may be findings which are present prior to arthroplasty. When the posterior approach to the joint is used the piriformis tendon is usually divided and is not necessarily repaired.26,27

Figure 14 THR with a metal-on-metal reaction. The left image shows the sciatic nerve (arrow) with surrounding fat with an adjacent metal-on-metal soft tissue reaction. The image on the right shows enlargement of the collection with has now engulfed the sciatic nerve (arrow) resulting in a sciatic nerve palsy.

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Metallosis Metallosis is an uncommon condition that occurs when excessive wear produces shedding of a large number of metallic particles into the joint. It typically occurs when there has been failure or fracture through the polyethylene liner of the acetabular component. The resultant abnormal articulation of the femoral head with the metal backing of the acetabular component causes generation of the particles. Metallosis can also occur in excessive wear in metal on metal arthroplasty.29,30 Titanium components are more commonly associated with metallosis than chromium cobalt prosthesis.31 The metallic debris causes a chronic inflammatory reaction and stimulates periprosthetic osteolysis.32 The metallosis may result in a linear radiodensity which outlines the periphery of the joint capsule. This appearance has also been termed the bubble sign.33 It may also appear as homogeneous increased density of the pseudocapsule of the joint on plain radiography. The lack of corticomedullary differentiation differentiates it from heterotopic ossification. Aspiration of affected joints typically reveals thick black oily liquid. The periprosthetic tissues may be stained black and be infiltrated with histiocytes containing metal debris.15,34

11 Wimhurst JA. The pathogenesis of aseptic loosening. Curr Orthop 2002; 16: 407e10. 12 Harris WH, McCarthy JCJ, O’Neill DA. Femoral component loosening using contemporary techniques of femoral cement fixation. J Bone Joint Surg Am 1982; 64: 1063e7. 13 Chiang PP, Burke DW, Freiberg AA, Rubash HE. Osteolysis of the pelvis: evaluation and treatment. Clin Orthop Relat Res 2003; 164e74. 14 Puri L, Lapinski B, Wixson RL, Lynch J, Hendrix R, Stulberg SD. Computed tomographic follow-up evaluation of operative intervention for periacetabular lysis. J Arthroplasty 2006; 21: 78e82. 15 Cahir JG, Toms AP, Marshall TJ, Wimhurst J, Nolan J. CT and MRI of hip arthroplasty. Clin Radiol 2007; 62: 1163e71 (discussion 1172e3). 16 Potter HG, Nestor BJ, Sofka CM, Ho ST, Peters LE, Salvati EA. Magnetic resonance imaging after total hip arthroplasty: evaluation of periprosthetic soft tissue. J Bone Joint Surg Am 2004; 86-A: 1947e54. 17 DeBoer DK, Christie MJ, Brinson MF, Morrison JC. Revision total hip arthroplasty for pelvic discontinuity. J Bone Joint Surg Am 2007; 89: 835e40. 18 Berry DJ, Lewallen DG, Hanssen AD, Cabanela ME. Pelvic discontinuity in revision total hip arthroplasty. J Bone Joint Surg Am 1999; 81: 1692e702. 19 Choplin RH, Henley CN, Edds EM, Capello W, Rankin JL, Buckwalter KA. Total hip arthroplasty in patients with bone deficiency of the acetabulum. Radiographics 2008; 28: 771e86. 20 Toms AP, Marshall TJ, Cahir J, et al. MR Imaging of early symptomatic metal-on-metal total hip arthroplasty: a retrospective review of radiological findingsin 20 hips. Clin Radiol 2008; 63: 49e58. 21 Park YS, Moon YW, Lim SJ, Yang JM, Ahn G, Choi YL. Early osteolysis following second-generation metal-on-metal hip replacement. J Bone Joint Surg Am 2005; 87: 1515e21. 22 Davies AP, Willert HG, Campbell PA, Learmonth ID, Case CP. An unusual lymphocytic perivascular infiltration in tissues around contemporary metal-on-metal joint replacements. J Bone Joint Surg Am 2005; 87: 18e27. 23 Fang CS, Harvie P, Gibbons CL, Whitwell D, Athanasou NA, Ostlere S. The imaging spectrum of peri-articular inflammatory masses following metal-on-metal hip resurfacing. Skeletal Radiol 2008; 37: 715e22. 24 Willert HG, Buchhorn GH, Fayyazi A, et al. Metal-on-metal bearings and hypersensitivity in patients with artificial hip joints. A clinical and histomorphological study. J Bone Joint Surg Am 2005; 87: 28e36. 25 Pfirrmann CW, Notzli HP, Dora C, Hodler J, Zanetti M. Abductor tendons and muscles assessed at MR imaging after total hip arthroplasty in asymptomatic and symptomatic patients. Radiology 2005; 235: 969e76. 26 Weeden SH, Paprosky WG, Bowling JW. The early dislocation rate in primary total hip arthroplasty following the posterior approach with posterior soft-tissue repair. J Arthroplasty 2003; 18: 709e13. 27 Stahelin T, Vienne P, Hersche O. Failure of reinserted short external rotator muscles after total hip arthroplasty. J Arthroplasty 2002; 17: 604e7. 28 Blankenbaker DG, Ullrick SR, Davis KW, De Smet AA, Haaland B, Fine JP. Correlation of MRI findings with clinical findings of trochanteric pain syndrome. Skeletal Radiol 2008; 37: 903e9. 29 Gambera D, Carta S, Crainz E, Fortina M, Maniscalco P, Ferrata P. Metallosis due to impingement between the socket and the femoral head in a total hip prosthesis. A case report. Acta Biomed 2002; 73: 85e91. 30 Cipriano CA, Issack PS, Beksac B, Della Valle AG, Sculco TP, Salvati EA. Metallosis after metal-on-polyethylene total hip arthroplasty. Am J Orthop 2008; 37: E18e25.

Conclusion Relatively simple modifications in imaging protocols can produce adequate metal artefact reduction on standard equipment. CT and MRI are now effective tools in the evaluation of the symptomatic hip arthroplasty. A

REFERENCES 1 Looney RJ, Boyd A, Totterman S, et al. Volumetric computerized tomography as a measurement of periprosthetic acetabular osteolysis and its correlation with wear. Arthritis Res 2002; 4: 59e63. 2 Public Accounts Comittee. Hip replacements: getting it right first time. House of Commons; 2000. 3 Kurtz S, Mowat F, Ong K, Chan N, Lau E, Halpern M. Prevalence of primary and revision total hip and knee arthroplasty in the United States from 1990 through 2002. J Bone Joint Surg Am 2005; 87: 1487e97. 4 White LM, Kim JK, Mehta M, et al. Complications of total hip arthroplasty: MR imaging-initial experience. Radiology 2000; 215: 254e62. 5 Cyteval C, Hamm V, Sarrabere MP, Lopez FM, Maury P, Taourel P. Painful infection at the site of hip prosthesis: CT imaging. Radiology 2002; 224: 477e83. 6 Bozic KJ, Durbhakula S, Berry DJ, et al. Differences in patient and procedure characteristics and hospital resource use in primary and revision total joint arthroplasty: a multicenter study. J Arthroplasty 2005; 20: 17e25. 7 Leung S, Naudie D, Kitamura N, Walde T, Engh CA. Computed tomography in the assessment of periacetabular osteolysis. J Bone Joint Surg Am 2005; 87: 592e7. 8 Johnston C, Kerr J, Ford S, O’byrne J, Eustace S. MRI as a problemsolving tool in unexplained failed total hip replacement following conventional assessment. Skeletal Radiol 2007; 36: 955e61. 9 Sofka CM, Potter HG. MR imaging of joint arthroplasty. Semin Musculoskelet Radiol 2002; 6: 79e85. 10 White LM, Buckwalter KA. Technical considerations: CT and MR imaging in the postoperative orthopedic patient. Semin Musculoskelet Radiol 2002; 6: 5e17.

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31 Weissman BN, Scott RD, Brick GW, Corson JM. Radiographic detection of metal-induced synovitis as a complication of arthroplasty of the knee. J Bone Joint Surg Am 1991; 73: 1002e7. 32 Heffernan EJ, Alkubaidan FO, Nielsen TO, Munk PL. The imaging appearances of metallosis. Skeletal Radiol 2008; 37: 59e62. 33 Su EP, Callander PW, Salvati EA. The bubble sign: a new radiographic sign in total hip arthroplasty. J Arthroplasty 2003; 18: 110e2. 34 Ottaviani G, Catagni MA, Matturri L. Massive metallosis due to metalon-metal impingement in substitutive long-stemmed knee prosthesis. Histopathology 2005; 46: 237e8.

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C

C C

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CT is better than plain radiographs for assessing bone stock around a THR. Metal artefact reduction sequences can successfully be implemented on most clinical MR machines. MR is useful for assessing peri-prosthetic soft tissues. In a painful THR with normal radiographs MR is a useful diagnostic tool.

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SPINE

Lumbar pars injury or spondylolysis – diagnosis and management Ujjwal K Debnath N Harshavardhana Brigitte E Scammell Brian JC Freeman Abstract Lumbar pars injury or spondylolysis is a unique lesion occurring only in human beings representing a stress fracture of the pars interarticularis and occurs most commonly at L5. Symptoms of low back pain relating to this lesion are more common in young athletes involved in trunk twisting sports. Diagnosis is dependent on plain radiography, computed tomography (CT) scan and magnetic resonance imaging (MRI) scans. Unilateral pars defect are less common than bilateral defects and run a more benign course. Treatment is dependent on symptoms as well as radiographic stage of the lesion. Conservative management is the mainstay of treating early lesions. Professional sporting individuals are at increased risk of failure of resolution of symptoms that may require early operative repart of the pars defect. Modified Buck’s technique of direct repair using screws has a high success rate in patients who have persistent low back pain. Preoperative ODI and SF-36 physical component scores (PCS) are significant predictor of a good functional outcome

Figure 1 Fifth lumbar vertebrae in an 600 year old skeleton with a unilateral pars defect of the left pars (From Hamann Todd Collection, Natural History Museum, Cleveland, USA).

a ‘stress’ or ‘fatigue’ fracture, seen most commonly in children and adolescents. Early subtle stress reactions within the bone of the posterior arch of the lumbar spine appear to be the first signs of a developing stress fracture.1 The PI defect is most commonly observed at L5 lumbar segment followed by others.

Historical review George Murray Humphrey in 1858, a surgeon from Cambridge in his book “Treatise on the Human Skeleton”, has quoted the first description of spondylolysis in the English literature.2,3 It was Robert du Coblenz, a professor of medicine at the university of Marburg, Germany who first recognised the importance of the pars defect in 1855.3 The term pars interarticularis (PI) was in use a few years later but the first published use of the word spondylolysis appears to have been by Franz Neugebauer in 1884 from Warsaw.3 Wiltse (1957) provided the theory of “fatigue fracture” which was supported by many authors in the subsequent literature.4 Reviews from the archaeological remains of skeletons from the past have suggested the prevalence to be about 6% in Caucasian Romano-British populations.5 The prevalence has been found to be 20% in Native American skeletons dating back 6000–1000BC.2 This prevalence rises to approximately 50% in skeletal remains of Eskimos from 12th Century AD.6 Eisenstein (1978) observed no significant variation between races and sexes in 485 skeletons.7

Keywords lumbar pars injury; lumbar spondylolysis; pars interarticularis; stress fracture of pars

Introduction Spondylolysis is derived from the Greek ‘spondylo’ meaning spine and ‘lysis’ meaning to dissolve. It is defined as a defect in the pars interarticularis (PI) of the spine (Figure 1). It represents

Ujjwal K Debnath FRCS MS (Orth) is a Spine Fellow at The Centre for Spinal Studies and Surgery, Nottingham University Hospitals NHS Trust, Queen’s Medical Centre Campus, Nottingham, UK. N Harshavardhana MRCS MS(Orth) is a Research Fellow at The Centre for Spinal Studies and Surgery, Nottingham University Hospitals NHS Trust, Queen’s Medical Centre Campus, Nottingham, UK.

Aetiology The PI defect or spondylolysis is unique to humans.1,8–10 By the age of six years this incidence has been reported to be 4.4% and by adulthood it reaches 6%.11 The incidence in the young athletic population is much higher than the general population and varies between 15% and 47%.12–15 It is believed that excessive loading in repetitive hyperextension in the young sporting population is a significant risk factor. Ciullo (1985) suggested that when an inherited weakness exists, a resulting defect of

Brigitte E Scammell FRCS FRCS(T&O) DM(Orth) is a Reader, Division of Accident & Orthopaedics Surgery, Consultant Orthopaedic Surgeon at The Centre for Spinal Studies and Surgery, Nottingham University Hospitals NHS Trust, Queen’s Medical Centre Campus, Nottingham, UK. Brian JC Freeman FRCS FRCS(T&O) DM(Orth) is a Consultant Spine Surgeon at The Centre for Spinal Studies and Surgery, Nottingham University Hospitals NHS Trust, Queen’s Medical Centre Campus, Nottingham, UK.

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the PI may develop.16 Support for this theory exists in animal studies where neural arch defects have not been demonstrated in other primates and animals. The Eskimos have an unusually high incidence (20–50%) of the defect.17 The effect of spondylolysis on these Eskimos is difficult to determine but it es highly unlikely that it caused severe disability. The relative frequency of spondylolysis in the Canadian Eskimos doubles from adolescence to early adulthood, being almost equally divided between complete and incomplete in the young adults.6 This is suggestive of genetic influence in the genesis of spondylolysis, which was first thought by Wiltse in 1962 through his study on “families” with ­spondylolysis.18 Currently, it is thought of as an acquired lesion, which may have developed between infancy and early adulthood. During embryological development two factors may contribute towards the developmental dysplasia of the PI. Firstly, the ossification does not progress uniformly in the lower lumbar segment. Secondly, there appears to be a transition between dense trabecular bone in the PI and the inferior articulating facet and less dense trabecular bone at the base of the pedicle only in the lower segments. If this differential in tissue type and density were to persist into childhood, a potential area of weakness or a stress riser may be present. Further mechanical stress may lead to the fatigue failure of an already weak PI.19 Further anatomic studies confirmed the increased sequential separation between facet joints which allows adjacent segments to imbricate during hyperextension thereby protecting the intervening PI from pressure. Insufficient increases in the inter-facet distance raises the pressure resulting from contact, which leads to development of pars defect.8 A feedback cycling model was developed recently suggested that although the three elements (anatomical features, microfracture and posture/activity) may cause lumbar spondylolysis independently, it is the nature and intensity of the interaction between the three during growth which determines the onset of PI lesions.20

onset LBP. Symptoms of LBP can vary according to age of the pars defect and sporting activities. The sporting population suffer from greater relative loss of function than PI defects existing in the general population. It is generally thought that the incidence of LBP increases with age. But Beutler et al (2003) in their 45 year follow-up study on subjects with spondylolysis suggested that pain was not their prominent feature at any age even though there was onset of slip.25 But this concept is debatable since a degenerate disc is noted frequently at L4/5 in cases of a PI defect at L5 without a slip.26 It has been further suggested that the L5/ S1 disc was more stable due to strong iliolumbar ligaments even though there is a defect at L5. Thus, if the pain continues to progress in the aging population in patients with spondylolysis it may be either due to the degenerate disc at L4/5 or the spondylolytic defect.

Why pars defect is painful? Typically patients present with extension related low back pain without radicular involvement. Immunolocalization techniques showed the ‘spondylolysis ligament’ (soft tissue at the PI defect) to contain neuropeptides associated with sensory or nociceptive transmission implicating a distinct source of pain.27 Connective tissue and scar harvested from the pars defect of symptomatic patients contain a high density of neural tissue which may be a source of back pain.28 The defective healing of the pars defect is probably due the stretching of these neural elements.29 Alternative sources of pain include an associated degenerate disc or facet joint. Ciullo (1985) suggested two possible sources of a painful PI defect. The pain is often experienced with the development of an acute stress fracture and the pain also subsides once the acute processes associated with the fracture subside. Recent studies by Boszczyk et al (2006) suggest that the ‘spondylolysis ligament’ has the hallmarks of a normal ligament i.e. fibrocartilaginous entheses at either end of an ordered collagenous fibre structure. The fibrocartilage is believed to dissipate stress concentration at the hard/soft tissue boundary.30 The second type of pain is due to segmental instability caused by the structural defect in the PI.16 However, segmental instability as a source of pain remains a controversial issue.31 But not all developmental defects of the PI cause pain. In one survey of 32,600 asymptomatic individuals a lumbar spondylolysis was present in 7.2%.32

Symptomatology Young sporting individuals present with symptoms of low back pain which develop at an earlier age than those of the more asymptomatic normal population.21 However, in many athletes, a new acute symptomatic defect develops from repeated microtrauma. Rossi and Dragoni (1990) reported 95% of 390 sportsmen with spondylolysis were involved in weight lifting, American football, gymnastics, wrestling and tennis.12 The condition is also associated with cricket, swimming and soccer.22 During repeated sheer and compression associated particularly with hyperextension, as characterised by actions in fast bowling (cricket) and many gymnastic exercises, the inferior articular facet is subjected to repeated loading and stress. Cortical fatigue reproduced in vitro, results in PI stress fractures.23 Chosa et al (2004) analysed a detailed 3-D L4/L5 motion segment model and concluded that PI stress was lower under compressive loading alone but higher under a combination of compression and extension or rotation.24 The diagnosis is based on clinical symptoms and radiological evidence of a pars defect. Not all stress reactions develop into a fracture and not all are painful. Most commonly patients present with either an acute onset low back pain (LBP) or a gradual

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Natural history The natural history of the defect seems to lie in the continuum, beginning with subtle stress reactions and ending in olisthesis, but the progression along this continuum is very unpredictable.11,25 Slippage is rare after the vertebral growth is complete (18–21 years), and the period of most likely and rapid slipping is between 9 and 15 years.16 A >10% displacement was observed in 23% subjects with symptomatic spondylolisthesis.33 Competitive sports did not affect the progression of spondylolyic spondylolisthesis.34,35 Muschik et al (1996) observed only 13% of athletes had increased displacement of >10% and suggested that participation in school and competitive sports is possible for children and adolescents with spondylolisthesis when the following conditions are met: a) limited spondylolyic spondylolisthesis, 110

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b) lordosis in the displaced segment, c) absence of symptoms, d) regular medical monitoring.35 Early or late development of pars defects was not associated with early or late segmental laxity. Later slip progression could not be predicted by the age of the subject at time of the initial slip. Unilateral pars defects were not associated with spondylolisthesis or significant disability.25 Bilateral pars defects develop symptomatic progression in only a small percentage of subjects in long-term follow-up studies.25 It has been suggested that while counselling parents of a child or adolescent presenting with bilateral L5 pars lesions it is appropriate to suggest a 5% incidence of progression of slip to adulthood.25

by the standing one-leg lumbar extension manoeuvre. Some of the more symptomatic patients may have lumbar paraspinous muscle spasms and pain throughout the lumbar spine range of motion. Imaging Plain radiographs (antero-posterior and lateral views) are essential preliminary imaging for the diagnosis of a pars defect (Figures 2a and b). Both planar bone scintigraphy (PBS) and single-photon-emission computed tomography (SPECT) are more sensitive than plain radiographs in detecting pars lesions.37 SPECT offers a more sensitive indicator of low intensity metabolic bone activity and bony remodelling, especially in early subtle stress reactions, than PBS.38 Sometimes increased stress response has been observed in the pedicles suggesting weakening of the neural arch from a contralateral spondylolysis.39 As spondylolysis becomes chronic, SPECT reverts to normal even though the spondylolysis has not healed completely.40–42 Computerised tomography (CT) is most often applied using the reverse gantry angle technique so that the scan plane is perpendicular to the defect. CT scans with thin slices are the most specific investigation for demonstrating a spondylolysis (Figures 2d and e). It is the investigation of choice for identifying radiographically occult lesions.38 Combinations of these two imaging modalities (SPECT & CT) increase the probability of diagnosis of a pars defect.43 Preoperative CT scanning is essential in planning since it gives valuable information about the morphology of the defect in terms of its width, site, orientation and gapping.44,45 MRI scans are nowadays routinely used for the early diagnosis and treatment of patients with

Diagnosis Clinical A high index of suspicion is required in a young patient complaining of exacerbation of LBP with activity. Typically, a young sporting individual e.g. a fast bowler (cricket) or a gymnast with a stress reaction in the posterior elements of the lumbar spine has aching low back pain, usually unilateral, that is exacerbated by motions such as twisting and hyperextension. Patients often volunteer that the pain is on one side “along the belt line.” But occasionally non-sporting young individuals may present with LBP unrelated to activity. Only 13% reported periods of disabling pain.34 Most commonly pars defects occur at L5 and are usually bilateral. It occurs less commonly in the upper lumbar spine but commonly occurs in fast bowlers in cricket as well as gymnasts.36 Physical examination reveals accentuation of pain

a and b Plain antero-posterior and lateral radiograph of a 29-year-old footballer showing a left L5 pars defect. c Screening radiograph of the same patient showing the pars injection with local anaesthetic. d and e Sagittal and reverse gantry axial CT scan showing left L5 pars defect and sclerosis in the right L5 pars. f and g T1w and T2w Sagittal MRI scans showing left L5 pars defect. h and i Six months post-operative plain antero-posterior and lateral radiograph of the above patient showing the repair of the L5 pars defect by Buck’s technique. Figure 2

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sportsmen experience disabling symptoms that are unresponsive to conservative treatment and prevent them in participation of their sports. Historically, postero-lateral arthrodesis with or without excision of the posterior elements has been performed. However, the loss of a motion segment at the level that is fused increases the load on the adjoining segment. Kimura (1968) was the first to describe the direct repair of a lumbar spondylolysis without instrumentation.56 This technique demonstrated that the motion at the segment could be preserved although he confined the patient to bed for two months followed by a corset for 4–6 months. The rationale for direct repair of the defect of PI relies on the fact that the pars defect is the main locus of pain. Injection of the pars defect with local anaesthetic has been recommended to determine if the pain generator is the pars (Figures 2c).57 The finding of nociceptive nerve endings within the pars defect lends credibility to pars injection as a diagnostic test in the evaluation of LBP in spondylolysis. An algorithm has been developed to plan a strategy for young patients with symptomatic lumbar pars defects (Figure 3).51 Several techniques have been developed to stabilize a spondylolytic defect in the lumbar spine. Commonly used methods include the direct repair described by Buck (1970), the Morscher hook screw (1984), the Scott wiring technique (1987) and many other screw-hook combinations.58–67 Several authors have analyzed the effectiveness of various systems but their series remain small.58–67 Good results of screw fixation have been reported in both non sporting and sporting populations.51,68–72

suspected stress injuries to the lumbar PI. With the use of high magnetic field strength, fat saturation techniques, and dedicated coil ­technology, high resolution MR images can be obtained that demonstrate the subtle bone marrow edema of early stress injuries, thus providing greater sensitivity than any other imaging modalities.46 MRI detects 98% of pars defects on T1W images and 93% on T2W images (Figures 2f and g). Hollenberg et al (2002) classified the PI defect into five grades on the basis of MRI scans. The following grading scheme was applied: grade 0 – normal; grade 1 – T2 signal abnormalities consistent with edema but no true spondylolysis; grade 2 – T2 signal abnormalities visible on T1 or T2W images; grade 3- visible complete unilateral or bilateral spondylolysis with associated abnormal T2 signal; grade 4 – complete spondylolysis without abnormal T2 signal (old ununited fracture).47

Management Conservative treatment Treatment depends on the severity of symptoms, age of the patient and level of sporting activity. Conservative options include: avoidance of sporting activity, trunk stability, core strength training, analgesic medication or brace treatment. The aim of managing painful lesions in young active individuals is to achieve bony union or at least a fibrous union of the PI defect in order to eliminate movement across the pars defect. The basic components of conservative treatment can be split into 4 areas of practice, 1) Reduction of activity level that causes the pain and relative immobilization, 2) Stretching hamstrings and glutei, 3) Abdominal strengthening exercises and back extensors, ­including core stability and functional stabilizing programs, 4) Graded return to provocative exercise when symptoms subside to allow comfortable exercise. Trials suggest that the functional integration of specific exercises directed at the deep abdominals and lumbar multifidus muscles are effective in reducing pain and functional disability in patients with chronically symptomatic spondylolysis or spondylolisthesis.48 Steiner and Micheli (1985) treated symptomatic patients with a brace (modified version of the Boston brace used for scoliosis) which was worn for 23 hours per day for six months, followed by a weaning period of the same time.49 Participation in sports was permitted, provided the brace was worn and the activity did not produce symptoms. Physical therapy includes hamstring and lumbosacral stretching, and abdominal (core) strengthening.50 Criteria for return to sport are dominated by residual symptoms following treatment.51 The healing potential for a symptomatic unilateral pars defect is higher than bilateral spondylolytic defects.51–53 Fuji et al (2004) suggested that the stage of the defect was the most predominant predictor of successful union.54 Non-operative management for six to twelve months is the gold standard for managing patients with either unilateral or bilateral spondylolyses.22,53,55

Biomechanical basis of surgical treatment Artificially induced bilateral pars defects in fresh frozen calf lumbar spines increase the intervertebral mobility not only at the involved level but also at the upper level adjacent to the lysis.73 The increased mobility of both the spondylolytic segment and the adjacent level are significantly reduced by Buck’s screw repair.58 The biomechanics of increased disc stresses in spondylolysis was studied on lumbar spondylolysis simulation models by Sairyo et al (2006).74 Buck’s direct repair model was simulated with 4.0 mm cannulated Titanium screws, placed bilaterally across the defect. The stresses at the annulus and nucleus pulposus decreased to 125% and 120% respectively in the Buck’s repair model suggesting that the Buck’s technique may be able to restore the disc stresses back to normal at both cranial and caudal disc levels. Deguchi et al (1999) compared four techniques of direct repair of the pars defect. The screw-rod-hook (Morscher) and Buck’s technique allowed the least motion across the pars defect when tested in flexion.75 Kip et al (1994) suggested that Buck screws provided the stiffest and strongest construct followed closely by Morscher’s hook-screw technique.76 An ideal instrumentation of the PI defect should have the following characteristics: 1) be able to counteract the high stress in extension and torsional forces, 2) must be of low profile and not irritate the adjacent facet joint 3) allows good surface area for bone grafting. Direct repair of pars defect In 1970, Buck described bilateral screw fixation applied transversely cross the PI defect.58 In this technique, the exposed PI defect is debrided and decorticated before the insertion of the cortical bone screw through the inferior laminar edge like ­fixing

Operative treatment A small percentage of patients need surgical intervention. The incidence of unmanageable LBP because of a pars defect in the young, competitive athlete is low. However, some young

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MANAGEMENT ALGORITHM History

Examination

VAS, ODI, SF36, BPSQ

X-rays AP and Lateral - No Oblique

SPECT Scan (before 2001)

Conservative Rx x 6-12m

rG CT + 3D CT

MRI Scan

Failed Conservative Rx Normal Disc

Disc Degeneration

HIZ +

Lysis Block

HIZ -

? Discogram - ive

+ ive

?

Repair Repair

Figure 3 Algorithm followed at QMC, Nottingham, proceeding to surgical repair of lumbar spondylolysis.

compress and stabilize the defect.64 This technique needs wide exposure and sublaminar wire passage. Most recently, Bozarth et al (2007) described a modified version of Songer’s cable-screw technique in three patients with return to active sports.65 Roca et al (2005) prospectively analysed 19 consecutive cases of spondylolysis repair using a new hook screw. They reported 12/13 patients below 20 years had union of the defect while 6 patients above the age of 20 years had non-union. Despite the non-union in six, four patients had an excellent clinical outcome.66 Debusscher & Troussel (2007) performed direct repair of the isthmus with a new type of pedicle screw hook system in 23 patients whose mean age was 34 years (range16–52 years). They reported 87% good outcome (100 % radiological union) in patients below 30 years of age against the 73% good outcome (82% radiological union) in patients above 30 years of age. All patients below 30 years had no degenerate disc disease. They

a fracture (Figures 2h and i). Morscher (1984) introduced the hook-screw construct which was effective in direct repair of the pars.59 Hefti et al (1992) reported only 58% of 33 patients to have union of the defect bilaterally.63 In 1985, Bradford and Iza first reported 21 patients with a successful outcome following the “Scott” wiring technique.70 Scott himself reported good results in their seven patients in 1986.60 Simple wiring technique is the least stable construct when tested against a flexion load and it is less likely to lead to sound healing across the defect.76 Pedicle screw-sublaminar hook technique described by Kakiuchi produced 100% union of PI defect.61 In their series, concomitant disc degeneration was not an exclusion criteri on and 7/16 patients were beyond 30 years of age.61 Songer & Rovin (1998) treated seven patients with PI defects successfully with a special pedicle cable-screw construct with a view that this will provide the strongest anchors at the pedicle and lamina which will

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recommended that direct repair can be carried out on patients with moderate degenerative disc disease.67These two studies used newer techniques of fixation and had CT scans to provide radiological evidence of successful union. Of all the techniques evolved in the last 40 years, Buck’s screw fixation has provided the best clinical outcome in the general population as well as well motivated professional athletes in many centres around the world. Although technically difficult, it provides a safe, reliable method and is reproducible (Figures 2a–i).10,22,51,53,57,58, 68,69,71,72

4 Wiltse LL. Etiology of spondylolisthesis. Clin Orthop 1957; 10: 48–60. 5 Waldron HA. Variations in the prevalence of spondylolysis in early british populations. J Royal Soc Med 1991; 84: 547–9. 6 Merbs CF. Incomplete spondylolysis and healing. Spine 1995; 20(21): 2328–33. 7 Eisenstein SM. Spondylolysis: a skeletal investigation of two population groups. J Bone Joint Surg Br 1978; 60(4): 488–94. 8 Ward CV, Latimer B. Human evolution and the development of spondylolysis. Spine 2005; 30(16): 1808–14. 9 Standaert CJ, Herring SA. Spondylolysis: a critical review. Br J Sports Med 2000; 34: 415–22. 10 Pedersen AK, Hagen R. Spondylolysis and spondylolisthesis – treatment by internal fixation and bone grafting of the defect. J Bone Joint Surg Am 1988; 70(1): 15–24. 11 Fredrickson BE, Baker D, McHolick WJ, Yuan HA, Lubicky JP. The natural history of spondylolysis and spondylolisthesis. J Bone Joint Surg Am 1984; 66(5): 699–707. 12 Rossi F, Dragoni S. Lumbar spondylolysis: occurrence in comnpetitive athletes. Updated achievements in a series of 390 cases. J Sports Med Phys Fitness 1990; 30(4): 450–2. 13 Blanda J, Bethem D, Moats W, et al. Defects of pars interarticularis in athlete: a protocol for nonoperative treatment. J Spinal Disord 1993; 6: 406–11. 14 Micheli LJ, Wood R. Back pain in young athlete: significant differences from adults in causes and patterns. Arch Pediatr Adolesc Med 1995; 149: 15–8. 15 Soler T, Calderon C. The prevalence of spondylolysis in the Spanish elite athlete. Am J Sports Med 2000; 28: 57–62. 16 Ciullo JV, Jackson DW. Pars interarticularis stress reaction, spondylolysis, and spondylolisthesis in gymnasts. Clin Sports Med 1985; 4(1): 95–110. 17 Kettlekamp DB, Wright DG. Spondylolysis in Alaskan Eskimo. J Bone Joint Surg Am 1971; 53(3): 563–6. 18 Wiltse LL. The etiology of spondylolisthesis. J Bone Joint Surg Am 1962; 44: 539–60. 19 Sagi HC, Jarviss JG, Uhthoff HK. Histomorphic analysis of the development of the pars interarticularis and its association with isthmic spondylolysis. Spine 1998; 23(15): 1635–9. 20 Masharawi Y, Dar G, Peleg S, et al. Lumbar facet anatomy changes in spondylolysis: a comparative skeletal study. Eur Spine J 2007; 16: 993–9. 21 Stinson JT. Spondylolysis and spondylolisthesis in the athlete. Clin Sports Med 1993 Jul; 12(3): 517–28. 22 Debnath UK, Freeman BJC, Gregory P, de la Harpe D, Kerslake RW, Webb JK. Clinical outcome and return to sport after the surgical treatment of spondylolysis in young athlete. J Bone Joint Surg Br 2003; 85(2): 244–9. 23 Cyron BM, Hutton WC, Troup JD. Spondylolytic fractures. J Bone Joint Surg Br 1976; 58(4): 462–6. 24 Chosa E, Totoribe K, Tajima N. A biomechanical study of lumbar spondylolysis based on a three-dimensional finite element method. J Orthop Res 2004; 22(1): 158–63. 25 Beutler WJ, Fredrickson BE, Murtland A, Sweeney CA, Grant WD, Baker D. The natural history of spondylolysis and spondylolisthesis: 45-year follow-up evaluation. Spine 2003 May 15; 28(10): 1027–35. 26 Ishida Y, Ohmori K, Inoue H, Suzuki K. Delayed vertebral slip and adjacent disc degeneration with an isthmic defect of the fifth lumbar vertebra. J Bone Joint Surg Br 1999; 81(2): 240–4.

Predictors of successful outcome following surgery It was established that the predictors of successful surgical outcome include age less than 25 years, spondylolysis of less than 4 mm, absence of disc degeneration, positive response to local anaesthetic infiltration of the pars defect, method of surgical repair and psychological motivation of the individual undergoing surgery.22,53 Further evaluation of studies at Nottingham suggests that results of direct repair of a PI defect in a patient over the age of 25 years old may sometimes run an unpredictable course. Ivanic et al (2003) reported a pseudarthrosis rate of 8.6% in patients less than 20 years of age compared to 35% in patients over the age of 20 years.77 Wu et al (1999) confirmed the successful outcome of surgery in patients with a positive response to a pars injection.78 Current analysis of data from Nottingham suggests that three factors had significant effect on the final outcome following Buck’s direct repair viz. 1) preoperative ODI 2) SF-36 scores and 3) professionalism in sports.51 Low back pain is the single most important predictor for one having a surgical ­intervention.51

Summary Surgery is indicated when 6–12 months of conservative therapy has failed to improve disabling low back pain in patients with lumbar spondylolysis. In the absence of pain arising from the disc or facet joint, attempts may be made to repair the pars defect. Commonly used methods include the direct repair with a cortical screw (Buck’s repair), the Morscher hook screw and combination of hook, cables & wires. Low back pain is the single most important predictor for one having a surgical intervention. If disc or facet joint degeneration is established at the time of diagnosis, instrumented spinal fusion is advised. Professionalism in sports has a high impact on the outcome of an individual following surgical repair of the defect. Unilateral spondylolyses do slightly better than bilateral spondylolyses following Buck’s repair. Preoperative ODI and SF-36 physical component scores (PCS) are significant predictors of a good functional outcome. Buck’s repair at L5 and L4 level has excellent to good short to mid-term outcome. ◆

References 1 Wiltse LL, Widell, Jackson DW. Fatigue fracture: the basic lesion in isthmic spondylolisthesis. J Bone Joint Surg Am 1975; 57: 17–22. 2 Gumphry GM. A treatise on the human skeleton, Cambridge. UK: Macmillan & Co., 1858 p. 143n. 3 Newell RLM. Historical perspective spondylolysis: an historical review. Spine 1995; 20(17): 1950–6.

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27 Eisenstein SM, Ashton IK, Roberts S, et al. Innervation of the spondylolysis “ligament”. Spine 1994; 19(8): 912–6. 28 Schneiderman GA, McLain RF, Hambly MF, Nielsen SL. The pars defect as a pain source. A histologic study. Spine 1995; 20(16): 1761–4. 29 Nordström D, Santavirta S, Seitsalo S, et al. Symptomatic lumbar spondylolysis. Neuroimmunologic studies. Spine 1994; 19(24): 2752–8. 30 Boszczyk BM, Boszczyk AA, Boos W, et al. An immunohistochemical study of the tissue bridging adult spondylolytic defects–the presence and significance of fibrocartilaginous entheses. Eur Spine J 2006; 15(6): 965–71. 31 Bogduk N. The anatomical basis for spinal pain syndromes. J Manipulative Physiol Ther 1995; 18(9): 603–5. 32 Moreton RD. Spondylolysis. JAMA 1966; 195(8): 671–4. 33 Seitsalo S, Osterman K, Hyvãrinen H, Tallroth K, Schlenzka D, Poussa M. Progression of spondylolisthesis in children and adolescents. A long-term follow-up of 272 patients. Spine 1991; 16(4): 417–21. 34 Saraste H, Brostrom LA, Aparisi T. Prognostic radiographic aspects of spondylolisthesis. Acta Radiol 1984; 25(5): 427–32. 35 Muschik M, Hahnel H, Robinson PN, Perka C, Muschik C. Competitive sports and the progression of spondylolisthesis. J Pediatr Orthop 1996; 16(3): 364–9. 36 Elliott BC. Back injuries and the fast bowler in cricket. J Sports Sci 2000; 18(12): 983–91. 37 Collier BD, Johnson RP, Carrera GF, et al. Painful spondylolysis or spondylolisthesis studied by radiography and single-photon emission computed tomography. Radiology 1985; 154(1): 207–11. 38 Harvey CJ, Richenberg JL, Saifuddin A, Wolman RL. The radiological investigation of lumbar spondylolysis. Clin Radiol 1998; 53(10): 723–8. 39 Bellah RD, Summerville DA, Treves ST, Micheli LJ. Low-back pain in adolescent athletes: detection of stress injury to the pars interarticularis with SPECT. Radiology 1991; 180(2): 509–12. 40 Lusins JO, Elting JJ, Cicoria AD, Goldsmith SJ. SPECT evaluation of lumbar spondylolysis and spondylolisthesis. Spine 1994; 19(5): 608–12. 41 Dutton JA, Hughes SP, Peters AM. SPECT in the management of patients with back pain and spondylolysis. Clin Nucl Med 2000 Feb; 25(2): 93–6. 42 Debnath UK, Freeman BJC, et al. SPECT imaging in posterior lumbar stress injuries. In: Proceedings of the British Orthopaedic Association XXII Annual Meeting 2002, Published in Proceedings JBJS Supp III, 2003. 43 Gregory Pl, Batt ME, Kerslake RW, Scammell BE, Webb JK. The value of combining SPECT and CT in the investigation of spondylolysis. Eur Spine J 2004; 13: 503–9. 44 Campbell RS, Grainger AJ, Hide IG, Papastefanou S, Greenough CG. Juvenile spondylolysis: a comparative analysis of CT, SPECT and MRI. Skeletal Radiol 2005; 34(2): 63–73. 45 Saifuddin A, White J, Tucker S, Taylor BA. Orientation of lumbar pars defects: implications for radiological detection and surgical management. J Bone Joint Surg Br 1998; 80(2): 208–11. 46 Udeshi UL, Reeves D. Routine thin slice MRI effectively demonstrates the lumbar pars interarticularis. Clin Radiol 1999; 54(9): 615–9. 47 Hollenberg GM, Beattie PF, Meyers SP, Weinberg EP, Adams MJ. Stress reactions of the lumbar pars interarticularis: the development of a New MRI classification system. Spine 2002; 27(2): 181–6. 48 O’Sullivan PB, Phyty GDM, Twomey LT, Allison GT. Evaluation of specific stabilizing exercise in the treatment of chronic low back

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pain with radiologic diagnosis of spondylolysis or spondylolisthesis. Spine 1997; 22(24): 2959–67. 49 Steiner ME, Micheli LJ. Treatment of symptomatic spondylolysis and spondylolisthesis with the modified Boston brace. Spine 1985; 10(10): 937–43. 50 McCleary MD, Congeni JA. Current concepts in the diagnosis and treatment of spondylolysis in young athletes. Curr Sports Med Rep 2007; 6(1): 62–6. 51 Debnath UK. Factors predicting the outcome following treatment for lumbar spondylolysis. Thesis submitted to University of Nottingham for Doctor of Medicine, Jun 2008. 52 Sys J, Michielsen J, Bracke P, Martens M, Verstreken J. Nonoperative treatment of active spondylolysis in elite athletes with normal X-ray findings: literature review and results of conservative treatment. Eur Spine J 2001; 10(6): 498–504. 53 Debnath UK, Freeman BJ, Grevitt MP, Sithole J, Scammell BE, Webb JK. Clinical outcome of symptomatic unilateral stress injuries of the lumbar pars interarticularis. Spine 2007; 32(9): 995–1000. 54 Fuji K, Katoh S, Sairyo K, Ikata T, Yasui N. Union of defects in the pars interarticularis of the lumbar spine in children and adolescents: the radiological outcome after conservative treatment. J Bone Joint Surg Br 2004; 86(2): 225–31. 55 Standaert CJ, Herring SA. Expert opinion and controversies in sports and musculoskeletal medicine: the diagnosis and treatment of spondylolysis in adolescent athletes. Arch Phys Med Rehabil 2007; 88(4): 537–40. 56 Kimura M. My method of filling the lesion with spongy bone in spondylolysis and spondylolisthesis. (in Japanese) Orthop Surg 1968; 19: 285–95. 57 Suh PB, Esses SI, Kostuik JP. Repair of pars interarticularis defect. The prognostic value of pars infiltration. Spine 1991; 16(8 Suppl): S445–8. 58 Buck JE. Direct repair of the defect in spondylolisthesis – preliminary report. J Bone Joint Surg Br 1970; 52(3): 432–8. 59 Morscher E, Gerber B, Fasel J. Surgical treatment of spondylolisthesis by bone grafting and direct stabilization of spondylolysis by means of a hook screw. Arch Orthop Trauma Surg 1984; 103(3): 175–8. 60 Nicol RO, Scott JH. Lytic spondylolysis. Repair by wiring. Spine 1986; 11(10): 1027–30. 61 Kakiuchi M. Repair of the defect in spondylolysis. Durable fixation with pedicle screws and laminar hooks. J Bone Joint Surg Am 1997; 79(6): 818–25. 62 Tokuhashi Y, Matsuzaki H. Repair of defects in spondylolysis by segmental pedicular screw hook fixation. A preliminary report. Spine 1996; 21(17): 2041–5. 63 Hefti F, Seelig W, Morscher E. Repair of lumbar spondylolysis with a hook-screw. Int Orthop 1992; 16(1): 81–5. 64 Songer MN, Rovin R. Repair of the pars interarticularis defect with a cable-screw construct. A preliminary report. Spine 1998; 23(2): 263–9. 65 Bozarth GR, Fogel GR, Toohey JS, Neider A. Repair of pars interarticularis defect with a modified cable-screw construct. J Surg Orthop Adv 2007; 16(2): 79–83. 66 Roca J, Iborra M, Cavanilles-Walker JM, Albertí G. Direct repair of spondylolysis using a new pedicle screw hook fixation: clinical and CT-assessed study: an analysis of 19 patients. J Spinal Disord Tech 2005(18 Suppl): S82–9. 67 Debusscher F, Troussel S. Direct repair of defects in lumbar spondylolysis with a new pedicle screw hook fixation: clinical,

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functional and CT-assessed study. Eur Spine J 2007; 16(10): 1650–8. 68 Gillet P, Petit M. Direct repair of spondylolysis without spondylolisthesis, using a rod-screw construct and bone grafting of the pars defect. Spine 1999; 24(12): 1252–6. 69 Hardcastle PH. Repair of spondylolysis in young fast bowlers. J Bone Joint Surg Br 1993; 75(3): 398–402. 70 Bradford DS, Iza J. Repair of the defect in spondylolysis or minimal degrees of spondylolisthesis by segment wire fixation and bone grafting. Spine 1985; 10: 673–9. 71 Bonnici AV, Koka SR, Richards DJ. Results of Buck screw fusion in grade I spondylolisthesis. J R Soc Med 1991; 84: 270–3. 72 Jeanneret B. Direct repair of spondylolysis. Acta Orthop Scand Suppl 1993; 251: 111–5. 73 Mihara H, Onari K, Cheung BC. The biomechanical effects of spondylolysis and its treatment. Spine 2003; 28: 235–8.

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74 Sairyo K, Goel VK, Faizan A, Vadapalli S, Biyani S, Ebraheim N. Buck’s direct repair of lumbar spondylolysis restores disc stresses at the involved and adjacent levels. Clin Biomech (Bristol, Avon) 2006; 21(10): 1020–6. 75 Deguchi M, Rapoff AJ, Zdeblick TA. Biomechanical comparison of spondylolysis fixation techniques. Spine 1999; 24(4): 328–33. 76 Kip PC, Esses SI, Doherty BI, Alexander JW, Crawford MJ. Biomechanical testing of pars defect repairs. Spine 1994; 19(23): 2692–7. 77 Ivanic GM, Pink TP, Achatz W, et al. Direct stabilization of lumbar spondylolysis with a hook-screw. Mean 11-year follow-up period for 113 patients. Spine 2003; 28: 255–9. 78 Wu SS, Lee CH, Chen PQ. Operative repair of symptomatic spondylolysis following a positive response to diagnostic pars injection. J Spinal Disord 1999; 12(1): 10–6.

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Arthroplasty

Is infection inevitable in some arthroplasty patients?

there may be an underlying genetic/immunological component responsible for infection in this vulnerable sub-group. The role of a major susceptibility gene in infection acquisition has yet to be shown, although a number of minor components may contribute to a polygenetic background of susceptibility in different patient groups. The identification of genetic polymorphisms associated with protection from some infectious diseases form the basis of genetic selection consistent with significant selective pressure by a particular agent.6 The problem when one tries to associate an opportunistic infection with a genetic predisposition is that in evolutionary terms, for an infection to exert selective pressure over a prolonged period of time it must significantly affect morbidity and mortality within a population prior to reproduction.6 This is simply not the case in terms of opportunistic infections in older patients with joint replacement. Therefore, when one attempts to identify a potential genetic factor linked to an increased risk of infection and subsequent failure of joint arthroplasty, one must look at three possibilities; 1) a subtle alteration in antigenic presentation or in the initial response to antigen that would otherwise not present unless the patient became compromised by, for example, surgery, 2) the presence of a polymorphism in a gene naturally selected to provide benefit that now may increase the susceptibility to opportunistic infection, and 3) a combination of both. Despite the fact that many risk factors have been identified for the development of surgical infection following arthroplasty, such as underlying comorbidities7 (for example obesity, malignancy, diabetes mellitus, and rheumatoid arthritis) or interferon gamma deficiency (IFN γ),8 this report will focus on the important role of cytokines, in particular interleukin-6 (IL-6) and the acute phase protein mannose binding lectin (MBL).

RJ Langley DI Rowley

Abstract Infection is a rare complication of arthroplasty surgery, yet the consequences of such an event lead to significant costs both in terms of finance and patient morbidity. This review describes the current literature examining a possible genetic link between post-surgical infections, cytokines and polymorphisms in the gene encoding the acute phase protein mannose binding lectin.

Keywords arthroplasty; cytokines; genetic; infection

Introduction Surgery is as old as civilization itself, and since its beginnings two great challenges have been faced; one pain, the other infection. The former can now be more or less controlled with modern anaesthetic techniques and powerful analgesics. In contrast, the latter, once thought to be under control with the discovery of antibiotics, has proven to be a significant challenge yet to be fully conquered. Modern surgical techniques of joint replacement can achieve what the forefathers of surgery, such as Paré or Lister, could only dream of. Ironically, modern day surgeons have a similar foe to their historical mentors, with approximately 1% of total hip replacements complicated by infection.1 Total hip and knee arthroplasty have been a significant breakthrough in restoring mobility to a large number of patients in whom conventional therapy was no longer of use. Unfortunately, over time, a certain percentage of prosthetic implants will fail, with the main reason being aseptic loosening/periprosthetic osteolysis.2 In terms of early failure, deep infection with the Gram-positive bacteria Staphylococcus aureus or coagulasenegative Staphylococci, is the most common cause.3,4 Therefore, the initial management of a patient receiving joint arthroplasty is focussed on preventing sepsis, by aseptic surgical techniques and the appropriate administration of peri-operative antibiotics. Despite these preventative measures, there remains a subset of patients who appear to acquire prosthetic joint infections without an obvious predisposition.5 This raises the possibility that

Cytokines & surgery In the likelihood of an increased susceptibility to infection, the patient’s ability to generate an appropriate cytokine response may play a significant role. A recent study has highlighted several cytokines that may be important in the post-surgical period.9 Despite the limited number of patients (n = 13), it has been demonstrated that the concentrations of both IL-6 and IL-8 appear to elevate following total hip replacement when compared with preoperative values. Furthermore, elevated levels of IL-6 have also been shown to be predictive of knee or hip prosthetic infection.10 The function of these proinflammatory cytokines is, amongst other things, to release acute phase proteins and chemo-attract neutrophils. The diverse immunological role of IL-6 is shown (Figure 1). In addition, further studies have reported that single promoter gene polymorphisms in the IL-6 and transforming growth factor-beta1 (TGF-β1),11 and IL-6 levels12 are predictive of aseptic loosening following total hip arthroplasty. Both studies indicate that the cytokine response, in particular IL-6, can greatly affect the outcome of total joint arthroplasty either via aseptic loosening or infection. In summary, one may expect to find elevated levels of IL-6 during an infection and that it would be predictive of post-surgical complications. With respect to a sub-group of patients with an increased incidence of infection, it may then be important to consider a deficiency in IL-6 expression or polymorphisms in the IL-6 gene

RJ Langley PhD is a Post-doctoral Researcher, in the Section of Orthopaedic and Trauma Surgery, Ninewells Hospital and Medical School, Dundee, UK. DI Rowley FRCS is a Professor in Orthopaedic and Trauma Surgery Department, Ninewells Hospital and Medical School, Dundee, UK.

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Interleukin-6

Liver: Acute phase proteins eg. C-RP and MBL

- Activation of complement - Opsonisation

Bone Marrow: Neutrophil mobilisation

Hypothalamus: Increased body temperature

B & T Iymphocytes: Increased activation

-Decreased viral and bacterial replication

Phagocytosis

-Increased antigen processing -Increased specific immune response

Figure 1 The Immunological roles of IL-6: IL-6 activates hepatocytes to produce acute phase proteins, including C-reactive protein (C-RP) and mannose binding lectin (MBL), and acts on the bone marrow to increase the number of circulating neutrophils. IL-6 is an endogenous pyogen that acts on the hypothalamus to increase the core body temperature; the effect of which is to decrease bacterial and viral replication coupled with an increase in antigenic processing. IL-6 enhances the activation of B- and T-lymphocytes and thus the adaptive immune response (Adapted from13).

MBL levels have been described17–20 (Figure 3). Polymorphisms at codon 52, 54 and 57, on exon 1, encode variant alleles A/D, A/B and A/C respectively (wild-type allele is A).17,18 The D, B, C alleles result in amino acid substitutions arginine to cysteine, glycine to aspartic acid and glycine to glutamic acid ­respectively.21 When one considers MBL structural variants, individuals can be designated A/A for wild-type homozygotes, A/O for heterozygotes (A/B, A/C, A/D) and O/O for structural variant homozygotes (B/B, C/C, or D/D) or compound heterozygotes (for example B/C).22 The phenotypic consequences of polymorphisms in the structural gene are that the efficiency of MBL oligomerization is reduced resulting in poor complement fixation and higher rate of MBL turnover.23 There is considerable variation between different populations and MBL allele frequency. The B allele is found with high frequency in healthy Caucasians, but is very rare in East African populations.24,25 The C allele is common in West Africans, but is rare in Caucasian populations and absent in Asians.21 Both the B and C allele have a dominant reducing effect on the level of MBL in serum.21 The D allele is found in East African and Caucasian populations, but, as with C, is absent in Asians.17 The population variation suggests that MBL variation may have been selected to provide benefit against infectious agents.22 This would therefore fulfil the criteria above, that in evolutionary terms for genetic polymorphisms to exist within a population selective pressure must have been exerted over a prolonged period of time and such must significantly effect morbidity and mortality within a population prior to reproduction.6 As implied earlier, although the presence of the mutant allele would provide benefit in evolutionary terms, it may have resulted in an increase in genetic susceptibility to opportunistic infection in certain ­individuals.

that reduce its effectiveness. If such a deficiency was observed then it would affect the capacity to mount a suitable challenge via IL-6 and acute-phase proteins, increasing patient susceptibility to developing a recalcitrant infection. The patient would, in effect, be immunocompromised. The deficiency may only be evident when the immune system is under significant stress, such as during arthroplasty, leading to failure in dealing with an infectious insult acutely, with the subsequent chronic sequelae of prosthetic failure. When one considers the importance of IL-6 it is also important to address the downstream affects of this cytokine, in particular its affect on the induction of the acute phase protein mannose binding lectin (MBL).

Mannose Binding Lectin Mannose binding lectin (MBL) is a hepatic derived acute phase protein with an important role in the innate immune system.14 MBL synthesis is induced by IL-6, which is derived from bacterial stimulation of macrophages.13 MBL is a member of the collectin family, which possess a carbohydrate recognition domain (CRD) and a collagenous domain (Figure 2).15 MBL, a 96 kDa trimer, has the capacity to form oligomers (2 to 6 trimer units) resulting in a large fan-shaped structure with considerable molecular similarity to the complement component C1q (Figure 2).15

MBL genetics The MBL gene has four exons (and three introns) and is found on the long arm of chromosome ten (10q11.2-q21).16 Currently, five single nucleotide polymorphisms (SNPs) that alter serum

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Figure 2 Mannose binding lectin (MBL): Mannose binding lectin is derived from the liver and secreted during the acute phase response to infection. It consists of an N-terminal cysteine (Cys)-rich region, a collagenous domain, a neck region with flexion and a calcium dependent carbohydrate recognition domain (CRD). The subunit molecular weight (MW) = 32 kDa. The MBL molecule is able to dimerise and trimerise via disulfide bonds formation (MW = 96 kDa). The formation of trimers leads to high order oligomerization and the formation of the active MBL molecule (Adapted from15).

organisms via the CRD domain, 2) activation of complement through the mannose-binding lectin associated serine proteases (MASPs),22 and 3) activation of macrophages via the C1q receptor.5 MBL has been shown to have high-level binding for S. aureus,32 Candida albicans, Aspergillus fumigatus, and Streptococcus pyogenes.33 The first account of a common opsonic defect was described in 1968,34 and it was subsequently recognised that an MBL deficiency was the cause.35 Many studies have since reported a link between MBL deficiency and a predisposition to serious infection35–37 and rheumatoid arthritis.28 However, there has been considerable debate within the scientific community over the importance of MBL and its immunological role.38–40 Interestingly, Fidler et al. demonstrated an association between MBL variant alleles and a seven-fold increased risk of sepsis in

Promoter region polymorphisms at −550 and −221 encode alleles H/L and X/Y respectively (Figure 3), and can greatly influence serum MBL concentrations in both wild-type individuals and heterozygotes for structural gene mutations.26 Six common haplotypes are formed; HYA, LYA, LXA, HYD, LYB, and LYC.15 The HYA haplotype has been shown to produce high MBL levels, LYA intermediate levels and LXA producing the lowest27 (Table 1). Mutations in these regions are associated with increased susceptibility in inflammatory arthritis,28 inflammatory bowel disease29 and autoimmune conditions.30

MBL, immunity & infection MBL can be thought of as a primitive non-specific antibody produced in response to non-specific stimuli and lacks the structural diversity associated with antibodies. MBL has three distinctive roles in innate immunity: 1) opsonisation of a wide variety of

Concentration of mannose binding lectin (MBL) in the Japanese population with varying MBL haplotypes (Adapted from31)

Figure 3 MBL gene: There are currently five common single nucleotide polymorphisms (SNP). Each polymorphism can greatly affect the concentration of serum MBL. The common SNPs are named H/L, X/Y, A/D (arginine to cysteine), A/B (glycine to aspartic acid) and A/C (glycine to glutamic acid). Therefore six common haplotypes are formed; HYA, LYA, LXA, HYD, LYB, and LYC (Adapted from15).

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Haplotypes

MBL concentration (mg/L)

HYA/LYA HYA/HYA LYA/LYA HYA/LXA LYA/LXA HYA/LYB LYA/LYB LXA/LYB LYB/LYB

1.411 1.177 1.210 0.830 0.584 0.333 0.119 0.013 0.002

Table 1

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paediatric patients.41 This study found that individuals with the wild-type MBL haplotype (A/A) had a 50% reduction in risk of systemic inflammatory response syndrome (SIRS). In contrast, all homozygotes or heterozygotes for structural variant alleles plus reduced promoter expression developed SIRS. Furthermore, once the individual became infected, the response was significantly increased in the presence of the variant allele. A number of other studies have examined levels of MBL pre-colorectal surgery,42 and have also found that low MBL concentrations predispose to infection.43 Thus, it seems likely that MBL plays a critical role in the host’s response to bacteria, and any deficiency has the potential to greatly increase severity.

mechanisms of failure are complex and appear to involve environmental, surgical and genetic factors. The latter will perhaps prove to be the most complex, involving a number of candidate genes and their interactions. Thus, this review highlights the need for further research examining patient genotypes and outcome of arthroplastic surgery. A future prospective study may wish to evaluate IL-6 levels, MBL polymorphisms and MBL serum concentration pre- and post- operatively to determine if a functional deficit may increase the likelihood of post-operative infection and ultimately prosthetic failure. Furthermore, prospective genotypic screening of patients prior to surgery may allow more tailored management, with the inclusion of MBL replacement therapy. ◆

MBL and arthroplasty

References 1 Imman R, Gallegos K, Brause B, Redecha P, Christian C. Clinical and microbiological features of prosthetic joint infection. Am J Med 1984; 77: 47–53. 2 Harris W. The problem is osteolysis. Clin Orthop 1995; 311: 46–50. 3 Tunney M, Patrick S, Gorman S. Improved detection of infection in hip replacements. A currently underestimated problem. J Bone Joint Surg 1998; 80B: 568–75. 4 Lidgren L, Knutson K, Stefansdottir A. Infection of prosthetic joints. Best Pract Res Clin Rheumatol 2003; 17: 209–218. 5 Malik M, Bayat A, Jury F, Kay P, Ollier W. Genetic susceptibility to total hip arthroplasty failure-positive association with mannosebinding lectin. J Arthroplasty 2007; 22: 265–270. 6 Cooke G, Hill A. Genetics of susceptibility to human infectious disease. Nat Rev Genet 2001; 2: 967–977. 7 Minnema B, Vearncombe M, Augustin A, Gollish J, Simor A. Risk factors for surgical-site infection following primary total knee arthroplasty. Infect Control Hosp Epidemiol 2004; 25: 477–480. 8 Honstettre A, Mege J, Lina G, Aubaniac J, Drancourt M. Relationship of relapsing hip prosthesis infection by Staphylococcus aureus with gamma interferon deficiency. J Clin Microbiol 2003; 41: 5344–5346. 9 Bjornsson GL, Thorsteinsson L, Gudmundsson KO, Jonsson Jr. H, Gudmundsson S, Gudbjornsson B. Inflammatory cytokines in relation to adrenal response following total hip replacement. Scand J Immunol 2007; 65: 99–105. 10 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: American Edition 2005; 87: 1921–1927. 11 Kolundzic R, Orlic D, Trkulja V, Pavelic K, Troselj KG. Single nucleotide polymorphisms in the interleukin-6 gene promoter, tumor necrosis factor-alpha gene promoter, and transforming growth factor-beta1 gene signal sequence as predictors of time to onset of aseptic loosening after total hip arthroplasty: preliminary study. J Orthop Sci 2006; 11: 592–600. 12 Konttinen YT, Xu JW, Waris E, et al. Interleukin-6 in aseptic loosening of total hip replacement prostheses. Clin Exp Rheumatol 2002; 20: 485–90. 13 Janeway C, Travers P. Non-adaptive host response to infection. Immunobiology: The immune system in health and disease. 3rd edn. New York: Garland Publishing, 1997:9:20-9:22. 14 Thiel S, Holmskov U, Hviid L, Laursen SB, Jensenius J. The concentration of C-type lectin, mannan-binding protein, in human plasma increases during an acute phase response. Clin Exp Immunol 1992; 90: 31–35.

Despite improvements to both surgical technique and materials used, a percentage of arthroplasties will always fail. A study by Malchau et al. has identified aseptic loosening as the main cause (75%), with deep infection leading to failure in 7% of cases of failure.44 Interestingly, survival of an implant appears to be largely independent of implant material and design, suggesting an underlying biological cause of failure.5 The immune system is compromised by the trauma associated with major surgery and there is a significant risk of infection in the post-surgical period.45 As has been discussed previously, MBL deficiency appears to increase the likelihood and severity of SIRS and sepsis. MBL may also play a role in aseptic loosening by activating the complement cascade and instigating loosening of the tissue-implant interface.5,46 A recent seminal study examined the interaction between MBL deficiency (associated with mutations at codon 52, 54 and the promoter region) and prosthetic joint failure by either aseptic loosening or deep infection.5 Malik et al. described a case-control study whereby the patient’s (n = 312, 150 control cases, 91 aseptic cases, 71 septic cases) MBL genotype was determined and related to the outcome of total hip arthroplasty (aseptic loosening or deep infection). The authors found an association between the promoter −550 and codon 54 SNP and increased failure of total hip arthroplasty. The promoter polymorphism results in reduced MBL transcription, and both lead to reduced serum MBL concentrations. The promoter −550 SNP was also shown to be increased in the septic failure group. MBL therapy Two methods of MBL replacement therapy are currently under consideration: MBL derived from human plasma47,48 and recombinant MBL.49,50 The former has been used in two clinical situations, MBL deficient patients47 and in a cystic fibrosis adult.51 Although neither study demonstrated clear clinical benefit, MBL was shown to be well tolerated and safe. These early studies provide hope that future surgical management plans may include the administration of MBL to reduce the risk of arthroplastic implant failure.

Summary The clinical outcomes of failure of joint arthroplasty are costly, both in terms of the increase in patients’ physiological and psychological morbidity as well as the financial implications. The

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mannose-binding lectin with mannose-binding lectin-associated serine protease after binding to Staphylococcus aureus. J Immunol 2002; 169: 4430–4436. 33 Neth O, Jack D, Dodds A. Mannose-binding lectin binds to a range of clinically relevant microorganisms and promotes complement deposition. Infect Immun 2000; 68: 688–693. 34 Miller M, Seals J, Kaye R, Levitsky R. A familial, plasma associated defect of phagocytosis: a new cause of recurrent bacterial infection. Lancet 1968; ii: 60–63. 35 Super M, Lu J, Thiel S, Levinsky R, Turner M. Association of low levels of mannan binding protein with a common defect of opsonisation. Lancet 1989; 334: 1236–239. 36 Turner M. Mannose-binding lectin: the pluripotent molecule of the innate immune system. Immunol Today 1996; 17: 532–540. 37 Roy S, Knox K, Segal S. MBL genotype and risk of invasive pneumococcal disease: a case controlled study. Lancet 2002; 359: 1569–1573. 38 Kronberg G, Weis N, Madsen H. Variant mannose-binding lectin alleles are not associated with susceptibility to or outcome of invasive pneumococcal infection in randomly included patients. J Infect Dis 2002; 185: 1517–1520. 39 Klein N. Mannose-binding lectin: do we need it? Mol Immunol 2005; 42: 919–924. 40 Casanova J, Abel L. Human mannose-binding lectin in immunity: Friend, foe or both? J Exp Med 2004; 10: 1295–1299. 41 Fidler K, Wilson P, Davies J, Turner M, Peters M, Klein N. Increased incidence and severity of the systemic inflammatory response syndrome in patients deficient in mannose binding lectin. Intensive Care Med 2004; 30: 1438–1445. 42 Ytting H, Christensen I, Jensenius J, Thiel S, Nielsen H. Preoperative mannan-binding lectin pathway and prognosis in colorectal cancer. Cancer Immunol Immunother 2005; 54: 265–272. 43 Siassi M, Hohenberger W, Riese J. Mannan-binding lectin (MBL) serum levels and post-operative infections. Biochem Soc Trans 2003; 31: 774–775. 44 Malchau H, Herberts P, Ahnfelt L. Prognosis of total hip replacement in Sweden. Follow up of 92, 675 operations performed 1978–1990. Acta Orthop Scan 1993; 64: 497. 45 Thiel S, Frederiksen P, Jensenius J. Clinical manifestations of manna binding lectin deficiency. Mol Immunol 2006; 43: 86–96. 46 Wooley P, Fitzgerald R, Song Z. Proteins bound to polyethylene components in patients who have aseptic loosening after total joint arthroplasty. J Bone Joint Surg: American Edition 1999; 81: 616. 47 Valdimarsson H, Stefansson M, Vikingdottir T, et al. Reconstitution of opsonizing activity by infusion of mannan-binding lectin (MBL) to MBL deficient humans. Scand J Immunol 1998; 48: 116–123. 48 Valdimarsson H, Vikingdottir T, Bang P, et al. Human plasma-derived mannose binding lectin: a phase I safety and pharmacokinetic study. Scand J Immunol 2004; 59: 97–102. 49 Vorup-Jensen T, Sorensen E, Jensen U. Recombinant expression of human mannan binding lectin. Int Immunopharmacol 2001; 1: 677–687. 50 Jensenius J, Jensen P, McGuire K, Larsen J, Thiel S. Recombinant mannan-binding lectin (MBL) for therapy. Biochem Soc Trans 2003; 31: 763–767. 51 Garred P, Pressler T, Lanng S, et al. Mannose-binding lectin (MBL) therapy in an MBL-deficient patient with severe cystic fibrosis lung disease. Pediatr Pulmonol 2002; 33: 201–207.

15 Tsutsumi A, Takahashi R, Suminda T. Mannose binding lectin: genetics and autoimmune disease. Autoimmun Rev 2005; 4: 364–372. 16 Sastry K, Herman G, Day L, Deignan E, Bruns G, Morton C. The human mannose binding protein gene. Exon structure reveals its evolutionary relationship to a human pulmonary surfactant gene and localisation to chromosome 10. J Exp Med 1989; 170: 1175–1189. 17 Madsen H, Garred P, Kurtzhals J, Lamm L, Ryder L, Thiel S. A new frequent allele is the missing link in the structural polymorphism of the human mannan binding protein. Immunogenetics 1994; 40: 37–44. 18 Suminya M, Super M, Tabona P, Levinsky R, Arai T, Turner M. Molecular basis of opsonic defect in immunodeficient children. Lancet 1991; 337: 1569–1570. 19 Lipscombe R, Suminya M, Hill A, Lau Y, Levinsky R, Summerfield J. High frequencies in African and non African populations of independent mutations in the mannose binding protein gene. Hum Mol Genet 1992; 1: 709–715. 20 Madsen H, Satz M, Hogh B, Svejgaard A, Garred P. Different molecular events result in low protein levels of mannan-binding lectin in populations from southeast Africa and South America. J Immunol 1998; 161: 3169–3175. 21 Garred P, Larsen F, Seyforth J, Fujita R, Madsen H. Mannose binding lectin and its genetic variants. Genes Immun 2006; 7: 85–94. 22 Eisen D, Minchiton R. Impact of mannose binding lectin on susceptibility to infectious diseases. Clin Infect Dis 2003; 37: 1496–1505. 23 Peterson S, Thiel S, Jensenius JC. The mannan binding lectin pathway of complement activation: biology and disease association. Mol Immunol 2001; 38: 133–149. 24 Garred P, Thiel S, Madsen H, Ryder L, Jensenius JC, Svejgaard A. Gene frequency and partial protein characterization of an allelic variant of mannan binding protein associated with low serum concentrations. Clin Exp Immunol 1992; 90: 517–21. 25 Garred P, Madsen H, Kurtzhals J, Lamm L, Thiel S, Hey A. Diallelic polymorphisms may explain variations of blood concentrations of mannan-binding protein in Eskimos, but not in black Africans. Eur J Immunogenet 1992; 19: 403–412. 26 Minchiton R, Dean M, Clark T, Heatley S, Mulligan C. Analysis of the relationship between mannose binding lectin (MBL) genotype, MBL levels and function in Australian blood donor population. Scand J Immunol 2002; 56: 630–641. 27 Madsen H, Garred P, Thiel S. Interplay between promoter and structural gene variants control basal serum level of mannanbinding protein. J Immunol 1995; 155: 3013–3020. 28 Jacobsen S, Madsen H, Klarlund M, et al. The influence of mannose binding lectin polymorphisms on disease outcome in early polyarthritis. J Rheumatol 2001; 28: 935–942. 29 Rector A, Lemey P, Laffut W. MBL gene polymorphisms in ulcerative colitis and Crohn’s disease. Genes Immun 2002; 2: 323. 30 Garred P, Madsen H, Halberg P. MBL polymorphisms and susceptibility to infection in systemic lupus erythematosus. Arthritis Rheum 1999; 42: 2145. 31 Tsutsumi A, Sasaki K, Wakamiya N, Ichikawa K, Atsumi T, Ohtani K. Mannose binding lectin gene: polymorphisms in Japanese patients with systemic Lupus erythematosus, rheumatoid arthritis and Sjogrens syndrome. Genes Immun 2001; 2: 99–104. 32 Neth O, Jack D, Johnson M, Klein N, Turner M. Enhancement of complement activation and opsonophagocytosis by complexes of

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self-assessment

Radiology quiz Questions

Case 2 A 20 year old man presented with an asymptomatic swelling on the volar aspect of the right wrist. What are the MRI ­findings?

Case 1 A 13 year old boy presented with a history of valgus injury to the knee one week ago. What are the main imaging features and the likely diagnosis?

Figure 1

Asha Ramakrishnan FRCR is a Specialist Registrar, Musculoskeletal Centre, Chapel Allerton Hospital, Leeds Teaching Hospitals, Leeds, UK. Philip Robinson FRCR is a Consultant Musculoskeletal Radiologist, Musculoskeletal Centre, Chapel Allerton Hospital, Leeds Teaching Hospitals, Leeds, UK.

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Figure 2

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self-assessment

Case 4 A 42 year old male presented with a two month history of swelling of the right knee. He underwent surgery of the right knee six months ago. What are the relevant findings and likely diagnosis?

Case 3 This 24 year old woman gave a three month history of pain along the left proximal thigh. What do the MRI images show? What is the likely diagnosis?

Figure 3

Figure 4

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Case 5 This 14 year old boy presented with a history of trauma to the left knee. What is the demonstrated abnormality?

Case 6 This 27 year old man developed clinical signs of brachial plexus injury and Horner’s syndrome following a motor bike accident one month ago. What are the findings on axial and coronal MRI images? What is the likely diagnosis?

Figure 5

Figure 6

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Answers

Case 3 On MRI, there is evidence of previous avulsion of the iliopsoas tendon at its insertion into the lesser trochanter with accompanying ossification (arrow). There are no acute features and no significant underlying bone marrow oedema. The radiological diagnosis was an old iliopsoas avulsion with accompanying myositis ossificans. Avulsion of the lesser trochanter occurs due to hip flexion in adolescent sport participants causing failure of the apophysis. When this is seen in adults without a history of significant trauma, it should be considered as a secondary to a metastatic neoplasm unless proved otherwise. Chronic or old injuries may be associated with a protuberant mass of bone and may occasionally resemble a neoplastic or infectious process clinically.

Case 1 There is marked oedema in the medial patellar retinaculum (arrowheads) which is grossly intact. Normal lateral patellar retinaculum (arrow). There is bone marrow oedema in the lateral femoral condyle and around the femoral origin of the medial collateral ligament. Imaging features are in keeping with previous patellar dislocation. Disruption or sprain of the medial patellar retinaculum, lateral patellar tilt or subluxation, lateral femoral condyle contusion, osteochondral injury and joint effusion are the constellation of MRI findings that distinguish transient lateral patellar dislocation from other knee injuries.

Case 2 There is an accessory muscle (*) arising from the antebrachial fascia passing anterior to the ulnar artery and nerve in Guyon’s canal. This passes on the radial side of the pisiform and distally the fibers merge with the main abductor digiti minimi muscle. This represents an accessory abductor digiti minimi muscle. Accessory muscles are usually asymptomatic and represent incidental findings. Clinical presentation may be either as a swelling or due to neurovascular compression in fibroosseous tunnels.

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Case 4 There is effusion, synovitis and focal haemosiderin deposition. There is synovitis lateral to the patella, posterior to the tibiofemoral joint (arrows), posteromedially and in the medial tibiofemoral joint. Menisci and cruciate ligaments were intact. The diagnosis is pigmented villonodular synovitis of the knee with anterior synovectomy performed six months ago. Pigmented villonodular synovitis is a benign condition resulting in a hyperplastic layer of synovium containing haemosiderin with the knee most commonly affected. Typical MRI findings are low signal intensity synovial masses on all sequences due to hemosiderin and include osseous cyst like areas or erosions. The differential diagnosis of so called “black synovium” include amyloid deposition and any condition where there is repeated intraarticular haemorrhage such as haemophilia.

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Case 5 In the medial femoral condyle there is an osteochondral defect (bent arrow) with underlying cystic change and bone marrow oedema. The overlying cartilage is intact. There was no evidence of internal ligamentous disruption in the knee. An incidental finding is a well defined lesion involving the posteromedial diaphyseal region of the left femur (arrow) which is low in signal on T1 and high signal on T2 with a low signal intensity rim. The overlying periosteum, physis and epiphysis are intact. There is no significant soft tissue component. There are a few internal septations but no fluid fluid levels. The appearances are in keeping with a non ossifying fibroma. Non ossifying fibroma is a benign tumour which is usually asymptomatic. Symptoms arise only when it is large enough to cause a pathological fracture. These are mostly seen in the second decade of life. The lesions are metaphyseal or diametaphyseal and intracortical. They may have a lobulated soap bubble appearance with enlargement into the medullary cavity. They are usually oval with their long axes in the line of bone. On MRI the majority are low signal on T1w sequences while on T2w sequences 80% are hypointense and the remainder hyperintense. Marginal sclerosis appears as a hypointense rim.

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Case 6 There are pseudomeningocoeles at C7/T1 (arrow) and T1/T2 levels (T1/T2 level not shown) consistent with avulsion of the nerve roots on the left. Nerve roots seen proximally and on the contralateral side were normal. Differentiation between pre-and post-ganglionic injury is crucial in the management of brachial plexus injury and imaging can play a significant role in this. The common causes of traction brachial plexus injuries include traffic accidents especially motor bike accidents and birth injuries. A traumatic meningocoele is caused by laceration in the dural sleeve of the nerve allowing CSF to leak in an extradural location and is a sign of a preganglionic lesion. Until recently, nerve transfers were the only treatment option for preganglionic injuries. Nerve root repair and reimplantation are some of the newer techniques which are being used for preganglionic injuries.

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ADULT HIP

Hip pain in young adults and the role of hip arthroscopy

hip conditions in young adults and allowed treatment of some of these conditions, with some promising early results.

What is the objective of this article? The aim of the article is to provide the reader with an overview of the most common causes of hip and groin pain in the young adult. Inflammatory conditions, idiopathic osteoarthritis of the hip, and lower back and sacro-iliac joint pathology are excluded. The role of hip arthroscopy and its results will be discussed, highlighting individual conditions in more detail. As the literature concerning hip arthroscopy is rapidly evolving, the reader is advised to update himself regularly.

Ernest Schilders Alexandra Dimitrakopoulou J Charles Talbot Quamar Bismil

History and clinical examination The majority of pathologies that will be discussed tend to present in an age group between 20 to 40. The history should try to distinguish between hip-related conditions, trochanteric pain, and conditions causing groin pain and inguinal problems such as the sportsman’s hernia. However several of these conditions can be present at the same time, which adds to complexity of the decision making and treatment plan. Table 1 provides an overview of the most common hip and groin conditions seen in young adults. Sportsman’s herniae are uncommon in young athletes (below the age of 18 years), and hip or psoas pathology needs to be considered when they present with hip or groin pain. Hip pain is

Abstract The spectrum of recognisable hip conditions has broadened significantly over the past five years through improved imaging techniques and hip arthroscopy. Hip arthroscopy may increasingly provide new treatment options for the plethora of hip pathologies. Femoro-acetabular impingement (FAI), a condition relatively unknown until its introduction by Ganz, is now thought to be the most common cause of hip pain in the young adult with an incidence around 10–15% of the population. FAI is responsible for labral tears and chondral injuries and there is growing evidence that it is a precursor of osteoarthritis. Although there are few studies assessing open and arthroscopic treatment of FAI, the early results are promising. Labral tears may be associated with dysplasia and instability, and can be degenerative or post-traumatic. With regard to articular degeneration hip arthroscopy appears to offer some benefits in treating localized articular cartilage lesions although its role for more diffuse ­osteoarthritis is limited. It is likely that the hip arthroscopist will become a valuable addition to the staffing in an orthopaedic department.

Most common musculoskeletal conditions of hip and groin pain in young adults

Keywords dysplasia; femoro-acetabular impingement; hip arthroscopy; hip instability; hip pain; labral tear; young adults

Groin

Trochanter pain

Femoro-acetabular impingement Dysplasia

Sportman’s hernia Adductor pathology Psoas tendonitis/ bursitis Osteitits pubis

Trochanteric bursitis

Labral tear

Introduction The diagnosis of hip pain in young adults can be difficult. Over the last decade improved techniques in hip arthroscopy and MR arthrography (MRA) of the hip have broadened our knowledge of

Articular cartilage lesions.

Gluteus medius and minimus tears. Thickening posterior portion of the iliotibial band (snapping hip) Thickening anterior portion of gluteus maximus (snapping hip)

Instability Loose body Synovial chondromatosis Osteoarthritis Ligamentum teres pathology Synovitis (RA) Adhesions following surgery Transient osteoporosis

Ernest Schilders MD is a Consultant Orthopaedic Surgeon at the Orthopaedic Department, Bradford Teaching Hospitals, Bradford, UK. Alexandra Dimitrakopoulou MD is a Orthopaedic Surgeon, c/o Prof. Schilders Secretary, Bradford Teaching Hospitals, Bradford, UK. J Charles Talbot MBChB MSc(Eng) MRCS is a Specialist Registrar in Trauma and Orthopaedic Surgery, c/o Prof. Schilders Secretary, Bradford Teaching Hospitals, Bradford, UK. Quamar Bismil MBCHB Hons MRCS DipSEM MFSEM FRCS(Tr & Orth) is a Specialist Registrar in Trauma and Orthopaedics SW Thames, c/o Prof. Schilders Secretary, Bradford Teaching Hospitals, Bradford, UK.

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Hip conditions

Table 1

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abducted and flexed position, and the adductor longus is an easily palpable cord-like structure. Patients who present with adductor pain who do not have tenderness on palpation may have referred pain from the hip joint itself. Assessment of the passive range of motion of the hip is performed in the supine and prone positions. Flexion, abduction and adduction are best assessed supine whilst internal and external rotation are best examined with the patient prone. In athletes involved in sports where rotation of the hip takes place, such as golf, tennis, soccer and dance, it is not uncommon to see increased internal rotation of the stance leg due to gradual stretching out of the ilio-femoral ligament and anterior capsule. In FAI internal rotation, flexion and abduction are reduced. Similarly, a reduction in the range of motion of the hip is seen with cartilage lesions and labral tears.

often activity-related and it is important to elicit which activities reproduce the symptoms. This may be very specific, for instance a golfer who is not able to follow through because of a restricted range of motion with FAI, or a hurdler who is unable to hyperflex and internally rotate the hip jumping over hurdles. Similarly, a golfer who presents with pain on following through and striding out may have instability associated with a labral tear. Patients who have difficulties walking up a slope or have problems rising up from a deep chair may have trochanteric bursitis. Soccer players with an articular cartilage lesion can present with pain when they are sprinting and twisting and turning but might be symptomfree when running in a straight line. Patients presenting with an altered gait pattern, particularly with a tendency to walk with the foot in external rotation, wearing out the lateral part of the heel of their shoes, may have FAI. Pain on sitting and getting in an out of the car also suggests reduced flexion of the hip. Patients may complain about instability and a sensation that the hip is popping out, but pain can also occur when standing causing the patient to shift weight from the affected leg to the other one. Clicking of the hip historically refers to labral tears although the majority of tears present without this symptom, and clunking tends to refer to a snapping psoas tendon, which is usually painless. The majority of patients present with hip pain which is anterolateral and deep seated. It is not uncommon for patients to have had numerous investigations such as hysteroscopy and colonoscopy or even previous surgery which failed to improve their condition. A history of a fall on the greater trochanter may indicate a ligamentum teres injury or an articular cartilage lesion of the femoral head. Difficulties in putting on socks or shoes may be secondary to restriction of hip flexion and rotation. In contrast, inguinal pain on coughing and sneezing suggests a problem of the abdominal wall musculature such as a sportsman’s hernia. Localising hip pain can be difficult and the C-sign described by Byrd may help: hip joint pain is likely when patients hold index and thumb over the hip trochanter area. However, hip problems can also give rise to pain in the buttock area. Sacro-iliac joint problems result in a combination of lower back pain and pain radiating to the groin area. Pain and tenderness predominantly localised over the trochanteric area is usually indicative of trochanteric bursitis. Pain over the adductor area may arise from an adductor-related problem, but can sometimes be the only presentation of an intra-articular hip problem. Only the clinical assessment of musculoskeletal conditions will be discussed, excluding lower back pathology. The examiner should employ an anatomical approach when examining the hip and groin area. Gait should be assessed for an antalgic or Trendelenburg pattern and external rotation of the foot should be noted if present. Palpation of the hip joint is difficult and tenderness is often non-specific. The trochanteric region can be palpated to assess patients with suspected trochanteric bursitis and the psoas tendon can be palpated superficially, as it lies subcutaneously below the inguinal ligament lateral to the femoral nerve and artery. The psoas tendon can also be palpated in the iliac fossa; to perform this the patient is asked to lift his leg to about 15 degrees of flexion and the muscle can be palpated with the finger tips.1 The examiner should be able to reproduce a clunk from the psoas tendon by bringing the hip from flexion, abduction and external rotation (FABER) to extension, adduction and internal rotation. The adductors are best examined in the

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Additional special tests for hip pathology should be performed The impingement test (Figure 1) This is performed with the hip in flexion and slight adduction; an internal rotation manoeuvre is performed and the test is positive if the pain is reproduced. The impingement test is positive in 95% of the patients with FAI but can also be positive in patients with labral tears un-related to FAI. The FABER distance (Figure 2) This measures the distance from the lateral joint line of the knee to the examination couch when the hip is in flexion, abduction and external rotation with the foot resting on top of the ­contralateral

Figure 1 Impingement test.

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test this endpoint is absent. This test can be false positive when a patient has reduced internal rotation and the resting position of the foot is in external rotation. Some clinicians use the log rolling manoeuvre as an indicator for intra-articular hip pathology.

Imaging Initially, patients presenting with hip or groin pain should have a plain antero-posterior pelvic X-ray (Figure 3a), to diagnose or exclude stress fractures, osteoarthritis, neoplasms, ­dysplasia, FAI and slipped capital femoral epiphysis or apophyseal injuries in younger patients.

Figure 2 Faber distance is measured between the lateral joint line of the knee and the examination couch. The distance is increased in >90% of the patients with femoro acetabular impingement.

knee. This distance is increased in more than 90% of the patients with FAI but this distance needs to be interpreted with caution in patients with associated sacro-iliac joint problems. The Thomas test Detects fixed flexion deformity (FFD) of the hip. A patient with FFD of the hip may be able to lay the limb flat on the couch by extension of the pelvis through increased lumbar lordosis. Abolishing this lumbar lordosis by flexing the contralateral hip will unmask this FFD. The McCarthy hip extension sign Should help to determine if the hip pain is intra-articular. This test is performed by placing both hips in flexion. The pain will be reproduced by placing the hip in extension first in external and then in internal rotation. Anterior apprehension sign This test is performed with patients in a sitting position. The patient is asked to externally rotate the hip from a position of full passive internal rotation. Pain with extension and external rotation is a positive test and often found in patients with dysplasia. In order to assess laxity of the anterior capsule and insufficiency of the ilio-femoral ligament the Log Roll Test can be performed. With a normal hip in the supine position an internal torque is applied to the leg; once released the foot will fall into external rotation with an endpoint similar to the opposite leg. In a positive

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a X ray true pelvis. Demonstrating the cross over sign. The centeredge angle of Wiberg which is normally >25°. b X ray L hip demonstrating the cross over sign that is indicative of a retroverted acetabulum. The anterior acetabular rim is in red, the posterior acetabular rim is in black. Figure 3

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with a cam type of FAI. The alpha angles differ for men and women: the average for men is 52 degrees and for women 48 degrees. The control group with FAI had an average angle of 72 degrees. Philippon found that increased alpha angles correlate with the presence of articular cartilage lesions. Alpha angles above 60 correlate with the presence of articular cartilage lesions, whilst alpha angles above 70 usually correlate with full thickness and more extensive cartilage lesions. MRA also provides excellent details about the ligamentum teres since tears or hypertrophy can be visualised (Figure 6). In summary MRA will provide information about FAI, labral tears, and tears of the ligamentum teres, as well as assessment of articular cartilage defects and capsulo-iliofemoral ligament injury. This will aid preoperative planning and help to provide prognostic information.

The radiological features of FAI include a cam lesion, a pincer deformity or both. A cam lesion describes a deformity of the femoral head-neck junction and is characterised radiologically by increased bone seen at the head-neck junction. In the absence of a cam lesion, sclerosis of the superior aspect of the femoral neck can be seen as a secondary feature of pincer deformity. A pincer deformity describes the excess bony overhang of the acetabulum and is recognised by the cross-over sign (Figure 3b) of the anterior and posterior acetabular wall. This will however be inaccurate if the pelvic inclination is not taken into account, and therefore the plain X-ray needs to be performed in the neutral position. In a more advanced type of pincer or coxa profunda deformity, the centre of the femoral head will lie medial to the posterior acetabular wall and the teardrop will have lost its normal shape and will be a straight line. Preoperative templating should include the centre edge angle, Sharp’s angle and assessment of the acetabular version. To further assess the cam deformity, a cross table view and Lauenstein or frog view can be used, though there is a reluctance to do cross table views in the UK because of the high radiation dose delivered. Magnetic resonance imaging is the next step in the diagnostic work up, and the MRA is the investigation of choice. Toomayan2 reported 92% sensitivity when diagnosing labral tears (Figure 4) with MRA, compared to only 8% for conventional MRI. However, while MRA is an excellent test to diagnose labral tears it is less reliable in identifying articular cartilage lesions. MR will also provide information about the soft tissue structures around the hip where classic ultrasound will be of limited use. The alpha angle (Figure 5) described by Notzli3 quantifies the deformity of the femoral head neck junction with a cam deformity. The angle helps to measure the anterior margin of the waist of the femoral neck. Increased alpha angles are found in patients

Diagnostic injections When there is uncertainty about the aetiology of the pain, diagnostic intra-articular injections can be helpful; they are performed under either X-ray or ultrasound guidance. A particular diagnostic challenge is the athlete with adductor-related symptoms and with x-ray findings suggesting FAI. In this instance pubic cleft injections4 can be used to identify adductor enthesopathy as the main source of the pain. Similarly, diagnostic ultrasound guided injection of the psoas bursa can be helpful in diagnosing snapping psoas tendonitis, even if previous imaging has been ­negative.

Overview of the most common conditions Femoro-acetabular impingement FAI is a newly recognized condition and was first described by Ganz in 2003.5 The overall incidence has been estimated to be around 10 to 15% and there is growing scientific evidence that FAI leads to arthritis of the hip. There are 3 types of FAI: cam deformity, pincer deformity and a mixed type. A cam deformity refers to an increased offset of bone at the antero-lateral aspect of the head neck of the femur. The femoral head has lost its spherical shape. When the hip is flexed and internally rotated, the abnormal head impinges against the

Figure 5 The alpha angle can be demonstrated on an axial oblique MRI scan through the femoral neck. This is a patient with FAI and an abnormal alpha angle of 73°.

Figure 4 MRI arthrogram of the hip demonstrating a tear (white arrow) at the interval between labrum and articular cartilage.

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Figure 6 MRI arthrogram of the hip demonstrating a hypertrophic ligamentum teres (arrow).

labrum and acetabulum. Because of the shear forces delamination of the articular cartilage occurs gradually leading to full thickness cartilage lesions. The delamination typically starts at the junction between labrum and articular cartilage (Figure 7a and b). The main difference from idiopathic osteoarthritis, therefore, is that in FAI the cartilage degeneration starts at the acetabular side instead of the femoral side (Figure 8a and b). Cam abnormalities can occur after a minimal slipped femoral capital epiphysis or after a malunion of a neck of femur fracture. A pincer abnormality means that there is acetabular over-coverage of the femoral head. There are 2 types of pincer abnormalities: a more focal type, and coxa profunda when there is global over-coverage. With 90 degrees flexion and internal rotation, the labrum and acetabulum abut against the femoral neck. This leads to labral degeneration, labral tears and ossification of the labrum and articular cartilage damage. MR images demonstrate herniation pits (Figure 9) and sclerosis at the neck area and often a reactive cam lesion is seen more distally on the femoral neck than the classic cam deformity. In his analysis of 302 hips, Beck6 et al found 9% isolated cam lesions and 5% isolated pincer lesions, but in the majority (86%) combined lesions were seen. Ganz7 reported that a cam deformity was more common in young males, whilst a pincer abnormality was more common in middle aged females, and most hips show a mixed FAI pattern with cam predominance. At the present time no long-term results are available following surgical treatment of FAI. The current proposed treatment consists of trimming down the cam abnormality (Figure 10a and b) thereby restoring a more normal femoral head-neck offset and restoring the spherical shape of the femoral head to alleviate further abutment against the ­ acetabular rim. Treatment of the pincer deformity consists of trimming down the overhang of the acetabulum (Figure 11a and b). Associated lesions involving articular cartilage should be addressed at the same time. Labral pathology should be treated with a debridement or repair. Currently open and arthroscopic approaches are used to treat FAI. Espinosa8 reported on treatment of FAI using a surgical dislocation of the hip to perform the femoral osteoplasty and

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Figure 7 a Drawing demonstrating the typical delamination of the acetabular articular cartilage associated with cam type impingement. The delamination starts at the interval between labrum and articular cartilage. b Arthroscopic picture of the hip demonstrating a full thickness articular cartilage lesion of the hip and labral tear at the interval with acetabular articular cartilage.

rim-trimming of the acetabulum and found superior results when the intact portion of the labrum was re-fixed. Epinosa reported 94% good and excellent results at 2 year follow-up. There have only been limited outcome studies about the arthroscopic treatment of FAI. Philippon9 reported 93% of athletes returning to professional competition following arthroscopic decompression for FAI; outcome was poorer for patients who had osteoarthritis at the time of arthroscopy. Stahelin10 also reports a good outcome in patients who had an arthroscopic offset ­ 132

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Figure 9 Axial oblique MRI scan through the femoral neck demonstrating the typical herniation pits (arrow) that can occur with pincer impingement.

a Arthroscopic picture of a patient with FAI. The picture taken in the peripheral compartment demonstrates the cam deformity and fraying of the labrum. b Athroscopic view of the central compartment showing delamination of the articular cartilage and a small grade 4 zone adjacent to the labrum. Figure 8

restoration in FAI. He showed that it was possible to do an accurate resection of the cam deformity by reducing a preoperative mean alpha angle of 75 to a postoperative mean angle of 54 and also reported a good outcome in patients with no or mild osteoarthritis. It is therefore crucial that we will be able to stage FAI. Currently we are unaware of the ideal time to intervene for FAI, but we do know that patients with FAI and diffuse ­osteoarthritis have a poorer outcome at present. Future research should address what the outcome is in patients with early delamination of the articular cartilage or full thickness tears and help us to determine at what stage it might be reasonable to offer curative surgical treatment for FAI. Ganz7 advocates restoring the normal anatomy at an early stage before major cartilage damage is ­present. Labral tears Most patients present with a gradual onset of groin and hip pain which they class as moderate to severe. Only a small percentage present with a labral tear as a result of major trauma. Most

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a X ray demonstrating the cam abnormality/osteophyte at the femoral head neck junction. b X ray after resection of the cam deformity. Figure 10

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The evidence suggests that simple arthroscopic debridement of a labral tear can only be expected to succeed when there is no associated pathology such as FAI, chondral lesions or dysplasia. Otherwise, it would seem that the future for labral tears is arthroscopic repair. Hines14 reports an improvement of function and high patient satisfaction reviewing 52 patients which had undergone a labral repair (Figure 12a–c). This study suggests a role for labral repairs in pain management and joint preservation, provided that the skeletal anatomy is normal. Articular cartilage lesions Articular cartilage lesions can be post-traumatic and the result of a fall, but the majority of articular cartilage lesions are associated with FAI. Arthroscopic treatment options include resection of unstable chondral flaps and microfracture of a full thickness cartilage lesions. Crawford15 reported encouraging early results following this technique. Philippon16 reported 95 to 100% coverage of the articular defect in eight out of nine patients when a second look arthroscopy was performed on average 20 months following arthroscopy with microfracture. Extensive chondral damage is associated with a less impressive outcome. Kim17 reported on the results of arthroscopic debridement for early osteoarthritis. Two groups were assessed; the first had X rays and degenerative changes of the labrum and cartilage seen on MRA and at arthroscopy; the second group also had degenerative changes on the plain X rays. A good outcome was reported after 50 months except in the cases where FAI was present. Dysplasia We can define hips with a centre edge angle less then 20 degrees as dysplastic. This condition predominantly affects females. Patients often present with an acute onset of pain during walking or running, intermittent locking, painful clicking and symptoms of instability and giving away. It is suggested that labral tears are responsible for hip pain in patients with dysplasia, the pain occurring when the torn labrum is incarcerated in the joint space. Yamamoto18 reported on the treatment of labral tears with limbectomy. He found that most tears were bucket handle tears located in the antero-superior part of the acetabulum. After an eight year follow up rapid progression to osteoarthritis was not observed. The function of the labrum in association with the maintenance of the stability of the hip joint remains unclear. The successful outcome of labral limbectomy in patients with dysplasia contradicts the results of Bonnomet.

a X ray demonstrating the cross over sign and the pincer abnormality of the hip. b X ray following resection of the pincer abnormality. The X ray demonstrates the absence of the cross over sign indicating an adequate resection. Figure 11

patients report activity-related symptoms. The majority have a positive impingement sign on clinical examination. Labral tears are increasingly diagnosed with the use of MRA and arthroscopy. Causes for labral tears are FAI, degenerative tears, dysplasia, instability and post-traumatic tears. The most common cause of labral tears is FAI. Treatment consists of debridement of the tear or a labral repair depending on the type of tear. Streich11 reports excellent results after resection of labral tears if there is no radiographical evidence of dysplasia. May12 reported on a series of 5 patients who had persistent pain in the hip following isolated arthroscopic debridement of labral tears. All these patients were found to have cam-type FAI and had symptomatic improvement following osteoplasty of the femoral head-neck junction. Bonnomet13 reported on 12 patients with labral tears treated with an arthroscopic debridement. Only 5 patients had isolated tears and 7 patients had either associated cartilage lesions or osteoarthritis of the hip. In the latter group 3 patients subsequently required a total hip replacement. In the group of 5 patients only 3 had symptomatic relief at 4 year ­follow up. The two patients who failed to improve had dyplasia.

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Ligamentum teres pathology Ligamentum teres ruptures have increasingly been recognized as a source of hip pain. Byrd19 reported a 15% incidence of lesions (41 patients) of the ligamentum teres in the patients he arthroscoped. The pathology consisted of full and partial ruptures, hypertrophy and degenerative changes and 50% of the patients experienced mechanical symptoms such as catching, popping and locking, others just experienced pain. Traumatic rupture usually results from major trauma such as a ­dislocation, but the condition can also result from a twisting injury. In Byrd’s series the diagnosis of ligamentum teres lesions was only made in 2 of 41 patients preoperatively. With a high index of ­ suspicion, ­especially after significant trauma, allied with constantly improving imaging techniques, the diagnosis can now be reliably made. 134

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a Drawing demonstrating a labral repair of the hip. The suture anchor is placed parallel to the articular surface. b X ray taken intraoperatively demonstrating the position of the drill guide and the arthroscope at the anterolateral acetabular rim. c Arthroscopic view of a labral repair of the hip. Figure 12

release of the iliotibial band (ITB), resection of the bursa and decompression of the greater trochanter. The “snapping hip” syndrome results when the ITB subflexes over the greater trochanter. When the hip is flexed the band slides over the greater trochanter. For resistant cases a Z type release of the ilio-tibial tract is effective.

Instability The classic example of hip instability is the post-traumatic posterior dislocation. This is associated with labral tears and chondral lesions. It is advisable to follow the patient up for osteonecrosis. Non-traumatic laxity and instability of the hip can occur in patients with collagen disorders such as Ehlers-Danlos, Marfan’s or Down’s syndrome, arthrogryposis multiplex congenita, developmental dysplastia of the hip and for no obvious reason.

Tears of the gluteus medius and minimus20 Are newly recognised conditions and share similarities with rotator cuff tears in the shoulder. Gluteal tears are associated with increasing age. On clinical examination there is often a slight Trendelenburg gait, and pain and weakness with resisted abduction of the hip compared with the contralateral side. Resistant cases can be treated arthroscopically. The gluteus medius tendon

Snapping hip and greater trochanteric pain Trochanteric bursitis Is a well know condition. The history and examination are fairly typical as is the response to steroid injections. Recalcitrant trochanteric bursitis can be successfully treated with arthroscopic

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can be inspected in a similar way to the rotator cuff and tears can be repaired with suture anchors.

associated pathologies and return to sport following arthroscopic decompression. Knee Surg Sports Traumatol Arthrosc 2007; 15: 908–14. 10 Stahelin L, Stahelin T, Jolles BM, Herzog RF. Arthroscopic offset restoration in femoro-acetabular cam impingement: accuracy and early clinical outcome. Arthroscopy 2008; 24: 51–57. 11 Streich NA, Gotterbarm T, Jung M, Schmitt H. Outcome of arthroscopic resection of labral tears. Z Orthop Unfall 2007; 145: 633–8. 12 May O, Matar WY, Beaule PE. Treatment of failed arthroscopic acetabular labral debridement by femoral chondro-osteoplasty: a case series of five patients. J Bone Joint Surg Br 2007; 89: 595–8. 13 Bonnomet F, Lefebvre Y, Clavert P, et al. Arthroscopic treatment of acetabular labrum lesions: a series of 12 patients with a 4-year follow up. Rev Chir Orthop Reparatrice Appar Mot 2000; 86: 787–93. 14 Hines S, Philippon M, Kuppersmith D, Maxwell B. Early results of labral repair. Arthroscopy 2007; 23(6): e9–e10. 15 Crawford K, Philippon M, Sekiya J, Rodkey W, Steadman J. Microfracture of the hip in athletes. Clin Sports Med 2006; 25: 327–35. 16 Philippon M, Schenker ML, Briggs K, Maxwell RB. Can microfracture produce repair tissue in acetabular chondral defects? Athroscopy 2008; 24: 46–50. 17 Kim KC, Hwang DS, Lee CH, Kwon ST. Influence of femoroacetabular impingement on results of hip arthroscopy in patients with early osteoarthritis. Clin Orthop Relat Res 2007; 456: 128–32. 18 Yamamoto Y, Ide T, Nakamura M, Hamada Y, Usui I. Arthroscopic partial limbectomy in hip joints with acetabular hypoplasia. Arthroscopy 2005; 21: 586–91. 19 Byrd JW, Jones KS. Traumatic rupture of the ligamentum teres as a source of hip pain. Arthroscopy 2004; 20: 385–91. 20 Shindle M, Voos J, Heyworth B, et al. Hip arthroscopy in the athletic patient: current techniques and spectrum of disease. J Bone Joint Surg Am 2007; 89(suppl 3): 29–43. 21 Milgram JW. Synovial chondromatosis: a histopathological study of thirty cases. J Bone Joint Surg 1977; 59A: 792–801.

Snapping psoas Diagnosis is made by clinical examination because very often the imaging can be negative. Treatment consists of ultrasound-guided injections and are a good predictor of the outcome that can be achieved with an arthroscopic release. An endoscopic release in the peripheral compartment of the hip may relieve symptoms. Synovial chondromatosis Synovial chondromatosis is a synovial proliferative disease in which cartilaginous or osteocartilaginous metaplasia occurs within the synovial membrane of joints, bursae, or tendon sheaths. The disease may be intra- or extra-articular. Milgram21 described three phases of the disease: early, with synovial chondrometaplasia but no loose bodies; transitional, with active synovial disease and loose bodies; and late, with loose bodies but no synovial disease. Both synovial disease and loose bodies can be treated arthroscopically. ◆

References 1 Holmich P. Longstanding groin pain in sportspeople fall into three primary patterns, a clinical entity approach: a prospective study of 207 patients. Br J Sports Med 2007; 41: 247–52. 2 Toomayan GA, Holman WR, Major NM, Kozlowicz SM, Vail TP. Sensitivity of MR arthrography in evaluation of acetabular labral tears. AJR Am J Roentgenol 2006; 186: 449–53. 3 Notzli HP, Wyss TF, Stoecklin CH, Schmid MR, Treiber K, Hodler J. The contour of the femoral head-neck junction as a predictor for the risk of anterior impingement. J Bone Joint Surg Br 2002; 84: 556–60. 4 Schilders E, Bismil Q, Robinson P, O`Connor P, Gibbon WW, Talbot JC. Adductor related groin pain in competitive athletes. Role of adductor enthesis, magnetic resonance imaging, and entheseal pubic cleft injections. J Bone Joint Surg Am 2007; 89: 2173–8. 5 Ganz R, Parvizi J, Beck M, Leunig M, Notzli H, Siebenrock KA. Femoroacetabular impingement: a cause for osteoarthritis of the hip. Clin Orthop Relat Res 2003; 417: 112–20. 6 Beck M, Kalhor M, Leunig M, Ganz R. Hip morphology influences the pattern of damage to the acetabular cartilage: femoroacetabular impingement as a cause of early osteoarthritis of the hip. J Bone Joint Surg Br 2005; 87: 1012–8. 7 Ganz R, Leunig M, Leunig-Ganz K, Harris WH. The etiology of osteoarthritis of the hip: an integrated mechanical concept. Clin Orthop Relat Res 2008; 466: 264–72. 8 Espinosa N, Beck M, Rothenfluh DA, Ganz R, Leunig M. Treatment of femoro acetabular impingement: preliminary results of labral fixation. Surgical technique. J Bone Joint Surg Am 2007; 89: 36–53. 9 Philippon M, Schenker M, Briggs K, Kuppersmith D. Femoroacetabular impingement in 45 professional athletes:

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Research directions Does FAI lead to osteoarthritis of the hip? Can open or arthroscopic treatment of FAI delay or stop the progress to FAI? When do we have to intervene with patients with FAI? Is there a role for screening? How do we treat labral tears and when can we do a debridement and when a repair? What is the role for autologous grafting to substitute an absent labrum?

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Trauma

Stress fractures

fracture’.3 Since then, much of the published literature on stress fractures relates to military recruits because of the high incidence and because they are an easy to study cohort of athletes. Milgrom et al1 conducted a prospective study of 295 Israeli military recruits undergoing 14 weeks training. They reported a 31% incidence of stress fracture. This exceptionally high incidence is probably because recruits were encouraged to report any symptoms of possible stress fracture and all recruits with suspected stress fracture underwent a bone scan. It is likely that some of these would not ordinarily be diagnosed as having had a stress fracture. Other studies of military recruits have reported lower incidences. Royal Marine Commando recruits were found to have a 7% incidence of stress fracture over 30 weeks training4 and an incidence of 4% has been reported for US Marine recruits over 12 weeks of basic training.5 Studies reporting the incidence of stress fracture in civilian athletes are probably much less accurate than those reporting on military recruits because they are a disparate group. While there are reports in the sports medicine literature of stress fractures occurring in almost all parts of the skeleton and in almost all types of sport, running athletes appear to have the highest incidence.2 A survey of recreational athletes reported a prevalence (not incidence) of 8% and 13% in male and female athletes respectively6 and it has been reported that 10% of all civilian sports injuries are stress fractures.7 The timing of stress fracture occurrence after initiation of training is not predictable. There is a lag period between osteoclastic resorption and osteoblastic osteoid formation. Theoretically, the athlete is vulnerable to stress fracture during this period of relative osteopenia, which is thought to be maximal approximately six weeks into training.4 However, it is clear that many other factors influence the timing of stress fracture presentation. Talbot et al found that the peak incidence in British Army recruits occurred between 13 and 16 weeks.8 Ross and Allsopp found that the peak incidence in Royal Marine Commando recruits occurred in the week of maximal training load (week 29.)4 Milgrom et al’s study of Israeli Defence Force recruits found that 53% of stress fractures occurred in the first four weeks and only 15% after the eighth week of training.1 This remarkable difference in distribution presumably reflects the different training regimens of the British and Israeli Armed Forces. The part of the skeleton at risk of stress fracture clearly depends on the activity undertaken. The vast majority of stress fractures occur in the lower limb. Matheson et al2 reported that the tibia (Figure 2) was the most common site in civilian athletes (49.1%), followed by the tarsals (25.3%), metatarsals (8.8%) and femur (7.2%). Milgrom et al2 reported a stress fracture distribution in military recruits of 51.2% tibial, 29.8% femoral, and 7.6% in the metatarsals. Interestingly, a large number of the femoral fractures in Milgrom’s study were asymptomatic and diagnosed incidentally in recruits receiving a bone scan for skeletal pain at another site.

Mark R Philipson Paul J Parker

Abstract Stress fractures are a major cause of morbidity in the athletic and military population. Long distance running and female sex are major risk factors. Clinicians must have a high index of suspicion as early diagnosis and treatment is crucial. Provocative tests such as one-foot hopping are helpful in diagnosis. MRI (or isotope bone scanning) is much more useful than plain radiography. Treatment is usually by avoidance or modification of the stressful activity, but some fractures may need internal fixation and possibly bone grafting.

Keywords military recruit training; overuse injury; sports injury; stress fracture

Introduction Stress fractures are the result of cyclical loading with stresses below the ultimate strength of the bone, i.e. sub-threshold loading. They are described as either insufficiency fractures or fatigue fractures. The former are fractures of abnormally weak or inelastic bone, the latter failure of normal bone, but there is often some overlap between the two types of stress fracture, e.g. in thin female athletes with oligomenorrhoea. Stress fractures are a significant cause of morbidity in the athletic and military population. An incidence as high as 31%1 has been reported in military recruits and it is estimated they make up 10% of all athletic injuries.2 Prompt diagnosis and appropriate management is very important to avoid prolonged time away from training and progression to catastrophic fracture. This article discusses the pathophysiology, risk factors, ­diagnosis, and management of stress fractures.

Epidemiology Military service and stress fractures are closely linked. The first report of a stress fracture in the literature was in 1855. The Prussian Army Physician Briethaupt described the syndrome of a painful swollen foot associated with marching hence ‘march

Mark R Philipson MBChB MRCS FRCS(Tr and Orth) is a Specialist Registrar in Trauma and Orthopaedics at the York District Hospital, York, UK.

Pathophysiology

Paul J Parker FIMC FRCSEd(Orth) is a Consultant Orthopaedic Surgeon at the Friarage Hospital, Northallerton and a Senior Lecturer in Orthopaedics at the Academic Department of Military Surgery and Trauma, UK.

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Bone is a dynamic tissue constantly remodelling under the influence of multiple hormonal and mechanical factors. There is a balance between bone resorption, carried out by osteoclasts, 137

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Training surface Load through the lower limb is related to the ground reaction force. It therefore follows that more shock absorbing elastic ground or training shoes should reduce the risk of stress fracture. A study has shown that athletes experience lower strains within the tibia when running on a treadmill compared to running on asphalt.14 Running shoes should be replaced every 6 months, especially with cheaper EVA foam shoes, as the foam compacts, losing shock absorption, over time.

and bone synthesis, carried out by osteoblasts. Bone has a ­remodelling response to mechanical stress so that the greatest amount of bone is laid down in areas of greatest applied stress (Wolff’s Law). Piezoelectric currents produced by bone under strain are thought to be responsible for stimulating this remodelling response to stress.9 Mature bone is composed of a matrix of parallel stress­oriented collagen fibres arranged in sheets known as lamellae. In cortical bone these are organised in concentric rings to form cylindrical structures known as osteons or Haversian systems. Cement lines exist between the osteons which are an area of relative ­weakness.10 When bone is subject to repetitive daily subthreshold loading, microcracks may occur within cement lines: the normal remodelling process repairs these cracks. However, if the bone continues to be subjected to high stresses then crack propagation occurs. If crack propagation outstrips repair then over a period of time a painful established stress fracture will develop. Given time, bone which is subjected to increased stress will lay down more bone. It has been shown that during this process, osteoblastic activity lags behind resorptive osteoclastic activity.11 Bone that is subject to a sudden increase in repetitive stress is particularly vulnerable to stress fracture during this lag period. Military recruit training and poorly designed ‘get fit quick’ training programs are ­examples of this phenomenon.

Intrinsic factors Bone anatomy The ability of a cylinder to resist bending and torsional stress is proportional to the fourth power of the cylinder radius. It follows that a wider long bone is stronger than a thin long bone. Studies have demonstrated that small tibial bone width, such as in females, correlates with stress fracture risk.15 Sex Women are at increased risk of stress fracture16 for a number of reasons. They have narrower bones and lower bone mineral density. Women training for events where low body weight is considered advantageous, such as gymnastics and long distance running, are particularly at risk from a syndrome known as the Female Athlete Triad: disordered eating, amenorrhoea, and osteoporosis.17 Inadequate calorie intake leads to menstrual dysfunction and low basal oestrogen levels.12 This causes a diminution in bone density. Multiple studies have shown an increased incidence of stress fracture in women with menstrual ­dysfunction.18–20 Studies have reported a high incidence of pubic ramus stress fracture (Figure 1) in female military recruits and it has been suggested that this is because of abnormal stresses created by over-striding in an attempt to match the stride length of taller male recruits during marching exercises.21 Hill et al22 reported a decrease in incidence of pubic stress fracture after the marching stride length was decreased from 30 to 27 inches.

Risk factors Risk factors for stress fractures are either extrinsic or intrinsic. Extrinsic factors pertain to the environment in which the athlete trains and intrinsic factors pertain to the athlete. Extrinsic risk factors Training regimen Activities with the highest loads for the most number of cycles confer the highest risk of stress fracture such as long distance running which has been shown to have an increased stress fracture risk.6 Carrying a weighted backpack, as in military training, increases the risk further. Abrupt increases in training intensity without adequate rest days also predisposes to stress fracture for a number of reasons. As osteoblastic bone synthesis lags behind osteoclastic bone resorption, hence there is period of decreased bone strength following increased bone stress. Microcracks form along cement lines. This can be seen on MRI scanning as bone oedema or ‘stress response’. If the athlete does not rest sufficiently to allow repair of the cracks, then crack propagation occurs and an established stress fracture can develop. Training with fatigued muscles increases risk of stress fracture12 because muscles play a vital role in reducing load through the skeleton. For example, the spine is subjected to loads several times body weight during sport, yet in vitro studies have shown that the spinal column can buckle with loads as little as 9 kg in the absence of normal musculature.13 Research at the Commando Training Centre Royal Marines found that 7% of recruits suffered some sort of stress fracture during their 30 week training. Training programmes where therefore altered to incorporate more rest days and specific strengthening exercises early on in training following which the proportion of recruits suffering stress fractures dropped ­significantly to 3.8%.14

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Nutrition Inadequate calcium and vitamin D intake may increase the risk of stress fracture.12 Inadequate caloric intake is probably of greater relevance in athletes, as dietary energy restriction has been found to be accompanied by reduced bone mass.23

Figure 1 Stress fracture of the right inferior pubic ramus in a female military recruit.

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they have undergone an abrupt increase in training and in women whether they have had any disruption of their menstrual cycle. Typically, the athlete describes an insidious onset localised dull aching pain which is worse with activity. On examination, the fracture site will normally be tender and percussion of the bone at a site away from the fracture may reproduce the pain. A high index of suspicion is necessary, especially for femoral stress fractures which cannot be directly palpated and frequently present with poorly localised pain. Finestone et al28 report a case of asymptomatic femoral stress fracture presenting as a displaced unstable mid-shaft fracture. They suggest that femoral stress fracture often presents with very non-specific symptoms such as thigh stiffness, groin and knee pain. Provocative tests such as pain on hopping can be helpful when establishing a diagnosis of femoral stress fracture.2 Stress fractures can occur in the upper limb in throwing athletes and rowers (Table 1). Plain radiographs can be useful because they are very specific and if a stress fracture is seen then further imaging is rarely necessary. However, plain radiographs can be falsely negative for up to three months after symptom onset.29 Isotope bone scans (scintigrams) are very sensitive for stress fracture; some authors define stress fracture by the presence of scintigraphic abnormality,30 and a normal scintigram usually excludes stress fracture. However, scintigrams are not very specific and give a radiation exposure of approximately 3mSv (a chest radiograph typically delivers 0.04mSv.)31 Magnetic resonance imaging is both sensitive and specific for stress fracture (Figure 3) and involves no radiation exposure. For further information on imaging of stress fractures, the reader is referred to Miller’s article in Current Orthopaedics April 2003.32

Figure 2 Stress fracture of the proximal tibia.

Fitness A number of studies have demonstrated that the aerobic fitness and previous sporting experience of military recruits prior to starting training are protective against stress fracture.5,18 This is likely to be because their skeleton is better adapted to stress and because they suffer less muscle fatigue.

Management The most important aspect of management is early diagnosis. The vast majority of stress fractures can be successfully treated non-operatively by avoidance of the stressing activity.29,33 The general principles of non-operative treatment are to avoid activity levels which reproduce pain and a very gradual return to training. For example by using special buoyancy jackets, athletes can return to ‘running’ training in a swimming pool.

Smoking A survey of 915 female military recruits found that those who smoked one or more cigarettes in the year prior to commencement of basic training were more likely to suffer a stress fracture, with an increased relative risk of 2.2.24 Non-steroidal anti-inflammatory drugs There is theoretical evidence based on animal studies that nonsteroidal anti-inflammatory drugs (NSAIDs) can have an adverse effect on fracture healing.25,26 The evidence available regarding the effect in humans is inconclusive.27 Until better quality evidence is available it is reasonable to minimise the use of NSAIDs during the management of stress fractures.

Reported locations of stress fracture in the upper body Scapula Rib Medial clavicle C7/T1 spinous processes Humeral shaft Olecranon Ulna shaft Radius Scaphoid Metacarpal

Diagnosis Early diagnosis is important to minimise not only time away from training but to preclude non-union or a catastrophic displaced fracture. Delay in diagnosis can lead to medical discharge from the Services4,8 for military personnel or early retirement from sport. A thorough history should establish whether the athlete has been exposed to any of the risk factors discussed above; whether

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Table 1

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Ivkovic et al34 have published an algorithm for non-operative management of stress fractures of the femoral shaft (Figure 4) which can be applied with modification to other fracture sites. Most authors recommend operative treatment for cases of delayed union or failed non-operative treatment.33 However, the evidence in the literature for different modes of operative ­treatment is poor and largely confined to small case series. The aims of surgical treatment are to improve the mechanical environment for fracture healing with a fixation device and/or improve the biological environment with debridement or bone graft. Treatment of the commoner stress fracture patterns is discussed below.

Specific regional injuries Femoral neck Femoral neck fractures constitute 8% of all stress fractures in military personnel,8 but the incidence appears to be less in civilian athletes.2 As always, the key to management is early diagnosis; the diagnosis should be considered in any high risk patient with

Figure 3 Stress fracture of the sacral ala.

DIAGNOSIS

SYMPTOMATIC PHASE 3 weeks non-weightbearing

positive

TESTS* negative

ASYMPTOMATIC PHASE 3 weeks walking, swimming, upper body work

positive

TESTS

negative

BASIC PHASE 3 weeks cycling, light weights, graduated running

positive

TESTS negative

RESUMING PHASE Gradual resumption of normal training *Provocative tests for the presence of pain: the fulcrum test where a bending stress is applied to the fracture, and the hopping test. Figure 4 Algorithm for the management of stress fractures of the femoral shaft Ivkovic et al 2006.34

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groin pain. Femoral neck fractures in athletes usually occur in the medial cortex which is under compression. Undisplaced fractures are stable and can be successfully treated non-­operatively with an initial period of non-weightbearing.8,33 Displaced fractures should always be reduced and fixed surgically with large cannulated screws. Stress fractures can affect the lateral cortex which is subject to tensile forces, but this is usually an insufficiency type fracture occurring in older patients. These lateral stress fractures are associated with a high risk of displacement and avascular necrosis of the femoral head.33 Therefore, even undisplaced fractures of the lateral cortex should normally be internally fixed. Figure 5 shows an algorithm for the management of femoral neck stress fractures (FNSF.)8 In the series reported by Talbot et al,8 50% of military personnel presenting with femoral neck stress fracture were eventually discharged from the military on medical grounds Figure 6.

in a randomised controlled trial. Overall, no difference in time to healing was detected between placebo and treatment groups, though they did observe an improved time to healing in the more ‘severe’ fractures. The less common stress fracture affecting the anterior tibial cortex is more difficult to manage because the incidence of delayed union is much higher.37 This is probably because the anterior cortex is subject to repetitive tensile rather than compressive loading. Non-operative management will normally take at least six months38 so early surgical management may be an option. Borens et al39 report good results with anterior tension band plating in a four high performance female athletes. Metatarsals The metatarsals most commonly affected by stress fractures are the second and third – the classic ‘march fracture.’ These are prone to stress fracture because they have a thin shaft but are subject to high levels of strain during the propulsive phase of running. They usually do well with non-operative management. Stress fractures of the fifth metatarsal typically occur at the proximal junction of diaphysis and metaphysis and have a higher incidence of delayed and non-union.33 Torg et al outlined guidelines for management of these difficult fractures.40 They suggest fractures which appear ‘acute’ radiologically with a sharp fracture line and no sclerosis can be treated non-operatively in a nonweightbearing cast for six to eight weeks. They concluded that fractures with radiological evidence of intramedullary sclerosis

Tibial shaft Approximately 50% of all stress fractures in runners and military recruits occur in the tibial shaft.1,2 They can occur anywhere in the tibial shaft, but most commonly affect the posteromedial cortex.33 The majority can be successfully managed non­operatively; the use of a pneumatic leg brace has been shown to be ­helpful.35 Beck et al36 investigated the effect of capacitively coupled electric fields on healing of posteromedial tibial stress fractures

Hip/groin pain > 3 days

High risk factors

yes

Consider other diagnosis

No FNSF

no

Urgent plain films & MRI

Plain films

FNSF FNSF

Normal

FNSF diagnosed

FNSF

MRI

Warn of prognosis* No FNSF Displaced

Operative treatment

Undisplaced

Non-operative treatment

Consider other diagnosis

* 50% risk of medical discharge in military personnel Figure 5 Algorithm for the management of femoral neck stress fractures (FNSF) Talbot and Parker.

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3 Briethaupt MDS. Zur pathologie des menschlichen fusses. Medizin Zeitung 1855; 24: 169–71, 175–177. 4 Ross RA, Allsopp A. Stress fractures in Royal Marines recruits. Mil Med 2002; 167: 560–5. 5 Shaffer RA, Brodine SK, Almeida SA, et al. Use of simple measures of physical activity to predict stress fractures in young men undergoing a rigorous physical training programme. Am J Epidemiol 1999; 149: 236–42. 6 Brunet ME, Cook SD, Brinker MR, et al. A survey of running injuries in 1505 competitive and recreational runners. J Sports Med Phys 1990; 30(3): 307–15. 7 Hulkko A, Orava S. Stress fractures in athletes. Int J Sports Med 1987; 8: 221–6. 8 Talbot JC, Cox G, Townend M, Langham M, Parker PJ. Femoral neck stress fractures in military personnel. EFORT May 2007. 9 Carter DR, Caler WE. A cumulative damage model for bone fracture. J Orthop Res 1985; 3(1): 84–90. 10 Bates P, Ramachandran M. Bone injury, healing and grafting. In: Ramachandran M, ed. Basic orthopaedic sciences. London: Hodder Arnold 2007; p. 123–34. 11 Pouilles JM, Bernard J, Tremollires F, Louvet JP, Ribot C. Femoral bone density in young male adults with stress fractures. Bone 1989; 192: 105–8. 12 Narvani AA, Hsu B, Wilson L. Biomechanics of the spine. In: Ramachandran M, ed. Basic orthopaedic sciences. London: Hodder Arnold, 2007; p. 180–6. 13 Milgrom C, Finestone A, Segev S, et al. Are overground or treadmill runners more likely to sustain tibial stress fractures? Br J Sports Med 2003; 37: 160–3. 14 Giladi M, Milgrom C, Simlin A, et al. Stress fractures and tibial bone width: a risk factor. J Bone Joint Surg 1987; 69-B: 326–9. 15 Jones BH, Thacker SB, Gilchrist J, et al. Prevention of lower extremity stress fractures in athletes and soldiers: a systematic review. Epidemiol Rev 2002; 24: 228–47. 16 Nattiv A, Agostini R, Drinkwater B, et al. The female athlete triad: the inter-relatedness of disordered eating, amenorrhoea, and osteoporosis. Clin Sports Med 1994; 13: 405–18. 17 Pepper M, Akuthota V, McCarty EC. The pathophysiology of stress fractures. Clin Sports Med 2006; 25: 1–16. 18 Winfield AC, Moore J, Bracker M, et al. Risk factors associated with stress reactions in female marines. Milit Med 1997; 162: 698–702. 19 Bennell KL, Malcolm SA, Thomas SA, et al. Risk factors for stress fracture in track and field athletes: a twelve month prospective study. Am J Sports Med 1996; 24: 810–8. 20 Warren MP, Brooks-Gunn J, Hamilton LH, et al. Scoliosis and fractures in young ballet dancers: relation to delayed menarche and secondary amenorrhoea. N Engl J Med 1986; 314: 1348–53. 21 Oxburn MS, Nichols JW. Pubic ramus and adductor insertion stress fractures in female basic trainees. Milit Med 1981; 146: 332–4. 22 Hill PF, Chatterji S, Chambers D, Keeling JD. Stress fractures of the pubic ramus in female recruits. J Bone Joint Surg 1996; 78-B: 383–6. 23 Ihle R, Loucks AB. Dose-response relationships between energy availability and bone turnover in young exercising women. J Bone Miner Res 2004; 19: 1231–40. 24 Altarac M, Gardner JW, Popovich RM, et al. Cigarette smoking and exercise-related injuries among young men and women. Am J Prev Med 2000; 18: 96–102.

Figure 6 Stress fracture of the 3rd MT with surrounding tissue oedema.

are best treated surgically with curettage of the medullary canal, tibial bone graft and a non-weightbearing cast for six weeks. Other authors have described good results with simple intramedullary screw fixation.33,41

Prevention In summary, trainers, athletes and orthopaedic surgeons must be aware of the risk of stress fracture. Training intensity should be built up gradually with rest periods built in to the regimen. Signs of stress fracture should be identified and treated early. The experience of Commando Training Centre Royal Marines8 demonstrates that a more physiologically progressive training regimen reduces the incidence of stress fracture. Female athletes and their trainers should be aware of the high risk associated with menstrual dysfunction. Diet should be optimised to avoid oligomenorrhoea. Early MRI scanning is the key to diagnosis, prognosis and intervention. Future research Does early access MRI reduce the time out from training due to stress fractures in military personnel? Do NSAIDs have an adverse effect on stress fracture healing in humans? Do osteoinductive agents such as BMP accelerate stress fracture healing? Is the converse piezoelectric field effect of an applied electric field beneficial in selected cases? ◆

References 1 Milgrom C, Giladi M, Stein M, et al. Stress fractures in military recruits. J Bone Joint Surg 1985; 67-B: 732–5. 2 Matheson GO, Clement DB, McKenzie DC, et al. Stress fractures in athletes. Am J Sports Med 1987; 15: 46–58.

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34 Ivkovic A, Bojanic I, Pecina M. Stress fractures of the femoral shaft in athletes: a new treatment algorithm. Br J Sports Med 2006; 40: 518–20. 35 Swenson Jr. EJ, DeHaven KE, Sebastienelli WJ, et al. The effect of a pneumatic leg brace on return to play in athletes with tibial stress fractures. Am J Sports Med 1997; 25: 322–8. 36 Beck BR, Matheson GO, Bergman G, et al. Do capacitively coupled electrical fields accelerate tibial stress fracture healing? Am J Sports Med 2007; 36: 545–53. 37 Orava S, Sulkko A. Delayed union and non-unions of stress fractures in athletes. Am J Sports Med 1988; 16: 378–82. 38 Rettig AC, Shelbourne KD, Beltz HF, et al. The natural history and treatment of delayed union and non-union stress fractures of the anterior cortex of the tibia. Am J Sports Med 1988; 16: 250–5. 39 Borens O, Sen MK, Huang RC, et al. Anterior tension band plating for anterior tibial stress fractures in high performance female athletes: a report of 4 cases. J Orthop Trauma 2006; 20: 425–30. 40 Torg JS, Balduini FC, Zelko RR, et al. Fractures of the base of the fifth metatarsal distal to the tuberosity. Classification and guidelines for non-surgical and surgical management. J Bone Joint Surg 1984; 66A: 209–14. 41 Rosenberg GA, Sferra JJ. Treatment strategies for acute fractures and non-unions of the proximal fifth metatarsal. J Am Acad Orthop Surg 2000; 8: 332–8.

25 Allen H, Wase A, Bear W. Indomethacin and aspirin: effect of nonsteroidal anti-inflammatory agents on the rate of fracture repair in rats. Acta Orthop Scand 1980; 51: 595–600. 26 Altman RD, Latta LL, Kear R, et al. Effect of nonsteroidal antiinflammatory drugs on fracture healing: a laboratory study in rats. J Orthop Trauma 1995; 9: 392–400. 27 Wheeler P, Batt ME. Do non-steroidal anti-inflammatory drugs adversely affect stress fracture healing? A short review. Br J Sports Med 2005; 39: 65–9. 28 Finestone AS. The completely asymptomatic displaced femoral stress fracture: a case report and review of the literature. Milit Med 2006; 171: 37–9. 29 Tuan K, Wu S, Sennett B. Stress fractures in athletes: risk factors, diagnosis, and management. Orthopedics 2004; 27: 583–91. 30 Jones BH, Harris JM, Vinh TN, Rubin C. Exercise-induced stress fractures and stress reactions of bone: epidemiology, etiology and classification. In: Pandolf KB, ed. Exercise and sports sciences reviews. American college of sports medicine series; vol. 17. Baltimore: Williams and Wilkins, 1989; p. 379–422. 31 Also available from: http://irb.ucsd.edu/RadiationEquivalents.pdf. 32 Miller JH. The radiological aspects of stress fractures and chronic stress injuries. Curr Orthop 2003; 17: 150–5. 33 Puddu G, Cerullo G, Selvanetti A, De Paulis F. Stress fractures. In: Harries M, Williams C, Stanish WD, Micheli LJ, eds. Oxford textbook of sports medicine. Oxford University Press, 1995, p. 546–63.

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Patello-femoral arthrosis F Rayan FS Haddad

Abstract Patello-femoral arthrosis is common but poorly understood and its pathophysiology and even clinical significance remain controversial. The aetiology, diagnosis and management are reviewed. To achieve a successful treatment outcome it is vital to differentiate between global and patello-femoral knee arthrosis, requiring careful clinical and radiological assessment before selecting appropriate treatment for each patient.

Keywords arthrosis; patella; patello-femoral; treatment

Introduction The prevalence of patello-femoral arthrosis was reported by Davies et al as 9%.1 Other (radiological) studies have ranged from 8% in women to 3.8%.2,3 The aetiology of patello-femoral pain, one of the commonest knee complaints, is multifactorial.4–6 Identification and treatment of isolated patello-femoral arthrosis is always a test for an orthopaedic surgeon.7 There are a number of surgical procedures for failure of nonoperative treatment, but all have their limitations, but advanced prosthetic designs and improved surgical techniques have led to successful outcomes.4,8 The main objective of treatment is a bone sparing procedure in younger patients and minimising surgical dissection and post-operative complications in older patients.

Figure 1 Lateral radiograph showing severity of patellofemoral arthrosis.

of both medial and lateral patellar ligament complex and muscular activity which together determine the dynamic position of the patella.12–15 Anterior knee pain was ascribed to patellar malalignment in the 1970s.16 It was defined by a combination of factors like bony alignment, joint geometry, soft tissue restraints, neuromuscular control, and functional demands giving rise to symptoms as a result of abnormally directed loads exceeding the physiologic threshold of the tissues.8,17,18 Degeneration of articular cartilage is a common problem in the patello-femoral joint; in a review of more than 30000 arthroscopies, 4% had grade IV lesions. Among these patellar wear and trochlear wear were seen in 21% and 15% respectively.19 Articular damage arises from mechanical overload secondary to obesity, repetitive deep knee flexion, malalignment, dysplasia and blunt trauma (Figures 2 and 3). Activities like ascending stairs, rising from a chair, bending down cause increased patellofemoral joint stresses. Rotational malalignment in the axial plane and trochlear dysplasia can also lead to abnormally high loads and the development of patello-femoral arthritis.20,16,21 The highest incidence of chondral wear is seen in the lateral facet of patella and lateral facet arthrosis is the most frequent clinical presentation of patello-femoral arthrosis suggesting that patellar malalignment is the precursor to the chondral damage.15,22 In a study of patello-femoral arthroplasties, 75% were associated with patellar malposition.23 Abnormal tilt of the patella was observed in 25% of patients in preoperative x-rays of 184 patients who underwent total knee arthroplasty.24 Trochlear dysplasia is frequently associated with malalignment. Four types have been described, based on the depth and the concavity of the

Aetiology and pathogenesis The three compartments of the knee (medial and lateral tibiofemoral and patello-femoral joints) form a complex synovial joint of which the patello-femoral joint including the entire extensor mechanism of the knee, is one (Figure 1). It is a synovial gliding joint between the patella and the trochlear surface of the femoral condyles and the shape of the patella, trochlear geometry and the cartilaginous layers play a crucial role in patello-femoral anatomy,9 but the cartilaginous surface of patella and trochlea do not align exactly parallel to its bony surface.10 The central portion of the patella is most heavily loaded and has the thickest cartilage.11 It is the alignment of the limb, soft tissue stabilisation

F Rayan D Orth MRCSEd is a Clinical Research Fellow at the Department of Orthopaedics, University College London Hospitals, London, UK. FS Haddad MCh (Orth) FRCS (Orth) is a Consultant Orthopaedic Surgeon at the Department of Orthopaedics, University College London Hospitals, London, UK.

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signs include squinting of the patella, foot pronation, patellar tilt, presence of the J sign (i.e. visible lateral subluxation of patella as the knee proceeds from flexion to terminal 20 degrees of extension, seen in patellar malalignment or muscular imbalance) patellofemoral crepitus and tenderness of the lateral patellar facet.8,26 Radiologically it is imperative to rule out tibio-femoral arthritis by standing anteroposterior and true lateral views.27 Merchant’s view is important as trochlear dysplasia presents more proximally and it is crucial to visualise this portion of the patello-femoral compartment.16 Merchant et al. classified the severity of the disease based on the 45° skyline view as: Stage 0 is normal, Stage 1 is mild with more than 3 mm joint space, Stage 2 is moderate with less than 3 mm joint space but no bony contact, Stage 3 is severe with bony surfaces in contact over less than one quarter of the joint surface, and Stage 4 is very severe with bony contact throughout the joint surfaces. MRI and CT my be useful.8 Technetium-99 m-MDP bone scan may give an idea about the metabolic activity of the compartment.5,28 It is prudent to rule out infection and inflammatory pathology.29

Management Figure 2 AP radiograph depicting a patello-femoral joint replacement.

The initial management of patello-femoral arthrosis is non­operative.30,31 The objective is to improve muscle fitness and flexibility with adequate pain control. Weight control, activity modification (e.g. avoiding stair climbing and impact activities), knee support with an anterior cut-out to minimise focal pressure on the patello-femoral joint, anti-inflammatories, analgesics and viscose supplementation may be useful.7 Physical therapy with prone stretching of the quadriceps mechanism decreases patello-femoral joint stresses by softening and elongating the peripatellar retinacula,32,33 and closed chain exercises may be beneficial.34,35 Patellar taping as described by McConnell has decreased pain and increased exercise tolerance.36

trochlear groove. In types 3 and 4 there is no groove for patellar tracking, and the trochlear can even be convex. Thus the aim of surgical treatment is to recreate the groove (Figure 4).

Diagnosis Patello-femoral arthrosis is a clinical and radiological diagnosis. McAlindon et al found isolated patello-femoral arthritis in 35% of patients of which half were asymptomatic.17 The clinical diagnosis is challenging as there are multiple conditions that can cause anterior knee pain e.g. direct patello-femoral trauma, malalignment, impingement of intra-articular structures, localized peripheral neuropathy, painful neuroma, tendinopathy, synovitis, focal lesions within the patella, and referred pain from the hip and spine. Patients with patello-femoral arthrosis complain of anterior, retro-patellar or peri-patellar knee pain, particularly when rising from a seated position or going up or down a flight of stairs which then diminishes while walking on a level ground.25 The clinical

Surgical treatment Only when conservative measures fail should surgical options be considered. These include lateral retinacular release, removal of osteophytes, facetectomy, spongialisation, patellar denervation, tibial tuberosity transfer, autologous chondrocyte implantation, patellectomy, patellar resurfacing, total knee arthroplasty

Figure 3 Skyline view of a patello-femoral arthroplasty.

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patients with lateral patello-femoral arthrosis and worst results in global arthrosis, gross trochlear involvement, defective cartilage at the proximal pole and crush injuries.44 Complications associated with this procedure are post-operative fracture of tibial shaft and non-union of the osteotomy site.32 The main disadvantage is the necessity for two bony cuts and it may displace medially even when it is not indicated i.e. in patients with a normal Q angle.32 Autologous chondrocyte implantation Autologous chondrocyte implantation (ACI) comprises harvesting articular cartilage, culturing the chondrocytes and reimplantation into the chondral defect. Minas and Bryant (2005) had good results using autologous chondrocyte transplantation to resurface trochlear and patellar lesions.45 Before this can be recommended as a standard option, studies both with longer followup and comparing autologous chondrocyte implantation with other alternatives are required. Ateshian et al resurfaced the entire patellar articulation with anatomically shaped moulds to contour chondrocyte seeded gels into the desired shape.43 If autologous chondrocyte implantation can be used to fill discrete defects, it is possible that similar technology could be utilized for larger surfaces. Figure 4 Lateral radiograph of a patellofemoral joint replacement.

Patellectomy As a last resort in a grossly degenerate patella with an intact trochlea, patellectomy is an acceptable.32 It is a safe single radical procedure but does not alleviate trochlear pain and reduces the mechanical advantage of the extensor mechanism of the knee. In a review by Lennox et al good results were seen in only 54% of patients with arthritis.46 During patellectomy care should be taken to centralize the extensor mechanism and avoid transecting the tendinous portion. Stripping the patella through a longitudinal split is the best approach. Persistent weakness and length of rehabilitation are the main problems.

and patello-femoral arthroplasty. Differentiation between global and trochlear patello-femoral arthrosis, careful clinical and ­radiological assessment of the patello-femoral joint and the selection of appropriate treatment option suitable for each individual patient are vital for a successful outcome; unfortunately to date there are no studies to compare alternative procedures. Lateral retinacular release aims to shift the patello-femoral contact area medially. It may provide temporary relief when there is a clear tilt and lateral patello-femoral arthritis37 but to date the success rate is not clearly known. Some patients with patello-femoral arthrosis treated with targeted resection of localised osteophytes may get relief. Yercan et al found lateral facetectomy to be palliative in patello-femoral arthrosis but the extent of resection should be limited up to 1 cm in small patellae to preserve the bone stock.38 The most common complication was haemarthrosis. Poor results were attributed to progression to patello-femoral arthrosis. The reduction of patellar thickness at its centre has good results, but weakening of the osseous bed is a case of concern.39,40 Spongialisation as described by Ficat et al involves removal of subchondral bone down to the cancellous bone; it is still used during resurfacing of patella.41 Patellar denervation can reduce the pain level in patellofemoral arthrosis, but is less effective for trochlear lesions.42

Total Knee Arthroplasty (TKA) Meding et al in 2007 retrospectively compared the outcome of 33 total knee arthroplasties in 27 patients with patello-femoral arthrosis less than 60 years of age (average 52 years) against a matched group of patients with primarily tibio-femoral arthritis.47 They showed favourable results with total knee arthroplasties in the patello-femoral group. Despite the success of total knee arthroplasty, many surgeons consider it to be too big a sacrifice of healthy tissue and too great a surgical dissection for a patient with disease involving mainly one compartment. TKA removes all present and future sources of arthritis and the present designs offer greater longevity. Patellar resurfacing Resurfacing of the patella is a controversial topic. Recent studies have shown no significant association between patello-femoral function parameters and the condition of the cartilage.48 Re-surfacing is most beneficial in younger patients with anterior knee pain49 but patients should be warned that they may require a further additional procedure at a later date.49

Tibial tubercle transfer The anteromedial tibial tubercle transfer by oblique osteotomy sloped in an anteromedial – posterolateral direction achieves realignment and anteriorisation gives pain relief and improves function. Advantages are that there is no need for a bony wedge and the vascular plane is avoided (as the screw is directed perpendicular to the plane of osteotomy). Ateshian et al reported medial displacement results only in 10% reduction in patello-femoral joint stress. They also showed that an 8 mm anteromedial displacement results in 4.5 mm medial displacement of patello-femoral contact area.43 Pidriano et al reported that the best results were noted in

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Patello-femoral arthroplasty McKeever first described a patellar arthroplasty in 1955 using a vitallium prosthesis transfixed with a screw.50 Various designs 146

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the patella are essential.53 Tilt and subluxation can be addressed with the help of lateral retinacular release.53 Any malalignment of the patellar extensor mechanism should be corrected. If the Q angle is excessive tibial tubercle transfer should be performed before or along with the main procedure.56 Post-operatively patients are encouraged to do full weightbearing using crutches until they gain quadriceps strength. ◆

followed i.e. Aglietti designed a patellar replacement in 1975, later Blaziina and Lubinus introduced a patello-femoral replacement which resurfaced both surfaces.51,52 There has been a resurgence of interest due to improved implant designs, strict patient and prosthetic selection criteria and improved surgical technique. The indications include: • isolated primary arthrosis of the patello-femoral joint • post-traumatic arthritis • patello-femoral malalignment or dysplasia induced degeneration with or without instability • failed extensor unloading procedure • severe symptoms unresponsive to non-surgical treatment and/or failed previous conservative procedures • extensive grade 3 chondrosis (i.e., loss of joint space without osseous deformation of the patello-femoral joint space, particularly pantrochlear, medial facet, or proximal half of patella).53 Contraindications include: • systemic inflammatory arthropathy • patella infera • uncorrected patello-femoral instability • uncorrected tibio-femoral valgus greater than 8 degrees and varus more than 5 degrees • active infection • reflex sympathetic dystrophy • fixed flexion deformity.53 Other factors which can adversely affect outcome are patella alta, obesity, chondromalacia, arthrofibrosis, quadriceps atrophy, age less than 40 years and ligamentous instability of the tibio-femoral compartment.53 The advantages of patello-femoral replacement are simplicity, bone conservation and preservation of uninvolved tibio-­femoral compartment, meniscus and cruciate ligaments. Even if the common cause of failure of patello-femoral arthroplasty is progression of tibio-femoral arthritis, its continued use is reasonable because the surgical revision to a TKA does not pose any specific difficulties and revision is straightforward.54 Reported patellofemoral complications are attributable to design of the trochlear components, e.g. sagittal radius of curvature, implant breadth, constraint, and proximal extension. Most clinical failures are due to progressive tibio-femoral arthritis. Other failures are due to patellar maltracking and implant malposition.54 The third generation patello-femoral arthroplasties should give better results and reduce the complications of earlier implants55 but long-term follow-up studies are required.55

References 1 Davies AP, Vince AS, Shepstone L, Donell ST, Glasgow MM. The radiologic prevalence of patellofemoral osteoarthritis. Clin Orthop Relat Res 2002; 402: 206–12. 2 McAlindon TE, Snow S, Cooper C, Dieppe PA. Radiographic patterns of osteoarthritis of the knee joint in the community: the importance of the patellofemoral joint. Ann Rheum Dis 1992; 51(7): 844–9. 3 Barrett Jr. JP, Rashkoff E, Sirna EC, Wilson A. Correlation of roentgenographic patterns and clinical manifestations of symptomatic idiopathic osteoarthritis of the knee. Clin Orthop Relat Res 1990; 253: 179–83. 4 Fulkerson JP. Patellofemoral pain disorders: evaluation and management. J Am Acad Orthop Surg 1994; 2(2): 124–32. 5 Dye SF. The pathophysiology of patellofemoral pain: a tissue homeostasis perspective. Clin Orthop Relat Res 2005; 436: 100–10. 6 Saleh KJ, Arendt EA, Eldridge J, Fulkerson JP, Minas T, Mulhall KJ. Symposium. Operative treatment of patellofemoral arthritis. J Bone Joint Surg Am 2005; 87(3): 659–71. 7 Post WR. Patellofemoral pain: results of nonoperative treatment. Clin Orthop Relat Res 2005; 436: 55–9. 8 Grelsamer RP, Stein DA. Patellofemoral arthritis. J Bone Joint Surg Am 2006; 88(8): 1849–60. 9 Arendt E. Anatomy and malalignment of the patellofemoral joint: its relation to patellofemoral arthrosis. Clin Orthop Relat Res 2005; 436: 71–5. 10 Staubli HU, Durrenmatt U, Porcellini B, Rauschning W. Anatomy and surface geometry of the patellofemoral joint in the axial plane. J Bone Joint Surg Br 1999; 81(3): 452–8. 11 Grelsamer RP, Weinstein CH. Applied biomechanics of the patella. Clin Orthop Relat Res 2001; 389: 9–14. 12 Arendt EA, Fithian DC, Cohen E. Current concepts of lateral patella dislocation. Clin Sports Med 2002; 21(3): 499–519. 13 Bohannon RW, Gajdosik RL, LeVeau BF. Relationship of pelvic and thigh motions during unilateral and bilateral hip flexion. Phys Ther 1985; 65(10): 1501–4. 14 Conlan T, Garth Jr. WP, Lemons JE. Evaluation of the medial softtissue restraints of the extensor mechanism of the knee. J Bone Joint Surg Am 1993; 75(5): 682–93. 15 Ficat P. The syndrome of lateral hyperpressure of the patella. Acta Orthop Belg 1978; 44( 1): 65–76. 16 Merchant AC, Mercer RL, Jacobsen RH, Cool CR. Roentgenographic analysis of patellofemoral congruence. J Bone Joint Surg Am 1974; 56(7): 1391–6. 17 McAlindon T, Zhang Y, Hannan M, et al. Are risk factors for patellofemoral and tibiofemoral knee osteoarthritis different? J Rheumatol 1996; 23(2): 332–7. 18 Grelsamer RP. Patellar malalignment. J Bone Joint Surg Am 2000; 82-A(11): 1639–50.

Technique The skin incision used should be adaptable for use in total knee replacement later should the need arise allowing adequate exposure, preservation of normal anatomy, evaluation of the tibiofemoral compartment and removal of osteophytes to eliminate impingement on the patellar prosthesis.53,56 After removal of a minimal amount of subchondral bone from the trochlear bed the femoral component is introduced with 3° to 6° of external rotation with reference to the epicondylar line.53 It is imperative to make a smooth surface interface between the prosthesis and the articular cartilage of the femoral condyles. The edges of the trochlear component should either be flush with or recessed approximately 1 mm from the adjacent articular cartilage of the femoral condyles.53 Restoration of thickness and medialisation of

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36 Cowan SM, Bennell KL, Crossley KM, Hodges PW, McConnell J. Physical therapy alters recruitment of the vasti in patellofemoral pain syndrome. Med Sci Sports Exerc 2002; 34(12): 1879–85. 37 Aderinto J, Cobb AG. Lateral release for patellofemoral arthritis. Arthroscopy 2002; 18(4): 399–403. 38 Yercan HS, Ait Si Selmi T, Neyret P. The treatment of patellofemoral osteoarthritis with partial lateral facetectomy. Clin Orthop Relat Res 2005; 436: 14–9. 39 Nerubay J, Katnelson A. Osteotomy of the patella. Clin Orthop Relat Res 1986; 207: 103–7. 40 Vaquero J, Arriaza R. The patella thinning osteotomy. An experimental study of a new technique for reducing patellofemoral pressure. Int Orthop 1992; 16(4): 372–6. 41 Ficat RP, Ficat C, Gedeon P, Toussaint JB. Spongialization: a new treatment for diseased patellae. Clin Orthop Relat Res 1979; 144: 74–83. 42 Dellon AL, Mont MA, Mullick T, Hungerford DS. Partial denervation for persistent neuroma pain around the knee. Clin Orthop Relat Res 1996; 329: 216–22. 43 Ateshian GA, Hung CT. Patellofemoral joint biomechanics and tissue engineering. Clin Orthop Relat Res 2005; 436: 81–90. 44 Pidoriano AJ, Fulkerson JP. Arthroscopy of the patellofemoral joint. Clin Sports Med 1997; 16(1): 17–28. 45 Minas T, Bryant T. The role of autologous chondrocyte implantation in the patellofemoral joint. Clin Orthop Relat Res 2005; 436: 30–9. 46 Lennox IA, Cobb AG, Knowles J, Bentley G. Knee function after patellectomy. A 12- to 48-year follow-up. J Bone Joint Surg Br 1994; 76(3): 485–7. 47 Meding JB, Wing JT, Keating EM, Ritter MA. Total knee arthroplasty for isolated patellofemoral arthritis in younger patients. Clin Orthop Relat Res 2007; 464: 78–82. 48 Han I, Chang CB, Lee S, Lee MC, Seong SC, Kim TK. Correlation of the condition of the patellar articular cartilage and patellofemoral symptoms and function in osteoarthritic patients undergoing total knee arthroplasty. J Bone Joint Surg Br 2005; 87(8): 1081–4. 49 Kolettis GT, Stern SH. Patellar resurfacing for patellofemoral arthritis. Orthop Clin North Am 1992; 23(4): 665–73. 50 McKeever DC. Patellar prosthesis. J Bone Joint Surg Am 1955; 37A(5): 1074–84. 51 Aglietti P, Insall JN, Walker PS, Trent P. A new patella prosthesis. Design and application. Clin Orthop Relat Res 1975; 107: 175–87. 52 Blazina ME, Fox JM, Del Pizzo W, Broukhim B, Ivey FM. Patellofemoral replacement. Clin Orthop Relat Res 1979; 144: 98–102. 53 Leadbetter WB, Seyler TM, Ragland PS, Mont MA. Indications, contraindications, and pitfalls of patellofemoral arthroplasty. J Bone Joint Surg Am 2006; 88(Suppl 4): 122–37. 54 Kooijman HJ, Driessen AP, van Horn JR. Long-term results of patellofemoral arthroplasty. A report of 56 arthroplasties with 17 years of follow-up. J Bone Joint Surg Br 2003; 85(6): 836–40. 55 Ackroyd CE, Chir B. Development and early results of a new patellofemoral arthroplasty. Clin Orthop Relat Res 2005; 436: 7–13. 56 Lonner JH. Patellofemoral arthroplasty: pros, cons, and design considerations. Clin Orthop Relat Res 2004; 428: 158–65.

19 Curl WW, Krome J, Gordon ES, Rushing J, Smith BP, Poehling GG. Cartilage injuries: a review of 31,516 knee arthroscopies. Arthroscopy 1997; 13(4): 456–60. 20 Cohen ZA, Roglic H, Grelsamer RP, et al. Patellofemoral stresses during open and closed kinetic chain exercises. An analysis using computer simulation. Am J Sports Med 2001; 29(4): 480–7. 21 Iwano T, Kurosawa H, Tokuyama H, Hoshikawa Y. Roentgenographic and clinical findings of patellofemoral osteoarthrosis. With special reference to its relationship to femorotibial osteoarthrosis and etiologic factors. Clin Orthop Relat Res 1990; 252: 190–7. 22 Casscells SW. Gross pathological changes in the knee joint of the aged individual: a study of 300 cases. Clin Orthop Relat Res 1978; 132: 225–32. 23 Cartier P, Sanouiller JL, Grelsamer R. Patellofemoral arthroplasty. 2–12-year follow-up study. J Arthroplasty 1990; 5(1): 49–55. 24 Bindelglass DF, Cohen JL, Dorr LD. Patellar tilt and subluxation in total knee arthroplasty. Relationship to pain, fixation, and design. Clin Orthop Relat Res 1993; 286: 103–9. 25 Cartier P, Sanouiller JL, Khefacha A. Long-term results with the first patellofemoral prosthesis. Clin Orthop Relat Res 2005; 436: 47–54. 26 Lonner JH. Patellofemoral arthroplasty. J Am Acad Orthop Surg 2007; 15(8): 495–506. 27 Maldague B, Malghem J. Significance of the radiograph of the knee profile in the detection of patellar instability. Preliminary report. Rev Chir Orthop Reparatrice Appar Mot 1985; 71(Suppl 2): 5–13. 28 Dye SF, Chew MH. The use of scintigraphy to detect increased osseous metabolic activity about the knee. Instr Course Lect 1994; 43: 453–69. 29 Steere AC, Malawista SE, Snydman DR, et al. Lyme arthritis: an epidemic of oligoarticular arthritis in children and adults in three connecticut communities. Arthritis Rheum 1977; 20(1): 7–17. 30 Dehaven KE, Dolan WA, Mayer PJ. Chondromalacia patellae in athletes. Clinical presentation and conservative management. Am J Sports Med 1979; 7(1): 5–11. 31 Ernst GP, Kawaguchi J, Saliba E. Effect of patellar taping on knee kinetics of patients with patellofemoral pain syndrome. J Orthop Sports Phys Ther 1999; 29(11): 661–7. 32 Fulkerson JP. Alternatives to patellofemoral arthroplasty. Clin Orthop Relat Res 2005; 436: 76–80. 33 Biedert RM, Stauffer E, Friederich NF. Occurrence of free nerve endings in the soft tissue of the knee joint. A histologic investigation. Am J Sports Med 1992; 20(4): 430–3. 34 Tang SF, Chen CK, Hsu R, Chou SW, Hong WH, Lew HL. Vastus medialis obliquus and vastus lateralis activity in open and closed kinetic chain exercises in patients with patellofemoral pain syndrome: an electromyographic study. Arch Phys Med Rehabil 2001; 82(10): 1441–5. 35 Witvrouw E, Lysens R, Bellemans J, Peers K, Vanderstraeten G. Open versus closed kinetic chain exercises for patellofemoral pain. A prospective, randomized study. Am J Sports Med 2000; 28(5): 687–94.

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CME SECTION

CME questions based on the Mini-Symposium on ‘‘Imaging for Joint Replacement’’ E. It decreases for the first 2 years then increases to near normal levels by 10 years

The following series of questions are based on the MiniSymposium on ‘‘Imaging for Joint Replacement’’. 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 Orthopaedics and Trauma Editorial Office at the address at the bottom of the RESPONSE sheet. Please photocopy this page if you wish to keep your copy of Orthopaedics and Trauma. Replies received before the next issue of the journal 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, via email, for your records.

4. What is the significance of osteolysis of the teardrop shadow in the radiological review of total hip replacements A. It can be discounted as being indicative of loosening B. It indicates definite loosening C. It implies contained bone loss that can be managed by impaction grafting D. It implies discontinuity of the anterior column E. It implies disruption of the quadrilateral plate 5. Which of the following observations is least strongly associated with the detection of early acetabular migration due to loosening A. A change in cup position measured by RSA B. A change in cup position observed between two plain AP radiographs C. Early osteolysis adjacent to the superolateral acetabulum D. Radiolucency demarcating the whole margin of the cup E. The absolute position of the cup

Questions 1. Which radiographic projection appears to be optimal for assessing the cement bone interface of the acetabular component after total hip replacement A. B. C. D. E.

AP pelvis Iliac Oblique Inlet view Lateral hip Obturator oblique

6. Radiologically a neocortex after hip replacement is a feature of which of the following A. Cement mantle fracture B. Distal pedestal formation in prosthesis with poor proximal support C. Loose uncemented stem D. Stem fracture E. Tuberculous infection

2. A radiolucent line, 1 mm thick with a sclerotic edge, appears around the bone cement interface of an acetabular component 3 months after a total hip replacement. What is the likely explanation A. B. C. D. E.

A layer of blood at the interface during cementation Deep sepsis Fibrous tissue replacing necrotic bone Granulation tissue as a reaction to polyethylene It is a layer of dead bone killed by exothermic cement setting

7. Which of the following attributes of an MRI scan will not reduce the artefact secondary to metallic implants A. B. C. D. E.

3. Which of the following correctly describes the sequence of changes in bone mineralisation in the proximal femur surrounding a newly implanted femoral component at THR

8. Which of the following parameters has the lowest value (%) when CT is used to investigate periprosthetic infection in a painful prosthesis

A. It decreases for the first six months to a new steady state and remains there indefinitely B. It decreases for the first six months then slowly increases to near normal levels two years after surgery C. It decreases for the first six months then increases bu never reaches near-normal levels D. It decreases for the first 2 years then increases but never approaches normal levels

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Employing spectral fat suppression Increasing the frequency of encoding gradients Reducing the volume of voxels Using fast spin echo techniques Using STIR sequences

A. The accuracy in detecting joint distension B. The sensitivity in detecting fluid collections in perimuscular fat C. The sensitivity in detecting periostitis D. The sensitivity in identifying fluid filled bursae E. The specificity in detecting periostitis

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9. What is the best MRI sequence for imaging the short external rotators of the hip A. B. C. D. E.

address and fax number is given after the response section.

Axial T1 Axial T2 Coronal T1 Coronal T2 Fat saturated T2

Responses Please shade in the square for the correct answer.

10. Which of the alternatives below best represents the equivalent exposure to radiation of a patient undergoing a 2 phase bone scan to investigate periprosthetic infection A. B. C. D. E.

One chest X ray One pelvic X ray Twenty Chest X rays Twenty five pelvic X rays Three hundred chest X rays

11. For which of the following is bone scintigraphy most useful A. B. C. D.

Proving infection five years after hip replacement Proving infection six months after knee replacement Ruling out infection after shoulder replacement Ruling out significant infection two years after hip replacement E. Ruling out infection 3 months after hip replacement

C

D

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NAME................................................................................. ADDRESS............................................................................

PET PET-CT Radionuclide arthrography SPECT White blood cell scintigraphy

........................................................................................... EMAIL ................................................................................ RETURN THE COMPLETED RESPONSE FORM by fax to þ44-113-392-3290, or by post to CME, Orthopaedics and Trauma, Academic Department of Orthopaedic Surgery, ‘‘A’’ Floor Clarendon Wing, Leeds General Infirmary, Great George Street, Leeds LS1 3EX, UK.

Please fill in your answers to the CME questionnaire above in the response section provided to the right. A return

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B

Your details (Print clearly)

12. Which of the following nuclear medicine techniques has the best spatial resolution A. B. C. D. E.

1 A

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Answers to CME questions based on the Mini-Symposium on “Osteoporosis” Please find below the answers to the Current Orthopaedics CME questions from Vol. 22, issue 6 which were based on the MiniSymposium on “Osteoporosis”

1 A

B

C

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2 A

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(i) Irritable hip and septic arthritis of the hip

symptomatic and there is no risk of long-term adverse consequences. The clinical presentation is classically an acute onset of limp associated with a variable degree of restriction of the range of movement at the hip. There may be a prodromic illness, but there are no clinical signs to suggest ongoing sepsis. The original description of Lovett and Morse in 1892 - ‘‘.. short lived and ephemeral form of hip disease which presents at first the characteristics of common hip disease, but the symptoms of which disappear in a few months instead of continuing for years’’1 e though accurate, was aimed at distinguishing irritable hip from tuberculosis of the hip. The peak age of presentation (between 3 and 8 years of age) coincides with the peak age of presentation of Perthes’ disease, and non specific irritability of the hip may very well be the first clinical presentation of Perthes’ disease. However, Perthes’ disease is clearly distinct from transient synovitis, with the characteristic radiographic changes becoming evident with the passage of time. It is the differentiation from septic arthritis of the hip which is critical and more difficult.

M Padman BW Scott

Abstract Transient synovitis needs to be differentiated from septic arthritis of the hip when a child presents with features of an irritable hip. Although there is considerable overlap in the clinical presentation of the two conditions, the natural history, treatment strategy and potential range of outcomes are quite distinct. While transient synovitis is a self limiting condition, emergent surgical intervention in the form of arthrotomy and wash out of joint is the mainstay of treatment of septic arthritis. Clinical decision algorithms have been developed using a combination of clinical and laboratory parameters to help differentiate the two conditions.

Evaluation and treatment protocol Where the clinical picture is unequivocal, children with transient synovitis of the hip do not require further investigations apart from baseline haematological tests including inflammatory markers. If the clinical diagnosis is supported by the results of the blood investigations, no further imaging is required. However, the child needs to be brought back for a further review after 7 to 10 days and most emergency departments have a protocol wherein this follow up appointment can be arranged. The treatment during this period is based entirely on the level of symptoms, with activity modification and analgesics as required. There is some evidence that NSAID’s speed up the recovery process, but this is not conclusive. The earlier practice of complete bed rest and traction is not recommended at present. Further radiological investigations are indicated when the clinical picture is not well defined at the first presentation and/or if there is an element of overlap with the features of septic arthritis. Ultrasound examination of the hips is the preferred mode of imaging2e4 in order to a: detect the presence of an effusion, b: determine its characteristics in terms of size and echogenicity, c: exclude any evidence of osteomyelitis e for example a subperiosteal collection and d: to exclude soft tissue infection. Figure 1 illustrates the comparative ultrasound images of a normal hip and a hip with an effusion. Plain radiographs of the hip are more useful in the older child, although most emergency departments routinely use a frog leg lateral view along with the ultrasound evaluation of the hips at all ages. Radiological imaging and referral to the Orthopaedic clinic is also indicated when there is no resolution of symptoms at the follow up visit.

Keywords clinical algorithms; irritable hip; post septic sequelae; septic arthritis; transient synovitis

Introduction An acutely irritable hip in a child is very often a diagnostic challenge with a myriad of pathologies characterised by irritability of the hip as their first clinical presentation. The common causes are infection, transient synovitis, Perthes’ disease, slipped upper femoral epiphysis, trauma, inflammatory arthritis and tumours. An awareness of the natural history of these various conditions, including the age at presentation and the characteristic features, coupled with a careful history and thorough physical examination, will help narrow the differential diagnosis in the vast majority of cases. However, one can frequently be left with the crucial decision of having to differentiate quickly between transient synovitis and true infection around the hip (septic arthritis and osteomyelitis of the proximal femur). Despite a remarkable similarity between these two conditions at the time of presentation, it is imperative that they are differentiated at an early stage in view of the adverse consequences of delayed treatment of septic arthritis. Various diagnostic algorithms, using a combination of clinical and laboratory parameters, have been proposed to help differentiate these two conditions.

Transient synovitis Transient synovitis is a benign condition of non specific aetiology, which has a self-limiting course and often the diagnosis is established by exclusion of other pathologies. The treatment is

Septic arthritis of the hip Pathogenesis The hip joint is the second most frequent joint to be affected by infection after the knee joint, but the consequences of infection are much more dramatic. Bacteria enter the hip joint by either of two routes, either by the haematogenous route following bacteraemia, or by direct spread from an osteomyelitic focus within

M Padman FRCS(Tr & Orth) is a Specialist Registrar at Sheffield Children’s Hospital, UK. BW Scott FRCS(Orth) is a Consultant Orthopaedic Surgeon at Leeds General Infirmary, Leeds, UK.

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Microbiology The causative organisms depend significantly on the age of presentation. Staphylococcus aureus remains the commonest organism across all age groups, responsible for 40 to 90% of all cases of musculoskeletal infection.9 Table 1 illustrates the pattern of microbial infection in the various age groups. With the widespread use of H1B vaccine, the incidence of Haemophilus influenzae infection has dramatically reduced. With the changing bacteriological pattern, unusual organisms like Kingella kingae are being recognised as responsible for an increasingly greater percentage of infections. K. kingae is a fastidious Gram negative bacillus, normally residing in the oropharynx of young children, but can become involved in musculoskeletal infection when it gains access to the bloodstream as an opportunistic pathogen. The increasing detection of K. kingae as the causative organism may be related to our greater understanding of how this organism can be isolated and cultured. Clinical features A child with septic arthritis of the hip presents with the systemic features of sepsis coupled with localised signs confined to the extremity in question. The systemic features may range from  generalised irritability and pyrexia (temperature> 38.5 centigrade) to florid signs of septicaemia. The local symptoms are pseudoparalysis in the smaller child and a limp in the older, ambulant child. The clinical symptoms may be preceded by a non-specific prodromal illness or occasionally by trauma. The limb itself is held in a position of flexion, abduction and external rotation to accommodate the increased joint volume due to effusion. There is very little spontaneous movement of the extremity and any attempt to passively move the joint is resisted. The pelvis, including the sacroiliac joints and the lumbosacral spine, must be examined to exclude other foci of infection. A thorough systemic examination is necessary to identify any potential source of infection which may require input by other specialists.

Ultrasound images of hips. a Normal hip. b Hip with an effusion showing capsular distension, thickening and distortion of soft tissue planes due to oedema. Figure 1

that part of the metaphysis which is intra articular. The proximal femur, proximal humerus, distal lateral tibia and proximal radius all share the common anatomic characteristic of having part of their metaphysis within the joint.5 The synovium has a rich vascular network from where bacteria gain access to the joint through the highly permeable blood vessels. The clinical outcome is determined by the host response to the bacterial burden, which is influenced by the virulence of the organism and the local and systemic resistance of the host. The acute inflammatory response, mediated by polymorphonuclear leukocytes, results in an exudative reaction into the joint producing a tense effusion. Articular cartilage is destroyed by a combination of enzymatic degradation, mediated by the various proteolytic enzymes released during the inflammatory cascade and by the disruption of blood supply following thrombosis within the microcirculation and by the elevated intracapsular pressure.6 Animal studies have demonstrated the rapidity with which irreversible articular damage occurs7 and also the incomplete protection of articular cartilage with intravenous antibiotic treatment alone,8 hence the need for immediate surgical decompression and wash out of the joint as the mainstay of treatment. Delayed treatment of septic arthritis of the hip can cause significant problems as a consequence of damage to the physis or preosseous cartilage, ischaemia and avascular necrosis of the femoral epiphysis, spread of infection to involve the proximal femur and generalised sepsis.

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Investigations The diagnosis of septic arthritis remains fundamentally a clinical one, based on a high index of suspicion and backed by appropriate investigations. The initial evaluation of a child with an irritable hip should include baseline haematological investigations; namely a total and differential white cell count (WCC), erythrocyte sedimentation rate (ESR) and C-reactive protein

Common organisms responsible for septic arthritis at various ages Age group

Commonest causative organisms

Neonate

Group B Streptococcus, Staph. aureus, Gram negative bacillus 1 monthe3 years Staph. aureus, Pneumococcus, Strep. pyogenes, (H. influenzae) 3 yearse12 years All of the above Adolescent Staph. aureus, N. gonorrhoeae Table 1

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(CRP). Typically the WCC is raised to> 12 000 cells per mm3 with a polymorphonuclear leukocystosis of 40e60%, the ESR is elevated to 50 mm per hour and the CRP is greater than 20. It is important to remember that the neonate may not show a significant elevation of the inflammatory markers due to the relative immaturity of their immune system. Blood cultures are positive in 40 to 60% of cases, and samples should be taken as part of the screening for sepsis before any antibiotics are administered. Ultrasound evaluation of the hips is a useful adjunct to identify an effusion within the hip where the clinical picture is not clear. The volume of fluid within the joint can be compared to the opposite side and the quality of the effusion can be assessed to see whether there is any debris, which would indicate an exudative reaction, and the presence of any subperiosteal collection detected.

joint. A follow up ultrasound scan is necessary to confirm that there is no residual instability before the harness is discontinued. The response to treatment is monitored clinically (temperature, spontaneous movement of the extremity and weight bearing) as well as with serial haematological investigations. Normalisation of the CRP level is the earliest laboratory parameter to indicate that the infective process is controlled and is a useful adjunct to determine the duration of antibiotic therapy. Controversy exists as to the total duration of antibiotic therapy as well as the optimum point for conversion from parenteral to oral antibiotics. Parenteral broad spectrum antibiotics are continued until formal culture and sensitivity results are obtained. Once switched to the appropriate antibiotics, as dictated by sensitivity results, the decision regarding the duration of antibiotic treatment is made based on several factors, including the virulence of the organism identified and the clinical response. A two to six week course is the standard regimen, with the longer duration reserved for more virulent organisms, protracted clinical course and when associated with concomitant osteomyelitis.10 Occasionally the clinical response to surgical drainage and antibiotic therapy is less than optimal, and when there is concern that there may be ongoing sepsis repeat ultrasound scans and Magnetic Resonance Imaging is indicated to exclude other foci of infection, especially within the pelvis.

The role of aspiration Evidence of pus on aspiration of the joint is diagnostic of suppurative arthritis, especially when done under ultrasound guidance.6,10 Diagnostic criteria have been established for confirmation of the diagnosis based on biochemical and cytological analysis of synovial fluid aspirate.11 However, the procedure is not well tolerated by the conscious child and therefore its routine use in clinical practice is limited. In practical terms, aspiration of the joint under fluoroscopic guidance is useful when done under anaesthesia before a formal arthrotomy, where there is a strong clinical suspicion of septic arthritis and the ultrasound evaluation has been either inconclusive or when facilities for sonography are unavailable.

Osteomyelitis of the proximal femur The clinical picture of osteomyelitis (Figure 2) is identical to septic arthritis, but for the absence of a hip effusion on ultrasound examination. Occasionally the ultrasound scan may show a subperiosteal collection and plain xrays may show an area of lucency in the proximal femoral metaphysis. The mainstay of treatment for osteomyelitis is antibiotic therapy, with the caveat that the total duration, as well as the duration of parenteral therapy, need to be more prolonged than for septic arthritis. The presence of concomitant osteomyelitis is a poor prognostic factor for the development of long term adverse sequelae.

Treatment Septic arthritis is a true emergency and the cornerstone of treatment is surgical drainage of the joint followed by copious irrigation. The hip joint is exposed through a mini bikini line incision, using the internervous plane between the tensor fascia lata and sartorius (modified Smith-Peterson approach). The capsule and pericapsular tissues may be oedematous as a consequence of the ongoing inflammation, which may distort tissue planes. Once the pericapsular soft tissues are cleared, the capsule is opened through a cruciate incision. Samples of fluid from the joint are taken at the first available opportunity and are sent for urgent Gram staining and microbiological analysis. To maximise the chances of isolating an organism, synovial fluid is injected into blood culture broths before sending to the lab. Empirical intravenous antibiotics are started as soon as specimens are obtained, based on the common patterns of microbiological isolation and sensitivities locally. It is helpful if advice is sought from the hospital microbiologist for the appropriate broad spectrum antibiotic, which would cover the common pathogens for the particular age group. The same anaesthetic sitting can be used for securing peripheral venous access (PICC line e peripherally inserted central catheter) for prolonged parenteral antibiotic therapy. The capsule and fascial layers are left open to facilitate continuous drainage of the joint, but the skin and subcutaneous layers can be closed. The neonate and the infant are at the greatest risk of developing subluxation or dislocation of the joint, and it may be necessary to immobilise the hip in a dynamic flexion-abduction brace (Pavlik harness) to maintain concentric reduction of the

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Figure 2 Concomitant septic arthritis & proximal femoral osteomyelitis. Evidence of hip subluxation which needed Pavlik harness immobilisation. Periosteal reaction of proximal femur.

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Sequelae of septic arthritis

Post septic sequelae and their possible mechanisms

The hip joint accounts for a substantial majority of poor outcomes when the adverse consequences following septic arthritis of all joints are assessed. The poor prognostic factors are: onset in a child under 6 months of age, delay in diagnosis by more than 4 days, concomitant proximal femoral osteomyelitis and infection with Staph. aureus.10,12,13 The catastrophic sequelae of delayed diagnosis of septic arthritis of the hip are a consequence of destruction of the articular hyaline cartilage and irreversible damage to the epiphysis, physis and metaphysis of the proximal femur and occasionally the triradiate cartilage of the acetabulum (Figure 3). The damage is brought about by a combination of enzymatic degradation, ischaemia and mechanical factors. Bacterial toxins, break down products of cells, proteolytic enzymes and inflammatory mediators (Interleukin-1) released as part of the inflammatory cascade all contribute to chondrolysis. Ischaemia to the preosseous cartilage is a consequence of septic emboli, endarteritis and mechanical factors. The mechanical factors that disrupt the subsynovial vasculature are capsular distension by the tense effusion and capsular stretching by the subluxing/dislocating femoral head. The various clinical and radiological sequelae of septic arthritis of the hip are listed in Table 2, along with their putative pathomechanisms. The sequelae were first classified by Hunka et al.14 on the basis of their radiological appearances, and several authors have attempted to devise reconstructive strategies to address the gross deformity and instability.15e18 The treatment strategies include conservative measures to maintain hip mobility in mild deformity, realignment proximal femoral osteotomies to correct varus/valgus deformities, pelvic osteotomies (Pemberton/Dega acetabuloplasties) to address acetabular dysplasia and instability, trochanteric distal transfer for abductor insufficiency plus the various measures to address the consequences of significant leg length discrepancy. Gross deformity and instability arising from a complete destruction of femoral head and neck (Hunka Type V hips) remain a challenge, and recent reports have indicated reasonable results with Pelvic Support Osteotomy along with Ilizarov hip reconstruction.19,20

Mechanism

Coxa magna

Transient disruption of the blood supply

Avascular necrosis of femoral head

Partial or total disruption of the blood supply

Acetabular dysplasia

Premature closure of the triradiate cartilage Persistent hip instability

Subluxation/Dislocation

Mechanical factorsecapsular distension

Abductor insufficiency/ Trochanteric overgrowth

Premature closure of proximal femoral physis

Coxa vara/coxa valga Torsional abnormalities

Asymmetric closure of the proximal femoral physis

Leg length discrepancy

Damage to the proximal femoral physis

Pseudoarthrosis of the femoral neck

Damage to the femoral neck and physis

Complete destruction of femoral head & neck

Damage to the preosseous cartilage and physis

Ankylosis of the hip

Natural consequence or following surgical treatment

Table 2

the hip, but have found considerable overlap between the two.21 Kocher et al.22 proposed a clinical prediction algorithm for differentiating between the two conditions, based on the retrospective evaluation of various clinical and laboratory features in children who presented to a tertiary centre with an irritable hip. Although several variables were found to differ significantly between the two groups, they also found that the overlap made it quite difficult to make the distinction based on individual variables alone. Four independent multivariate clinical predictors were evaluatedehistory of fever, non weight bearing, an Erythrocyte Sedimentation Rate (ESR) greater than 40 mm/hour and elevated White Cell Count of more than 12 000 cells per cubic millimetereas predictors for septic arthritis. The predictive values for a probable diagnosis of septic arthritis were 99.6% when all four variables were present, 93.1% in the presence of three variables, 40% for two variables and 3% for one variable. Subsequently, the authors validated the same four clinical variables in a prospective study within a different population although the predictive values were diminished (93% for all four variables, 72.8% for three variables).23 Although some investigators have found similar predictive values on prospective evaluation of the four variables plus C reactive protein,24 others have found the algorithm to be not

The differentiation between transient synovitis & septic arthritiseclinical diagnostic algorithms Clinicians have empirically used various parameters to establish clinical prediction rules that would help to objectively make a distinction between transient synovitis and septic arthritis of

Figure 3 Post septic sequelae.

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Clinical/Radiological abnormality

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13 Gillespie R. Septic arthritis of childhood. Clin Orthop Relat Res 1973; 96: 152e9. 14 Hunka L, Said SE, MacKenzie DA, Rogala EJ, Cruess RL. Classification and surgical management of the severe sequelae of septic hips in children. Clin Orthop Relat Res 1982; 171: 30e6. 15 Choi IH, Pizzutillo PD, Bowen JR, Dragann R, Malhis T. Sequelae and reconstruction after septic arthritis of the hip in infants. J Bone Joint Surg Am 1990; 72-A(8): 1150e65. 16 Choi IH, Shin YW, Vhung CY, Cho TJ, Yoo WJ, Lee DY. Surgical treatment of the severe sequelae of infantile septic arthritis of the hip. Clin Orthop Relat Res 2005; 434: 102e9. 17 Forlin E, Milani C. Sequelae of septic arthritis of the hip in children: a new classification and a review of 41 hips. J Pediatr Orthop. 2008; 28(5): 524e8. 18 Wada A, Fujii T, Takamura K, Yanagida H, Urano N, Surijamorn P. Operative reconstuction of the severe sequelae of infantile septic arthritis of the hip. J Pediatr Orthop 2007; 27(8): 910e4. 19 Rozbruch SR, Paley D, Bhave A, Herzenberg JE. Ilizarov hip reconstruction for the late sequelae of infantile hip infection. J Bone Joint Surg Am 2005; 87-A(5): 1007e18. 20 Pafilas D, Nayagam S. The pelvic support osteotomy: Indications and preoperative planning. Strategies Trauma Limb Reconstr 2008; 3: 83e92. 21 Del Beccaro MA, Champoux AN, Bockers T, Mendelman PM. Septic arthritis versus transient synovitis of the hip: the value of screening laboratory tests. Ann Emerg Med 1992; 21(12): 1418e22. 22 Kocher MS, Zurakowski D, Kasser JR. Differentiation between septic arthritis and transient synovitis of the hip in children: an evidencebased clinical prediction algorithm. J Bone Joint Surg Am 1999; 81-A(12): 1662e70. 23 Kocher MS, Mandiga R, Zurakowski D, Barnewolt C, Kasser JR. Validation of a clinical prediction rule for the differentiation between septic arthritis and transient synovitis of the hip in children. J Bone Joint Surg Am 2004; 86-A(8): 1629e35. 24 Caird MS, Flynn JM, Leung YL, Millman JE, D’Italia JG, Dormans JP. Factors distinguishing septic arthritis from transient synovitis of the hip in children. A prospective study. J Bone Joint Surg Am 2006; 88-A(6): 1251e7. 25 Luhmann SJ, Jones A, Schootman M, Gordon JE, Schoenecker PL, Luhmann JD. Differentiation between septic arthritis and transient synovitis of the hip in children with clinical prediction algorithms. J Bone Joint Surg Am 2004; 86-A(5): 956e62.

useful in distinguishing between transient synovitis and septic arthritis with predictive values as low as 59% even with the presence of four variables.25

Conclusion The diagnosis of septic arthritis of the hip fundamentally remains a clinical one despite the development of various clinical diagnostic algorithms. Laboratory and imaging studies are useful adjuncts to support the clinical decision. A

REFERENCES 1 Lovett RW, Morse JL. A transient or ephemeral form of hip-disease, with a report of cases. Boston Med Surg J 1892; 127: 161e3. 2 Bickerstaff DR, Neal LM, Booth AJ, Brennan PO, Bell MJ. Ultrasound examination of the irritable hip. J Bone Joint Surg Br 1990; 72-B(4): 549e53. 3 Zieger MM, Dorr U, Schulz RD. Ultrasonography of hip joint effusions. Skeletal Radiol 1987; 16(8): 607e11. 4 Hill SA, MacLarnon JC, Nag D. Ultrasound-guided aspiration for transient synovitis of the hip. J Bone Joint Surg Br 1990; 72-B(5): 852e3. 5 Dormans JP, Drummond DS. Pediatric hematogenous osteomyelitis: new trends in presentation, diagnosis and treatment. J Am Acad Orthop Surg 1994; 2(6): 333e41. 6 McCarthy JJ, Dormans JP, Kozin SH, Pizzutillo PD. Musculoskeletal infections in children. Basic treatment principles and recent advancements. J Bone Joint Surg Am 2004; 86-A(4): 850e63. 7 Daniel D, Akeson W, Amiel D, Ryder M, Boyer J. Lavage of septic joints in rabbits: effects of chondrolysis. J Bone Joint Surg Am 1976; 58-A(3): 393e5. 8 Smith RL, Schurman DJ, Kajiyama G, Mell M, Gilkerson E. The effect of antibiotics on the destruction of cartilage in experimental infectious arthritis. J Bone Joint Surg Am 1987; 69-A(7): 1063e8. 9 Morrissy RT, Weinstein SL, eds. Lovell and Winter’s Pediatric Orthopaedics. 6th edn., No. 1. Lippincott Williams & Wilkins; 2006. 10 Sucato DJ, Schwend RM, Gillespie R. Septic arthritis of the hip in children. J Am Acad Orthop Surg 1997; 5(5): 249e60. 11 Nade S. Acute septic arthritis in infancy and childhood. J Bone Joint Surg Br 1983; 65-B(3): 234e41. 12 Jackson MA, Nelson JD. Etiology and medical management of acute suppurative bone and joint infections in pediatric patients. J Pediatr Orthop 1982; 2(3): 313e23.

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(ii) Surgical approaches to the hip in children

both potentially injurious and will also cause seepage of contrast material around the extra-capsular tissues, making interpretation of the arthrogram difficult. A suitable radio-opaque medium such as Radiografin is used and may be diluted with saline to give greater clarification of the intra-articular structures.

M F Macnicol

Lateral This is of value in the older child, for instance, when Perthes’ disease is being investigated. The tip of the greater trochanter is palpated and the spinal needle inserted immediately anterior to this (Figure 1). The needle is advanced transversely, in the horizontal plane, so that the tip enters the superior capsular recess at the lateral margin of the femoral neck. Once again, saline is injected for a trial assessment before the contrast medium is inserted.

Abstract The relevant anatomical structures around the hip are considered in relation to medial, anterolateral and posterior approaches to the joint. Paediatric conditions that make this surgical facility necessary include developmental dysplasia and dislocation of the hip, septic arthritis, slipped upper femoral epiphysis and the removal of benign tumours and loose bodies.

Anterior Other sites of insertion are less commonly required. The anterior is 2 cm lateral to the femoral artery, aiming directly posterior. A more medial approach is risky owing to the proximity of the femoral vessels. Any extravasation of contrast will obscure the details of the hip joint.

Keywords anterolateral; arthrography; arthroscopy; hip joint; medial and posterior approaches; surgical anatomy

Medial The medial or adductor approach inserts the needle immediately posterior to the adductor longus tendon. The leg should be abducted and the needle aimed at the opposite anterior iliac spine in the horizontal plane and at 45 degrees to the long axis of the patient.

Introduction The most common indications for exposing the paediatric hip joint are developmental dysplasia with femoral head displacement, and septic arthritis. Occasional indications are loose body removal, reduction of major slippage of the upper femoral epiphysis, excision of a proximal femoral tumour such as an osteochondroma, and femoro-acetabular impingement in the adolescent.

Caudal A caudal insertion is possible if the hip is flexed 45 degrees, allowing the ischial tuberosity to be palpated. The needle tip is introduced immediately anterior and lateral to the tuberosity in a horizontal plane, allowing the medial recess of the capsule of the joint to be penetrated.

Arthrography and arthroscopy Surgical operations principally comprise anterolateral or medial dissections; the posterior approach is rarely required. Before discussing the incisions and anatomical details of these two common approaches the surgeon should also be conversant with the different techniques for arthrography and arthroscopy.

Arthroscopy This technique currently has a very limited role in the adolescent. In the child, the spaces available for the tip of the arthroscope are curtailed and longitudinal traction may be damaging. The portals for access are lateral (proximal to the greater trochanter), anterolateral (to view the inferior recess under the femoral neck) and the rarely used posterior portal. In the older and larger child and adolescent removal of loose bodies, particularly synovial chondromatosis debris, and drilling of osteochondral defects may be technically possible. This is provided that the femoral head is not deformed, as loss of sphericity will frustrate vision and access. Labral tears can be reduced by punch forceps or a shaver, although progressive disruption of the labrum is likely when the acetabulum is dysplastic and offers little or no support. Femoro-acetabular impingement is generally treated in the young and often athletic adult, both by partial labrectomy and by increasing the femoral head/neck offset. The long term outcome after these interventions merits critical review.

Arthrography Anterolateral (cranial) A 20-gauge spinal needle is attached to a syringe containing normal saline. The central stylet prevents the needle from blocking during its insertion. After preparing and draping the region the needle is inserted one finger breadth distal and posterior to the anterior superior iliac spine.1 The needle should be held horizontally as there is a tendency to direct it posterior to the hip joint capsule. Once the needle tip meets the lateral wall of the iliac wing it is ‘walked down’ to the lateral aspect of the capsule. The labrum or an inverted limbus should be avoided, aiming the needle approximately 45 degrees caudally (Figure 1). When the joint is entered the saline can be injected deep to the capsule and into the joint; a free return of fluid confirms success. Repeated insertions of the needle should be avoided as they are

Surgical approaches Medial (median adductor) approach This surgical approach is ascribed to Ludloff (1913)2 although his longitudinal skin incision, parallel with adductor longus, is less cosmetic than the transverse incision usually employed today

M F Macnicol BSc(hons) MCh FRCS FRCP FRCSEd(Orth) is a Consultant Orthopaedic Surgeon at the Royal Hospital for Sick Children, Scienne Road, Edinburgh, UK.

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P

VAN

Superior anterolateral

AL Direct lateral IP G AB

45˚

F

AM

Adductor (medial) AL= proximally- released adductor longus; P= pectineus; G= gracilis; AB= adductor brevis; AM= adductor magnus; IP= iliopsoas tendon; F= femur and lesser trochanter; VAN= femoral vein, artery and nerve

Figure 1 The appropriate sites of needle insertion for hip arthrography. Copyright 1996 M.F. Macnicol.1

Figure 3 The different approaches to the medial aspect of the hip joint.

(Figure 2). On exposing the pectineus muscle the dissection proceeds either anterolateral or posteromedial to this muscle (Figure 3). Ludloff developed the interval between pectineus and the iliopsoas by retracting adductor brevis and pectineus medially after detaching the adductor longus tendon proximally. Chiari popularised the approach in 19573 and Weinstein and Ponseti4 preferred its direct access to the joint. More posterior and medial dissections are also shown in Figure 3. These keep pectineus anteriorly, retracted laterally. If the approach is over the anterior surface of adductor brevis the branches of the anterior obturator nerve must be protected. Ferguson (1973) utilised an approach between between the adductor brevis (and longus) anteriorly and gracilis and adductor magnus posteromedially5 although the exposure is limited. All techniques are made easier by release of adductor longus proximally and the iliopsoas tendon distally at the lesser trochanter. The approach should not be attempted in children over 12 to 18 months of age.

The dissection requires that the medial circumflex vessels be divided, as they lie across the capsule of the hip joint. Avascular necrosis rates of between 0e60 per cent have been recorded, Morcuende et al6 describing a 24 per cent rate although more recent reviews have suggested that a rate of less than 5 per cent can be achieved. Zamzam et al7 reported a rate of 2 per cent, excluding the type I, possibly benign and temporary, irregularity of proximal femoral epiphyseal ossification. They considered that diathermy or ligation of the medial circumflex vessels was not the direct cause of avascular changes since a similar rate affected their patients when operated upon using an iliofemoral approach. The medial approach offers no access to the limbus nor can it be combined with a pelvic osteotomy. Anatomical reduction can be confirmed with a medial metallic marker and a preoperative radiograph. When draining a septic arthritis through the medial route, good dependent drainage can be achieved so that the insertion of a drain is unnecessary provided the medial capsule has been opened widely. Anterolateral (iliofemoral) approach The skin incision may be either transverse (‘‘bikini’’ line) or iliofemoral (Figure 4), curving distally and medially. For drainage of the septic hip a relatively short incision of approximately 4 cm is centred a centimetre below the anterior superior iliac spine8,9 and can be extended medially or laterally as required. Salter10 described a curved iliofemoral (Smith Petersen) incision when promoting his innominate osteotomy but the bikini incision is more cosmetic and allows adequate exposure for the Salter procedure11 and allied pelvic operations in the younger child. The bikini incision usually offers good access for the Chiari12 and other major pelvic osteotomies after skeletal maturity. For most hip exposures the incision is one-third (in length) medial to the anterior superior iliac spine and two-thirds lateral to it. The femoral nerve and inferior epigastric vessls should not be transgressed. The interval between tensor fascia lata and the sartorius muscle can be palpated as a slight cleft beneath the

Figure 2 The medial approach is best undertaken through a transverse, skin crease incision.

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iliopsoas tendon; but for drainage of the septic hip the exposure can be more limited. Adherent muscle, fat and areolar tissue can be swept away from the capsule so that it is well defined, including the overlying Bigelow’s ligament. If a high dislocation of the femoral head is present the capsule will need to be opened fully, preferably through a T cut with the transverse arm parallel and 5 mm lateral to the acetabular margin. The round ligament is usually bulky and should be resected, following its deep attachment to define the true acetabulum. The transverse acetabular ligament is divided and adhesions or capsular retrictions released fully to allow deep reduction of the femoral head. Radial cuts of a few millimetres allow an inverted limbus (outer labrum and attached capsule) to be everted. The pulvinar (fat pad) is rarely bulky and obstructive so it should be preserved. Combining an anterior or anterolateral incision with a proximal lateral thigh longitudinal incision is not advised. The resultant scar is extensive and ugly. Instead, if a proximal femoral shortening/derotation osteotomy is indicated along with open reduction of a high dislocation and/or an acetabuloplasy, the approach should employ the standard, separate incisions. When carrying out the Dunn osteotomy,13 or one of its variants for severe slippage of the proximal femoral epiphysis, an anterolateral approach is preferred to the lateral incision with trochanteric osteotomy employed by Dunn. Since the patient is usually an adolescent the plane between gluteus medius and tensor fascia lata can be developed sufficiently widely to give adequate access to the femoral neck proximally. The fascia lata should be split immediately posterior to the tensor, curving further posteriorly when extended distally over the upper, lateral thigh so that the femoral shaft can be exposed for the subsequent insertion of fixation screws. Fat overlying the capsule is excised and the gluteus medius released distally, for later reattachment. Dissection around the capsule should define it fully but retractors must not be passed posterior to the femoral neck (Figure 6) as they may damage the only blood supply to the posteriorly displaced epiphysis. A circumferential cut is made around the rim of the acetabulum and another at right angles to this. The femoral neck is exposed fully laterally, anteriorly and medially. Since the patient is supine the leg is supported by an assistant at this stage, gradually externally rotating and extending the adducted leg. This manoeuvre brings the anterolateral edge of the displaced epiphysis into view. Retractors can be placed against or over the ilium in order to improve access and the labrum may need to be reflected. The details of the femoral neck shortening osteotomy1,13 are beyond the scope of this contribution.

Iliofemoral

“Bikini”

Figure 4 The ‘bikini’ incision is preferred to the iliofemoral incisions which cross the groin crease when undertaking the anterolateral approach.

deep fascia, more apparent distally. This natural, intermuscular plane of cleavage should therefore be developed distally with round-tipped dissecting scissors before completing the intermuscular separation proximally towards the iliac wing (Figure 5). The lateral femoral cutaneous nerve should be protected and usually has to be retracted medially. It has a variable course and is easily injured during subsequent operative procedures. Proximally, the superior gluteal nerve branch to the tensor fascia lata should be avoided, although a leash of vessels may require division. In the child or early adolescent the iliac apophysis is split down to cancellous bone by sharp dissection along the anterior 3e4 cm, cracking open and then reflecting the two halves of the apophysis away from the wing subperiosteally. The straight head of rectus femoris is identified by blunt dissection, lifted off the anterior capsule of the hip joint and then transected. This helps to expose the anterolateral capsule more fully (Figure 5) when carrying out an open reduction of the hip, as will release of the

TFL

AIIS

S

Posterior approach This is familiar to most surgeons, necessitating a splitting of the fibres of gluteus maximus and division of the short, external rotators in order to expose the hip joint capsule. The access is relatively easy with the patient lying on the normal side but in the younger child the buttock fat is a very thick layer and the resultant scar is not always cosmetic. Therefore, although excellent dependent drainage can be ensured, this approach is not recommended in paediatric practice.

RF

Figure 5 The capsule of the hip joint is exposed by careful separation of the sartorius [S] and tensor fascia lata [TFL] muscles. The straight head of rectus [RF] is lifted away from the capsule by blunt dissection, released from the anterior inferior iliac spine [AIIS], and retracted distally.

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determine whether a posterior approach is more appropriate; careful preoperative planning is therefore essential. A

REFERENCES 1 Macnicol MF. Color atlas and text of osteotomy of the hip. London: Mosby-Wolfe; 1996. pp. 167. 2 Ludloff K. The open reduction of the congenital dislocation of the hip using a median adductor approach. Am J Orthop Surg 1913; 10: 438e54. 3 Chiari K. Die operative Behandlung am Huftgelenk bei der angeborenen Huftgelenksverrenkung. Wien Med Wochenschr 1957; 107: 1020e7. 4 Weinstein SL, Ponseti IV. Congenital dislocation of the hip. J Bone Joint Surg Am 1979; 61-A: 114e24. 5 Ferguson Jr AB. Primary open reduction of congenital dislocation of the hip using a median adductor approach. J Bone Joint Surg Am 1973; 55-A: 671e89. 6 Morcuende JA, Meyer MD, Dolan LA, Weinstein SL. Long-term outcome after open reduction through an anteromedial approach for congenital dislocation of the hip. J Bone Joint Surg Am 1997; 79-A: 176e80. 7 Zamzam MM, Koshhal KI, Abak AA, Bakerman KA, AlSiddiky AMM, Kremli MK. One-stage bilateral open reduction through a medial approach in developmental dysplasia of the hip. J Bone Joint Surg Br 2009; 91-B: 113e8. 8 Macnicol MF. Surgical management of qcute bone and joint infections. In: Rob, Smith, eds. Operative surgery, 4th edn. Orthopaedics Part 1. Butterworth; 1991. pp. 54e60. 9 Macnicol MF. Septic arthritis and osteomyelitis in children. In: Kaelin A, Lemaire R, Duparc J, eds. Surgical techniques in orthopaedics and traumatology. EFFORT publication; 2004. 10 Salter RB. Innominate osteotomy in the treatment of congenital dislocation and subluxation of the hip. J Bone Joint Surg Br 1961; 43-B: 518e39. 11 Macnicol MF, Al Rawashdeh H, Auld J. Technical aspects of the Salter innominate osteotomy. Curr Orthop 2000; 14: 209e14. 12 Hogh J, Macnicol MF. The Chiari pelvic osteotomy: a long term review of clinical and radiographic results. J Bone Joint Surg Br 1987; 69-B: 365e73. 13 Dunn DM, Angel JC. Replacement of the femoral head by open reduction in severe adolescent slipping of the upper femoral epiphysis. J Bone Joint Surg Br 1978; 60-B: 394e403.

Figure 6 Retractors are placed anterior and proximal to the femoral neck but not posteriorly.

Summary Reduction of the congenitally dislocated hip up to the age of 12e18 months can be achieved relatively atraumatically by a medial (median adductor) or anterolateral approach. After this age the anterolateral dissection ensures a better access to the pathology and permits a concurrent pelvic osteotomy. Drainage of the septic hip is effective through both a limited anterolateral incision or the medial approach. A posterior incision is not advised. Removal of loose bodies can be achieved through the anterolateral approach, possibly combined with femoral head dislocation surgically if a medial fragment or osteochondral separation is present. In the adolescent hip arthroscopy is an option. Note that in the older child, with associated deformity of the femoral head resulting from Perthes’ disease or avascular necrosis, therapeutic dislocation of the femoral head may prove very difficult so a posterior approach is occasionally of value. An extended, anterolateral approach is advised for major slippage of the proximal femoral epiphysis when femoral neck shortening and epiphyseal reduction are required. This approach is also effective for femoro-acetabular impingement and tumours of the femoral neck. The site and extent of the neoplasm will

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As Connolly2 points out, DDH has both anatomical and radiological definitions. The anatomical definition refers to abnormal development of the femoral head and acetabulum, while the radiological definition refers to a break in Shenton’s line. To this definition can be added a hip with an increased acetabular index.

(iii) Developmental dysplasia of the hip Benjamin Holroyd John Wedge

Aetiology The underlying aetiology, although hypothesized, is not clear but is likely to be multi-factorial. In this review we have concentrated on non-teratological and non-neurological dislocations. For want of simplicity and clarity we have chosen to leave dislocated hips in these two groups to another discussion, as we feel there is doubt as to whether they should be included in the definition of DDH at all. DDH is predominantly a female condition (5:1), giving rise to hypotheses pertaining to a hormonal aetiology. Relaxin is the hormone most commonly implicated. It may however be the fact that up to twice as many females as males are born breech. Males with the disease are often more resistant to treatment. It is more common in the left hip as this is the adducted hip lying against the sacrum in the most commonly occurring intrauterine position. The disease is bilateral in 20% of patients. There is a geographical predilection. It is common in Native American Indians (1 in 20) and rare in sub-Saharan Africans, supporting postnatal influences such as swaddling as a causative factor. The close association with torticollis and foot deformities support the ‘‘tight packaging’’ theory. Other than female sex, risk factors for DDH and ones that may be used to rationalize ultrasound hip screening include breech presentation, primiparous babies, high birth weight, family history, multiple pregnancies and oligohydramnios.

Abstract Developmental dysplasia of the hip (DDH) is a spectrum of pathologies affecting the infant hip ranging from asymptomatic subtle radiographic signs through mild instability to frank dislocations with an abnormal acetabulum. Patients with developmental hip dysplasia account for around 10% of all primary hip arthroplasties, and around 30% in those under sixty. Early detection and appropriate management can prevent or delay the requirement for total hip replacement. In this article we aim to provide a broad overview of the aetiology, natural history, pathology and management of developmental dysplasia of the hip.

Keywords developmental dysplasia of the hip (DDH); open reduction; pelvic osteotomy; screening; spica

‘‘It is difficult to portage a canoe with a man who limps e he dips and you don’t’’.1 The week beginning 23rd February 2009 marked Baby Hip Health Awareness Week organized by the STEPS charity. This coincided with a Parliamentary Early Day Motion proposed by the MP for Blaydon, Mr David Anderson, calling for the Government to improve shortcomings in screening for and patient information about developmental dysplasia of the hip (DDH).

Natural history Why intervene at all? The reason is that patients with DDH account for 10% of all total hip replacements,3 and up to 30% in the under 60’s. Complete dislocations may have little functional disability. Patients will have leg length discrepancies if unilateral and a Trendelenberg gait. Perceived disability is largely dependent on socio-economic factors. Walker1 reports that Navajo Indians consider dislocated hips in much the same way as urban societies view left handedness. The development of a false acetabulum is the best predictor of outcome.4 A false acetabulum undergoes degenerative change in much the same way as a native joint. Based upon an early modification of the Harris hip score only a quarter of patients with well-developed acetabula have a good result into adulthood, compared to half of those with no or poor false acetabula. Hips that sublux usually develop significant osteoarthritic changes in the third or fourth decades. Stable hips with radiological evidence of dysplasia are less predictable, although it is uncommon to see hips without any degenerative change beyond the fifth decade. The concentration of forces through a reduced weight bearing area is the primary cause of early onset osteoarthritis, although the inherent quality of the cartilage may also play a role. The more dysplastic a hip, the smaller the weight bearing area between articular surfaces.

Introduction DDH, despite a recent change in nomenclature, is not a new diagnosis, having been described as early as Hippocrates. It is a spectrum of pathologies affecting the infant hip ranging from asymptomatic subtle radiographic signs through mild instability to frank dislocations with acetabular abnormality. Many authors have attempted to subdivide the condition into distinct entities. Although popular opinion now favors a continuous spectrum, adolescent and young adult patients presenting with acetabular dysplasia may represent as an entirely distinct entity. Initially referred to as congenital dislocation of the hip, recognition that apparently normal hips on examination at birth did not exclude the disease led to a change of nomenclature to developmental dysplasia of the hip.

Benjamin Holroyd MBBS BSc FRCS (Tr & Orth) Orthopaedic Fellow at The Hospital for Sick Children, Toronto, Ontario, Canada M5G 1X8. John Wedge OC MD FRCS(C) Professor of Surgery at University of Toronto and a Chair of Advisory Council for Sick Kids International, Canada.

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Presentation

authors, although debate exists where the cut-off between each of the four groups (six in the modified classification) lies. The radiographic findings in DDH are problematic in that there are no sharp distinctions between pathology and normality. This subtle spectrum is the core of the problem for the management of DDH.

A patients’ presentation can broadly be categorized into early or late. Arbitrarily, six months of age is often used as a cut-off between the two groups, although it may again be considered a spectrum. Early presenting patients may arrive in the hip clinic as a result of findings on baby checks, as detected by screening of at risk babies, or because of parental concern. Parents often report clicking in a baby’s hip when handling the child, particularly when changing nappies. This reported sign is a notoriously poor predictor of hip pathology as it often arises from the knee, the iliopsoas tendon moving over the femoral head or the fascia lata moving over the greater trochanter. Abnormality of soft tissue creases also corresponds poorly with DDH, despite being an often quoted finding in textbooks. Leg length discrepancy as assessed by Galeazzi’s test may not pick up more subtle differences, and is obviously absent in bilateral dislocations. We along with many authors have found a limitation of hip abduction and obvious tightness in the adductor longus tendon to be the most sensitive examination to detect a dislocated hip. Very infrequently does a child with a dislocation have full, symmetrical abduction. Late presenting hips often present at the time of walking. There is a weak association between delayed walkers and DDH. A Trendelenberg gait may be noted, although in toddlers this may be difficult to appreciate even to the experienced. Leg length discrepancy is a common reason to present but children never present with pain. The first referral may be as a result of symptomatic OA in the young adult.

Screening There is little debate that an early diagnosis in DDH is beneficial to patient outcome. The subject of how patients are detected however is more contentious. A meta-analysis by Lehmann6 found the incidence of DDH revealed from examination by a paediatrician to be 8.6/1000, from examination by an orthopaedic surgeon to be 11.5/1000 and from ultrasound examination to be 25/1000. In the UK, neonates have their hips examined for stability and range of movement by a member of the paediatric team, often a junior member. Jones recognized this as an issue in his 1998 JBJS editorial7 and called for surgeons to be more involved with screening or, as he preferred to call it, surveillance of DDH and with education of other healthcare professionals. Performing a reductive test (Ortolani) or a provocative test (Barlow) is not a completely benign process. The hip may theoretically be damaged by direct means as the head is pushed over the acetabulum, disrupting the labrum or potentially the iliac or ischial secondary growth plates. Multiple examinations by inexperienced examiners or when findings are equivocal are said to increase the likelihood of iatrogenic damage. Even in experienced hands, it has been postulated that a disruption of the negative intra-articular pressure within the hip joint can lead to dysplasia in an otherwise healthy joint. Jones8 examined ten neonatal hips in stillborns after repeated Barlow testing and found that the posterior capsule was not a strong or important structure, but that the vacuum fit between femur and acetabulum was. Positioning a hip to take a forced, frog lateral X-ray is enough to disrupt the labral seal containing the negative intra-articular pressure as evidenced when an air arthrogram is inadvertently created. Other than iatrogenic hip injury, examination as a hip screening tool is problematic on account of its low sensitivity. Jones9 reports sensitivity likely to be less than 60% despite the high specificity, approaching 100%, as there are few false positives. Combining clinical examination with an ultrasound investigation (Figure 1) increases the sensitivity to approximately 90%.10 Some authors would argue that screening all births by examination and ultrasound leads to parental anxiety. But Schoenecker11 points out that this is ‘‘a fallacious reason not to screen, as with any healthcare issue in infancy in which early detection can lead to a simple and definitive treatment of a potentially pathological condition’’. Barlow12 demonstrated hip instability in 1 in 60 of newborns. Untreated, 60% will stabilize in the 1st week, 88% by 2 months. As it is not possible to predict which of the unstable hips will normalize, the consequences of not treating an unstable hip are severe and the risks associated with early treatment relatively low, most authors recommend that all unstable hips should be treated. However, follow up with regular ultrasound and delaying treatment until four to six weeks of age is probably safest.

Radiological findings Before something can be considered pathological it is important to consider what is normal. The work by Tonnis5 from 1975 described normal values in both adults and children and is considered the classic description. The acetabular index changes with age from 30 (þ/5 ) at birth to 20 (þ/5 ) at 5 years. Tonnis reported that values falling two standard deviations above the mean were definitely pathological, but that a grey area existed between one and two standard deviations. He concluded that all those above a single standard deviation should be treated as only 25% become normal. As with all radiographic measures inaccuracies are common if positioning of the child allows postural artefacts to occur. The centre edge angle of Wiberg is notoriously difficult to measure in the under 5’s, as it is difficult to pinpoint the centre of the femoral head. For this reason there are no meaningful data of normal values and it is therefore of very limited clinical value at this age. It does, however, offer an indication of femoral head lateralization. Tonnis described the lower limit of normal, in other words one standard deviation below the mean to increase from 19 in 5 year olds, to 25 in 10 year olds. Wiberg considered the adult normal range to be 20 to 40 . Although it is difficult to attach numerical values to Shenton’s line this is one of the most useful radiological findings in DDH. A break in Shenton’s line may best be considered a binary event, and denotes proximal or lateral migration of the femoral head. The Severin radiographic classification (1941) is popular with

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a cartilaginous model of the hip. By the 11th week the femoral head is spherical, the acetabulum reciprocally shaped and the capsule, synovium and ligamentum teres identifiable. The acetabulum continues to develop through intrauterine life, the labrum contributing significantly to its depth. Having initially been deeply set, it becomes shallowest and therefore least stable in late pregnancy, presumably to facilitate delivery. After birth, it again becomes more deeply set. This perinatal period is the time of greatest risk of instability. Sequential ultrasound investigations around this time can demonstrate how in a matter of weeks the hips can significantly deepen. The immature hip may only need observation as it normalizes, rather than commencing potentially damaging treatment. During the adolescent growth spurt, three secondary ossification centres develop, further deepening the joint. The os acetabuli in the pubis contributes to the anterior wall. The acetabular epiphysis of the ilium forms a major part of the superior margin of the acetabulum. This structure is at risk from the inexperienced surgeon when performing open reductions and pelvic osteotomies, and must be given due respect. Finally, a secondary centre on the ilium contributes to the posterior wall. Most of the primary pathological changes that happen occur on the acetabular side of the hip joint.14 The abnormal growth and development is related to primary pathology of the acetabular growth plates. Secondary changes from misdirected pressure from the femoral head also contribute. Somerville15 felt that femoral neck version played an important role and that changing this and the valgus/varus angle to redirect the head to the centre of the hip would facilitate remodeling on the acetabular side. It is worth mentioning that the same author amongst others believe ligamentous laxity may play a role. Without adequate pressure from the anterior hip ligaments, femoral neck anteversion remodeling is less likely to occur, increasing the chances of eccentric loading of the acetabulum and altering the growth potential on the acetabular side. Salter was not concerned by femoral anteversion, provided that a concentric reduction could be maintained during walking, as he considered the version would correct spontaneously. Although we have described DDH as a continuous spectrum we would specifically like to highlight one type of dislocation that we believe merits special consideration. We have observed in our own institution as well as elsewhere, surgeons experience greater trepidation when dealing with the higher dislocation. We suggest that the low dislocation that ‘‘slides’’ out requires more careful consideration. In our experience these hips are more likely to re-dislocate or not resolve as satisfactorily post-reduction. This may be because of pressure on the lateral acetabular epiphysis as the hip dislocates, inhibiting growth potential of the acetabulum post-reduction. The high dislocation exerts little or no pressure on this important growth centre, so once the femoral head is reduced and covered by the acetabulum the socket can grow and remodel reasonably well.

Figure 1 A normal hip on ultrasound.

The exception to this is the hip that is dislocated at rest, with an entry clunk, which should be treated urgently (Figure 2). There have been many ultrasound techniques described, those by Harcke, Terjesen, Suzuki and Graf being the most commonly used. The Graf13 technique is the most popular technique employed in the UK. He popularized hip ultrasound in 1978 with his classification from 1, a normal hip, through to 4, a dislocated hip with no discernable acetabulum. The ultrasound must meet strictly defined criteria in order to avoid faulty diagnosis. Graf reports a misdiagnosis of normal hips that later require surgical intervention to be as high as 20% in patients who he felt had inadequate ultrasound scans. Clearly adequate training of ultrasonographers or clinicians is integral to the success of the diagnosis and hence treatment.

Pathophysiology From studies that have examined aborted foetuses, we know that the normal hip begins to form as early as the 7th week of gestation. Primitive mesenchymal cells give rise to the limb buds that differentiate into the four extremities. A cleft first appears in the mesoderm at the end of 8 weeks and represents

Treatment We do not feel that describing our treatment algorithm in depth would be useful as there will always be debate as to how and when

Figure 2 A dislocated hip on ultrasound.

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to initiate various treatments. We do however want to highlight the basic treatment principles and options available, along with the reasoning behind commonly adopted timings for interventions. It would seem logical that an early concentric reduction would give the optimal result. Several authors16,17 have reported that this is not necessarily the case and that hip reduction does not automatically lead to normal acetabular growth. Using the acetabular index as a marker of growth, Harris18 concluded that ‘‘the later the age of congruity, the more likely it is that the acetabulum will be dysplastic’’. He went on to state that ‘‘the critical age for obtaining a congruous reduction in the functional position is four years and that above this age an unsatisfactory acetabulum is the probable outcome’’. The timing of a reduction appears to be key to the prognosis. Albinana19 observed the timing of appearance and morphology of the teardrop in unilateral DDH treated non-operatively, using the normal side in his study as the control group. He found that a widened teardrop in the dislocated hip, presumably because of abnormal joint reaction forces, correlated strongly with a poor outcome at skeletal maturity. The use of the teardrop unfortunately cannot be used to time interventions, as by the time it is widened the intervention window has been missed. It may be useful however to predict outcome. Albinana also found that the age at which the hip reduction was achieved was the most important factor predicting outcome by Severin class at maturity, and that the earlier the reduction is achieved, the greater the remodeling capacity of the hip. Kalamchi however reports better results with waiting until patients are older than six months, as he feels this decreases the risk of avascular necrosis.20 Although an early reduction is desirable this has to be offset against technical difficulties associated with operating on younger patients. Salter for example does not recommend performing an innominate osteotomy before the age of 18 months. The most controversial timing of intervention is between six and eighteen months. It is becoming an increasingly popular view that intervention should be delayed until after the appearance of the ossific nucleus as this radiographic sign is thought to be protective from the risk of avascular necrosis.21 One problem with this approach is that in a small number of children, the ossific nucleus may not be visible until the latter part of this time frame. This could result in a hip reduction that is delayed by nearly a year, which may have a potentially detrimental effect on remodeling and hence the long term result.

harness because of disappointment at the high rates of avascular necrosis (AVN) with other methods of conservative treatment, predominantly using ‘‘passive mechanical treatment’’. Pavlik felt that movement was essential to the treatment of dysplasia. With the hips flexed, infants are unable to keep the hips adducted because of fatigue. This positioning leads to a gradual, spontaneous and non-violent reduction of the dysplastic hip. Movement of the legs generates a cyclical loading of the acetabulum, stimulating remodeling. The Pavlik harness is only suitable for hips that can be reduced on examination. An irreducible hip is a contraindication and an operative course of treatment should be initiated. The high rate of AVN that Pavlik observed was likely to be the result of forced abduction and/or flexion. Ramsey22 describes a ‘‘safe zone’’ when managing hips non-operatively. This is between the abduction and flexion necessary to maintain reduction, but not so far as to lead to interruption of the vascular supply of the femoral head. Success rates with Pavlik harness treatment are as high as 95% with corresponding AVN rates as low as 0.3%23 if used early in the course of the disease. Other than AVN and occasional parental compliance issues, the only significant side effect of harness treatment is femoral nerve palsy associated with hyperflexion. This usual resolves on adjustment of the harness. It is easily detected because active knee extension is lost, a movement that the harness does not restrict. Operative treatment If a hip has failed to respond to non-operative measures, is irreducible, or is diagnosed late, operative interventions are indicated. Closed reductions A hip manipulation under general anaesthetic with radiographic evaluation may be all that is required to achieve a satisfactory reduction. Although it is common practice to use an intra-operative arthrogram, we believe that this is not an essential requirement, and that the reduction can be assessed without radio-opaque medium. Proponents of arthrography accept no medial pooling of contrast when judging the reduction position and can identify residual soft tissue obstructions which may impair the acetabular response after femoral head reduction. The potential risk of anaphylaxis and sepsis with this procedure are over-stated. In the thirty year follow up paper of closed reductions, Malvitz24 placed his patients in hip spicas with 90 e100 of flexion and 60 of abduction, with the cast down to the ankle on the affected side and to above the knee on the unaffected side, thus stabilising the pelvis. The spica was left on for twelve weeks. It is fairly common practice to change the spica after six to eight weeks, to account for growth and soiling. Attention has to be paid to the ‘‘safe zone ‘‘mentioned earlier, and to performing an adductor tenotomy either percutaneously or open if this arc is insufficient. Confirmation of reduction in the spica is usually achieved with either MRI or CT scans. CT scans provide a clear view of bony architecture, but involve ionizing radiation, whereas an MRI involves no radiation but often requires general anaesthesia in order for the child to be still enough to gain meaningful images.

Non-operative treatment Once identified at a baby check, a child with an unstable hip is often placed into double nappies whilst awaiting an ultrasound scan or referral to an orthopaedic surgeon. The idea of increased abduction is a logical one but with little scientific basis. The same may be said for children spending time prone whilst awake and being observed. In the light of sudden infant deaths, few if any would continue to recommend prone sleeping. These two activity modifications although unproven to be beneficial are unlikely to cause damage, so may in our opinion continue to be employed but with advice to parents that they are an adjunct rather than as the primary treatment modality. Pavlik first described the use of his harness to the Czechoslovak Orthopaedic Society in Prague in 1946. He developed the

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The rate of AVN varies widely from 0 to 73%.25 The true rate clearly lies in between and depends very much on the diagnostic criteria and how rigorously and for how long they are sought. It is likely that the hips that go on to develop avascular necrosis are those that are dislocated rather than dislocatable. Open reductions The requirement for open reductions has declined since hip screening programs have become more widespread. Failure to achieve a closed reduction by the methods described previously, or late presentations, may necessitate an open procedure. In the child under six months of age, our preference is for a medial approach. Over eighteen months a concomittant innominate osteotomy can be performed through an anterior approach. The treatment between six and eighteen months as mentioned above is more controversial. We tend to favour an anterior open reduction, often postponing the pelvic osteotomy until after eighteen months of age if the acetabular index is not improving towards the expected normal values. The predominant structures that prevent reduction and need addressing at the time of open reduction, regardless of the approach used are the iliopsoas tendon, ligamentum teres, transverse acetabular ligament and pulvinar. The labrum and capsular infolding do not usually a cause a block to reduction if the capsule is opened and later plicated to remove the ‘‘dead space’’ into which the hip can redislocate. A very deformed, inverted labrum can be brought out over the femoral head if radial cuts are inserted into it, without damaging the lateral acetabular epiphysis. The thickened ligamentum teres often requires to be excised, after its proximal end has been used to define the true acetabulum in the high dislocation. The transverse acetabular ligament and any other medial bans should be released prior to reduction, but the pulvinar (fat pad) is a useful structure and does not merit excision as it is not obstructive.

Figure 3 Pre-operative radiograph of left hip dysplasia.

Two thirds of the surviving hips had little or no evidence of osteoarthritis. The results of any author describing their own technique are almost universally better than those who try to replicate it. This however is not necessarily the case following the innominate osteotomy if the author’s original technical description is understood and adhered to. As pelvic osteotomies rely on flexibility of either the tri-radiate cartilage or the pubic symphysis, there is obviously an age limit beyond which they should not be performed, and an adult periacetabular osteotomeis then considered more appropriate. We consider the upper age limit for reduction to be ten years in unilateral high dislocations and five years in bilateral, high dislocations. Bilateral dislocations treated with pelvic osteotomies should be staged to avoid creating a pelvic discontinuity. Femoral osteotomies Studies trying to compare the outcomes of femoral osteotomies versus pelvic osteotomies have been undertaken, but attempting to glean meaningful conclusions from them is difficult, on account of the large number of variables.

Pelvic osteotomies As discussed under hip pathophysiology, the primary pathology lies on the acebular side of the joint, with secondary changes occurring on the femoral side, such as femoral head deformation and increased anteversion. It is for this reason that we believe the principal correction should also take place on the acetabular side. There are numerous pelvic osteotomies described in the literature. Broadly speaking, they can be divided into two categories. There are those that rely on rotating the acetabulum around the open pubic symphysis, therefore not changing the volume of the joint but merely redirecting it. These ostetomies are used when a congruent reduction can be achieved and additional head coverage is required. The second group rotates the acetabulum about the tri-radiate cartilage, reducing the volume of the joint. These may be appropriate when there is an incongruence between the femoral head and acetabulum after reduction. Our preferred osteotomy is the innominate osteotomy (Figures 3, 4 and 5) described by Salter. This yields predictable results as demonstrated by post-operative follow to up to 45 years.26 Patients treated with an innominate osteotomy and open reduction had hip survival rates of 99% at thirty year follow up, 86% at forty year follow up and 54% at forty five year follow up.

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Figure 4 Post operative radiograph after innominate osteotomy.

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Figure 5 Radiograph demonstrating acetabular remodeling after innominate osteotomy.

Figure 7 Post operative radiograph in a hip spica following open reduction, innominate osteotomy and shortening femoral osteotomy. Note: Staging of bilateral procedures.

Femoral osteotomies do have a place, but rarely, in our opinion, as the sole procedure. The commonest indication is a high dislocation that requires a femoral shortening osteotomy in order to reduce the hip without tension (Figures 6 and 7). The coronal alignment (varus/valgus) does not need much correction, and needs careful to be carefully controlled when adjusting femoral neck version.

affecting the ossific nucleus resulted in excellent long term function, whereas avascular necrosis affecting the proximal femoral physis was associated with an unpredictable but usually poor outcome. Kalamchi found the highest rate of avasular necrosis to be in those treated under six months of age. This however was in the pre-Pavlic era, when it was not uncommon to place a child in a hip spica without general anaesthesia. He correctly points out that ‘‘this is not to suggest a delay in initiating treatment, but rather a plea for extra care when treating infants’’. Ultimately the sequelae of DDH, whether affected by avascular necrosis or not, is arthritic change requiring total hip replacement. Although implant design and materials have advanced over the years, arthroplasty in the untreated DDH hip with no recognizable acetabulum or in one that is proximally placed with marked limb shortening remains a challenge. Long standing shortening is often only partially correctable, limited by soft tissue distraction tolerance. The acetabular component is often sub-optimally supported even with augmented implants or bone grafting procedures. The increase in arthroplasty options should not detract from solving the underlying problem.

Sequelae Despite advances in our understanding of the pathophysiology and hence treatment of DDH, avascular necrosis of the femoral head remains a relatively common and serious complication. It is difficult to place a figure on the rate of avascular necrosis in DDH, not only as the treatment options are so varied, but also because diagnostic criteria for it differ, depending on author. This is likely to account for the wide range in quoted rates from 0e73%. Kalamchi20 developed a classification system for avascular necrosis by reviewing 1072 patients treated for DDH, 119 of whom had avascular necrosis. He found that avascular necrosis

Conclusions The healthcare economics that surround hip dysplasia are extremely complex. However the morbidity spared the child and family as well as the potential savings for the country if a national strategy is appropriately implemented through resource availability could be substantial. There is an enormous volume of literature written about DDH. What has become abundantly clear is that it is unlikely to be a single disease entity requiring a single simple solution. Early diagnosis is clearly beneficial to both the child and family, and to the wider community in terms of healthcare economics. What remain the greatest challenges in the management of DDH are interpretation of hip imaging, timing of the intervention and the treatment choices. A

Figure 6 Radiograph of bilateral late presenting hip dislocations.

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REFERENCES 1 Walker JM. Congenital hip disease in a Cree-Ojibwa population: a retrospective study. Can Med Assoc J 1977; 116: 501. 2 Connolly P, Weinstein SL. The natural history of acetabular development in developmental dysplasia of the hip. Acta Orthop Traumatol Turc 2007; 41(Suppl 1): 1e5. 3 Dezateux C, Rosendahl K. Developmental dysplasia of the hip. The Lancet 2007; 369. 4 Wedge JH, Wasylenko MJ. The natural history of congenital disease of the hip. J Bone Joint Surg Br 1979; 61: 334e8. 5 Tonnis D. Normal values of the hip joint for the evaluation of X-rays in children and adults. Clin Orthop Relat Res 1976; 119: 39e47. 6 Lehmann HP, Hinton R, Morello P, Santoli J. Developmental dysplasia of the hip practice guideline: technical report. Committee on quality improvement and subcommittee on developmental dysplasia of the hip. Pediatrics 2000; 105: 57e82. 7 Jones D. Neonatal detection of developmental dysplasia of the hip. J Bone Joint Surg Br 1998; 80: 943e5. 8 Jones DA. Neonatal hip stability and the Barlow test. A study in stillborn babies. J Bone Joint Surg Br 1991; 73: 216e8. 9 Jones D. An assessment of the value of examination of the hip in the newborn. J Bone Joint Surg Br 1977; 59: 318e22. 10 Rosenberg N, Bialik V, Norman D, Blazer S. The importance of combined clinical and sonographic examination of instability of the neonatal hip. Int Orthop 1998: 431e4. 11 US Preventive Services Task Force. Screening for developmental dysplasia of the hip: recommendation statement. Pediatrics 2006; 117: 898e902. 12 Barlow TG. Early diagnosis and treatment of congenital dislocation of the hip. J Bone Joint Surg Br 1962; 44: 292e301. 13 Graf R. Hip sonography. Diagnosis and management of hip dysplasia. 2nd edn. New York: Springer Verlag, 2006. 14 Ponsetti IV. Morphology of the acetabulum in congenital dislocation of the hip. Gross, histological and roentographic studies. J Bone Joint Surg Am 1978; 60: 586e99.

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15 Somerville EW, Scott JC. The direct approach to congenital dislocation of the hip. J Bone Joint Surg Br 1957; 39: 623. 16 Bost FC, Hagey H, Schottstaedt ER, Larsen JJ. The results of treatment of congenital dislocation of the hip in infancy. J Bone Joint Surg Am 1948; 30: 454. 17 Trevor D. Treatment of congenital hip dislocation in older children. Proc R Soc Med 1960; 53: 481. 18 Harris NH. Acetabular growth potential in congenital dislocation of the hip and some factors upon which it may depend. Clin Orthop Relat Res 1976; 119: 99e106. 19 Albinana J, Morcuende JA, Weinstein SL. The teardrop in congenital dislocation of the hip diagnosed late. A quantitative study. J Bone Joint Surg Am 1996; 78: 1048e55. 20 Kalamchi A, MacEwen GD. Avascular necrosis following treatment of congenital dislocation of the hip. J Bone Joint Surg Am 1980; 62: 876e88. 21 Clarke NMP, Jowett AJL, Parker L. The surgical treatment of established congenital dislocation of the hip: results of surgery after planned delayed intervention following the appearance of the capital femoral ossific nucleus. J Pediatr Orthop 2005; 25(4): 434e9. 22 Ramsey PL, Lasser S, MacEwen GD. Congenital dislocation of the hip. Use of the Pavlik harness in the child during the first six months of life. J Bone Joint Surg Am 1976; 58: 1000e4. 23 Taylor GR, Clarke NM. Monitoring the treatment of developmental dysplasia of the hip with the Pavlik harness. The role of ultrasound. J Bone Joint Surg Br 1997; 79: 719e23. 24 Malvitz TA, Weinstein SL. Closed reduction for congenital dislocation of the hip. Functional and radiographic results after an average of thirty years. J Bone Joint Surg Am 1994; 76: 1777e92. 25 Zionts LE, MacEwan 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: 829e46. 26 Thomas SR, Wedge JH, Salter RB. Outcome at forty five years after open reduction and innominate osteotomy for late presenting developmental dislocation of the hip. J Bone Joint Surg Am 2007; 89: 2341e50.

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(iv) Slipped upper femoral epiphysis

Endocrine disorders are causative in approximately 8% of SUFE patients, and the majority are of short stature [10th percentile or less]. Height can be used as a screening tool to identify those who should be investigated by an endocrinologist, as 91% of those with an endocrinopathy are on the 10th percentile or below.3 The disorders particularly associated with SUFE are hypothyroidism (40%), growth hormone deficiency (25%), with other endocrinopathies accounting for the other 35%. The endocrinopathies that present under the age of 10 are hypothyroidism and growth hormone deficiency. Those with a diagnosis of hypothyroidism usually slipped prior to, or during treatment, whilst those with growth hormone deficiency usually slipped during or after treatment. The majority of other endocrine disorders present after the age of 16.4 Bilaterality of slip occurs in 61%, suggesting the need for prophylactic pinning of the other hip in endocrine disorders. Apart from endocrine disorders, many other conditions have been linked to SUFE:- renal failure osteodystrophy with secondary hyper-parathyroidism, radiation therapy, steroid treatment, paraplegia, tuberculosis, and malnutrition. Racial differences appear significant. The highest relative incidence appears to be in Pacific Islanders (4.5), and blacks (2.2). Whites are in the middle of the incidence scale (1). The incidence in North Africa, Middle East, India (0.1) &Asia (0.5) is low. How much of this apparent racial difference is actually due to differences in weight, diet, or climate, is unknown.

Richard J Montgomery

Abstract The incidence of slipped upper femoral epiphysis is 10 per 100 000 in the age groups most at risk. The commonest presenting features include groin, thigh, or knee pain, with limp, hip ‘irritability’, external rotation, and restriction of flexion and abduction. In girls the peak incidence is between 10 and 13 and in boys between the ages of 12 and 15. Most cases are idiopathic and associated with a high body mass index. Slips usually occur through the proliferative and hypertrophic zones of the growth plate. The chief complications are avascular necrosis and chondrolysis. The treatment of a slip is usually by pinning in situ. A severe slip is very disabling, even if AVN is avoided. Surgery to correct the deformity is either by some variant of intra-capsular neck osteotomy, or by an extra-capsular osteotomy. In the past, intra-capsular osteotomy was blamed for causing AVN, but recent experience suggests that it is the setting in which it is considered [severe, often unstable slips] which is the cause of the AVN, not the procedure itself.

Keywords avascular necrosis; chondrolysis; slipped upper femoral epiphysis

Pathogenesis Incidence

The pathology of the condition has been established only through study of the established slip. We cannot be certain which of the changes we see were present before the slip occurred, and which are a consequence of the slip process. A study of the pathology of ‘pre-slip’ and of the contralateral side in unilateral cases may determine this question. ‘Pre-slip’ refers to the situation when the hip is painful prior to detectable displacement. The use of MR scanning may help to detect early abnormality. It is also assumed when the other side has already slipped. It should be treated by pinning in situ. The slip occurs through the proliferative and hypertrophic zones of the growth plate, which are thickened and appear abnormal both under light and electron microscopy. There appears to be down-regulation of gene expression for type II collagen and aggrecan in the growth plate, although whether this is cause or effect is not known. The chief complication of a slip is avascular necrosis of the epiphysis [AVN]. This mostly commonly follows an unstable slip, defined by Loder5 as one where the patient is unable to walk; a patient who is able to walk is defined as stable. However it must be appreciated that this stability is relative, and that a stable slip can at any stage become unstable, with all the undesirable consequences that brings. Therefore all slips, presently stable or unstable, need urgent assessment and treatment. Increasing degrees of slip are also associated with an increased risk of AVN, though that might be because of an association between instability and severe grade slip. Chondrolysis refers to the breakdown of articular cartilage in the joint. The hip is relatively stiff, and joint space narrowing

The incidence of slipped upper femoral epiphysis [SUFE] varies with sex, age, and racial group.1 Overall, the incidence is in the order of 3.41 per 100 000 of the population under 25; in the age groups found to be at most risk, it is 10.08 per 100 000. This is an under-estimate, as mild cases may not be diagnosed until arthritis supervenes many years later. The lowest annual incidence appears to be in white females, at 1.64 per 100 000. White males are next with an incidence of 4.74 per 100 000. Black females have an incidence of 6.68, black males an incidence of 7.79 per 100 000. 80% of male cases are diagnosed between the ages of twelve and fifteen; 83% of female cases are diagnosed between the ages of ten and thirteen. Boys, therefore, tend to have their slips two years older than girls. The majority of cases diagnosed below or above these ages have other associated systemic diagnoses; late cases may be associated with conditions that delay skeletal maturation and physeal closure.

Aetiology Patients with SUFE have a significantly higher Body Mass Index during growth than normally developing children.2 Most cases are idiopathic.

Richard J Montgomery MB BS FRCSEd is a Consultant Trauma & Orthopaedic Surgeon at The James Cook University Hospital, Middlesbrough, UK.

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becomes apparent on X-ray. It can occur where there is persistent pin penetration of the joint following internal fixation of the slip, but usually occurs spontaneously. It is commoner in black races, and can be seen at the time of presentation in nearly half of the cases. Most joint space narrowing occurs within the first year, and a subsequent increase in joint space and range of movement occurs for up to three years thereafter. Pain resolves but some stiffness persists in over one third of cases.6 Recently, femoro-acetabular impingement [FAI] has been identified as a problem after slips in some cases [Figure 1]. Some surgeons are interventionist in treating this surgically, the belief being that FAI will lead inevitably to osteoarthritis, and that surgical dislocation and anatomical replacement of the head, or subsequent treatment of the impingement may prevent this. This belief in the almost inevitable progression to arthritis does not match the known rates of progression to arthritis of slips pinned in situ [see below]. It will be many years before we know whether this surgical enthusiasm translates into patient benefit. Long term results of pinning in situ are perhaps better than one might expect, given the amount of deformity of the femur that remains. At 30 years follow up, 20% of cases with up to 30 degrees slip angle have mild osteoarthritis, 2.5% have severe arthritis.7 Slip angles between 30 and 50 degrees lead to 33% mild osteoarthritis, and 16% severe arthritis. Results for slips more severe than 50 degrees were not recorded, and are expected to be considerably worse given that the AVN rate may exceed 50% in slips of this severity.

to move, there is a reduction in the range of internal rotation, and of abduction. A late case presents the findings of a displaced femoral neck fracture, for that is what it is. The leg is shortened, and lies in fixed external rotation, with a obvious loss of flexion and abduction. The very much rarer valgus slip presents with different physical findings on late presentation, but the symptoms are similar at its onset.

Investigation If any of the clinical patterns above is presented, the case for radiography is made. This is definitely a scenario where, if the diagnosis is even suspected, urgent radiography is the right course. The patient should be managed as if they were an adult suspected of having a femoral neck fracture. They should be kept non-weight bearing, and be conveyed to the nearest hospital with an accident and emergency department and X-ray facilities. If the patient has been able to weight bear up to this point [stable slip], anteroposterior and frog lateral radiographs should be done. There is no need for a lateral radiograph in the unstable slip if the first anteroposterior radiograph is diagnostic as frog-leg positioning is extremely painful and could worsen the slip [Figure 2]. In a mild case of SUFE, one may see widening and lack of definition of the physeal plate. Klein’s line, drawn along the superior edge of the femoral neck, may not intersect with the femoral head [Trethowan’s sign]. There may be metaphyseal blanching, due to increased X-ray absorption caused by superimposition of the head behind the metaphysis. Chronic cases may show new bone formation on the posterior/ inferior part of the femoral neck. Over time, the superior edge of the metaphsis becomes blunted and round due to erosion caused by abutment against the acetabular labrum or acetabular edge. The extent of an unstable or severe slip can be determined best by tomography. Because of the difficulty in pure abduction, the lateral film obtained tends to incorporate a varying degree of flexion and external rotation; rarely are the two films at right angles to each other. Judging the degree of slip purely by plain radiography is therefore often misleading. The true situation is sometimes far worse than the plain films indicate. CT can reveal

Clinical features The clinical presentation may be sudden, or insidious; the latter may progress to the former. The relative rarity of the condition, its insidious onset, the referral of pain to the ipsilateral knee and sometimes the vagueness of symptoms are responsible for the common delay in diagnosis. SUFE is a regular cause of litigation. Since the difference in outcome between an early-diagnosed case and a late case is great, settlements are correspondingly large. The typical case is an overweight boy approaching puberty who develops groin, thigh, or knee pain, perhaps after a trivial injury. However it must be emphasized that neither sex is immune; it can happen in slim children, and outside the typical age band, particularly if an endocrine disorder is present. Clinical findings in the early case are subtle. There may be no signs except an antalgic limp, discomfort, or ‘irritability of the hip’ on examination. The symptoms may be intermittent, in which case a link to activity is usually present. As the slip starts

Figure 1 Case A. The prominence of the exposed metaphysis could lead to femoroacetabular inpingement.

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Figure 2 Case A. AP pelvic radiograph showing left sided SUFE, in this case unstable.

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classification does not help to determine the treatment, nor is it of prognostic significance. Classification by stability is useful. A stable slip is one where the patient can walk, whereas an unstable slip is one where the patient cannot walk, with or without crutches. An unstable slip carries a higher risk of complications, principally avascular necrosis, which occurred in 47% of unstable slips in Loder’s series, but in none of the stable slips. There are also two anatomical classifications, which measure displacement either by proportion of slip, or by angle of slip. A mild slip is one where the displacement of the physis as a proportion of neck width is less than one third. In a moderate slip, displacement is by between one third and one half of neck width, and severe slip has displacement of greater than one half of neck width. Angular displacement can be measured by comparing the Southwick angle of the slipped side with that of the normal side. This of course assumes that there is a normal side, which is often not the case. The Southwick angle is drawn on the lateral radiograph. It is the angle between a line drawn from the posterior to the anterior edge of the physis, and the axis of the neck. A mild slip has an angle difference of less than 30 degrees, a moderate slip has an angle difference of between 30 and 50 degrees, and a severe slip has a difference of over 50 degrees. In practice, one tends to use a combination of the Loder classification and one of the anatomical classifications [for example: ‘a severe unstable slip’]. There is some crossover between the classifications but severe slips are more likely to be unstable.

Figure 3 Case A. MRI showing widespread oedema, and a severe slip.

new bone formation on the postero-inferior aspect of the neck, which would imply a degree of chronicity. Apart from this it adds little. MRI can reveal pre-slip, the extent of slip, oedema, and vascular changes [Figure 3 and 4]. Although avascularity does not in fact alter management, it is considered good practice to share information about likely prognosis with parents at the earliest opportunity. Endocrine investigations are not routine, but should be done in cases outside the usual age range, or those showing characteristics such as restricted growth, delayed maturation, or features suggestive of hypothyroidism.

Management

Traditionally, SUFE was classified as acute [where symptoms had been present for less than three weeks], chronic, or acute on chronic [where there had been a recent deterioration against a background of previous symptoms]. This is more of a description than a classification. The recall of symptom duration is unreliable, and some slips are asymptomatic. This temporal

Management is often contentious. The reason for this is the lack of high quality evidence, due to rarity, uncertainty regarding long term outcomes, and the difficulty in comparing like with like. It is only relatively recently that the influence on prognosis of the Loder classification has become starkly apparent. Older studies in which no distinction is drawn between cases that could, or could not walk, or which do not stratify the severity of slip are no longer considered to be very useful. Caution should be exercised in interpreting studies that give very low postoperative AVN rates in unstable slips, as a selection bias is likely to have been operating.

Figure 4 Case A. MRI shows that the slip angle is approaching 90 degrees. The upper femoral epiphysis and the trochanteric epiphysis are almost in contact.

Reduction of displaced slips, and timing of surgery Forceful reduction of a slipped epiphysis should never be performed. A stable slip cannot be reduced without turning it into an unstable slip, with the likelihood of vascular damage. Stable displaced slips should therefore be pinned in situ unless the degree of slip is severe, when the option of femoral neck osteotomy should be discussed, with its benefits and drawbacks. If the slip is unstable and recent, it is commonly found that some reduction takes place while transferring the patient onto the operating table. This should be accepted. Phillips et al8 reported good results from reducing and pinning unstable slips within 24 hours of the onset of significant symptoms. Kalogrianitis et al9 found that of sixteen unstable slips, half developed AVN. Those that did not develop AVN were operated on before 24 hours or after a week. Other authors advise waiting for three

Classification

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weeks, with bed rest to allow the femoral head circulation to recover before surgery for the severe unstable slip.10 Pinning in situ Stable or unstable slips of mild degree can be pinned in situ, and a good result is usually obtained. A single screw into the central third of the physis on AP & lateral planes is the ideal fixation. The screw does not need to be removed, and should not be removed prior to physeal arrest, otherwise progression of the slip may resume. It is usually possible to place the screw percutaneously, over a guide-wire under image intensifier control; descriptions of how to find the skin entry point for this are published. The entry point for the wire is more anterior than for an adult hip fracture. The worse the slip deformity, the harder the intra-operative radiography becomes to perform and interpret. The wire should pass obliquely in a posterior direction, passing out of the proximal end of the metaphysis [not out through the posterior cortex of the neck], and into the central third of the head. If the slip is so severe that this placement is not possible, then it is unlikely that pinning in situ will lead to a good result. It is the author’s view that this is the indication for open reduction and femoral neck osteotomy [see below]. When less than 50% contact remains between the corresponding surfaces of the physis, the biomechanics of the fixation changes. If the screw is placed anteriorly in the head, a shorter screw has to be used, or it will penetrate the articular surface. Little grip is then obtained, and the screw may simply cut out as the slip progresses. If, on the other hand, it is placed posteriorly, where the femoral head is overhanging the neck, it may tip the head further when compression is applied. If the initial wire placement is wrong, then the spinning threaded tip may pass into the posterior vascular pedicle upon which the femoral head depends. If the slip is so severe that the femoral head is lying on the back of the neck, there are now two incongruous surfaces. The dished under-surface of the physis contacts the cylindrical neck in only two places. A single screw will not convert this into a stable situation. Since the slip has gone as far as it can, and since pinning would not make it stable, there is very little point in attempting to pin in situ at this stage; referral to a surgeon who performs surgical reduction is a much better option. Don’t make a hole in the femoral head before you do that! There are relatively few specific complications associated with the pinning process itself. Slip progression can occur if early full weight bearing is allowed before the physis stabilises, and is reported to be commoner if less than five screw threads engage the epiphysis. If AVN does occur [Figure 5], the screw may protrude into the joint as the head collapses. Removal of the screw is not usually difficult in these circumstances, because the bone becomes soft. However, if screw removal is attempted later, after a successful pinning, it can prove very difficult or impossible. The use of a hip screw with threads that cut in reverse, and an outside hex that fixes firmly to a wrench, can minimise these problems.

Figure 5 Case B. A severe unstable slip has been pinned in situ, in a dispaced position. The occurrence of avascular necrosis means that the hip is painful & stiff in a position of adduction, external rotation and extension.

slip seems unrelated to age at first slip, and may be more severe.11 In addition, patients with an underlying endocrine or metabolic disorder are very likely to experience a slip on the contra-lateral side. Against prophylactic pinning is that in many cases one is performing an operation that would not have proved necessary otherwise. However the risks seem smaller than waiting for the other side to slip. For all these reasons, I routinely pin the opposite side if the patient and parent(s) consent after explanation.12 Operative reduction by femoral neck osteotomy Whilst pinning in situ has good results in mild slips, unfortunately the same is not true when the technique is applied to severe slips, particularly if they are unstable. The worst outcomes of all follow pinning in situ of a severely displaced hip, followed by AVN. AVN with the epiphysis in a good position is bad enough, but AVN with the head still behind the femoral neck is far worse [see Figure 5]. The hip is exceedingly stiff in adduction and external rotation, and flexion restriction makes sitting difficult. If it is not too painful, then femoral osteotomy can realign the leg into a more functional position. If it is painful and disabling, then the only reasonable solution may be arthrodesis with deformity correction, for which the patient & family are usually very grateful. Because of the limitations of pinning in situ of severely displaced hips, various authors have treated the condition by surgical reduction of the deformity. The most logical site to do this is at the site of the deformity itself. This approach has been taken by Dunn, Fish, and Ganz.13,14,15 The operation has the merit of reducing the chance of impingement and allows an excellent return of hip function provided that AVN does not occur. The Ganz technique of surgical dislocation prior to the reduction reportedly has a low rate of AVN in the hands of its originators, but whether this record will be maintained if it is used more widely, only time will tell. The Dunn technique involves a trochanteric osteotomy, which potentially could put the vascular supply to the head at risk. Nevertheless, the results

Prophylactic pinning of the contra-lateral side The reasons given for prophylactic pinning are that slipping may be painless, or sudden, and that some patients cannot be relied upon to return if symptoms occur on the other side. The second

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practice, the osteotomy needs to be carefully thought through so that it addresses the individual needs of that patient. The surgeon must bear in mind that the patient will likely need a hip arthroplasty in time, and take care not to complicate that eventuality by excessive angulations or translations. If pain is a big feature, then arthrodesis of the hip should at least be discussed with the parents, even if it is not eventually selected. Arthroplasty of the hip in adolescents has an overall failure rate of 45% at 15 years, but the risk of failure is even higher in unilateral cases, in active individuals, and after noninflammatory conditions. This translates to a risk of revision arthroplasty before the thirtieth birthday. The alternative of arthrodesis is at least durable. Although it is said that arthrodesis causes back pain, some of the arthrodeses performed in the past were achieved in less than ideal positions that may have contributed to this outcome. One should consider that back pain may also occur after arthroplasty. Back pain after arthrodesis does not appear to be as disabling as a failed arthroplasty or a Girdlestone procedure. Arthroplasty is the only realistic solution on those rare occasions when SUFE has resulted in bilateral painful hips. A

Figure 6 Case A. Healing after Fish osteotomy on the left, prophylactic pinning on right.

REFERENCES 1 Kelsey JL, Keggi KJ, Southwick WO. The incidence & distribution of slipped capital femoral epiphysis in Connecticut & Southwestern United States. J Bone Joint Surg Am 1970; 52-A: 6. 2 Poussa M, Schlenzka D, Yrjonen T. Body mass index and slipped capital femoral epiphysis. J Pediatr Orthop B 2003; 12960: 369e71. 3 Burrow SR, Alman B, Wright JG. Short stature as a screening test for endocrinopathy in slipped capital femoral epiphysis. J Bone Joint Surg Br 2001; 83-B: 263e8. 4 Loder RT, Wittenberg B, DeSilva G. Slipped capital femoral epiphysis associated with endocrine disorders. J Pediatr Orthop 1995 MayeJun; 15(3): 349e56. 5 Loder RT, Richards BS, Shapiro PS, Reznick LR, Aronson DD. Acute slipped capital femoral epiphysis: the importance of physeal stability. J Bone Joint Surg Am 1993; 75: 1134e40. 6 Vrettos BC, Hoffman EB. Chondrolysis in slipped upper femoral epiphysis. Long-term study of the aetiology and natural history. J Bone Joint Surg Br 1993 Nov; 75(6): 956e61. ¨gstedt B, Jerre R, Wallin J. Long-term results 7 Hansson G, Billing L, Ho after nailing in situ of slipped upper femoral epiphysis. A 30-year follow-up of 59 hips. J Bone Joint Surg Br 1998 Jan; 80(1): 70e7. 8 Phillips SA, Griffiths WEG, Clarke NMP. The timing of reduction and stabilisation of the acute, unstable, slipped upper femoral epiphysis. J Bone Joint Surg Br 2001; 83-B: 1046e9. 9 Kalogrianitis S, Tan CK, Kemp GJ, Bass A, Bruce C. Does unstable slipped capital femoral epiphysis require urgent stabilization? J Pediatr Orthop B 2007 Jan; 16(1): 6e9. 10 Biring GS, Hashemi-Nejad A, Catterall A. Outcomes of subcapital cuneiform osteotomy for the treatment of severe slipped capital femoral epiphysis after skeletal maturity. J Bone Joint Surg Br 2006; 88-B: 1379e84. 11 MacLean JG, Reddy SK. The contralateral slip. An avoidable complication and indication for prophylactic pinning in slipped upper femoral epiphysis. J Bone Joint Surg Br 2006 Nov; 88(11): 1497e501.

in chronic slip are impressive, with 3 cases of AVN out of 70 patients. In acute-on-chronic cases, 9 out of 38 developed AVN. Many of these were probably unstable, although the term had not been coined at that stage. This incidence of AVN might just be a reflection of their instability. Fish described cuneiform osteotomy of the femoral neck, carried out through a Smith-Petersen approach, which spares the abductors. The access for the femoral neck reduction is good, and it is not necessary to dislocate the hip. He reported remarkably low AVN rates, which may be a reflection of the stability/severity of the slips that he was referred. An audit of severe unstable slips presenting to our hospital showed that when treated by pinning in situ, the AVN rate was 40%; when treated by cuneiform osteotomy the incidence was 35%, not significantly different. The implication here is that the osteotomy is not the cause of the AVN, it is the vascular damage due to the instability of the slip that is responsible. We therefore take the view that we might as well reduce the deformity, and the majority of cases will benefit, whether or not they ultimately develop AVN. Not all cases of AVN are severe, and the patient may do quite well unless a major collapse of the head occurs. With any femoral neck osteotomy it is important not to resect too much neck. Firstly this will adversely affect function, and secondly it can lead to a post-operative dislocation because of slackness in the joint. Femoral neck osteotomy after fusion of the displaced physis carries a high incidence of AVN, and an extra-capsular osteotomy is a better choice [Figure 6]. Salvage surgery Circumstances arise where severe displacement remains after physeal healing, or the hip becomes stiff in a poor position, whilst the patient is still young. Here a trochanteric or subtrochanteric realignment osteotomy may improve function. The Southwick osteotomy is the best known example. However, in

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12 Schultz WR, Weinstein JN, Weinstein SL, Smith BG. Prophylactic pinning of the contralateral hip in slipped capital femoral epiphysis: evaluation of long-term outcome for the contralateral hip with use of decision analysis. J Bone Joint Surg Am 2002 Aug; 84-A(8): 1305e14. 13 Broughton NS, Todd RC, Dunn DM, Angel JC. Open reduction of the severely slipped upper femoral epiphysis. J Bone Joint Surg Br 1988 May; 70(3): 435e9.

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14 Fish JB. Cuneiform osteotomy of the femoral neck in the treatment of slipped capital femoral epiphysis. J Bone Joint Surg Am 1984 Oct; 66(8): 1153e68. 15 Leunig M, Slongo T, Kleinschmidt M, Ganz R. Subcapital correction osteotomy in slipped capital femoral epiphysis by means of surgical hip dislocation. Oper Orthop Traumatol 2007 Oct; 19(4): 389e410.

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Basic Science

Biofilm and orthopaedic practice: the world of microbes in a world of implants

Biofilms that colonise orthopaedic devices have been studied extensively, but there are many areas that need further clarification about their structure, cell community composition and pathophysiologic activity. On every implanted biomaterial surface a “race for the surface” occurs, involving extracellular matrix (ECM) proteins, host cells (fibroblasts, osteoblasts, endothelial cells), and bacteria (Table 1). The ECM is a biologically active layer composed of a complex mixture of macromolecules, such as fibronectin, fibrinogen, albumin, vitronectin, and collagen. The composition and structural organization of the ECM influences host cell adhesion, migration, proliferation, and differentiation. However it not only serves as a substrate for host cells, but also for colonizing bacteria. Thus, if host cells such as fibroblasts arrive at the biomaterial surface and establish secure bonds, bacteria are confronted with a living, integrated cellular surface. Such integrated viable cell layers with functional host defense mechanisms can resist bacterial attachment and colonization. However bacteria such as Staphylococcus aureus express many surface adhesion molecules that promote attachment to plasma and ECM proteins of host cells, or those ECM proteins anchored onto metal or polymer surfaces.3,4

Spyridon P Galanakos Stamatios A Papadakis Konstantinos Kateros Ioannis Papakostas George Macheras

Abstract Biofilms are complex communities of surface-attached micro-organisms made up of single or multiple species. They grow in three stages, attachment of bacteria to the substratum followed by bacterial growth and division and then colonization of the surrounding area and the formation of the biofilm. While the basic mechanisms of biofilm-associated antimicrobial resistance are understood, research continues into biofilmassociated antimicrobial resistance.

History Biofilms were known to exist in aquatic systems before 19785,6 but not in much detail. In 1978 Geesey et al.7 adapted recovery methods for quantitative determination of biofilm bacteria in a pristine mountain stream and were able to compare the in number and activity of planktonic or free-living and biofilm bacteria in the same aquatic ecosystem. They showed that biofilm bacteria predominated both numerically and in metabolic activity. This led to widespread application of the same methods in natural, industrial, and medical ecosystems. Such biofilm populations have a very significant metabolic activity and predominate in virtually all nutrient sufficient aquatic systems irrespective of system geometry and type of ecosystem involved.8 Rodriguez et al.9 used the same methods to predict the extent of biofilm formation in a particular aquatic system, based on the following principles: • Metabolically active (vegetative) bacteria show a remarkable avidity for adhesion to surfaces, which is especially pronounced in wild-type cells in natural environments.

Keywords antimicrobial resistance; biofilm; colonization; community; formation

Introduction The pathogenesis of many orthopaedic infections is related to the presence of microorganisms in biofilms.1,2 Bacteria grow predominantly in biofilms and when they do so adopt a different phenotype and the component cells communicate by intercellular signals.

Spyridon P Galanakos MD is a Resident in Orthopaedics at Fourth Orthopaedic Department, General Hospital of Athens “KAT”, Kifissia, Greece.

The most common microorganisms causing implant-associated infections

Stamatios A Papadakis MD is a Consultant in Orthopaedics at Fourth Orthopaedic Department, General Hospital of Athens “KAT”, Kifissia, Greece. Konstantinos Kateros MD is a Consultant in Orthopaedics at Second Orthopaedic Department, Medical School, University of Athens, Konstantopoulion Hospital, Greece. Ioannis Papakostas MD, MSc, PhD is a Consultant in Orthopaedics at Orthopaedic Department, General Hospital of Thiva, Greece. George Macheras MD is a Head of Department at Fourth Orthopaedic Department, General Hospital of Athens “KAT”, Kifissia, Greece.

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Microorganism

Frequency (%)

Staphylococcus aureus Coagulase-negative staphylococci Gram-negative bacilli Anaerobes Enterococci Streptococci Polymicrobial Unknown

30 22 10 5 3 1 27 2

Table 1

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environment. All major classes of macromolecules – proteins, polysaccharides, DNA and RNA– can be present, in addition to peptidoglycans, lipids, and phospholipids.10 Within biofilms, microorganisms organize communities with structural and functional heterogeneity similar to that of a multicellular organism; interstitial voids between micro-colonies, can be considered to serve as a rudimentary circulatory system. Cellto-cell signaling (i.e. quorum-sensing) induces biofilm microorganisms to change patterns of gene expression. Quorum-sensing is the ability of a bacterial colony to sense its size and in response to regulate its activity. At a certain population density, intercellular signals activate genes involved in biofilm differentiation.3 Living within a biofilm represents a basic survival mechanism against environmental influences including host immune responses (i.e. opsonization, phagocytosis, and complementmediated lysis) and antimicrobial agents. Polymorphonuclear neutrophils can attach to, penetrate, and produce cytokines in, maturing and fully matured Staphylococcus aureus biofilm; nevertheless, these efforts are usually unable to clear the bacteria. Furthermore, ineffective attempts at phagocytosis may result in release of cytotoxic and proteolytic substances contributing to tissue injury and ultimately, in the case of orthopaedic implants, to periprosthetic osteolysis.11 The genetic basis of biofilm formation has been investigated for a number of bacterial species, including Escherichia coli, Pseudomonas aeruginosa and Vibrio cholera. These studies use randomly generated mutant species grown on plates. After removal of planktonic forms and staining with crystal violet, cells with no staining correspond to mutants that are defective for mature biofilm formation. These genetic screens for biofilm-defective mutants have shown that the initial interaction with the surface is accelerated by force-generating organelles such as type IV pili and flagella. Once temporary contact with the surface is made, bacteria use either flagella or type IV pili to move along the surface until other bacteria are encountered and micro-­colonies are

• The extent of biofilm accretion on surfaces in any aquatic system is controlled by quantity of nutrients available for cell replication and for exopolysaccharide production. • In extremely oligotrophic environments, organic nutrients tend to associate with available surfaces, and to trigger local biofilm development, but bacteria generally do not adhere on ­surfaces in nutrient-deficient environments.

Biofilm: definition and formation A biofilm is a layer-like aggregation of cells and cellular products attached to a solid surface or substratum. An established biofilm structure is made up of microbial cells and extracellular polymeric substances and provides an environment for the exchange of genetic material between cells9 (Figure 1). The biofilm architecture is spatially heterogeneous, constantly changing through external and internal processes. Although ­macroscopically an idealized biofilm is a thin homogeneous layer, microscopically it is a non-uniform structure of variable thickness and polymer densities. This may play an important role in hydrodynamic fouling of ships and boats, microbial influenced corrosion, substrate conversion and biocide efficacy. Furthermore, due to their irregular surface, biofilms increase the fluid’s functional resistance and shear stress. These effects, in turn, influence the effective diffusion coefficient in aerobic biofilms, where the oxygen distribution strongly depends on flow conditions and on biofilm’s structure. A large portion of biofilm matrix, depending on the specific system under investigation, is actually water (up to 97%), either bound within the capsules of microbial cells or as a solvent with physical properties such as viscosity determined by the solutes dissolved in it. Viscosity within the biofilm matrix is integral to the diffusion processes that occur. In addition to water and microbial cells, the biofilm matrix includes secreted polymers, absorbed nutrients and metabolites, products from cell lysis and particulate material and detritus from the immediate surrounding

Planktonic bacterial cells (free living)

Stage 1

Stage 2

Stage 3

Stage 4

Stage 5

Adapted from the original artwork by Dr Antonopoulos Dimitrios MD

Figure 1 Diagram showing the development of a biofilm as a five-stage process. Stage 1: initial attachment of cells to the surface. Stage 2: production of extracellular polymeric substance. Stage 3: early development of biofilm architecture (colonization). Stage 4: maturation of biofilm architecture. Stage 5: dispersion of single cells from the biofilm. In the final stage, when environmental conditions become unfavorable, some of the bacteria may detach and swim away to find a surface in a more favorable environment.

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­ umber of benefits such as resistance to environmental changes, n distribution of the metabolic burden, gene transfer, and selfless ­behavior.11

formed or enlarged. Finally, exo-polysaccharide production is necessary to stabilize the pillars of the biofilm.12

Why do bacteria form biofilms? Implant associated infections – pathogenesis

The most important fact is that bacteria normally grow as biofilms; planktonic cultures are an in vitro artifact i.e. biofilms are the default mode of growth. There are three reasons for biofilm formation during infection: • protection from harmful conditions in the host (defense) • sequestration in a nutrient-rich area (colonization) • utilization of cooperative benefits (community)13 Within biofilms organisms can withstand nutrient deprivation, pH changes, oxygen radicals, disinfectants, and antibiotics better than planktonic organisms. Biofilms are also resistant to phagocytosis, and the phagocytes that attempt an assault on the biofilm may actually do more harm to surrounding tissues than to the biofilm itself. The chronic nature of certain infections is usually due to the development of a resilient biofilm. The invulnerability of biofilms is not completely understood but is likely dependent upon a number of biofilm specific characteristics including slow growth and physiologic heterogeneity of the inhabitants. Another important aspect that fortifies biofilm resistance is the sticky matrix which may contain DNA and other polymers but in general, is predominantly composed of exopolysaccharides.14 Bacteria have a number of strategies to ensure their viability in the human host. They produce an impressive array of autolysin/adhesins that actually appear to have evolved as a means to inhabit the human host. In further support of the hypothesis that biofilm formation is a mechanism for organisms to remain viable in the favorable environment of the human host, is the finding that carbon catabolite induced gene regulation, plays a critical role in biofilm formation.15 Bacterial cells do not differentiate, but rather respond to the environment by adapting their gene expression to meet occasional needs. For this reason, it is more accurate to refer to biofilms as interactive communities rather than multi-cellular organisms. Nonetheless living in a community gives its ­ members a

The presence of a foreign body such as an orthopaedic implant has been shown to significantly increase susceptibility to infection. While this is at least partially due to a locally acquired granulocyte defect, biofilm formation is of major importance. Haematogenous infection is less frequent and is commonly associated with bacteraemia originating from skin, respiratory, dental, or urinary tract infections.17 Adherence of micro-organisms to the surface of the implant involves rapid attachment by specific (e.g. adhesins) or non­specific factors (e.g. surface tension, hydrophobicity, and electrostatic forces). This initial phase is followed by an accumulative phase during which bacterial cells adhere to each other and form a biofilm. Depletion of nutrients and/or waste product accumulation in biofilms causes micro-organisms to enter a slow or non-growing (stationary) state making them up to 1,000 times more resistant to most antimicrobial agents than their planktonic (free living) counterparts.16 Infections associated with fracture fixation can occur • exogenously in cases of open trauma i.e. pre-operatively • during insertion of the fixation device i.e. intra-operatively • during disturbed wound healing i.e. post-operatively Stainless steel, titanium and titanium alloys are the most commonly used materials for orthopaedic implants, but biodegradable polymers such as poly -L-lactide are also used in orthopaedic and maxillofacial surgery. The differences between stainless steel and titanium are well documented, with stainless steel implants being associated with significantly greater infection rates than titanium implants.18 A possible reason is the fact that soft tissue adheres firmly to titanium-implant surfaces. Another factor is the formation of a fibrous capsule which is a recognised reaction to steel implants. This encloses a liquid filled non-vascularised

Protected biofilm bacterial cells

Lysis of planktonic bacterial cells

Antibiotic Macrophage

Antibody

Implant surface

Periimplant tissue Adapted by Dr Antonopoulos Dimitrios MD from Trampuz and Zimmerli

25

Figure 2 Schematic representation of planktonic bacterial cells killed by antibiotics and the immune system, and biofilm microorganisms, attached to a surface and protected in an extracellular matrix.

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space which is less accessible to the host defense mechanisms in which bacteria can spread and multiply freely. From a clinical point of view, the prevention of initial bacterial adhesion is of utmost importance because mature biofilms are very difficult to treat. Possible solutions include implant ­surface modifications such as altering the topography and/or surface chemistry of the biomaterial, or by using an antimicrobial or protein-resistant coating.6

Several tests based on molecular and immunologic methods are currently available for the diagnosis of biofilm infections of bones and joints. These new methods can be combined with imaging modalities so that bacterial communities can be located with some degree of accuracy. Anti-biofilm antibodies can be tagged with specific “opacity markers” for various types of scans. Positive enzyme-linked immunosorbent assay (ELISA) tests could be informative as a diagnostic tool, and antibody based imaging could help localization and clinical treatment. 22

Anti-microbial resistance mechanisms Is colonization and formation of biofilm preventable?

It has been suggested that the exo-polysaccharide matrix, or glycocalyx, characteristic of biofilms, among other functions, prevents the access of antibiotics by restricting their diffusion (Figure 2). Further, nutrient and/or oxygen depletion and waste product accumulation may cause bacteria to enter a non-growing (i.e. stationary) state, which gives protection to growth ­dependent antimicrobial action. A subpopulation of bacteria may differentiate into a phenotypically resistant state and organisms may express biofilm specific antimicrobial resistance genes that are not required for biofilm formation.3 Anderl et al.19 cultured Klebsiella pneumoniae colony biofilms on agar plates with and without antibiotics. By placing a filter on top of the colony, they were able to look for antibiotic diffusion through the colony, using a standard zone of inhibition assay with the filter. Ampicillin was unable to diffuse even in mutant colonies which lacked the ability to produce β-lactamase, suggesting that other mechanisms contribute to the resistance of these colonies. Pseudomonas aeruginosa biofilms formed by an alginate overproducing strain, show a highly structured architecture and are more resistant to tobramycin than biofilms formed by an isogenic non-mucoid strain. Mah et al.20 recently have identified a gene (ndvB), the absence of which results in the formation of P. aeruginosa colonies without biofilm specific resistance to antimicrobial agents. The ndvB locus is required for the synthesis of periplasmic glucose polymers that interact with tobramycin apparently preventing the drug from reaching its site of action. Whether such a process occurs in staphylococci as well is not known, but could explain the poor activity of glycopeptides against S. epidermidis biofilms Table 1.

Research by the water industry has shown that surfaces are very similar in their tendency to attract planktonic cells and that the contamination of surfaces by organic materials ­(especially residual biofilm matrices) accelerates this process at least ­tenfold.1 In the process of manufacturing orthopaedic implants, machining techniques (especially those that use a wet interface between the tool assembly and the implant) can lead to biofilm development. Sterilization (e.g. ethylene oxide) kills the bacteria in these biofilms but fails to remove the residue of their matrices. These deposits must be removed before the devices can be implanted. Techniques with enzyme treatments are available for the removal of biofilm residues. One of the most practical strategies for the prevention of colonization and consequent biofilm formation is the use of materials and coatings that release antibiotics into the surrounding tissues and fluids. Ideally, these materials will release antibiotics in ­concentrations lethal for any local planktonic cell to prevent biofilm formation. Topography and chemical properties of biomaterial surfaces could be modified to alter the propensity for bacteria adhesion and subsequent biofilm formation. Electro-polished titanium or titanium alloy (Ti-6Al-7Nb) may be a solution for avoiding infections associated with intramedullary nailing systems as there are indications that staphylococci tend to adhere more to standard titanium alloy nails both in vitro and in vivo. Another possibility is to coat titanium or stainless steel with nitrogen ions, which affects the resistivity and chemical topography of the surface; titanium nitride coatings induce fibroblast attachment and growth, minimizing the adhesion of S. aureus, S. epidermis, Streptococcus mutans and P. aeruginosa.4 Other methods to reduce protein absorption, bacterial attachment and biofilm formation on biomaterial surfaces include protein coatings, e.g., heparin or albumin, surface modification by hydrophilic chains, phosphorylchiline-modified polymer coatings and poly(ethylene glycol)-based coatings.4 Local antibiotics to supplement systemic therapy have been proven effective in controlling orthopaedic infections. Thus there has been an interest in coating implants (stainless steel, titanium, or titanium alloy) with a thin layer of antibiotic-loaded biocompatible, biodegradable polymer, such as polylactic-co-glycolic acid (PLGA), and poly (D,L-lactide) (PDLLA). Various antibiotics have been studied, including gentamicin, ciprofloxacin, and vancomycin. To prevent the development of resistant bacteria, which is more likely if a combination of antibiotics is used, the concentration of the antibiotic eluted from the implant must remain above the minimal inhibitory concentration (MIC) value for an adequate amount of time.23

Diagnosis of orthopaedic biofilm infections Diagnosis of biofilm infections is always complicated by the fact that matrix-enclosed sessile bacteria are less immunogenic and elicit a reduced inflammatory response compared with the response elicited by an analogous amount of planktonic or free living bacterial cells.21 Because of lack of sensitivity of conventional microbiologic methods, molecular methods [e.g. polymerase chain reaction (PCR) and fluorescence in situ hybridization (FISH)] are more suitable for detection of biofilm infections. The humoral and cellular response of patients is very useful for detection of developing biofilms in cases of implanted orthopaedic materials. The humoral system reacts to immunogenic epitopes on the surface of bacteria by producing specific antibodies. These antibodies are not useful against biofilms, because bacteria in biofilms produce surface proteins that are very distinct from those on the surface of planktonic cells of the same species.3

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Forster et al described a novel way to prevent bacterial colonization on external fixation pins and wires.24 They fitted gentamicin coated polyurethane sleeves over the pins and wires which substantially reduced the incidence of pin tract infections caused by S. epidermidis, and elution tests revealed that the concentration of gentamicin in the pin tract remained above the 4 μg/ml MIC value recommended for gentamicin for up to 26 weeks. A new approach to the prevention of the colonization of prostheses is under investigation which may be to alter or interrupt intercellular communication in the biofilm.2

9 Rodriguez RF, Zamora JM, Salinas- Rodriguez E, Izquierdo E. Stochastic modeling of some aspects of biofilm behavior. Rev Mex Fis 2003; 49(2): 132–143. 10 Sutherland IW. The biofilm matrix – an immobilized but dynamic microbial environment. Trends Microbiol May 2001; 9(5): 222–7. 11 Wagner C, Kondella K, Bernschneider T, et al. Post-traumatic osteomyelitis: analysis of inflammatory cells recruited into the site of infection. Shock 2003; 20: 503–510. 12 Donlan RM, Costerton JW. Biofilms: survival mechanisms of clinically relevant microorganisms. Clin Microbiol Rev 2002; 15: 167–193. 13 Jefferson KK. What drives bacteria to produce a biofilm? FEMS Microbiol Lett Review 2004 Jul 15; 236(2): 163–73. 14 Shirtliff ME, Mader JT, Camper AK. Molecular interactions in biofilms. Chem Biol 2002; 9: 859–871. 15 O’Toole G, Kaplan HB, Kolter R. Biofilm formation as microbial development. Annu Rev Microbiol 2000; 54: 49–79. 16 Donlan RM. Biofilms: microbial life on surfaces. Emerg Infect Dis 2002; 8(9): 881–890. 17 Zimmerli W, Waldvogel FA, Vaudaux P, Nydegger UE. Pathogenesis of foreign body infection: description and characteristics of an animal model. J Infect Dis 1982; 146(4): 487–497. 18 Chang CC, Merritt K. Infection at the site of implanted materials with and without preadhered bacteria. J Orthop Res 1994; 12(4): 526–531. 19 Anderl JN, Franklin MJ, Stewart PS. Role of antibiotic penetration limitation in Klebsiella pneumonia biofilm resistance to ampicillin and ciprofloxacin. Antimicrob Agents Chemother 2000; 44: 1818–1824. 20 Mah TF, Pitts B, Pellock B, Walker GC, Stewarts PS, OToole GA. A genetic basis for Pseudomonas aeruginosa biofilm antibiotic resistance. Nature 2003; 426: 306–310. 21 Mah TF, O’Toole GA. Mechanisms of biofilm resistance to antimicrobial agents. Trends Microbiol 2001; 9: 34–39. 22 Costerton JW. Biofilm theory can guide the treatment of devicerelated orthopaedic infections. Session I: biofilms in orthopaedic infections. Clin Orthop 2005; 437: 7–11. 23 Tambe SM, Sampath L, Modak SM. In vitro evaluation of the risk of developing bacterial resistance to antiseptics and antibiotics used in medical devices. J Antimicrob Chemother 2001; 47(5): 589–598. 24 Forster H, Marotta JS, Heseltine K, Milner R, Jani S. Bactericidal activity of antimicrobial coated polyurethane sleeves for external fixation pins. J Orthop Res 2004; 22(3): 671–677. 25 Trampuz A, Zimmerli W. Diagnosis and treatment of infections associated with fracture-fixation devices. Injury 2006; 37: S59–S66.

Conclusion Biofilm formation is a crucial step in the pathogenesis of many sub-acute and chronic bacterial infections, particularly foreign body related infections. They are difficult to eradicate with ­conventional antimicrobial agents as they have several potential antimicrobial resistance mechanisms which may act concurrently, and in some cases, synergistically. Understanding that microbes are communal rather then individual organisms and how microbes gather into biofilm communities maintaining diversity and the mechanisms involved in biofilm-associated antimicrobial resistance is key to developing new therapeutic strategies and remains one of the central questions of microbiology. ◆

References 1 Costerton JW, Lewandowski Z, Caldwell DE, Korber DR, Lappin Scott HM. Microbial biofilms. Ann Rev Micro 1995; 49: 711–745. 2 Davies DG, Parsek MR, Pearson JP, Iglewski BH, Costerton JW, Greenberg EP. The involvement of cell-to-cell signals in the development of a bacterial biofilm. Science 1998; 280: 295–298. 3 Patel R. Biofilms and antimicrobial resistance. Clin Orthop 2005; 437(437): 41–47. 4 Harris LG, Richards RG. Staphylococci and implant surfaces: a review. Injury 2006; 37: S3–S14. 5 Marshall KC, Stout R, Mitchell R. Mechanisms of the initial events in the sorption of marine bacteria to surfaces. J Gen Microbiol 1971; 68: 337–48. 6 Zobell CE. The effect of solid surfaces upon bacterial activity. J Bacteriol 1943; 46: 39–56. 7 Geesey GG, Mutch R, Costerton JW, Green RB. Sessile bacteria: an important component of the microbial population in small mountain streams. Limnol Oceanogr 1978; 23: 1214–23. 8 Lappin-Scott HM, Costerton JW, eds. Microbial biofilms. Cambridge: Cambridge Univ. Press, 1995.

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Facioscapulohumeral muscular dystrophy assessment and treatment

FSHD was first described by Louis Landouzy and Joseph Dejerine in the late 1800’s, based upon a family that they followed for 11 years.2 Tyler and Stephens3 in 1950 described a lineage from America including 1,249 people over six generations, all descended from a single affected individual who had migrated to Utah in 1840. A total of 240 family members were examined, of whom 58 were affected. This provided the basis of much of what is now known regarding the inheritance pattern and clinical characteristics. Padberg’s series of 107 FSHD patients from 19821 has also provided additional detailed information of this condition.

Samuel J Parsons Andrew McMurtrie Stephen Cooke Birender Balain David Jaffray

Clinical features Patients with FSHD characteristically present with difficulties in overhead activities. They have asymmetrical involvement of the serratus anterior, rhomboids, trapezius, and teres muscles. The pectoralis major and minor, biceps and triceps are also frequently involved to varying degrees. The deltoid, however, is usually spared, as are the supraspinatus, infraspinatus and subscapularis.4 The weakness of scapular stabilisers means that the shoulder blade is abnormally mobile and rotates causing cephalad displacement and winging.5 The increased mobility means that deltoid is also at a mechanical disadvantage and the additional effort required causes the deltoid to fatigue easily. At rest there is an elevated scapular position due to weakness of the middle and lower thirds of trapezius and internal rotation of shoulder. On active shoulder flexion or abduction, there is marked winging of the scapula and reduction in the strength and magnitude of these movements (Figures 1e4). Padberg1 reported that 82% of patients presented initially with shoulder girdle weakness as their first complaint, 10% with facial muscle weakness and 8% had ankle dorsiflexor weakness. However on examination he found that 94% had facial muscle weakness, 93% had shoulder girdle weakness and 67% had ankle dorsiflexor weakness. Although the commonest presentation is of shoulder girdle weakness, other patterns of presentation do occur. A thorough examination of facial, pelvic girdle and lower limb muscles should be performed to avoid confusing FSHD with other forms of muscular dystrophy. FSHD is characteristically asymmetrical but it is not clear why. Over-work and handedness have been suggested. It is the asymmetrical weakness that distinguishes FSHD from other limb girdle dystrophies. Despite this asymmetry, the incidence of contractures and scoliosis is low, with 10% developing ankle contractures and a 30% risk of scoliosis.6 There is a more severe infantile form (probably autosomal recessive), which has a rapid and progressive course. The features are similar to the adult onset form but in addition to the facial and shoulder girdle features, they develop a severe lumbar lordosis. This is a compensatory curve due to fixed flexion of the hips, which in turn is due to almost complete absence of gluteus maximus, compounded by weakness of the postural abdominal musculature. They have foot drop deformities and sensorineural deafness. These children are usually wheelchair dependant by the age of 8e9. By the third decade thoracic and respiratory compromise becomes clinically significant.

Abstract Facioscapulohumeral dystrophy (FSHD), is a muscular dystrophy that classically affects the shoulder girdle and facial muscles. It should be considered in the differential diagnosis of patients presenting with limb girdle weakness. Progression is usually slow, and the condition is rarely fatal. Treatment is mostly supportive, although a number of patients can be helped with scapulo-thoracic fusion. This paper summarises the current understanding of this form of muscular dystrophy.

Keywords

facioscapulohumeral

dystrophy;

muscular

dystrophy;

shoulder

Introduction Facioscapulohumeral dystrophy (FSHD) is the third most common form of muscular dystrophy after Duchenne dystrophy and Myotonic dystrophy.1 It has an estimated prevalence of 1 in 20 000 and exhibits a high level of new mutations, which represent 10e30% of all new FSHD cases. It has a characteristic pattern of initially regional involvement, with mild muscle weakness and slow progression, although 20% of patients will eventually become wheelchair dependent.1

Samuel J Parsons FRCS (Tr & Orth) is a Orthopaedic Specialist Registrar at North Staffordshire Royal Infirmary, University Hospital of North Staffordshire NHS Trust, Stoke on Trent, UK. Andrew McMurtrie MRCS is a Orthopaedic Specialist Registrar at North Staffordshire Royal Infirmary, University Hospital of North Staffordshire NHS Trust, Stoke on Trent, UK. Stephen Cooke MRCS is a Orthopaedic Specialist Registrar at North Staffordshire Royal Infirmary, Stoke on Trent, UK. Birender Balain FRCS is a Orthopaedic Specialist Registrar at North Staffordshire Royal Infirmary, University Hospital of North Staffordshire NHS Trust, Stoke on Trent, UK. David Jaffray FRCS is a Consultant Orthopaedic Surgeon at Robert Jones and Agnes Hunt Hospital, Oswestry, Shropshire, UK.

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Figure 1 Patient with FSHD, resting position. Left side has previously undergone scapulo-thoracic arthrodesis.

Figure 2 Same patient viewed from behind, scars visible from scapulothoracic fusion and bone graft site.

Other features Lower limb involvement Pelvic girdle weakness and ankle dorsiflexor weakness can both occur; an MRI study8 showed this involvement is most marked in the hamstrings, tibialis anterior and medial gastrocnemius.

Face Other features include facial muscle weakness, orbicularis oculi and oris being most commonly involved. Classically patients cannot purse their lips or blow out their cheeks and are said to be unable to blow out candles or whistle as a result. The facial signs that may be present in infancy include a lack of mobility, incomplete eye closure, pouting lips with transverse smile and an absence of eye and forehead wrinkles. Difficulties in swallowing can occur though this is felt to be secondary to orofacial muscle weakness as there is no involvement of pharyngeal or laryngeal muscles.

Other features Other disease features include cardiac arrhythmias (12%) and high tone hearing loss (25e65%). Up to one third of patients also complain of pain which may be exertional or postural. The quality of life of FSHD patients is often severely impaired by fatigue with up to 60% complaining of reduced levels of activity and motivation.

Shoulder girdle In addition to the elevated scapular position and internal rotation of the shoulder, there is flattening of the anterior chest wall due to atrophy of the pectoralis major (especially the sternal head) and the clavicular portion of sternocleidomastoid.

Diagnostic criteria The criteria for the diagnosis of FSHD were established in 1991 by Padberg and Lunt9 and include: 1. Onset of the disease in the facial or shoulder girdle muscles and sparing of the extra-ocular, pharyngeal and lingual muscles and the myocardium. 2. Facial muscle weakness in more than 50% of affected family members. 3. Autosomal dominant inheritance in familial cases 4. Electromyography and muscle biopsy evidence of myopathy, in the absence of biopsy features specific for alternative diagnoses.

Abdominal muscles Weakness of abdominal muscles is another early feature of the disease. This can lead to a lordotic posture with a protuberant abdomen. A positive Beevor sign (upward movement of the umbilicus on an attempt to sit up) has been reported in a majority of patients with FSHD,7 and it is felt that this should become another diagnostic criterion.

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Figure 3 Patient attempting abduction, left shoulder has undergone scapulo-thoracic arthrodesis.

Since these were published myocardial involvement has been documented.

Disease progression One third of familial cases never progress beyond shoulder weakness.1 Of the remaining two thirds, 80% will go on to develop weakness of ankle dorsiflexion, and 20% pelvic girdle weakness. The humeral component of FSHD progresses to involve the biceps and triceps, which become weak and wasted. Wrist extensor muscles can become involved leading to a weak grip and limitation of hand use. 10% of all patients and 20% of those over 50 years become wheelchair-bound, although their lifespan is normal. Progression is very slow, occurring over a period of decades, thereby allowing a degree of functional adaptation to compensate.

Figure 4 Same movement, viewed from behind. Note the position of the right scapula, compared to the left side.

Treatment There is no effective medical or genetic treatment. The mainstay of management is symptomatic relief, prevention of secondary problems, improvement of functional abilities and quality of life within the constraints imposed by this progressive condition.

Pathophysiology Facioscapulohumeral dystrophy is transmitted as an autosomal dominant condition with 95% penetrance. Onset is in late childhood or early adulthood. Those affected having a good life expectancy although the more severe infantile form does shorten life span. FSHD is diagnosed by physical examination with DNA confirmation. Genetic testing is 95% sensitive. CPK levels are normal and help to differentiate FSHD from Duchenne muscular dystrophy. The pathophysiology is unknown despite genetic localisation of FSHD to the long arm of chromosome 4 (4q35). Clear identification of the molecular lesion, the causative gene or its protein product has not yet been made and the underlying pathological mechanism involved in disease expression remains unexplained. The genetic defect is a tandem deletion on chromosome 4 at the region D4Z4. Although it codes for no protein, normal individuals do have more copies of this repeat. An approximate inverse correlation has been reported between the exact number of D4Z4 repeats retained by a patient and the level of disease severity. The muscles of affected individuals show pseudohypertrophy due to fibrous and fatty infiltration.

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Conservative General measures should be instituted to ensure that patients maintain a good level of fitness and avoid obesity. A Cochrane review of strength and muscle training in myotonic dystrophy and FSHD10 suggested that it appears to do no harm but there was insufficient evidence to establish that it offers benefit. The orthotist has an important role, helping to correct, accommodate or compensate for weakness and/or deformity, especially when the lower limbs are involved. Medical Some drugs have been trialled in FSHD; unfortunately none has been universally successful. Corticosteroids have been used in the past, but a prospective trial where patients were administered large doses of prednisolone for three months failed to show any measurable improvement in muscle strength.11 Albuterol (known as salbutamol in the UK), a beta-2-agonist, has muscle anabolic effects in several animal models of muscle wasting as well as in normal humans in the setting of disuse atrophy.12 In a randomised double blind placebo controlled trial

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in FSHD patients, it failed to show any increase in muscle strength or improvement in function. However, there was an increase in lean body mass and hand grip strength suggesting some anabolic effect.13 The authors felt that it may have a role if combined with other anabolic agents or used together with an exercise regime. Creatine has been shown to improve muscle force in healthy adults and to increased lean body mass, most of which is muscle. This has been proposed as a potentially useful treatment in muscle dystrophies, but a Cochrane review14 of pooled trial data15 suggested that it had no role to play in FSHD. Surgical treatment Surgical stabilisation of the scapula against the posterior chest wall increases the functional range of motion of the shoulder, as it allows the deltoid to move the humerus without the excessive scapular motion present in patients with FSHD. Functional abduction and flexion of the upper limb is thus restored.16 It can also alleviate discomfort and improve the appearance of the shoulder.5 Various methods of scapulothoracic stabilisation have been described. Although muscle transfers, including those involving trapezius, teres major, rhomboids, latissimus dorsi and pectoralis major, have been used to treat scapular winging due to poliomyelitis, these procedures are contraindicated in FSHD because of the widespread muscle weakness and uncertainties of progression of muscle involvement.17 The use of fascial18 or Mersilene slings17 to restrict scapular motion has also been described; however, such methods have almost always been associated with progressive loss of stability due to stretching or breakage of the biological or artificial graft. Scapulothoracic arthrodesis restores scapular stability, providing a stable fulcrum for the deltoid to act upon, allowing the arm to be abducted (Figures 5 and 6)4. The operation should only be performed if deltoid strength is at least MRC grade 4, as greater deltoid weakness will lead to limited motor effectiveness and a greater possibility of diminished function with time.5 Improvement relies upon deltoid strength being maintained. The progressive nature of FSHD means patients need to be forewarned regarding deterioration. Surgery also leaves patients with a square-shouldered appearance. Fusion of the scapula to the thorax has been described using a combination of screws, wires or plates with or without cortical or cancellous bone graft.4,19,20 This is typically followed by a period of postoperative immobilisation. The procedure may be complicated by rib fractures, loss of fixation, pneumothorax or pleural irritation by the screw tips.5 Twyman et al reported that forced vital capacity decreased by an average of 21% (range, 3.2% to 30%) in all five patients in his series who had bilateral scapulothoracic fusion.21 Others have reported minimal or no reduction in vital capacity, respiratory volume or forced expiratory volume following scapulothoracic fusion.

Figure 5 Post scapulo-thoracic fusion radiograph, lateral view. Note for this case supplementary screws were used.

risk of metal failure/cut-out and are more likely not to be tolerant of the postoperative rehabilitation. Preoperative lung function tests should be normal because of the potentially restrictive pulmonary defect after fusion. Smoking, due to its effect on bone graft incorporation, wound healing and pulmonary function is a contra-indication to surgery. To assess whether scapulothoracic fusion is likely to be of benefit, place and then hold the scapula in the abducted position. If normal abduction can be achieved from this position then

Senior author’s practice Ideally patients are screened and referred from a specialist muscle clinic. In general, surgical results are better in younger patients with mild or slowly progressive disease. Patients over 40 are less likely to achieve scapulothoracic fusion, tend to have a higher

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Figure 6 Post scapulo-thoracic fusion radiograph, antero-posterior view.

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fusion has a chance of functional success. In general, the inferior angle of the scapula should be 15 cm from the midline.

Preoperative assessment The patient should be cross-matched, though in the senior author’s practice (DCJ), transfusion has not yet proved necessary. Dissection around the scapula, if slow, should be bloodless. The anaesthetist should be experienced in managing patients suffering from any muscular dystrophy and be ready to deal with the rare but serious associated complications, for example, malignant hyperpyrexia. Position of patient The patient should be positioned prone on spinal cushions in a similar manner to a posterior spinal procedure. The arm is placed on a hand table. The patient is prepped and draped from the posterior iliac crest to the neck, including the arm, allowing it to be moved during surgery. Adrenaline infiltration is not necessary. Procedure The incision is made obliquely and follows the line of the medial border of the scapula. Meticulous attention must be paid to haemostasis throughout. The atrophic muscle layers should be preserved to facilitate closure. The scapula is then mobilised from the chest wall by reflecting tissues subperiosteally. At least five ribs, from the second inferiorly, should be exposed, again by subperiosteal dissection. Double spinal sub-laminar wires are passed around the ribs avoiding the intercostal neurovascular bundle. This should not be difficult if adequate exposure has been obtained and the bones are exposed subperiosteally. The inferior border of the scapula is placed 15 cm from the midline and drill holes are made in the solid portion of its medial border, through which the wires are passed. The five exposed ribs are decorticated with a burr along with the under surface of the scapula. It is absolutely essential to get quality bone graft in sufficient quantity. There is an abundant source in the iliac crest. Make an incision following the iliac crest from the posterior superior iliac spine arcing laterally. The muscles must be reflected clearly in a subperiosteal fashion. This minimises donor site pain. It also allows greater exposure of the crest and reduces the chance of inadvertently entering the sciatic notch. Cortico-cancellous strips should be cut from the lateral pelvic wall using an osteotome and seams of cancellous bone can be harvested using Capener gouges. The harvested autograft is placed between the ribs and the scapula before tightening the wires. Once tight, the scapula is rigidly fixed against the chest. Screws into the ribs are unnecessary. Corticocancellous strips are placed across the medial border of the scapula and held in place by folding the wires over them. The wounds are closed without drains and the patient given a sling.

Figure 7 Post operative range of abduction.

Postoperative management Around the third post-operative day, a shoulder spica is applied down to the wrist. A large abdominal blowhole centred on the umbilicus avoids the potentially life-threatening complications of superior mesenteric thrombosis, gastric dilatation and caval thrombosis. The anterior shell of the spica covering the arm can be removed after three weeks to allow elbow mobilisation. The remainder is removed at two months.

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Figure 8 Post operative range of internal rotation.

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3

4

5

6

7

8

9 10

11 Figure 9 Post operative range of forward flexion. 12

Using this technique, the senior author has not yet encountered a failure. Every patient thus far has elected to undergo the rigours of the same procedure on the contralateral side following the successful primary operation. A spica is essential as patients are liable to remove slings and other orthotic devices. No significant restrictive pulmonary deficit has been measured. All patients have returned to work, more able to cope than prior to surgery. Bilateral scapulo-thoracic fusions are therefore of value for a select group of patients but the rehabilitation will take the best part of a year (Figures 7e9).

13

14

15

16

Conclusion Though rarely seen in everyday practice the diagnosis of FSHD should be borne in mind when seeing any muscular dystrophy patients or those complaining of limb girdle weakness. Although treatment options are currently limited, ongoing research may identify the genetic deficiency. Perhaps gene therapies aimed specifically at the defect may in the future provide targeted treatments. A

17

18 19

20 REFERENCES 1 Padberg GW. Facioscapulohumeral disease: thesis. University of Leiden; 1982. 2 Rogers MT. Facioscapulohumeral muscular dystrophy: historical background and literature review. In: Upadhyaya M, Cooper DN, eds.

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Facioscapulohumeral muscular dystrophy. New York, NY: Bios Scientific Publishers, 2004; p. 17e40. Tyler FH, Stephens FE. Studies in disorders of muscle, II: clinical manifestations and inheritance of facioscapulohumeral dystrophy in a large family. Ann Intern Med 1950; 32: 640e60. Letournel E, Fardeau M, Lytle JO, Serrault M, Gosselin RA. Scapulothoracic arthrodesis for patients who have facioscapulohumeral muscular dystrophy. J Bone Joint Surg Am 1990; 72-A(1): 78e84. Diab M, Darras B, Shapiro F. Scapulothoracic fusion for facioscapulohumeral muscular dystrophy. J Bone Joint Surg Am 2005; 87-A(10): 2267e75. Padberg GW. Facioscapulohumeral muscular dystrophy: a clinician’s experience. In: Upadhyaya M, Cooper DN, eds. Facioscapulohumeral muscular dystrophy. New York, NY: Bios Scientific Publishers 2004; p. 41e54. Shahrizaila N, Wills AJ. Significance of Beevors sign in FSHD and other neuromuscular diseases. J Neurol Neurosurg Psychiatr 2005; 76: 869e70. Olsen DB, Gideon P, Jeppesen TD, Vissing J. Leg muscle involvement in facioscapulohumeral muscular dystrophy assessed by MRI. J Neurol 2006; 253: 1437e41. Padberg GW, Lunt PW, Fardeau M. Diagnostic criteria for FSHD. Neuromuscul Disord 1991; 1: 231e4. Van der Kooi EL, Lindeman E, Riphagen I. Strength training and aerobic exercise training for muscle disease. Cochrane Database Syst Rev 2005; Issue 1. Art. No.: CD003907. doi: 10.1002/14651858. CD003907.pub2. Tawil R, McDermott MP, Pandya S, et al. A pilot trial of prednisolone in facioscapulohumeral muscular dystrophy. FSH-DY Group. Neurology 1997; 48(1): 46e9. Kissel JT, McDermott MP, Natarajan R, et al. Pilot trial of albuterol in facioscapulo-humeral muscular dystrophy. FSH- DY Group. Neurology 1998; 50(5): 1402e6. Kissel JT, McDermott MP, Mendell JR, et al. Randomized, double-blind, placebo-controlled trial of albuterol in facioscapulohumeral dystrophy. Neurology Oct 2001; 57: 1434e40. Rose MR, Tawil R. Drug treatment for facioscapulohumeral muscular dystrophy. Cochrane Database Syst Rev 2004; Issue 2. Art. No.: CD002276. doi: 10.1002/14651858.CD002276.pub2. ¨ller H, Reilich P, et al. Creatine monohydrate in Walter MC, Lochmu muscular dystrophies: a double-blind, placebo-controlled clinical study. Neurology May 2000; 54: 1848e50. Bunch WH, Siegel I. Scapulothoracic arthrodesis in facioscapulohumeral muscular dystrophy. J Bone Joint Surg Am 1993; 75-A(3): 372e6. Ketenjian A. Scapulocostal stabilization for scapular winging in facioscapulohumeral muscular dystrophy. J Bone Joint Surg Am 1978; 60-A(4): 476e80. Dickson FD. Fascial transplants in paralytic and other conditions. J Bone Joint Surg Am 1937; 19(2): 405e12. Copeland SA, Howard RC. Thoracoscapular fusion for facioscapulohumeral dystrophy. J Bone Joint Surg Br 1978; 60-B(4): 547e51. Copeland SA, Levy O, Warner GC, Dodenhoff RM. The shoulder in patients with muscular dystrophy. Clin Orthop Relat Res 1999; 368: 80e91. Twyman RS, Harper GD, Edgar MA. Thoracoscapular fusion in facioscapulohumeral dystrophy: clinical review of a new surgical method. J Shoulder Elbow Surg 1996; 5: 201e5.

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Ætiology of extraosseous wrist ganglia; the published evidence

Histological evidence The aetiology remains obscure, but the most popular theories are mucoid degeneration.4,7 the production of mucin by ­ modified synovial cells or fibroblasts at the synovial capsular junction ­following tissue trauma8 or the ganglion contents being produced by mesenchymal cells within the ganglion wall.9 WE Sanders 198510 In attempting to clarify various theories on the pathogenesis of the ganglion, histopathologic examinations indicate that the ganglion develops from connective tissue by myxoid degeneration and disintegration of collagen fibres. Increasing amounts of mucinous fluid accumulate by the progressive liquefaction of collagen fibres and are surrounded by densifying collagen bundles which form a delimiting capsule.11 Razemon stated that histologic examination confirms the non-synovial nature of ganglion cysts of the wrist and that there is a mucoid degeneration of the capsule and surrounding tissue with numerous neighbouring microcysts.12 In a detailed electronmicroscopic study, Psaila and Mansell were able to show that the ganglion wall consists of multidirectional strata of collagen fibres and has no cellular lining. The wall has a sponge-like appearance and does not appear degenerate or necrotic. Comparison with synovial membrane and adventitious bursa confirmed that these are distinct structures that have a cellular lining. The authors concluded that ganglia probably arise from the multifunctional mesenchymal cells that are found within their walls. The ganglion fluid may also originate from these cells.9 Mucoid degeneration does not explain, however, why the process is self-limiting, solitary and may occur in adolescents and young adults. Angelides has produced a more recent theory that microtrauma causes stretching of capsular tissues and ligaments stimulating the production of hyaluronic acid. The mucin producing cells may be modified synovial cells, mesenchymal cells or fibroblasts that, in tissue culture, have been shown to synthesize hyaluronic acid.13 The mucin then dissects through the ligamentous and capsular structures forming capsular ducts and lakes that eventually coalesce to form the main cyst.14 Kapral et al have support Angelides’ microtrauma-mucoid degeneration concept15 as have Nahra and Bucchierei in a review article.14 de Villiers et al have shown that the dorsal ganglion arises as a ‘herniation’ from the dorsal scapholunate ligament. This ‘herniation’ increases in size (according to La Place’s law) owing to a unidirectional pinchcock effect of the mucosal folds of the duct and the pressure of the overlying extensor retinaculum until the distending pressure inside the ganglion equals the overlying tissue pressure. They used wrist gangliography, retrograde wrist arthrography, histology and nuclear magnetic resonance imaging to prove this ‘conclusively’. They concluded that conservative therapy is illogical since the communicating duct remains and synovial fluid from the scapholunate joint will cause a reherniation and recurrence of the ganglion.16

AJ Thurston

Abstract Ganglia represent the most common soft-tissue tumour in the hand. They usually occur singly and although they arise in specific locations, they have been reported to arise from almost every joint of the hand and wrist. The ætiology of ganglia remains controversial. They may develop from connective tissue by myxoid degeneration and disintegration of collagen fibres. However, there is no evidence in the literature to support trauma as an ætiologic factor.

Keywords ætiology; ganglion; histology; trauma; wrist

History Conflicting views have been put forward on the origin of ganglia. Some believe that they represent a degenerative process. ­ Others claim that they are benign tumours of tendon sheath or joint ­capsule.2 J Crawford Adams, 1956 Hippocrates provided the first description of knots of tissue containing mucoid flesh.3 Initially, a ganglion cyst was regarded as being a synovial herniation from a joint and then as a synovial dermoid caused by “arthrogenesis blastoma cell nests” or embryonic periarticular tissue. Henle regarded them as new growths from synovial membranes and Voigt considered them to be modifications of bursæ or degenerative cysts. Ledderhose produced a theory of mucoid degeneration and this was supported by Carp and Stout.4 It is this theory that has endured and still pertains.

Prevalence The most common soft-tissue tumour in the hand is the ganglion.5 In a recently published paper by Lowden et al the findings of MRI scans of the wrists of 103 asymptomatic volunteers were reported. The inclusion criteria were that the wrists had never been injured, investigated or treated. Wrist ganglia were identified in 53 out of the 103 wrists. The study showed that volar wrist ganglia are more common than dorsal wrist ganglia and that these asymptomatic ganglia occur without associated ligamentous disruption.6

The rôle of trauma

AJ Thurston ED MB ChB MSc(Oxon) FRACS FNZOA is an Associate Professor of Orthopaedics and Hand Surgery, Department of Surgery, Wellington School of Medicine & Health Sciences, University of Otago, Wellington, New Zealand.

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Cheng and Rockwell stated that the cause of these cysts is unknown, although trauma has been postulated as an inciting factor,17 without evidence that trauma is an ætiologic factor. 186

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Kerrigan et al reported on 12 patients with volar ganglia that encroached on the carpal tunnel, in six of whom the cysts were coincidentally associated with direct trauma, usually with the wrist in hyperextension.18 Angelides1 has stated “A specific antecedent traumatic event is present in at least 10 percent of cases…” This statement was unsupported by any evidence of his own, nor did he cite any evidence from the literature. He went on to say that “…repeated minor trauma may be an a etiologic factor in their development.” Once again, there was no evidence to support this. He concluded with “I believe that the factor stimulating the production of hyaluronic acid (a tissue lubricant) is tissue trauma or irritation, such as stretching of the capsular and ligamentous supporting joint structures”.3 Watson et al reviewed their experience with rotary subluxation of the scaphoid after ganglion excision in 17 patients. Only single case reports of rotary subluxation of the scaphoid after ganglion excision had been previously reported. Of the 17 patients in the cohort, two had been involved in motor vehicle accidents and a third had fallen. Seven others were covered by Workers’ Compensation and had also described ‘accidents’. The authors reviewed the x-rays of four patients and the x-ray reports of a further six patients, all taken before the ganglion excision surgery, and in none was there any evidence of carpal malalignment or carpal instability. Although the authors suggested that the development of the ganglia was a secondary manifestation of rotatory instability of the scaphoid, part of the surgical management of a dorsal wrist ganglion is to excise the associated portion of the dorsal scapho-lunate ligament.3 This has the potential to cause instability between the scaphoid and lunate bones.19–21 They suggested that their data supports an hypothesis that the ganglion may be a secondary manifestation of underlying periscaphoid ligamentous injury.22 This was by association rather than with substantive evidence. This report by Watson et al is of a retrospective, uncontrolled study, although they did review a group of 10 patients, all of whom had undergone excision of dorsal wrist ganglia some time previously. No history of injury was given for any of these patients.22 The paper by Sanders10 (vide supra) is a report of only nine patients with chronic wrist pain for between four months and six years. In none of these patients was a history of trauma given. In two of three patients whose wrists were explored for occult ganglia no ganglia were found but, instead, isolated tears of the dorsal scapho-lunate were found. It was considered by the author that the condition most likely to mimic an occult ganglion is such a tear of the scapho-lunate ligament. Sanders also stated “Damage to the dorsal scapho-lunate ligament complex could be postulated either from compression of this area against the dorsal edge of the radius in hyperdorsiflexion of the wrist,23 or from tension on the scapho-lunate ligament as the scaphoid transmits the force produced by the wrist flexors and extensors to the proximal carpal row.24” Sanders went on to say that the diagnosis of “chronic wrist sprain” (suggesting a traumatic ætiology) has been replaced by a number of differential diagnoses indicating a more precise understanding of wrist pathomechanics.10 Lister has stated “The origin of ganglia remains controversial. It may develop from connective tissue by myxoid degeneration and disintegration of collagen fibres.”25 While lack of evidence is not proof that there is no causal relationship between trauma

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and wrist ganglia, it remains to be proven that this relationship exists.

Other coincidental pathology The author’s experience of investigating wrist ganglia is that they are seldom painful. If a patient presents with wrist pain and a ganglion then a separate explanation for the wrist pain should be sought. This approach is supported by evidence from a retrospective study by Povlson and Peckett who, investigated the link between a painful dorsal wrist ganglion and wrist joint abnormalities. Of 16 wrists that were arthroscoped 12 were abnormal, 10 had an abnormal scapholunate joint and two had abnormal lunotriquetral joints. These authors suggested that ‘painful’ dorsal wrist ganglia, like popliteal cysts in the knee, are markers of underlying joint abnormalities.26 On the other hand, Sanders has stated that the dorsal ganglion can cause chronic wrist discomfort and the diagnosis of ‘occult dorsal carpal ganglion’ should be included in the differential diagnosis. The concept of ‘dorsal wrist syndrome’ (DWS) was developed by Watson27 and is manifest as dorsal wrist pain with or without a palpable dorsal wrist ganglion. Watson considered it as an entity encompassing pre-dynamic rotary subluxation of the scaphoid and the overloaded wrist. An explanation for the pain was provided by Dellon and Seif. Prompted by the finding of a neuroma, which clinically simulated a recurrent ganglion, they dissected the terminal branches of the posterior interosseous nerve and found that there was a constant relationship between the terminal branches of the nerve and the scapholunate ligament. They suggested that the aching wrist pain associated with a dorsal wrist ganglion may be due to a compression neuropathy of the posterior interosseous nerve.28 Yasuda et al reviewed 20 cases of DWS treated surgically. At operation, they observed scapholunate ligament tears in eight wrists and dorsal ganglia in 12 cases. They stated that excision of the posterior interosseous nerve and the dorsal capsule including the ganglion, if present, provides pain relief in DWS.29

Conclusion The ætiology of ganglia remains controversial. They may develop from connective tissue by myxoid degeneration and disintegration of collagen fibres. However, there is no scientific evidence in the literature to support trauma as an ætiologic factor. ◆

References 1 Angelides A, ed. 4th edn. Ganglions of the hand and wrist; vol. 2 New York, Edinburgh, London, Philadelphia, San Francisco: Churchill Livingston, 1999, p. 2171–83. 2 Crawford Adams J. Outline of Orthopaedics, 6th edn. Edinburgh & London: E & S Livingston Ltd., 1969, 293–4. 3 Angelides A, ed. 2nd edn. Ganglions of the hand and wrist; vol. 3 New York: Churchill Livingstone, 1988, p. 2282–3. 4 Carp L, Stout A. A study of ganglion, with special reference to treatment. Surg Gynecol Obstet 1928; 47: 460–8.

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18 Kerrigan J, Bertoni J, Jaeger S. Ganglion cysts and carpal tunnel syndrome. J Hand Surg [Am] 1988; 13A(5): 763–5. 19 Palmer A, Dobyns J, Linscheid R. Management of post-traumatic instability of the wrist secondary to ligament rupture. J Hand Surg 1978; 3(6): 507–32. 20 Kauer JMG. Functional anatomy of the wrist. Clin Orthop Relat Res 1980; 149: 9. 21 Ruby L, An K, Linscheid R, Cooney W, Chao E. The effect of scapholunate ligament section on scapholunate motion. J Hand Surg [Am] 1987; 12A(5 pt 1): 767–71. 22 Watson H, Rogers W, Ashmead D. Reevaluation of the cause of the wrist ganglion. J Hand Surg [Am] 1989; 14A: 812–7. 23 Jones J. The occult wrist ganglion AAOS index - Catalogue of the film library. J Bone Joint Surg [Am] 1965; 47A: 879. 24 Linscheid R, Dobyns J, Beabout J, Bryan R. Traumatic instability of the wrist: Diagnosis, classification and pathomechanics. J Bone Joint Surg [Am] 1972; 54A: 1612–32. 25 Lister G, ed. 4th edn. Tumours, benign swellings and ulceration; vol. 1 London, New York, Philadelphia, St Louis, Sydney, Toronto: Churchill Livingstone, 2002, p. 399–455. 26 Povlsen B, Peckett W. Arthroscopic findings in patients with painful wrist ganglia. Scand J Plast Reconstr Surg Hand Surg 2001; 35(3): 323–8. 27 Weinzweig J. Dorsal wrist syndrome. In: Watson H, Weinzweig J, eds. The Wrist Philadelphia: Lippincott, Williams & Wilkins, 2001, p. 483–90. 28 Dellon A, Seif S. Anatomic dissections relating the posterior interosseous nerve to the carpus, and the etiology of dorsal wrist ganglion pain. J Hand Surg [Am] 1978; 3A(4): 326–32. 29 Yasuda M, Masada K, Takeuchi E. Dorsal wrist syndrome repair. Hand Surg 2004; 9(1): 45–8.

5 Young L, Bartell T, Logan A. Ganglions of the hand and wrist. South Med Ass J 1988; 81(6): 751–60. 6 Lowden C, Attiah M, Garvin G, Macdermid J, Osman S, Faber K. The prevalence of wrist ganglia in an asymptomatic population: magnetic resonance evaluation. J Hand Surg [Br] 2005; 30B(3): 302–6. 7 Nelson C, Sawmiller S, Phalen G. Ganglions of the wrist and hand. J Bone Joint Surg [Am] 1972; 54A(7): 1459–64. 8 Angelides AD, Wallace PF. The dorsal ganglion of the wrist. Its pathogenesis, gross and microscopic anatomy and surgical treatment. J Hand Surg 1976; 1: 228–35. 9 Psaila J, Mansel R. The surface ultrastructure of ganglia. J Bone Joint Surg [Br] 1978; 60B(2): 228–33. 10 Sanders W. The occult dorsal carpal ganglion. J Hand Surg [Br] 1985; 10B(2): 257–60. 11 Soren A. Pathogenesis, clinic and treatment of ganglion. Arch Orthop Trauma Surg 1982; 99(4): 247–52. 12 Razemon J. Surgical treatment of ganglions of the wrist by partial excision of the joint capsule. Report on 303 cases. Ann Chir Main 1983; 2(3): 230–43. 13 Morris C, Godman G. Production of acid mucopolysaccharides by fibroblasts in cell cultures. Nature 1960; 188: 407–9. 14 Nahra M, Bucchieri J. Ganglion cysts and other tumor related conditions of the hand and wrist. Hand Clin 2004; 20(3): 249–60. 15 Kapral W, Zawodsky F, Bien I. Das typische Handgelenksganglion. Chirurg 1978; 49(3): 184–8. 16 de Villiers C, Birnie R, Pretorius L, Vlok G. Dorsal ganglion of the wrist–pathogenesis and biomechanics. Operative v. conservative treatment. S Afr Med J 1989; 75(5): 214–6. 17 Cheng C, Rockwell W. Ganglions of the proximal interphalangeal joint. Am J Orthop 1999; 28(8): 458–60.

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Current concepts in articular cartilage repair

This review will focus on the structure and function of AC. It will review the pathophysiology of AC defects, and what treatment modalities are available to halt the progression of degeneration. We will also provide an insight into what may be available in the future.

A Getgood TPS Bhullar N Rushton

The structure and function of articular cartilage Hyaline cartilage is a specialised tissue. In many ways it should be thought of as an organ, as it is made up from a number of tissue types and exhibits regional organisation (Figure 1). The osteochondral unit is made up of subchondral bone, the calcified cartilage, and the radial, transitional and tangential, or superficial zones, of the AC itself. AC contains 60e80% water. The predominant cell type is the chondrocyte (5% wet weight) which is responsible for extracellular matrix (ECM) production. They are spherical in shape, surrounded by lacunae, but become more flattened as they get closer to the superficial zone, where they are fibroblastic in shape. They often clump together in columns forming chondrons (2e4 cells), which are orientated along collagen fibres. The ECM is made up of collagen fibres (25% wet weight) of which Type II predominates (95%), but also includes types VI, IX and XI with type X in the calcified layer. These fibres are anchored to the calcified layer running perpendicularly to it, crossing each other in arcs at the superficial zone. The horizontal cellular orientation combined with the collagen network in the superficial zone, provide resistance to shear forces. Chondrocytes secrete lubricin (also known as Superficial Zone Protein), a molecule which is responsible for reducing the coefficient of friction and thus providing cartilage with such favourable tribiological properties. In the spaces formed by the cross linking of collagen fibres, large negatively charged hydrophilic proteoglycan molecules reside, with aggrecan and hyaluronan predominating. The dense collagen network restricts the hydration of these molecules to about 40e60%. As a result, the swelling pressure which is generated provides the compressive stiffness of cartilage. During the early degenerative process, when the collagen fibres are disrupted, the proteoglycans can become more hydrated causing the cartilage to soften. Smaller glycoproteins also exist, including fibronectin and cartilage oligomeric protein (COMP), which have a role in cell adhesion. In addition there are growth factors present, such as Bone Morphogenetic Proteins (BMP’s). Their role is under intense investigation and in many ways remains poorly understood. Tissue turnover is mostly governed by a balance between the matrix metalloproteinases (MMP-3, MMP-8, MMP-9, MMP-13 and aggrecanases 4&5 predominating) and the Tissue Inhibitors of Metalloproteinases (TIMPS). Over expression of one or other is a likely contributor of osteoarthritis (OA).5 AC is avascular and aneural. It receives its nutrition from the synovial fluid, as a result of mechanical movement of the tissue producing a diffusion gradient. Chondrocytes are isolated within the ECM, therefore appropriate mechanical stresses are essential for metabolism to occur. AC is immunopriveledged; it does not contain immune cells therefore chondrocytes secrete lysozyme to counteract microorganisms.

Abstract Our knowledge of articular cartilage pathophysiology has advanced hugely in the last 20 years. Although once thought of as a structure incapable of intrinsic repair, we now have a selection of treatment options available in clinical practice, which we can use to attempt to reproduce the specific zonal architecture and mechanical composition of hyaline cartilage. This review will focus on the structure and function of articular cartilage, the aetiology of cartilage injury, and how the disease process can be investigated and treated. Different treatment options will be described providing an up to date review of the spectrum of treatment modalities, from the simple marrow stimulation techniques, to osteochondral transfer, chondrocyte transplantation and finally tissue engineering. Each will be illustrated with examples from the literature, providing a current concepts review on the outcomes following these repair strategies.

Keywords articular cartilage repair; chondrocyte implantation; microfracture; tissue engineering

Introduction Articular cartilage (AC) injury is a common disorder of joints which can affect people of all ages, resulting in a spectrum of clinical presentations. Recent large studies which have looked at the prevalence of AC defects at the time of arthroscopy have found them to be present in 63%1 and 60%2 of knees; however, it is unclear how many of these defects are actually symptomatic and require surgical intervention. The population continues to live longer and remain active into later life, and as a result the number of cartilage surgeries performed is increasing, with over 500,000 procedures performed per year in the USA alone.3 William Hunter observed in 1743 that ‘‘cartilage once destroyed never heals’’.4 Although AC has a poor ability to regenerate itself, there is potential for repair. Our understanding of AC pathophysiology is improving, yet the mechanism for the regeneration of hyaline cartilage continues to elude us.

A Getgood MRCS MPhil Clinical Research Associate, The University of Cambridge Orthopaedic Research Unit, Addenbrooke’s Hospital, Cambridge, UK. TPS Bhullar FRCS Consultant Orthopaedic Surgeon, Edith Cavell Hospital, Peterborough, UK. N Rushton MD FRCS Consultant Orthopaedic Surgeon and Director, The University of Cambridge Orthopaedic Research Unit Cambridge, UK.

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Figure 2 Partial thickness chondral defect.

Inflammatory mediators such as cytokines may play a role in this process with Interleukin 1 (IL-1) having been implicated as one of the main protagonists. IL-1 and tumour necrosis factoralpha (TNF-a) have been shown to stimulate chondrocytes to produce nitric oxide, MMP’s, aggrecanases(ADAMTS) and suppress the synthesis of aggrecan and collagen. Drugs have been developed to target these mediators which have shown promising results. However, it is likely that more than one causative factor will need to be addressed, especially as the severity of the disease progresses.

Figure 1 The zonal architecture of articular cartilage.

Articular cartilage pathophysiology Articular cartilage pathology may be traumatic or degenerative. Degenerative disease can be further sub-classed as either primary or secondary. The aetiology of secondary arthrosis is multifactorial and many different risk factors have been implicated.6 Mechanical factors such as direct trauma, instability, malalignment and loss of meniscal chondroprotection have a role, as do metabolic factors such as diabetes, alcohol abuse and obesity. It is evident that often more than one may need to be addressed if attempting to prevent disease progression. The manner in which AC defects behave will differ depending on their aetiology and the depth of injury. Traumatic partial thickness cartilage defects do not spontaneously heal (Figure 2). The paucity of chondrocytes within the ECM, their inability to migrate to the zone of injury, and their relative inability to regenerate large amounts of ECM, mean these defects will usually progress. Full thickness defects, which penetrate the subchondral bone, do have the potential for intrinsic repair due to the communication gained with the marrow cavity and the mesenchymal stem cell (MSC) population (Figure 3). However a regenerate tissue is not formed, as the repair tends to be fibroblastic in origin. In early OA an increase in matrix molecule synthesis is often recognised. However, once loss of matrix eventually exceeds that which is deposited, a net loss of ECM results. The chondrocytes are noted to proliferate and form clusters, and cell hypertrophy is often observed. Loss of chondrocytes in the superficial zone occurs followed by fibrillation, fissuring, erosion, subsequent denudation of bone and finally deformity. The role of the subchondral bone continues to receive attention. Radin et al. recognised its importance back in 1986, but still we are unsure as to the extent of its involvement in modulating disease progression.7

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Diagnosis and imaging The main presenting symptoms of AC injury are pain and mechanical symptoms, such as locking or catching. As the degenerative process worsens, pain, loss of movement and reduced function predominate. Diagnosis may be made on clinical grounds, however imaging modalities are often utilised to assess the degree of damage, and help with the planning of future treatment.

Figure 3 Full thickness chondral defect.

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Magnetic Resonance Imaging (MRI) is the mainstay of diagnostic imaging at present. New techniques such as delayed Gadolinium Enhanced MRI (dGEMRIC) and T2 mapping not only allow morphological detailing of the cartilage surface and subchondral bone, but also give information on its biochemical and biomechanical status. To be able to use MRI as an assessment tool a 1.5 T magnet or stronger must be used with a dedicated extremity coil. The main sequences employed are T2 weighted Fast SpinEcho (FSE) (Figure 4a,c) with or without fat suppression, and T1 weighted 3D gradient echo (GRE). The FSE images show cartilage to be dark in contrast to the high signal of synovial fluid and bone marrow. Surface and matrix irregularities will be shown with increased signal. GRE sequences produce high signal intensity in the cartilage compared to that low in bone and synovial fluid. The 3D nature of these images allows improved visualisation and volume measurements. Biochemical assessment utilises the relaxation times of water within the tissue. T2 mapping is a sensitive technique which seems to show T2 relaxation times as having a relationship with collagen orientation and concentration (Figure 4b,d). Studies have shown that these T2 relaxation times are sensitive to load and that the response differs between normal, degraded and repair cartilage.8

As glycosaminoglycan (GAG) is one of the first molecules of the ECM to be lost in early degeneration, dGEMRIC is considered the method of choice for detecting proteoglycan depletion in articular cartilage. Following injection of gadolinium, which binds to the negatively charged GAG molecules, T1 images can be used to quantify tissue GAG concentration. T1 signal is high in normal cartilage and low in GAG depleted cartilage. The drawback of this technique is that a double dose of gadolinium is required followed by a 90 minute period of exercise to provide homogenous enhancement of cartilage. For many centres this is impractical. As these techniques evolve, it is likely that MRI will form the mainstay of diagnosis, and more importantly, the assessment of clinical outcome in correlation with the biomechanical and biochemical characteristics of the repair tissue.

Repair strategies Before undertaking a cartilage repair procedure, the surgeon must take into consideration both the biology of the defect and the physical condition and requirements of the patient. The demands which the patient will place on the joint should be considered, and their willingness to partake in an extended rehabilitation programme should be ascertained. The nature of the patient’s employment and sporting activities will have a significant impact on what procedure is chosen.

Fast spin echo MRI of microfracture (black arrow) a pre-operatively, b pre-operative T2 map, c 1 year post-operatively and d 1 year post-operative T2 map, showing increase in repair tissue. (Courtesy of the Hospital for Special Surgery, New York, MRI). Figure 4

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Debridement This is the most simple of procedures but has been shown to have the least predictable outcome. The removal of unstable flaps of cartilage, loose bodies and meniscal tears can be performed if the patient exhibits mechanical symptoms. Early mobilisation and weight bearing as tolerated is encouraged with concurrent strengthening programmes. In a prospective study performed in 76 knees, over 50% of patients improved, however, the therapeutic effect generally only lasted for one year.9 Moseley et al performed a study which compared arthroscopic lavage to placebo, in this case sham surgery, and found that neither arthroscopic lavage nor debridement were better than placebo.10 We therefore would not advise debridement being offered as a treatment apart from in patients who elicit mechanical symptoms and signs, in whom more aggressive treatments are not appropriate.

Studies have shown microfracture to produce a fibrocartilagenous reparative response, which mostly provides symptom relief for up to 2 years. Steadman et al. have published data on 72 patients with defects less than 4 cm2 who underwent microfracture with follow-up of 7e17 years.15 Eighty percent of patients improved, with Lysholm scores improving from 59 to 89, and Tegner activity scores improving from 6 pre-operatively to 9 post-operatively. Gobbi reported similar results in a group of athletes, but at 2 years noted that 80% of patients had a reduction in Tegner score.16 This may be as a result of the less durable fibrocartilage which is produced, but also the poor tissue fill of the defect, particularly around the margins, with poor integration with the native articular cartilage. This may be related to the size of the defects treated. Dorotka et al. showed in an ovine model, that improved defect fill was found when the clot was stabilised with a collagen membrane.17 As a result, microfracture has been augmented with a collagen I/III matrix (Chondro-Gide, Geistlich Biomaterials) which soak up the blood clot from the subchondral holes, providing a scaffold for cells and chemotactic factors to reside. The membrane can be fixed with fibrin glue or 6/0 vicryl sutures. Autologous Matrix Induced Chondrogenesis (AMIC) has shown promising results, although we await long term data.18 It is possible that this may represent the future of marrow stimulation techniques.

Marrow stimulation Marrow stimulation involves penetrating the subchondral bone plate to allow communication with the marrow cavity. This allows marrow stromal cells containing mesenchymal stem cells (MSC’s), platelets and other chemotactic factors to collect within the defect. The original techniques described, such as Pridie drilling, have gone out of favour for the more refined microfracture technique described by Steadman11 (Figure 5). Following debridement of the perilesional cartilage, producing a perpendicular shoulder of cartilage, 3e4 mm deep holes are made in the subchondral bone 2e3 mm apart, starting in the periphery, working into the centre of the defect. Unlike Pridie drilling, this maintains greater mechanical stability of the subchondral bone and collapse is not seen as readily as in previous techniques. Frisbie et al. showed in a study in horses the importance of removing the calcified cartilage layer to allow satisfactory repair tissue.12 The rehabilitation seems to form an integral part of the procedure, and the original authors maintain that the intensive rehab period must be adhered to for the procedure to be successful.13 Unfortunately, many centres are unable to adhere to this degree of rehab. However, microfracture is relatively easy to perform, is cheap, minimally invasive and well tolerated by the patient.

Autologous osteochondral grafting Osteochondral autograft transfer (OAT) has been employed in articular cartilage repair since the mid-1990’s.19 Osteochondral plugs are harvested from the ‘non-weight bearing’ lateral trochlear ridge or intercondylar notch of the ipsilateral knee and transferred to a pre-prepared cylindrical hole within the defect. It is the only procedure which produces hyaline cartilage within the defect. However, the biomechanical and topographical properties will differ between donor and recipient sites. For single plug transfer, the size of the defect will be the limiting factor. Problems such as joint congruency and donor site availability are encountered; hence mosaicplasty techniques have been developed. Mosaicplasty involves the transfer of a number of smaller plugs, producing a congruent joint surface (Figure 6). It is

Arthroscopic view of the microfracture technique. Figure 5

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Mosaicplasty. a recipient site preparation and b osteochondral plugs insitu. Figure 6

extremely technically demanding and donor site morbidity remains a problem, as the lateral trochlear ridge is not truly nonweight bearing. Both techniques suffer from poor graft incorporation, with mosaicplasty particularly suffering with poor integration in gaps between the plugs and native cartilage.20 Attempts to counteract this problem have included microfracturing the gaps and inserting Osteogenic Protein-1 (BMP-7) in a collagen matrix.21 Mosaicplasty has shown mixed results, with a number of studies showing superior outcomes to marrow stimulation techniques. Hangody et al. showed that 87% of patients had good to excellent results at 5 years following mosaicplasty, compared with 0e34% of patients who were randomised to one of three marrow stimulation techniques.19 In a further study looking at a group of competitive athletes, the same group found 100% of patients had a good to excellent result at greater than one year, with 63% returning to full sports. However, the follow-up in this group was short.22 Bentley et al. have since shown improved outcomes with Autologous Chondrocyte Implantation (ACI) over mosaicplasty, with 88% showing good to excellent results with ACI compared to 69% with mosaicplasty at a mean of 19 months.23 Although good results have been reported, the use of mosaicplasty seems to be less widely employed due to the technical difficulty, problems with congruency and donor site morbidity. There does seem to be a trend back towards the use of single osteochondral transfer in small isolated defects.24

defect during the second stage procedure, and held in place with a periosteal patch, harvested from the proximal tibia, sutured over the defect to keep the cells in place. This procedure has since evolved to using a collagen membrane; however the cell expansion in-vitro persists. Large defects (>4 cm2) can be treated, as can multiple or even in some cases, ‘kissing’ lesions26 (Figure 7). A variation of ACI, Matrix Assisted Chondrocyte Implantation (MACI) (Genzyme, Cambridge, MA) has been in clinical use for a number of years (Figure 8). MACI employs a collagen matrix on which chondrocytes are expanded in-vitro and then transferred into the defect. The membrane can be held with fibrin glue and/ or sutures. Benefits of this include the ease of application of the membrane, and the possibility of performing the procedure arthroscopically. Good to excellent results have been reported in 85e92% 0f patients at 2 years in a number of observational cohort studies.25,27,28 A number of randomised studies have been published comparing ACI/MACI to other cartilage repair procedures. Horas et al. showed that an improvement in symptoms could be established with both ACI and OATS, however, the speed of recovery of ACI was slower.29 Bentley et al. compared ACI to mosaicplasty in 100 patients with similar demographics and lesion size. At a mean of 19 months, 89% of patients who had ACI showed good to excellent results, compared with 69% in that of mosaicplasty.23 Dozin et al., however, found an improvement in 88% of mosaicplasty patients in their study, compared to 68% in the ACI group. The numbers in this study were small, and interestingly, 31.4% of patients were excluded due to improvement in symptoms following debridement at the time of the arthroscopic assessment/biopsy. They were not included in the final analysis thus an intention to treat protocol was not followed.30 At present, only two randomised controlled trials exist comparing ACI to microfracture.31,32 Knutsen et al. has showed

Autologous chondrocyte transplantation The process of transplanting autologous chondrocytes in suspension to a cartilage defect was first described clinically by Brittberg et al. in 1994.25 A biopsy of normal cartilage from the non-weight bearing aspect of the ipsilateral knee is taken during the initial arthroscopic procedure. Chondrocytes are then isolated and expanded in-vitro. The cell suspension is returned to the

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Autologous chondrocyte implantation (ACI). a debridement kissing lesions in lateral compartment of the knee, b & c collagen membranes in situ (courtesy of Mr Tim Spalding, University Hospitals Coventry and Warwickshire NHS Trust) Figure 7

no difference in clinical and radiographic outcome between the groups at 5 years, although this study was underpowered.31 No correlation was found between histology grade and clinical outcome; however, those with the best histology at two years did not exhibit any failures. The more recent study by Saris et al. incorporated a novel chondrocyte characterisation system which supposedly correlates with improved histology and outcome.32 One year results favour characterised chondrocyte implantation (CCI, Tigenix, Leuven) over microfracture in terms of histomorphometry, however, functional outcome as measured by the Knee Injury and Osteoarthritis Outcome Score (KOOS) was similar in both groups at 12e18 months assessment. Two further randomised trials, the first by Bartlett et al. has shown ACI and MACI to be comparable at 1 year.33 The second, by Gooding et al,34 has shown similar functional outcome at two years between ACI with periosteum patch, compared to a collagen membrane. Of note, 36% of the periosteum group required debridement of the graft due to periosteal hypertrophy.

Other problems with this technique exist. Two operations are required, it is very expensive to culture cells and the repair tissue still is not hyaline cartilage. At best, histology can be described as ‘hyaline-like’. But does this matter? Our ultimate goal is to produce a repair tissue which is durable and reliably reduces patient symptoms in the longer term. Tissue engineering Tissue engineering applies to the concept of applying combinations of biomaterials, cells and bioactive signalling molecules to the goal of regenerating tissue. This is an exciting field which has been around since the early 1990’s, and is extremely prevalent in current literature. It remains in its infancy in clinical practice as novel products continue to be developed. Second and third generation ACI Combination products are currently used in clinical practice and include MACI (Genzyme, Cambridge MA), Hyalograft C (Fidia Farmaceutia, Italy),

MACI graft of the patella. a chondral defect prior to debridement, b post debridement and c MACI graft insitu (courtesy of Mr Tim Spalding, University Hospitals Coventry and Warwickshire NHS Trust). Figure 8

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collagen based scaffolds such as Osseofit (Kensie Nash, Exton, PA) and Chondromimetic (Orthomimetics, Cambridge, UK).

Bioseed-C (BioTissue Technologies, Freiburg, Germany), CaRes (Arthrokinetics, Macclesfield, UK), Cartipatch (TBF Tissue Engineering, Bron, France) and Novocart (TETEC AG, Reutlingen, Germany). Each utilises in-vitro culture of chondrocytes in the scaffold matrix followed by implantation. This enables 3D culture of chondrocytes, aiming to prevent de-differentiation down a fibroblastic lineage and loss of phenotype. Novel methods of implantation and fixation are being developed, allowing minimally invasive and arthroscopic techniques to be used. Although many of these products have produced satisfactory clinical outcomes, we wait to see if they provide any benefit over other aforementioned cartilage repair techniques.

Allograft Osteochondral allografts (Figure 10) have been employed particularly in cases of large osteochondral defects, where there is substantial loss of bone and cartilage, for example in osteochondritis dissecans.36 They are particularly useful in the young where joint replacement is not a viable option. Osteochondral allograft transplantation allows the implantation of biomechanically and topographically similar hyaline cartilage into an AC defect. Allograft tends to be more popular in North America, with a number of studies having been published reporting good results with this technique. Bugbee et al. have shown a greater than 75% success (91% at 5 years and 75% at 10 years) with femoral37,38 and patellofemoral allografting.39 Indeed, if the problem of graft incorporation is overcome, good outcomes are established. Ghazavi et al. have shown similar results with an 85% success rate in those with traumatic defects at 7.5 years. They found that age greater than 50 years old, malalignment leading to overstressing the grafts and workers compensation cases were associated with graft failure.40 Although good results are reported, the main issues associated with allograft are chondrocyte viability, graft incorporation and

Synthetic osteochondral plugs The introduction of the Trufit CB plug (Smith & Nephew Endoscopy, Andover, MA) has allowed ‘off the shelf’ implantation of a scaffold to replace the osteochondral unit. It is a biphasic porous scaffold made of polylactide co-glycolide (PLG) polymer, mineralised with calcium sulphate employing surfactant as a lubricant on its most superficial layer (Figure 9). Its use has been reported in small observational cohorts and results have been promising in smaller defects.35 It is an exciting concept which may allow combinations of cells and growth factors, which could be applied at the time of implantation, negating the need for two stage surgeries. Other scaffolds which are currently undergoing clinical analysis include

a&b The Trufit osteochondral scaffold (Smith & Nephew Endoscopy, Andover, MA), c chondral defect on the medial femoral condyle, d checking the depth of the recipient hole in medial femoral condyle and e the Trufit plug inserted into the medial femoral condyle. Figure 9

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Intraoperative pictures showing a an osteochondral defect of the medial femoral condyle, b a harvested dowel osteochondral allograft and c the dowel allograft inserted into the defect reconstructing the contour of the condyle. (Courtesy of Dr William Bugbee MD, Scripps Clinic, La Jolla, CA). Figure 10

risk of disease transmission. Fresh allografting has been advocated over frozen, due to the improved chondrocyte viability.41 This comes at the expense of increased risk of delayed graft incorporation, due to the immunogenic response of the donor bone, and the increased risk of infection. A stringent donor screening programme is therefore essential, as is detailed informed patient consent.

Varus/Valgus osteotomy In physiological loading of the knee, 60% is transmitted through the medial compartment and 40% through the lateral. The concept of physiological varus becoming pathological in the presence of pathology is becoming a more accepted view.42 Although there is no good clinical evidence to support it, more authors suggest performing staged or simultaneous osteotomy (Figure 11) to unload a defect/repair if the mechanical axis falls within the affected compartment. Mina et al. have demonstrated in a cadaveric model that load is equally distributed in both compartments if a corrective osteotomy is performed to 0e4 degrees valgus. Complete unloading of the medial compartment can be achieved with 6e10 degrees of valgus.43 The problem with trying to prove this concept is that if procedures are performed simultaneously it is difficult to ascertain which has the biggest impact on the functional outcome. To perform a randomised controlled trial would take large numbers

Adjuvant procedures It is becoming more evident that the joint environment is integral to successful repair outcomes. If malalignment, instability, or the lack of meniscus is not corrected, the repair will undergo abnormal mechanical loads. Combinations of distal femoral, high tibial or tibial tubercle osteotomy with anterior cruciate ligament reconstruction and meniscal allograft/collagen meniscal implant insertion can be done simultaneously or staged, depending on the degree and amount of correction required.

Osteotomies a Distal femoral and proximal tibial closing wedge valgus osteotomy, b medial opening wedge valgus osteotomy with Tomofix plate (Synthes). Figure 11

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reduces the load transmitted through the PFJ45 (Figure 12). Farr has shown improved results in complex PFJ defects treated with ACI and osteotomy þ/ MPFL reconstruction, with improvements seen in Cincinnati rating, Lysholm and visual analogue score (VAS) at a mean of 1.2 years.46 Again, no studies have been performed to conclude which procedure has the greatest impact. Meniscal allograft transplantation/collagen meniscal implant It is well documented how loss of meniscal tissue can lead to progressive degenerative change.47,48 The chondroprotective role of the meniscus is recognised and thus transplantation with allograft (Figure 13), or tissue engineered meniscus, is an accepted procedure.49 Although good results have been reported with both allograft transplantation50,51 and Collagen Meniscal Implantation52 alone, a study by Deie et al. found an unsatisfactory outcome when allograft transplantation was performed in the presence of a medial femoral condyle AC defect.53 We would therefore suggest that the procedures should be performed in combination so as to benefit from the load sharing role of the new meniscus tissue, thereby protecting the cartilage graft.

Figure 12 Anteromedialisation tibial tubercle osteotomy.

and likely be very difficult to recruit to achieve statistical power. We are therefore left with case series such as that by Sterett et al., who published a series of combined high tibial osteotomy (HTO) and microfracture showing satisfactory outcome, with mean Lysholm scores improving from 43.5 to 78 at two years.44 Minas reported a group of 71 salvage cases, where multiple defects were treated simultaneously with osteotomy and ACL reconstruction. An improvement in Cincinnati rating scale and SF-36 scores were seen at two years.32 Ninety percent of these salvage patients were happy with their treatment at last follow-up.

Viscosupplementation The use of hyaluronic acid (HA) injections in the treatment of OA is well documented and covered in a number of review papers.54,55 Each establishes that there is objective evidence to show that HA can provide symptom relief in degenerative conditions. Further randomised controlled trials continue to be published, looking at specific preparations and delivery to maximise its affect.56,57 Evidence pointing toward the role of HA in chondroprotection is less prevalent. A study by Tytherleigh-Strong et al. demonstrated its potential positive role in cartilage repair when used in conjunction with osteochondral autograft transfer.58 Further evidence will be required before it should be incorporated as standard into cartilage repair procedures.

Tibial tubercle osteotomy A similar concept is found within the patellofemoral joint (PFJ). Increased loading of chondral defects associated with maltracking should be corrected along with cartilage restoration procedures.24 Combinations of lateral release, medial patellofemoral ligament (MPFL) reconstruction and tibial tubercle osteotomy can be employed. The Fulkerson tibial tubercle osteotomy employs the anteromedialisation of the tibial tubercle, which not only corrects maltracking, but also

Rehabilitation A key aspect of all of these treatments is the rehabilitation protocol which is employed. It is well established from

a Lateral meniscal allograft, b intra-operative picture of prepared lateral compartment, c meniscal allograft held in place with bone block, screw and peripheral sutures. (Courtesy of Dr William Bugbee MD, Scripps Clinic, La Jolla, CA). Figure 13

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Figure 14 Treatment algorithm for articular cartilage pathology (courtesy of Dr B Cole, Rush University, Chicago).

preclinical studies that chondrocytes require mechanical load to stimulate the production of ECM and remain in a chondrogenic phenotype.59,60 The type of surgery performed will govern how early weight bearing can commence. The benefit of osteochondral grafting is that early weight bearing can be tolerated due to the stability of the graft.61,62 This is not the same with ACI/MACI or microfracture, as the graft has to be given time to embed in the subchondral bone.16 Mechanisms of fixation therefore continue to evolve, to allow early range of motion, weight bearing and hopefully a quicker return to function or sport.

biologics and tissue engineering into clinical practice will see an increase in production of functional tissue regeneration, and the longevity of improved patient outcome. A

REFERENCES 1 Curl WW, Krome J, Gordon ES, Rushing J, Smith BP, Poehling GG. Cartilage injuries: a review of 31,516 knee arthroscopies. Arthroscopy 1997 Aug; 13(4): 456e60. 2 Widuchowski W, Widuchowski J, Trzaska T. Articular cartilage defects: study of 25,124 knee arthroscopies. Knee 2007 Jun; 14(3): 177e82. 3 Haasper C, Zeichen J, Meister R, Krettek C, Jagodzinski M. Tissue engineering of osteochondral constructs in vitro using bioreactors. Injury 2008 Apr; 39(Suppl 1): S66e76. 4 Hunter W. On the structure and diseases of articular cartilages. Philos Trans R Soc Lond 1743; 42B: 514e21. 5 Murphy G, Lee MH. What are the roles of metalloproteinases in cartilage and bone damage? Ann Rheum Dis 2005 Nov; 64(Suppl 4): iv44e7. 6 Jordan KM, Arden NK, Doherty M, et al. EULAR Recommendations 2003: an evidence based approach to the management of knee osteoarthritis: Report of a Task Force of the Standing Committee for International Clinical Studies Including Therapeutic Trials (ESCISIT). Ann Rheum Dis 2003 Dec; 62(12): 1145e55. 7 Radin EL, Rose RM. Role of subchondral bone in the initiation and progression of cartilage damage. Clin Orthop Relat Res 1986 Dec; (213): 34e40. 8 Kaufman JH, Regatte RR, Bolinger L, Kneeland JB, Reddy R, Leigh JS. A novel approach to observing articular cartilage deformation in vitro via magnetic resonance imaging. J Magn Reson Imaging 1999 May; 9(5): 653e62. 9 Hubbard MJ. Articular debridement versus washout for degeneration of the medial femoral condyle. A five-year study. J Bone Joint Surg Br 1996 Mar; 78(2): 217e9.

Treatment algorithm It can be assumed that no one procedure is best for all types of defect. Indeed, the procedure should also be tailored to the patient’s requirements. We therefore require a method of differentiating which procedures should be used, and for which lesion and patient. The treatment algorithm presented (Figure 14) is an example of how the information required can be structured and easily called upon. The algorithm takes into account the anatomical location and size of defect, and the mechanical environment to which it resides. Options are then given as to which procedure may be used, depending on the availability of equipment and skill set of the surgeon.

Conclusion The treatment of articular cartilage pathology continues to evolve. It is clear that the majority of current treatments are still unable to regenerate hyaline cartilage, although patient centred outcomes continue to improve. To halt the process of degeneration, more aggressive tactics may need to be utilised to counteract the development of osteoarthritis. It is likely that tissue engineering will form the basis of future cartilage repair innovation. The delivery of signalling molecules via genetically modified cells may provide the correct stimulus to produce hyaline cartilage. Ultimately, we hope the further introduction of

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10 Moseley JB, O’Malley K, Petersen NJ, et al. A controlled trial of arthroscopic surgery for osteoarthritis of the knee. N Engl J Med 11 Jul 2002; 347(2): 81e8. 11 Steadman JR, Rodkey WG, Rodrigo JJ. Microfracture: surgical technique and rehabilitation to treat chondral defects. Clin Orthop Relat Res 2001 Oct;(391 Suppl): S362e9. 12 Frisbie DD, Morisset S, Ho CP, Rodkey WG, Steadman JR, McIlwraith CW. Effects of calcified cartilage on healing of chondral defects treated with microfracture in horses. Am J Sports Med 2006 Nov; 34(11): 1824e31. 13 Steadman JR, Rodkey WG, Briggs KK. Microfracture to treat full-thickness chondral defects: surgical technique, rehabilitation, and outcomes. J Knee Surg 2002; 15(3): 170e6. 15 Steadman JR, Briggs KK, Rodrigo JJ, Kocher MS, Gill TJ, Rodkey WG. Outcomes of microfracture for traumatic chondral defects of the knee: average 11-year follow-up. Arthroscopy 2003 May; 19(5): 477e84. 16 Gobbi A, Nunag P, Malinowski K. Treatment of full thickness chondral lesions of the knee with microfracture in a group of athletes. Knee Surg Sports Traumatol Arthrosc 2005 Apr; 13(3): 213e21. 17 Dorotka R, Windberger U, Macfelda K, Bindreiter U, Toma C, Nehrer S. Repair of articular cartilage defects treated by microfracture and a three-dimensional collagen matrix. Biomaterials 2005 Jun; 26(17): 3617e29. 18 Steinwachs MR, Guggi T, Kreuz PC. Marrow stimulation techniques. Injury 2008 Apr; 39(Suppl 1): S26e31. 19 Hangody L, Kish G, Karpati Z, Szerb I, Udvarhelyi I. Arthroscopic autogenous osteochondral mosaicplasty for the treatment of femoral condylar articular defects. A preliminary report. Knee Surg Sports Traumatol Arthrosc 1997; 5(4): 262e7. 20 Lane JG, Massie JB, Ball ST, et al. Follow-up of osteochondral plug transfers in a goat model: a 6-month study. Am J Sports Med 2004 Sep; 32(6): 1440e50. 21 Chubinskaya S, Hurtig M, Rueger DC. OP-1/BMP-7 in cartilage repair. Int Orthop 2007 Dec; 31(6): 773e81. 22 Kish G, Modis L, Hangody L. Osteochondral mosaicplasty for the treatment of focal chondral and osteochondral lesions of the knee and talus in the athlete. Rationale, indications, techniques, and results. Clin Sports Med 1999 Jan; 18(1): 45e66. vi. 23 Bentley G, Biant LC, Carrington RW, et al. A prospective, randomised comparison of autologous chondrocyte implantation versus mosaicplasty for osteochondral defects in the knee. J Bone Joint Surg Br 2003 Mar; 85(2): 223e30. 24 Cole BJ. Surgical management of articular cartilage defects of the knee. 2008. 25 Brittberg M, Lindahl A, Nilsson A, Ohlsson C, Isaksson O, Peterson L. Treatment of deep cartilage defects in the knee with autologous chondrocyte transplantation. N Engl J Med 1994 Oct 6; 331(14): 889e95. 26 Minas T. Autologous chondrocyte implantation for focal chondral defects of the knee. Clin Orthop Relat Res 2001 Oct;(391 Suppl): S349e61. 27 Gillogly SD, Voight M, Blackburn T. Treatment of articular cartilage defects of the knee with autologous chondrocyte implantation. J Orthop Sports Phys Ther 1998 Oct; 28(4): 241e51. 28 Peterson L, Brittberg M, Kiviranta I, Akerlund EL, Lindahl A. Autologous chondrocyte transplantation. Biomechanics and long-term durability. Am J Sports Med 2002 Jan; 30(1): 2e12.

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29 Horas U, Pelinkovic D, Herr G, Aigner T, Schnettler R. Autologous chondrocyte implantation and osteochondral cylinder transplantation in cartilage repair of the knee joint. A prospective, comparative trial. J Bone Joint Surg Am 2003 Feb; 85-A(2): 185e92. 30 Dozin B, Malpeli M, Cancedda R, et al. Comparative evaluation of autologous chondrocyte implantation and mosaicplasty: a multicentered randomized clinical trial. Clin J Sport Med 2005 Jul; 15(4): 220e6. 31 Knutsen G, Drogset JO, Engebretsen L, et al. A randomized trial comparing autologous chondrocyte implantation with microfracture. Findings at five years. J Bone Joint Surg Am 2007 Oct; 89(10): 2105e12. 32 Saris DB, Vanlauwe J, Victor J, et al. Characterized chondrocyte implantation results in better structural repair when treating symptomatic cartilage defects of the knee in a randomized controlled trial versus microfracture. Am J Sports Med 2008 Feb; 36(2): 235e46. 33 Bartlett W, Skinner JA, Gooding CR, et al. Autologous chondrocyte implantation versus matrix-induced autologous chondrocyte implantation for osteochondral defects of the knee: a prospective, randomised study. J Bone Joint Surg Br 2005 May; 87(5): 640e5. 34 Gooding CR, Bartlett W, Bentley G, Skinner JA, Carrington R, Flanagan A. A prospective, randomised study comparing two techniques of autologous chondrocyte implantation for osteochondral defects in the knee: periosteum covered versus type I/III collagen covered. Knee 2006 Jun; 13(3): 203e10. 35 Williams RJ, Gamradt SC. Articular cartilage repair using a resorbable matrix scaffold. Instr Course Lect 2008 Jan 15; 57: 563e71. 36 Emmerson BC, Gortz S, Jamali AA, Chung C, Amiel D, Bugbee WD. Fresh osteochondral allografting in the treatment of osteochondritis dissecans of the femoral condyle. Am J Sports Med 2007 Jun; 35(6): 907e14. 37 Bugbee WD, Convery FR. Osteochondral allograft transplantation. Clin Sports Med 1999 Jan; 18(1): 67e75. 38 Bugbee WD. Fresh osteochondral allografts. J Knee Surg 2002; 15(3): 191e5. 39 Jamali AA, Emmerson BC, Chung C, Convery FR, Bugbee WD. Fresh osteochondral allografts. Clin Orthop Relat Res 2005 Aug;(437): 176e85. 40 Ghazavi MT, Pritzker KP, Davis AM, Gross AE. Fresh osteochondral allografts for post-traumatic osteochondral defects of the knee. J Bone Joint Surg Br 1997 Nov; 79(6): 1008e13. 41 Williams SK, Amiel D, Ball ST, et al. Prolonged storage effects on the articular cartilage of fresh human osteochondral allografts. J Bone Joint Surg Am 2003 Nov; 85-A(11): 2111e20. 42 Amendola A. Surgical management of articular cartilage defects of the knee. 2008. 43 Mina C, Garrett Jr WE, Pietrobon R, Glisson R, Higgins L. High tibial osteotomy for unloading osteochondral defects in the medial compartment of the knee. Am J Sports Med 2008 May; 36(5): 949e55. 44 Sterett WI, Steadman JR. Chondral resurfacing and high tibial osteotomy in the varus knee. Am J Sports Med 2004 Jul; 32(5): 1243e9. 45 Fulkerson JP. Anteromedialization of the tibial tuberosity for patellofemoral malalignment. Clin Orthop Relat Res 1983 Jul;(177): 176e81.

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46 Farr J. Autologous chondrocyte implantation improves patellofemoral cartilage treatment outcomes. Clin Orthop Relat Res 2007 Oct; 463: 187e94. 47 Lee SJ, Aadalen KJ, Malaviya P, et al. Tibiofemoral contact mechanics after serial medial meniscectomies in the human cadaveric knee. Am J Sports Med 2006 Aug; 34(8): 1334e44. 48 McDermott ID, Amis AA. The consequences of meniscectomy. J Bone Joint Surg Br 2006 Dec; 88(12): 1549e56. 49 Alford JW, Cole BJ. Cartilage restoration, part 2: techniques, outcomes, and future directions. Am J Sports Med 2005 Mar; 33(3): 443e60. 50 Cole BJ, Dennis MG, Lee SJ, et al. Prospective evaluation of allograft meniscus transplantation: a minimum 2-year follow-up. Am J Sports Med 2006 Jun; 34(6): 919e27. 51 Verdonk PC, Verstraete KL, Almqvist KF, et al. Meniscal allograft transplantation: long-term clinical results with radiological and magnetic resonance imaging correlations. Knee Surg Sports Traumatol Arthrosc 2006 Aug; 14(8): 694e706. 52 Zaffagnini S, Giordano G, Vascellari A, et al. Arthroscopic collagen meniscus implant results at 6 to 8 years follow up. Knee Surg Sports Traumatol Arthrosc 2007 Feb; 15(2): 175e83. 53 Deie M, Sumen Y, Adachi N, et al. The long-term results of meniscus transplantation for articular cartilage defects in the knee joint. Knee Surg Sports Traumatol Arthrosc 2007 Jan; 15(1): 61e6. 54 Bellamy N, Campbell J, Robinson V, Gee T, Bourne R, Wells G. Viscosupplementation for the treatment of osteoarthritis of the knee. Cochrane Database Syst Rev 2006;(2). CD005321.

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55 Divine JG, Zazulak BT, Hewett TE. Viscosupplementation for knee osteoarthritis: a systematic review. Clin Orthop Relat Res 2007 Feb; 455: 113e22. 56 Huskin JP, Vandekerckhove B, Delince P, et al. Multicentre, prospective, open study to evaluate the safety and efficacy of hylan G-F 20 in knee osteoarthritis subjects presenting with pain following arthroscopic meniscectomy. Knee Surg Sports Traumatol Arthrosc; 7 Jun; 2008. 57 Reddi AH. Cartilage morphogenetic proteins: role in joint development, homoeostasis, and regeneration. Ann Rheum Dis 2003 Nov; 62(Suppl 2): ii73e8. 58 Tytherleigh-Strong G, Hurtig M, Miniaci A. Intra-articular hyaluronan following autogenous osteochondral grafting of the knee. Arthroscopy 2005 Aug; 21(8): 999e1005. 59 Williams JM, Moran M, Thonar EJ, Salter RB. Continuous passive motion stimulates repair of rabbit knee articular cartilage after matrix proteoglycan loss. Clin Orthop Relat Res 1994 Jul;(304): 252e62. 60 Salter RB, Simmonds DF, Malcolm BW, Rumble EJ, MacMichael D, Clements ND. The biological effect of continuous passive motion on the healing of full-thickness defects in articular cartilage. An experimental investigation in the rabbit. J Bone Joint Surg Am 1980 Dec; 62(8): 1232e51. 61 Bartha L, Vajda A, Duska Z, Rahmeh H, Hangody L. Autologous osteochondral mosaicplasty grafting. J Orthop Sports Phys Ther 2006 Oct; 36(10): 739e50. 62 Szerb I, Hangody L, Duska Z, Kaposi NP. Mosaicplasty: long-term follow-up. Bull Hosp Jt Dis 2005; 63(1e2): 54e62.

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CHILDREN

The management of spastic equinus in cerebral palsy

a mixture of these conditions. Spasticity is the commonest. Among patients with cerebral palsy 70% have spasticity, which results in asymmetric muscle function.1 The altered innervation of individual muscles produces either spasticity or weakness, causing imbalances of muscle activity across joints. With growth, the imbalance between agonists and antagonists often progresses to joint and bony deformities and muscle contracture. Cerebral palsy is considered to be the main cause of motor disability in children, affecting 1e6 of 1000 newborns. Foot equinus is the most common deformity in children with spastic cerebral palsy.2 Equinus deformity of the foot is defined as the inability to dorsiflex the ankle sufficiently enough to allow the heel to contact the supporting surface without some form of compensation in the mechanics of the lower limb and foot (Figure 1). Methods to compensate for equinus include hip flexion, knee flexion, lumbar lordosis or genu recurvatum (hyperextension of the knee) and abducted gait. It is also defined as a limitation of passive dorsiflexion of the foot in the ankle joint beyond the neutral position (the neutral position is at an angle of 90 between the lower leg and the foot in the sagittal plane).

Goran Cobeljic Marko Bumbasirevic Aleksandar Lesic Zoran Bajin

Abstract Equinus of the foot is the most common deformity in children with spastic cerebral palsy. Patients with cerebral palsy who are able to walk may have different problems because of an equinus deformity. They may have a clumsy gait and often stumble, fall and suffer injuries. Secondary hip and knee deformities, forefoot callosities and pain, shoe fitting problems and excessive wear on shoes are common. The treatment of equinus is either nonoperative or operative. Nonoperative treatment is indicated in dynamic equinus, during the fast-growth phase of a child’s development. The most favourable results can be expected with a combination of different forms of such treatment including repeated injections of Botulinum toxin type A together with orthotics and physical therapy. If there are simultaneous contractures in the hip and/or knee joints, multilevel surgery with nonoperative treatment of dynamic equinus may be the best solution. Operative treatment is indicated in patients with fixed equinus. In diplegia and quadriplegia the most favourable outcome can be expected with either a procedure on the gastrocnemius muscle or triceps surae muscle. In hemiplegia the best results may be expected with procedures on the triceps surae muscle. Multilevel surgery at the hip and knee joints is the rule in cases of contractures or deformity.

Prevalence Equinus is the most common deformity in patients with spastic cerebral palsy.3 Around 90% of the deformities in cerebral palsy occur in the ankle and foot region.4 The incidence of equinus is around 75%.5

Aetiopathogenesis and spontaneous evolution Spastic equinus is caused by muscular imbalance, by one of the following mechanisms: (1) spastic plantarflexor muscles (gastrocnemius, triceps surae, of which soleus is the main plantar-flexor muscle along with plantaris, tibialis posterior, flexor hallucis longus and flexor digitorum longus; the last three muscles also have a supination function) versus weaker spastic dorsiflexors (tibialis anterior and all toe extensors), (2) spastic plantarflexors versus normal dorsiflexors, or (3) spastic plantarflexors versus flaccid dorsiflexors. In the majority of patients with spastic diplegia the gastrocnemius muscle demonstrates abnormal spasticity with relative sparing of the soleus. In most patients with spastic hemiplegia the gastrocnemius and soleus are affected equally, while the muscles in spastic quadriplegic patients are variably affected.6 Tonic foot reflexes can also be the cause of both foot deformity and equinus in the spastic form of cerebral palsy. These reflexes occur on stimulation of the plantar surface of the foot. They normally disappear by the age of one year. However, they can persist due to the absence of inhibitory activity of the immature and impaired central nervous system. The existence of these reflexes, along with a progressive muscle imbalance, result in forced positions and deformities.7 The most important reflex implicated in equinus deformity is the plantar grasp reflex: tonic flexion and adduction of the toes will occur upon light digital pressure on the plantar surface of the foot, just proximal to the toes (Figure 2). This reflex is present in the newborn infant and disappears by the end of the first year, but it may persist in children with cerebral palsy.

Keywords cerebral palsy; orthopaedic management; spastic equinus

Introduction Cerebral palsy is a central nervous system disorder; a group of persistent postural or movement dysfunctions secondary to a nonprogressive lesion in the developing brain. Dysfunction is manifest as spasticity, athetosis, dystonia, ataxia, hypotonia, or

Goran Cobeljic MD PhD is a Professor at the Institute for Orthopaedic Surgery ‘‘Banjica’’, Mihajla Avramovica 28, 11040 Belgrade, Serbia. Marko Bumbasirevic MD PhD is a Professor at the Institute for Orthopaedic Surgery and Traumatology, Clinical Center of Serbia, Visegradska 26, 11000 Belgrade, Serbia. Aleksandar Lesic MD PhD is a Professor at the Institute for Orthopaedic Surgery and Traumatology, Clinical Center of Serbia, Visegradska 26, 11000 Belgrade, Serbia. Zoran Bajin MD PhD is a Consultant Orthopaedic Surgeon at the Institute for Orthopaedic Surgery ‘‘Banjica’’, Mihajla Avramovica 28, 11040 Belgrade, Serbia.

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the joints are generated. Therefore, equinus in cerebral palsy is caused by spasm, fibrosis and contracture of a part or the whole triceps surae muscle, which is a plantarflexor. If equinus persists, further changes occur which tend to fix the deformity. The plantarflexors of the toes, tibialis posterior muscle and peroneal muscles become shorter, the posterior parts of the talocrural and talocalcaneal joints decrease in length, a part of the talus neck becomes thicker which leads to further limitation of foot dorsiflexion. Due to the plantarflexion, part of the joint surface of the talus lies outside the joint surfaces of the tibia and fibula (Figure 3). Such a condition causes degenerative changes in the frontal part of the lower surface of the tibial joint surface and a corresponding part of the talus.9 Cartilage degeneration occurs when the opposing articular surfaces are not in contact. Articular cartilage needs movement to survive and to repair itself.10 The deformity is dynamic and correctible at first, but with time, especially if it is not treated, becomes fixed due to fibrous changes in the surrounding tissues. As the child develops, spastic muscles fail to grow as rapidly as neighbouring structures, transforming dynamic into fixed equinus.11 Secondary adaptive changes occur in major neighbouring joints. If a patient bears weight on the forefoot, a flexion deformity develops at the hip and knee (Figure 1). If a patient bears weight on the full plantar surface, a hyper-extension deformity develops (Figure 4).12 Equinus gait in cerebral palsy can result in knee and ankle problems, abnormal motion during gait, impaired balance and proprioception. The loss of the smooth mechanism of weight transfer along the foot during gait leads to increased muscle

Figure 1 Equinus in a patient with spastic hemiplegia. Flexion deformity of the hip and the knee as a form of compensation for the equinus deformity.

The spasm reduces not only the strength and contractility of muscles, but also their elasticity, which leads to diminished range and precision of movement. A spastic muscle has shorter muscle fibres, an elongated tendon and the overall volume is reduced. There is insufficient relaxation of antagonists when agonists are active, which decreases the amplitude and efficiency of movement. Fibrosis and hypotrophy of muscle fibers occur.8 Fibrosis leads to shortening, which is progressive and leads to further reduction of contractility. This shortening is more prominent if a child does not walk. The tendency increases with age, therefore bone growth is not followed by appropriate muscles growth. This is how deformations and contractures in

Figure 2 Plantar grasp reflex.

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Figure 3 Hypertrophic changes in the neck of the talus in spastic equinus.

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manoeuvre, then contracture of the soleus or triceps surae muscle is present.15 However, electromyographic studies of these muscles during the Silfverskio¨ld test demonstrate that both muscles show increased action potentials regardless of the position of the knee joint. No clear-cut difference between gastrocnemius and soleus or triceps surae muscle spasticity/contracture were found in spite of a positive Silfverskio¨ld test.16 Other authors also concluded that this test may not reflect the true functional status of the triceps surae during walking and/or weightbearing.17 Although unreliable in conscious patients, the Silfverskio¨ld test can give consistent results when carried out under anaesthesia. In patients with cerebral palsy examination under general anaesthesia is the only absolute test to determine whether a muscle is contracted or not. This test should be done at the beginning of surgery to confirm which muscle is in contracture.18 Spastic equinus caused by calf muscle imbalance (when the plantarflexors are stronger) is a primary equinus. On the other hand spasticity and flexion contractures at the hip and knee may dictate an equinus posture at the ankle, when there is no calf contracture, and it is a secondary equinus.

Diagnosis The diagnosis of spastic equinus is based on clinical findings indicating the existence of a deformity together with a diagnosis of cerebral palsy. The clinical finding of equinus is also possible in cases of upper motor neuron lesions after maturation of the central nervous system, in leg length discrepancy, congenital or postural shortening of the Achilles tendon, poliomyelitis, myelomeningocele, peroneal muscular atrophy, progressive muscular dystrophy, arthrogryposis multiplex congenita, peroneal nerve palsy, congenital pseudarthrosis of the tibia, congenital angulation of the tibia, malunited/nonunited fractures of the leg and as a consequence of a variety of injuries to the lower leg muscles accompanied by secondary contractures, etc.

Figure 4 Hyperextension of the knee-genu recurvatum in a patient with spastic equinus deformity.

activity across the more proximal joints to maintain an upright posture, which is not energy efficient. The heel, ankle and forefoot optimise the shock-absorbing, stabilising and propulsive functions of the foot. The forefoot strike and small area of support in equinus affect stability during the stance phase of gait; there is a loss of the smooth transition of the body over the foot and inadequate foot clearance in the swing phase of gait, with an increased risk of tripping and falling. Stride length is decreased and the gait is clumsy.13 Patients with equinus can present with a variety of conditions such as forefoot callosities (Figure 5c), plantar ulceration, metatarsalgia, Achilles tendinopathy, calcaneal apophysitis, plantar fascitis, low back pain, chondromalacia patellae, hallux valgus or rigidus, excessive wear on shoes and shoe fitting problems.14

Treatment Spastic equinus deformity must be treated in patients able to walk. Untreated foot disorders may lead to fixed contractures and proximal compensatory deformities requiring surgical intervention.19 Treatment can either be nonoperative or operative. Nonoperative treatment Nonoperative (conservative) treatment is indicated for dynamic equinus during the fast-growth phase of a child’s development, starting between the ages of 1 and 4 up to 6 to 8 years old. By this age (7 years on average) neurological control has matured to the adult pattern of walking, thereby minimising the risk of selecting the wrong surgical procedure, in cases where it is indicated. Furthermore, delaying surgery is important when possible because the results of early surgery are less predictable, especially before 6 years of age. In children with hemiplegia the principal risk associated with early surgery is recurrent equinus and the need for another operation. In children with diplegia or quadriplegia, the principal risk of early surgery is overcorrection and the development of calcaneus deformity of the foot. On the other hand, there should be no need to delay until the end of growth, because progression of bone deformities compromises soft tissue procedures.20,21

Classification There are three types of equinus deformity:  dynamic, without muscle contracture,  fixed, with contracture of the soleus or triceps surae muscle and  contracture of the gastrocnemius muscle. The third type is correctable only with flexion of the knee. Distinction between the last two types is possible using the classical Silfverskio¨ld test. If dorsiflexion of the foot with the knee flexed is greater than that with the knee extended, then the gastrocnemius is implicated as the main site of contracture. If there is no change in dorsiflexion of the ankle with this

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a, b Patient with spastic equinus deformity. c Forefoot calluses in the same patient. Figure 5

Nonoperative treatment aims at functional improvement, postponing surgery to at least the age of 6 years or at avoiding surgery by prevention of a fixed deformity. Additional rationales include improving the patient’s ability to wear shoes, the acceptance of orthoses, ease of physical therapy and elimination of disturbances. Physical therapy, casting, orthotics, special shoes and arch supports, biofeedback devices, phenol, alcohol, botulinum toxin type A and various pharamaceutical agents are options for nonoperative treatment.

for bathing, may be associated with significant discomfort and pressure sores can occur under the cast. Therefore, casts are not suitable for long-term treatment of spastic equinus.21 Orthotics There are knee-ankle-foot orthoses (KAFO) and anklefoot orthoses (AFO). KAFO are rarely indicated; only at night, postoperatively, to prevent recurrence of equinus in patients with flexion deformity of the knee. There are several AFO orthoses: rigid AFOs for preventing equinus in the stance and swing phases of gait; more flexible types with posterior leaf springs to prevent equinus only in the swing phase of gait; flexible hinged AFOs and supramalleolar dynamic AFOs (DAFO). DAFO are designed to improve postural control and balance through unrestricted neural feedback mechanisms, including a highly contoured footplate that is proposed to influence muscle tone, inhibiting pathological foot reflexes.22 A rigid AFO, made of thermoplastic material, is the best alternative for most patients.18 Rigid AFOs must incorporate adequate dorsiflexion. The wall test should be included in the assessment of a rigid AFO. If the calf or upper portion of the brace contacts the wall while the foot portion of the brace is flat on the floor, the brace is probably positioned in equinus. This should be avoided and the brace adjusted to more dorsiflexion (the heel portion should make contact with the wall). Rigid AFOs, with adequate dorsiflexion, are also a suitable solution for patients with equinus who walk with the knee in hyperextension. Rigid AFO, leaf spring AFO and hinged AFO designs with a plantarflexion stop can prevent equinus deformities. DAFO does not prevent equinus, but improves the temporal parameters of gait, such as walking speed and stride length and thereby improves gait efficiency. However, for activities such as climbing stairs, moving from sitting to standing or controlling perturbed balance, children with less severe impairments often perform better in leaf spring AFO, hinged AFO or DAFO.23 Rigid KAFO and AFO can be used postoperatively as night splints or for daily

Physical therapy Exercises, hydrotherapy and electrotherapy, all supplemented by occupational therapy are the most frequent manual interventions used to treat equinus deformity. It is generally agreed that physical therapy is necessary to rehabilitate patients with a dynamic equinus foot, usually alongside other forms of nonoperative treatment. It is also included before and after the surgical correction of fixed equinus. However, formal trial evidence is still lacking in order to establish the real benefit of physical therapy and occupational therapy in the rehabilitation of equinus foot patients.1 Casting Some authors have successful results (95%) with closed below-knee plaster treatment, which is wedged upwards at the ankle at four-day intervals until the deformity has been over corrected. Those children who are resistant to this treatment are encouraged to walk in the plaster in which the foot has been dorsiflexed as fully as possible. With each step the calf muscles are stretched and the process can be hastened by further wedging of the foot. Treatment is completed at 6e8 weeks.9 However, most authors have failed to produce sufficiently good results using this regimen and most would now advocate serial casting on three occasions with a below-knee walking plaster for periods of 4e6 weeks in a neutral or dorsiflexed position. Around 30% success is claimed. Plaster of Paris is cheap and easy to apply. Children readily adapt to walking in plaster casts, but the cast cannot be removed

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splinting to prevent the recurrence of equinus for a period of 3e6 months to 1 year or until the end of growth.6

soleus and 200 U in the gastrocnemius (both muscles should be injected laterally and medially). A clinical effect may be expected within two weeks after injection and in that period any other conservative treatment should be avoided. Injections may be repeated every 6e12 months, not less than 3 months. Larger doses used less frequently are safe, more effective, better tolerated by children, more acceptable to their families and the functional outcomes are longer lasting.3,21 Injections of BT-A into the gastrocnemius and soleus allow active strengthening of the dorsiflexors. Relaxation of the spastic plantarflexor muscles facilitates stretching, promotes growth, prevents contractures and delays surgery. To improve their effect, injections may be combined with short periods of casting or with intensive physical therapy and orthotics to maximize muscle stretching. Today, BT-A is the first-choice pharmacological agent because of its reversible effects, low adverse reaction rate, painlessness and the fact that it offers repetition. The disadvantage of BT-A is the cost of the medication.26

Shoes and arch supports Shoes and arch supports are accessory devices to other forms of nonoperative treatment. They have no corrective effect. Tennis shoes provide good ground contact and possibly force more muscle coordination. Hiking-boots with heavy rubber soles, with or without arch supports, seem to help ankle stability. These also add a bit of weight and might help control balance. High-top shoes can hide the deformity. Biofeedback devices Biofeedback devices may be worthwhile in selected groups of patients. Biofeedback means that the patient is able to monitor the action of a muscle by some mechanical/ electrical device. Devices used include a pressure-sensitive on/off switch inside the shoe and under the heel. The switch is connected to a battery-powered bleeper (auditory feedback). When the bleep is heard the child knows that heel contact occurred. After instruction by the physical therapist the device is used 3 hours per day for 3 months at home. This regimen appeared more effective than daily visits to a physical therapist. Biofeedback devices are indicated in patients over 4 years of age, with IQ of more than 70 who have mild spasticity of the triceps surae with a dynamic equinus deformity.24

Drugs Antispasticity drugs (baclofen, the benzodiazepines, dantrolene, tizanidine, some anticonvulsants and the cannabinoids) are not specific for treatment of spastic equinus. Orally administered they are nonselective in action, so generalised weakness, functional disability and toxic effects may result from their use, especially with high doses. Furthermore, the clinical benefit of these drugs usually becomes less evident after a few months of treatment because tolerance to their effects on spasticity frequently develops with chronic use. Intrathecal baclofen infusion has been shown to be effective in carefully selected patients. However, its application is complicated, expensive and can result in potentially serious complications, mainly technical, but local sepsis and spinal meningitis are possible.27 The most favourable results could be expected with a combination of different forms of nonoperative treatment, such as repeated injections of BT-A with a short period of casting or orthotics and with physical therapy. Also, if there are simultaneous contractures in the hip and/or knee joints, multilevel surgery with nonoperative treatment of dynamic equinus is the best solution.28

Phenol and alcohol Spasticity of a specific muscle or group of muscles can be relieved for up to 6 months by injection of 3e5% phenol into the sheath of the motor nerve (peripheral nerve block of branches for the gastrocnemius-soleus muscle).25 However, because phenol can denature any protein with which it comes in contact, injection into a mixed nerve can cause chemical neuritis. Therefore, it is preferable to identify and inject the motor nerve during surgery. Phenol nerve block is more often used in the upper than in the lower extremity. Unfortunately it has a shortterm anaesthetic effect and a long-term destructive effect. Nerve fibres of all diameters can be destroyed and it is difficult to control the degree of tissue destruction.24 Alcohol has been used as neurotoxic agent to block motor endplates chemically. About 3e4 ml ethyl alcohol is injected into the motor points of the muscle (intramuscular injections of gastrocnemius-soleus) and spasticity can be relieved temporarily for 2e6 weeks.6 Alcohol injections can be uncomfortable because of a burn sensation. Although phenol and alcohol are inexpensive and effective, their use has been largely supplanted by botulinum toxin.

Operative treatment Operative treatment is indicated in patients with fixed equinus. Patients with fixed equinus treated nonsurgically continue to have a deformity and there is no trend towards improvement despite physical therapy and brace use.29 In hemiplegia it is worthwhile, when possible, to postpone surgery at least to the age of 6 years by nonoperative treatment. The younger the age of surgical correction, the more likely the recurrence of equinus, due to rapid bone growth that is faster than muscle and tendon growth.20,28 In diplegia and quadriplegia the timing of surgery is also important. Girls over 7 years old and boys over 8 show much better results, but delayed development of gait or difficulty in predicting the final length and strength of plantarflexors of the foot can be problematic. With early surgery there is a possibility of overcorrection and development of calcaneus deformity.20 There are many surgical procedures for the correction of equinus deformity in cerebral palsy and they can be classified in five groups:

Botulinum toxin type A Botulinum toxin type A (BT-A) prevents release of acetylcholine at the neuromuscular junction from the presynaptic axon of the motor endplate. Therefore BT-A reduces the spasticity of muscles, providing a temporary 2e6 months weakening of the injected muscle.19 BT-A is injected intramuscularly into the medial and lateral heads of the calf muscle at two to four sites per leg. The dose of BT-A is individualized for each patient. There are two formulations of BT-A: BotoxÒ with a recommended dose of 4e12 U/kg body weight, with a maximum of 300 U per child on one occasion and 50 U per injection site and DysportÒ with a recommended dose of 15e30 U/kg body weight. The maximal dose administered must not exceed 1000 U per patient and with minimal individual dosages of 100 U in the

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 neurectomy of motor branches of the tibial nerve to the calf muscles (gastrocnemius mainly, but also soleus or gastrocnemius or soleus alone  tendon transfers  procedures on the gastrocnemius muscle  procedures on the triceps surae muscle  tarsectomy

Subcutaneous lengthening of the Achilles tendon is the most unpredictable procedure, particularly in younger patients, possibly because the size of the tendon is very variable and complete transection is not uncommon. Other disadvantages include intraoperative oversliding during forced dorsiflexion and calcaneus deformity, sural neuritis, adhesions etc. Control of the tendon ends is poor and this procedure has been condemned by most surgeons.47,48 The other procedures are indicated in children with contracture of the gastrocnemius muscle, soleus muscle or the whole triceps surae muscle. Equinus in hemiplegia is more likely to be due to contracture of the whole triceps surae muscle. However, in Z-lengthening of the Achilles tendon it is difficult to determine precisely the value of proper tendon lengthening and often there are some problems with skin adhesions.24 Most surgeons consequently prefer the other procedures listed in this group.

Neurectomy of motor branches of the tibial nerve to the calf muscles This procedure cannot correct fixed equinus and the results with dynamic equinus are unpredictable. Recurrences of equinus or calcaneus deformity are possible and this procedure has been abandoned because there was often too much or too little motor paralysis.30 Tendon transfers include - anterior transfer of the tibialis posterior31 - tritendon anastomosis between the tendons of the tibialis posterior, peroneus longus and tibialis anterior - Birdle procedure32 - anterior transfer of the long toe flexors33 - heel cord advancement34 These procedures are not fully accepted because the results are not superior to procedures on gastrocnemius and triceps surae, yet they are more complex. Frequent complications include recurrent deformity, planovalgus deformity and difficulty in obtaining complete correction, particularly in patients with severe pes equinus. Some authors combine heel cord advancement with lengthening of the gastrocnemius but this procedure is complex35,36 and success rates equivocal.

Tarsectomy Tarsectomy or triple arthrodesis is indicated in patients with fixed equinus and hypertrophic changes in the neck of the talus (Figure 3) after 12 years of age.5,9 In such cases it is impossible to correct fixed equinus by soft tissue surgery, even with posterior capsulotomy of the tibiotalar and talocalcaneal joints, as additional procedures. The Lambrinudi procedure, a tarsectomy, is a suitable choice.49 In diplegia and quadriplegia the most favourable outcome could be expected either with procedures on the gastrocnemius muscle or with one of the cited procedures on the triceps surae muscle (Figure 6) and in hemiplegia with procedures on the triceps surae muscle. Multilevel surgery on the hip and knee joints is the rule in cases involving their contracture or deformity. Simultaneous lengthening of both the gastrocnemius or triceps surae and the distal hamstrings addresses equinus and crouch. Increased knee flexion deformity could result from shortening of the gastrocnemius or triceps surae muscles, which span the knee and ankle joints. Coexisting hamstring spasticity exacerbates crouch following isolated lengthening of the gastrocnemius or triceps surae muscle, as the ankle becomes more dorsiflexed.12 No single surgical procedure emerges as being consistently superior to others.6 Whatever procedure is used, postoperative management includes a long leg walking cast with the knee in full extension for 2e3 weeks followed by a below-knee walking cast for 3e4 weeks. Immobilisation in a long leg cast ensures that the gastrocnemius heals in the desired position. A long leg cast also stretches the hamstring muscles.18 Bracing is indicated in patients with hemiplegia, especially during growth. As a night splint it may prevent or delay recurrence of equinus deformity. It is used for a period of 3e6 months to 1 year, or in patients with inadequate dorsiflexor strength until the end of growth.47 It is important to place the foot in the neutral position of 90 in the postoperative walking cast, especially after procedures on the triceps surae muscle, where a position of more than 90 can lead to calcaneal deformity of the foot.24

Procedures on the gastrocnemius muscle These include: - the Vulpius and Sto¨ffel technique: a chevron-like incision of the gastrocnemius aponeurosis37; - the Silfverskio¨ld procedure: proximal recession of the gastrocnemius muscle15; - the Green and Mc Dermott procedure: lengthening of the gastrocnemius muscle at its origin with/without neurectomy of the tibial nerve38; - the Strayer procedure: distal recession of the gastrocnemius muscle39; - the Baker procedure: tonge-in-groove lengthening of the gastrocnemius aponeurosis40 These procedures are indicated in children with contracture of the gastrocnemius muscle. Most patients with spastic diplegia or quadriplegia with equinus deformity have contracture of the gastrocnemius muscle, without contracture of the soleus muscle.20 Equinus with contracture of the gastrocnemius muscle is diagnosed by the Silfverskio¨ld test under general anesthesia. Procedures on the triceps surae muscle These include: - Z-lengthening of the Achilles tendon41; - White slide lengthening of the triceps surae muscle (2-cut)42; - subcutaneous lengthening of the Achilles tendon43; - the Strayer procedure with Z-lengthening of the Achilles tendon44; - Hoke slide lengthening of the triceps surae muscle (3-cut)45; - Baumann intramuscular lengthening of the gastrosoleus muscle (in the anterior aponeurosis of gastrocnemius and the adjacent fascia of soleus)46

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Complications of operative treatment There are three possible complications of operative treatment: recurrence of the equinus deformity, overcorrection of the equinus-calcaneus deformity and flexion deformity of the toes.

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a, b Patient with spastic diplegia and equinus deformity of both feet before operation. c The same patient after bilateral correction of the equinus (Hoke sliding lengthening of the triceps surae muscle). Figure 6

Recurrence of equinus deformity Most investigators have observed a greater risk of recurrent deformity in hemiplegic children with severe spasticity of the triceps surae muscle who fail postoperative casting and bracing and who are operated before 6 years of age. There is also some risk of recurrence in patients who have developed hamstring contractures.18 Longitudinal growth is reduced in spastic limbs. Spastic muscle grows at only 55% of the rate of bone and this explains the development of recurrent equinus during periods of rapid growth after surgery before 6 years of age.50,51 Some studies have shown that quadriplegic and especially diplegic patients exhibit a lower recurrence rate of equinus deformity than hemiplegic patients. This may be explained by the observation that dorsiflexors of the foot in hemiplegic patients are significantly weaker than in quadriplegic and diplegic patients. The recurrence rate of equinus deformity is approximately 10e40% in hemiplegic, about 15e20% in quadriplegic and about 10e15% in diplegic patients.6,20 Other variables that have been suggested to influence the recurrence rate include: post operative rehabilitation programs; parental and patient cooperation and compliance; an adequate assessment of antagonist muscles; trunk and hip control; skill of the surgeon; gender (in one study a significantly higher recurrence rate in boys than girls was reported).6,20 The treatment of recurrent equinus deformity is surgical, involving procedures on the triceps surae muscle, with or without posterior capsulotomy of the ankle and subtalar joint. Tarsectomy is indicated in cases where it is impossible to correct equinus by soft tissue procedures. Simultaneous correction of hamstring contractures is important.

This deformity or hypercorrection of equinus is the most significant complication because effective bracing or operative correction is difficult to achieve. The triceps surae muscle becomes overly long, it allows the tibia to fall forwards resulting in a requirement to flex both the hips and knees, i.e. crouch gait develops. Crouch gait requires continual activity of the quadriceps and hip extensors to resist gravity. Once the ground reaction force is behind the knee throughout the stance phase of gait, a persistent stretch is applied to the calf muscle, which becomes too long and biomechanically incompetent. Patients with calcaneus deformity usually have heel calluses, shoe fitting problems, excessive wear of the shoes, walking becomes difficult and is not energy efficient. A little equinus is better than any calcaneal deformity.53 The risk of calcaneal deformity is about 60% in quadriplegic patients, about 30e40% in diplegic and about 5% in hemiplegic patients.20,53 The risk is about 15% higher for patients subject to procedures on the triceps surae muscle than for those with procedures on the gastrocnemius muscle alone.54 The treatment of calcaneal deformity is surgical. In mild cases the inverse Strayer procedure is a satisfactory solution.9 Achilles tendon shortening and/or posterior transfer of the tibial, peroneal tendons and/or long toe flexors to strengthen the Achilles tendon are procedures which can be used, with simultaneous correction of the hip and knee deformity. Flexion deformity of the toes In fixed longstanding equinus deformity, the flexors of the toes are shortened. Often, after correction of the equinus and with the foot in a neutral position, the shortened flexors of the toes will become tighter, which causes flexion deformity of the toes (Figure 7). These deformities can cause shoe fitting problems. Treatment is usually conservative with suitable shoes and arch supports. Sometimes, surgery is indicated by elongation or

Calcaneus deformity Calcaneus deformity is limitation of passive plantarflexion of the foot at the ankle joint of over 4 compared to foot dorsiflexion.52

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foot in patients with diplegia and quadriplegia, a more favourable outcome is obtained over 7 years of age. In these conditions the best results could be expected with procedures on the gastrocnemius muscle or triceps surae muscle and in hemiplegia with procedures on the triceps surae muscle alone. Multilevel surgery on the hip and knee joints is the rule in cases of their associated contracture or deformity. Tarsectomy or triple arthrodesis is indicated in patients with fixed equinus and hypertrophic changes in the neck of the talus after 12 years of age. In such cases it is impossible to correct fixed equinus by soft tissue surgery. A

REFERENCES 1 Cardoso E, Rodrigues B, Barroso M, et al. Botulinum toxin type A for the treatment of the spastic equinus foot in cerebral palsy. Pediatr Neurol 2006; 34: 106e9. 2 Rutter M. Graham P, Yule W. A neuropsychiatric study in childhood. in: Clinics in developmental medicine, No 35/36. London: Spastics International Medical Publications with Heinemann Medical, 1970. 3 Metaxiotis D, Siebel A, Doederlein L. Repeated Botulinum toxin A injections in the treatment of spastic equinus foot. Clin Orthop 2002; 394: 177e85. 4 O’Connell P, D’Souza L, Dudeney S, et al. Foot deformities in children with cerebral palsy. J Pediatr Orthop 1998; 18: 743e7. 5 Banks H, Green W. The correction of equinus deformity in cerebral palsy. J Bone Joint Surg 1958; 40-A: 1359e79. 6 Koman A, Smith B, Barron R. Recurrence of equinus foot deformity in cerebral palsy patients following surgery: a review. J South Orthop Assoc 2003; 12: 125e33. 7 Duncan R. Tonic reflexes of the foot. Their orthopaedic significance in normal children and in children with cerebral palsy. J Bone Joint Surg 1974; 56-A: 1598e602. 8 Tardieu G, Rondot R, Dalloz J, et al. Essai de classification de raideurs musculaires d’origines cerebrales. Rev Neurol 1957; 4: 264e75. 9 Pollock G. Surgical treatment of cerebral palsy. J Bone Joint Surg 1962; 44-B: 68e81. 10 Sood S. A study of the effects of experimental immobilization on rabbit articular cartilage. J Anat 1971; 188: 497e507. 11 Cosgrove A, Graham H. Botulinum toxin prevents the development of contractures in the hereditary spastic mouse. Dev Med Child Neurol 1994; 36: 379e85. 12 Gage J. Principles of treatment in cerebral palsy, hemiplegia, diplegia and quadriplegia. In: Gage J, ed. Gait analysis in cerebral palsy. Oxford: Mac Keith Press, 1991; p. 118e72. 13 Gage J, DeLuca P, Renshaw T. Gait analysis: principles and applications, emphasis on its use in cerebral palsy. J Bone Joint Surg 1995; 77-A: 1607e23. 14 Simpson D. Clinical trials of Botulinum toxin in the treatment of spasticity. Muscle Nerve 1997; 6(Suppl): 169e75. ¨ld N. Reduction of the uncrossed two-joints muscles of the 15 Silfverskio leg to on-joint muscles in spastic conditions. Acta Chir Scand 1923; 56: 315e30. 16 Perry J, Hoffer M, Giovan P, Antonelli D, Greenberg R. Gait analysis of the triceps surae in cerebral palsy - a preoperative and postoperative clinical and electromyographic study. J Bone Joint Surg 1974; 56-A: 511e20.

Figure 7 Flexion deformity of the toes after surgical correction (Hoke procedure) of the equinus deformity in a patient with spastic diplegia.

tenotomy of the long flexors of the toes, with or without plantar capsulotomy of the proximal and/or distal interphalangeal joints.

Conclusions The orthopaedic treatment of equinus deformity in patients with spastic cerebral palsy who are able to walk is almost always necessary. Nonoperative treatment is indicated in dynamic equinus during the fast-growth phase of a child’s development, starting at 1 to 4 years of age up until 7 years old. It is reasonable to avoid early surgery. In children with hemiplegia the principal risk associated with early surgery is recurrent equinus and the need for repeated surgery. In children with diplegia or quadriplegia the principal risk of early surgery is overcorrection and development of calcaneus deformity of the foot. On the other hand, one should not wait until the end of growth, because progression of bone deformities compromises future soft tissue procedures. The most satisfactory results could be expected from a combination of different forms of nonoperative treatment, such as repeated injections of BT-A with a short period of casting, orthotics and physical therapy. If there are simultaneous contractures in the hip and/or knee joints, multilevel surgery associated with nonoperative treatment of dynamic equinus is the best solution. Operative treatment is indicated for patients with fixed equinus. In hemiplegia it is worthwhile, when possible, to postpone surgery until at least the age of 6 years by nonoperative treatment. Due to delayed development of gait or difficulty in predicting the final length and strength of plantarflexors of the

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17 Lemperg R, Hagberg B, Lundberg A. Achilles tenoplasty for correction of equinus deformity in spastic syndromes of cerebral palsy. Acta Orthop Scand 1969; 40: 507e19. 18 Green W. Cerebral palsy. Evaluation and management of equinus and equinovarus deformities. Foot Ankle Clin 2000; 5: 265e80. 19 Koman L, Mooney III J, Smith B, et al. Botulinum toxin type A neuromuscular blockade in the treatment of lower extremity spasticity in cerebral palsy: a randomized, double-blind, placebo-controlled trial. BOTOX Study Group. J Pediatr Orthop 2000; 20: 108e15. 20 Borton D, Walker K, Pirpiris M, Nattrass G, Graham H. Isolated calf lengthening in cerebral palsy. J Bone Joint Surg 2001; 83-B: 364e70. 21 Houltram J, Noble I, Boyd R, et al. Botulinum toxin type A in the management of equinus in children with cerebral palsy: an evidencebased economic evaluation. Eur J Neurol 2001; 8(Suppl.): 194e202. 22 Hylton N. Postural and functional impact of dynamic AFO’s and foot orthoses in a pediatric population. J Prosthet Orthot 1990; 2: 40e53. 23 Morris C. A review of the efficacy of lower-limb orthoses used for cerebral palsy. Dev Med Child Neurol 2002; 44: 205e11. 24 Bleck E. Orthopaedic management in cerebral palsy. In: Clinics in Developmental Medicine. No. 99/100. London: Mac Keith Press Oxford Blackwell Scientific Publications Ltd. Philadelphia J B Lippincott Co. 1987. 25 Spira R. Management of spasticity in cerebral palsied children by peripheral nerve block with phenol. Dev Med Child Neurol 1971; 13: 164e73. 26 Detrembleur C, Lejeune T, Renders A, Van den Bergh P. Botulinum toxin and short-term electrical stimulation in the treatment of equinus in cerebral palsy. Mov Disord 2002; 17: 162e9. 27 Bakheit M. Botulinum toxin treatment of muscle spasticity. Dublin: Blackhall Publishing Colour Books Ltd., 2001. 28 Saraph V, Zwick E, Steinwender C, Steinwender G, Linhart W. Conservative management of dynamic equinus in diplegic children treated by gait improvement surgery. J Pediatr Orthop B 2001; 10: 287e92. 29 Damron T, Greenwald T, Breed A. Chronologic outcome of surgical tendoachilles lengthening and natural history of gastroc-soleus contracture in cerebral palsy. Clin Orthop 1994; 301: 249e55. 30 Banks H. The management of spastic deformities of the foot and ankle. Clin Orthop 1977; 122: 70e6. 31 Ober F. Tendon transplantation in the lower extremity. N Engl J Med 1933; 209: 52e9. 32 Srinivasasn H, Mukherjee S, Subramaniam R. Two-tailed transfer of the tibialis posterior for correction of drop foot in leprosy. J Bone Joint Surg 1968; 50-B: 623e8. 33 Ono K, Doi T, Kajiura I, Inoue A, Mizuno S. Reconstructive surgery of the limb in the brain damaged adult. Med J Osaka Univ 1970; 20: 245e71. 34 Pierrot A, Murphy O. Heel chord advancement: a new approach to the spastic equinus deformity. Orthop Clin North Am 1974; 5: 117e26.

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35 Engsberg J, Oeffinger D, Ross S, et al. Comparsion of three heel cord surgeries in children with cerebral palsy. J Appl Biomech 2005; 21: 322e33. 36 Yoshimoto M, Kura H, Matsuyama T, et al. Heel cord advancement combined with Vulpius’ lengthening of the gastrocnemius. Clin Orthop 2005; 434: 213e6. ¨ffel A. Orthopaedishe operationslehre. 1st edn. 37 Vulpius O, Sto Stuttgart: Ferdinand Enke; 1913. 38 Green W, Mc Dermott L. Operative treatment of cerebral palsy of spastic type. J Am Med Assoc 1942; 118: 434e40. 39 Strayer L. Recession of the gastrocnemius, an operation to relieve spastic contracture of the calf muscles. J Bone Joint Surg 1950; 32-A: 671e6. 40 Baker L. Triceps surae syndrome in cerebral palsy: an operation to aid in its relief. Arch Surg 1954; 68: 216e21. 41 Bayer H. Die Verein fachung der plastichen Achillotomie. Zentralbl f Chirurg, 1901. 42 White J. Torsion of the Achilles tendon, its surgical significance. Arch Surg 1943; 46: 784e7. 43 Hatt R, Lamphier T. Triple hemisection: a simplified procedure for lengthening the Achilles tendon. N Engl J Med 1947; 236: 166e9. 44 Craig J, Van Vuren J. The importance of gastrocnemius recession in the correction of equinus deformity in cerebral palsy. J Bone Joint Surg 1976; 58-B: 84e7. 45 Lee C, Bleck E. Surgical correction of equinus deformity in cerebral palsy. Dev Med Child Neurol 1980; 22: 287e92. 46 Baumann J, Koch H. Ventrale aponeurotische Verla¨ngerung des Musculus gastrocnemius. Operat Orthop Traumatol 1989; 1: 254e8. 47 Graham K, Fixsen J. Lengthening of the calcaneal tendon in spastic hemiplegia by the white slide technique. J Bone Joint Surg 1988; 70-B: 472e5. 48 Haro A, DiDomenico L. Frontal plane-guided percutaneous tendo Achilles’ lengthening. J Foot Ankle Surg 2007; 46: 55e61. 49 Lambrinudi C. New operation on drop-foot. Br J Surg 1927; 15: 193e8. 50 Truscelli D, Lespargot A, Tardieu G. Variations in the long-term results of elongation of the tendo Achilles in children with cerebral palsy. J Bone Joint Surg 1979; 61-B: 466e9. 51 Ziv I, Blackburn N, Rang M, Koreska J. Muscle growth in normal and spastic mice. Dev Med Child Neurol 1984; 26: 94e9. 52 Yngve D, Chambers C. Vulpius and z-lengthening. J Pediatr Orthop 1996; 16: 759e64. 53 Segal L, Thomas S, Mazur J, et al. Calcaneal gait in spastic diplegia after heel cord lengthening: a study with gait analysis. J Pediatr Orthop 1989; 9: 697e701. 54 Kay R, Rethlefsen S, Ryan J, Wren T. Outcome of gastrocnemius recession and tendo-Achilles lengthening in ambulatory children with cerebral palsy. J Pediatr Orthop 2004; 13: 92e8.

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Computer assisted hip resurfacing

g­ iving better long-term implant survival and superior clinical ­outcomes.

Wolfram H Kluge

Implant positioning in the anterior-posterior direction has significant impact on the mobility of the joint. For example, posterior implant shift can cause anterior neck impingement in flexion/ internal rotation. The angle between implant axis and femoral shaft should be more valgus compared to the natural neck-shaft angle. The aim is for an implant position which covers the femoral neck sufficiently (head/neck ratio), and while adequate bone preparation around the entire femoral head is required, erosion of the femoral neck (notching) is to be avoided. These goals are not easy to achieve consistently using mechanical tools, which led to the introduction of computer assistance. Such joint replacement navigation systems have been in use for more than a decade, but hip resurfacing has been included only recently and the published studies have been of smaller case numbers than of conventional hip replacement. There are two main technologies, image-guided (CT and fluoroscopy) and imageless navigation systems. CT guided systems use a three dimensional image reconstruction of the pelvis and femur, match the image with the actual anatomy during the operation and help to perform the surgery according to the pre-operative plan. Pre-operative radiological assessment is generally performed on the anterior-posterior x-ray with the hip in slight internal rotation. A lateral view is helpful to recognise possible shift of the head on the femoral neck. Fluoroscopic navigation uses pre-operative x-ray images uploaded by the navigation software. During the actual surgical procedure no further x-ray exposure is required because the computer generates an image of the anatomy derived from the pre-operative imaging. Such image-guided systems are popular, but the market seems to be dominated by imageless navigation, which uses point/surface acquisition during a registration process following a standard surgical approach to the joint to generate a three dimensional model of the femoral neck and head, The computer generates an animation bone model which illustrates the underlying structure and allows precise measurement of the individual natural neck-shaft angle in all planes. Data display is manufacturer specific. In general the surgeon can use a three dimensional animation and/or two dimensional split images (anterior-posterior plane, axial plane, coronal split images). The navigation system outlines the femoral head in order to position a correctly sized implant in the direction of the acquired neck axis, allowing the surgeon to adjust the size and position of the implant. Additionally most navigation systems display a warning and indicate the areas potentially in danger of notching. The key procedure for navigated preparation of the femoral side is the guide wire insertion into the femoral head to determine implant orientation. On line display of the actual wire position in three dimensions allows for immediate correction and best match with the pre-planned pin alignment. The wire is then over-drilled and replaced by the instrumentation guide for final head preparation. Most systems offer navigation of the femoral

Navigated hip resurfacing

Abstract Hip resurfacing has generally favourable results. Complications such as femoral neck fracture and implant loosening are often related to surgical technique. Recent published results suggest that the revision rate for hip resurfacing could be reduced by accurate implant positioning. This article is a review of the characteristics of computer assisted navigation systems which aim to achieve best possible alignment of the femoral head surface replacement in relation to the individual head-neck axis.

Keywords computer assistance; femoral notching; head-neck axis; hip resurfacing; image-guided; impingement; navigation

Introduction Until the introduction of total hip replacement, the resurfacing/ mould femoral cup arthroplasty introduced by Smith-Petersen in Massachusetts dating back to 1923 was the standard method of hip reconstruction.1–4 The development of this, hip resurfacing, has the advantage over stemmed hip arthroplasty of preservation of femoral bone, superior postoperative joint stability and kinematic properties as well as low rates of articular bearing wear.5–7 However while some of the early implants demonstrated satisfactory implant survival,8 the results of hip resurfacing were never as good as those of stemmed hip arthroplasty. Clinical and radiological results vary, and concerns have been raised over metal-on-metal bearings and their possible effects on patient health as increased levels of metal ions in body cells and fluids have been detected, and pseudo-tumours associated with metal-on-metal hip resurfacings have been reported.9,10 As with any joint replacement there appears to be a link between implant position and clinical outcome. Implant failures from operations undertaken during a surgeon’s learning period suggest that the surgical technique is challenging,11 Such early implant failures have shown that experienced hip surgeons needed to undertake over fifty procedures using a manual jig before they were able to place the implant consistently within 5 degrees of the intended position12 as mechanical jig positioning can produce highly variable pin positions.13 Implant malposition during the surgeon’s learning period can be avoided by use of computer assistance.14 This article reviews the potential benefits of computer assisted hip resurfacing in

Wolfram H Kluge Dr.med.habil. is a Consultant Orthopaedic Surgeon, Hon. Senior Lecturer University Leeds, Bradford Royal Infirmary, Bradford, UK.

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Figure 1 Pin insertion guided in three planes (screenshot BrainLAB system).

to the BrainLAB optical reference arrays. The workflow can be saved in a surgeon-specific user profile. Adjustment of the implant position on the planning screen is surgeon-driven and based on the individual neck axis and femoral head anatomy and includes display of possible neck notching. BrainLAB tools facilitate guide pin navigation (Figure 1) but reaming depth along the pin axis is not navigated. The Ci ASR navigation system (Articular Surface Replacement, DePuy) has been developed in cooperation with BrainLAB. It is a versatile implant-specific product. Passive optical tracking allows for detailed guide wire planning and positioning and safety advice is given on line if there is danger of femoral neck damage (Figure 2). Reaming is navigation-controlled offering precise depth measurement. A verification tool provides accurate check of the trial and final implant position which is helpful in checking the compression of the cement mantel. Stryker provide an implant-specific active optical navigation system (iNfinitus hip resurfacing) for the Mitch implant. Guide wire insertion is navigated and the depth of femoral head reaming is guided by pointer controlled positioning of the mechanical tools. Again, the system offers safety checks to avoid notching (Figure 4). The PiGalileo navigation platform is a passive optical system currently being developed by Smith&Nephew for navigation of the Birmingham hip resurfacing. This implant-specific system offers navigation of the guide wire and the manufacturer plans to

head and chamfer reamer in order to preserve as much bone as possible without significant alteration of the biomechanical hip centre. Pelvic cup navigation is beyond the scope of this article; but the essential steps are included for completeness. The procedure is identical to that used in total hip replacement navigation. A reference frame is mounted to the pelvis and planes are recorded which is usually done by taking landmarks from the anterior superior iliac spine and the pubic symphysis on both sides. Following exposure further points are recorded from the acetabulum. With the navigated impactor anteversion, inclination and impaction depth of the cup can be controlled. As with femoral head navigation the general principles of commercially available systems are comparable.

Manufacturer specific review Imageless (image-free) systems based on optical tracking are most commonly used because they require less pre-planning and no intra-operative radiation exposure. BrainLAB (Vector Vision Hip SR) is an open navigation platform for use with various femoral resurfacing implants based on imageless passive optical tracking. The Birmingham hip resurfacing system (Smith&Nephew), Durom hip resurfacing (Zimmer), Cormet hip resurfacing (Corin) and the ASR hip resurfacing (DePuy) require manufacturer specific instruments adapted/calibrated

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Figure 2 Initial planning screens (Ci ASR, DePuy) for implant positioning and sizing in order to achieve best alignment on the neck and appropriate cover of the femoral head. Note: warning of potential neck notching.

common indication for revision, followed by aseptic loosening in four joints.21 Although these results are encouraging, early failures particularly those related to fracture need to be addressed. Fractures predominantly occur during the first post-operative year and are thought to be due to interruption of the femoral blood supply during surgery.22 There appears to be a link between accuracy of component placement in relation to femoral neck notching, fracture and revision rate.23 In a multicentre study, Shimmin reported 50 fractures in 3497 resurfaced hips and identified femoral notching and varus ­position of the femoral component as the main reasons for complications.24 Neutral or slight valgus orientation of the implant has been recommended in order to prevent fracture or limitations in range of motion25–27 as finite element analysis has shown increased stress to the femoral neck in varus as compared to valgus implant position28 and cadaver studies have shown that an increase in valgus position of ten degree significantly lessens the risk of a femoral neck fracture.29 Beaule et al. have confirmed that valgus placement of the femoral component reduces the risk of femoral neck fractures and implant loosening.30 However, exaggerated valgus position of the implant is potentially hazardous as it can lead to femoral neck notching. To avoid this’ more proximal positioning of the implant on the femoral head could be considered but this can lead to insufficient bone contact and inadequate fixation. The same is true for a very large head implant which would also require removal of excessive acetabular bone. The introduction of navigation allows for intra-operative simulation of different implant positions and sizes. In a cadaver study Hodgson et al. demonstrated improved consistency in computer-assisted guide pin placement for varus/valgus and

include navigation of the femoral reamer allowing for axial depth control. The default implant positioning on the femoral head will be based on a number of models incorporated in the software. Further imageless systems available for femoral head resurfacing are Localite HipNavigator and Orthosoft partial hip resurfacing navigation system (Zimmer). Various CT and fluoroscopy based systems are available in association with established resurfacing implants. Acrobot’s CT guided navigation system for hip resurfacing is being distributed by Corin using the Cormet implant. Belei et al. recently proposed a new method using calibrated multi-planar fluoroscopy in combination with adaptive model-based planning tools.15

Discussion Hip resurfacing is a successful bone sparing alternative to conventional hip replacement. A study from Germany, which appears to be representative of other Western countries, showed that in 4.1% of hip arthroplasties hip resurfacing was the preferred technique. This is mainly driven by long-term implant survival.16 The study showed that most surgeons consider guide pin placement straight forward when using navigation systems and fluoroscopic control can be avoided when using imageless technology, further reducing operating time. There are now large outcome studies on hip resurfacing available.17–20 Steffen et al. reported on 610 ‘Birmingham’ hip resurfacing arthroplasties. At a minimum of five years follow-up 93% had an excellent or good outcome according to the Harris hip score. There were no patients with definite radiological evidence of loosening or narrowing of the femoral neck exceeding 10% of its width. There was an overall survival of 95% at seven years. Neck of femur fracture occurred in 12 hips and was the most

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Figure 3 Planning screen (ASR, DePuy) for hip resurfacing in a Type 1 deformity. Note: The centre of the femoral head is aligned with the femoral neck axis.

mid-neck placement.13 This study supports the view that navigated pin placement is relatively independent of the surgeons’ operative experience. One of the prerequisites for hip resurfacing should be sufficient femoral bone quality. As position and shape of the femoral head might vary with CAM deformity, osteophyte formation and alignment of the head centre on the femoral neck axis, it is useful to classify two subtypes of femoral head/neck anatomy: Type 1: Femoral head centre aligned on the neck axis (Figure 3). Type 2: Femoral head centre has drifted away from the neck axis (Figure 4). While a general idea about the anatomy can be gained from plain two-dimensional x-rays, it is difficult to plan hip resurfacing from these standard films. Navigation offers a three-­dimensional planning display which allows the surgeon to identify and ­correct abnormalities of the femoral head. As long as the femoral head centre falls in line with the neck axis, guide wire position and head sizing depend mainly on the femoral head anatomy (Figure 3).

If the femoral head centre is not aligned with the neck axis (Type 2), the surgeon will find guide wire placement more ­difficult. Although one should aim for central neck alignment, as discussed, slight valgus is preferable (Figure 4). A relative anterosuperior bone deficiency on the femoral head might appear and the femoral component will possibly have to be downsized not to lose bone contact in this area. Smaller components in valgus make the head/neck junction prone to anterior neck impingement and notching and patients might experience groin pain despite satisfactory x-ray appearance. These considerations emphasize the importance of careful planning. Navigation enables the surgeon to simulate various scenarios for implant size and position. Only if planning screens suggest optimal component alignment should reaming be started. Pelvic cup position is equally significant. Any antero-superior overhang of the cup can lead to the same impingement effect as a pincer deformity but worse because the metal rim will rapidly

Figure 4 Planning screen (Mitch, Stryker) for hip resurfacing in a Type 2 deformity. Note: The left planning screen demonstrates how the femoral head drops away from the neck axis causing a “pistol grip” appearance.

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destroy the femoral neck or the head implant. Subluxation can occur in flexion and internal rotation. Early aseptic loosening of the acetabular component might be caused by inadequate impaction. Hip resurfacing cups have no central perforation to give certainty about the depth of implant impaction towards the acetabular floor. Cup navigation enables the surgeon to better control inclination, anteversion and impaction depth of the implant. An open pelvic implant (high inclination) will uncover the femoral head leading to lateral/superior subluxation and uneven wear of the metal-on-metal bearing. Cobb suggested that pelvic cup inclination over 55 degree leads to excessive wear which can result in high serum levels of metal ions.31 Hess recommended that navigation of the pelvic implant can be used to avoid impingement of the femoral neck against a protruding anterior rim of the socket or irritation of the psoas tendon.

5 National Institute for Clinical Excellence. Guidance on the use of metal-on-metal hip resurfacing arthroplasty. London: National Institute for Clinical Excellence, 2002. 6 Beaule PE, Lee JL, Le Duff MJ, Amstutz HC, Ebramzadeh E. Orientation of the femoral component in surface arthroplasty of the hip. A biomechanical and clinical analysis. J Bone Joint Surg 2004; 86-A: 2015–21. 7 Treacy RB, McBryde CW, Pynsent PB. Birmingham hip resurfacing arthroplasty. A minimum follow-up of five years. J Bone Joint Surg 2005; 87-B: 167–70. 8 Mahalingham K, Reidy D. Smith Petersen Vitallium Mould Arthroplasty: a 45 year follow up. J Bone Joint Surg 1996; 78-B: 497–8. 9 McCalden RW. Erythrocyte, urine metal ion levels remain elevated in metal-on-metal patients. Orthopaedics Today International 2008; 11: 6. 10 Pandit H, Glyn-Jones S, McLardy-Smith P, et al. Pseudotumours associated with metal-on-metal hip resurfacings. J Bone Joint Surg 2008; 90-B: 847–51. 11 Mont MA, Ragland P, Bezweda H, Thomas CM, Etienne G. The results of metal-on-metal resurfacing hip arthroplasty: learning curve stratification of results. Washington, DC: Presentation at the American Academy of Orthopaedic Surgeons, February 2005. 12 Back DL, Smith JD, Dalziel RE. Establishing a learning curve for hip resurfacing. American Academy of Orthopaedic Surgeons 74th Annual Meeting, San Diego 2007 Proceedings: p. 14–18. 13 Hodgson A, Helmy N, Masri BA, et al. Comparative repeatability of guide-pin axis positioning in computer-assisted and manual femoral head resurfacing arthroplasty. Proc Inst Mech Eng 2007; 221(7): 713–24. 14 Romanowski JR, Swank ML. Imageless navigation in hip resurfacing: Avoiding component malposition during the surgeon learning curve. 8th Annual Meeting of CAOS-International Proceedings. Hong Kong, China; 2008 p. 153–6. 15 Belei P, Skwara A, De La Fuente M, et al. Fluoroscopic navigation system for hip surface replacement. Comput Aided Surg 2007; 12(3): 160–7. 16 Sendtner E, Boluki D, Grifka J. Current state of doing minimal invasive total hip replacement in Germany, the use of new implants and navigation–results of a nation-wide survey. Z Orthop Unfall 2007; 145(3): 297–302. 17 Gill HS. The five-year results of the Birmingham hip resurfacing arthroplasty. An independent study. J Bone Joint Surg 2008; 90-B: 436–41. 18 Pollard TC, Baker RP, Eastaugh-Waring SJ, Bannister GC. Treatment of the young active patient with osteoarthritis of the hip: a five- to seven-year comparison of hybrid total hip arthroplasty and metalon-metal resurfacing. J Bone Joint Surg 2006; 88-B: 592–600. 19 Amstutz HC, Beaule PE, Dorey FJ, Le Duff MJ, Campbell PA, Gruen TA. Metal-on-metal hybrid surface arthroplasty: two to six-year follow-up study. J Bone Joint Surg 2004; 86-A: 28–39. 20 Amstutz HC, Antoniades JT, Le Duff MJ. Results of metal-on-metal hybrid hip resurfacing for Crowe type-I and II developmental dysplasia. J Bone Joint Surg 2007; 89-A: 339–46. 21 Steffen RT, Pandit HP, Palan J, et al. The five-year results of the Birmingham Hip Resurfacing arthroplasty. J Bone Joint Surg 2008; 90-B: 436–41. 22 Murray DW, Little JP, Steffen RT, et al. Femoral neck fractures following resurfacing. Procs IMechE 2007: 137–9. 23 Mont MA, Rajadhyaksha AD, Hungerford DS. Outcomes of limited femoral resurfacing surgeries compared with total hip arthroplasty

Conclusions Recent publications have confirmed that accurate implant positioning is crucial in order to achieve best clinical results and longterm implant survival and have shown that implant alignment is consistently superior when using navigation in comparison to mechanical tools.32–35 The continuing debate is whether to use fluoroscopy-based, CT based or imageless techniques. Fluoroscopy based navigation systems require at least two but preferably three views to provide a reasonable guarantee that notching can be avoided.36,37 Magnification errors encountered with x-ray can lead to significant planning mistakes. Imageless navigation on the other hand is based on accurate mechanical registration of the femoral neck in order to avoid cortical damage. The procedure requires a more extensive surgical approach in comparison to the limited access procedures using fluoroscopy or CT based systems. Fixation of the tracking array (dynamic reference base) to the femur has improved with the introduction of small two pin systems. Manufacturers were recently advised to withdraw 3  mm pins because of reported breakage. There is scope for future development in providing rigid but even less invasive tracker fixation. Ultimately surgeon’s preferences, hospital infrastructure, cost factors and radiation exposure determine which particular navigation system is employed for hip resurfacing. Navigation can help to obtain best possible alignment of the surface replacement along the head-neck axis. The implant thereby maintains optimal contact to the existing femoral head bone while impingement and notching can be avoided, and give optimal clinical results. ◆

References 1 Hettfleisch J, Wissenbach R. Fourty-year survival of a Judet hip prosthesis: a case report. J Bone Joint Surg 1994; 76-B: 671–2. 2 Judet J, Judet R. The use of an artificial femoral head for arthroplasty of the hip joint. J Bone Joint Surg 1950; 32-B: 166–73. 3 Smith-Petersen MN. Evolution of mould arthroplasty of the hip joint. J Bone Joint Surg 1948; 30-B: 59–75. 4 Charnley J. Arthroplasty of the hip: a new operation. Lancet 1961; i: 1129–32.

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system for implantation of the femoral component in hip resurfacing – An in-vitro and cadaver study within the scope of the ORTHOMIT project. 8th Annual Meeting of CAOS-International Proceedings. Hong Kong China; 2008 p. 149–52. 35 Schnurr C, Michael WP, Eysel P, König DP. Imageless navigation of hip resurfacing arthroplasty increases the implant accuracy. Int Orthop 2007 Springer Berlin/Heidelberg, ISSN 0341-2695 (Print) 1432–95 (On line). 36 Hess T. Navigation for hip resurfacing. In: Stiehl JB, Konermann WH, Haaker RG, DiGioia AM, eds. Navigation and MIS in orthopedic surgery. Springer Berlin Heidelberg, 2007, p. 373–9 [chapter 48]. 37 Hess T, Gampe T, Koettgen C, Szawlowski B. Intraoperative navigation for hip resurfacing. Methods and first results. Orthopade 2004; 33(10): 1183–93.

for osteonecrosis of the femoral head. J. Arthroplasty 2001; 16(8 Suppl. 1): 134–9. 24 Shimmin AJ, Bare J, Back DL. Complications associated with hip resurfacing arthroplasty. Orthop Clin North Am 2005; 36: 187–93. 25 Amstutz HC, Campbell PA, Le Duff MJ. Fracture of the neck of the femur after surface arthroplasty of the hip. J Bone Joint Surg 2004; 86-A: 1874–7. 26 Daniel J, Pynsent PB, McMinn DJ. Metal-on-metal resurfacing of the hip in patients under the age of 55 years with osteoarthritis. J Bone Joint Surg Br 2004; 86(2): 177–84. 27 Shimmin AJ, Back D. Femoral neck fractures following Birmingham hip resurfacing: a national review of 50 cases. J Bone Joint Surg 2005; 86-B: 463–4. 28 Long JP, Bartel DL. Surgical variables affect the mechanics of a hip resurfacing system. Orthop Relat Res 2006; 453: 115–22. 29 Anglin C, Masri BA, Tonetti J, Hodgson AJ, Greidanus NV. Hip resurfacing femoral neck fracture influenced by valgus placement. Orthop Relat Res 2007; 465: 71–9. 30 Beaule PE, Amstutz HC, Le Duff M, Dorey F. Surface arthroplasty for osteonecrosis of the hip: Hemisurfacing versus metal-on-metal hybrid resurfacing. J Arthroplasty 2004; 19(8 Suppl. 3): 54–8. 31 Cobb JP. Personal conversation and discussion at the 8th Annual Meeting of CAOS-International 2008, Hong Kong, China. 32 Davis ET, Gallie P, Macgroarty K, Waddell JP, Schemitsch E. The accuracy of image free computer. 33 Cobb JP, Kannan V, Dandachli W. Which CAOS systems can deliver adequate accuracy and precision in hip resurfacing? 8th Annual Meeting of CAOS-International Proceedings. Hong Kong, China; 2008 p. 145–8. 34 Gravius S, Belei P, de la Fuente M, et al. Evaluation on the functionality and accuracy of a new fluoroscopic-based navigation

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Practice points • Computer assisted hip resurfacing can give consistent optimum implant alignment. • Navigation helps to improve results during the learning period. • Navigated hip resurfacing can save operating time and radiation exposure. • Navigation systems can be particularly helpful with difficult head-neck anatomy.

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Why do joints swell?

Understanding joint effusions requires a knowledge of joint anatomy and physiology, pressure gradients, fluid resistance and Starling’s principle, among other factors, such that a simple answer as to why joints swell, and often remain swollen, is not easily forthcoming. One must then go back to basics.

Les Grujic Sydney Nade

The anatomy of joints Abstract

The most common joint is a diarthrodial (synovial) joint (Di ¼ Apart, Arthron ¼ Joint). In contrast an amphiarthrodial joint (Amphi ¼ both or around) is a fibrous joint with limited motion, such as the symphysis pubis. A synarthrodial joint (Syn ¼ together) generally has no motion and is only seen in the adult e.g. skull sutures. Effusions occur in diarthrodial joints. We all know the anatomy of a synovial joint. The articulating ends of the bones are covered with hyaline cartilage. The remainder of the interior of the joint lumen is lined by synovium, often called synovial membrane, which attaches to the periarticular margin of the bone. This creates the synovial cavity. Most of us have been led to believe that this synovial cavity, the lumen of the joint, is ‘filled’ with synovial fluid. In normal circumstances, however, it consists of only a thin film between joint surfaces. Our experience with the anatomy of the human joint lining lies with what we see at arthroscopy or arthrotomy (Figure 1). Some joints do contain menisci, but for most normal synovial joints the only content inside the joint is synovial fluid. Hyaline (‘translucent’) cartilage covers the articular surface of a joint. Hyaline cartilage is avascular. though it contains metabolically active chondrocytes. Articular cartilage has very little direct blood supply from the underlying bone, thus the nutrition and viability of the metabolically active chondrocytes is dependent on synovial fluid. Nutritional support of articular cartilage occurs over a relatively long distance compared to most other tissues. The primary functions of synovial fluid are to transmit nutrients and to lubricate the joint. Articular cartilage consists of more than 70% water. One to two per cent of the total volume of articular cartilage is chondrocytes. Over 90% of the dry weight of cartilage is accounted for by collagen and proteoglycans.

Orthopaedic surgeons see patients with effusions in joints very frequently. The reasons why effusions occur in joints, and sometimes remain in joints, requires an understanding of the physiology of production of synovial fluid, and the ways in which it enters and leaves joints. Most orthopaedic surgeons do not understand the basic physiology of this common clinical sign, and this article attempts to answer the question of ‘‘why do joints swell?’’.

Keywords joint physiology; joint swelling; synovial fluid

Introduction This is the third article we have written about Science and Symptoms. Previous articles appeared in Current Orthopaedics under the titles Clicks, Clunks, Creaks and Crepitus (vol. 6. pp60e64, 1992) and Joint Stiffness (Vol. 11. pp48e50, 1997). The common symptoms described by patients with pathology of joints are pain, stiffness and swelling. However, the scientific basis of the common symptoms and signs of joint physiology and pathology, seen frequently by the orthopaedic surgeon, are rarely understood.

What is joint swelling? Why do joints swell? How many of us actually understand the pathogenesis of a joint effusion? An initial attempt at an answer seems quite simple. A swollen joint is due to accumulation of fluid or tissue. Fluid accumulation within a joint can be a consequence of:  Effusion (of synovial fluid)  Blood  Pus  Iatrogenic interference (arthroscopy or injection) Tissue accumulation at a joint can consist of:  Bone  Capsule  Synovium  Neoplasm Do you now fully understand joint swelling? While seven of the above eight causes are self-evident, understanding how and why an effusion forms is not so simple.

Les Grujic MBBS FRACS FA(OrthA) is a Consultant at the Orthopaedic and Arthritis Specialist Centre, 445 Victoria Avenue, Chatswood, NSW 2067, Australia. Sydney Nade Dsc MD FRACS FRCS MRCP(UK) is a Professor in the Discipline of Surgery, The University of Sydney, Sydney, NSW 2006, Australia.

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Figure 1 Ankle arthroscopy showing articular cartilage, periarticular bone and hyperaemic synovium.

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Synovium (Syn ¼ like, Ovum ¼ [white of] egg) lies between the fibrous joint capsule and the synovial cavity. It consists of two layers:  Synovial intima (also known as the ‘synovial lining’)  Subsynovium (also referred to as ‘subintima’ or ‘synovial stroma’) The synovial intima is a very thin layer lining the interior of the joint cavity. Its thickness is only 2e3 cell layers. In the human knee the thickness of the intima is approximately 60 microns. The intimal layer has an extremely rich micro-circulation and a very high blood flow. The ultrastructure of the synovial intima is interesting. The synovial lining is discontinuous, with gaps between synovial cells. The cells have no intercellular junctions, producing an open intercellular pathway. A collagen fibril interstitial matrix fills the intercellular gaps. The intimal capillaries, which form a rich network within the intima, have their fenestrated outer capillary walls facing the joint cavity (Figure 2). The intima consists of cells and an extra-cellular matrix. The synovial cells consist of two types:  Type A synoviocytes  Type B synoviocytes Type A synoviocytes are derived from macrophages and serve a phagocytic function. They form the minority of the cell population: approximately 10e20%. The Type B synoviocytes (80%) are fibroblast-derived and their primary function involves synthesis of the extra-cellular matrix. The subsynovium backs the intimal layer and is formed from loose connective tissue and fat cells. It contains terminal arteries, veins and a rich lymphatic plexus. This lymphatic plexus is very important as it drains away fluid and macromolecules seeping through the synovial lining from the joint cavity and from the breakdown of articular cartilage. In general terms the subsynovium acts as a ‘sink’. It has an important role in response to inflammatory arthritis as it is a host to inflammatory cell infiltrates and lymphoid follicles. The synovial vasculature is critical in synovial fluid dynamics. The subsynovial layer contains the larger vessels and the lymphatics. The intimal layer hosts a rich capillary micro-circulatory network. The capillary density in the intimal layer is 3 times greater than in rabbit hamstring. The synovial intimal

Synovium

Synovial fluid

capillaries are in close proximity to the joint lumen, as this is the site of fluid and cellular exchange. They are essential in the generation of synovial fluid. Synovial capillaries have 3 important adaptations to aid in synovial fluid production:  High capillary density  Location close to the joint  Fenestrations which face the joint These adaptations are the reason for the common occurrence of spontaneous haemarthroses in haemophiliacs - a less common cause of why joints can swell!

Basic physiology of synovial joints Apart from synovial structure (anatomy and histology), we need to understand a little about synovial joint physiology. Intra-articular pressure in normal joints is slightly sub-atmospheric in a joint that is not moving and has adopted a ‘comfortable’ posture. It may decrease further with exercise. Because of Boyle’s Law, the change in volume of a joint as it moves causes an inversely proportional change in pressure within the joint. Movement of joints is an essential component of producing flow of synovial fluid into and out of joints. Change in volume with movement occurs as the capsule unfolds and folds, not unlike a drawn curtain. Under normal physiological conditions a joint does not distend (swell) with movement. Distension implies further unfolding, as the capsule tissue is not elastic. However, there are other factors apart from the pressure-volume relationships that must be understood in order to know what determines the volume of fluid inside a joint. Intra-articular pressure is dependent on a number of factors including:  Joint size  Synovial fluid volume  Position of the joint and periarticular tissues  Membrane permeability  Capsular compliance  Movement of fluid into and out of the joint. It has been shown that the resting intra-articular pressure in rheumatoid arthritis can be as much as 20 mm Hg and increase to greater than 100 mm Hg with exercise. This is well above capillary perfusion pressure and can occasionally be above arterial pressure! Intra-articular pressure in rheumatoid arthritis can interrupt synovial blood flow and cause synovial hypoxia. In the past textbooks were written about synovial fluid analysis, and the changes in the fluid seen in various disease states. Apart from performing cell counts and micro-biological tests, there seems to be little interest nowadays in the constituents of synovial fluid. Those constituents warrant further exposition. What is synovial fluid? Essentially it is an ultrafiltrate of plasma with a few additives (Hyaluronan, Lubricin). Urine is also an ultrafiltrate of plasma as it emerges from a glomerulus! Hyaluronan is a glycosaminoglycan, synthesised by the fibroblastic B cells in the intima. The concentration of hyaluronan in synovial fluid is approximately 3 g/l whereas in plasma it is found at 30 mcg/l. Its primary function does not lie with joint lubrication, as most of us are led to believe the primary role of hyaluronan is water retention. As the cells in the intima have no basement membrane, it serves as a filtration screen to regulate

Cartilage

Synovial B cell Capillary Note the gaps between the cells JOINT LUMEN Lymph vessel

Synovial A cell

Figure 2 A diagrammatic representation of the relationship between the cells and vessels of the synovium to the joint lumen and articular cartilage. Note the gaps between the synovial cells that allow for movement of ultra-filtrated plasma from capillaries into and out of the joint lumen, and the proximity of lymphatic vessels through which fluid can leave the joint.

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synovial fluid turnover. Levick has described hyaluronan as the ‘molecular filtercake’ or ‘dynamic waterproofing’. Hyaluronan tends to be selectively retained in the joint. The turnover time for synovial fluid and protein is approximately one hour whereas Levick has shown that hyaluronan turnover time in the rabbit knee is approximately 30 hours. Lubricin is also a glycosaminoglycan synthesised by the B cells and it functions as an articular lubricant. A swollen joint with an effusion contains an increased amount of synovial fluid. The amount of synovial fluid in a joint is the difference between the amount produced and the amount removed. Inflow and outflow are going on continuously and the net rate of movement is the synovial fluid turnover. Synovial fluid turnover is dependent on three key elements:  Synovial capillaries  The interstitium (intima)  The lymphatic drainage system The synovial membrane thus acts as a permeability barrier and has been termed the ‘blood e joint barrier’. This permeability barrier is governed by Starling’s principle of micro-vascular fluid exchange. The direction of fluid drive is dependent on intra-capillary and intra-articular hydrostatic pressure as well as the colloid osmotic pressure of plasma and synovial fluid. The pressure drop from capillary plasma to the synovial interstitium minus the difference of colloid osmotic pressure across the capillary wall, (i.e. higher protein concentration in plasma tends to draw fluid into capillary) tends to draw fluid from capillary to joint cavity. In other words, when the capillary pressure is greater than intra-articular pressure, plasma ultrafiltrate is forced into the interstitium through the capillary fenestrations. Hyaluronan is added by secretion from the synovial A cells and the combined ultra-filtrate and added molecules passes into the joint as synovial fluid. Low molecular weight solutes, including glucose, diffuse freely. The protein in synovial fluid is inversely proportional to the molecular size. Albumin concentration in joints is approximately 45% that of plasma. The removal of synovial fluid is predominantly lymphatic. Flow into lymphatics is independent of molecular size. Joint movement plays an integral part in aiding fluid clearance. As a joint moves the volume of its lumen changes and that alters the intra-articular pressure. If the volume decreases it affects net flow across the interstitium and opposes capillary filtration by increasing peri-capillary interstitial pressure. This promotes drainage into the subsynovial sink.

nutrients. Controlled escape of fluid occurs through the sieve and is removed by the lymphatics. So what causes an effusion? Remember the three key elements of synovial fluid turnover discussed above. In general terms this is clearly related to a disturbance of balance between the plasma and the joint cavity. That is:  A disturbance in the microcirculation (capillary network)  A disturbance of the synovial interstitium  A disturbance of lymphatic drainage (subsynovium) In addition we need to consider:  An alteration in the water holding capacity of molecules in synovial fluid (in disease states there may be other macromolecules produced by the synovium that affect its chemical and physical characteristics e such as colour, viscosity, thixotropy) All of the above factors are involved in the physiology of ‘normal’ joints. Effusions occur in joints that reflect a pathological state. What do we know of the architectural changes in arthritis? We know there is a disturbance of micro-vasculature. In chronic arthritis, capillaries become buried under hypertrophied synovial lining. This can increase the distance between the capillary and the joint and reduce capillary density. In some forms of acute inflammatory arthritis we see (at arthroscopy) an increased vascularity and assume there is a raised synovial metabolic rate. Increased capillary permeability leads to an increase in (plasma) proteins within synovial fluid, larger macromolecules, oedema, intra-articular polymorph migration and less hyaluronan. It is possible that the water-retaining properties of some macro-molecules, apart from hyaluronan, might be a cause of joint effusions. Such molecules might be secreted by synovial cells in different disease states, perhaps even stimulated by the presence of fragments of articular cartilage in the joint. There is also recent evidence from experimental models, principally from Levick, that the amount of hyaluronan secreted into synovial fluid is influenced by impulses that travel along nerves from mechano-receptors, and hence by the pattern of movement of a joint.

Summary While this article adds to an understanding of synovial fluid dynamics, much still remains to be discovered. The physiology of synovial joints is a field of endeavour that has been undersubscribed in relation to the frequency of joint effusions found in clinical practice. Joints are richly innervated, principally with mechano-receptors that signal position, velocity and acceleration. They may also signal intra-articular pressure. It is likely that this neural signalling mechanism also plays a significant part in providing impulses that are centrally interpreted as pain. Being able to understand the physiological mechanisms that produce the common physical sign of joint swelling may lead to better ways of controlling joint pain e a very common symptom related by your patients! A

The role of the synovium From the above considerations of anatomy and physiology it can be seen that the synovium has vital roles in:  Generating synovial fluid  Containing and maintaining synovial fluid within the joint  Draining synovial fluid from the joint The synovium is best thought of as a metabolically active mesh between the capillary and the joint. Synovial fluid dynamics can be summarised as follows: plasma ultrafiltrate exits the capillary through the fenestrations into the synovial interstitium. Here hyaluronan (and lubricin) is added forming synovial fluid. This passes freely into the joint cavity. Hyaluronan acts as a molecular sieve to retain solutes and

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FURTHER READING Levick JR, McDonald JN. Fluid movement across synovium in healthy joints: role of synovial fluid macromolecules. Ann Rheum Dis 1995; 54: 417e23.

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CME SECTION

CME questions based on the Mini-Symposium on ‘‘Children’s Hip Problems’’ The following series of questions are based on the MiniSymposium on ‘‘Children’s Hip Problems’’. 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 Orthopaedics and Trauma Editorial Office at the address at the bottom of the RESPONSE sheet. Please photocopy this page if you wish to keep your copy of Orthopaedics and Trauma. Replies received before the next issue of the journal 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, via email, for your records.

5 Which of the following falls outside the normal range for the parameter being measured A Acetabular index of 15 degrees at birth B Acetabular index of 35 degrees at birth C Centre Edge angle of 20 degrees in a 5 year old D Centre edge angle of 30 degrees in a 10 year old E Centre edge angle of 40 degrees in an adult 6 Which of the following statements concerning the use of clinical examination as a screening tool for DDH is incorrect A Combining with Ultrasound results in a sensitivity of about 90% B If positive at birth, approximately 50% will have stabilized by 6 weeks C The normally negative intra articular pressure is over come, disrupting stability D The sensitivity is less than 60% E The specificity is almost 100%

Questions 1 In the adductor approach to the hip ascribed to Ludloff the interval between pectineus and which other muscle is exploited? A Adductor brevis B Adductor longus C Gracilis D Iliopsoas E Rectus femoris

7 Which of the following statements concerning Pavlik harness treatment of DDH is incorrect A It allows movement of the hip in the acetabulum, stimulating remodeling B It can be associated with femoral nerve palsy C It discourages adduction as maintaining this position in the harness leads to fatigue D It permits gradual reduction of the dislocated hip that cannot be reduced on examination E It was introduced in an effort to reduce the risk of avascular necrosis

2 Which pair of nerves is most at risk during the initial development of the anterolateral approach to the hip A Femoral nerve and branch of obturator nerve B Femoral nerve and branch of superior gluteal nerve C Lateral femoral cutaneous nerve and branch of obturator nerve D Lateral femoral cutaneous nerve and branch of supe rior gluteal nerve E Obturator nerve and branch of superior gluteal nerve

8 Which of the following endocrine disorders is most strongly associated with slipped upper femoral epiphysis A Gigantism B Growth hormone deficiency C Hyperparathyroidism D Hyperthyroidism E Hypothyroidism

3 Which of the following is not a recognized risk factor for DDH A Breech presentation B Female sex C Low birth weight D Multiple pregnancies E Oligohydramnios

9 If a large cohort of patients with slipped upper femoral epiphysis treated by in-situ pinning with slip angles of 30e50 degrees are followed in the long term, approximately what proportion with develop severe osteoarthritis A 5% B 15% C 25% D 40% E 60%

4 Which of the following clinical signs is most sensitive in detecting DDH A Assymetrical skin creases B Clicking hip found at newborn screening C Galeazzi’s test D Limitation of abduction with tight adductor longus E Parental reports of hip clicking at nappy change

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Responses

10 Which of the following organisms is least likely to be responsible for septic arthritis of the hip in childhood A Gram negative bacilli B Haemophilus Influenzae C Kingella kingae D Staphylococcus aureus E Streptocioccus sp.

Please shade in the square for the correct answer.

11 Which of the following is not one of the characteristic poor prognostic signs in septic arthritis of the hip in childhood A Age of onset under 6 months B Concomitant proximal femoral osteomyelitis C Delay in diagnosis of more than 4 days D Heterogenous effusion on ultrasound E Infection with Staphylococcus aureus

12 Which of the following sets of blood results points best to a diagnosis of septic arthritis rather than irritable hip A Afebrile, ESR 100, not weight bearing, White count 5  103/mm3 B Fever, ESR 20, weight bearing, White count 14  103/mm3 C Fever, ESR 60, not weight bearing, White count 14  103/mm3 D Fever, ESR 100, weight bearing, White count 6  103/mm3 E Fever, ESR 120, not weight bearing, White count 4  103/mm3

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Your details (Print clearly) NAME..................... ADDRESS..................... ........................ EMAIL..................... RETURN THE COMPLETED RESPONSE FORM by fax to þ44-113-392-3290, or by post to CME, Orthopaedics and Trauma, Academic Department of Orthopaedic Surgery, ‘‘A’’ Floor Clarendon Wing, Leeds General Infirmary, Great George Street, Leeds LS1 3EX, UK.

Please fill in your answers to the CME questionnaire above in the response section provided to the right. A return address and fax number is given below the response section.

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Answers to CME questions based on the Mini-Symposium on “What’s new in hip replacement — basic principles” Answers 1 a



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(i) Epidemiology of bone and soft-tissue sarcomas

data are presented in terms of the primary site of the cancer rather than its histological type. The most commonly used system is the International Classification of Diseases (ICD), as used by the Office for National Statistics in compiling the cancer statistics for the UK.4 The ICD enables malignant bone and cartilage neoplasms to be defined as a single group, though it is impossible to further subdivide this group in order to distinguish between osteosarcoma and chondrosarcoma, for example. There are further problems when trying to interpret the statistics as regards soft tissue sarcomas. One code ‘malignant neoplasm of connective and other soft tissue’ includes both sarcomas and nonsarcomatous neoplasms, whilst many sarcomas can be found in other diverse groups, such as ‘malignant neoplasms of the retroperitoneum’ and ‘malignant neoplasms of other and illdefined sites’. This reflects the complexity of the treatment of sarcoma, with over 50 different histiological sub-types and emergence at all body sites, demanding input from a range of clinicians, each with a site-specific interest.

Benjamin JF Dean Duncan Whitwell

Abstract Sarcomas are malignant tumours of connective tissue and account for around 1% of all the cancer diagnoses in the UK each year. Sarcomas can be categorized as being of either bone or soft tissue in origin and both categories consist of a wide variety of histological subtypes. Most sarcomas (about 55%) affect limbs, most frequently the leg; about 15% affect the head and neck area or are found externally on the trunk, while the remainder are internal and located in the retroperitoneum or abdomen. A number of environmental factors including radiation exposure, viral infection, occupation and chemical exposure have been linked to the development of sarcomas. A number of heritable conditions, including LieFraumeni syndrome, neurofibromatosis, retinoblastoma and Werner’s syndrome, are associated with an increased risk of sarcoma development. This article reviews the epidemiology of bone and softtissue sarcomas and highlights its relevance with regard to sarcoma diagnosis and the potential development of new treatments.

Age and site distribution Soft tissue sarcoma Three quarters of soft tissue sarcomas are located in the limbs and the median age at diagnosis is 65 years. Sarcomas are histologically classified by their presumed cell of origin. The most common types are malignant fibrous histiocytoma (MFH), leiomyosarcoma and liposarcoma. In children rhabdomyosarcoma is predominant. For all cell types combined, and for most individual types, there is a male preponderance. This is especially true for blood vessel sarcomas largely because of Kaposi’s sarcoma, which has an increased incidence in white males attributable to the acquired immune deficiency syndrome (AIDS). The age related incidence depends on the histological sub-type of tumour; for example synovial sarcoma is most common in young adults whilst liposarcoma and leiomyosarcoma dominate in the elderly.

Keywords bone; epidemiology; sarcoma; soft-tissue

Introduction Sarcomas are malignant tumours of connective tissue. Soft tissue sarcomas are tumours arising from mesechymal tissue, which consists of muscle, fat, blood vessels, fibrous and other supporting tissue, whereas bone sarcomas are tumours of the skeleton.1 The incidence of soft tissue sarcoma is approximately 30 per million2 and accounts for less than 1% of all malignant neoplasms. There are no data to suggest a change in the incidence of soft tissue sarcoma over time or any geographic variation. Bone sarcomas occur at a rate approximately one third that of their soft tissue counterparts3 and there are approximately 300 to 400 cases a year in the UK.4 Osteosarcoma is the most common and accounts for over 35% of primary bone sarcoma cases. Chondrosarcoma (26%) and Ewing’s sarcoma (16%) are the next most common primary bone sarcomas.3 Several factors conspire to leave a relative paucity of information on the descriptive epidemiology of bone and soft tissue sarcomas. The main reason for this is the fact that cancer registry

Bone sarcoma The age-related incidence rates of bone sarcomas are bimodal. The first peak occurs in the second decade of life (Figures 1 and 2), while the second peak is after the age of sixty years. This is clearly different to the age-related incidence rates of soft tissue sarcomas, which increase gradually with increasing age (Table 1). The most common bone sarcoma, osetosarcoma, predominates in patients under the age of twenty and the majority are located in the long bones. This predilection for the long bones tends to decrease with increasing age. Ewing’s sarcoma has a similar peak incidence in the second decade of life and tends to arise in the diaphyseal areas of the long bones, as opposed to osteosarcoma, which is more frequently found in the metaphyseal areas (Figure 3). Ewing’s sarcoma occurs almost exclusively in the white population, unlike osteosarcoma which is equally distributed across different racial groups. Chondrosarcoma shows a gradual increase in incidence that continues into the eighth decade of life. There is no clear difference in incidence between races and sexes.

Benjamin JF Dean MRCS(Ed) Specialist Trainee at the Nuffield Orthopaedic Centre, Headington, Oxford, UK. Duncan Whitwell FRCS (Orth) Orthopaedic Consultant at the Nuffield Orthopaedic Centre, Headington, Oxford, UK.

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A review of 344 cases of post-radiation sarcoma10 revealed osteosarcoma to be the most common, followed respectively by malignant fibrous histiocytoma and lymphangiosarcoma. It was hypothesized that the high incidence of bone tumours was related to a greater absorption of radiation by bone. A large number of these post-radiation sarcomas presented relatively late and the prognosis was generally poor. The incidence of soft tissue sarcoma following radiotherapy in the treatment of breast cancer has been studied by Karlsson et al.11 Over 100 000 women from the Swedish Cancer Register were followed up for soft tissue sarcoma, and it was found that, for all sarcomas other than angiosarcoma, the integral dose of radiotherapy was a predictor of risk. Other studies have suggested that young children may be more susceptible to the carcinogenic effects of radiation. Ron et al.12 observed 10 834 children who had received radiotherapy to the scalp for the treatment of ringworm over a twelve year period from 1948 to 1960. Six of these children developed bone or soft tissue sarcomas, with five of the six occurring in the irradiated field.

Figure 1 The incidence of bone sarcomas by type (SEER 1975e2000).5

Environmental factors Radiation There is strong evidence that radiation exposure increases the risk of developing both bone and soft tissue sarcomas. Numerous studies of patients treated with ionizing radiation have observed an increased risk of sarcoma. The incidence of sarcomas after radiotherapy ranges from one in several thousand to around one percent. This association was first noticed in the early 20th century by Beck, who commented on an unusually high incidence of sarcomas in patients who had previously been irradiated for tuberculous arthritis.6 Further work from Martland and Humphreys7 in 1929 went further to confirming the causal link. They reported 42 bone sarcomas in 1468 female watch-dial painters, representing an incidence of 2.8%. Over the following years there were several more reports of sarcomas in patients who had previously been irradiated, and in 1948, Cahan8 proposed a series of diagnostic criteria for radiation-induced sarcoma of bone, which have since been modified by Arlen.9 These criteria include the need for histologically proven sarcoma development after an appropriately long latent period (3e5 years) in an irradiated area that was without evidence of such tumour before the irradiation. The majority of post-radiation sarcomas occur in bone, though soft tissue sarcomas may also occur following radiation.

Viral infection and immunodeficiency Kaposi’s sarcoma is a very rare malignancy except in association with human immunodeficiency virus 1 (HIV-1) infection, when its risk of occurrence is increased by up to seventy thousand times. Human herpes virus 8 (HHV-8) has been found to be associated with all forms of Kaposi’s sarcoma and is necessary for the development of this tumour.13 Some evidence suggests that HIV-1 plays a more indirect role in the aetiological process by causing immunosuppression and facilitating coninfection with HHV-8, though other data supports a more direct involvement of HIV-1 in the tumour development process.14 An increased risk of soft tissue sarcoma has been reported among patients receiving therapeutic immunosuppression for renal transplants and other conditions. Soft tissue sarcoma is also excessively common amongst patients with primary immunodeciciency syndromes, certain lymphoproliferative conditions and some autoimmune diseases. Epstein Barr virus has been associated with smooth muscle tumours in immunodeficient patients. Stewart-Treves syndrome indicates the development of angiosarcoma in patients with long-standing chronic lymphoedema and some authors have attributed this phenomenon to acquired regional immunodeficiency. Occupational and chemical Soft tissue sarcomas have been associated with phenoxyherbicides, chlorophenols and dioxin exposure. However, not all studies have found elevated risks associated with exposure to these agents.15 Specifically, malignant fibrous histiocytoma and leiomyosarcoma appear to be the soft tissue sarcomas that are most associated with the aforementioned agents. Occupational factors linked to soft tissue sarcomas include woodworking, construction work, solvent exposure, farming and leather tanning. Carpentry, medical research, arsenic exposure, meat packing and oil refinery work have all been linked to bone sarcoma. The inconsistent evidence in this area may well be as a result of different disease aetiologies across the sarcoma subtypes. Various implant materials, including chromium, nickel, cobalt, titanium and polyethylene, have been suspected as risks

Figure 2 Incidence of All Bone Sarcomas by Race/Ethnicity, SEER 1990e2000.5

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Age distribution (%) of incidence cases by site, 2000e200416 Site

All cancers Bones and joints Soft tissues

Age <20

20e34

35e44

45e54

55e64

65e74

75e84

85D

All ages

Cases

1.1 28.7 10.4

2.7 16.5 10.8

5.9 11.5 11.5

13.6 13.0 15.1

20.9 10.1 15.1

25.8 8.6 15.4

22.6 7.8 15.8

7.4 3.8 5.9

100 100 100

1 671 579 3368 11 229

Table 1

factors for bone sarcoma development, though the epidemiological evidence for a causative role is lacking. Further epidemiological studies on patients who have undergone the orthopaedic implantation of various foreign materials are needed.

syndrome and Gardner’s syndrome. Recent advances in technology have resulted in significant moves in our understanding of the cytogenetics of sarcoma and the list of chromosomal translocations present in several different subtypes of sarcoma is now extensive (Table 2).21 Genetic alterations cause tumour cell deregulation and genomic instability at a number of levels in the cell cycle. Rapid advancement in our basic biological understanding and investigations using microarray techniques is leading to novel therapy development with the aim of reducing the mortality from the development of metastatic disease.

Chemotherapeutic agents There have been reports linking the use of cyclophosphamide with the development of bone sarcomas in patients who underwent radiation treatment as part of their therapy.17 A large study that followed 9170 children who had survived childhood malignancies found that treatment with alkylating agents was an independent risk factor for the subsequent development of bone sarcoma, with the risk increasing as cumulative drug exposure rose.18

LieFraumeni syndrome This rare autosomal dominant syndrome was first described by Li and Fraumeni in 196919 and is characterized by an early age of tumour onset with a wide tumour spectrum. The classical Lie Fraumeni tumour spectrum includes soft tissue sarcomas, osteosarcomas, pre-menopausal breast cancers, brain tumours and adrenocortical tumours. Patients are also at a higher risk of other malignancies including leukaemias and lymphomas, as well as gastric, lung and colorectal cancers. Of children with soft tissue sarcomas, around five percent have family histories of

Host factors Genetic factors can be both acquired or inherited. The first reports suggesting a role for heritable factors in the development of sarcomas were published the 1960s.19,20 Since these early reports a slightly increased incidence of sarcoma has been linked to various syndromes including neurofibromatosis, Werner’s

Figure 3 The distribution of bone sarcomas by anatomical site.5

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of several malignancies including soft tissue sarcomas, thyroid carcinomas, melanomas, osteosarcomas and leukaemias.1,23

Chromosomal changes in sarcoma Tumour

Translocation

Fusion protein

Ewing’s sarcoma

t(11;22)q24;q12) t(21;22)(q22;q12) t(7;22)(p22;q12) t(17;22)(q12;q12) t(2;21;22) t(21;13)(q34;q14) t(;13)(p36;q14) t(12;22)(q13-q14;q12) t(11;12)(p13;q12)

EWS-FLI1 EWS-ERG EWS-ETV1 EWS-E1AF EWS-FEV PAX3-FKHR PAX7-FKHR EWS-ATF1 EWS-WT1

t(9;22)(q22;q12) t(9;17)(q22;q11.2) t(X;18)(p11;q11) t(12;16)(q13;p11) t(12;22)(q13;q12) t(12;22;20) (q13;q12;q11) t(12;15)(p13;q25) t(17;22)(q22;q13)

EWS-CHN RBP56-CHN SYT-SSX1 or SSX2 TLS(FUS)-CHOP EWS-CHOP EWS-CHOP

Alveolar rhabdomyosarcoma Clear cell sarcoma Desmoplastic small round-cell tumour Extraskeletal myxoid chondrosarcoma Synovial cell sarcoma Myxoid liposarcoma

Congenital fibrosarcoma Dermatofibrosarcoma protuberans Alveolar soft-part sarcoma T(X;17)(p11.2;q25)

RothmundeThompson syndrome RothmundeThompson syndrome (RTS) is an extremely rare autosomal recessive disorder attributed to mutations of the RECQL4 helicase gene on 8q24. It is characterized by early photosensitivity and poikilodermatous skin changes, juvenile cataracts, skeletal dysplasias, and a predisposition to osteosarcoma and skin cancer. The development of osteosarcoma occurs in around one third of cases and the median age of osteosarcoma diagnosis is 11.5 years.24 Enchondromatosis Ollier’s disease is a rare developmental disorder characterized by the formation of multiple enchondromas. When also associated with haemangioma formation it is termed Maffucci syndrome. Typically, the short and long tubular bones of the extremities are affected, though other bones may also be involved (Figures 4,5,6 and 7). There is a considerable risk of malignant transformation in Ollier’s disease: the incidence of secondary chondrosarcoma formation is around 25% at the age of 40 years and the development of other bone sarcomas has been reported.25 The incidence of chondrosarcoma formation is even higher in Maffucci syndrome, with malignant degeneration said to be a virtual certainty.25

ETV6-NTRK3 COL1A1-PDGFB ASPL-TFE3

Hereditary multiple exostoses Hereditary multiple exostoses (HME), or multiple osteochondromas, occurs at a rate of approximately 1:50 000 in the general population and involves the formation of multiple osteochondromas as a result of mutations in one of the EXT genes. The most important complication of HME is malignant transformation of an osteochondroma, which is reported to occur at

Table 2

malignancies consistent with LieFraumeni syndrome or other syndromes with an autosomal dominant inheritance pattern. Lie Fraumeni syndrome has been linked to germline heterozygous mutations of the tumor suppressor gene p53.22 Retinoblastoma Retinoblastoma (RB) is a malignant tumour of the developing retina that usually occurs before the age of five. The bilateral form is more common and makes up 60% of cases, whilst the unilateral form accounts for the remaining 40%. RB may occur sporadically (60%), or it may be inherited (40%). RB occurs in cells that have cancer-predisposing mutations in both copies of the gene RB1. Individuals heterozygous for a cancer-predisposing mutation in one RB1 allele are said to have a germline mutation and thus have a hereditary predisposition to RB. Mutations in the RB gene (RB1) are also associated with the development of the following tumours (once disease free having been treated for the initial disease): osteosarcoma, malignant fibrous histiocytoma, chondrosarcoma, Ewing’s sarcoma, melanoma, brain tumours and pinealoblastoma. Werner’s syndrome Werner’s syndrome (WS) is a rare autosomal recessive genetic instability syndrome and is caused by mutations in the WRN gene. It is the most common of the premature ageing disorders and affects connective tissue throughout the body. The most common clinical findings develop after the age of ten and include bilateral cataracts, short stature, premature graying and a loss of scalp hair. Werner’s syndrome predisposes to an increased risk

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Figure 4 Malignant transformation within multiple enchondromas of the hand in Mafucci’s syndrome.

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Figure 6 A resected humerus showing a proximal humeral chondrosarcoma in Ollier’s disease. Figure 5 A distal femoral enchondroma in Ollier’s disease.

15 000, and the majority of cases are sporadic. Patients with BWS have a risk of approximately 7.5% of developing tumours in childhood. The most commonly reported are Wilm’s tumour, adrenocortical carcinoma, embryonal rhabdomyosarcoma and hepatoblastoma.

a rate of just under 1%.26,27 In the majority of cases the malignant transformation involves the formation of a secondary peripheral chondrosarcoma. Neurofibromatosis Neurofibromatosis (NF) is a multisystem genetic disorder commonly associated with cutaneous, neurologic, and orthopaedic manifestations. In type 1 NF cutaneous or subcutaneous neurofibromas, optic nerve gliomas, spinal cord tumors, and brain tumors are among the nerve-related tumors (Figure 8). Of note, malignant peripheral nerve sheath tumors (MPNSTs) or neurosarcomas are not uncommon in adolescents and adults with type 1 NF; some studies have estimated the lifetime risk to be in the order of 10%. Type 1 NF, like LFS, involves an abnormality with a tumour suppressor gene. In type 1 NF this is the NF1 gene which serves to produce neurofibromin, a tumour suppressor. Type 2 NF is also known as bilateral acoustic neurofibromatosis, it is characterised by multiple tumours and lesions on the brain and spinal cord.

McCuneeAlbright syndrome McCuneeAlbright syndrome (MAS) is a sporadically occurring disorder that consists of polyostotic fibrous dysplasia (Figures 9 and 10), cafe´ au lait skin pigmentation and autonomous endocrine hyperfunction. The syndrome is caused by mutations in the GNAS1 gene. Malignant bone tumours have been associated with the fibrous dysplasia in MAS. Osteosarcomas and chondrosarcomas appear to occur at an increased frequency in MAS, although other sarcomas that have been linked to fibrous dysplasia, such as malignant fibrous histiocytoma, are not at increased in frequency in MAS. Paget’s disease Paget’s disease is a metabolic disorder characterized by abnormal bone remodeling; it is more common in the elderly population and of uncertain aetiology. The most lethal complication is the development of bone sarcoma, which has a reported incidence of 0.7%.28 The majority of these bone sarcomas are osteosarcomas, with the remainder largely being malignant

BeckwitheWeidemann syndrome BeckwitheWeidemann syndrome (BWS) is a complex overgrowth disorder caused by the disrupted imprinting of one or more genes. It is rare, with an incidence of approximately 1 in

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Figure 8 Large nerve-related tumour in a patient with NF1.

Malignant fibrous histiocytoma has been found in individual cases after a great range of chronic repair processes including tuberculosis, following prosthesis insertion, ulcers and scars. This association may be more than just a coincidence, however other than evidence from various studies carried out upon animal models there is not enough good quality evidence to reach a definitive conclusion on this matter.

Conclusions Bone and soft tissue sarcomas are relatively rare; however a significant number of patients who develop these tumours will die as a result of metastatic disease. The grade and size of tumours at presentation are important prognostic factors and patients continue to present late for treatment. Our current understanding is that the majority of sarcomas occur spontaneously. However, the identification of aetiologic agents provides a valuable opportunity for earlier diagnosis and hopefully a better prognosis. For example, the discovery that radiation increases the risk of sarcoma formation has led to the closer monitoring of patients following radiotherapy. It has also led to clinicians and patients maintaining a higher index of suspicion for the development of post-radiation sarcomas. The knowledge that radiation can induce sarcomas is also taken into account when considering whether a course of radiotherapy is in a patient’s best interests. The role of other factors, such as chemicals and occupational exposure, need further definition. A better understanding of sarcoma genetics and biology is beginning to lead to new therapeutic strategies. An example of this is mdm2, an inhibitor of the p53 gene, which is increased in a number of different sarcoma subtypes.21 Potentially the inhibition of mdm2 may activate p53 to result in growth arrest and enhance chemotherapy induced apoptosis. This strategy resulted in tumour regression in an osteogenic sarcoma xenograft model.30 Molecular genetic tests for translocated gene products are now used to aid diagnosis in a large number of sarcomas. Continued progress in these areas promises to revolutionise the

Figure 7 A bone scan showing multiple hot spots in a patient with Mafucci’s syndrome.

fibrous histiocytomas. The prognosis when malignant transformation occurs is notoriously poor, with 5-year survival rates of near to zero. Hormones Several studies suggest an involvement of hormonal stimulation in the tumorigenesis of leiomyosarcoma. Leiomyosarcoma is more common in women than men, partly and not solely due to uterine leiomyosarcoma. In humans, hormone receptors have been found in both uterine leiomyosarcomas and leiomyosarcomas of blood vessels, while leiomyosarcoma has been induced in hamsters by hormone exposure. The use of oral contraceptives has also been shown to be associated with a significantly reduced risk of developing soft tissue sarcoma. Lymphoedema and chronic repair Stewart and Treves29 were the first to describe the development of lymphangiosarcoma in patients with chronic postmastectomy lymphoedema. This observation has since been further developed by others. A case of lymphangiosarcoma has been reported in a patient with lymphoedema secondary to chronic filarial infection.

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Polyostotic fibrous dysplasia in McCuneeAlbright syndrome: proximal femoral lesion treated with intramedullary device and free fibular graft. Figures 9 and 10

way in which sarcomas are diagnosed and treated in the future, and ideally these advances can be translated into improved outcomes for patients with sarcoma. A

6

7 REFERENCES 1 Fletcher CDM, Uni KK, Mertens F, eds. World Health Organistion classification of tumours. Pathology and genetics. Lyon: IARC Press, 2002. 2 Gustafson P. Soft tissue sarcoma. Epidemiology and prognosis in 508 patients. Acta Orthop Scand Suppl 1994; 259: 1e31. 3 Dorfman HD, Czerniak B. Bone cancers. Cancer 1995; 75: 203e10. 4 Office for National Statistics. Registrations for cancer diagnosed in 2006, England. Series MB1, No 37. 5 Bleyer A, O’Leary M, Barr R, Ries LAG, eds. Chapter 8: malignant bone tmours. cancer epidemiology in older adolescents and young adults 15 to 29 years of age, including SEER incidence and survival:

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1975e2000. Bethesda, MD: National Cancer Institute; 2006. NIH Pub. No. 06-5767. Beck A. Zur Frage des Rontgensarkoms, zugleich ein Beitrag zur Pathogenese des Sarkoms. Munchener Med Wochenschr 1922; 69: 623e5. Martland H, Humphries RE. Osteogenic sarcoma in dial painters using luminous paint. Arch Pathol 1929; 7: 406e17. Cahan WG, Woodward HQ, Higinbotham NL, Stewart FW, Coley BL. Sarcoma arising in irradiated bone: report of eleven cases. Cancer 1948; 1: 3e29. Arlen M, Higinbotham NL, Huvos AG, et al. Radiation-induced sarcoma of bone. Cancer 1971; 28: 1087e99. Robinson E, Neugut AI, Wylie P. Clinical aspects of postirradiation sarcomas. J Natl Cancer Inst 1988; 80: 233e40. Karlsson P, Holmberg E, Samuelsson A, Johansson KA, Wallgren A. Soft tissue sarcoma after treatment for breast cancerea Swedish population-based study. Eur J Cancer 1998 Dec; 34(13): 2068e75.

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¨e´ R, Baert-Desurmont S, et al. French LFS 22 Bougeard G, Sesbou working group. Molecular basis of the LieFraumeni syndrome: an update from the French LFS families. J Med Genet 2008; 45: 535e8. 23 Goto M, Miller RW, Ishikawa Y, Sugano H. Excess of rare cancers in Werner syndrome (adult progeria). Cancer Epidemiol Biomarkers Prev 1996 Apr; 5(4): 239e46. 24 Wang LL, Levy ML, Lewis RA, et al. Clinical manifestations in a cohort of 41 RothmundeThomson syndrome patients. Am J Med Genet Jul 22 2001; 102(1): 11e7. 25 Schwartz HS, Zimmerman NB, Simon MA, Wroble RR, Millar EA, Bonfiglio M. The malignant potential of enchondromatosis. J Bone Joint Surg Am 1987; 69: 269e74. 26 Legeai-Mallet L, Munnich A, Maroteaux P, Le Merrer M. Incomplete penetrance and expressivity skewing in hereditary multiple exostoses. Clin Genet 1997; 52: 12e6. 27 Peterson HA. Multiple hereditary osteochondromata. Clin Orthop 1989; 239: 222e30. 28 Hadjipavlou A, Lander P, Srolovitz H, Enker IP. Malignant transformation in Paget disease of bone. Cancer 1992 Dec 15; 70(12): 2802e8. 29 Stewart FW, Treves N. Lymphangiosarcoma in postmastectomy lymphedema: A report of six cases in elephantiasis chirurgica. Cancer 1948; 1: 64e81. 30 Wang H, Zeng X, Oliver P, et al. MDM2 oncogene as a target for cancer therapy: an antisense approach. Int J Oncol 1999 Oct; 15(4): 653e60.

12 Ron E, Modan B, Boice Jr JD. Mortality after radiotherapy for ringworm of the scalp. Am J Epidemiol 1988 Apr; 127(4): 713e25. 13 Bagni R, Whitby D. Kaposi’s sarcoma-associated herpesvirus transmission and primary infection. Curr Opin HIV AIDS 2009 Jan; 4(1): 22e6. 14 Blattner WA. Human retroviruses: their role in cancer. Proc Assoc Am Physicians 1999 NoveDec; 111(6): 563e72. 15 Hoppin JA, Tolbert PE, Flanders WD, et al. Occupational risk factors for sarcoma subtypes. Epidemiology 1999 Nov; 10(6): 788. 16 Ries LAG, Melbert D, Krapcho M, eds. SEER cancer statistics review, 1975e2004. Bethesda, MD: National Cancer Institute. Also available at: http://seer.cancer.gov/csr/1975_2004/; 2007. based on November 2006 SEER data submission, posted to the SEER web site. 17 McClay EF. Epidemiology of bone and soft tissue sarcomas. Semin Oncol 1989 Aug; 16(4): 264e72. 18 Tucker MA, D’Angio GJ, Boice Jr JD, et al. Bone sarcomas linked to radiotherapy and chemotherapy in children. N Engl J Med 1987 Sep 3; 317(10): 588e93. 19 Li FP, Fraumeni Jr JF. Soft-tissue sarcomas, breast cancer, and other neoplasms. A familial syndrome? Ann Intern Med Oct 1969; 71(4): 747e52. 20 Howard GM, Casten VG. Rhabdomyosarcoma of the orbit in brothers. Arch Ophthalmol 1963; 70(3): 319e22. 21 Skapek SX, Chui CH. Cytogenetics and the biologic basis of sarcomas. Curr Opin Oncol 2000 Jul; 12(4): 315e22.

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(ii) Investigation of musculoskeletal malignancy

In confirmed cases of Ewing’s sarcoma (both the primary bone type and the rarer primary soft tissue form) as well as the related rarer small round blue cell tumours such as PNET (Primitive Neuro-Ectodermal Tumour) a bone marrow aspirate is necessary to complete staging.

Robert U Ashford K Julia Fairbairn

Imaging Primary malignant bone tumours Radiography The majority of primary malignant bone tumours are clearly visible on plain radiographs (two views at right angles) and this is usually how the diagnosis is made. Computerised tomography (CT) is often used for complex sites such as the shoulder girdle, pelvis and the spine as CT shows additional bony detail without overlap of structures, allowing assessment of calcified matrix, especially if the mineralization is subtle. Radiographically the lesion may be described as lytic (less dense than adjacent bone), sclerotic (more dense than adjacent bone) or mixed. However within an area of lytic destruction there may be areas of mineralization which may be characteristic of the type of tumour; two classic types are of ‘cotton wool’ or ‘cumulo-nimbus cloud’ matrix seen in osteosarcoma and the ‘curvi-linear’ or ‘popcorn’ like matrix in chondrosarcoma. The amount of mineralised matrix is variable but generally an obvious, well defined matrix is seen in the less aggressive tumours such as a low grade chondrosarcoma and less matrix is seen in the more aggressive forms such as a telangiectatic osteosarcoma (Figure 1). Some benign lesions can display a characteristic mineralization pattern such as the ‘ground glass’ pattern seen in fibrous dysplasia; typically a long lesion in long bones or ribs with associated expansion and possible areas of chondroid-like matrix. An unusual variant includes associated adjacent soft tissue myxomata (Mazzabraud’s syndrome). Another example is an osteoid osteoma which has a lytic nidus or centre that may have stippled calcification within that can be mistaken for a chondroid matrix. The usually associated cortical thickening with sclerosis or, in the rare intra-capsular form, an accompanying effusion, should avoid confusion. The relationship to the medullary cavity (including primary trabeculae) and the cortex especially the periosteum of the parent bone is also important. The margin of the lesion often suggests how aggressive it is. The most aggressive part should be used to characterise the lesion not the more benign part e.g. a chondrosarcoma of the tri-radiate cartilage of the acetabulum may have a variable thickness of sclerosis extending from the roof of the acetabulum as a ‘‘mechanical’’ response to the tumour related to weight bearing but an intermediate margin at the nonweight bearing inferior aspect extending into the ischium. The most benign bone margin is a thin rim of sclerotic bone, almost like a thin cortex, surrounding the lesion For example a bone cyst which may also have a characteristic ‘‘falling fragment’’ sign within following recent trauma. Aneurysmal bone cysts may have a similar but more ‘bubbly’ shape at the margin and accompanying expansion. Moving towards the aggressive end of the spectrum is a margin with a surgical cut off, then an intermediate type followed by an aggressive margin that is often referred to as ‘‘moth eaten’’ or permeative. The latter margin

Abstract Diagnosis and assessment of the extent of tumour burden are key to managing musculoskeletal malignancy to avoid the risk of inappropriate treatment when palliation would be appropriate. This review sets out the principles of investigating suspected musculoskeletal malignancies for the non-specialist with a focus also on the musculoskeletal imaging rather than oncological staging. It is not intended to be a comprehensive review of all musculoskeletal malignancies.

Keywords biopsy; investigation; metastases; MRI; sarcoma

Introduction Musculoskeletal malignancy falls into three broad types:  Primary malignant bone tumours - bone sarcomas  Primary soft tissue sarcomas  Metastatic malignancy While separate entities there is considerable overlap in their investigation, and to preclude errors, investigation strategies must be systematic.

History & examination A thorough history and examination is mandatory. As well as a systemic review, the history must include any previous history of malignancy and its treatment, especially radiotherapy, and any family history of malignancy. A full examination should include examination of the breasts in female patients and the prostate in males. Regarding the tumour itself, the red flag symptoms and signs for soft tissue masses are:  pain  size greater than 5 cm  deep to deep fascia  increasing size.

Blood investigations Full haematological and biochemical work-up forms part of the initial assessment and includes FBC, U&Es, LFTs, ESR or PV, CRP, tumour markers & serum electrophoresis.

Robert U Ashford FRCS(Tr & Orth) Consultant Orthopaedic and Musculoskeletal Tumour Surgeon for the East Midlands Sarcoma Service at Leicester Royal Infirmary, Infirmary Square, Leicester, LE1 5WW and Nottingham City Hospital, Hucknall Road, Nottingham, NG5 1PB, UK. K Julia Fairbairn FRCR Consultant Musculoskeletal Radiologist for the East Midlands Sarcoma Service at Nottingham City Hospital, Hucknall Road, Nottingham, NG5 1PB, UK.

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other localised changes to the classic Paget’s disease are suspicious for malignant change including involvement by metastatic disease which is actually probably more common than the rare secondary sarcomas.

Magnetic Resonance Imaging (MRI) MRI complements the radiographic and CT findings prior to biopsy. It is not as good at assessing any mineralised matrix but may show a characteristic ‘‘bubbly’’ pattern like the ‘‘cut surface of a pomegranate’’ in a chondrosarcoma (also in the rarer soft tissue form). In the unusual but aggressive telangiectatic osteosarcoma, there may be little or no mineralised matrix but there may be other features such as fluid-fluid levels that are seen in some more aggressive tumours which may help to suggest the diagnosis (Figure 2). MRI is crucial for local staging and evaluation of primary malignant bone tumours. It will delineate the intra-osseous and extra-osseous extent of the tumour including joint involvement, the presence or absence of skip lesions within the involved bone and the relationship of nerves and vessels to the tumour which can be either involved in the tumour precluding limb salvage, abutting the tumour or displaced by the tumour but not involved, or free from the tumour. This is critical in planning surgical resectionethe first group requiring amputation, the middle group usually being appropriate for limb salvage (unless the disease progresses during chemotherapy) and the latter group usually being appropriate for limb salvage. Most tumours will have low signal similar to muscle on T1 scans and high signal similar to fluid on T2 and Fat Suppressed scans (Short Tau Inversion Recovery ¼ STIR or spectral fat suppression techniques which are often faster but more susceptible to artefacts). Apart from low signal from a matrix, there are other unusual signal patterns that help suggest a diagnosis e.g. in giant cell tumours there is a relative lack of high signal on T2 and STIR scans from increased collagen or haemosiderin. This is especially helpful for Giant Cell Tumours (GCTs) that are not in the typical long bone meta-epiphyseal location e.g. the odontoid peg, in epiphyseal equivalents (carpus and tarsus) and in the rarer soft tissue form. This may also be helpful in assessing for recurrence. GCTs have another unusual trait that cross-sectional imaging may detect. They can cross joints such as the sacro-iliac joints without overt destruction of the joint on imaging, a trait they also share with bone lymphomas and also angiosarcomas although the latter may cause more joint destruction. Spinal tumours. A solitary metastasis, plasmacytoma or lymphoma are all more common than primary bone tumours. A solitary spinal lesion should be carefully assessed on imaging prior to biopsy. Apart from the signal pattern and odontoid or sacral prevalence of GCTs, a chordoma has similar high or low spinal predominance and may have some mineralization within on CT. Ten per cent of osteosarcomas are spinal; again CT may help confirm their typical matrix pattern. Typically osteoid osteomas or the larger osteoblastomas may cause a short angled scoliosis and occur in the posterior elements with a surrounding halo of oedema. CT is again recommended as an adjunct to assess the nidus and a three phase bone scan will be active on all three phases. Vascular tumours are common in the spine especially vertebral haemangiomas with a fatty stroma which are of no clinical

Figure 1 Plain AP radiograph of the knee demonstrating a destructive lesion of the proximal tibia with osteolysis, periosteal reaction and faint mineralization. Biopsy confirmed the lesion to be an osteosarcoma.

may be over 1e2 cm or more whilst the surgical cut off is very sharp or localised with the intermediate margin somewhere in between. The margins of sclerotic lesions can also be assessed in a similar fashion e.g. sclerotic metastases have ill-defined or blurred margins compared to a bone island/enostosis which is irregular but blends with the adjacent trabeculae. The cortex may act as a partial barrier to the tumour, but once this is breached, the periosteum offers little barrier to the spread of tumour. Various periosteal reactions can help characterize different bone tumours; the ‘‘onion skin’’ pattern of a Ewing’s sarcoma with layers of mineralization parallel to the diaphysis of a long bone. A ‘‘sunburst’’ pattern may be seen in osteosarcomas with mineralization at right angles to the cortex centred on the tumour. At the tumour margin there may be mineralization of an angled elevation of the periosteum known as a Codman’s triangle. This is seen in aggressive tumours such as an osteosarcoma but also may be seen with sub-periosteal collections such as haematomas and infection. Sequestra (bone fragments) and cloacae (cortical openings containing a dead fragment of bone) are usually thought of as features of infection but they may also be seen in some tumours e.g. lymphoma of bone. Some of these are seen in Paget’s disease which has a characteristic pattern of thickened, sclerotic primary trabeculae in a woven pattern and similar thickening and mild expansion of the cortex. The pelvis is a common site as well as the long bones which lesions typically start at the epiphysis, although there is also the rare diaphyseal form. The early stage is lytic and often described as a lytic ‘‘flame’’ as it progresses away from the end of a long bone. As rarely Paget’s can undergo malignant change to secondary sarcoma (usually osteosarcoma), areas of lysis or

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Figure 3 Isotope bone scan of the same patientethe proximal tibia shows marked increased uptake. There is no evidence of skeletal metastases.

author’s experience) or angiosarcomas may have an association with consumptive coagulopathy, thrombocytopenia and purpura known as the Kasabach-Merritt Syndrome1,2 with subsequent risk to biopsy/surgery. It is always worth remembering that an unusual appearance for a metastasis is more common than an unusual primary.

Systemic staging: isotope bone scan & CT chest Systemic staging of bone sarcomas requires a chest radiograph and CT for pulmonary metastases and an Isotope Bone Scan for skip lesions and osseous metastases (Figure 3). The Bone Scan is a map of osteoblastic activity and is often increased at a primary bone tumour site and metastases but can appear unremarkable or reduced in aggressive tumours where the osteoclastic activity is the dominant finding. This would be classically seen in patients with plasmacytomas or perhaps renal cell metastases where the lesions are often sizable before they are detected as areas of reduced activity. A very aggressive bone primary such as a telangiectatic osteosarcoma could have a similar appearance. Care needs to be taken when reviewing scans as osteoblastic activity is common when there is sclerosis at degenerative sites. Also, not all areas of increased activity at other sites are malignant tumours e.g. fibrous dysplasia, bone islands/enostosis especially larger ones and Paget’s disease.

a Coronal T2 MRI of the same tibial osteosarcoma showing the medullary and soft tissue extent of the tumourethe matrix is difficult to characterise. b Axial T2 MRI showing the popliteal vessels being encased/involved in the tumour. The fluid-fluid levels suggest an aggressive lesion. Vessel involvement precludes limb salvage.

Soft tissue sarcomas Plain radiographs The majority of probable soft tissue sarcomas should undergo plain radiography for the following reasons:  To exclude a bone lesion with soft tissue extension or vice versa  To assess any invasion of bone by an extra-osseous tumour  To assess the presence or absence of phleboliths (remember rim calcification like soft centred chocolates as seen in the pelvis on IVU’s for renal colic) which are often present in arterio-venous malformations and other vascular tumours  To assess matrix calcification or ossification such as dystrophic calcification that has no form seen in synovial cell sarcomas, more

Figure 2

significance. Haemangiomas with a vascularised stroma may cause confusion if the typical ‘‘polka dot’’ pattern on axial images or ‘‘corduroy cloth’’ pattern on sagittal or coronal scans is not recognised. The intermediate grade haemangio-endothelioma and haemangio-pericytoma may share some of these features. Angiosarcomas usually have a more aggressive appearance, may be multiple at presentation and also cross joints. Haemangioma, haemangio-endothelioma, (also haemangio-pericytoma in

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a Axial T1 b Axial T2 c Coronal STIR images demonstrating a large soft tissue mass in the adductor compartment of the thigh with fluid-fluid levels, consistent with a high grade sarcoma of the thigh. Figure 4

determine its local extent and to determine the need and best site for biopsy. The ultimate goal of imaging is to predict malignancy and an approximately 25% correct histological diagnosis can be made from imaging.4 The signal pattern of a lot of soft tissue tumours is nonspecific; (Figure 4) on T1 scans, masses are often low signal similar to muscle but without the normal fatty marbling. They are often high signal similar to fluid on T2 and Fat Suppressed scans (Short Tau Inversion Recovery e STIR - or spectral fat suppression techniques). Intravenous contrast in the form of chelated gadolinium (Gd) shows enhancement depending on the vascularity of the lesion but this can also be seen with oedema and at the margins of abscesses and other fluid collections if there is a vascularised capsule. The use of gadolinium is variable across the UK; we use it sparingly especially since the recognition of nephrogenic systemic fibrosis (NSF) which can occur in patients with grade 3 or higher renal failure. Our main use would be in lesions that have uniform signal and thus the potential to be just fluid or a predominantly myxoid tumour that could be benign or malignant. The contrast will confirm any nodular, cellular areas that should then be targeted at biopsy e.g. myxoid liposarcomas, fibrosarcomas or chondrosarcomas. Dynamic uptake curves have been used in Europe, but rarely in the UK, to try and differentiate benign from malignant lesions but with only limited success. There are some tumours that show signal variations of the common pattern of low on T1 and high on T2. The signal may be

structured calcification or ossification in liposarcomas, rare curvilinear matrix in mesenchymal chondrosarcomas and the even rarer ‘‘cotton wool’’ or ‘‘cumulo-nimbus cloud’’ like matrix in soft tissue osteosarcomas  To assess any associated underlying skeletal deformityetypically vascular tumours or hamartomatous lesions can have under- or overdevelopment of the limb and some mesenchymal syndromes have bony and soft tissue tumours e.g. Maffucci’s which has multiple enchondromas with malignant potential to form chondrosarcomas and associated overlying haemangiomas.

Computerised tomography CT is occasionally useful for the assessment of soft tissue tumours. It is superior to plain films for assessing calcification, ossification and air and also identifies adipose tissue well and can thus be complementary to MRI. CT is especially useful in assessing large lipomatous tumours in patients unsuitable for MRI due to claustrophobia or for other absolute reasons i.e. metallic foreign body in the eye, previous brain surgery with use of vascular clips and a cardiac pacemaker as there is reduced artefact from implants using modern multi-slice scanners. Magnetic Resonance Imaging It has been said that ‘‘Soft tissue tumours should be diagnosed and staged before biopsy’’.3 While the gold standard must be histology, MRI is the investigation of choice to assess soft tissue malignancy. It is used to detect and characterise a tumour, to

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increased or high signal on T1 where there is adipose tissue, methaemaglobin and slow flowing blood; the signal may be decreased or low signal on T2 where there is fibrous tissue, calcification/ossification, haemosiderin (and hyper-acute blood more in the neuro-axis than peripheral) and high flowing blood or flow voids. Examples of the high T1 pattern are adipose tumours such as an Atypical Lipomatous Tumour (ALT) or smaller quantities may be seen in liposarcomas. Examples of the low T2 pattern would include aggressive fibromatosis (a variant of a desmoid tumour with variable local infiltration) which often involves the trunk, mineralization in a mesenchymal chondrosarcoma and haemosiderin in pigmented villo-nodular synovitis (PVNS). Patterns are also helpful in suggesting specific diagnoses such as the shape (bubbly in cartilaginous tumours, serpiginous in vascular tumours), location and signal (close to joints with low signal from dystrophic calcification in synovial cell sarcomas) fluid-fluid levels (from organising haematomas to highly malignant sarcomas such as synovial cell sarcomas), signal voids (high flow, mineralization, implants and susceptibility artefact) and lastly multiplicity (fibrous tumours such as desmoids to fibrosarcomas, neural tumours both benign and malignant, vascular tumours both benign and malignant, myxomata and of course metastases especially mucinous tumours from ovary or GI tract). Assessment of malignancy can be relatively straightforward if there is a large, deep mass of mixed signal with a high growth rate. There may also be further clues such as an aggressive, infiltrating tumour margin, adjacent soft tissue and/or bone involvement, neurovascular invasion and extension beyond a compartment. These are the easy cases that obviously require a biopsy to confirm and then staging to formulate al treatment plan. There are however some major pitfalls. Some malignant tumours may have a very indolent appearance; some may even fool the unwary into thinking that they are simple cysts for example a myxoid sarcoma such as a myxoid liposarcoma. Hence the need for referral to a specialist tumour service for thorough clinical assessment, imaging review and, if necessary, repeat MRI with contrast and a targeted biopsy at a nodular, cellular part of the tumour to confirm the diagnosis. All lesions that are not small, superficial, mobile and distinct in character should have an MRI performed. A normal MRI virtually excludes an underlying malignancy. There are a number of difficulties imaging soft tissue sarcomas, many non-specific e.g. the experience and ability of the interpreter will vary. Then, while MRI is highly specific it is of low sensitivity, there are a range of appearances within histological groups and there are evolutionary changes and therapy changes. Despite these, as already stated, 25% correct histological diagnoses can be made from imaging alone. MRI also assesses structures at risk with marginal and wide resections, facilitates pre-operative surgical planning and has a further role in surveillance and follow-up, but this is controversial; some units use regular MRI to form a baseline postsurgery scan to monitor for local recurrence. In particular impalpable deep tumours are amenable to such surveillance.

centre. The fact that scanning detail decreases further from the probe means that deep large lesions are not scanned well. However small superficial lesions are more amenable to ultrasound assessment. Additionally ultrasound can assist in characterising lesions - especially aneurysms - that mimic tumours and for targeting of biopsy. It also has a role in assessing regional spread (nodal), can be used to assess vascularity and can differentiate a mass from a cyst and from oedema.

Systemic staging: CT chest and isotope bone scan As with bone sarcomas, systemic staging of soft tissue sarcomas comprises a chest radiograph with CT for pulmonary metastases (Figure 5). If the primary is retroperitoneal, abdominal, pelvic or spinal, CT assessment of the abdomen and pelvis are included. Unlike bone sarcoma work up, an isotope bone scan is only occasionally of help to assess for any periosteal involvement but it is again a standard requirement in staging soft tissue Ewing’s and other small round blue cell tumours such as a PNET and for rhabdomyosarcomas. A brain CT is included if there are relevant clinical symptoms or signs. New & novel techniques Positron Emission Tomography (PET eCT) PET-CT scanning is a functional imaging modality. 18F-fluorodeoxyglucose (FDG) is a labeled glucose substrate that is administered to the patient. The patient is then PET scanned followed by a low dose CT scan (Figure 6). The images are viewed independently as well as fused. It is an evolving technique that has a well defined role in the management of lung and oesophageal cancers as well as lymphoma. The role in sarcoma is less well defined but potential roles are for staging at primary diagnosis and detecting metastases (apart from in the lung where the CT resolution precludes accurate diagnosis and for brain metastases as diagnosis is masked by the avid glucose uptake of brain activity).

Ultrasound Ultrasound has a limited role in the management of sarcomas. It is operator and reader dependant whereas an MRI scan can be reported locally, and still be available for review by a specialist

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Figure 5 Chest radiograph demonstrating multiple metastases from the previous soft tissue sarcoma.

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a PET and b fused PET-CT images showing areas of avid glucose uptake in the proximal femora, right thigh muscles, left lung and axilla, consistent with a primary lung cancer with skeletal and soft tissue metastases (Reproduced from Current Orthopaedics 2006, Volume 20(4); 299e315). Figure 6

One area of sarcoma management where PET-CT appears to have a clear role is in neurofibromatosis type 1 where a lesion is suspected of having undergone change into a MPNST (Malignant Peripheral Nerve Sheath Tumour). FDG PET-CT has been shown to be both sensitive and specific in detecting these tumours.5 Malignancy is not the only condition that will result in an area of increased uptakeeother causes are inflammation, brown fat and exercise. It remains to be seen whether there are further clear definable roles for PET-CT in the management of sarcomas.

different methods, either a moving table in combination with the body coil or a specially designed rolling table platform with multiple phase array coils. A series of images are obtained, (typically coronals in our institution) which are electronically pasted together to produce whole body images (Figure 7). There is also recent interest in using diffusion weighted imaging (DWI) in whole body scans. Diffusion weighted imaging is a novel technique used in brain imaging to reflect the degree of restriction to water diffusion in biological tissues. This is inversely correlated to the cellularity and the integrity of cell membranes.8 DW imaging is acquired at multiple stations, reviewed as separate images and then fused producing a composite DW image of the whole body.

Whole Body MRI Whole Body MRI (WBMRI) is also an evolving technique for the assessment of bone marrow involvement, tumour staging and screening which has been developed in recent years using

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Whole Body MRI: Single Coronal a T1, b STIR and c Summated DWI images of a patient who presented with metastatic sarcoma. WBMRI demonstrated the primary tumourea large mixed signal tumour in the right thigh on T1 and STIR and also a right external iliac lymph node adjacent to the bladder. Figure 7

 Well or poorly defined  Permeative and/or destructive  Varied in their soft tissue involvement.

WBMRI protocols usually include T1 weighted and STIR (short tau inversion recovery) imaging which have proven highly efficient for the assessment of bone and soft tissue structures6,7 and therefore may have an evolving role in the assessment of bone and soft tissue sarcomas. It may especially be helpful for locating the primary when a patient presents with an unusual lung secondary or secondaries and there is no obvious primary site after a thorough clinical assessment. Similarly in a patient presenting with lymphadenopathy in one of the small round blue cell tumours (e.g. rhabdomyosarcoma) and the primary is not clinically evident. MR imaging is limited in its ability to detect small lung metastases. WBMR imaging shares this difficulty especially as there may be reduced image resolution compared to conventional MR images and this is currently compounded in the DWI technique. Unlike PET-CT, however, brain metastases may be assessed. The role of WBMRI in sarcoma remains to be fully established but promises to be of value.

Cross sectional imaging Dependent on the site of the lesion, CT or MRI scan may be appropriate. CT scans are best for looking at bone quality, bone destruction, calcified tumour matrix and cortical erosions whereas MRI is highly sensitive but relatively non-specific and is superior at demonstrating marrow replacement, skip lesions, quantifying oedema and assessing neurovascular involvement. Isotope bone scanning Bone scintigraphy may show multiple hot lesions, but beware the cold lesions (myeloma, renal cell carcinoma). It is also useful for demonstrating multiple lesions, and for identifying asymptomatic lesions. Positron Emission Tomography (PET) scanning is increasing in frequency and can be useful to determine the extent of tumour burden. The uptake of F18-FDG (fluorine-18 fluorodeoxyglucose), a glucose analogue, into tumour cells enables the most active and viable part of the tumour to be identified and targeted for biopsy. These modalities will help to identify other sites (metastases) both skeletal and visceral that may potentially require treatment.

Metastatic musculoskeletal malignancy Radiography Radiographs should be in two planes including the joint above and below to enable all lesions within the bone to be identified (Figure 8). Plain radiographs offer good integration of the overall bone structure and alignment. Radiographic features of skeletal metastases are variable. Tumours can be:  Lytic (osteoclastic), sclerotic (osteoblastic) or mixed  Solitary or multiple with a differential diagnosis of metastasis, myeloma or lymphoma for a patient with multiple lesions

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Summary of imaging As an aide memoire, Gilbert Jr. and Thompson Jr. summarised the major imaging modalities and their relative (Table 1) strengths in musculoskeletal malignancy:

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The incidence of complications of biopsy is up to five times more common in referring hospitals than in specialist centres.18e20 Thus all likely primary bone and soft sarcomas should be biopsied in the specialist centre that will be managing the patient. However, to avoid over-burdening the specialist centres, lesions felt highly likely to be bone secondaries of systemic malignancies (particularly where the lesion is multiple) can usually be safely or adequately assessed at a non-specialist centre and secondarily referred for a further opinion and/or repeat biopsy if an unexpected primary bone sarcoma is biopsied. Nonetheless, such biopsies should however be done along sarcoma principles. There are a number of situations in the management of metastatic disease where biopsy is desirable. Salai grouped these into five types of patient11 for whom biopsy is necessary:  A patient with a known primary malignancy but no known metastases who develops a new (first) bony lesion.  A patient with a history of long stable malignancy (breast, prostate cancer) who was considered cured, who develops a new bony lesion.  A patient with a known malignancy who presents with a pathological fracture.  A patient, previously healthy, who presents with new multiple bony lesion suspicious of disseminated metastatic disease, as yet of unknown origin.  A healthy patient who presents with a pathological fracture suspected of being metastatic in origin. The commonest types of biopsy are:  core needle biopsy (CNB)  fine needle biopsy (FNB)  excisional and incisional biopsies Most primary bone malignancies are amenable to core needle biopsy. The advantages of CNB are decreased morbidity, less haematoma formation, avoidance of open biopsy and they can be performed on an outpatient basis. Excision biopsy is only applicable to small superficial lesions smaller than 2 cm diameter or where a diagnosis has been made from imaging. It is not suitable for large lesions or lesions without a diagnosis.17 Care should be made when undertaking these lest the tumour bed requires further resection. Incision biopsies can be used for bone or soft tissue lesions. They should be performed following consultation with the surgeon who will be performing any definitive surgical procedure. There are a number of principles:  The surgeon performing the biopsy should be aware of the definitive resection approach so that the biopsy site and approach can be removed en bloc with the tumour.  Transverse incisions should be avoided (especially on limbs).  A tourniquet (if used) should be deflated prior to closure and haemostasis should be meticulous. If used a drain should be brought out through or at the tip of the incision. Haematoma must be avoided as it contaminates uninvolved tissue.  Uninvolved compartments should not be breached, tissue layers should not be developed and neurovascular structures must not be exposed and contaminated.  Tissue should be sent for both microbiology and histopathology.  A frozen section should be utilised for diagnostic representative tissue12

Figure 8 AP radiograph of right proximal femur with a large lytic lesion in the greater trochanter with permeative margins and cortical breakthrough consistent with a breast cancer metastasis (Reproduced from Current Orthopaedics 2006, Volume 20(4); 299e315).

Biopsy For primary tumours, tissue biopsy is critical to guide appropriate initial patient management. It is essential that it is carefully planned. This usually requires assessment with appropriate radiological imaging9,10 to assess the anatomical extent of the tumour prior to biopsy. Soft tissue lesions that are indeterminate on MRI need a tissue sample to be obtained for diagnosis. Poorly performed biopsies have a number of potential consequences, including pathological misdiagnosis due non-representative sampling), functional impairment, amputation and death.

Strengths of Imaging Modalities in assessment of musculoskeletal malignancy (from (4)) Bone lesions Soft tissue Metastases Strengths lesions Radiograph U

U

Ultrasound

U

Bone Scan CT MRI

U U U

U

Bone lesions & invasion Cystic lesions & aneurysms

U U

U

Delineates tumour extent

Table 1

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 Biopsy of bone should be taken away from any site of pathological fractureereaction of the bone to the fracture can be difficult to interpret. The majority of sarcoma services use mainly core needle biopsy. In specialist centres accuracy exceeds 80%.12e14 These can be image guided where necessary.15,16

13 Heslin MJ, Lewis JJ, Woodruff JM, Brennan MF. Core needle biopsy for diagnosis of extremity soft tissue sarcoma. Ann Surg Oncol 1997; 4(5): 425e31. 14 Stoker DJ, Cobb JP, Pringle JA. Needle biopsy of musculoskeletal lesions. A review of 208 procedures. J Bone Joint Surg 1991; 73-B(3): 498e500. 15 Altuntas AO, Slavin J, Smith PJ, et al. Accuracy of computed tomography guided core needle biopsy of musculoskeletal tumours. ANZ J Surg 2005; 75(4): 187e91. 16 Saifuddin A, Mitchell R, Burnett SJ, Sandison A, Pringle JA. Ultrasound-guided needle biopsy of primary bone tumours. J Bone Joint Surg 2000; 82-B(1): 50e4. 17 Papp DF, Khanna AJ, McCarthy EF, Carrino JA, Farber AJ, Frassica FJ. Magnetic resonance imaging of soft-tissue tumors: determinate and indeterminate lesions. J Bone Joint Surg Am 2007; 89(Suppl. 3): 103e15. 18 Mankin HJ, Lange TA, Spanier SS. The hazards of biopsy in patients with malignant primary bone and soft-tissue tumors. J Bone Joint Surg Am 1982; 64(8): 1121e7. 19 Mankin HJ, Mankin CJ, Simon MA. The hazards of the biopsy, revisited. Members of the Musculoskeletal Tumor Society. J Bone Joint Surg Am 1996; 78(5): 656e63. 20 Pollock RC, Stalley PD. Biopsy of musculoskeletal tumoursebeware. ANZ J Surg 2004 Jul; 74(7): 516e9.

Conclusion The aim of investigation of musculoskeletal malignancy is to establish the diagnosis and the extent of the disease burden and to enable treatment planning. Investigation should be meticulous, thorough and ordered. A

REFERENCES 1 Hall GW. Kasabach-Merritt syndrome: pathogenesis and management. Br J Haematol 2001; 112(4): 851e62. 2 Murphey MD, Fairbairn KJ, Parman LM, Baxter KG, Parsa MB, Smith WS. From the archives of the AFIP. Musculoskeletal angiomatous lesions: radiologic-pathologic correlation. Radiographics 1995; 15(4): 893e917. 3 Sundaram M, McLeod RA. MR imaging of tumor and tumorlike lesions of bone and soft tissue. AJR Am J Roentgenol 1990; 155(4): 817e24. 4 Gilbert Jr TJ, Thompson Jr RC. Imaging of Soft Tissue Tumors. Curr Orthop 1997; 11: 83e97. 5 Ferner RE, Golding JF, Smith M, Calonje E, Jan W, Sanjayanathan V, et al. [18F]2-fluoro-2-deoxy-D-glucose positron emission tomography (FDG PET) as a diagnostic tool for neurofibromatosis 1 (NF1) associated malignant peripheral nerve sheath tumours (MPNSTs): a longterm clinical study. Ann Oncol 2008; 19(2): 390e4. 6 Lauenstein TC, Semelka RC. Emerging techniques: whole-body screening and staging with MRI. J Magn Reson Imaging 2006; 24(3): 489e98. 7 Schaefer JF, Schlemmer HP. Total-body MR-imaging in oncology. Eur Radiol 2006; 16(9): 2000e15. 8 Vilanova JC, Barcelo J. Diffusion-weighted whole-body MR screening. Eur J Radiol 2008; 67(3): 440e7. 9 Peabody TD, Gibbs CP, Simon MA. Current concepts review - evaluation and staging of musculoskeletal neoplasms. J Bone Joint Surg 1998; 80-A(8): 1204e18. 10 Simon MA, Finn HA. Diagnostic strategy for bone and soft-tissue tumors. J Bone Joint Surg Am 1993; 75(4): 622e31. 11 Salai M, Dudkiewicz I. Surgical biopsy of bone metastases. In: Jasmin C, Coleman RE, Coia LR, Capanna R, Saillant G, editors. Textbook of bone metastases. 1st ed. Chichester: Wiley; 2005. p. 123e31. 12 Ashford RU, McCarthy SW, Scolyer RA, Bonar SF, Karim RZ, Stalley PD. Surgical biopsy with intra-operative frozen section. An accurate and cost-effective method for diagnosis of musculoskeletal sarcomas. J Bone Joint Surg 2006; 88-B(9): 1207e11.

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FURTHER READING Kransdorf MJ, Murphey MD. Imaging of soft tissue tumors. Lippincott Williams & Wilkins; 2005. Levesque J, Marx R, Bell RS, et al. A clinical guide to primary bone tumors. Lippincott Williams & Wilkins; 1998. Pollock RE. Soft tissue sarcomas: a volume in the American Cancer Society Atlas of Clinical Oncology Series. Decker; 2002.

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C

C

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For primary musculoskeletal tumours biopsy is the FINAL diagnostic step Biopsy should be performed by or at the very least after consultation with a regional sarcoma service All imaging modalities can provide useful information but plain radiographs and MRI remain the gold standard for local staging of sarcomas (bone and soft tissue) Systemic staging is usually a chest radiograph followed by CT chest and an isotope bone scan for all bone sarcomas and for a limited number of (specific) soft tissue sarcomas PET-CT and Whole Body MRI are evolving techniques for systemic staging

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(iii) The management of softtissue sarcomas

Diagnosis Benign soft tissue lesions outnumber STS by at least a factor of 100 and therefore the diagnosis of malignancy is often overlooked.4 In the United Kingdom, referral guidelines within cancer networks attempt to facilitate and streamline prompt referral to specialist diagnostic clinics.6 Under these guidelines, soft tissue masses larger than 5 cm in maximum diameter, those deep to the fascia, or those which are painful or growing in size are suspicious for malignancy and should be urgently referred.6 Clinical history taking should include enquiry about a personal or family history of malignancy, the rapidity of growth, whether or not the lesion is painful, and if it is solitary. Lesions that fluctuate in size are often fluid-filled bursae or ganglia. Clinical examination should include an assessment of the mass, of adjacent neurovascular structures, of regional lymph nodes and of the chest and abdomen. Radiological investigations should include plain x-rays to look for calcification within the lesion and local bone involvement. Local site imaging is conventionally performed with MRI or CT scans to determine the constituent tissues of the mass, its size and anatomical location, and its relationship to nearby neurovascular and bony structures. MRI scanning is generally preferred to CT, as it can give more information about the tumour pseudocapsule and it’s surrounding inflammatory zone. Imaging studies are used to plan the most appropriate route for biopsy. At the present time, core needle biopsy is probably the most common technique used in the diagnosis of STS. Needle biopsies reliably provide enough information to plan further treatment and are associated with a low rate of complications.7 Although the assessment of necrosis and mitotic index is less reliable on core needle biopsy than incision biopsy, this seldom influences management.1,7 Incisional biopsies can be used if a needle biopsy has failed, or if more tissue is required. Biopsy planning is important: all tissues contaminated by the biopsy and its track must be removed in the definitive resection. For this reason, biopsies are best performed by, or after discussion with, a surgeon who is experienced in performing definitive resections. Where open biopsies are performed, the incision should be placed along the longitudinal axis of the limb so that the biopsy track can be excised en bloc with the tumour. Close attention to haemostasis and minimal tissue dissection are important during incisional biopsy to minimise tissue seeding. Tumours are histologically classified according to the WHO system, which relies principally on morphological appearance.8 Histological grading is most often performed using either the Trojani or the National Cancer Institute grading systems. The Trojani grading system (published by the French Fe´de´ration Nationale des Centres de Lutte le Cancer), uses tumour differentiation, mitotic count and proportion of tumour necrosis to grade tumours 1e3.1,9 Staging investigations conventionally include chest CXR and chest CT, and, where appropriate, isotope bone scan. Although metastases to the lung is the most common route of dissemination, some tumour types (eg synovial sarcoma and clear cell sarcoma) can metastasise to lymph nodes and these may require additional imaging. Myxoid liposarcomas may spread to other soft tissues, particularly the paraspinal muscles. Imaging studies are used in conjunction with histological grading to stage the tumour. The most common staging systems in use are the 2002 American Joint Committee on Cancer (AJCC) Staging System for

Thomas B Beckingsale Craig H Gerrand

Abstract Soft-tissue sarcomas are a heterogeneous group of malignant tumours of connective tissue. The investigation, diagnosis and treatment of these rare tumours should be co-ordinated by specialist multi-disciplinary teams. Here we discuss the surgical principles involved in the management of these tumours, and explore the literature on surgical margins and adjuvant treatment. The management of local and systemic recurrence and prognosis are discussed and the evidence base reviewed.

Keywords chemotherapy; margins; radiotherapy; sarcoma; surgery

Introduction Soft-tissue sarcomas (STS) (from the Greek sarkoma, meaning fleshy growth), are malignant tumours of mesenchymal or connective tissue origin. They are rare, comprising less than 1% of all adult cancers, and heterogeneous, having an extensive range of histological types and biological behaviours.1,2 In Europe, the overall 5-year survival is 59%, although prognosis varies with histological type and grade.3 In England and Wales, the incidence is approximately 21 cases per million per year, with a crude mortality rate of 11 per million per year.4 It is recommended that evaluation and management of patients with STS is performed by specialist sarcoma multidisciplinary teams. The National Institute for Health and Clinical Excellence (NICE) in the UK4 and The National Comprehensive Cancer Network (NCCN) in America,5 provide comprehensive, evidence based guidelines for the treatment of STS.

Practice point C

Documentation from NICE (UK) and NCCN (USA) include detailed reviews of the literature and set out guidelines for investigation, management and follow-up.

Thomas B Beckingsale MSc(Durham) MBBS(Newcastle) MRCS(England) is a Specialist Registrar Orthopaedics and Trauma at Sunderland Royal Hospital, Sunderland, UK. Craig H Gerrand MBChB FRCS Trauma and Orth(Edinburgh) MD is a Consultant in Orthopaedic Oncology and Honorary Senior Lecturer at Newcastle University, Northern Centre for Bone and Soft Tissue Tumours, Freeman Hospital, Newcastle upon Tyne, UK.

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Soft Tissue Sarcoma and the Musculoskeletal Tumour Society (MSTS) (Enneking) system. The AJCC system stages tumours I e IV by size (greater or less than 5 cm) and site (superficial or deep), the presence or absence of regional lymph nodes, the presence or absence of distant metastases and the histological grade of the tumour.10 The Enneking system uses grade (low or high), site (intra-compartmental or extra-compartmental) and presence or absence of metastases (defined as any skip lesions, regional lymph nodes or distant metastasis). Low grade tumours are defined as stage I, high grade tumours as stage II and metastatic tumours as stage III. Intracompartmental tumours are further classified as ‘‘A’’ and extracompartmental as ‘‘B’’.11

and micronodules of tumour, which is known as the reactive zone. In high grade tumours, micronodules and extensions of the tumour into, and through, this reactive zone can lead to satellite and skip lesions.12 To avoid local recurrence, therefore, the resection should be performed outside the reactive zone if possible (Figure 1). Importantly, STS respect anatomical boundaries. Enneking recognised that tissues such as bone and fascia resist invasion by tumour, and this observation lead to the concept of anatomical ‘‘compartments’’. For example, three compartments are recognised in the thigh: the anterior, posterior and medial compartments. Anatomical spaces with less well defined boundaries (such as the popliteal fossa) are termed ‘‘extracompartmental’’ sites. He recognised that STS tend to remain within the compartment from which they arise. Extension of STS outside an anatomical compartment tends to occur late in the disease process and tumours often follow the path of perforating vessels. Tumours which arise in extra-compartmental spaces grow rapidly and extend longitudinally to a greater extent than those contained within fascial compartments. Extension of tumour from a fascialbound muscle compartment through an avascular tendinous insertion into bone is exceptionally rare, as is direct extension through the sheath of a major nerve, even one encased in tumour.12 The boundaries of anatomical compartments (eg fascia) can be used by surgeons to ensure complete resection.

Practice points C

C

Soft tissue masses larger than 5 cm in maximum diameter, deep to the fascia, or which are painful or growing in size should be urgently referred to a multi-disciplinary team. Biopsy planning is important and is best performed by, or after discussion with, a surgeon who is experienced in performing definitive resections.

Principles of surgery The local treatment of STS most often involves surgical resection, with or without radiotherapy. In order to gain local control, the whole tumour must be removed. Enneking made a major contribution to the understanding of the local behaviour of STS, which underpins surgical treatment.12 Most STS grow in a centrifugal fashion leading to compression, and thence atrophy, of the normal surrounding tissue. Surrounding the compression zone, or pseudocapsule, is an area of oedema and neovascularity, characterised by the presence of inflammatory cells

Practice point C

C

STS respect anatomical boundaries. Tissues such as bone and fascia resist invasion by tumour. Key reference: Enneking et al. The effect of anatomic setting on the results of surgical procedures for soft parts sarcoma of the thigh. Cancer 1981;47(5):1005e1022.12

This T2 weighted image shows a Grade 3 myxofibrosarcoma in the lateral thigh. The tumour is surrounded by a zone of oedema, which may or may not contain tumour cells. A decision has to be made about whether or not to remove this area of oedema along with the main tumour mass. In this anatomic location, it was straightforward to remove the whole of the vastus lateralis muscle, including the zone of oedema, although it did not contain tumour cells histologically. Figure 1

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Surgical margins The completeness of surgical excision is usually assessed by histological examination of the resection margins of the surgical specimen. In Enneking’s system, margins are described as, intralesional, marginal, wide or radical depending on the relationship between the plane of resection, the tumour, the pseudocapsule and the compartment. An intralesional margin is one in which macroscopic tumour deposits are left within the wound. Microscopic deposits within the reactive zone and possible skip lesions in surrounding normal tissue may be left behind. With a marginal margin, the tumour is excised with an intact pseudocapsule but the reactive zone is violated and there is the piossibility of leaving residual microscopic satellites and skip lesions within the wound. A wide margin implies that the tumour has been resected with a complete surrounding cuff of normal tissue. In high grade tumours there is a risk that microscopic skip lesions within the normal tissue will remain. To achieve a radical margin, the entire compartment, within which the tumour resides, must be excised en bloc. In theory, a radical excision leaves no microscopic disease in situ. (Figure 2): Given the size of most tumours and their relationship to critical structures, many resections are technically marginal in the Enneking system. Others have sought to refine the Enneking system in order to provide further detailed prognostic information on the risk of local recurrence. Rydholm and Rooser, for example, subclassified wide margins as wide-S (subcutaneous) when a subcutaneous tumour was excised with a cuff of subcutaneous tissue and deep fascia, wide-F (fascia) when a deep tumour was excised with an intact envelope of uninvolved fascia and wide-AM (areolar tissue and muscle) when a deep tumour was excised with a wide margin, some or all of which comprised muscle or areolar tissue. In their paper, the crude

rates of local recurrence after wide-S, wide-F and wide-AM, were 6%, 7% and 27% respectively.13 Kawaguchi et al. proposed a classification of wide margins as curative, adequate or inadequate depending on the thickness and quality of the tissue comprising the margin. In their paper, inadequate wide margins did not ensure local control for highgrade sarcoma even with adjuvant radiotherapy, but were sufficient for low-grade tumours.14 Surgical margins may also be described as microscopically positive or negative. However, it is clear that not all positive surgical margins are equal. For example, a focally positive surgical margin accepted by the surgeon in order to preserve a critical anatomical structure such as a major nerve is likely to be associated with a lower risk of local recurrence than a positive surgical margin following an unplanned resection, in which there is likely to be more tumour left in the wound. In the series by Gerrand et al, where positive surgical margins were planned before surgery in order to preserve critical structures, the subsequent risk of local recurrence remained low (3.6%) (Figure 3). This was in contrast to patients who had positive margins after unplanned excisions at non-specialist centres and patients who had unplanned, inadvertent positive margins at the specialist centre, who both had high rates of local recurrence (31.6% and 37.5% respectively).15

Practice point C

Amputation versus limb-sparing surgery Limb sparing surgery became widely accepted after the publication by Rosenberg in 1982 of a study in which patients were randomised to receive either primary amputation or limb-sparing surgery with radiotherapy. The paper reported that although there was a higher rate of local recurrence in limb-sparing surgery, there was no significant difference in either five year disease free survival or five year overall survival.16 Limb-sparing surgery continues to be associated with a higher risk of local recurrence than amputation, and although it is generally accepted that limb-sparing is not associated with a higher risk of tumour related mortality, at least one study has suggested that positive surgical margins are associated with lower diseasespecific survival than negative surgical margins.17 The currently accepted indications for amputation are narrow. Greater familiarity with limb sparing techniques mean that major arteries can be resected and reconstructed, there is better understanding of the implications of the resection of complete muscle groups, and plastic surgical flap reconstruction can be used to cover skin and soft tissue defects.18,19 The traditional view that the need to perform major motor nerve resection makes the residual limb not worth saving has been challenged by Brooks et al. who demonstrated that resection of the sciatic,

Figure 2 Diagrammatic representation of a soft tissue tumour within the anterior thigh in cross section. The tumour (red) is surrounded by a reactive zone of compressed normal tissue and inflammatory cells (pink), within an osteofascial compartment (green). Examples of planes of resection are shown. In an intralesional excision, the plane of resection passes through the tumour, in a marginal excision through the reactive zone, and in a wide excision through normal tissue. In a radical excision the whole of the compartment (green) would be excised.

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Enneking described surgical margins as, intralesional, marginal, wide or radical depending on the relationship between the plane of resection, the tumour, the pseudocapsule and the compartment.

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These axial and sagittal MR images show a large (20 cm in maximum dimension), heterogenous soft tissue sarcoma arising in the calf. There is a broad plane of contact with the tibia, but no bone involvement radiologically. A microscopically positive margin can be accepted against the tibia if the resection is wide elsewhere, and a subperiosteal dissection is performed. A multidisciplinary approach is helpful in planning preoperative radiotherapy and soft tissue cover of the tibia following resection of the tumour and overlying skin. Figure 3

peroneal or tibial nerves gives acceptable objective and subjective functional results in most patients, and represents an excellent alternative to amputation. All patients in their series preferred their status over having an amputation.18 There is no doubt though, that resection of motor nerves in limb-sparing surgery leads to decreased Musculoskeletal Tumor Society Rating Scale (MSTS) scores and increased disability, as measured by the Toronto Extremity Salvage Score (TESS).20 Amputation should generally be reserved for cases where: the tumour bridges several compartments or extensively involves neurovascular structures, thus precluding adequate surgical margins; a below-knee prosthesis would provide a better functional result than a lower limb extensively damaged by surgery and radiation; or the dose and field of radiation would be so large that there would be a significant risk of major complications.21 It is important to note that several studies have shown that patients who have limb sparing surgery and those who have amputations tend to have similar general health status and quality of life scores. However, there a trend towards increased disability after amputation verses limb-sparing surgery and a significantly increased level of handicap in patients who have amputation.22

modalities. The World Health Organisation’s International Classification of Functioning, Disability and Health (ICF), defines impairments as any loss or abnormality of psychological, physiological or anatomic structure or function; activity limitations (disabilities) as any restriction or lack of ability to perform an activity in the manner or within the range considered normal for a human being; and participation restrictions (handicaps) as any limitation in performing roles considered normal for that individual.23 Most of the current literature focuses on impairments, few papers tackle activity limitations and almost none deal with participation restrictions.24 Approximately 50% of patients treated for STS have significant impairments.25 After limb sparing surgery, most studies use the MSTS or TESS scores to measure physical functioning. Motor nerve resection, bone resection, large tumour size and post-operative complications are predictive of lower MSTS scores. Patients with large, high-grade tumours who require motor nerve resection are also more disabled as reflected by lower TESS scores.20 The treatment of superficial tumours does not usually lead to significant changes in functional scores. The anatomical location of tumours has not been shown to significantly affect aggregated MSTS and TESS scores, although there is significant variation in individual score items within the scoring systems. For instance, tumours in the buttock and posterior thigh are associated with difficulty in sitting compared to tumours in other anatomical locations. This information can be of value in counselling patients about their likely impairment and disability after treatment.26

Practice point C

Limb-sparing surgery is associated with a higher rate of local recurrence but no significant difference in either five year disease free survival or five year overall survival.16

Adjuvant treatment Radiotherapy In order to achieve local control of STS in adults, surgery is generally combined with radiotherapy, particularly for tumours that are large, high-grade or which have been incompletely excised.27,28 Small, low grade tumours, excised with adequate

Functional outcomes Assessing physical function after the surgical treatment of STS is important in order to explore the impact of different treatment

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margins can be treated by surgery alone.21 Although radiotherapy is associated with a lower rate of local recurrence, a positive impact on survival has not been demonstrated.27,28 Radiotherapy is most often given as external beam radiotherapy, although some centres advocate brachytherapy, in which the radiation source (usually radioactive wires) is placed within or close to the area being treated.29 Intensity-modulated radiation therapy (IMRT) has the potential to better target the delivered radiation dose, and is under investigation. Complications associated with radiotherapy include second malignancies, wound complications, oedema, and fibrosis.

in which the use of higher doses of doxorubicin in combination with ifosfamide became common practice. A benefit of chemotherapy for local, distant, and overall recurrence-free survival, and a statistically significant increase in overall survival were demonstrated. The odds ratio for overall survival using doxorubicin alone was 0.84 ( p ¼ 0.09) and for doxorubicin combined with ifosfamide was 0.56 ( p ¼ 0.01), equating to an absolute risk reduction of death of 11%.34 Unfortunately the side effects of these regimens (particularly the cardiotoxicity of doxorubicin) are significant and their use outside the trial setting is generally reserved for younger patients at high risk of relapse, in the presence of metastatic disease, or in some specific tumour types (eg. rhabdomyosarcoma, soft-tissue Ewing’s sarcoma and primitive neurectodermal tumours [PNET]).35,36 Isolated limb perfusion is a surgical technique in which the major vessels to an affected limb are isolated and the limb is perfused with cytotoxic agents, most often melphalan and tumour necrosis factor alpha (TNF-alpha), often with hyperthermia. This is a useful technique when used to down-size locally-advanced tumours to facilitate limb salvage when amputation is being considered. Despite this positive effect, there are currently no randomised data to suggest an increase in overall survival, compared to surgery alone,37 and the technically demanding nature of its delivery means that it is only available in a small number of centres in the United Kingdom.

Pre or post-operative radiotherapy? External beam radiotherapy can be given before or after surgery. The advantages of pre-operative radiotherapy include a smaller field and a lower dose of radiation (typically 50 Gy compared with 66 Gy given postoperatively). The major disadvantage is a higher rate of post-operative wound complications, particularly when tumours are located in the thigh.21,30 Although post-operative radiotherapy is associated with a lower rate of wound complications, the higher dose increases the risk of other late complications, such as tissue fibrosis and lymphoedema, which lead to poorer functional outcomes.21,30 At the present time therefore, one approach is to consider using external beam radiotherapy pre-operatively for tumours in anatomical sites at low risk of wound complications (such as the upper limb), when the tumour is adjacent to radiosensitive structures like the lung and brachial plexus, or for some large tumours, when the size of the surgical field may be significant.30 Tumours that are particularly radiosensitive, such as myxoid liposarcomas, may respond well to pre-operative radiotherapy and reduce in size,before operative excision.31

Complications of local treatment The extensive surgery required, large skin flaps and the resulting soft tissue defect mean that surgery for STS is associated with a high rate of wound complications. The liberal use of free flaps or skin grafts may help.30 Radiotherapy increases the risk of wound complications, particularly given preoperatively. In the longer term, radiotherapy is associated with soft tissue fibrosis, joint stiffness, lymphoedema, pathological fracture and second malignancy.38,39 Risk factors for pathological fracture include age, female gender, periosteal stripping and radiotherapy dose. Thromboembolic events occur at around the same overall rate as after lower limb arthroplasty. However, large thigh tumours appear to be a particular risk for thromboembolism. The use of thrombo-prophylactic agents remains controversial due to a perceived increased risk of bleeding complications.40

Practice points C

C

Radiotherapy reduces rates of local recurrence but has no impact on overall survival. Pre-operative radiotherapy is associated with a higher rate of post-operative wound complications.

Chemotherapy The use of chemotherapy in the treatment of STS is debated. Perhaps the best evidence for chemotherapy comes from the Sarcoma Meta-analysis Collaboration (SMAC) meta-analysis of individual patient data, first published in 1997 and updated for the Cochrane Collaboration in 2000.32,33 Data from 14 randomised trials of doxorubicin-based adjuvant chemotherapy involving a total of 1568 patients were included. This meta-analysis demonstrated a small but significant difference in both local recurrence-free survival, and distant recurrence-free survival, as well as overall recurrence-free survival corresponding to absolute benefits of 10% at 10 years. Although a trend towards increased overall survival in patients receiving chemotherapy was demonstrated, it did not reach statistical significance.32 More recently however, Pervaiz et al. updated this metaanalysis by including 4 trials performed in the intervening decade

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Follow up After treatment, patients are usually followed up with regular clinic visits and radiological investigations. The rationale for follow up is to detect local or systemic recurrence early in the belief that this will improve outcomes, or in some patients, particularly those who have received chemotherapy, to detect the late effects of treatment. Unfortunately there is a financial burden for the healthcare system and a psychological burden for the patient associated with follow up. Furthermore, patients or their General Practitioners are capable of detecting most local recurrences.41 As a result, follow up protocols vary significantly. The National Comprehensive Cancer Network (NCCN) in the USA recommends follow-up initially with a chest x-ray (CXR) every 6e12 months for stage I tumours and with CXR or CT every 3e6 months for stage II and III tumours, with periodic imaging of the

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primary site based on the risk of loco-regional recurrence.5 Other authors suggest that in the absence of other risk factors, CXR surveillance is not indicated in grade I tumours, as the risk of lung metastasis is extremely low.42 A postal survey of UK clinicians demonstrated that most STS patients are followed up with clinic visits and CXR, although the interval between visits is variable, and partly determined by the perceived risk of recurrence. CT chest and imaging of the primary site are used less frequently. The most cost-effective follow-up protocol that will maximise patient survival, quality of life, psychological outcomes and function remains to be determined.41 In the United Kingdom, patients are commonly reviewed with clinical examination and CXR every 3 months in years one to 3, at six monthly intervals in years 4 and 5, and annually thereafter to 10 years.

The future

Local and systemic recurrence

The management of soft tissue tumours should be coordinated through a multidisciplinary team. The biopsy of suspicious lesions should best be carried out by someone capable and prepared to carry out definitive treatment. Suspicious lesions are those that are more than 5 cm in diameter, deep to fascia, painful and rapidly growing. Limb sparing surgery is preferred, as an increased risk of local recurrence is not associated with any difference in long term survival. Furthermore there can be a role for adjuvant radiotherapy in some cases to reduce the risk of local recurrence. Local recurrence, if it does occur, is teeated using the same principles which govern the management of primary disease. Whilst there are exciting developments in systemic treatment, much can currently be achieved by improving access to the highest standards of care for all patients with STS. Early referral to an appropriate team is key. A

Looking to the future, there is a need to refine the local therapy of STS and to develop new systemic agents. The development of imatinib has transformed the care of patients with gastro-intestinal stromal tumours and the hope is that similar progress can be made for other tumour types. New drug strategies under investigation include targeting tumour angiogenesis with antivascular endothelial growth factor (VGEF) agents, the inhibition of the Bcl-2 anti-apoptotic genes, the use of heat shock protein modulators or cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) inhibition.50 Gene therapies may offer new treatments in the future.50

Summary

The two most important predictors of local recurrence are surgical margin status and histological grade.17,41,43 Other factors associated with an increased risk of local recurrence include age >50 years, locally recurrent disease at presentation, size >5 cm, upper extremity tumours and tumours located deep to the investing muscle fascia.17,43e45 Unfortunately, patients with a local recurrence are at risk of distant metastasis and therefore need to undergo local and systemic staging investigations.5 The principles of the surgical treatment of local recurrence are similar to those for treatment of a primary tumour. Wherever possible, limb sparing surgery is performed. As in the primary setting, amputation has been shown to reduce the risk of further local recurrence but not to improve overall survival.43 Hence, amputation is generally reserved for patients with multi-focal or multi-compartmental extremity recurrences and those with significant bone, joint or neurovascular involvement. Radiotherapy may be given, depending on local tissue toxicity and the previous radiation dose. Brachytherapy is useful if radiotherapy has been given in the past as the tumour bed can be treated without increasing toxicity.46 Systemic metastases pose a risk to life in patients with extremity sarcomas, compared with those with abdominal tumours for whom local recurrence may represent the biggest risk. The principal risk factors for tumour metastasis are tumour grade, size and depth.47 Age at diagnosis, tumour site and histological subtype are also included as risk factors on a nomogram developed by Kattan et al., which predicts the 12-year risk of tumour-related death.48 Wherever possible, patients with metastases should be considered for surgical resection. There is some evidence that aggressive surgical treatment of pulmonary metastases is associated with improved survival, even if the metastases recur.49 Patients with unresectable or high risk metastatic disease may be considered for chemotherapy.

REFERENCES 1 Coindre J-M. Grading of Soft Tissue Sarcomas. Arch Pathol Lab Med 2006; 130: 1448e53. 2 Zahm SH, Fraumeni JF. The epidemiology of soft tissue sarcoma. Semin Oncol 1997; 24(5): 504e14. 3 Storm HH. Survival of adult patients with cancer of soft tissues or bone in Europe. European Journal of Cancer 1998; 34: 2212e7. 4 NICE. Guidance on Improving Cancer Services: Improving Outcomes for People with Sarcoma. The Manual. London: National Institute for Health and Clinical Excellence; 2006. 5 NCCN. National Comprehensive Cancer Network Clinical Practice Guidlines in Oncology: Soft Tissue Sarcoma. V.2.2008. National Comprehensive Cancer Network; 2008. 6 NICE. Clinical guidline 27: Referral guidelines for suspected cancer. London: National Institute for Health and Clinical Excellence. 2005. 7 Welker JA, Henshaw RM, Jelinek J, Shmookler BM, Malawer MM. The percutaneous needle biopsy is safe and recommended in the diagnosis of musculoskeletal masses. Cancer 2000; 89(12): 2677e86. 8 WHO. International Statistical Classification of Diseases and Health Related Problems. Tenth Revision. (ICD-10) Second ed. Geneva: World Health Organization; 2005. 9 Trojani M, Contesso G, Coindre JM, et al. Soft-tissue sarcomas of adults; study of pathological prognostic variables and definition of a histopathological grading system. International Journal of Cancer 1984; 33(1): 37e42.

Practice points C

C

The principles of the surgical treatment of local recurrence are similar to those for treatment of a primary tumour. Wherever possible, patients with metastases should be considered for surgical resection.

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10 Greene FL, Page DL, Fleming ID, et al. In: American Joint Committee on CancerCancer Staging Manual, editor. 6th ed. New York, NY: Springer; 2002. 11 Enneking WF, Spanier SS, Goodman MA. Current concepts review. The surgical staging of musculoskeletal sarcoma. J Bone Joint Surg Am 1980; 62(6): 1027e30. 12 Enneking WF, Spanier SS, Malawer MM. The effect of the anatomic setting on the results of surgical procedures for soft parts sarcoma of the thigh. Cancer 1981; 47(5): 1005e22. 13 Rydholm A, Rooser B. Surgical margins for soft-tissue sarcoma. J Bone Joint Surg Am 1987; 69(7): 1074e8. 14 Kawaguchi N, Ahmed AR, Matsumoto S, Manabe J, Matsushita Y. The concept of curative margin in surgery for bone and soft tissue sarcoma. Clinical Orthopaedics & Related Research 2004; 419: 165e72. 15 Gerrand CH, Wunder JS, Kandel RA, et al. Classification of positive margins after resection of soft-tissue sarcoma of the limb predicts the risk of local recurrence. Journal of Bone and Joint Surg [Br] 2001; 83-B: 1149e55. 16 Rosenberg SA, Tepper J, Glatstein E, et al. The treatment of softtissue sarcomas of the extremities - prospective randomized evaluations of (1) limb-sparing surgery plus radiation therapy compared with amputation and (2) the role of adjuvant chemotherapy. Annals of Surgery 1982; 196(3): 305e15. 17 Stojadinovic A, Leung DHY, Hoos A, Jaques DP, Lewis JJ, Brennan MF. Analysis of the Prognostic Significance of Microscopic Margins in 2,084 Localized Primary Adult Soft Tissue Sarcomas. Annals of Surgery 2002; 235(3): 424e34. 18 Brooks AD, Gold JS, Graham D, et al. Resection of the Sciatic, Peroneal, or Tibial Nerves: Assessment of Functional Status. Annals of Surgical Oncology 2002; 9(1): 41e7. 19 Ghert MA, Davis AM, Griffin AM, et al. The Surgical and Functional Outcome of Limb-Salvage Surgery With Vascular Reconstruction for Soft Tissue Sarcoma of the Extremity. Ann Surg Oncol 2005; 12(12): 1102e10. 20 Davis AM, Sennik S, Griffin AM, et al. Predictors of functional outcomes following limb salvage surgery for lower-extremity soft tissue sarcoma. Journal of Surgical Oncology 2000; 73(4): 206e11. 21 Pisters PWT, O’Sullivan B, Maki RG. Evidence-Based Recommendations for Local Therapy for Soft Tissue Sarcomas. J Clin Oncol 2007; 25(8): 1003e8. 22 Davis AM, Devlin M, Griffin AM, Wunder JS, Bell RS. Functional outcome in amputation verses limb sparing of patients with lower extremity sarcoma: a matched case-control study. Achives of Physical Medicine and Rehabilitation 1999; 80(6): 615e8. 23 WHO. World Health Organization. International Classification of Functioning. Disability and Health (ICF). Geneva: World Health Organization; 2001. 24 Parsons JA, Davis AM. Rehabilitation and Quality-of-Life Issues in Patients with Extremity Soft Tissue Sarcoma. Current Treatment Options in Oncology 2004; 5: 477e88. 25 Davis AM. Functional outcome in extremity soft tissue sarcoma. Seminars in Radiation Oncology 1999; 9(4): 360e8. 26 Gerrand CH, Wunder JS, Kandel RA, et al. The Influence of Anatomic Location on Functional Outcome in Lower-Extremity Soft-Tissue Sarcoma. Annals of Surgical Oncology 2004; 11(5): 476e8. 27 Khanfir K, Alzieu L, Terrier P, et al. Does adjuvant radiation therapy increase loco-regional control after optimal resection of soft-tissue sarcoma of the extremities? European journal of cancer 2003; 39(13): 1872e80.

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28 Yang JC, Chang AE, Baker AR, et al. Randomised Prospective Study of the Benefit of Adjuvant Radiation Therapy in the Treatment of Soft Tissue Sarcomas of the Extremity. Journal of Clinical Oncology 1998; 16: 197e203. 29 Pisters PW, Harrison LB, Leung DH, Woodruff JM, Casper ES, Brennan MF. Long-Term Results of a Prospective Randomised Trial of Adjuvant Brachytherapy in Soft Tissue Sarcoma. Journal of Clinical Oncology 1996; 14: 849e68. 30 O’Sullivan B, Davis AM, Turcotte R, et al. Preoperative verses postoperative radiotherapy in soft-tissue sarcoma of the limbs: a randomised trial. The Lancet 2002; 359: 2235e41. 31 Pitson G, Robinson P, Wilke D, et al. Radiation response: An additional unique signature of myxoid liposarcoma. International Journal of Radiation Oncology, Biology, Physics 2004; 60(2): 522e6. 32 SMAC. Adjuvant chemotherapy for localised resectable soft tissue sarcoma in adults. Cochrane Database of Systematic Reviews 2000(Issue 4). 33 SMAC. Adjuvant chemotherapy for localised resectable soft-tissue sarcoma of adults: meta-analysis of individual data. The Lancet 1997; 350(9092): 1647e54. 34 Pervaiz N, Colterjohn N, Farrokhyar F, Tozer R, Figueredo A, Ghert M. A systematic meta-analysis of randomized controlled trials of adjuvant chemotherapy for localized resectable soft-tissue sarcoma. Cancer 2008; 113(3): 573e81. 35 Judson I. State-of-the-art approach in selective curable tumours: soft tissue sarcoma. Annals of Oncology 2008; 19(Suppl 7): vii166evii9. 36 DeLaney TF, Spiro IJ, Suit HD, et al. Neoadjuvant chemotherapy and radiotherapy for large extremity soft-tissue sarcomas. International Journal of Radiation Oncology, Biology, Physics 2003; 56(4): 1117e27. 37 Hohenberger P, Wysocki WM. Neoadjuvant Treatment of Locally Advanced Soft Tissue Sarcoma of the Limbs: Which Treatment to Choose? Oncologist 2008; 13(2): 175e86. 38 MacDougall RH, Kerr GR, Duncan W. Incidence of sarcoma in patients treated with fast neutrons. International Journal of Radiation Oncology, Biology, Physics 2006; 66(3): 842e4. 39 Davis AM, O’Sullivan B, Bell RS, et al. Function and Health Status Outcomes in a Randomized Trial Comparing Preoperative and Postoperative Radiotherapy in Extremity Soft Tissue Sarcoma. J Clin Oncol 2002; 20(22): 4472e7. 40 Mitchell SY, Lingard EA, Kesteven P, McCaskie AW, Gerrand CH. Venous Thromboembolism in Patients with Primary Bone or SoftTissue Sarcomas. Journal of Bone and Joint Surg [Am] 2007; 89: 2433e9. 41 Gerrand CH, Billingham LJ, Woll PJ, Grimer RJ. Follow up after Primary Treatment of Soft Tissue Sarcoma: A Survey of Current Practice in the United Kingdom. Sarcoma 2007: 1e6. 42 Lord HK, Salter DM, MacDougall RH, Kerr GR. Is routine chest radiography a useful test in the follow up of all adult patients with soft tissue sarcoma? Br J Radiol 2006; 79(946): 799e800. 43 Stojadinovic A, Jaques DP, Leung DHY, Healey JH, Brennan MF. Amputation for Recurrent Soft Tissue Sarcoma of the Extremity: Indications and Outcome. Annals of Surgical Oncology 2001; 8(6): 509e18. 44 Pisters PW, Leung DH, Woodruff J, Shi W, Brennan MF. Analysis of prognostic factors in 1,041 patients with localized soft tissue sarcomas of the extremities. Journal of Clinical Oncology 1996; 14: 1679e89. 45 Espat NJ, Lewis JJ. The biological significance of failure at the primary site on ultimate survival in soft tissue sarcoma. Seminars in Radiation Oncology 1999; 9(4): 369e77.

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46 Pearlstone DB, Janjan NA, Feig BW, et al. Re-resection with brachytherapy for locally recurrent soft tissue sarcoma in a previously irradiated field. Cancer J Sci Am 1999; 5(1): 26e33. 47 Coindre J-M, Terrier P, Guillou L, et al. Predictive Value of Grade for Metastasis Development in the Main Histologic Types of Adult Soft Tissue Sarcomas. A Study of 1240 Patients from the French Federation of Cancer Centers Sarcoma Group. Cancer 2001; 91(10): 1914e26.

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48 Kattan MW, Leung DHY, Brennan MF. Postoperative Nomogram for 12-Year Sarcoma-Specific Death. J Clin Oncol 2002; 20(3): 791e6. 49 Rehders A, Hosch SB, Scheunemann P, Stoecklein NH, Knoefel WT, Peiper M. Benefit of Surgical Treatment of Lung Metastasis in Soft Tissue Sarcoma. Arch Surg 2007; 142(1): 70e5. 50 Kasper B, Gil T, D’Hondt V, Gebhart M, Awada A. Novel treatment strategies for soft tissue sarcoma. Critical Reviews in Oncology/Hematology 2007; 62(1): 9e15.

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(iv) Management of benign bone tumours

ever been substantiated except multiple hereditary osteochondromatosis (also known as diaphyseal aclasis) which is inherited as an autosomal dominant. Two genes are responsible, namely the EXT 1 and EXT 2 genes found at the 8q24 and 11p11-12 loci respectively. Approximately 15% of patients with osteochondromas have the inherited form of the condition.

Rob Pollock

Clinical features Abstract

The clinical features are non-specific and variable. Some long standing lesions present as an incidental finding. For example, an adolescent who attends the accident and emergency department after a knee injury and a fibrous cortical defect is found on X-ray (Figure 1). Some tumours such as osteochondroma present with a long history of a painless swelling (Figure 2), but more aggressive lesions, such as giant cell tumour, usually present with a short history of a pain, swelling and loss of function.

Benign primary bone tumours are rare, occurring most commonly in skeletally immature patients, arising from cartilage or bone. The commonest locations are the distal femur, proximal tibia and proximal humerus. They present with pain, swelling or pathological fracture. Diagnosis is by plain x-rays, MRI scans and a core needle biopsy if indicated. More aggressive tumours may appear radiologically to be similar to malignant tumours. Treatment depends on the anatomical location, symptoms, the natural history of the tumour and the morbidity of treatment and in most cases involves either simple excision or curettage although occasionally it is necessary to perform a complete excision using the same principles as for malignant tumours.

Investigation As some benign bone tumours can be difficult to distinguish from their malignant counterparts, investigation should be carried out in a multidisciplinary setting, ideally in a specialist musculoskeletal tumour centre.3 The bare minimum is adequate imaging by plain x-ray and a magnetic resonance imaging (MRI) scan. The radiological features may be so clear that, if compatible with the clinical picture, tissue diagnosis is not necessary before definitive treatment. However, if there is any doubt about the diagnosis, a tissue diagnosis should be obtained, which is best done by core needle biopsy using a Jamshedi needle.

Keywords benign bone tumour; non-neoplastic tumour-like conditions of bone

Introduction Primary bone tumours are extremely rare, accounting for only 0.2% of human tumours.1 The majority are benign and affect the skeletally immature patient but some are difficult to distinguish from their malignant counterparts, have a significant incidence of local recurrence and may undergo malignant transformation. Diagnosis and treatment of bone tumours is complex and management of this group of patients is best undertaken at specialist centres in a multidisciplinary setting.

Management General principles Treatment is dependant on many factors, particularly:  patient’s symptoms  natural history of the tumour  morbidity of treatment. Treatment varies from simple observation with repeat imaging through to wide excision using the same surgical principles as for malignant tumours. When treating bone tumours the surgeon has to balance excision margin against function. With wider margins, there may be greater functional loss but a lesser chance of local recurrence. Conversely, intralesional surgery has less morbidity but a greater risk of local recurrence.

Classification Two classification systems are commonly used, see Tables 1 and 2. The first is histological, based on the cell of origin. The second is more clinically orientated and based on the pattern of behaviour of the tumour.2 While tumours may arise from chondrocytes, osteoblasts, osteoclasts, periosteum or soft tissue within bone such as fat or smooth muscle, some fall into a ‘‘miscellaneous’’ group and their pathogenesis is unclear. Their behaviour dictates their clinical presentation, varying from being an incidental finding on an x-ray in the case of a latent lesion to a rapidly growing, painful lesion associated with functional loss in the case of an aggressive lesion. This is reflected in Enneking’s classification.

Non-operative Asymptomatic lesions that fall into the Enneking latent group of tumours can simply be observed, for example the natural history of lesions such as non-ossifying fibromas and is well documented and predictable and it is safe to leave them alone. If the diagnosis has been made on imaging alone and non-operative treatment has been chosen, obviously histological confirmation of the diagnosis is not going to be available. Thus it is advisable to repeat the plain x-ray after three to six months to ensure that the tumour is showing no signs of progression. If radiological or clinical progression does occur, then there must be a low threshold for biopsy.

Aetiology The aetiology of the vast majority of benign bone tumours is unclear. Numerous theories have been proposed but none has

Rob Pollock BSc (Hons) FRCS (Tr & Orth) Consultant Orthopaedic Surgeon, Royal National Orthopaedic Hospital, Stanmore, UK.

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Classification of tumour by histological subtype Cell type

Tumour subtype

Chondrocyte

Enchondroma Osteochondroma Chondroblastoma Chondromyxoid fibroma Osteoid osteoma Osteoblastoma Giant cell tumour Periosteal chondroma Bizarre periosteal osteochondromatous proliferation Haemangioma Lipoma Leiomyoma Simple bone cyst Aneurysmal bone cyst Langerhans cell histiocytosis Fibrous dysplasia Osteofibrous dysplasia Fibrous cortical defect Non ossifying fibroma

Osteoblast Osteoclast Periosteum

Vascular Fat Smooth muscle Miscellaneous

Table 1

Curettage Curettage is the treatment of choice for the majority of benign bone tumours requiring surgical intervention. It is, by definition, intralesional surgery. The intention is to achieve macroscopically clear margins, accepting that microscopic disease is likely to be left behind. The technique involves exposing the affected bone and creating a bone window with osteotomes. The window needs to be big enough to obtain an adequate view of the tumour but small enough to ensure that the grafting material can be contained within the bone at the end of the procedure. It is helpful to use an image intensifier per-operatively to ensure that the curettage has cleared the entire lesion. After curettage, dependant on the histology of the tumour, its anatomical location of the tumour, the age of the patient, the

Figure 1 Fibrous cortical defect in the medial aspect of the proximal tibia.

likelihood of local recurrence and the risk of pathological fracture, the resulting cavity may be left unfilled or filled with iliac crest autograft, morcellised allograft, synthetic bone substitute or polymethylmethacrylate cement (PMMA). Additionally, the curetted bone can be augmented with internal fixation to prevent a pathological fracture (Figure 4). After curettage some tumours have a higher incidence of local recurrence than others, such as giant cell tumours, osteoblastomas, chondroblastomas and aneurysmal bone cysts. When treating these, it has been shown that using some form of

Classification of tumour by biological behaviour according to Enneking2 Classification

Behaviour

Example of tumour

Latent

Slow growth with spontaneous healing. Often incidental finding on x-ray. No treatment required Progressive growth over time and usually symptomatic. Treatment of choice; curettage. Low incidence of local recurrence Rapid growth of tumour often extending beyond periosteum into the soft tissues. Treatment of choice curettage or excision. 10e15% chance of local recurrence

Fibrous cortical defect, non ossifying fibroma,

Active Aggressive

Chondromyxoid fibroma, enchondroma, LCH, simple bone cyst Chondroblastoma, osteoblastoma, giant cell tumour, aneurysmal bone cyst

Table 2

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targeted thermal destruction of bone (Figure 3). Under general anaesthesia, guided by computerized tomography (CT), a Jamshedi needle is inserted percutaneously into the centre of the lesion. The radiofrequency wire is then passed down the needle and its position checked. When the device is switched on, heat is generated at the tip of the wire using microwave energy. The target temperature is 80e90 degrees Celsius and the duration of treatment is typically five to ten minutes. For lesions greater than 1 cm. in diameter two probes can be used. The advantage of RFA is that the tumour is treated with minimal destruction of surrounding bone and permits treatment of tumours in surgically inaccessible locations with minimal morbidity. In reality, the perceived disadvantage that a tissue diagnosis is rarely obtained doesn’t matter as the diagnosis is clear cut both clinically and radiologically. Excision and reconstruction Complete excision of a benign bone tumour is indicated when the tumour is particularly aggressive. This may manifest as bone expansion, bone destruction, extra-osseous extension of disease,

Figure 2 Osteochondroma arising from the medial aspect of the right distal femur. This presented as a painless lump with symptoms of impingement on the hamstring tendons.

adjuvant treatment reduces the risk of local recurrence.4 These include treating the cavity wall with a high speed burr, phenol, hydrogen peroxide or liquid nitrogen and filling the defect with PMMA. Which of these adjuvants is used depends on the surgeon’s preference, but the incidence of local recurrence after curettage of these more aggressive tumours is 10e15% even with adjuvant treatment. Radiofrequency ablation (RFA) RFA is the technique of choice for small, symptomatic lesions less than 1.5 cm in diameter e.g. osteoid osteomas. It causes

Curettage practice points C C C

C

C

Intralesional surgery leaving residual microscopic disease Image intensifier ensures clearance of tumour Adjuvant treatment to cavity reduces incidence of local recurrence Choice of filler depends on histology, location of tumour, age of patient and risk of fracture Internal fixation strengthens construct and helps prevent pathological fracture

a CT scan showing an osteoid osteoma in the femoral head. b CT guided radiofrequency ablation. Figure 3

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The surgical principles are similar to those used when treating a malignant bone tumour. The intention is to perform a marginal but complete excision and remove both macroscopic and microscopic disease. After a section of bone has been excised, some form of reconstruction will be necessary, which may be a biological reconstruction such as a vascularised fibula graft or a massive endoprosthesis (Figure 5). The reconstruction used is dependant on many factors, particularly anatomical location and the individual surgeon’s preferences.

Management of specific tumours Cartilage tumours Osteochondroma (synonym: exostosis) Osteochondromas are cartilage capped bony projections with a marrow cavity continuous with the underlying bone. They account for approximately 35% of all benign bone tumours and present within the first three decades of life.5 Most occur close to the physis of long bones but they can also arise from flat bones such as the scapula and pelvis. The commonest sites are the distal femur and proximal tibia, followed by the proximal humerus and proximal fibula. Symptoms are most commonly mechanical and caused by impingement of the osteochondroma on nearby tendons, especially around the knee. In about 15% of cases they are multiple, a condition known as diaphyseal aclasis (Figure 6), which in most of cases are familial and inherited as an autosomal dominant, but sporadic cases are well recognised. The genetic defect again appears to be in the tumour suppressor genes EXT1 and EXT2. Malignant transformation of a solitary osteochondroma into chondrosarcoma occurs in approximately 1% of cases and up to 3% patients with diaphyseal aclasis.5 The warning signs include rapid increase in size of an osteochondroma associated with increasing pain. Of particular concern are pelvic osteochondromas that may be large and silent until they transform. If there is any suspicion of malignant transformation the osteochondroma should be imaged with an MRI scan and the cartilage cap assessed. Cartilage caps greater than 1 cm suggest a high probability of malignant transformation. Surgical excision of osteochondromas is usually curative but it is important to excise the cartilage cap in its entirety or local recurrence is likely. In patients with diaphyseal aclasis it is impractical to excise every osteochondroma and surgery is reserved for those which are symptomatic, unsightly or which are suspicious for malignant transformation. Enchondroma Enchondromas are benign, intramedullary cartilage neoplasms which account for approximately 10e25% of all benign bone tumours and present at any age.5 They mainly affect the long bones and are most commonly solitary. The hands and feet are most commonly affected followed by the proximal humerus and proximal and distal femur. While enchondromas in the larger long bones such as the humerus or femur may be asymptomatic and discovered incidentally, the most common presentation is with a palpable swelling on the hands or feet. Pain may or may not be present and some are associated with a pathological fracture. The radiological features of enchondromas of the hands and feet are those of a well defined, radiolucent lesion exhibiting punctate mineralization, and may be associated with bone

a Plain x-ray showing a haemangioma of the proximal femur. The patient is at risk of pathological fracture. b Post-operative x-ray following curettage and internal fixation with a dynamic condylar screw and plate. Figure 4

pathological fracture or combinations of the above. If the tumour is subarticular, there may even be no alternative but to sacrifice the joint.

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enchondromas in the long bones of the hands, feet and limbs. When associated with soft tissue or visceral haemangiomas the condition is known as Mafucci syndrome (Figure 7). The aetiology is unclear; most cases are sporadic rather than inherited. The condition usually presents in early childhood with lumps in the hands and feet, limb deformity and/or multiple pathological fractures. Diagnosis is based on the clinical picture and x-ray appearances. Treatment is aimed at maintaining function, preventing deformity and careful surveillance in order to pick up malignant transformation early. The incidence of malignant transformation into chondrosarcoma is approximately 15e30% in patients with Ollier’s and probably even greater in those with Mafucii’s.6

Osteochondroma practice points C C C C C C

C

Commonest benign bone tumour Most commonly seen in the metaphyseal region of long bones Distal femur and proximal tibia are the commonest sites 15% cases are multiple Autosomal dominant inheritance 1% risk of malignant transformation in solitary cases (3% if multiple) Surgical excision if symptomatic, unsightly or suspicious for malignant transformation

Chondroblastoma Chondroblastoma is a cartilage producing tumour typically arising in the epiphysis of skeletally immature patients. There is a slight male preponderance. 75% occur in long bones and the commonest sites are the proximal and distal femur, the proximal tibia and the proximal humerus.7 Symptoms vary from mild pain of many years duration to recent onset of severe pain. Clinically, patients may develop an effusion in the hip or knee associated with stiffness. Plain x-rays show a well-defined, lytic lesion within the epiphysis and MRI

expansion. They are usually ‘‘hot’’ on bone scan. In larger bones chondral tissue is seen in the metaphyseal region. Lesions greater than 5 cm in length and causing endosteal scalloping on MRI should be considered as possible low-grade chondrosarcoma. The majority of enchondromas are successfully treated with curettage and the local recurrence rate is extremely low. Ollier’s disease and Mafucci syndrome Ollier’s disease is a developmental disorder characterized by multiple

a Lateral view of the wrist showing a GCT of the distal radius. b Axial T1 weighted MRI scan showing expansion of the distal radius with cortical thinning. The extensor tendons are closely applied to the pseudo-capsule of the lesion. c A free, vascularised fibula graft has been inserted with a paddle of soft tissue to aid wound closure. d One year post-operative x-ray showing complete bone union and successful wrist arthrodesis. Figure 5

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Figure 7 AP x-ray of the foot showing multiple enchondromas and a haemangioma in the 4th web space. These are the features of Mafuccci syndrome. Figure 6 Classic appearances of diaphyseal aclasis.

They are too small to biopsy and the diagnosis is made on the basis of clinical presentation and imaging. The findings of sclerosis on plain x-ray, high uptake on bone scan or single photon emission computed tomography (SPECT), a nidus on CT and the presence of oedema on MRI are enough to make the diagnosis. The treatment of choice is percutaneous, CT guided radiofrequency ablation described above.4 The success rate in most series is 90e95% after a single treatment and 100% after two treatments. The complication rate is extremely low.9

shows a sharply demarcated chondral lesion with surrounding oedema (Figure 8). Core needle biopsy will confirm the diagnosis. Curettage is the treatment of choice and is successful in 80e90%. Chondromyxoid fibroma This is one of the least common bone tumours. It most commonly affects the long bones, particularly around the knee, of patients in their second and third decades. The clinical presentation is very similar to a chondroblastoma and the treatment and prognosis is also the same.

Osteoblastoma This is a rare, bone forming tumour that typically affects young adults aged 10e30 years. It is twice as common in men as women. Over 50% of cases affect the posterior elements of the spine, pelvis or the sacrum (Figure 9). In the rest of the skeleton the proximal and distal femur and the proximal tibia are the commonest sites.10 The clinical features are similar to those of an osteoid osteoma i.e. chronic pain. Imaging reveals a well defined, lytic lesion somewhere between 3 and 10 cm in diameter. Some osteoblastomas are associated with aneurysmal bone cyst (ABC) change. Osteoblastomas can be hard to differentiate from osteoblastic osteosarcoma and thus core needle biopsy is recommended before definitive treatment is carried out. The treatment of choice is curettage and cementation. The prognosis is good and the incidence of local recurrence after curettage is low.

Bone tumours Osteoid osteoma This is a small, bone forming tumour which can occur in any bone but is most commonly seen in the proximal femur (See Figure 3). It usually affects skeletally immature patients but it is also seen in young adults. Histologically the features are the same as an osteoblastoma.8 The clinical presentation is classic with a history of constant, unremitting pain often worse at night, which usually responds to aspirin and non-steroidal anti-inflammatory drugs (NSAIDs). The site of the lesion often determines the clinical findings; in the spine it may cause scoliosis, in fingers it may cause significant swelling and loss of function and if the lesion is subarticular, it may cause a joint effusion. The differential diagnosis includes Brodie’s abscess, stress fracture or subtle area of osteomyelitis.

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a MRI scan showing the classic appearance of a chondroblastoma. b Post-operative x-ray following curettage. Figure 8

Giant cell tumour Giant cell tumours (GCT) are locally aggressive lesions which account for about 20% of all benign bone tumours. They occur in adults between the ages of 20 and 40 years with a slight female preponderance. They affect the metaphyseal regions of the long bones and are commonest in the distal femur, proximal tibia, proximal humerus and distal radius. About 5% of GCTs affect the flat bones especially those of the pelvis. Patients usually present with a short history of pain, swelling and functional loss. Plain x-rays show a lytic lesion with

a narrow zone of transition extending to the sub-articular surface. MRI reveals a haemosiderin rich lesion with low to intermediate signal on T1 weighted images and high intensity on T2 weighted images (Figure 10). Campanacci classified GCTs according to their radiological appearance.11 Type 1 or quiescent tumours have a well-defined margin, surrounding sclerosis and no cortical involvement. Type 2 or active tumours lack surrounding sclerosis and demonstrate cortical expansion but are still well-defined. Type 3 or aggressive tumours have ill-defined margins, show cortical destruction and extend into the soft tissues. The differential diagnosis includes hyperparathyroidism, aneurysmal bone cyst and telangiectatic osteosarcoma and thus again core needle biopsy is essential. Treatment of GCTs depends on the anatomical location, the aggressiveness of the tumour clinically and radiologically, and the functional expectations of the patient. If the joint can be saved, the initial treatment of choice is curettage with some form of adjuvant treatment and cementation with PMMA. If the lesion is very destructive, i.e. Campanacci type 3 tumour or if there is a pathological fracture or if a joint is involved then, wide excision may be necessary. Following a wide excision, tumours around the knee are best reconstructed with a massive endoprosthesis to allow immediate weight bearing and early recovery of function. Tumours around the wrist are better treated with a vascularised fibula graft with or without wrist fusion12 (See Figure 5). The incidence of local recurrence after curettage in most series is 10e15% and usually occurs within the first two years.4,12,13

Figure 9 CT scan of the pelvis showing a lytic lesion in the posterior ilium. Biopsy confirmed the diagnosis of osteoblastoma and the lesion was curetted.

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a Plain x-ray showing a giant cell tumour of the proximal tibia. Note the narrow zone of transition and extension of tumour up to the sub-chondral region. b MRI scan showing classical appearances of a GCT. Figure 10

Some studies have suggested that bisphosphonates post-operatively may reduce the incidence of local recurrence.14 Despite them being histologically benign, pulmonary metastases are seen in up to 2% of patients with giant cell tumours, on average three to four years after diagnosis. Most grow slowly, some regress and some progress leading to the death of the patient. True malignant transformation of a giant cell tumour is extremely rare.

unclear. They fall into the latent category by Enneking’s classification and are most commonly seen as an incidental finding in skeletally immature patients. They are rarely symptomatic and can be safely observed. Occasionally a large non-ossifying fibroma can cause a stress fracture in the adjacent bone in which case curettage and internal fixation are indicated. Simple bone cyst (synonym: unicameral bone cyst) Simple bone cysts (SBC) are fluid filled, metaphyseal cysts of unclear aetiology. They are most commonly seen in the fist two decades of life with a male to female ratio of 3:1. The proximal femur, proximal tibia and proximal humerus account for 90% of cases.15 Most patients present with a pathological fracture after minimal trauma (Figure 11). Plain X-rays are diagnostic and show a metaphyseal lucency often extending into the diaphysis but never involving the epiphysis. The cortex is usually thin and may be mildly expanded but never beyond the width of the physis. If a fracture is present a ‘‘fallen fragment’’ sign may be seen. Numerous methods of treating SBCs have been described including; aspiration and injection with steroid, injection with bone marrow, inserting a cannulated screw to decompress the cyst, fixation with Nancy nails and curettage combined with internal fixation.16 Even after curettage recurrence rates of 10e20% are reported. By the time the patient is skeletally mature the cyst will have healed. The treatment modality chosen depends partly on the anatomical location of the cyst. Cysts of weight bearing bones such as those in the femoral neck are more

Miscellaneous lesions Non-ossifying fibroma/fibrous cortical defect By convention, a fibrous cortical defect measures less than 1 cm in diameter and a non-ossifying fibroma is larger than 1 cm but histologically these two conditions are identical (Figure 5). Their aetiology is

GCT practice points C C C

C C C C

Locally aggressive Distal femur, proximal tibia, proximal humerus, distal radius Differential diagnosis ABC, telangiectatic osteosarcoma, hyperparathyroidism Campanacci types 1, 2 & 3 Treat with curettage and some form of adjuvant 10e15% local recurrence rate Bisphosphonates may reduce incidence of local recurrence

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Figure 11 Typical x-ray appearance of a simple bone cyst. Note the mild expansion but not wider than the physis. Figure 12 Plain x-ray showing an aneurysmal bone cyst. Note that the bone is expanded beyond the width of the physis.

frequently curetted, grafted and internally fixed than those in the non- weight bearing bones.

Patients present with pain and swelling and the imaging features may be aggressive. The differential diagnosis includes osteomyelitis and Ewing’s sarcoma and thus biopsy is essential. Treatment varies from surveillance through to curettage and for those with multiple sites of disease, chemotherapy.

Aneurysmal bone cyst Aneurysmal bone cysts (ABC) are multilocular, expansile, aggressive, destructive lesions that may expand into the soft tissues. They are most common in the first two decades of life and typically affect the metaphyseal regions of the long bones (Figure 12). They can arise de novo or they can complicate other benign tumours i.e. they show ‘‘ABC change’’. Most patients present with a short history of pain and swelling. The characteristic radiological findings are those of an eccentric, expansile, well-defined, lytic lesion on plain x-ray with the presence of multiple fluid-fluid levels on MRI. The differential diagnosis includes giant cell tumour and telangiectatic osteosarcoma. Biopsy should be attempted although, frequently, only blood clot is obtained. The majority of ABCs are suitable for curettage and grafting. They can be extremely vascular and it is advisable to perform arteriography and embolisation pre-operatively in lesions where a tourniquet cannot be used. Local recurrence occurs in approximately 25% and is usually apparent within a year of surgery.17 ABCs at the aggressive end of the spectrum may require marginal but complete excision.

Fibrous dysplasia Fibrous dysplasia (FD) is a developmental abnormality rather than a tumour and may affect any bone. Clinical presentation with pain, deformity or pathological fracture can occur at any age. It may be monostotic or polyostotic. McCune-Albright syndrome is polyostotic FD, pigmented skin lesions resembling ‘‘the coast of Maine’’ and endocrinopathy. X-ray appearances are diagnostic showing a ground glass appearance of the affected bone. ABC change can occur. Treatment is aimed at symptom control. Bisphosphonates have been shown to be effective in reducing pain.18 Surgery is reserved for pathological fractures or severe deformity. Osteofibrous dysplasia Osteofibrous dysplasia (OFD) is a slow growing, fibro-osseous lesion classically affecting the cortical bone of the tibial diaphysis. It is most commonly seen in skeletally immature males. Presentation varies from an incidental finding to a painful deformity. It is usually self limiting and spontaneous healing often occurs. The differential diagnosis includes adamantinoma; a low-grade malignant lesion with similar radiological appearances. Indeed there is controversy as to whether OFD has the potential to transform into adamantinoma, but others think they are two separate entities. A

Langerhans cell histiocytosis. (Synonyms: Histiocytosis X, Eosinophilic granuloma) Langerhans cell histiocytosis (LCH) is a rare disorder that can affect any bone and be monostotic or polyostotic. Visceral structures can also be involved. There is a wide age range from the first to the eighth decade but 80% of patients are under thirty.

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REFERENCES 1 Dorfman H, Vanel D, Czerniak B, Park Y, Kotz R, Unni K. WHO classification of bone tumours. In: Fletcher C, Unni K, Mertens F, eds. World Health Organization classification of tumours. Pathology and genetics of tumours of soft tissue and bone. Lyon: IARC Press; 2002. p. 226e32. 2 Enneking W. Musculoskeletal tumor surgery, vol. 1. New York: Churchill Livingstone; 1983. 1e60. 3 Mankin H, Lange T, Spanier S. The hazards of biopsy in patients with malignant primary bone and soft tissue tumors. J Bone Joint Surg 1982; 64A: 1121e7. 4 Balke M, Schremper L, Gebert C, et al. Giant cell tumor of bone: treatment and outcome of 214 cases. J Cancer Res Clin Oncol 2008; 134(9): 969e78. 5 Unni K. Dahlin’s bone tumors: general aspects and data on 11,087 cases. Philadelphia: Lippincott-Raven; 1996. 6 Schwartz H, Zimmerman N, Simon M, Wroble R, Miller E, Bonfiglio M. The malignant potential of enchondromatosis. J Bone Joint Surg Am 1987; 69: 269e74. 7 Springfield D, Capanna R, Gherlinzoni F, Picci P, Campanacci M. Chondroblastoma. A review of seventy cases. J Bone Joint Surg Am 1985; 67: 748e55. 8 Klein M, Parisien M, Schneider-Stock R. Osteoid osteoma. In: Fletcher C, Unni K, Mertens F, eds. World Health Organization classification of tumours. Pathology and genetics of tumours of soft tissue and bone. Lyon: IARC Press; 2002. p. 260e1. 9 Lindner N, Ozaki, Roedl R, Gosheger G, Winkelman W, Worler K. Percutaneous radiofrequency ablation in osteoid osteoma. J Bone Joint Surg 2001; 83(3): 391e6. 10 Malcolm A, Schiller A, Schneider-Stock R. Osteoblastoma. In: Fletcher C, Unni K, Mertens F, eds. World Health Organization classification of tumours. Pathology and genetics of tumours of soft tissue and bone. Lyon: IARC Press; 2002. p. 262e3. 11 Campanacci M, Baldini N, Boriani S, Sudanese A. Giant-cell tumor of bone. J Bone Joint Surg Am 1987; 69: 106e14. 12 Pollock R, Stalley P, Lee K, Pennington D. Free vascularized fibula grafts in limb salvage surgery. J Reconstr Microsurg 2005; 21(2): 79e84.

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13 Meldenhall W, Zlotecki R, Scarborough M, Gibbs C, Meldenhall N. Giant cell tumor of bone. Am J Clin Oncol 2006; 29(1): 96e9. 14 Tse L, Wong K, Kumta S, Huang L, Chow T, Griffith J. Bisphosphonates reduce local recurrence in extremity giant cell tumour of bone: a case control study. Bone 2008; 42(1): 68e73. 15 Kalil R, Araujo E. Simple bone cyst. In: Fletcher C, Unni K, Mertens F, eds. World Health Organization classification of tumours. Pathology and genetics of tumours of soft tissue and bone. Lyon: IARC Press; 2002. p. 340. 16 Wilkins R. Unicameral bone cysts. J Am Acad Orthop Surg 2000; 8(4): 217e24. 17 Kransdorf M, Sweet D. Aneurysmal bone cyst: concept, controversy, clinical presentation and imaging. AJR Am J Roentgenol 1995; 164(3): 573e80. 18 DiMeglio L. Bisphosphonate therapy for fibrous dysplasia. Pediatr Endocrinol Rev 2007; 4(Suppl 4): 440e5. FURTHER READING Fletcher C, Unni K, Mertens F, eds. World Health Organization classification of tumours. Pathology and genetics of tumours of soft tissue and bone. Lyon: IARC Press; 2002.

Research directions C

C

C

257

Phase 2 clinical trial studying the use of Denosumab in the management of GCTs. This agent is a monoclonal antibody that targets the RANK ligand, part of the signaling pathway that stimulates osteoblasts Use of novel bone substitutes to promote bone healing after curettage Molecular genetic studies to identify genes and chromosomal aberrations responsible for these tumours

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(v) The non-surgical management of musculoskeletal malignancy

and lung. The incidence of bone metastases varies depending on the site of the primary cancer. It occurs in approximately 70% of patients with prostate and breast cancer and 30% of patients with lung, bladder and thyroid cancer. Patients may present with bone metastases or they may become apparent during treatment. Bone metastases can cause significant morbidity which adversely impacts on the patient’s quality of life and survival. The most frequent cause of pain in cancer patients is metastatic bone lesions. ‘Skeletal Related Events’ (SRE) help to objectively measure the impact of bone metastases and are frequent end points which are measured in clinical studies. These events include pain, pathological fracture, hypercalcaemia, spinal cord compression, need for palliative radiotherapy or surgical intervention.2 The aim of all palliative treatment for bone metastases should be pain relief, preservation of function and skeletal integrity. There are two different, but by no means exclusive, approaches to treatment: 1) treating the underlying malignancy 2) palliating the symptoms of SRE. Chemotherapy, radiotherapy, hormone treatment and biological agents are modalities which can actually reduce the burden of cancer cells which in some cancers can help improve survival as well as improve symptoms and quality of life. Treatment is different for each cancer subtype and will also vary for each individual patient depending on patient choice, performance status and previous treatments. Simple analgesia, bisphosphonates, radiotherapy, radiological interventions and surgery are treatment modalities to help improve symptoms and quality or life but do not generally reduce the burden of malignancy or improve survival (Table 1).

Claire Esler

Abstract Metastatic bone disease is a common clinical problem that requires a multidisciplinary approach in order to reduce patient suffering and maintain quality of life. Almost all patients with metastatic bone disease will have incurable cancer and this needs to be remembered when considering how to treat these patients. Conversely primary musculoskeletal cancers are rare conditions that need to be managed by specialist centres. Multimodality treatment is needed which may last for many months and may be associated with considerable toxicity. Patients with localised disease can possibly be cured but those with sarcoma remain with a guarded prognosis.

Keywords bisphosphonates; bone metastases; chemotherapy; Ewing’s sarcomas; osteosarcoma; radiotherapy; soft tissue sarcoma

Introduction Musculoskeletal malignancy can be divided up into two main categories: 1) primary malignancy including osteosarcomas, Ewing’s sarcoma, chondrosarcoma, solitary plasmacytoma, primary bone lymphoma and soft tissue sarcomas etc. 2) secondary malignancy i.e. bone metastases. The incidence of metastatic bone disease is far higher than that of both primary bone malignancy and soft tissue sarcomas (STS).1 Whereas the treatment of these two groups is vastly different, what is crucially important is that both need a multidisciplinary approach to the diagnosis, treatment and ongoing management. It is not unusual for a patient with a musculoskeletal malignancy, primary or secondary, to require the input of specialist nurses, medical and clinical oncologists, orthopaedic surgeons, spinal surgeons, plastic surgeons, radiologists, pathologists, palliative care teams, occupational and physio therapists etc. This review will cover the basic non-surgical, oncological management of bone metastases, primary bone tumours and extremity soft tissue sarcomas. However, a thorough discussion of all these topics is beyond the scope of this article.

Palliative radiotherapy for bone metastases There are three ways of using radiation therapy to treat bone metastases: local external beam radiotherapy, hemi-body radiotherapy and radiopharmaceuticals.

Local external beam radiotherapy Local external beam radiotherapy is a reliable and effective modality for treating bone metastases. It is an outpatient treatment and is generally well tolerated. The definition of response to radiotherapy varies, however there are consistent reports of partial response rates of approximately 70e80% and complete responses 30e40%. Many different radiotherapy fractionation schedules have been reported. In the UK a single 8 Gy fraction or 20 Gy in 5 fractions are the most commonly used schedules. There is an abundance of level 1a evidence including three recent metanalyses3e5 that conclude that shorter fractionation schedules are as effective as longer schedules in controlling pain. Single fraction treatment is far easier on a frail patient where quality of life is paramount. The need for retreatment is higher in the shorter schedules and the greater the dose per fraction, the ‘‘potentially’’ higher the risk of significant late toxicity. The review by Sze et al. showed a higher fracture rate after a single fraction of radiotherapy but the absolute frequencies were very low. There is a tendency for oncologists to prescribe longer fractionation schedules for those patients in whom the prognosis indicates survival for several years. This reduces the need for retreatment

Metastatic bone disease Metastases are a frequent sequelae of malignancy with bone being the third most common site of metastatic disease after liver

Claire Esler BMedSci BMBS MRCP MMedSci FRCR Consultant Clinical Oncologist at the Department of Oncology, Leicester Royal Infirmary, Infirmary Square, Leicester, LE1 5WW, UK.

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Table demonstrating the treatment options for patients with bone metastases General

Systemic treatment

Radiotherapy

Surgery

Radiological

Analgesia

Chemotherapy

Prophylactic internal fixation

Cementoplasty

Palliative care Multidisciplinary Care Input

Hormone therapy Biological agents Bisphosphonates Novel bone targeting biological agents

Localised external beam radiotherapy Hemibody irradiation Radioisotopes

Fracture Stabilisation Spinal cord decompression

Vertebroplasty Radiofrequency ablation

Table 1

and limits late toxicity. An example of this would be a patient with breast cancer and bone metastases as the only site of metastases. However, there is little evidence to support this practice and for the majority of such patients, a single 8 Gy fraction is entirely appropriate. It usually takes at least one week before any relief in pain and response may subsequently increase until a plateau is reached at 4e6 weeks. Radiotherapy to bone metastases is well tolerated especially in long bones where there is little normal tissue to be damaged. If large volumes of the pelvis or thoraco-lumbar spine are treated, acute toxicity from the small bowel may cause nausea and diarrhoea. Pain flare is defined as temporary worsening of pain in an irradiated bone metastatic site immediately after radiotherapy. Reported rates of bone flare range from 2e44%.6 Fractures should be internally fixed or where there is a significant risk of pathological fracture secondary to bone metastasis, prophylactic internal fixation is recommended prior to radiotherapy. This is considered standard care in the UK despite little evidence to support this practice. A single 8 Gy fraction is usually appropriate post-operatively. In patients with a very poor life expectancy and deteriorating condition surgery may be inappropriate and palliative radiotherapy alone may help to reduce pain and aid healing. There are varying opinions about what volume should be irradiated after a long bone has had surgical fixation. One argument is to irradiate the entire long bone on the basis that the marrow cavity may have been contaminated with tumour cells at the time of surgery. The alternative is to only irradiate the prosthesis plus a margin as this is the area most at risk of residual tumour and hence recurrence. It is the author’s preference to irradiate the entire bone if possible although this is based only on personal experience. Patients may present with a pathological fracture as their first manifestation of malignancy and it is always important to send bone reamings for histological diagnosis. Even when a patient is known to have a malignancy occasionally a second malignancy is identified and this may alter future treatment decisions.

unsatisfactory results. HBI can be an alternative option for such patients. HBI was traditionally considered as upper or lower hemibody radiotherapy with the ‘‘cut off’’ at the umbilicus. Nowadays it is planned as a large field of external beam radiotherapy covering the areas of painful bone metastases either in the upper or lower body. A typical linear accelerator will be able to produce a radiation field size of 40  40 cm. Treatment to the upper hemibody is 6 Gy in a single fraction and to the lower hemibody is typically 8 Gy in a single fraction. HBI has also been shown to delay the appearance of new painful bone metastases in the treatment field.7 When treating large volumes with radiotherapy, acute toxicity can be a major problem especially gastrointestinal toxicity and bone marrow toxicity. Prophylactic 5HT3 antagonist antiemetics e.g. ondansetron, and monitoring of a full blood count are usually necessary. The response to HBI is similar to that seen in localised radiotherapy with a 60e70% improvement in pain. In 25% of patients a rapid response to pain is seen within twenty four hours.

Radioisotopes Strontium 89 (89St) is a bone targeting radioisotope which, when administered intravenously, localizes to areas of osteoblastic bone activity.8 It is a beta admitting radioisotope with a half life of 50.5 days. Prostate cancer patients with widespread, predominantly osteoblastic metastases are ideal candidates for this therapy. It is used to treat pain not controlled by other treatments. 89St can cause significant bone marrow toxicity and should not be given to bone marrow suppressed patients. The onset of pain relief occurs seven to twenty days after injection. Doses can be repeated after three months. 89St needs to be handled by radiation oncologists who are experienced with its use and the associated radioprotection issues. Financial cost limits it use in the UK. Bisphosphonates Bisphosphonates are a group of compounds that are stable analogues of naturally occurring inorganic pyrophosphate. They are potent inhibitors of osteoclast mediated bone resorption and effect the cells in the bone microenvironment. Bisphosphonates also have a direct effect on cancer cells by inhibiting tumour cell invasion and adhesion to bone matrix. In animal models bisphosphonates can inhibit development of bone metastases and there are ongoing trials in humans looking at the role of bisphosphonates in preventing bone metastases.

Hemi-body irradiation (HBI) Bone metastases are frequently multiple and patients may complain of poorly localised pain that flits around. Attempts to ‘‘chase’’ the cause of pain may lead to multiple visits to the radiotherapy department for localised radiotherapy with

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There are three generations of bisphosphonates available; from first generation clodronate to second generation pamidronate and more recently third generation zoledronic acid and ibandronate. With increasing generations of bisphosphonates the in-vitro potency significantly increases. Many studies have confirmed the effectiveness of bisphosphonates in treating hypercalcaemia of malignancy and in preventing skeletal related events in patients known to have bone metastases (secondary prophylaxis). Most supportive evidence is for patients with breast cancer, multiple myeloma and prostate cancer. A systematic review by Ross et al.9 included 21 randomised controlled trials (RCTs) of patients with bone metastases from myeloma and solid malignancies (predominantly breast and prostate cancer). Primary end-points were time to first SRE and reduction in skeletal morbidity. It did not assess pain relief. The risk of non-vertebral fracture, vertebral fracture, need for radiotherapy and hypercalcaemia was significantly improved compared with patients receiving radiotherapy. There was no benefit seen with regards to spinal cord compression. Time to SRE was also reduced with bisphosphonates. The review concluded that patients needed to be on bisphosphonates for at least twenty four months before significant reductions in the need for orthopaedic surgery were seen, twelve months before hypercalcaemia and non-vertebral fractures were reduced, and six months before there was a reduction in the need for radiotherapy. Studies giving less than six months of bisphosphonates showed no significant benefit in any end-point. Treating patients with a prognosis of less than six months, is probably not beneficial or cost-effective. Evidence for the use of bisphosphonates for pain control from bone metastases is inconsistent. A Cochrane review concluded there was sufficient evidence to support the effectiveness of these drugs in providing some pain relief for bone metastases but that there was insufficient data to recommend them as first line treatment. There was insufficient data to conclude which bisphosphonate was most efficacious or to say which primary tumour type responded most.

bisphosphonates. Intravenous pamidronate, zoledronic acid and ibandronate and oral ibandronate have all been shown to reduce SRE. As an oral agent ibandroante is logistically and economically easier to give to large numbers of patients as it does not require a hospital day case attendance for intravenous infusions. Recent NICE guidelines for advanced breast cancer state that clinicians should consider offering bisphosphonates to patients with newly diagnosed bone metastases to prevent SRE and reduce pain. NICE does not make recommendations on which bisphosphonate to use.

Bisphosphonates in breast cancer Approximately 70% of patients with advanced breast cancer will develop bone metastases. They are predominantly osteolytic but osteoblastic metastases may also be present. Untreated, 50% of these patients will have an SRE, 40% will sustain a pathological fracture and an even greater percentage will have problems with severe pain. Systemic treatment options for metastatic breast cancer patients with bone metastases include analgesia, hormone treatments, chemotherapy, biological agents e.g trastuzumab, and bisphosphonates. Bisphosphonates are considered the normal standard of care for breast cancer patient with bone metastases who have a reasonable prognosis. Grade 1 evidence from five RCTs and three systematic reviews conclude that bisphosphonates reduce the risk of predefined SRE. The Cochrane review reported a 17% reduced risk of SRE and a delay in median time to first SRE in patients taking bisphosphonates as secondary prophylaxis in bone metastases.10 There was no benefit seen in overall survival in patients taking

Bisphosphonates in prostate cancer Skeletal metastases from prostate cancer are usually osteoblastic. It was initially thought that purely osteoblastic/sclerotic bone metastases would not respond to bisphosphonates. It is now known that there is an element of increased bone resorption in metastatic prostate cancer.This probably explains the response seen to zoledronic acid which is the only bisphosphonate that has demonstrated clinical benefit in reducing SRE in this patient group.12 Compared to placebo, three weekly intravenous doses of zoledronic acid reduced the risk of SRE by 11% and significantly prolonged the time to first SRE by 5.5 months.

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Bisphosphonates in myeloma Myeloma is a malignancy of plasma cells which is characterised by osteolytic bone destruction throughout the skeleton resulting in pain, pathological fractures and hypercalcaemia. Interleukin 1 and 6, tumour necrosis factor and receptor for activation of nuclear factor kappa B ligand are all cytokines produced by the myeloma cells and the stroma of the bone marrow. These cytokines help stimulate osteoclastic resorption of bone without accompanying bone formation leading to purely osteolytic metastases. Berenson et al. looked at myeloma patients with at least one lytic bone lesion and randomised them to four weekly intravenous pamidronate infusions or placebo for nine cycles. In addition, first or second line myeloma chemotherapy was given.11 Time to first SRE and percentage of patients sustaining a SRE were significantly reduced in the patients receiving a bisphosphonate (41% of patients in the placebo group versus 24% in the pamidronate group) Bone pain was significantly reduced with pamidronate but there was no difference in overall survival between the two groups. The benefit of long term use of bisphosphonates has now been confirmed. The incidence of osteonecrosis of the jaw is higher in myeloma patients compared to patients with other malignancies receiving bisphosphonates. Zoledronic acid is perceived to have a higher risk of osteonecrosis of the jaw than other bisphosphonates and recent guidelines from the USA have recommended against the use of zoledronic acid in myeloma patients.

Bisphosphonates in other solid malignancies There is less evidence on the efficacy of bisphosphonates in other types of malignancy. In the UK only patients with breast, prostate cancer and myeloma patients are routinely prescribed bisphosphonates. However, a large RCT comparing zoledronic acid with palcebo in patients with lung cancer, renal cancer and a variety of other primary cancers did conclude that zoledronic

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acid was beneficial.13 A significantly lower proportion of patients receiving zoledronic acid had an SRE and in those that did, there was a longer time to first SRE. Lung cancer patients receiving zoledronic acid from this trial had a non-significant reduction of SRE’s. However, when hypercalcaemia was included as an SRE for the purposes of analysis, the reduction in SRE with zoledronic acid became significant. Based on these data, zoledronic acid is the only bisphosphonate to have worldwide regulatory approval for patients with bone metastases from solid tumours other than breast cancer.

years old there are new guidelines addressing where they should have their non-surgical oncological treatment. They should be offered treatment in an oncology centre where there is a specialised teenage and young adult oncology department. For some patients this may mean travelling a significant distance. Until the 1970’s surgical resection, which usually meant amputation, was the sole radical treatment for osteosarcoma. Despite good local control, 80e90% of patients subsequently died of metastatic disease. It was thought, and has subsequently been demonstrated, that the majority of osteosarcomas have subclinical micrometastases at the time of presentation and that a systemic approach to treatment is required. Two randomised controlled trials in the1980s confirmed a survival benefit with adjuvant chemotherapy in high grade localised osteosarcoma.14,15 There is still uncertainty about whether preoperative (neoadjuvant) or post operative (adjuvant) chemotherapy is superior. The theoretical benefits of neoadjuvant chemotherapy are: that treatment starts immediately allowing time for a customized endoprosthesis to be made, micrometastases can be treated earlier, the tumour may shrink making surgery easier and allowing improved limb sparing surgery, chemotherapy may sterilize the surgical bed making contamination less of a problem at the time of surgery and it allows assessment of the tumour response to chemotherapy which is an important prognostic feature. The risks of neoadjuvant chemotherapy are that it delays definitive treatment and if the cancer does not respond to chemotherapy a potentially curable cancer may become inoperable. Neoadjuvant chemotherapy allows an in-vivo drug trial to determine the chemosensitivity of the tumour. A good response is defined as 90% or greater cell necrosis and this indicates a five year survival between 71e80%. In patients with less tumour necrosis the 5 year survival rate is between 45e60%. The POG trial 8651 randomised patients with high grade osteosarcoma to surgery and adjuvant chemotherapy or 10 weeks of neoadjuvant chemotherapy then surgery. There was no statistically significant difference between five year recurrence free survival in the two arms, 65% for the adjuvant arm versus 61% in the neoadjuvant arm.16 Currently the standard treatment for patients with localised high grade osteosarcoma is two to three cycles of cisplatin and doxorubicin and high dose methotrexate followed by limb preserving surgery followed by a further three or four cycles of the same chemotherapy. The benefit of adding in high dose methotrexate is controversial although there seems to be more benefit in younger patients. This combination chemotherapy is a highly toxic regimen which needs to be given as an inpatient via a central line (Table 2). There are two questions that are currently being addressed in the EURAMOS study, which is an international phase 3 RCT looking at patients under the age of forty with localised high grade osteosarcoma. The first question is whether changing chemotherapy drugs in patients with less than 90% necrosis after two cycles of neoadjuvant cisplatin, doxorubicin and methotrexate improves survival. These patients are randomised to either continue with the same chemotherapy or to switch to ifosfamide and etoposide chemotherapy. The second question is whether maintenance treatment with interferon after the completion of standard treatment can improve survival. Patients

Urinary markers One of the major difficulties in comparing the results of trials that look at different treatments for bone metastases is the varying primary end-points. End-points include assessment of SRE, pain scores, pain relief, need for narcotic analgesia etc. Similarly the timing of these assessments is not consistent. Radiological assessment of bone metastases can also be misleading, as response to treatment may induce a sclerotic reaction which can make the radiological appearance look like apparent progressive disease. Biochemical surrogate markers have therefore been sought to try and make assessment more objective. Urinary and blood markers of bone remodelling that have been shown to be useful in assessment of bisphosphonates include pyridinoline and deoxypyridinoline, N-telopeptide and C-telopeptide. New agents to treat bone metastases Denosumab is a fully humanised monoclonal antibody that binds to and neutralises RANK ligand, resulting in inhibition of osteoclast function and bone resorption. Phase III RCTs comparing denosumab and bisphosphonates in patients with metastatic bone disease are ongoing.

Primary musculoskeletal tumours Malignant primary bone and connective tissue tumours are rare, accounting for about 1e2% of all new cancers diagnosed in the UK each year. In 2005 1988 people in the UK were diagnosed with a primary bone or connective tissue malignancy.1 The treatment of soft tissue sarcoma is very different from the treatment of primary bone tumours. Similarly the treatment of each type of primary bone tumour is different. For the purposes of this review the main principles for the more common primary musculoskeletal tumours will be discussed. Primary bone malignancies Less than 0.2% of all cancers are primary bone malignancies. The most common is osteosarcoma. Other histological types include Ewing’s sarcoma, chondrosarcoma, chordoma, solitary plasmacytoma and primary lymphoma. In England all patients presenting with a suspected primary bone sarcoma should be referred to one of the specialist bone sarcoma centres for their surgical treatment. Tumours such as osteosarcoma and Ewing’s sarcoma should ideally be treated in clinical trials in order to standardise treatments, improve outcomes and help to establish new treatments.

Osteosarcoma There are two peaks in the age-related incidence of osteosarcoma. The first and largest is in adolescents and young adults and a second smaller peak in older adults. For patients under 24

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Table showing the more common and serious toxicities from chemotherapy regimens used to treat sarcoma patients Doxorubicin

Doxorubicin D Ifosfamide

VIDE

Doxorubicin D cisplatin

Sarcoma type Soft tissue sarcoma Common toxicities Nausea, Vomiting, Sore mouth, Alopecia, Neutropenic sepsis, Thrombocytopenia Anaemia, Diarrhoea, Fatigue, Skin necrosis, Nail changes.

Soft tissue sarcoma As Doxorubicin þ CNS toxicity

Rare but serious toxicities

As Doxorubicin þ Bladder, renal and liver toxicity, Infertility, Second malignancy.

Ewing’s sarcoma Nausea, Vomiting, Sore mouth, Alopecia, Neutropenic sepsis, Thrombocytopenia Anaemia, Diarrhoea, Constipation Fatigue, Skin necrosis if leakage, Nail changes, CNS toxicity. Cardiotoxicity, Infertility, Bladder, renal and liver toxicity, Second malignancy

Osteosarcoma Nausea, Vomiting, Sore mouth, Alopecia, Neutropenic sepsis, Thrombocytopenia, Anaemia, Diarrhoea, Renal impairment, Hearing loss, Peripheral nerve toxicity, Nail changes, Fatigue, Skin necrosis. Cardiotoxicity, Infertility, Liver toxicity.

Cardiotoxicity, Infertility, Liver toxicity.

VIDE: vincristine, ifosfamide, doxorubicin and etoposide. CNS: central nervous system.

Table 2

Ewing’s sarcoma Ewing’s sarcoma is the second commonest primary bone malignancy in childhood and adolescence. The issues about treating in a specialist paediatric or teenage and young adult department apply as in osteosarcoma. Ewing’s sarcoma is a tumour that has arisen from the neural crest and is one of the small, round blue cell tumour types. The actual diagnosis can be confirmed by cytogenetic testing, a translocation between the part of the EWS gene on chromosome 22 and part of the ETS transcription factors. In 85% of cases it is a (11:22) translocation resulting in the gene fusion of EWS and FLI1. Ewing’s sarcoma is a systemic disease. Without systemic treatment more than 90% of patients die from secondary metastases.17 Since the 1970’s aggressive chemotherapy has increased survival rates to 55e65% for local disease and up to 35% in primary metastatic disease. The actual treatment a patient receives depends on the site of the primary and the presence and distribution of any metastatic disease. Most patients, treatment will consist of six cycles of in-patient vincristine, ifosfamide, doxorubicin and etoposide (VIDE) chemotherapy. If they have localised operable disease, then they will have surgery and or radiotherapy followed by further chemotherapy. If there is more than 90% necrosis of the tumour after initial chemotherapy, the prognosis is improved compared to patients where they have less than 90% necrosis. Further chemotherapy decisions are depend on this tumour necrosis. Ewing’s sarcoma is a far more radiosensitive tumour than osteosarcoma and most soft tissues sarcomas. Lower doses of radiotherapy are needed, usually around 50e55 Gy. If the position of the primary tumour makes surgery impossible then radiotherapy alone without surgery can be used as radical treatment to the primary. Patients with metastatic disease at presentation have a very poor prognosis with five year survival often significantly less than 25%. The prognosis depends on the site of metastases with lung only metastases doing better than those patients who have

who have a good response to chemotherapy are randomised to two years of interferon or observation. Osteosarcoma is a relatively radioresistant malignancy. Unlike soft tissue sarcomas and Ewing’s sarcoma adjuvant radiotherapy has a very small role in the treatment of osteosarcomas. The only indication for adjuvant radiotherapy is after an incomplete surgical resection when further surgery is not possible. The most common sites of metastases in osteosarcoma are lung and bone. The presence of bone metastases is a dismal prognostic feature. The only potential for long term survival for patients with lung metastases is metastatectomy and chemotherapy and this should at least be considered in all patients with disease confined to the thorax. The number of metastases resected depends on the distribution of the lesions and the underlying lung function. Five year survival of 30% can be obtained with this multimodality approach. Radiofrequency ablation (RFA) is a new method for treating lung metastases and has been used in sarcoma patients with good early results. It is a minimally invasive technique which is used when surgical resection is not an option. An electrode is placed in the area to be treated and causes tissue destruction with thermal energy. Heat is generated by an alternating electric current in the frequency of radio waves. Currently there is no evidence from randomised controlled trials comparing RFA to surgery but such studies are currently being considered. In patients with unresectable disease, treatment is with palliative intent and options include chemotherapy with doxorubicin, cisplatin, ifosfamide and etoposide, palliative radiotherapy for bone or obstructing lung metastases, or consideration of early phase trials. Phase 1 trials are trials designed to assess new drugs and establish their maximum tolerated dose in humans. They may or may not be specific for sarcoma patients and are essentially undertaken to find the maximum tolerated dose in humans. Phase 2 studies are more likely to be specific for a certain malignancy and are to establish early efficacy data for the drug. Patients need to be in good performance status for these trials and they often require multiple hospital visits and investigations.

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bone, bone marrow or other metastatic sites. Patients with lung metastases who respond well to chemotherapy should have their primary tumour treated radically and then receive low dose irradiation to their whole lungs. Patients with other sites of metastatic disease who respond well to conventional chemotherapy regimens may be considered for high dose chemotherapy with stem cell rescue. The evidence to support this approach is small and this approach is included in the international trial EuroEwings 99 protocol.

radiotherapy was designed to assess any difference in the incidence of wound complications.19 The trial was stopped prematurely because of increased acute wound complications in the preoperative treatment arm. 35% of patients developed wound complications in the preoperative arm versus 17% in the postoperative arm ( p ¼ 0.01). Updated data from this trial with a median follow up of 6.9 years show over 90% local control in both arms but the post-operative radiotherapy arm had significantly more patients with late toxicity (86% versus 68%). In the UK preoperative radiotherapy may be used in order to try and shrink the STS to allow limb preserving surgery in a patient who otherwise may need an amputation. Toxicity seen from radiotherapy varies depending on the site being treated, the volume being irradiated and a patient’s individual sensitivity to radiotherapy (Table 3). Patient education and physiotherapy are important to aid recovery after surgery and radiotherapy in order for patients to recover to their maximum potential. Until recently the use of adjuvant chemotherapy was controversial with some suggestion that it may be beneficial in high grade, extremity sarcomas. A recent pooled analysis from two EORTC trials showed no benefit from adjuvant chemotherapy.20,21 In the UK adjuvant chemotherapy is no longer used outside the setting of clinical trials. Occasionally neoadjuvant chemotherapy is given in an attempt to make a surgical excision possible or to try and avoid an amputation. There are no data from randomised controlled trials to support this approach. Patients with localised inoperable disease because of surgical reasons, patient comorbidity or patients choice can be treated radically with radiotherapy alone. Doses in excess of 66 Gy need to be used. Local control of 61% has been reported with this approach. Fifty percent of patients with STS will either present with, or develop locally advanced or metastatic disease. When they do, the median survival is 8e12 months. Similar to bone sarcomas, the commonest site of metastatic disease is the lung and the possibility of metastatectomy should always be considered as this is the only possible option for long term survival (Figure 1).

Soft tissue sarcoma Soft tissue sarcomas (STS) can occur in any part of the body where mesenchymal tissue exists. There are over fifty different histiological types of STS in the WHO sarcoma classification. The non-surgical treatment for the majority of these is similar however, for some sub-types such as rhabdomyosarcoma, Gastro Intestinal Tumours (GISTs) and Kaposi’s sarcoma,the treatment is very different and beyond the scope of this article. The goal of treatment for localised extremity STS is a functioning limb without local recurrence. In the 1980’s it became clear that wide local excision (limb conservation) and adjuvant radiotherapy could produce local control rates similar to amputation without prejudicing overall survival. Yang et al. randomised patients with STS to adjuvant radiotherapy or not, after wide excision.18 In high grade sarcomas the ten year local recurrence rate was 0% versus 22% in favour of radiotherapy. In the low grade sarcomas the ten year local recurrence rates were 4% versus 33% in favour of radiotherapy. There was no benefit in overall survival for either low or high grade sarcomas with radiotherapy. In the UK, the standard of care is adjuvant radiotherapy for patients with either high grade, >5 cm in size or deep tumours. Patients who have positive margins after surgery in whom further surgery is not possible should receive post-operative radiotherapy. To plan radiotherapy treatment the oncologist needs to outline on a CT planning scan where the original tumour was, add a margin for possible subclinical spread, and a margin to allow for patient movement and daily radiotherapy set up error. They need to have the pre-operative imaging, histopathology report, surgical operation notes and ideally the sarcoma surgeon will have placed clips around the tumour bed which can be seen on imaging. It also helps if the oncologist sees the patient preoperatively and can talk to the surgeon after surgery about what the intraoperative appearances of the tumour were i.e. which margins might the surgeon be concerned about. Patients typically are treated daily, Monday to Friday, for 6e7 weeks with a dose of 66 Gy in 33 fractions. Historically, large volumes of tissue have been irradiated with margins of 5e7 cms superiorly and inferiorly to where the original tumour was. However, these large volumes can cause significant morbidity and there is evidence that local recurrences occur much closer to the initial tumour. The Vortex study is an National Cancer Research Network (NCRN) trial which is currently is investigating whether such large treatment margins are really necessary. In Canada, standard care is to give preoperative radiotherapy. There are potential benefits from both pre and post-operative radiotherapy. An RCT comparing pre and post-operative

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Table showing the acute and long term radiotherapy toxicities from adjuvant radiotherapy for soft tissue sarcoma of the extremities Acute toxicity

Chronic toxicity

Skin erythema Skin desquamation Limb oedema Hair loss in radiation field Skin break down and ulceration Tiredness

Soft tissue fibrosis and induration Skin atrophy Chronic oedema Hair loss in treatment field Arthritis (if a joint is irradiated) Muscle fibrosis Osteoporosis and fracture risk Second malignancy Halting of growth in pre pubertal patients

Table 3

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which may have features of bone or soft tissue high grade sarcoma. The prognosis is very poor with a median survival of six months. In view off this, patients may be offered neoadjuvant and adjuvant chemotherapy with cisplatin and doxorubicin.22

Solitary plasmacytoma of the bone Solitary plasmacytoma is a proliferation of monoclonal plasma cells in a solitary lesion which usually presents with a bony mass lesion, neurological compression or pain. They are most common in the axial skeleton and vertebrae where they can cause spinal cord compression. Before the diagnosis of solitary plasmacytoma can be made, multiple myeloma needs to be excluded (bone marrow aspirate and trephine, skeletal survey, urine Bence Jones protein, plasma paraprotein levels, calcium, renal function and full blood count). An MRI of the spine should also be done to ensure that the lesion is truly solitary. These tumours are very radiosensitive and should be treated with radical radiotherapy with a dose 45e50 Gy. Local control rates are reported between 88e100%. These patients have about a 50e80% risk of developing multiple myeloma usually within two to five years but this may occur twenty years later.

Figure 1 CXR of a patient with a metastatic soft tissue sarcoma who has had a left pneumonectomy for metastatic disease and now has a metastases in her right lung five years later.

Primary lymphoma of bone Primary lymphoma of bone accounts for about 3% of primary bone malignancies. The vast majority are diffuse large B cell lymphomas. They usually present with a palpable mass secondary to soft tissue around bone. B symptoms (night sweats, fever and weight loss) may be present. Non-Hodgkins Lymphoma (NHL) is both chemo and radiosensitive. Treatment consists of R CHOP chemotherapy i.e. rituximab, cyclophosphamide, vincristine, doxorubicin and prednisolone. Rituximab is a humanised monoclonal antibody against CD 20 (an antigen on B lymphocytes). This is usually followed by involved field radiotherapy with a dose of 40e45 Gy.

For the majority of patients however, treatment is with palliative intent. Chemotherapy with doxorubicin alone or in combination with ifosfamide is the standard option. Response rates for doxorubicin alone are approximately 20%. Ifosfamide and doxorubicin together have a higher response rate of approximately 30e40% but at the cost of considerably more toxicity, the need for inpatient treatment and no benefit in overall survival. In 2007 Trabectedin, a novel DNA binding compound derived from the marine turbicate Ecteinascidia Turbinate was licensed for treatment for patients with STS who progress after treatment with ifosfamide and doxorubicin. This is the first newly licensed drug for STS in over 20 years. Studies have showed Trabectedin can stop tumour growth or induce a partial response in 50% of patients with one year survival rates of 50%. At the time of writing Trabectedin is not routinely funded on the NHS and NICE is due to consider it in Autumn 2009. Inevitably like most metastatic cancers, patients will deteriorate and need active symptom control and palliative care. Palliative radiotherapy can be very effective in locally advanced STS to control symptoms of bleeding, pain or compression. Occasionally palliative surgery can be a very useful treatment for intractable local symptoms.

Conclusion Malignancy affects the musculoskeletal system in many ways. The incidence of metastatic bone disease is much higher than that of primary musculoskeletal malignancy. Even though there are many treatment options, it is almost always with palliative intent. Primary bone or soft tissue malignancy is rare but can be truly challenging to treat. The primary sarcomas still have a disappointingly poor prognosis even for localised disease particularly as patients are often young. Other primary bone tumours such as NHL and plasmacytoma have a much better prognosis. What is the same for all patients with these conditions is the need for a truly multidisciplinary approach in order to ensure these patients are diagnosed and treated to the highest possible level. A

Chondrosarcoma Chondrosarcomas are a heterogeneous group of malignant bone tumours that produce a cartilaginous matrix. They account for 20e 27% of primary bone malignancies. Approximately 90% of these tumours are low or intermediate grade and are treated by surgical management alone. The conventional high grade and rarer mesenchymal chondrosarcomas have a high metastatic potential and less than 30% ten year survival. Adjuvant radiotherapy is recommended for these tumours if surgical excision is incomplete. Similarly to soft tissue sarcomas, a dose above 60 Gy is required. Dedifferentiated chondrosarcomas are highly aggressive tumours which have the additional component of high grade sarcoma

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a randomised phase III double blind, placebo controlled trial. Cancer 2004; 100: 2613e21. Eilber F, Giuliano A, Eckardt J, et al. Adjuvant chemotherapy for osteosarcoma: a randomized prospective trial. J Clin Oncol 1987; 5(1): 21e6. Link MP, Goorin AM, Miser AW, et al. The effect of adjuvant chemotherapy on relapse free survival in patients with osteosarcoma of the extremity. N Engl J Med 1986; 314(2): 1600e6. Goorin AM, Schwartzentruber DJ, Devidas M, et al. Pre-surgical chemotherapy compared with immediate surgery and adjuvant chemotherapy for non metastatic osteosarcoma: pediatric Oncology Group Study POG-8651. J Clin Oncol 2003; 21(8): 1574e80. Patricio MB, Vilhena M, Neves M, et al. Ewings’ Sarcoma in children: twenty five years of experience at the Instituto Portuges do Oncologia de Francisico Gentil. J Surg Oncol 1991; 47: 37e40. Yang JC, Chang AE, Baker AR, et al. Randomized prospective study of the benefit of adjuvant radiation therapy in the treatment of soft tissue sarcomas of the extremity. J Clin Oncol 1988; 16: 197e203. O’Sullivan B, Davis AM, Turcotte R, et al. Preoperative versus postoperative radiotherapy in soft tissue sarcoma of the limbs: a randomised trial. Lancet 2002; 359: 2235e41. Woll PJ, van Glabbeke M, Hohenberger P, et al. Adjuvant chemotherapy with doxorubicin and ifosfamide in resected soft tissue sarcoma (STS): interim analysis of a randomised phase III trial [abstract]. J Clin Oncol 2007; 25: 547s. Pervaiz N, Colterjohn N, Farrokhyar F, et al. A systematic metaanalysis of randomized controlled trials of adjuvant chemotherapy for localized resectable soft-tissue sarcoma. Cancer 2008; 113: 573. Mitchell AD, Ayoub K, Mangham DC, Grimer RJ, et al. Experience in the treatment of dedifferentiated chondrosarcoma. J Bone Joint Surg 2000; 82B: 55e61.

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Management of articular cartilage defects

of patients in all age groups and reported chondral lesions in 19,827 (63%) of patients; 5% of all cases were found in patients younger than 40 years of age who had grade IV lesions.4 A review of 1,000 arthroscopies by Hjelle et al reported chondral or osteochondral lesions of any type in 610 patients (61%), out of which 190 patients had focal lesions (19% of all cases). Many of these lesions were clinically silent at the time of detection.5 In conclusion OCD appears to be relatively commonly associated with knee problems which affect young active patients

Ehab Kheir David Shaw

Grades of OCD (Figure 2)

Abstract

The most popular arthroscopic classification system of cartilage lesion was developed by Outerbridge6 (Figure 1). Other less widely used grading systems have been developed7,8 including the International Cartilage Repair Society (ICRS) index, which evaluates both the cartilage injury and degree of repair.9

This paper discusses the management of articular cartilage defects. ­Osteochondral defects (OCD) may be traumatic or degenerative in origin. Arthroscopic surgery is the gold standard diagnostic and therapeutic tool for the management of OCD. The management of OCD remains controversial and over the last five decades various treatment options and surgical techniques have been tried to maximise the clinical outcome. In this article we review the current practice of management of OCD. We also highlight the most recent approaches and research and look to the future of management of OCD.

Outerbridge classification: (Figure 1) • grade 0: normal cartilage; • grade I: cartilage with softening and swelling; • grade II: a partial-thickness defect with fissures on the ­surface that do not reach subchondral bone or exceed 1.5 cm in diameter; • grade III: fissuring to the level of subchondral bone in an area with a diameter more than 1.5 cm; • grade IV, exposed subchondral bone.

Keywords articular cartilage; osteochondral defect

Introduction Hyaline cartilage is a complex and highly specialized tissue. It is a formidable challenge to replace or repair cartilage once damaged. The predominant repair tissue found in such defects is fibrocartilage, which is mechanically and chemically inferior to hyaline cartilage.1 The management of OCD remains controversial and over the last five decades various treatment options and surgical techniques have been tried to optimise the clinical outcome.

Epidemiology The true incidence of articular cartilage injury is still debated. Several studies have described a wide range of incidences. Noyes reviewed results of 85 knee arthroscopies of young patients (14 to 43 years old) following acute traumatic haemarthrosis. The study reported on acute chondral fractures associated with or without anterior cruciate ligament (ACL) disruption as 10% and 4% respectively.2 In a review of 993 knee arthroscopies in patients with a mean age of 35 years, there was an 11% incidence of full-thickness lesions (International Cartilage Repair Society grade III or IV) that could have benefited from surgical treatment.3 In a larger and more generalised study, Curl et al reviewed 31,516 knee ­arthroscopies

Ehab Kheir MRCS is Registrar Trauma and Orthopaedics, Bradford Royal Infirmary, UK. Outerbridge grading system of cartilage damage. David Shaw Msc FRCS Ed FRCS (Orth) is Consultant Orthopaedic Surgeon, Bradford Royal Infirmary, UK.

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Figure 1

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Figure 2 ICRS grading system of cartilage damage.

debris and debridement of friable inflammatory tissues as well as removal of unstable chondral flaps which were proposed as the main cause of symptoms.11 Good or excellent short term results were achieved in 52% of the patients following arthroscopic joint lavage alone.12 When combined, arthroscopic lavage and debridement appear together to improve results and provide a better sustainable outcome.13 This treatment option is the least expensive and not technically demanding.

Current practice in the management of hyaline cartilage defects Arthroscopic lavage and debridement Background and advantages This method of treatment was first described by Magnusson more than 6 decades ago.10 This involves arthroscopic washout of

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Disadvantages This technique does not provide any reparative cartilage formation and cannot be used in large OCD. The outcomes after arthroscopic lavage or arthroscopic debridement in arthritic knees has been reported to be no better than those after a placebo procedure.14 Marrow stimulation techniques (Microfractures) Background and advantages In continuation of the work of Magnasson, Pridie15 drilled a series of holes into the subchondral bone using a quarter-inch drill. These drill holes allowed the vascular bone beneath to provide regenerative cells to the surface and the OCD becomes filled with fibrocartilage. Johnson introduced arthroscopic abrasion arthroplasty in 1986.16 This contemporary technique, popularised by Steadman,17 uses especially designed punches to produce microfractures in the area of cartilage loss. The technique is relatively safe and does not pose a risk of thermal necrosis and is now the most popular treatment option for OCD.

Figure 3 a Most superior and lateral (marginal). b Most inferior and lateral (marginal).

Osteochondral allograft Background and advantages This technique is similar to the previous one except that the osteochondral allografts are harvested from cadaveric donors.29 Fitzpatrick & Morgan suggested that osteochondral allograft could represent a biologic alternative to knee replacement.30 Osteochondral allografts have also been used following bone tumours resection.31,32 The advantage of osteochondral allografts is the ability to provide fully formed articular cartilage without specific limitations with respect to defect size. In addition, there is no concern for donor site morbidity. Subjective improvement in 75% to 85% of patients after osteochondral allograft implantation treatment of properly selected chondral lesions has been reported. Careful patient selection and accurate identification of the pathology is recommended.33

Disadvantages There are two main disadvantages to this technique: first it is designed to stimulate primitive mesenchymal cells to differentiate into fibrocartilage18 and the biomechanical properties of the repair fibrocartilage are inferior to those of hyaline cartilage.19 The second disadvantage is that following microfracture the extent of fill has been reported to be rarely more than 75% of the total volume of the chondral defect.19 Osteochondral defect substitutes Osteochondral autografts Background and advantages This technique involves the transfer of intact hyaline cartilage and the underlying subchondral bone to replace an OCD.20 The success of this technique is dependant on chondrocyte viability because only living chondrocytes can produce and maintain the extracellular matrix of proper load-bearing capacity.21 Several studies have been conducted since and have investigated the ideal donor site and plug size.22–26 Grafts taken from the most marginal (medial or lateral) aspect of the patellar groove have been shown to provide a significantly better topographic match than did grafts taken from the central intercondylar notch or from the side of the notch (Figure 3). It was also shown that the most inferior donor sites on the medial and lateral edges of the patellar groove provided a better match to the weight-bearing portions of the condyles than did the more superior sites of the patellar groove.27 Bottomed and unbottomed osteochondral plugs are demonstrated in Figure 4. Bottomed plugs were found generally to provide much more stability than unbottomed ones. Short bottomed plugs were more stable than long bottomed plugs. Thus, in clinical practice it is advisable to use short bottomed plugs.28

Disadvantages Disadvantages of fresh osteochondral allograft include the relative paucity of donor tissue, complexities in procurement and handling, and the possibility of disease transmission through the transplantation of fresh tissue.33,34 Studies have confirmed a significant immunologic response in humans to histocompatibility antigens (Class I and II) presented by frozen osteochondral allografts.35,36 This favours the use of decellularised cartilage to minimise the risk of immunologic rejection. Periosteal and perichondral grafting Periosteum can differentiate to produce new bone.37 In the case of using a periosteal graft for full thickness chondral defects reconstruction, the cells may originate either from periosteal chondrocyte precursor cells or from bone marrow mesenchymal cells. This technique is performed in a limited number of centres, and there are few reported outcomes that have validated its use.38–41 Autologous chondrocyte implantation (ACI) Autologous chondrocyte implantation (ACI) involves two stages; first a hyaline cartilage biopsy is harvested arthroscopically and the cells are cultured in-vitro, the second stage involves reimplantation of the cultured chondrocytes into the chondral defect underneath a periosteal patch. The first reported ACI in humans was described by Brittberg in 1994.42 They reported that the number of cells in the initial biopsy was the key factor ­affecting

Disadvantages The main disadvantage of this technique is the donor-site morbidity after osteochondral harvest which can be significant. Reddy et al. (2007) showed a significant decline in knee function following osteochondral graft harvesting.

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(Kock et al. 2006) a 3 bottomed plugs of different lengths (8–16 mm). The bottoms of the plugs are exactly positioned at the bottom of the defect. b 3 unbottomed plugs of same lengths as in A. The bottoms of the plugs “float” about 5 mm above the bottom of the recipient site defect. Figure 4

success,43 to date the precise number of cells required for a successful clinical implantation of chondrocytes has not been studied sufficiently. In 2004 a randomized trial, comparing autologous chondrocyte implantation with microfractures, showed that the improvement with microfractures was significantly better in comparison to autologous chondrocyte implantation, but the authors recommended that mid-term and long-term follow-up was needed to determine if one method was better than the other for generating long-lasting hyaline cartilage and alleviating symptoms.44

and maintain their differentiated function, and its architecture defines the ultimate shape of the new bone and cartilage.51 Natural scaffolds These include fibrin, collagen, hyaluronan, gelatin, agarose and alginate, chitosan, bacterial cellulose (Table 1). The major advantages of natural biomaterials are their low toxicity and low capacity to induce an inflammatory response. They are degraded by naturally occurring enzymes into non toxic absorbable degradation products. However their mechanical strength is weak and their complex structure makes manipulation difficult. As they can easily be denatured, further chemical manipulation will potentially lead to toxicity.52–54 To overcome these difficulties natural scaffolds have been used in combination with other natural or synthetic materials to enhance their mechanical strength.

Recent tissue engineering approaches Tissue engineering is an emerging field in biomedical science. The two essential component of tissue engineering are biomaterials and cells.45 Biomaterials represent the gap filler or the scaffold into which cells will differentiate to form the new desired tissue. In hyaline articular cartilage biomaterials are akin to the extracellular matrix (ECM). The properties of biomaterials are the key for the success of tissue engineering. High porosity is an important character of biomaterials to promote integration of cells into the scaffold which would allow them to generate their own ECM.46 Other characteristics such as biocompatibility and mechanical properties are also important.47 The second component of tissue engineering, the cells, involves cell isolation and appropriate differentiation.48 Every effort should be made to maintain this state trying to avoid dedifferentiation,49 to allow these cells to generate ECM proteins and form new tissues.50 Scaffolds or three-dimensional (3-D) ­constructs provide the necessary support for cells to proliferate

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Natural scaffolds for cartilage tissue engineering Scaffold

References

Collagen Fibrin Gelatin Hyaluronan Agarose and alginate Bacterial cellulose Chitosan

55,56 57,58 59 60,61 62,63 64,65 66,67

Table 1

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Synthetic scaffolds Synthetic scaffolds are more durable and easier to handle and manipulate than natural materials, they also effectively integrate with the host tissues. Hitherto their biochemical properties remain inferior to native cartilage. Examples of some synthetic scaffolds used in articular cartilage tissue engineering are shown in Table 2. Similar to natural scaffolds, synthetic scaffolds can be used in isolation although they are more commonly used in combination with other natural or synthetic materials.

Acellular scaffolds for tissue engineering

Acellular scaffolds Acellular grafts have been used in other fields of clinical practice. Since they have no cells they do not lead to cell necrosis as compared to autografts or allografts which have shown deterioration of mechanical strength following implantation.78 Acellular scaffolds have the advantage of being composed of ­ natural ECM, giving them numerous advantages in terms of mechanical behaviour and biocompatibility.79 Some examples of acellular scaffolds used in tissue engineering are shown in Table 3. Acellular cartilage bone matrix could potentially provide a favourable substitute in the treatment of OCD or as a biological joint replacement. The authors of this article are currently developing a technique to decellularise cartilage/bone matrix scaffold for use in cartilage tissue engineering. The primitive results showed that it is possible to decellularise a porcine cartilage-bone matrix that can be used as a biological scaffold for recellularisation with autologus chondrocytes with a view to use as an osteochondral implant.

68,69 70 71,72 73,74 75 76,77

Table 2

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80,81 82,83

84,85 86 87,88

References 1 Furukawa T, Eyre DR, Koide S, Glimcher MJ. Biochemical studies on repair cartilage resurfacing experimental defects in the rabbit knee. J Bone Joint Surg Am 1980; 62(1): 79–89. 2 Noyes FR, Bassett RW, Grood ES, Butler DL. Arthroscopy in acute traumatic hemarthrosis of the knee. Incidence of anterior cruciate tears and other injuries. J Bone Joint Surg Am 1980; 62(5): 687–695, 757. 3 Aroen A, Loken S, Heir S, et al. Articular cartilage lesions in 993 consecutive knee arthroscopies. Am J Sports Med 2004; 32(1): 211–215. 4 Curl WW, Krome J, Gordon ES, Rushing J, Smith BP, Poehling GG. Cartilage injuries: a review of 31,516 knee arthroscopies. Arthroscopy 1997; 13(4): 456–460. 5 Hjelle K, Solheim E, Strand T, Muri R, Brittberg M. Articular cartilage defects in 1,000 knee arthroscopies. Arthroscopy 2002; 18(7): 730–734.

Synthetic scaffolds for articular cartilage tissue engineering

Polylactic acid (PLA) Polyglycolic acid (PGA) PLA-PGA Copolymer, Dacron Teflon Hydroxyapatite

Pericardial acellular matrix Small intestinal submucosa (SIS) as a vascular graft Acellular vascular matrix Acellular meniscus Acellular tendons

OCD autograft does provide a native hyaline osteochondral constructs, although the major drawback of this surgical technique is donor site morbidity.20 The large OCD remains an obstacle to using this technique.24 OCD allograft can provide greater coverage for large OCD.29 However the risks of disease transmission, as well as immunological rejection,36 are the main disadvantages.35 The availability of cartilage donors can add difficulties for using this treatment option.33 Tissue engineering has developed rapidly over the last decade and there are a number of biomaterials being tried for cartilage substitution.89 The properties of biomaterials are key to the success of tissue engineering.45 High porosity is important to promote integration of cells into the scaffold which would allow them to generate their own ECM, biocompatibility and mechanical properties are crucial for a scaffold to mimic the host tissues.45 Decellularised tissues and organs have been successfully used in both pre-clinical animal studies and in human clinical applications.90 Decellularisation and generation of biological acellular scaffolds was achieved in cardiac valves,91 vascular tissues,79 pericardial matrix,81 porcine meniscus86 and different other tissues and organs. An acellular osteochondral scaffold will potentially provide functioning hyaline cartilage and primary healing of these constructs will be clinical integration through bone-to-bone healing providing the best results. ◆

The management of OCD remains controversial and over the last five decades, various treatment options and surgical techniques have been tried to optimise the clinical outcome. Microfractures or marrow stimulation techniques remain the gold standard and are most commonly used. Currently this is the least technically demanding option with the longest follow up results and it is the least expensive. For these reasons it is the current “gold standard”.17 Nevertheless the basic concept of this treatment is to replace hyaline cartilage with fibrocartilage, which has inferior mechanical properties compared to hyaline cartilage and microfracture is not suitable for large osteochondral defects.

References

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Table 3

Conclusion

Scaffold

Scaffold

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48 Koechlin N, Pisam M, Poujeol P, Tauc M, Rambourg A. Conversion of a rabbit proximal convoluted tubule (PCT) into a cell monolayer: ultrastructural study of cell dedifferentiation and redifferentiation. Eur J Cell Biol 1991; 54(2): 224–236. 49 Minuth WW, Aigner J, Kubat B, Kloth S. Improved differentiation of renal tubular epithelium in vitro: potential for tissue engineering. Exp Nephrol 1997; 5(1): 10–17. 50 Sittinger M, Bujia J, Rotter N, Reitzel D, Minuth WW, Burmester GR. Tissue engineering and autologous transplant formation: practical approaches with resorbable biomaterials and new cell culture techniques. Biomaterials 1996; 17(3): 237–242. 51 Hutmacher DW. Scaffolds in tissue engineering bone and cartilage. Biomaterials 2000; 21(24): 2529–2543. 52 van Luyn MJ, van Wachem PB, Damink LO, Dijkstra PJ, Feijen J, Nieuwenhuis P. Relations between in vitro cytotoxicity and crosslinked dermal sheep collagens. J Biomed Mater Res 1992; 26(8): 1091–1110. 53 Olde Damink LH, Dijkstra PJ, van Luyn MJ, van Wachem PB, Nieuwenhuis P, Feijen J. Cross-linking of dermal sheep collagen using a water-soluble carbodiimide. Biomaterials 1996; 17(8): 765–773. 54 Gough JE, Scotchford CA, Downes S. Cytotoxicity of glutaraldehyde crosslinked collagen/poly(vinyl alcohol) films is by the mechanism of apoptosis. J Biomed Mater Res 2002; 61(1): 121–130. 55 Sams AE, Minor RR, Wootton JA, Mohammed H, Nixon AJ. Local and remote matrix responses to chondrocyte-laden collagen scaffold implantation in extensive articular cartilage defects. Osteoarthritis Cartilage 1995; 3(1): 61–70. 56 Lee CR, Grodzinsky AJ, Hsu HP, Spector M. Effects of a cultured autologous chondrocyte-seeded type II collagen scaffold on the healing of a chondral defect in a canine model. J Orthop Res 2003; 21(2): 272–281. 57 Hendrickson DA, Nixon AJ, Grande DA, et al. Chondrocyte-fibrin matrix transplants for resurfacing extensive articular cartilage defects. J Orthop Res 1994; 12(4): 485–497. 58 Brittberg M, Sjogren-Jansson E, Lindahl A, Peterson L. Influence of fibrin sealant (Tisseel) on osteochondral defect repair in the rabbit knee. Biomaterials 1997; 18(3): 235–242. 59 Chang CH, Lin FH, Lin CC, Chou CH, Liu HC. Cartilage tissue engineering on the surface of a novel gelatin-calcium-phosphate biphasic scaffold in a double-chamber bioreactor. J Biomed Mater Res B Appl Biomater 2004; 71(2): 313–321. 60 Solchaga LA, Yoo JU, Lundberg M, et al. Hyaluronan-based polymers in the treatment of osteochondral defects. J Orthop Res 2000; 18(5): 773–780. 61 Solchaga LA, Gao J, Dennis JE, et al. Treatment of osteochondral defects with autologous bone marrow in a hyaluronan-based delivery vehicle. Tissue Eng 2002; 8(2): 333–347. 62 Rahfoth B, Weisser J, Sternkopf F, Aigner T, von der Mark K, Brauer R. Transplantation of allograft chondrocytes embedded in agarose gel into cartilage defects of rabbits. Osteoarthritis Cartilage 1998; 6(1): 50–65. 63 Mierisch CM, Wilson HA, Turner MA, et al. Chondrocyte transplantation into articular cartilage defects with use of calcium alginate: the fate of the cells. J Bone Joint Surg Am 2003; 85-A(9): 1757–1767. 64 Muller FA, Muller L, Hofmann I, Greil P, Wenzel MM, Staudenmaier R. Cellulose-based scaffold materials for cartilage tissue engineering. Biomaterials 2006; 27(21): 3955–3963. 65 Pulkkinen H, Tiitu V, Lammentausta E, et al. Cellulose sponge as a scaffold for cartilage tissue engineering. Biomed Mater Eng 2006; 16(4 Suppl): S29–35.

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66 Nettles DL, Elder SH, Gilbert JA. Potential use of chitosan as a cell scaffold material for cartilage tissue engineering. Tissue Eng 2002; 8(6): 1009–1016. 67 Griffon DJ, Sedighi MR, Schaeffer DV, Eurell JA, Johnson AL. Chitosan scaffolds: interconnective pore size and cartilage engineering. Acta Biomater 2006; 2(3): 313–320. 68 Chu CR, Dounchis JS, Yoshioka M, Sah RL, Coutts RD, Amiel D. Osteochondral repair using perichondrial cells. A 1-year study in rabbits. Clin Orthop Relat Res 1997(340): 220–229. 69 Giurea A, Klein TJ, Chen AC, et al. Adhesion of perichondrial cells to a polylactic acid scaffold. J Orthop Res 2003; 21(4): 584–589. 70 Liu Y, Chen F, Liu W, et al. Repairing large porcine full-thickness defects of articular cartilage using autologous chondrocyteengineered cartilage. Tissue Eng 2002; 8(4): 709–721. 71 Cohen SB, Meirisch CM, Wilson HA, Diduch DR. The use of absorbable co-polymer pads with alginate and cells for articular cartilage repair in rabbits. Biomaterials 2003; 24(15): 2653–2660. 72 Zwingmann J, Mehlhorn AT, Sudkamp N, Stark B, Dauner M, Schmal H. Chondrogenic differentiation of human articular chondrocytes differs in biodegradable PGA/PLA scaffolds. Tissue Eng 2007; 13(9): 2335–2343. 73 McGibbon B. Use of Dacron backing on the cartilage framework in the construction of ears. Plast Reconstr Surg 1977; 60(2): 262–266. 74 Mola F, Keskin G, Ozturk M, Muezzinoglu B. The comparison of acellular dermal matric (Alloderm), Dacron, Gore-Tex, and autologous cartilage graft materials in an experimental animal model for nasal septal repair surgery. Am J Rhinol 2007; 21(3): 330–334. 75 Defrere J, Franckart A. Teflon/polyurethane arthroplasty of the knee: the first 2 years preliminary clinical experience in a new concept of artificial resurfacing of full thickness cartilage lesions of the knee. Acta Chir Belg 1992; 92(5): 217–227. 76 Pan Y, Xiong D, Gao F. Viscoelastic behavior of nano-hydroxyapatite reinforced poly(vinyl alcohol) gel biocomposites as an articular cartilage. J Mater Sci Mater Med 2008; 19(5): 1963–1969. 77 van Susante JL, Buma P, Homminga GN, van den Berg WB, Veth RP. Chondrocyte-seeded hydroxyapatite for repair of large articular cartilage defects. A pilot study in the goat. Biomaterials 1998; 19(24): 2367–2374. 78 Ingram JH, Korossis S, Howling G, Fisher J, Ingham E. The use of ultrasonication to aid recellularization of acellular natural tissue scaffolds for use in anterior cruciate ligament reconstruction. Tissue Eng 2007; 13(7): 1561–1572. 79 Schmidt CE, Baier JM. Acellular vascular tissues: natural biomaterials for tissue repair and tissue engineering. Biomaterials 2000; 21(22): 2215–2231. 80 Courtman DW, Pereira CA, Kashef V, McComb D, Lee JM, Wilson GJ. Development of a pericardial acellular matrix biomaterial: biochemical and mechanical effects of cell extraction. J Biomed Mater Res 1994; 28(6): 655–666. 81 Mirsadraee S, Wilcox HE, Korossis SA, et al. Development and characterization of an acellular human pericardial matrix for tissue engineering. Tissue Eng 2006; 12(4): 763–773. 82 Badylak SF, Kropp B, McPherson T, Liang H, Snyder PW. Small intestinal submucosa: a rapidly resorbed bioscaffold for augmentation cystoplasty in a dog model. Tissue Eng 1998; 4(4): 379–387. 83 Robotin-Johnson MC, Swanson PE, Johnson DC, Schuessler RB, Cox JL. An experimental model of small intestinal submucosa as a growing vascular graft. J Thorac Cardiovasc Surg 1998; 116(5): 805–811.

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observations. J Vet Med A Physiol Pathol Clin Med 2003; 50(10): 520–526. 88 Lee DK. A preliminary study on the effects of acellular tissue graft augmentation in acute Achilles tendon ruptures. J Foot Ankle Surg 2008; 47(1): 8–12. 89 Martin I, Miot S, Barbero A, Jakob M, Wendt D. Osteochondral tissue engineering. J Biomech 2006. 90 Gilbert TW, Sellaro TL, Badylak SF. Decellularization of tissues and organs. Biomaterials 2006; 27(19): 3675–3683. 91 Booth C, Korossis SA, Wilcox HE, et al. Tissue engineering of cardiac valve prostheses I: development and histological characterization of an acellular porcine scaffold. J Heart Valve Dis 2002; 11(4): 457–462.

84 Wilson GJ, Yeger H, Klement P, Lee JM, Courtman DW. Acellular matrix allograft small caliber vascular prostheses. ASAIO Trans 1990; 36(3): M340–M343. 85 Schaner PJ, Martin ND, Tulenko TN, et al. Decellularized vein as a potential scaffold for vascular tissue engineering. J Vasc Surg 2004; 40(1): 146–153. 86 Stapleton TW, Ingram J, Katta J, et al. Development and characterization of an acellular porcine medial meniscus for use in tissue engineering. Tissue Eng Part A 2008; 14(4): 505–518. 87 Ramesh R, Kumar N, Sharma AK, Maiti SK, Kumar S, Charan K. Acellular and glutaraldehyde-preserved tendon allografts for reconstruction of superficial digital flexor tendon in bovines: Part II–Gross, microscopic and scanning electron microscopic

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ADULT PATHOLOGY

Charcot Marie Tooth Disease

(Box 1). In general they are classified by their inheritance pattern and which part of the nerve cell is affected. CMT can either be autosomal dominant, recessive or X-linked. These genetic abnormalities affect gene expression for vital proteins in myelin sheaths, peripheral nerve cell axons, or sometimes both. It is the large variety of genetic abnormalities on each chromosome resulting in CMT that has resulted in the ever-increasing recognition of subtypes.

DWJ Howcroft S Kumar N Makwana

Clinical history The onset of symptoms can be variable, depending on the type, but is often during adolescence or early adulthood. Research has shown that children as young as 2 years of age show electrical evidence of nerve dysfunction in CMT-1,1 without any clinical signs. CMT affects both upper and lower limbs, but usually affects the lower legs first. Patients may present with increasing deformity, a history of recurrent ankle sprains, or the development of a high stepping (foot drop) gait (the latter being rare). In the early stages of CMT foot drop may occur with fatigue, at the end of the day. Alternatively, sufferers may

Abstract Charcot Marie Tooth (CMT) disease was first described in 1886. It describes a spectrum of genetic disorders that affects peripheral nerves, either by slowing action potential transmission along the axons, or by reducing the amplitude, or both. It is this variety of underlying genetic findings and subtleties of clinical presentation that has resulted in the varying nomenclature over the years. Patients with CMT commonly present to orthopaedic surgeons with lower and upper limb symptoms including ankle sprains, cavus feet and weakness of the intrinsic hand muscles. More rarely, they present with spinal and hip manifestations. It is not usually a life threatening or painful condition and therefore lends itself to the FRCS (Tr & Orth) exam.

CMT types and subtypes

Keywords Charcot Marie Tooth (CMT); Hereditary Motor Sensory Neuropathy (HMSN)

CMT1 (50%) C Myelin sheath abnormality C Autosomal dominant C Further division into CMT1A,B,C, etc. C CMT1A e duplication of PMP* 22 on chromosome 17

Introduction

CMT2 (20e40%) C Abnormal peripheral nerve cell axons C Autosomal dominant

It was in Paris in 1886 that Jean-Martin Charcot and his student Pierre Marie described the clinical manifestations of CMT. They initially attributed this to a myelopathy, but it was Henry Tooth from Cambridge, later in the same year, who correctly recognised this to be due to a dysfunction of peripheral nerves. It is the most common genetic neurological condition. Though there is no known cure, it is usually painless and only rarely fatal.

CMT3 (rare) C Dejerine-Sottas disease C Specific point mutation of PMP 22 or P(0) gene C Severe demyelinating disease affecting infants and children

Epidemiology CMT4 (rare) C Several subtypes C Genetic basis not yet fully understood C Demyelinating disease C Autosomal recessive C Childhood leg weakness, non-ambulatory by adolescence

CMT appears to affect all races equally. The global prevalence is thought to be in the region of 1 in 2500e3500 people. A total of 2.6 million people probably suffer from CMT worldwide. There is often a strong genetic component with CMT so that a positive family history can be very helpful in diagnosis. It is recognised that patients can develop CMT despite a negative family history by spontaneous genetic mutations. The incidence of this is not known. Other terms, such as ‘‘Peroneal Muscle Atrophy’’, have been used previously, making a detailed review of management over the years difficult.

CMTX (10e20%) C Connexin-32 gene affected C Schwann cells affected C Males moderate to severely affected C Females mild or no symptoms

Classification Over the last decade numerous types and subtypes of CMT, which affects both motor and sensory nerves, have been described genetically

Intermediate CMT (rare) C Autosomal dominant C Myelin AND axons affected

DWJ Howcroft MBBS iMRCS is a Specialist Registrar at Wrexham Maelor Hospital, 24 School Drive, Lymm, Cheshire, UK.

HNPP C Hereditary Neuropathy with predisposition to Pressure Palsy C Closely related to CMT1 C Deletion instead of duplication C Episodic, recurrent demyelinating neuropathy

S Kumar MBBS iMRCS is a Core Trainee 2 at Wrexham Maelor Hospital, Croesnewydd Road, Wrexham, UK. N Makwana MBBS FRCS (Tr & Orth) is a Consultant Foot & Ankle Orthopaedic Surgeon at Wrexham Maelor Hospital, Croesnewydd Road, Wrexham, UK and Robert Jones & Agnes Hunt Hospital, Oswestry, UK.

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have noticed that their feet (cavus, occasionally planus) or toes (clawing) have changed shape. This is almost always bilateral. They, too, may complain of ‘‘pins and needles’’ and sometimes pain, in upper and lower extremities as well as clumsiness and weakness of the hands. In children, parents may say children are clumsy or inactive. Though generally considered painless, neuropathic pain is seen in CMT. This appears to be under-reported.2 A detailed family history in these patients is important. On discovering these progressive feet abnormalities it is always worth considering the differential diagnoses, particularly in cavus feet (Table 1).

of the hindfoot (Figure 2) which should be considered before deciding upon treatment. By standing the patient on a block at the angle shown, the 1st ray can be offloaded and the hindfoot can then be assessed for full or partial correction of its apparent varus.7 Occasionally the lesser metatarsals may also be depressed, which means a slight modification of the Coleman block test (i.e. angle the foot so the lesser metatarsal heads are also offloaded).

Diagnosis Once the above history and findings have suggested a diagnosis of CMT, a number of further tests can be used to confirm it. These consist of electrophysiological and genetic assessmen, and occasionally nerve biopsy.

Clinical examination The classical appearances of ‘‘inverted champagne bottle’’ legs with pes cavus and hammer toes (Table 2) are not always present, but should be sought. Specific distal lower limb muscle wasting should be assessed and MRC graded power in these groups should be documented. Deep tendon reflexes are commonly diminished or absent. Patients may have sensory ataxia, resulting in a positive Rhomberg’s test. It is not uncommon to be able to palpate thickened posterior auricular nerves, and some patients may also develop sensorineural deafness. Patients usually don’t perceive sensory deficit, but formal testing can elicit diminished proprioception and vibration sense, and later problems with pain and temperature may be encountered. Other orthopaedic manifestations of CMT include hip dysplasia3 and scoliosis, the incidence of which is approximately 25%, but this depends on the CMT type, with CMT-1 appearing to predispose most strongly to spinal deformity.4

Electrophysiology  Nerve conduction velocities and amplitudes are tested for reductions of either or both.  Electromyography is also performed to assess which muscle groups are affected, and to what extent.  CMT1 usually exhibits reduced velocities (abnormal myelin) and normal amplitudes.  CMT2 demonstrates normal velocities but reduced ampli tudes (dysfunctional axons).  Other forms can manifest with a variety of combinations of the above. Genetic testing  Only some forms of CMT1 can be recognised by this means.  May be useful for patients concerned about transmission to offspring.

Pathophysiology The pattern of weakness in the distal leg muscles in CMT is characteristic. There is a critical distribution of muscles affected which results in the classical deformity. The anterior compartment is principally affected, while in the lateral compartment the peroneus brevis is more severely affected than the longus.5,6 The intrinsics are weak; these are usually the first muscles affected in the hand too. Clawing of the lesser toes is due to weakness of the intrinsic muscles and relative sparing of the extrinsics. The cavus foot, in part, is produced by extension contractures of the metatarso-phalangeal joints, causing tightening of the plantar fascia, but more importantly by the relatively intact peroneus longus muscle plantarflexing the first ray by overpowering the weakened tibialis anterior. This in turn contributes to the varus of the hindfoot, further exaggerated by the action of tibialis posterior, which is relatively unopposed because of the more weakened peroneus brevis muscle. Figure 1 illustrates a classical pattern of deformity seen in CMT. The hindfoot varus is usually correctable, often until late in the disease. The ‘‘Coleman block test’’ is useful in assessing this flexibility

Nerve biopsy  Outdated practice  Rarely used

Potential causes of Cavus Foot Neuromuscular C Peripheral neuropathy e CMT C Spinal cord disease e poliomyelitis, neoplasia, syringomyelia. C CNS disease e Freidrich’s ataxia, cerebral palsy C Myopathy e muscular dystrophy Congenital C Arthrogryposis C Residual clubfoot deformity Trauma C Post compartment syndrome Idiopathic Figure 1 Classical appearance in the lower legs in a patient with Charcot Marie Tooth Disease.

Table 1

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ADULT PATHOLOGY

Operative The surgical treatment of CMT foot deformity tends to follow a stepwise approach that may include:

 soft tissue procedures  osteotomies  arthrodeses. The principle of treatment is to align the foot under the tibia and the sole flat to the ground. The muscles around the foot are then balanced. Orthoses may still be needed. In general, soft tissue procedures are reserved for children, osteotomies and soft tissue procedures are beneficial in adults, and fusions should be reserved for the older patient with degenerative changes and/or deformity. There is no agreement on the timing of surgical intervention, but generally the soft-tissue procedures and osteotomies are best performed in mobile joints, and the arthrodesis reserved for more severe fixed deformities.

Figure 2 Correction of hindfoot varus with Coleman Block Test.

C C C C C C

C

Soft tissue procedures The philosophy of these procedures is to use the relatively spared muscles to bolster those that are most severely affected. The weak peroneus brevis predisposes to ankle instability and the relatively preserved peroneus longus muscle tends to promote the cavus deformity. By transferring the longus to the brevis both problems may be lessened. The Jones procedure may be useful. EHL is detached from the hallux and transferred to the neck of the first metatarsal, often with a synchronous fusion of the interphalangeal joint. This allows the EHL to dorsiflex the ankle, without worsening of the claw deformity. It sometimes needs to be supplemented with a closing wedge osteotomy of the first metatarsal to allow full correction. There is little evidence to show that these procedures delay the onset of more severe deformity. Plantar fascial release proximally is no longer recommended.

Often genetic transmission Affects motor and sensory nerves Upper and lower limbs affected History of unsteadiness/clumsiness and ankle sprain Classical pattern of nerves involved Lower limbs more severely affected B inverted champagne bottle legs B cavus feet with hammer toes Clumsiness and intrinsics wasting most common findings in upper limbs

Osteotomies These are usually used when the majority of the deformities are correctable but one or two are not. For example, a dorsiflexion closing wedge osteotomy at the base of the first metatarsal may be used if fixed plantarflexion at the first ray has occurred. Alternatively various calcaneal osteotomies may be use to correct heel position in fixed situations, or allow lateralisation of the tendo achilles (TA).

Table 2

Management

Arthrodeses Triple arthrodesis is the most widely used skeletal procedure for the fixed cavovarus foot. Evidence suggests that the operation produces good long-term results10 although others have reported that over three quarters of CMT patients experience only fair to poor results at 20 years.11 It is thought that the main reason for this is recurrence of deformity and the development of ankle degenerate change. Many patients go on to require pantalar athrodesis. Due to the risk of recurrent deformity, particularly with fusions in the young patient, most advocate the use of soft tissue balancing procedures in combination with fusion (Table 3).

As already discussed, CMT is a progressive disease and as yet there is no known cure. Management of these patients is aimed at keeping them mobile and independent for as long as possible. It is influenced by symptoms and the extent to which the patient complains, whether from footwear problems, ankle instability, pain, ulcers or stress fractures.

Non-operative Lifestyle factors, such as reducing weight and keeping fit, can help ensure patient mobility. Patients should also avoid drugs that can potentiate neuropathy, such as nitrofurantoin, isoniazid and also alcohol to excess. The mainstay of non-operative treatment involves a combination of keeping the joints supple with regular stretches and a resort to static and dynamic bracing. Though useful in controlling symptoms. Evidence is unconvincing regarding improvement,8 and most reports suggest it makes no difference.9 In the early stages regular stretching of the calf is useful, and simple ankle supports may reduce the incidence of ankle sprains. Once more severe foot- drop occurs lightweight ankle-foot-orthoses (AFOs) with assisted dorsiflexion can be used. Later. when the deformities are more pronounced, patients often need specifically moulded AFOs. Devices are available that appear to maintain movement and muscle bulk by electric stimulation. These threshold electrical stimulation machines are not widely used and there is to date no evidence supporting their use.

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Treatment of CMT Non-operative C weight loss C avoidance of certain drugs C accommodative footwear C simple bracing C AFO Operative C soft tissues/tendon transfers C osteotomies (midfoot and hindfoot) C arthrodeses Table 3

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Summary Charcot-Marie-Tooth disease remains a very challenging condition to treat. As no cure exists at present the mainstay of treatment is to maintain mobility and independence. Though affecting both upper and lower limbs, it is the legs that are usually more severely affected and often require orthotic or surgical treatment. Other manifestations, such as hip dysplasia and scoliosis, may require surgery if symptomatic or progressive. Surgical treatment remains a challenge as there is very little strong evidence to support the different options, and complications and recurrence of deformity are relatively common. It is clear that genetic or medical management remains the only hope for a true cure. Bracing and surgery only provide symptomatic relief and a slight improvement in gait. Genetic counselling should be offered for all patients affected with CMT, thus giving a clear idea of the risks of inheritance. A

5 6

7 8

9

10 REFERENCES 1 Berciano J, Garcia A, Calleja J, Combarros O. Clinicoelectrophysiological correlation of extensor digitorum brevis muscle atrophy in children with Charcot Marie Tooth disease 1A duplication. Neuromuscul Disord 2000; 10: 419e24. 2 Carter GT, Jenson MP, Galer BS, et al. Neuropathic pain in CharcotMarie-Tooth disease. Arch Phys Med Rehabil 1998; 79(12): 1560e4. 3 Walker JL, Nelson KR, Heavilon JA. Hip abnormalities in childrenwith Charcot-Marie-Tooth diease. J Pediatr Orthop 1994; 14: 54e9. 4 Horacek O, Mazanec R, Morris CE, Kobeova A. Spinal deformities in hereditary motor and sensory neuropathy: a retrospective

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qualitative, quantitative, genotypical, and familial analysis of 175 patients. Spine 2007; 32(22): 2502e8. Mann RA, Missirian J. Pathophysiology of Charcot-Marie-Tooth disease. Clin Orthop 1998; 234: 221e8. Tynan MC, Klenerman L, Helliwell TR, Edwards RH, Hayward M. Investigation of muscle imbalence in the leg in symptomatic forefoot pes cavus: a multidisciplinary study. Foot Ankle 1992; 13: 489e501. Coleman SS, Chestnut WJ. A simple test for hindfoot flexibility in the cavovarus foot. Clin Ortop Relat Res 1977; 123: 60e2. Guzian MC, Bensoussan L, Viton JM. Orthopaedic shoes improve gait in Charcot-Marie-Tooth patient: a combined clinical and quantified case study. Prosthet Orthot Int 2006; 30(1): 87e96. Refshauge KM, Raymond J, Nicholson G. Night splinting does not increase ankle range of motion in people with Charcot-Marie-Tooth disease: a randomised, cross-over trial. Aust J Physiother 2006; 52(3): 193e9. Saltzman CL, Fehrle MJ, Cooper RR. Triple arthrodesis: twenty-five and forty-four year average follow-up of the same patients. J Bone Joint Surg Am 1999; 81(10): 1391e402. Wetmore RS, Drennan JC. Long-term results of triple arthrodesis in Charcot-Marie-Tooth disease. J Bone Joint Surg Am 1989; 71: 417e22.

Acknowledgement With thanks to Mr. P Cooke MB,ChB,FRCS,ChM, Consultant Orthopaedic Surgeon, Nuffield Orthopaedic NHS Centre, Oxford.

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SYNDROME

Ollier’s disease and Maffucci syndrome

Investigations and diagnosis Conventional radiography along with clinical evaluation remains the most reliable method of diagnosing Ollier’s disease, whilst histological analysis is only indicated if malignant transformation is suspected.1,8

Sean Fang

Major radiographic features:1,5,8–11 • Oval/elongated radiolucent lesions, often with longitudinal striations • Erosion of the cortices and subsequent calcification of the ­lesions producing a diffusely speckled appearance typical of ­enchondromata (Figure 1) • Long bones and small bones of hands and feet typically the most commonly affected sites • Enchondromata almost exclusively in the metaphyseal region in long bones, possibly extending to the diaphysis (Figure 2) • Epiphysis affected at later age after closure of the growth plate • Affected areas substantially enlarged and shortened • Cortical thinning associated with pathological fracture.

Donna Dimond Rouin Amirfeyz Martin Gargan

Introduction Enchondromata are benign cartilaginous tumours which arise in intramedullary bone, predominantly affecting the metaphyses of long bones.1 Lesions can occur in isolation or at numerous sites, with the latter termed multiple enchondromatosis. Ollier’s disease (WHO terminology),2 named after French surgeon Louis Ollier who first reported on the condition in 1898, is defined as the presence of multiple enchondromata with predominantly unilateral distribution.3 The major orthopaedic manifestations usually appear in the first decade of life, consisting of skeletal deformity, limb length discrepancy and pathological fractures.1,4,5 Enchondromata may be associated with soft tissue hemangiomas in a condition called Maffucci syndrome.6

Orthopaedic manifestations The vast majority of these enchondromata affect the long bones and the tubular bones of the hands and feet.5,10,11 Orthopaedic manifestations are most commonly asymmetrical in nature due to the unilateral nature of the condition. Main orthopaedic manifestations:1,5,8 • Asymmetrical limb shortening and deformity • Swelling and deformity of the hands or feet • Pathological fracture

Epidemiology and genetics The prevalence of Ollier’s disease is approximately 1/100,000, with females more commonly affected.1 Lesions may be observed at birth and grow until puberty, with symptoms appearing in the first decade of life.5 The disease is a non-hereditary developmental disorder which occurs spontaneously, producing lesions which are variable in size and location.1,5 This has led to proposals suggesting it is a disorder of enchondral bone formation, substantiated by mutations found in the PTH/PTHrP type I receptor (PTHR1 gene) in patients with enchondromatosis. The mutant receptor decreases chondrocyte differentiation which may lead to the formation of enchondromata.5,7

Pathophysiology The lesions develop from proliferation of ectopic hyaline cartilage in intramedullary bone, where normal bone is replaced with cartilaginous tumours that usually become calcified with time.

Sean Fang is a Medical Student, Faculty of Medicine and Dentistry, The University of Bristol, Bristol, UK. Donna Dimond DCR(R) BSc PgC is a Superintendent Paediatric Radiographer, Bristol Royal Hospital for Children, Bristol, UK. Rouin Amirfeyz MRCS MSc MD is a Specialist Registrar in Trauma and Orthopaedics, Bristol Royal Infirmary, Bristol, UK.

Figure 1 Radiograph of left hand. Enchondromata localised in the phalanges and metacarpals of the ring and little fingers. The cartilaginous lesions contain areas of calcification generating a speckled appearance typical of enchondromata.

Martin Gargan FRCS(Trauma & Orth) MA is a Consultant Paediatric Orthopaedic Surgeon, Bristol Royal Hospital for Children, Bristol, UK.

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Figure 2 Radiograph of the proximal tibia showing an enchondroma, the intramedullary radiolucent lesion affecting the metaphyseal region with epiphyseal involvement. Note the expansion of bone and thinning of the cortex.

Asymmetrical limb shortening Affected long bones can be substantially shortened and grossly enlarged.5,10 Limb length discrepancy is therefore one of the earliest detectable signs, usually manifesting as a limp in the child with lower limb involvement.8 In severe disease there may be gross deformation of the long bone, particularly angulation, resulting in bowing of limbs and occasionally abnormal joint function.11,12 There is no medical treatment for enchondromatosis. Orthopaedic management is aimed at restoring function by correction of deformities and limb length discrepancy using osteotomy and frame reduction.5,13

Figure 3 Radiograph showing enchondromatosis of the fourth and little fingers of the left hand. The affected fingers are shortened and lesions would be visible and palpable on examination.

• enlargement of a lesion after skeletal maturity • onset of pain in an affected bone • pathological fracture of a long bone Radiographic signs of malignant transformation are:1,8 • extensive cortical erosion with expansion into the surrounding soft tissues • poorly demarcated border of the tumour • foci of unmineralised cartilage within a mineralised tumour. Treatment of malignancy requires excision with wide surgical margins by resection or amputation.9,15 If this is achieved the recurrence rate is relatively low. If the excisional margins are inadequate or there is tumour cell contamination, recurrence rates of nearly 70% have been reported due to the ease of spillage of cells from chondrosarcomas. Treatment by radiotherapy and chemotherapy are ineffective as chondrosarcomas lack the vascular supply required for such methods to be ­therapeutic.15

Bony swellings of fingers and feet The small bones of the hands and feet are one of the most common sites to be affected; typically the phalanges and metacarpals.1,10 Lesions usually manifest as a painless swelling of the fingers or toes, with the affected bones becoming progressively enlarged as the tumour grows, resulting in a globular shape11 (Figure 3). Function can be impaired in severe cases, an indication for surgical intervention, principally curettage with or without bone grafting.5,11,12 Pathological fracture As enchondromata grow the cortical bone thins, sometimes resulting in a pathological fracture8,14 (Figure 4). Malignant transformation is highly unusual in peripheral sites but pathological fracture of a long bone is suggestive of chondrosarcoma formation.1,8

Maffucci syndrome The Maffucci syndrome is a genetic disorder where soft tissue haemangiomas form in addition to enchondromata. Like Ollier’s disease the condition is not hereditary but is much rarer, fewer than 200 cases having been reported in the medical literature.16 The haemangiomas (venous malformations) may be deep or superficial, manifesting as bluish, subcutaneous nodules commonly found in the extremities16 (Figure 5). Clinical signs are usually detectable before puberty.17 ­However, cases exist where a diagnosis of Ollier’s disease has been later revised to the Maffucci syndrome because of the formation of a

Malignant transformation The incidence of malignancy has been reported to be approximately 25–30% from long term studies.5,9 However, this risk is variable, with reports of malignant transformation in up to 50% of cases.1,10,11 Prognosis is difficult to predict but a normal life expectancy can be expected in those where malignancy does not develop. Regular and long-term follow up is imperative. Clinical signs which are highly suggestive of chondrosarcoma include:5,8,12

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Maffucci-specific glioma after enchondromata. This ­phenomenon suggests that the two conditions are simply elements of the same spectrum of enchondromatosis.18 The prognosis is much worse for Maffucci’s syndrome which is associated with a high rate of malignancy, not just of chondrosarcoma but also other highly aggressive tumours. ◆

References 1 Silve C, Juppner H. Ollier’s disease. Orphanet J Rare Dis 2006; 1: 37. 2 Fletcher CDM, Unni K, Mertens F. World Health Organisation classification of tumors. Pathology and genetics. Tumors of Soft Tissue and Bone. Lyon: IARC Press, 2002; 427. 3 Ollier’s LXEL. Dyschondroplasie. Lyon Med 1898; 88: 484–92. 4 Unni KK. Cartilaginous lesions of bone. J Orthop Sci 2001; 6: 457–72. 5 Spranger JW, Brill PW, Poznanski A. Enchondromatosis. Bone Dysplasias; an atlas of genetic disorders of skeletal development, 2nd edn. Oxford University Press, 2002; 554–555. 6 Maffucci A. Di un caso encondroma ed angioma multiplo. Contribuzione alla genesi embrionale dei tumori Movimento medico-chirurgico, Napoli 1881; 3: 399–412 and 565–575. 7 Hopyan S, Gokgoz N, Poon R, Gensure RC, Yu C, Cole WG, et al. A mutant PTH/PTHrP type I receptor in enchondromatosis. Nat Genet 2002; 30: 306–310. 8 Chew FS, Maldjian C. Enchondroma and enchondromatosis. www.emedicine.com, 2006. 9 Bulstrode C, Buckwalter J, Carr A, Marsh L, Fairbank J, Wilson-Macdonald J, Multiple enchondromatosis. Oxford Texbook of Orthopaedics and Trauma, 1st edn. Oxford University Press, 2002; 190–1. 10 Benbouazza K, Hassani SE, Hassikou H, Guedira N, Hajjaj-Hassouni N. Multiple enchondromatosis: a case report. Joint Bone Spine 2002; 69: 236–9. 11 Simon NP, Simon MW. Multiple enchondromatosis: Ollier’s disease. Int Pediatr 2002; 17: 231–2. 12 Miyawaki T, Kinoshita Y, Lizuka T. A case of Ollier’s’ disease of the hand. Ann Plast Surg 1997; 38: 77–80. 13 Jesus-Garcia R, Bongiovanni JC, Korukian M, Boatto H, Seixas MT, Laredo J. Use of the Ilizarov external fixator in the treatment of patients with Ollier’s disease. Clin Orthop Relat Res 2001; 382: 82–86. 14 Margolis J. Ollier’s disease. Arch Intern Med 1959; 103: 279–84. 15 Bulstrode C, Buckwalter J, Carr A, Marsh L, Fairbank J, WilsonMacdonald J. Multiple enchondromatosis. Oxford Texbook of Orthopaedics and Trauma, 1st edn. Oxford University Press, 2002; 241. 16 McDermott A-L, Dutt SN, Chavada SV, Morgan DW. Maffucci’s syndrome: clinical and radiological features of a rare condition. J Laryngol Otol 2001; 115: 845–7. 17 Lewis RJ, Ketcham AS. Maffucci’s syndrome: functional and neoplastic significance: case report and review of the literature. J Bone Joint Surg Am 1973; 55: 1465–1479. 18 Mellon CD, Carrer JE, Owen DB. Ollier’s disease and Maffucci’s syndrome. Distinct entities or a continuum. A case report – enchondromatosis complicated by an intracranial glioma. J Neurol 1988; 235: 376–8.

Figure 4 Radiograph showing an enchondroma of the left femur that has resulted in a pathological fracture.

Figure 5 Radiograph showing both hands of a patient with Maffucci’s syndrome. Enchondromatosis is seen in the bones, along with soft tissue masses and phleboliths consistent with the haemangiomas that characterise the condition.

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The use and abuse of locking plates

In the late 1950s the Swiss AO group, led by Maurice Muller, launched a battle against ‘fracture disease’ by promoting early mobilization of injured patients and their limbs. To achieve this, fractures were anatomically reduced and compression fixation was applied in order to achieve sufficient stability to enable patients to mobilize the injured limb free of the constraints of plasters and splints. When successful this technique produced a marked reduction in ‘fracture disease’ and the compression fixation led to direct bone healing with no callus formation by producing absolute stability. However, it required open reduction and anatomical fixation of even the most complex fractures. The price paid for focusing on mechanical stability was slower bone healing and, particularly in less experienced hands, severe damage to the blood supply of the soft tissue envelope and underlying periosteum. Critics often cited examples of increased nonunion, infection and re-fractures after premature plate removal. In the late 1980s Stephen Perren and colleagues,1,2 studied the potential of plates and internal fixators with reduced bone surface contact (LC-DCP and PC-Fix). Animal studies confirmed the reduced damage to periosteal blood supply and the formation of substantial amounts of early solid bridging callus. Infection was also noted to be significantly reduced. A new era was born to respect the biology of the soft tissue envelope, and tools and techniques were developed to reduce damage to the bone blood supply during fracture surgery; so called ‘Biological Fixation’.3,4 This entailed not only new implants but also new techniques to minimize soft tissue damage. Fracture reduction by closed indirect means using traction and ligamentotaxis (Indirect Reduction), less invasive surgery and minimal disturbance of the fracture hematoma are all important contributors to a successful outcome using these techniques. The need for anatomical reduction and absolutely stable fixation was confined to intra-articular fractures and non-unions. In extra-articular fractures of the metaphyseal and diaphyseal regions, there was a realization that general re-alignment with correction of the overall position, length and rotation would suffice (the radius and ulna being exceptions to this, due to their unique anatomical relationship with each other). This could be achieved using internal and external splints, thus preserving blood supply and accelerating healing by callus formation, indirect bone healing. Locked intra-medullary fixation using nails, and extra-medullary fixation using bridge plating techniques, are both examples of internal splinting, which allows controlled movement at the fracture site, so called relative stability. Providing the blood supply is preserved this will usually lead to reliable callus formation, even in multi-fragmentary fractures, without the need to bone graft. Locking plates are part of this evolution of extra-medullary techniques to preserve biology, allow controlled movement (relative stability), encourage more rapid fracture healing and yet still allow early mobilization of the injured patient and their limb. In order to understand the role of locking plates in modern day fracture surgery we need to consider the following: What are locking plates? How have they evolved? Clinical indications & particular uses Tips and pitfalls Cost

Paul Szypryt Daren Forward

Abstract The concept of locking plates is now more than 15 years old and represents a clear advance in the management of fractures by internal fixation using plate technology. Fractures in osteoporotic bone, fractures with short metaphyseal segments and fractures treated with biological fixation are all better managed with lockable plates. There are, of course, additional and unique problems that arise from their use. Locking plates evolved through the recognition that in order to get a fracture to heal quickly and satisfactorily it was not always necessary to achieve rigid internal fixation and absolute stability. The biology of the fracture would be better preserved by using low contact implants combined with minimally invasive surgical techniques. These implants also offered the ability to confer angular stability to a fixation construct. In this article we use the term locking plates and lockable plates. Locking plates refer to those plates that have holes that will only accommodate locking head screws and are therefore used to bridge across the fracture like an internal splint or fixator e.g. Less Invasive Stabilisation System (LISS). In contrast, lockable plates refer to implants that can accept either standard screws or locking screws. This hybrid implant can, therefore, be used to produce internal splintage with locking screws or the more traditional compression, buttressing and neutralization when standard techniques are employed. Failure to recognize that a lockable plate does not necessarily need to have locking head screws inserted is discussed as one of the pitfalls in using these implants.

Keywords fractures; locking plates; osteoporosis

Introduction Historically, internal fixation of fractures was used as a last resort to achieve bony union. This frequently followed prolonged periods of failed non-operative treatment, which resulted in joint stiffness, muscle wasting and disuse osteoporosis: so called ‘fracture disease’. In addition, the techniques of fracture fixation were often poorly understood and poorly executed, resulting in high rates of failure.

Paul Szypryt Consultant Trauma & Orthopaedic Surgeon, Nottingham University Hospitals, Queen’s Medical Centre, United Kingdom. Daren Forward Consultant Trauma & Orthopaedic Surgeon, Nottingham University Hospitals, Queen’s Medical Centre, United Kingdom.

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a Standard cortical screw e compressing plate to surface of the bone, providing friction and stabilty. b Locking head screw e providing angular stability and preservation of periosteal blood supply. Figure 1

What are locking plates?

implant into an internal fixator, which functions mechanically more like an external fixator buried beneath the skin (Figure 2). The usual mode of failure with standard plates and screws, especially in osteoporotic, bone is sequential screw loosening. However, with angularly stable implants the locking head screws lock into the plate so that sequential loosening does not occur and this greatly enhances the resistance to bending forces (Figures 3 and 4). The progression of this concept led to the development of the LISS system of plates for the distal femur and proximal tibia (1995 and 1997 respectively) and later the Philos plate for the proximal humerus. This created a generation of anatomically pre-contoured locked fixed-angle systems.

Locking plates are surgical tools used to stabilize fractures. They differ from standard plates in that the screw heads lock into the plate, providing a composite unit, or ‘fixed-angle device’. Standard plates are compressed against the underlying bone by the pressure applied using normal screws. This creates friction that abolishes movement but also damages the blood supply to the underlying periosteum. This compression, and hence stability, will reduce with time, particularly in osteoporotic bone. In contrast, locking plates are not usually compressed against the bone and therefore have less of a biological footprint on the periosteum (Figure 1). In addition the effect of locking the screws to the plate greatly enhances fixation especially in osteoporotic bone and reduces the risk of implant failure from screw pullout.

The development of locking head screws (LHS) Unlike conventional screws, which compress against the plate creating friction, locking head screws are locked into the plate giving axial and angular stability. The locking head screws of the internal fixator are actually more like threaded bolts. No compression of the plate onto the bone occurs and the forces from the bone to the fixator occur across the neck of the screws. For this reason the geometry of the LHS is different to a corresponding cortical screw.

How have they evolved? The first uses of locking plates were reported in Craniomaxillofacial and Spinal surgery.7e9 In general trauma, various types of experimental plate systems were tested to try and improve bone blood supply and improve fixation in osteoporotic bone (the Schuhli nut10 and PC-Fix1,2). The main driving force behind these developments was a realization that preserving biology was probably more important than creating absolute stability in every case, no matter what the cost to the bone blood supply. The concept of the locked internal fixator specifically addresses the issues around ‘biological fixation’, namely, indirect reduction techniques, minimally invasive surgery and preservation of bone blood supply and the fracture haematoma, whilst allowing some movement to help stimulate callus formation (relative stability). Although they resemble a plate the function of the device is more like a fixator buried sub-muscularly/subcutaneously; because the screw heads are locked into the plate holes they provide angular stability and the plate is not compresses against the bone surface, as with standard plates and screws. This angular stability of the locking head screws (LHS) provides excellent anchorage, even in osteoporotic bone, and the lack of compression improves bone biology. This turns the

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a Standard plate and screws acting as a load sharing device. b Locking plate acts like an internal splint and load sparing device. Figure 2

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a, b Sequential screw failure with standard plates. Figure 3

 The head is conical rather than hemispherical to improve locking fixation in the screw hole, with better distribution of forces between the screw head and the threaded holes.  The core diameter is increased giving much greater strength in bending (200%) and shear (100%).  The shaft of the screw is slightly larger than the screw hole and tapered to produce radial preload and prevent bone reabsorption and reduce micro-movement. Locked screws provide better anchorage both in flexible bridging fixation and in absolutely stable fixation, thus offering advantages to fixation in osteoporotic bone.

reduction techniques, minimally invasive surgical exposure and flexible internal splinting to facilitate callus formation. They are 100% locked fixators because only locking head screws are used and the plates are pre-shaped to match the expected anatomy of the lateral femoral and tibial condyles. They are designed with matching jigs to facilitate percutaneous fixation with unicortical, self-drilling, self-tapping locking head screws for use in the diaphyseal region. Whilst there are definite advantages of ‘biological’ fixation using locking plates there were also noted to be potential disadvantages to such an inflexible system. Essentially, they provide internal splinting only.

Less Invasive Stabilization System (LISS) Advantages (i) Locking of the screw head to the plate means that the bone thread can no longer be stripped during insertion.

The AO Less Invasive Stabilization System (LISS) was initially developed for fractures of the distal femur (1995) and proximal tibia (1997). This greatly facilitated fixation and stabilization using all the principles of ‘biological’ fixation, including indirect

a, b Increased resistance to bending forces with locked plates. Figure 4

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The combination hole of the LCP combines the use of compression/lag and locking screws in one implant. Figure 5

Progression to Locking Compression Plate (LCP) Two separate systems therefore came into existence. Traditional compression plates, LC-DCP with oval holes and the ability to compress, buttress and neutralize or protect primary lag screw fixation. New locked internal fixators, such as the LISS/Philos (Figure 6) for use in specific areas, but only as internal splints. By merging both systems a new plate evolved, the Locking Compression Plate (LCP).

(ii) Compression between plate and bone is unnecessary and does not occur, therefore periosteal blood supply is preserved. (iii) The fixed-angle connection between the LHS and plate offers improved stability when bending and torsional forces are applied. It is much less likely that the plate will pull away from the bone because the screws will not sequentially loosen and fail, as in a standard plating system. This enhances the fixation in osteoporotic bone considerably and has the same benefit in peri-articular fractures where there may be a small articular block. (iv) The plates do not need to be anatomically contoured and do not sit flush against the surface of the bone.

Locked Compression Plate (LCP) The LISS system was designed as a device that would provide angular stability and would only accommodate locking head screws (all the holes in the plate are threaded). This made it incompatible with other standard plate systems, usually made of stainless steel. The LISS technology was considered by some to be too restrictive. Thanks to the ingenious work of Professor Michael Wagner (Vienna), Robbie Frigg (AO Institute, Davos) and other colleagues a hybrid system evolved including a combination hole, which has been incorporated into the latest generation of Locking Compression Plates (LCP, Synthes).5,6 The LCP combination hole allows internal fixation to be achieved by inserting either a conventional screw into the unthreaded part of the hole or a locking head screw into the threaded half of the hole (Figure 5). This makes the implant much more versatile and allows the surgeon to choose whether to use all standard screws, all locking head screws or a combination of both.

Disadvantages i. Lack of ability to introduce lag screws through the plate in intra-articular fractures and simple oblique fractures. ii. Loss of tactile feel when inserting screws in bone. iii. Fixed orientation of LHS. iv. Over tightening of the LHS, producing cold-welding of the screw head to the plate making removal difficult. v. Loss of ability to use the plate as a reduction tool, compression or buttress device. vi. If the plate is not pre-shaped to match the local anatomy then in areas of the body where there is minimal subcutaneous tissue the locked plates may be prominent beneath the surface of the skin and can cause pain and irritation necessitating removal. The LISS system can truly be considered to be a locking plate in that it can only have locking head screws inserted through it.

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a, b Locking (Philos) plate for fixation of short metaphyseal segments, in this case in the proximal humerus. Figure 6

The LCP can therefore provide the usual functions of a standard LC-DCP, i.e. compression, buttress and neutralisation/ protection and also function as a pure bridging internal fixator with locked screw options. This system has two plating techniques to choose from combined in a single implant. This makes it a lockable plate, a term which highlights that locking head screw use in this situation is an application of a technique, not a prerequisite with the use of these plates e the same metal plate can be used in different ways depending on which screws are used and the order in which they are inserted.

There are three specific indications for use of a locking/ lockable plate: 1. Osteoporotic fractures including use in peri-prosthetic fractures. 2. Peri-articular fractures with short metaphyseal segments. For these, pre-shaped anatomical plates can be used as reduction tools. 3. Biological fixation including percutaneous plating of multifragmentary fractures. It is clear that overall, lockable plates have enabled a change in the approach to treatment of certain fractures, such as the distal radius, where lockable plates allow control of the short articular segment from the volar surface, or in the proximal humerus with a much greater purchase possible in the humeral head (Figure 6). The control of peri-prosthetic fractures (Figure 7) with mono-cortical locked screws is also significantly greater than with previously used standard techniques. There are also identifiable fracture types where lockable plates are generally not required because standard implants work well, such as appropriate hip fractures (DHS), partial articular fractures (buttress plate), diaphyseal forearm fractures, fractures around the ankle, metastatic diaphyseal fractures treatable with intra-medullary nails, and simple fractures involving normal quality diaphyseal bone.

Other locking plate systems Apart from Synthes many other companies now have lockable plate systems on the market which work in slightly different ways. Each system may well offer different locking options some with variable screw/pin angulation and most with pre-shaped anatomical plates. The general principles of their application are as outlined in this article. However, there is not enough information available to the authors to compare the various systems and offer an objective appraisal.

Clinical indications and examples of use Most common fractures do not require fixation using a locked plate. The majority will heal using either non-operative treatment or conventional methods of internal fixation. The key to correct use of a locked compression plate (LCP) is to understand that it is a versatile implant and not a technique. The surgeon should consider how they would treat a fracture in the absence of a LCP i.e. does the surgeon want to achieve absolute stability or relative stability, since a locked compression plate (LCP) can be used to achieve either type of stability, and sometimes both within the same fracture. Certain fractures are associated with higher risk of non-union or loss of stability and lockable plates can reduce the risk of failure of fixation.

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Osteoporotic bone: In cortical bone of good quality, the use of a locked screw within a plate offers a minimal improvement in the pullout strength of the construct compared to a standard screw, and comes with possible disadvantages of the locking technique. In osteoporotic bone however, the increase in pullout strength is significant enough to overcome any potential disadvantages of locking. This is afforded by the increased rigidity of the fixed-angle construct delivered by the locking head screws/ plate composite and lack of toggle (Figure 4). Peri-articular fractures: The control of short segments of metaphyseal bone is improved with a locked construct (Figures 6 and 8) Anatomical plates with locking options also provide the option of

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a, b Locking screws used to gain purchase in limited bone around a prosthesis. Figure 7

applying the pre-contoured plate to the articular segment and using the construct to aid in the reduction of the articular segment onto the metaphysis, e.g. in the distal femur and distal radius. The locking construct is also angularly stable, so that it can resist collapse (for example typically into varus in the proximal tibia), thereby avoiding secondary loss of alignment and position.

of soft tissue attachments to a comminuted fracture by percutaneous insertion and bridging of the zone of injury. The preservation of blood supply and controlled movement at the fracture site allows the formation of an abundance of callus and rapid bone healing without the need for bone grafting. Planning This is more important than ever and should include not only plate length, number of screws and order of insertion etc., but considerable thought should be given to the surgical

Biological fixation: This may be considered to be using the plate as an ‘internal external fixator’e the plate can be used in much the same way as an external fixator would be, with preservation

a, b Hybrid fixation e locked screws proximally bridging the comminuted fracture, but using regular screws for purchase in good cortical bone distally. Figure 8

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Post operative regime - Wound care, antibiotics and VTE prophylaxis (starting before surgery if appropriate) - Physiotherapy (range of movement, bracing/splintage) - Weight bearing status - X-rays and follow up arrangements

tactic and purpose of the implant. The surgeon should consider in detail. Patient factors - Fracture location (diaphysis v metaphysis v articular) and configuration (simple v multi-fragmentary) - Condition of the soft tissues (high v low energy, open v closed) - Condition of the patient (isolated v multiple injuries) - Presence of other implants (peri-prosthetic fractures)

Reduce the fracture first This is the principle of ‘lag, then lock’. Any articular element should be anatomically reduced and fixed using the principles of absolute stability. The articular block is then realigned to the diaphysis, using a pre-shaped anatomical plate as a reduction tool, before anchoring the plate to the diaphysis. The plan must also include the reduction technique. The plate will not reduce the fracture if only locking screws are used, as these do not ‘drag’ the bone to the plate. Therefore, the surgeon should be clear whether direct or indirect reduction techniques are being used, and how the reduction is to be held e by lag screws, clamps, cerclage wires or pre-shaped plates pressed to the bone.

Intended outcome - Absolute stability with direct bone healing - Relative stability with indirect bone healing - Combination of both (complex articular and complex metaphyseal fractures) Direct or indirect reduction - Patient position and surgical approach (direct open reduction v indirect closed reduction) - Type of operating table (traction v radiolucent) - Additional equipment (reduction aids, image intensifier)

Clinical uses Conventional plating - anatomical reduction (usually direct) and absolute stability, using inter-fragmentary compression is used for: - Displaced intra-articular fractures - Simple transverse/oblique fractures - Non-unions - Precision osteotomies A standard LC-DCP or new hybrid LCP using standard screws can achieve the usual plate functions of compression þ/ lag screws, buttressing and neutralisation/protection of lag screw fixation (Figure 9).

Choice of implants - Type of plate (anatomically pre-shaped v standard) - Length of plate and purpose (locked plates are usually longer than conventional plates to allow a longer working length and reduced stress concentration at the fracture site) - Number of screws and purpose (standard v locked v mixed) - Order of screw insertion and purpose (far-far, near-near for locked internal fixators. If a mixture of standard and locking head screws are used then the standard screws must be inserted first)

aec LCP used with standard cortical screws to produce compression at the fracture. Figure 9

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a, b LCP with locking screws producing bridging fixation with an increased working length of the implant. Figure 10

Biological plating - anatomical alignment (indirect reduction), minimally invasive approach and relative stability is often appropriate for: - Multi-fragmentary fractures of the diaphysis/metaphysis - Peri-prosthetic fractures - Opening wedge osteotomies Locked plates (LISS, Philos) or LCP using locking head screws would function as an internal fixator or bridging internal splint (Figure 10).

- Diaphyseal/metaphyseal fractures with extension into the adjacent joint - Segmental fractures - Fractures involving osteoporotic bone e.g. the proximal humerus (Figures 6e8). The versatility of the LCP can offer the option of two biomechanical principles in certain situations where a combination of inter-fragmentary compression and the internal fixator (bridging) techniques are required. If mixed techniques are used within the same implant then the surgeon should be clear what he/she is trying to achieve. When a combination of standard screws and locking head screws are used at the same time then the standard screws must be inserted first. The locking head screws are usually used to

Combination plating - in fractures that require a mixture of techniques, combining compression, buttressing and angular stability can be used: - Intra-articular fractures with complex metaphyseal components

a A short working length of implant produces high stress and strain over a small area of implant. b Longer working length produces less stress and strain reducing risk of implant failure. Figure 11

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achieve angular stability either in a short articular block, to avoid late deformation, or to provide better fixation in osteoporotic bone.

 

Tips and pitfalls Attention to detail is important:  the drill guide must be screwed into the threaded hole correctly to ensure the bone hole is drilled correctly. All debris should be cleared from the hole, and contouring the plate can compromise the threaded hole.  contouring may also disadvantageously alter the fixed trajectory of the screws, so that the locking screws come to be directed toward the joint.  locked screws are usually inserted with a torque-limited screwdriver to avoid cold-welding of the screw head to the plate, particularly in titanium systems. Failure to achieve sufficient tightening, however, can lead to screw backout, particularly in mobile regions such as the proximal humerus.  when using combination techniques involving lockable and non-lockable screws, the non-locked screws should be inserted first. Once the lockable screws are inserted the



 

distance between the plate and the bone is fixed and cannot be changed. damage to the bone blood supply, either at the time of the original injury or by subsequent surgery, will lead to delayed union. unlike conventional plates, which often fail by sequential screw loosening, locked implants usually do not loosen but there may be sudden catastrophic failure resulting in plate or screw breakage. This is particularly a problem in unreduced simple fractures, where there is a residual fracture gap and too stiff a construct with a short working length of implant, producing high stress over a small area (Figures 11 and 12). locked constructs should not be too rigid and should be longer and use fewer screws than a non-locked construct applied to the same fracture. This allows controlled movement with a longer working length to reduce the stress on the implant (Figures 10 and 12). locking plates are not necessary for simple articular/diaphyseal fractures in normal quality bone. when using indirect reduction methods, adequate reduction of the fracture may be very difficult to ascertain using the limitations of per-operative image intensifier. It is especially important to assess the limb clinically, particularly rotation, as this is often overlooked.

aec An imperfectly reduced fracture within a stiff construct with a short working length can lead to catastrophic implant failure. Figure 12

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Cost

3 Ganz R, Mast J, Weber B, et al. Clinical aspects of ‘biological plating’. Injury 1991; 22(1): 4e5. 4 Perren SM. Evolution of internal fixation of long bone fractures: the scientific basis of biological internal fixation: choosing a new balance between stability and biology. J Bone Joint Surg Br 2002; 84: 1093e110. 5 Frigg Robert. Development of the locking compression plate. Injury 2003; 34(2): SB6e10. 6 Wagner M, Frigg R. Locking compression plate (LCP). Einneuer AO standard. OP J 2000; 16(3): 238e43. 7 Morscher E, Sutter F, Jenny H, Olerud S. Anterior plating of the cervical spine with the locking screw plate system. Chirug 1986; 57: 702e7. 8 Egol KA, Kubiak EN, Fulkerson E, Kummer FJ, Koval KJ. Biomechanics of locked plates and screws. J Orthop Trauma 2004; 18: 488e93. 9 Ogr S, derholm AL, Lindquist C, Skuttnabb K, Rahn B. Bridging of mandibular defects with different reconstruction systems: an experimental study. J Oral Maxillofac Surg 1991; 49: 10. 10 Kolodziej P, Lee FS, Patel A, Kassab SS, Shen KL, Yang KH, Mast JW. Biomechanical evaluation of the Schuhli nut. Clin Orthop Related Res 1998; 347: 79e85.

Invariably, because of the newer technology and increased manufacturing costs, these implants are in general much more expensive than the previous non-locking options. Both the locking screws and the pre-shaped anatomical plates command a premium and cost up to 4 as much as corresponding standard implants. The surgeon should therefore, be quite specific about the indications and benefits of using this new technology. Usage should be limited to essential cases then costs can be contained. The indiscriminate use of locking head screws and plates should be discouraged.

Summary Lockable plates have clearly advanced the treatment of certain fractures such as those of the proximal humerus and distal radius, but require careful planning to maximize their benefits. There is no substitute for poor planning or poor surgery. Careful attention to detail is required in pre-op planning and plate insertion to realize these benefits. Fractures involving osteoporotic bone, with short metaphyseal segments and biological fixation are the three situations that lockable plates are of greatest use. A

Acknowledgment

REFERENCES 1 Tepic S, Peren SM. The biomechanics of the PC-Fix internal fixator. Injury 1995; 26(2): SB5e10. 2 Haas N, Hauke C, Scheutz M, et al. Treatment of diaphyseal fractures of the forearm using the Point Contact Fixator (PC-Fix): results of 387 fractures of prospective multicentre study. Injury 2001; 32(2): SB51e62.

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The authors would like to thank the AO Foundation for help in providing the illustrations for this article. No financial inducement has been received by either of the authors in the preparation of this article.

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Shoulder arthroscopy, anatomy and variants - part 1

earlier use of the arthroscope has been reported by the Danish surgeon Nordentoft (1912),2 Takagi in Japan (1918),3 Dr Eugen Bircher (1922)4 and Dr Phillip Kreuscher (1925).5 These pioneering arthroscopists however, performed these early procedures primarily on knee joints. In addition, Burman also defined several arthroscopic principles in his work that are still applied today. These include joint distension (using fluid or air), the use of traction and the importance of positioning. The advent of World War II slowed progression, and it was not until the 1950’s, when the work of Takagi was revived by Dr Masaki Watanabe, that arthroscopy began to move forward again. Watanabe modified existing arthroscopic equipment, and in 1958 he introduced the Watanabe 21, which led to the complete revision of the Atlas of Arthroscopy. Further advances in the 1970’s and 80’s included the introduction of smaller diameter arthroscopes, higher quality lenses, the use of fibre optic light sources and later, the introduction of the charge coupled device (CCD) camera. The development of shoulder arthroscopy remained slow, its first recorded clinical use being by Andren and Lundberg in 19656 for the treatment of frozen shoulder. Watanabe subsequently described the posterior portal in 19787 and through this he began to describe shoulder pathology as viewed through the arthroscope.8 Conti shortly after described the anterior portal which he used to perform brisement (capsular distension) and capsular release in 18 patients with frozen shoulders.9 The first documented use of the arthroscopic shaver in the shoulder appeared in 1980.10 Thereafter shoulder arthroscopy became increasingly popular, especially in the management of dynamic gleno-humeral joint and sub-acromial disorders. More recently, the arthroscope has been used to perform acromio-clavicular joint stabilisations and excision, suprascapular nerve releases, bone block transfers and even latissimus dorsi transfers. These developments are beyond the scope of this article and innovative techniques continue to be introduced with regularity.

Simon Boyle Manuel Haag David Limb Laurent Lafosse

Abstract Arthroscopy is increasingly the modality of choice for interventional procedures in shoulder surgery. It is often learned after a basic grounding in knee arthroscopy, but the wide variation in normal anatomy and unfamiliarity with the 3D arrangement of the joint can easily confuse. This article therefore describes the technicalities of shoulder arthroscopy and introduces the many structures that are encountered. In part 1 we will discuss the indications for arthroscopy and the process of setting up and performing the procedure in a clinical setting, with useful concepts and technical tips. In part 2 we will move on to discuss the range of findings that can be encountered, both normal and pathological, as correct recognition is critical to safe subsequent management.

Keywords arthroscopy; patient positioning; portals; shoulder anatomy

Introduction Since the early 1980’s there has been an exponential rise in the use of the arthroscope in shoulder surgery. The minimally disruptive nature of arthroscopic surgery along with the benefit of magnification, has resulted in an improved understanding of shoulder anatomy, its variants and the pathophysiology of shoulder dysfunction. This, combined with developments in instruments, pumps and cameras, has led to a natural increase in the proportion of therapeutic procedures that can be performed arthroscopically, and therefore an expansion in the indications for shoulder arthroscopy.

Indications The indications for shoulder arthroscopy are continually expanding. Its early use was as a diagnostic tool but this role now encompasses many complex procedures. Both intra- and extraarticular shoulder girdle structures are seen as being accessible to the arthroscope and a combination of approaches can be adopted. The arthroscope has the advantage of causing minimal disruption to the existing joint anatomy and its use has led to a better appreciation of several pathological entities, most notably the Superior Labrum Anterior Posterior (SLAP) lesion. The gleno-humeral joint (GHJ), sub-acromial space, acromioclavicular joint (ACJ) and scapulo-thoracic articulation are all accessible to the arthroscope. Furthermore, neurovascular structures such as the axillary nerve, supra-scapular nerve, brachial plexus and axillary vessels are all within reach of the skilled (or clumsy!) arthroscopist (Table 1).

History The first shoulder arthroscopy is generally credited to the American Dr Michael Burman in 1931.1 He performed his initial arthroscopies on cadaveric shoulders, although evidence of the

Simon Boyle MSc FCRS(Tr&Orth) Shoulder Fellow, Alps Surgery Institute, Annecy, France. Manuel Haag MD Shoulder Fellow, Alps Surgery Institute, Annecy, France. David Limb BSc FRCSEd(Orth) Consultant Orthopaedic Surgeon Leeds General Infirmary, Leeds, UK. Laurent Lafosse France.

MD

Anaesthesia for shoulder arthroscopy As shoulder surgery has advanced, so has the familiarity and enthusiasm for regional nerve blockade for both anaesthesia and postoperative pain control. Consequently, shoulder arthroscopy

Shoulder Surgeon, Alps Surgery Institute, Annecy,

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The indications for shoulder arthroscopy Diagnostic Therapeutic

Gleno-humeral joint

Instability

Cuff pathology Capsular pathology Biceps tendon

Synovial disorders

Sub-acromial space (Bursoscopy)

Acromio-clavicular joint

Septic arthritis Ganglia/cysts Cartilage lesions (OA) Impingement Cuff pathology

Supra-scapular nerve Scapulo-thoracic articulation

Instability Dislocation Degeneration Entrapment Snapping scapula

Muscle transfers

Large irreparable cuff tears

Bankart repair Capsular plication Capsular shrinkage Latarjet procedure Calcific tendinitis Rotator cuff tears Adhesive capsulitis SLAP lesions Subluxing/dislocating tendon Biceps tendinopathy Synovitis Synovial chondromatosis PVNS Washout Decompression Graft procedures Calcific tendinitis Rotator cuff tears

Nerve release Bursitis Osteochondromas Arthroscopic Latissimus dorsi transfer

Table 1

is now routinely performed under inter-scalene block, general anaesthesia, or both. A basic knowledge of these anaesthetic techniques is essential for shoulder surgeons, especially with regard to their risks and complications and these will be discussed in a forthcoming issue of Orthopaedics and Trauma.

components to improve access to the posterior part of the shoulder. We insist on being able to place two fingers medial to the medial aspect of the scapula to ensure adequate access. The arm is prepared and draped, after which it can either be placed in traction, rested on a custom support or on a Mayo table. We prefer to use 2e3.5 kg of traction with the shoulder flexed to 60 and 20 abduction (see Figure 1). Advantages of the beach chair position - familiar anatomic upright position - easier to convert to an open procedure without re-positioning or re-draping - regional anaesthesia alone is better tolerated in this position

Patient positioning11,12 Shoulder arthroscopy is performed in either the lateral decubitus or beach chair positions. The choice often comes down to surgeon familiarity and this is usually a reflection of experience and exposure to a particular setup during training. There are, however, practical differences to consider when determining the optimal position for the patient. As with any surgical procedure, correct positioning is vital and many intra-operative difficulties can be avoided if time and diligence are taken at this stage of the setup. Beach chair Positioning begins with the patient in the supine position on a table equipped with a suitable back, neck and headrest. A cushion is placed behind the patients knees, which are flexed to approximately 30 . The table is then adjusted to bring the patients trunk into a more upright position with their hips flexed to 60 . Most modern tables allow the removal of different

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Figure 1 Beach chair position.

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- this position permits easier access for the anaesthetist should conversion to general anaesthesia be necessary - allows greater mobility of the arm and shoulder during surgery - the option of not using traction means less distortion of the soft tissues This is especially important during stabilisation procedures. Disadvantages - bubbles can accumulate superiorly in the subacromial space or the joint after using diathermy - increased risk of cardiovascular complications - increased risk of air embolus.

In both positions, care must be taken to support the head, neck and airway in conjunction with the anaesthetist. All pressure points should be well padded and the eyes protected. The amount of traction applied depends on surgeon preference, the procedure being performed and the body habitus of the patient.

Examination under anaesthesia The majority of diagnoses regarding shoulder pathology are made through good history taking, clinical examination and supplementary radiology. However, an examination under anaesthesia (EUA) can yield valuable information that may even lead to a change in the surgical management plan eg. unmasking unrecognised instability that was not detected on awake examination due to pain.

Lateral decubitus In this position, the patient is placed laterally on the operating table and supports are placed behind the upper lumbar spine and anterior to the anterior superior iliac spine. Alternatively, a bean bag type support can be used. An axillary roll is used to help protect the neurovascular structures of the non-operated side. The head is supported in a neutral position and the lower ear protected. A pillow is placed between the knees and these are flexed to 30 . The operative arm is placed in traction at approximately 30 abduction and 15 forward flexion, although this can be varied according to the procedure being performed (see Figure 2). Additional lateral traction can be added with a sling around the upper humerus. Finally, the table can be tilted laterally to bring the plane of the glenoid more horizontal, parallel to the floor. Advantages - familiarity if trained in this technique - traction improves the view in the subacromial space and glenohumeral joint - lower cardiovascular and cerebrovascular risk - an assistant may not be needed. Disadvantages - more difficult to convert to an open procedure - it is necessary to reach forwards and around for the anterior portals - patients do not tolerate isolated regional anaesthesia well in this position - the use of traction is associated with decreased limb perfusion and brachial plexus neuropraxia - peroneal nerve neuropraxia - increased risk of nerve injury with antero-inferior portal.

Passive range of movement This is assessed with particular attention to the point at which scapulo-thoracic motion commences. Passive range of movement is recorded in all planes and referenced against the pre-operative examination and in comparison to the opposite shoulder. This is particularly relevant in cases of adhesive capsulitis. It is useful to use the forearm as a goniometer for this assessment. Gleno-humeral stability Anterior and posterior translation should be performed and graded. We prefer to use the Load and Shift test13 in which the examiner stands behind the patient and with one hand stabilises the scapula whilst the other hand centres the humeral head with an axial load applied to the humeral shaft. Humeral translation is then applied in an anterior and posterior direction and graded as follows: Grade I - the humeral head can be translated to the glenoid rim Grade II - the head can be felt riding over the glenoid rim but reduces spontaneously with the release of the translating force Grade III - the head rides over the glenoid rim and remains dislocated on release of the translating force. This test is then repeated in increasing the degrees of abduction and rotation of the arm where occult subluxation is suspected and also allows assessment of any engaging Hill-Sachs lesion. Inferior translation is then assessed with inferior traction force applied to the arm. When a hollow or sulcus appears below the acromion, it can be graded as follows I - less than 1 cm II - 1e2 cm III - >2 cm If a sulcus is seen, then the test is repeated with the shoulder in external rotation. A persistent sulcus sign in external rotation suggests laxity of the rotator interval.14

The shoulder as a house Before introducing the arthroscope and proceeding to a formal joint evaluation, it is important for the surgeon to have a clear understanding of the anatomy of the shoulder. To improve spatial awareness and to gain a better appreciation of the 3 dimensional nature of the shoulder, the Alps Surgery Institute find it useful to create an analogy of the shoulder as a house (see Figure 3), with a ground floor, a first floor and a basement.

Figure 2 Lateral position.12

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Arthroscopic portals

The ground floor The glenohumeral joint is the main room on the ground floor. It’s ceiling is formed by the supraspinatus tendon, the anterior wall by the subscapularis tendon, and the posterior wall by the infraspinatus and teres minor tendons. The rotator cuff interval, including the superior glenohumeral ligament and the coracohumeral ligament, closes the junction between the supraspinatus and subscapularis tendon. Inside the glenohumeral joint, the biceps leaves the glenoid and exits the room through the rotator interval, like a chimney. Remaining on the ground floor but anterior and medial to the main room is the coracoid process. This is a key landmark and serves as the attachment of two musculotendinous structures: the pectoralis minor and the conjoint tendons. These structures help define the sub-coracoid and supra-coracoid spaces. The subcoracoid space is the second room on the ground floor, located between the subscapularis tendon (posteriorly) and the conjoint tendon (anteriorly). Medial to the coracoid, the brachial plexus including the axillary nerve and the subscapular nerves can be found. The ceiling of the sub-coracoid space is the coracoid process and the pectoralis minor tendon. Posterior to the infraspinatus and teres minor tendons exists the back room on the ground floor, lying between the rotator cuff and the deltoid muscle. This posterior sub-deltoid space can provide access like a staircase up to the subacromial space on the first floor and also down to the basement where the axillary nerve can be found.

Arthroscopic portal selection, and correct siting, are fundamental steps essential for a good view of the joint and associated pathology. The portals must be placed with the subsequent procedure in mind, to permit unhindered instrument access to relevant anatomical structures. The portals may just be required for suture management but they must be placed to minimise risk to local neurovascular structures. General technique Firstly the bony landmarks of the shoulder are palpated and marked with a surgical site pen (see Figure 4). The clavicle, acromioclavicular joint (ACJ), acromion, and scapula spine should be clearly marked, followed by the coracoid. One may choose to draw in the biceps tendon, in the bicipital groove, and the conjoint tendon. A bursal orientation line can be made which begins at the posterior edge of the ACJ to extend 4 cm laterally down the arm. This indicates the start of the subacromial bursa and demonstrates the anterior nature of its position. This is particularly helpful for the placement of the lateral portal. It is also helpful to recall that moving the scope through a portal resembles moving it within an hourglass, with the constriction or pivot at the level of the portal. We use a 30 scope and regularly change the direction of the lens by rotating the light cable to optimise our view. It is also important to review a structure through different portals, to give a better 3 dimensional perspective of the anatomy in question. To confirm that instrument access to an anatomical structure will be adequate, we introduce a needle at the potential portal site and probe the anatomy prior to making that definitive portal. We name our basic arthroscopic portals A to E, after which the more advanced and procedure specific portals can be labelled F to K (Figures 4 and 5).

The first floor The subacromial space is on the first floor. The supraspinatus tendon and the coracohumeral ligament now form the floor. The acromion, the clavicle, and the deltoid muscle all represent roof. The subacromial bursa is found here in the anterior part of the sub-acromial space, like a room within a room. Moving medially on the first floor is the supra-coracoid space beneath the clavicle. Herein lie the coracoclavicular ligaments and the suprascapular nerve. The coracoacromial ligament forms the division between the supra-coracoid space and the subacromial space.

Portal A e the posterior portal This is often the first portal established, as it is the standard viewing portal for the gleno-humeral joint. The entry point is located in the ‘‘soft spot’’, a location found approximately 2 cm

The basement Finally, at the level of the basement, the quadrilateral space is located beneath the gleno-humeral joint. The quadrilateral space communicates anteriorly with the most inferior part of the subcoracoid space and posteriorly with the inferior part of the posterior sub-deltoid space. Importantly, it contains the axillary nerve, the teres major and the latissimus dorsi tendons.

Figure 4 Skin markings of shoulder anatomy with basic and advanced portals.

Figure 3 The shoulder as a house.

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the scope over the posterior edge of the glenoid just above its equator, prior to advancing it into the joint. There is a feeling of ‘‘give’’ once the scope successfully enters the joint and this can be confirmed by attaching the camera. Structures seen e anterior capsule, gleno-humeral ligaments, rotator interval, subscapularis (superior 1/3), intra-articular biceps tendon, labrum, inferior recess, glenoid and humeral articular surfaces, supraspinatus and infraspinatus. Internervous plane e between infraspinatus (suprascapular nerve) and teres minor (axillary nerve) Structures at risk e posterior deltoid and/or infraspinatus fibres may be traversed with this portal - axillary nerve - posterior circumflex humeral vessels.

Posterior subacromial portal Figure 5 3D graphical representation of portal placement.

This utilises the same skin incision as the posterior A portal and is used to gain access to the subacromial space. This takes place after completion of the gleno-humeral joint inspection and the scope is withdrawn and the blunt trocar reinserted. The scope and trocar are reintroduced but redirected towards the anterolateral corner of the acromion. A sweeping motion is also used to clear any adhesions prior to recommencing fluid distension. The trocar is then replaced by the camera and a bursoscopy is performed. Structures seenesubacromial space, bursal side of rotator cuff, ACJ, extra-articular biceps, coracoid, coraco-acromial ligament. Structures at riskeposterior deltoid fibres may be traversed.

inferior and 1cm medial to the posterolateral corner of the acromion. A needle is inserted and directed towards the coracoid, into the inferior apex of a triangle formed by the acromion (superiorly), humeral head (laterally) and the glenoid (medially) (Figure 6). The needle serves as a guide to the correct direction of the joint and occasionally a hiss can be heard confirming its intra-articular location. A 5 mm skin incision is then made and the arthroscope containing a blunt trocar is introduced into the joint. To assist in the correct placement, the scope can be directed towards the middle finger of the opposite hand which is placed on the tip of the coracoid. In more difficult cases, the apex of this triangle and therefore the joint line, can also be identified by gently flicking the tip of

Portal Bepostero-lateral subacromial This portal is used to provide access to the posterior cuff and posterior labrum (posterior Bankart repair). Its position is generally located 1 cm antero-inferior to the postero-lateral edge of the acromion. Structures seeneposterior rotator cuff, often used for instrumented repair and suture management. Intra-articular advancement reveals the posterior labrum and joint structures as seen from a slightly different angle to the A portal. Structures at riskeposterior fibres of deltoid and if used to instrument articular structures, then infraspinatus is also breached. The axillary nerve is 4e5 cm inferior to this portal. Portal Celateral subacromial We use this portal as our initial portal in cases of large cuff tears and adhesive capsulitis. It is located at the level of the mid-acromion and provides excellent access to the subacromial space, but also allows visualisation, manipulation and repair of rotator cuff tears. As with the initial A portal, a needle is used confirm correct placement and to aid direction of the scope after the skin incision. This is an excellent working portal for many procedures. Structures seen - subacromial space, bursal side of rotator cuff, ACJ, suprascapular nerve, coraco-clavicular ligaments, extra-articular biceps, coracoid, coraco-acromial ligament, coracohumeral ligament and rotator interval, extra-articular subscapularis, conjoint tendon. Structures at riskelateral fibres of deltoid traversed, axillary nerve well inferior.

Figure 6 Triangle used for posterior portal placement.

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Summary

Portal Desupero-lateral This is known as the sub-bicipital portal and provides good access to the biceps tendon and the subscapularis insertion. It is positioned optimally using a spinal needle but is generally placed 1 cm lateral to the antero-lateral edge of the acromion. It can also provide access for single or double row repairs of the anterior labrum (Cassiopeia technique) as it gives excellent access to the anterior glenoid rim and neck. When the cuff is intact, intraarticular access is gained by traversing the CHL and rotator interval, where the CHL can be safely identified at its origin on the coracoid. This allows access not only to the joint but also to the sub-coracoid space for subscapularis releases and plexus exploration. It is also used for instrumenting the supra-coracoid space for suprascapular nerve exposure. Structures seen e supraspinatus, subscapularis, rotator interval, coracoid, sub-coracoid space/bursa, intra-articular access through the RI, suprascapular nerve, Structures at risk e antero-lateral deltoid, rotator interval, biceps tendon.

Shoulder arthroscopy still has a critical role in the diagnosis of shoulder pathology and for a range of conditions it allows better visualisation and interpretation of the pathoanatomy than other imaging modalities. Experience with arthroscopy has led to an explosion of interest and expertise in the technical skills that have made arthroscopic surgery the mainstay of surgical management for a wide range of shoulder conditions. In part 2 of this article we will consider the wide range of findings that can confuse the newcomer, as the spectrum of normal findings is wide yet the pathological lesions can be obscure. A

REFERENCES 1 Burman MS. Arthroscopy or the direct visualisation of joints: An experimental cadaver study. J Bone Joint Surg 1931; 13: 669e95. 2 Kieser CW, Jackson RW. Severin Nordentoft: the first arthroscopist. Arthroscopy 2001; 17-5: 532e5. 3 Watanabe M, Takeda S, Ikeuchi H. Atlas of arthroscopy. Tokyo: IgakinShoin; 1957. 4 Bircher E. Die Arthroendoskopie. Zentralbl Chir 1921; 40: 1460e81. 5 Kreuscher PH. Semi-lunar cartilage disease, a plea for early recognition by means of the arthroscope and early treatment of this condition. Illionois Med J 1925; 47: 290e2. 6 Andren L, Lundberg BJ. Treatment of rigid Shoulders by joint distension during arthrography. Acta Orthop Scand 1965; 36: 45e53. 7 Watanabe M, Takeba S, Ikeuchi H. Atlas of arthroscopy. 3rd edn. New York: Igaku-Shoin; 1978. 8 Watanabe M. Arthroscopy: the present state. Orthop Clin North Am 1979; 10e13: 505e22. 9 Conti V. Arthroscopy in rehabilitation. Orthop Clin North Am 1979; 10e13: 709e11. 10 Johnson LL. Arthroscopy of the shoulder. Orthop Clin North Am 1980; 11e12: 197e204. 11 Abrams JS, Bell RH. Arthroscopic rotator cuff surgery. New York: Springer; 2008. 12 Peruto CM, Ciccotti MG, Cohen SB, (in press). Shoulder arthroscopy positioning: lateral decubitus versus beach chair. Arthrocopy. 13 Silliman JF, Hawkins RJ. Classification and physical diagnosis of instability of the shoulder. Clin Orthop Relat Res 1993; 291: 7e19. 14 Fitzpatrick MJ, Powell SE, Tibone JE, Warren RF. The anatomy, pathology, and definitive treatment of rotator interval lesions: current concepts. Arthroscopy 2003; 19(Suppl. 1): 70e9.

Portal Eeanterior This portal provides a useful adjunct in diagnostic arthroscopy by allowing instrument access and therefore a means of palpating and dynamically stressing shoulder anatomy. The key to portal placement here is visualisation of the biceps tendon and rotator interval as seen through the posterior portal. A needle is first placed using an outside in technique, to confirm the best position of the portal and also to probe the relevant anatomy. The surface landmark is found halfway on a line joining the coracoid and acromion. It is important to remain lateral to the coracoid to minimise risk to the neurovascular structures. The intra-articular view confirms correct needle placement and the skin is then incised. The blade is advanced following the direction of the needle into the rotator interval, being cautious not to injure the adjacent structures. Alternative methods include the use of a blunt trocar to puncture the anterior capsule, use of a cannulated portal or techniques employing a switching stick. Structures seen e this portal is generally used for anterior instrumentation but it does provide alternative views of the biceps anchor, anterior labrum and glenoid neck, subscapularis and good views of the glenoid, infraspinatus, teres minor, posterior labrum and capsule. Structures at risk - this portal transgresses the anterior deltoid, and the rotator interval. - medially lies the brachial plexus and axillary vessels - infero-laterally lies the musculocutaneous nerve - cephalic vein.

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CME SECTION

CME questions based on the Mini-Symposium ‘‘Orthopaedic Oncology’’ C D E

The following series of questions are based on the MiniSymposium on ‘‘Orthopaedic Oncology’’. 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 Orthopaedics and Trauma Editorial Office at the address at the bottom of the RESPONSE sheet. Please photocopy this page if you wish to keep your copy of Orthopaedics and Trauma. Replies received before the next issue of the journal 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, via email, for your records.

5 For any given musculoskeletal tumour, in which of the following anatomical sites is it’s growth and spread likely to be most rapid A Anterior thigh B Calf C Medial thigh D Popliteal fossa E Posterior thigh

6 Which of the following layers does a marginal resection margin critically violate A The tumour B The pseudocapsule C The reactive zone D The compartment that may contain skip lesions E The boundaries of the compartment

Questions 1 In the assessment of soft tissue masses for malignant potential, which of the following is not a red flag A Deep to deep fascia B Firmly attached to skin C Increasing size D Pain E Size >5 cm

7 In which of the following situations is postoperative radiotherapy most likely to be preferred to preoperative radiotherapy in the adjuvant treatment of a musculoskeletal tumour A Lower limb tumour B Deeply situated pelvic tumour in sciatic notch C Tumour adjacent to lung D Tumour in supraclavicular fossa E Very large upper limb tumour

2 Which of the following tumours is most likely to show an unusual pattern of low T2 signal on MRI scanning A Aggressive fibromatosis B Atypical lipomatous tumour C Liposarcoma D Myxoma E Synovial cell sarcoma 3 Which of the following suggested principles governing the biopsy of suspected malignant musculoskeletal tumours is not appropriate A Biopsy can be performed under tourniquet control B Drains, if used, should be brought out through one end of the incision C Transverse incisions should be avoided D Tissue samples should be sent for microbiologiocal investigation E When a pathological fracture has occurred through a lesion, bone should be sampled from the fracture line

8 Which of the following factors has the weakest positive relationship to local recurrence after tumour excision A Age >50 B Histological grade C Size >5 cm D Tumours superficial to investing fascia E Surgical margin status

9 Approximately how many new cases of osteosarcoma occur in the UK annually A <1 B 1e5 C 20 D 50 E 100

4 Which of the following tumour attributes is not considered when staging using the AJCC system A Confinement or otherwise to one compartment B Involvement of regional lymph nodes

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Responses

10 Which of the following sarcomas is most likely to arise as a consequence of radiation exposure A Angiosarcoma B Lymphangiosarcoma C Malignant fibrous histiocytoma D Osteosarcoma E Rhabdomyosarcoma

Please shade in the square for the correct answer.

11 Which of the following conditions has the weakest association with the development of osteosarcoma A BeckwitheWeidemann syndrome B LieFraumeni syndrome C McCune Albright syndrome D Rothmund Thompson syndrome E Werners syndrome

12 Which of the following tumours is most likely to be eradicatable by radiotherapy alone A Chondrosarcoma B Ewings sarcoma C Multiple myeloma D Osteosarcoma E Plasmacytoma

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Your details (Print clearly) NAME..................... ADDRESS.................... ........................ EMAIL..................... RETURN THE COMPLETED RESPONSE FORM by fax to þ44-113-392-3290, or by post to CME, Orthopaedics and Trauma, Academic Department of Orthopaedic Surgery, ‘‘A’’ Floor Clarendon Wing, Leeds General Infirmary, Great George Street, Leeds LS1 3EX, UK.

Please fill in your answers to the CME questionnaire above in the response section provided to the right. A return address and fax number is given below the response section.

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Answers to CME questions based on the Mini-Symposium on ‘‘Imaging for Joint Replacement’’ Please find below the answers to the Current Orthopaedics CME questions from Vol. 23, issue 2 which were based on the MiniSymposium on ‘‘Imaging for Joint Replacement’’

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MINI-SYMPOSIUM: REVISION HIP SURGERY

(i) Evaluation of a painful total hip replacement

in error and other causes of the pain should be excluded. If the pain is different from that felt pre-operatively then a cause related to the surgery is more likely. Persistent pain with no pain free interval suggests infection, fracture, impingement or, in the case of uncemented prostheses, failure of initial stability. Late onset pain is seen in aseptic loosening, low grade infection, osteolysis or instability. Constant pain, rest and night pain is suggestive of sepsis or malignancy. Pain brought on by starting to walk from sitting - start up pain - is indicative of prosthetic loosening, but activity related pain relieved by rest suggests neurogenic or vascular claudication , bursitis, iliopsoas tendinitis or loosening. The site of the pain is important; pain localized to the greater trochanter can be due to trochanteric wires, bursitis or non union. Groin pain is often related to acetabular problems but occasionally is due to inguinal hernia or iliopsoas irritation. Occasionally deep gluteal pain arises from acetabular loosening, but is more commonly associated with lower back, sacroiliac joint or neurogenic problems especially combined with radicular pain. The latter should be distinguished from thigh pain or referred knee pain which may be indicative of femoral loosening. In particular, loosening at the tip of the stem, if it is in contact with posterior femoral cortex, can cause pain felt at the back of the thigh. However, some patients with a well fixed cemented or cementless stem can still experience thigh pain for no apparent reason. As well as noting any precipitating cause of the pain such as trauma or a fall which might indicate a fracture or the onset of loosening, factors related to the surgery must be sought as delayed wound healing, postoperative haematoma formation, persistent wound ooze, prolonged inpatient stay or antibiotic administration and distant sites of infection may indicate joint sepsis. Co-morbidities such as obesity, diabetes, rheumatoid arthritis and immuno-suppression are common in infection and in female patients any relationship between the pain and menses, such as can occur with endometriosis and other gynaecological conditions, should be noted. Obviously previous hospital records including operation details (surgical approach, implants etc) should be reviewed to gather as much information as possible.

Ardeshir Y Bonshahi Anil K Gambhir

Abstract Total hip replacement is a common and effective operation with a high success rate. This article discusses the aetiology and evaluation of persisting pain after total hip replacement. A thorough history and physical examination and appropriate investigation can determine the cause of the painful total hip replacement in most patients, allowing appropriate treatment.

Keywords evaluation; hip replacement; pain

Introduction In the US alone, it has been estimated that nearly 600 000 hip replacements and 1.4 million knee replacements will be performed in the year 2015.1 Long term results for Total Hip Replacement (THR) are excellent; it is a procedure that is successful in reducing pain and improving function and quality of life in patients with debilitating hip disease, and it is regarded as one of the most cost-effective interventions in health care.2,3 Patient expectation to a large extent predicts post operative satisfaction. Mancuso et al4 found that 60% of patients expected pain relief and those who wanted to return to nonessential activities were least satisfied (75%). A small proportion of patients continue to experience pain, some with no obvious cause, making these cases difficult to treat. Britton et al5 suggest the use of pain scores as the main outcome measure after THR, as postoperative pain remains one of the most sensitive predictors of success. They studied the natural history of pain after THR in more than 2000 patients and confirmed a large improvement in pain in the first six months, followed by a further small improvement for the next two years. After four years there was a gradual, sustained deterioration in pain levels.

Examination The clinical examination begins by observing the patients gait and looking for abnormalities, such as antalgic, Trendelenburg (which may be related to abductor deficiency after a direct lateral approach) or short limb gait.6 Leg length discrepancy should be measured with the patient standing on graduated blocks until the pelvis is level in order to determine true and apparent leg length discrepancy, seen with pelvic obliquity and scoliosis. Progressive leg shortening may be related to the subsidence of one of the components.7 The skin is inspected for scar location, sinuses and inflammation or swelling around the hip and is palpated to localize areas of tenderness, such as that due to trochanteric bursitis or underlying neuromas. Range of movement is assessed, paying particular attention to any pain provocation. Pain at an extreme of movement may be related to impingement or loosening, whereas pain throughout the range of movement may indicate an inflammatory process or infection. Pain on resisted flexion is suggestive of iliopsoas

History A detailed history and physical examination is important to narrow the differential diagnosis and allow more focussed investigations. It is important to note the nature of pain, its onset, duration, frequency, site, relieving and exacerbating factors. Pain similar to that felt preoperatively might suggest that the original diagnosis/pathology, for which the THR had been performed was

Ardeshir Y Bonshahi FRCS(Tr&Orth) Lower Limb Arthroplasty Fellow, Wrightington Hospital, Hall Lane, Appley Bridge, Wigan, Lancashire WN6 9EP, UK. Anil K Gambhir FRCS(Tr&Orth) Consultant Orthopaedic Surgeon, Wrightington Hospital, Hall Lane, Appley Bridge, Wigan, Lancashire WN6 9EP, UK.

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tendinitis. The examination should include the ipsilateral knee and a neurovascular examination of both lower limbs.

Differential diagnosis Possible causes of a painful total hip replacement can be divided into intrinsic and extrinsic: (Table 1) Intrinsic causes Aseptic loosening: This accounts for more than 70% of the hip revisions in Sweden8 and it is important to know what prosthesis was used, as some designs are associated with early failure. Among the most dramatic reports of early stem failure is that of the Capital THA (3-M Healthcare Limited, Loughborough, UK). Definite loosening was present in 16% with an additional 8% possibly loose at follow-up of 26 months. Approximately 5,000 stems were implanted throughout Great Britain with a failure rate at 5 years estimated at 20%.9 Loosening is usually asymptomatic in the early stages, particularly on the acetabular side. Late presentation may be as groin or thigh pain and sometimes as deep gluteal discomfort in cases of acetabular loosening (Figure 1).

Figure 1 Painful right hip replacement. Differential diagnosis of aseptic osteolysis or infection. Hip aspiration - no growth. One stage revision resulted in pain relief.

sensitive staphylococcus aureus (MSSA, 44% patients). 8% grew methicillin resistant staphylococcus aureus (MRSA) and 7% grew anaerobes.14

Infection: Deep infection is a challenging complication for both the patient and the surgeon. The incidence of infection post joint arthroplasty ranges from 0.3%, reported by the British Medical Research Council10 to 2.2% described in a large review.11 Fitzgerald et al12, classified prosthetic joint infections:  Stage I Acute fulminating infections, usually presenting within six weeks  Stage II Delayed sepsis or chronic indolent infection  Stage III Late haematogenous infection in a previously well functioning hip replacement. Tsukayama et al13 proposed a fourth type where a positive culture is found at the time of revision without previous evidence of infection. In a large study the most frequently isolated organisms were coagulase negative staphylococci (47% patients) and methicillin

Instability: Dislocation is one of the most common complications of total hip arthroplasty. The reported incidence varies from 0.3% to 7% in primary total hip replacement and up to 25% in revision hip replacement. While frank dislocation of the hip is obvious from the history and radiographs, subluxation is less obvious. It is related to cup position, wear or deficient abductor mechanism. It can produce discomfort from soft-tissue stretch, and may be associated with mechanical clunking. Early dislocation occurs within the first 3 months postoperatively and carries a better prognosis and a lower rate of recurrence with non operative treatment compared to late dislocation.15 In comparison, late dislocations have a multifactorial aetiology including polyethylene wear and soft-tissue laxity which in turn leads to a higher recurrent dislocation rate.2,16 Larger femoral heads have reduced the incidence of dislocation by increasing the head-neck ratio thus improving the primary arc of motion and by allowing a greater amount of translation before dislocation occurs.17

Differential diagnoses of painful THR Intrinsic causes C C C

C C C C C C

Infection Mechanical loosening Tip of stem pain (modulus mismatch) Stress fracture Periprosthetic fracture Nonunion Osteolysis Instability Inflammatory bursitis, tendonitis (trochanteric, iliopsoas)

Extrinsic causes C

Lumbar spine disease Stenosis B Disc herniation B Spondylolysis or spondylolisthesis Peripheral vascular disease Nerve injury or irritation (sciatic, femoral, meralgia paresthetica) Causalgia or complex regional pain syndrome Metabolic disease (Paget’s disease, osteomalacia) Malignancy or metastases Hernia (femoral, inguinal, obturator) Referred pain

Periprosthetic fractures: Berry reported an periprosthetic fracture incidence of 0.3% in 20 859 primary cemented and 5.4% in 3121 uncemented total hip arthroplasties and an intraoperative fracture rate of 3.6% in cemented and 20.9% in uncemented revision total hip arthroplasties.18 The location of the fracture and bone quality needs careful evaluation. The Vancouver classification is based on fracture location  Type A the fracture involves the trochanteric region  Type B the fracture is around or just distal to the femoral stem B1 the femoral implant is well fixed B2 the femoral implant is loose but the remaining bone stock is good B3 severe bone stock loss in the presence of a loose implant.19  Type C the fracture is so far below the stem that the treatment is independent of the hip replacement.

B

C C

C

C

C C C

Table 1

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Inflammatory conditions: Trochanteric bursitis is reported to occur in 17% of arthroplasties performed with a trochanteric osteotomy and in 3% without, and can result from increasing the offset in the operated hip or from trochanteric wires.20 The pain is well localized and increases upon lying on the affected side. Iliopsoas tendonitis can arise from impingement with the leading anterior edge of a relatively under anteverted or retroverted cup. Thigh pain - tip of stem pain: The aetiology of thigh pain is multifactorial and it has a variable reported incidence. Engh and Massin noted an 8% incidence of thigh pain in patients with bony ingrowth and 35% with fibrous ingrowth.21 There are two basic aetio-pathogenic mechanisms, tip micromotion and tip overload. In the former, stem loosening or fibrous fixation allows tip of stem movement during cyclic loading of the joint which in turn irritates the densely innervated endosteum. The latter is due to a mismatch in the modulus of elasticity between a stiff, largediameter uncemented femoral implant and the surrounding, less stiff host bone. Here the stem does not transmit the applied load to the femur along its full length, but concentrates it around the tip producing excessive bone localized strain and endosteal irritation.

Figure 2 Painful left hip replacement: Trochanteric pain, heterotrophic bone formation or pain from underlying Pagets disease?

However, the leucocyte count is not particularly helpful in diagnosing infection. Canner et al22 reported an elevated leucocyte count in only 15% of cases with confirmed prosthetic infection. Spangehl et al23 too reported an elevated leucocyte count to be a poor indicator of infection, with a sensitivity of 20%, a specificity of 96%, a positive predictive value of 54%, and a negative predictive value of 85%. ESR is a non specific marker of inflammation. After an uncomplicated THR it decreases to less than 20 mm per hour at approximately 6 months. Patients with a documented infection of a prosthesis had a significantly higher ESR (mean 60 mm/hour).24 The CRP level returns to normal more rapidly than ESR after total hip arthroplasty . Aalto et al25 recorded that the CRP peaked at postoperative Day 2, and was normal after 3 weeks. Thus an elevated CRP after that may be indicative of infection. A combination of a normal ESR and CRP has a specificity of 100% for excluding the diagnosis of infection in patients with a painful THR.26

Extrinsic causes of pain If the pain experienced after hip replacement is similar to that experienced before, then it is likely that hip pathology may not have been the cause of symptoms. For example, lumbar spine and sacroiliac pathology can mimic symptoms of an arthritic hip, giving rise to thigh, buttock and occasionally groin pain. Spinal stenosis is one of the common differential diagnoses; passive hip movements in such cases should be pain free, but occasionally pre-existing spinal stenosis is unmasked by increased patient activity levels after THR, but such pain is of a different character from that experienced preoperatively. Other degenerative and inflammatory spinal or sacro-iliac joint problems can be differentiated by a detailed history and examination, and can be confirmed with radiographs, computed tomography, or magnetic resonance imaging. However, in some cases it is difficult to exclude a spinal contribution to pain based on examination and investigation alone and diagnostic local anaesthetic hip injection may be useful. Pain also may be related to Paget’s disease which can coexist with osteoarthritis of the hip (Figure 2). It can produce postoperative pain but should respond well to medical management. The femoral, sciatic and lateral cutaneous nerves of the thigh can be injured either directly at operation or indirectly by limb lengthening due to the hip replacement giving rise to causalgia. Metastatic disease affecting the pelvis, lumbar spine, or femur can give symptoms suggestive of a malfunctioning painful THR. Such metastases may not be evident on plain radiographs and may be obscured by implants. They have a typical history of rest or night pain.

Plain radiography: All patients should have an AP and a lateral X Ray of the affected hip. Evaluation of serial x-rays is more informative than a single image in assessing signs of loosening. Cemented implants are assessed for the presence of radiolucencies in the bone cement interface around the stem and acetabular components. The acetabulum was divided into three zones by DeLee and Charnley27 and the femur has been divided into seven zones by Gruen.28 The development of progressive radiolucent lines in these zones either in cemented or uncemented components suggests loosening. This should be differentiated from age related radiolucent lines, which do not have an area of adjacent sclerosis, and non-progressive radiolucent lines typically in femoral zones 1 and 7 due to imperfect cement interlocking was not associated with adverse outcome.29 Cemented femoral stem loosening was classified by O’Neill and Harris30  Possible loosening is defined as a radiolucent line at the bonecement interface occupying between 50% to a 100% of the whole bone-cement interface.  Probable loosening is defined as a radiolucent line that is either continuous around the entire cement mantle or is 2 mm in width at some point.

Investigation Blood tests: Routine blood tests including a full blood count and inflammatory markers, erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), are essential.

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Engh et al32 predicted cementless component stability by major and minor radiographic signs. Major signs of osseointegration are absence of reactive, radio dense lines around the porous-coated portion of the implant and the presence of endosteal ‘spot-welds’. Minor signs of osseointegration include absence of pedestal or calcar atrophy and a stable distal stem. An extensive reactive line around the porous coated portion of the implant is a major sign of failure of osseointegration, whereas the absence of endosteal spot welds is considered a minor sign. Infection can be difficult to diagnose radiographically in the early stages. Rapidly progressive osteolysis within the first year of a total hip replacement is highly indicative of infection and periosteal new bone formation, endosteal scalloping and osteolysis are late changes highly suggestive of infection.33

 Definite loosening is defined as component migration, cement or component fracture. Cemented acetabular component loosening was classified by Hodgkinson et al31 depending on the extent of demarcation at the bone cement interface.  Type 0 had no radiolucencies  Type 1 involved the outer third  Type 2 involved the outer and middle third  Type 3 had complete demarcation  Type 4 had a migrated socket. This correlated with intraoperative findings of loosening; none of the type 0 sockets, 7% of type 1, 71% of type 2, 94% of type 3 and 100% of type 4 sockets were loose.

Evaluation algorithm Painful THR – History & Physical examination

Plain Radiographs

Loose components

Normal ESR/ CRP

Hip aspirate negative

Well fixed components

Normal ESR/ CRP

Raised ESR/CRP

Hip aspirate positive

Well fixed component – do technetium bone scan

Technetium bone scan

Positive – indium scan

Negative = look for extrinsic causes

Negative indium scan = look for extrinsic causes

Aseptic loosening = Single stage revision

Positive indium scan

CT assessment for occult loosening

Infection = Two stage revision

Table 2

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Nuclear Medicine: There is enhanced uptake of Technetium-99 methylene diphosphonate (99Tc MDP) in metabolically active bone apparent as localized hot spots-a positive bone scan. Increased uptake is seen in aseptic loosening, infection, heterotopic bone formation, stress fractures, tumours, metabolic bone disease, and reflex sympathetic dystrophy.34 However, increased uptake is seen for up to two years after uncomplicated THR,35 which reduces the value of this investigation in evaluating suspected loosening or infection in its early stages. In a series of 54 patients with painful hip arthroplasties who had surgical exploration, Lieberman et al36 reported that technetium bone scanning had a lower sensitivity and specificity than serial plain radiographs for diagnosing femoral and acetabular component loosening and they recommended using bone scanning only when plain radiography was inconclusive. Technetium-99 methylene diphosphonate scan is most useful as a negative predictor, asd if normal it eliminates of many of the potential hip related causes of pain. Merkel et al37 have shown that indium 111-labeled (111In) leucocyte scans have a higher sensitivity and specificity for excluding infection than 99Tc MDP or Gallium scan, either alone or in combination. Thus if infection is suspected an indium labelled white cell scan is usually performed following a positive technetium bone scan.

Surgical exploration to establish the diagnosis is rarely useful and can leave the patient even more distressed. If no known cause is established in spite of thorough evaluation, then a period of observation with serial radiographs is recommended. A

REFERENCES 1 Kim S. Changes in surgical loads and economic burden of hip and knee replacements in the US: 1997e2004. Arthritis Rheum 2008 Apr 15; 59: 481e8. ¨derman P, Malchau H, Herberts P. Outcome after total hip arthro2 So plasty: part I. General health evaluation in relation to definition of failure in the Swedish National Total Hip Arthoplasty Register. Acta Orthop Scand 2000; 71: 354e9. ¨derman P, Malchau H, Herberts P, Zu ¨gner R, Regne´r H, Garellick G. 3 So Outcome after total hip arthroplasty: part II. Disease-specific followup and the Swedish National total hip arthroplasty register. Acta Orthop Scand 2001; 72: 113e9. 4 Mancuso CA, Salvati EA, Johanson NA, Peterson MGE, Charlson ME. Patients. expectations and satisfaction with total hip arthroplasty. J Arthroplasty 1997; 12: 387e96. 5 Britton AR, Murray DW, Bulstrode CJ, McPherson K, Denham RA. Pain levels after total hip replacement: their use as endpoints for survival analysis. J Bone Joint Surg Br 1997; 79: 93e8. 6 Baker AS, Bitounis VC. Abductor function after total hip replacement: an electromyographic and clinical review. J Bone Joint Surg Br 1989; 71B: 47e50. 7 Cuckler JM, Star AM, Alavi A, Noto RB. Diagnosis and management of the infected total joint arthroplasty. Orthop Clin North Am 1991; 22: 523e30. 8 Herberts P, Malchau H. Long-term registration has improved the quality of hip replacement: a review of the Swedish THR Register comparing 160 000 cases. Acta Orthop Scand 2000; 71: 111e21. 9 Muirhead-Allwood SK. Lessons of a hip failure: if we want improved prostheses we must regulate their use. BMJ 1998; 16: 644. 10 Lidwell OM. Clean air at operation and subsequent sepsis in the joint. Clin Orthop 1986; 211: 91e102. 11 Sculco TP. The economic impact of infected total joint arthroplasty. Instr Course Lect 1993; 42: 349e51. 12 Fitzgerald Jr RH, Nolan DR, Ilstrup DM, et al. Deep wound sepsis following total hip arthroplasty. J Bone Joint Surg Am 1977; 59-A: 847e55. 13 Tsukayama DT, Estrada R, Gustilo RB. Infection after total hip arthroplasty: a study of the treatment of one hundred and six infections. J Bone Joint Surg Am 1996; 78-A: 512e23. 14 Moran E, Masters S, Berendt AR, McLardy-Smith P, Byren I, Atkins BL. Guiding empirical antibiotic therapy in orthopaedics: the microbiology of prosthetic joint infection managed by debridement, irrigation and prosthesis retention. J Infect 2007 Jul; 55: 1e7. 15 Woo RY, Morrey BF. Dislocations after total hip arthroplasty. J Bone Joint Surg Am 1982; 64: 1295. 16 von Knoch M, Berry DJ, Harmsen WS, et al. Late dislocation after total hip arthroplasty. J Bone Joint Surg Am 2002; 84-A: 1949. 17 Berry Daniel J, Knoch Marius von, Schleck Cathy D, Harmsen William S. Effect of femoral head diameter and operative approach on risk of dislocation after primary total hip arthroplasty. J Bone Joint Surg Am Nov 2005; 87: 2456e63. 18 Berry DJ. Epidemiology of periprosthetic fractures after major joint replacement: hip and knee. Orthop Clin North Am 1999; 30: 183e90.

Hip aspiration/anaesthetic injection: Hip aspiration should be performed in all suspected cases of infection and should be offered to patients with an elevated ESR and CRP beyond the early post operative period i.e. after 3 months. We perform these under image intensifier guidance in theatre combined with an arthrogram to confirm the intra-articular location of the needle in case of a dry tap. In such cases, some authors recommend instilling sterile saline and re-aspirating it for microbiological investigation.38 Spangehl et al.39 reported that aspiration had an 89% probability of confirming infection if the ESR and CRP level were both elevated. One advantage of aspiration is the ability to inject local anaesthetic in case of a dry tap. It can help localize intrinsic versus extrinsic causes of pain which is particularly helpful if hip and lumbar spine pathologies coexist. Computed Tomography (CT): CT scanning has been described to assess loosening in an apparently radiographically stable cementless femoral stem.40 The CT scan is obtained with the leg in maximum internal rotation and then repeated with it in maximum external rotation. Using the posterior femoral condyles as a reference, a change in position of the component between the two views greater than 2 is strongly indicative of loosening.

Summary Painful THR can be a diagnostic challenge and a systematic approach using an algorithm can be helpful (Table 2). While mechanical loosening may not be a diagnostic challenge, even in such cases a high index of suspicion for infection is essential. History, examination, plain radiographs, and blood tests including ESR, and CRP are the mainstays of the workup for sepsis. Hip aspiration should be attempted in the case of elevated or equivocal markers. Bone scans are rarely necessary to confirm the diagnosis.

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19 Duncan CP, Masri BA. Fractures of the femur after hip replacement. Instr Course Lect 1995; 45: 293e304. 20 Parker HG, Wiesman HG, Ewald FC, Thomas WH, Sledge CB. Comparison of preoperative, intraoperative and early postoperative total hip replacements with and without trochanteric osteotomy. Clin Orthop 1976; 121: 44e9. 21 Engh CA, Massin P. Cementless total hip arthroplasty using the anatomic medullary locking stem: results using a survivorship analysis. Clin Orthop 1989; 249: 141e58. 22 Canner GC, Steinberg ME, Heppenstall RB, Balderston R. The infected hip after total hip arthroplasty. J Bone Joint Surg Am 1984; 66: 1393e9. 23 Spangehl MJ, Masri BA, O’Connell JX, et al. Prospective analysis of preoperative and intraoperative investigations for the diagnosis of infection at the sites of two hundred and two revision total hip arthroplasties. J Bone Joint Surg Am 1999; 81A: 672e83. 24 Forster IW, Crawford R. Sedimentation rate in infected and uninfected total hip arthroplasty. Clin Orthop 1982; 168: 48e52. 25 Aalto K, Osterman K, Peltola H, et al. Changes in erythrocyte sedimentation rate and C-reactive protein after total hip arthroplasty. Clin Orthop 1984; 184: 118e20. 26 Spangehl MJ, Masri BA, O’Connell JX, et al. Prospective analysis of preoperative and intraoperative investigations for the diagnosis of infection at the sites of two hundred and two revision total hip arthroplasties. J Bone Joint Surg 1999; 81A: 672e83. 27 DeLee JG, Charnley J. Radiological demarcation of cemented sockets in total hip replacement. Clin Orthop 1976; 121: 20e32. 28 Gruen TA, McNeice GM, Amstutz HC. ‘‘Modes of failure’’ of cemented stem-type femoral components: a radiographic analysis of loosening. Clin Orthop 1979; 141: 17e27. 29 Iwaki H, Scott G, Freeman MA. The natural history and significance of radiolucent lines at a cemented femoral interface. J Bone Joint Surg Br 2002 May; 84: 550e5. 30 O’Neill DA, Harris WH. Failed total hip replacement: assessment by plain radiographs, arthrograms, and aspiration of the hip joint. J Bone Joint Surg Am 1984; 66: 540e6.

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31 Hodgkinson JP, Shelley P, Wroblewski BM. The correlation between the roentgenographic appearance and operative findings at the bone-cement junction of the socket in Charnley low friction arthroplasties. Clin Orthop 1988; 228: 105e9. 32 Engh CA, Massin P, Suthers KE. Roentgenographic assessment of the biologic fixation of porous-surfaced femoral components. Clin Orthop Relat Res 1990; 257: 107e28. Erratum in: Clin Orthop Relat Res. 1992; 284: 310e2. 33 O’Neill D, Harris WH. Failed total hip replacement: assessment by plain radiographs, arthrograms, and aspiration of the hip joint. J Bone Joint Surg 1984; 66A: 540e6. 34 Mittal R, Kheterpal R, Malhotra R, et al. The role of Tc-99 m bone imaging in the management of pain after complicated total hip replacement. Clin Nucl Med 1997; 22: 593e5. 35 Oswald SG, Van Nostrand D, Savory CG, Callaghan JJ. Three-phase bone scan and indium white blood cell scintigraphy following porous coated hip arthroplasty: a prospective study of the prosthetic tip. J Nucl Med 1989; 30: 1321e31. 36 Lieberman JR, Huo MH, Schneider R, et al. Are technetium bone scans necessary? J Bone Joint Surg 1993; 75B: 475e8. 37 Merkel KD, Brown ML, Dewanjee MK, et al. Comparison of indiumlabeled-leukocyte imaging with sequential technetium-gallium scanning in the diagnosis of low-grade musculoskeletal sepsis: a prospective study. J Bone Joint Surg 1985; 67A: 465e76. 38 Spangehl MJ, Masri BA, O’Connell JX, Duncan CP. Prospective analysis of preoperative and intraoperative investigations for the diagnosis of infection at the sites of two hundred and two revision total hip arthroplasties. J Bone Joint Surg Am 1999; 81: 672e83. 39 Spangehl MJ, Masri BA, O’Connell JX, Duncan CP. Prospective analysis of preoperative and intraoperative investigations for the diagnosis of infection at the sites of two hundred and two revision total hip arthroplasties. J Bone Joint Surg Am 1999; 81: 672e83. 40 Berger R, Fletcher F, Donaldson T, Wasielewsk R, Peterson M, Rubash H. Dynamic test to diagnose loose uncemented femoral total hip components. Clin Orthop Relat Res 1996; 330: 115e23.

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(ii) Implant removal in revision hip surgery

surgery. Some are uncommon, used locally and for a relatively short time. Many of the components were implanted many years prior to revision. Identification of the type of implant can assist the surgeon to determine the extent, nature and quality of component fixation. While there might be specific instrumentation available to remove particular implants, there are other component design features that the experienced surgeon can exploit to facilitate removal. This might reduce the requirement for more extensive/destructive surgical approaches. The surgeon must assess pre-operative radiographs carefully and should be aware of radiological features that directly or indirectly indicate the degree of ongoing implant fixation. From that point of view, radiographs should visualize the entire implant, on both AP and lateral views. Surgical exposure in revision hip arthroplasty can be complicated and can influence implant removal. Indeed, the choice of surgical exposure and approach should only be made having considered both the planned reconstruction and the technique to be used for implant removal. While surgical exposure will not be dealt with specifically in this article, a surgeon performing significant numbers of revision hip procedures should be aware of, and familiar with, the various approaches and techniques available. The surgical procedure should be discussed with anaesthetic colleagues, to ensure that relevant techniques are employed to provide sufficient time and a satisfactory surgical field to facilitate surgery. The overall aim of planning is to make this technically challenging procedure both less stressful and time-consuming for the surgeon. Additionally, and more importantly, careful planning can reduce complication rates and improve clinical outcomes for our patients. Implant removal technique differs on the acetabular and femoral sides, and according to whether cemented or uncemented fixation was used at the time of index surgery. In this article, removal of cemented and uncemented implants will be discussed in separate sections, further subdivided into the acetabulum and the femur. Subsequently, specific and potentially challenging situations will be discussed.

Andrew R J Manktelow

Abstract Implant removal is a major part of revision hip surgery. A complication, such as fracture or perforation during implant removal, more common in the presence of surrounding osteopenia, can compromise subsequent reconstruction. Similarly, care must be taken to avoid additional bone loss during implant removal. Various techniques are available on both the femoral and acetabular sides that can facilitate the procedure. Recent developments in instrumentation can prove helpful. In this article the techniques are reviewed. In addition, the importance of pre-operative planning and exposure is discussed. The techniques used to remove both cemented and uncemented implants are detailed with examples, illustrations and practical tips. The overall aim of the article is to make this potentially complicated procedure less challenging for the surgeon, but more importantly, to reduce complication rates in implant removal, improving clinical outcomes for patients.

Keywords cemented and uncemented implant removal; revision hip surgery

Introduction While much of the interest and development in revision hip arthroplasty surgery surrounds the techniques available to effect femoral and acetabular reconstruction, the potential complexity of implant removal should not be disregarded. Indeed, successful revision hip reconstruction starts with careful removal of the implants. This requires planning. During implant removal the surgeon must ensure that no additional bone loss occurs, and that the technique and exposure used do not compromise reconstructive options. Thus, implant removal is an extremely important and frequently challenging component of revision hip arthroplasty surgery. A number of systems and instruments are available for implant removal, with different techniques available for the removal of cemented and uncemented components. It is important that any surgeon in training, or in practice in this area, should be aware of and have experience in these techniques. The complexities involved in surgical exposure, implant removal and subsequent reconstruction support revision hip surgery being performed by surgeons with specialist training and experience. When planning the procedure, it is helpful if the surgeon is able to identify the component to be removed. Numerous implants have been used over the years in hip arthroplasty

Removal of implants Removal of cemented implants While there has been a more recent increase in the number of uncemented implants used in hip arthroplasty surgery in the United Kingdom, cemented implants still remain more common. In planning to remove cemented implants, it is important to determine whether the implant is loose and if so, whether loosening has occurred at the bone-cement interface, cement-implant interface or both. This can be identified easily when the implant has migrated or the orientation has changed over time. Otherwise, radiolucency around the implant should be identified, along with its location, extent and any progression. This provides corroborating evidence of component loosening. Similarly, an assessment of the surrounding bone quality should be made to reduce the potential for additional bone loss with implant removal. A wide variety of instruments are required to remove cemented components safely and within a reasonable time. Standard cemented revision instrument trays should include

Andrew R J Manktelow BSc MB BS FRCS (Ed) FRCS (Ed) Orth Consultant Orthopaedic Surgeon, The Queen’s Medical Centre University Hospitals NHS Trust, Derby Road, Nottingham, UK.

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curved and straight osteotomes, curettes, rongeurs and drills (Figure 1). Additional equipment such as high speed burrs, flexible reamers, ultrasound devices, ballistic chisels and external light sources are also helpful.

elevating the cement, which is removed in sections. The entire technique is demonstrated in Figure 2. Small residual cement plugs can be elevated using curved osteotomes and rongeurs. Larger plugs can be removed as above, using ultrasonic devices or drills, taps and screws. Great care should be taken with cement plugs, particularly those that have ‘mushroomed’ beyond their entry point, resulting in a larger diameter than the hole into which the cement was introduced. Particular care should be taken when removing intra-pelvic cement in these circumstances. Indeed, frequently, in an aseptic case the surgeon might choose to leave these ‘in-situ’, rather than risk significant bone damage/loss and/or haemorrhage. A specific approach for the extraction of intra-pelvic components will be discussed below. Other techniques have been described to remove well-fixed cemented acetabular components. An acetabular reamer can be used to ‘ream out’ the implant. While this can be successful, it can result in considerable debris. Similarly, this will blunt reamers that should not then be used in primary hip arthroplasty. The technique may, however, allow consideration of a ‘cement in cement’ technique for acetabular reconstruction in the presence of a perfect remaining acetabular bone-cement interface. The use of the ‘Explant’ device (Zimmer, Warsaw, IN), more popular in the removal of well-fixed uncemented components, can be helpful. In my own practice, the vast majority of cemented acetabular components, both fixed and indeed loose, can be removed using the techniques described above.

Removal of the cemented acetabulum The removal of any acetabular component starts with full exposure of the entire acetabulum, including the rim. Adequate visualization, both proximally and distally, must be achieved. Retractors should be used with care, to avoid damaging the surrounding bone. Subsequently, where the implant is loose, any peripheral soft tissue ‘securing’ the implant around the rim should be removed. Residual areas of fixation can be released using sequentially longer curved osteotomes. The implant should be completely detached before it is removed. Devices such as the Moreland extractor (Figure 2) can be attached to the socket to facilitate removal, though this should be used with care. If an attempt is made to remove an implant that remains sufficiently fixed with this device additional bone loss can result. Removal of a well-fixed cemented acetabular component can be more difficult. A number of techniques have been described. In principle, my practice in this circumstance is first to remove the socket from the cement. Once this has been achieved, the cement mantle is visualized and can then be sectioned, carefully and under direct vision. The cement can then be released from the bone using straight and curved osteotomes or a high-speed burr, and removed in small segments. This ensures that no additional bone loss occurs as the implant is removed from frequently osteopenic surrounding host bone. When removing a well-fixed cemented socket, the initial step is to remove the ‘flange’ of the socket. This is done using straight osteotomes. Subsequently, curved osteotomes are introduced at the implant-cement interface, carefully releasing this so that the socket can be extracted. The well-fixed mantle is then ‘sectioned’, with sharp straight osteotomes. Curved osteotomes are then introduced at the bone-cement interface, gently

Removal of the uncemented acetabular component The removal of a well-fixed uncemented acetabular component can be a technical challenge. As detailed above, the surgeon needs to have a good understanding of the design of the component, including the extent, location and type of coating. Additional fixation devices, such as screws, fins, spikes and pegs need to be addressed. Manufacturers may provide specific tools that attach to a particular socket design to facilitate removal.

Figure 1 The various instruments used in the removal of cemented implants.

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A technique for removal of a cemented socket. Circumferential exposure is achieved with careful soft tissue release. Of note, in this case the femoral component has been translated antero-superiorly above the socket. Subsequently, the flange is excised. The component itself is removed from the cement mantle with curved osteotomes. The Moreland extractor can be used, with care, to remove the component. In this circumstance, the majority of the cement was relatively loose and was removed with the implant. Figure 2

Frankly loose uncemented sockets can be removed without difficulty. Many failed uncemented sockets, however, are surrounded by osteopenic bone, frequently with associated lysis. This can occur even in the presence of a relatively secure implant (Figure 3). As can be seen in this example, the socket, while damaged and surrounded by severe lysis, has two or three small areas of residual ‘fixation’ that have prevented the implant from ‘collapsing’ into the surrounding defects. Such implants can be ‘released’, and removed using curved osteotomes, with care to avoid unnecessary additional damage to the grossly deficient surrounding bone, albeit leaving a demanding reconstruction. The removal of a well-fixed uncemented acetabular component, for infection, mal-orientation and/or wear, remains one of

the more challenging procedures in revision hip arthroplasty, though the morbidity associated with this has been significantly reduced by the development and widespread use of devices such as the ‘Explant’. Removal of a well-fixed uncemented socket starts with a thorough exposure of the entire acetabular rim. Again, care should be taken with retraction to avoid additional bone loss on both the acetabular and femoral sides. There are circumstances in which the surgeon may choose to perform an extended trochanteric osteotomy (ETO) or trochanteric slide, solely to facilitate mobilisation of the femur to allow good acetabular exposure. Similarly, the use of a ‘cement in cement’ femoral revision technique can be useful. This allows a well-fixed

Figure 3 A damaged cementless socket that remains ‘stable’ despite extensive surrounding lysis. The patient presented not with pain, but merely a grating sensation in the hip as he walked.

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Figure 4 A technique for removal of a polyethylene liner from a cementless socket using a cortical screw.

cemented component to be removed, albeit temporarily, at the time of acetabular revision, potentially solely to facilitate acetabular exposure. Having identified the rim of the socket, the next step is to remove the liner and any screws. Loose liners can be removed easily, however in other cases, and specifically those in which there is no release mechanism, a cortical screw can be used. As the screw is advanced into the polyethylene liner, it contacts the internal shell surface. Further turning of the screw will disengage the locking mechanism (Figure 4). Alternatively, the liner may need to be sectioned to gain access to back surface fixation devices. Removal of hard bearing liners presents a particular problem. Many systems have specific devices with which the surgeon can simultaneously impact against the rim of the intact shell, while a spring-tensioned suction device, attached to the liner, extricates the liner. Essentially, the morse taper is released as the surgeon strikes the rim of the socket. Other systems provide specific instruments that can be introduced through gaps in the periphery of the shell and behind the morse taper, to allow the liner to be levered out of the shell. This particular issue should be discussed with the implant manufacturer or colleagues prior to the case. No attempt should be made to remove the shell without removing screws. This is likely both to be challenging and to result in catastrophic bone loss. While the surgeon should try to locate specific screwdrivers for a particular system, many generic implant and broken implant removal sets have various modular heads that can be attached to a driving system. Periodically, screw heads will fail and broken screw removal instrumentation will be required. In addition, a metal cutting burr can be used, with irrigation and soft tissue protection, to remove the head of a damaged screw to allow removal of the socket. The remaining screw shaft can be removed subsequently, using curettes, crown reamers and reverse threaded screw removal systems. After the rim has been exposed and the screws have been removed, sequential curved osteotomes can be introduced and impacted carefully into the implant-bone interface, gradually releasing the implant, allowing it to be removed. Alternatively, more recently, and perhaps now in the majority of cases, the use of the ‘Explant’ (Zimmer, Warsaw, IN) system has become the standard technique. The ‘Explant’ device (Figure 5) comprises detachable heads that centralize the device within the socket. Subseqently, short then long blades in 2 mm diameter increments, are used to ‘cut’ the well-fixed implant out of the acetabular bone.

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Prior to the ‘Explant’ system being used, the rim of the bone-implant interface should be identified and the surgeon must ensure that the device is satisfactorily centralized within the component. Where there has been gross acetabular polyethylene lysis, either a trial liner or a definitive liner

The ‘Explant’ system, primarily used in the removal of uncemented sockets. The system provides different sized heads that attach to the handle and centralize the cutting blades around the shell. Initially a short, then a long blade, is attached then passed around the socket. The blades disrupt fixation and allow the implant to be removed with minimal bone loss. Figure 5

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temporarily cemented into the shell can be used. Subsequently, the short Explant blade, corresponding to the diameter of the socket to be removed, is passed around the rim of the implant, using both rotational and longitudinal ‘stabbing’ movements. This steadily deepens disruption of the boneimplant interface. Gentle taps with a mallet can be used in a linear direction to deepen penetration at the interface, though great care should be taken not to fracture the blade. As the interface is developed, the short blade is changed to the longer one. Thus, the implant is functionally ‘cut out’ from the surrounding bone (Figure 6). With experience, removal of a well-fixed uncemented socket can become a relatively straightforward procedure and can be achieved in a reasonably short time, with little if any additional bone loss (Figure 7). Indeed, frequently it is possible to remove the implant and subsequently implant a new socket with only a 2 or 4 mm increased diameter. The blades on the ‘Explant’ device should be inspected carefully after each use, to ensure that they have not been damaged. While hemispherical sockets can be removed relatively easily, peripherally expanded sockets can be more difficult. There remains the potential for removing slightly more bone medially than is necessary. While this is a possibility, with careful use of the ‘Explant’ device and with curved osteotomes, bone loss in this circumstance can be minimized. With the increasing numbers of hip resurfacing implants inserted, removal of a well-fixed uncemented resurfacing acetabular component has become a more common procedure. Where the centre radius of curvature of the socket is not at the centre of the socket internal geometry, there are specific conversion devices that can be introduced into the resurfacing socket, allowing for the altered hip centre, into which the ‘Explant’ device can be introduced (Figure 8). Similarly successful extraction is possible using this technique (Figure 9). The potential use of this system will depend on design of the acetabular component. This should be discussed with the implant manufacturer.

Figure 7 The preserved acetabular bone stock after removal of a well fixed acetabular implant using the ‘Explant’ device.

Removal of intra-pelvic components Intra-pelvic components constitute a challenge in revision hip arthroplasty. Quite apart from access and technical difficulties in retrieving the implants, there is major concern regarding potential intra-pelvic disruption, which could cause major haemorrhage and other complications. As such, the removal of intra-pelvic components needs to be planned carefully. Pre-operative imaging is important. The use of CT scans is helpful, along with the use of CT or MRI arthrography, to identify the proximity of the components to major vessels (Figure 10). The procedures should be discussed pre-operatively with general surgical, vascular or other colleagues who have experience and the ability to provide retroperitoneal access to the pelvic vessels and the internal aspect of the acetabulum. Where a truly intra-pelvic implant is to be removed, there are a number of options available to the surgeon (Figure 11). It may still be possible to remove the implant via a traditional approach.

Figure 6 A cementless socket that has been removed using the ‘Explant’ system. Note the close proximity of the resection blade to the contour of the shell and the minimal amount of bone removed with the previously well fixed implant.

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Figure 8 Internal conversion devices that compensate for the difference in internal and external radius of curvature of a resurfacing socket, allowing the ‘Explant’ device to be used safely to remove these implants.

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Figure 9 A resurfacing socket that has been removed using the system demonstrated in Figure 8.

However, in this circumstance, care must be taken in planning and practice to ensure adequate exposure. As previously detailed, the use of an extended trochanteric osteotomy or trochanteric slide can facilitate mobilization of the femur, improving acetabular access. If this is to be attempted, it is prudent to have a colleague with vascular experience available. Vascular instruments should be available in case a rapid change of plan is required. If, while removing the implant through a traditional approach, excessive bleeding occurs, a more extensive approach with proximal control of the vessels is likely to be required. Therefore, the patient needs to be prepared and draped to allow patient position to be changed rapidly, intra-operatively, for an additional surgical procedure, frequently a retroperitoneal approach, to be performed to gain urgent control of any bleeding. The alternative is to combine the traditional hip approach with a retroperitoneal approach. This technique allows the implant to be mobilized and delivered more safely through either approach. Simultaneously, the surgeon gains primary access and control of potential bleeding prior to the implant being removed. Typically, the retroperitoneal approach is performed and the

vessels are identified and mobilized before the traditional hip approach is performed. Frequently, nothing further will be required from the retroperitoneal approach if the surgeon is able to remove the implant via the traditional approach, however, with unexpected bleeding the surgeon has access for rapid control. The approach chosen in this circumstance depends on planning, surgical experience and the availability of colleagues with the required surgical expertise. It is outwith this article to discuss this in detail, however, this complex procedure should be performed by an experienced revision arthroplasty team. One other area of concern surrounds intra pelvic-cement, particularly in the presence of infection. Typically, it is essential that all foreign material is removed at the time of revision, or the first stage of a two-stage procedure. Therefore, with truly intrapelvic cement, it is important that the surgeon has other adjunctive techniques available to ensure that all foreign material is removed. Small cement plugs can be removed using gouges. Longer cement plugs can be removed using ultrasonic devices, such as the ‘plug puller’. In other circumstances, particularly with large pieces of intra-pelvic cement, a similar approach to

Figure 10 The use of CT angiography to investigate the proximity of mal-positioned screws to intra-pelvic vessels. This imaging can be used to help plan the surgical approach required to remove the implants safely.

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Figure 11 A cemented socket that has collapsed centrally into the pelvis. CT scans demonstrate the proximity of the component to the intra-pelvic vessels. The component was removed via a combined posterior hip and retroperitoneal approach.

that detailed above will need to be considered. It should be appreciated that the intra-pelvic cement can become adherent to local soft tissues. Great care should be taken to avoid merely pulling on these cement pieces as significant bleeding, which can be difficult to control, can result.

identify any specific aspects of the component that will facilitate removal. The surgeon should discuss the implant with the manufacturer, if necessary, to determine whether any specific instrumentation is available to facilitate removal. Factors that should be considered for the implant itself include whether the implant is modular or monoblock. A monoblock component allows the use of devices that attach at the femoral head/neck junction to facilitate removal. If the implant has a collar, again, this can be used as the point against which a punch can be positioned to facilitate extraction. There are specific devices that can be used to gain purchase at the neck/stem junction on a modular component that will allow a slap hammer to be attached to facilitate removal (Figure 12).

Removal of cemented femoral components Removal of a cemented femoral component for loosening, wear, component failure, infection, instability or periprosthetic fracture is a common procedure in revision hip arthroplasty surgery. The procedure starts with planning. The surgeon should identify the implant to be removed, both from the point of view of the likely areas and extent of residual fixation, but also to

Figure 12 Removal instrumentation that attaches to the neck region of the implant, facilitating removal of a modular femoral component.

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Prior to this, a specific head-neck separation device should be used to remove the femoral head. This prevents both loosening of the stem and potential damage to the taper. The surgeon should assess whether the implant is loose or well-fixed. If the implant is loose, the surgeon should determine whether loosening has occurred at the bone-cement or the cement-implant interface. If the implant is loose, within a membrane, it can be removed with ease. Similarly, a smooth cemented implant can frequently be removed, even from an intact mantle, without too much difficulty. ‘Matt’ finished and pre-coated stems, however, may be well fixed to the surrounding cement mantle. Any attempt to remove this type of stem without first disrupting the implant cement interface bond could result in fracture and/or femoral bone loss. With regard to the surrounding cement, the extent of the distal cement column should be assessed with adequate imaging. The surgeon should identify whether a cement restrictor was used and whether the cement mantle is central or eccentric (Figure 14). The latter may increase the chance of perforation, which may well influence plans for reconstruction. It can be difficult to assess the extent of residual radiolucent cement on radiographs. Alternative imaging techniques, such as MRI scans, can be useful in this regard. The surgeon should determine whether all the cement needs to be removed or if there are options for a ‘cement in cement’ revision technique that might simplify reconstruction. Revision hip surgery requires extensive instrumentation. The surgeon should have at their disposal a variety of instruments to remove implants safely and expeditiously (Figure 1). With experience and patience, the majority of cement removal can be performed with hand instruments. These include series of curved and flat osteotomes, cement splitters, cement drills, rongeurs, reverse hooks and cement taps. In addition, flexible reamers can be used, passed over an olive tipped guide wire, once the column has been perforated. Beyond that, there are specific tools, such as ultrasonic and ballistic devices, that can be used. The surgeon should have a mental picture of the cement mantle, its position and the extent of residual fixation relative to the host femur. The significance of a complication during implant removal, such as canal perforation or fracture, should be appreciated for subsequent plans for reconstruction. Typically, the first stage of removal of the cemented implant will be to remove any cement overhanging the collar of the implant, in the lateral ‘runway’ within the greater trochanter (Figure 13). Failure to clear this area before the stem is removed can result in fracture of the trochanter. Management of trochanteric fracture in this circumstance can be a technical challenge in terms of reduction, fixation and gaining satisfactory union within the relatively porotic bone of the greater trochanter and proximal femur. Once the implant has been removed, and when there is loosening at the bone-cement interface, residual cement can be removed without too much difficulty. Careful use of osteotomes to develop and sequentially disrupt the residual bone-cement interface is followed by the use of rongeurs to extract segments of cement. It is important to prevent small fragments of cement falling into the canal. I find it helpful to use small ‘mastoid’ swabs, recorded and tagged, placed into the canal to prevent this.

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Figure 13 Cement overhanging the shoulder of an implant. This should be removed with care prior to stem extraction to prevent fracture of the greater trochanter.

The surgeon should be able to see the bone-cement interface clearly. Careful use of standard theatre lighting is helpful, along with head lights and/or a hand held external light source. It may be helpful to elevate the table, with the patient in a lateral position. Similarly, the patient can be rolled away from the surgeon slightly to improve visualization and lighting. Beyond this I find it essential to have developed lateral access to the femoral canal to improve visualization of the residual cement mantle. A decision should be made as to whether to remove the cement, leaving the femur intact, or whether to use an extended trochanteric osteotomy (ETO) or transfemoral approach to facilitate cement clearance. The use of the ETO, described elsewhere in this article, can, on occasion, greatly facilitate cement removal. The technique should be used particularly if there has been significant varus remodeling, where the osteotomy can be used to help realign the femur, particularly when a straight uncemented femoral stem is to be used in reconstruction. The osteotomy has been shown to heal satisfactorily and can significantly reduce the time taken to remove well-fixed cement. Once the osteotomy has been elevated, drills, hand instruments and high-speed burrs can all be used to remove cement. Particular care should be taken in the trochanteric region to avoid fracture when elevating the lateral fragment. The extent of the ETO needs to be determined dependent on the extent, location and degree of residual fixation of the cement to be removed. Typically, the ETO will extend down to the area of tip lysis, therefore, a small part of the cement column may remain distal to it. However, the ETO, in its own right, will aid visualization of any residual cement, facilitating extraction. Where the cement is well-fixed, and with an intact femur, cement removal techniques can be split into regions. Within the metaphysis, the surgeon is likely to encounter relatively thick cement alongside thin bone. This part of the cement mantle can be removed successfully with hand instruments. The surgeon should carefully disrupt the bone-cement interface circumferentially, with curved or flat osteotomes. Care should be taken to avoid levering on the cement, while gently elevating it away from the bone. Sections of cement can then be developed, with care, using a cement splitter and removed with cement rongeurs. Using a splitter to section the mantle

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Figure 14 Two mal-aligned cemented femoral stems. Particular care should be taken to avoid femoral perforation during cement removal in these cases.

longitudinally reduces hoop stress. The surgeon should avoid being over-greedy, removing only small sections of well-fixed cement at any one time, to reduce the chance of unexpected and undesirable complications. The regular use of lavage is helpful, to identify the bone-cement interface clearly. Similarly, hypotensive anaesthesia reduces the intra-operative blood loss, but also facilitates visualization within the femoral canal. With sequential and careful cement extraction in the metaphysis and proximal diaphysis, cement is removed using rongeurs or curettes down to the distal extent of the stem and into the diaphysis. The next step in cement removal is removal of the residual cement plug within the diaphysis. In the first instance, the surgeon should be aware of whether stem alignment was central or eccentric within the femur (Figure 14). When eccentric, particularly in the presence of osteoporotic bone or tip lysis, further attempts at cement column perforation in the same alignment as the stem can result in canal perforation.

Initially, the removal of the cement column involves first penetrating the cement column, avoiding femoral canal perforation. While centralisation devices exist that can be positioned within the femoral diaphysis, the use of ultrasound can be particularly helpful. When there is difficulty, and particularly in the early cases of an inexperienced surgeon, the image intensifier can be used intra-operatively to guide extraction. The C-arm can be draped and introduced over the patient, with the patient in a lateral position. This then allows the surgeon to drill or use ultrasound and to penetrate the cement column under radiographic control (Figure 15).

Figure 16 A long cement column, extending into and beyond the isthmus, removed using an ultrasonic cement removal system (by kind permission Ms S K Muirhead-Allwood).

Figure 15 The use of an ultrasound probe, under image intensification, to locate and remove intra-femoral cement.

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Figure 17

These segments can then be removed, with care, either with reverse curettes or rongeurs. Care must be taken with the use of reverse curettes. While they are excellent at removal of small segments of cement that remain against the diaphyseal wall, if the surgeon is not careful and if a femoral perforation has not been identified, reverse curettes introduced into a small perforation can result in that perforation being turned into a large femoral defect. An image intensifier can be helpful, along with the guide wire acting as a probe, if there is any concern that a femoral perforation might have occurred. Long cement grabbers of different sizes, straight and curved, can be used to remove all residual cement from the canal. It is traditional that the extraction of the final part of the cement restrictor should be accompanied by an encouraging response from all those in theatre, thereby keeping the surgeon’s spirits up at the end of one of the more challenging parts of the procedure! The surgeon must be sure that all cement has been removed from the femur. The use of reverse curettes, probes or the image intensifier can confirm this. Any residual cement within the canal can give the surgeon an inaccurate impression of an interference fit if the surgeon is to use an uncemented reconstruction. The presence of residual cement can compromise implant fixation and result in early failure of the revision. In addition to probing the canal, another reassuring technique is to fill the canal with lavage. In the presence of a significant femoral perforation or fracture, lavage will leak from the femur. However, if the lavage is retained within the canal, this can be further reassurance that no perforation or fracture has occurred. Once the surgeon is clear that all cement has been cleared, attention can be turned to reconstruction. Techniques available for this will be described elsewhere.

The principles and practice regarding the use of ultrasound in cement extraction will be described below. Once the column has been penetrated, an ‘olive tipped’ guide wire can be passed down through the perforation in the column and into the distal diaphysis. Prior to any reaming, the surgeon must ensure that the guide wire remains intraosseous by using it as a probe. Subsequently, sequentially larger flexible reamers can be passed over the wire, both removing residual cement and improving distal visualization. Once adequate sized flexible reamers have been introduced, further use of osteotomes, elevators and splitters will disrupt the residual thinned cement at the bone-cement interface.

The use of ultrasound in femoral cement removal While the use of ultrasound had been investigated in Germany previously, its use in cement removal was popularised in the early 1990s. Its effectiveness in cement removal in revision hip surgery is now established. The systems, such as OSCAR (Orthosonic System for Cemented Arthroplasty Revision), function by delivering ultrasonic energy from a handset, via a probe, directly to the cement. The cement is changed from its solid form, albeit temporarily, and can then be extracted, in its altered state, using curettes and back scrapers. Alternatively, the cement can be extracted in segments from the column using a plug puller. In this

An ultrasound system used in cement removal. The hand piece is attached to various probes that are introduced into the cement. The cement can then be extracted in various forms, dependent on the tool tip used.

Figure 18 Specific instrumentation available to facilitate implant removal, in this particular case of an SROM stem that remained well fixed in the presence of infection. Cases should be discussed with colleagues and/or implant manufacturers to identify whether specific removal instrumentation exists.

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Removal of well fixed uncemented femoral component Again, while the removal of a loose uncemented femoral component can be a relatively straightforward procedure, the removal of a securely fixed uncemented femoral component can be a major challenge. Implant removal in the presence of an extensively coated and well-fixed component is often made more technically demanding by the presence of surrounding osteopenia. In addition, proximal stress shielding increases the risk of perforation and fracture. Once again, it is important that the surgeon knows as much about the implant to be removed as is possible. Uncemented femoral implants differ in terms of their geometry and the extent and principles of fixation. All of these factors must be considered when planning removal. The technique used to remove the component will have a significant impact on the options in reconstruction. As detailed previously, it is important that the surgeon discusses the stem with the manufacturer, to explore specific instrumentation to facilitate removal (Figure 18). Figure 19 The basic instrumentation required for the removal of a well fixed uncemented stem.

Required instrumentation With regard to general equipment, the surgeon will need to have a range of slim flexible osteotomes of different shapes and sizes. Flat and curved osteotomes will be required for different stems and different parts of the procedure. On occasions, a stem may need to be sectioned and a number of metal cutting burrs are required for this. Similarly, trephines may be required, passed down over the cylindrical part of the stem, to disrupt implant fixation and facilitate removal. The surgeon will need to be aware of the component dimensions, to determine the size of trephine required. An example of the required instrumentation is shown in Figure 19. With regard to the trephines, when the bone implant interface is sound the cutting teeth of the trephines can be damaged, splay apart or blunt relatively rapidly. Therefore, it is likely that a number of appropriately sized trephines will be used to facilitate successful implant extraction. Proximally, it is important that a mechanism of gaining purchase on the stem is available. Many uncemented stems have introducing systems or holes into which an introducer or a hook, attached to a slap hammer, can be positioned. Similarly, many stems have collars onto which punches can be applied to facilitate extraction. In addition to this, there are systems available that clamp onto the neck region of the component, gaining proximal purchase to facilitate removal

circumstance the ultrasonic probe is passed into the cement, the altered cement subsequently ‘sets’ around the probe, and a slap hammer is used to extract segments of the cement column. This is particularly useful in a relatively long cement column (Figure 16). There are various probe tips available to provide the versatile options for cement removal described above (Figure 17). While the ultrasound probe generates heat, cement has an ability to maintain a significant temperature gradient across a small distance. Therefore, the temperature to which endosteal bone is exposed, when used with lavage, has not been shown to be sufficiently high to cause necrosis. The probe itself should be used with care. There is both audible and tactile feedback from the probe if the tip contacts bone. With gentle pressure, the probe will pass through the changed cement steadily. If resistance is encoutered, specifically in the presence of an audible ‘screech’, it is likely that the probe is in contact with femoral bone. The probe should then be realigned to pass satisfactorily through the column. Again, the use of the image intensifier in conjunction with the ultrasound probe, particularly in the surgeon’s early experience, is helpful. There are systems available that combine this use of ultrasound with femoral canal endoscopy. This can be helpful when used with lavage, frequently with additional external lighting.

Figure 20 An uncemented stem, with proximal fixation, which can be released by disrupting ingrowth at the anterior and posterior ‘fibremesh’ pads.

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A metal cutting burr being used to create a groove into the lateral aspect of the failed stem. A punch can be impacted against the groove to facilitate removal after initial release with narrow curved osteotomes and subsequent trephining of the stem. Figure 21

(Figure 12). Slim oscillating saw blades can be used to disrupt the interface. Counter-intuitively, in some circumstances, the regions of ingrowth can be disrupted by gently impacting the stem against the areas of fixation. Similarly, a corticotomy into the lateral aspect of the femur can reduce hoop fixation forces and allow the stem to be removed. Frequently, a gigli saw may be helpful to interrupt the interface within the medial metaphyseal and calcar region.

The surgeon should appreciate that careful planning is required for this procedure. A large instrumentation inventory is required. While hiring in the instrumentation can be costly if it is not already on the shelf, this type of case should not be undertaken without the required equipment. The procedure is difficult enough with all the necessary instrumentation; without it, extraction can result in catastrophic destruction of the femur, seriously compromising reconstructive options.

Figure 22 A failed but well fixed Furlong stem with extensive HA coating.

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Figure 23 The failed Furlong stem from Figure 22, after it has been sectioned and removed. Evidence of sound bony integration is seen around the proximal body and distal stem. The component has been sectioned and the distal stem removed within a trephine.

Stems with proximal metaphyseal fixation When the stem is loose or if there are easily accessible or limited regions of ingrowth, such as the stems demonstrated in Figure 20, it is possible to remove the stem having disrupted the ingrowth proximally, from above, using slim flexible osteotomes. Once the surgeon is absolutely sure that all of the ingrowth is disrupted, the stem can be extracted with the femur intact. In the absence of significant lysis or bone loss, this would leave numerous femoral reconstructive techniques available. Where ingrowth is circumferential and sound, while it may be impossible to disrupt this satisfactorily using osteotomes proximally, it is frequently better to perform a relatively short ETO to gain access to the interface area. Care should be taken when elevating the osteotomy over a well-fixed stem, to ensure that the elevated segment or the residual femur is not fractured. Once the osteotomy is elevated, good access is available to disrupt anterior and posterior ingrowth with osteotomes or an oscillating saw. Medial ingrowth can be accessed, via the calcar, with curved osteotomes or a gigli saw. If there is a collar this may need to be removed with a metal cutting burr to gain access. The stem can then be removed, though it may be helpful to create a small groove in the lateral aspect of the femoral component into which a punch can be positioned to aid extraction (Figure 21).

Soft tissues should be protected with damp swabs and a metal cutting burr can be used to section the stem. This can be a time-consuming procedure that should be undertaken carefully. Lavage should be used to prevent over heating of the stem and surrounding soft tissues. Care should be taken to protect surrounding host bone from damage by the burr. Once the stem is sectioned and full release anteriorly and posteriorly has been carried out, the gigli saw can be passed from lateral to medial, through the defect in the stem, to disrupt the medial metaphyseal and calcar interface, facilitating removal of the proximal part of the stem. The distal stem can then be trephined.

Stems with more extensive fixation With stems with more extensive ingrowth (Figure 22), it may be necessary to section the stem in situ, removing the proximal part prior to trephining out the distal well-fixed part of the component. With standard length stems, access is gained, as above, via an extended trochanteric osteotomy. The length of the osteotomy needs to be planned carefully preoperatively to ensure the segment elevated is sufficiently distal to gain access to the diaphyseal portion of the stem.

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Figure 24 A failed tapered modular revision stem. The component has failed via a cantilever mechanism, with insufficient proximal support, 8 years after implantation for a B3 peri-prosthetic fracture. The tapered stem itself remains solidly fixed to host bone.

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Figure 25 The tapered stem from Figure 24 after removal. Sound bony ongrowth is clear distally. The cylindrical section of bone removed with the trephine is shown. Within this column the tapered component itself remains well fixed. This demonstrates the potential for bone loss when using this technique in this circumstance.

The required size trephine should be estimated and/or determined prior to surgery. This can then be checked against the sectioned end of the stem. The smallest possible trephine that will pass over the stem should be used to reduce the amount of host bone lost. As previously stated, the trephines can blunt relatively rapidly and a number of short and long trephines are required. Subsequently, with time, patience, irrigation and gentle pressure, the stem is eventually ‘trephined’ from the diaphysis (Figure 23). Once this is removed, the femur can be reconstructed. Specific difficulties can be encountered when attempting to remove long revision stems, when there might an extensive length of a straight or indeed a bowed stem to be removed. The surgeon can consider sectioning the stem at a number of locations, to trephine short sections sequentially. Alternatively, particularly with a long well fixed tapered stem or a long curved stem, the surgeon may consider performing a transfemoral approach, with a ‘step cut’ osteotomy over the fixed length of the stem. Again, care should be taken to elevate the lateral wall of the femur away from the stem. The component can subsequently be released under direct vision, from the lateral side. A ‘gigli’ saw or curved osteotomes can be used to release areas of ingrowth on the medial side. In general in this situation, it is safer to perform an elective, albeit extensive osteotomy, than to risk what could be a catastrophic intra-operative femoral fracture. Following this approach, with care taken during the soft tissue exposure, the femoral diaphysis can be re approximated to allow reconstruction. While subsequent reconstruction may be possible using a stem loading the intact proximal femur, frequently a long stemmed device, with the potential for distal locking, will be necessary, particularly should there be unexpected femoral complication.

The removal of failed, frequently modular, tapered uncemented stems is becoming a more common problem. This occurs with cantilever failure of the component in the absence of adequate proximal support. The failure occurs most frequently around the region of the modular junction (Figure 24). These stems have very good ingrowth characteristics. While the ‘aggressive’ nature of their conical design means the true conical ‘zone of fixation’ is potentially relatively short, many of the stems are ‘grit blasted’ distally, with cutting flutes. In addition, many achieve ‘three point fixation’ on the lateral view, over the anterior femoral bow, giving rise to sound bony integration throughout their length. To trephine these failed stems from the top can result in the loss of excessive bone more distally, which might compromise reconstruction. Similarly, it can be difficult to release the conical stem from within a cylinder of bone, cut out by the trephine. These concerns are both illustrated in Figure 25. The tapered revision stem shows excellent ingrowth and the cylinder of bone required to be removed during its extraction is clearly identified. In these circumstances it may be helpful to perform a slightly longer extended trochanteric osteotomy than necessary. Subsequently, the stem is sectioned below its widest part and the proximal segment is removed. Finally, the slightly narrower

Figure 27 A long modular uncemented revision stem, with distal locking, used to reconstruct the femur following successful removal of the failed modular revision stem shown in Figure 24.

Figure 26 A trephine being passed over the well fixed distal tapered section of the stem from Figure 24.

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a major problem. The surgeon should always bear in mind, however, the presence of relatively osteopenic bone or localized areas of lysis that can increase the risk of iatrogenic fracture. When the implants are well-fixed on either the acetabular or femoral side, the procedure can become more challenging. The surgeon should plan carefully, be patient, and should be aware of all of the numerous technical advances in instrumentation that can facilitate the procedure. The surgeon should feel comfortable to discuss these cases with colleagues and indeed to refer them on to specialist units when appropriate. The surgeon should always be aware that successful reconstruction starts with successful removal of the implants. A

distal segment is trephined out. This technique can remove the implant successfully while minimizing bone loss. The removal of the well-fixed tapered distal segment in the case shown in Figure 24 is demonstrated in Figure 26. Similarly, the technique employed in femoral reconstruction is shown in Figure 27. Removal of a well-fixed uncemented femoral component is, as previously detailed, a challenge. The surgeon should not undertake this lightly. The surgeon should plan carefully and ensure that all potentially useful instrumentation is available before starting the procedure. The loan of much of this equipment and indeed the purchase of the trephines is expensive. The surgeon should not compromise in this regard. In a number of lectures on the subject, I have made lighthearted mention of the benefit of ‘encouraging and sycophantic’ assistants. Both can be helpful! This procedure is not always for the faint hearted. Reconstruction must be planned carefully and, as previously detailed, it is my advice to have a salvage type stem, with options for distal locking, or indeed a proximal femoral replacement available, that will bypass any femoral fracture, allowing sound, albeit perhaps more extensive than initially planned, femoral reconstruction.

FURTHER READING Della Valle CJ. Component removal In Master techniques in orthopaedic surgery part VI revision total hip arthroplasty. Barrack and Rosenberg (pub Lippincott Williams and Wilkins). pp 319e332. Hozack WJ, Wade FA. Removal of components and cement In The adult hip. (2nd edn.) (pub Lippincott and Williams). Callaghan, Rosenberg and Rubash Chapter 91: pp1352e1370. Petrera P, Trakru S, Mehta S, et al. Revision total hip arthroplasty with a retroperitoneal approach to the iliac vessels. J Arthrop 1996; 11: 1704e9.

Summary Implant removal is an extremely important part of revision hip arthroplasty. Removal of loose implants, on the whole, is not

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(iii) Reconstruction/revision of acetabular failure in revision hip replacement

Keypoints C

C

Peter W Howard C

C

Abstract C

Reconstruction of the acetabulum following acetabular failure in hip arthroplasty presents a wide array of challenges. The extent of bone loss present at revision may require a number of different potential techniques, aiming wherever possible to restore bone stock to that of the primary arthroplasty situation. Gaining primary implant stability is the key to success for all revision methods. Success rates are generally inferior to primary hip arthroplasty, and more so the greater the loss of bone stock.

Classification systems seek to place the varying amounts and directions of bone stock loss into differing categories, to help guide which method is to be used, and for comparing the literature results of differing methods and implants. Most widely used are the AAOS3 and Paprosky4 grading systems, briefly summarised in Tables 1 and 2. In the assessment of bony defects, a key issue is containment. If a defect is well contained by surrounding bone, it is readily amenable to bone grafting. If not, then containment can become a major factor in achieving primary stability. Most defects requiring bone grafting will necessitate the use of allograft bone by virtue of the quantity required; host bone is usually in short supply, with the exception of patients requiring a contra-lateral primary hip or a knee replacement at around the same time. In such instances, the bone can be harvested and frozen for use at the subsequent revision. There are several substitutes for allograft bone that can be used by themselves or to supplement allograft, for example hydroxyapatite granules, coral and bovine bone, each with their advocates. Differing indications for revision will have an influence on choice of method and implant. The commonest indication for revision of the acetabulum is aseptic loosening, with or without bone loss and/or osteolysis; for this the implant choice is widest. For recurrent dislocation with a relatively well positioned and well fixed implant the options narrow; they would include cup augmentation, revision to a much larger bearing size, and revision to a constrained component. When the implant to be revised has been infected, and significant reconstruction with allograft is the chosen option, then a staged revision is often considered to be a safer choice.

Keywords acetabular reconstruction; allograft; impaction grafting; revision hip arthroplasty

Introduction Revision surgery of the acetabulum covers a wide spectrum of complexity, with a myriad of techniques for dealing with the difficulties that can arise. Careful pre-operative assessment and planning is vital, as is having alternative plans and the inventory to support them if the (not infrequently) unexpected occurs. Many of the techniques and implants are applicable to more than a few of the scenarios; often there is little to choose between them in terms of reported outcomes. The main goals are to provide a stable and lasting fixation, and where possible to improve the bone stock, most commonly with the use of allograft bone. Excellent results have been reported with both cemented and cementless options.1,2

Pre-operative assessment The plain radiograph often gives sufficient information in what could be termed straight-forward cases. The standard views are an antero-posterior (AP) view, combined with a horizontal beam lateral (not a turned lateral). Oblique or Judet views are helpful in further assessment, but these are perhaps now being supplanted by the use of computer tomography (CT) with modern software that can remove the artefacts produced by the scatter from the metal implants (Figure 1). It is always worth emphasising that these studies only quantify the bone present; the quality of the bone can be quite different to that which is expected, and this is one of the factors that can dictate a change of plan per-operatively.

Techniques for specific instances The well fixed or minimally loose cup with good bone stock The first key, where bone stock restoration does not seem to be required, is that implant removal does not compromise that situation. A well fixed cementless cup can be removed with virtually no loss of bone by specific tools for the purpose, such as the ‘‘Explant’’. A well fixed cemented component can be removed with the aid of an ultrasonic tool, or by cutting the plastic into quarters and removing it piecemeal. Once the cup is removed and the quality and quantity of the bone assessed as not requiring restoration, the choice of implant and method of fixation is essentially the same as for a primary

Peter W Howard MB ChB FRCS Consultant Orthopaedic Surgeon, Royal Derby Hospital N.H.S. Foundation Trust, Uttoxeter Road, Derby, UK.

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Bone stock restoration and primary implant stability are the main aims Investigation reveals the extent of bone present but not its quality Bone stock loss identified at surgery is generally greater than anticipated pre-operatively Implants, bone and consent need to be in place to deal with the unexpected Success rates diminish with greater bone stock loss

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X-ray and CT scan showing the extent of osteolysis behind a well fixed resurfacing cup. Figure 1

hip replacement. It is, however, often the case that there is more compromise to the bone stock than initially anticipated, and it is therefore vital that the tools for restoration are to hand, including allograft bone, and that the patient has been both appropriately informed and consented in advance.

the technique are not well defined; there is some suggestion that greater graft thickness, perhaps over 2 cm, may be associated with a higher failure rate.5 A minor lack of containment is acceptable so long as the vast majority of the graft is well contained and the cup well supported e as in Figure 3. Techniques of graft preparation vary; a mixture of sizes and shapes has some biomechanical advantage for impaction, and this can be produced readily by a combination of chips from a bone mill and morcellising 1 cm slices of allograft femoral head with a bone nibbler. Washing the graft is recommended. The long term reported success rates of cementless acetabular fixation are comparable.4 With larger contained defects, when a rim fix (cementless) can be obtained the depth of the graft becomes less important. Remodelling often accompanies incorporation (Figure 4).

The well fixed cementless cup with osteolysis The situation of a well fixed cup with polyethylene wear and osteolysis of the pelvis is usually associated with cementless metal backed components. Depending on the extent of the problem, there are a number of options. Curettage of the lytic area and allograft bone grafting is a viable option (Figure 2), followed by replacement with a new polyethylene liner, with replacement of the femoral head (if modular), as this is likely to be scratched. A similar technique is to graft the lesion and then cement a polyethylene socket into the shell. This is suited to a well fixed reasonably large shell, where osteolysis is recognised as a frequent problem for that particular implant. Alternatively, the cup can be removed and one may proceed as in next section. This is preferable if the cup is well fixed but fixation is only in a few contact areas.

Uncontained defects (excluding pelvic discontinuity) There are several well established techniques for managing uncontained defects. These are less common procedures and generally regarded as a special field in themselves. As in the other sections, the aim is to gain primary stability and restore bone stock; these two aims are better achieved by some methods than others. Solutions in cemented arthroplasty include the use of mesh screwed onto the pelvis to contain morcellised graft, the use of block/bulk and morcellised allograft combined, the use of a variety of shapes and sizes of supporting rings with graft and a cemented cup, and pegged/stemmed prostheses. Filling a large defect with cement can be considered when only a short term solution is required (eg short life expectancy), but this does not improve bone stock and stability can be short lived.

The contained defect with an intact rim This is the ideal situation for allograft bone grafting, either with a cemented or cementless component. Morcellised allograft with a cemented component has been widely reported.2 The limits to

Paprosky grading system, based on the ability to use a hemispherical cementless cup Type 1 Type II

Undistorted rim Distorted but intact rim, will support cup

Type III Non supportive rim

IIa Supero-medial defect IIb Supero-lateral defect IIc Medial/protrusio defect IIIa 1/3e rim defect, 40e60% host bone contact IIIb > rim defect, <40% host bone contact. Includes discontinuity

The AAOS Classification Contained Segmental Combined contained and segmental Pelvic discontinuity Ankylosis

Table 1

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Table 2

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A large osteolytic lesion above a well fixed shell, with marked wear of the polyethylene liner, treated with curettage and bone grafting, and liner change. Figure 2

A loose socket pre- and 1 year post-operatively after impaction bone grafting and cemented arthroplasty. Figure 3

An infected hip replacement with protrusio, 1 and 10 years after staged reconstruction. Note the medial wall remodelling. Figure 4

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Staged revision for infection, 6 weeks and then 2 years post-operatively, with block allograft femoral head. Figure 5

An uncontained lateral/postero-lateral deficiency is one of the commoner scenarios (Figure 5), where the bone stock has been eroded by the loosening prosthesis. Containment is achieved in this example with a portion of an allograft femoral head (distal femur is another option), shaped and fixed to the pelvis with screws. The resultant construct is then reamed. Morcellised allograft is then impacted, thereby sealing any small gaps, and a cup cemented in. Longer term concerns with this method are that revascularisation of the graft might result in collapse and loosening,7 but many grafts gain bony union without this happening (Figure 6). Supporting rings or roof re-enforcement rings,6 almost all available in titanium, can often achieve a reasonable press fit, which is then supplemented with screws. The bone stock is then augmented with morcellised graft prior to cup cementation; in general, their use is for larger uncontained defects. Similar support can be given by titanium mesh screwed onto the pelvis to augment the stability of impacted graft with cementation. Cementless fixation with large uncontained defects has a number of different options. An oversized (or ‘‘jumbo’’) cup can give a reasonable press fit to limited host bone after careful reaming, with

cavities then filled with morcellised graft and with screws passed through the cup to enhance early stability. Any exposed/uncovered component can then have bone onlaid. Favourable results have been reported although the technique is limited by the ability to get stable primary fixation, with often less bone available in smaller patients.8 Bilobed (or dual diameter) cups were introduced to fill the acetabulum and a lateral defect with implant. Variable results have been reported. The shortcoming of the technique is that bone stock is not restored, and more bone might have to be removed to get the implant to fit. There are a variety of stemmed and pegged implants (Figure 7) reported for gaining stability where there is insufficient host bone to gain a press fit. They are technically demanding, but good results have been reported.9 Trabecular metal implants are a relatively recent advance, and are showing great promise. Essentially, a very porous titanium surface enhances very rapid bony ingrowth as well as providing good grip for primary stability. The implants are available as augments and press fit sockets, but come with not inconsiderable expense. Short term reported results have to date been excellent, offering good versatility.

Revision with allograft femoral head at 6 weeks and 1 year. Note graft host union occurring superiorly. Figure 6

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Figure 8 Pelvic discontinuity, 3 years after reconstruction with BurchSchneider cage. No bone graft was used, but solid bony union is evident.

and replacing lost bone stock with bone optimises implant longevity and potentially improves options should subsequent revision ever be needed. A

REFERENCES 1 Park DK, Della Valle CJ, Quigley L, Moric M, Rosenberg A, Galante G. Revision of the acetabular component without cement. A concise follow-up, at twenty to twenty-four years, of a previous report. J Bone Joint Surg Am 2009; 91: 350e5. 2 Schreurs W, Busch V JJF, Marianne L, et al. Acetabular reconstruction with impaction bone-grafting and a cemented Cup in patients younger than fifty years old. J Bone Joint Surg Am 86: 2385e2392. 3 Paprosky WG, Peron PG, Lawrence JM. Acetabular defect classification and surgical reconstruction in revision arthroplasty. A 6 year follow-up evaluation. J Arthroplasty 1994; 9: 33e4. 4 D’Antonio JA. Peri-prosthetic bone loss of the acetabulum. Classification and management. Orthop Clin North Am 1992; 23: 279e90. 5 van Haaren EH, Heyligers IC, Alexander FGM, Wuisman PIJM. High rate of failure of impaction grafting in large acetabular defects. J Bone Joint Surg Br 2007; 89-B: 296e300. 6 Gill TJ, Sledge JB, Muller ME. The Burch-Schneider anti-protrusio cage in revision total hip arthroplasty: indications, principles and long term results. J Bone Joint Surg Br 1998; 80: 946e53. 7 Hooten JP, Engh Jr CA, Engh CA. Failure of structural acetabular allografts in cementless revision hip arthroplasty. J Bone Joint Surg Br 1994; 76-B: 419e22. 8 Whaley AL, Berry DJ, Harmsen WS. Extra large uncemented hemispherical acetabular components for revision hip arthroplasty. J Bone Joint Surg Am 2001; 83-A: 1352. 9 Badhe N, Howard PW. A stemmed acetabular component in the management of severe acetabular deficiency. J Bone Joint Surg Br 2005; 87-B: 1611e6. 10 Paprosky WG, Sekundiak TD. Total acetabular allografts. J Bone Joint Surg Am 1999; 81-A: 280e9.

Figure 7 10 years after a stemmed cup reconstruction with morcellised allograft.

Pelvic discontinuity Perhaps the most challenging situation of all is where there is a complete pelvic discontinuity, or transverse pelvic fracture, involving usually the acetabular floor and the adjacent anterior and posterior columns. The accompanying loss of bone stock can be variable, and whilst often obviously discontinuous by the alteration of the inner pelvic contour, the finding of a discontinuity at revision surgery is occasionally unexpected. Stability of the fracture must be obtained, usually by internal fixation either through a cage with multiple screws, by combined plate/screw fixation, or via the screw-holes of a cementless cup. The BurchSchneider cage (Figure 8) has been widely used and reported. It is versatile for its wide choice of screw placement, although there are concerns in the longer term over loosening of these large stiff implants. Trabecular metal implants are starting to be used in this situation, with some encouraging results reported. Where bone loss is massive, there is a place for the use of massive (whole) acetabular allografts,10 but this is in the surgical repertoire of very few surgeons, with an excision arthroplasty the remaining option for the hip that is otherwise un-reconstructable.

Conclusion There is a wide variety of techniques and options available for acetabular reconstruction; each with differing merits and some with definite drawbacks. Where possible, the principle of ‘‘building for the future’’ holds sound; gaining primary stability

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(iv) Reconstruction and revision of femoral failure in revision hip arthroplasty

has been ruled out as a cause of failure. Investigation should include the measurement of plasma viscosity erythrocyte sedimentation rate (ESR), full blood count (FBC) and C-Reactive protein (CRP). If inflammatory markers are raised a pre-operative aspiration of the joint is a sensitive and specific method to confirm the presence and sensitivities of the infecting organism.1 Bone stock is assessed radiographically. This should include an antero-posterior view of the pelvis in conjunction with an antero-posterior and lateral view of the hip to include the full length of any prosthesis and cement tail present. Obtaining previous radiographs where possible is essential to assess progression of any bone stock loss and assessment of subtle but significant changes.15 An attempt to classify residual bone stock should be made, bearing in mind the known inter/intra-observer limitations of all classification systems. Our unit classifies femoral bone stock abnormalities via the Endo-Klinik system2 (Table 2) though other systems such as that of the American Academy of Orthopaedic Surgeons, and Paprosky,8 are commonly used within the literature. Radiographs should be used for pre-operative templating of components. This gives the surgeon a plan to work towards during the reconstruction and also allows for component selection based on bone size or stock in more difficult cases. If the patient is a tertiary referral then all previous surgical operative notes should be obtained. This will confirm current implant type and size/configuration and may also reveal any technical difficulties encountered during the previous procedures.

Alexander Acornley Robin Banerjee Robert Kerry

Abstract Suitable techniques for femoral reconstruction and revision are dependent on the status of femoral bone stock. The pre-operative planning and operative strategies utilised increase in complexity as the bone stock diminishes. The options range from proximal to distal fixation techniques using cemented or cementless prostheses. Bone stock augmentation in the form of impacted morcellised or structural strut allografts may be required. In the most severe cases bone stock may need to be restored with bulk allograft or restored with a mega-endoprosthesis. A structured reconstruction cascade discussing these options is presented.

Keywords arthroplasty; femur; hip Joint; re-operation

Introduction Operative surgery

The number of patients undergoing total hip arthroplasty (THA) continues to increase, with 66 839 primary and 6757 (10%) revision THA procedures being recorded in the National Joint Registry for the United Kingdom in 2007/8. Femoral revision and/or reconstruction at the time of THA can range from the simple to the extremely technically demanding, but will essentially revolve around the status of the bone stock within the femur. The potential methods employed are summarised in Table 1. If bone stock is acceptable then revision can be performed using either proximal or distal fixation. If bone stock is unacceptable then the main question is whether bone augmentation or replacement is required.

Surgery should be carried out in a laminar flow theatre, with appropriate prophylactic intravenous antibiotics administered after specimens have been obtained. Impervious, non-woven, disposable drapes should be used. The use of an extensile approach should be encouraged to facilitate implant and cement removal, as appropriate. Many units perform revision hip arthroplasty with the patient in a lateral decubitus position and utilise a posterior approach. This can then easily be combined with either a trochanteric slide or extended trochanteric osteotomy based on the pre-operative plan and requirements at the time of surgery.

Pre-operative planning

Femoral reconstruction ladder

Pre-operative planning starts with a thorough history and examination of the patient. This is vital to ensure that infection

Alexander Acornley MBChB FRCSEd (Tr & Orth) Cavendish Hip Fellow at the Sheffield Teaching Hospitals NHS Foundation Trust Northern General Hospital, Sheffield, UK. Robin Banerjee MBChB FRCSEd (Tr & Orth) Cavendish Hip Fellow at the Sheffield Teaching Hospitals NHS Foundation Trust, Northern General Hospital, Sheffield, UK. Robert Kerry MBBS FRCS(Orth) Consultant Orthopaedic Surgeon at the Sheffield Teaching Hospitals NHS Foundation Trust, Northern General Hospital, Sheffield, UK.

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Reconstruction Method

Bone Stock Status

Implantation Devices

Proximal Fixation

Adequate

Distal Fixation

Adequate

Bone Augmentation

Inadequate

Bone Replacement

Inadequate

Cement in Cement Cementless (Metaphyseal fit) Cemented (Long stem) Cementless (Diaphyseal fit) Impaction grafting Cortical Strut Allograft Bulk Allograft Mega-Endoprosthesis

Table 1

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Endo-Klinik classification system of femoral bone loss Grade

Definition

I

Radiolucent lines confined to the upper half of the cement mantle; clinical signs of loosening. Generalised radiolucent zones and endosteal erosion of the proximal part of the femur, leading to widening of the medullary canal. Widening of the medullary canal by additional expansion of the proximal femur. Gross destruction of the proximal third of the femur with concomitant involvement of the middle third, precluding the insertion of an even-stemmed prosthesis.

II III IV

Table 2

Femoral reconstruction is preceded by acetabular reconstruction, if required, aimed at restoring the anatomical hip centre, and choice of an appropriate bearing surface. Potential fixation strategies and techniques for bone augmentation/replacement will now be discussed in more detail.

use of cemented femoral components can be justified as the proximal bone stock remains supportive. The most important technical point, as in a primary THA, is bone preparation for cementation. Meticulous removal of any fibrous tissue and exploration of osteolytic areas with curettage of granulation tissue must be performed. Often there has been the formation of a neo-cortex, which must also be debrided; a high speed burr is a useful tool in this situation. Care must be taken to remove any pedestal formed distally if it is likely to impede the correct placement of a cement restrictor. Implantation of a standard cemented femoral component into the cancellous bed can then be performed with the use of third generation cementation techniques.

Proximal fixation (Endo-Klinik Grade 1 bone loss) Femoral reconstruction using proximal fixation can be either cemented or cementless; Cemented: The situation often arises where there is a loose acetabular component but well fixed femoral cemented component. Complete removal of a well fixed femoral cement mantle in an aseptic revision THA can be avoided using the cement-incement technique. This is advantageous in that it avoids the potential complications of removing a well fixed cement mantle, as well as reducing blood loss and operative time. This technique involves cementing a new smaller femoral component into a complete or distally intact cement mantle, most commonly using a polished, tapered stem design. The main indications are after; - removal of a stable stem to aid acetabular exposure, - removal of a broken stem, - removal of a monoblock or inadequate offset stem in instability cases to allow increased offset or larger head sizes to be utilised. The most important technical details of the technique are; - the distal mantle must be intact and not damaged by extraction of the old implant, - the shoulder of the implant should be completely clear of cement before extraction is attempted, - any defects or osteolysis in the proximal mantle, i.e. corresponding to Gruen zones 1 and 7,3 need to be extracted and the bone-cement interface debrided until a surface that would support osseo-integration can be confirmed and - the old distal cement interface must be kept meticulously clean and dry to avoid debris and blood entering the interface at the time of cementation of the new implant. The technique was first described by Eftekhar in 19784 and recent good short-term clinical and radiological results have now been reported.5,6 Removal of a cementless femoral component without a biological ingrowth surface often yields a femur with minimal metaphyseal cancellous bone loss and an intact diaphysis. The

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Cementless: Complete removal of a cemented femoral component would not normally yield enough bone stock proximally to allow for a metaphyseal fit cementless system to be used. Removal of a cementless femoral component without a biological ingrowth surface often yields a femur with minimal metaphyseal cancellous bone loss and an intact diaphysis. The use of cementless metaphyseal fit femoral components is justified as the proximal bone stock remains supportive. In revision THA for instability, where malalignment of the primary components is an issue, the use of modular systems that allow metaphyseal fit and fill to be reconstructed as an independent variable to stem version can be an advantage. If required both mechanical and biological modifications such as proximal internal collars and hydroxyapatite coatings can be used, avoiding the need for distal fixation. Strict attention to detail in the surgical technique of implantation of the femoral component remains identical to that of cementless primary THA. Distal fixation (Endo-Klinik group 2 and 3) Cemented e long stem: In the context of adequate distal but reduced proximal bone stock the use of a long stemmed cemented implant can be considered. Early series using standard length components in combination with first generation cementation techniques did yield relatively poor results but 98% stem survival for aseptic loosening has now been reported with the use of polished long-stemmed, double tapered, collarless prostheses without the addition of any bone augmentation.7 This is certainly an attractive option in the elderly, osteoporotic population with their associated co-morbidities and osteopaenia; risk

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factors that increase the potential for complications with the use of impaction grafting or cementless implants. A double taper design allows for the taper slip principle of stem engagement and the slim profile distally allows for a large cement mantle to aid load transfer (Figure 1). Meticulous removal of all fibrous tissue and exploration of osteolytic areas with curettage of granulation tissue must be performed. Neocortex must be debrided to provide an acceptable cancellous base for cement osseo-integration. Cementation should proceed with the use of: - distal cement restriction, - pulsatile lavage of the cancellous bed, - retrograde canal filling via a long nozzle cement gun, - proximal seal and - cement pressurisation prior to insertion.

(metaphyseal) fit stems, such as may be used in primary total hip arthroplasty, and longer stems designed for revision purposes to fit distally within the diaphysis. After initial preoperative planning and confirmation of findings at operation, appropriate implant choice can be made. If proximal metaphyseal bone stock is adequate then shorter stems designed to fit and fill the metaphysis can be used, but if the metaphyseal bone stock is inadequate distal fit stems are appropriate. At the preoperative planning stage one must make a decision on the amount of bone available above the isthmus. According to Paprosky, if there is more than 4 cm of bone stock within the diaphysis above the isthmus then a distal fit stem is suitable8 (Figure 2). If there is less than 4 cm then a distal fit stem can still be used but augmentation in the form of graft or interlocking screws across the distal stem must be employed. The adequacy of distal support is ultimately a decision based on experience and the design characteristics of the particular implant. On-table axial and rotational stability are mandatory. A number of stem designs and surface finishes are available in order to help ensure this. The length of the stem is also of vital importance as one must assure that the stem progresses at least two full cortical diameters below any significant defect. This can be difficult as after removal of a cemented stem, distal cement and cement restrictor the distance to the isthmus may be greatly reduced. As the length of the stem increases one must also be aware of the natural bow of the distal femur and if possible use

Cementless: The two main types of cementless stems of use in femoral reconstruction are broadly divided into shorter proximal

a Endo-Klinik Grade 3 Bone loss associated with 1st stage revision for infection. b Reconstruction with cemented double polished long tapered stem. Figure 2 Reconstruction with long stem scratch-fit prosthesis after utilisation of extended trochanteric osteotomy for exposure.

Figure 1

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Bone augmentation In the presence of significant bone stock loss it may be advisable to augment the revision THA with bone. This can take the form of either impaction grafting of morcellised allograft bone chips or extramedullary bypass support in the form of allograft cortical strut fixation. It is important to highlight that avoiding unnecessary compromise of bone stock in the distal femur through appropriate choice of primary or revision implant leaves more options for future revision THA surgery. This is especially important in the young patient where multiple revision procedures can be anticipated in a lifetime. Regardless of the reconstruction chosen, the end result must be a stable implant.

a stem that matches this to avoid a stress riser on the anterior cortex of the femur or even perforation. During the approach in such cases, an extended trochanteric osteotomy offers many advantages for the following reasons: - ease of exposure, - ease of removal of cement along with products of osteolysis, - with larger and bulkier stems it still allows secure abductor reattachment and - proper placement of the level of the abductor mechanism, especially when the limb has been shortened for some time. Even when care is taken, there is still the risk of a distal fracture of the diaphysis below the stem and appropriate clamps/ cerclage wiring around the femur distally at the time of prosthesis insertion may be required. When attention is turned to the proximal portion of these longer modular stems, both offset and version must be addressed. With more modern prostheses there is a range of bodies available and care must be taken to restore optimal offset and version so as to leave the surgeon with a full set of available head lengths to fully balance the hip (Figure 3). If appropriate care is taken with all of these points then a full set of plus and minus heads is still available to the surgeon to finely balance the tension of the reduced hip and ensure adequate stability without excessive lengthening.

Impaction grafting: Impaction grafting of the femoral canal as a technique for revision THA was first described by the Exeter group in 1991.9 Morcellised allograft bone chips created by milling donated bone are impacted into the proximal femur to replace deficient bone stock. Any uncontained defects require prior containment. This is achieved with the application of fine stainless steel mesh or occasionally plates or cortical strut allografts, which are secured with the use of wires. Once impacted, the canal is retrograde filled with low viscosity bone cement, proximally sealed, pressurised and the

a Endo-Kinik Grade 3 Bone loss associated with aseptic loosening and osteolysis. b Reconstruction with cementless modular long stem prosthesis after utilisation of extended trochanteric osteotomy for exposure. Figure 3

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new standard or long-stemmed polished, tapered, collarless component is implanted (Figure 4). Concerns about subsidence and ultimately failure of the reconstruction have been raised with this method. The technique has now evolved to include dedicated instrumentation for impaction and certain technical considerations are now recommended to lower the risk of subsidence10: - use of larger bone chips (5 mm) within the femur if the canal is capacious, - good distribution of particle size, - washing of the bone chips, - tight impaction within the femur to the point where the impaction device cannot be removed or rotated from the femur unless it is physically disimpacted with the backslapping hammer and - the use of long stems in severe cases to reduce the risk of fracture. It must be remembered that due to the very nature of tight impaction of the allograft, femoral fracture either intra- or postoperatively is a potential complication and a low threshold for investigation of this possibility should be employed.

with stronger cables to avoid damaging the periosteal supply to the host bone. To promote healing to the host bone supplementary autograft bone may be used. In a study of 52 patients over 4 years the average time to union was 10 months, with a 4% rate of non-union and graft resorption.11 Bone replacement There will come a point in the reconstructive cascade that bone loss has become so severe that its total replacement becomes the only remaining option. This is most commonly the case in the young patient who has had multiple revision procedures and in cases of severe infection where the radical debridement required has resulted in massive bone stock loss.

Cortical strut allograft: These can be used as an adjunct to fixation in several scenarios: - to restore uncontained non-circumferential defects in the diaphysis, - to bypass stress risers or - to stabilise a proximal femoral allograft at the junction of host bone. The struts are cut from diaphyseal bone. They are placed over the required area and should be wired in place rather than held

a Bulk proximal femoral allograft composite prior to implantation. b Bulk proximal femoral allograft union and remodelling. Figure 4 Reconstruction via impaction grafting with cortical defect closed with mesh.

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Figure 5

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a/b Massive bone loss associated with 1st stage debridement for severe infection of previous revision hip arthroplasty. c/d Reconstruction with total femoral replacement. Figure 6

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The options for replacement are either bulk allograft or megaendoprosthetic replacement.

Mega-endoprostheses: Replacement of the proximal femur with a large endoprosthesis has been used in neoplastic cases for many years. The long term outcome of these procedures can be limited by the poor life expectancy of the patients. In the case of revision hip arthroplasty in non-neoplastic scenarios, proximal femoral endoprosthetic replacement has a high morbidity rate, with such complications as dislocation in 10% of patients and eventual revision in up to 30% of patients at an average follow up of 11 years.14 To this end, endoprosthetic replacement must be viewed as the last option in the reconstructive surgeon’s armamentarium. When there is gross destruction of the proximal third of the femur with concomitant destruction of the isthmus then insertion of any stemmed prosthesis is precluded and endoprosthetic replacement must be considered. Numerous different systems are available but the basic principles of insertion are the same. Most systems offer cemented and uncemented fixation but the majority of cases require cement fixation distally, as the isthmus has been passed. One of the main problems is dislocation due to the lack of abductor function and soft tissue attachment. The proximal bone is not supportive of the implant but can be left in the sterile case and wired around the prosthesis to offer some soft tissue attachment. When there is no proximal bone whatsoever, great care is required to ensure the correct tension and ensure stability. Some implants offer the option of trabecular metal at the shoulder of the implant to allow any remnant of greater trochanter the potential to fix to the replacement, but in our experience this seldom occurs. All other opportunities to reduce the high risk of dislocation should be considered, such as increasing the head size and captive acetabular components, despite the inevitable associated disadvantages. In cases where the patient has an ipsilateral knee replacement then the use of long endoprosthetic proximal femoral replacement carries a very high risk of periprosthetic fracture between the knee and the hip. In these cases total femoral replacement should be considered (Figure 6).

Bulk allograft:12,13 The use of bulk proximal femoral allografts (BPFA), harvested from cadaveric donors gained popularity in the late 20th century both within the United States, Canada and the United Kingdom. The main indication is a circumfrential defect that is more than five centimetres in length. The use of BPFA has several theoretical advantages: - restoration of proximal femoral bone stock, - good soft tissue reattachment around the hip aiding muscle function and stability, and - dry virgin surface for cementation proximally and distal press-fit, with limited compromise of the remaining distal femur. All donors are screened for known transmissible diseases. The grafts are usually harvested under sterile conditions and then processed so as to decrease their immunogenicity and ensure sterility. The most common methods used are freezing ( 70  C) or freeze drying, which can be combined with irradiation. Minus seventy degree Celsius stored samples have a storage life of five years. The surgical approach is usually dictated by remaining host bone, which is often kept to allow it to be wrapped around the BPFA at the end of the procedure. This allows good restoration of the soft tissue envelope and can aid stability. The host junction is sectioned as a step-cut osteotomy to allow initial rotational stability and this can be further augmented with cerclage wires. Bone ingrowth cannot occur within the BPFA, therefore the prosthesis should be secured to it with cement proximally. The stem protrudes distally out of the composite to allow insertion and a press-fit into the host. The BFPA, can be held in a vice on a sterile trolley within the operating theatre and prepared as for a standard cemented stem. The cement should be pressurised. This can be achieved by thumb occlusion of the distal end, retrograde cement insertion with a gun and the use of a proximal seal. The prosthesis is then inserted in a standard fashion into the BFPA, allowing further pressurisation. It is essential to ensure that no cement enters the interface between the graft and host. The stem/BFPA composite, is then placed into the host and the step cuts matched, conferring initial stability. This can then be further secured with cerclage wires (Figure 5). The remaining host bone can then be folded back over the BPFA, and held with cerclage wires. Post-operatively patients can weight-bear protected until radiological evidence of trochanteric and graft-host union is present. Unsurprisingly significant though very variable complication rates have been reported for this major procedure: - infection (4e13%) - instability (0e35%) - non-union of graft-host (4e23%) - non-union of trochanter (usually not an issue if distal soft tissue attachment has been preserved and trochanteric escape has been avoided) - resorption (8e34%) and - fracture. Failure of such a construct, or bone stock loss which is not suitable for reconstruction with BPFA, may be salvaged with a mega-endoprosthesis.

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Summary In summary, cases higher up the reconstruction ladder will require more complex reconstructions and have greater potential for complications. A surgeon and unit with adequate experience of that type of case are essential if an optimal outcome is to be achieved. A

REFERENCES 1 Ali F, Wilkinson JM, Cooper JR, et al. Accuracy of joint aspiration for the preoperative diagnosis of infection in total hip arthroplasty. J Arthroplasty 2006; Feb; 21(2): 221e6. 2 Engelbrecht E, Heinert K. Klassifikation und behandlungsrichtlinien von knochensubstanzverlusten bei revisionsoperationen am ¨ftgelenk. Hrsg Endo-Klinik Hamburg. [[Classification and guidelines hu for treatment of loss of bone stock during revision surgery on the hipdmedium-term results]]. In: Endo-Klinik, editor. ¨rund revisionsalloarthroplastik. Hamburg, Berlin: Springer; Prima 1987. p. 189e201. German.

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3 Gruen TA, McNiece GM, Amstutz HC. ‘‘Modes of failure’’ of cemented stem-type femoral components: a radiographic analysis of loosening. Clin Orthop 1979; 141: 17e27. 4 Eftekhar NS. Principles of total hip arthroplasty. St Louis: Mosby; 1978. 5 Quinlan JF, O’Shea K, Doyle F, Brady OH. In-cement technique for revision hip arthroplasty. J Bone Joint Surg Br 2006; 88-B: 730e3. 6 Goto K, Kawanabe K, Akiyama H, Morimoto T, Nakamura T. Clinical and radiological evaluation of revision hip arthroplasty using the cement-in-cement technique. J Bone Joint Surg Br August 1, 2008; 90-B(8): 1013e8. 7 Howie DW, Wimhurst JA, McGee MA, et al. Revision total hip replacement using cemented collarless double-taper femoral components. J Bone Joint Surg Br 2007; 89-B: 879e86. 8 Valle CJ, Paprosky WG. Classification and an algorithmic approach to the reconstruction of femoral deficiency in revision total hip arthroplasty. J Bone Joint Surg Am 2003; 85-A(Suppl 4): 1e6. 9 Simon JP, Fowler JL, Gie GA, et al. Impaction cancellous grafting of the femur in cemented total hip revision arthroplasty. In: Proceedings of the British Orthopaedic Association. J Bone Joint Surg Br 1991; 73(Suppl 1): 73.

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10 Halliday BR, English HW, Timperley AJ, et al. Femoral impaction grafting with cement in revision total hip replacement. Evolution of the technique and results. J Bone Joint Surg Br 2003 Aug; 85(6): 809e17. 11 Gross AE, Wong PK, Hutchison CR, King AE. Onlay cortical strut grafting in revision arthroplasty of the hip. J Arthroplasty 2003 Apr; 18(3 Suppl. 1): 104e6. 12 Haddad FS, Garbuz DS, Masri BA, et al. Instructional Course Lectures, The American Academy of Orthopaedic Surgeons. Femoral bone loss in patients managed with revision hip replacement: results of circumferential allograft replacement. J Bone Joint Surg Am Mar 1999; 81: 420e36. 13 Graham NM, Stockley I. The use of structural proximal femoral allografts in complex revision hip arthroplasty. J Bone Joint Surg Br 2004 Apr; 86(3): 337e43. 14 Malkani AL, Settecerri JJ, Sim FH, Chao EY, Wallrichs SL. Long-term results of proximal femoral replacement for non-neoplastic disorders. J Bone Joint Surg Br 1995; 77(3): 351e6. 15 Andoni P Toms, Rajesh Botchu, John F Nolan. Diagnostic plain film radiology of the failing hip replacement. Ortho & Trauma 2009; 23(2): 88e100.

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(v) The management of dislocation in hip arthroplasty

topic (Volume 23:1 2009). By selecting the correct implant for each specific patient, ensuring that optimal component position is achieved and performing a thorough intra-operative trial reduction, subsequent instability should be minimised. Despite our best efforts, dislocations will occur, which serves to underline the multi-factorial nature of dislocation in THA. Therefore, when dislocation does occur following THA the cornerstone of subsequent successful management depends upon a detailed and accurate assessment, with the expectation that when as many of these factors are addressed as possible in the treatment strategy then a successful outcome should be more likely.

R Yarlagadda SA Jones

Abstract Hip dislocation and the sequel of recurrent instability continues to be a problem following Total Hip Arthroplasty (THA), and is one of the leading causes of revision surgery. The cause of instability is often multi-factorial, including patient factors, surgeon factors, implant position and design, together with soft tissue related factors. Successful management of hip instability depends on an accurate assessment and, thereafter, addressing as many of these factors as possible. This article concentrates on the assessment and surgical management of hip instability following THA.

Assessment Patient history Deciding what factors caused a specific patient’s hip to dislocate requires a systematic approach, involving taking a targeted history, examination of the patient, gathering information from the notes and ordering appropriate investigations. When considering patient history in hip instability, details can be considered in three groups: - History of events surrounding dislocation and details of any subsequent instability - History of progress since index THA - History and patient factors prior to index THA Most of the patient factors for dislocation can be discovered in the clinical history. Questions relating to the dislocation include the number of dislocations and when they started. Dislocations that start to occur later in the life of the implant may be due wear of the articulating surfaces and change in the position of the implants. In the case of multiple dislocations, one should question what the original cause of the dislocation was. Was it associated with trauma or was it a positional event? The position in which the hip dislocates gives information on the direction of dislocation (i.e. anterior or posterior) and an idea of the primary arc of the implants. Previous hip surgery, surgery for hip fractures and revision hip surgery all predispose a patient to the risk of dislocation. Compliance of the patient also needs to be assessed, as a lack of compliance could have compromised the original operation and will have to be taken into account for subsequent treatment. Patient-related factors involve the patient’s co-existing morbidities. Patients with a history of alcoholism, neurological conditions such as Parkinsonism, epilepsy and strokes are also at a higher risk of dislocation. Patients who are suffering from dementia and other psychiatric conditions may have issues surrounding compliance post hip surgery.

Keywords dislocation; hip replacement; instability; treatment

Introduction Dislocation occurs after 0.3% to 10% of primary total hip arthroplasty (THA) and after up to 28% of revision THA.1 Early dislocation, which has been defined as occurring within the first three months following THA, is more common but the cumulative risk of dislocation increases with the number of years following implant insertion. Half of those patients who dislocate suffer a single episode; however, for the other half recurrent instability and often further surgical intervention are required.2 The patient with a dislocating THA is functionally impaired and this leads to patient apprehension and dissatisfaction. Clinical outcome scores and global outcome measures in patients who have had a dislocation of their hip are significantly worse than those without dislocation3 and do not improve despite successful revision surgery. The burden of revision surgery for instability to both patient and surgeon is considerable, in terms of both morbidity and cost. In North America instability is now the main reason for revision surgery, accounting for 22% of cases undergoing revision THA.4 Instability following THA is most often multi-factorial and the underlying causes can be considered to fall into five major subgroups (Box 1). Prevention and avoidance of dislocation and instability in the first instance is obviously preferable and a recent Orthopaedics and Trauma article has addressed this

Factors related to instability in THA 1. 2. 3. 4. 5. 6.

R Yarlagadda FRCS (Orth) Lower limb arthroplasty fellow, University Hospital Llandough, Cardiff, UK. SA Jones MSc FRCS (Orth) Consultant Orthopaedic Surgeon, University Hospital Llandough, Cardiff, UK.

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Patient factors Surgeon factors Implant design Implant alignment Soft tissue factors Most commonly multi-factorial

Box 1

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Woolson et al found that ‘‘cerebral dysfunction’’, which included a state of mental confusion during stay in hospital, a history of senile dementia/mental disorder and excessive alcohol consumption increased the risk of dislocation significantly.5 Increasing age, especially patients over the age of 80, also carries a greater risk of dislocation; up to 12%.6 The notion that age itself is related to dislocation risk is controversial but it certainly may lead to increased risk of falls, decreased muscle control and degradation of cognitive ability; all of which can increase the risk of dislocation. From the patient’s medical records it is important to gather information from the operation details such as the implants used and the size and type of the articulating surfaces. Information is also gathered regarding the operation itself, including the surgical approach used. The large majority of dislocations and therefore subsequent instability occur in the direction of the original surgical approach. Were any difficulties encountered during the procedure for any reason and was stability assessed intra-operatively? If the THA has previously dislocated and been treated with a closed reduced in theatre, was there an assessment of stability performed and in particular what was the safe arc of movement and status the soft tissue tension?

opposite side? Assess the range of movement of the joint and whether is it excessive in any particular direction, and assess the rotational profile of the THA. The neurological status of the lower limb (in particular the superior gluteal and sciatic nerve function) should be assessed and documented, as damage from previous surgery or dislocation may have occurred. Radiological investigations Standardised radiographic views, including AP pelvis for hips and a lateral of the affected hip, can yield valuable information regarding the leg length, offset, and the implants used. Evidence of wear and loosening must be looked for. Varus or valgus alignment of the femoral component can affect the soft tissue tension. Component orientation is obviously important; although it can be difficult to comment on the cup anteversion, vital information can be gained from good quality AP (Figures 1 and 2) and lateral radiographs (Figures 1 and 2). If infection is being considered clinically then blood tests for CRP and ESR should be performed and aspiration arthrogram performed if indicated. If there is concern about the alignment of the implants then CT scanning is an excellent way of gaining further information regarding the position of the implants (Figure 3). In particular, the acetabular component anteversion can be difficult to determine on plain radiographs and as this is frequently an issue resulting in instability, accurate assessment is required.7

Clinical examination On examination, as well as standard assessment, one must specifically inspect for leg length discrepancies and assess the function of the abductor muscles. Look at the attitude of the limb; does it appear more internally or externally rotated than the

Figure 2 Surgery included cup and stem revision to correct mal-position, the head-neck ratio was maximised with a large diameter metal-on-metal bearing to provide the largest possible primary arc of movement and soft tissue tension addressed by trochanteric cable plate fixation. With several factors addressed a successful outcome was achieved.

Figure 1 Cemented THA presenting with recurrent instability. Assessment demonstrated poor implant position and soft tissue factors with trochanteric non-union. Also patient compliance was an issue.

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Assessment of patient with THA dislocation C C C C C

Targeted history Clinical examination Information from clinical records Investigations (plain radiographs, CT scan, fluoroscopy) Examination under anaesthesia

Box 2

component fixation and indeed implant design as it is possible with loose or indeed certain implant designs to disturb the prosthesis during reduction (Figure 6). Intra-operative fluoroscopy can then be used to confirm reduction and assess the stability and status of the implants. There is evidence to suggests that 2/3rds of patients with an early dislocation will not dislocate again as long as the implants are well positioned.1 It is therefore imperative to confirm that implants are well positioned and this may require further radiological imaging. Although abduction braces and knee immobilizers are frequently used, their benefit in the peer-reviewed literature is of questionable value. Cesare et al braced 91 first time and 58 recurrent dislocations with no obvious mal-positioned implants and found bracing to be ineffective in preventing further dislocations when compared to a control group that was not braced.8 Physiotherapy with an emphasis on patient re-education may well be worthwhile. The question then is how many dislocations one allows before treating the patient surgically? Although there is no specific evidence to support such a decision, generally most surgeons would intervene when more than two dislocations have occurred. The indications for operative intervention include recurrent instability, chronic dislocation, irreducible dislocations, mal-positioned implants and lack of adequate soft tissue tension leading to instability.

Figure 3 CT scan demonstrating significant acetabular component retroversion.

Examination under anaesthetic and fluoroscopy screening can be a useful assessment tool in THA instability (Figure 4). The impingement free range of movement can be defined as well as the stable arc of movement. In particular, soft tissue tension can be assessed, which can be difficult to determine by other methods as it may well occur in a well-orientated THA with a functional primary arc of movement. All of the information gathered helps formulate the plan for treatment and the further prevention of dislocation in the patient (Box 2).

Treatment of dislocations following THA Early post-operative first time dislocation A first time dislocation is treated with a closed reduction. It is generally recommended that this be performed under anaesthesia in the operating theatre. It is important to ensure that the dynamic muscle stabilisers are overcome with the reduction manoeuvre and that potential damage to the components and patient’s own tissues is avoided. Both failed and successful reductions have been shown to cause bearing surface damage (Figure 5). The history, clinical examination and radiographs should allow the direction of the dislocation to be confirmed, as this will determine the reduction technique. Reduction techniques are similar to those manoeuvres for traumatic dislocations of the native hip. Radiographs should also be studied to appreciate both

Instability and component mal-position Implant orientation obviously has a major effect on implant stability, and cup mal-position in particular is found to be a major cause of dislocation. Parvizi reported on their series of

Figure 4 Examination under anaesthesia and fluoroscopy screening demonstrates that in a case of recurrent instability the THA exhibits a stable ROM but gentle axial traction results in joint subluxation confirming significant soft tissue insufficiency.

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Figure 5 Dislocated primary cementless THA with ceramic on ceramic bearing. Damage to head evident at time of subsequent revision surgery.

patients with recurrent instability that required revision surgery.9 Socket mal-position was identified as the major cause in 33 (35%) of 93 patients. Revision surgery was successful in preventing recurrence of instability in 91% in their series. Historically, however, the recurrence rates after component revision have been much higher (39e47%).10,11 If the components are mal-positioned then the implants should be revised to implants with the appropriate alignment. The recommended ‘‘safe zone’’ as described by Lewnineck for acetabular orientation is cup abduction of 40 þ/10 degrees and anterversion 15 þ/10 degrees.12 Exceeding the abovementioned measurements has been to show to increase the rates of dislocation from 1.5% to 6.1 %. The use of the transverse ligament has been shown to be a dependable landmark for the anteversion of the cup, as shown by Archbold and Beverland et al.13 By placing the cup parallel to the transverse ligament this prevents excessive anteversion or retroversion of the cup, thus placing the cup in the centre of the patient’s functional range, enhancing the joint’s stability. On the femoral side, the recommended anteversion angle is 10 to 25 degrees. An overall combined cup and stem anteversion of 45 degrees should be aimed for.14

removal. Impingement can also be related to the implant characteristics or the patient’s femoral and pelvic anatomy. If the natural femoral offset of the patient was not restored at the time of the index surgery, then poor soft tissue tension may be problematic; also the greater trochanter may impinge against the pelvis, effectively levering the hip out of joint. This can be addressed by restoring the offset at the time of the revision. The two issues involving implant design and impingement are the primary arc and the excursion distance. The primary arc is the range of movement possible in the articulation before it impinges on the edge of the liner, which is followed by leveringout, and when the excursion or jump distance is exceeded dislocation occurs (generally the jump distance¼radius of the femoral head). The range of movement possible before impingement occurs is determined by the head:neck ratio. The larger the head is compared to the size of the neck, the further the hip has to travel before it impinges on the edge of the cup and thus the greater the primary arc of movement. Therefore, skirted femoral heads and elevated rim profile cups affect the primary arc and can cause impingement by virtue of their design. Various implants have been used to optimise the head:neck ratio and the excursion distance of the revised implant. They include the use of large diameter femoral heads, modular component exchange and the use of bipolar and tri-polar articulations.

Instability and well-positioned components The two principal reasons why well-positioned implants dislocate are because of either impingement or soft tissue (principally abductor) deficiency. Dislocation may be due to impingement of bony or soft tissue, causing the hip to lever out. Occasionally a lump of scar tissue may be found to cause enough impingement to result in a dislocation. This tissue should be looked for at the time of revision and excised. Similarly, bony impingement can be caused by osteophytes around the acetabulum or a remnant of femoral neck not excised at the time of the primary surgery, and will require

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Large diameter femoral heads Advances in manufacture, together with our knowledge of the wear of modern bearing surfaces, has resulted in the ability to use larger diameter femoral heads, thereby increasing THA stability. The larger diameter heads also allow for an increased neck length to be achieved without the incorporation of a skirt into the head design. Head sizes of 36mm and larger are now available for use with most

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Figure 7 In this patient modular exchange was taken to the extreme with exchange of the SROM stem from within its ingrown modular collar, to allow increased offset. Due to abductor deficiency, a constrained liner was also used.

Figure 6 Attempted closed reduction of an early dislocation in a patient who had a cemented polished tapered femoral stem resulted in displacement of the stem from the cement mantle and required open reduction.

bearing surfaces, including Highly Cross-linked UHMWPE, ceramic and metal articulations, each of which have their own advantages and disadvantages. The use of jumbo-sized femoral heads is commonly employed in an attempt to prevent dislocation and is increasingly reported for management of recurrent instability. Beaule et al reported on 12 patients treated with large femoral heads (mean diameter 44 mm) for recurrent instability; in their series patients had an average of four previous operations and seven prior dislocations. At an average follow-up of 6.5 years, 10 patients had no further episodes of instability.15

the primary arc of movement of the articulation surface and may result in increased impingement in other positions. For the same reason, skirted femoral heads should be avoided. Toomey et al reported a success rate of 92% at a mean of 5.8 years in a series of 13 hips using modular component exchange, and recommended the use of this technique only in selected cases.16 In general, the cup and stem have to be both well positioned and well fixed and the cup must also be of a sufficient size to allow for the use of a liner of sufficient thickness for the size of femoral head chosen. However, this technique is associated with complications, as reported by Barrack et al,17 including detachment of the femoral head, dislodgement of the polyethylene liner from the acetabular shell and asymmetrical rotation of the liner. In general, isolated modular exchange has had a relatively poor track record of success in treating recurrent instability in THA.

Modular component exchange Exchange of the modular components that comprise the THA can be undertaken as a method to improve stability (Figure 7). Modularity allows for alteration in neck length, acetabular offset and head diameter. Acetabular liners can be offset to improve soft tissue tension. Also, face-changing liners can re-direct the articulation interface by a limited amount. Elevated rim liners, whilst potentially increasing stability in a particular direction, will overall reduce

Bi-polar and tri-polar arthroplasty A bi-polar device is a small femoral head placed inside a polyethylene shell that is within a larger femoral head. The larger head then articulates with the native acetabulum. In theory, the movement occurs between the small head and the poly liner and also between the large head and the patient’s acetabulum. When the larger head articulates with an acetabular component it is called a tri-polar arthroplasty. Grigoris et al first described using tri-polar arthroplasty in a series

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of 8 patients with no further dislocations at a mean of 4.2 years.18 Parvizi et al reported on a series of 27 recurrent dislocations treated with bipolar arthroplasties. At a mean of 5 years, 81 % had no further dislocations.19 However, there are problems associated with the use of bipolar arthroplasty. Not infrequently patients complain of groin pain and there is always potential for the implant to migrate, for what are modest gains in function. For these reasons, this should not be the first line of treatment for a dislocating arthroplasty and it is mainly indicated in salvage cases. Abductor function and soft tissue factors A lack of soft tissue tension in THA can lead to instability. Certainly, failing to restore the offset of the hip can lead to instability and this must be looked for in the radiographs in the investigations leading up to surgery. In such cases, the offset should be restored at the time of surgery. Non-union of the torchanteric osteotomy performed as part of the approach can lead to instability by defunctioning the abductors, reported to be as high as 17.6% when compared to 2.8% when the osteotomy healed.1 If present, the non-union should be treated with fixation at the time of surgery. Trochanteric advancement has been suggested as a method of treating recurrent dislocators where neither component malpositioning nor impingement was the cause of the dislocations. Kaplan et al reported on 21 recurrent dislocators treated with an average of 16mm of trochanteric advancement.20 The surgery was successful in 17 of the patients. They noted that in the failures, two of the patients had non-union of the trochanter leading to a proximal migration of 1cm; these patients continued to dislocate repeatedly and thus it was suggested that proximal migration of the trochanter by 1 cm or more may result in an increased risk of dislocation.

Figure 8 Dislocation of a tri-polar constrained liner e the underlying mechanism at revision surgery was found to be poor component position.

corrected before using a constrained liner. The insertion of a constrained liner into a mal-positioned cup will increase impingement and will lead to early if not catastrophic failure. Although isolated case reports exist of successful closed reduction of constrained articulations, it is certainly the general rule that a dislocated constrained device cannot be reduced by closed means and requires an open reduction.22

Constrained acetabular liners Constrained acetabular liners are a very powerful weapon in the armamentarium to treat THA instability. They are designed to resist dislocation of the femoral head by physically locking the head into the acetabular component, and their use is gaining in popularity. One potential reason for this may be their ease of use. Two commonly used designs are a constrained UHMWPE liner with a metal reinforcement ring or a tri-polar constrained construct. Unfortunately, the advantage of increased stability of these systems can result in a decreased range of motion, increased wear, increased interface stresses and loosening, together with component failure of the constrained mechanism (Figure 8). The definitive indications for a constrained liner are recurrent dislocations with inadequate soft tissue, especially deficient abductor mechanism or neuromuscular disorders. Berend et al reported on 755 consecutive constrained acetabular components and reported a dislocation rate of 17.5% overall. When used for patients with recurrent instability there was a 29% dislocation rate.21 Certain patient factors cannot be changed. Lack of muscular control for any reason can, as mentioned, lead to instability of an arthroplasty. Similarly, lack of compliance is another issue that may not change. In such patients a constrained cup can be used. Important to note with regard to the use of constrained liners is that any mal-alignment of the implants still needs to be

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Other methods of treatment In cemented acetabular cups, screw on lip augmentation devices have been used with some success.23 Although, just like elevated cementless acetabular liners, they effectively reduce the primary arc of movement, they can present a relatively conservative surgical option, particularly in elderly high-risk patients. Other novel methods of treating recurrent dislocators are reported in the literature. These methods generally represent one centre, single surgeon series with small patient numbers. The use of Achilles tendon grafts24 and synthetic ligaments that act as check reigns to prevent dislocation have been described.

Summary Dislocation of a THA is both a common and a serious complication. It is usually caused by multiple factors. A systematic approach to both the diagnosis and treatment of dislocation is required for its management. The success of revision arthroplasty largely depends upon identifying the underlying aetiology. Implant position should be defined accurately and if sub-optimal,

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11 Lind M, Krarup N, Petersen LG, et al. Acetabular revision for recurrent dislocations: results in 14 cases after 3 years follow-up. Acta Orthop Scand 2002; 73: 291. 12 Lewinnek GE, Lewis JL, Tarr R, Compere CL, Zimmerman JR. Dislocations after total hip replacement arthoplasties. J Bone Joint Surg Am 1978; 60: 217e20. 13 Archbold HAP, Mockford B, Molloy B, et al. The transverse acetabular ligament: an aid to orientation of the acetabular component. J Bone Joint Surg Br 2006; 88-B: 883e6. 14 Ranawat CS, Rao RR, Rodriguez JA, Bhende HS. Correction of limblength inequality during total hip arthroplasty. J Arthroplasty 2001; 16: 717e20. 15 Beaule PE, Schmalzried TP, Udomkait P, Amstutz HC. Jumbo femoral heads for the treatment of recurrent dislocation following total hip replacement. J Bone Joint Surg Am 2002; 84-A: 256. 16 Toomey SD, Hooper RH, McAuley JP, et al. Modular component exchange for treatment of recurrent dislocation of total hip replacement in selected patients. J Bone Joint Surg Am 2001; 83: 1529. 17 Barack R. Dislocation after total hip arthroplasty: implant design and orientation. J Am Acad Orthop Surg March/April 2003; 11(No 2): 89e99. 18 Grigoris P, Grecula MJ, Amstutz HC, et al. Tripolar hip replacement for recurrent prosthetic dislocation. Clin Orth Related Res 1994 Jul; 304: 148e55. 19 Parvizi J, Morrey BF. Bipolar hip arthroplasty as a salvage treatment for instability of the hip. J Bone Joint Surg Am 2000; 8: 629. 20 Kaplan SJ, Thomas WH, Poss R. Trochanteric advancement for recurrent dislocation after total hip arthroplasty. J Arthroplasty 1987; 2: 119. 21 Berend KR, Lombardi A, Mallory T, et al. The long-term outcome of 755 consecutive constrained acetabular components in total hip arthroplasty, examining the successes and the failures. J Bone Joint Surg Am 2005; 20: 93. 22 Miller CW, Zura RD. Closed reduction of a dislocation of a constrained acetabular component. J Arthroplasty June 2001; 16: 504e5. 23 Campbell D. The posterior lip augmentation device for recurrent dislocation. J Bone Joint Surg Br 2002; 84-B: 154. 24 Lavigne M. Recurrent dislocation after total hip arthroplasty: Treatment with an achilles tendon allograft. J Arthroplasty 2001; 16: 13e8.

revised to the appropriate alignment. If the alignment is acceptable then impingement and soft tissue factors are a likely cause. Revision surgery should attempt to address all implant factors to maximise success rates. Many of the techniques that are described in this article can be used in combination, with a polymodal approach to a multi-factorial problem. A

REFERENCES 1 Woo RY, Morrey BF. Dislocations after total hip arthroplasty. J Bone Joint Surg Am 1982; 64: 1295e306. 2 Blom AW, Rogers M, Taylor AH, Pattison G, Whitehouse S, Bannister GC. Dislocation following total hip replacement: the Avon Orthopaedic Centre experience. Ann R Coll Surg Engl 2008; 90: 658e62. 3 Kotwal RS, Ganapathi M, John A, Maheson M, Jones S. Outcome of treatment for dislocation after primary total hip replacement. J Bone Joint Surg Br 2009; 91-B: 321e6. 4 Bozic KJ, Kurtz SM, Lau E, et al. The epidemiology of revision total hip arthroplasty in the United States. J Bone Joint Surg Am 2009; 91: 128e33. 5 Woolson ST, Rahimtoola ZO. Risk factors for dislocation during the first 3 months after primary total hip replacement. J Arthroplasty 1999 Sept; 14: 662e8. 6 Newington DP, Bannister GC, Fordyce M. Primary total hip replacement in patients over 80 years of age. J Bone Joint Surgery Br 1990; 72-B: 450e2. 7 Wines AP, McNicol. Computed tomography measurement of the accuracy of component version in total hip arthroplasty. J Arthropalsty 2006; 21: 696e702. 8 DeWal H, Maurer SL, Tsai P, et al. Efficacy of abduction bracing in the management of total hip arthroplasty dislocation. J Arthroplasty 2004; 19: 733e8. 9 Parvizi J, Kim KI, Goldberg G, et al. Recurrent Instability after Total Hip Arthroplasty: beware of subtle component mal-positioning. Clin Orthop Relat Res 2006; 447: 60. 10 Morrey BF. Instability after total hip arthroplasty. Orthop Clin North Am 1992; 23: 237.

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(vi) Management of periprosthetic infection in total hip arthroplasty

Infection following THA can be a diagnostic challenge, there is no gold standard for determining whether an infection is present and none of the tests available are 100% sensitive and 100% specific.7 The treatment of an infected THA leads to a long and difficult course for the patient, and frequently leads to a suboptimal functional outcome. An infected THA should be approached with careful preoperative assessment and a well defined treatment plan, which depends on many factors including:  acute or chronic infection  infecting organism, its antibiotic sensitivity and its ability to manufacture glycocalyx  the health of the patient  fixity of the prosthesis  bone stock  the particular philosophy and training of the surgeon.8

MTS Sukeik FS Haddad

Abstract Total hip arthroplasty (THA) is one of the most commonly preferred orthopaedic procedures. Although the rate of deep infection after primary hip arthroplasty is relatively low, the economic burden, associated morbidity and mortality make it potentially devastating. Because of an ageing population will need an increasing number of arthroplasties, prevention, diagnosis and treatment of infection must be optimised in order to reduce both direct and indirect costs to patients and healthcare systems.

Prevention of infection and microbiologic considerations While infection after THA may be caused by haematogenous seeding, it is more commonly due to bacteria entering the wound at the time of surgery, either from the patients skin flora or airborne bacteria from the operating theatre environment including from theatre staff. Many studies have demonstrated that individuals moving around the operating theatre contribute the largest proportion of pathogenic bacteria to the wound. This led to the introduction of a controlled operating environment, such as laminar air flow and Charnley’s ultraclean air system with sterile hoods and a body-exhaust system. Together with prophylactic antibiotics, these have reduced rates of infection from 9% to 1.3%.9,10 To use the appropriate antibiotics for prophylaxis and treatment, a good understanding of potential pathogens contaminating surgical wounds is essential. Staphylococcus aureus and Staphylococcus epidermidis are the most common infecting organisms in periprosthetic hip infections, accounting for approximately 85%e90% of cases. Some common but less frequent organisms include Streptococcus species and gram negatives such as Pseudomonas, Klebsiella, and Escherichia coli. These are usually secondary invaders of open, draining wounds in patients with deep sepsis of a hip arthroplasty. Anaerobic microorganisms are isolated in 10% of such patients.11 Occasionally, the treatment of the infected arthroplasty is complicated by polymicrobial infections with particularly virulent organisms such as Group D Streptococci, Pseudomonas, fungal or mycobacterial infections which can be difficult to both diagnose and treat due to recurrent sepsis.12 Increasing infection involving methicillin-resistant strains of Staphylococcus aureus and Staphylococcus epidermidis has also emerged. Resistance has been attributed to the ability of the organism to produce a slime layer, or a biofilm of glycocalyx. This layer is made up of a variety of polysaccharides synthesised by the bacteria, as well as a range of host molecules which enables the organism to adhere to and survive on synthetic surfaces. Bacteria that exist within a biofilm are at least 500 times more resistant to antibiotics than bacteria which exist as individual free-floating cells.13 Antimicrobial prophylaxis has been established as the single most significant factor in the prevention of deep wound infection

Keywords infection; management; presentation; revision; total hip arthroplasty

Introduction Periprosthetic infection in THA was one of its most common and dangerous complications in the early years of total hip replacement, with a rate as high as 9.5% reported by Charnley.1 More recently, the incidence has decreased significantly due to improvements in operating room discipline, surgical technique, more assiduous preoperative assessment of the patient, and the prophylactic administration of antimicrobial agents.2 Although rates now are around one to two percent of all primary hip replacements and five percent of revision hip arthroplasties,3 their management, for both patient and surgeon is challenging, often requiring prolonged treatment. It is also expensive; estimated at four times the cost of a primary hip replacement without infection.4 Additionally the infection may recur with septic loosening of the prosthesis.5 Multiple risk factors for developing infection after THA have been identified including  length of the procedure  number of previous operative interventions  rheumatoid arthritis  diabetes mellitus  sickle cell disease  obesity  poor nutrition  immunosuppressive medications including systemic steroids  history of osteomyelitis or septic arthritis  presence of open skin lesions on the affected extremity.6

MTS Sukeik MD MRCSEd Clinical Research Fellow, University College London Hospital, UK. FS Haddad BSc MCh(Orth) FRCSEd FRCS(Tr & Orth) Consultant Orthopaedic Surgeon, University College London Hospital, UK.

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following total hip arthroplasty.14 The classes of antibiotics used include the b-lactams such as cephalosporins, penicillin and its derivatives, glycopeptides such as teicoplanin, and aminoglycosides such as gentamicin. Al-Maiyah et al.15 reported an increased resistance of coagulase negative staphylococci to cephalosporins and recommended a revised prophylaxis strategy avoiding cephalosporins, but Al Buhairan et al.16 showed in a systematic review of antibiotic prophylaxis in joint arthroplasty that there is no evidence that any type of antibiotic prophylaxis has better results than any other and that selection should be on the basis of cost and local availability. There is insufficient evidence to determine if there is a threshold prevalence of MRSA at which switching from non-glycopeptide to glycopeptide antibiotic prophylaxis might be clinically effective and cost-effective.17 Furthermore, the American Academy of Orthopaedic Surgeons has suggested routine antibiotic prophylaxis for 2 years after THA prior to various procedures associated with significant risk of bacteraemia such as dental cleaning and extraction.18 The role of antibiotic loaded cement (ALC) in primary hip arthroplasties has also been assessed in prospective studies in over 1600 cases. In data from the Scandinavian arthroplasty registers, with an exhaustive follow-up of more than 2,400,000 hip replacements, infection rate was reduced by 50%. Human pharmacokinetics during total hip replacement showed antibiotic concentrations 20 times the minimal inhibitory concentration (MIC) in drainage fluids. No toxic concentrations have been detected in blood or urine, and no allergies, toxic effects, mechanical failures or selection of resistant microorganisms have been observed. Therefore, ALC prophylaxis is now widely used in countries with prostheses registers. The most commonly used antibiotics in ALC include tobramycin, gentamicin and vancomycin.21 The combination of vancomycin and one of the aminoglycosides provides a broad spectrum of coverage for organisms commonly encountered with deep periprosthetic infections. The presence of tobramycin has a synergistic like effect on the bactericidal activity of vancomycin. A low dose of ALC ( 1 g of antibiotic per batch of cement) should be used for prophylaxis. However, when used in treatment of infected THA, ALC is used in higher doses as an adjuvant to excision of infected and devascularised tissues and systemic antibiotic treatment.22 Antibiotics leach from Palacos bone cement in higher concentrations and for longer periods than from Simplex-P, CMW, and Sulfix acrylic bone cements.19 Furthermore, Palacos with gentamicin is more resistant to fracture than Zimmer or Simplex-P cement mixed with gentamicin.20 Other general measures to prevent infection include stopping smoking, weight loss in the obese and control of co-morbid diseases, such as diabetes, sickle cell disease and rheumatoid arthritis. Temporary cessation of medications such as methotrexate also decreases infection risk23 although this needs to be balanced against the risk of a rheumatoid flare. In theatre, staff should be kept to a minimum, appropriate use of gowns, face masks, double gloving and hand-washing should always be implemented and duration of surgery should be kept as short as possible. The use of pulsatile lavage has also been reported to remove up to 87% of all organisms from wounds.24 In the perioperative period, periodontal and urinary tract sepsis must be

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eradicated early to prevent haematogenous seeding of the prosthesis.25

Classification Classification systems are based on the time of onset of symptoms after surgery and the route by which the infecting organism gained access to the joint space. Coventry26 in 1975, classified infections after THA into three stages:  Stage I acute infections developing within three months of surgery caused by contamination at the time of operation  Stage II delayed infections which are more indolent and may not become apparent until several months after the hip replacement but are also related to contamination at the time of surgery  Stage III haematogenous infections associated with an infection remote from the hip joint e.g. respiratory, dental and urinary tract infection, which may develop soon after the remote infection or as late as two or even several years after the hip replacement. Tsukayama et al.27 expanded the classification into four categories to aid the management of these patients:  positive intra-operative cultures found when undertaking a revision THA. The infection should be treated with six weeks of intravenous antibiotics and no additional operative intervention  early postoperative infections (occurring less than 1 month postoperatively) when treatment should include debridement, retention of the prosthesis, and intravenous antibiotics  late chronic infections (occurring more than 1 month postoperatively with an insidious onset) requiring removal of the prosthesis and a staged revision  acute haematogenous infections. If the prosthesis is well fixed debridement is sufficient. If the prosthesis is loose, treatment should be the same as for a late chronic infection.

Clinical presentation History and examination A thorough history and physical examination are essential. Acute prosthetic infections are caused by infected haematomas or superficial wound infections spreading into the deep periprosthetic space and present in the immediate postoperative period with continuous pain. The patient may have an erythematous, swollen and fluctuant wound with purulent discharge and systemic signs of infection including fever, chills and sweating. Chronic infections are characterised by gradual deterioration of function and persistent pain from the time of the operation, classically presenting after a few months from the index procedure. A history of prolonged hospital stay after the surgery, a prolonged course of antibiotics and continuous wound discharge are important in the diagnosis, as symptoms and signs may be nonspecific.28 Haematogenous infections can occur early or late in relation to joint surgery. However, the typical case is of a prosthesis that has been functioning well for months or years that suddenly becomes painful and swollen associated with systemic manifestations, such as fever and chills. This type of infection is more likely to occur in immunocompromised patients. Early diagnosis

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et al.33 reported in a recent meta-analysis of antigranulocyte scintigraphy with monoclonal antibodies a reasonably high discriminating ability to identify prosthesis infection in patients who underwent THA (sensitivity 90%, specificity 80%). Intra-operative evaluation at revision THA, including tissue appearance combined with intra-operative gram stains, are unreliable for detecting periprosthetic sepsis, and neither is adequate alone for ruling out infection.7 Intra-operative frozen section has been shown to be a useful tool for identifying infection during the revision procedure, depending on the area and number of tissue samples obtained, the availability of an experienced pathologist to interpret the results and the number of white blood cells visualised per high power field. Lonner et al.34 in a prospective study of 175 revision arthroplasties recommended using 10 white blood cells/high power field for diagnosing periprosthetic infection (sensitivity 0.84 specificity 0.99). Intra-operative culture, although assumed to be the gold standard for identifying periprosthetic infection, is subject to false-negative and false-positive results.27,35 As with joint aspiration, careful technique and withholding antibiotics for a few weeks preoperatively are essential in reducing false results. A minimum of five tissue samples should be sent to the laboratory for processing to rule out infection.36

may allow salvage of the prosthesis by means of a thorough debridement, whereas a delay in diagnosis may necessitate a staged exchange procedure in order to eradicate the infection. Investigations It is essential that the relative utility of preoperative and intraoperative tests used to diagnose periprosthetic sepsis are thoroughly understood.7 Helpful laboratory investigations include the erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). The white blood cell count is usually unhelpful and is often normal even in patients with an actively infected hip and cannot relied upon to exclude infection.29 CRP level is a sensitive indicator of postoperative infection; it reaches maximum values within 48 hours from surgery, returning to normal levels within 2 to 3 weeks. However the ESR may remain elevated for months after an uncomplicated THA. Therefore, a persistently elevated CRP is more accurate in identifying patients with a deep infection.30 In a study of 202 hip replacements, Spangehl et al.29 demonstrated that all thirty-five cases complicated by deep infection were in patients who had an ESR of >30 mm/hr (sensitivity 0.82, specificity 0.85) or a CRP of >10 mg/L (sensitivity 0.96, specificity 0.92). They suggested that a normal ESR and CRP effectively excludes the possibility of infection at the site of a THA and that combining both tests should improve the accuracy of diagnosis. It is essential though to recognise that both ESR and CRP are nonspecific markers of inflammation that may be elevated in other conditions such as rheumatoid arthritis, neoplasia, collagen vascular disease, other inflammatory conditions and after a recent operation. Plain radiographs should be taken of all failed arthroplasties and can occasionally provide clues to infection, but they are neither sensitive nor specific for detection of infection. Radiographic findings including loosening, osteolysis and endosteal scalloping are common to both septic and aseptic failures. Periosteal new bone formation has been considered by some to be suggestive of infection.29 Hip joint aspiration is used to evaluate patients with noninflammatory arthritis with a painful total hip arthroplasty and an elevated ESR or CRP levels. It is also useful when ESR and CRP levels are elevated in chronic inflammatory conditions. However, the reported rates of sensitivity and specificity have varied widely in the literature, with the sensitivity ranging from 0.50 to 0.93 and the specificity ranging from 0.82 to 0.97.29,31,32 Therefore, a strict aseptic technique is imperative to reduce false positive results as well as preventing iatrogenic periprosthetic infection. It is also essential that all antibiotics are discontinued several weeks prior to joint aspiration to reduce the number of false negative test results. Nuclear medicine studies are second-line investigations of patients with infected THA when serologic tests may be falsely elevated and aspiration cultures from the hip joint unreliable because of the administration of antibiotics. However, its use is limited by cost, the time to undertake the procedure and because scans can remain positive for as long as one year after a hip replacement due the surgery itself or complications such as heterotopic ossification. Various isotopes including Technetium99 m, Gallium-67 citrate, and Indium-111-labeled white blood cells have been used, resulting in a wide range of sensitivities and specificities in detecting periprosthetic infection. Pakos

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Management The goals of treatment are the eradication of infection and the restoration of function of the affected limb. Treatment options include  debridement with retention of components  single-stage revision  two-stage revision  multi-stage revision and long term suppressive antibiotics  salvage procedures. The extent of infection and the length of time it has been present affect the choice of the revision procedure and the success rate following revision.3 Classifying infection into acute or late infection aids in the treatment plan. Treatment of mycobacterial infections follows the same guidelines.37

Acute infection Debridement with component retention For early or late infections with a short duration of symptoms, stable components, no significant immunosuppression and overlying soft tissue and skin of good condition, irrigation and debridement with exchange of mobile parts (femoral heads and acetabular inserts) but retention of the infected implant has been advocated.38,39 The aim of rapid intervention with thorough debridement is the prevention of the production of a biofilm by the infecting organism which is essential for a successful outcome.40 Difficulties include determination of the time of onset of infection and the establishment of a point beyond which it is no longer reasonable to retain the implant. Davis et al.38 suggested up to two weeks for early infection and up to 72 hours for acute haematogenous, late infection whereas Zimmerli et al.39 recommended a period of three weeks for both early and late infections. Despite expeditious management with irrigation and debridement, acute total hip infections may lead to recurrent infections. Success rates in the literature range between less than 10% and more than

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50%.41,42 Thus patients should be advised that further treatment may be necessary if the attempt to retain the prosthesis is unsuccessful including a staged revision or salvage procedures.

a THA infection is over 90%.49,50 Furthermore, it permits uncemented reconstruction and the use of allografts, which is particularly important given the frequency of femoral and acetabular defects associated with THA infections.51e53 Alexeff et al.54 used massive structural allografts in the second stage of a two-stage procedure in 11 patients. They reported no additional sepsis at a mean follow-up of 4 years. The principles of two-stage revision include removal of the implant along with all cement and necrotic tissue which contain the infecting organisms, administration of systemic antibiotics postoperatively for 6 to 12 weeks followed by implantation of a new prosthesis. A patient is deemed free of infection and able to proceed to second-stage arthroplasty when repeat joint aspirates after 4 weeks of discontinuing antibiotics are negative, and the ESR and CRP return to normal values. Two-stage revision arthroplasty using ALC but without a prolonged course of antibiotic therapy has also been reported by Stockley et al.63 in a series of 114 patients for chronic THA infections. Infection was successfully eradicated in 100 patients (87.7%) at a mean follow-up of two years.

Debridement with single-stage revision At our institution, for acutely infected uncemented prosthesis following aggressive debridement, we then proceed to a singlestage revision with ALC. This is an ideal opportunity to remove both the implant and biofilm, prior to in-growth. Over the past 7 years, in a series of 28 patients with acutely infected hip prostheses, 21 patients (75%) are now infection free at a minimum 1-year follow-up. 10 were treated within 5 days of the onset of symptoms, and of this group only one went on to have a reinfection. In contrast, of the remaining 18 patients that were treated more than 5 days after the onset of symptoms, 7 had reinfections. We emphasise the importance of a swift and accurate diagnosis, ensuring prompt treatment to maximise the likelihood that the prosthesis will be salvaged.

Chronic infection Multi-stage revision A three-stage reimplantation procedure is suitable for treatment of extensive bone defects in which the use of a large amount of morcellised allograft can be anticipated. The bone bed created is allowed to incorporate for about 6 months and, in most cases, a cementless implant is then inserted.64 Multi-stage revision is also indicated when clinical presentation, blood parameters and cultures are suggestive of persistent infection requiring further debridement and possible repeat of PROSTALAC to eradicate infection after the first stage of revision.

Reimplantation into a sterile bed is the goal of treatment and can either be performed at the same stage as debridement as part of a single-stage procedure, using cemented components with ALC or, alternatively, as part of a two or multi-stage procedure where debridement and reimplantation are separated by a period of antibiotic delivery, both locally and systemically.43,44 Single-stage revision The advantages of simultaneous debridement and exchange of the prosthesis include the avoidance of additional surgical procedures for patients who have major medical problems, for whom the risks of additional procedures are cumulative. Success rates for eradication of infection with single-stage revisions ranged between 7682% in most studies when ALC has been utilised in comparison to only 58% without ALC.35,45,46 When ALC is used for prosthesis fixation in single and two or multi-stage revisions, the dosage recommended is usually 1 or 2 g per 40 g of bone cement to avoid mechanical weakening.47 However, Jackson et al.48 in a review of the literature reported that the indications for direct exchange are limited by several factors including  Failures associated with polymicrobial infection, gram-negative organisms (especially Pseudomonas sp) and certain gram-positive organisms such as methicillin-resistant Staphylococcus epidermidis and Group D Streptococcus  Patients with significant bone stock deficiency cannot be managed with this technique because single-stage revision requires that the implant be inserted with ALC  Lack of data on the use of bone graft in association with single-stage revision  Difficulties with removal of a solidly fixed cemented prosthesis without destroying the remaining proximal femoral bone stock should the procedure fail to eradicate the infection. Nevertheless, single-stage revision remains a viable option which is associated with less morbidity and is cheaper than delayed exchange when used in carefully selected patients.

Long term suppressive antibiotics Chronic suppressive therapy for periprosthetic infections is indicated when an operation is refused by the patient or is has an unacceptable risk in medically unfit patients.65 Infection is controlled rather than eradicated. The infecting organism must be identified and sensitive to the chosen antibiotic which should be effective orally and tolerable by the patient. Failures of treatment are due to the patient developing side effects or recurrent candidiasis and the emergence of resistant strains.

Salvage procedures Girdlestone arthroplasty In life threatening or intractable hip infection or when limb viability is at risk, hip excision arthroplasty should be considered.50 Other indications include the elderly patient incapable of mobilising independently, those who are mentally impaired and may be unable to cooperate with the postoperative rehabilitation process, uncooperative patients such as intravenous drug abusers and immuno-compromised patients.8 Girdlestone arthroplasty is primarily aimed at pain relief and infection control. However, such patients must be warned to expect at least 2e3 cm of limb shortening and reliance upon a walking aid postoperatively.66 The greater the bone loss, the more unsatisfactory an excision arthroplasty becomes. Arthrodesis This is an alternative treatment in THA infection described by Kostuik and Alexander67 in a series of 14 patients where the

Two-stage revision Two-stage reimplantation is the gold standard for the treatment of infected total hip replacements. The successful eradication of

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indications were a young age, male gender and strenuous functional demands. Although all hips eventually fused and patients were able to mobilise independently, patients had an average of 4.6 cm limb-length discrepancy.

PROSTALAC system now consists of a constrained cemented acetabular component with an articulating polyethylene liner and a femoral component with a modular head made intraoperatively using a series of moulds with ALC surrounding a stainless steel endoskeleton. Whilst providing high doses of local antibiotic delivery, this system also allows earlier mobilisation out of bed and accelerated rehabilitation and permits discharge from the hospital between stages of treatment avoiding the complications associated with prolonged hospital stay and immobilisation.8 Recently a preformed PROSTALAC equivalent with fixed low-dose antibiotic content has become available. Prefabricated moulds of different sizes are also now available, allowing the surgeon to select antibiotic dose and content. The disadvantages of preformed mobile spacers include limitation in implant sizes and antibiotic dose, often allowing delivery of only a single antibiotic. Mobile spacers formed in the operating room have the advantage of adjustable antibiotic dosing; a combination of antibiotics and the addition of an antifungal option as necessary. Disadvantages of mobile spacers formed in the operating room include additional time to construct the implant in the operating room, a limited number of sizes, additional cost, and complications may similarly occur (Figures 1e3).

Amputation Amputation is rarely necessary and is generally reserved for patients with life threatening infections, multiple unsuccessful revisions and vascular injuries.

ALC spacers Using ALC as spacers during the intervening treatment period to deliver antibiotics locally has been popular due to the even higher rates of eradicating infection achieving up to 95% in several studies.55,56 It increases local antibiotic levels up to 200 times higher than those for systemic administration and prevents debris from accumulating in the potential joint space and softtissue contractures.57 When used in temporary spacers, antibiotic dosages up to 20 g per 40 g of bone cement can be achieved without reported systemic side effects.58 For fungal infections, 100 to 150 mg of amphotericin B is typically added to the 40 g of bone cement in addition to other antibiotics chosen. There are various types of spacers. Although ALC beads were used previously, they are rarely used today in the treatment of the infected THA due to the associated scarring and as a result, the difficulty in identifying and removing them at the 2nd stage procedure.59

Complications of spacers Implant and periprosthetic fractures Surgeon made spacers in the operating room may be at higher risk for a fracture, especially with a mobile spacer, as a result of cement heterogeneity and mixing inconsistencies. The use of higher antibiotic doses also leads to increased risk of fracture. A noncongruent femoral component fit on host femoral bone may lead to subsidence and fracture of the implant. Therefore, the surgeon should avoid impacting the mobile cement spacer during cementing which may predispose both the prosthesis and the bone stock deficient proximal femur to fracture.60

Static/nonarticulating spacers Static or simple block spacers aim to maintain the dead space and are mostly used in the acetabulum. They facilitate surgical dissection at reimplantation and allow delivery of the antibiotics of choice according to sensitivities. Typically 20 g of bone cement mixed with at least 2 or 3 g of powdered antibiotic provides an adequate volume for the acetabular defect. The disadvantage of a static spacer is that it does not allow physiological motion of the joint but this has been associated with less generation of debris in comparison with mobile spacers.60,61

Antibiotic toxicity This rare complication may be more common with surgeon constructed spacer implants when high doses of antibiotics are

Medullary dowels A tapered cement dowel fashioned from the nozzle of a cement gun provides an excellent size and shape for a spacer to be inserted into the medullary canal of the femur during treatment of an infected THA. A small bulb is left at the end of the dowel to prevent distal migration and help facilitate removal. Disadvantages include the potential for proximal femoral migration and they cannot be used in patients with severe femoral bone loss.60,61 Mobile/articulating spacers The aim of this technique is to allow the patient to move the joint through a range of motion between prosthesis removal and insertion of the new prosthesis. The Prosthesis of Antibiotic Loaded Acrylic Cement (PROSTALAC) first developed by Duncan and Beauchamp62 was composed of a metal femoral endoskeleton component covered with ALC. The cement of the femoral head articulated with the bone of the acetabular bed, which unfortunately could lead to bone erosion and discomfort. Therefore an acetabular cement component was introduced; preventing loss of acetabular bone, but the cement-on-cement articulation limited motion and caused discomfort. The

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Figure 1 Infected primary left total hip replacement with evidence of periprosthetic loosening.

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Figure 2 Prosthesis with antibiotic-loaded acrylic cement (PROSTALAC) inserted as a temporary spacer at 1st stage revision of infected left total hip replacement.

added to the cement.57 As renal failure may potentiate antibiotic toxicity include renal failure, renal function and antibiotic levels monitoring is crucial in this group of patients and should this complication occur, removal of the implant must be considered.

Figure 3 Proximal femoral prosthesis inserted at 2nd stage revision of infected left total hip replacement.

Instability This occurs more frequently with knee spacers. However, in the hip, the use of a snap-fit polyethylene liner has reduced the incidence.60

infection in culture negative cases. However, Panousis 70 in a prospective study of 91 patients undergoing revision total hip or knee arthroplasties for infection concluded that PCR cannot be recommended for the routine detection of prosthetic infection due to the low positive predictive value (34%). Molecular biology continues to develop in the meantime, and may well have an essential role in the future in identifying infection with the advantage of reducing the amount of time needed to obtain results in comparison with conventional culture methods.

Challenges and future plans for management The management of THA infection can be challenging and advances in diagnosis, treatment and prevention may improve the outcome of patients with an infected prosthesis. Investigations Bottner68 investigated the role of Interleukin-6, procalcitonin and tumour necrosis factor (TNF-alpha) and compared them with CRP and ESR in a prospective study of 78 patients undergoing revision total hip or knee replacement. Results showed that CRP >3.2 mg/dl and interleukin-6 >12 pg/ml had the highest sensitivity (0.95). However, Interleukin-6 was less specific than CRP (0.87 versus 0.96) and combining CRP and interleukin-6 identified all patients with deep infection of the implant. An advantage of interleukin-6 over both CRP and ESR is that levels return to normal within 48 to 72 hours after operation; this may have an essential role in the future for detecting early infection post THA.69 Procalcitonin (> 0.3 ng/ml) and TNF-alpha (> 40 ng/ml) were very specific (0.98 versus 0.94) but had a low sensitivity (0.33 versus 0.43). Molecular diagnostic techniques including polymerase chain reaction (PCR) have enabled the detection of

ORTHOPAEDICS AND TRAUMA 23:5

Antibiotics The growing incidence of resistant microorganisms has led to the introduction of new antibiotics with good antimicrobial and pharmacokinetic properties, such as linezolid, the first approved oxazolidinone. This has been reported in several studies to be an effective agent against methicillin-resistant staphylococcus aureus, vancomycin-resistant enterococci, resistant coagulasenegative staphylococci and macrolide-resistant streptococci.71,72 It is well absorbed and oral administration gives serum levels comparable with those following intravenous injection of the same dose which has markedly reduced hospital stay costs when long term antibiotic therapy is indicated. Linezolid has also demonstrated acceptable elution kinetics from ALC when tested in vitro in combination with gentamicin; however, further experimental research and animal studies should clarify any

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14 Hanssen AD, Osmon DR. Prevention of deep wound infection after total hip arthroplasty: the role of prophylactic antibiotics and clean air technology. Semin Arthroplasty 1994; 5(3): 114e21. 15 AlBuhairan B, Hind D, Hutchinson A. Antibiotic prophylaxis for wound infections in total joint arthroplasty: a systematic review. J Bone Joint Surg Br 2008; 90(7): 915e20. 16 Al-Maiyah M, Hill D, Bajwa A, Slater S, et al. Bacterial contaminants and antibiotic prophylaxis in total hip arthroplasty. J Bone Joint Surg Br 2005; 87(9): 1256e9. 17 Cranny G, Elliott R, Weatherly H, et al. A systematic review and economic model of switching from non-glycopeptide to glycopeptide antibiotic prophylaxis for surgery. Health Technol Assess 2008; 12(1): 1366e5278. 18 Orthopaedic knowledge update. 3rd ed. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2006. 19 Penner MJ, Duncan CP, Masri BA. The in vitro elution characteristics of antibiotic-loaded CMW and Palacos-R bone cements. J Arthroplasty 1999; 14: 209e14. 20 Callaghan JJ, Salvati FA, Brause BD, Rimnac CM, Wright TM. Reimplantation for salvage of the infected hip: rationale for the use of gentamicinimpregnated cement and heads. The hip proceedings of the thirteenth open scientific meeting of the hip society. 1985; pp. 65e94, The Hip 1985. 21 Scott CP, Higham PA. Antibiotic bone cement for the treatment of pseudomonas aeruginosa in joint arthroplasty: comparison of tobramycin and gentamicin-loaded cements. J Biomed Mater Res 2003; 64B: 94e8. 22 Langlais F, Belot N, Ropars M, Thomazeau H, Lambotte JC, Cathelineau G. Antibiotic cements in articular prostheses: current orthopaedic concepts. Int J Antimicrob Agents 2006; 28(2): 84e9. 23 Bridges Jr SL, Lo´pez-Me´ndez A, Han KH, Tracy IC, Alarco´n GS. Should methotrexate be discontinued before elective orthopedic surgery in patients with rheumatoid arthritis? J Rheumatol 1991; 18(7): 984e8. 24 Hope PG, Kristinsson KG, Norman P, Elson RA. Deep infection of cemented total hip arthroplasties caused by coagulase-negative staphylococci. J Bone Joint Surg Br 1989; 71(5): 851e5. 25 Sandiford A, Skinner J. Mini-Symposium: What’s new in hip replacementdBasic principles: the prevention of infection in total hip arthroplasty. Orthop Trauma 2009; 23(1): 8e16. 26 Coventry MB. Treatment of infections occurring in total hip surgery. Orthop Clin North Am 1975; 6: 991e1003. 27 Tsukayama DT, Estrada R, Gustilo RB. Infection after total hip arthroplasty: a study of the treatment of one hundred and six infections. J Bone Joint Surg 1996; 78A: 512e23. 28 Fitzgerald Jr RH. Infected total hip arthroplasty: diagnosis and treatment. J Am Acad Orthop Surg 1995; 3: 249e62. 29 Spangehl MJ, Masri BA, O’Connell JX, Duncan CR. Prospective analysis of preoperative and intraoperative investigations for the diagnosis of infection at the sites of two hundred and two revision total hip arthroplasties. J Bone Joint Surg Am 1999; 81: 672e83. 30 Haaker R, Senge A, Kramer J, Rubenthaler F. Osteomyelitis after arthroplasty. Orthopade 2004; 33(4): 431e8. 31 Lachiewicz PF, Rogers GD, Thomason HC. Aspiration of the hip joint before revision total hip arthroplasty. Clinical and laboratory factors influencing attainment of a positive culture. J Bone Joint Surg Am 1996; 78(5): 749e54. 32 Kraemer WJ, Saplys R, Waddell JP, Morton J. Bone scan, gallium scan, and hip aspiration in the diagnosis of infected total hip arthroplasty. J Arthroplasty 1993; 8(6): 611e5. 33 Pakos EE, Trikalinos TA, Fotopoulos AD, Ioannidis JP. Prosthesis infection: diagnosis after total joint arthroplasty with antigranulocyte

possible side effect of linezolid-loaded cement before definitive use in the clinical practice.73 ALC substitutes Antimicrobial therapy and eradication of infection improved with the introduction of ALC. However, using polymethylmethacrylate (PMMA) as the standard material for delivering depot antibiotics has raised concerns as it is surface friendly to biofilm-forming bacteria. Therefore, many biodegradable materials have been evaluated as alternatives including proteinbased materials (collagen, fibrin, thrombin, clotted blood), bonegraft, bone-graft substitutes and extenders (hydroxyapatite, betatricalcium phosphate, calcium sulphate, bioglass), and synthetic polymers. Unfortunately, considering the limited clinical data that is currently available, the use of these materials still is experimental and clinical application should be cautious, limiting the total antibiotic load.74

Conclusion Revision THA remains a very expensive procedure to the patient and healthcare systems and no matter how much progress in diagnostic and treatment methods are achieved, the cost and morbidity of infected THA suggest that preventative measurements as discussed earlier are the single most important factor in managing this problem. A

REFERENCES 1 Charnley JA. clean-air operating enclosure. Br J Surg 1964; 51: 202e5. 2 Kaltsas D. Infection after total hip arthroplasty. Ann R Coll Surg Engl 2004; 86: 267e71. 3 Wolfe RM. Total hip arthroplasty revision for sepsis. Trauma 2002; 43: 29e47. 4 Dreghorn CR, Hamblen DL. Revision arthroplasty: a high price to pay. 11. Br Med J 1989; 298(6674): 648e9. 5 Burnett RS, Kelly MA, Hanssen AD, Barrack RL. Technique and timing of two-stage exchange for Infection in TKA. Clin Orthop Relat Res 2007; 464: 164e78. 6 Luessenhop CP, Higgins LD, Brause BD, Ranawat CS. Multiple prosthetic infections after total joint arthroplasty. Risk factor analysis. J Arthroplasty 1996; 11(7): 862e8. 7 Della Valle CJ, Zuckerman JD, Di Cesare PE. Perioperative sepsis. Clin Orthop Relat Res 2004; 420: 26e31. 8 Haddad FS, Masri BA, Garbuz DS, Duncan CP. The treatment of the infected hip replacement, the complex case. Clin Orthop Relat Res 1999; 369: 144e56. 9 Charnley J. Postoperative infections after total hip replacement with special reference to air contamination in the operating room. Clin Orthop 1972; 87: 167e87. 10 Ha’eri GB, Wiley AM. Total hip replacement in a laminar flow environment with special reference to deep infection. Clin Orthop 1980; 148: 163e8. 11 HCh Vogely, Fleer A, Dhert WJA, Verbout AJ. Infection of an orthopaedic implant: epidemiology and diagnosis. Rev Med Microbiol 2000; 11(3): 115e25. 12 Nestor BJ, Hanssen AD, Ferrer-Gonzalez R, Fitzgerald RH. The use of porous prostheses in delayed reconstruction of total hip replacements that have failed because of infection. J Bone Joint Surg 1994; 76A: 349e58. 13 Costerton JW, Lewandowski Z, Caldwell DE, et al. Microbial biofilms. Annu Rev Microbiol 1995; 49: 711e45.

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55 Hofmann AA, Goldberg TD, Tanner AM, Cook TM. Ten-year experience using an articulating antibiotic cement hip spacer for the treatment of chronically infected total hip. J Arthroplasty 2005; 20(7): 874e9. 56 Younger AS, Duncan CP, Masri BA, Mc-Graw RW. The outcome of twostage arthroplasty using a custom-made interval spacer to treat the infected hip. J Arthroplasty 1997; 12(6): 615e23. 57 Masri B, Duncan CP, Beauchamp CP. Long-term elution of antibiotics from bone cement: an in vivo study using the PROSTALAC system. J Arthroplasty 1998; 13: 331e8. 58 Springer BD, Lee Gwo-Chin, Osmon D, Haidukewych GJ, Hansen AD, Jacofsky DJ. Systemic safety of high-dose antibiotic loaded cement spacers after resection of an infected total knee arthroplasty. Clin Orthop Relat Res 2004; 427: 47e51. 59 Taggart T, Kerry RM, Norman P, Stockley I. The use of vancomycinimpregnated cement beads in the management of infection of prosthetic joints. J Bone Joint Surg 2002; 84B: 70e2. 60 Burnett RJ, Kelly MA, Hanssen AD, Barrack RL. Technique and timing of two-stage exchange for infection in TKA. Clin Orthop Relat Res 2007; 464: 164e78. 61 Hanssen AD, Spangehl MJ. Practical applications of antibiotic-loaded bone cement for treatment of infected joint replacements. Clin Orthop Relat Res 2004; 427: 79e85. 62 Duncan CP, Beauchamp C. A temporary antibiotic-loaded joint replacement system for management of complex infections involving the hip. Orthop Clin North Am 1993; 24: 751e9. 63 Stockley I, Mockford BJ, Hoad-Reddick A, Norman P. The use of twostage exchange arthroplasty with depot antibiotics in the absence of long-term antibiotic therapy in infected total hip replacement. J Bone Joint Surg Br 2008; 90(2): 145e8. 64 Landor I, Vavrik P, Jahoda D. General principles of infection treatment in joint replacements. Acta Chirurgiae Orthopaedicae et Traumatologiae Cechoslovaca 2005; 72(3): 183e90. 65 Goulet JA, Pellici PM, Brause BD, et al. Prolonged suppression of infection in total hip arthroplasty. J Arthroplasty 1988; 3: 109e16. 66 Sharma H, De Leeuw J, Rowley DI. Girdlestone resection arthroplasty following failed surgical procedures. Int Orthop 2005; 29(2): 92e5. 67 Kostuik J, Alexander D. Arthrodesis for failed arthroplasty of the hip. Clin Orthop 1984; 188: 173e82. 68 Bottner F, Wegner A, Winkelmann W, Becker K, Erren M. Interleukin-6, procalcitonin and TNF-{alpha}: markers of peri-prosthetic infection following total joint replacement. J Bone Joint Surg Br 2007; 89B/1: 94e9. 69 Wirtz DC, Heller KD, Miltner O, Zilkens KW, Wolff JM. Interleukin-6: a potential inflammatory marker after total joint replacement. lnt Orthop 2000; 24: 194e6. 70 Panousis K, Grigoris P, Butcher I, Rana B, Reilly JH, Hamblen DL. Poor predictive value of broad-range PCR for the detection of arthroplasty infection in 92 cases. Acta Orthop 2005; 76(3): 341e6. 71 Oussedik SI, Haddad FS. The use of linezolid in the treatment of infected total joint arthroplasty. J Arthroplasty 2008; 23(2): 273e8. 72 Bassetti M, Vitale F, Melica G, et al. Linezolid in the treatment of Gram-positive prosthetic joint infections. J Antimicrob Chemother 2005; 55(3): 387e90. 73 Anagnostakos K, Kelm J, Grun S, Schmitt E, Jung W, Swoboda S. Antimicrobial properties and elution kinetics of linezolid-loaded hip spacers in vitro. J Biomed Mat Res - Part B Appl Biomaterials 2008; 87(1): 173e8. 74 McLaren AC. Alternative materials to acrylic bone cement for delivery of depot antibiotics in orthopaedic infections. Clin Orthop Relat Res 2004; 427: 101e6.

scintigraphy with 99mTc-labeled monoclonal antibodiesea metaanalysis. Radiology 2007; 242(1): 101e8. Lonner JH, Desai P, Dicesare PE, et al. The reliability of analysis of intraoperative frozen sections for identifying active infection during revision hip or knee arthroplasty. J Bone Joint Surg 1996; 78A: 1553e8. Buchholz HW, Elson RA, Engelbrecht E, et al. Management of deep infection of total hip replacement. J Bone Joint Surg 1981; 63B: 342e53. Matthews PC, Dean BJ, Medagoda K, et al. Native hip joint septic arthritis in 20 adults: delayed presentation beyond three weeks predicts need for excision arthroplasty. J Infect 2008; 57(3): 185e90. Boeri C, Gaudias J, Jenny JY. Total hip replacement complicated by tuberculous infection. Revue de Chirurgie Orthopedique et Reparatrice de l’Appareil Moteur 2003; 89(2): 163e6. Davis JS. Management of bone and joint infections due to Staphylococcus aureus. Intern Med J 2005; 35(Suppl.): 79e96. Zimmerli W, Trampuz A, Ochsner PE. Prosthetic-joint infections. N Engl J Med 2004; 351: 1645e54. Moyad TF, Thornhill T, Estok D. Evaluation and management of the infected total hip and knee. Orthopedics 2008; 31(6): 581e90. Crockarell JR, Hansen AD, Osmon DR, Morrey BF. Treatment of infection with debridement and retention of the components following hip arthroplasty. J Bone Joint Surg Am 1988; 80(9): 1306e13. Deirmengian C, Greenbaum J, Stern J, et al. Open debridement of acute gram-positive infections after total knee arthroplasty. Clin Orthop Relat Res 2003; 416: 129e34. Mitchell PA, Masri BA, Garbuz DS, Greidanus NV, Duncan CP. Cementless revision for infection following total hip arthroplasty. Instr Course Lect 2003; 52: 323e30. Krbec M, Cech O, Dzupa V, Pacovsky V, Klezl Z. Infection complications of total hip arthroplasty. Acta Chirurgiae Orthopaedicae et Traumatologiae Cechoslovaca 2004; 71(3): 179e88. Raut VV, Siney PD, Wroblewski BM. One-stage revision of total hip arthroplasty for deep infection: Long-term follow-up. Clin Orthop 1995; 321: 202e7. Sanzen L, Carlsson AS, Josefsson G, et al. Revision operations on infected total hip arthroplasties: Two- to nine-year follow-up study. Clin Orthop 1988; 229: 165e72. Hanssen AD, Osmon DR. Assessment of patient selection criteria for treatment of the infected hip arthroplasty. Clin Orthop 2000; 381: 91e100. Jackson WO, Schmalzried TP. Limited role of direct exchange arthroplasty in the treatment of infected total hip replacements. Clin Orthop Relat Res 2000; 381: 101e5. Lin J, Yang X, Bostrom MP. Two-stage exchange hip arthroplasty for deep infection. J Chemother 2001; 13(1): 54e65. Bottner F, Sculco TP. Infection in revision total hip arthroplasty. Techniques in Orthopaedics 2001; 16(3): 310e22. Lai KA, Shen WJ, Yang CY, et al. Two-stage cementless revision THR after infection. 5 recurrences in 40 cases followed 2.5e7 years. Acta Orthop Scand 1996; 67: 325e8. Berry DJ, Chandler HP, Reilly DT. The use of bone allografts in twostage reconstruction after failure of hip replacement due to infection. J Bone Joint Surg 1991; 73A: 1460e8. Haddad FS, Muirhead-Allwood SK, Manktelow AR, BacareseHamilton I. Two-stage uncemented revision hip arthroplasty for infection. J Bone Joint Surg Br 2000; 82(5): 689e94. Alexeff M, Mahomed N, Morsi E, Garbuz D, Gross A. Structural allograft in two-stage revisions for failed septic hip arthroplasty. J Bone Joint Surg 1996; 78B: 213e6.

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(vii) Management of periprosthetic fractures in the lower limb

fractures are usually caused by the insertion of the stem in the femur or the tibia. The incidence varies with different fixation methods. In the femur, uncemented stems carry a higher risk; Berry et al. report a rate of 0.3% in cemented and 5.4% in uncemented. The rates are significantly higher in revision surgery. The post-operative incidence of periprosthetic fractures in primary total hip arthroplasties (THA) has been reported by the Mayo clinic registry as 1.1% of total hip replacements done between 1969 and 1999).

Panos Makrides Harpal Singh Uppal Steve Krikler

Aetiology Abstract

According to the Swedish Hip registry, trauma accounts for 75% of all PPFs.5 The majority are low velocity falls from a standing or sitting position. There are numerous possible risk factors for periprosthetic fractures; while patients with long standing THA are probably at higher risk of developing periprosthetic fracture but there are many possible confounders for this variable including the increased age of this patient group, other co-morbidities, poor bone stock and osteoporosis. Tsiridis6 suggests that female gender is associated with increased risk of PPF which is supported by various studies, and is probably related to the increased prevalence of osteoporosis in females. Beals and Tower reported that 38% of PPF in their study were associated with previous osteoporotic vertebral or metaphyseal fractures. However, the most common cause of PPF in older implants is osteolysis.7,8 The terms osteolysis and aseptic loosening are often used interchangeably and are essentially in reference to a common pathway. Osteolysis is believed be caused by the host’s response to particulate wear debris associated with cement failure and subsequent loosening of the prosthesis. The choice of implant, cementation technique (or un-cemented) and operative technique are therefore directly related to the processes which are most likely to be important risk factors for late periprosthetic fracture. The original diagnosis is relevant to the risk of periprosthetic fracture; rheumatoid arthritis has been shown to be a risk factor for PPF by both the Finnish and Swedish Registries.9 Fractures of the proximal femur treated by arthroplasty are at higher risk for sustaining periprosthetic fracture; osteoporotic fractures of the neck of femur are regarded as pathological fractures and the ongoing pathological process is likely to be responsible for the increased incidence of PPF which increases with age, and from the index operation.10,11 Lindahl, based on the Swedish Registry, shows that initially PPF is the third commonest reason for revision, but from four years onwards, it is the second commonest reason.12

The incidence of periprosthetic fractures is rising significantly as more replacement arthroplasties are performed. They are a potentially devastating complication associated with high morbidity and mortality. Their management is a sub-specialty in itself. This article outlines the principles of the management of periprosthetic fractures of the lower limb.

Keywords bone graft; internal fixation; peri-prosthetic fracture

Introduction An aging population with higher standards of living has led to a steady increase in replacement arthroplasties in developed countries as recorded by the Scandinavian, Australian, UK and Mayo Clinic Registers. The positive outcome of an otherwise successful procedure can be compromised by a periprosthetic fracture (PPF). It is a major problem, associated with high rates of morbidity and mortality.1,2 The prevalence is difficult to ascertain but the consensus is that they are increasing both numerically and in complexity. In 2006 Lindahl et al. reported the cumulative incidence of periprosthetic hip fractures as 0.4%.3 According to the Swedish Hip Registry, PPF is the third commonest reason for revision arthroplasty, after aseptic loosening and dislocation.4 Periprosthetic fractures around a total knee arthroplasty are less common but equally important. They are more common in the distal femur (0.3e2.5%) compared with the proximal tibia (0.39% to 0.5%). Periprosthetic fractures can be divided into those occurring intra-operatively and post-operatively. Intra-operative

Panos Makrides Department of Trauma and Orthopaedic Surgery University Hospital Coventry and Warwickshire NHS Trust, Clifford Bridge Road, Coventry, UK.

Classification of periprosthetic fractures around the hip

Harpal Singh Uppal Department of Trauma and Orthopaedic Surgery University Hospital Coventry and Warwickshire NHS Trust, Clifford Bridge Road, Coventry, UK.

While classification is essential to aid communication and for research, it is of most use to assist management. Numerous classification systems have been devised. Most, like Parrish (Table 1), classify the fracture according to its location. While simple and straightforward it does not help in deciding the correct treatment.

Steve Krikler Department of Trauma and Orthopaedic Surgery University Hospital Coventry and Warwickshire NHS Trust, Clifford Bridge Road, Coventry, UK.

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the management of these patients is at least discussed with and ideally managed by surgeons who have experience in the field. Assessment of a periprosthetic fracture should be standardised. The patient should be investigated biochemically and haematologically to assess their fitness for surgery. Radiologically, it is of paramount importance to obtain good quality radiographs which should be assessed carefully, comparing them with previous X-Rays. CT scanning may be useful, provided there is adequate suppression of artefact from the implant.

Parrish classification Group

Site of fracture

Group Group Group Group

1 2 3 4

Fractures Fractures Fractures Fractures

in in in in

the the the the

trochanteric area proximal part of the shaft mid-shaft distal part of the femur

Table 1

Management If the patient is unfit for surgical treatment, closed reduction can be attempted; but the associated prolonged bed rest can lead to serious complications. Malunion is a major concern in this group as it can be detrimental to function, and can make future revision, if that becomes possible, extremely challenging. The surgical management of periprosthetic fractures depends on the site of the fracture, the bone quality and the stability of the components. When the stem is stable, fixation of the fracture should be performed, either open or closed. Special consideration should be given to transverse fractures at the tip of the stem. These are very difficult to treat conventionally and many surgeons advocate stem revision despite the prosthesis itself being stable.

Coventry classification (Modified from Ninan et al.13) Ninan et al. produced the Coventry classification for PPF.13 We find this is comprehensive, easy to apply and also helpful in decision making for what is difficult and challenging problem. They divided periprosthetic fractures into two types; Type 1 hips include the ‘happy hips’, did not have problems pre-injury, and whose X-Ray shows that the stem is generally well-fixed with no evidence of loosening, or bone loss. In these cases treatment should focus on treating the fracture without interfering with the prosthesis. In Type 2, or ‘unhappy hips’ the fixation is compromised and the implant has to be revised as part of the treatment of the fracture.

No

Loose?

Standard or Long Stem, depending on whether there is significant proximal bone loss, adequate isthmus, or intact distal femur

Very Distal?

Retro Nail or Locking Plate +/- cables

Locking Plate +/cables +/- graft

Vancouver classification The Vancouver Classification can be used similarly, but is far more complex. Types A, B1 and C can be managed in the same way as the type 1(happy hips), whereas types B2 and B3 can be thought of as type 2 (unhappy) hips, which require revision (Table 2).

Historically Ogden in 1972 used a long plate designed to accommodate pre-existing intramedullary devices. It had slots to accommodate wires and bands. However, biomechanical analysis showed that these resulted in high tensile stress at the fracture site and stress shielding at the proximal lateral cortex, leading to fractures below the plate and component loosening. The Partridge system, introduced in 1982, consisted of a nylon plate and straps which were introduced around the fracture. Over time it proved to be unsuccessful, with poor results, especially in more distal fractures, largely due to band loosening. Another popular device was the Mennen Plate, a paraskeletal clamp-on plate device, but reports of its use were controversial. It gave semi-rigid stability and was first introduced for non weight-bearing bones, but Lam et al. advocated its suitability and use for femoral periprosthetic fractures.14 The general consensus is that they give sub-optimal results were technically difficult to apply, and the surgical approach and exposure were not soft tissue friendly. Current concepts for the treatment of any fracture should follow AO principles. If the prosthesis is satisfactory both clinically and radiologically the focus should be on treating the fracture on its own merits. Thus if the fracture is distal to the tip of the femoral stem, the use of conventional DCP, DCS or LCP plates should be considered (Figure 1). The LCP plate is a newer development in plate osteosynthesis which has revolutionised

Clinical assessment Revision arthroplasty and the management of periprosthetic fractures is a sub-specialty in its own right. It is important that

Type

Site and type of fracture

Type AG Type AL Type B1

Fractures of greater trochanter Fractures of lesser trochanter Fracture around the stem or extending just below (femoral component solid) Around or just extending below stem - femoral component is loose Around or just extending below stem - femoral component is loose associated with severe bone loss Fractures distal to tip of stem

Type B2 Type B3 Type C Table 2

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Yes

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the principles of internal fixation, providing better purchase in low quality bones, and gives excellent angular stability. Chakravarthy et al. confirmed this.15 The angular stability provided by the locking screws abolishes the need to compress the plate on to the bone, thus avoiding compression and strangulation of the periosteal blood supply. A further development of locking plate osteosynthesis is the concept of Less Invasive Stabilization System (LISS system). This is a pre-shaped plate applied to the extra-medullary surface using locking screws. It combines a locking device conferring good angular stability with a minimally invasive approach to the fracture. The plate can be inserted antegrade or retrograde (Figure 2). This minimal approach results in less periosteal stripping and less disruption to the soft tissues, leading to more favourable biology for bone healing and union. Kobbe et al. reported good mid-term functional results of the use of the LISS system in the treatment of periprosthetic fracture.3 The LISS is most commonly used for more distal diaphyseal fractures and it widely used for supracondylar fractures above a knee arthroplasty as will be discussed later. Combining screw fixation with cerclage wires with a locking system remains controversial. The combination is said to give better fixation of the plate and hence give a more stable construct, but critics suggest that the good hold provided by the locking system renders the use of cerclage wires unnecessary and they also regard them as dangerous as they can act as stress risers. For conventional plate fixation onto bone the consensus is that screws, cerclage wires or bands have proven to be inefficient when used on their own. A combination has been shown to give good results. Tsiridis et al. showed good results using the DallMiles plate, essentially a development of the Ogden plate, which uses a combination of cable and screw fixation proximally and conventional screw fixation distally. Special attention should be given to the proximal screw fixation. In this case the use of uni-cortical screws is recommended around the stem of the implant and bi-cortical screws below this level. The more proximal the periprosthetic fracture the more challenging the fixation is. The prosthesis and the cement mantle restrict the options for screw and plate placement and insertion of the screws can fracture the cement or act as stress risers, altering the biomechanical properties of the cement and leading to instability and interference with the prosthesis/bone interface with consequent loosening and long term osteolysis. In type 2, the unhappy fractures, where the prosthesis is affected or there is evidence of loosening, revision of the prosthesis should be undertaken. When revising a femoral stem in the presence of a periprosthetic fracture, most authors advocate the use of long stems. A long stem can give good results when bone loss is proximal to the isthmus. Larson at al state that cortical perforations and femoral fractures should be bypassed by at least 2 femoral diameters.16 Both cemented and uncemented implants can be used (Figures 3 and 4). The latter depend on good fixation in the femoral diaphysis for initial stability.17 A short stem can be used but it is generally accepted that the fracture should be bypassed distally by at least 5e10 cm. Overall, uncemented porous implants have given the best results.18 Revision of a prosthesis is challenging and more so in the presence of a periprosthetic fracture. The removal of the old prosthesis and cement requires great care as it can lead to further

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bone loss, development of a new fracture or extension of the existing one. The surgeon is usually left with significant bone loss and poor remaining bone stock. There are various techniques to overcome these problems, such as the use of cortical onlay grafts. These are usually hemi-cylindrical diaphyseal or cortical fibular allografts, which are fixed to the host bone by circumferential wires. The aim is to provide structural support to the femur by replacing uncontained non-circumferential femoral defects, reducing stress risers and speeding up the healing process. Another technique is impaction grafting, which is usually reserved for severe osteolysis. Firstly, the proximal femur is re-constituted forming a cortical scaffold or containment created using wires, plates or meshes or a combination. Then bone graft is impacted into this tube. Once completed, the reconstructed bony tube can accommodate the femoral component. This technique can also be applied to acetabular defects when compressed graft is used to fill the defect followed by insertion of either a cemented or cementless acetabular component.19 If a patient is not fit for such a major procedure, there are a few more options available. If the patient is of average functional demand, or if definitive surgery may be possible in the future, in a happy hip external fixation can be considered. If the patient has low functional demand and a loose prosthesis, then a Girdlestone procedure can be considered. Finally, if the defect is very extensive, using a mega-prosthesis, such as are used after tumour resection, can be considered. The femur is osteotomised just below the level of abnormal bone stock and the prosthesis is fixed to the distal diaphysis. The abductor mechanism is then attached to the mega-prosthesis. Satisfactory results with an average Harris hip score of 71 have been reported by Klein et al. 20 In PPFs around the hip most attention is focussed on the femoral component as periprosthetic fractures around the acetabulum are extremely rare, but they are potentially life threatening. Acetabular fractures most frequently occur intraoperatively, but they are also associated with loosening or severe osteolysis around the acetabular component. Obviously loose sockets should be revised.

Classification of periprosthetic fractures around the knee Various classifications have been proposed for periprosthetic fractures around the knee. Backstein21 et al. described a system based on the position of the fracture, the bone stock and if the prosthesis was loose (Table 3).

Site Femur 1: Adequate bone on distal fragment for distal locking screws 2: Inadequate

Bone stock

Prosthesis

Tibia 1: Large proximal fragment to allow internal fixation

g ¼ good bone stock

S ¼ stable

2: Insufficient proximal fragment

l ¼ loose prosthesis

L ¼ Loose

Table 3

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Periprosthetic fracture associated with an un-cemented hemi-arthroplasty, revised to a cemented stem reducing the fracture with cables. Figure 1

Management

The Rorabeck-Lewis classification is a good guide for management, again based on the condition of the prosthesis22 (Table 4).

If, which is quite rare, the fracture is undisplaced and the prosthesis is stable, non-surgical treatment is appropriate using a brace to restrict joint movement and protected weight-bearing. In most cases surgical treatment is necessary. Fractures more than 15 cm away from the femoral implant should not be considered as periprosthetic and should be managed conventionally. The commonest and most widely advocated method to manage them is by using a retrograde intramedullary nail. The two pre-requisites are a large enough distal fragment to allow fixation of the distal locking screws, and a femoral component that allows access to the medullary canal. Hence, closed box devices are absolute contraindications. If the fracture is too distal, or there is a closed box implant, locking plates are advocated and have been shown to do well (Figure 5). Patellar fractures are the second commonest periprosthetic fracture of the knee, with a reported incidence of patello-femoral

Type Type I

Undisplaced, Intact Component

Type II

Displaced, Intact Component Loose Implant

Type III

Cast, protect WB ORIF if cannot tolerate cast/brace LCP, DCS, LISS, Ex-Fix, Nail Treat Fracture and address implant later Revise acutely

Table 4

‘‘Unhappy hip’’ revised using a longer stem and cables. Figure 2

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Periprosthetic Fracture following hip resurfacing, using the Ganz approach, fixed with a fixed angle locking plate, as there is no loosening of the components (‘‘happy hip’’). Figure 3

implant is loose), internal fixation, or patellectomy (partial or total). Internal fixation is associated with poor union rates, increased infection and a post-operative extension lag of 10 degrees.25,26 Tibial periprosthetic fractures are far less common. If the component is stable, the fracture can be treated using a buttress plate; peri-articular plates have also been advocated for complex metaphyseal fractures in the presence of a stable component. These plates are anatomically pre-contoured, so require minimal intra-operative bending. The use of locking screws may give a more stable fixation. If the prosthesis is loose and there is radiological evidence of osteolysis is a difficult problem. Removal of the prosthesis and cement and poor bone stock, can result in significant bony

complications (fracture, loosening, radiolucency) from 0.15%e 12%. Most occur with no evidence of injury within the first two years after surgery.23 Specific risk factors that apply to patellar fracture/component loosening include excessive bone resection or lateral release during the index procedure with resulting maltracking. Patellar resurfacing during the index procedure has a clear correlation. Management of patellar periprosthetic fractures is determined by fracture displacement, the degree of component loosening and whether the extensor mechanism is intact. Type III fractures are the commonest according to Ortiguera and Berry.24 Management varies according to the type, but the majority (70%) are managed nonoperatively. Other options include revision arthroplasty (if the

‘‘Happy hip’’eperiprosthetic fracture with no loosening of the femoral component with was therefore retained, and fracture fixed with a locking plate. Figure 4

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Supracondylar femoral periprosthetic fracture. As the components remain well fixed (‘‘happy’’), the fracture was fixed with a locking plate. Figure 5

5 Lindahl H, Malchau H, Herberts P, Garellick G. Periprosthetic femoral fractures: classification and demographics of 1049 periprosthetic femoral fractures from the Swedish National Hip Arthroplasty Register. J Arthroplasty 2005; 20: 857e65. 6 Tsiridis E, Haddad FS, Gie GA. The management of periprosthetic femoral fractures around hip replacements. Injury 2003; 34: 95e105. 7 Pazzaglia U, Byers PD. Fractured femoral shaft through an osteolytic lesion resulting from the reaction to a prosthesis: a case report. J Bone Joint Surg Br 1984; 66: 337e9. 8 Schmidt H, Kyle RF. Periprosthetic fractures of the femur. Orthop Clin North Am 2002; 33: 143e52. 9 Franklin John, Malchau Henrik. Risk factors for periprosthetic femoral fracture. Injury June 2007; 38(6): 655e60. 10 Fawzy Ernest, de Steiger Richard, Gundle Roger, McLardy-Smith Peter, Murray David W. The management of periprosthetic fractures oxford trimodular femoral stem: a survivorship study. J Arthroplasty November 2008. 11 Tsiridis Eleftherios, Krikler Steve, Giannoudis Peter V. Periprosthetic femoral fractures: current aspects of management. Injury June 2007; 38(6): 649e50. 12 Lindah Hans. Epidemiology of periprosthetic femur fracture around a total hip arthroplasty. Injury June 2007; 38(6): 651e4. 13 Ninan TM, Costa ML, Krikler SJ. Classification of femoral periprosthetic fractures. Injury June 2007; 38(6): 661e8. 14 Lam SJS, Purkaystna A. The Mennen plate: a unique indication for internal fixation. Dentsply: CMW laboratories; 1982. 15 Chakravarthy Jagannath, Bansal Rajeev, Cooper Julian. Locking plate osteosynthesis for Vancouver type B1 and type C periprosthetic fractures of femur: a report on 12 patients. Injury June 2007; 38(6): 725e33. 16 Duncan CP, Masri BA. Fractures of femur after hip replacement. Instr Course Lect 1995; 44: 293e304. 17 Emerson Jr RH, Malinin TI, Cuellar AD, Head WC, Peters PC. Cortical strut allografts in the reconstruction of the femur in revision total hip

deficiency. This can be made up relatively easily by using a combination of thicker polyethylene implants and metal augments. Small defects can also be filled using cement (poly-methylmethacrylate) but as this has no biological properties, it may prevent fracture healing. In cases of severe bone loss, a custom made mega-prosthesis may have to be considered as this allows reconstruction of fractures with significant bone defects. The disadvantages however are the cost and the lack of intra-operative flexibility. In all cases where there is loss of bone with comminution and poor bone stock, bone grafting is extremely helpful. Autologous graft is best due to its osteoconductive and osteoinductive properties, but in the majority of patients sufficient volume is not available, limiting its usefulness. Another option is the use of a structural allograft/implant composite; Engh et al. reported good results using structural allograft in cases of severe tibial bone loss.27 Problems have also been reported with periprosthetic fractures after unicompartmental knee replacement, presenting with significant loosening of the components and tibial bone loss. They should be managed by conversion to a total knee replacement with allograft to cover the tibial bone defect which has been shown to have good results.28 A

REFERENCES 1 Lewallen DG, Berry DJ. Periprosthetic fracture of the femur after total hip arthroplasty: treatment and results to date. Instr Course Lect 1998; 47: 243e9. 2 Tower SS, Beals RK. Fractures of the femur after hip replacement: the Oregon experience. Orthop Clin North Am 1999; 30: 235e47. 3 Kobbe Philipp, Klemm Ralf, Reilmann Heinrich, Hockertz Thomas J. Less invasive stabilisation system (LISS) for the treatment of periprosthetic femoral fractures: a 3-year follow-up. Injury April 2008; 39(4): 472e9. 4 Lindahl Hans. Epidemiology of periprosthetic femur fracture around a total hip arthroplasty. Injury June 2007; 38(6): 651e4.

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18

19

20

21 22

23 Chalidis Byron E, Tsiridis Eleftherios, Tragas Adamantios A, Stavrou Zois, Giannoudis Peter V. Management of periprosthetic patellar fractures: a systematic review of literature. Injury June 2007; 38(6): 714e24. 24 Ortiguera CJ, Berry DJ. Patellar fracture after total knee arthroplasty. J Bone Joint Surg Am 2002; 84-A: 532e40. 25 Brick GW, Scott RD. The patellofemoral component of total knee arthroplasty. Clin Orthop Relat Res; 1988: 163e78. 26 Chun KA, Ohashi K, Bennett DL, El-Khoury GY. Patellar fractures after total knee replacement. AJR Am J Roentgenol 2005; 185: 655e60. 27 Engh Loss Gerard A, Ammeen Deborah J. Use of structural allograft in revision total knee arthroplasty in knees with severe tibial bone. J Bone Joint Surg Am 2007; 89: 2640e7. 28 Kumar Arun, Chambers Iain, Wong Paul. Periprosthetic fracture of the proximal tibia after lateral unicompartmental knee arthroplasty. J Arthroplasty June 2008; 23(4): 615e8.

arthroplasty. A basic science and clinical study. Clin Orthop Relat Res 1992; 285: 35e44. Springer BD, Berry DJ, Lewallen DG. Treatment of periprosthetic femoral fractures following total hip arthroplasty with femoral component revision. J Bone Joint Surg Am 2003; 85(11): 2156e62. Oakes Daniel A, Cabanela Miguel E. Impaction bone grafting for revision hip arthroplasty: biology and clinical applications. J Am Acad Orthop Surg October 2006; 14(No. 11): 620e8. Klein GR, Parvizi J, Rapuri V, et al. Proximal femoral replacement for the treatment of periprosthetic fractures. J Bone Joint Surg Am 2005; 87(8): 1777e81. Backstein David, Safir Oleg, Gross Allan. Knees. J Arthroplasty June 2007; 22(4, Suppl. 1): 45e9. Su Edward T, De Wal Hargovind, dI Cesare Paul E. Periprosthetic femoral fractures above total knee replacements. J Am Acad Surg Jan/Feb 2004; 12(no. 1): 12e20.

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BASIC SCIENCE

Arthroscopic powered instruments: a review of shavers and burrs

The demand for appropriate and specific instrumentation is increasing. Arthroscopic shavers have become increasingly important in routine arthroscopic work, both for improving visualisation and also for therapeutic work. However, to use these instruments safely and optimally a sound knowledge of their specific function and mode of action is required.

S Singh

History

A Tavakkolizadeh

Powered cutting instruments have been proven to be extremely useful in arthroscopic procedures. The first such power-driven device was a patellar shaver that was introduced in 1975 by Dr. Lanny Johnson2 and made by Dyonics Corporation (Figure 1).

A Arya J Compson

Shaver blades and cutting tips Shaver blades with a wide range of cutting tips have been developed by the orthopaedic instrument companies. They are designed for use in different clinical situations and for specific functions. However, the principles of the design remain similar (Figure 2).

Abstract There has been rapid development in the field of arthroscopic surgery in the last decade. Hand in hand with this the instrumentation has also become more specific and sophisticated. Powered arthroscopic instruments such as shavers and burrs are commonly used in all forms of arthroscopy and a large range is now available to the orthopaedic surgeon. This large array can cause confusion, especially since many have very specific intended functions. This article reviews the types of blades and burrs available and the principles underlying the mechanism of how they work. A better understanding of the subject should hopefully make the surgery easier and also minimize the potential damage these instruments can cause.

Blades The blade consists of an outer hollow sheath and an inner hollow rotating cannula with corresponding windows for suction and cutting; a “tube within a tube” mechanism.3 The window of the inner sheath functions as a two-edged cylindrical blade that spins within the outer hollow tube.1 The shape and geometry of the edges of the inner and outer tube tips determines the degree of aggression of the blade.

Keywords arthroscopy; blades; burrs; instruments; shavers

Introduction The evolution of arthroscopic surgery has been one of the major developments in orthopaedic surgery in the recent past. It has dramatically changed the orthopaedic surgeon’s approach to joint pathology. A high degree of clinical accuracy combined with low morbidity has encouraged its use in diagnosis, assessment and treatment. Progressive improvements in arthroscopic systems, equipment and accessory operative instruments, such as powered cutters, have made advanced intra-articular operative techniques possible.1

S Singh MBBS MS(Orth) MRCSEd Dip. Sports & Exercise Med (Edin) is a Registrar at the Department of Orthopaedics, William Harvey Hospital, Ashford, UK. A Tavakkolizadeh MBBS MSc FRCS(Tr & Orth) is a Locum Consultant Orthopaedic Surgeon, Department of Orthopaedics, King’s College Hospital, London, UK. A Arya MBBS MS(Orth) MChOrth FRCS(Tr & Orth) is an Associate Specialist, Department of Orthopaedics, King’s College Hospital, London, UK.

Figure 1 Photograph of first patella shaver (Dyonics Corporation). A shaver system consists of a number of components, broadly these include: A. Shaver blades with variable cutting tips and shaft. B. A Hand piece and grip. C. A Power source. D. Irrigation and suction.

J Compson MBBS BSc FRCS(Tr & Orth) is a Consultant Orthopaedic Surgeon, Department of Orthopaedics, King’s College Hospital, London, UK.

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Figure 2 Different parts of a shaver blade.

They are available in standard and long lengths, curved and straight styles, and shaft diameters ranging from 1.9 to 5.5 mm, depending on the joint involved and the procedure to be performed. Smaller blades allow access to smaller or more constrained joints. We have tried to broadly divide the shavers according to the type of tissue they cut, though there is some overlap:Figure 3 Different cutting tips give the shaver different levels of aggressiveness (Courtesy: Smith & Nephew). a Smooth inner tube and smooth outer tube. b Smooth outer tube with toothed inner tube. c Toothed inner and outer tube (can be razor edged).

(I) Blades designed for cutting soft tissue These function best at lower speeds, in the range of 1800–2000 rpm in the oscillate mode. Because these tips require tissue to be introduced into the opening of the outer tube, higher revolutions per minute effectively close the aperture and permit insufficient time for soft tissue fragments to enter. Unless the blade is extremely sharp, the internal component will push firmer tissue back out of the aperture or will spool thinner tissue without ­cutting it. The key points in design when selecting a soft tissue shaver blade include: • Size of the aperture: This is the window at the tip, which can be large, as in a full radius blade, or smaller. The larger the window the greater the ability to resect tissue. • Location of aperture: ‘Side cutting’ is the normal mode of function in most shavers as access is normally tangential, but additionally some designs allow ‘end cutting’ when only almost perpendicular access is possible. End cutting is normally prevented in most shavers by a hood at the tip of the shaft. Choosing the right design is crucial to avoid collateral damage within the joint. • Edges of the aperture: The design of the edges of the soft tissue blade can affect its role. There are generally three designs with increasing levels of aggressiveness (Figure 3): a) smooth inner tube and smooth outer tube,

b) smooth outer tube with toothed inner tube, and c) Toothed inner and outer tube (can be razor edged) (II) Blades designed for bony resection These perform best at speeds of about 5000 rpm in forward mode. The deeper the flute pattern in the burr, the more important higher speed becomes. Deep flutes, widely spaced, tend to chatter and vibrate at lower speeds. Shallower flutes turning at higher speeds present inadequate cutting surface to the tissue. Cutting, therefore, becomes a function of the angle at which the burr edge approaches the bone surface and the velocity at which it turns.3 The burrs generally cut better on forward but they can be used to polish a surface on reverse. The newer designs ­provide an outer coating on the blade that works as lubricant. This prevents and reduces the release of metal debris when using the blade against a hard surface. The two different designs of burr blades are: (a) Barrel Shape: used in standard procedures such as acromioplasty. With these, the less the number of flutes, the more

Figure 4 a Barrel shaped burrs for acromioplasty with different flute and end cutting designs. Note the V-shaped flutes (in II) vs. diagonal ones (in I). b Shielded ball burrs. (Courtesy: Smith & Nephew).

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be secured to the drapes with enough length to allow free movement of the hand piece and minimize “drag”. Careful setting up will save time and effort in the procedure.

aggressive the blade. Aggressiveness is further increased by having V-shaped flutes rather than the standard diagonal one. The tips can be tapered in some designs. (b) Ball Shape: can be hooded or unhooded and commonly used for preparing the labrum for stabilisation procedures or notchplasty in ACL reconstructions (Figure 4).

Power source Control unit The control unit provides for variable speed of operation of the tools, and has digital displays showing the mode of function and speed. The footswitch or hand controls allow forward or reverse blade rotation, or oscillation mode, in which the blade alternates between forward and reverse rotation. The shaver system control unit can also drive high powered arthroscopic instruments such as drills, wire drivers and saws. Some shaver systems sense the type of blade installed in the connected hand piece and automatically set the shaver blade speed based on a preset programme.4 Some systems can also recall the adjusted settings for a specific blade in future use. This recognition is achieved through a magnet in the blade handle.

(III) Blades designed for bony and soft tissue resection These instruments either: – have an extra coating which reduces blade friction and allows both soft tissue and bone cutting, or – have an inner tube with helical shape that allows cutting of both bone and soft tissue including periosteum without clogging (Figure 5). It has been shown in animal models that the tissue cutting rate for synovial tissue is better in a slower oscillating mode (Graph 1), which is generally more aggressive at cutting, whereas bone cutting ability is better with the forward moving shaver at higher speeds (Graph 2).

Irrigation and suction system Suction is provided through the central cylinder of the blade and brings the fragments of soft tissue into the window. As the blade rotates, the tissue is cut, sucked out through the central tube and collected in a suction trap. The suction window is the same as the cutting window in the soft tissue shavers whereas in the bony burrs the suction window is proximal to the tip on the inner tube as the mode of action is different (Figure 6).1 The blade action alternately opens and closes the window to the suction flow in the oscillate mode of the soft tissue shavers. With different hand piece designs, there is a variation in location of control buttons as well as levers for suction control (Figure 7).

Hand piece and Grip Hand-piece The shaver hand-piece drives a variety of surgical blades and provides manual control of suction flow. Hand pieces are available in different sizes and weights. The optional Hand Control Shaver hand piece features push-button controls for blade operation. The Mini Shaver hand-piece uses smaller blades for small-joint surgery. New high torque lightweight designs respond quickly to variations in tissue and bone. This helps to maintain speed and performance and avoid stalling. Lightweight and flexible cords and tubing further reduce the drag on the hand by their weight.3 Grip Since the cutting tip of a shaver is placed distally, the weight of the hand piece is important for control. There are two types of grips that are commonly used, these are: – Pencil grip - used for finer manoeuvres and delicate procedures. It is controlled by the thumb, index and long fingers. Most of the weight should be in the front of the hand-piece, held distal to the 1st web space. – Pistol grip - used for those procedures requiring more power instead of finer delicate movements. It is controlled by strength coming from ulnar side of the hand with weight concentrated in the handle, which is held in the centre of the palm. The balance of the shaver is also affected by the position, weight and tension of the power lead and suction tube, which should

Sterilisation Most current shaver blades are single use only, due to both physical damage to the blades during use,5 as well as the potential risk of infection.6 In 2006 a study5 showed that of 27 reprocessed single-use only shaver blades 13 (48%), had detectable levels of protein and 17 (63%), had detectable levels of nucleic acid. Additionally, 20 of the reprocessed shaver blades had visual damage to the teeth.

Figure 5 HELICUT™ Burr (Smith & Nephew) allows both soft tissue and bone cutting functions.

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Graph 1 Synovial tissue response to different modes of cutting (Courtesy: Smith & Nephew).

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Figure 6 The suction window above the tip in the burrs (Courtesy: Smith & Nephew).

the shaver to “hoover up” fragments like loose bodies or debris from hand instruments. Graph 2 Bone tissue response to different modes of cutting (Courtesy: Smith & Nephew).

Over-suction If outflow exceeds inflow this causes over-suction and turbulence, which creates bubbles in the joint. It is important to balance the two to maintain joint distension and optimal evacuation of tissue.13

Traditionally, when blades were commonly re-used, gluteraldehyde was used for sterilisation in between cases and ethylene oxide gas was used every few days for further ­sterilisation.2,7 For the initial cleaning of the hand piece, the suction control lever is fully opened and the hand piece is cleaned thoroughly with soapy water. The drain tube is cleaned with a brush. After rinsing with water, formal sterilisation is carried out by steam at 132° C for 4 to 10 minutes, depending on the presence or absence of a vacuum.

Heat injury Heat injury can occur to the surrounding structures especially in absence of adequate irrigation.13 With the practice of blade re-use, if the blades are blunt there is a risk of heat injuries and infection.5,6 However, most modern shaver blades are for single use only to reduce these risks. Damage to surrounding tissues and arthroscope The cutting tip should always be within the visual field to minimise the risk of unintended tissue or arthroscope damage.2 Both the tip and the edge of the cutting window can scour and damage the articular surface. The shaver should not be forced into joint spaces or used to produce distraction. Adequate joint space or distension is necessary for arthroscopic inspection and use of arthroscopic shaver. Therefore, shavers should be used cautiously in patients with ankylosis or stiff joints.

Window lock Most shaver systems have a window lock that stops the blade in the closed position following shaving. This has to be set at the start of the procedure, usually by closing the shaver aperture either before insertion (watch for over heating) or after insertion once the shaver is in the joint (and suction off). A button on the foot piece or hand piece will turn the inner blade slowly until the window is closed. When a blade is changed this needs to be reset. This is a very useful function to keep the joint distended between bouts of shaving, although it does not work for burrs.

Shaver failure Dried blood, saline, and other deposits inside the hand-pieces can be a major cause of equipment malfunction or infection unless cleaned and sterilised regularly and adequately. Most shaver blades now on the market are for single use only.

Complications Breakage There are cases in the literature that report breakage of shaver tips in joints that were discovered on x-rays post operatively. It is therefore important to check the tip of blade for breakage at the end of a procedure.8–11

Heat damage to instruments Irreversible damage to burrs will result if they are run without the flow of irrigation.13 Post-operative inflammation and limitation of joint movement Debris left within the joint space has the potential to cause postoperative symptoms due to an inflammatory reaction or mechanical interference with joint function.

Clogging Clogging can be troublesome and may be kept to a minimum if suction is well regulated,8,12 It also commonly occurs when using

Figure 7 a Suction lever on the standard shaver hand-piece b suction levers on the hand control hand-piece c suction lever on the mini shaver hand-piece.

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7 Johnson LL, Shneider DA, Austin MD, Goodman FG, Bullock JM, DeBruin JA. Two per cent glutaraldehyde: a disinfectant in arthroscopy and arthroscopic surgery. J Bone Joint Surg Am. 1982; 64(2): 237–239. 8 In Y, Bahk WJ, Park JB. Detachment of the tip of a motorised shaver within the knee joint: A complication of Arthroscopic Surgery. Arthroscopy 2003; vol. 19(Issue 6): e25–e27. 9 Small NC. Complications in arthroscopy: the knee and other joints. Arthroscopy 1986; 2: 253–8. 10 Small NC. Complications in arthroscopic surgery performed by experienced arthroscopists. Arthroscopy 1988; 4: 215–21. 11 McGinty JB. Complications of arthroscopy and arthroscopic surgery. In: McGinty JB, ed. Operative arthroscopy. 2nd edn. Philadelphia: Lippincott-Raven, 1996, p. 71–81. 12 Strobel MJ. Surgical instruments. In: Strobel MJ, ed. Manual of arthroscopic surgery. Berlin: Springer-Verlag, 2002, p. 22–48. 13 Ogilvie-Harris DJ, Weisleder L. Fluid pump systems for arthroscopy: a comparison of pressure control versus pressure and flow control. Arthroscopy 1995; 11(5): 591–595.

Conclusion The development of shaver systems and blades has made arthroscopic surgery more versatile. It allows controlled management of the soft tissue and bony resections as part of reconstructive arthroscopic procedures. We hope to have given an overview of the principles that are important to both surgical trainees and established surgeons alike, to help them use these powerful and useful but potentially damaging tools. It is crucial that before using any shaver system for the first time, all available product information is reviewed. ◆

References 1 Phillips BB. General principles of arthroscopy. In: Canale ST, ed. Campbell’s Operative Orthopaedics. 10th edn. Mosby-Year Book Inc. 2002, 1463–1469. 2 Dandy D. Arthroscopic management of the knee, 2nd edn. Churchill Livingstone, 1987, p. 23–27. 3 Whipple TL. Powered instruments for wrist arthroscopy. Arthroscopy: The Jornal of Arthroscopic and Related Surgery 1988; 4(4): 290–294. 4 Caspari RB. Current Development of Instrumentation for Arthroscopy. Clin Sports Med 1987; vol 6(3): 619–635. 5 King JS, Pink MM, Jobe CM. Assessment of reprocessed arthroscopic shaver blades. Arthroscopy 2006; 22(10): 1046–1052. 6 Backrest-Hamilton IA, Bhamra M, Jackson AM. Arthroscopic meniscal shavers: a potential hazard of sepsis. Ann R Coll Surg Engl 1991; 73(2): 70–1; Discussion 72.

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Acknowledgements We would like to thank Smith & Nephew Inc. 150 Minuteman Road, Andover, Massachusetts 01810, U.S.A. for kindly providing all the figures for this article.

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SYNDROME

Nail-patella syndrome

the LMX1B gene which is located on the distal end of the long arm of chromosome 9 in the region 9q34.6 It is thought to occur in 1 in 50,000 newborns.7 The severity and incidence of each feature of nail patella syndrome is unpredictable and can vary within the same family. The mutation in the LMX1B gene is in the majority inherited, however spontaneous mutations can occur.

Charlotte Jones Donna Diamond Rouin Amirfeyz Martin Gargan

Clinical features Nail dysplasia This is the commonest abnormality in nail-patella syndrome and is seen in 98% of patients. Nails may be missing completely, hypoplastic, ridged, pitted or separated into two by a skin ridge. The thumbnails are most affected and the severity tends to decrease towards the little finger. The ulnar border of the thumb is more involved than the radial. Finger nails are more commonly affected than the toenails and the changes are often symmetrical. Changes are usually present at birth. Triangular lunula are also seen and are sometimes the only abnormality of the nail.8

Abstract Nail patella is one of the familial syndromes commonly asked on the FRCS (Trauma & Orth) exam. This article reviews the latest scientific information available and high-lights the key features.

Keywords iliac horn; Nail-patella syndrome; radial head dislocation; patella dyslasia

Introduction Patella hypoplasia The patellae in patients with NPS are small, irregularly shaped or completely absent.9 When present the patella is unstable, often causing the presenting complaint of NPS to be recurrent lateral dislocation. This is exacerbated by hypoplasia of the lateral femoral condyle. A septum which runs from the patella to the intercondylar groove divides the knee into two compartments. Due to the lateral femoral condyle hypoplasia, genu valgum (knock knees) occurs, although infrequently genu varum is also seen.9 Knee pain is the main complaint of patients with NPS in the longer term.10

Nail-patella syndrome (NPS), also know as hereditary onychoosteodysplasia, displays a quartet of main findings: nail dysplasia patella hypoplasia elbow dysplasia iliac horns. Other features seen in this syndrome include renal problems, ophthalmological problems and other orthopaedic manifestations. The earliest description of nail dysplasia associated with skeletal dysplasia dates back to 1820 when Chatelain described a patient with congenital anomalies of the nails, elbows and knees.1 In 1897, Little quoted the description by Sedgewick suggesting the hereditary nature of the disorder in the description of a family with 18 members, from four generations, having absent thumbnails and patellae.2 The presence of iliac horns was first noted by Fong in 1946 during routine urography. Fong saw conical bony projections on the dorsolateral aspects of the ilia, which he termed ‘‘iliac horns’’3 or ‘‘Fong’s horns’’. These were not associated with the syndrome until a few years later by Mino et al. 1948 and Thompson et al. 1949 (Figure 1).4,5

Elbow dysplasia Straightening the elbow may be difficult and there is a varying cubital valgus. The elbow joint is characteristically dysplastic with hypoplasia of the lateral side of the elbow joint, involving the radial head, capitellum and lateral humeral condyle. Abnormal articulation of radial head and capitellum often results in a dislocated radial head.9,11 Pterygia (webbing) may occur across the elbow joint (Figure 2).

Genetics Nail patella syndrome is a genetic disorder that is transferred via autosomal dominant inheritance. It is caused by a mutation in

Charlotte Jones Medical Student, Faculty of Medicine and Dentistry, University of Bristol, Bristol, UK. Donna Diamond DCR(R) BSc PgC Superintendent Paediatric Radiographer, Bristol Royal Hospital for Children, Bristol, UK. Rouin Amirfeyz FRCS (Trauma & Orth) MSc MD Specialist Registrar in Trauma and Orthopaedics, Bristol Royal Infirmary, Bristol, UK. Martin Gargan FRCS (Trauma & Orth) MA Consultant Paediatric Orthopaedic Surgeon, Bristol Royal Hospital for Children, Bristol, UK.

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Figure 1 Radiograph of adult pelvis showing centrally placed iliac horns.

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SYNDROME

population. Once a diagnosis of NPS is established regular screening for glaucoma should be implemented.

Orthopaedic treatments Treatment of NPS is mainly supportive and, since a significant number of people with NPS are asymptomatic, surgical treatment is not necessary. In a review of 44 patients with NPS only 20 received surgical intervention for knee contractures or a mal-aligned patella. The best results were obtained using a combination of full posterior capsular release for flexion contractures and quadricepsplasty for flexion contracture along with proximal and distal patellar realignment.9 A case report of a patient with NPS having an established congenital dislocation of the patella describes successful treatment using the Stanisavljevic procedure.21 Arthroscopic management often proves difficult due to the presence of an intraarticular septum. Asymptomatic dislocation of the radial head is common in younger children with symptoms occasionally becoming apparent later on in life. Surgical excision of the radial head does little to improve range of movement, however does provide symptomatic relief. Excision in the premature skeleton does not appear to be associated with significant problems, despite the procedure traditionally being carried out post skeletal maturity.9 Poor results following the treatment of anticubital pterygium with a 90 fixed flexion deformity were reported in 1998 by Song et al. Poor function and recurrence of deformity occurred following a soft tissue release with Ilizarov external fixation and distraction.22 Iliac horns are largely impalpable, asymptomatic and require no treatment. Foot deformities are frequently the primary complaint in children with NPS. These are treated using the standard methods, but can often be more resistant to successful treatment.9,23 A

Figure 2 Radiograph showing hypoplastic elbow with radial head dislocation.

Iliac horns Iliac horns are pathognomonic of NPS and present in over 80% of patients.9e12 They arise bilaterally at the site of attachment of the gluteus medius muscles and project posterolaterally.13 They may be palpable. Other orthopaedic manifestations Frequently described features of NPS that do not contribute to the diagnosis include: Shoulder girdle dysplasia14 Short stature15 Talipes equinovarus (club feet)8 Calcaneo-valgus feet8,15 Dislocation of the hips15 Madelung’s deformity16 Large joint contractures Generalised joint hyperextensibility is a common feature, particularly of the fingers.

REFERENCES 1 Chatelain (1820), quoted by Roeckherath W. The Nail-patella syndrome. Fortschr Geb Rontgenstr 1951; 75: 700e4. 2 Little EM. Congenital absence or delayed development of the patella. Lancet 1897; 2: 781e4. 3 Fong EE. ‘‘Iliac horns’’ (symmetrical bilateral central posterior iliac processes). Radiology 1946; 47: 517e8. 4 Mino RA, Mino VH, Livingstone RG. Osseous dysplasia and dystrophy of the nails. Review of the literature and report of a case. Am J Roentgenol 1948; 60: 633e41. 5 Thompson EA, Walker ET, Weens HS. Iliac horns. An osseous manifestation of hereditary arthrodysplasia associated with dystrophy of the fingernails. Radiology 1949; 53: 88e92. 6 Sato U, Kitanaka S, Sekine T, Takahashi S, Ashida A, Igarashi T. Functional characterization of LMX1B mutations associated with nailpatella syndrome. J Pediatr Res 2005; 57: 783e8. 7 Wynne-Davies R, Hall C, Apley AG. Atlas of skeletal dyplasias. Edinburgh: Churchill-Livingstone; 1985. p. 614. 8 Beals R, Eckhardt AL. Hereditary onycho-osteodysplasia (Nail-patella syndrome): a report of nine kindreds. J Bone Joint Surg Am 1969; 51: 505e16. 9 Guidera KJ, Satterwhite Y, Ogden JA, et al. Nail-patella syndrome: a review of 44 orthopaedic patients. J Pediatr Orthop 1991; 11: 737e42.

Kidney involvement The most important non-orthopaedic condition in NPS is nephropathy, which is reported to be present in more than 60% of cases.17 The course of the nephropathy is variable between patients, with around 30% of cases resulting in end-stage renal failure.18 Renal biopsy is diagnostic. Immediate referral to nephrology is essential following diagnosis of NPS. Ophthalmological findings Another non-orthopaedic manifestation of NPS is open-angle glaucoma.19,20 Lester’s sign, a clover-leaf shaped area of darker pigmentation on the inner margins of the iris, is also seen at a higher prevalence in patients with NPS than in the general

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10 Beguiristain JL, de Rada PD, Barriga A. Nail-patella syndrome long term evolution. J Pediatr Orthop B 2003; 12(1): 13e16. 11 Yakish SD, Fu FH. Long-term follow-up of the treatment of a family with nail-patella syndrome. J Pediatr Orthop 1983; 3: 360e3. 12 Goshen E, Schwartz A, Zilha LR, Zwas ST. Bilateral accessory iliac horns: pathognomonic findings in nail-patella syndrome. Scintigraphic evidence on bone scan. Clin Nucl Med 2000; 25: 476e7. 13 Lazzeri S, Nori G, Matocci GP, Di Filippo P. Hereditary osteo-onychodysplasia of nail-patella syndrome: description of one case and literature review. J Orthop Trauma 2005; 6: 105e9. 14 Loomer RL. Shoulder girdle dysplasia associated with nail-patella syndrome. A case report and literature review. Clin Orthop Relat Res 1989; 238: 112e6. 15 Maini PS, Mittal RL. Hereditary onycho-osto-arthrodysplasia. J Bone Joint Surg Am 1966; 48: 924e30. 16 Duthie RB, Hecht F. The inheritance and development of the nailpatella syndrome. J Bone Joint Surg Br 1963; 45B: 259e67. 17 Knoers NVAM, Bongers EMHF, Van Beersum SEC, Lommen EJP, Van Bokhoven H, Hol FA. Nail-patella syndrome: identification of

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20

21

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mutations in the LMx1B gene in Dutch families. J Am Soc Nephrol 2000; 11: 1762e6. Meyrier S, Rizzo R, Gubier MC. The nail-patella syndrome. A review. J Nephrol 1990; 2: 100e40. Farley FA, Lichter PA, Downs CA, McIntosh I, Vollrath D, Richards J. An orthopaedic scoring system for nail-patella syndrome and application to a kindred with variable expressivity and glaucoma. J Pediatr Orthop 1999; 19: 624e31. Lichter PR, Richards JF, Downs CA, Stringham HM, Boehnke M, Farley FA. Cosegregation of open-angle glaucoma and the nail-patella syndrome. Am J Ophthalmol 1997; 124: 506e15. Marumo K, Fujii K, Tanaka T, Takeuchi H, Saito H, Koyano Y. Surgical management of congenital permanent dislocation of the patella in nail patella syndrome by Stanisavljevic procedure. J Orthop Sci 1999; 4: 446e9. Song HR, Cho SH, Koo KH, Jung ST, Shin HS. Treatment of antecubital pterygium in the nail-patella syndrome. J Pediatr Orthop 1998; 7B: 27e31. Hogh J, Macnicol MF. Foot deformities associated with onychoosteodysplasia. A familial study and review of associated features. Int Orthop 1985; 9: 135e8.

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Shoulder arthroscopy, anatomy and variants e part 2

structure that exhibits restraint but also permits the great mobility we see in the shoulder joint. The volume of the joint, as dictated by the capsule, varies significantly and the extremes include the small restrictive volume found in adhesive capsulitis, to the capacious capsule in those patients with connective tissue disorders or multidirectional laxity. From an anatomical perspective, the rotator cuff tendons fuse with the capsule near their insertions. Supraspinatus and infraspinatus merge with the capsule about 15 mm proximal to their insertions on the humerus and cannot be separated from the capsule by blunt dissection. The capsule importantly contains several localised areas where there are definable thickenings representing the glenohumeral ligaments. It is also necessary to remember that the capsule is lined by synovium and is therefore subject to inflammatory disorders, malignancy and tumour-like conditions.

Simon Boyle Manuel Haag David Limb Laurent Lafosse

Abstract In part 1 of this article we have described the history of shoulder arthroscopy and its current indications. We introduced concepts useful in the execution and interpretation of shoulder arthroscopy and introduced some technical tips to help those starting out, or developing their expertise, in this surgical skill. In part 2 we will focus on the range of findings that arthroscopy can yield, which can at first be daunting and confusing. The spectrum of normal findings is quite wide and substantial experience is needed simply to recognise what is within this spectrum and what should be considered pathological. Furthermore some pathological findings can be subtle or obscure, and easily missed if the arthroscopy is not complete and correlated carefully with the examination under anaesthesia.

Superior gleno-humeral ligament (SGHL) This structure is found to be present in 40e94% of shoulders1,2 and, when present, tends have the most consistent anatomy of the three anterior ligaments. It arises from the 12 o’clock position at the supra glenoid tubercle but can also take origin from the biceps anchor and labrum. It travels parallel to the biceps tendon to insert on the medial edge of the bicipital groove and the fovea capitus (just superior to the lesser tuberosity). Laterally, at its insertion, the SGHL joins the coracohumeral ligament,3 contributes to the biceps pulley and forms part of the rotator interval. The lateral insertion of the SGHL means that this structure plays a crucial role in the stabilisation of the biceps tendon against anterior shearing stress as part of the pulley system. Arthroscopically it is best seen from the A portal and can be made more visible by bringing the shoulder into adduction (Figure 1).

Keywords arthroscopy; patient positioning; portals; shoulder anatomy

Gleno-humeral joint arthroscopy Once intra-articular access has been gained with the arthroscope, as described in part 1 of this article, it is important to conduct a systematic and thorough examination of the shoulder. This usually, but not always, starts with the gleno-humeral joint. Fundamental to any surgical procedure is a good knowledge of anatomy and its variants to ensure that all abnormalities are recognised, and just as importantly, that variants are not misdiagnosed as being pathological. Shoulder capsule The use of arthroscopy has led to a better appreciation of the structure and function of the capsule and its definable anatomic components. The capsule can be considered as a watertight

Simon Boyle MSc FRCS(Tr&Orth) Shoulder Fellow, Alps Surgery Institute, Clinique Generale, Annecy, France. Manuel Haag MD Shoulder Fellow, Alps Surgery Institute, Clinique Generale, Annecy, France. David Limb BSc FRCSEd(Orth) Consultant Orthopaedic Surgeon, Department of Orthopaedics and Trauma, Leeds General Infirmary, Leeds, UK. Figure 1 HH e humeral head, SSc Subscapularis, SGHL Superior glenohumeral ligament, MGHL Middle glenohumeral ligament, BT Biceps tendon.

Laurent Lafosse MD Shoulder Surgeon, Alps Surgery Institute, Clinique Generale, Annecy, France.

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Middle gleno-humeral ligament (MGHL) This ligament is present in 84e92% of shoulders1,2,4 and arises variably from the upper part of the glenoid, the labrum, or with the SGHL. It then runs diagonally downward and across the subscapularis tendon at 45 to insert into the inferior part of the lesser tuberosity. Its superior border is usually easily identifiable as it courses away from the SGHL. The interval between the two ligaments forms the entrance to the subscapular bursa through the foramen of Weitbrecht. The appearance of the MGHL is also subject to common variations  a cord like MGHL (17e22%1,2)  Buford complex19 which comprises  cord like MGHL  arising from the superior labrum  with an absent anterior superior labrum between the MGHL origin and the mid-glenoid notch  an absent or thin MGHL The importance of the morphology of the MGHL may well affect the stress that certain anatomical variations put on the biceps anchor, potentially predisposing to SLAP tears. Arthroscopically, the MGHL can be seen through the A or D portals (Figure 2). Special care should be taken to ensure it is carefully assessed at its humeral insertion to avoid missing a humeral avulsion of the gleno-humeral ligaments (HAGL) lesion at this level.

Figure 3 IGHLa. The prominent anterior edge of the IGHLa can be seen easily in some shoulders.

Arthroscopically the anterior band of the IGHL is best seen through the A portal and occasionally a thickened anterior edge can be discerned7 (Figure 3). Improved visualisation of this band may require abduction and external rotation of the arm to bring it under tension and into view. Further dynamic testing of these ligaments involves performing translational movements of the humeral head and observing the structures and their tension (Figure 4). Disruption of the IGHL should be carefully looked for due to its important role in shoulder stability. The glenoid or humeral attachment may be disrupted on either band predisposing to instability (Figure 5). The ability to pass the arthroscope between the humeral head and the glenoid at the level of the IGHLa is known as the drive through sign. This was originally considered to be a sign of shoulder instability but more recent work suggests that it is associated with shoulder laxity and is not specific for instability.8

Inferior gleno-humeral ligament (IGHL) Cadaveric studies have revealed that this structure is found in 75e93% of shoulders.4,6 The IGHL has an anterior band (IGHLa) which takes origin from the glenoid between the 2 and 5 o’clock positions and a posterior band (IGHLp) which takes origin from the 7e9 o’clock position. These converge to form a sling which inserts onto the humerus in the 4e8 o’clock position. This anatomical arrangement dictates that the IGHL acts as the main static stabiliser of the GHJ in abduction. The intervening capsular tissue between the two bands represents the axillary pouch.

Figure 4 IGHLa. These fibres can be seen forming a sling around the humeral head as they descend into the axillary pouch.

Figure 2 Cord like MGHL. SSc subscapularis, HH humeral head.

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Figure 7 Sagittal schematic of subscapularis recess.24

bursa when present. This is a useful area to park sutures when performing intra-articular procedures such as subscapularis repairs and biceps tenodeses. A final bursa may be found between the coracobrachialis anteriorly and subscapularis posteriorly corresponding to our previously described sub-coracoid space. This is generally approached from the subacromial region after identifying the coracoid via the CAL. Occasionally this communicates with the subscapular bursa. These areas can be sites of loose body settling and should therefore always be examined.

Figure 5 Inferior HAGL lesion.

Gleno-humeral joint recesses and bursae Between the gleno-humeral ligaments exist a variable number of recesses in the anterior capsule. Their existence is dependant on the presence of the gleno-humeral ligaments and their variation has been classified by DePalma into six different types.9 The synovial recess seen above the MGHL is known as the superior subscapular recess or foramen of Weitbrecht, and in most cases this opens into the subscapular bursa (Figure 6). This bursa lies between the subscapularis tendon and the glenoid neck and saddlebags the top of the subscapularis tendon10 (Figure 7). It can be followed along the superior border of the subscapularis tendon and reaches further medially between the subscapularis muscle and the coracoid process for several centimetres. This space is utilised arthroscopically to perform subscapularis releases and to approach the brachial plexus and subscapular nerves when needed. The synovial recess below the MGHL is known as the inferior subscapular recess and corresponds to the sub-coracoid foramen of Rouvie`re. This communicates with an inferior subscapular

Labrum This ring of fibrous tissue produces a circumferential lip on the glenoid. It would be convenient to compare the labrum to the menisci of the knee but in actual fact, there is very little fibrocartilaginous tissue in the labrum.11 Its fibres are arranged in a predominantly circumferential pattern although a superficial randomly arranged layer and a deep layer organised into dense insertional fibre bundles can be discerned on electron microscopy.12,13 The labrum, as well as forming an origin for the glenohumeral ligaments and biceps anchor, also provides a static role in gleno-humeral stability. It deepens the socket by up to 50% leading some authors to attribute to it a ‘‘chock block’’ function, limiting humeral translation. It also aids in the concavity compression role of the rotator cuff. Anatomical variations are seen most commonly in the anterosuperior segment of the labrum. A sub-labral foramen (Figure 8) has been reported in 12e19% of shoulders2,5 and a Buford complex (Figure 9) reported in up to 1.5% of shoulders.1,5 These areas should be carefully assessed and probed so as not to be confused with a traumatic anterior labral injury (Bankart lesion). As these lesions are not pathological, an unwarranted repair can lead to a poor outcome. A non-pathological meniscal variant has also been described in up to 15% of shoulders giving the appearance of a free edge.14 Again this should be probed to prevent unnecessary treatment. Below its equator, the labrum attaches to the glenoid in a consistent manner with good fixation to bone. The labrum is best viewed initially through the A portal and probed through the D or E portal to assess its integrity. The view of the posterior labrum can be improved by either displacing the

Figure 6 Foramen of Weitbrecht.

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The function of the RI and its components is to restrict inferior and posterior translation of the humeral head via the SGHL and CHL as well as limiting external rotation. A second, more subtle, role for the RI is to maintain a negative intra-articular pressure. Its lateral components are essential to maintain the stability of the biceps tendon. Arthroscopy has promulgated the study of the function of the RI and its disorders. Lesions of the RI have been classified by Nobuhara and Ikeda16 into two types. Type I lesions are those leading to a contracture of the RI eg. adhesive capsulitis and type II lesions lead to RI laxity. Alternative methods of classification include naming the lesion according to the individual structure involved and newer entities such as coracoid impingement and biceps instability are described. The normal dimensions of the RI have been reported at the level of the glenoid, and these define a normal RI of 21.6 mm without joint distension and 27.8 mm with fluid distension. These measurements serve as guidelines for assessing laxity during arthroscopic procedures although practically this is difficult to measure. The RI can be viewed intra-articularly through the A portal or extra-articularly through the C or D portals, where it also serves to provide access to the GHJ.

Figure 8 Sublabral hole.

humeral head anteriorly or changing the viewing portal to the D portal. The rotator interval The rotator interval (RI) remains an area of great fascination, debate and confusion. It is located in the anterior shoulder and continues to be implicated in various pathologies, particularly with regard to instability and stiffness. It is triangular in shape with its base at the coracoid process, its apex is the inter-tubercular groove, the inferior margin is the superior border of the subscapularis tendon and its superior margin is the inferior border of the supraspinatus tendon. The contents of the RI are the SGHL, biceps tendon, the coracohumeral ligament and the gleno-humeral joint capsule. The organisation of the layers of the rotator interval has been studied, and these differ from the medial part of the interval, where two layers can be defined, to the lateral part where four layers can be identified.15

The coracohumeral ligament (CHL) This irregular trapezoidal structure is located in the rotator interval. It originates from an extra-articular location via two roots; a ventral root arising from the anterior part of the dorsolateral coracoid and the dorsal root arising from the base of the coracoid. Both of these roots lie beneath the CA ligament, after which the CHL takes a course parallel to the long head of biceps tendon, through the interval, although its insertion laterally is subject to enormous variation. The most common variant is insertion into the interval itself, and less commonly the CHL inserts into supraspinatus tendon, subscapularis tendon or occasionally both17 (Figure 10). The CHL is thought to represent a phylogenetic remnant of a redundant pectoralis minor tendon.32 However debate

Figure 9 Buford complex.

Figure 10 CHL running parallel to the biceps in the RI.

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continues as to whether the CHL truly represents a distinct anatomical entity or whether it is a further capsular thickening. Its function is considered to be one of limiting external rotation with the arm in adduction29,33 but it also has a role in providing resistance to inferior translation of the humeral head.20,29,34 The CHL as a structure is particularly important to shoulder arthroscopists for several reasons. The first is that it is considered to be the primary structure affected by adhesive capsulitis21 and therefore any arthroscopic surgical release should address this. Secondly, it acts as an anatomic landmark to guide the arthroscopist towards the coracoid process and therefore the conjoint tendon, plexus etc. Finally, its ablation or transgression provides a route of entry to the glenohumeral joint through anterior portals. The biceps tendon The long head of biceps tendon (LHBT) is an intra-articular shoulder structure but remains extra-synovial. The tendon is enveloped in a synovial sheath which terminates in a blind pouch at the distal end of the bicipital groove. The LHBT is important to the arthroscopist both in terms of its landmark function but also as a source of pathology and symptoms. It can be considered to have three different sections: the biceps anchor, the intra-articular tendinous portion and the pulley system.

Figure 12 Intra-articular biceps tendon (BT). RI Rotator interval.

exiting through the pulley system. This intra-articular part of the tendon is on average 100 mm in length. Its cross section changes from an oval shape near the glenoid after which it becomes more tapered as it approaches the bicipital groove to finally become more rounded.

The biceps anchor (Figure 11): 40e60% of the LHBT fibres arise from the supra-glenoid tubercle, and this lies 5 mm medial to the superior rim of the glenoid.22 The remaining fibres arise from the glenoid labrum. The anchor is the site of the Superior Labral Anterior Posterior lesion (SLAP) as coined by Snyder in 1990,23 commonly seen in overhead throwing athletes and after traction injuries. Arthroscopically, SLAP lesions can be assessed using the Peel back test,24 whereby the anchor is visualised whilst the arm is placed in abduction and external rotation. The integrity of the anchor can be seen and graded.

The pulley system (Figures 13 and 14): The LHBT is stabilised as it exits the shoulder via the pulley system prior to entering the bicipital groove. The pulley has four components, these being the supraspinatus and subscapularis tendons, the CHL and the SGHL. Floor e this is formed largely by fibres from subscapularis, intermingled with the other three components of the pulley and becomes fibrocartilaginous in the groove. Medial Sling e the SGHL parallels the LHBT in the RI but as it enters the pulley, it forms a U shaped sling inserting just above subscapularis on the lesser tuberosity.

Intra-articular tendinous portion (Figure 12): From its site of attachment, the LHBT then passes obliquely along the RI before

Figure 11 Biceps anchor. BT Biceps tendon.

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Figure 13 Medial sling of pulley.

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Figure 15 Anterior 3D representation of Type II subscapularis tear. Figure 14 Lateral sling of pulley.

Subscapularis tears can be classified as follows.29 I e partial lesion only involving the upper 1/3 of subscap II e complete lesion of the upper 1/3 (see Figures 15 and 16) III e complete lesion of the upper 2/3 IV e complete lesion of the tendon but the head remains centred and Goutallier 3 V e complete lesion with an eccentric head position and coracoid impingement and Goutallier 4 (Goutallier grades refer to fatty degeneration of the muscle belly) In retracted tears, the subscapularis can be traced medially and may require the use of a supplementary portal to effect a release eg. portal C for viewing with an instrument such as a shaver or radiofrequency probe in D or E.(Figure 17).

Roof and Lateral wall e this is formed by the fibres of the CHL crossing the groove and also from a tendinous slip from supraspinatus extending to join subscapularis.25 These intimate relations dictate that the arthroscopist should carefully evaluate the tendons of supraspinatus and subscapularis in cases of biceps tendon instability.26,27 After probing the anchor and pulley, the LHBT can be dynamically tested by performing internal and external rotation manoeuvres. Dislocation is manifested by the tendon moving completely out of the groove. The intra-tubercular potion of the tendon can be visualised by pulling it into the joint using a probe. The macrostructure of the LHBT can be graded as follows with treatment recommendations for each of these.28 0 e normal I e <50% of tendon affected (localised lesion or fibre rupture) II e >50% of tendon affected (erosion/partial rupture) III e tendon rupture

Supraspinatus: This muscle arises from the supraspinous fossa via 2 muscle bellies to insert onto the greater tuberosity. From the anterior fusiform belly arises a central tendon which migrates

The rotator cuff The rotator cuff tendons lie beneath the deltoid and are vital in enabling movement and providing stability to the shoulder joint. The cuff comprises of 4 muscles e subscapularis, supraspinatus, infraspinatus and teres minor. Subscapularis: This is the largest and most powerful of the rotator cuff muscles. Its large origin from the upper 2/3 of the anterior surface of the scapula condenses laterally to pass under the coracoid. The upper 2/3 has a tendinous morphology whilst the fibres of the lower 1/3 remain muscular. It attaches to the lesser tubercle adjacent to the biceps groove. The upper 1/3 of the subscapularis tendon can be viewed intra-articularly through the A portal and its integrity can be assessed by probing. To improve the view of the subscapularis insertion, internal rotation should be applied to the arm. There should be a high index of suspicion for a subscapularis tear in the presence of an anterior pulley rupture.

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Figure 16 Intra-articular view of type II subscapularis tear seen through the posterior A portal.

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Infraspinatus: This thick, triangular, multipennate muscle arises from the infraspinous fossa after which its fibres converge into a tendon that passes across the posterior aspect of the glenohumeral joint. The tendon overlaps the posterior border of the supraspinatus tendon, where it is almost impossible to distinguish the two. Footprint e the tendon inserts via a trapezoidal footprint onto the middle facet of the greater tuberosity with average dimensions of 29  19 mm33 (Figure 18). As with the supraspinatus tendon, this area provides a good base for tendon to bone healing. The infraspinatus insertion lies immediately adjacent to the articular cartilage at its superior aspect but a gap of 16 mm develops inferiorly. This gap between the superior and inferior insertions represents the bare area (Figure 19). Teres minor: This muscle takes origin from the dorsal surface of the lateral border of the scapula and the dense fascia of infraspinatus. It then passes laterally, across the back of the shoulder joint, to form a tendon which inserts onto the inferior facet of the greater tuberosity. As the tendon passes over the capsule, its fibres become adherent and impossible to separate with blunt dissection. The inferior border of the teres minor tendon forms the superior boundary of the quadrilateral space which transmits the posterior circumflex humeral artery and axillary nerve.

Figure 17 Cable and crescent configuration in Supraspinatus.

anteriorly, thickens and forms an external extra-muscular tendon comprising 40% of the overall width of the tendon. The posterior 60% is flatter and arises from a unipennate muscle belly. These differences in muscle belly sizes and tendon dimensions results in a 2.88 times greater stress in the anterior supraspinatus tendon which may be a risk factor for this common site of tearing.18 The supraspinatus tendon has been divided into four structurally independent subunits based on histological and biomechanical studies30 as follows: 1. Tendon proper e extends from the musculotendinous junction to 2 cm medial to the greater tuberosity. The collagen fibres in this region are parallel. 2. Rotator Cable (Figure 13) e this band of densely packed unidirectional collagen fibres extends from the CHL anteriorly to the inferior border of infraspinatus posteriorly. The rotator cable surrounds the thinner crescent where the cable here is thought to act as a stress shield to protect the weaker crescent. Because of this effect, a tear of the rotator crescent may have no discernable functional deficit in the shoulder when the integrity of the rotator crescent is maintained. A suspension bridge analogy has been drawn here by Burkhart31 to explain this phenomenon where the cuff can be anatomically deficient but biomechanically intact. In these situations, the cable ensures that a balance of the force couples is maintained. 3. Fibrocartilage attachment e extends from the tendon proper to the greater tuberosity 4. Capsule e composed of thin collagen sheets with a uniform fibre alignment. The supraspinatus tendon inserts into the superior and middle facets of the greater tuberosity. Normally, a margin of 0.9 mm (0e4 mm) exists between the articular cartilage and the supraspinatus insertion, extending from the top of the bicipital groove to the top of the bare area. From this initial insertion, the tendon extends w16 mm laterally onto the tuberosity forming the footprint. This gives a wide zone of tendon to bone contact and recreating this forms the basis of the double row technique of rotator cuff repair (see Figure 18).

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Bones and cartilage The glenoid: The glenoid concavity has three components; bone, articular cartilage and the soft tissue labrum. It is shaped like an inverted comma with a broader inferior portion and a thinner superior tail. The average vertical dimension is 35 mm and average horizontal dimension is 25 mm. 75% of glenoids are retroverted overall with regard to the plane of the scapula with an average superior tilt of 15 , though the situation in reality is more complex than this and the version alters as one moves from superior to inferior parts.34 It is formed from two ossification centres that can be roughly separated by a transverse line between the two regions of the glenoid (Figure 20).

Figure 18 Anatomical model showing the footprint of the supraspinatus tendon (green), infraspinatus (red), teres minor (black) and subscapularis (blue).46

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Figure 19 Bare area.

Figure 21 Glenoid bare spot.

The glenoid fossa is covered by hyaline cartilage, which is thicker at the periphery than in the centre. This serves to deepen the concavity of the glenoid. The thin area of discolouration in the centre corresponds to the bare spot of the glenoid (Figure 21). This represents an area of cartilage thinning with underlying subchondral bone thickening35 probably due to the increased loads experienced in this region. The geometry of the glenoid bone and cartilage contributes 50% of the depth of the glenoid concavity, with the remaining 50% coming from the labrum. Arthroscopically the glenoid should be inspected in its entirety with regard to shape, size, fractures, cartilage defects and the course of the labrum. Probing of these structures may be necessary the extent and depth of any cartilage lesions. The glenoid is best visualised initially through the A portal and

a probe introduced through the D portal. For ease of description and communication of cartilage lesions we prefer to use the classification introduced by Outerbridge.36 We also use a system of letters (AeF) representing six segments of the glenoid to describe the location of any pathology. The A segment represents the superior segment and these progress to the postero-superior F segment (see Figure 22). The three division lines for these are a transverse line through the equator and a two further lines passing at 60 to this passing through the centre. Humeral head: The humeral head articular surface forms 1/3 of a near true sphere37 which is retroverted a mean of 25e3538 and has a superior inclination of 130 . The anterior border is limited by the lesser tuberosity and the lateral border by the greater tuberosity. The inter-tubercular groove lies between the two. A bare area exists on the posterolateral humeral head, adjacent to the infraspinatus tendon. This contains osseous pits

Figure 20 Glenoid ossification centres.

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Figure 22 Sectors of the glenoid.

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Figure 23 Humeral head with anterior translation in hyperlaxity. Figure 24 Traumatic Hill-Sachs lesion. Note the area of cartilage lateral to the Hill-Sachs (HS) lesion.

which represent previous sites of vessel penetration. The bone here should be assessed carefully and not confused with a traumatic Hill-Sachs lesion. The humerus is best examined through the A portal and probed through an anterior portal for any suspected fractures or cartilage defects. Cartilage lesions are classified by the Outerbridge system and, like the glenoid, the humerus can be divided into 6 segments for ease of description in a similar fashion to the glenoid. These are based on a line passing through the equator, and two further lines at 60 to this. The segments are named as follows: I e antero-superior III e centro-superior V e postero-superior II e antero-inferior IV e centro-inferior VI e postero-inferior Arthroscopy of the humeral head is very much a dynamic process, with rotation, translation, abduction and adduction movements all essential to enable an adequate inspection. It is also important to inspect for any soft tissue or bony avulsions of the gleno-humeral ligaments (HAGL lesions) especially in cases where instability is suspected. Stability can also be dynamically assessed by repeating translational movements (Figure 23). The size depth and position of engagement of a Hill-Sachs lesion can be assessed at this point (see Figure 24).

The scope is best directed towards the antero-lateral corner of the acromion when performing bursoscopy through the A portal to ensure successful entry. Not infrequently, the SA bursa extends laterally into the sub-deltoid bursa. Where adhesions are present from inflammation or previous surgery, a bursectomy is needed to improve visualisation. During bursoscopy, the bursal side of the rotator cuff can be seen, although the overlying bursal tissue may need to be removed with a shaver. The bursal side of the cuff is then inspected for tears, their shape, the tendon involved, its reducibility and the quality of the tendon involved. Calcific deposits can be probed for and evacuated on this side of the cuff. The C portal is the best portal for assessing antero-superior cuff tears in the SA space after an initial view has be obtained from the A portal. Extra-articular subscapularis tendon evaluation can be performed by moving anteriorly and inferiorly from the subacromial space back down to the ground floor. This is best performed through the C or D portal. Acromion: The acromion is one of the most studied parts of the shoulder largely due to its presumed role in impingement and rotator cuff pathology. The main role of the acromion in bipeds is to provide a lever arm and a strong arched origin for the powerful deltoid muscle. The acromion forms from three ossification centres, which usually fuse by the age of 25,40 and failure of any of these centres to unite can lead to an os acromiale. This has a mean incidence of 8% and most commonly it is an incidental finding. These lesions can be defined as a pre-acromion, meso-acromion (most common), met-acromion and basi-acromion. The morphology of the intact acromion has been described and classified by Bigliani into three different types. I e Flat II e Curved III e Hooked

Sub-acromial space Sub-acromial bursa: The subacromial bursa lies between the anterior rotator cuff and the acromion and provides an excellent bloodless field for the initial visualisation of the first floor of the house.39 It is a synovial-lined sac that acts to reduce friction and improve gliding between the rotator cuff and the coraco-acromial arch. The SA bursa lies more anteriorly than many surgeons appreciate, which may explain the difficulty that some arthroscopists have in gaining access to the bursa first time. As a guide, the mean distance to the posterior aspect of the bursa from the antero-lateral edge of the acromion is 2.8 cm or 55% of the AP acromial length. The degree to which the bursa crosses the ACJ is variable and in some cases it does not cross not at all.

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Numerous authors have associated the type III hooked acromion with rotator cuff tears. A convex41 and a keeled42 acromion have also been described. The acromion also takes the attachment of the coraco-acromial ligament and forms an articulation with the clavicle, both of which are discussed below.The acromion is visualised through the A portal and C portals, both of which can be used for instrumented resections. The undersurface of the acromion should normally be seen to be covered with the CAL and periosteum. The shape of the tip and the presence of an os acromiale should also be checked. Dissection of the anterior aspect of the acromion and ACJ often leads to bleeding due to the inadvertent division of the acromial branch of the thoracoacromial trunk.

A third centre at the tip ossifies later although occasionally this fails. The coracoid forms the site of attachment for several tendons and ligaments and can almost be considered to have a starfish type appearance when viewed from the front. Superiorly are the coraco-clavicular ligaments (conoid and trapezoid), inferiorly lies the conjoint tendon, laterally emanates the CHL and CAL and infero-medially courses the pectoralis minor tendon. Inferomedial to the coracoid lie the neurovascular structures of the plexus and axillary vessels and passing directly beneath the coracoid is the tendon of subscapularis. Arthroscopically the coracoid is a vital landmark which serves to orientate the surgeon prior to commencing several procedures eg. the origin of the CHL for an extra-articular arthroscopic arthrolysis in adhesive capsulitis, and the graft site for the arthroscopic Latarjet procedure. The coracoid is best visualised through the C portal with instrumented dissection through the D portal (Figure 26).

Coraco-acromial ligament (CAL): This strong triangular ligament forms the anterior part of the coracoacromial arch. It is separated from the rotator cuff by the subacromial bursa and is strongly implicated in impingement syndrome. Its origin is from a broad area on the lateral aspect of the coracoid. Its apex inserts onto the antero-medial and anteroinferior surfaces of the acromion. Commonly, distinct bands can be found e antero-lateral and postero-medial e although this is subject to variation.43 Spurs of the ligament occur preferentially in the antero-lateral band so it is important to completely visualise the antero-lateral corner of the acromion when examining this ligament with regard to a subacromial decompression.33 The CAL is best viewed through the A and the C portals (Figure 25). When viewed through the A portal, the fibres can be seen on the undersurface of the acromion passing obliquely to the coracoid. In its degenerate state, the normal white fibres can be seen to be frayed. Coracoid: The coracoid is found at the base of the neck of the glenoid and projects anteriorly before hooking antero-laterally and flattening. It has two and occasionally three ossification centres, the second of which appears at around 10 years of age and contributes to the formation of the upper part of the glenoid.

Acromio-clavicular joint (ACJ) This articulation between the clavicle and the acromion is often the ‘site of degeneration associated with pain, osteophyte formation or traumatic separation, hence its importance in arthroscopic surgery. It is a diarthrodial joint with the articular surfaces being separated by an intra-articular disc of varying size and shape. The angle of the joint is variable, but in most cases it is orientated supero-lateral to infero-medial. The lateral end of the clavicle has a convex articular surface whereas that of the acromion is concave. The joint capsule is thickest on is anterior, medial and superior surfaces although dissection of this area is required to identify this joint fully. Further aids to identification include applying pressure to the clavicle and observing its movement and the placement of a needle directly in the joint. The ACJ can be viewed through the A portal (Figure 27) and the lateral C portal and it is instrumented through the C and E portal most easily.

Figure 25 Coracoacromial ligament.

Figure 26 Coracoid process (CP) and Conjoint tendon (CT) post dissection.

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8 McFarland EG, Neira CA, Gutierrez MI, Cosgarea AJ, Magee M. Clinical significance of the arthroscopic drive-through sign in shoulder surgery. Arthroscopy 2001; 17: 38e43. 9 DePalma AF. In: Regional, variational and surgical anatomy. Surgery of the shoulder. 3rd edn. Philadelphia: JB Lippincott, 1983. 10 Grainger AJ, Tirman PF, Elliott JM, Kingzett-Taylor A, Steinbach LS, Genant HK. MR anatomy of the subcoracoid bursa and the association of subcoracoid effusion with tears of the anterior rotator cuff and the rotator interval. AJR Am J Roentgenol 2000; 174: 1377e80. 11 Moseley HF, Overgaard B. The anterior capsular mechanism in recurrent anterior dislocation of the shoulder. Journal of Bone and Joint Surgery Br 1962; 44: 913e27. 12 Nishida K, Hashizume H, Toda K, Inoue H. Histologic and scanning electron microscopic study of the glenoid labrum. J Shoulder Elbow Surg 1996; 5: 132e8. 13 Tamai K, Higashi A, Tanabe T, Hamada J. Recurrences after the open Bankart repair: a potential risk with use of suture anchors. J Shoulder Elbow Surg 1999; 8: 37e41. 14 Snyder SJ. Shoulder arthroscopy. Philadelphia: Lippincott Williams and Wilkins, 2003. 15 Jost B, Koch PP, Gerber C. Anatomy and functional aspects of the rotator interval. J Shoulder Elbow Surg 2000; 9: 336e41. 16 Nobuhara K, Ikeda H. Rotator interval lesion. Clin Orthop Relat Res 1987; 223: 44e50. 17 Yang HF, Tang KL, Chen W, et al. An anatomic and histologic study of the coracohumeral ligament. J Shoulder Elbow Surg 2009; 18: 305e10. 18 Di Giacomo G, Pouliart N, Costantini A, De Vita A. Atlas of functional shoulder anatomy. Milan: Springer-Verlag Italia, 2008. 19 Ferrari DA. Capsular ligaments of the shoulder. Anatomical and functional study of the anterior superior capsule. Am J Sports Med 1990; 18: 20e4. 20 Ovesen J, Nielsen S. Experimental distal subluxation in the glenohumeral joint. Arch Orthop Trauma Surg 1985; 104: 78e81. 21 Bunker TD, Anthony PP. The pathology of frozen shoulder. A Dupuytren-like disease. J Bone Joint Surg Br 1995; 77: 677e83. 22 Vangsness Jr CT, Jorgenson SS, Watson T, Johnson DL. The origin of the long head of the biceps from the scapula and glenoid labrum. An anatomical study of 100 shoulders. J Bone Joint Surg Br 1994; 76: 951e4. 23 Snyder SJ, Karzel RP, Del Pizzo W, Ferkel RD, Friedman MJ. SLAP lesions of the shoulder. Arthroscopy 1990; 6: 274e9. 24 Burkhart SS, Morgan CD. The peel-back mechanism: its role in producing and extending posterior type II SLAP lesions and its effect on SLAP repair rehabilitation. Arthroscopy 1998; 14: 637e40. 25 Clark JM, Harryman 2nd DT. Tendons, ligaments, and capsule of the rotator cuff. Gross and microscopic anatomy. J Bone Joint Surg Am 1992; 74: 713e25. 26 Walch G, Nove-Josserand L, Boileau P, Levigne C. Subluxations and dislocations of the tendon of the long head of the biceps. J Shoulder Elbow Surg 1998; 7: 100e8. 27 Walch G, Nove-Josserand L, Levigne C, Renaud E. Tears of the supraspinatus tendon associated with ‘‘hidden’’ lesions of the rotator interval. Journal of Shoulder and Elbow Surgery 1994; 3: 353e60. 28 Lafosse L, Reiland Y, Baier GP, Toussaint B, Jost B. Anterior and posterior instability of the long head of the biceps tendon in rotator cuff tears: a new classification based on arthroscopic observations. Arthroscopy 2007; 23: 73e80. 29 Lafosse L, Jost B, Reiland Y, Audebert S, Toussaint B, Gobezie R. Structural integrity and clinical outcomes after arthroscopic repair of isolated subscapularis tears. J Bone Joint Surg Am 2007; 89: 1184e93.

Figure 27 ACJ post resection of soft tissue and bone ends.

Summary With the correct equipment, skilled anaesthesia and careful positioning shoulder arthroscopy is safe and has proved itself to be one of the most powerful investigative tools for the diagnosis of shoulder pathology. There is a significant learning curve not only because of the awkward anatomical arrangement of the joint, but also because no two shoulders are the same and there is a very wide spectrum of normal findings. However, once triangulation within the joint is mastered and the range of pathological and normal findings is understood it proves to be an excellent tool not only for establishing a diagnosis, but in also providing a minimally invasive method of treatment with success rates catching up with, or surpassing, those reported with open surgical treatment. A

REFERENCES 1 Ide J, Maeda S, Takagi K. Normal variations of the glenohumeral ligament complex: an anatomic study for arthroscopic Bankart repair. Arthroscopy 2004; 20: 164e8. 2 Ilahi OA, Labbe MR, Cosculluela P. Variants of the anterosuperior glenoid labrum and associated pathology. Arthroscopy 2002; 18: 882e6. 3 Pouliart N, Somers K, Eid S, Gagey O. Variations in the superior capsuloligamentous complex and description of a new ligament. J Shoulder Elbow Surg 2007; 16: 821e36. 4 Steinbeck J, Liljenqvist U, Jerosch J. The anatomy of the glenohumeral ligamentous complex and its contribution to anterior shoulder stability. J Shoulder Elbow Surg 1998; 7: 122e6. 5 Williams MM, Snyder SJ, Buford Jr D. The Buford complex e the ‘‘cord-like’’ middle glenohumeral ligament and absent anterosuperior labrum complex: a normal anatomic capsulolabral variant. Arthroscopy 1994; 10: 241e7. 6 De Palma AF, Callery G, Bennett GA. Shoulder joint: Variational anatomy and degenerative regions of the shoulder joint. Vol. 6, 1949. 7 Turkel SJ, Panio MW, Marshall JL, Girgis FG. Stabilizing mechanisms preventing anterior dislocation of the glenohumeral joint. J Bone Joint Surg Am 1981; 63: 1208e17.

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30 Nakajima T, Rokuuma N, Hamada K. Histological and biomechanical characteristics of the supraspinatus tendon: reference torotator cuff tearing. J Shoulder Elbow Surg 1994; 3: 79e87. 31 Burkhart SS, Esch JC, Jolson RS. The rotator crescent and rotator cable: an anatomic description of the shoulder’s ‘‘suspension bridge’’. Arthroscopy 1993; 9: 611e6. 32 Curtis AS, Burbank KM, Tierney JJ, Scheller AD, Curran AR. The insertional footprint of the rotator cuff: an anatomic study. Arthroscopy 2006; 22: 609.e1. 33 DeFranco MJ, Cole BJ. Current concepts: current perspectives on rotator cuff anatomy. Arthroscopy 2009; 25: 305e20. 34 Monk AP, Berry E, Limb D, Soames RW. Laser morphometric analysis of the glenoid fossa of the scapula. Clin Anat 2001; 14: 320e3. 35 Warner JJ, Bowen MK, Deng XH, Hannafin JA, Arnoczky SP, Warren RF. Articular contact patterns of the normal glenohumeral joint. J Shoulder Elbow Surg 1998; 7: 381e8. 36 Outerbridge RE. The etiology of chondromalacia patellae. J Bone Joint Surg Br 1961; 43-B: 752e7.

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37 Boileau P, Walch G. The three-dimensional geometry of the proximal humerus. Implications for surgical technique and prosthetic design. J Bone Joint Surg Br 1997; 79: 857e65. 38 Rockwood CA, Matsen FA, Wirth MA, Lippitt SB. The shouler. 4th edn., vol. 1. Saunders Elsevier, 2009. 39 Yepes H, Al-Hibshi A, Tang M, Morris SF, Stanish WD. Vascular anatomy of the subacromial space: a map of bleeding points for the arthroscopic surgeon. Arthroscopy 2007; 23: 978e84. 40 Liberson F. Os acromiale e a contested anomaly. J Bone Joint Surg Am 1937; 19: 683e9. 41 Vanarthos WJ, Monu JU. Type 4 acromion: a new classification. Contemp Orthop 1995; 30: 227e9. 42 Tucker TJ, Snyder SJ. The keeled acromion: an aggressive acromial variant e a series of 20 patients with associated rotator cuff tears. Arthroscopy 2004; 20: 744e53. 43 Fealy S, April EW, Khazzam M, Armengol-Barallat J, Bigliani LU. The coracoacromial ligament: morphology and study of acromial enthesopathy. J Shoulder Elbow Surg 2005; 14: 542e8.

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Safer surgery: how a checklist can make orthopaedic surgery safer

database has revealed that a high proportion of all surgical patient safety incidents are related to the specialty of orthopaedics and trauma (145,743/446,184 ¼ 32.6%). Other high-risk industries have made great progress in managing the challenges of improving safety and reducing harmful events.5 These industries have all addressed the following issues:  They have accepted that errors are inevitable and provide opportunities to learn and improve from them.  They have built systems that reliably deliver what is required, identify errors that occur and mitigate these to prevent them causing harm.  They have used an understanding of human factors to make the right thing the easiest thing to do, create teams of employees trained in technical and non-technical skills and developed formal models of communication. These changes have delivered significantly safer air travel, a safer nuclear power industry and in some healthcare organizations, substantially better outcomes. Checklists have formed a critical part of these changes for all these industries.

Mark Emerton Sukhmeet S Panesar Kirsty Forrest

Abstract ‘‘Medicine today has entered its B-17 phase. Substantial parts of what hospitals (do) .... are now too complex for clinicians to carry them out reliably from memory alone.’’ 6 In January 2007 the World Health Organization (WHO) began a programme aimed at improving the safety of surgical care globally. The initiative, called ‘‘Safe Surgery Saves Lives’’ aimed to identify minimum standards of surgical care that could be universally applied across countries and settings. One component of the initiative was the introduction of a peri-operative checklist.1 In February 2009 the National Patient Safety Agency (NPSA) issued an alert requiring all hospitals in England and Wales to implement the perioperative checklist by February 2010.2 The main reason for the checklist is to improve patient care by making the operative environment a safer place. But why the need for this checklist and how can it help? What evidence exists that it makes any difference to patient care? What are the essential component parts to the checklist and how can is it introduced? We hope to answer these questions for you in the following text.

Origins of checklists The origins of checklists lie in the aviation industry, where technological advancement surpassed a pilot’s capability to remember all the procedures necessary to fly a new advanced plane. Box 1 is an anecdote taken from of a piece that first appeared in the New Yorker by Atul Gawande.6

The modern day checklist A core set of safety checks has been identified in the form of a WHO surgical safety checklist that can be used in any surgical setting and operating theatre environment. Each step on the checklist is simple, widely applicable, and measurable. It has already been demonstrated that its use can reduce death and major complicationsas a result of Surgery. This has been modified for England and Wales.2 Eight hospitals in different cities, representing a variety of economic circumstances and diverse populations of patients, participated in the introduction of the WHO checklist. Data was collected prospectively on 3955 consecutive surgical procedures before and after the introduction of the Surgical Safety Checklist. The primary end point was the rate of complications, including death, during hospitalization within the first 30 days after the operation. The rate of death was 1.5% before the checklist was introduced and decreased to 0.8% after its introduction (P ¼ 0.003). Inpatient complications occurred in 11.0% of patients at baseline and in 7.0% after introduction of the checklist (P < 0.001).7 An adapted version of the checklist has been developed by the National Patient Safety Agency (NPSA) in collaboration with a multi professional expert reference group for use in England and Wales and can be found at the web address www.npsa.nhs.uk/checklist. The checklist consists of a short series of questions to be asked at three points in time in the peri-operative period. These are: before anaesthesia, before the skin incision and during or just after wound closure. It is to be used for every surgical intervention, including those under local anaesthesia, and it contains the core elements that are expected to be used for most

Why the need? Surgery has been categorised as a very unsafe industry, with a rate of fatal adverse events (catastrophic events per exposure) of 1 per 10 000. In trauma surgery the rate of serious complications is 1 per 100 patient exposures. In contrast, civil aviation, railway transport and nuclear power the rate of death is less than 1 per million exposures.3 In one US surgical centre a death rate due to error of 1 in 270 (0.4%) cases was found, of which 65% (12.6% of all deaths) were deemed preventable.4 The National Health Service (NHS) in the UK, through the National Patient Safety Agency’s (NPSA) National Reporting and Learning System (NRLS), has the largest database of patient safety incidents (PSIs) in the world and has a repository of 900 000 errors annually. To date, over three million incidents have been reported. A soon to be published review (personal communication) of the

Mark Emerton MA FRCS Consultant orthopaedic surgeon and senior fellow NHS Institute for Innovation and Improvement, UK. Sukhmeet S Panesar BSc(Hons) MBBS Chief Medical Officer’s, Clinical Advisor National Patient Safety Agency, National Patient Safety Agency (NPSA)Patient Safety Division, London, UK. Kirsty Forrest FRCS MMEd Consultant anaesthetist, Leeds Teaching Hospital Trust, Clinical training advisor Yorkshire and Humber Deanery, UK.

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Checklists, teamwork and communication

The origins of the checklist

The challenge for the surgical community is to match recent technical improvements with new ways of working that ensure that we achieve safe care for our patients. Having a formal method of communication can improve team performance. It can reduce hierarchy and the fear of speaking up and prepare team members for the expected as well as the unexpected by ensuring everyone understands the plan. Surgeons assume that the scrub nurse remembers what might happen, that the system has delivered the appropriate amount of cross-matched blood, that the correct antibiotics have been given, the images are ready and available and that everyone else knows what is going to happen. This is far from the truth and the rate of surgical error has been shown to be between 47.7% and 50.4%. Almost half of these are preventable.8 Many definitions of a team exist and historically the surgical team would have been seen to be the consultant, registrar and the junior staff for that senior surgeon. However, with the many changes in healthcare and training this perception has to change. The definition of team is those at any point in time that are caring for that patient. Teams are therefore not rigid and stable structures but fluid, changeable and adaptable. This transfers very easily into the theatre environment. All staff groups in theatre are aware of the impact of poor teamwork on the patient. Staff turnover and sickness rates are directly affected by the quality of team performance.9 The most discerning element is whether team members feel safe to speak up if they see something going wrong. Our hierarchical systems prevent junior members of the team from speaking up when an error is set in motion.10 In principle, good teamwork helps avoid error-inducing situations (through anticipation and workload management), improves error detection (through mutual monitoring and support), and generates a better response in a crisis.11 Many studies have shown that errors in surgery are associated with lack of situation awareness and teamwork failure.12,13 Others have identified sustained failure of communication leading to poorer performance in the team.14 Surgical trainees were particularly vulnerable to failures of communication, often through mimicking their poor senior surgical role models. Reasons for communication failures included; poor timing, missing information, unclear purpose, and the wrong audience. In short, critical items of information were delivered incomplete, at the wrong time to the wrong people in the wrong way. The checklist addresses these issues by clarifying communication in the team for that patient at three points in time. This may be something that you think you do already, but when you are under stress, tired and busy things can be missed and do go wrong.

In 1935, the U.S. Army Air Corps held a flight competition for aeroplane manufacturers vying to build its next-generation longrange bomber. In early evaluations, the Boeing plane had trounced other designs. The flight "competition," was regarded as a mere formality. With the most technically gifted test pilot in the army on board, the plane roared down the tarmac, lifted off smoothly, and climbed sharply to three hundred feet. Then it stalled, turned on one wing, and crashed in a fiery explosion. Two of the five crew members died, including the pilot. An investigation revealed that nothing mechanical had gone wrong. The crash had been due to pilot error. Substantially more complex than previous aircraft, the new plane required the pilot to attend to the four engines, a retractable landing gear, new wing flaps, electric trim tabs that needed adjustment to maintain control at different airspeeds, and constant-speed propellers whose pitch had to be regulated with hydraulic controls. While doing all this, the pilot had forgotten to release a new locking mechanism on the elevator and rudder controls. The Boeing model was deemed, as a newspaper put it, "too much aeroplane for one man to fly." The Army Air Corps declared another smaller design the winner. Boeing nearly went bankrupt. Surprisingly, the Army purchased a few aircraft from Boeing as test planes, and some "less technically able" army pilots remained convinced that the aircraft was flyable. They came up with an ingeniously simple approach: they created a pilot’s checklist, with step-by-step checks for takeoff, flight, landing, and taxiing. In the early years of flight, getting an aircraft into the air might have been nerve-racking, but it was hardly complex. But this new plane was too complicated to be left to the memory of any person, however expert. With the checklist in hand, the pilots went on to fly the model a total of 1.8 million miles without one accident. The plane was dubbed the B-17. And with this plane, the American Army gained a decisive air advantage in the Second World War, which enabled its devastating bombing campaign across Nazi Germany.6 Box 1

surgical procedures. The process of implementation differs from previously published checklists in a number of ways. To begin with, the alert has been issued 12 months before it is expected to be in place to allow time for it to be adopted and implemented by the teams of staff that will use it, rather than as an enforced overnight change. There is a lot of evidence that changes developed and delivered by the staff responsible for clinical care are much more effective than edicts from ‘‘on high.’’ The checklist can also be adapted to suit individual hospitals, processes and clinical environments. The layout and timing of particular questions can be changed. The governance arrangements and who asks the questions or records the answers is entirely up to the teams involved. The checklist is deliberately based on an expectation that mistakes happen and can be identified and corrected. In this way it helps deliver the three essential changes, as discussed above, which have improved safety in other high risk industries.

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NOTSS e Non-technical skills for surgeons All of these problems mentioned above can be classified as nontechnical skills that need to be learnt by trainees. These have been researched and catagorised into the following: 1. Situation awareness 2. Decision making 3. Communication and teamwork 4. Leadership There are behavioural markers associated with each category so that they can be modeled, taught and assessed in the workplace. Interestingly many of the behavioural markers are seen by

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putting into practise the peri-operative checklist, showing the importance of non-technical skills and how they are inherently linked to patient safety.15

Every surgeon will have experienced the frustrations of a list that is full of delays and appears poorly prepared. These lists are often performed amidst growing friction and failing communication. These feel difficult: errors and poorer clinical outcomes are much more likely.6 Most surgeons will also have experienced a really good list where things flow smoothly and everything falls into place. The work is completed more quickly, with less effort and better outcomes. The second scenario is much more likely with the use of a checklist. As with many things in life ‘it’s not what you do but the way that you do it’. It is not just the specific points on the checklist that make safer healthcare but it is the spirit in which it is used, and the team building that goes alongside it that are the important factors.

Briefings The WHO checklist is a simple means of preventing potentially catastrophic error and harm to patients. Further improvements in teamwork with all the associated benefits for patients and staff can be delivered through briefings before and de-briefings at the end of a theatre list. These are particularly effective at flattening hierarchy and making all team members feel comfortable about speaking up. In one local hospital a checklist for briefings and debriefings has been developed. It begins with each member of the team introducing themselves and stating their role for the day. The briefing goes on to discuss equipment, anaesthetic and other issues (such as positioning and patient placement post surgery), any expected risks such as blood loss, staff leaving for other meetings and x-ray requirement. The briefing finishes with the question ‘are any of the staff are concerned about patient safety for that day’. At the end of the list a debriefing takes place. This goes though the following questions: What went well today? Did anyone have any concerns about the list? Were there any specific equipment issues? Is there anything we could do to make the list safer? Is there anything that could do to make the list more productive? In addition, comments and ‘glitches’ are collected so that any recurrent problems can be highlighted. The very first step of introducing yourself by name and role in the team could be seen by outsiders as redundant. But we would like to ask you to think in the next theatre list that you participate in (that does not have a briefing beforehand!) e can you name everyone in the theatre and do you know what they doing there? Briefings help identify potential hazards such as list changes, missing equipment and staff problems and allow team members to highlight individual or technical problems easily and safely. In some ways this could be seen like a sports team meeting, defining roles, what to do when it doesn’t go as expected and sorting out the game plan. It is not uncommon on the flight deck to hear pilots specifically asking their colleagues to support them if they recognize a potential reason for sub-optimal performance such as fatigue or personal issues. When raised at a briefing these can strengthen the team and focus all the resource in the room on the patients’ needs rather than causing in increased tension and failing communication as stress levels rise. Where briefings have been added to the checklist the growing, as yet anecdotal, evidence suggests that it delivers major improvements in team performance. These include reduced errors, better preparedness, more motivated happier staff and smoother lists. It also appears that the efficiency of lists is improved with reduced turn round and procedure time due to fewer delays and staff being more proactive in creating the perfect list. (Personal communication)

Conclusion Training in surgery focuses on technical skills. Whilst essential, this fails to recognize that surgeons cannot perform to the best of their technical ability unless in a well functioning team. Better teamwork and communication in operating theatres improves outcomes. Teamwork is definable and measurable and can be improved through formal structured communication, such as checklists. Healthcare, and surgery in particular, is a team game yet we have ignored the experience of other high risk industries to our patients cost. The WHO checklist and associated briefings and debriefings are a major step forward in our approach to delivering the safe reliable care we would want for our family, to all our patients. ‘‘It’s ludicrous, though, to suppose that checklists are going to do away with the need for courage, wits, and improvisation. The body is too intricate and individual for that: good medicine will not be able to dispense with expert audacity. Yet it should also be ready to accept the virtues of regimentation.’’6 A

REFERENCES 1 World Health Organisation (WHO). Safe surgery saves lives. The second global patient safety challenge. Available online at: http://www.who.int/ patientsafety/safesurgery/en/index.html. Last accessed on 25 Jul 2009. 2 National Patient Safety Agency (NPSA). The safer surgery alert. Available online at: http://www.npsa.nhs.uk/nrls/alerts-anddirectives/alerts/safer-surgery-alert/. Last accessed on 25 Jul 2009. 3 Amalberti R, Auroy Y, Berwick D, et al. Five system barriers to achieving ultrasafe health care. Ann Intern Med 2005; 142: 756e64. 4 Calland JF, Adams RB, Benjamin DK, et al. Thirty-day postoperative death rate at an academic medical center. Ann Surg 2002; 235: 690e6. 5 Helmreich RL. On error management: lessons from aviation. BMJ 2000; 320: 781e5. 6 Gawande A. The Checklist. The New Yorker 10th December 2007. Available online at: http://www.newyorker.com/reporting/2007/12/10/ 071210fa_fact_gawande?currentPage ¼ all. Last accessed on 25 Jul 2009. 7 Haynes AB, Weiser TG, Berry WR, et al. Safe surgery saves lives Study Group. A surgical safety checklist to reduce morbidity and mortality in a global population. N Engl J Med 2009; 360: 491e9. 8 Sarker SK, Vincent C. Errors in surgery. Int J Surg 2005; 1: 75e81. ¨ki M, Vanhala A, Pentti J, et al. Team climate, intention to leave 9 Kivima and turnover among hospital employees: prospective cohort study. BMC Health Serv Res 2007; 23: 170. 10 Bromiley M. Have you ever made a mistake? The royal college of anaesthetists bulletin 2008; 48: 2442e5.

How to introduce the checklist The use of checklists is gathering pace. Where the checklist is used, by early adopter’s, their lists appear to be running more smoothly, word gets out and its use spreads. You can download the WHO checklist online and adapt it to your local area of work.2

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11 Mishra A, Catchpole K, Dale T, et al. The influence of non-technical performance on technical outcome in laparoscopic cholecystectomy. Surg Endosc 2008; 1: 68e73. 12 Catchpole K, Bell MD, Johnson S. Safety in anaesthesia: a study of 12 606 reported incidents from the UK National Reporting and Learning System. Anaesthesia 2008; 63: 340e6. 13 Elbardissi AW, Wiegmann DA, Henrickson S, et al. Identifying methods to improve heart surgery: an operative approach and

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strategy for implementation on an organizational level. Eur J Cardiothorac Surg 2008; 34: 1027e33. 14 Lingard L, Espin S, Whyte S, et al. Communication failures in the operating room: an observational classification of recurrent types and effects. Qual.Saf Health Care 2004; 13: 330e4. 15 Yule S, Flin R, Maran N, et al. Surgeons’ non-technical skills in the operating room: reliability testing of the NOTSS behaviour rating system. World J Surg 2008; 32: 548e56.

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CME SECTION

CME questions based on the Mini-Symposium ‘‘Revision Hip Surgery’’ C Explant device D Screwdriver E Spring tensioned suction device

The following series of questions are based on the MiniSymposium on ‘‘Revision Hip 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. After completing the questionnaire, either post or fax the answer page to the Orthopaedics and Trauma Editorial Office at the address at the bottom of the RESPONSE sheet. Please photocopy this page if you wish to keep your copy of Orthopaedics and Trauma. Replies received before the next issue of the journal 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, via email, for your records.

5 An acetabular component is investigated prior to revision and it is found that there is a distorted but intact rim with a superomedial defect. How would this be classified according to Paprosky A Type I B Type IIa C Type IIb D Type IIc E Type IIIa 6 How much bone stock is required above the isthmus to allow revision of a femoral stem using a distal fit stem without augmentation A None B 1cm C 2cm D 4cm E 6cm

Questions 1 Which of the following organisms is most commonly isolated from an infected hip replacement at revision surgery A Anaerobes B Coagulase negative Staphylococcus aureus C Corynebacterium acnes D Methcillin sensitive Staphylococcus aureus E Methicillin resistant Staphylococcus aureus

7 For how long can cadaveric bulk allografts be stored at L70 degrees Celcius A 3 months B 6 months C 1 year D 2 years E 5 years

2 A periprosthietic fracture occurs around a femoral stem. There is a severe deficiency of bone stock and the implant was clearly loose before the fracture occurred. How would this fracture be classified according to the Vancouver system A A B B1 C B2 D B3 E C

8 What is currently the commonest reason for undergoing revision total hip replacement in North America A Aseptic loosening B Deep sepsis C Instability D Loss of material from bearing surface E Periprosthetic fracture

3 Approximately how long after total hip replacement does the CRP return to normal levels A 24 hours B 3 days C 3 weeks D 3 months E 1 year

9 A patient sustains a dislocation 3 months after undergoing a primary total hip replacement. It is carefully reduced under general anaesthesia and imaging afterwards suggests that the implants are well positioned. What is the approximate risk that further dislocations will occur? A Less than 2% B 5% C 10% D 30% E 60%

4 The following equipment is all used to remove a well fixed, uncemented acetabular component during revision total hip replacement. Which item is most likely to have been used last A Cortical screw B Drill

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Responses

10 Which of the following positions of an acetabular cup is least likely to predispose the joint to dislocation A 25 degrees abduction, 15 degrees anteversion B 35 degrees abduction, 15 degrees anteversion C 35 degrees abduction, 15 degrees retroversion D 45 degrees abduction, 15 degrees retroversion E 55 degrees abduction, 15 degrees anteversion

Please shade in the square for the correct answer.

11 What is the single most significant factor in the prevention of deep wound infection following total hip replacement A Antibiotic prophylaxis B Body exhaust C Bone cement with added antibiotics D Early debridement of suspected infection after surgery E Laminar flow ventilation

12 Which of the following pairs of investigations has been shown to be the most sensitive in identifying patients with deep infection after total hip or knee replacement A CRP and ESR B CRP and Interleukin-6 C CRP and TNF-alpha D Procalcitonin and Interleukin-6 E Procalcitonin and TNF-alpha

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Your details (Print clearly) NAME..................... ADDRESS..................... ........................ EMAIL..................... RETURN THE COMPLETED RESPONSE FORM by fax to þ44-113-392-3290, or by post to CME, Orthopaedics and Trauma, Academic Department of Orthopaedic Surgery, ‘‘A’’ Floor Clarendon Wing, Leeds General Infirmary, Great George Street, Leeds LS1 3EX, UK.

Please fill in your answers to the CME questionnaire above in the response section provided to the right. A return address and fax number is given below the response section.

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CME SECTION

Answers to CME questions based on the Mini-Symposium on ‘‘Children’s Hip Disorders’’ Please find below the answers to the Current Orthopaedics CME questions from Vol. 23, issue 3 which were based on the MiniSymposium on ‘‘Children’s Hip Disorders’’

Answers 1

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MINI-SYMPOSIUM: FOOT AND ANKLE

(i) The principles of foot and ankle arthrodesis

treatment of primary degenerative osteoarthritis and in secondary arthritis due to trauma, inflammation, infection, and avascular necrosis. It is also employed to stabilise joints with ligamentous injury or neurological deformity where gross instability cannot be treated with soft tissue procedures alone.

Lee Parker Dishan Singh

Pre-operative preparation The aetiology of a patient’s joint disease is important. Diabetic patients with Charcot’s arthropathy inevitably have microvascular disease, with the potential for compromise of skin and bone healing. Associated, progressive neurological deformity is difficult to control with standard internal fixation techniques due to associated osteoporosis. Patients with avascular necrosis require resection of devitalised bone, which can lead to limb shortening and mal-alignment.3 The presence of mal-alignment in the coronal and sagittal planes, areas of maximal tenderness, restricted range of movement, ligament instability, tendonopathy, adjacent joint degeneration, as well as the patient’s skin condition and neurovascular status, should all be considered in the surgical plan.

Abstract Successful arthrodesis of a diseased joint for pain relief and stability in the appropriate patient is achieved by thorough pre-operative planning and attention to risk factors for non-union, meticulous surgical technique including respect for soft tissues, adequate joint surface preparation and co-aptation of joint surfaces with stable fixation in the position of most useful function. Here we outline how these principles are applied in the foot and ankle.

Keywords ankle joint; arthrodesis; osteoarthritis; subtalar joint

Introduction

Investigations Plain x-rays are the most useful investigation and should be taken weight-bearing to represent the patient’s physiological alignment. Due to the close-packed arrangement of the joints of the foot, pain is often poorly localised by the patient and radiographic changes do not always correlate with the site of reported pain. Fluoroscopic-guided Injections of local anaesthetic and contrast (Figure 1), after which a pain diary is kept, are helpful in

Arthrodesis is the surgical fusion of a diseased joint for the purposes of obtaining pain relief and stability. The bones are fused in a position permitting most useful function but lose their natural motion. Henry Park is said to have performed the first arthrodesis of a tuberculous knee joint with a fixed flexion deformity, in Liverpool in 1781.1 However, Edward Albert later introduced the term ‘‘arthrodesis’’ in 1882 when he realised its potential in stabilising the foot and ankle of polio sufferers.2 Orthopaedic trainees are often exposed to the principles of arthroplasty; the aim of this article is to introduce and reinforce the basic principles of arthrodesis as applied to foot and ankle surgery. Extra-articular arthrodeses, where the joint surface is not prepared, relies on osteoconduction along a bone graft and is not usually useful in foot and ankle surgery, except possibly for fusion of the subtalar joint in paediatric cases. It is preferable to rely on intra-articular arthrodesis, where all cartilage is denuded and primary bone healing proceeds between two apposed cancellous surfaces. The technique of dowel grafting, where only part of the joint surface is prepared and union is attempted by osteoconduction along an interposed bone graft, generally gives inferior results to full joint preparation in foot and ankle surgery.

Indications Arthrodesis is a suitable alternative to arthroplasty in the painful, stiff, deformed or unstable joint where loss of motion will not significantly compromise overall function. It is used in the Lee Parker BM MRCS Specialist Registrar Trauma and Orthopaedic Surgery, North East Thames (Stanmore) Rotation, Foot and Ankle Unit, Royal National Orthopaedic Hospital, Brockley Hill, Stanmore, Middlesex, UK.

Figure 1 Ankle arthrogram under fluoroscopy. Contrast is seen in the ankle joint but does not penetrate the subtalar joint (30% of patients may have a connection between the ankle joint and the subtalar joints in which case the study may not be of diagnostic value). This rheumatoid patient obtained almost complete pain relief after injection alone and a subsequent ankle fusion has improved her mobility.

Dishan Singh MB ChB FRCS FRCS (Orth) Consultant Orthopaedic Surgeon, Foot and Ankle Unit, Royal National Orthopaedic Hospital, Brockley Hill, Stanmore, Middlesex, UK.

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can be allied with fracture healing in cancellous bone and those factors which influence it should be considered. The literature on fracture healing has previously been extensively reviewed12: Patients with significant co-morbidity, in particular cardiovascular disease and diabetes with microangiopathy and those rheumatoid patients on long-term immunosuppressive steroids, are at particular risk of infection and non-union. In patients with peripheral vascular disease, local tissue hypoxia can lead to delayed bone union and poor wound healing. Oxygen is required for the hydroxylation of proline residues during collagen formation and iron is essential for cellular electron-transport systems. Studies in iron-deficient, anaemic rats have shown poor rates of union and decreased strength of bony union.13 Tight glycaemic control is also important in diabetics to minimise the risks of delayed and non-union, which are significantly higher in this group of patients.14 Animal studies have demonstrated reduced levels of cellular proliferation, osteoblastic activity and collagen synthesis in diabetics as a result of growth factor inhibition, ultimately leading to a reduction in the tensile strength and stiffness of callus.15 While it is unlikely that patients who are being considered for arthrodesis will be malnourished, it has been shown in animal studies that deficiencies of vitamins B6, C, D, E, calcium and phosphorus all delay the synthesis and maturation of callus.16e18

confirming the source of pain, particularly when adjacent joints are also degenerate. Relief of pain after injection is highly predictive of pain relief after fusion.4 With severe arthritis, or when the anatomy is disordered (for example after previous fracture), or when there is pseudoarthrosis, CT-guided injections allow better joint access and subsequent assessment of the joint disease.5 Adjacent joint degeneration The joints adjacent to the proposed arthrodesis should never be ignored. A scannogram of the whole lower limb is helpful in determining how a single joint deformity affects overall limb alignment. It is preferable to deal with more proximal joint degeneration and mal-alignment first. For example, meticulous alignment of an ankle fusion can later be upset by a knee replacement that alters coronal lower limb alignment by as little as 2 . A fused joint becomes less able to dissipate the forces placed through it, thereby potentially accelerating adjacent joint degeneration. The incidence of subtalar fusion five years following ankle fusion has been quoted to be 2.8%6 but retrospective analyses of pre-operative x-rays of patients with ankle arthrodesis report that co-existent hind or midfoot arthritis was present in 95.8% of cases.7 Alternative treatments All patients should have a trial of conservative management before being offered an arthrodesis. Patients with ankle arthritis benefit from activity modification, weight-loss, analgesics antiinflammatories and walking aids. Orthoses, such as a moulded Ankle-Foot-Orthosis (AFO), Solid Ankle Cushion Heel insert (SACH) or insoles, work by limiting the motion of the joint that brings about pain and by mechanical unloading. Patients with tarso-metatarsal arthritis may benefit from localised steroid injections, insoles and rigid soled shoes with a rocker. Patients with MTPJ arthritis of the hallux may benefit from similar footwear adaptation or from a manipulation and steroid injection, particularly for milder grades of arthritis.8 Cheilectomy (excision of dorsal osteophytes and up to a third of the metatarsal articular surface) leads to pain relief and improvement in joint motion,9 thereby delaying the need for an arthrodesis in properly chosen patients. Similarly, for those patients with anterior ankle impingement pain, arthroscopic debridement can give good long-term pain relief in those with anterior osteophytes and minimal joint space narrowing.10 The role of ankle arthroplasty in the treatment of ankle arthritis is controversial. The early major revision rate for arthroplasty is far higher than for arthrodesis at five years (23% vs. 11%).6 Its use is therefore to be avoided in younger patients, though in the elderly or rheumatoid patient where stiffness of the remainder of the foot is a concern, preservation of ankle motion with arthroplasty may be appropriate.11

Medications Continual use of non-steroidal anti inflammatory agents (NSAID’s) can be regarded as a risk factor for the development of non-union. Even the use of Celecoxib (a selective COX-2 inhibitor) has been shown in the rat model to lead to unfavourable histological and mechanical properties in the healing bone and the effect is more profound the longer the drug is administered.19 It would seem prudent, therefore, to reduce the use of NSAIDs in patients undergoing arthrodesis. In the rheumatoid patient, DMARDS (Disease Modifying Anti-rheumatic Drugs) such as methotrexate, cyclosporine and anti-TNF-a, are often used in low doses. There is no evidence to suggest they adversely affect bony union. The long-term administration of corticosteroids is known to be detrimental to tissue healing and fracture repair. Short term administration seems to have little effect on bone healing20 whereas continual administration leads to high rates of nonunion in animal models.21 Bisphosphonates are osteoclast inhibitors and are used in the treatment of post-menopausal osteoporosis, steroid-induced osteoporosis, Paget’s disease and neoplastic conditions associated with bone destruction. There is no evidence that they increase bone union rates in the setting of either fracture or arthrodesis. Smoking Smokers have a higher risk of wound healing complications, non-union and poor outcome in ankle fusion.22 The relative risk of non-union of ankle arthrodesis is 3.75 times higher than that of non-smokers and, when confounding factors for non-union such as diabetes, cardiovascular disease and use of NSAIDS are excluded, the relative risk of non-union in smokers is 16 times that of non-smokers.23 When patients give-up smoking for their hindfoot fusion, their rate of non-union reduces from 18.6% to 11.1%, compared with 7.1% in non-smokers.24 Despite the wellknown detrimental effects of smoking on foot and ankle fusion,

Managing co-morbidity, medications and smoking Co-morbidity The patient as a host must always be considered in determining whether arthrodesis will be successful. Union of an arthrodesis

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as few as 23% of foot and ankle surgeons take measures to reduce their patients’ smoking before surgery and only 9% record non-union as a direct complication of smoking on the preoperative consent form.25 In our opinion smokers should give up smoking at least 2 weeks prior to surgery and remain off cigarettes until soft tissue healing and bony union have occurred.

require a rocker outsole. Patients who undergo a triple arthrodesis only lose inversion and eversion, but patients often wrongly believe that they will also lose plantarflexion/dorsiflexion. In our institution we have found that our patients’ concerns are best managed in a nurse-practitioner-led ‘‘fusion forum’’. This is set-up as an informal group meeting between patients considering fusion and the orthotist, plaster technicians and patients who have previously undergone fusion. Such a forum enables the patient to understand the surgery and its potential benefits and risks as well as addressing concerns over gait issues.30

Managing infection Arthrodesis is the treatment of choice for limb-threatening septic arthritis of the ankle and subtalar joint. The surgery is often complicated by limb oedema, scarring from previous surgery, chronic osteomyelitis and poor bone stock. The patient is often unemployed, or becomes unemployed because of prolonged sickness, and compliance with treatment can be poor.26 A two stage arthrodesis is required in infected cases, with the initial removal of implanted metal-work, radical soft tissue debridement with excision of secretory fistulae and sinuses, removal of osteonecrotic bone and implantation of antibiotic beads and spacers with concomitant administration of parenteral intravenous antibiotics. The second stage depends on the filling of large bone voids with bone graft, obtaining length, alignment and stability, usually with a combination of internal and external fixation. Adequate soft tissue coverage may necessitate a muscle transfer procedure.27 Stability is paramount in the eradication of infection. Internal fixation reduces the effective surface area of cancellous bone that is able to take part in fusion and has potential to loosen in the presence of on-going infection. External fixators can achieve interfragmentary compression without interfering with the local blood supply and loose wires can always be re-tensioned, however, pin-tract infections and irritation of the soft tissues can be a problem. When internal and external fixation are used in combination in the ankle, union rates of 86.6%, 84.2% and 93% have been reported.26e28 The patient’s expectations, and the alternative of below knee amputation, with a shorter period of convalescence and lower potential complications, should be explored before salvage surgery for infection.

Operative preparation Surgical approaches and arthroscopy Planning the initial incision is important in order to avoid neurovascular structures and to be able to carry-out meticulous and thorough joint preparation through an adequate exposure. This has to be balanced against the detrimental effect of excessive soft-tissue dissection and periosteal stripping on the healing of the skin and indeed the arthrodesis itself. The Charnley anterior transverse approach to the ankle, with division of the extensor tendons,31 has now been abandoned in favour of the anterior approach between the tendons of tibialis anterior and extensor hallucis longus. Previous scars and frail skin should be avoided and occasionally the surgical approach has to be modified in order to avoid areas of excessive soft tissue tension, which can be a particular problem with the valgus hindfoot.32 The Ollier approach to the subtalar and Chopart joints has largely been abandoned by adult foot and ankle surgeons because of the difficulty exposing and preparing the medial part of the talonavicular joint and the significant risks of nerve damage leading to painful neuromata. It is however still used in paediatric orthopaedics and in polio surgery. The preferred approach is to use the lateral utility incision from the tip of the fibula to the base of the 4th metatarsal to expose the subtalar joint and the calcaneocuboid joint if necessary (Figure 2). If a triple arthrodesis is being performed, a separate medial utility incision is used between the tibialis anterior and tibialis posterior tendons to prepare the boat-shaped talonavicular joint (Figure 3). Arthroscopic fusion of the subtalar and Chopart joints is possible but as yet is not common in practice. Providing there is only minor mal-alignment and bone loss, and there is no need for bone graft, arthroscopic ankle arthrodesis has proven to yield similar fusion rates to open ankle arthrodesis.33 Arthroscopic ankle arthrodesis has gained popularity, since it addresses concerns about excessive soft tissue dissection and improves post-operative pain and recovery, yielding high patient satisfaction rates.34 A skilled arthroscopic surgeon can perform most ankle fusions,35 though conversion to an open procedure is occasionally necessary and the patient should be warned of this pre-operatively.

Patient education Managing patient expectations is a priority when considering fusion. Patients should be informed of the risks specific to fusion, which include: infection requiring subsequent surgery or even amputation, neurovascular injury, delayed union and non-union, painful hardware requiring removal and the development of adjacent joint arthritis. They should be told that a small minority of patients require subtle footwear modification to improve gait after foot and ankle fusion. Patients often wrongly imagine that they will walk with a marked limp after surgery. A patient with a fused ankle has an average of a 75% reduction in total sagittal motion of the foot; however, the successful outcome of ankle fusion is not reliant on compensatory tarsal hypermobility, which only occurs in 27% of cases.29 What is more likely is that patients undertake subtle modifications to their gait, which are aided by having a normally functioning ankle in the contralateral leg, some normal residual motion in the tarsal joints of the ipsilateral leg (not necessarily hypermobility) and suitable footwear,11 which might on occasion

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Joint surface preparation An arthrodesis is essentially a controlled fracture and although there is considerable interest in the development of biomatrices and growth factors to promote union, there is great innate potential for union, which can be optimised by enhancing the natural biology of the fusion site through adequate

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congruous surfaces, which can be brought into close coaptation. Maintenance of natural joint shape and congruity has been shown to be more biomechanically stable than flat arthrodesis cuts.37 Following decortication, the exposed cancellous surfaces should be ‘‘feathered’’, ‘‘fish-scaled’’ or ‘‘petalised’’ in two perpendicular directions to create pits and furrows thereby maximising the area of interdigitation between surfaces and exposing pluripotent marrow-derived stem cells (Figure 4). All decortication and petalisation should be carried out with sharp chisels wherever possible: the use of saws and power burrs should, in our opinion, be avoided due to the generation of high localised temperatures which are known to impair bone healing in animal models.38 Power burrs are acceptable in arthroscopic arthrodesis, where high cold water inflow and outflow control heat exchange. Thorough decortication may not be necessary for certain patients, Percutaneous and spontaneous arthrodesis is possible in the joint which has undergone chondrolysis as a result of immobility or in the rheumatoid joint as a result of synovitis.37 However, thorough joint preparation by meticulous removal of all cartilage and feathering in two perpendicular directions provides a better environment for successful bony healing.

Figure 2 ’The lateral utility incision for subtalar arthrodesis passes from just below the tip of the fibula to towards the base of the 4th metatarsal. The extensor digitorum brevis is reflected distally to expose the joint and sinus tarsi. At the anterior aspect of the incision the calcaneocuboid joint can be approached as part of a triple arthrodesis. The incision can also be used to fix a fracture of the lateral process of the talus and to excise a calcaneo-navicular coalition.

Filling of cancellous defects e bone void fillers Charnley stated that union of an arthrodesis takes place between perfectly co-apted cancellous surfaces with intact circulation, making it comparable to fracture healing in an undisplaced fracture under ideal conditions, with both surfaces participating equally in osteogenesis. He concluded that bone grafts acted as little more than ‘‘passengers for three or four months until they secure a blood supply’’.39 Charnley was also of the opinion that bone graft is slow to become incorporated and can occasionally fracture and fail to unite.31 In hindfoot fusion only local graft from the excised joint surfaces is needed to achieve comparable

decortication.36 All articular cartilage should first be removed to expose the underlying subchondral bone. The use of a laminar spreader to distract the articular surfaces is invaluable for this purpose. Thorough decortication of the surfaces down to bleeding cancellous bone is then carried out while taking care to maintain

Figure 3 The medial utility incision for talonavicular arthrodesis passes mid-way between the tendons of tibialis anterior and tibialis posterior over the talonavicular joint. The incision can be extended to the knot of Henry to harvest the flexor hallucis or flexor digitorum tendons and its anterior extension can be used to expose the first tarso-metatarsal joint.

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Figure 4 The prepared arthrodesis surface of the medial cuneiform during a first tarsometatarsal arthrodesis (Lapidus procedure). Removal of articular cartilage, decortication and feathering/petalising/shingling in two perpendicular directions are performed to improve coaptation.

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union rates.40 We tend to avoid the use of bone graft in uncomplicated primary fusion procedures, but accept that its use is occasionally necessary when the anatomy of the joint does not lend itself well to internal fixation, when there is significant bone loss from the primary pathology or when revising from an arthroplasty to a fusion. Bone void fillers include autograft, which can be obtained locally or from the iliac crest, freeze dried or fresh frozen acellular cadaveric allograft and bone substitutes such as DBX (de-mineralized bone matrix). OP-1 or recombinant BMP-7 (bone morphogenic protein) has been used as a safe alternative to iliac crest bone graft in achieving posterolateral spinal fusion,41 in tibial nonunion42 and has been shown to reduce time to bony union in tibial fractures treated with external fixation43; however, it has not come into popular use in foot and ankle surgery.

calcaneocuboid joint may not be apposed, in which case a small bone block may be required to achieve lateral column lengthening. In all forefoot and midfoot fusions, it is important to test the proposed position of fusion by asking the operative assistant to press a flat surface against the sole of the foot to simulate optimal foot position when weight-bearing (Table 1). In first tarsometatarsal fusion there is considerable opportunity to reposition the metatarsal into a more plantarflexed or dorsiflexed position to assist with correction of forefoot pronation or supination respectively and this can be combined with a calcaneal osteotomy or ‘‘heel shift’’. Co-aptation, fixation and compression In his early work on knee arthrodesis, Charnley proposed that optimal cancellous healing occurred across an arthrodesis when the cancellous surfaces were held rigidly in compression,39 which encourages union by several means: when co-aptation of cut bony surfaces is imperfect, space exists between the cut surfaces in which fibrous union can occur. When compression is applied across an arthrodesis, the pressure is initially concentrated on the proudest parts of the cut surfaces which, as a result, undergo resorption by osteoclasis. This brings the surfaces into closer co-aptation. Under the influence of moderate dynamic compression, osteoblasts are then stimulated to achieve union across the arthrodesis39 (Figure 5a). Compression, rigidity and co-aptation are highly interrelated. With imperfect co-aptation between bone ends held with high compression, considerable rigidity can be achieved since compression neutralises shear and bending forces and prevents separation of the surfaces. Excessive compression, however, leads to bone resorption46 and so the ideal arthrodesis should have moderate compression and near perfect coaptation, which in fact provides conditions for considerable rigidity. Rigidity of fixation alone is probably less important than compression and co-aptation. The difference between very rigid and less rigid fixation is revealed in the histological characteristics of bone healing prevailing within the respective mechanical

Obtaining correct position and alignment The optimum position for ankle arthrodesis is important to note and has been found, through gait analysis, to be approximately 5 of ankle and subtalar valgus, neutral ankle dorsiflexion and 5 of external rotation with slight posterior positioning of the talus under the tibia.44 The valgus position of the hindfoot maintains the mobility of the midfoot by ‘‘unlocking’’ the transverse tarsal joint; the neutral/slight dorsiflexion and external rotation of the ankle guard against a varus-thrusting gait where the patient vaults over the instep, leading to high stresses on the medial collateral ligament of the knee.45 It may be necessary to perform soft tissue releases to achieve a plantigrade foot prior to fusion; for example, an equinus ankle may require a percutaneous lengthening of the Achilles tendon. Similarly, lengthening of the peroneal tendons may be necessary when performing a triple arthrodesis for correction of planovalgus. When planovalgus is corrected, the medial column of the foot is effectively shortened by the correction manoever, which is internal rotation of the calcaneum on the talus, reduction of subtalar valgus and re-alignment of the talonavicular joint which is fixed first. When the talonavicular joint is aligned, apposed and fixed, the

The optimum position of foot and ankle fusions Ankle Arthrodesis

Subtalar Arthrodesis Talonavicular Arthrodesis Calcaneocuboid Arthrodesis

First MTPJ Arthrodesis

Neutral dorsi/plantarflexion 5 hindfoot valgus Same external rotation as other side Talus posterior Neutral dorsi/plantarflexion 10 heel valgus Neutral dorsi/plantarflexion 10 heel valgus Neutral forefoot ad/abduction Neutral forefoot pro/supination Flat surface should be applied to sole of foot intra-operatively to determine correct dorsi/plantarflexion 15 proximal phalanx valgus Neutral phalangeal rotation

If the ankle is fused in varus, the supinated foot becomes rigid and does not adapt to the ground during the second rocker phase The lever arm of the foot becomes too long and impairs the third rocker phase if the talus is fused in an anterior position

Talonavicular joint should be fixed before calcaneocuboid joint during a triple arthrodesis

Simulated weight-bearing can be performed by using the cover of the screw set Best assessed by assessing alignment with second toe Plane of movement of interphalangeal joint more important than alignment of nail plate

Table 1

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a Contact stresses are concentrated at high spots across the arthrodesis leading to bony resorption by osteoclasis and flattening of the arthrodesis surface, b When crossed screws are used in a fusion, the screws must cross a short distance away from the joint to avoid rotation occurring at the fixation; we prefer 2 parallel screws, c Correct screw positioning with all threads crossing the fusion (on the left) ensures good interfragmentary compression. Figure 5

environment. Direct or primary bone healing is seen after rigid stabilisation with perfect co-aptation and minimal interfragmentary motion. Osteoid is laid down behind ‘‘cutting cones’’ of osteoblasts which traverse the fracture or arthrodesis line. Small gaps are filled by woven bone that is later remodelled to lamellar bone. External callus is not seen and bone strength is not restored for many months. In contrast, more external callus is seen in less rigidly fixed fractures and in arthrodeses, when mechanical integrity is restored more rapidly to physiological levels as bone is remodelled in accordance with Wolff’s law. Decreased stiffness of fixation and the application of short duration controlled micromotion are also known to improve the healing characteristics of tibial fractures providing the boundaries of strain magnitude and force of application are not exceeded.47 Various methods are available for the stabilisation of the arthrodesis. Internal fixation can be carried out with screws, plates, intra-medullary nails and k-wires. External fixation can be carried out with mono-axial or circular frames, or even plaster of Paris. A combination of techniques can also be used. Internal fixation with screws is likely to be the most stable construct for ankle arthrodesis, particularly when the screws are crossed just above the joint line in the tibia37 (Figure 5b). Our preference, however, is to use two parallel partially-threaded cannulated cancellous screws with washers, ensuring both screw threads entirely cross the joint-line to obtain adequate compression of the fusion, (Figures 5c and 6). A retrograde

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Figure 6 Lateral radiograph 3 months after ankle fusion in a patient with Charcot Marie Tooth presenting with pes cavus and a painful arthritic ankle with a fixed varus deformity; injection studies into the ankle joint had abolished his pain and the arthritic subtalar joint was therefore not fused. The plantarflexed first ray was corrected by a dorsiflexion osteotomy of the first metatarsal and a tibialis posterior tendon transfer to the peroneus tertius were carried out at the time of the ankle fusion.

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This 40 year old patient from the Middle East had developed a hindfoot varus with osteoarthritic ankle and subtalar joints after sustaining a peroneal tendon laceration at the age of 5. a The fixed hindoot varus led to the patient walking on the lateral border of her foot and caused painful callosities. b Arthritis of the ankle and subtalar joints with a varus hindfoot is seen on the mortise view of the ankle. c Due to the amount of deformity, a talectomy and tibio-calcaneal fusion using an intramedullary nail were carried out through a lateral approach; the radiographs at four months demonstrate union of the arthrodesis. Figure 7

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intramedullary nail inserted through the calcaneum across the ankle and subtalar joint is an excellent way of achieving coronal stability when both the ankle and subtalar joint are arthritic and mal-aligned (Figure 7a-c). The ‘‘chisel test’’ is a useful intra-operative technique used to assess the stability and co-aptation of an arthrodesis after fixation. It is performed by inserting the chisel between the prepared, immobilised surfaces and attempting to separate the arthrodesis by twisting the chisel (Figure 8). If no separation is observed then further augmentation of the fixation with more screws is unnecessary.

Treatment of non-union Identify biological causes

Identify mechanical causes

Identify infection Revision principles

Post-operative care The arthrodesis is splinted until evidence of union occurs clinically and radiographically, with bony trabeculae crossing the fusion line on X rays. There is wide variation in clinical practice concerning postoperative immobilisation. Our own regimen for ankle arthrodesis is to allow protected weight-bearing in a cast after 4 weeks, provided the stability of the internal fixation is deemed acceptable. With arthroscopic ankle arthrodesis, earlier weight-bearing has been shown to be safe with no impact on union rates compared to those patients conventionally managed with longer periods of restricted weight-bearing.48 Patients undergoing a subtalar arthrodesis are allowed to fully weight-bear after 2 weeks but are managed in a cast until radiographic union. Patients undergoing a Chopart or tarsometatarsal arthrodesis are managed non-weight-bearing for six weeks and then gradually allowed to increase weight-bearing in

Poor blood supply Smoking Inadequate joint surface preparation Inadequate compression/rigidity Too early weight-bearing Poor patient compliance Blood markers Bone biopsy if necessary Adequate surface preparation Adequate apposition of surfaces in optimal position Bone graft to fill bone voids/add structural support Rigid internal þ/ external fixation Longer period of splintage Staged revision procedures for infection

Table 2

a cast until union, at an average of 12 weeks post-operatively. For first MTPJ and TMTJ fusions, patients tend to be managed with 6 to 8 weeks in a wedge shoe, which offloads the forefoot.

Complications The most significant complication of any arthrodesis procedure is failure of union. Union rates for ankle arthrodesis have improved with modern surgical techniques from 80% at 6 months in Charnley’s era31 to as high as 94% with fusion times of 8.7 weeks using arthroscopic techniques.33 Non-union rates for triple arthrodesis as high as 10% have been reported with most non-union occurring at the talonavicular joint.49 Improvements in surgical techniques have yielded non-union rates as low as 4%40 without the use of supplementary bone graft, although the modern trend may also reflect fewer polio/neuromuscular cases. Table 2 summarises the principles of dealing with non-union of an attempted arthrodesis. Deep infection rates are low (0.4% acute osteomyelitis) for ankle arthrodesis6 but are serious and require prolonged antibiotics and staged revision procedures often using bone graft and additional or alternative fixation methods. Below knee amputation rates of 0.3% have been reported.6 Mal-alignment producing gait abnormalities and painful metalwork requiring removal are less common complications which can often be remedied with footwear modification and minor surgery.

Conclusions 1 Arthrodesis is surgical fusion of a diseased joint for the purposes of pain relief and stability. 2 Consider the aetiology of joint abnormality, for example, uncorrected muscle imbalance will lead to deforming forces at adjacent joints. 3 Image-guided injections of local anaesthetic and contrast with provision of pain diary are helpful in confirming the

Figure 8 The ‘‘Chisel test’’ is performed by inserting the blade of the chisel between the prepared and fixed joint surfaces and twisting the handle of the chisel. Further fixation with additional screws or plates is carried out if the surfaces can be separated by twisting the chisel handle.

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4 5 6 7 8

9 10

18 Einhorn TA, Bonnarens F, Burstein AH. The contributions of dietary protein and mineral to the healing of experimental fractures: a biomechanical study. JBJS Am 1986; 68: 1389e95. 19 Simon AM, Manigrasso MB, O’Connor JP. Cyclo-oxygenase 2 function is essential for bone fracture healing. J Bone Miner Res 2002; 17: 963e76. 20 Aslan M, Simsek G, Yildirim U. Effects of short-term treatment with systemic prednisilone on bone healing: an experimental study in rats. Dent Traumatol 2005; 21: 222e5. 21 Waters RV, Gamradt SC, Asnis P, Vickery BH, Avnur Z, Hill E, Bostrum M. Systemic corticosteroids inhibit bone healing in a rabbit ulnar osteotomy model. Acta Orthop Scand 2000; 71: 316e21. 22 Perlman MH, Thordarson DB. Ankle fusion in a high risk population: an assessment of non-union risk factors. Foot Ankle Int 1999; 20: 491e6. 23 Cobb TK, Gabrielsen TA, Campbell DC, Wallrichs SL, Ilustrup DU. Cigarette smoking and non-union after ankle arthrodesis. Foot Ankle 1994; 15(2): 64e7. 24 Ishikawa SN, Murphy GA, Richardson EG. The effect of cigarette smoking on hindfoot fusions. Foot Ankle Int 2002; 23(11): 996e8. 25 Bhargava A, Greiss ME. Effects of smoking in foot and ankle surgery e an awareness survey of members of the British Orthopaedic Foot and Ankle Society. The Foot 2007; 17(3): 132e5. 26 Richter D, Hahn MP, Laun RA, Ekkernkamp A, Muhr G, Ostermann PA. Arthrodesis of the infected ankle and subtalar joint: Technique, indications and results of 45 consecutive cases. J Trauma 1999; 47(6): 1072. 27 Hulscher JBF, te Velde EA, Schuurman AH, Hoogendoorn JM, Kon M, van der Werken C. Arthrodesis after osteosynthesis and infection of the ankle joint. Injury 2001; 32(2): 145e52. 28 Kollig E, Esenwein SA, Muhr G, Kutscha-Lissberg F. Fusion of the septic ankle: experience with 15 cases using hybrid external fixation. J Trauma 2003; 55(4): 685e91. 29 Jackson A, Glasgow M. Tarsal hypermobility after ankle fusion e fact or fiction? JBJS Br 1979; 61(4): 470e3. 30 Patten L, Singh D, Cullen N. Setting up a nurse-led patient forum to inform choice. Nurs Times 5th Feb 2008. 31 Charnley JC. Compression arthrodesis of the ankle and shoulder. JBJS Br 1951; 33(2): 180e91. 32 Jackson WFM, Tryfonidis M, Cooke PH, Sharp RJ. Arthrodesis of the hindfoot for valgus deformity. An entirely medial approach. JBJS Br 2007; 89(7): 925e7. 33 Myerson MS, Quill G. Ankle arthrodesis. A comparison of an arthroscopic and an open method of treatment. Clin Orthop 1991; 268: 84e95. 34 Sagaras NP. Results of arthroscopic arthrodesis of the ankle. Foot Ankle Surg 2004; 10(3): 141e3. 35 Winson IG, Robinson DE, Allen PE. Arthroscopic ankle arthrodesis. JBJS Br 2005; 87: 343e7. 36 Slappey G, Toribatake Y, Ganey TM, Ogden JA, Hutton WC. Guidelines to decortications in posterolateral spine fusion. J Spine Disord 1998; 11(2): 102e9. 37 Lauge-Pedersen H. Percutaneous arthrodesis Thesis. Acta Orthop Scand Supplement 2003; 307(74):1e30. 38 Jacobs RL, Ray RD. The effect of heat on bone healing. A disadvantage in the use of power tools. AMA Arch Surg 1972; 104(5): 687e91. 39 Charnley JC. Positive pressure in arthrodesis of the knee joint. JBJS Br 1948; 30: 478e86. 40 Rosenfeld PF, Budgen SA, Saxby TS. Triple arthrodesis: is bone grafting necessary? The results in 100 consecutive cases. JBJS Br 2005; 87: 175e8.

source of pain, particularly when the adjacent joint is also degenerate. Infection must be treated before attempting arthrodesis. Smoking significantly increases the risk of non-union. In the lower limb, deformity of proximal joints must be corrected before attempting fusion of more distal joints. Respect for the soft tissue envelope is important. Meticulous removal of all cartilage and perpendicular feathering of the subchondral bone provide better bone coaptation. The arthrodesed joint must be placed in the optimum position of function. Compression and rigid internal fixation promote bony union. A

REFERENCES 1 Klenerman L. Development of foot and ankle surgery. In: Klenerman L, ed. The evolution of orthopaedic surgery. London: Royal Society of Medicine Press Ltd., 1998. p. 167e8. 2 Rang M. Anthology of orthopaedics. Churchill Livingstone Edinburgh, 1966. pp. 208e211. 3 Kitaoka HB, Patzer GL. Arthrodesis for the treatment of arthrosis of the ankle and osteonecrosis of the talus. JBJS Am 1998; 80: 370e9. 4 Khoury NJ, El-Khoury GY, Saltzman CL, Brandser EA. Intraarticular foot and ankle injections to identify source of pain before arthrodesis. Am J Roentgenol 1996; 167: 669e73. 5 Saifuddin A, Abdus-Samee M, Mann C, Singh D, Angel JC. CT guided diagnostic foot injections. Clin Radiol 2005; 60(2): 191e5. 6 SooHoo NF, Zingmond DS, Ko CY. Comparison of reoperation rates following ankle arthrodesis and total ankle arthroplasty. JBJS Am 2007; 89: 2143e9. 7 Sheridan BD, Robinson DE, Hubble MJW, Winson IG. Ankle arthrodesis and its relationship to ipsilateral arthritis of the hind- and midfoot. JBJS Br 2006; 88(2): 206e7. 8 Solan MC, Calder JDF, Bendall SP. Manipulation and injection for hallux rigidus - Is it worthwhile? JBJS Br 2001; 83: 706e8. 9 Mann RA, Clanton TO. Hallux rigidus: treatment by cheilectomy. JBJS Am 1988; 70(3): 400e6. 10 Tol JL, Verheyen CPPM, van Dijk CN. Arthroscopic treatment of anterior impingement in the ankle. A prospective study with a five to eight year follow-up. JBJS Br 2001; 83(1): 9e13. 11 Mazur JM, Schwartz E, Simon SR. Ankle arthrodesis. Long-term follow-up with gait analysis. JBJS Am 1979; 61(7): 964e75. 12 Gaston MS, Simpson AHRW. Inhibition of fracture healing. JBJS Br 2007; 89: 1553e60. 13 Rothman RH, Klemek JS, Toton JJ. The effect of iron deficiency anaemia on fracture healing. Clin Orthop 1971; 77: 276e83. 14 Cozen L. Does diabetes delay fracture healing? Clin Orthop 1972; 82: 134e40. 15 Beam HA, Parsons JR, Lin SS. The effects of blood glucose control upon fracture healing in the BB Wistar rat with diabetes mellitus. J Orthop Res 2002; 20: 1210e6. 16 Dodds RA, Catterall A, Bitensky L, Chayen J. Abnormalities in fracture healing induced by vitamin B6 deficiency in rats. Bone 1986; 7: 489e95. 17 Sarisozen B, Durak K, Dincer G, Bilgen OF. The effects of vitamins E and C on fracture healing in rats. J Int Med Res 2002; 30: 309e13.

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41 Vaccaro AR, Whang PG, Patel P, et al. The safety and efficacy of OP-1 (rhBMP-7) as a replacement for iliac crest autograft for posterolateral lumbar arthrodesis: minimum 4-year follow-up of a pilot study. The Spine J 2008; 8(3): 457e65. 42 Pecina M, Haspl M, Jelic M, Vukicevic S. Repair of a resistant tibial non-union with a recombinant bone morphogenetic protein-7 (rh-BMP-7). Int Orthop 2003; 27: 320e1. 43 Ristini J, Flinkkila T, Hyvonen P, et al. RhBMP-7 accelerated the healing of distal tibial fractures treated by external fixation. JBJS Br 2007; 89: 265e72. 44 Coughlin MJ, Mann RA, Saltzman CL. Surgery of the Foot and Ankle. 8th edn., 1. Mosby Inc., 2007. pp. 934.

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45 Buck P, Morrey BF, Chao EY. The optimum position of arthrodesis of the ankle. A gait study of the knee and ankle. JBJS Am 1987; 69: 1052e62. 46 Cunningham JL, Richardson JB, Soriano RMG, Kenwright J. A mechanical assessment of applied compression and healing in knee arthrodesis. Clin Orthop 1989; 242: 256e64. 47 Kenwright JK, Goodship AE. Controlled mechanical stimulation in the treatment of tibial fractures. Clin Orthop 1989; 241: 36e47. 48 Cannon LB, Brown J, Cooke PH. Early weight bearing is safe following arthroscopic ankle arthrodesis. Foot Ankle Surg 2004; 10(3): 135e9. 49 Wilson F, Fay G, Lamotte P, Williams J. Triple arthrodesis: a study of factors affecting fusion after three hundred and one procedures. JBJS Am 1965; 47: 340e8.

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(ii) Flatfoot deformity: an overview

Therefore, it is vitally important for the treating orthopaedic surgeon to be clear about the different types of flatfoot deformity: congenital or acquired, flexible or rigid, adult or paediatric. It is also important to understand the biomechanics of the foot and the relations of forefoot to midfoot to hindfoot in order to identify and treat the underlying cause correctly. In this article we give an overview of the current concepts regarding flatfoot deformity, its diagnosis and management, bearing in mind that the patients’ symptoms, disability or expected disability (if left untreated) are the driving forces to instigate treatment, not the flatfoot deformity itself, which in the majority of cases causes no, or minimal, symptoms.

Kurt Thomas Haendlmayer Nick John Harris

Abstract Flatfoot deformity is a common complaint with various etiologies. It causes confusion as to when and how to treat it. Unnecessary treatment is a problem, especially in asymptomatic flexible paediatric flatfoot. The human foot is a sophisticated biomechanical structure. Interference with this complicated system of joints, ligaments, tendons and muscles has to be based on a sound knowledge of anatomical structures and their interactions. It is therefore important for every doctor dealing with this condition to be able to differentiate between cases needing treatment and cases that simply need reassurance. Historically, flatfoot deformities have been over treated with the aim to correct deformity, in the process not only failing to achieve the desired correction but also creating symptoms in previously symptom free individuals. A lot has been learned about flatfoot deformity and a more sensible approach based on symptoms and expected disability has been adopted. The adult acquired flatfoot is a complex condition, commonly caused by posterior tibial tendon deficiency (PTTD). Management of these patients is based on a thorough assessment of the underlying pathology. In this article we give an overview of the condition, with emphasis placed on assessment and management of the more common causes.

Definition Flat feet (Figure 1) is a medical condition with varying aetiology, in which the entire sole of the foot comes into complete or nearcomplete contact with the ground.

Aetiology of flatfoot deformities Table 1 lists the most common causes of flatfoot deformity in the adult and paediatric population. By far the most common in both groups is the physiological or idiopathic flatfoot. The commonest cause for acquired adult flatfoot is dysfunction of the posterior tibial tendon. Anatomical considerations Flatfoot deformity is always a result of a combination of several anatomic factors. Hyperpronation and/or increased eversion in the subtalar joint is often present. The calcaneum in relation to the talus is in external rotation and valgus. The navicular bone might be subluxed in a dorso-lateral direction in relation to the talus. This talo-navicular subluxation is either a contributing factor to pes planus or a biomechanical consequence of existing flatfoot of other causes. As a consequence of the varying anatomic conditions, the lateral column of the foot is short in relation to the medial column. Recognition of these anatomic factors is especially important when surgical intervention is indicated.

Keywords acquired adult flatfoot; flatfoot; paediatric flatfoot; posterior tibial tendon

Introduction Flat foot (pes planus) in its various types is a common complaint in general orthopaedic or more specialised foot and ankle clinics. A large number of these present in patients without symptoms of pain or functional deficit. These simply need advice and reassurance, especially for the parents of young children under the age of seven, where flat feet are very common, asymptomatic and should not cause any concern; they do not need surgical management, and only very rarely orthotic treatment. Pfeiffer et al1 found flat feet (valgus 5e20 ) in 44% of children age 3e6. In the same study group, they found less than 1% pathological (valgus more than 20 ) flat feet (7 from 835).1

Paediatric flatfoot Flexible flatfoot The physiological flatfoot is usually flexible, and normal arches can be observed in non-weight-bearing feet and when standing on tip toes. It is a mostly asymptomatic condition, but mild symptoms can occur. Asymptomatic flexible flatfoot: all children are born with flat feet and it might take until the age of 7e10 before the normal arch develops fully. The vast majority of these children are asymptomatic, with no functional deficit. The natural history is of gradual improvement over time and treatment is not indicated. Advice to parents is usually sufficient. Even after the age of 10, a full arch might not develop, accounting for the fact that mostly asymptomatic flexible flat feet are present in about 20% of the adult population.2 The management of asymptomatic, non-physiological flat feet consists of observation initially, to check for progression.

Kurt Thomas Haendlmayer FRCS (Trauma & Orthopaedics and Sportsmedicine) Foot & Ankle Fellow Leeds Teaching Hospitals NHS Trust, Leeds General Infirmary, Great George Street, Leeds, UK. Nick John Harris FRCS (Trauma & Orthopaedics) Consultant Orthopaedic Surgeon at the Leeds Teaching Hospitals NHS Trust, Leeds General Infirmary, Great George Street, Leeds, UK.

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Treatment consists of activity modification, orthoses and physiotherapy. In severe cases, non-steroidal anti-inflammatory medication can be administered. Patients can present with comorbidities such as obesity, ligamentous laxity, hypotonia or proximal limb problems. These need to be identified and addressed then patients need observation at regular intervals. If the response to non-operative measures is satisfactory and the clinical symptoms are resolving, observation and orthoses might be sufficient. Surgical intervention can be considered if the clinical response is inadequate. Surgery can consist of soft tissue procedures, bony procedures or combinations thereof. Soft tissue procedures alone are rarely successful in the long term treatment of the flexible flatfoot. Bony procedures include osteotomies of the forefoot, midfoot and hindfoot, lateral column lengthening and medial displacement osteotomy of the calcaneum. These can be combined with Achilles tendon lengthening and medial plication.

Figure 1 Lateral X-ray showing flatfoot with increased talo-metatarsal angle.

Rigid paediatric flatfoot Features of rigid flatfoot are a low arch in both weight-bearing and non-weight-bearing feet, with motion in the midfoot and hindfoot reduced or absent. The differential diagnosis includes congenital vertical talus, tarsal coalition, peroneal spastic flatfoot without coalition, iatrogenic and post-traumatic flatfoot. The underlying primary pathology can be diagnosed with a good history, clinical examination and appropriate imaging.

Patients with a tight Achilles tendon might benefit from stretching, with the aim of preventing progression. Orthoses are sometimes helpful. Symptomatic flexible flatfoot: symptomatic forms of flexible flatfoot produce subjective complaints and can have an effect on function. Patients complain of pain along the medial border of the foot, in the sinus tarsi, but pain can also be produced in knees, hips and the lower back. Gait disturbances and reduced endurance are features. Findings on examination are a prominent talar head, everted heel and tight Achilles tendon. Pathological flexible flatfoot is characterised by a more severe degree of the deformity and progression over time. Other findings in pathological flat feet can include excessive heel eversion, an unstable talo-navicular joint, a tight Achilles tendon and on occasions gait disturbances.

Tarsal coalition: Tarsal coalition is an abnormal, congenital union between two or more tarsal bones. It can be osseous (synostosis), cartilagenous (synchondrosis) or fibrous (syndesmosis). The prevalence is 1e2%. Autosomal dominant inheritance with reduced penetrance has been proposed.3,4 Calcaneonavicular and talocalcaneal (middle facet) coalitions are the most common, accounting for about 90% of tarsal coalitions.3 Other rarer coalitions are talonavicular, calcaneocuboid, naviculocuboid and naviculocuneiform. About 50% of coalitions are bilateral. The degree of deformity varies, and particularly in calcaneonavicular coalitions the coalition can be minimal, with little evidence of pes planus. Most patients, however, have fixed hindfoot valgus, loss of subtalar motion and loss of the normal longitudinal arch. Tarsal coalitions are most probably present at birth but cause symptoms only with increasing maturation of the skeleton, increasing bodyweight and activity levels. Symptoms might first present after bouts of vigorous activity. Symptoms in very young children are rare due to the flexibility of the cartilage surrounding the primary ossification centres. With progressing ossification, hindfoot stiffness increases and the ability to withstand external stresses decreases, leading to symptoms. Incomplete coalitions (fibrous or cartilagenous) often lead to vague, non-specific foot pain and walking difficulties, especially on uneven surfaces. Symptoms worsen with increasing age. If peroneal spasticity due to shortening of the peroneal muscles is observed, the condition is also called peroneal spastic flatfoot.

Causes for flatfoot deformity in children and adults Paediatric flatfoot

Adult flatfoot

Physiological

Physiological ongoing from childhood Inflammatory - Rheumatoid arthritis - Seronegative spondylarthropathies Posterior tibial tendon dysfunction Osteoarthritis Neurological Accessory navicular bone Connective tissue disorders Post-traumatic Adult tarsal coalition Iatrogenic

Inflammatory - Juvenile rheumatoid arthritis

Connective tissue disorders - Marfan, Ehlers-Danlos Neurological disorders - Cerebral palsy Tarsal coalition - Talcalcaneal - Calcaneonavicular - Rarer other coalitions

Calcaneonavicular coalition e calcaneonavicular coalition most commonly manifests in children aged 8e12. The coalition runs from the anterior process of the calcaneus to the lateral and dorso-lateral extra-articular surface of the navicular bone. It can

Table 1

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fibrous or cartilaginous coalitions is, however, recommended by most authors. As described for calcaneonavicular coalitions, the presence of arthritic changes makes excision of the coalition alone less likely to be successful and arthrodesis procedures are more likely to be required. The decision making process should be individualised for each case.

be up to 2 cm long and 2 cm wide. Symptoms consist of pain, often directly over the abnormal coalition, but can be unspecific and mimic simple sprains. Clinical examination reveals hindfoot valgus, a reduced longitudinal arch and reduced subtalar movement, which can be subtle and difficult to determine, especially in bilateral cases. Some coalitions are asymptomatic and can present as coincidental findings on radiographs, CT or MRI scans that have been performed for other indications. The diagnosis can usually be made with standard radiographs, including a 45 lateral oblique view. In some cases an ‘anteater nose sign’ can be observed on lateral radiographs.5 CT and MRI are also important diagnostic tools. CT is useful for pre-operative planning. MRI scans show surrounding or intraosseous oedema. Treatment initially should include activity and footwear modification or cast immobilisation for 4e6 weeks. If symptoms are not relieved by these methods, or if they return after initial success, surgical treatment can be recommended. Early onset of the symptoms of calcaneonavicular coalitions (below age 10) is more likely to lead to surgical intervention, as symptoms are expected to worsen with progressing skeletal maturity. The chosen surgical procedure depends on the age of the patient and the presence of secondary degenerative changes in adjacent joints. Resection of the calcaneonavicular bar, with or without interposition of fat or muscle tissue, is indicated in young adolescents after failed conservative treatment and in the absence of secondary arthritic changes. If beaking of the talar neck is observed, this indicates early degenerative changes in the subtalar joint. In these cases simple excision of the bar can still be attempted but is less likely to lead to a complete eradication of symptoms. In the presence of advanced arthritic changes in the subtalar joint, triple arthrodesis is the treatment of choice.

Congenital vertical talus: congenital vertical talus (CVT), also named rocker-bottom flatfoot or congenital rigid flatfoot, can usually be detected directly after birth (Figures 2 and 3). It can be isolated or part of a syndromic disorder. It is associated with arthrogryposis and myelomeningocele.10 The normal longitudinal arch of the foot is reversed to the extent that the sole of the foot becomes convex. This is caused by the talus being in abnormal plantar flexion with the talar head pointing medially. The calcaneum also takes up an equinus position, causing shortening of the Achilles tendon. The talonavicular joint is dislocated, with the navicular lying on the dorsal aspect of the talar head, with resulting dorsiflexion of the whole forefoot. This causes deep creases on the dorsal and lateral aspect, in front and inferior to the lateral malleolus. Without treatment, adaptive changes in bones and soft tissues will occur and correction of the deformity becomes more and more difficult with time. Weightbearing leads to callosities underlying the anterior aspect of the calcaneus and the medial border of the foot over the talar head. The forefoot becomes severely abducted and the heel cannot touch the ground. Contractures of soft tissues occurs. Tendon units will either loose function or adapt to abnormal function, for example the peroneal tendons come to lie anterior to the ankle and act as dorsiflexors. CVT can be diagnosed by clinical examination and adequate radiographs, which should include anteroposterior views and plantar flexion lateral stress views. In the normal situation, the long axis of the first metatarsal passes plantarward to the long axis of the talus in a lateral plantar flexion stress view, whereas in CVT the long axis of the first metatarsal runs dorsal to the long axis of the talus, reversing the normal angle. Correction of CVT is difficult and can rarely be achieved without surgery. Non-surgical methods involve gentle manipulations followed by casting. This helps to prevent contractures of the dorsal structures and facilitates surgical correction later. The

Subtalar coalition e subtalar coalition tends to become clinically symptomatic in 12e14-year-old children. The most consistent sign is a reduction or absence of subtalar motion. The symptoms are similar to calcaneonavicular bars, with pain in the hindfoot and loss of the longitudinal arch. Peroneal muscle spasm is more common in talocalcaneal coalition, compared to calcaneonavicular coalition. Subtalar coalitions can involve multiple facets but most consistently affect the middle facet.6 Anterior or posterior facet coalitions are very rare. The diagnosis is made on CT scan. Coronal views with the feet plantarflexed are recommended for best visualisation.7 It is rarely possible to diagnose subtalar coalitions with X-rays alone. The great variability in hindfoot anatomy makes standard radiographs unreliable, even when using special angles. Therefore, CT is the gold standard for diagnosis of talocalcaneal coalitions. Treatment consists of activity modification, adjusting footwear or cast immobilisation. Should initial non-operative treatment fail, surgery is indicated. Options for the surgical treatment of subtalar coalition includes excision of the coalition or triple arthrodesis, with or without calcaneal osteotomy. There is debate in the literature as to what extent talocalcaneal coalitions can be successfully excised. Some recommend excision of all symptomatic coalitions when conservative treatment has failed, regardless of the extent of the coalition, whereas others recommend that only those coalitions involving less than 50% of the talocalcaneal joint should be exicsed.8,9 Excision of early, small

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Figure 2 Clinical photograph showing rocker-bottom deformity in congenital vertical talus.

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military recruits did not find significant differences in injury rates for different arch heights.13 Jones et al concluded after an extensive search of the literature, that arch height is likely to be a risk factor for metatarsal fatigue fractures.14 Posterior tibial tendon dysfunction (PTTD) PTTD (Figure 4) is the most common cause of adult acquired flatfoot. It has been suggested that PTTD is not solely responsible for causing acquired adult flatfoot, and that other structures are also failing in the development of acquired flatfoot. Deland et al15 examined cadaver models after severing the PTT. They then subjected the foot to axial loads in an attempt to reproduce the adult acquired flatfoot. Cutting the PTT alone produced minimal arch collapse or valgus rotation of the hindfoot. To achieve significant collapse of the hindfoot and midfoot (as seen in Stage II and Stage III PTTD), the spring ligament complex, plantar aponeurosis, deltoid ligament, talocalcaneal ligament, long and short plantar ligament, and medial calcaneal-cuboid ligament had to be cut as well. This supports the theory that the adult acquired flatfoot is not caused by rupture of the PTT alone. Other ligaments must also fail to produce deformities and the clinical pictures seen in Stage II and Stage III deformities. Similar conclusions have been drawn from examinations of feet after PTT transfer that did not develop a flatfoot deformity after 6 years of follow-up.16 The development of a flatfoot in tibialis posterior tendon dysfunction is unlikely to be the result of PTTD alone. The adult acquired flatfoot is more likely the result of complex biomechanical failures in the foot and ankle that ultimately cause overload of the PTT during life. The underlying pathology is within the posterior tibial tendon itself, which is usually unilateral. Typically, it affects women aged 45e65years. The history often reveals pre-existing flatfoot deformity, positive family history for flatfoot, or minor trauma. Patients often report overuse activity before the onset of initial symptoms. Symptoms may present at any stage of this condition, but are often not immediately recognised as relating to PTTD, which can lead to delayed diagnosis.

Figure 3 X-ray showing congenital vertical talus.

talo-navicular joint cannot usually be reduced by manipulation alone and needs open reduction in almost all cases. Surgery depends on the age of the child and the severity of the deformity. Children from 1 to 4 years old are treated with open reduction of the talo-navicular and subtalar joints, which involves extensive dorsal soft tissue releases, posterior capsular releases of the ankle and subtalar joint and lengthening of the Achilles tendon with a Z-plasty. In older children (3þ years) with severe deformity, excision of the navicular has been described. Children aged 4e8 might need extra-articular subtalar arthrodesis in addition to open reduction and soft tissue releases. Children older than 12 years need triple arthrodesis for deformity correction. Procedures are often performed in several stages in order to allow the soft tissues to adapt to the new position.

Adult flatfoot Flexible adult flatfoot In the adult population, flexible flatfoot deformity is common, and in most cases it is asymptomatic. It usually represents a progression from paediatric flatfoot. The most common cause of acquired adult flatfoot is dysfunction of the posterior tibial tendon, which is typically unilateral and progresses from flexible to rigid adult flatfoot. Other causes are trauma, types of arthritis, prolonged or unusual stresses to the foot, defective biomechanics or it can simply develop as part of the normal ageing process. Most commonly, it is a combination of several of these factors. Flat feet can also develop during pregnancy, due to increased elasticity combined with increased strain due to increased weight. Flat feet acquired as an adult will usually remain flat as normal arches can only develop in the growing skeleton. The adult flexible flatfoot can develop into a rigid flatfoot, where the soft tissue structures are stretched out and as a result in the end stage, the bony skeleton develops arthritic changes, with fixed positions. Treatment of adult flexible flatfoot should be reserved for symptomatic cases, as it will not make any difference to asymptomatic patients. It will not create a lasting arch and overenthusiastic treatment can even be the cause of symptoms. No amount of exercise, however useful it might be overall for the individual, can change the appearance of a flatfoot. Studies comparing two groups of individuals with high arches and low arches found a tendency to a lower injury rate in individuals with low arches.11 A study of Israeli soldiers found an almost four times higher incidence of stress fractures in those with high arches compared to those with low arches.12 Other studies of

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Anatomy: the posterior tibial muscle originates from the posterior surface of the interosseous membrane and the adjacent tibia

Figure 4 Intra-operative photograph showing diseased posterior tibial tendon with longitudinal split and synovitis within the opened tendon sheath.

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and fibula. The tendon curves at an acute angle around the posterior medial malleolus in a shallow groove. The groove is covered by the flexor retinaculum, which ties the tendon firmly down. It passes underneath the calcaneonavicular ligament and inserts into the navicular tuberosity, but it is unique in that it also has insertions into the sustentaculum tali, all the cuneiforms, the cuboid and into the bases of metatarsals two, three and four. It passes posterior to the axis of the ankle joint and medial to the subtalar axis, therefore acting as plantar flexor and inverter of the hindfoot. Through its many insertions into the midfoot, it acts as a forefoot supinator and adductor. The posterior tibial tendon runs in a synovial sheath, which extends from approximately 4e5 cm proximal to 3 cm distal to the tip of the medial malleolus. Its sheath is unique as it does not contain a complete mesotenon, and the tendon therefore relies on its blood supply via other routes. Apart from inversion, plantar flexion, supination and forefoot adduction, the posterior tibial tendon also acts as a hindfoot stabiliser against valgus forces. It is active in the stance phase of the gait cycle, from heel strike to toe lift-off, decelerating the pronation forces to the subtalar joint after heel contact, and then it stabilises and locks the transverse tarsal joint at midstance. This maximises the effects of the soleusegastrocnemius complex during plantar flexion. By adducting and supinating the forefoot, the PTT also allows the soleusegastrocnemius complex to become the primary invertor of the subtalar joint. This optimises the leverage so that forces can be transferred efficiently, especially in the propulsive phase of the gait cycle. The peroneus brevis muscle is the primary antagonist, abducting the midfoot and everting the hindfoot. Stabilisation of the longitudinal arch is provided by static and dynamic forces. There is still debate whether the static forces act as a truss or a beam. A truss has two struts meeting at an apex, represented in the foot by the arch.17 These struts are connected at their base by a tie, the plantar aponeurosis, and as long as the tie remains intact the arch cannot collapse. This is closely represented by a windlass mechanism. A beam is a less rigid structure. In the foot the beam is curved, which on loading creates compression at the convex side and tension on the concave side. Tension therefore directly affects the plantar ligaments stabilising the arch, namely the long and short plantar ligament, the spring ligament (calcaneonavicular) and the bifurcate ligament. All of these ligaments are insertion sites for the posterior tibial tendon.18 The posterior tibial tendon and the intrinsic muscles of the foot act as dynamic arch supports.

Trauma is rare as a cause for PTT rupture but cases have been reported, especially with medial malleolar fractures.19 Reports of an initiating traumatic event leading to rupture range from 14% in elderly patients20 to 50% in a younger patient group.21 Again, trauma leading to rupture of the PTT is more likely on the basis of an already diseased tendon, even in the absence of pre-existing symptoms. Repetitive microtrauma to the tendon can lead to tendon disruption through an inflammatory response. Microtears can be caused by overloading and if these are repetitive, the damage cannot be repaired and chronic inflammation can result. Inflammation as a primary cause for PTT dysfunction and rupture is also debated. In rheumatoid arthritis it is difficult to ascertain which pathological process is responsible for PTT failure. It is most likely a combination of effects specific to rheumatoid arthritis. Rheumatoid disease can lead to flatfoot via several pathways, e.g. joint destruction with resulting hindfoot valgus and destruction of the ligament complexes of the subtalar and talo-navicular joints. The resulting valgus deformity puts enormous stresses on the PTT to counteract the deformity. Several studies suggest that rheumatoid arthritis might not be linked directly to destruction of the PTT. Kirkham and Gibson found no PTTD in 50 patients with rheumatoid arthritis, collapsing arches and hindfoot valgus.21 Similarly, Jahss found a normal PTT in patients undergoing arthrodesis for symptomatic flatfoot.22 There is evidence that the PTT is actually working harder to counteract the valgus forces caused by rheumatoid arthritis, as shown in an electromyographic study by Keenan et al.23 An epidemiological study by Holmes and Mann found a correlation between PTTD and obesity, hypertension, diabetes and steroid use.24 All of these conditions can compromise the blood supply to the posterior tibial tendon directly or indirectly. The blood supply to the PTT arises mainly from the posterior tibial artery, with the most distal portion of the tendon receiving a supply from the dorsalis pedis artery. Several authors have examined the blood supply to the PTT. Frey et al found a hypovascular zone of approximately 14 mm length at a distance of 40 mm from insertion.25 This corresponds roughly with the tip of the medial malleolus. In this zone the authors found no mesotenon and also a hypovascular synovial sheath. This theory is supported by the fact that the common location for tendon rupture falls within this zone. Peterson et al found this zone to be avascular using a different method.26 The avascular area is exactly where the PTT is in direct contact to the bone at the level of the medial malleolus. Further anatomical factors restricting the tendon’s blood supply have been suggested. Jahss states that the overlying flexor retinaculum can cause compression and constriction through synovial swelling and as a consequence causes degeneration of the tendon.22 Other authors state that excessive friction at the sharp turn around the medial malleolus can contribute to an inflammatory process.27 Another contributing factor to PTTD is thought to be changes in the collagen content, type and orientation of the fibres. Given the fact that in a normal tendon the collagen works perfectly, any changes in the collagen content or type or orientation may reduce the elastic qualities. Ageing changes the collagen structure. Myxoid degeneration with increased mucin content, alters the normal linear orientation of the collagen bundles of the tendon, leading to a haphazard configuration of the collagen, which leads

Aetiology: the cause of posterior tibial tendon dysfunction is subject to much debate. It is most likely multifactorial. Although many underlying causes have been identified, a clear uniform opinion does not exist. Possibilities are spontaneous rupture, progression from congenital flexible flatfoot, trauma, repetitive microtrauma, inflammatory causes, collagen disorders, vascular causes or the presence of an accessory navicular bone. Spontaneous rupture of an intact tibialis posterior tendon is unlikely, and what might appear to be a spontaneous rupture is likely to be the endstage of a degenerative process within the tendon that might not have caused noticeable symptoms until rupture occurs.

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to decreased tensile strength with the potential endpoint of spontaneous rupture. Several authors found a wavy and irregular configuration of the collagen in histopathological examinations of diseased posterior tibial tendons.28e30 Another detiological factor is congenital pes planus. The abnormal position of the hindfoot and forefoot places greater stresses on the posterior tibial tendon, which in line with the theory of repetitive microtrauma, can ultimately lead to PTTD. The presence of an accessory navicular bone is also associated with development of PTTD. Posterior tibial tendon dysfunction is also correlated with seronegative spondyloarthropathies. Especially in younger patient groups with PTTD, Myerson found HLA markers in the majority of patients, whereas in the older age group HLA markers are rarely found. Seronegative inflammatory disease affects tissues outside the synovium, and involves multiple attachment sites of tendons, ligaments and capsules to bone (enthesopathy). The younger patient group is mostly female, and in this group a disproportionately high number of concurrent connective tissue disorders such as inflammatory bowel disease, psoriasis, urethritis, uveitis, conjunctivitis and oral ulcers are found.20

The patient is first inspected standing with the lower extremities exposed to above the knee from the front, the sides and from behind. The gait is observed from front, back and sides. With the patient sitting on the examination couch, the sole of the foot can be inspected. Features of PTTD on inspection are flatfoot deformity (unilateral or bilateral), swelling along the PTT, fullness around the medial aspect of the ankle, lateral skin wrinkling (lateral impingement), ‘too-many-toes’ sign when inspected from posterior, and hindfoot valgus. All these should be observed with the patient standing. With the patient seated the sole can be inspected for callosities, which in PTTD are typically plantar to the talar head. Palpation must again follow a systematic approach, with special attention paid to the course of the posterior tibial tendon around the medial malleolus to its insertion into the midfoot. In stages of active inflammation, palpation along the course of the PTT can be extremely painful but in later stages it might be painfree. Palpation is performed along all the hindfoot and midfoot joints to detect potential signs of arthritis. The examiner should also look for warmth and increased fluid within the tendon sheath. The range of movement is examined for ankle, subtalar and midfoot joints bilaterally. Specific tests concerning the function of the tibialis posterior tendon are the heel rise test and direct strength testing. The heel rise test is first performed bilaterally with the examiner observing from posterior. The hindfeet should inverse symmetrically from a valgus position going into slight varus (Figure 5). Asymmetry indicates an insufficient PTT unable to invert the subtalar joint, lock the transverse tarsal joint and thereby allow the soleusegastrocnemius complex to lift the heel off the

Physical examination and findings: the physical examination of the foot and ankle should follow a systematic approach in order to get a complete picture without missing physical signs. Every surgeon can create their own system, and the following paragraph is simply a guideline. In our unit we follow the look, feel, move principle with inspection first, then palpation and finally examination of movement followed by specific tests. As with all foot and ankle problems, the patient’s shoes should be inspected for abnormal wear patterns.

Figure 5 Examination of hindfoot movement. Note shift from valgus to varus when tiptoeing. (Reproduced with kind permission of Cambridge University Press from ‘‘Advanced Examination Technique in Orthopaedics’’).

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ground. The examiner must exclude primary pathology in the subtalar or talo-navicular joints, which can give similar results on testing. Confirmation is obtained by asking the patient to perform a single-limb heel rise. For single-limb heel rise the patient is allowed to rest some fingers against a wall or table for balance, but the examiner must be aware of the patient’s overall position, which must be upright without leaning forward or bending the knee. The PTT is mainly used to initiate heel rise, which is then maintained by the soleusegastrocnemius complex. This means the patient with a PTTD can appear to have PTT function by altering the body’s centre of gravity and recruiting adjacent muscles to get the heel to rise and then maintaining the position. The power of the PTM is assessed in the seated patient. To isolate the PTT the ankle is placed in a plantarflexed position and the foot everted. This eliminates the effect of the anterior tibial tendon. The examiner’s hand is placed against the medial aspect over the first metatarsal and the patient is asked to invert the foot against the examiners resistance. The strength is noted and compared against the contralateral side. Pain when performing the test is also noted.

In patients with congenital flatfoot, X-rays of the contralateral foot are recommended for comparison. Radiographs are usually normal in stage I disease, but are useful as a screening tool to look for other pathology contributing to the patients symptoms like arthritic changes, tarsal coalition, an accessory navicular bone or Lisfranc injury. Characteristic changes are seen with progressing disorder. The talo-navicular joint will show lateral subluxation on an AP view and sag on lateral views. The first tarso-metatarsal joint is viewed in the lateral view, as it can contribute to the flatfoot deformity through subluxation and arthritis. Subluxation of the subtalar joint is difficult to detect on a lateral view, as it only shows as an indistinct joint surface. Radiography is also used to quantify deformity by measuring angles, which can then be used for monitoring progression of disease and for pre-operative planning. The angles measured on lateral radiographs are the talocalcaneal angle (normal ¼ 25e30 ), the talo-metatarsal angle (normal ¼ 4 to þ4 ) and the cuneiform height. On AP radiographs the relevant angles are the talocalcaneal angle, the talo-metatarsal angle and the articular congruity angle for the talo-navicular joint.

Classification: The system used the most in PTTD is the classification system proposed by Johnson and Strom, which originally included stages 1, 2 and 3.31 More recently, stage 2 was subclassified into stages 2A and 2B and then in 1996 Myerson added a stage 4.32 The staging includes clinical presentation, disorder and radiographic findings (Table 2).

Imaging e Magnetic Resonance Imaging: MRI scanning is excellent in detecting detailed changes in the PTT. It is superior to computed tomography for showing tissue degeneration, tendon definition, highlighting synovial fluid and soft tissue oedema. The sensitivity of MRI is 95%, compared to 90% for CT. The specificity is 100% for both MRI and CT.33 MRI detects longitudinal splits easily, which often do not show on CT scanning. Rosenberg et al also found the percentage of tears correctly diagnosed and classified with MRI to be 73%, with CT as low as 59%.33

Imaging e Radiography: radiographs are the first line of investigation in suspected PTTD. Weight-bearing films should be obtained of the foot in three planes and the ankle in two planes.

Johnson and Strom classification of PTTD with associated clinical, pathological and radiological features Stage

Clinical findings

Pathology

Imaging

I

Medial pain and swelling Single-limb heel rise þ

Normal tendon length Tenosynovitis

X-ray: normal MRI/USS: tenosynovitis

IIA

Obvious but flexible deformity Medial pain and swelling Single-limb heel rise þ Too many toes sign þ

Tendon elongation Tenosynovitis Flatfoot deformity

X-ray: lateral increased talo-metatarsal angle AP: uncovering of talar head MRI: tenosynovitis, splits USS: tenosynovitis, splits

IIB

Obvious deformity Medial and lateral pain Single-limb heel rise ve Too many toes sign þ

Tendon elongation Degenerative changes Lateral impingement

X-ray: arthritic changes MRI: soft tissue changes

III

Rigid valgus deformity forefoot varus >15 Tight tendo Achilles Lateral pain Pain at rest

Subtalar osteoarthritis Lateral impingement

X-ray: arthritic changes CT: pre-operative planning of fusion procedures MRI: soft tissue changes

IV

Lateral ankle pain Rigid deformity

Advanced osteoarthritis Now also in ankle joint

X-Ray: ankle OA with ankle tilt CT/MRI: pre-operative planning

Table 2

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MRI is also used to assess the muscle belly of the posterior tibial muscle, which helps with pre-operative planning. In a physiological study by Wacker et al, the muscle underwent significant fatty degeneration only 10 months after complete PTT rupture, and atrophy in incomplete tears.34 At the same time the muscle belly of the flexor digitorum longus hypertrophied as a compensatory mechanism. This is especially important since the FDL is used in reconstructive procedures for PTTD. Imaging e Ultrasound: ultrasound is a very accurate and costeffective tool for diagnosing PTT pathology. It has the advantage of allowing dynamic examination. It is, however, very dependant on the radiologist’s skill and experience, which might be the reason why the interobserver reliability was found to be poor with USS (0.37) and excellent with MRI (0.86).35 In some units ultrasonography is used as the primary diagnostic tool for detection of PTTD.

Figure 6 Intra-operative photograph showing FDL transfer with fixation of the FDL in a drill hole through the navicular bone with biotenodesis screw.

Treatment e Operative: surgical treatment is dependant on the stages of the disease. There are different principles and procedures for each stage. This article cannot go into great detail about individual surgical procedures but instead focuses more on the principles and aims. Although stage 1 should be reserved for conservative management, tenosynovectomy can be indicated. Stage 2 dysfunction usually requires a combination of procedures. Meticulous pre-operative assessment is mandatory for surgical planning and choice of procedures. Flexor digitorum longus tendon transfer (Figure 6) is often combined with medial displacement calcaneal osteotomy.37 These can be combined with spring ligament repair or reconstruction and gastrocnemius slide. A plantar flexion opening wedge osteotomy of the medial cuneiform is added if, after correction of the hindfoot, the forefoot remains in a supinated position with the first ray not touching the ground. In more advanced stages (2B), a lateral column lengthening procedure might be indicated. Subtalar arthrodesis is performed if inversion is restricted but a stable correctable transverse tarsal joint is present. If the transverse tarsal joint is in fixed abduction, or if there is fixed forefoot varus, then triple arthrodesis is indicated.

Imaging e Computed Tomography: CT has largely been replaced by MRI and is now mainly used if MRI is contraindicated. It shows anatomy well but has limitations in distinguishing tenosynovitis from tendon rupture. Longitudinal tears, in particular, are frequently missed.33 Treatment e Non-operative: a multidisciplinary approach is useful, including services from physiotherapy, podiatry, and the orthotic department. The non-operative options should be exhausted before surgical reconstruction is planned. These include rest, anti-inflammatory medication, physiotherapy and orthotics. Rest should include unloading of inversion excursion, which can be achieved in ankle crossing braces or walker boots, although this is only successful in mild cases. If more immobilisation is required for pain relief, a period in a below knee cast provides best rest for the PTT. Weightbearing can be allowed according to pain tolerance. Cast immobilisation can be combined with anti-inflammatory medication. Physical therapy can also reduce inflammation. Iontophoresis with dexamethasone, cryotherapy or pulsed ultrasound can be used. Strengthening exercises aimed at the PTT are limited by pain and can only be started once other methods have greatly reduced or eliminated the pain. According to Kulig et al, resisted adduction with elastic bands had the greatest effects on activation of the posterior tibial muscle.36 Orthotics and braces aim to reduce stresses and strain on the PTT by elevating the arch and reducing PTT excursion. The type of orthosis used depends on the stage of disease and whether the deformity is flexible or fixed. With flexible deformities (stages 1 and 2A), the orthotics are corrective tools, whereas fixed deformities require accommodating rather than correcting devices. Examples of devices used are the UCBL (University of California Biomechanics Laboratory) for flexible deformities, and the moulded ankleefoot-orthosis (AFO) for rigid deformities. These are only a few examples out of a wide variety of orthotic tools available. Each surgeon treating patients with PTTD should be familiar with the type of devices available in their unit. There is debate whether prolonged non-operative management allows the condition to worsen, but most authors agree that a 3e6-month trial of non-operative treatment is indicated unless there is significant structural deformity present.22

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Other causes for acquired adult flatfoot Other causes for acquired adult flatfoot include post-traumatic flatfoot, osteoarthritis and Charcot arthropathy. In all of these diagnoses, the aim is to provide the patient with a functional, stable, plantigrade foot with operative or non-operative methods as appropriate.

Conclusion From reviewing the literature, it is clear that a great deal of progress has been made in the diagnosis and treatment of flatfoot deformity. There is now a consensus about flexible or physiological paediatric flatfoot that treatment is not necessary in the vast majority of cases and simple observation and advice to parents and their children is sufficient. Controversy still exists about the aetiology of acquired adult flatfoot, especially concerning the events leading up to posterior tibial tendon dysfunction or rupture. The large number of potential contributory causes for posterior tibial dysfunction makes it clear that the cause is most probably multifactorial. The

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19 De Zwart DF, Davidson JS. Rupture of the posterior tibial tendon associated with fractures of the ankle. A report of two cases. J Bone Joint Surg Am 1983; 65: 260e2. 20 Myerson M, Solomon G, Shereff M. Posterior tibial tendon dysfunction: its association with seronegative inflammatory disease. Foot Ankle 1989; 9: 219e25. 21 Kirkham BW, Gibson T. Comment on the article by Downey et al. Arthritis Rheum 1989; 32: 359. 22 Jahss MH. Spontaneous rupture of the tibialis posterior tendon: clinical findings, tenographic studies, and a new technique of repair. Foot Ankle 1982; 3: 158e66. 23 Keenan MA, Peabody TD, Gronley JK, Perry J. Valgus deformities of the feet and characteristics of gait in patients who have rheumatoid arthritis. J Bone Joint Surg Am 1991; 73: 237e47. 24 Holmes GB, Mann RA. Possible epidemiological factors associated with rupture of the posterior tibial tendon. Foot Ankle 1992; 13: 70e9. 25 Frey C, Shereff M, Greenidge N. Vascularity of the posterior tibial tendon. J Bone Joint Surg Am 1990; 72: 884e8. 26 Petersen W, Hohmann G, Stein V, Tillmann B. The blood supply of the posterior tibial tendon. J Bone Joint Surg Br 2002; 84(1): 141e4. 27 Supple KM, Hanft JR, Murphy BJ, Janecki CJ, Kogler GF. Posterior tibial tendon dysfunction. Semin Arthritis Rheum 1992; 22(2): 106e13. 28 Delmi M, Kurt AM, Meyer JM, Hoffmeyer P. Calcification of the posterior tibialis tendon: a case report and literature review. Foot Ankle Int 1995; 16: 792e5. 29 Mueller TJ. Acquired flatfoot secondary to tibialis posterior dysfunction: biomechanical aspects. J Foot Surg 1991; 30: 2e11. 30 Trevino S, Gould N, Korson R. Surgical treatment of stenosing tenosynovitis at the ankle. Foot Ankle 1981; 2: 37e45. 31 Johnson KA, Strom DE. Tibialis posterior dysfunction. Clin Orthop Relat Res 1989; 239: 196e206. 32 Myerson MS. Adult acquired flatfoot deformity: treatment of dysfunction of the posterior tibial tendon. J Bone Joint Surg Am 1996; 78: 780e92. 33 Rosenberg ZS, Jahss MH, Noto AM, Norman A, Leeds NE. Rupture of the posterior tibial tendon: CT and surgical findings. Radiology 1988; 167(2): 489e93. 34 Wacker JT, Calder JD, Engstrom CM, Saxby TS. MR morphometry of posterior tibialis muscle in adult acquired flat foot. Foot Ankle Int 2003; 24: 354e7. 35 Gerling MC, Pfirrmann CW, Farocki S, et al. Posterior tibial tendon tears: comparison of the diagnostic efficacy of magnetic resonance imaging and ultrasonography for the detection of surgically created longitudinal tears in cadavers. Invest Radiol 2003; 38(1): 51e6. 36 Kulig SA, Burnfield JM, Requejo SM, Sperry M, Terk M. Selective activation of tibialis posterior. Evaluation by magnetic resonance imaging. Med Sci Sports Exerc 2004; 36(5): 862e7. 37 Wacker JT, Hennessey MS, Saxby TS. Calcaneal osteotomy and transfer of the flexor digitorum longus for stage-II dysfunction of tibialis posterior. Three- to five-year results. J Bone Joint Surg Br 2002; 84-B: 54e8.

acquired flatfoot deformity is only the endstage of a complicated sequence of biomechanical failures in the architecture of the normal foot and ankle. A

REFERENCES 1 Pfeiffer M, Kotz R, Ledl T, Hauser G, Sluga M. Prevalence of flat foot in preschool-aged-children. Pediatrics 2006; 118: 634e9. 2 Staheli LT, Chew DE, Corbett M. The longitudinal arch. A survey of 882 feet in normal children and adults. J Bone Joint Surg Am 1987; 69: 426e8. 3 Newman JS, Newberg AH. Congenital tarsal coalition: multimodality evaluation with emphasis on CT and MR imaging. RadioGraphics 2000; 20: 321e32. 4 Leonard MA. The inheritance of tarsal coalition and its relationship to spastic flat foot. J Bone Joint Surg Br 1974; 56B: 520e6. 5 Chapman VM. The anteater nose sign. Radiology 2007; 245: 604e5. 6 Sartoris DJ, Resnick DL. Tarsal coalition. Arthritis Rheum 1985; 28: 331e8. 7 Herzenberg JE, Goldner JI, Martinez S, Silverman PM. Computerized tomography of talocalcaneal tarsal coalition: a clinical and anatomic study. J Foot Ankle 1986; 6: 273e88. 8 Kumar SJ, Guille JT, Lee MS, Couto JC. Osseous and non-osseous coalition of the middle facet of the talocalcaneal joint. J Bone Joint Surg Am 1992; 74: 530e5. 9 Scranton Jr PE. Treatment of symptomatic talocalcaneal coalition. J Bone Joint Surg Am 1987; 69: 539e53. 10 Lloyd-Roberts GC, Spence AJ. Congenital vertical talus. J Bone Joint Surg Br 1958; 40B: 33e41. 11 Esterman A, Pilotto L. Foot shape and its effect on functioning in Royal Australian Air Force recruits. Part 1: Prospective cohort study. Mil Med 2005; 170: 623e8. 12 Giladi M, Milgrom C, Stein M, et al. The low arch, a protective factor in stress fractures: a prospective study of 295 military recruits. Orthop Ref 1985; 14: 709e12. 13 Kaufman KR, Brodine SK, Shaffer RA, Johnson CW, Cullison TR. The effect of foot structure and range of motion on musculoskeletal overuse injuries. Am J Sports Med 1999; 27(5): 585e93. 14 Jones BH, Thacker SB, Gilchrist J, Kimsey CD, Sosin DM. Prevention of lower extremity stress fractures in athletes and soldiers: a systematic review. Epidemiol Rev 2002; 24: 228e47. 15 Deland JT, Arnoczky SP, Thompson FM. Adult acquired flatfoot deformity at the talonavicular joint: reconstruction of the Spring ligament in an in vitro model. Foot Ankle 1992; 13: 327e32. 16 Mizel MS, Temple HT, Scranton Jr PE, et al. Role of the peroneal tendons in the production of the deformed foot with posterior tibial tendon dysfunction. Foot Ankle Int 1999; 20(5): 285e9. 17 Lapidus PW. Kinesiology and mechanical anatomy of the tarsal joints. Clin Orthop Relat Res 1963; 30: 30e6. 18 Saraffian SK. Anatomy of the foot and ankle. Philadelphia: JB Lippincott, 1983. pp. 43e61; 216e19; 375e425.

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(iii) Entrapment neuropathies of the foot and ankle

A third, smaller, branch, the medial calcaneal nerve (MCN), pierces the retinaculum to supply sensation to the heel and medial hindfoot. The two plantar nerves each pierce the fascia of abductor hallucis (AbH) before supplying the musculature of the foot and sensation to the sole of the foot. The flexor retinaculum (syn: lancinate ligament) roofs the fibro-osseous tarsal tunnel which as well as the tibial neurovascular bundle contains the flexor tendons; tibialis posterior, flexor digitorum longus and flexor hallucis longus. The tunnel extends from approximately 10 cm proximal to the medial malleolus to the sustentaculum tali distally. The medial wall of the tunnel is comprised successively of the distal tibia and medial malleolus, the talus, the infero-medial portion of the navicular, the sustentaculum tali and the medial surface of the calcaneum. As the tunnel is fully enclosed, the volume and pressure within the tunnel is critical. Significant decreases in the volume of the tunnel or increases in the pressure within it will compress the neural bundle.4,5 Tarsal Tunnel Syndrome is caused by compression of the tibial nerve or its terminal branches between the proximal origin of the flexor retinaculum and its exit from the tarsal tunnel, where the plantar nerves pierce the AbH fascia. This can result from an intrinsic problem of the nerve itself or from an external compressive force. Specific causes (Table 1) are both local and general. While in many cases the aetiology remains idiopathic, a recognisable cause can be identified in up to 80% of cases 6 and the commonest underlying problem is of proliferation or oedema of the connective tissues within the tunnel reducing its volume.

Timothy HD Williams Andrew HN Robinson

Abstract Any of the 5 nerves supplying the foot and ankle (tibial, superficial & deep peroneal, sural, saphenous) can suffer compression neuropathy. The diagnosis is usually made clinically, supported by imaging and electrodiagnostic studies. Treatment is conservative or surgical. The known nerve entrapments about the foot and ankle are presented with a discussion of their aetiology, clinical findings and treatment options.

Keywords ankle; foot; nerve compression; nerve entrapment; neuropathy

Introduction Entrapment neuropathies are a source of significant morbidity, but they are rare. They must be differentiated from radicular back pain caused by nerve root entrapment, and peripheral neuropathies secondary to systemic disease such as diabetes mellitus.1 The nerve supply to the foot comprises five peripheral nerves. Four of these (tibial, deep peroneal (DPN), superficial peroneal (SPN) and sural) are branches of the sciatic nerve and the fifth, the saphenous, is a terminal branch of the femoral nerve. Entrapment of any of these nerves along their entire length can give symptoms in the foot and ankle, which can range from intermittent pain and paraesthesia to motor weakness and muscle wasting.

Clinical Features: The presentation of TTS is with an insidious onset of heel pain, radiating to the sole of the foot and occasionally proximally. It is aggravated by activity and relieved by rest, and, as with carpal tunnel syndrome, is often worse at night. There is intermittent paraesthesia and occasionally anaesthesia. In the later stages, there is wasting of the intrinsic muscles most obviously in AbH. It is usually unilateral; bilateral symptoms should lead the clinician to look for a systemic cause. Examination begins with the patient standing to assess heel and foot alignment, especially valgus heel malalignment. Varicosities may only be apparent at this point, disappearing once the patient is supine. A general examination of the back and peripheral nervous system is essential. Proximal compression of the tibial nerve itself can occur, particularly at the tendinous arch of the soleus origin or with soft tissue masses around the popliteal fossa. L5 radicular pain can be experienced in the medial side of the foot. A negative straight leg raise test, persistent deep tendon reflexes and maintained power in the long extensors and flexors should raise the suspicion of TTS. Spinal nerve root compression, peripheral neuropathy and peripheral vascular disease should always be considered, with the caveat that they can co-exist with TTS. Then the tibial nerve is palpated from proximal to distal to assess for thickening or an adjacent tumour. The foot is then assessed, inspecting for intrinsic muscle wasting, particular attention is paid to the AbH as a site or result of the entrapment. Any change in sensibility should be mapped using a 10 gram Semmes-Weinstein monofilament (Figure 3) as a dermatomal distribution of sensibility changes would be suggestive of nerve

Tibial nerve entrapment Tarsal tunnel syndrome Tarsal tunnel syndrome (TTS) is caused by entrapment of the tibial nerve around the ankle. It was first described in 1932 and named by Keck and Lam in 1962.2 It is an uncommon condition predominantly of adults, with a slight female predominance.2 Aetiology: The tibial nerve is a terminal branch of the popliteal nerve that descends deep to soleus with the posterior tibial vessels. It passes behind the medial malleolus in the tarsal tunnel. In 93% of the population3 it divides into its two main branches, the medial and lateral plantar nerves (MPN & LPN).

Timothy HD Williams MBBS MRCS FRCS(Orth) Specialist Registrar, Department of Orthopaedics, BOX 37, Addenbrooke’s Hospital, Cambridge, UK. Andrew HN Robinson MBBS BSc FRCS (Orth) FRCS ECFMG Consultant Foot & Ankle Surgeon, BOX 37, Addenbrooke’s Hospital, Cambridge, UK.

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ankle or hindfoot orthoses, varicose vein management, ganglion aspiration, anti-inflammatories and occasionally local steroid injections can provide symptomatic relief, but TTS is often refractory to such measures, necessitating surgical release. First described by Lam,5 this is performed through a curvilinear incision centred posterior to the medial malleolus and tracing the course of the nerve. The flexor retinaculum is released from its proximal origin to the sustentaculum tali and the tibial nerve is decompressed and tracked distally to enable identification and release of the MPN, LPN and the perforating medial calcaneal nerve. The fascial openings in AbH should be incised. The tarsal tunnel needs careful exploration; it is not uncommon to find space occupying lesions pressing on or even intrinsic to the nerve. Figure 4 shows a schwannoma, but ganglia etc can present in this way. The retinaculum is left open and the skin closed. Post-operative management comprises two weeks cast or rigid boot immobilisation with elevation for wound healing, followed by early range of motion exercises. Protected weight bearing is allowed from the outset. Reported results differ with series varying from 44 to 90% good/excellent results. The commonest cause of recurrence or persistence of symptoms is inadequate release, usually proximally, and associated with scarring.4 Revision surgery is much less predictable and a careful search for a more proximal or general cause should be undertaken first.

Causes of tarsal tunnel syndrome7 Local Causes

General Causes

Idiopathic Trauma/Scarring Venous varicosity Neuroma Ganglion Fibrosis Tarsal Coalition Tumour (Fig xxx) AbH fascia constriction Heel varus/valgus

Diabetes Rheumatoid Arthritis Hypothyroidism Hypercholesterolaemia Systemic Lupus Erythematosus Ankylosing Spondylitis Acromegaly Obesity Alcoholism

Table 1

root compression or the examination might show the more generalised abnormal findings of a peripheral neuropathy. Tinel’s8 tap test, percussing along the route of the nerve from proximal to distal, can reproduce the patient’s symptoms distally in the foot the the site of compression is tapped. This is often associated with pain. (The Valleix phenomenon4 is the production of parasthesia and pain proximally as well as distally along the course of the nerve from the damaged area when percussed.) A more subtle test uses an inflated blood pressure cuff wrapped around each ankle which may elicit paraesthesia and pain in the affected foot before the contralateral.4 Passive ankle inversion reduces the volume of the tarsal tunnel and eversion and dorsiflexion stretches the nerve. Thus either of these movements may reproduce the patient’s symptoms. Peripheral pulses and capillary refill should be checked to exclude peripheral vascular disease. Local differentials to be considered include plantar fasciitis, soft tissue trauma, metatarsalgia, Morton’s neuroma and a tarsal coalition.

Medial plantar nerve entrapment (syn: joggers foot)7 After piercing the AbH muscle fascia the MPN runs with flexor digitorum longus (FDL) tendon. MPN lies in close proximity to the knot of Henry, the decussation of the FDL and flexor hallucis longus tendons. Entrapment here causes intermittent medial midfoot pain and parasthesia. It occurs in athletes or associated with use of medial arch orthoses which compress the medial midfoot. A valgus hindfoot, positive Tinel’s test, pain with ankle eversion and exacerbation when on tiptoe will help narrow the differential diagnosis. If conservative management fails, particularly alteration of shoes, orthoses and training modification, surgical release is performed through a medial arch incision. In essence the release is a continuation of a tarsal tunnel decompression, extended toward the plantar aspect of the navicular to expose the knot of Henry.

Investigations: Standing plain radiographs of the foot and ankle should be performed to assess alignment and to exclude tarsal coalitions, fractures or space occupying lesions. Serological tests for general causes including inflammatory markers should be performed. Ultrasound and MRI can detect and often identify space occupying lesions within the tarsal tunnel itself, as well as subtle coalitions or fractures. Electrodiagnostic studies provide further diagnostic support; reduced conduction velocity and delayed latency compared with the contralateral foot is seen with greater sensitivity in sensory, rather than motor nerves.9 Positive electrophysiological studies are supportive of a clinical diagnosis, but negative findings do not rule out TTS, but they may point to a more proximal or systemic cause. Even in this situation a double crush phenomenon (see below) with entrapment of the nerve at two levels synchronously should be considered.

Entrapment of the first branch of the lateral plantar nerve (lpn)10 This is an uncommon condition predominantly of male athletes.10 It should be considered in chronic heel pain sufferers unresponsive to conservative measures. Importantly, this is a differential diagnosis of plantar fasciitis. The first branch of the LPN, also known as Baxter’s nerve,10 passes obliquely between the deep AbH fascia and the medial quadratus plantae (QP) fascia. It then runs under flexor digitorum brevis and supplies sensory innervation to the periosteum of the medial process of the calcaneal tuberosity and the lateral heel, and the motor innervation of flexor digitorum brevis and abductor digiti minimi. The patient presents with heel pain radiating to the ankle, typically not accompanied by paraesthesia. Initial treatment is non-operative, including cushioning heel cup orthoses and anti-inflammatory medication. If non-operative

Treatment: Systemic causes, such as diabetes mellitus and rheumatoid arthritis should be treated Alignment correcting

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treatment fails surgical release of the superficial and deep AbH fascia to decompress the nerve is undertaken. Surgery is performed through a medial approach, as an extension of a tarsal tunnel release in the majority of cases. The LPN is traced distally until its first branch is decompressed.

If, when a thumb is pushed into the web space from the plantar aspect with the foot dorsiflexed and the forefoot is squeezed in a medio-lateral direction, a painful crunch or click (palpated on the dorsal aspect of the web space) is elicited, it is diagnostic (Mulder’s click14) (Figure 5). On careful examination, the sensibility of the toes is often altered or reduced.

Common digital nerve entrapment e Morton’s neuroma This is a common condition, first described by Morton in 1876. Morton’s neuroma has become recognised as an entrapment neuropathy affecting the plantar digital nerves below and distal to the transverse metatarsal ligament caused by entrapment and crushing of the nerve between the metatarsal heads. Histologically an amorphous eosinophilic material is deposited within the nerve, which is followed by slow degeneration,7,11 the perineurium thickens and fibroses, local demyelination occurs and although the overall nerve and vesicular thickness increases, the nerve fibres are thinned. Thus Morton’s neuroma is not a true neuroma.

Investigation: Standing AP and lateral X-rays of the foot should be obtained to identify possible degenerate change, Freiberg’s disease, dislocated MTPJ’s or exostoses. Ultrasound, whilst operator dependant, has been shown to have a sensitivity of up to 92% and a specificity of 100%15 in identifying a Morton’s neuroma and MRI has been shown to produce similar results, we consider the diagnosis is primarily clinical. Treatment: Initial treatment is conservative with shoes with a wide toe box and low heels combined with insoles with a metatarsal pad proximal to the neuroma to off-load it, and possibly widen the inter-space can be beneficial. Injection of the inter-space with steroid has been shown to give short term relief in up to 80% of patients. However, Rasmussen and colleagues showed that 47% of those injected still ended up requiring surgery, and the remainder had some residual symptoms.16 Higher success rates have been reported with repeated injection with alcohol under sonographic guidance, Hughes et al17 reporting partial or total symptomatic improvement in 94% of 101 patients after an average of four injections. Ultrasound sonography at six months following injections in 30 of the patients demonstrated a 30% reduction in the size of the neuroma. However further reports are awaited and long term results are, as yet unknown. If non-operative measures fail, surgical treatment is by local neurectomy. The approach to the common digital nerve can be either dorsal or plantar, and there is continuing debate as to which approach is better. While we prefer a dorsal incision in the primary case, other experienced foot surgeons use a plantar approach with few reported problems. A Cochrane review in 2004 concluded that there is ‘at best, very limited indications to suggest that dorsal incisions may result in less symptomatic postoperative scars when compared to plantar’.18 Both dorsal or plantar approaches utilise longitudinal incisions over the appropriate inter space. If approached dorsally, the inter-metatarsal ligament must be divided to identify the nerve. Then the nerve is exposed proximally, close to the intrinsic muscle and traced distally towards each toe to a point 1 cm beyond its bifurcation. The nerve is sharply divided at all three points. Proximally this is performed with the nerve under slight tension so that the cut end retracts into the intrinsic muscle. The specimen (Figure 6) should undergo histological examination to confirm the diagnosis. Post-operatively, cautious full weight bearing in a soft dressing is allowed, with rest and elevation until wound healing is sound. Great care must be taken if exploring two adjacent web spaces at one time. It is the senior author’s practice not to undertake simultaneous resection of adjacent neuromata. If two neuromata are identified, the largest is resected, and the inter-metatarsal ligament of adjacent space is divided. If at the conclusion of surgery a toe is cyanotic toe, the dressings should be reduced, the

Aetiology: It is more common in women (w8:1), usually affecting those aged between 40 and 60. The third web space is the most commonly affected, followed by the second. It is almost unrecognised in the first and fifth web spaces and synchronous involvement of two interspaces is not uncommon. The reason for the predominance of lesions in the third web space is not certain; there are three principal theories.  The third web space is the junction between the relatively stable 1st, 2nd and 3rd metatarsals and the more mobile 4th and 5th rays.  Anatomical studies have shown that the 2nd and 3rd interspaces are smaller, making entrapment more likely.12  The third web space has an accessory, interconnecting branch from the LPN to its MPN in 27%13 of individuals. The consequent increase in overall neural diameter and tethering is proposed as contributing to the high incidence of Morton’s neuromas in the third web space. Clinical: Classically the patient presents with plantar pain between the MT heads worsened by walking, often in a high heeled or narrow toe box shoe. The pain is relieved by removing the shoe, or bare foot walking. The pain is burning in nature and radiates to the adjacent toes supplied by the involved common digital nerve. Later, sufferers may complain of numbness or tingling in the toes, as well as a feeling of walking on a pebble. Examination begins with the patient standing. Obviously, a full spinal and peripheral nerve examination should be performed to exclude more proximal causes including TTS, peripheral neuropathies and sciatica. Then, deviation of the toes should be sought. While this is not a specific feature of a Morton’s neuroma, it can be indicative of synovitis of the metatarsophalangeal joint (MTPJ) which can cause inter-digital nerve compression, and the symptoms of Morton’s neuroma. Thus each MTPJ should be examined for signs of inflammation evidenced by tenderness or reduced range of motion. In patients with synovitis, this should be treated before treating the Morton’s neuroma. If the tenderness is in the webspace when squeezed between finger and thumb, rather than over the MTPJ, the diagnosis is more likely to be Morton’s neuroma.

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foot placed dependant and warmed, which usually restores the blood supply. The procedure leaves the web space partially anaesthetic. Other complications include wound-healing problems, scar pain, haematoma formation and vascular insufficiency from vasospasm or division of the inter-digital artery; amputation as a result of gangrene has been reported. The most troublesome complication is a painful stump neuroma. The incidence can be reduced by adequate proximal division at the level of the interosseous muscle, and even burying the resected stump in the muscle. Because of this complication, there is renewed interest in local, decompressive neurolysis by releasing the inter-metatarsal ligament through a dorsal approach.19

Weight bearing AP and lateral X-rays of the foot and ankle will show any osseous abnormality. Electrodiagnostic studies will demonstrate increased latency (>5ms) and reduced distal velocity, but with preserved function proximally.21 However, electro-diagnostic abnormalities of innervation of EDB is neither sensitive nor specific.4,22 Any soft tissue mass encountered such as a lipoma, ganglion synovial cyst etc. should be investigated with MRI or ultrasound. Conservative treatment starts with advice on footwear; alteration of the lacing pattern, or the tongue of the shoe maybe all that is required! If operative treatment is necessary, the site of the preoperative Tinel’s sign can be used as a guide. Operative decompression of the tunnel following the lateral border of EHL allows exposure and decompression of the nerve. It is important to remove any space-occupying lesion, such as osteophytes, and ganglia. However full release of the retinaculum should not be undertaken to avoided the risk of tendon bowstringing. If a full release is necessary, a ‘‘Z- plasty’’ of the retinaculum should be performed, allowing the retinaculum to be re-constituted without tension.

Deep peroneal nerve (dpn) entrapment Anterior tarsal tunnel syndrome Named anterior tarsal tunnel syndrome (ATTS) in 1968 by Marinacci20 this condition is caused by entrapment of the DPN as it crosses in front of the ankle to the foot. As common in men as women, it affects adults from adolescence into the 60’s.

Superficial peroneal nerve (spn) entrapment The SPN is a branch of the CPN below the fibular neck (Figure 8). The nerve runs in and supplies the peroneus longus and brevis muscles. It pierces the deep fascia 10 cm to 15 cm above the tip of the fibula, becoming subcutaneous. Its terminal branches are the medial and intermediate, which supply sensation to the dorsum of the foot and ankle, ending over all five toes, but there is a considerable overlap with the other cutaneous nerves. Entrapment occurs as it pierces the fascia above the ankle as a result of direct irritation by a tight fascial band. This can result from trauma, especially repetitive ankle sprains which can also give rise to perineural fibrosis of the nerve. Local masses or muscle hernias at the fascial orifice or proximally can also compromise the nerve. Additionally the nerve can be injured as a complication of ankle fractures involving the fibula or of the surgery to treat such fractures as the SPN is at risk when the fibula, particularly distally, is operatively exposed.23

Aetiology: The DPN is a branch of the common peroneal nerve arising as it passes around the fibular neck. It supplies the anterior compartment of the leg. Distally it passes under the superior and inferior extensor retinacula between the tendons of the extensor digitorum longus and the extensor hallucis longus. The anterior tarsal tunnel is a fibro-osseous, flattened space between the inferior extensor retinaculum and the fascia overlying the talus and navicular. (Figure 7). There is a motor branch to extensor digitorum brevis (EDB), but symptoms relate to the terminal sensory branch, which supplies the dorsal skin of the first web space. Entrapment can occur anywhere along its course but commonly at the superior and inferior edges of the inferior retinaculum, within the anterior tarsal tunnel itself and under the extensor hallucis brevis tendon. Accessory ossicles or osteophytes at the level of the talonavicular joints can also cause irritation of the DPN. One of the commonest sites of entrapment leading to clinical symptoms is over the tarsometatarsal joint, where the nerve may be stretched over osteophytes and in the older population a common site of entrapment is by osteophytes over the second tarso-metatarsal joint. While not strictly ATTS, these present in an identical manner.

Clinical Typically a young adult presents with intermittent symptoms related to activity often of a long duration. They complain of burning pain radiating from the ankle to the dorsum of the foot, accompanied by paraesthesia in about a third of patients.7 Night pain is uncommon. Any history of ankle trauma and especially local surgery should be noted (Figures 1e9). As with other peripheral nerve entrapments, the clinician must consider more proximal entrapments including sciatica and CPN entrapment at the fibular neck. Localised tenderness proximal to the lateral malleolus may be elicited and there may be a palpable fascial defect or muscle hernia. Styf’s provocative test24 is performed by palpating the fascial defect combined with active dorsiflexion and eversion of the foot against resistance. If positive, this elicits pain. Tenderness elicited with passive plantarflexion and inversion of the foot and percussion over the local area is also highly suggestive of SPN entrapment. Symptomatic relief can be achieved with steroid and local anaesthetic injections which is also a diagnostic tool.

Clinical: ATTS predominantly affects sportsmen or women. Pressure from shoes, particularly running shoes and ski boots, often exacerbates the symptoms as does the excessive plantar flexion whilst running or wearing high heels. The pain is over the dorsum of the foot radiating to the first and second toes. It is burning in nature and accompanied by paraesthesia. Inspection of the patient’s shoes should be part of the examination. Local tenderness of the nerve and a positive Tinel’s test may be elicited. Permanent dysaesthesia in the first webspace is uncommon. Wasting of EDB muscle belly implies compression of the DPN proximal to its bifurcation and the differential diagnosis then includes more proximal lesions of both the DPN and CPN. Any tenderness at the fibular neck with wasting of the anterior compartment should be noted as this suggests a more proximal lesion, such as an exertional compartment syndrome or CPN irritation.

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Figure 1 Medial side of the ankle illustrating the course and branches of the tibial nerve.

Figure 3 Semmes Weinstein monofilaments. The fine fibres are applied to the skin. When the fibre bends, the patient is asked if they can feel it. The fibres are calibrated, and the 10 gramme is the most commonly used threshold (this is the central of the three filaments shown).

Pharmacological management with gabapentin can be effective. Refractory cases may require local fasciotomy and neurolysis through an incision over the point of maximum tenderness. Then a fasciotomy and neurolysis is carried out to fully decompress the nerve. Reported results have shown 75% satisfaction or symptom improvement,24 but in athletes the outcome appears to be less predictable.

Sural nerve entrapment Anatomy The sural nerve arises from the tibial nerve in the popliteal fossa, and then passes between the two heads of gastrocnemius. It pierces the deep fascia in the mid third of the calf, and is then joined by the peroneal communicating branch of the lateral sural cutaneous nerve. It then runs subcutaneously approximately 1 cm lateral to the Achilles tendon, onto the lateral border of the foot. It is a purely sensory nerve and its terminal branches supply the skin of the lateral side of the heel and border of the 5th metatarsal and toe. There is commonly overlap with the intermediate branch of the SPN supplying the 4th webspace. Aetiology Entrapment can occur anywhere along the course of the sural nerve. Proximal compression has been reported following gastrocnemius muscle tears and at the fascial orifice through which the sural nerve emerges. Entrapment in athletes may be due to muscle hypertrophy or fascial scarring from microtrauma.25 More distally, recurring instability of the ankle and acute fractures of the 5th metatarsal can cause symptoms. Lateral

Figure 2 Plantar aspect of the foot illustrating the branches of the tibial nerve.

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Figure 4 A Schwannoma of the tibial nerve.

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Figure 5 Eliciting Mulder’s click. (See text for details).

Chopart joint ganglia compressing the nerve have also been reported.26 Figure 7 Dorsal view of the foot and ankle illustrating the course of the deep peroneal nerve.

Clinical There is often a history of intense athletic training or trauma. Pain and paraesthesia affecting specific areas can help localise the lesion. Again, examination should include the spine and spinal nerves, particularly looking for S1 sciatica. Sites of specific tenderness should be noted, as should a Tinel’s sign. Treatment is by surgical release of the nerve at the site of entrapment and any predisposing ankle instability should be treated with physiotherapy, bracing or reconstruction as appropriate.

thigh with the superficial femoral artery. After exiting the adductor canal through the fascia lata it divides into an infrapatellar branch, which supplies the skin over the lower knee, and a descending branch. The descending branch continues with the long saphenous vein to the foot. Two terminal branches supply the medial ankle and medial midfoot, the latter overlapping the medial branch of the SPN. Aetiology Lying subcutaneously anterior to the medial malleolus, the saphenous nerve is not prone to distal entrapment. It may be entrapped more proximally in Hunter’s (adductor) canal. Acute traumatic causes, particularly around the knee are also well

Saphenous nerve entrapment Anatomy The saphenous nerve is an entirely sensory branch of the femoral nerve. It arises within the femoral triangle, passing down the

Figure 8 Anterolateral view of the lower leg and foot illustrating courses of the nerves.

Figure 6 A surgical specimen of a Morton’s neuroma. Note the proximal nerve, and two distal digital nerves.

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REFERENCES 1 Pickard JD, Robinson AH, Bearcroft PW. Posterior tarsal tunnel syndrome: an unusual unrelated cause of late pain after lumbar spine surgery. Br J Neurosurg 2006 Oct; 20: 331e2. 2 Keck C. The tarsal tunnel syndrome. J Bone Joint Surg Am 1962; 44: 180e2. 3 Dellon AL, Mackinnon SE. Tibial nerve branching in the tarsal tunnel. Arch Neurol 1984; 41: 645e6. 4 Wallach DM, Katchis SD. Tarsal tunnel syndrome. In: Ranawat CS, Positano RG, eds. Disorders of the heel, rearfoot, and ankle. Churchill Livingston, 1999: p. 125e34. 5 Lam SJ. Tarsal tunnel syndrome. J Bone Joint Surg Br 1967; 49: 87. 6 Cimino WR. Tarsal tunnel syndrome: review of the literature. Foot Ankle 1990; 11: 47e52. 7 Mann RA. Diseases of the nerves. In: Mann RA, ed. Surgery of the foot and ankle. Mosby, 1999. Chapter 11. 8 Tinel J. ‘‘Tingling’’ signs with peripheral nerve injuries 1915. J Hand Surg Br 2005 Feb; 30: 87e9. 9 Patel AT, Gaines K, Malamut R, et al. Usefulness of electrodiagnostic techniques in the evaluation of suspected tarsal tunnel syndrome: an evidence-based review. Muscle Nerve 2005 Aug; 32: 236e40. 10 Baxter DE, Pfeffer GB. Treatment of chronic heel pain by surgical release of the first branch of the lateral plantar nerve. Clin Orthop 1992; 279: 229e36. 11 Lassmann G. Morton’s toe. Clinical, light, and electron microscopic investigations in 133 cases. Clin Orthop 1979; 142: 73. 12 Levitsky KA, Alman BA, Jevsevar DS, Morehead J. Digital nerves of the foot: anatomic variations and implications regarding the pathogenesis of interdigital neuroma. Foot Ankle 1993 May; 14: 208e14. 13 Jones JR, Klenerman L. A study of the communicating branch between the medial and lateral plantar nerves. Foot Ankle 1984; 4: 313. 14 Mulder JD. The causative mechanism in Morton’s metatarsalgia. J Bone Joint Surg 1951; 33: 94e5. 15 Kankanala G, Jain AS. The operational characteristics of ultrasonography for the diagnosis of plantar intermetatarsal neuroma. J Foot Ankle Surg 2007 JuleAug; 46: 213e7. 16 Rasmussen MR, Kitaoka HB, Patzer GL. Nonoperative treatment of plantar interdigital neuroma with a single corticosteroid injection. Clin Orthop; 1996 May: 188e93. 17 Hughes RJ, Ali K, Jones H, Kendall S, Connell DA. Treatment of Morton’s neuroma with alcohol injection under sonographic guidance: follow-up of 101 cases. AJR Am J Roentgenol 2007 Jun; 188: 1535e9. 18 Thomson CE, Gibson JN, Martin D. Interventions for the treatment of Morton’s neuroma. Cochrane Database Syst Rev 2004; (3): CD003118. 19 Villas C, Florez B, Alfonso M. Neurectomy versus neurolysis for Morton’s neuroma. Foot Ankle Int 2008 Jun; 29: 578e80. 20 Marinacci AA. Neurological syndromes of the tarsal tunnels. Bull Los Angeles Neurol Soc 1968 Apr; 33: 90e100. 21 Zongzhao L, Jiansheng Z, Li Z. Anterior tarsal tunnel syndrome. J Bone Joint Surg Br 1991; 73: 470e3. 22 Anderson BL, Wertsch JJ, Stewart WA. Anterior tarsal tunnel syndrome. J Bone Joint Surg 1984; 66: 786e7. 23 Redfern DJ, Sauve PS, Sakellariou A. Investigation of superficial peroneal injury following ankle fracture. Foot Ankle Int 2003; 24: 771e4. 24 Styf J. Entrapment of the superficial peroneal nerve: diagnosis and results of decompression. J Bone Joint Surg 1989; 71B: 131.

Figure 9 Dorsal view of the foot and ankle illustrating the peripheral nerve sensory supply.

recognised and isolated entrapment of the infrapatellar branch is recognised, giving rise to localised symptoms. Iatrogenic damage during surgery of the knee or varicose vein surgery with stripping or avulsions may occur giving rise to entrapment with perineural fibrosis. Clinical The presenting symptoms are of medial knee and calf pain with associated paraesthesia over the dorsum of the medial foot, particularly the 1st ray. As it is a sensory nerve, the findings of weakness or dysreflexia should alert the clinician to a more proximal lesion, such as L3/L4 radiculopathy. A tender point with a positive Tinel’s test along the course of the nerve will be diagnostic. Local anaesthetic injection can assist in making the diagnosis and electro-diagnostic studies can be helpful. Surgical management is best avoided and treatment is usually directed at the more proximal symptoms. Judicious use of corticosteroids and local anaesthetic blocks around Hunter’s canal have been suggested in the literature.

A general caveat e the double crush phenomenon Whenever considering the aetiology of a distal nerve entrapment, consideration should always be given to search for a second, often primary, proximal lesion. This can be synchronous or metachronous, general (e.g. diabetes) or local (e.g. radiculopathy). The proximal nerve insult can change the physiology of the distal nerve, increasing its sensitivity to entrapment. Both sites of compression must be addressed in order to achieve a satisfactory clinical outcome.27 A

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25 Fabre T, Montero C, Gaujard E, Gervais-Dellion F, Durandeau A. Chronic calf pain in athletes due to sural nerve entrapment. A report of 18 cases. Am J Sports Med 2000 Sep-Oct; 28: 679e82.

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26 Pringle RM, Protheroe K, Mukherjee SK. Entrapment neuropathy of the sural nerve. J Bone Joint Surg 1974; 56B: 465. 27 Augustijn P, Vanneste J. The tarsal tunnel syndrome after a proximal lesion. J Neurol Neurosurg Psychiatry 1992 Jan; 55: 65e7.

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(iv) Imaging of foot and ankle disorders

assessment of acute osseous injury and most injuries can be managed without resorting to any other imaging modality. It has very limited value in the assessment of chronic soft tissue disorders. The standard views of the ankle are the AP and lateral. The AP should be performed routinely with 15 of internal rotation giving the ‘‘mortise view’’. A variety of measurements of the syndesmosis have been reported to assess the integrity of the distal tibiofibular joint but all the measurements are prone to inaccuracy, as they are subject to marked variation with slight alterations in the degree of rotation. A good rule of thumb is that the fibula and tibia should overlap by at least 1 mm. The medial joint space should be less than or equal to the superior joint space (Figure 1). In this situation a radiograph of the whole fibula may be required to detect the Maisonneuve fracture. On the lateral view Boehler’s angle can be measured to assess disruption of the subtalar joint due to a calcaneal fracture. The normal Boehler’s angle should measure between 28 and 40 . A variety of other views have been described, including oblique and subtalar views. Most centres have now abandoned these and proceed straight to CT if further imaging is required. The presence of a cast on the limb is no hindrance to CT or MRI scanning of the ankle. Weight bearing views of the ankle allow assessment of the thickness of the articular cartilage and joint congruity under loading, but are not used in the context of acute trauma. Stress views can be performed on both the AP and lateral views for the assessment of chronic ligamentous instability but in a lot of situations this adds little to the clinical assessment and US and MRI provide a more direct assessment of ligamentous integrity. Standard trauma views of the foot are the dorsi-plantar (DP), the 30 oblique and the lateral projection. The tarsal metatarsal

James J Rankine

Abstract This article gives an overview of the imaging modalities used in the assessment of acute and chronic foot and ankle disorders in the adult patient. The relative merits of each imaging modality are explained and examples are given of the common conditions.

Keywords ankle; computed tomography; foot; magnetic resonance imaging; ultrasound

Introduction Virtually every patient with a foot and ankle disorder will have conventional radiography performed. This is clearly quick and easy to perform and has a pivotal role to play in the assessment of acute bony injury. Whilst the bony alignment can suggest the integrity of the ligamentous structures, it is generally of limited use in the assessment of soft tissue injuries. Computed tomography (CT) adds sectional imaging to the assessment of the foot and ankle, can demonstrate undisplaced fractures not seen on conventional radiography and can show good anatomical definition, even in the presence of a substantial amount of metalwork. It shares conventional radiography’s limited ability to assess the soft tissues. Ultrasound (US) is now far more widely available in the UK since it became a core part of the training for musculoskeletal radiologists. In many aspects it is superior to MRI in the assessment of tendons and ligaments, having a greater resolution and the ability to scan dynamically. It is limited in the assessment of the bony structures and the articular surfaces. MRI therefore provides the best overall assessment of combined bone and soft tissue injuries. These imaging modalities cover the vast majority of techniques, and their use in the adult patient will be explored in greater detail in this article. MR arthrography has a very limited role in the assessment of the stability of osteochondral fractures and in the assessment of ankle impingement syndromes. Isotope scanning may have a very limited role in assessing infection or chronic bone injury in patients who have contraindications to MR scanning, or where the quantity of metalwork renders the images non-diagnostic. Box 1 summarizes the advantages and disadvantages of each imaging modality.

Summary of the advantages and disadvantages of each imaging modality Modality Advantages Radiography Readily available Good bone detail CT Good bony anatomical detail Multiplanar reformatting capabilities Quick scanning times Metalwork artefact is limited on modem CT scanners US High resolution images of the soft tissues Dynamic scanning ability e partial v. complete tendon tear, ligament tears MRI Best overall imaging of the bone and soft tissues

Conventional radiography Conventional radiography is the initial imaging modality for the majority of foot and ankle disorders. It’s main role remains in the

James J Rankine MRCP MRad FRCR MD Consultant Radiologist at the MRI Department, Leeds General Infirmary, Leeds, UK.

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Disadvantages Poor soft tissue detail Poor soft tissue definition therefore of limited use in tendon, ligament and cartilage injury

Poor bony definition e only demonstrates bone surface Can not image the articular surface Lengthy scanning times Images prone to motion and metalwork artefact

Box 1

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a There is a slight widening of the medial joint space. There remains overlap of the distal tibia and fibula. b A repeat radiograph shows more obvious widening of the medial joint space and there is a clear evidence of disruption of the syndesmosis with no overlap between the tibia and fibula. c Radiograph of the whole fibula confirmed a proximal fibula fracture, a Maisonneuve fracture. Figure 1

alignment requires particular attention in order to diagnose a Lisfranc injury. The tarsal metatarsal joint spaces are not well visualized on the DP view due to the normal plantar arch resulting in an oblique projection of the articular surfaces. Particular care should be given to the alignment of the joints on the oblique projection (Figure 2). Small bony avulsions around the Lisfranc joint should not be dismissed, since these are indications that severe stress has been applied to the joint and a Lisfranc disruption is very likely. The lateral view is particularly helpful in assessing disruption of the talo-navicular and calcanealecuboid joints, the Chopart fracture (Figure 3).

entrapment of the peroneal tendons within a calcaneal fracture being a particular example (Figure 4). CT also plays a role in the assessment of post-operative complications following internal fixation, where the presence of metalwork would result in too much artefact on an MRI scan. (Figure 5). Box 2 summarizes the uses of CT.

Ultrasound US provides images of soft tissue structures at a greater resolution than MRI. It can distinguish the internal fasicular structure of tendons, allowing small partial tears to be detected. The ability to

Computed tomography

Summary of the uses of CT

Advances in CT technology, with multi-detector imaging the norm for state of the art scanners, ensure that a scan of the ankle can be performed in a matter of seconds giving high quality coronal and sagittal re-formats. Radiation dose is minimal since none of the vital organs enters the radiation beam. CT is either used to further characterize and plan an operation for a fracture seen on conventional radiographs, or to detect occult injury not visible on the radiographs. Common occult injuries include undisplaced talus, calcaneal and cuboid fractures and Lisfranc disruption. Whilst the primary role of CT is in the assessment of bony pathology it is worth remembering that some information can be gleaned about the soft tissues, with

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Acute Trauma Pre-operative planning prior to internal fixation Detection of radiographically occult fractures Chronic pain Complications following previous fracture particularly in the presence of metalwork-assessment of post traumatic osteoarthritis eg subtalar following calcaneal fracture, mid foot following Lisfranc injury. Box 2

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a Very subtle widening between the bases of the first and second MTs. The second MT aligns normally with the intermediate cuneiform. b Weight bearing view. The second MT shifts laterally and no longer aligns with the intermediate cuneiform. This is a Lisfranc disruption. Figure 2

dynamically scan whilst putting the tendons and ligaments through a range of motion is an advantage over MRI, which only visualizes static structures. Moving the foot whilst scanning an achilles tendon tear can distinguish a high grade partial tear from a full thickness tear and give an accurate measurement of the tendon gap (Figure 6). Subluxation of the peroneal tendons due to rupture of the peroneal retinaculum can be demonstrated whilst scanning the tendons in resisted eversion.

US can demonstrate acute ligamentous ankle disruption, most commonly the anterior talo-fibular (ATFL) component of the lateral collateral ligament (Figure 7). Scanning is infrequently performed acutely since it rarely affects the immediate management of the patient. It is more commonly employed in the assessment of chronic ankle instability following a previous inversion, or a series of inversion injuries. Scanning the lateral collateral ligament in inversion can demonstrate a ligament

a Chopart disruption. There is malalignment of the calcanealecuboid joint. b The disruption of the calcanealecuboid and talo-navicular joints is much easier to appreciate on the true lateral projection. Figure 3

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Figure 4 Bilateral calcaneal fractures. On the left the peroneal tendons lie free of the fracture (large arrow). On the right the peroneal longus is lying within the fracture (small arrow).

which, though it may have healed with scar tissue, has lengthened resulting in laxity. US is frequently used in the assessment of chronic tendonopathy, most frequently in the evaluation of the achilles tendon. The most common finding is degenerative tendonopathy (Figure 8). Inflammation of the surrounding soft tissues, the socalled paratenon, or a retrocalcaneal bursa are important

diagnoses to make, since these may respond to a steroid injection, a treatment which is not recommended for an intrinsic degenerative tendonopathy since the steroid may further weaken the tendon. A Morton’s neuroma occurs between the metatarsal heads, most commonly in the third/fourth intermetatarsal space. US can be used to detect these neuromas and dynamic scanning whilst

a AP and b lateral radiographs of the ankle. The patient was complaining of continued pain following internal fixation. c Sagittal CT shows part of the metalwork is sitting within the subtalar joint. Figure 5

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a Normal ATFL (arrows). b Acute rupture of the ATFL with complete disruption of the ligament. Figure 7

a High grade partial rupture of the achilles tendon (arrows). The superficial fibres of the tendon are intact. b There is no opening out of the tendon gap with the foot in dorsiflexion confirming the functionally intact superficial fibres. c Complete full thickness tear (arrows). There are apparent intact fibres superficially. d In dorsiflexion the gap widens. One small strand of tissue bridges the gap but the widening in dorsiflexion confirms a full thickness tear. Figure 6

compressing the toes can displace the neuroma, demonstrating that it is the cause of the clinical finding known as a Mulder’s click. Conventional radiography is frequently requested for the assessment of a calcaneal spur in patients with chronic foot pain, because of its association with plantar fasciitis. In fact a calcaneal spur can occur in completely asymptomatic individuals and if any imaging is required, then US is the imaging modality of choice (Figure 9). US can also be used to target a steroid injection into the area of inflamed plantar fascia.

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a Thickening and loss of the normal fasicular structure of the achilles tendon in degenerative tendonopathy. b Retrocalcaneal bursa (arrows) with a normal achilles tendon. This may respond to an US guided injection. Figure 8

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The assessment of chronic heel pain. a A lateral calcaneal radiograph demonstrating a calcaneal spur. Whilst this is associated with plantar fasciitis it can occur in asymptomatic individuals and if conformation of the diagnosis is required it is much better to demonstrate the plantar fascia directly with US. b Thickening of the plantar fascia in plantar fasciitis. US can be used to direct a steroid injection into the affected area. c Lateral calcaneal radiograph showing a sclerotic area in a typical site for a calcaneal stress fracture. If a radiograph is performed in chronic heel pain it should be done to exclude other causes of pain, such as a stress fracture, rather than the demonstration of a calcaneal spur. Figure 9

One disadvantage of US is the limited ability to assess the bones and articular surfaces. US can assess the surface of the bone but not the internal structure. Stress fractures are only demonstrated if there is a periosteal reaction. If a combination of bone and soft tissue injury is suspected it is much better to perform an MRI. Box 3 summarizes the use of US.

lateral collateral ligament, which in 70% of cases involves an isolated injury of the ATFL. More severe injury involves the calcaneo-fibular ligament as well as the ATFL. Injury of the posterior talo-fibular ligament is very rare. Since the ATFL is the most susceptible component of the lateral collateral ligament to injury, an intact ATFL usually implies there is no injury to the lateral collateral ligament. It runs close to the axial plane of the ankle and is therefore usually best seen on the axial sections, where it is identified on one or two contiguous slices. Signs of ligamentous disruption include non-visualization of the ligament, ligament discontinuity and a contour alteration with a wavy or curved ligament (Figure 10). Osteochondral injury is commonly associated with severe inversion injuries. A common pattern of injury is an impaction injury of the medial talus and an osteochondral fracture of the lateral talus which impacts on the fibula during a severe inversion injury (Figure 10). Osteochondral fractures can be seen on conventional radiographs, but impaction injuries and purely cartilage damage can only be diagnosed with MRI. The normal articular cartilage of the ankle is very thin so assessment of cartilage defects and flaps can be very difficult. Visualization is aided in acute injury by the presence of a joint effusion, which acts as a natural contrast agent outlining the cartilage. In subacute and chronic osteochondral injury assessment of the cartilage may be improved by performing an MR arthrogram. In addition to osteochondral injuries, chronic lateral collateral ligament injury can lead to a number of consequences, all of which can be assessed by MRI. These include post-traumatic arthritis, peroneal tendon injury and subtalar instability leading to the sinus tarsi syndrome (Figure 11).

Summary of the uses of US Acute Trauma Tendon and ligament injury in the absence of clinical osteochondral fracture Chronic Pain Chronic tendonopathy Chronic ligament instability in the absence of clinical osteochondral injury Plantar fasciitis Morton’s neuroma

Box 3

Magnetic resonance imaging Ligament and osteochondral injury The great advantage of MRI over US is the ability to assess the bony structures as well as the soft tissues, and specifically the ability to assess the articular surfaces. MRI is useful both in acute ligamentous and osteochondral injuries and in subacute/ chronic ankle and foot pain. Bone contusion is reliably demonstrated on T2-weighted fat suppressed sequences and usually resolves 8e12 weeks after the injury. Continued bone oedema following this is evidence of continued abnormal stress forces. The commonest mechanism of ankle injury is the supinationeadduction injury, which is commonly referred to as an inversion injury. This can result in ligamentous injury of the

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Ankle impingement Anterior impingement occurs in young athletic patients and is the result of repeated stress in ankle dorsiflexion with impingement

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a Axial T2-weighted, fat suppressed MRI. Rupture of the ATFL. There is discontinuity of the ligament and a wavy contour (arrow). b Acute osteochondral fracture of the lateral dome of the talus (arrow). There is joint fluid between the fragment and the talus indicating that the fragment is unstable. Figure 10

of soft tissues between bony spurs at the anterior rim of the tibial plafond and the apposing margin of the talus. Whilst MRI can assess the extent of the soft tissue impingement, most cases are simply diagnosed by clinical assessment and conventional radiography (Figure 12). Posterior impingement occurs as a result of repetitive plantarflexion of the foot which compresses the talus or os trigonum and adjacent soft tissues between the tibia and the calcaneus. Anatomical variants which pre-dispose to the development of this condition are the presence of an os trigonum and

a prominent posterior process of the talus. Whilst conventional radiography can demonstrate these anatomical variants, they are so common that their demonstration is not diagnostic of posterior impingement. MRI demonstrates oedema, either within the os trigonum or the posterior process of the talus and oedema of the adjacent soft tissues (Figure 13). Anterolateral impingement can cause chronic ankle pain in the anterolateral gutter and typically occurs following an ankle inversion sprain. MRI can demonstrate synovial thickening when an ankle effusion is present. In the absence of an effusion MR

a Sagittal T1-weighted MRI. Inflammation within the sinus tarsi is demonstrated as low signal with loss of definition of the interosseous and cervical ligaments (arrow). b T2-weighted fat suppressed MRI. There is high signal inflammation within the sinus tarsi (arrow). Figure 11

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Figure 14 Axial T2-weighted MRI demonstrating bone oedema and a fracture line in the navicular (arrow). Figure 12 Anterior bony spurring in a case of anterior impingement.

arthrography is required. Medial impingement is an uncommon cause of chronic medial ankle pain. Again MR arthrography is required in the absence of a joint effusion and careful clinical correlation of the MR findings is required.

Summary of the uses of MRI Acute injury Severe acute ligamentous injury particularly when acute osteochondral fracture also suspected Chronic pain Chronic osteochondral injury Ligament laxity and impingement syndromes Chronic bone stress fracture Infection eg in the diabetic foot

Chronic bone injury Common sites of chronic stress injury in the ankle and foot include the metatarsals, the navicular and the calcaneum. Changes on conventional radiography are a relatively late feature, particularly in the navicular, and MRI is very useful to demonstrate the bone oedema of micro-trabecular stress fracture in the early stages and fracture lines when they are present (Figure 14). Box 4 summarizes the uses of MRI.

Box 4

Summary Conventional radiography is useful in acute bone injury but has a limited role in chronic pain, with the exception of osteoarthritis, anterior impingement and established stress fractures. CT gives the best anatomical bone detail and is useful for the assessment of occult acute bone injury and in the presence of extensive metalwork, which renders MRI non-diagnostic. Ultrasound is the investigation of choice for isolated tendon and ligament injury that allows dynamic assessment of integrity and direct correlation of patient’s pain and tenderness with pathological findings during the scan. MRI gives the best overall assessment of soft tissue and bone injury and is the most useful investigation for chronic ligament instability and impingement syndromes, osteochondral injury and chronic stress fractures.A

FURTHER READING Stoller DW, Tirman PF, Bredella MA. Diagnostic imaging: orthopaedics. Elsevier, 2004.

Figure 13 Sagittal T2-weighted fat suppressed MRI. There is a large os trigonum which shows high signal oedematous change (arrow).

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The anatomy, investigations and management of adult brachial plexus injuries

Introduction Brachial plexus injuries range from transient nerve dysfunction to a completely flail upper limb associated with life-threatening injuries. Significant injuries lead to physical disability in addition to psychological and financial hardship. The management of such cases is complicated by concurrent injuries that may delay or cloud the neurological assessment. In addition to this, anatomical variations within the brachial plexus make these injuries a considerable challenge to clinicians responsible for their care. Traumatic lesions are most commonly the result of motorcycle accidents and typically affect young men.1e3 Lesions can also occur following penetrating or sports related injuries, falls, industrial accidents, radiation therapy and iatrogenic causes (first rib resection, shoulder surgery, interventional radiology). The most common mechanism is a traction injury to the nerves secondary to forceful separation of the neck from the shoulder.1

Jonathan Gregory Alex Cowey Matthew Jones Simon Pickard David Ford

Abstract Brachial plexus injuries have increased in numbers since the turn of the twentieth century in line with the increased use of motorcycles. Advances in microsurgical and tissue transfer techniques have seen the management of such injuries change dramatically during this time period. As a result, surgery for plexus injuries is now considered a legitimate option. Such injuries require extensive medical input in a multidisciplinary environment. All patients should be thoroughly investigated to establish the exact extent of the injury and managed on an individual basis. The options available are conservative or surgical. Conservative options include physiotherapy, orthotics and pain control. Surgical reconstruction of the plexus may involve neurolysis, nerve grafting, nerve transfer and late peripheral reconstruction including arthrodesis, tendon transfers, free muscle transfers and amputation. Despite many advances in the field, injuries still result in considerable disability and loss of working days.

History Brachial plexus reconstruction began in earnest in the mid 20th century with work by Barnes, Brooks, Bonney, Seddon and Leffert and later Narakas. Despite their work the role of surgery was confined to exploration in order to determine prognosis, more complex interventions being associated with poor results.1e4 The extent of this belief is highlighted by Seddon’s comments in 1961 ‘The results of reconstructive operations have been so disappointing that we believe that this type of treatment should be abandoned’.5 Towards the end of the 20th century advances in microsurgical techniques and tissue transfer procedures have improved the functional outcome of these injuries. However, many of these patients still require extensive medical input and a multidisciplinary approach to their care.

Keywords anatomy; brachial plexus; management; nerve injury; neurophysiology

Assessment A full assessment to establish the aetiology, and clearly define the level and severity of the injury must be performed. It is important to ascertain whether the lesion is pre- or post ganglionic, as this significantly affects both management and prognosis, and this may require supplementary tests such as electrophysiological or radiological investigations. Concurrent severe injuries occur in up to 80% of patients, and the attending clinician must be alert to this. Commonly associated injuries include dislocated shoulders, fractures of the proximal humerus, clavicle, scapula and cervical spine, in addition to major upper limb vascular injuries (subclavian or axillary artery). These injuries require management in their own right but can also provide vital clues to the extent and nature of the plexopathy. A lesion can be classified using a variety of systems, which often differentiate between upper plexus and lower plexus injuries. Leffert’s classification system6 based on aetiology and level of the injury is commonly used (Table 1), but it must be remembered that lesions may occur at more then one level. Following a full evaluation the management plan should be tailored to an individual patient’s needs and a time scale set out, with consideration given to both conservative measures and secondary reanimation of the limb.

Jonathan Gregory BSc MB ChB FRCS (TþO) Specialist Registrar Trauma and Orthopaedics, Robert Jones and Agnes Hunt Orthopaedic & District General Hospital, Shropshire, UK. Alex Cowey MB ChB FRCS (TþO) Specialist Registrar Trauma and Orthopaedics, Robert Jones and Agnes Hunt Orthopaedic & District General Hospital, Shropshire, UK. Matthew Jones MB ChB MRCP Clinical Research Fellow and Specialist Registrar in Neurology, University of Manchester, Wolfson Molecular imaging Centre, Manchester, UK. Simon Pickard MB ChB FRCS FRCS(Orth) Consultant Orthopaedic Surgeon and Specialist in Hand, Upper limb and Nerve Injury Surgery, Nerve Injury Unit, The Robert Jones and Agnes Hunt Orthopaedic & District General Hospital, Shropshire, UK. David Ford MB ChB FRCS FRCS(Orth) Consultant Orthopaedic Surgeon and Specialist in Hand, Upper limb and Nerve Injury Surgery, Nerve Injury Unit, The Robert Jones and Agnes Hunt Orthopaedic & District General Hospital, Shropshire, UK.

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Two anatomical triangles contain the proximal plexus. The interscalene triangle is formed between the anterior and middle scalene muscles superiorly and the first rib inferiorly and contains the roots of the plexus. The posterior triangle of the neck contains the trunks of the plexus and is formed by the sternocleidomastoid muscle anteriorly, trapezius laterally and the clavicle inferiorly. Dorsal (sensory) and ventral (motor) rootlets arise from the spinal cord and merge to form a root as they pass through the vertebral foramen. Just prior to the formation of the root the sensory rootlet enlarges in diameter forming the dorsal root ganglia (DRG). The DRG contains the cell bodies of the sensory nerves (motor nerve cell bodies are within the spinal cord). An injury proximal to the DRG is described as pre-ganglionic. This may be avulsion of the rootlets from the spinal cord or an injury, which is still intradural, but just proximal to the DRG. The rootlets have no connective tissue or meningeal covering as they originate from the spinal cord; this contributes to their susceptibility to avulsion from the cord. The roots have a protective layer formed by the dura and are able to move freely within the foramen. As the C4, C5, C6 and C7 roots emerge from the foramen they are tethered to the transverse processes of their respective vertebrae. C8 and T1 are not tethered in this way, which leads to a higher incidence of root avulsion from the spinal cord being seen at these levels compared to the upper plexus. The roots enter the scalene triangle, being found between anterior and middle scalene muscles. The first terminal nerves to arise from the plexus do so at this level. The C5 root has 3 branches at this point: contributions to the phrenic, long thoracic and dorsal scapular nerves. The roots descend and move laterally into the posterior triangle of the neck.

Leffert classification of brachial plexus injuries I II

Open Closed

IIa

IIb IIc

Supraclavicular Preganglionic e nerve root avulsion Postganglionic e traction injuries Infraclavicular Combined

III Radiotherapy induced IV Obstetric IVa Upper root (Erb’s palsy) IVb Lower root (Klumpke’s palsy) IVc Mixed Table 1

Anatomy of the brachial plexus The anatomy of the brachial plexus demonstrates a large degree of variability, both between individuals and between the left and right limbs of the same individual.7 Most commonly the brachial plexus is formed by the confluence of the ventral rami of the spinal nerve roots from C5 to T1. Common variations include contributions to the plexus by the C4 nerve root (described as a pre-fixed plexus) or the T2 nerve root (a post-fixed plexus). The 5 roots normally contributing to the plexus merge into 3 trunks, each of which splits into anterior and posterior divisions. The divisions become 3 cords which give rise to the terminal branches (Figure 1).

Figure 1 Diagrammatic representation of the Brachial Plexus.

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PERIPHERAL NERVE

Terminal branches of the roots, trunks and cords of the brachial plexus Nerve

Origin from plexus

Root value

Muscle/area innervated

Phrenic Dorsal scapular Long thoracic Subclavius Suprascapular Lateral pectoral

Root Root Root Upper trunk Upper trunk Lateral cord

C345 C5 C567 C56 C56 C56

Medial pectoral

Medial cord

C678

Medial brachial cutaneous Medial antebrachial cutaneous Upper subscapular Thoracodorsal Lower subscapular

Medial cord Medial cord Posterior cord Posterior cord Posterior cord

C567 C678 C567

Ipsilateral hemidiaphragm Rhomboids Serratus anterior Subclavius Supraspinatus, infraspinatus Clavicular and sternocostal heads Pectoralis major, Pectoralis minor Sternocostal head Pectoralis major, Pectoralis minor Medial arm above the elbow Medial forearm Subscapularis Latissimus dorsi Subscapularis, Teres Major

Table 2

The C5 and C6 roots combine to form the upper trunk of the plexus. The point at which they become confluent is known as Erb’s point. The C7 root becomes the middle trunk and the C8 and T1 roots merge into the lower trunk. If, on clinical examination, the rhomboids (dorsal scapular nerve) and serratus anterior (long thoracic nerve) are functional the lesion must be distal to Erb’s point. The trunks divide to form anterior and posterior divisions, which are located behind the clavicle. The upper trunk gives off the nerve to subclavius and the suprascapular nerve, supplying supraspinatus and infraspinatus, prior to forming its 2 divisions. There are no branches given off by the divisions of the brachial plexus. The posterior divisions all combine to form the posterior cord located behind the axillary artery. The anterior divisions of the upper and middle trunks form the lateral cord, lateral to the axillary artery, and the anterior division of the lower trunk forms the medial cord, medial to the axillary artery. There are terminal branches arising from all of the cords. The lateral

cord gives off the lateral pectoral nerve to pectoralis major. The posterior and medial cords each give rise to 3 terminal branches. The posterior cord forms the upper subscapular, thoracodorsal and lower subscapular nerves. The medial cord gives rise to the medial pectoral nerve, the medial brachial cutaneous nerve and the medial antebrachial cutaneous nerve. The terminal branches of the plexus arise from the cords. The posterior cord terminates as the axillary and radial nerves. The lateral cord contributes to the median nerve and forms the musculocutaneous nerve. The medial cord forms the ulnar nerve and contributes to the median nerve (Table 2).

Clinical clues to the anatomical location of pathology When considering the level of an injury to the brachial plexus injury, the most important step is determining whether a lesion affects the roots and is therefore pre-ganglionic (proximal to the dorsal root ganglion) or post ganglionic (Figure 2).

A vulsion

Posterior

PREGANGLIONIC

A C-spine Stretch Dorsal root ganglion

B

Rupture POSTGANGLIONIC

Figure 2 Preganglionic and Postganglionic nerve lesions.

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There are clinical clues that indicate that an injury has occurred in the vicinity of the DRG. If the rhomboids or serratus anterior are weak then pre-ganglionic injury should be suspected, as the dorsal scapular and long thoracic nerves arise at the proximal ends of their roots. In a non-acute situation fasiculations may be seen in the paraspinal muscles. These are not supplied by the plexus but from the dorsal rami, which arise from the spinal nerves as they exit the intervertebral foramen. The T1 root is in close proximity to the T1 sympathetic ganglion. The inference is that if the T1 sympathetic ganglion is injured then it is probable that the T1 root will also have been injured. Injury to the T1 sympathetic ganglion will produce a Horner’s syndrome of the ipsilateral eye. The 4 components of Horner’s syndrome are; meiosis (unopposed parasympathetic function), mild ptosis (weakness of Muller’s muscle which assists levator palpebrae superioris), enopthalmos and facial anhydrosis.

Comparison of the Seddon and Sunderland classification of peripheral nerve injury Seddons classification Neurapraxia

2

Axonotmesis

3 4 5

Axonotmesis Axonotmesis Neurotmesis

Histology Physiological not anatomical disruption Endoneurium and perineurium intact Intact Perineurium Intact Epineurium All layers disrupted

Table 3

Classification of peripheral nerve injury

swelling of the cell body and the nucleus moves to the periphery of the cell body. Approximately 10% of the cell bodies may undergo apoptosis. The rough endoplasmic reticulum changes, with dispersal of the Nissl granules, which are usually involved in neurotransmitter production, in a process called chromatolysis. These changes occur as the cell switches its synthetic output from neurotransmitters to the structural proteins required for nerve repair. There is increased synthesis of mRNA, actin, tubulin and growth factors. The axon proximal to the injury undergoes retrograde degeneration to the node of Ranvier proximal to the zone of injury. The nerve stump distal to the point of injury undergoes Wallerian degeneration after 48 to 96 hours. There is demyelination and axonal degeneration. Schwann cells proliferate and act to phagocytose the degenerating nerve in a calcium dependent process. Macrophages rapidly invade the distal nerve stump removing debris14 and secreting neurotrophic factors to commence repair. The neurobiology of nerve repair has been discussed in a recent Current Orthopaedics article.15 Once Wallerian degeneration is complete the Schwann cells begin to align themselves along their basal laminae. This leads to the formation of columns of Schwann cells called Bynger bands. These columns provide a structural framework for regeneration. A growth cone emerges from the proximal end of the divided nerve. This has finger-like projections called filopodia, which explore the microenvironment. The axon grows and contracts by the addition and removal of actin polypeptides. The filopodia guide the growing axon towards the distal stump and its Bynger bands. It responds to four classes of substances; neurotrophic factors, neurite promoting factors, matrix forming precursors and metabolic factors. Pathological changes also occur in the target organs for the nerve. When their motor supply is lost, muscle cells reduce in volume leading to atrophy and interstitial fibrosis. Denervation hypersensitivity is produced by an increase in the number of motor endplates. The muscle then responds to smaller amounts of acetylcholine than is normally effective, which is detected as fibrillations on electromyography (EMG) and clinically may produce fasciculation. Motor endplates start to be lost irretrievably after 3 months. Sensory end organs such as Meissner corpuscles also degenerate, although over a less clearly defined time scale than muscle. These end organ changes are the factor

Myelinated peripheral nerve fibres are surrounded by Schwann cells. Each nerve fibre and its accompanying Schwann cell are surrounded by loose vascular tissue called endoneurium. Bundles of nerve fibers are grouped together into fascicles. Each fascicle is covered in a layer of collagen called the perineurium. Most nerves consist of numerous fascicles, which are held together by loose collagenous tissue, which is condensed peripherally into a strong outer layer; the epineurium. Seddon’s classification of nerve injury is widely used and describes nerve injuries as neurapraxia, axonotmesis and neurotmesis.8 Neurapraxia is due to a physiological dysfunction leading to a blockade of nerve conduction. The axon of the nerve fibre remains in continuity, without any degeneration of the nerve distal to the site of injury. There may be a local area of myelin damage that is repaired by the Schwann cells9 and normal conduction is restored. Axonotmesis describes loss of axonal continuity of individual nerve fibres but the perineurium is preserved. Neurotmesis is the most severe injury where all the connective tissue elements and axons of the peripheral nerve are disrupted. The category of axonotmesis is very broad and contains a variety of nerve injuries that have very different outcomes. Therefore Seddons’s classification was refined by Sunderland.10 Sunderland’s classification is based upon 5 groups. The benefit of Sunderland’s classification is that it subdivides axonotmesis in to injuries that recovery very well (type 2) from those that have a poor outcome, (type 4) (Table 3). The classification systems of Sunderland and Seddon can only be applied retrospectively or at the time of surgical exploration. Birch and Bonney developed a classification system based upon neurophysiological testing.11 They defined injuries as those producing a conduction block and those without a conduction block with the hope of producing a more clinically useful classification system.

Pathophysiology of nerve regeneration Axonotmesis and neurotmesis involve axonal damage, which leads to pathological changes along the entire nerve, from the nerve distal to the injury up to the cell body.12,13 There is

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Histamine test Now rarely performed, it was of use in differentiating preganglionic from post ganglionic lesions. A drop of histamine is placed on the skin and the skin is scratched through the histamine. When the nerve is intact a triple response will occur (vasodilatation, wheal formation and a flare response). The histamine causes vasodilatation. The wheal is localised tissue swelling due to increased capillary permeability secondary to histamine and substance P. The flare is a mottled reddening around the area of skin injury due to mechanical stimulation of nociceptive nerve endings and C fibres. This leads to antidromic conduction in axon branches, which then release substance P, which causes vasodilatation and histamine release from mast cells in the surrounding tissues. When there is nerve disruption proximal to the DRG there will be a normal response in an area of skin that is anaesthetic. If the nerve is injured distal to the DRG there will be vasodilatation and wheal formation in an anaesthetic area of skin but no flare response will occur as this is an axon-mediated response requiring a functioning axon in continuity with its cell body.

that limits the time available for nerve repair. If the recovering nerve does not reach the end effectors within approximately 18 months following injury then little functional improvement will occur. In addition to the type of nerve injury other factors determine prognosis (Table 4).

Investigations The aim of investigations is to localise the level of the brachial plexus lesion and determine the prognosis for spontaneous recovery. Knowledge of these two features determines the subsequent patient management. Radiological During the initial assessment of the patient, plain films of the clavicle and cervical spine may identify bony injuries and raise the clinical suspicion for a brachial plexus injury e.g. displaced fracture of the transverse process of the cervical spine, fracture of the 1st and 2nd ribs. The complexity of the anatomical structure of the plexus, combined with the number of air/fluid/fat interfaces (due to its proximity to the lungs and vasculature structures) make interpretation of brachial plexus imaging difficult. The main role of imaging in traumatic brachial plexus injuries is to differentiate root avulsions from more distal injuries. Roots are approximately 1 mm thick and, until recently, the conventional slice thickness of CT and MR imaging was greater than this. Improvements in hardware and scanning sequences mean that useful information can now be obtained. MR scanning is useful in the investigation of non-traumatic lesions because of the wide variety of pathology that may be responsible for non-traumatic brachial plexus dysfunction; infiltrating tumours, compressive tumours, radiation injury, idiopathic brachial neuritis and vasculitic/granulomatous conditions may all result in a brachial plexopathy. Oedema on a T2 weighted scan indicates the zone of injury and if it is within or around the plexus it implies injury if the clinical situation correlates with a plexus injury.

Basic electrophysiology Action potentials (AP) are transient changes in axon membrane potential, which are conducted over considerable distances without any change in amplitude. Neurons have a negative resting membrane potential - their internal charge is negative relative to the surrounding environment. This is due to the relative levels of Kþ, Naþ and Cl across the membrane. The resting membrane potential for neurons is approximately 70 mV. When a neuron is stimulated above its threshold for activation there is a rapid influx of Naþ, which causes depolarisation. The membrane potential usually reaches approximately þ30 mV before the Naþ channels are inactivated. Voltage sensitive Kþ channels open and release potassium into the surrounding environment and Cl channels allow chloride into the cell to re-establish the negative membrane potential of 70 mV. The sodium channels are then capable of reactivation should another stimulus arrive. The period during which the Naþ channels are

Factors affecting outcome of peripheral nerve injury Factor Mechanism of injury

Effect High energy poorer prognosis related to severity of injury. Traction poorer than sharp division Poorer outcome if arterial injury Age of patient Better outcome in younger patients. Cerebral cortex plasticity allows adaption to new sizes of motor units and changes in sensory input. Type of nerve Purely motor or sensory nerves have better functional recovery than mixed nerves (growth cones more likely to reach an end organ that they can usefully supply). Some pure nerves do poorly for unknown reasons eg superficial radial nerve. Level of injury Supraclavicular injuries have a poorer prognosis than infraclavicular injuries. Upper trunk lesions have the best prognosis. Pain Patients who have persistent pain for 6 months after a brachial plexus injury have a poorer prognosis with regard to neurological recovery. Time interval injury to surgery If surgery is delayed for months then fibrosis and degeneration of end organs make for a poorer outcome Patient factors Other medical co-morbidities, infections. Effect of smoking unknown but thought to be detrimental. Table 4

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20

m al

PERIPHERAL NERVE

No r

Velocity Reduced

15

ting

ylina

mV 10

ix ed

Dem

10

15

20

25

30

35

40

45

50

Amplitude

5

Axon al

M

5

m/s

Figure 3 CMAP recording - biphasic, large amplitude and long duration of the potential. Reduced

closed as the cell repolarises is called the refractory period, as the cell is unable to respond in this period to standard stimuli. At any time only a small area of the axon is depolarised as the AP passes along it. The flow of the AP is unidirectional, as the area the AP has passed through will enter a refractory period and reversal of the direction of flow is thereby prevented. AP velocity is increased by increasing nerve fibre size, as in these circumstances there are more ions within the cell to carry the current. Myelination means that depolarisation is limited to the nodes of Ranvier. This reduces the number of depolarisations required to travel the length of the nerve (salutatory conduction).

Figure 4 Differentiating types of nerve lesions using changes in conduction velocity and amplitude.

m/s but absolute values vary between patients and with different recording apparatus. Intra-examiner variability is low but there can be considerable inter-observer variability of sensory and motor amplitudes.16 For this reason serial studies should be performed by the same neurophysiologist. The amplitude of the CMAP relates to the number of working muscle fibres in the muscle sampled. The conduction velocity is proportional to the nerve diameter. Conduction velocity is lower in unmyelinated axons and axons which have undergone demylination. Motor and sensory conduction velocity decreases with age; 0.4e1.7 m/s per decade after 20 years of age for motor and 2e4 m/s for sensory.17 After the CMAP has been recorded there may be observed the appearance of a small F wave. This is a rebound phenomenon. The nerve has been stimulated somewhere along its length therefore the AP can move proximally and distally (unlike under normal circumstances where the AP begins either proximally or distally). The AP therefore passes up the nerve to the motoneurone cell body and then comes back down the nerve, eventually reaching the recording electrode after the CMAP. F waves are a sensitive marker of nerve pathology and are useful when the lesion is very proximal and not therefore easily accessible by routine NCS techniques. Changes in conduction velocity and amplitude can be used to help differentiate between types of nerve injury and may indicate whether demyelination or axonal damage or both has occurred (Figure 4).

Nerve conduction studies (NCS) Motor studies (Figure 3): An electrical stimulus is applied to the skin directly over a nerve. The electrical stimulus intensity is gradually increased until a further increase in stimulus does not have an effect on the amplitude of the motor potential. This is a supra-maximal stimulus. A supra-maximal stimulus is used to obtain greater reproducibility of results. The response of the distal motor unit is usually recorded by a surface electrode placed on the skin overlying the belly of the target muscle. Needle electrodes are occasionally required if there has been profound muscle wasting. The recording from the muscle is called the motor action potential (MAP) or the compound muscle AP (CMAP). The CMAP represents a summation of the voltage responses from individual muscle fibre action potentials. The time from the stimulus being applied and the appearance of the MAP is called the distal motor latency. This period of time is a composite of the time taken for nerve excitation, conduction of the AP, Acetylcholine release at the NMJ and generation of a post synaptic muscle potential to trigger the muscle response. To calculate conduction velocity the nerve must be stimulated at 2 points along its course with the MAP being measured by the same muscle electrode. To remove the effect of the distal apparatus the conduction velocity is then calculated. The normal conduction velocity in the upper limbs is between 45 and 60 m/s, whilst in the lower limb it is between 40 and 55

Conduction Velocityðm=sÞ ¼

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Sensory studies (Figure 5): A sensory nerve is stimulated distally and the response is recorded proximally. The proximal response is called the Sensory Nerve Action Potential (SNAP). In the upper limb sensory nerves are often stimulated by the use of a ring electrode placed on a digit served by the nerve of interest e.g. middle finger for median nerve. SNAPs are much smaller than CMAPs e in the micro-volt range. The conduction velocity and

Distance between the 2 sites of nerve stimulus proximal latencyðmsÞ  distal latencyðmsÞ

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denervation changes are localized to deltoid, triceps and extensor digitorum communis a posterior cord lesion should suspected. EMG is able to differentiate myopathic from neuropathic causes of muscle weakness. EMG can also identify the first signs of recovery after nerve injury. As the regenerating motor axons start reforming motor units they initially conduct at a slower velocity, leading to low amplitude complex polyphasic waveforms being recorded from the muscle. These are called nascent potentials and are an early sign of reinnervation. Nascent potentials are the only way to differentiate temporary from permanent denervation. As recovery continues the waveforms become greater in amplitude and have a simpler waveform. When reinnervation is complete the EMG will still not be completely normal, as the size of the motor units will be larger than prior to injury. To compensate for this the firing pattern of each motor unit will be different, usually with increased firing rates to try and maintain force production. For further information regarding the technical aspects of electromyography the following reference is suggested.18 The neurophysiologic findings seen in nerve injuries are shown in Table 5.

40 30

uv 20 10

1

2

3

4

5

6

7

8

9

10

m/s Figure 5 SNAP recording - triphasic, small amplitude and short duration of potential.

amplitude can be calculated. The amplitude of the SNAP gives an indication of the number of functioning axons. It is also affected by the synchrony of the AP arriving at the recording site e i.e. AP arriving over a prolonged period will cause reduced peak SNAP amplitude. Demylination will lead to a small SNAP as the AP will have greater temporal spread. Axonal degeneration will lead to an absent SNAP. Age does have an effect on the SNAP. For further information regarding the technical aspects of nerve conduction studies the following reference is suggested.17

Neurophysiological assessment of the brachial plexus Neurophysiology can confirm the diagnosis of a brachial plexus injury. It can localise the site of the lesion, attempt to quantify the degree of axonal loss and identify if recovery is occurring. Initial NCS should be performed 3e4 weeks after injury, as Wallerian degeneration will have been completed. Denervation changes maybe seen in 10e14 days but can take up to 40 days to appear. Proximal muscles are affected prior to distal muscles. When denervation changes occur in the cervical paraspinal muscles, rhomboids or serratus anterior it implies the lesion is proximal to the brachial plexus. Motor responses are affected before sensory responses when measured on NCS .16 The CMAP will be reduced in amplitude, reflecting the loss of axons if an injury of greater severity than neurapraxia/Sunderland 1 has been sustained. The SNAP can indicate if a lesion is pre- or post-ganglionic. If a SNAP is present the lesion is proximal to the sensory nerve bodies in the DRG. If the SNAP is absent or reduced the lesion is distal to the DRG. The number of intact axons dictates the amplitude of the SNAP. One limitation is that a SNAP may be absent due to a post-ganglionic injury but there may also be a coexistent injury at the pre-ganglionic level.

Electromyography (EMG) A needle is placed into a muscle to record the activity of motor units at rest and on muscle contraction. The needle records from a radius of approximately 1 mm around the needle. The number of motor units in this field will vary between muscles. A normal muscle will not have any spontaneous activity. A sub-maximal contraction will allow individual motor unit potentials to be identified and a maximal contraction will produce complex discharges. Spontaneous discharges are a sign of partial or complete denervation, compression of spinal nerve roots or anterior horn cell diseases. They are caused by hypersensitivity to acetylcholine as receptor numbers are up-regulated to compensate for the reduced/lost innervation. The acetylcholine receptors are also found outside the confines of the previous neuromuscular junction spreading across the whole muscle surface. Fasciculations may be seen; these represent spontaneous discharges. They develop approximately 7e14 days after denervation. Muscles are sampled by EMG to map the distribution of denervation changes. This information can then be interpreted to allow localization of a brachial plexus lesion. For example if

Summary of neurophysiological findings for the categories of peripheral nerve injury as defined by Seddon. Neurophysiological differentiation between axonotmesis and neurotmesis can be challenging

Conduction velocity CMAP Amplitude SNAP Amplitude Spontaneous Activity on EMG

Neurapraxia

Axonotmesis

Neurotmesis

Normal in most cases Normal/Reduced Reduced Absent

Normal/slight reduction Reduced Reduced Maybe present

Absent Absent Absent Present

Table 5

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There is a lot of overlapping innervation of the paraspinal muscles. One root injury may cause fibrillation potentials in more than one paraspinal level. Therefore the number of paraspinal fibrillations cannot tell you how many root injuries there are, only that at least one root injury is present. However if no paraspinal fibrillations are recorded then it is possible to say that no root injuries have occurred. Nascent potentials on EMG and reduced fibrillations can point to nerve recovery long before clinical recovery is apparent. Nascent potentials indicate that nerve fibres have reached the muscles and established motor end-plate connections. However EMG recovery does not always equate to useful clinical recovery. Some centres use intra-operative nerve conduction studies. The nerves of the plexus are stimulated across their damaged areas to identify whether there are functional axons. These are NAPs e nerve action potentials. They measure activity in sensory and motor fibres in mixed nerves along the length of nerve tested with no distal organ effect being measured. The nerve is stimulated directly with an electrode and the recording is performed with a hook or forceps type electrode at least 4 cm away from the stimulating electrode. Four cm of separation between the stimulating and recording electrodes is essential to produce reliable recording of NAPs intra-operatively. There is a lot of stimulus artefact when recording NAPs. If no NAP is recordable across a lesion then grafting is performed if the proximal nerve root is in continuity. The presence of a NAP across a lesion indicates either preserved axons or that recovering axons have now traversed the lesion. If the nerves are judged to be functional neurolysis rather than grafting may be appropriate. Somato-sensory evoked potentials (SSEP) and cortical evoked potentials have also been used for intraoperative monitoring. If an SSEP is present then there is contact between the peripheral sensory nerve and the CNS suggesting that the DRG is intact.19

required in these cases. In one of the biggest series in the literature of stab wounds to the plexus Dunkerton reported good results with early exploration, with a better prognosis associated with C5/C6 lesions.20 Open injuries secondary to low-velocity missiles (gunshot wounds), do not warrant early exploration. This is because the resultant injuries are mostly neurapraxic.21 It must be added, though, that as technology advances more powerful weapons are being produced leading to an increase in severe stretch injuries (lesions in continuity) to the plexus. If there is no associated vascular or thoracic injury, conservative management with local wound care is advocated. If no recovery is seen by 3 months exploration with repair/grafting is indicated. Kline reported on a large series of civilian gunshot wounds in the era of lowvelocity weapons and found the best surgical outcomes were associated with upper trunk and lateral and posterior cord injuries.

Management of closed injuries In the absence of any open wounds and life-threatening injuries surgery is not traditionally the first line of treatment. The initial management is observation, pain control and physiotherapy. Electromyography is performed at 3e4 weeks and a myelogram or magnetic resonance imaging at 6e8 weeks if a neurological deficit persists. If function fails to return, or if initial neurological recovery ceases, then surgical exploration is justified at 3 to 6 months, although there is no uniformly accepted algorithm for these injuries. Non-surgical management The goals are to maintain passive motion, to strengthen those muscles that remain functional, to protect anaesthetic skin areas and to control pain. Physiotherapy plays an important role in maintaining passive motion as well as strengthening muscles. A home programme of physiotherapy should run alongside structured departmental sessions, to maximise the functional outcome of the limb. Functional splinting will complement physiotherapy. Chronic oedema can develop secondary to dependent positioning, loss of vascular tone due to sympathetic nerve denervation and concurrent soft tissue injury to the limb. Elevation, bracing and compression garments can all be used to reduce the oedema that, if ignored, can lead to stiffness, particularly in the hand. The mainstay of the management of anaesthetic skin is education, and the program is essentially the same as for diabetic neuropathy with patients avoiding extreme temperatures and inspecting the insensate area daily. The management of pain can be difficult and significant pain is more common with total plexus injuries than partial, particularly with root avulsions. Pain, in addition to being very distressing, can also compromise rehabilitation, and its control is paramount. Restoration of function, both of the limb and the patient, including the return to employment, is often the most effective form of pain control. The use of pharmacological agents is vital, but dependency and side effects must be taken into account. Non-steroidal anti-inflammatories and opioids instigated at the time of injury may become ineffective with time, particularly in relation to neuropathic pain. In these cases there is

Management of open injuries Open injuries are not common and range from minor penetrating wounds to complex major blast injuries with near amputation of the upper limb. These injuries are usually caused by sharp penetrating implements or missiles, resulting in a neurotmesis. In this situation, with sharp division of the nerve(s), primary exploration and repair in the acute setting should be attempted if the patient’s other injuries allow. It is not unusual however for additional injuries to the major vessels or thoracic viscera to preclude immediate exploration and in these cases repair must be delayed. If a cursory plexus inspection and tagging of the injured nerves is possible during the management of concurrent injuries the opportunity should be taken. If there is a delay between the initial injury and presentation to the clinician responsible for the management of the brachial plexus injury, then all wounds and other injuries should be left to stabilise before considering any further surgical intervention. The opportunity may be taken to perform EMG during this period at 3e4 weeks, aiming for exploration and repair at 4e6 weeks. Due to the delay, in these cases primary nerve repair may not be possible because of nerve retraction or following the resection of neuromatous stumps, necessitating the need for nerve grafting. Neurolysis of scarred nerve ends may also be

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a role for carefully titrated doses of anti-epileptics (gabapentin and carbamazipine) or tricyclic anti-depressant (amitriptyline). It should be noted, though, that only one third of patients report significant pain relief with these medications.22 Other modalities including counseling, biofeedback, hypnosis, acupuncture and transcutaneous nerve stimulation have all been used with mixed results. Severe cases of intractable pain, which do not respond to the above non-surgical measures, can be considered for dorsal root entry zone (DREZ) ablation, described by Nashold23 or the use of implantable dorsal root stimulators. Pain control should be managed by a multi-disciplinary team and customised to the character of the pain and to the patient. Access to a pain clinic is an important adjunct.

formation. Omohyoid muscle, which signals the transition from superficial to deep dissection, is divided and the supraclavicular fat pad is swept away from the operative site. Below the fat pad is the transverse cervical artery with Erb’s point deep to this. The phrenic nerve is identified, closely applied to scalenus anterior, and is followed proximally to identify the root of C5 at the lateral edge of the muscle. The lower roots can be visualised distally by retraction of scalenius anterior, taking care with the subclavian vein anteriorly and the subclavian artery posteriorly. For proximal foraminal exposure scalenius anterior is divided. The upper trunk is located by tracing the C5 and C6 roots distally, the middle trunk being found both deeper and medial to this. Access may be limited by the transverse cervical artery, which is ligated if necessary. To access the lower trunk the subclavian vasculature is mobilised and retracted with care as the origin of the vertebral artery lies close, as does the lung pleura. Clavicular osteotomy can be performed to increase exposure, facilitating closure by preparing a pre-contoured plate and predrilling the lateral screws. The clavicle should be divided via a low energy osteotomy at an oblique angle. The infraclavicular plexus is exposed through the deltopectoral groove (Figure 6aef). To expose the entire plexus the supraclavicular and infraclavicular approaches are linked over the lateral clavicle. The cephalic vein is preserved and mobilised laterally with the deltoid. The delto-pectoral interval is developed and the clavicular attachments of pectoralis major and deltoid may be partially released to optimise exposure. Distal exposure requires the release of the humeral attachment of pectoralis major. Pectoralis minor is divided close to its insertion onto the coracoid (a stay suture is placed in the tendon) to expose a fat pad which is swept aside bringing the cords of the brachial plexus into view. The lateral cord is the most readily identifiable and deep to this is the axillary artery which requires mobilisation and protection. The medial and posterior cords are identified in relation to the artery. The cords can be traced both distally, to identify the branches, and proximally, to locate the divisions.

Surgical management Considerable advances have been made since the early 1900s, when attempts at surgical repair and neurolysis proved almost futile. Modern microsurgical techniques have led to improved results, but as of yet no definitive management algorithm has been constructed and uniformly accepted. There are several general statements concerning surgical intervention of closed injuries that can be made: 1. Patients who have complete loss of C5, C6 and C7 root functions have the most to gain 2. Nerve grafting of the upper roots is often possible as rupture, not avulsion, is the usual mechanism of injury. 3. Grafting C8 and T1 is often not an option, as at this level avulsion injuries are likely to have occured. If grafting is possible it is only likely to provide protective sensation and no meaningful motor recovery. This is because muscle atrophy occurs prior to reinnervation of the finger flexors and intrinsics due to the considerable distance the regenerated nerves have to travel. 4. In a child any complete lesion regardless of level should be repaired and grafted if possible. 5. Across the literature, timing of surgery most commonly occurs between 3e6 months.

Surgical options A variety of surgical strategies exist to improve function and the choice used will depend on the extent and location of the injury. A clear surgical plan with realistic expectations of the outcome should be discussed with the patient. Surgical options available include:

Surgical approach to the brachial plexus The plexus can be exposed in its entirety or partially, depending on the procedure being performed and the extent of the injury. The patient is positioned for primary exposure allowing for intraoperative adjustment. Any potential nerve grafts and transfer sites and must also be readily accessible (intercostals or sural nerve, for example). Under general anaesthesia, with the use of a short acting muscle relaxant for intubation to allow for intra-operative nerve stimulation, the patient is placed in the semi-recumbent beach chair position with the neck slightly extended and turned to the contralateral shoulder. The arm is prepared so that it can be moved intra-operatively to aid dissection. The surface markings for exploration of the supraclavicular plexus are the posterior border of sternocleidomastoid and a line just superior and parallel to the clavicle. The skin and superficial fascia are incised and subplatysmal flaps are raised to improve exposure. Deep to the platysma are the external jugular vein, which is retracted medially, and the cervical plexus, which should be preserved where possible to prevent neuroma

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Neurolysis Lesions in continuity, with external compression or scarring, can be treated with neurolysis. For these procedures to be successful the fascicular pattern and endoneural tissue must be preserved. If there is concern or doubt over the integrity of the fascicle pattern, resection of the segment and grafting is preferred. Nerve grafting This forms the basis of modern post-ganglionic plexus surgery. Anatomical reconstruction, with connection of the proximal and distal stumps is attempted. The limiting factors in reconstruction tend to be the length of the gap that requires grafting and the availability of a sufficient nerve graft. Therefore, priority is given to 1, restoration of elbow flexion, 2, restoration of shoulder abduction, and 3, restoration of sensation on the medial border

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Intra-operative photographs demonstrating exposure of the terminal branches of the brachial plexus. Figure 6

the function of the axon donor, but new end-to-side26 techniques mean this is not necessarily the case. From a surgical point of view it must also be considered whether the donor nerve can be transferred without tension. Table 6 shows the donor nerves commonly used for transfers. Some surgeons prefer to use intraplexus donors suggesting they give better results, due to the greater number of axons compared with extraplexus donors, therefore increasing the chances of successful neurotization27. Despite this viewpoint, some extraplexus donors give consistently good results in clinical practice; the intercostals when used for shoulder and elbow function are reported to give up to 70% good to excellent results.27 The accessory nerve, according to published studies, is also a reliable donor.27

of the forearm. The commonly used donor sensory nerves for grafting are, sural, saphenous, medial brachial and antebrachial cutaneous and superficial radial nerves. Vascularised nerve grafts24 have added another possibility and the most commonly used is the ulnar nerve. In these cases the ulnar nerve should be split into minor units roughly the size of the sural nerve before grafting, in order to increase chances of success.25 Nerve transfer (Neurotization) Neurotization is used more often in pre-ganglionic lesions. Nerve fibres from one nerve are transferred to a denervated nerve, in order to ‘neurotize’ the nerve. Motor nerves have to be used as donors to restore motor function and sensory nerves to restore sensory function. Classically this technique involves sacrificing

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most benefit. In essence, peripheral reconstruction is aimed at restoring shoulder stability, with or without movement, in addition to restoring elbow flexion and hand function.

Donor nerves used for transfer Donor nerve for transfer Intercostal (to Musculocutaneous) Ipisilateral Cervical Plexus Contralateral Lateral Pectoral Accessory Hypoglossal Phrenic Contra lateral C7 Ulnar nerve to Musculocutaneous

Described Seddon 1961 Brunelli 1980 Gibert 1992 Bonnel 1984 Narakas 1984 Zhen 1989 Chen 1991 Oberlin 1997

Late reconstruction

Shoulder arthrodesis The role of shoulder arthrodesis is two-fold. Firstly, in total plexus palsies, by stabilising the shoulder it enables the surgeon to concentrate all available nerve grafts and transfers, which maybe limited, on restoring elbow and hand function. Secondly, in upper plexus palsies, it may be of benefit in unstable shoulders (painful, subluxing or dislocating) where attempts to stabilise have failed or where it is not appropriate to undertake such procedures in the first place. Certain aspects are worth considering when planning shoulder arthrodesis:  Good scapulothoracic muscle function is vital  Good distal function of the arm is needed for the procedure to be worthwhile. If the hand is completely paralysed there is unlikely to be any substantial gain in function from shoulder arthrodesis.  Integrity of the acromioclavicular, sternoclavicular and scapulothoracic joints should be considered. Stiffness of these joints may limit the success of arthrodesis and it is also important to ensure the acromioclavicular joint is not incorporated into the arthrodesis With advances in bone fixation, especially rigid compression plating, the need for prolonged postoperative immobilisation is no longer required. The most common position for arthrodesis is 20 of abduction, 30 of flexion and 30 internal rotation. Excessive abduction must be avoided, as it leads to chronic fatigue around the shoulder girdle. This position should give a strong and functional shoulder to feed and address personal hygiene with an average movement of 60 of abduction and flexion32 being possible via the scapulothoracic articulation. Shoulder arthrodesis gives predictable results and can improve the function of the limb considerably. The strength and movement is greater than is achieved with muscle transfers, but does depend on the scapulothoracic muscles. It should be born in mind when combining shoulder arthrodesis with other distal procedures, that following the arthrodesis it can be difficult to position the arm and thus the distal procedures may be more easily performed first.

In cases where spontaneous recovery has not occurred, or when surgical intervention has failed to yield any functional benefit, then late reconstructive options should be considered. In such cases there needs to be conclusive evidence that neurological recovery is unlikely, or sufficient time has elapsed without functional improvement following the injury. Many of the techniques used in reconstruction have been adapted from use in poliomyelitis and peripheral nerve injuries. It must be acknowledged, however, that in poliomyelitis there is no loss of sensation and thus in plexus injuries the functional benefits from motor improvement maybe less. The primary procedures in peripheral reconstruction are arthrodesis and tendon transfers, with the newer technique of free muscle transfers becoming an option. There is also a limited place for amputation. Numerous procedures have been described to improve the function of the upper limb and, as previously stated, it is important to assess each individual patient carefully and to determine from which procedures they are likely to derive the

Tendon transfers to the shoulder In cases where only partial paralysis of the shoulder has occurred arthrodesis may not be necessary and tendon transfers are sufficient to restore function. Many transfers have been described including:  Trapezius to deltoid insertion on the humerus (Bateman procedure)  Latissimus dorsi and teres major to the posterolateral humerus (L’Episcopo) to improve external rotation  Anterior advancement of the posterior portion of deltoid to replace non-functioning anterior segment.  Transfer of the long head of triceps to the acromion There are many other described transfers and the final decision as to which is used will depend on the exact nature of the paralysis and donor muscles available. Thus, no precise management algorithm can be constructed, although Alnot in 199633 outlined his surgical approach to shoulder muscle palsies (Table 7).

Table 6

Repair of avulsed spinal nerve roots has been attempted by many, with Bonney and Jamieson reporting on a case in 1979. Both Jamieson and Carlstedt have published experimental work on animal models with some functional success28,29 and early work has emerged on human subjects.30,31 Despite this, to date, this surgical option has not reached the stage where it warrants inclusion in the standard surgical armamentarium. As with all peripheral nerve injuries, a considerable number of factors influence the results of surgery to the brachial plexus. As a result, firm statements regarding the prognosis of surgery are difficult to justify. The literature indicates overall that younger patients do better, as do upper plexus injuries. This almost certainly reflects the fact that in upper lesions the target organs are much closer to the plexus, making regeneration more likely. Terzis27 in a series of over two hundred surgically managed plexus injuries reported good to excellent results in 75% of suprascapular nerve reconstructions, 40% of biceps reconstructions, 30% of triceps reconstructions, 35% finger flexion reconstructions and 15% of finger extension reconstructions. Restoration of hand function secondary to a lower plexus injury remains the most difficult area to address, but with aggressive management, according to Terzis, it is not out of the question.

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Free muscle transfers Free muscle transfers are a feasible option in reconstruction of elbow flexion and prehensile reconstruction of the hand.34,35 In order for these transfers to function it is necessary for the proximal joints to be stable. Thus in reconstruction of elbow flexion function is compromised if the shoulder is not stable, and this must be addressed either at the same time or before the free muscle transfer. When addressing finger function, stability of the elbow and wrist is mandatory. In addition to proximal joint stability the presence of an antagonistic muscle greatly influences functional outcome. The weight of the limb and the effects of gravity to a certain extent act as antagonists, but this is often not enough, and thus when addressing finger flexion in the absence of active extension, splinting may be required. Double free muscle transfers may deal with this potential problem.35 The donor muscles commonly used are latissimus dorsi, gracilis and rectus femoris. Consideration must be given to donor muscle blood supply, length, volume and shape. Latissimus dorsi and rectus femoris are mainly used for restoration of elbow flexion whereas gracilis due to its shape and amplitude of contraction is the preferred donor for wrist and finger function.

Alnot’s surgical approach to shoulder muscle palsies Deltoid muscle palsy only

Deltoid & Infraspinatus palsy Deltoid, Infraspinatus & Supraspinatus

Trapezius to deltoid (Bateman) or Long head triceps to Acromion Derotation osteotomy of humeral shaft for external rotation Stabilisation shoulder with long head of biceps Derotation osteotomy Shoulder arthrodesis Trapezius transfer

Table 7

Tendon transfers to restore elbow flexion Elbow flexion plays a vital role in upper limb function and its restoration can significantly improve a patient’s functional outcome. Depending on the level of the lesion and the degree of successful reinnervation different reconstructive procedures are available. Once again the final decision depends on the precise functional deficit and on available donor muscles. When considering which transfer to use, muscle excursion, alignment, cosmesis and pre-existing range of movement must be considered. The aim of surgery is to restore good strength through a functional range of 30 to 130 without excessive pronation. The common donors used in transfers to restore elbow flexion are:  Proximal advancement of the common origin of the forearm flexor-pronator muscles (Steindler) - historically most popular, but can be weak and can lead to flexion contractures and excessive pronation.  Latissimus dorsi - good power and excursion but frequently denervated along with elbow flexors and thus unavailable.  Pectoralis major (Clarke) - requires stable or arthrodesed shoulder to establish correct tension  Pectoralis minor - stable or arthrodesed shoulder  Triceps - good strength, excursion and cosmesis but loss of extension is a high price to pay.  Sternocleidomastoid - rarely used due to web appearance in neck and the occasional need to preposition the head to achieve elbow flexion.

Orthotics The role of orthotics should not be forgotten in brachial plexus injuries, in both the non-surgically and surgically managed cases. They can be used to immobilise, stabilise, and support a joint in a desired position, protect weak muscles from overstretch, prevent contractures and support structures following surgical repair. They can be used instead of, or alongside, late reconstruction to enhance the function of the limb. A static orthosis is primarily intended to stabilise joints or place the limb in a position of function. Dynamic orthoses are often more complex and intended to more than simply stabilise a joint. Multiple dynamic orthoses are available including shoulder, elbow, wrist and hand orthotics. The exact orthoses used will depend on the functional deficit and needs of the patient as assessed by a trained orthotist. Consideration must be given to ease of use, wear and application as well as the risks of skin problems, particularly with anaesthetic skin. Despite some patients finding orthotics undesirable, they can be a very useful adjunct to management.

Amputation With the advent of the modern techniques in brachial plexus injuries discussed above there has been a significant shift away from amputation. This has occurred to the extent that Tervis in 1999 claimed ‘Amputation has no place in the modern treatment of traumatic plexopathies’. With that considered, in some cases where reconstruction has failed and the patient is left with a flail useless arm, struggles with the weight of it and fails to properly care for the anaesthetic skin, amputation is a viable option. The amputation can be at any level, depending on the needs of the patient and maybe combined with shoulder arthrodesis. Amputation is not an appropriate option for those who request it for neurological pain relief.

Tendon transfers to restore hand function This is a very difficult area to address and there are no simple solutions. In essence the tendon transfers available are those commonly used for isolated peripheral nerve injuries and to cover them exhaustively is beyond the scope of this review. The most notable difference is that often the donor muscles used in isolated median, ulnar and radial nerve palsies are not necessarily available or expendable in a brachial plexus lesion, due to the more global effect they have on hand function. As with all tendon transfers, consideration must be given to the potential gains from the procedure and also the functional loses that will occur. Ultimately the treating clinician must assess and discuss with the patient the available options including risks and benefits and come to a mutual conclusion as to what is the best management plan.

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Summary Unfortunately brachial plexus injuries are becoming increasingly common and they result in a very significant disability, whilst

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19 Hetreed MA, Howard LA, Birch R. Evaluation of sensory evoked potentials recorded from nerve roots to the cervical epidural space during brachial plexus surgery. In: Jones SJ, Boyd S, Hetree M, Smith NJ, eds. Handbook of spinal cord monitoring. Dordrecht: Kluwer Academic Publishers, 1994. p. 171e8. 20 Dunkerton MC, Boome RS. Stab wounds involving the brachial plexus. J Bone Joint Surg 1988; 70B: 566e70. 21 Kline Dg. Civilian gunshot wounds to the brachial plexus. J Neurosurg 1989; 70: 166e74. 22 Leffert RD. Brachial plexus injuries in the adult. In: Norris TR, ed. Orthopaedic knowledge update: shoulder and elbow 2. J Am Acad Orthop Surg 2002: 394. 23 Nashold BS. Current status of the DREZ operations. J Neurosurg 1984; 15: 942e4. 24 Taylor GI, Ham FJ. The free vascularized nerve graft: a further experimental and clinical application of microvascular techniques. Plast Reconstr Surg 1976; 57: 413e26. 25 Eberhard D, Millesi H. Split nerve grafting. J Reconstr Microsurg 1994; 12: 71e6. 26 Viterbo F, Trindale JC, Hoshino K, Mazzoni A. Two end-to-side neurorhaphies and nerve graft with removal of the epineural sheath: experimental study in rats. Br J Plast Surg 1994; 47: 75e80. 27 Terzis JK, Vekris MD, Soucacos PN. Outcomes of brachial plexus reconstruction in 204 patients with devastating paralysis. Plast Reconstr Surg 1999; 104: 1221e40. 28 Jamieson A, Earnes RA. Reimplantation of avulsed brachial plexus roots: an experimental study on dogs. Int J Microsurg 1980; 2: 75e80. 29 Carlstedt T, Grane P, Hallin RG. Return of function after spinal cord implantation of avulsed spinal nerve roots. Lancet 1995; 346: 1323e5. 30 Carlstedt T, Anand P, Hallin R. Spinal nerve root repair and reimplantation of avulsed ventral roots into the spinal cord after brachial plexus injury. J Neurosurg 2000; 2(Suppl): 237. 31 Fournier H, Mercier P, Menei P. Repair of avulsed ventral nerve roots by direct ventral intraspinal implantation after brachial plexus injury. Hand Clin 2005; 21: 109. 32 Rouholamin E, Wootton R, Jamieson AM. Arthrodesis of the shoulder following brachial plexus injury. Injury 1991; 22: 271e4. 33 Alnot JY. Brachial plexus palsies: palliative surgery. In: J-Y and Narnkas A, eds. Traumatic brachial plexus injuries. Expansion Scientifique Francaise: Paris 218e220. 34 Doi K, Sakai K, Fuchigami Y, Kawai S. Reconstruction of irreparable brachial plexus injuries with reinnervated free-muscle transfer. J Neurosurg 1996; 85: 174e7. 35 Doi K, Sakai K, Kuwata N, et al. Double-muscle technique for reconstruction of prehension after complete avulsion of brachial plexus. J Hand Surg Am 1995; 20: 408e14.

occurring in young individuals, usually of working age. Conservative management helps control pain and maintain movement and function. Recent technical advances, however, have significantly increased the role of early surgery employing neurolysis, nerve grafting and nerve transfer. Function may also be helped by, or in combination with, shoulder arthrodesis and a range of tendon transfers to capitalise on any remaining functioning muscle units. The care of patients with plexus injuries is complex and requires a multiskilled, multidisciplinary approach for the best results. A

REFERENCES 1 Barnes R. Traction injuries of the brachial plexus in adults. J Bone Joint Surg 1949; 31B: 10e6. 2 Bonney G. Prognosis in traction lesions of the brachial plexus. J Bone Joint Surg 1959; 41B: 4e35. 3 Leffert RD, Seddon H. Infraclavicular brachial plexus injuries. J Bone Joint Surg 1965; 49B: 9e22. 4 Narakas A. Surgical treatment of traction injuries of the brachial plexus. Clin Orthop 1978; 133: 71e90. 5 Yeoman PM, Seddon HJ. Brachial plexus injuries: treatment of the flail arm. J Bone Joint Surg 1961; 43B: 493e500. 6 Leffert RD. Brachial plexus injuries. N Engl J Med 1974; 291: 1059e67. 7 Kerr A. Brachial plexus of nerves in man. the variations in its formation and branches. Am J Anat 1918; 23: 285. 8 Seddon HJ. Three types of nerve injury. Brain 1943; 66: 238e88. 9 DeVries GH. Schwann cell proliferation. In: Dyck PJ, Thomas PK, Griffin JW, et al., eds. Peripheral neuropathy. Philadelphia: WB Saunders, 1993. p. 290e8. 10 Sunderland S. A classification of peripheral nerve injuries producing loss of function. Brain 1951; 74: 491e516. 11 Birch R, Bonney G, Wynn Parry CB. Surgical disorders of the peripheral nerves. Edinburgh: Churchill Livingstone, 1998. 12 Lieberman AR. The axonal reaction. a review of the principal features of perikaryal responses to axon injury. Int Rev Neurobiol 1971; 14: 49e124. 13 Price DL, Porter K. The response of ventral horn neurns to axonal transaction. J Cell Biol 1972; 53: 24e37. 14 Stoll G, Griffin JW, Li CY, Trapp BD. Wallerian degeneration in the peripheral nervous system: participation of both schwann cells and macrophages in myelin degredation. J Neurocytol 1989; 18: 671e83. 15 Dahlin LB. Nerve Injuries. Curr Orthop 2008; 22: 9e16. 16 Chaudhry V, Cornblath DR, Mellits ED, et al. Inter and intra examiner reliability of nerve conduction measurements in normal subjects. Ann Neurol 1991; 30: 841e3. 17 Mallik A, I Weir A. Nerve conduction studies: essentials and pitfalls in practice. J Neurol Neurosurg Psychiatry 2005; 76(Suppl. II): ii23e31. 18 Mills KR. The Basics of electromyography. J Neurol Neurosurg Psychiatry 2005; 76(Suppl. II): ii32e5.

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Acute compartment syndrome of the lower extremity: an update

The key element in its pathogenesis is an elevation of tissue pressure within encapsulated muscles as a consequence of increased vascular permeability and interstitial oedema formation. Elevated compartment pressure results in progressive skeletal muscle microvascular ischaemia with subsequent muscle cell death, loss of motor function, or loss of the limb. Evidence suggests that reactive oxygen metabolites may be decisively implicated in the occurrence of this clinical entity.16 The clinical diagnosis of compartment syndrome depends on the presence of pain, tenseness, swelling, and diminished motor and/or sensory function in the affected limb. Even though some authors recommend that the diagnosis of compartment syndrome should rely on clinical symptoms,17 others have highlighted the significance of intracompartmental pressure measurement.18e20 Nevertheless it remains a fact that the subjectivity of symptoms and the ambiguous nature of the clinical signs emphasize the necessity of intracompartmental pressure measurement in the diagnosis or exclusion of compartment syndrome. However there is no specific, reliable and reproducible test that could confirm the diagnosis of ACS.21 Delay in the diagnosis or treatment may result in permanent sequelae, including paralysis, painful dysthaesias, contractures, and occasionally loss of the limb. Thus, a systematic evaluation should include a repeatable physical examination and compartment pressure monitoring. The definitive treatment for acute compartment syndrome is fasciotomy. This involves a skin incision, and splitting the fascia of the compartment to relieve pressure and allow tissue perfusion. Single or double incisions along the limb axis may be required. Failure to recognise the syndrome has significant functional consequences for the patient and may involve the surgeon in a malpractice litigation.22 Thus, a knowledge of the pathogenesis, methods of evaluation and treatment are extremely important. In this paper the current concepts of the pathophysiology, diagnosis, and treatment of compartment syndrome of the lower limb are discussed.

Christopher Tzioupis George Cox Peter V Giannoudis

Abstract Acute Compartment Syndrome (ACS) represents a limb threatening condition characterised by increased intracompartmental pressure and decreased tissue perfusion leading to cellular anoxia, muscle ischemia, and death. Musculoskeletal trauma, as well as other medical conditions, initiate this syndrome. Most commonly the lower leg is involved. Basic science data shows the involvement of reactive oxygen metabolites in the development of this clinical entity. Diagnosis is principally clinical, reportedly delayed by certain anaesthetic techniques, such as nerve blocks and other forms of regional and epidural anaesthesia. Measurement of the intracompartmental pressure is required for the confirmation of the syndrome. Complete fasciotomy of all compartments involved is mandatory to reinstate perfusion to the affected tissues. Recognising a compartment syndrome requires a high index of suspicion, accurate evaluation. Early treatment.prevents irreversible damage and subsequent disability as well as avoiding medico-legal problems.

Keywords compartment; fasciotomies; intracompartment pressure; tibial fractures

Introduction Acute compartment syndrome (ACS) is a true orthopaedic emergency representing a unique form of ischaemia that affects a group of muscles enclosed within a relatively non-compliant fascial sheath.1e3 ACS can occur as a result of any extremity fracture, crush injuryto a limb, prolonged tourniquet use under anaesthesia, compression by casts or dressings, burns, bleeding from trauma or anticoagulation therapy, soft tissue injuries or, from exercise in chronic compartment syndrome.1e12 ACS may cause irreversible muscle or nerve damage, leading to a poor functional result.13,14 The most frequently affected site is the anterior compartment of the leg following a tibial fracture but it can also occur in the hand, forearm, foot, or proximal portions of the limbs.15

Historical aspects The risks of elevated intracompartmental pressure have long been recognized. Hippocrates (ca. 400 B.C.) recommended: ‘‘apply the linen bandage putting the head of it at the fracture so as to give support, but without much pressure’’.23 In the modern era, compartment syndrome was originally described by Richard von Volkman.24 in 1881. He described a classic presentation of forearm muscle contractures following the application of a tight bandage for the treatment of an elbow fracture. Jepson in 192625 described the effect of prompt decompression to prevent such a disastrous condition. Sir Robert Jones in 192826 concluded that ‘‘pressure from both within or without, or both’’ could be the cause. Bywater and Beall in 194127 reported on the victims of the London Blitz, highlighting the systemic consequences of severe crush injuries including renal failure and death. In the early 1900s, interventional devices were used to measure pressure in the compartments. In 1975 Whitesides et al.28 advocated the use of a simple pressure monitoring device employing a manometer, catheter, and needle. Owen et al.29 contributed to our understanding of the pathogenesis of ACS in

Christopher Tzioupis MD Trauma Fellow, Trauma and Orthopaedic Surgery, School of Medicine, University of Leeds, Leeds, UK. George Cox MRCS Research Fellow, Trauma and Orthopaedic Surgery, School of Medicine, University of Leeds, Leeds, UK. Peter V Giannoudis MD FRCS Professor of Trauma and Orthopaedic Surgery, School of Medicine, University of Leeds, Leeds, UK.

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Pathophysiology of ACS

their elegant description of 11 cases of crush syndrome following a period of prolonged compression. Matsen30 suggested that the underlying features of compartment syndrome are the same, irrespective of aetiology or location. He described the role of compartment pressure measurement in ambiguous situations and the importance of prompt surgical decompression. The vivid account by Rorabeck and Macnab31 deserves special reference. They pointed out the four main entities that could lead to the syndrome:post-exercise, post-traumatic, post-ischaemic and post-arterial occlusion. Mc Queen and Court-Brown32 more recently reported the role of Delta pressure as the critical determinant of need for decompression.

Phillips45 defined the pathophysiology of compartment syndrome as an insult to normal local tissue homeostasis that results in increased tissue pressure, decreased capillary blood flow, and local tissue necrosis caused by oxygen deprivation. Tissue metabolism normally requires an oxygen tension of 5e7 mmHg. This is readily maintained by capillary perfusion pressure (CPP) of 25 mm which is well above the normal interstitial tissue pressure (IP) of 4e6 mm. The tissue perfusion pressure equals capillary perfusion pressure minus interstitial pressure. As compartment pressure increases, progressive decrease in perfusion leads to ischaemia and necrosis which then triggers a chain of events including an increased capillary permeability due to toxins. Tissue ischaemia, a direct result of increased compartment pressure, is also compounded by: 1. Arterial spasm directly due to increasing interstitial pressure.46 2. Effect of critical closing pressures on the arterioles.47 Due to a small luminal radius and high mural tension, arterioles naturally have high transmural pressure (arteriolar pressure minus tissue pressure). When the transmural pressure equals zero (due either to increasing tissue pressure or decreasing arteriolar pressure), the arterioles close (critical closing pressure [CCP] is reached) and ischemia ensues.47 3. The rising tissue pressure causes collapse of the veins as their walls are thin and susceptible. Initially the unabated arterial flow increases the venous pressure which re-establishes the flow, but the increased venous pressures adversely affect the arteriovenous gradient and result in ischemia. When interstitial pressure exceeds CCP, capillaries collapse causing reduced perfusion, ischaemia, and cell death.31 The hypoxic injury to cells releases vaso-active substances, which increase the endothelial permeability. Subsequently an unabated shift of fluid occurs across the capillary endothelium into the extra-vascular space, causing high tissue pressure.48 Nerve conduction slows down as a result of ischaemia. Tissue pH falls and the degradation products contribute to a further increase in the tissue pressure. A vicious cycle of increased tissue pressure and ischemia ensues. Myocyte necrosis produces significant amounts of osmotically active particles (each milliosmole of such substance has been showed to exert 19.5 mmHg pressure8) drawing large quantities of fluid into the tissues.31 Rorabeck31 identified external pressure, trauma, and post-revasularisation swelling as the main causes of the pathological events leading to the compartment syndrome. The involvement of neutrophils in arterial occlusion models of ischaemic skeletal muscle injury has also been reported.49The mechanisms by which neutrophils induce microvascular dysfunction are unclear. It is believed that neutrophils once activated can produce large quantities of oxygen metabolites, which are involved in the occurrence of ACS in rabbits during revascularization.16 Furthermore, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and the enzyme xanthine oxidase are believed to be the main sources of oxidants in post-traumatic ischaemia. Sadasivan et al.50 showed that neutrophil reduction precludes microvascular dysfunction and muscle neutrophil infiltration. Furthermore, they correlated the occurrence of ACS with

Incidence and aetiology Musculoskeletal trauma and various medical conditions are linked to acute compartment syndrome (ACS) (Table 1).21,32e34 The commonest fractures associated with ACS are those of the tibial shaft35 with an incidence of 40%,21 and mainly involve the anterior and deep-posterior compartments.36 The incidence after open tibial fractures varies between 1.2 and 10.2%.8,35,37 Lower limb and ankle joint position have been reported to contribute to the establishment of ACS by altering compartment pressure.40 ACS has been reported to occur also after isolated femoral fractures,38 and after operative treatment of fractures with intramedullary nailing. However thigh compartment syndrome is seen more commonly in polytrauma patients and can be associated with various soft tissue injuries.39 Anticoagulation treatment in joint replacement surgery procedures has been implicated in the occurrence of ACS.44 Burns causing eschar formation and intersitial edema have been noted to cause ACS.41 Any revascularisation procedure can result in ACS, due to tissue swelling following reperfusion, with its incidence ranging from 0 to 21%.42 The use of military antishock trousers (MAST) for abdominal or pelvic haemorrhage has been associated with lower extremity compartment syndromes, although the key factor seems to be the inflation pressure rather than the time duration.43

Main aetiologies of acute compartment syndrome of the leg Closed Fractures61,77 Open fractures8 Nailing procedures 17,20,21 Soft tissue injuries51,75 Casting material71 Lithotomy position52 Burns41 Revascularization76 Military Antishock Trousers43 Anticoagulation treatment44 Skin traction81 Table 1

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a neutrophil chemotactic factor which facilitates the neutrophil endothelial cell interactions. Thus, a plethora of mechanisms are involved in the genesis of this devastating condition and once the chain of events starts, the vicious cycle of swelling and tissue death follows. Only immediate decompression helps to break the cycle. Once prolonged ischaemia is established, it leads to muscle infarct followed by fibrosis and contractures (Volkmann’s ischaemic contractures). The marked atrophy and contractures are instantly recognisable and have devastating functional results.28

Neurological symptoms in the early stages include reduced vibratory sensation, increased two-point discrimination, and paraesthesia. Altered sensation over the space between the first and the second toes may accompany the pain. The other classic Ps like paralysis (e.g.: foot drop), pallor, as well as poikilothermia are not only unreliable but, more importantly, can be late signs.55 In a meta-analysis, Ulmer et al.56 showed that if two clinical indicators were positive, the probability of a compartment syndrome was 25%, and if three were positive the probability was 93%. They concluded that, whereas association of clinical findings with compartment syndrome seems evident, the predictive value of the clinical findings for the diagnosis of compartment syndrome had yet to be delineated.

Diagnosis History and clinical examination The mechanism of injury is the first warning that a patient may be at risk for the development of ACS. According to Tscherne and Gotzen,51 the more severe the initial soft-tissue injury, the greater the probability that soft-tissue complications, including compartment syndrome, will develop. The diagnostic role and relative value of clinical findings are debated. Some authors conclude that the diagnosis of compartment syndrome is largely a clinical one and is based on signs and symptoms.17 Yet, the role of clinical findings is questioned by others who debate that few criteria are available to serve as guidelines for making the diagnosis of ACS.22 However, in most patients, an early diagnosis of an ACS can be made on the basis of a clinical evaluation, provided that the physician has a high index of suspicion that ACS may occur. The classic clinical criteria include the six Ps: pain, pressure, pulselessness, paralysis, paraesthesia, and pallor (Table 2).52 Pain is the most reliable symptom of ACS. However, pain is not easily assessed in the sedated, intoxicated, or unconscious patient; furthermore, pain may be absent in an established compartment syndrome.52 Pain reproduced by passive stretching has been described as a highly sensitive indicator of compartment syndrome in the lower leg.20 This may result from ischaemia-induced loss of intramuscular high-energy phosphates or alterations of intramuscular pressure.53 Paraesthesia is also a significant diagnostic sign and a valuable indicator for fasciotomy.54 Even though the pulse status has a restricted diagnostic value, the absence of pulses should also raise suspicion for a vascular laceration.52

Clinical signs Painful passive toe flexion First web space numbness Anterior tenseness Weak foot eversion Numbness at the dorsum of the foot Painful dorsiflexion Numbness at the lateral foot Painful passive toe extension Foot numbness

Intracompartmental pressure (ICP) measurement The intracompartmental pressure (ICP) of a normal muscle compartment at rest is less than 10 mmHg.57 Monitoring of ICP in patients at risk of developing ACS has no significant complications, but failure to monitor may lead to a missed diagnosis.2,10 The critical pressure that will lead to microcirculatory failure depends on the patient’s blood pressure, the duration of pressure elevation, and many other local and systemic factors.44 Both basic science and clinical studies have shown that muscle ischaemia in injured limbs generally occurs when the tissue pressure increases to within 20e30 mmHg of the diastolic pressure.58 Yet, controversy exists about the identification of a critical value that will lead to the development of tissue necrosis. Some researchers propose an absolute compartment pressure of 30 mmHg and others 45 mmHg.59 On the other hand, it has been suggested that this critical value must reflect a decrease in tissue perfusion. This critical difference between diastolic blood pressure (DP) and ICP, has been suggested to be 30 to 40 mmHg.60 Clinical assessment of ICP must be repeated, preferably by the same clinician, at frequent intervals (30 min to 2 h) to detect a progressive compartment syndrome. Continuous monitoring can alter management and allow early fasciotomy.32 There are both continuous and intermittent methods of monitoring ICP. There is no consensus about the ideal measuring device or the threshold pressure for fasciotomy in each anatomical region. The instruments that are currently used, such as the slit and the wick catheter, consist of a fluid-filled catheter attached to an extracorporeal transducer.61 Whitesides and colleagues28 created the simple needle manometry technique utilising an 18-G needle and a pressurised constant-infusion system. The infusion technique was evaluated by Matsen and colleagues.30 The drawback of this technique is that the need for continuous infusion of saline may lead to an increase of ICP of 2e4 mmHg. Furthermore, the results of the measurement of ICP depend on the position of the limb and the height of the pressure transducer above the tip of the catheter. Conversely, Willy et al.60 have developed an electronic transducer-tipped catheter system thereby avoiding problems commonly associated with fluid-filled systems. The catheter is readily available for measurements of intracompartmental pressure as it does not require any additional manipulation.

Compartment Leg anterior

lateral posterior-superficial posterior-deep

Table 2

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Heckman et al.,62 measuring intracompartmental pressures at multiple sites in patients with tibial fractures, recommended the measurement of pressure at multiple sites, especially at the level of the fracture, as well as the careful assessment of all adjacent compartments. Zweifach et al.63 reported that an ICP of 30 mmHg or greater can cause excessive muscle necrosis and recommended this threshold as a clinical indicator for fasciotomy. Whitesides et al.28 have suggested using a difference between the diastolic pressure and the ICP, with a differential pressure within 10e30 mmHg of the diastolic pressure as the threshold for performing a fasciotomy. This method was further assessed in 116 patients with tibial fractures by McQueen and Court-Brown,32 who utilised a differential pressure of 30 mmHg and showed that fasciotomy was needed in only three patients, with no adverse sequelae in the others. Matsen and colleagues64 showed that patients varied in their tolerance to raised ICP before neuromuscular deficits occurred, and used an ICP level of 45 mmHg for performing fasciotomy. Ouellette and Kelly65 used an ICP of between 15 and 25 mmHg when clinical signs were present and of more than 25 mmHg in the absence of clinical signs. Janzing and Broos66 recommended measuring ICP only in symptomatic patients or in those who were difficult to assess. Recently new non-invasive modalities have been utilised in order to obtain more accurate and reliable results from the measurement of ICP. Near InfraRed spectroscopy (NIRS) is a non-invasive method of detecting variations in the level of muscle haemoglobin and myoglobin. NIRS was found to differentiate between an induced acute compartment syndrome and both hypoxia and hypotension.67 However, this method has been utilised mostly in patients with the chronic exertional form of compartment syndrome (CECS). Magnetic resonance imaging (MRI) has a wide variety of diagnostic applications in modern medicine and some encouraging results have been obtained in studies examining its ability to diagnose both chronic exertional and acute compartment syndromes. Rominger et al.68 found that the changes on MRI in an established compartment syndrome with swollen compartments and loss of normal muscle texture correlated well with both the intraoperative findings and the tissue histology. Limited studies have been performed to assess invasive laser doppler flowmetry as a diagnostic aid particularly in CECS. Abraham et al.69 found that there were differences in patients with and without CECS but considered that further investigation was necessary.

Treatment General measures Once the diagnosis of ACS is made, immediate measures should be taken to prevent further increase of intracompartmental pressure. All the dressings and casts should be removed down to skin as it has been shown that splitting of the underlying dressings reduced the pressures by further 15%. complete removal of casts leads to a further decrease of 15%.71 The limb should be kept at the level of the heart rather than elevated, to maximise the tissue perfusion. Inadvertent pressure of the patient’s torso on the extremity was also shown to have dramatic effects on the compartment pressures as shown by Owen et al.29 Adequate hydration and blood pressure maintenance also help the tissue perfusion. Fasciotomy The purpose of fasciotomy is to achieve prompt and adequate decompression so as to restore the tissue perfusion. The surgeon should be familiar with the visual recognition of necrotic tissue because thorough debridement reduces the potential of infection and improves the chances of tissue recovery. Rorabeck72 reported that almost complete recovery of limb function is possible if adequate fasciotomy was done within 6 hours. Matsen73 demonstrated muscle necrosis after six hours. Irreversible changes in the nerve tissues appear after 12 to 24 hours. Muscle has significant regeneration potential and therefore immediate surgical decompression is crucial. An adequate skin incision is necessary as the skin can be a potentially limiting structure. In the leg there are four recognised compartments: the anterior, the lateral (or peroneal), the deep posterior and the superficial posterior. Tibialis anterior, extensor hallucis longus and peroneus tertius including the anterior tibial neurovascular structures comprise the anterior compartment. Peroneal muscles and the superficial peroneal nerve occupy the lateral compartment. In the posterior compartments, plantar-flexors including the gastrocnemius, soleus and plantaris with the sural nerve constitute the superficial compartment, while tibialis posterior, flexors of the big and lesser toes, posterior tibial nerve and vessels, and peroneal vessels form the deep compartment. Various fasciotomy techniques are described to facilitate an approach to all four compartments of the lower limb. Kelly and Whitesides described a single lateral incision technique with added fibulectomy.59 Jacob74 suggested the double incision technique with incisions placed on both the medial and the lateral sides of the lower limb. Regardless of the approach used, all four compartments of the leg must be thoroughly decompressed. In most instances, the two-incision technique affords better exposure of the four compartments and release of the soleus from the fibula is not required. At the lower leg, through the two-incision technique75 the anterior and lateral compartments are approached. A vertical incision is made over the leg midway between the fibular shaft and tibial crest. The intermuscular septum is identified, and the anterior and the lateral compartments are decompressed by separate incisions, taking care to avoid the superficial peroneal

Laboratory findings Previous studies have shown that elevation of serum CPK in an isolated compartment syndrome reflects the amount of muscular damage. Lactate dehydrogenase (LDH) has also been shown to be elevated in patients with ACS, especially secondary to ischaemia and crush syndromes.70 Continued elevated levels of CPK after decompression denote insufficient decompression and ongoing muscle necrosis. Coagulopathy has been described as a risk factor for the development of thigh compartment syndrome15 and may raise suspicion for an impending thigh compartment syndrome, if it is associated with a patient with a tense, swollen thigh.

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hyperbaric oxygen treatment,83 ischaemic preconditioning,84 as well as treatment with glycine, glutamine, and inhibitor of tumour necrosis factor.85,86 There are several investigational techniques that are currently being assessed for their efficacy in improving the diagnosis of ACS. These include measurements of the surface hardness of the compartment, transcutaneous oxygen measurements, measurement of mechanical impedance, NIRS, thallium stress testing, and laser Doppler flowmetry.69 Tissue ultrafiltration is a process in which small semipermeable hollow fibres are placed into tissues for removal of interstitial fluid. Tissue ultrafiltration was first described as a method of assaying the interstitial space and has been used experimentally in skin flaps.87 Compartment syndrome ultrafiltration (CSUF) promises to be a clinical tool that will improve diagnosis and treatment of ACS.

nerve in the lateral compartment. A vertical incision is made medially two centimetres behind the posterior border of the tibia, the saphenous vein is protected and through a small transverse incision the superficial and deep compartments are identified. The fascia over the flexor digitorum longus muscle is incised to expose and decompress the deep compartment including the tibialis posterior muscle. Some authors support limited incisions, while others suggest long incisions, underlining the fact that such are essential to decompress affected compartments sufficiently.42 Patman76 advocated long skin incisions only in the presence of massive soft tissue swelling or paralysis, utilising multiple small skin incisions for decompression in fasciotomy for vascular causes. On the contrary, Cohen et al., utilising the two-incision technique, defined the adequate skin incision length for the compartments’ decompression to be up to 16 cm.77 They concluded that long incisions do not influence either the complication rate or the late functional result. Janzing and Broos, summarising the techniques for the various fasciotomies described the fasciotomy incisions as either closed (small skin incision or primary skin closure), subcutaneous (limited skin incision and secondary closure) or open (extensive skin incision and secondary skin closure).66 Overall open fasciotomy is recommended for adequate decompression. The skin incision in the leg should be approximately 16 cm. This is because small, subcutaneous, and closed incisions may not decompress the compartments fully, and patients treated in this way may need further intervention to regain a normal ICP.

Complications and outcome It is well known that delay in fasciotomy is the single cause of a poor outcome in ACS, also increasing the incidence of septic wound complications.14,88e90 The use of broad-spectrum antibiotic prophylaxis and vacuum-assisted wound care techniques may help to reduce the incidence of septic complications after fasciotomy. Rorabeck studied a series of 18 patients requiring double incision four compartment fasciotomies of the lower limb.72 The results in thirteen patients (72%) were said to be acceptable, which implied a leg with normal function, no residual neurological sequelae and with no further reconstructive surgery required. Four patients (22%) yielded unacceptable results, as they had persistent neurological sequelae requiring either further reconstructive surgery or an orthosis, one patient (6%) required an amputation. This retrospective review of patients revealed that the patients’ wounds were associated with marked morbidity and of such an appearance that their lifestyles were altered. This study suggests that fasciotomy wound closure should be reappraised and techniques sought to reduce the size and subsequent morbidity of such wounds. Adequate and timely treatment of the acute compartment syndrome can lead to healing with good functional and cosmetic results. However, results are not always good. After fasciotomy, mortality rates of 11%e15%, amputation rates of 11%e21%, and other serious morbidities have been reported.42,78,90 If operative treatment is delayed or inadequate, excessive tissue necrosis may lead to amputation, renal insufficiency, and death.88 Although the aetiology, pathophysiology, and treatment of ACS have been well described in the literature, there is limited knowledge of the long-term impact of compartment syndrome on the quality of patients’ lives. The incidence of ischaemic contractures as a complication of tibial fractures has been reported to be 2%, However, the long-term effect of this is not known.90 Vandervelpen et al.91 assessed the functional outcome of 28 patients on an average of 17 months following tibial fasciotomies. They reported that more than one-fourth of the patients showed late functional disabilities mainly because of limitation of dorsiflexion of the ankle joint, reduction of the function strength of the foot extensors, contractures of the foot flexors, and abnormal superficial sensibility.

Wound closure The fasciotomy wound may be allowed to heal by secondary intention or undergo skin closure (primary, delayed primary, and secondary), skin grafting or flap coverage.78 During the last five years, multiple techniques have been proposed to close fasciotomy wounds with dermatotraction, which is the progressive closure of wounds by continuous traction on the skin margins. Examples are the shoelace or vessel loop technique,79 the STAR,80 and Sure-Closure (Comesa, Brussels, Belgium) skin-stretching device.81 Early secondary wound closure after fasciotomy has been advocated for some patients on the third or fourth day after operation, but only with concurrent ICP monitoring because closing the wound even on the fourth day can still increase ICP. Split-thickness skin grafting is usually performed after 7e21 days. Other authors have described techniques to avoid the need for skin grafting. These include employing plaster strips, rubber bands, skin staples and subcuticular non-absorbable sutures, all of which are used to close the wound gradually.80 There is little information in the medical literature regarding the use of vacuum assisted closure (VAC) dressings after fasciotomies for compartment syndrome. It seems though that the VAC dressing may be useful after fasciotomy for compartment syndrome to increase the ability to perform delayed primary closure.82 Alternative interventions There are no clear alternatives to fasciotomy, even in early or borderline cases. There has been little or only moderate success with attempts at non-invasive treatment of ACS including

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In another study of 27 patients,92 the long-term damage of muscle, surgically treated for ACS, was evaluated by means of sonography after anaverage of 98 months (43e154) following trauma. Twelve patients had fasciotomy for a manifest ACS and 15 for an imminent one. Comparison of the affected lower limb to the healthy one revealed changes of echogenicity reflecting the loss of typical muscle texture in all the patients with manifest ACS. Only two patients in the imminent group demonstrated sonographic changes. This study suggests that such symptoms as pain and discomfort as well as poor mobility may be long lasting following surgical treatment of compartment syndrome, and provides a benchmark for further longterm and comparative studies. In conclusion, compartment syndrome may be associated with long-term symptoms and a continuing shortfall in patients’ health-related quality of life.89

3 Avitzour M, Mintz Y, Liebergall M, Mosheiff R. The burden of terrorism: high rate of recurrent hospital referrals. Injury 2008; 39: 77e82. 4 Shaw CJ, Spencer JD. Late management of compartment syndromes. Injury 1995; 26: 633e5. 5 Kotak BP, Bendall SP. Recurrent acute compartment syndrome. Injury 2000; 31: 66e7. 6 Williams P, Shenolikar A, Roberts RC, Davies RM. Acute non-traumatic compartment syndrome related to soft tissue injury. Injury 1996; 27: 507e8. 7 Hocking G. Re: the use of regional anaesthesia in patients at risk of acute compartment syndrome. Injury 2007; 38: 872e3. 8 Mulvey JM, Awan SU, Qadri AA, Maqsood MA. Profile of injuries arising from the 2005 Kashmir earthquake: the first 72 h. Injury 2008; 39: 554e60. 9 Seroyer ST, Musahl V, Harner CD. Management of the acute knee dislocation: the Pittsburgh experience. Injury 2008; 39: 710e8. 10 Berben SA, Meijs TH, van Dongen RT, et al. Pain prevalence and pain relief in trauma patients in the Accident & Emergency department. Injury 2008; 39: 578e85. 11 Young H, Topliss C. Complications associated with the use of a titanium tibial nail. Injury 2007; 38: 223e6. 12 Dhar SA, Butt MF, Hussain A, et al. Management of lower limb fractures in polytrauma patients with delayed referral in a mass disaster. The role of the Ilizarov method in conversion osteosynthesis. Injury 2008; 39: 947e51. 13 Ferguson M, Brand C, Lowe A, et al. Outcomes of isolated tibial shaft fractures treated at level 1 trauma centres. Injury 2008; 39: 187e95. 14 Court-Brown CM, Brydone A. Social deprivation and adult tibial diaphyseal fractures. Injury 2007; 38: 750e4. 15 Ojike NI, Roberts CS, Giannoudis PV. Compartment syndrome of the thigh: a systematic review. Injury 2009. 16 Perler BA, Tohmeh AG, Bulkley GB. Inhibition of the compartment syndrome by the ablation of free radical-mediated reperfusion injury. Surgery 1990; 108: 40e7. 17 Bourne RB, Rorabeck CH. Compartment syndromes of the lower leg. Clin Orthop Relat Res 1989: 97e104. 18 Al-Dadah OQ, Darrah C, Cooper A, et al. Continuous compartment pressure monitoring vs. clinical monitoring in tibial diaphyseal fractures. Injury 2008; 39: 1204e9. 19 Giannoudis PV, Tzioupis C, Pape HC. Early diagnosis of tibial compartment syndrome: continuous pressure measurement or not? Injury 2009; 40: 341e2. 20 McQueen MM, Christie J, Court-Brown CM. Compartment pressures after intramedullary nailing of the tibia. J Bone Joint Surg Br 1990; 72: 395e7. 21 McQueen MM, Gaston P, Court-Brown CM. Acute compartment syndrome. Who is at risk? J Bone Joint Surg Br 2000; 82: 200e3. 22 Tornetta 3rd P, Templeman D. Compartment syndrome associated with tibial fracture. Instr Course Lect 1997; 46: 303e8. 23 Lloyd GER, ed. Hippocratic writings. Middlesex, England: Penguin Books 1978. 24 Volkmann RV. Die ischaemischen Muskellahmungen and Kontracturen. Zentralbl Chir 1881; 8: 801e3. 25 Jepson PN. Ischaemic contracture: experimental study. Ann Surg 1926; 84: 785e95. 26 Jones SR. Volkmann’s ischaemic contracture with special reference to treatment. Br Med J 1928; 2: 639e42. 27 Bywaters EG, Beall D. Crush injuries with impairment of renal function. 1941. J Am Soc Nephrol; 1998: 322e32.

Medical-legal aspects Compartment syndrome is one of the most litigated topics in orthopedic surgery. A misdiagnosed compartment syndrome creates a major liability risk for the treating surgeon.52 The management of compartment syndrome should therefore aim to avoid the sequelae of a missed diagnosis and minimise the risk of a malpractice claim. Templeman et al.93 conducting a study in 1987 revealed that awards after missed compartment syndrome averaged $280,000.00 and often involved young patients. Bhattacharyya et al.94 reviewed records on closed malpractice claims involving compartment syndrome over the past twenty-three years. They revealed nineteen closed claims involving sixteen patients and encompassing a total liability of $3.8 million between 1980 and 2003. They concluded that physician documentation of an abnormal finding on a neurological examination without intervention, poor physician-patient communication, and increased time to fasciotomy are associated with an indemnity payment.

Conclusion Acute compartment syndrome is a potentially devastating situation resulting from many different causes such as fractures, trauma, contusions, and burns. Recent studies have illuminated the issues of tissue ischaemia and the detailed location of insult to muscle in injured extremities. The diagnosis of ACS, usually based on clinical factors, remains a challenge for orthopaedic surgeons. Its presentation can be clouded by altered mental status, fluctuating physical signs or covered up by general anaesthesia or other anaesthetic procedures. Adjunctive use of compartment pressure measurements is reasonable in the majority of patients. A high suspicion index, prompt diagnosis and early fasciotomy are the key elements in limiting patient morbidity and mortality, as well as minimising the modern medical-legal implications. A

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28 Whitesides Jr TE, Haney TC, Harada H, et al. A simple method for tissue pressure determination. Arch Surg 1975; 110: 1311e3. 29 Owen CA, Mubarak SJ, Hargens AR, et al. Intramuscular pressures with limb compression clarification of the pathogenesis of the druginduced muscle-compartment syndrome. N Engl J Med 1979; 300: 1169e72. 30 Matsen 3rd FA, Krugmire Jr RB. Compartmental syndromes. Surg Gynecol Obstet 1978; 147: 943e9. 31 Rorabeck CH, Macnab I. The pathophysiology of the anterior tibial compartmental syndrome. Clin Orthop Relat Res 1975: 52e7. 32 McQueen MM, Court-Brown CM. Compartment monitoring in tibial fractures. The pressure threshold for decompression. J Bone Joint Surg Br 1996; 78: 99e104. 33 McQueen MM, Christie J, Court-Brown CM. Acute compartment syndrome in tibial diaphyseal fractures. J Bone Joint Surg Br 1996; 78: 95e8. 34 Gulli B, Templeman D. Compartment syndrome of the lower extremity. Orthop Clin North Am 1994; 25: 677e84. 35 Mullett H, Al-Abed K, Prasad CV, O’Sullivan M. Outcome of compartment syndrome following intramedullary nailing of tibial diaphyseal fractures. Injury 2001; 32: 411e3. 36 Frink M, Klaus AK, Kuther G, et al. Long term results of compartment syndrome of the lower limb in polytraumatised patients. Injury 2007; 38: 607e13. 37 Tielinen L, Lindahl JE, Tukiainen EJ. Acute unreamed intramedullary nailing and soft tissue reconstruction with muscle flaps for the treatment of severe open tibial shaft fractures. Injury 2007; 38: 906e12. 38 Mithofer K, Lhowe DW, Vrahas MS, et al. Clinical spectrum of acute compartment syndrome of the thigh and its relation to associated injuries. Clin Orthop Relat Res 2004: 223e9. 39 Winternitz Jr WA, Metheny JA, Wear LC. Acute compartment syndrome of the thigh in sports-related injuries not associated with femoral fractures. Am J Sports Med 1992; 20: 476e7. 40 Shakespeare DT, Henderson NJ. Compartmental pressure changes during calcaneal traction in tibial fractures. J Bone Joint Surg Br 1982; 64: 498e9. 41 Justis DL, Law EJ, MacMillan BG. Tibial compartment syndromes in burn patients. A report of four cases. Arch Surg 1976; 111: 1004e8. 42 Rush DS, Frame SB, Bell RM, et al. Does open fasciotomy contribute to morbidity and mortality after acute lower extremity ischemia and revascularization? J Vasc Surg 1989; 10: 343e50. 43 Aprahamian C, Gessert G, Bandyk DF, et al. MAST-associated compartment syndrome (MACS): a review. J Trauma 1989; 29: 549e55. 44 Nadeem RD, Clift BA, Martindale JP, et al. Acute compartment syndrome of the thigh after joint replacement with anticoagulation. J Bone Joint Surg Br 1998; 80: 866e8. 45 Phillips BB. Traumatic disorders. In: Crenshaw AH, Daugherty K, Campbell WC, eds. Campbell’s operative orthopaedics. 8th edn. St. Louis: Mosby, 1992. p. 1895e900. 46 Ashton H. The effect of increased tissue pressure on blood flow. Clin Orthop Relat Res 1975: 15e26. 47 Burton AC. On the physical equilibrium of small blood vessels. Am J Physiol 1951; 164: 319e29. 48 Shrier I, Magder S. Pressure-flow relationships in in vitro model of compartment syndrome. J Appl Physiol 1995; 79: 214e21. 49 Smith JK, Grisham MB, Granger DN, Korthuis RJ. Free radical defense mechanisms and neutrophil infiltration in postischemic skeletal muscle. Am J Physiol 1989; 256: H789e93.

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50 Sadasivan KK, Carden DL, Moore MB, Korthuis RJ. Neutrophil mediated microvascular injury in acute, experimental compartment syndrome. Clin Orthop Relat Res 1997: 206e15. 51 Tscherne H, Gotzen L. Fractures with soft tissue injuries. New York: Springer 1984. 52 Olson SA, Rhorer AS. Orthopaedic trauma for the general orthopaedist: avoiding problems and pitfalls in treatment. Clin Orthop Relat Res 2005: 30e7. 53 Schoenberg M, Brenner B, Chalovich JM, et al. Cross-bridge attachment in relaxed muscle. Adv Exp Med Biol 1984; 170: 269e84. 54 Mubarak SJ, Hargens AR. Acute compartment syndromes. Surg Clin North Am 1983; 63: 539e65. 55 Hargens AR, Mubarak SJ. Current concepts in the pathophysiology, evaluation, and diagnosis of compartment syndrome. Hand Clin 1998; 14: 371e83. 56 Ulmer T. The clinical diagnosis of compartment syndrome of the lower leg: are clinical findings predictive of the disorder? J Orthop Trauma 2002; 16: 572e7. 57 Mubarak SJ. A practical approach to compartmental syndromes. Part II. Diagnosis. Instr Course Lect 1983; 32: 92e102. 58 Heckman MM, Whitesides Jr TE, Grewe SR, et al. Histologic determination of the ischemic threshold of muscle in the canine compartment syndrome model. J Orthop Trauma 1993; 7: 199e210. 59 Matsen 3rd FA, Winquist RA, Krugmire Jr RB. Diagnosis and management of compartmental syndromes. J Bone Joint Surg Am 1980; 62: 286e91. 60 Willy C, Gerngross H, Sterk J. Measurement of intracompartmental pressure with use of a new electronic transducer-tipped catheter system. J Bone Joint Surg Am 1999; 81: 158e68. 61 Moed BR, Thorderson PK. Measurement of intracompartmental pressure: a comparison of the slit catheter, side-ported needle, and simple needle. J Bone Joint Surg Am 1993; 75: 231e5. 62 Heckman MM, Whitesides Jr TE, Grewe SR, Rooks MD. Compartment pressure in association with closed tibial fractures. The relationship between tissue pressure, compartment, and the distance from the site of the fracture. J Bone Joint Surg Am 1994; 76: 1285e92. 63 Zweifach SS, Hargens AR, Evans KL, et al. Skeletal muscle necrosis in pressurized compartments associated with hemorrhagic hypotension. J Trauma 1980; 20: 941e7. 64 Matsen 3rd FA, Mayo KA, Sheridan GW, Krugmire Jr RB. Monitoring of intramuscular pressure. Surgery 1976; 79: 702e9. 65 Ouellette EA. Compartment syndromes in obtunded patients. Hand Clin 1998; 14: 431e50. 66 Janzing H, Broos P. Fasciotomies of the limbs: how to do it? Acta Chir Belg 1998; 98: 187e91. 67 Arbabi S, Brundage SI, Gentilello LM. Near-infrared spectroscopy: a potential method for continuous, transcutaneous monitoring for compartmental syndrome in critically injured patients. J Trauma 1999; 47: 829e33. 68 Rominger MB, Lukosch CJ, Bachmann GF. MR imaging of compartment syndrome of the lower leg: a case control study. Eur Radiol 2004; 14: 1432e9. 69 Abraham P, Leftheriotis G, Saumet JL. Laser Doppler flowmetry in the diagnosis of chronic compartment syndrome. J Bone Joint Surg Br 1998; 80: 365e9. 70 Vrouenraets BC, Kroon BB, Klaase JM, et al. Value of laboratory tests in monitoring acute regional toxicity after isolated limb perfusion. Ann Surg Oncol 1997; 4: 88e94.

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84 Lepore DA, Morrison WA. Ischemic preconditioning: lack of delayed protection against skeletal muscle ischemia-reperfusion. Microsurgery 2000; 20: 350e5. 85 Prem JT, Eppinger M, Lemmon G, et al. The role of glutamine in skeletal muscle ischemia/reperfusion injury in the rat hind limb model. Am J Surg 1999; 178: 147e50. 86 Gaines GC, Welborn 3rd MB, Moldawer LL, et al. Attenuation of skeletal muscle ischemia/reperfusion injury by inhibition of tumor necrosis factor. J Vasc Surg 1999; 29: 370e6. 87 Odland R, Schmidt AH, Hunter B, et al. Use of tissue ultrafiltration for treatment of compartment syndrome: a pilot study using porcine hindlimbs. J Orthop Trauma 2005; 19: 267e75. 88 Finkelstein JA, Hunter GA, Hu RW. Lower limb compartment syndrome: course after delayed fasciotomy. J Trauma 1996; 40: 342e4. 89 Giannoudis PV, Harwood PJ, Kontakis G, et al. Long-term quality of life in trauma patients following the full spectrum of tibial injury (fasciotomy, closed fracture, grade IIIB/IIIC open fracture and amputation). Injury 2009; 40: 213e9. 90 Giannoudis PV, Nicolopoulos C, Dinopoulos H, et al. The impact of lower leg compartment syndrome on health related quality of life. Injury 2002; 33: 117e21. 91 Vandervelpen G, Goris L, Broos PL, Rommens PM. [Functional sequelae in tibial shaft fractures with compartment syndrome following primary treatment with urgent fasciotomy]. Acta Chir Belg 1992; 92: 234e40. 92 Kullmer K, Olivier L, Eysel P, et al. [Traumatically-induced compartment syndrome of the tibia. Ultrasound diagnosis for qualitative assessment of late sequelae for musculature after dermatofasciotomy]. Unfallchirurgie 1997; 23: 87e91. 93 Templeman D, Lange R, Harms B. Lower-extremity compartment syndromes associated with use of pneumatic antishock garments. J Trauma 1987; 27: 79e81. 94 Bhattacharyya T, Vrahas MS. The medical-legal aspects of compartment syndrome. J Bone Joint Surg Am 2004; 86-A: 864e8.

71 Weiner G, Styf J, Nakhostine M, Gershuni DH. Effect of ankle position and a plaster cast on intramuscular pressure in the human leg. J Bone Joint Surg Am 1994; 76: 1476e81. 72 Rorabeck CH. The treatment of compartment syndromes of the leg. J Bone Joint Surg Br 1984; 66: 93e7. 73 Matsen 3rd FA. Compartmental syndrome. An unified concept. Clin Orthop Relat Res 1975: 8e14. 74 Jacob JE. Compartment syndrome. A potential cause of amputation in battlefield vascular injuries. Int Surg 1974; 59: 542e8. 75 Mubarak SJ, Owen CA. Double-incision fasciotomy of the leg for decompression in compartment syndromes. J Bone Joint Surg Am 1977; 59: 184e7. 76 Patman RD. Compartmental syndromes in peripheral vascular surgery. Clin Orthop Relat Res 1975: 103e10. 77 Cohen MS, Garfin SR, Hargens AR, Mubarak SJ. Acute compartment syndrome. Effect of dermotomy on fascial decompression in the leg. J Bone Joint Surg Br 1991; 73: 287e90. 78 Jensen SL, Sandermann J. Compartment syndrome and fasciotomy in vascular surgery. A review of 57 cases. Eur J Vasc Endovasc Surg 1997; 13: 48e53. 79 Harris I. Gradual closure of fasciotomy wounds using a vessel loop shoelace. Injury 1993; 24: 565e6. 80 McKenney MG, Nir I, Fee T, et al. A simple device for closure of fasciotomy wounds. Am J Surg 1996; 172: 275e7. 81 Caruso DM, King TJ, Tsujimura RB, et al. Primary closure of fasciotomy incisions with a skin-stretching device in patients with burn and trauma. J Burn Care Rehabil 1997; 18: 125e32. 82 Kanakaris NK, Thanasas C, Keramaris N, et al. The efficacy of negative pressure wound therapy in the management of lower extremity trauma: review of clinical evidence. Injury 2007; 38(Suppl 5): S9e18. 83 Myers RA. Hyperbaric oxygen therapy for trauma: crush injury, compartment syndrome, and other acute traumatic peripheral ischemias. Int Anesthesiol Clin 2000; 38: 139e51.

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Regional analgesia and orthopaedic surgery

acting local anaesthetic agents, continue to give epidurals for lower limb arthroplasty surgery and continue to refuse regional techniques because of perceived risks of complications.

Pharmacokinetics of local anaesthetic agents

Andy Wilson

An in depth knowledge of LA pharmacology is not essential, however the basic principles are required to understand the mechanism of action of LA, toxicity, the choice of agent and future developments. Regional anaesthesia and regional analgesia can be considered the same entity, anaesthesia being a more profound and denser block than analgesia. Regional anaesthesia makes the operative site insensate for the duration of the surgery and is influenced by LA concentration. Regional analgesia decreases the operative site pain for a period well beyond the operative period. This duration of action is influenced by choice, concentration and volume of LA, additives and continuous catheter techniques. Regional analgesia can be obtained with opioids alone. With the exception of the ultra short acting chloroprocaine (Procaine) all local anaesthetic agents now in use are amides. The original ester agents were all associated with a high incidence of allergic reactions. All local anaesthetics produce their effects by blocking voltagegated sodium channels. Unfortunately this applies to all types of nerve fibres and, to date, no LA is available that can truly differentiate between motor and sensory fibres. Agents such as ropivacaine have been suggested to produce less motor block3 than other equipotent agents such as bupivicaine, but motor block still occurs and so the clinical significance of this differential effect is of questionable value. Recent developments may allow the goal of selecting specific sensory fibre sodium channels4, but despite this being realised in the laboratory no agent is as yet clinically available. The consequences of motor block are now of greater relevance than previously mentioned in reviews on the subject because of the pressures, both economic and medical, to get patients mobilized and discharged from hospital as quickly as possible. It must be recognized that all regional techniques have a risk: benefit ratio. Indeed it is this risk benefit ratio that has resulted in the adoption of the new surgical technique of Local Infiltration Arthroplasty5 surgery (LIA) because of the previous over-reliance

Abstract Regional Anaesthesia and Analgesia is a growing subspecialty, which impacts on all orthopaedic procedures. Advances continue to be made in the range of techniques available to the anaesthetist, which will influence patient outcomes. It is therefore essential that all practicing orthopaedic surgeons understand the background principles and practices of regional anaesthesia to aid in treatment planning and team decision making. All regional procedures have the potential to facilitate postoperative recovery, however all have inherent risks and if ‘‘overdone’’ may inhibit early rehabilitation. Only with a proper understanding of the techniques available can an informed choice be made by the patient and surgeon. This review examines the pharmacology of current local anaesthetics and additives, the pros and cons of central axial blocks and differing techniques including Local Infiltration Arthroplasty (LIA) and ultrasound guided blocks for major joint surgery in the upper and lower limbs. It is not intended as a literature review of all the latest esoteric techniques but as a background essential reading of what is currently happening in regional anaesthesia.

Keywords epidural anaesthetic; interscalene block; local anaesthetic; regional anaesthetic; spinal anaesthetic

Introduction It is 125 years since Koller 1 first described the use of cocaine to produce local anaesthesia for an ophthalmic surgical procedure. Following on from this landmark case in 1884 followed a decade of trials whereby cocaine was applied topically, injected subcutaneously, around specific nerves and then centrally, most notably by Bier2 in 1899. Techniques have grown from this basic principle of bathing the nerves supplying the surgical site with Local Anaesthetic (LA). Has the specialty moved on? The answer is of course yes. Over the last century advances have been made in LA potency, safety and efficacy, nerve localization techniques, central axial blockade and more recently in ultrasound guided regional analgesia (Figure 1). There is now a greater understanding as to how Regional anaesthesia/analgesia (RA) affects the surgical outcome. A basic knowledge of these principles, practices and developments is not only a requirement for the trainee orthopaedic surgeon but for any practicing surgeon, as there is no surgical site that is not amenable to RA. Unfortunately there are practices continuing that have no evidence base and indeed some which continue despite evidence that they potentially cause harm with no benefit at all. Surgeons and Anaesthetists, for example, continue to add drugs to long Andy Wilson MBChB FRCA Consultant Anaesthetist, Leeds Teaching Hospitals Trust, Leeds, UK.

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Figure 1 Out of plane ultrasound guided interscalene block for fixation of fractured neck of humerus.

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on epidural analgesia in lower limb arthroplasty surgery. This technique will be discussed in greater detail later in this review. The choice of LA is often dictated by the required duration of action, as differing surgical procedures have differing intra and postoperative analgesic requirements. For example, the pain after a surgical procedure on the shoulder compared with one on the hand is generally more intense and of a greater duration. The preference of hand units is often therefore for shorter acting agents, even though both shoulder and hand surgery may be of the same operative duration and may both be performed as day case procedures under regional anaesthesia alone. The duration of action is dependent on both protein binding of the drug and it’s clearance from the injection site. Both of these elements can be manipulated pharmacologically to increase the longevity of the block, but clinically only clearance can be altered. Protein binding of the longer acting agents, such as bupiviacine and ropivicaine, is approximately 95% whereas that of the shorter acting lidocaine is only 65%. The clearance from the injection site is dependent upon local blood flow and some LAs such as lidocaine, have intrinsic vasodilator properties that potentiate this. This flow can be manipulated by vasopressors, such as adrenaline or felypressin, but since the protein binding of the longer acting agents is so high, local blood flow has little if any effect on the duration of action on these agents. However the practice of adding adrenaline to these long acting agents unfortunately continues, despite the lack of any pharmacological basis. The onset time of local anaesthetics is dependent upon three factors; molecular weight (all are similar), pKa and diffusibility. Only pKa can be manipulated. A detailed understanding of molecular pKa is not required, save to say that the further the pKa of the molecule from the acid pH solution (all LA pKa are alkaline) the more ionised it is, and therefore the less able it is to cross the lipid membrane. Again, however, only the shorter acting agents are amenable to manipulation as the very high pKa of the longer acting agents makes a small increase in non-ionised molecules (by warming or alkalinisation with bicarbonate) of little significance. pKa is not therefore routinely manipulated, as the short acting agents already have a quick onset time. It should be noted that the agents with quickest onset time tend to be the those with the shortest duration of action and lowest potency.

potentiate any risk of axonotmesis. Of course superficial infiltration with adrenaline containing LA is given for it’s local vasoconstrictor actions and this has nothing to do with the duration of block, but this practice does not need to continue for nerve blocks as well. Mixing two agents, one short acting but of rapid onset and one long acting of slow onset, is commonplace but again has little pharmacological basis. However, ultrasound has allowed specific nerves to be targeted for postoperative analgesia using long acting agents whilst anaesthesia of the whole limb is produced with short acting agents applied to the remaining plexus. Other additives For peripheral nerve blocks there have been many agents added to LA to increase its effectiveness, but few have been shown to be of significant benefit.6 Even those that have been shown to be beneficial incur additional side effects. With peripheral nerve blocks the general rule is therefore not to use any additive with an agent that is already pharmacologically long acting. However this rule is often ignored, with many units routinely adding opioids or clonidine (and to a less frequent extent NSAIDs, midazolam, ketamine, neostigmine and relaxants) to agents such as bupivicaine and ropivacaine, despite the lack of evidence as described above. The a 2 receptor agonist Clonidine is the only adjuvant to be used routinely in the UK but there are as many papers refuting its benefits as there are showing it to improve the quality and duration of block. For central axial blocks, however, the addition of opioids or clonidine is far more evidence-based. They produce prolonged analgesia, or an improvement in block quality, because of their direct action on the dorsal and ventral horns respectively. The addition of morphine to a spinal anaesthetic is a now a routine procedure, providing excellent analgesia for up to 24 hrs without any residual motor block. However, side effects such as pruritis are common and there is also the threat of the far more serious problem of late respiratory depression. Late respiratory depression is far more common after the administration of hydrophilic, long acting agents such as morphine compared with the short acting lipophilic agents such as fentanyl. Many centres insist on a HDU bed postoperatively or at least a ratio of nurses to patient infrequently found on a busy orthopaedic ward and this often precludes their use.

Key points in pharmacology

Additive agents Adrenaline The use of vasopressors, as noted above, is effective with short acting agents. They increase the duration of action by decreasing clearance. The addition of a vasopressor will also allow an increased dose of relatively non-potent, short acting drugs to be used before reaching toxic levels, as plasma levels will not peak rapidly. This has little or no influence on the plasma levels of the longer acting agents; indeed, ropivacaine has been shown to have an intrinsic vasoconstrictor action of its own. The is some evidence that adrenaline may itself have specific analgesic properties, acting on a2 receptors, but the significance of this is again minor in long acting blocks. Putting it simply, if a long duration of action is required a long acting agent without an additive should be used, not a short acting one with adrenaline added. Vasopressors are not without their own potential complications, as they may reduce blood flow to the target nerves, which may

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C

C C

C

C

All local anaesthetics, with the exception of chloroprocaine, are Amides. To date all LA produce motor block as well as sensory block Adrenaline does not increase the duration of action of long acting LA The alpha 2 agonist clonidine is the only agent to have been shown to significantly improve the duration or quality of analgesia in peripheral blocks. The duration and quality of spinal/epidural analgesia can be significantly improved by opioids and clonidine but both have significant side effects especially in the elderly.

Regional techniques An outline of the basic principles of central axial (spinal and epidural), plexus (brachial and lumbar) and peripheral nerve blocks,

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as well as local infiltration, will aid background understanding when it comes to discussing RA for specific sites and procedures.

Central neuraxial block, CNB We now have more than 100 years experience in CNB and the basic principle of bathing the spinal cord in LA has not changed. Spinal Single shot spinal (subdural) anaesthesia remains a popular choice, as it is a safe and easy alternative to general anaesthesia with the added advantage of providing excellent analgesia in the very early postoperative phase. Spinal catheters can be used to prolong spinal blocks but their necessarily small size has limited their popularity. Extending the analgesia beyond the very early postoperative period has proved more problematical and attempts to do this with epidural catheters (combined epispinal) have potentially set back the rehabilitation phase because of the resulting prolonged motor block. There is now a general consensus that postoperative epidurals in routine lower limb surgery should not be used. However it is also true to say that lower limb arthroplasty surgery is painful well beyond the first postoperative hour and unless analgesia is effective, which is difficult to achieve with the standard analgesics (including parenteral morphine) rehabilitation will equally be set back. Therefore the addition of other regional techniques and/or spinal opiates is an essential part of the spinal anaesthesia protocol.

a Quincke cutting needle, b Sprotte pencil point needle. Figure 2

block is further influenced by patient positioning at time of introduction of the block and the first ten minutes thereafter, and to a lesser predictable degree by age, site of injection and obesity.

Spinal needle The major drive for change in needle design has been from obstetric RA, where the high incidence of post dural puncture headache (PDPH) led to research to find the least traumatic needle. The incidence of PDPH is secondary to continuing CSF leak and is influenced principally by needle size but also by needle tip design, with PDPH being more common with the older, large gauge needles. The standard bevelled cutting needle (Quincke) has largely been replace by a blunter pencil point needle (Sprotte), though variations on both themes are still in use, particularly in orthopaedic anaesthesia. PDPH is most common in the younger population and those that ambulate early after surgery. Fortunately PDPH is rarely seen following joint replacement surgery, and these are often patients in which the firmer, larger gauge cutting needle may be required to facilitate placement beyond the osteoarthritic spine Figure 2.

Epidural The indications for, and popularity of, epidurals for orthopaedic procedures have declined in recent years. There has been recognition that the best analgesia does not necessarily produce the best outcomes and it may not be too long before this is also shown for general surgical procedures. The advantage of an epidural, where the LA is placed in the extradural space with a Touhy needle between the ligamentum flavum and the dura, is that using a catheter technique the block can be established incrementally to achieve the desired height and it can be kept topped up well beyond the few hours possible with a single shot. The disadvantages, though, are potential patchy blocks with ‘‘missed segments’’, time to achieve adequate block height and misplacement of the catheter. Epidurals are therefore rarely used for anaesthesia but more as a method of achieving excellent intra and postoperative analgesia. Unfortunately it is this excellent postoperative analgesia with its concomitant motor block which often produces a pain free but relatively immobile patient with a subsequent delay in discharge. Other secondary effects include the requirement for urinary catheterisation and a potential increase in the rate of DVT and chest infections secondary to immobility. Hyperbaric solutions are not used in epidural blocks, as altering baricity has no influence on epidural spread. As with spinal anaesthesia, block height can be influenced, and the greatest influences on epidural spread and height of block are the site of injection and the volume of injectate used. For orthopaedic anaesthesia a lumbar epidural will always suffice for lower limb

Choice of LA The duration of block is largely determined by the agent used. Whilst there is renewed interest in shorter acting agents, such as preservative-free chloroprocaine for out patient surgery, lidocaine has an unacceptably high incidence of transient neurological symptoms and is no longer used. The majority of spinal anaesthetics are now performed with bupivicaine 0.5%. This agent gives a predictable block of approximately 120 minutes duration, although it has a relatively slow onset time. Most bupivicaine is administered as hyperbaric or ‘‘heavy’’ bupivicaine. With this hyperbaric solution the height of the block is less influenced by other factors and therefore is more predictable than with hypo or normo-baric solutions. Hypobaric solutions are far less predictable but do have the benefit of inducing unilateral anaesthesia in a nondependent limb, which is useful, for example, in fractured neck of femur patients. Height of

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and pelvic surgery, as the height of block does not need to extend beyond the lower thoracic dermatomes. Further influences are similar to those in spinal anaesthesia.

Example of UK regional centre guidelines

Safety and adverse effects There is a common misconception that CNB is safer than general anaesthesia, but this is not supported in the literature. There are specific examples of perioperative survival being influenced positively by spinal anaesthesia, but survival rates beyond the immediate operative period are comparable. Whilst it may appear intuitive that avoidance of general anaesthesia must be advantageous this does not take into account both the adverse effects of regional anaesthesia and the overall stress effects of surgery. The commonest adverse effect of a central axial block is hypotension, because when a block extends above T10 a sympathetic block occurs with subsequent vasodilatation. Height of block is the greatest influence of how much sympathectomy occurs but the degree of cardiovascular compromise is further influenced by pre-existing hypovolaemia, hypotension, treated hypertension, age and the addition of general anaesthesia. Pre-existing hypovolaemia is therefore an absolute contraindication to central axial blockade. Normal respiratory function is not affected by spinal anaesthesia, though patients with severe obstructive lung disease who rely on accessory muscles of respiration may well be compromised. The risk: benefit ratio of spinal versus general anaesthesia in patients with severe pulmonary disease will usually still come down on the side of a spinal technique. Cardiovascular function is, however, affected by spinal anaesthesia, as already mentioned. Therefore patients with significant cardiac disease may well do better with general anaesthesia if the height of block is such that significant sympathetic block is inevitable. If subsequent hypotension is well controlled (or no sympathectomy occurs) central axial blocks, particularly low blocks, are a very safe alternative to general anaesthesia in the presence of cardiovascular disease. Significant Aortic stenosis is a relative contraindication to spinal anaesthesia, as the fixed cardiac output will compromise the patient in the presence of vasodilatation. It can be seen therefore that spinal or epidural anaesthesia are ideal for patients with respiratory disease but less so for those with significant cardiac disease. Of course, many patients presenting for orthopaedic procedures have both lung and cardiac disease and therefore the decision is usually not quite so clear cut. Major complications of CNB have recently been the subject of a UK national audit7, the results of which showed that permanent nerve injury occurred at a rate of approximately 3 per 100,000 spinals, whilst paraplegia or death occurred in approximately 1 per 100,000 spinal anaesthetics. Notably two-thirds of initially disabling injuries resolved fully.

* **

Drug

Delay after drug before block

Delay after block before next dose

LMWH - prophylactic LMWH - therapeutic Unfractionated heparin Warfarin Aspirin NSAID Clopidogrel

12 hrs 24 hrs 4 hrs INR below 1.5 No delay** No delay 7 days

6 hrs 6 hrs 1 hr*

6 hrs following traumatic puncture. some authors recommend a delay of at least 24 hrs if LMWH is used in a patient already on Aspirin.

Table 1

thromboprophylaxis. Most regional centres have adopted their own adaptation of national guidelines Table 1.

Compartment syndrome Acute compartment syndrome (ACS) requires prompt recognition, diagnosis and treatment. The question is does RA influence time of diagnosis and subsequent outcome? A recent systematic review8 examined whether modern acute pain management techniques contributed to a delay in diagnosis. They found no good evidence of any adverse influence of RA on compartment syndrome diagnosis but did acknowledge that under-reporting is common and no comparative trials have been published. In fact there is evidence to the contrary, in that in the presence of RA, if significant break through pain occurs, ACS must be considered and this may aid diagnosis. A note of caution however; a dense block of either a CNB or PNB will delay diagnosis due to complete sensory and motor block. Anaesthesia with long acting agents or analgesia with high

Spinal/Epidural key points C

C

C

C

Anticoagulants Thromboprophylaxis for major orthopaedic surgery is now standard in many centres because of the high risk of DVT and PE following this type of surgery in an already ‘at risk’ group. Unfortunately with central axial blocks this increases the risk of spinal haematoma and subsequent neurological deficit. European and American guidelines have been published, differing slightly principally because of the differing techniques of administering

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C

C

C

444

Most spinal anaesthetics are single shot with bupivicaine and last approximately 120 minutes Spinal but not epidural spread is influenced by LA baricity and patient position. The commonest side effect is hypotension secondary to sympathetic block and this makes pre-existing hypovolaemia a contraindication. They are excellent for patients with respiratory disease but must be used with caution in patients with cardiac disease. Unlike peripheral blocks, central block analgesia can be extended without motor block by the use of opioids or clonidine. Delay in central block after thromboprophylaxis or antiplatelet therapy is essential to avoid a spinal heamatoma. No evidence of influence on Compartment syndrome but dense blocks must be avoided.

Ó 2009 Elsevier Ltd. All rights reserved.

ANAESTHESIA

concentration LA should therefore be avoided. Withholding analgesia (PCA or RA) has no evidence of benefit and is inhumane.

LIA key points

Local infiltration and LIA C

Local wound infiltration is not a new technique, of course, but the concept of Local infiltration analgesia, LIA, in arthroplasty surgery warrants further detailed discussion. Kohan and Kerr9, from Sydney Australia, have been credited with the introduction of a fast track programme for lower limb arthroplasty surgery, the central tenet of which is early ambulation. This early ambulation, in the first few hours in the immediate postoperative period, is possible because of excellent postoperative analgesia with no motor block achieved solely by local infiltration. The technique involves a spinal anaesthetic for the procedure itself and infiltration of all tissue planes with a mixture of ropivicaine and two adjuvants, ketorolac and adrenaline. An intra-articular catheter is placed and used for reinjection 15e20 hrs after surgery. Most are able to walk with assistance less than 6 hrs postoperatively and within 22 hrs independently. No paper has yet compared LA with and without these combined adjuvants but from previous published data it is likely that they are not necessary and may raise the complication rate. Whilst it is true to say that their early reported (usually through personal communications) but unpublished results of discharge after only 1 postoperative day have not been reliably replicated, it was their innovative programme that has stimulated research. Their subsequently published results of between 41% (Total hip replacement, THR) and 51% (Total knee replacement, TKR) discharge after a single overnight hospital stay are a still a target to achieve. The percentage of THR who stayed more than 3 nights in hospital however was still 33%. This is often overlooked, perhaps reflecting the understandable bias of surgeons wishing to achieve early discharge with excellent patient analgesia and satisfaction rates, and is still better than achieved in most centres. 3 days seems to be the ideal target to aim for, as few centres have the ability to provide physiotherapy and occupational therapy outside of the hospital at adequate intensity to support discharge before this period. Why then has this not become the gold standard and why do a third of THR patients stay more than three days? The answer is that what Kerr and Kohan have achieved is not the perfect analgesic regimen but an acknowledgement that a rethink of the whole postoperative pathway was required. It is no longer necessary or desirable to have patients rehabilitate only when they are ready, or when a resolving motor block dictates. The outcome may well improve if early mobilization and subsequent discharge is sought. Whatever analgesic regimen is chosen, in order for patients to ambulate early they must also be adequately analgesed with no residual motor block. Despite the hyperbole it is probably not the immediate (within 6 hrs) mobilization that is important, however impressive this appears, but the emphasis on excellent analgesia and early mobilization, with the implementation of a programme that facilitates the delivery of physiotherapy and occupational therapy in the early postoperative phase. Regional anaesthesia of any technique must therefore be adapted to allow this early mobilization and this therefore precludes the use of postoperative epidural and long lasting dense nerve blocks.

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C

C

C C

Should not be considered just a regional anaesthetic technique but a whole fast track programme. Early mobilization achieved because of excellent analgesia without motor block. Technique involves infiltrating the whole operative area with ropivacaine, ketorolac and adrenaline and an intraarticular catheter for second injection 20 hrs later. No study of LIA with GA, only spinal anaesthesia Approximately 50 % arthroplasty patients can be discharged after only 1 overnight hospital stay.

Nerve and plexus blocks The practice of peripheral nerve blocks has grown exponentially in the last decade, principally because of the drive to day-case surgery but also because orthopaedic anaesthesia has become a subspecialty in its own right and there is an increasing expertise in the use of ultrasound. The opiate sparing effect of regional blocks increases patient satisfaction rates and, for day-case surgery, decreases readmission rates. There is evidence that peripheral nerve blocks improve surgical outcomes both in upper and lower limb surgery, principally improving the range of movement achieved. At first glance, peripheral nerve blocks appear to be the ideal method of analgesia and this proves to be the case for upper limb procedures. However, as previously discussed, if the motor block is allowed to persist then rehabilitation after lower limb surgery may be inhibited. This does not mean that peripheral blocks are no longer the ideal for knee surgery in particular, but that care has to be taken to ensure that a dose and concentration of LA is chosen that minimises long lasting motor block. There are too many nerve blocks to go into detail, but individual blocks will be considered in relation to specific surgical procedures. The general practice of nerve blocks including localization, safety and efficacy and the needles used will be described. Safety and efficacy The greatest influence on efficacy is experience of the operator, whatever technique of localization is used. Different studies are therefore difficult to compare, but in general a failure rate of 5e10% is the norm with approximation to, but not achieving, 100% in very experienced hands. Some techniques that are still practiced, such as single shot axillary brachial plexus blocks, will always produce a low success rate (approx. 60%) because of a failure to appreciate the technique’s limitations. Peripheral nerve blocks have complications, which can be reduced but not eliminated by adhering to safe basic practices. There are two types of nerve damage which may occur, temporary neuropraxia or the potentially permanent axonotmesis. The former is very common and usually caused by direct needle trauma. This can be reduced by avoiding the elicitation of parasthesia, not searching for a low threshold current and possibly by using ultrasound, as the needle can be directed away from the nerve. The latter, axonotmesis, is usually caused by intrafascicular injection with a pressure effect causing ischaemia. This

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is a rare complication in the order of 1 in 10,000 regional blocks, although this may be significantly higher in relation to blocks of the smaller nerves, such as the roots of the brachial plexus. This can be reduced by avoiding direct nerve contact, not using approaches where the nerve is already stretched, not injecting under pressure and not injecting if the awake patient complains of pain. It is likely that in large nerves, with a lot of connective tissue, intraneural injection (subepineurial) is common but actual intrafascicular injection is fortunately very rare. Other important complications include toxic levels of LA producing central nervous or cardiovascular collapse. Toxic levels can be achieved either because of an overdose of drug or, more commonly, by rapid concentration increases secondary to intravascular injection. It is therefore a minimal standard to have reliable venous access before any peripheral nerve block is performed. The degree and length of CNS and CVS collapse is dependent on the LA used. Although maximum doses are quoted, they are only guidelines, as the absorption rate is dependent on site of injection. It is not the maximum dose that is important but the maximum plasma level of drug, with drugs being rapidly absorbed from the pleura, for example, compared with intraarticular injections, and of course intravascular injections cause a very rapid rise. Contrary to expectation, most maxima quoted by the manufacturers are not based on clinical trials and quoted maxima vary Table 2. There has been an increase in use of the newer and safer long acting agents such as levobupivicaine and ropivacaine in preference to bupivicaine. However these agents may still produce collapse and there is some evidence that the use of intralipid during cardiac resuscitation is beneficial. CNS collapse usually precedes CVS collapse and may be associated with warning signs, such as circum-oral tingling, but this is rapidly followed by a seizure if levels continue to rise. It is this initial warning sign that is lost if the patient has already been anaesthetised or heavily sedated, but this knowledge has not been translated into any evidence of more frequent toxicity in the anaesthetised patient.

nerve (Coulomb’s law). This threshold assessment has been taken a little further to suggest that a very low stimulating current, i.e. <0.3 mA, may indicate nerve epineurial penetration and possibly an increase in the risk of axonotmesis, but this has no clinical evidence base. Unfortunately, even with a low threshold current and the needle tip in close proximity to the target nerve, the needle tip and therefore spread of LA may be in the wrong tissue plane and block failure may be the result. Over the last 10 years there has been an increase in the use of ultrasound for nerve localization. Ultrasound has the benefit that both the target nerve and the needle can be visualized. Whilst this may suggest it to be a safer technique, because nerves and vessels can be identified, there have still been reports of both intraneural and intravascular injection occurring with ultrasound. Fortunately both complications, although catastrophic, are rare and it cannot therefore be shown that one technique is statistically safer than the other, however obvious it may appear. Ultrasound does allow visualization of tissue planes and the spread of LA. This has led to a change in practice from aiming the needle directly towards a nerve and placing it as close as possible, to now aiming next to nerves but in the same tissue plane. This will improve block success rates and facilitate teaching of techniques, therefore the risk: benefit ratio should improve. Ultrasound has also allowed new techniques and approaches to be described.

Nerve localization Peripheral nerve stimulation has been the mainstay of mixed nerve localization for the last 30 years. This involves the application of a stimulating current, of the order of 1.0 mA, applied via an insulated needle so that only the tip is exposed, maximising current density. A reduction in the applied current to a threshold current required to stimulate muscle contraction will allow the assumption of approximation of the needletip to the

The innervation of the shoulder joint is from the axillary and suprascapular nerves, derived from the upper trunk of the brachial plexus. The area medial to deltoid is, however, innervated by the supra-clavicular branches of the superficial cervical plexus and will require additional LA if the surgical site extends medial to the delto-pectoral groove. For shoulder surgery there is only one block that will reliably anaesthetise and analgese the shoulder and that is the interscalene block (ISB). The C5 and C6 roots are blocked at the upper trunk, between the middle and anterior scalene muscles in the neck. Lower brachial plexus blocks are possible but do not reliably block the suprascapular nerve, as it arises from the upper trunk fairly high in the neck and gives a sensory innervation to the posterior capsule of the shoulder. A single shot nerve block gives up to 17 hours of analgesia and is therefore excellent for many day case procedures. Unfortunately shoulder surgery is particularly painful and this pain often lasts for more than 24 hrs.10 This has led to the development of interscalene catheters which, providing there is robust support in the community, are safe for continuation out of the hospital following early discharge.11 However this level of support has proved difficult to obtain in the UK.

Upper limb All regional anaesthesia requires a detailed knowledge of the nerve distribution of the limb and this is especially true in the upper limb. There is no blanket block which is all encompassing, so the regional anaesthetist has to have a detailed knowledge of the brachial plexus and its surrounding anatomy. The brachial plexus and its terminal branches are easy to visualize and identify with ultrasound and this is therefore becoming the gold standard adjunct for brachial plexus blockade.

The shoulder

Maximum doses of commonly used local anaesthetic agents LA

Max dose without adrenaline mg/kg (mg)

Max dose with adrenaline mg/kg (mg)

Lidocaine Bupivicaine*

3 (300) 2 (150) 3 (200)

7 (500) 2 (150) 3 (200)

Ropivicaine *

Includes levo-bupivicaine.

Table 2

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It should be noted that because of a series of 5 serious untoward incidents in the United States the ISB is the only block that the ASRA guidelines require to be performed on awake patients. There is no such consensus in Europe and these guidelines did not take in to account the use of ultrasound. There is some evidence that a suprascapular nerve block alone provides analgesia of the shoulder, but it is inferior to the interscalene block. Intra-articular or subacromial LA appears to have little benefit over placebo. The ISB will not block the lower trunk (C8 and T1) and its divisions. It cannot therefore be used alone for surgery of the hand or elbow Figure 3. Elbow and distal arm For surgery below the shoulder a supra-clavicular block (SCB), or axillary brachial plexus block (ABPB), are ideal and again are facilitated by ultrasound. The Infra-clavicular approach is now less commonly used because of its proximity to the pleura, but is similar to the SCB. The SCB has been named the ‘‘spinal of the arm’’ as it is the only site where all of the trunks and divisions are in close proximity, lying superior and lateral to the subclavian artery. Even here it is a two injection technique.

The C8/T1 lower trunk has to be identified separately as it begins its descent behind the 1st rib by passing behind the subclavian artery to become the medial cord (and subsequently the ulna nerve). The SCB does carry a risk of pneumothorax and vascular puncture and this makes ultrasound an invaluable aid. Because of ultrasound, the use of the SCB has become much more popular in hand units where previously it was out of favour Figure 4. The ABPB has become at least a 3 if not 4 injection technique because of the unacceptable levels of missed terminal branches when the original single shot technique was used. LA is placed around the ulna, median and radial nerves separately, as well as the musculo-cutaneous nerve as it lies separated from the artery, between the biceps and coracobrachialis muscles. A recent development with ultrasound is the selective blocking of nerves supplying the operative site with long acting LA, such as the ulna and median nerves for hand surgery, whilst blocking the remaining nerves with short acting LA to cover the period of operation and tourniquet use only. Rescue blocks of peripheral nerves are easy to achieve at or below the elbow if a partial brachial plexus block is insufficient for surgery.

a Ultrasound image of interscalene space using Sonosite S nerve portable ultrasound machine. b with anatomical structures identified.

a Ultrasound image of supraclavicular region using Sonosite S nerve portable ultrasound machine. b with anatomical structures identified.

Figure 3

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Figure 4

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the PROSPECT review.14 However in experienced hands the SNB is an excellent block with high success rates. In combination with a FNB complete knee analgesia is achieved with no opiate requirement. Again the prolonged nature of this block makes early mobilization difficult if high concentration, long acting LA is used. A distal SNB at the popliteal crease causes far less problems with mobilization and it therefore remains the main stay for analgesia for foot and ankle surgery.

Key points in upper limb RA C C

All approaches are aided by Ultrasound. All carry the risk of vascular puncture.

Shoulder: C

C

Interscalene is the only reliable block but the area medial to deltoid is innervated by cervical plexus Significant postoperative pain extends beyond the duration of single shot block (consider interscalene catheter)

The hip The innervation of the hip joint is derived from the sciatic, obturator and femoral nerves whilst the overlying skin, lateral to the joint, is supplied by the lateral cutaneous nerve of the thigh (LCN). Because of this multiple innervation, peripheral nerve blocks are not ideal for hip surgery although significant analgesia is achieved with a lumbar plexus block when combined with a high sciatic nerve block. The lumbar plexus block is a fascial plane block of the lumbar plexus roots within the confines of the psoas muscle. It has the advantage of being a single shot block for femoral, obturator and LCN. However it has the significant disadvantages of requiring a high volume of LA and it has unpredictable epidural spread. Spinal anaesthesia and LIA, when combined with spinal opiates, is likely to become the gold standard for hip surgery analgesia as it provides excellent analgesia without prolonged motor block. However similar results for fast track surgery with discharge on day one have been achieved with short term epidural analgesia in hip arthroplasty surgery.15 It is quite possible therefore that early mobilization and discharge can be achieved in hip surgery whatever technique is employed, as long as long acting motor block is avoided.

Elbow and distal arm/hand: C C

C

Supra-clavicular or axillary blocks are suitable SCB is a two injection technique because of lack of spread of LA to the lower trunk ABPB is a multiple injection technique as a single injection does not reliably spread around all terminal branches.

Lower limb The sensory innervation of the lower limb originates from both the lumbar and sacral plexus which, although joined, are impossible to anaesthetise with a single plexus block. It is for this reason that central neuraxial block became the principal anaesthetic technique for lower limb surgery and until recently epidural catheters for postoperative analgesia were common. It is now more usual practice to provide anaesthesia with CNB or GA but to deliver postoperative analgesia with spinal opiates and/or peripheral nerve blocks or LIA. As mentioned above, the principle problem with lower limb RA is the associated motor block preventing early mobilization, but peripheral nerve blocks have been shown to improve perioperative outcomes after lower limb arthroplasty surgery.12 Bilateral lower limb procedures are a particular problem for RA, as even single side procedures require near maximum LA doses. CNB therefore remains the mode of analgesia most commonly used for bilateral lower limb arthroplasty.

The knee The innervation of the knee is derived from the femoral and the sciatic nerves. Historically it is believed that the obturator nerve gives a variable sensory innervation to the medial knee, though the clinical evidence for this is poor. Unlike the hip, complete analgesia of the knee is possible with just two peripheral nerve blocks, although the addition of a sciatic nerve block to a femoral nerve block remains contentious. The recent PROSPECT working group review, published in 2008, supported the use of GA plus a single shot femoral nerve block or spinal anaesthesia plus spinal opiates. Unfortunately this group have not considered LIA in their review. Total knee replacement surgery generally is more painful than total hip arthroplasty. The dose of intrathecal morphine required is significantly higher than for hip surgery and, as the concomitant side effects increase, so does the risk benefit ratio. To date there has been no paper comparing LIA with complete RA of the knee, i.e. combined femoral and sciatic nerve blocks. Even papers that have compared LIA with just a femoral nerve block have not shown a reduction in hospital stay. It does appear that analgesia is more difficult to obtain with Knee arthroplasty and hence the continued popularity of peripheral nerve blocks for this type of surgery. As with hip surgery, it is likely that it is the preoperative protocol combined with early mobilization that is important. For the anaesthetist it is a balancing act between adequate analgesia to allow mobilization and too much analgesia preventing it.

The femoral nerve block (FNB) It is easy to achieve and success rates have improved with the use of ultrasound. With ultrasound the fascial plane between the fascia iliaca and the iliacus muscle is easy to visualize and lateral spread of LA towards the lateral cutaneous nerve confirms that a large volume FNB is a 2 in 1 block, not 3 in 1. In some centres catheters have been placed in this fascial plane to prolong the block. Despite the use of low concentration LA, motor block is still a potential problem with catheters, but discharge home on the first postoperative day after TKR has been achieved13 with a catheter in situ. The sciatic nerve block (SNB) It is less easy to achieve this block in inexperienced hands. The nerve is less easy to define using ultrasound and access to the nerve can be difficult. Despite its significant innervation of the posterior capsule of the knee and the tibial plateau most studies have failed to show efficacy following TKR because of the high failure rate of this block. It is not therefore recommended in

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Analgesia and early discharge for soft tissue knee reconstructive surgery can be facilitated by a femoral nerve block alone. Some centres in the US discharge ACL patients with femoral catheters but in the UK a single shot femoral block is the norm and this does not prevent discharge on day of surgery, despite the loss of motor function.

by the surgeon and anaesthetist. It therefore is essential that both members of the team have a treatment plan that includes intraand post-operative needs and aims and neither is blinded to the others requirements. A

Foot and ankle surgery

REFERENCES 1 Koller C. On the use of Cocaine for producing anaesthesia on the eye. Lancet 1884; 2: 990. 2 Bier A. Versuche uber Coacinisirung des Ruckenmarkes. Dtsch Z Chir 1899; 5151: 361. 3 Borgeat A, Kalberer F, Jacob H, et al. Patient-controlled interscalene analgesia with ropivicaine 0.2% versus bupivicaine 0.15% after major open shoulder surgery: the effects on hand motor function. Anesth Analg 2001; 92: 218e23. 4 Ilfeld BM, Yaksh TL. The end of postoperative pain-a fast-approaching possibility? and, if so, will we be ready? Reg Anesth Pain Med 2009; 34: 85e7. 5 Rostund T, Kehlet H. High-dose local infiltration analgesia after hip and knee replacement-what is it, why does it work, and what are the future challenges? Acta Orthopaedica 2007; 78: 159e61. 6 Forster JG, Rosenberg PH. Clinical useful adjuvants in regional anaesthesia 2003; 16: 477e86. 7 Cook TM, Counsell D, Wildsmith JAW. Major complications of central neuraxial block: report on the third project of the Royal College of anaesthetists. Br J Anaesth 2009; 102(2): 179e90. 8 Mar GJ, Barrington MJ, McGuirk BR. Acute compartment syndrome of the lower limb and the effect of postoperative analgesia on diagnosis. Br J Anaesth 2009; 102(1): 3e11. 9 Kerr D, Kohan L. Local infiltration analgesia: a technique for the control of acute postoperative pain following knee and hip surgery. Acta Orthopaedica 2008; 79(2): 174e83. 10 Wilson AT, Nicholson E, Burton L, Wild C. Analgesia for day-case shoulder surgery. Br J Anaesth 2004; 92(3): 414e5. 11 Swenson JD, Bay N, Loose E, et al. Outpatient management of continuous peripheral nerve catheters placed using ultrasound guidance: an experience of 620 patients. Anesth Analg 2006; 103: 1436e43. 12 Hebl JR, Dilger JA, Byer DE, et al. A pre-emptive multimodal pathway featuring peripheral nerve block improves perioperative outcomes after major orthopaedic surgery. Reg Anesth pain med 2008; 33(6): 510e7. 13 Ilfeld BM, Gearden PF, Enneking F, et al. Total knee arthroplasty as an overnight-stay procedure using continuous femoral nerve blocks at home: a prospective feasibility study. Anesth Analg 2006; 102: 87e90. 14 Fischer HB, Simanski CJ, Sharp C, et al. A procedure-specific systematic review and concensus recommendations for postoperative analgesia following total knee arthroplasty. Anaesthesia 2008; 63(10): 1105e23. 15 Berger RA, Sanders SA, Thill ES, et al. Newer anaesthesia and rehabilitation protocols enable outpatient hip replacement in selected patients. Clin Orthop relat res 2009; 467: 1424e30.

The innervation of the foot and ankle is predominantly from the terminal branches of the sciatic nerve. There is a small supply from the saphenous branch of the femoral nerve, from the medial malleolus to the base of the first metatarsal. Excellent analgesia is therefore achieved either by blocking the sciatic nerve in the popliteal fossa or, for foot surgery, by blocking the terminal branches at the ankle. The popliteal block is amenable to catheter placement to prolong analgesia. The saphenous nerve can be blocked medial to the knee or at the ankle, adjacent to the saphenous vein. Major foot surgery can therefore be carried out on a day case basis and can be done under block alone, with little motor block delaying discharge.

Key points in lower limb RA C C

All procedures possible under GA or Central Neuraxial block Innervation of all major joints is from lumbar and sacral plexus making single plexus block inadequate

Hip: C

C C

Because of multiple innervation spinal anaesthesia  opiates  LIA is the preferred technique by many Alternatives include lumbar plexus block Early ambulation and discharge possible in most cases if long acting LA avoided

Knee: C C

TKR generally more painful than THR RA presents a more difficult balance between adequate analgesia to facilitate mobilization and too much motor block inhibiting it.

Conclusion Regional anaesthesia in orthopaedic surgery has moved to become more efficient, safer and evidence based. There is now a realization that simply giving a general anaesthetic is no longer the best technique for the vast majority of major orthopaedic procedures, as regional analgesia will improve surgical outcome as well as patient satisfaction. However, particularly in lower limb surgery, long acting RA may well be detrimental to the patient if early postoperative mobilization is inhibited by a dense regional block. RA must therefore be considered a balance both

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BASIC SCIENCE

Hyaline articular cartilage

in 1743 when he described articular cartilage damage as a problem that will not heal.3 The cellular component of the hyaline cartilage represents 3–5% of the total cartilage mass. More than 95% of the cartilage volume consists of extracellular matrix (ECM), which is the functional element of this tissue.4

Ehab Kheir David Shaw

Cellular component Chondrocytes are sparse but essential in the production and maintenance of the ECM including collagen, glycosaminoglycans (GAGs) and proteoglycans.5 They are distributed either singularly or in clusters known as isogenous groups. The latter group represents newly divided cells. The cytoplasm of chondrocytes varies in appearance depending on their level of activity.6 The newly divided chondrocytes that are active in the production of matrix material display areas of cytoplasmic basophilia, where protein is synthesised, and clear areas, containing large Golgi apparatus. In older less active chondrocytes, the Golgi apparatus is reduced in size and clear areas of cytoplasm usually indicate extracted lipid droplets and glycogen stores. Each chondrocyte is surrounded by a thin, pericellular matrix that provides hydrodynamic protection for the chondrocyte; a complex known as the chondron.7 Each chondron is composed of a chondrocyte linked to a high pericellular concentration of proteoglycans, as well as hyaluronan, biglycans and matrix ­glycoproteins.8 Figure 1 illustrates hyaline cartilage cross sections, stained with haematoxylin and eosin. This figure is extracted from MSc research undertaken by the first author. The stained tissue sections demonstrated cartilage to have four zones:

Abstract Hyaline articular cartilage forms an important component of synovial joints, the integrity of which is crucial for normal function. Knowledge of its composition and dynamics is important for a better understanding of joint diseases pathophysiology and management. This article describes the basic characters of hyaline cartilage, its biochemical and biomechanical properties and reviews the current concepts of cartilage diseases.

Keywords articular cartilage; collagen; glycosaminglycans; ­ osteochondral defect; osteoarthritis

Introduction Hyaline articular cartilage is the most important structure of a synovial joint. Its main function is to protect the articular surface of bones from abrasion and to provide a smooth lubricated surface for joint movement distributing load evenly.1 It can withstand an astonishing amount of repetitive physical stress. The complex and highly specialized composition of normal hyaline articular cartilage makes it a formidable challenge to replace or repair once damaged or lost. The predominant repair tissue found in damaged areas is fibrocartilage, which is mechanically and biochemically inferior to hyaline cartilage.2 Thus, chondral lesions often result in progressive deterioration and eventually osteoarthritis.

Tangential layer Chondrocytes were rather small, flattened and parallel to the surface. Transitional zone The chondrocytes were slightly larger, round and arranged both singly and in isogenous groups. Radial zone Fairly large chondrocytes oriented perpendicular to the articulating surface.

Structure of hyaline cartilage Hyaline cartilage is a tough, semi-transparent, elastic, flexible tissue consisting of cartilage cells (chondrocytes and chondroblasts) scattered through a complex woven network of collagen fibres and proteoglycans distributed within interstitial water, the extra-cellular matrix. The articular surface of cartilage is covered by a dense fibrous membrane called the perichondrium.1 Cartilage is an avascular and aneural tissue, and when damaged, it does not heal readily. This concept was first described by Hunter

Calcified cartilage layer This is adjacent to the underlying cortex of the bone. The matrix of the calcified cartilage layer stained slightly darker (H&E) than the matrix of the other layers.

Ehab Kheir MRCS MRCS is a Registrar in Trauma and Orthopaedics at Bradford Royal Infirmary, UK.

Biochemical component of the hyaline cartilage matrix The ECM of hyaline cartilage is mostly water (60-80%). The remaining organic component predominantly is collagen molecules amounting to 15% of the ECM, of which type II is the most abundant. The rest of the ECM is formed of proteoglycans (aggrecan) (10%) and multiadhesive glycoproteins (5%)9 (Figure 2).

David Shaw MSc FRCS Ed FRCS (Orth) is a Consultant Orthopaedic Surgeon at Bradford Royal Infirmary and a Consultant in Trauma and Orthopaedics, Honorary Senior Lecturer Medical & Mechanical Engineering at Leeds University, UK.

Collagen molecules Collagen represents the major ECM protein. It constitutes the only fibrillar component of the cartilage. 80% of the hyaline articular cartilage is type II collagen.10 Each collagen type

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Hyaline cartilage stained with haematoxylin and eosin. a Original magnification ×40, b original magnification ×100, c the Arrow points to chondrocytes cluster, original magnification ×200, d the arrow indicates a single chondrocyte, original magnification ×400. Figure 1

Proteoglycans and glycosamoniglycans The ECM in hyaline cartilage contains three kinds of GAGs: hyaluronan, chondroitin sulphate, and keratan sulphate (Figure 4). The hyaluronan molecule is exceptionaly important in the structure of the ECM as it forms a linear aggregate and is interwoven with the network of collagen fibrils.7 A proteoglycan monomer consists of a core protein joined by GAGs. The most important proteoglycan monomer in the ECM is aggrecan, which is joined by chondroitin sulphate and keratan molecules.15 Proteoglycans are hydrophilic; this property results in the ability of hyaline cartilage to retain water which is essential to its proper function.

has a specific role in maintaining the structure of cartilage (Table 1). The arcade concept Alfred Benninghoff first described the arcade concept which explained the three-dimensional (3-D) organization of the collagen fibres within the ECM.13 The arcade concept proposed that the collagen fibrils anchored deeply in the calcified zone, run vertically towards the articular surface in the radial zone, turn obliquely in the transitional zone and become parallel to the articular surface in the tangential zone14 (Figure 3).

Figure 2 a Cartilage constituents b Structure of the solid component of the extracellular matrix in hyaline cartilage.

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e­ lectromagnetic fields can produce a sustained up-regulation of growth factors in articular cartilage.17

Function of collagen in hyaline cartilage Collagen type

Function

II

forms the network of fibrils within which the proteoglycans are contained found mainly at the periphery of the chondrocytes where it helps to attach these cells to the matrix framework10 facilitates fibril interaction with the matrix proteoglycan molecules11 organizes the collagen fibrils into a threedimensional hexagonal lattice12 regulation of fibrils size Function in articular cartilage unknown

VI

IX X XI III, XII & XIV

Biochemical properties of hyaline cartilage The solid phase of hyaline cartilage consists of proteoglycan aggregates entrapped within the collagen meshwork forming a strong porous-permeable composite. Both molecules bind to water by different ways.18 Within the solid phase proteoglycans contain repeating sulphate and carboxylate groups along their chains, which become negatively charged when placed in an aqueous solution. These negatively charged molecules repel each other exerting a large swelling pressure which is resisted by the tensile stress of the surrounding collagen network.18 The balance of the expanding swelling pressure exerted by the proteoglycans and the constraining tensile force within the collagen network determines the degree of hydration in the cartilage. Any disruption of this balance, by damage to either component of the solid phase, causes an increase in tissue hydration.19

Table 1

Function The principal role of articular cartilage is to efficiently transmit weight loads to the underlying bone. Keratin sulfate and chondroitin sulfate on the GAGs carry a negative charge. This negative charge creates a high affinity for water that helps cartilage resist compressive loads and causes the aggrecans to repel one another, resulting in maximal volume expansion. The flow of water through charged regions of the proteoglycan-rich matrix generates piezoelectric charges that further modulate the rate of water flow contributing to the viscoelastic behaviour of articular cartilage.16 In addition, there is evidence that electric and

Biomechanical behaviour of hyaline cartilage Hyaline cartilage consists of a fluid component within a solid porous-permeable matrix. This biphasic nature profoundly influences its mechanical behaviour when loaded.20 Loading results in the flow of water through the solid permeable matrix generating a frictional drag on the matrix.21 Hyaline cartilage is permeable and fluid may flow through it.22 Permeability is a measure of the ability of fluid to flow through

Figure 3 The three-dimensional organisation of collagen in articular cartilage.

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a Proteoglycan aggregate structure, b The proteoglycan monomer. Figure 4

hydrated porcine hyaline cartilage was subjected to compression (1 Newton) using a flat pin (3 mm in diameter). The test allowed generation of results in the format of time against voltage. Results were converted to time against deformation (mm) on application of the calibration factor. The y-axis represents displacement (mm) and x-axis represents time (minutes).

a porous-permeable material such as an ECM and is inversely proportional to the friction drag exerted by the fluid.22 Thus, as the cartilage is compressed under load, fluid extrudes from it and this reduces the pore size and permeability of the ECM. As the permeability of the ECM decreases the drag forces on fluid movement increases.22 The overall result of this is to provide cartilage with a selfprotective mechanical feedback mechanism which stiffens the cartilage by limiting rapid fluid flow in response to high and increasing load. This behaviour is exhibited as creep and stress relaxation.20,23 Creep occurs when cartilage undergoes constant loading. Typically cartilage responds to loading by an initial rapid deformation followed by a more slow deformation as time goes on. This timedependant deformation continues until equilibrium is reached. At the same time cartilage will respond with high initial stress which progressively diminishes with time. This time-dependant stress response is known as stress relaxation.20

Cartilage response to injury – the three stages theory The extent of articular cartilage damage is dependent on the severity of the injury. With increasing traumatic insult the 1 0.9

Deformation (mm)

0.8

Laboratory simulation of cartilage mechanical behaviour The mechanical behaviour of hyaline cartilage in response to load can be investigated in vitro by the indentation test. This compressive testing of hyaline cartilage was first described by Mow24 in 1989. Mow demonstrated that hyaline cartilage initially deforms rapidly and as compression is sustained the rate of deformation slows down gradually until it reaches a plateau phase. Figure 5 illustrates the results of the indentation test as part of a Master of Science undertaken by the first author. Fully

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Figure 5 Compressive (Indentation) testing of hyaline cartilage. Data are expressed as the mean (n = 9) ± 95% confidence limits. 453

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Water

Softening Water permeability Water content

2

3 Proteoglycans

Stiffness of subchondral bone load transmission to the partially damaged cartilage

1

Figure 6 Schematic illustrations of the three stages of cartilage damage following low energy trauma and development of osteoarthritis.

effect may range from fibrillation to development of an osteochondral defect.25 Nevertheless low energy trauma has been reported to injure the chondrocytes, compromise their metabolic capacity to repair, and lead to decreased proteoglycan concentration,26 increased hydration (Figure 6 [1]), and altered fibrillar organization of collagen.19 This has been reported to result in softening of the cartilage due to increased water content and permeability which will eventually lead to increased force transmission to the underlying subchondral bone, which will increase its stiffness (Figure 6 [2]) and, in turn, cause impact loads to be more readily transmitted to the partially damaged cartilage (Figure 6 [3]). This vicious cycle is thought to contribute to the progression of partial-thickness articular cartilage injuries to full-thickness defects and the development of osteoarthritis (OA).19 ◆

8 Poole CA, Flint MH, Beaumont BW. Chondrons in cartilage: ultrastructural analysis of the pericellular microenvironment in adult human articular cartilages. J Orthop Res 1987; 5(4): 509–522. 9 Poole AR, Pidoux I, Reiner A, Rosenberg L. An immunoelectron microscope study of the organization of proteoglycan monomer, link protein, and collagen in the matrix of articular cartilage. J Cell Biol 1982; 93(3): 921–937. 10 Eyre DR, Wu JJ, Woods PE. The cartilage collagens: structural and metabolic studies. J Rheumatol Suppl 1991; 27: 49–51. 11 Mendler M, Eich-Bender SG, Vaughan L, Winterhalter KH, Bruckner P. Cartilage contains mixed fibrils of collagen types II, IX, and XI. J Cell Biol 1989; 108(1): 191–197. 12 Schmid TM, Linsenmayer TF. Immunohistochemical localization of short chain cartilage collagen (type X) in avian tissues. J Cell Biol 1985; 100(2): 598–605. 13 Benninghoff A. Form und Bau der Gelenkknorpel in ihren Beziehungen zu Funktion. II Tell: der Aufbau des Gelenkknorpel in semen Beziehungen zu Funktion. Z Zellforsch 1925; 2: 783–862. 14 Huber M, Trattnig S, Lintner F. Anatomy, biochemistry, and physiology of articular cartilage. Invest Radiol 2000; 35(10): 573–580. 15 Hardingham TE, Muir H. Hyaluronic acid in cartilage and proteoglycan aggregation. Biochem J 1974; 139(3): 565–581. 16 Vidal Bde C, Vilarta R. Articular cartilage: collagen II-proteoglycans interactions. Availability of reactive groups. Variation in birefringence and differences as compared to collagen I. Acta Histochem 1988; 83(2): 189–205. 17 Aaron RK, Boyan BD, Ciombor DM, Schwartz Z, Simon BJ. Stimulation of growth factor synthesis by electric and electromagnetic fields. Clin Orthop Relat Res 2004(419): 30–37. 18 Jaffe FF, Mankin HJ, Weiss C, Zarins A. Water binding in the articular cartilage of rabbits. J Bone Joint Surg Am 1974; 56(5): 1031–1039. 19 Mankin HJ. The response of articular cartilage to mechanical injury. J Bone Joint Surg Am 1982; 64(3): 460–466. 20 Mow VC, Kuei SC, Lai WM, Armstrong CG. Biphasic creep and stress relaxation of articular cartilage in compression? Theory and experiments. J Biomech Eng 1980; 102(1): 73–84.

References 1 Buckwalter JA. Articular cartilage. Instr Course Lect 1983; 32: 349–370. 2 Furukawa T, Eyre DR, Koide S, Glimcher MJ. Biochemical studies on repair cartilage resurfacing experimental defects in the rabbit knee. J Bone Joint Surg Am 1980; 62(1): 79–89. 3 Hunter W. Of the structure and disease of articulating cartilages. 1743. Clin Orthop Relat Res 1995(317): 3–6. 4 Anderson CE, Ludowieg J, Harper HA, Engleman EP. The Composition of the organic component of human articular cartilage: relationship to age and degenerative joint disease. J Bone Joint Surg Am 1964; 46(6): 1176–1183. 5 Stockwell RA. The cell density of human articular and costal cartilage. J Anat 1967; 101(Pt 4): 753–763. 6 Stockwell RA. The interrelationship of cell density and cartilage thickness in mammalian articular cartilage. J Anat 1971; 109(Pt 3): 411–421. 7 Poole CA. Articular cartilage chondrons: form, function and failure. J Anat 1997; 191(Pt 1): 1–13.

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21 Mow VC, Holmes MH, Lai WM. Fluid transport and mechanical properties of articular cartilage: a review. J Biomech 1984; 17(5): 377–394. 22 Maroudas A, Bullough P, Swanson SA, Freeman MA. The permeability of articular cartilage. J Bone Joint Surg Br 1968; 50(1): 166–177. 23 Kempson GE, Freeman MA, Swanson SA. The determination of a creep modulus for articular cartilage from indentation tests of the human femoral head. J Biomech 1971; 4(4): 239–250. 24 Mow VC, Gibbs MC, Lai WM, Zhu WB, Athanasiou KA. Biphasic indentation of articular cartilage–II. A numerical algorithm and an experimental study. J Biomech 1989; 22(8–9): 853–861. 25 Alford JW, Cole BJ. Cartilage restoration, part 1: basic science, historical perspective, patient evaluation, and treatment options. Am J Sports Med 2005; 33(2): 295–306. 26 Lohmander LS, Dahlberg L, Ryd L, Heinegard D. Increased levels of proteoglycan fragments in knee joint fluid after injury. Arthritis Rheum 1989; 32(11): 1434–1442.

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Practice Points • Cartilage is an avascular and aneural tissue • When cartilage is damaged, it does not heal readily • The predominant repair tissue found in such defects is fibrocartilage, which is mechanically and chemically inferior to hyaline cartilage • Hyaline cartilage consists of a fluid component within a solid porous-permeable matrix; the biphasic nature of hyaline cartilage • The balance of the expanding swelling pressure exerted by the proteoglycans and the constraining tensile force within the collagen network determines the degree of hydration in the cartilage

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Multiple hereditary exostoses

Other diagnoses to consider C C

Payam Tarassoli C

Rouin Amirfeyz

C

Martin Gargan

C C

C

Abstract

C

Multiple hereditary exostoses is an autosomal dominant condition with a prevalence of 1:50, 000. Orthopaedic manifestations are of deformity and compression syndromes. In this article, the genetics, clinical presentation and orthopaedic management are discussed.

C C

Trevors Disease (Dysplasia Epiphysealis Hemimelica) Cartilaginous overgrowth of a portion of one or more epiphyses Metachondromatosis Multiple synchronous osteochondromas and enchondromas Commonly affects hands and feet Lesions do not result in deformity; may spontaneously resolve Ollier’s Disease (enchondromatosis) Benign cartilage tumours of bone (multiple in Ollier’s Disease) Often with unilateral predominance Incidence of malignant transformation much higher (20e50%)

Keywords EXT; multiple hereditary exostoses; Osteochondroma Nuclear bone scanning is highly sensitive to malignant change but due to the active nature of benign exostoses it is not particularly specific.

Introduction Multiple Hereditary Exostosis (MHE, Multiple Osteochondromas (MO), diaphyseal aclasis, multiple cartilaginous exostoses) is a disorder in which multiple outgrowths of cartilage-capped bone (osteochondromas or exostoses) are found on the skeleton. The lesions commonly affect the metaphyses of long bones, often causing pain and deformity. They are the most common bone tumour in children, with a prevalence at roughly 1:50,000 in the general population; males are more commonly affected (male-to-female ratio 1.5:1).1

Clinical features Exostoses may be sessile or pedunculated, and vary in number and size, although for a diagnosis of MHE to be made two or more lesions must be radiographically identified. The onset of MHE may be at any time between early childhood (2e3 years) and puberty, with approximately four-fifths of all patients affected during the first decade of life. 3 Exostoses cease to grow when the epiphyses fuse, although, in rare cases spontaneous resolution has been reported during childhood and puberty. Exostoses are usually painless, and come to clinical attention for cosmetic reasons. Altered body growth is a common consequence, with many patients presenting with symmetrical or asymmetrical deformity. Any long bone in the body can be affected, although there are certain areas where exostoses tend to occur more frequently;  The forearm is commonly affected in MHE, and bowing may ensue when growth in either the radius or ulna is reduced due to an exostosis, and there is relative overgrowth of the unaffected bone. This may destabilise the radioulnar joint to the extent that subluxation occurs. The same mechanism can cause valgus angulation at the ankle, with a relative shortening of the fibula as the tibia overgrows, and in some cases subluxation of the talus in the unstable joint.  The rate of knee deformity in MHE has been reported to be as high as 84% in some studies.4 Of those patients with knee deformity, 50% have both knees affected.5 Lesions affecting the distal femur and proximal tibia commonly cause varus or valgus deformity in the knee, with valgus deformity being more frequent.5,6  Femoral exostoses (in particular proximal ones) can cause anteversion and valgus of the hip and impairment of flexion. Short stature in MHE is usually the result of disruption in the normal growth of the femur and/or tibia, the femur being more commonly affected.

Imaging After clinical examination plain radiography can easily identify the characteristic features which are common to most exostoses:  Sharply demarcated bony lesion projecting from the metaphysis2  Usually pointing away from the epiphysis (‘‘from the knee we flee but to the elbow we go’’)  Cortical and medullary continuity with the parent bone  Distal end often bulbous Computed tomography (CT) and Magnetic Resonance Imaging (MRI) are also useful in evaluating complex sites (pelvis and spine) and ascertaining the level of structural impingement and the size of the cartilage cap (which is indicative of malignant change3). Ultrasonography is frequently used to evaluate the size of the cartilage cap and vascular complications, and is useful in imaging surrounding soft tissue and tendon involvement.

Payam Tarassoli MbChb BSc F2 Doctor, Bristol Royal Infirmary, Bristol, UK. Rouin Amirfeyz FRCS (Trauma & Orth) MSc MD Specialist Registrar in Trauma and Orthopaedics, Bristol Royal Infirmary, Bristol, UK. Martin Gargan FRCS (Trauma & Orth) MA Consultant Paediatric Orthopaedic Surgeon, Bristol Royal Hospital for Children, Bristol, UK.

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Figure 1 Radiographic features and distribution.

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 The spine is less frequently affected. However, when they occur, lesions are most commonly found in the upper cervical spine and originate from the posterior element. Scoliosis may occur.7  Tarsal, carpal and phalangeal involvement is less common but involvement can cause restriction of movement of the joint as well as deformity. There exists no classification system for the severity of MHE, but it has been observed that greater forearm involvement correlates with a more severe disease process overall.8 Local effects of the exostoses include impingement on adjacent structures such as tendons or nerves (the spinal cord in some cases, and the peroneal nerve in tibial exostoses) causing pain, osteoarthritis, bursa formation and cosmetic deformity.9 Vascular compromise, resulting mainly from compression of arteries or veins has also been reported.10 Malignant transformation of an exostosis, usually to a low grade chondrosarcoma, is rare,1 but can occur and expedites urgent removal. Signs suggesting malignant transformation are:  Increasing size (especially after fusion of the epiphyses after puberty)  Increasing pain  Thick cartilaginous cap measuring more than 1 cm2 Solitary exostoses should be regarded with a certain degree of suspicion and surgical excision with tumour margins is the current practice in many centres.

Indications for Surgical Intervention/Complications of Osteochondromas C C C C C C C C C C

In addition to surgical removal, correction of deformities affecting the long bones, such as those causing limb-length discrepancy, can be achieved by osteotomy, with the option of using epiphysiodesis as an adjuvant intervention (Figure 1). A

REFERENCES 1 Ahn J, Ludecke HJ, Lindow S, et al. Cloning of the putative tumour suppressor gene for hereditary multiple exostoses (EXT1). Nat Genet 1995; 11: 137e43. doi: 10.1038/ng1095-137. 2 Resnick D, Kyriakos M, Greenway G. Tumors and tumor-like lesions of bone:imaging and pathology of specific lesions. In: Resnick D, Niwayama G, eds. Diagnosis ofbone andjoint disorders. 2nd edn., vol. 6. Philadelphia: WB Saunders Co, 1988. p. 3648e720. chap 91. 3 Greenspan A. Tumors of cartilage origin. Orthop Clin North Am 1989; 20: 347e66. 4 Pannier S, Legeai-Mallet L. Hereditary multiple exostoses and enchondromatosis. Best Pract Res Clin Rheumatol 2008 Mar; 22: 45e54. 5 Schmale GA, Conrad EU, Raskind WH. The natural history of hereditary multiple exostoses. J Bone Joint Surg 1994; 76A: 986e92. 6 Pierz KA, Stieber JR, Kusumi K, Dormans JP. Hereditary multiple exostoses: one center’s experience and review of etiology. Clin Orthop Relat Res 2002 Aug: 49e59. 7 Bess RS, Robbin MR, Bohlman HH, Thompson GH. Spinal exostoses: analysis of twelve cases and review of the literature. Spine 2005 Apr 1; 30: 774e80. 8 Taniguchi K. A practical classification system for multiple cartilaginous exostosis in children. J Pediatr Orthop Sep-Oct 1995; 15: 585e91. 9 Wicklund LC, Pauli RM, Johnston D, Hecht JT. Natural history study of hereditary multiple exostoses. Am J Med Genet 1995; 55: 43e6. 10 Tanigawa N, Kariya S, Kojima H, et al. Lower limb ischaemia caused by fractured osteochondroma of the femur. Br J Radiol Apr 2007; 80: e78e80. 11 Stickens D, Clines G, Burbee D, et al. The EXT2 multiple exostoses gene defines a family of putative tumour suppressor genes. Nat Genet 1996; 14: 25e32. doi: 10.1038/ng0996-25. 12 Lonie L, Porter DE, Fraser M, et al. Determination of the mutation spectrum of the EXT1/EXT2 genes in British Caucasian patients with

Genetic aetiology MHE is an autosomal dominant disorder with a very high penetrance. It exhibits genetic heterogeneity, and to date has been associated with 2 unique genes within the EXT (endoplasmic reticulum-resident type) loci.  EXT1 accounting for 50%  EXT2 accounting for 30% of MHE cases.11 More recently, there is mounting evidence of the possibility of a third EXT gene, with novel mutations arising from new techniques in genetic screening.12,13 The locus has been mapped to chromosome arm 19p; however the precise gene is yet to be localised. The majority of MHE sufferers exhibit mutations of the tumour suppressor genes (EXT1 and EXT2) whose gene products are involved in the catalysis of heparan sulphate (HS) polymerisation. Without this polymerisation, HS proteoglycans accumulate in the cell cytoplasm, rather than being transported to the cell surface at which they are expressed.14 This expression is essential for the binding of fibroblast growth factor (FGF) and for the diffusion of morphogens (hedgehog variety), both of which, during normal growth are involved in a feedback loop that regulates migration of chondrocytes to the growth plate and their subsequent differentiation in situ.15 It is stipulated that disruption of this feedback loop causes subsequent formation of osteochondromas.16

Management Surgical excision of an osteochondroma should be performed after fusion of the epiphyses as early intervention risks disruption of the plate. Asymptomatic and uncomplicated osteochondroma, are best managed conservatively with regular surveillance; however, complications may ensue which mandate surgical input.17

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Limb length discrepancy and deformity Pain Bursa formation leading to inflammation/infection Instability e exostoses likely to fracture Impingement of tendons Spinal involvement with nerve root or cord compression Interference with joint function/movement Malignant transformation Solitary osteochondromas Osteochondromas causing vascular insufficiency

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15 Benoist-Lasselin C, de Margerie E, Gibbs L, et al. Defective chondrocyte proliferation and differentiation in osteochondromas of MHE patients. Bone 2006; 39: 17e26. 16 Wuyts W, Van Hul W, De Boulle K, et al. Mutations in the EXT1 and EXT2 genes in hereditary multiple exostoses. Am J Hum Genet 1998; 62: 346e54. 17 Carpintero P, Leon F, Zafra M, Montero M, Berral FJ. Fractures of osteochondroma during physical exercise. Am J Sports Med 2003; 31: 1003e6.

multiple osteochondromas, and exclusion of six candidate genes in EXT negative cases. Hum Mutat 2006; 27: 1160. 13 Signori E, Massi E, Matera MG, et al. Combined analytical approach reveals novel EXT1/2 gene mutations in a large cohort of Italian multiple osteochondromas patients. Genes Chromosomes Cancer 2007; 46: 470e7. 14 Hameetman L, David G, Yavas A, et al. Decreased EXT expression and intracellular accumulation of HSPG in osteochondromas and peripheral chondrosarcomas. J Pathol 2007; 211: 399e409.

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CME SECTION

CME questions based on the Mini-Symposium on ‘‘Foot and Ankle Problems’’ The following series of questions are based on the MiniSymposium on ‘‘Foot and Ankle Problems’’. 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 Orthopaedics and Trauma Editorial Office at the address at the bottom of the RESPONSE sheet. Please photocopy this page if you wish to keep your copy of Orthopaedics and Trauma. Replies received before the next issue of the journal 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, via email, for your records.

4 Which of the following conditions is least likely to give rise to paraesthesiae in the foot? A Anterior tarsal tunnel syndrome B Common digital nerve entrapment C Entrapment of the 1st branch of the lateral plantar nerve D Medial plantar nerve entrapment E Sural nerve entrapment

Questions

6 Approximately what proportion of the adult population have asymptomatic flat feet? A 1% B 5% C 10% D 20% E 30%

5 Which of the following is not usually a component of adult flat foot deformity? A Dorsolateral subluxation of the navicular B Hyperpronation C Increased subtalar eversion D Internal rotation of the calcaneus in relation to the talus E Short lateral column in relation to medial column

1 Which of the following statements concerning the nerve supply to the foot and ankle is correct? A It is supplied entirely by branches of the sciatic nerve B It is supplied by four branches of the sciatic nerve and one of the femoral C It is supplied by three branches of the sciatic nerve, one of the femoral and one obturator D It is supplied by three branches of the sciatic nerve and two of the femoral E It is supplied by two terminal branches of the sciatic nerve and one of the femoral

7 Which of the following is the most common form of tarsal coalition? A Calcaneocuboid B Naviculocuboid C Naviculocuneiform D Talocalcaneal E Talonavicular

2 Which of the following most accurately describes the contents of the tarsal tunnel? A Medial and lateral plantar nerves alone B Tibial nerve alone C Tibial neurovascular bundle and tibialis posterior tendon D Tibial neurovascular bundle, and tibialis anterior tendon E Tibial neurovascular bundle, tibialis posterior, flexor hallucis longus and flexor digitorum longus

8 Into which of the following does the Tibialis posterior tendon NOT insert? A Cuboid B First metatarsal C Fourth metatarsal D Lateral cuneiform E Navicular 9 At what stage of posterior tibial tendon disorder (according to Johnson and Strom) does a lateral column lengthening procedure become indicated? A 1 B 2A C 2B D 3 E 4

3 Which of the following would give rise to symptoms most closely mimicking tarsal tunnel syndrome? A L4/5 central disc prolapse B L4/5 posterolateral disc prolapse C L4/5 far lateral disc prolapse D L5/S1 central disc prolapse E L5/S1 posterolateral disc prolapse

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CME SECTION

10 How do biphosphonates exert their therapeutic effect? A Decrease calcium excretion B Increase calcium absorbtion C Inhibit osteoclasts D Raise serum calcium E Stimulate osteoblasts

Responses Please shade in the square for the correct answer. B C D E 1 A

11 What happens to the rate of nonunion when smokers give up smoking prior to ankle arthrodesis and abstain throughout treatment? A It increases by 10% B No change C It decreases by 10% D It decreases by 20% E It decreases by 40% 12 Which of the following sets of criteria contains elements that are all favourable for ideal positioning of an ankle arthrodesis? A 5 of ankle valgus and external rotation, slight posterior positioning of talus under tibia B 5 of ankle varus and external rotation, slight posterior positioning of talus under tibia C 5 of ankle valgus and external rotation, slight anterior positioning of talus under tibia D 5 of ankle varus and internal rotation, slight anterior positioning of talus under tibia E 5 of valgus and internal rotation, slight anterior positioning of talus under tibia

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D

E

Your details (Print clearly) NAME..................... ADDRESS..................... .......................... EMAIL.....................

RETURN THE COMPLETED RESPONSE FORM by fax to 113-392-3290, or by post to CME, Orthopaedics and Trauma, Academic Department of Orthopaedic Surgery, ‘‘A’’ Floor Clarendon Wing, Leeds General Infirmary, Great George Street, Leeds LS1 3EX, UK.

Please fill in your answers to the CME questionnaire above in the response section provided to the right. A return address and fax number is given below the response section.

ORTHOPAEDICS AND TRAUMA 23:6

2

461

Ó 2009 Published by Elsevier Ltd.

CME SECTION

Answers to CME questions based on the Mini-Symposium on ‘‘Orthopaedic Oncology’’ Please find below the answers to the Current Orthopaedics CME questions from Vol. 23, issue 4 which were based on the MiniSymposium on ‘‘Orthopaedic Oncology’’

Answers 1

a

2

a

b

c

d

e

3

a

b

c

d

e

4

a

b

c

d

e

5

a

b

c

d

e

6

a

b

c

d

e

7

a

b

c

d

e

8

a

b

c

d

e

9

a

b

c

d

e

10

a

b

c

d

e

11

a

b

c

d

e

12

a

b

c

d

e

ORTHOPAEDICS AND TRAUMA 23:6

b

c

d

e

462

Ó 2009 Published by Elsevier Ltd.