Aims and Scope Current Orthopaedics presents a unique collection of international review articles summarizing the current state of knowledge and research in orthopaedics. Each issue focuses on a specific topic, discussed in depth in a mini-symposium; other articles cover the areas of basic science, medicine, children/adults, trauma, imaging and historical review. There is also an annotation, self-assessment questions and an exam section. In this way, the entire postgraduate syllabus will be covered in a 4-year cycle. The Journal is cited in: Cochrane Center, EMBASE/ Excerpta Medica, Infomed, Reference Update and UMI Microfilms.
Editor Professor R. A. Dickson MA, ChM, FRCS, DSc St James’s University Hospital Trust, Leeds, UK
Editorial Committee President of BOTA, M. A. Farquharson-Roberts (Gosport, UK), I. Leslie (Bristol, UK), D. Limb (Leeds, UK), M. Macnicol (Edinburgh, UK), J. Rankine (Leeds, UK)
Editorial Advisory Board A. Thurston (New Zealand) E. G. Pasion (Philippines) L. de Almeida (Portugal) G. P. Songcharoen (Thailand) R. W. Bucholz (USA) J. W. Frymoyer (USA) R. W. Gaines (USA) S. L. Weinstein (USA) M. Bumbasirevic (former Yugoslavia)
M. Torrens (Greece) J. C. Y. Leong (Hong Kong) A. K. Mukherjee (India) A. Kusakabe (Japan) A. Uchida (Japan) M.-S. Moon (Korea) R. Castelein (The Netherlands) R. K. Marti (The Netherlands) G. Hooper (New Zealand)
D. C. Davidson (Australia) J. Harris (Australia) S. Nade (Australia) R. Szyszkowitz (Austria) G. R. Velloso (Brazil) G. A. Hunter (Canada) J. H. Wedge (Canada) S. Santavirta (Finland) P. N. Smyrnis (Greece) P. N. Soucacos (Greece)
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Volume 19 (2005) contents Mini-Symposium: Radiology for the FRCS (Orth) (i) Ionising radiation and orthopaedics P. Dewey, S. George and A. Gray. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
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(ii) Basic science: magnetic resonance imaging S. McKie and J. Brittenden. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
13
(iii) Basic science: computed tomography D. Barron. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
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(iv) Basic science: ultrasound K. Colquhoun, A. Alam and D. Wilson . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
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(v) Basic science: nuclear medicine in skeletal imaging M. Calleja, A. Alam, D. Wilson and K. Bradley . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
34
The Foot Sesamoids of the foot R. Anwar, S.N. Anjum and J.E. Nicholl . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
40
Trauma Acute injuries of the extensor mechanism of the knee M. Bumbasˇirevic´ and A. Lesˇic` . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
49
Arthroplasty The outcome of total hip and knee arthroplasty in diabetics P.K.H. Chan, I.J. Brenkel and J. Aderinto. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
59
Tumours Sarcomatous degeneration in Paget’s disease of bone H. Sharma and M.J. Jane . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
68
CME Section CME Questions based on ‘‘Ionising radiation and orthopaedics’’. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
78
Answers to CME questions in Vol. 18, issue 5 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
81
Book Reviews . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
82
Mini-Symposium: The Foot (i) The structure and function of the foot in relation to injury P.J. Briggs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
85
(ii) The hindfoot: Calcaneal and talar fractures and dislocationsFPart I: Fractures of the calcaneum D.J. Mcbride, C. Ramamurthy and P. Laing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
94
(ii) The hindfoot: Calcaneal and talar fractures and dislocationsFPart II: Fracture and dislocations of the talus D.J. Mcbride, C. Ramamurthy and P. Laing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
101
(iii) Tarsometatarsal injuriesFLisfranc injuries N.K. Makwana. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
108
Tumors The role of chemotherapy in the treatment of bone and soft tissue sarcomas A. Longhi, E. Setola, M. Versari and G. Bacci . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
119
VI
CURRENT ORTHOPAEDICS
Spine Cervical spondylosis. Part III: Cervical arthroplasty M.J. Torrens . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
127
Orthopaedic Informatics Personal digital assistants in orthopaedic surgery K. Barbosa and L. Funk . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
135
Trauma Acetabular fractures J. McMaster and J. Powell. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
140
Pain Complex regional pain syndrome A. McBride and R. Atkins. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
155
CME Section CME Questions based on ‘‘Acetabular Fractures’’ . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
166
Answers to CME questions in Vol. 18, issue 6 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
169
Mini-Symposium: The Wrist (i) Examination of the wristFsurface anatomy of the carpal bones R.S. Reddy and J. Compson. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
171
(i) Examination of the wristFsoft tissue, joints and special tests R.S. Reddy and J. Compson. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
180
(ii) Management of Peri-Trapezial Osteoarthritis J.W.K. Harrison and N.R.M. Fahmy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
190
(iii) MR imaging of the wrist P. Robinson. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
196
Orthopaedic Information Digital imaging for orthopaedic surgeons L. Funk. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
209
Tumours Pigmented villonodular synovitis: Diagnostic pitfalls and management strategy H. Sharma, M.J. Jane and R. Reid . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
215
Children Developmental dysplasia of the hip (DDH) J.J. McCarthy, P.V. Scoles and G.D. MacEwen . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
223
Trauma Injuries of the midfoot N.K. Makwana and M.R. van Liefland. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
231
CME Section CME Questions based on ‘‘Examination of the wrist: Parts I and II’’. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
243
Answers to CME questions in Vol. 19, issue 1 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
246
Mini-Symposium: Hip replacement (i) A review of minimally invasive hip replacement surgeryFcurrent practice and the way forward N.A. Siddiqui, P. Mohandas, S. Muirhead-Allwood and T. Nuthall . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
247
VOLUME19 (2005) CONTENTS
VII
(ii) Conservative hip implants I.D. Learmonth . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
255
(iii) Resurfacing arthroplasty of the hip P. Roberts, P. Grigoris, H. Bosch and N. Talwaker . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
263
(iv) The science of metal-on-metal articulation J.L. Tipper, E. Ingham, Z.M. Jin and J. Fisher . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
280
(v) Silent osteolysis associated with an uncemented acetabular component: A monitoring and treatment algorithm J.H.M. Goosen, R.M. Castelein and C.C.P.M. Verheyen . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
288
Trauma Humeral nails: When to choose what and how to use C. Garnavos . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
294
Tumours Management of lung metastases from musculoskeletal sarcomas A. Briccoli, M. Rocca and M. Salone . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
305
Syndromes Spondyloepiphyseal dysplasia R. Amirfeyz, C. Clark and M. Gargan . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
309
Trauma Trauma-related sepsis and multiple organ failure: Current concepts in the diagnosis and management V. Bumbasirevic, A. Karamarkovic, A. Lesic and M. Bumbasirevic . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
314
CME Section CME Questions based on "Resurfacing arthroplasty of the hip". . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
322
Answers to CME questions in Vol. 19, issue 2 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
325
Book Review Essentials of musculoskeletal imaging J.J. Rankine. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
326
Mini-Symposium: Pelvic fractures (i) Injuries to the pelvic ring: Incidence, classification, associated injuries and mortality rates B.A. Petrisor and M. Bhandari . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
327
(ii) Acute management of pelvic ring fractures M. Keel and O. Trentz. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
334
(iii) Management of open pelvic fractures E. Katsoulis, E. Drakoulakis and P.V. Giannoudis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
345
(iv) Pelvic fractures and genitourinary injuries J. Yerasimides and C.S. Roberts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
354
(v) Delayed reconstruction of pelvic fractures J. Keating . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
362
Children Missed posttraumatic radial head dislocation S. Agarwal and B.W. Scott. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
373
Foot The surgical treatment of Morton’s neuroma S.K. Singh, J.P. Ioli and C.P. Chiodo . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
379
VIII
CURRENT ORTHOPAEDICS
Hip Girdlestone resection arthroplasty of the hip: Current perspectives H. Sharma, C.R. Dreghorn and E.R. Gardner. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
385
Tumours The use of massive bone allografts in bone tumour surgery of the limb D. Donati, C. Di Bella, M. Col angeli, G. Bianchi and M. Mercuri . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
393
CME Section CME Questions based on ‘‘Management of open pelvic fractures’’ . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
400
Answers to CME questions in Vol. 19, issue 3 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
403
Book Reviews . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
404
Mini-Symposium: Surgery for Knee Arthritis (i) Novel treatments for early osteoarthritis of the knee S.P. Krishnan and J.A. Skinner . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
407
(ii) Osteotomy for osteoarthritis of the knee V. Franco, G. Cerullo, M. Cipolla, E. Gianni and G. Puddu . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
415
(iii) Modern unicompartmental knee replacement G.C.R. Keene and M.C. Forster . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
428
(iv) Total knee replacement J. Bellemans, H. Vandenneucker and J. Vanlauwe . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
446
Tissue Engineering Current concepts and applications in the musculoskeletal and peripheral nervous systems P.N. Soucacos and E.O. Johnson . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
453
Children Hallux flexus: Review of current opinion on aetiology and management N.E. Ohly and M.F. Macnicol . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
461
Syndromes Achondroplasia R. Amirfeyz and M. Gargan . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
467
Case Study Hip A.A. Faraj. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
471
Quiz Radiology quiz M. Shaw and C. Wakeley . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
474
CME Section CME Questions based on ‘‘Novel treatments for early osteoarthritis of the knee’’. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
478
Answers to CME questions in Vol. 19, issue 4 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
481
Erratum Erratum to ‘‘Resurfacing arthroplasty of the hip’’ [Current Orthopaedics (2005) 263–279] P. Roberts, P. Grigoris, H. Bosch and N. Talwaker . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
482
Author Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
I
Subject Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
III
Contents of Volume 19 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
V
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 1–12
www.elsevier.com/locate/cuor
MINI-SYMPOSIUM: RADIOLOGY FOR THE FRCS (Orth)
(i) Ionising radiation and orthopaedics$ Peter Deweya,, Stame Georgeb, Angus Grayc a
P.O. Box 1763, Bowral, NSW 2576, Australia Royal North Shore Hospital of Sydney, St Leonards, NSW, 2065, Australia c Sydney Children’s Hospital, Randwick, NSW, Australia b
KEYWORDS Ionising radiation; X-ray; Surgeon; Cancer; Radiation protection
Summary Ionising radiation is a dangerous and potentially lethal modality yet its use is vital to surgical practice and patient care. It is necessary for the surgeon to understand the physical properties of ionising radiation and its effects on living tissue leading to the risk of induction of carcinogenesis and somatic effects such as cataract formation. These risks justify the statutory regulations that control its use, the need for protective equipment and garments and surgeons’ responsibility to minimise and monitor their radiation exposure together with that of patient and staff. These aspects are discussed in detail so that ionising radiation may be safely used in the workplace to the benefit of patient care with very minimal risk to surgeons and their staff. & 2005 Elsevier Ltd. All rights reserved.
Introduction Roentgen discovered X-rays in 1895 and in the medical setting X-rays developed pari passu with surgery with an explosive expansion in the last two decades. In orthopaedics X-ray usage increased dramatically with the concept that accurate $
The table and figures are reproduced with kind permission of the Australian Orthopaedic Association from the booklet Radiation Safety for Orthopaedic Surgeons by George S, Dewey P, McGrath J and Beh H. The figures are adapted from Bontrager KT, Textbook of Radiographic Positioning and Related Anatomy, 4th Ed. Corresponding author. Tel.: +61 2 4862 3970; fax: +61 2 4862 4149. E-mail addresses:
[email protected] (P. Dewey),
[email protected] (S. George),
[email protected] (A. Gray).
operative reduction and rigid fixation of fractures, often with the necessity of X-ray imaging, hastened recovery and shortened hospital admission times. During this period radiation education and protection practices lagged behind the clinical scene and the situation was worsened in that many hospital authorities were slow to accept their responsibility of the radiation protection of their staff. The recent finding of a cluster of Australian orthopaedic surgeons with thyroid cancer has highlighted the problem.1 That ionising radiation causes cancer is well established from the Second World War atomic explosions2 and the Chernobyl accident that saw a near 200-fold increase in childhood thyroid cancer.3 Thyroid cancer occurring after a latent period following radiotherapy to the face for acne, the scalp for tinea capitis and the
0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2005.01.002
ARTICLE IN PRESS 2 tonsillar bed for chronic infection is well recognised. The link between radiation and thyroid cancer has a documented genetic basis with a high incidence of the RET/PTC thyroid specific oncogene being described in children from the Chernobyl region.4 This oncogene has been produced from both in vivo and in vitro radiation exposure.5 This risk of cancer from exposure to radiation and the radiation somatic effects cannot be ignored and demands an understanding of the modality by surgeons with a continuing education process and a constant awareness and reaction to the risks throughout a surgical career.
Physical properties and generation of X-rays The X-ray tube, where X-rays are produced, is made up of a cathode and an anode, encased in an evacuated glass container which has a window for the X-rays to emerge but is otherwise encased in lead to prevent radiation escaping in all directions. The cathode is a filament that is heated by the passage of an electric current. The heat promotes electrons to leave the surface of the filament. A high potential of more than 50,000 V between the
P. Dewey et al. cathode filament and the anode accelerates the electrons from the filament and fires them towards the anode, called the target. The electrons hit the target anode and in the deceleration process electromagnetic radiation in the form of X-rays (bremsstrahlung or braking radiation) and heat are produced. See Fig. 1. A cooling system, normally using oil, is used to remove the large amount of heat generated where the electrons strike the target. The anode is made to rotate so that the heat and continuous bombardment do not damage it by constantly striking it at one spot. The target anode is normally made of tungsten as its higher atomic number allows the production of a greater number of X-rays. The X-rays are ‘‘filtered’’ on emerging from the X-ray tube by the glass window material (inherent filtration) and by other materials such as aluminium placed at the outlet (added filtration). This ‘‘filtration’’ removes the low energy X-rays that are useless in image production and only contribute to the unwanted exposure of the patient and staff. The spectrum of X-rays generated consists of the continuous bremsstrahlung X-rays as well as some ‘‘characteristic X-rays’’. The latter are so-called because they are characteristic of the target material (tungsten). The high voltage (kV) controls the energy or penetrating power as well as the number of X-rays
Figure 1 Schematic diagram of an X-ray tube assembly, showing the various components including the important aluminium filter.
ARTICLE IN PRESS Ionising radiation and orthopaedics
3
Figure 2 The bremsstrahlung continuous X-ray spectrum showing the effect of different voltages (kV).
produced. Increasing the kV increases the number of X-rays produced and their energy. The filament current controls the tube current (mA) and the number of X-rays only, without affecting their energy. The mA should be kept low and increased only if the high voltage alone cannot achieve the desired image quality. See Fig. 2. Since X-rays are produced by the deceleration of charged particles or electrons they are in essence electromagnetic waves, similar in nature to radiowave, microwave, infrared, visible light, ultraviolet, and gamma radiations. X-rays exist in the higher energy end of the electromagnetic spectrum, which explains their high penetrating power. Therefore, just like other electromagnetic radiations, X-rays travel at the speed of light (300,000 km/s), travel in straight lines, are not affected by electric or magnetic fields, and are absorbed or scattered by matter. Most importantly, they obey the inverse square law that says that the intensity of X-rays decreases as the square of the distance from the source increases. X-rays also are invisible and have the ability to ionise atoms and molecules. It is the effects of this ionisation that ultimately damage or kill living cells. The interaction of X-rays with matter, resulting in the ionisation of atoms and molecules, occurs in two main ways. If the X-ray hits an electron in one of the inner orbits of an atom, the X-ray is completely absorbed, and the electron is ejected from the atom, resulting in a positive–negative ion pair. This is called photoelectric absorption. If the X-ray hits an outer orbit electron, the electron is ejected from the atom, again resulting in an ion
pair. The X-ray, however, is not absorbed, but is deflected or scattered, to continue on with lower energy. This is called Compton scattering. Compton scattering creates the radiation field around the patient during X-ray exposure and constitutes the radiation hazard for the surgeon and attending staff. The quantities and units used to measure X-radiation are: 1. Dose—the amount of energy absorbed per unit mass of matter. The unit is the Gray (Gy) (1 J/ kg). 2. Equivalent Dose—used to stipulate the radiobiological effect of dose as the energy absorbed per unit mass (equal numerically to dose for X-rays). The unit is the Sievert (Sv) (1 J/kg). As the Sievert is a large unit, the millisievert (mSv), one thousandth of a Sievert, is used in medicine. The International Commission on Radiological Protection (ICRP) has a System of Radiological Protection based on three principles, first expounded in ICRP publication 26 and later refined in ICRP publication 60:6 1. Justification. No practice involving exposure to radiation should be adopted unless it produces a net benefit. 2. Optimisation. All exposures should be kept As Low As Reasonably Achievable (ALARA), economic and social factors being taken into account.
ARTICLE IN PRESS 4 3. Limitation. The exposure of individuals should be subject to dose limits. There are annual Dose Equivalent Limits set both for members of the public and for persons who are occupationally exposed. These limits do not include exposure to background radiation or exposures for medical purposes. 1. The annual whole body Dose Equivalent Limit for occupationally exposed persons is 20 mSv. 2. The annual whole body Dose Equivalent Limit for members of the public is 1 mSv.
Effects on living tissue Ionising radiations interact with matter through excitation and ionisation of atoms and molecules. This causes damage by direct or indirect action.
Direct action An X-ray track passing through a cell may directly disrupt the molecular bonds of cellular material such as DNA and cell membranes. The cell either dies or if the DNA is distorted will replicate to abnormal or cancerous cells. Damage to the DNA in the nucleus of a single cell probably represents the initial event of carcinogenesis. Low dose radiation to human fibroblasts has been shown to produce double strand DNA breaks that are irreparable.7 A single X-ray track has the ability to irreparably damage a cell, with the possibility of deleterious effects, and this leads to the concept that the effects of exposures to X-rays, regardless of how small the dose, are cumulative over the organism’s lifetime.
Indirect action Water molecules are ionised into HO, HO2 free radicals or hydrogen peroxide H2O2 that have the ability to disrupt molecular bonds. Most long term effects of radiation are caused by this process as water is the most abundant molecule in the cell. The effects of radiation are classified as stochastic (probabilistic) or non-stochastic (deterministic). Stochastic effects are those where the probability of an effect occurring increases as the radiation dose increases and a lower threshold of dose is thought not to exist.8 The lack of a lower threshold is logical when it is realised that a single X-ray track may damage a cell. A latent period exists between
P. Dewey et al. the radiation exposure and the appearance of the effect, often of many years. The risk factor for fatal cancers induced by radiation depends on the tissue radiated and dose (thyroid cancer that has a high cure rate and cancers that may occur in old age and not be the cause of death are not included in the risk assessment). For uniform acute exposure of the whole body the probability for fatal cancer given by UNSCEAR (1988)9 and BEIR V (1990)10 is about 1 in 10 per Sievert .With prolonged exposure ICRP 60 (1991)6 gives a value of 1 in 20 per Sievert for the probability of induced fatal cancer. Non-stochastic effects are those where the severity of the effect increases with the dose and a threshold probably exists. The effects are specific to the tissue, for example, cataract formation, non-malignant skin changes, gonadal cell damage leading to impaired fertility and bone marrow dysplasia. If the dose is not greatly above the threshold the effects are temporary and reversion to normal occurs. If the dose is greatly above the threshold cell death occurs.
Background radiation Everyone is exposed to a background radiation that is either naturally or artificially generated. The natural sources are cosmic radiation, gamma radiation from natural uranium, inhaled radon gas from the decay of uranium and radioisotopes in the diet and in our bodies. The artificial sources are medical generated X-rays and radionuclide studies and are estimated to form 15% of the total average background radiation dose to the population.11 The effective whole body dose equivalent from natural sources is about 2.1 mSv per annum in areas of average background radiation and in some areas can rise to levels of 8–20 mSv per annum. A return air trip between Europe and Australia will incur an additional dose of about 0.28 mSv.
Diagnostic exposure Table 1 compares the average exposures of common radiological examinations to background radiation and gives the risk of fatal cancer induction for each examination. Recent work12 based on statistical models using the annual rate of diagnostic radiological procedures to estimate the dose to various organs and then applied to a model for radiation induced cumulative cancer risk suggests that in the USA, UK and Australia the incidence of cancers per annum induced from diagnostic radiological
ARTICLE IN PRESS Ionising radiation and orthopaedics Table 1
5
Average Exposures of some Examinations compared to Background Radiation
Diagnostic procedure
X-ray examinations: Limbs and joints (except hip) Teeth (single bitewing) (panoramic) Chest (single PA film) Skull Cervical spine (neck) Hip Thoracic spine Pelvis Abdomen Lumbar spine Barium swallow IVU (kidneys and bladder) Barium meal Barium follow Barium enema Cholecystography Cholangiography Cardiac Catheterisation CT head CT cervical spine CT lumbar spine CT chest CT abdomen/pelvis Radionuclide studies: Lung ventilation (81Krm) Lung perfusion (99Tcm) Kidney (99Tcm) Thyroid (99Tcm) Bone (99Tcm) Dynamic cardiac (99Tcm) Myocardial perfusion (201Tl)
Typical effective dose (mSv)
Risk of fatal cancer per examination
Equivalent period of natural background radiation
o0.01 o0.01
1 in a few million 1 in a few million
o1.5 days o1.5 days
0.01 0.02 0.07 0.08 0.3 0.7 0.7 0.7 1.3 1.5 2.5 3 3 7 1 2.6 18.9 2 2.6 6 8 10
1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1
in in in in in in in in in in in in in in in in in in in in in in
2 million a million 300,000 200,000 67,000 30,000 30,000 30,000 15,000 13,000 8000 6700 6700 3000 20,000 8,000 1,000 10,000 8000 3300 2500 2000
1.2 days 2.4 days 8 days 1.6 weeks 5.6 weeks 3.2 months 3.2 months 3.2 months 5.6 months 6.4 months 1 year 13 months 13 months 2.6 years 5 months 13 months 6.8 years 10 months 13 months 2.3 years 3 years 3.6 years
0.1 1 1 1 4 6 18
1 1 1 1 1 1 1
in in in in in in in
200,000 20,000 20,000 20,000 5000 3300 1100
2 weeks 5 months 5 months 5 months 2 years 2.3 years 6.7 years
Approximate lifetime risk for patients from 16 to 69 years old: for paediatric patients multiply risks by about 2; for geriatric
patients divide risks by about 5. Australian average about 2.6 mSv/yr: regional averages range from 1.5 to 7.5 mSv/yr.
procedures is 5695, 700 and 413, respectively. There is epidemiological evidence of increased cancer risk with whole body exposures in the range of 10–50 mSv for acute exposures and 50–100 mSv for protracted exposures.13 Many diagnostic CT procedures would come within the former range and for many people a lifetime’s cumulative diagnostic exposure would fall within the latter range. This is shown in the US Scoliosis Cohort Study14 where adolescent females exposed to multiple diagnostic X-rays giving a mean breast dose of 108 mSv in 25 exposures have a statistically significant increased risk for breast cancer.
Although the risks are small the surgeon must justify exposing patients to ionising radiation. If the use is for a specific purpose that gives clinical benefit then that benefit outweighs the risk. If there is no potential patient benefit expected from the investigation then the risk is unacceptable and the investigation should not proceed. This concept determines that many current ‘‘follow up’’ X-rays are essentially for the surgical assessment of specific procedures and appliances and not for individual patient benefit. These X-rays must be considered as research investigations and the patient must be informed of the radiation risk and
ARTICLE IN PRESS 6 local research protocols followed. remembered that though the risk carcinogenesis may be small, if a applied to a large population then health problem could result.
P. Dewey et al. It must be of inducing small risk is a significant
Radiation protection This falls into five areas; a. minimisation of radiation use, b. maximising the distance between the individual and the X-ray source, beam and scatter, c. use of lead screens, d. personal protective garments, and e. monitoring personal exposure dose. These have particular application to the surgeon using image intensification or fluoroscopy in the operating room. In this situation the supervision of the radiation protection of the patient, the staff and the surgeon is the surgeon’s responsibility. Minimising radiation use is enshrined in the ALARA principle of optimisation that radiation dose, both in ordering diagnostic X-rays and in the operating room using the fluoroscope be kept As Low As Reasonably Achievable (ALARA is the acronym). With fluoroscopy the radiation exposure is minimised by careful positioning of the patient as close as possible to the intensifier or receptor, with minimal screening time, the smallest possible field size, the use of image memory facilities and an awareness of the scatter patterns around the fluoroscope. X-rays obey the inverse square law that the intensity of the X-rays (photons per unit area) is inversely proportional to the square of the distance from the X-ray source. This fact is vital to the understanding of radiation protection. The effect is that the exposure received at 2 m from a fluoroscope and beam is relatively minimal and it has been suggested that at distances greater than this, operating theatre staff need not wear lead gowns. However it is recommended that lead gowns be worn by all staff as even at 2 m there is some exposure and it is unreasonable to expect staff in the heat of the moment to always be thinking of their distance from a fluoroscope that may be hidden by the drapes with the direction of its beam being constantly manoeuvred by the surgeon. Lead screens reduce exposure to scatter considerably. They may be mounted on the operating table and hang between surgeon and fluoroscope or ceiling mounted and lowered as appropriate.
Mobile lead screens can be draped and placed between surgeon and beam. A mobile screen can easily be made by hanging a lead gown on the cross arm of a lowered drip stand and draping this as necessary to stand in the operating area. Surgeons should always consider the provision of lead screening with the purchase of new equipment and when consulted on operating theatre design. Personal protective garments are a lead gown, thyroid shield and lead acrylic glasses or head shield. The gown must be ‘‘wrap around’’ with overlap and of 0.5 mm lead equivalence (lead equivalence is the thickness of lead that would have the same absorption properties as the thickness of any other material placed in the path of the radiation beam). Two piece garments with a bodice and skirt are more comfortable but the bodice must overlap the skirt. A thyroid shield must protect the neck. The eyes must be protected by lead acrylic glasses or head shield. These may be made to specific prescription or lead acrylic protective glasses (wrap around glasses or clipons) may be worn over prescription glasses. The thyroid shield and lead acrylic glasses may be replaced by a head shield that has a full lead acrylic visor anchored to the gown or supported by a head band. The visor also acts as a surgical splash protector but has the drawback of being relatively heavy for prolonged wear. Lead gowns must be handled carefully and not thrown down and crumpled as the protective lining will crack and be ineffective. For this reason gowns must be visibly inspected before each wearing and regularly checked by the radiology department and the date of the last check marked on the gown. These inspections should be at least annually and ideally every six months. Protective garments still allow penetration of about 10% of the radiation and even when appropriately protected the wearer should move as far as possible away from the fluoroscope and area of scatter. All personnel exposed to radiation must wear a radiation personal dosimeter in a constant position beneath the protective gown to record any personal dose. Only in this way will one be aware of one’s dose, be able to vary practice if the dose increases and be able to record a lifetime’s work exposure. Ideal monitors are the optically stimulated luminescence dosimeter (OSL) and thermo-luminescent dosimeter (TLD). These must be safely stored away from radiation sources and never shared. The exposure of the patient for each operative procedure should be recorded in the operating note. A special area of radiation protection concerns the sexually active female surgeon and nurse not observing contraceptive precautions. Ideally these females should avoid being part of the ‘‘scrub
ARTICLE IN PRESS Ionising radiation and orthopaedics team’’ when ionising radiation is in use. If this is not practical then maximum protection with a recently tested 0.5 mm lead equivalence wrap around gown is essential and it is critical to maintain the maximum distance from the X-ray source, beam and area of scatter (special 0.5 mm lead equivalence gowns are available with a 1 mm lead equivalence thickness over the foetal area). If such staff are ‘‘unscrubbed’’ in the theatre they must follow the same regime and be made aware that they must be conscious of the position of the X-ray equipment since it may be moved at any time and compromise their safety distance. Once a pregnancy has been discovered these special precautions must be continued until term. Studies of childhood cancer risks following in utero diagnostic exposures conclude that exposures of 10 mSv cause a significant increase in the risk of childhood cancer.15
7
c.
Advice when operating with X-rays Fluoroscopy is essential to orthopaedic surgical practice but the dangers of ionising radiation pose a threat to all staff within the operating room and to the patient. For the staff the danger lies in the insidious cumulative effect of low dose exposure over time. A lack of appreciation of the risks leads to practices that include excessive and inappropriate use of the fluoroscope, poor supervision of junior surgeons often with an unrealistic expectation of their skills and inadequate application of approved protection regimes. The deleterious effects of ionising radiation can be minimised over a surgical career by strict observance of the following guidelines: a. Maximising distance from the energised fluoroscope. Moving away from the energised fluoroscope invokes the benefit of the inverse square law. Simply put, moving from 1 m from the energised fluoroscope to 2 m away reduces the intensity of the X-rays by a factor of four. The radiation exposure is greatest at the X-ray tube or generator end of the C arm and lowest behind the image receptor or intensifier. See Figs. 3–8. b. Decreasing the number and duration of exposures reduces the radiation dose in direct proportion. Correct positioning to anatomical landmarks or surgical features minimises exposure as it eliminates the need ‘‘to screen to search’’ for the desired feature. Once the position of an anatomical landmark has been established it can be marked on the drapes to
d.
e.
f.
g.
give future accurate positioning of the fluoroscope. Correct positioning of the fluoroscope is critical in minimising exposure of the surgeon both from the beam and scatter. It must be constantly remembered that the exposure is greater on the X-ray generator side of the fluoroscope than on the receptor or image intensification side of the fluoroscope. Positioning the image receptor as close as possible to the patient and the X-ray tube as far away as possible reduces primary radiation exposure of the patient and scatter to the surgeon. If more X-rays are needed for better image quality it is important to increase the kV rather than the mA. Increasing the kV increases the energy as well as the intensity of the X-rays allowing more X-rays to reach the receptor. This applies in lateral views of the femoral neck and trochanters when the patient must be on the edge of the operating table or even overhanging the edge to allow the image receptor to be close to the lateral aspect of the patient’s hip. A lead shield suspended from the operating table or ceiling or a mobile shield between surgeon and table gives a further significant reduction in the surgeon’s exposure to scatter. See Fig. 5. A mobile shield can be easily made by hanging a lead gown on the cross arm of a lowered drip stand. It may be sterile draped if appropriate. If the C arm is angled 15–201 with the receptor towards the surgeon the scatter to the surgeon’s head and neck is reduced but the scatter to the assistant on the opposite side is increased and the surgeon and assistant must recognise this and the assistant move away. If the C arm is angled with the image receptor away from the surgeon the scatter to the surgeon increases. See Figs. 6 and 7. The utilisation of image intensifier memory and image storage facilities in preference to further exposures reduces radiation dose. The fluoroscope must not be used as a convenience or expediency over the use of standard X-ray equipment. Intramedullary locked nailing systems are often associated with multiple and long exposures. If marked difficulty is encountered in introducing guide wires it is acceptable and wise to proceed to an open procedure rather than persist with closed manipulation and expose patient and staff to further radiation exposure. With locked nailing systems radiation dose can be reduced by using only one cross locking screw if stability is not compromised.
ARTICLE IN PRESS 8
P. Dewey et al.
Figure 3 With the X-ray generator above the table the maximal scatter is towards the surgeon’s head and neck. Note that the scatter at the generator end of the C arm exceeds that at the receptor end. Compare with Fig. 4.
Figure 4 With the X-ray generator beneath the operating table the receptor can be placed closer to the patient so reducing the primary radiation exposure to the patient. The scatter towards the surgeon’s head and neck is significantly reduced. Compare with Fig. 3.
h. Positioning the patient with airbags rather than water bags will reduce dose and scatter. i. Junior surgeons must be given senior assistance with difficult fractures, as there is evidence that in these situations the unsupervised and
inexperienced surgeon uses excessive exposures.16 The same problem occurs with junior radiographers and the surgeon should ask for senior radiographer supervision when operating on complex fracture patterns such as three and
ARTICLE IN PRESS Ionising radiation and orthopaedics
9
Figure 5 With the receptor close to the patient and with a mobile or table suspended shield the scatter is significantly reduced towards the surgeon. Compare with Figs. 3 and 4.
Figure 6 With the C arm angled 20 degrees with the image receptor towards the surgeon and adjacent to the patient the scatter to the surgeon’s head and neck is reduced. A table suspended or mobile screen would reduce the scatter to minimal levels (see Fig. 5). The scatter to the assistant on the opposite side of the table is increased and the assistant must move away during exposures.
ARTICLE IN PRESS 10
P. Dewey et al.
Figure 7 With the C arm angled 15 degrees with the image receptor away from the surgeon the scatter to the surgeon’s head and neck increases. The position of the generator interferes with the use of a rigid table suspended or mobile screen. The scatter to an assistant on the opposite side decreases but the assistant must utilise full protection methods.
Figure 8 The C arm is positioned to allow the surgeon operative access to the lower limb to insert cross screws to the lower femur or tibia. The closeness of the receptor to the limb and the small volume of tissue minimises radiation dose and back scatter. With real time operative manoeuvring the surgeon must avoid the X-ray beam and use long surgical instruments. A mobile screen in front of the surgeon greatly reduces scatter towards the surgeon (see Fig. 5).
ARTICLE IN PRESS Ionising radiation and orthopaedics
j.
k.
l.
m.
four part trochanteric or segmental femoral fractures. Constant use of high quality and properly maintained protection equipment, both personal and fixed table or ceiling mounted screens. The fluoroscope must never be used inappropriately such as when proudly displaying an anatomically fixed fracture, in real time, to the theatre staff or students. The receptor must not be used as an operating table. The radiation exposure is unacceptable and there is the risk of explosion should the fragile receptor be inadvertently punctured by a drill or other instrument. Constant supervision of radiation practices by senior surgeons and inclusion of ionising radiation and its hazards in the continuing education process.
Cross screwing the lower femur and tibia are scenarios where it is necessary to reverse the C arm and have the X-ray generator on the surgeon’s side and the receptor close to the patient on the opposite side of the limb to allow surgical access to the limb. As the volume of tissue being Xrayed in these cases is relatively small, the back scatter to the surgeon is diminished compared to the torso or hip but the surgeon should stand back during exposures and if it is necessary to have real time operative exposures the surgeon must use the longest possible instruments. Radiation protective gloves are useful in this instance. See Fig. 8.
Code of conduct As ionising radiation is dangerous and can induce cancer every surgeon must have a personal code of conduct for the safe use of the modality. This should encompass recognition of the dangers of radiation, compliance with protection procedures, ensuring staff and patient safety, continuing education and fulfilling all legislated regulations.
Regulations It is beyond the scope of this paper to list the ionising radiation regulations enacted in every country where this paper may be read. Suffice it to say that all surgeons using ionising radiation must be aware of the statutory regulations applicable to their workplace and conform to protection procedures. Ideally professional Orthopaedic
11 Associations should promulgate the local regulations and protection procedures to their members together with a code of conduct governing ionising radiation use. Practice hints
X-rays can have deleterious effects Effects of X-rays have no known safe lower threshold of dose Always wear a lead gown, thyroid shield, lead acrylic glasses and a personal dosimeter in the presence of ionising radiation Use lead or lead acrylic shields and barriers whenever possible Remember the inverse square law and maximise your distance from X-ray generators, beam and scatter Always practice the ALARA principle
Research directions
Non-ionising alternatives for cross screwing
References 1. Dewey P, Incoll I. Evaluation of thyroid shields for reduction of radiation exposure to orthopaedic surgeons. Aust N Z J Surg 1998;68:635–6. 2. Parker LN, Belsky JL, Yamamoto T, et al. Thyroid carcinoma after exposure to atomic radiation. Ann Int Med 1974;80:600–5. 3. Miccoli P, Antonelli A, Spinelli C, et al. Completion total thyroidectomy in children with thyroid cancer secondary to the Chernobyl accident. Arch Surg 1998;133:89–93. 4. Klugbauer S, Lengfelder E, Demidchik EP, Rabes HM. High prevalence of RET rearrangements in thyroid tumours of children from Belarus after the Chernobyl reactor accident. Oncogene 1997;15:2459–67. 5. Mizuno T, Kyoizumi SK, Suzuki T, Iwamoto KS, Seyama T. Continued expression of a tissue specific activated oncogene in the early steps of radiation induced human thyroid carcinogenesis. Oncogene 1997;15:1455–60. 6. ICRP 60. 1990 Recommendations on the International Commission on Radiological Protection, Annals of the ICRP 21 (1–3). Oxford: Pergamon Press; 1991. 7. Rothkamm K, Lobrich M. Evidence for a lack of DNA double strand break repair in human cells exposed to very low X-ray doses. Proc Natl Acad Sci USA 2003; 100(9):5057–62. 8. Upton AC. The state of the art in the 1990s: NCRP report No 136 on the scientific bases for linearity in the doseresponse relationship for ionizing radiation. Health Phys 2003;85:15–22.
ARTICLE IN PRESS 12 9. UNSCEAR. Sources, Effects and Risks of Ionising Radiation. Annex F. Radiation Carcinogenesis in Man. United Nations Scientific Committee on the Effects of Atomic Radiation. E. 88. IX. 7, United Nations, New York, 1988. 10. BEIR V Report. Health effects of exposure to low levels of ionising radiation. Natl Acad Sci. Washington, DC: National Academy Press; 1990. 11. Clarke RH. Managing radiation risks. J R Soc Med 1997; 90:88–92. 12. Berrington de Gonzalez A, Darby S. Risk of cancer from diagnostic X-rays: estimates from the UK and 14 other countries. Lancet 2004;363:345–51.
P. Dewey et al. 13. Brenner DJ, Doll R, Goodhead DT, et al. Cancer risks attributable to low doses of ionizing radiation: assessing what we really know. Proc Natl Acad Sci USA 2003; 100:13761–6. 14. Morin Doody M, Lonstein JE, Stovall M, Hacker DG, Luckyanov N, Land CE. Breast cancer mortality after diagnostic radiography: findings from the US Scoliosis Cohort Study. Spine 2000;25:2052–63. 15. Doll R, Wakeford R. Risk of childhood cancer from fetal irradiation. Br J Radiol 1997;70:130–9. 16. Giannoudis PV, McGuigan J, Shaw DL. Ionising radiation during internal fixation of extracapsular neck of femur fractures. Injury 1998;29(6):469–72.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 13–19
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MINI-SYMPOSIUM: RADIOLOGY FOR THE FRCS (Orth)
(ii) Basic science: magnetic resonance imaging S. McKiea,, J. Brittendenb a
St James Hospital, Leeds Teaching Hospital NHS Trust, Beckett Street, Leeds, LS9 7TF, UK Leeds General Infirmary, Leeds Teaching Hospital NHS Trust, Great George Street, Leeds, LS1 3EX,UK
b
KEYWORDS Magnetic resonance imaging; MRI physics; Orthopaedic; MRI sequences; MRI safety
Summary Plain film radiography is the mainstay of orthopaedic investigation. Magnetic resonance imaging (MRI) is however now being utilised more frequently and reveals pathology that may have been overlooked with the plain film. This paper describes the basic science of MRI. It also describes the most frequently used sequences in orthopaedic MRI, MRI safety, and types of scanner, artefacts and the use of gadolinium. & 2005 Published by Elsevier Ltd.
Introduction
The basic physics of MRI
Plain film radiology has been the mainstay of orthopaedic investigation since the discovery of Xrays but recently Magnetic Resonance Imaging (MRI) has become more widely available, and is now an indispensable tool in the investigation of musculoskeletal pathology. A thorough understanding of MRI physics is not necessary but a background knowledge is useful in order to appreciate why certain sequences are used and to assist in image interpretation. The main sequences used in daily practice are T1 and T2 sequences with STIR (FAT saturation), PD (proton density) and T1 post gadolinium sequences used as ancillary methods depending on the clinical question, with imaging performed in transverse, sagittal and coronal planes according to the anatomical site of interest.
MRI is based on the process of Nuclear Magnetic Resonance, a process involving the absorption and emission of energy by atomic nuclei in the presence of an externally applied magnetic field. Hydrogen proton nuclei are used to generate the image, as they are by far the most abundant nuclei in the body with the greatest concentration in water and lipid molecules. The patient is placed in the MRI scanner and energy is applied in the form of radiofrequency pulses which are designed to match the resonant frequency of hydrogen atoms, which absorb these energy pulses. After each radiofrequency pulse has been applied, the hydrogen atoms re-emit this energy as a magnetic resonance signal which induces a small voltage in a receiver coil placed next to the patient. The hydrogen atoms return to a relaxed state by two mechanisms known as T1 and T2 relaxation which are dependent on molecule size and binding to larger macromolecules. All tissues e.g bone,
Corresponding author. Fife Acute Hospital Trust, Victoria Hospital, Hayfield Road, Kirkcaldy, Fife, Scotland, KY2 5AH, UK.
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ARTICLE IN PRESS 14 marrow, fluid/oedema, tumours, muscle, cartilage, ligaments and tendons have different T1 and T2 relaxation times. This principle is used to detect the emitted energy from the hydrogen atoms after the radiofrequency pulse has been applied by varying the time to detect the signal (TE—time to echo) and the time to apply the next radiofrequency pulse (TR—time to repetition). Liquids have long T1 and T2 values whilst fat has short T1 and T2 values, thus varying the TE and TR can weight the sequences as either T1 or T2. For example, increasing the time to echo and time for pulse repetition will produce a T2 weighting which is sensitive for fluid which accumulates in pathological conditions such as oedema, inflammation infection and in tumours. On T1 weighted sequences fat returns a high signal but the converse is true for fluid. Therefore a region of bone bruising would appear as a region of low signal next to the high signal fatty marrow on T1 sequences but would appear bright on a T2 sequence.
S. McKie, J. Brittenden
Vascular lines Intrauterine contraceptive devices HALO spinal vest Penile prosthesis (compatibility must be checked) Heart valves (compatibility must be checked)
Patients may not tolerate the confined space of the MRI scanner and therefore prior to requesting an MRI it is advisable to ask the patient if they suffer from claustrophobia. Sedation can be administered if there are qualified staff available to supervise but in cases of severe claustrophobia where investigation is paramount and in infants, general anaesthesia can be given provided there is compatible anaesthetic equipment. It is imperative that conscious patients remain still during the examination as motion artefact dramatically degrades image quality.
Types of scanner MRI safety Any ferrous containing object is potentially dangerous within the MRI scanning room unless secure. Hearing aids, jewellery, watches, glasses, prostheses, credit cards and any type of implant should be removed before entering the scanner as they can potentially become a dangerous projectile. Orthopaedic implants including prosthetic joints, pins, rods, screws, nails, clips, plates or K wires are not contraindicated although they significantly degrade image quality with less artefact produced by titanium devices. Objects such as oxygen cylinders or trolleys must not be taken into the scanning suite unless they are MRI compatible. The following objects are contraindicated:
Cardiac pacemakers Implanted defibrillators, neurostimulators and insulin pumps Swan Ganz catheters Orbital metallic foreign bodies (if suspected then X-ray the orbits) Any intravascular coils, filters or stents (some may be compatible) Cochlear implants (possible compatibility) Aneurysm clips (possible compatibility)
The strength of a magnet correlates with image quality although very high field strengths may paradoxically lead to increased artefact. The optimal strength for orthopaedic work is regarded as 1.5 T (Tesla); however 0.5 T low field magnets can be used but image quality may be compromised. Low field strength magnets degrade image quality and lengthen examination time thus further degrading the image by movement artefact. Patients who are intolerant of standard tunnel MRI scanners due to claustrophobia may tolerate an open magnet, which is also suitable for very large patients. These magnets usually generally operate at lower field strengths (Fig. 1). Short bore magnets have also been developed that combine the high field strength and anatomical accuracy of a tunnel magnet with the comfort of an open magnet (Fig. 2). Recently the advent of standing or sitting MRI scanners are available which allow imaging, particularly of spines and weight bearing joints to be performed in more anatomical positions (Fig. 3).
MRI sequences (1) T1—short TR (TRo1000 ms), short TE (TEo60 ms)
The following are MRI compatible:
Surgical clips 6 weeks post procedure Superficial staples
This is a short sequence, which can be rapidly acquired. Anatomical detail and spatial resolution are excellent. Fat, sub acute haemorrhage and
ARTICLE IN PRESS Basic science: magnetic resonance imaging
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Figure 1 Open Magnet MRI. Figure 3 Standing/ Sitting MRI.
Figure 2 Short Bore MRI.
proteinaceous fluid are bright. Fluid is however dark on T1. T1 is good for looking for meniscal pathology and marrow. It is however less good at detecting oedema when either T2 or STIR would be optimal (Fig. 4).
Figure 4 T1 weighted sagittal lumbar spine image. Note that fat is bright and CSF returns a low signal. Marrow is brighter then disk due to its high fat content. Hydrated intervertebral disks should always be darker than bone marrow as.
(2) T2—long TR (TR41000 ms), long TE (TE460 ms) This is a long sequence. Fluid is bright and because most pathological processes involve oedema, it highlights the area of abnormality (Fig. 5).
(3) Proton density (PD)—long TR(TR41000 ms), short TE (TEo60 ms) This sequence is a mix of T1 and T2. The contrast is a function of the number of protons in the tissue
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S. McKie, J. Brittenden therefore fluid can be missed. This technique decreases the signal intensity from fat and strikingly enhances the signal from fluid and oedema. It is therefore a very sensitive tool for detecting soft tissue and marrow pathology. Some centres use a similar technique of fat suppressed T2 sequences. Fat suppression may be used to confirm the fatty nature of a lipoma (Fig. 7).
(5) T2*—gradient echo T2 (TR variable, TE o60 ms, flip angle ¼ 10–801)
Figure 5 T2 weighted sagittal lumbar spine image. The CSF returns a high signal due to its high water content as do the hydrated intervertebral discs.
This is an accelerated T2 sequence. Fluid appears bright as with other T2 sequences. It is particularly good at imaging ligaments and articular cartilage, particularly fibrocartilage such as the menisci and labrum of the hip and glenoid. The images can be acquired in extremely thin 3D volumes making it very useful in assessing small structures such as the ligaments of the wrist and reconstruction is possible in various planes. The sequence is however degraded significantly if adjacent tissues have widely differing magnetic properties such as metal and soft tissue resulting in susceptibility artefact. This phenomenon may however be put to use when looking for subtle haemorrhage which results in a ‘‘blooming artefact’’ due to breakdown products of haemoglobin.
(6) Fast spin (Turbo) echo
Figure 6 Proton density sagittal image of the knee demonstrating a complex tear of the posterior horn of the medial meniscus.
and is intermediate between T1 and T2. PD sequences are most commonly used in the assessment of the menisci as part of routine knee protocols (Fig. 6).
(4) STIR/SPIR—Fat suppressed inversion recovery techniques (TR41000 ms), (TE TE460 ms), (TI time to inversion) ¼ 120–150 ms) The contrast between fat and water is low on T2 sequences as both return a high signal, and
This is an accelerated method of acquiring T2 and PD images, as the normal acquisition time can be lengthy. In general accelerated, fast or ‘turbo’ techniques are utilised routinely for acquiring all sequences. Both T2 and PD sequences can be acquired at the same time, reducing imaging time and therefore decreasing motion artefact. However, on fast spin echo T2 sequences fat remains quite bright and lesions within bone marrow which would also be bright on T2, may be missed. This can be overcome by using fat saturated STIR/SPIR sequences (see section 4, above). In addition, on fast spin echo PD image degradation may result in meniscal pathology not being seen. The degradation in image quality is miniscule but this is offset by the dramatically reduced scanning time compared with standard T2 acquisitions. Metal prostheses obscure anatomy due to susceptibility artefact. Fast spin echo techniques however reduce the artefact and should be employed if there has been previous instrumentation. All sequences however will show artefact to a
ARTICLE IN PRESS Basic science: magnetic resonance imaging
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Figure 7 T1 axial image of the upper arm showing a high signal intramuscular soft tissue mass. The signal is suppressed on the STIR sequence and is diagnostic of a lipoma.
Figure 8 Previous removal of Harrington rods. T1 Sagittal thoracic spine image. The artefact is from tiny remnant metal fragments causing severe image degradation.
Figure 9 Wrist Arthrogram—T1 with fat suppression showing contrast in the mid carpal joint, proximal carpal joint and radiocarpal joint.
lesser or greater extent due to metallic foreign structures (Fig. 8). Gadolinium is a paramagnetic contrast agent that causes tissue enhancement in vascular structures when administered intravenously. Enhancement is best evaluated on T1 sequences and fat saturation may also be used to optimise the enhancement especially when the abnormality is situated within fatty tissue which would also be bright on T1.
It can help discriminate between a cystic or solid mass, viable from necrotic tissue, infection from inflammatory tissue and a recurrent intervertebral disc from postoperative scar tissue. Intra-articular dilute gadolinium is also used in detecting labral tears, meniscal tears in
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S. McKie, J. Brittenden Table 1 Clinical question
Optimal sequence
Bone Marrow Muscle Soft tissue
Fracture Malignancy/mets Injury Malignancy
Tendons/ligaments Menisci Labrum Synovium
Rupture/strain Tear Tear Inflammation
T1, STIR T1, T2* T1, STIR T1, STIR if mass and high signal on STIR then Gadolinium enhancement T1,T2*,STIR T1, PD, T2* Arthrogram T1, T2* Pre and post gadolinium T1
postoperative knees, ligamentous injuries, and osteochondral defects (Fig. 9).
Sequences specific for particular tissues (Table 1) Collagen: Some tissues such as ligaments, tendons and fibrocartilage do not contain free hydrogen atoms to contribute a signal and are therefore dark on T1 and T2 sequences. Structures containing collagen may demonstrate artefactual high signal due to the magic angle effect which occurs when the collagen bundles are orientated at 551 to the magnetic field. It is most prominent in T1, PD and T2*(short TE sequences), but disappears on T2W and STIR (long TE sequences) and can be a problem in particular when assessing the rotator cuff tendons. Marrow: Haemopoietic marrow seen in the paediatric population is brighter than muscle but darker than fat on T1 sequences and therefore must not be interpreted as pathology. STIR and fat suppressed T2 are the optimal sequences for looking for marrow pathology and bone bruising in trauma whilst T1 sequences are used to look for fracture lines which can be missed on T2 owing to the surrounding oedema. Muscle: T1 and STIR are used to depict muscle architecture and localise oedema indicating the site of pathology. Cartilage: STIR or fat saturated fast spin echo T2 are used to assess cartilage. Many MRI scanners have a specific cartilage sensitive sequence which may also be used. Fibrocartilage and hyaline cartilage return a dark and intermediate on all sequences respectively. Menisci are optimally visualised with T1, PD and T2*. The glenoid and acetabular labrum are best seen with T1W post intra-articular gadolinium and T2*.
Table 2 Body area
Sequence
Plane
Knee
SE PD/T2 SE T1 STIR PD SPIR
Sagittal Coronal Coronal Axial
Shoulder
T2 SE T1 T2 SPIR SE T1 STIR
Axial Coronal oblique Coronal oblique Sagital oblique Sagital olique
Ankle
STIR SE T1 T2 SPIR PD T2 SPIR
Coronal Coronal Sagittal Axial Axial
Lumbar spine
T1 T2 T1 T2 7T2 SPIR
Sagittal Sagittal Axial Axial Sagittal
Hip
T1 T2 SPIR T1 T2 SPIR
Axial Axial Coronal Coronal
Synovium: The synovium is difficult to visualise unless it is abnormal where it enhances post contrast administration but is indistinguishable from fluid on T2 and STIR sequences.
Sequence and planes The following sequences and planes are the most frequently used; the site of anatomy and the clinical question determine what protocol is used (Table 2).
ARTICLE IN PRESS Basic science: magnetic resonance imaging Axial, sagittal and coronal imaging are the mainstay, but oblique imaging particularly of the shoulder tendons is useful.
19 suppression. Fat in these cases will then be dark and the images are usually compared with the T1 images pre-contrast to ascertain the degree, if any of enhancement.
How do you determine the sequence from the film? Conclusion When confronted with a series of MRI images, the first thing to do is identify known areas of fluid, for example CSF, hydrated intervertebral discs, the urinary bladder and renal pelvis. If these areas return a high signal, then the image is T2 weighted. If the fluid is bright and the fat is dark then it is most likely a fat suppressed T2 image such as a STIR. If fat is bright and the fluid is dark then it is likely to be a T1 weighted image. PD may be difficult to determine but has intermediate signal fat and soft tissue. The contrast in a PD is not as great. Contrast enhanced scans are usually labelled and are usually T1 sequences with or without fat
Although there have been numerous advances in the number of imaging sequences in MRI, the basic principles still apply. The sequences used are tailored to yield the most amount of information in the shortest time. It is however important that there is good interaction between the orthopaedic surgeon and radiologist so that a succinct answer to the clinical question is achieved by optimising the sequences and planes used. Although the radiologist’s role is to protocol and report the MRI images, with some basic background knowledge the orthopaedic surgeon should be able to appreciate the sequences used and identify pathology on MRI studies, which will benefit them in patient assessment and management.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 20–26
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MINI-SYMPOSIUM: RADIOLOGY FOR THE FRCS (Orth)
(iii) Basic science: computed tomography Dominic Barron Department of Radiology, Leeds Teaching Hospitals, St James’s University Hospital, Leeds LS9 7TF, UK
KEYWORDS Computed tomography; Musculoskeletal; Physics
Summary Computed tomography utilises a rotating X-ray source combined with multiple detectors in the latest scanners. This data can then be processed in numerous ways to provide axial, multi-planar and 3D images for diagnostic purposes. This modality has rapidly developed since its inception in direct relationship to the exponential increase in computer technology with a corresponding increase in its range of applications. & 2005 Elsevier Ltd. All rights reserved.
History Computed Tomography (CT) scanners are a relatively recent invention and their inception and development are closely linked to advances in computer technology. It is therefore not surprising to learn that Godfrey Hounsfield, who is credited with the development of the first EMI CT scanner, also developed the first all transistor computer. He jointly received the 1979 Nobel Prize in Physiology or Medicine in recognition of his pioneering work in this field.
beam to varying amounts, i.e. the denser the tissues in a plane the fewer X-rays will reach the detectors. The multiple measurements from a slice are then taken, and using Fast Fourier Transformations, a map of different density tissues within the slice examined can be produced. This data is then converted into an image for radiological analysis. Dependant upon the scanner up to 3000 levels of attenuation can be demonstrated. The computer arbitrarily assigns a value to various tissues known as the Hounsfield scale:1 Bone +2000 Acute blood 60 Soft tissues 40 Water 0 Fat—100 Air—1000
Principle The underlying principle of CT is to irradiate a slice of tissue from multiple angles measuring the output from the opposite side. Tissues have differing densities and will attenuate the incident X-ray Tel.: +44 0 113 206 5331; fax: +44 0 113 206 4587.
E-mail address:
[email protected].
To generate an image, the computer then assigns a grey scale to the values obtained. Unfortunately, the eye can only appreciate 11 different shades of grey rather limiting what can be viewed. To take
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ARTICLE IN PRESS Basic science: computed tomography
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Figure 1 This is an axial image through the mid-thorax. The window settings have been set to optimally visualise the bones. This demonstrates a posterior left rib fracture. This window setting is also useful to look fro free air and the large left tension pneumothorax is clearly visible displacing the mediastinum to the right.
advantage of the large amount of data available different ‘‘windows’’ are used. For example, in an abdominal CT scan the soft tissues of the abdomen are the most important structures to visualise so the grey scale is arbitrarily centred at a value of 20 with the width of the window being restricted to no more than 200 (Fig. 1). This means that any structure with a number less than 80 will show up as black and any structure registering 120 or above will be white. However, the subtle density differences of the abdominal soft tissues will be well demonstrated.
the patient obtaining data from a single location for processing before moving onto the next point. Various advances on this technique were produced but the next big step forward came with the development of spiral scanning. Instead of the source and detector rotating around a fixed point and then moving down the patient in a stepwise manner, the table moves down during the scan resulting in a ‘‘spiral’’ data acquisition through the volume of interest. The spacing between the spirals directly affects how detailed the scan obtained is. Therefore, the smaller the distance the more detailed the resultant scan. However, the payback is that this limits the volume that can be covered. The radiologist therefore has to balance the choice between the detail and volume.
Different types of CT scanner Single slice Multi-slice The first CT scanners were very slow and limited to examination of the head and brain. Indeed, the scan time for the pre-production scanner was measured in hours and took several days to process with a mainframe computer. The original clinical scanners required a water bath around the area of interest limiting the range of applications. The hardware used consisted of a single X-ray source and a single detector, these were rotated around
The latest leap in technology has been the development of multi-slice technology. This means the use of multiple detectors at the same time vastly increases the amount of data that can be acquired in a single acquisition. It is possible to get a far more accurate representation of the anatomy and reduce the artefact, particularly from metalwork.
ARTICLE IN PRESS 22 From a practical point of view, multi-slice scanners are far faster and it is now possible to scan from the top of the head down to the pubis in a single acquisition taking about 30 s. This means that the previous constraints upon coverage and detail no longer apply. Careful use of this technology has led to a decrease in the dose required for image production; however, because multi-slice scanners are so flexible and fast there is now a trend to scan far larger areas leading to an increase in overall dose for the patient. One of the current challenges in radiology is to optimise the scan protocols to take advantage of the multi-slice technology and at the same time keep the doses reasonable.
Slice thickness Careful choice of scanning parameters, in particular the slice thickness is key to any examination. This equates to the interval between consecutive passes of the scanning beam as this spirals down the patient. Choosing a small slice thickness results in a more detailed examination of the area in question and significantly better quality reformats or 3D models. At first glance, it would seem attractive to perform all CT examinations using the smallest slice thickness possible to obtain the most detailed examination and to facilitate high-quality postprocessing. Unfortunately, the thinner the slice thickness the greater the dose required for a set tissue volume and the greater the data acquired. The increase in dose must then be justified on the basis of what information is required. The result is usually a compromise where the largest slice thickness is used which will allow the relevant pathology to be demonstrated. The volume of data generated can lead to problems of its own. For example, a CT examination of the whole cervical spine using a 1.25 mm slice thickness will generate 180 images not including the reformats. If a slice thickness of 0.625 mm is used although the quality of data is substantially better, this results in 550 images.
Contrast Enhancement All scans have natural contrast, however, difference between soft tissues can be very subtle (Fig. 2). This can be of particular problem when trying to differentiate acute haematoma from the liver and spleen (the most commonly injured solid
D. Barron organ with blunt trauma). Fortunately, there are a variety of ways in which the contrast can be enhanced: 1. Air—as air has a very low Hounsfield number, this is easily identifiable. Air in an abnormal location is pathognomonic for certain conditions, for instance, a pnemoperitoneum indicates a perforation. Air can also be introduced to enhance structure, for example, air per rectum is used to evaluate the large bowel. 2. Intravenous contrast—Iodine containing preparations can be injected. The timing of the scan can then be tailored to assess different structures. An early scan will show arteries and arterial phase filling of solid structures. A slightly delayed scan will show venous anatomy, venous filling of solid structures and to a lesser extent the arteries. For general abdominal examination, the scans are timed to coincide with portal venous filling of the liver as this tends to demonstrate most abdominal organs well. 3. Oral contrast—iodine containing preparations can be taken to more clearly demonstrate the bowel. In the acute abdomen, this needs, ideally, to be an hour before the scan to clearly demonstrate the stomach, duodenum and as much of the small bowel as possible. For oncology scans, the patient takes further oral preparations on the day before to demonstrate the large bowel as well. 4. Rectal contrast—iodine containing preparations can be introduced per rectum to ensure high quality imaging of the large bowel. This is particularly useful where there is pelvic or large bowel pathology. 5. Bladder contrast—the bladder can be filled with contrast enhancing either by performing a delayed scan by which time iodine will have been excreted by the kidneys or by directly filling the bladder with very dilute contrast agent using a urinary catheter. This latter technique is particularly useful in the acute trauma case where there is clinical concern for bladder rupture. 6. Tampons—these are clearly visible and for pelvic pathology are routinely used to clearly define the location of the vagina.
Applications CT has benefited greatly from the exponential development in computer software, and with the
ARTICLE IN PRESS Basic science: computed tomography
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Figure 2 Post-contrast-enhanced axial abdominal image. The aorta (A), IVC (I), spleen (Sp), liver (L) and kidneys (K) are all seen to enhance due to vascular contrast media. Irregular vascular enhancement of the spleen is shown secondary to a Grade 4 splenic laceration.2 The stomach (St) is seen to contain oral contrast media. The free air in the tension pneumothorax is demonstrated displacing the spleen and stomach.
advent of smaller slice thickness it is now possible to post-process the data in a multitude of ways. The most widely used post-processing is MultiPlanar Reformats (MPRs) (Fig. 3). This is the reconstruction of the data into any plane desired although usually this is a sagittal and coronal reformat. Curved reformats are possible and are of particular use for spinal imaging in patients with scoliosis. 3D images (Fig. 4). There are multiple software packages available to produce these images. These either create surface-rendered images or true volumetric images. These used to be considered purely as a toy; however, careful selection of patients means that these can find a place in the interpretation of complex fractures or complex spinal abnormalities to give the surgeon an overview. The only potential problem with these is that there is an inevitable loss of definition associated with this form of post-processing which means that subtle fractures can ‘‘fade away’’ or alternatively be created. A recent development of this principle is the ability to ghost out structures (Fig. 5). For
Figure 3 Sagittal reformat through the ankle demonstrating the distal end of an intra-medullary nail with a multi-segmental fracture of the distal tibia. Note: the lack of artefact secondary to the nail. Prior to multi-slice this imaging was not possible.
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D. Barron examination than endoscopy itself. The main downside to this technique remains the large radiation dose necessary for the investigation; although this is less of a problem in the older patient this does rather limit this application for the younger age group.
Terminology
Figure 4 A 3D surface rendered image of a fracture dislocation of the right hip joint with the femur removed.
Figure 5 The same case as in Fig. 4 with the femur ghosted out to give perspective on the relative positions of the fracture and the femoral head.
example, with acetabular fractures this allows a ghost outline of a femoral head to be maintained to show its relationship to the fracture but with full view of the fracture itself still possible. Virtual endoscopy is a technique which is fast becoming popular as a non-invasive way of looking for luminal tumours. Multiple software packages are available and certainly in frail elderly patients this is far safer and a more patient friendly
There are a number of common misconceptions mainly because of the very fast development in CT technology. Spiral—this describes the underlying technique used and now applies to most scans performed. Therefore, asking for a spiral scan will usually elicit a smile from the radiologist as virtually all scanners now used are these. High resolution—this is limited to a specific type of chest CT examination (Fig. 6). A very thin slice is obtained specifically to look at the lung parenchyma. Only a small number of slices are taken through the lung at 10 mm intervals. This technique is limited to assessing diffuse parenchymal lung disease. The usual misconception is that this provides a detailed look at all of the lungs. If the examination is performed to look for small lung deposits then a more general scan is indicated, as large volumes of lung are not assessed by the highresolution technique. ‘‘A Contrast scan’’—all scans have natural contrast and it is not always necessary to give contrastenhancing agents to make the diagnosis. Part of a radiologist’s job is to understand how to tailor examinations for each patient. A scan is always necessary—the quality of the imaging is so good now that few surgeons are willing to perform a blind operation. It is, however, essential that the patient is not forgotten in this and if they are unstable or if they still need an operation regardless of the scan results, then they should not be delayed just to get a pre-op scan. Every year, patients die in the CT department when they should have been on the operating table and hence the other name for CT Scanners is ‘‘The doughnut of death.’’
Radiation protection CT is a tremendously versatile modality with a wide range of applications and an almost limitless variety of ways in which the data can be manipulated. It is also, by dint of its speed with the new
ARTICLE IN PRESS Basic science: computed tomography
25
Figure 6 High-resolution CT scan of the lungs. This gives high-quality information about the lung parenchyma but provides little information about the mediastinum or bones.
Table 1
CXR Pelvic X-ray CT head CT chest CT abdomen/pelvis
Typical effective dose (mSv)
Equivalent number of chest radiographs
Equivalent period of natural background radiation
0.02 0.7 2.0 8.0 10.0
1 35 100 400 500
3 days 4 months 10 months 3.6 years 4.5 years
multi-slice technology, very quick and is now very much the modality of choice for trauma patients. The major drawback of CT is that it uses ionising radiation to generate the images. This means that it is a legal requirement to justify all investigations as there is the potential to cause harm to the patient. CT unfortunately not only uses ionising radiation but the actual amounts are very high3 (Table 1).
In acute life-threatening trauma, this is easy to justify as for a patient to be at risk of a cancer, they must first survive the life threatening state that they are in. By the same argument, it is easy to justify the initial diagnostic examination in patients undergoing oncological investigation. However, it can be seen that this becomes more difficult to justify when repeat CTs are requested or alterna-
ARTICLE IN PRESS 26 tively whole body CT for minor trauma. This is a particular problem with oncology where a significant number of patients are entered into clinical trials which rely upon regular CT follow-up. Careful choice of areas to scan is important, the pelvis (reproductive organs), the neck (thyroid gland) and the face (orbits) are very radiosensitive and where possible these areas should be avoided. The other factor to balance is the scan parameters. Multi-slice technology now means that there is no real limit on the volume scanned and down to 0.4 mm slices are possible. Unfortunately, the thinner the slice thickness and the greater the volume of tissue scanned, then the greater the dose the patient is subjected to.
Availability A cursory read through of this article will lead the reader to correctly assume that this is one of the key investigations available to the clinician. However, for any diagnostic investigation to be of major benefit, the waiting times for the test needs to be as short as possible. In North America, this is certainly the case with in-patient waiting times measured in hours and out-patient times in days. This is certainly not the case in the majority of UK centres. The US centres achieve this as they operate on fee per service agreements and so the greater the demand the greater the revenue allowing for appropriate increases in staffing and equipment. In the UK, most radiology departments receive a lump sum to provide all their services and although this has steadily increased, few centres have taken
D. Barron account of the massive increase in demand for imaging associated with the technological advances. This leaves most radiology departments now with too few CT scanners and too few staff to operate them and interpret the results. To put this into context, most UK hospitals will have one or two CT scanners, in North America similar size institutions will usually have between six and ten scanners! Until such time, as proper service led agreements become commonplace in the UK, it is difficult to see this changing. The end result is that waiting times in the UK are more usually measured in days for in-patients and months for out-patients.
Summary CT scanning has made dramatic improvements since its inception in the 1970s. It is now the modality of choice for the acute trauma patient with a wide range of software packages available. The challenges, in the UK, are to improve its availability and to address the increasing concern over the dose associated with this technique.
References 1. Hounsfield GN. Nobel award Address. Computed medical imaging. Med Phys 1980;7(4):283–90. 2. Becker CD, Spring P, Glattli A, Schweizer W. Blunt splenic trauma in adults: can CT findings be used to determine the need for surgery? Am J Roentgenol 1994;162:343–7. 3. Making the best use of a department of clinical radiology. 5th ed. The Royal College of Radiologists; 2003. p. 12.
Current Orthopaedics (2005) 19, 27–33
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MINI-SYMPOSIUM: RADIOLOGY FOR THE FRCS (Orth)
(iv) Basic science: ultrasound Kate Colquhoun, Adeeb Alam, David Wilson Nuffield Orthopaedic Centre, NHS Trust, Headington, Oxford OX3 7LD, UK
KEYWORDS Ultrasound; Musculoskeletal; Physics
Summary Ultrasound is the investigation of choice for imaging soft tissue disease, offering resolution significantly greater than CT or MRI. It is low cost and readily accessible allowing dynamic imaging which is particularly useful for assessing musculoskeletal abnormalities. It also allows real-time image-guided interventional procedures including biopsies and injections. & 2005 Elsevier Ltd. All rights reserved.
Basic physics
Transmission of ultrasound
Ultrasound involves the use of very high-frequency sound waves typically in the range of 3–15 MHz. Sound waves over 20 KHz are inaudible to the human ear. Unlike CT, plain X-rays and scintigraphy, ultrasound does not employ ionising radiation.
The ultrasound beam will be produced at a particular frequency, depending on the transducer used. These waves are then transmitted from the probe, through a coupling device ‘gel’ and into the patient. The transmission through the layers can be summarised in the following diagram:
Production of ultrasound The transducer of an ultrasound machine contains a material which has the ability to produce ultrasound waves when an electric current is passed through it. This phenomenon is called the piezoelectric effect. The material can be a crystal, such as lead zirconate titanate (PZT) or a plastic such as polyvinylidine difluoride (PVDF). Each substance has a ‘Curie temperature’ above which the basic structure is destroyed and the piezoelectric property lost permanently. For PZT, this is approximately 350 1C. Therefore, transducers should not be placed in an autoclave.
US Probe Gel Skin Subcutaneous fat Muscle
Corresponding author. Tel.: +44 1865 227257;
fax: +44 1865 227347. E-mail address:
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Bone
28 The density of a transmission substance will determine the velocity and wavelength with which the ultrasound travels through it. At the junction of each interface (e.g. skin and subcutaneous fat) a proportion of the ultrasound waves will be reflected back to the probe and it is these reflected waves which are analysed and converted into a 2D grey-scale image seen on the monitor. The remaining waves are transmitted into the next layer at a different velocity and wavelength. The waves then travel to the next interface where again a proportion of waves are reflected and some are transmitted. This process of transmission and reflection is also occurring at a much smaller level within each layer. For example, the muscle layer contains muscle fibres surrounded by a thin membrane of connective tissue (epimysium) and since these have different densities, a few waves will be reflected back to the probe which is then able to create a detailed image of the muscle. The probe is therefore able to make a detailed 2D image of not only the different tissue layers, but also the finer structures within each compartment, giving a resolution significantly greater than CT or MRI. The superficial structures (e.g. skin and subcutaneous fat) will reflect waves first and will be seen at the top of the monitor. To image deep structures, a lower frequency probe must be used at the expense of resolution. The proportion of waves that are reflected at each junction is determined by the differences in acoustic impedance between the two structures. The acoustic impedance is the product of density of the material and velocity of the sound traveling through it. The difference in acoustic impedance between, say, fat and muscle is not great and so the majority (99%) of sound will be transmitted at a fat–muscle interface and only 1% reflected back to the probe. However, the difference between, say, gas and tissue is very great and less than 0.1% of the waves will be transmitted at this interface. That is why viewing retro-peritoneal structures in an abdomen distended with bowel gas is virtually impossible as all the waves are reflected back. Likewise, the difference in acoustic impedance between soft tissue and the cortex of bone is high and therefore structures beyond the cortex cannot be visualised. The importance of removing air between the ultrasound probe and skin by using a coupling agent can also be explained. If no gel is used, then the difference in acoustic impedance between the probe and an air pocket is so large that all the waves would be reflected and none transmitted into the body.
K. Colquhoun et al.
Doppler effect During ultrasound examination of a stationary tissue (e.g. muscle), the frequency of the ultrasound which is produced by the probe is the same as that which is reflected back to it. The only changes are in the velocity and wavelength, depending on the density of the tissue. However, if the object is moving (e.g. flowing blood in a vessel), the frequency of the waves reflected back would be different to that produced by the probe. This frequency shift will be proportional to the velocity of the flowing blood. If the angle of incidence of the ultrasound beam to the vessel is also known, an equation can be used to calculate the precise velocity. The direction of flow and the velocity can be represented on a colour flow image and duplex scanning is when this colour image is superimposed on a grey-scale image. In normal grey-scale imaging, the angle of incidence of the ultrasound beam should be 901 to optimally view a structure. However, with Doppler imaging, the beam must not be at 901 to the blood vessels otherwise it would not be possible to calculate the shift in frequency. The optimum angle of incidence, which has been shown to give the most accurate measurements of velocity is 601 and the beam can be electronically steered to produce this angle (Fig. 1).
Choice of probe The choice of probe depends on the area being imaged. Probes can vary in frequency, shape and size. Transducer frequency is proportional to the spatial resolution achieved but inversely proportional to the depth of penetration. Most musculoskeletal ultrasound examinations are of relatively superficial structures and a high-frequency transducer (e.g. 10–20 MHz) can be used to give the best resolution. If the depth has to be increased, for example, adult hip examination or intra-abdominal scanning, then the frequency of the transducer needs to be reduced at the expense of resolution. A low frequency transducer is typically 3–6 MHz. Probes also come in different shapes. When a wide field of view is required, for example for abdominal scanning, then a curvilinear probe is used which has a divergent beam and excellent depth of penetration. However, poor gel contact at the curved periphery of the probe, can occasionally be a problem. Most musculoskeletal ultrasound examinations involve localised imaging of an area and rectangular probes are used which provide
Basic science: ultrasound
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Figure 1 Transverse US image of the long head of biceps tendon in the bicipital groove (arrowheads). Angling the US probe obliquely to the long axis of the tendon reduces the reflection of sound giving a dark appearance: an anisotropic artefact (a). Adjusting the angle towards 901 increases the reflected sound giving a bright appearance (b).
uniform linear beam giving excellent resolution but poor depth penetration.
structure. This artefact can be used to diagnose calcific tendonitis.
Common artefacts
Acoustic enhancement Structures containing fluid allow more sound to be transmitted through adjacent structures resulting in an area of increased brightness. Fluid-filled cavities, such as the bladder and cystic lesions will demonstrate this effect. Certain homogeneous mass lesions, for example, neuromas and lymph nodes, which are less echogenic than muscle may also show acoustic enhancement (Fig. 3).
Anisotropy For ordinary grey-scale imaging the angle of incidence of the ultrasound beam needs to be 901 to the target structure to get the best possible image. When this does not happen, an artefact called anisotropy occurs and the target tissue may appear artificially dark and may give the impression of being abnormal. This artefact is a particular problem in musculoskeletal ultrasound where the topography of the body may not allow a perpendicular beam to the target structure and it is commonly seen in tendons curving around a joint (Fig. 2). Reverberation This artefact can occur at strongly reflective interfaces where sound waves are transmitted back and forth between the probe and the interface. The result is a series of strongly echogenic lines separated by short distances. Reverberation is commonly seen at bone surfaces. Acoustic shadowing Strongly reflective structures, such as bone, calculi and gas do not transmit ultrasound beyond them and this is seen as a shadow posterior to the
Limitations of ultrasound Ultrasound is an operator-dependant technique that requires a long learning curve and inexperience can lead to failure to identify an abnormality or misinterpretation. One of the major difficulties is the inability to review another operator’s examination, particularly when only single images are presented and body markers and annotations are not used. The hardware required can be expensive and the cheaper portable machines do not have the quality or resolution for diagnostic imaging. There have been tremendous technical advances in recent years and machines available today are significantly better than those available even 3 years ago. However, not all high-frequency probes and machines are good for musculoskeletal imaging.
30
K. Colquhoun et al.
Figure 2 Extended field of view longitudinal image of the right index finger. The flexor tendons have a bright fibrillar structure where they are perpendicular to the angle of insonation (arrows). Anisotropy of the curved tendons where they are tethered by the annular pulleys (*).
Figure 3 Longitudinal view of the pulp of the index finger tip showing a wood splinter that has stimulated a foreign body reaction with a dark rim of soft tissue oedema (low reflectivity) (a), and increased vascularity on power Doppler imaging (b).
Applications of sonography in orthopaedics Ultrasound provides a safe targeted imaging tool in the investigation of disease of the soft tissues of the musculoskeletal system. The exquisite nearfield resolution lends itself perfectly to interrogation of superficial soft tissue structures such as muscle, tendons and ligaments of the appendicular skeleton. Ultrasound is patient centred with additional information available in the form of an up to date history, clinical examination and dynamic real-time assessment of the tissue under investigation, both at rest and during active or passive movement. More information is available during dynamic examination than in static images. This limits the ability to review someone else’s examination. Musculoskeletal US is a challenging technique to acquire with a long learning curve even for individuals possessing core US skills. Not all US equipment has sufficient near-field resolution for musculoskeletal imaging, which demands advanced and expensive hardware
and software to produce images of diagnostic quality.
Muscle Although limited resolution at great depth, many muscles and their entheses are readily examined using US. The disruption of the normal pennate arrangement of muscle fibres by collections of fluid, haematoma or solid tumour can be demonstrated. In the acute trauma or sports setting, muscle tears can be diagnosed and graded according to severity to predict the clinical coarse and healing time. These are readily followed up with serial US studies. Complications of trauma such as myositis ossificans, fascial herniae, denervation and contractures are also well demonstrated (Fig. 4). A dynamic tool with real time interaction with the patient, US can identify masses that are not seen on MR of resting muscle but become apparent with contraction of the muscle, such as muscle herniae, and chronic scars. Comparison with the
Basic science: ultrasound
31
Figure 4 Acute Achilles tendon tear. Extended field of view longitudinal US image showing a full thickness tear of the Achilles tendon 7 cm from its distal insertion (arrowheads) (a and b). The gap between the tendon ends is shown to reduce with the ankle in equinus (c).
asymptomatic side, and careful respect of the anatomy can diagnose accessory or deviant muscle slips presenting as masses or nerve entrapment phenomena.
Tendons Normal tendon structure: regular tightly packed fibrillar linear arrangement of fibres aligned in the direction of the pull of the muscle. High-frequency (10–20 MHz) linear array probes with compound imaging and Doppler software can be used to define clearly the presence of this normal anatomy and detect sub-millimeter disruptions in the tendon fibres, degenerative clefts, micro-tears and calcification, through to full thickness tears of the tendon. Extended field of view software can be used to display the entire length of the tendon. This makes it easier to demonstrate in a static image the nature and location of disease. In the acute setting, the position and size of the tear can be documented and the function of the tendon can be dynamically assessed in the presence of an incomplete tear or repair. In chronic tendinopathy, the presence of cystic degeneration
and calcification, peritendinous oedema, paratenonitis or synovitis, and neovascular injection of the tendon substance can be easily demonstrated. Care must be taken to identify and adjust for anisotropic artefact as described above. Having said that, anisotropy can be advantageous, delineating a tendon from surrounding structures by tilting the probe and demonstrating that the tendon becomes more or less reflective. This may be used to confirm that the tendon is normal. US soft tissue contrast resolution is far superior to that afforded by MRI, such that US is replacing other methods in the assessment of rotator cuff disease of the shoulder, and tendinopathy of the wrist, ankle and foot (Fig. 5).
Ligaments US is useful when an isolated injury of superficial ligamentous structures is suspected, or dynamic assessment of joint stability is required. Ligaments share a closely packed linear arrangement of fibres offering isometric stability to joints. The collateral stabilisers of the knee, elbow and the medial and lateral ligamentous complexes of the ankle are
32
K. Colquhoun et al.
Figure 5 Schwannoma of the axillary nerve. Grey scale and power Doppler images of a 3 cm well-defined soft tissue mass arising from a thickened axillary nerve (a). The mass has heterogenous reflectivity with solid and cystic areas and foci of calcification (c). There is increased marginal vascularity (b). The nerve fibres divide around the mass. The afferent axillary nerve is seen to be thickened in transverse view (d).
frequently studied with US. A sound knowledge of anatomy is, as always, essential. However oedema, thickening or absence of the ligament can be readily demonstrated with reinforcement of the diagnosis by visualising the joint space opening under gentle dynamic stress.
Joints Although unable to define the deep internal arrangement of large joints, US provides useful information about the superficial supporting tissues of these joints and has a proven record in assessment of smaller joints such as those of the hands and feet. US is sensitive at detecting the presence of joint fluid, and synovitis, and directing diagnostic needle aspiration especially where blind attempts have failed. Recent advances in near field high-resolution technology have been applied to
imaging the relatively accessible metacarpophalangeal and interphalangeal joints of the hands. Early erosion of the articular cartilage and juxta-articular bone can be demonstrated in inflammatory arthropathies where disease-modifying drugs such as anti-TNF agents are being considered. US has practical advantages over MRI for this purpose and has recently become the primary imaging method for such patients.
Soft tissue masses It is much easier to localise a soft tissue mass with the patient present, able to point out their lump. A brief history also reveals important information such as how long it has been there, whether it is painful or growing, any previous trauma, and whether there are any other lumps or other
Basic science: ultrasound relevant medical or surgical history e.g. diabetes or seropositive arthritis. Ultrasound is then used to define the dimensions and morphology of the mass with respect to its surface contour and definition, internal reflectivity, relationship to surrounding structures, and other specific features such as internal calcifications, and vascularity. This process might yield an easy diagnosis such as a simple cyst: a well-defined, clearly marginated lesion containing anechoic fluid (low reflectivity, acoustic enhancement of its deep wall) with no internal vascularity; or a intralipomatous lipoma: a superficial well-defined fat reflectivity mass containing internal striations but no non-fatty solid reflectivity complexity or increased vascularity. The diagnosis may be less obvious in cases with more non-specific features. In these cases, the differential diagnosis may be narrowed by typical location, history or behaviour on follow-up scanning. Correlation with findings of other imaging may be helpful but ultimately a biopsy will be required for tissue diagnosis.
US guided intervention Percutaneous fine needle aspiration, core tissue biopsy or injection of local anaesthetic and corticosteroid are commonly performed interventional musculoskeletal procedures. US is ideally suited to safely guide the needle tip to the correct location for the injection or biopsy, avoiding important vascular or neural tissue. Acquiring the necessary skills requires patience, a respect for anatomy and practice. In US skills courses, chicken fillets are a useful substitute for a volunteer! A common approach to enhance the visualisation of
33 the needle is to keep the angle of the probe surface as near parallel to the long axis of the needle as possible, causing the barrel of the needle to reflect maximum amount of sound. A careful initial US examination is essential to plan the safest, most effective route to the target. The position of the probe and planned entry site of the needle are marked with indelible pen or the impression of the blunt hub of a needle. The skin is prepared with sterilising fluid and drapes. US is used both to direct the placement of local anaesthetic and the subsequent biopsy or injection.
Conclusion Ultrasound is dynamic and patient centered providing a safe, low-cost, targeted imaging tool for the investigation of disease of the soft tissues of the musculoskeletal system. US has many advantages over other cross-sectional imaging techniques with the best available soft tissue contrast resolution, lack of ionising radiation and the potential for realtime guided intervention. There is increasing recognition of these benefits in many clinical centres and the future will see further development of this exciting imaging field.
Recommended reading 1. Van Holsbeeck MT, Introcaso JH. Musculoskeletal ultrasound. St. Louis: Mosby; 2001. 2. McNally E, editor. Practical musculoskeletal ultrasound. Amsterdam: Elsevier; 2004. 3. Farr RF, Roberts PJ, Weir J. Physics for medical imaging. Tindall: Bailliere; 1996.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 34–39
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MINI-SYMPOSIUM: RADIOLOGY FOR THE FRCS (Orth)
(v) Basic science: nuclear medicine in skeletal imaging Michele Callejaa, Adeeb Alama, David Wilsonb,, Kevin Bradleyc a
Nuffield Orthopaedic Centre, Oxford, UK Nuffield Orthopaedic Centre, Headington, Oxford OX3 7LD, UK c John Radcliffe Hospital, Oxford, UK b
KEYWORDS Nuclear medicine; Musculoskeletal; Physics
Summary Radiopharmaceutical agents are used for a variety of diagnostic purposes; their application to musculoskeletal imaging provides a powerful diagnostic tool for the detection and analysis of abnormal bone metabolism. & 2005 Elsevier Ltd. All rights reserved.
Basic physics A stable nucleus is one where the number of protons and neutrons are equal or nearly equal. However, this equilibrium can be disturbed by adding an extra neutron, a process that occurs in a nuclear reactor, or removing a neutron, which occurs in a cyclotron. The resulting nuclide (or isotope) is unstable and will decay to a more stable state by emitting energy (radiation), such as alpha, beta and gamma rays. This process is called radioactive decay and its application in medicine is for both diagnostic and therapeutic purposes. Diagnostic nuclear medicine involves injecting a radioactive agent, intravenously. The agent is then taken up by organs and radioactive decay within the patient begins. Emitted gamma rays have high energy and a significant proportion leaves Corresponding author. Tel.: +44 1865 227337;
fax: +44 1865 227347. E-mail address:
[email protected] (D. Wilson).
the body and can be detected and measured by a gamma camera. The majority of those radiopharmaceuticals used in diagnostic imaging are gamma emitters. A gamma camera is a device that contains crystals that will react to particles of radiation producing a point light source (scintillation). The light is multiplied by a photomultiplier tube and recorded. The images are acquired over a period of time that ranges from a few minutes to half an hour depending on the amount of radiation emitted. The camera is placed next to the patient who will need to remain still for the duration of the study. As radiation is partly absorbed by tissues, it is usually necessary to image the area of interest from different angles and directions in each study. Alpha and beta particles have much less energy and most of the energy will be absorbed by the patient. Radiopharmaceuticals that use alpha or beta radioactive decay as a marker will lead to much higher radiation dose than a gamma-emitting compound. Alpha and beta rays are charged
0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2005.01.009
ARTICLE IN PRESS Basic science: nuclear medicine in skeletal imaging
35
particles which are directly ionising, causing damage to DNA. These particles are therefore potentially more dangerous. However, this property can also be used, under controlled conditions, to target cells (e.g. Y90 synovectomy). Currently, alpha and beta particle emitting agents have no useful role in diagnostic imaging. The most widely used nuclide in diagnostic nuclear medicine is the metastable isotope of Technetium (Tc99m). Its main advantages are that it is a pure gamma emitter and has a half-life of only 6 h which is long enough to perform a diagnostic study such as bone scintigraphy, but short enough to keep patient dose to a minimum. Tc99m can be labelled with a variety of compounds called chelators, which stabilise the nuclide and direct it to the part of the body that needs to be imaged. For example, methyl diphosphonate (MDP) is taken up by osteoblasts and therefore Tc99m-MDP is used for bone scintigraphy. Areas which have higher osteoblastic activity (e.g. metastatic deposits) will therefore take up more isotope and show up as hot areas on scintigraphy. However, a tumour that does not cause significant bone reaction (e.g. multiple myeloma) can be invisible on bone scan. Single-photon emission computed tomography (SPECT) is a tomographic examination achieved by rotating the gamma camera 3601 around a patient who has been injected with a radioisotope. The camera stops at regular intervals (every 61), to detect and measure the gamma ray emissions. Computations allow the construction of an image that represents a slice of tissue in a similar way to a conventional CT scanner. However, compared to CT the resolution and noise are significantly worse. SPECT can improve the sensitivity for detecting small lesions by improving contrast and anatomic localisation compared to planar imaging. Its main applications are in bone scintigraphy, cerebral and myocardial perfusion imaging.
produces two photons of gamma radiation of exactly 511 keV emitted simultaneously at 1801 to each other. This energy is detected and measured by a coincidence camera. Modern machines allow combined PET-CT imaging. This provides attenuation correction improving lesion detection at depth and providing anatomic localisation.
Positron emission tomography (PET) scanning is one of the most recent developments in imaging and although currently limited in availability in the UK, the number of PET scanners is likely to increase rapidly over the next few years. The most widely used nuclide in PET scanning is deoxyglucose labelled with 18Fluorine. This isotope is taken up by metabolically active cells, most avidly by malignant cells. Radioactive decay then occurs with a half-life of 112 min. The radioactive decay produces a positron which is very rapidly destroyed by an electron inside the patient’s body. This interaction
Radionuclide examination of the skeletal system remains a useful diagnostic method. Bone-seeking radiopharmaceuticals are used, most commonly Tc99m-MDP (mono-diphosphonate). The initial accumulation of the technetium-labelled radiopharmaceutical in bone is primarily related to blood supply, although other factors such as the quantity of mineralisable bone, bone turnover, as well as hormonal influences play a part. Factors that may be responsible for greater-thanusual activity are: (1) (2) (3) (4)
Increased osteoid formation Increased blood flow Increased mineralisation of osteoid Interrupted sympathetic nerve supply
The converse is also true. Thus, in cases of cardiac failure and reduced cardiac output, bone scintigraphy may be of poor quality due to reduced delivery of radiopharmaceutical.
The normal study It varies markedly in appearance between children and adults. In the child, areas of active epiphyseal growth are hot’’ on bone scintigraphy. In the adult, skeletal uptake can be somewhat patchy in relation to the patient’s age; the older the patient, and the more osteoporotic, the patchier the uptake is likely to be. In addition, age-related degenerative changes within joints, discs, etc. can lead to foci of increased bone uptake. Areas of tendon insertion, constant stress and osseous remodelling will show increased activity. On the anterior view, there is prominent visualisation of the sternum, sterno-clavicular joints, shoulders, iliac crests and hips. Anterior views are, however, poor at demonstrating posterior structures as the radiation emitted from these areas will be largely absorbed by the body before it reaches the camera. As a consequence, it is important to use different views and to recognise that only those structures within 15–20 cm of the surface will be well visualised. ’’
The basic physics of PET scanning
Bone scintigraphy
ARTICLE IN PRESS 36
M. Calleja et al.
Indications for bone scintigraphy (1) (2) (3) (4) (5)
Detection and staging of metastatic disease Bone pain in patients with normal radiographs Investigation of abnormal X-ray findings Assessment of possible arthropathy Prosthetic joints for signs of infection or loosening (together with MRI) (6) Differentiation between osteomyelitis and cellulitis The principal use of bone scintigraphy is in searching for metastatic disease as it has a high sensitivity for this purpose. Bone scintigraphy typically will demonstrate metastases weeks or months before plain radiography. However, some tumours may produce false-negative bone scintigraphy. This phenomenon occurs most commonly with multiple myeloma deposits. Breast cancer metastases are occasionally cold on bone scintigraphy. Approximately 80% of patients with known malignancy and bone pain will have metastases documented by bone scintigraphy.
The abnormal study (Fig. 1) Most metastases are multiple and relatively easy to detect by scintigraphy. However, in the case of solitary lesions, interpretation may be difficult. A single focus of increased uptake is usually secondary to benign disease. In the thorax, if two consecutive ribs are involved, this is most likely secondary to trauma. However, if multi-focal noncontiguous areas of increased uptake are detected, these are more likely due to metastatic disease. Diffuse involvement of the axial skeleton by metastases can be deceptive; it may look simply like a remarkably good bone scan, with uniform uptake throughout. Closer inspection will show relative lack of renal uptake indicating the excessive bone activity; this constitutes a Superscan’’, and is most commonly due to metastatic prostate carcinoma. When searching for metastatic disease, cold lesions on bone scintigraphy are also important. If the tumour is extremely aggressive and there is disruption to blood supply or if there is significant marrow involvement, then photon-deficient lesions may occur. ’’
Some causes of hot lesions on bone scintigraphy Localised:
Figure 1 Anterior and posterior views of a radioisotope bone scan showing multiple areas of increased tracer uptake throughout the bony skeleton consistent with multiple metastases in a patient with prostate cancer.
Generalised:
Metastatic disease Primary malignant bone tumour (Fig. 2)
Primary hyperparathyroidism Renal osteodystrophy Multiple metastases (prostate, lung, breast) Haematologic disorders
Some causes of cold lesions on bone scintigraphy
Osteomyelitis Trauma including stress fractures, non-accidental injury, loose prosthesis Osteoid osteoma Paget’s disease Fibrous dysplasia Arthritis Locally increased blood flow
Overlying artefact from, e.g. pacemaker, barium, etc. Radiation therapy
ARTICLE IN PRESS Basic science: nuclear medicine in skeletal imaging
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Figure 2 (a) Plain X-ray of the left humerus in a 13-year-old shows an aggressive bone-forming lesion in the proximal humeral diaphysis. (b) Radioisotope bone scan shows an area of markedly increased tracer uptake corresponding to the abnormality seen on plain film. This was biopsied and histology showed an osteosarcoma. The foci of increased uptake in both proximal humeri represent normal activity around the growth plates.
Local vascular compromise, e.g. infarction, early aseptic necrosis Early osteomyelitis Tumour, e.g. Myeloma, plasmacytoma, breast carcinoma
Bone scintigraphy is of limited value in the local staging of primary malignant bone tumours such as osteosarcoma, since the assessment of tumour extent is usually complicated by reactive hyperaemia and thus markedly increased tracer uptake in much of the affected limb. In this situation, MRI is the examination of choice. In the case of benign bone tumours, bone scintigraphy is even less useful since these do not
usually accumulate tracer. The major exception to this is in osteoid osteomas, which demonstrate intense activity at the site of the nidus. Soft tissue uptake On occasion, soft tissue visualisation may be a confusing issue. There are various potential causes for this, the most important being:
Poor radiopharmaceutical preparation Renal failure Urine contamination Tissue infarction Myositis ossificans and other causes of soft tissue calcification/ossification
ARTICLE IN PRESS 38 Amyloidosis Certain soft tissue tumours, e.g. mucinous ovarian, colon, uterine fibroids, hepatic mets.
Use of bone scintigraphy in trauma In general, an examination will be abnormal within 24 h after a fracture, and usually remains active for a length of time, which is variable and agedependant. Typically, bone scintigraphy has been used in the assessment of subtle trauma such as that from stress fractures which are often difficult to identify on plain film, and also in the detection of occult scaphoid fractures. Nuclear medicine studies will only be reliable a few days after the injury as the bone needs time to react to the insult to change in its vascular supply and to alter the metabolic turn over. On the other hand, MRI will detect fractures as soon as they occur and it has greater resolution. For these reasons, MR is superseding bone scintigraphy in trauma. In the case of the suspected non-accidental injury in children, bone scintigraphy is of limited use in excluding areas of increased bone activity that may represent fractures. Interpretation must be cautious, however, in view of the markedly increased activity around the growth plates. Scintigraphy is particularly useful for detecting stress or fatigue fractures, which are among the most common skeletal injuries in physically active patients, when most stress fractures result from repetitive local stress on normal bone that causes excessive bone resorption, collapse of the bony trabeculae, and micro-fracture. Insufficiency fractures result from routine physical stress on a weakened bone (Fig. 3). Osteoporosis, corticosteroid therapy, and metabolic bone diseases are common predisposing factors for insufficiency fractures. In addition to the vertebrae, the sacrum is a common site for an insufficiency fracture that can cause unexplained low-back pain, especially in elderly women with osteoporosis. The bone scintigraphy typically demonstrates bilateral linear uptake in the region of the sacral alae with transverse uptake in the mid-sacrum which appear as an H shape on the posterior image and this is described as a Honda’’ sign. All these lesions may be detected by MRI. ’’
Assessment of joint prostheses In the initial post-surgical period, activity is noted around the prosthesis, although this usually decreases rapidly and returns to normal within 12 months around the hip, and 18 months around the knee. Persistent activity around the tip of the prosthesis may be taken as an indication of loosening. More generalised activity can be due to
Figure 3 Radioisotope bone scan showing markedly increased uptake around the sacrum in a Honda distribution, together with foci of increased uptake in two adjacent lower right ribs. These represent classical sacral insufficiency fractures, together with rib fractures.
infection around the prosthesis. This issue may be studied further by means of labelled white cell scintigraphy which will be positive in the case of infection. However, aspiration of the joint and instillation of local anaesthetic is also an efficient way of detecting sepsis, that will additionally identify the organism and prove that it is the joint that hurts. In many practices, joint puncture has replaced scintigraphy as the primary means of diagnosis in potentially infected prostheses. Use of bone scintigraphy in benign, nonneoplastic disease Paget’s disease of bone classically displays marked increased activity in the involved skeleton. Scintigraphy may be used to search for occult disease but is not normally indicated in the routine management of this condition. Fibrous dysplasia, will be active on bone scintigraphy; therefore the technique may be a useful tool in searching for polyostotic involvement. Diagnosis of osteomyelitis Three-phase skeletal scintigraphy, consisting of a radionuclide angiogram, an immediate post-injection blood-pool’’ image, and 2–3 h delayed images can be used when the diagnosis of osteomyelitis is in question. In these cases, increased tracer uptake will be observed during both the angiographic and the blood pool images at the site of infection. ’’
M. Calleja et al.
ARTICLE IN PRESS Basic science: nuclear medicine in skeletal imaging
39
However, MRI has virtually replaced scintigraphy for this indication.
and Tc99m-hexamethyl propylenamineoxime. Labelled WBCs usually accumulate in areas of infection but not in areas of increased bone turnover. Due to the increasing use of MRI in diagnosing bone and joint infection, WBC imaging is mainly used in the case of suspected multi-focal infection. The delineation of infected prostheses is also a potential use. When the appearance of the white cell scan is controversial, further information may be obtained by performing a marrow scan using technetium labelled with sulphur colloid. This will show up any areas of marrow rests’’ which have been implanted during surgery.
This may be used to identify bone marrow replacement by tumour or locate active sites for biopsy. It has also been used to assess femoral head blood supply. 99mTc-sulphur colloid is used, which localises to marrow since it is phagocytosed by the native reticuloendothelial cells. Again MR is generally the preferred imaging method for tumours and marrow involvement.
SPECT (single-photon emission computed tomography) The development of SPECT has enhanced the contrast resolution of bone scintigraphy by screening out overlying or underlying tissue. This results in improved detection and localisation of small abnormalities, especially in the spine, pelvis, and knees. In some cases, increased activity not clearly seen on the planar images can be definitively demonstrated with SPECT. Tc 99m-MDP is employed, and the use of SPECT makes it possible to generate tomographic, multi-planar images of skeletal structures within the field of view of the camera.
White blood cell (WBC) imaging This examination technique involves labelling the patient’s own WBCs with the radioactive tracer. The agents used most often for labelling are indium
’’
Bone marrow scintigraphy
PET (positron emission tomography) Better diagnosis and follow up of bone and softtissue infections, particularly in joint replacement patients, are major benefits of PET. A patient undergoing a PET scan is injected with the radiopharmaceutical 18-fluorodeoxyglucose about 45 min before the examination. The radiopharmaceutical tracer emits signals which are picked up by the PET scanner. A computer then reformats the signals into images that display the distribution of metabolic activity as an anatomic image. The more metabolic areas show up more brightly on the scan. The most important emerging use of PET in skeletal radiology is in the assessment of metallic implant-associated infection, owing to its superior spatial resolution. The role for PET is, however, limited by the fact that prosthetic joint loosening can give rise to a positive PET scan as can degenerative joint change. WBC scanning is certainly more specific for infection and joint aspiration has a primary role in most cases.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 40–48
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THE FOOT
Sesamoids of the foot R. Anwara,, S.N. Anjumb, J.E. Nichollc a
Registrar, Department of Trauma & Orthopaedics, Kent & Sussex Hospital, Tunbridge Wells, Kent DA6 8DR, UK b Staff Grade Surgeon, Department of Trauma & Orthopaedics, Warrington Hospital, Lovely Lane, Warrington WA5 1QG, UK c Consultant Orthopaedic Surgeon, Department of Trauma & Orthopaedics, Kent & Sussex Hospital, Tunbridge Wells, Kent TN4 8AT, UK
KEYWORDS Sesamoids; Foot; Anatomy; Clinical findings; X-ray findings; Treatment
Summary Sesamoids are inter-tendinous bones and the constant ones are the medial and lateral sesamoids of the first metatarsophalangeal joint. Accessory sesamoids occur elsewhere and are rare. Sesamoiditis, infection, fracture and bipartite sesamoid are the common associated conditions. Treatment should be conservative in the first instance. Sesamoidectomy may be necessary but removal of both big toe sesamoids in contra-indicated. & 2005 Elsevier Ltd. All rights reserved.
Introduction The term ‘sesamoid’, coined by Galen,1 is derived from the flat, oval seeds of Sesanum Indicum, an ancient East Indian plant used by Greek physicians as a purgative.2 Sesamoids occur in the substance of tendons and may be completely or partially ossified or fully cartilaginous bodies. The degree of ossification is responsible for their radiographic presence or absence and the appearance of bipartism.3 The patella, the largest of the sesamoids, ossifies Address for correspondence: 77 Standard Road, Bexleyheath,
Kent DA6 8DR, UK. E-mail addresses:
[email protected] (R. Anwar),
[email protected] (S.N. Anjum),
[email protected] (J.E. Nicholl).
between 3 and 6 years, but the ossification of the sesamoids of the foot occurs quite late. However, the exact timing of ossification is unclear.4 Their function is to modify the direction of muscle action.
Anatomy Some sesamoids are described as ‘constant’, e.g. the sesamoids of the first metatarsophalangeal (MTP) joint contained within the tendons of flexor hallucis brevis, which play a significant role in the function of hallux. The ‘variable’ or ‘accessory sesamoids are often described as ‘accessory’ bones or ossicles. They occur relatively infrequently beneath any weightbearing bone of the foot, especially the lesser metatarsal heads or phalanges and are rarely of
0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2005.01.001
ARTICLE IN PRESS Sesamoids of the foot
41
Table 1 Some examples of constant and accessory sesamoids. Constant sesamoids
Accessory sesamoids
Tibial (medial) sesamoid (I MTP Jt)
Tibialis anterior tendon
Fibular (lateral) sesamoid (I MTPJt)
Tibialis posterior tendon Os trigonum Accessory navicular Os vesalianum Os intermetatarsum
clinical significance except by causing diagnostic confusion! Hence it is important to be able to differentiate them from an acute fracture or injury. (Table 1).
Sesamoids of the first meta-tarsophalangeal Joint The sesamoids of the first MTP joint are the most important sesamoids of the foot as they play a significant role in the function of the hallux. They absorb the majority of the weight of the first ray, protect the tendon of flexor hallucis longus under the first metatarsal head and help to increase the fulcrum of the intrinsic musculature of the first ray to provide a strong plantarflexion force at the first MTP joint.
Anatomy The two sesamoids within the double tendon of flexor hallucis brevis are entirely intratendinous except dorsally, where they articulate with the plantar facets of the first metatarsal head. A crista or inter-sesamoidal ridge separates the two metatarsal facets and provides intrinsic stability to the sesamoid complex. They are connected to the plantar base of the proximal phalanx through the plantar plate and are suspended by a sling-like mechanism formed by the collateral ligaments of the MTP joint and the sesamoid ligaments (Fig. 1) on both the medial and lateral aspects of the MTP joint. The plantar aponeurosis is attached, with the capsule, to the sesamoids. On the medial side of MTP joint, the abductor hallucis tendon inserts into the plantar-medial base of the proximal phalanx as
Figure 1 Metatarsophalngeal (MTP) joint viewed from dorsally showing the intersesamoidal ligament (1), lateral sesamoid (3), medial sesamoid (2), lateral metatarsosesamoid ligament (plantar plate) (5), medial metatarsosesamoid ligament (plantar plate) (4), lateral joint capsule with extension into the distal plantar plate (6), and lateral joint capsule (7) and medial joint capsule that merge centrally with the distal plantar plate.(Reproduced from Coughlin MJ Roger MA. In Surgery of the Foot & Ankle, ed 7, 1999, C.V. Mosby, pp 437–499).
well as medial sesamoid and provides stability. On the lateral aspect, the adductor hallucis tendon inserts into the lateral base of the proximal phalanx and into the lateral sesamoid to provide lateral stability to the sesamoid complex. The intersesamoidal ligament that forms the base of the tendinous tunnel around the flexor hallucis longus tendon connects the two sesamoids. The medial sesamoid is slightly larger, 9 and11 mm in width and 12–15 mm in length. It lies more distal than the lateral sesamoid which is between 7 and 9 mm wide and of 9–10 mm.5
Blood supply Pretterklieber and Wanivenhaus6 described three types of arterial circulation of the sesamoid bone. The type A (52%) is supplied from the medial planter artery and the plantar arch. The less common type B (24%) is supplied predominantly from the plantar arch, and in type C (24%)
ARTICLE IN PRESS 42 circulation was derived from the medial planter artery. Sobel et al.7 showed that the major vascular supply enters the sesamoids from the proximal and plantar aspect, with a minor arterial supply entering through the distal pole of the sesamoids from its capsular attachments. The proximal arterial supply enters via the flexor hallucis brevis supplying one to two thirds of the sesamoid. There is an anastomasis between the proximal and distal supplies. Thus the distal part of sesamoid has the most tenuous blood supply, and this may lead to delayed healing or nonunion after fracture. The number of arterial branches may affect both healing and the incidence of avascular necrosis (Fig. 2).
Common Conditions of the First MetaTarspophalangeal Sesamoids They may be affected by congenital anomaly, arthritis, trauma, infection, osteochondritis and
R. Anwar et al. Table 2
Conditions affecting Sesamoids.
Sesamoiditis Infection Fracture Bursitis Subluxation and Dislocation Bipartite sesamoid Hypertrophied sesamoid Intractable plantar keratosis
sesamoiditis (see Table 2). Additionally the position of the sesamoid is important in the assessment and correction of hallux valgus deformity.
Clinical findings Symptoms and signs arising from the sesamoids of the MTP include pain on direct palpation or on movement of the first MTP joint, restricted range of motion, swelling of the first MTP joint and decreased plantar/dorsiflexion strength. Synovitis of first MTP joint may be noted and sometimes a plantar callosity may be present under the sesamoids. A hallux valgus or varus deformity should be noted as progressive hallux valgus or varus may develop secondary to disruption of the sesamoid by trauma, particularly fracture or following surgical excision. Examination of the digital nerves of the first ray is important to diagnose a compression that may present as isolated neuritic symptoms or numbness; a positive Tinel’s sign may be elicited along the border of the sesamoid.
Radiological examination
Figure 2 (A) The major vascular supply enters the sesamoid proximally. An anastomosis occurs between the distal and proximal surface. (B), The plantar vascular supply to the sesamoid is significant. (Reproduced from Sobel M et al: Foot Ankle 13:359–363, 1992).
Radiological examination is useful in the assessment of sesamoid pathology. However, routine antero-posterior and lateral views provide limited information. The lateral sesamoid is best demonstrated in lateral oblique views (Fig. 3). The medial sesamoid is best seen in medial oblique views (Fig. 4). Often the most useful X-ray is the axial sesamoid view (Fig. 5A & B). Bone scans may demonstrate increased uptake before any significant radiographic change such as sclerosis, fragmentation, or disintegration. The Research committee of American Orthopaedic Foot and Ankle Society8 has proposed a method for the assessment of the degree of displacement of
ARTICLE IN PRESS Sesamoids of the foot
43
Figure 3 Oblique view clearly demonstrate the fibular (lateral oblique) sesamoid.
Figure 4 Oblique view clearly demonstrates the tibial (medial oblique) sesamoid.
sesamoids in hallux valgus deformity on a weightbearing anteroposterior radiograph (Table 3). The classification is helpful in assessing the degree of deformity and correction achieved after metatarsal osteotomies.
hallux. However, in general, the congenital absence of a sesamoid is usually asymptomatic.
Bipartite sesamoid The incidence of this condition is relatively rare and 80% of bipartite sesamoids involve the medial sesamoid.9 It may be difficult to differentiate between a bipartite sesamoid and a fractured sesamoid. It is not clear in the literature whether these bipartite sesamoids, especially if asymmetrical, have a congenital origin or they are actually fracture nonunions. Congenital absence Absence of a medial sesamoid may lead to the development of a progressive post-operative hallux valgus deformity or produce a clawing of the
Distorted or hypertrophic sesamoids and plantar keratosis An irregularity in shape or congenital hypertrophy, especially over the plantar surface may lead to the development of symptomatic plantar keratosis. Subsequent ulceration and chronic osteomyelitis may result. Unrelenting pain with ambulation is the most common presentaion. Diffuse keratosis underneath the head of the first metatarsal is usually associated with a plantar flexed first ray and a cavus deformity. Conservative measures such as a metatarsal pad or custom orthotic device may redistribute the weight and alleviate symptoms. However, in refractory cases, sesamoid shaving and very rarely, sesamoidectomy may be considered. The associated deformities,
ARTICLE IN PRESS 44
R. Anwar et al.
Figure 5 (A) Position of foot and direction of X-ray beam for an adequate sesamoid view. (B) Sesamoid view showing tibial and fibular sesamoids.
Table 3 Grade Grade Grade Grade
0 1 2 3
Classification to assess the degree of displacement of medial sesamoid. No displacement of medial sesamoid relative to the axis of first metatarsal Overlap of o50% of medial sesamoid to the axis of the first metatarsal Overlap of 450% of medial sesamoid to the axis of the first metatarsal Medial sesamoid completely displaced beyond the axis of the first metatarsal
especially in cases of intractable plantar keratosis may also require correction. Fracture Fracture is rare but may occur after significant trauma to the first MTP joint e.g. a fall, sudden
loading of the foot or a crush injury. Pain excacerbated by weight bearing is the predominant symptom. Passive dorsiflexion and plantar flexion of the big toe reproduces the pain. X-rays help in diagnosis but are very often difficult to interpret.
ARTICLE IN PRESS Sesamoids of the foot Orthotic devices and metatarsal pads may help in relieving symptoms. Taping of the first toe to reduce dorsiflexion may also diminish pain. Sesamoidectomy may be necessary if conservative methods fail.
Bursitis Any form of prolonged irritation (cavus deformity, excessive ambulation etc) may result in chronic inflammation of a bursa present under the metatarsal head and sesamoids.10 The treatment is usually conservative. Nerve compression Impingement of either the medial or lateral plantar digital plantar nerve by sesamoids may be the cause of local pain. Occasionally Tinel’s sign may be elicited. The treament is the same as for any other condition involving medial or lateral sesamoids. Arthritis Degenerative arthritis of the first metatarsal sesamoid articulation may present as pain, swelling, erythema and localised tenderness around the joint. This may follow localised trauma, sesamoiditis or chronic conditions like rheumatoid arthritis, psoriasis, diffuse idiopathic skeletal hyperostosis etc. Insoles, metatarsal pads and anti-inflammatory medication are the initial treatment. Resection of the involved sesamoid may be necessary in cases not responding to conservative mangement. Resection of both sesamoids is contraindicated as it disturbs the intrinsic musculature and causes clawing.11 Subluxation and dislocation This is commonly seen in patients with a moderate to severe hallux valgus deformity, especially those associated with pronation of the great toe and medial migration of the metatarsal head. The sesamoids tend to maintain their relationship with the second metatarsal while subluxating or dislocating from the first metatarsal head. The intersesamoidal ridge is eroded in severe cases. Surgical correction of hallux valgus may restore the relationship of sesamoids to the first metatarsal head. The release of adductor tendons and capsular structures may also become necessary. Infection Trauma, plantar keratosis and neuropathic conditions like diabetes, myelodysplasia etc, may lead to
45 the development of chronic osteomyelitis of sesamoids and/or infection of the MTP joint. Pain, especially on ambulation and passive joint movement, localised tenderness with swelling and eryhtema are the presenting clinical features. The symptoms and signs (e.g. reduced sensibility in diabetes) of the underlying cause may also be present. Treatment of the underlying cause combined with conservative measures may help in the initial stages. However, sesamoidectomy with wound debridement and irrigation is necessary in advanced cases. A double sesamoidectomy should be avoided for the reasons mentioned before. Osteochondritis of the sesamoids Local trauma is the most common cause of osteochondritis of the sesamoids. Any injury, causing disruption of the intra-osseus circulation of the sesamoids, may predispose an injured sesamoid to osteonecrosis. Pain and tenderness are localised to the involved sesamoid and the metatarsal head is usually non-tender. A radiological examination may show fragmentation, mottling, flattening and elongation of the sesamoid. However, a bone scan may be required if the X-ray findings are normal and there is a high clinical suspicion of this condition. The bone scan usually shows high uptake without MTP joint involvement. The treatment recommendations are the same as for any chronic disorder of sesamoids. Conservative measures include orthoses, metatarsal pads, antiinflammatory medication. Sesamoidectomy, is reserved for sesamoids showing collapse and fragmentation. Sesamoiditis This condition is more common in teenagers and young adults and in the past has been described as ‘chondromalacia’.12 Dobas and Silver9 defined it as the inflammation of the peritendinous structures involving sesamoids. It may be associated with trauma (dancing, wearing high heels, jumping etc). Surgical excision is only indicated if conservative treatment fails. Subhallux sesamoid or interphalangeal sesamoid It may occur as an accessory bone beneath the head of the proximal phalanx of the hallux. This is related to the substance of flexor hallucis longus tendon and articulates with the interphalangeal joint. It may be associated with a hyperkeratotic lesion. Surgical excision is indicated
ARTICLE IN PRESS 46
R. Anwar et al. Table 4
Treatment of disorders affecting medial and lateral sesamoids.
Conservative
Surgical
1. Reduce pressure Decrease in activity Low heeled shoes Below knee walking cast Custom made insole Metatarsal pad 2. Reduce inflammation Anti-inflammatory medication Steroids (very rarely) 3. Reduce dorsiflexion Taping of hallux
1. Sesamoidectomy Plantar medial or plantar-lateral approach is used depending upon the sesamoid involved. Removal of both tibial and fibular sesamoids should be avoided 2. Shaving of sesamoids — plantar keratosis 3. Fixation of sesamoids — painful non union (rare)13 4. Correction of the underlying condition — hallux valgus
if conservative measures fail to relieve direct pressure (Table 4).
Uncommon sesamoids and accessory bones of the foot Accessory bones of the foot are developmental anomalies that may occur as subdivisions of normal bones or as a separate prominence of an ordinary tarsal bone.14 They may occur bilaterally or unilaterally. In general, their major significance lies in differentiating them from fractures of the adjacent bones.
Os trigonum Rosenmuller15 first described the os trigonum. Shepherd16 initially considered it as a fracture of the posterolateral tubercle of the talus but later realised that it was not a fracture. However, forced plantar flexion may lead to a fracture of the trigonal process of the talus or may cause impingement of the os trigonum against the tibial plafond. This is especially seen in athletes. These symptoms are sometimes referred to as ‘os trigonum syndrome’. Pain may be increased with direct digital pressure around os trigonum. The os trigonum may cause pain in the retrocalcaneal space aggravated by walking. Plantarflexion is the most uncomfortable position of the foot in symptomatic patients. This condition must be differentiated from retrocalcaneal bursitis in which the pain is acute and tenderness is just posterior to the Achilles tendon. X-ray is diagnostic. However, in some cases, especially in those associated with os trigonum syndrome, MRI may give additional information.17
Conservative measures include limitation of activity, casting and anti-inflammatory medication. Local steroids are best avoided due to proximity of the bone to the Achilles tendon. The os trigonum may be excised through a medial or lateral approach18–20 if conservative treatment fails to relieve symptoms.
Accessory Navicular First described by Bauhin,21 this is a congenital anomaly where the tuberosity of the navicular develops from a secondary centre of ossification. It is located on the medial side of the arch of the foot in association with the navicular and has been termed as ‘prehallux’, ‘os externum’, ‘accessory scaphoid’. It has been regarded as a cause of pes planus deformity22 and is occasionally mistaken for a fracture of the tuberosity of the navicular. It is closely related to the tibialis posterior tendon. Children and adults, both may present with symptoms. In children, the symptoms are primarily related to pressure or progressive arch flattening. However, adults usually present with severe tenderness over a prominence on the medial arch following trauma. Radiographs and in some cases bone scan may be helpful. The treatment is initially conservative with a cast, archsupports and sometimes, local steroid injections (Table 5). According to Grogan et al,23 the majority of the symptomatic cases require surgical treatment; excision of the accessory navicular (anteromedial approach) with or without rerouting of tibialis posterior tendon through the navicular (Kidner procedure).24
ARTICLE IN PRESS Sesamoids of the foot Table 5
47
Accessory bones and other uncommon sesamoids of the foot.
Name (s) of the bone
Location/origin
Clinical significance
Os trigonum
Posterior process of talus
Mistaken as a fracture of the posterior process of the talus
Os trigonum syndrome Fracture, when fused to the talus Accessory navicular
Os peroneum
Medial arch of the foot in association with the navicular. Congenital anomaly in which the tuberosity of the navicular develops from a secondary ossification centre
Mistaken for a fracture of the
Substance of the peroneus longus tendon in the ‘calcaneo-cuboid’ region
Mistaken for a fracture Fracture of os peroneum Disruption of the Peroneal longus
tuberosity of the navicular
Pes planus22
tendon Os vesalianum
Proximal to the base of the fifth metatarsal
Differentiation from a frature of the base of fifth metatarsal
Differentiation from a failure of fusion of apophysis of the base of fifth metatarsal or apophysitis Differentiation from os peroneum Os intermetatarseum
Between the base of the first and second metatarsals and medial cuneiform
Associated with Hallux Valgus25 Differentiated from a calcified dorsalis paedis artery, osteophyte or a fracture
Os subtibiale
Inferior to the medial malleolus
Mistaken for a fracture
Os subfibulare
Posterior to the tip of the lateral malleolus
Mistaken for a fracture
Calcaneus accessorius
Lateral aspect of calcaneus just distal to the tip of the lateral malleolus
Mistaken for a fracture
Os calcaneus Secondarius
Dorsal beak of the calcaneus close to the head of talus (antero-medial)
Mistaken for a fracture of the
Posterior aspect of sustentaculum tali
Mistaken for a fracture Pes planus26
Os sustentaculi
Other rare sesamoids that may be mistaken for a fracture are:
Sesamoids of the tibialis posterior tendon Sesamois of the tibialis anterior tendon Os subcalcis Os aponeurosis plantaris Os cuboides secondarium Os talonaviculare dorsale Os supratalare Os intercuneiforme Os cuneo-I metatarsale-II dorsale Bipartite first cuneiform Bipartite navicular
tuberosity of the calcaneus
ARTICLE IN PRESS 48
References 1. Inge GAL, Ferguson AB. Surgery of the sesamoid bones of the great toe. Arch Surg 1933;27:466–88. 2. Hubay CA. Sesamoid bones of the hand and feet. Am J Roentgen 1949;61:493–505. 3. Sarrafian SK. osteology. In: Anatomy of the foot and ankle. Philadelphia: JB Lippincott; 1983. p. 83–7. 4. Williams PL, Warwick R, Dyson M, Bannister LH. Osteology. In: Gray’s Anatomy. New York, NY: Churchill Livinstone; 1989. p. 457–8. 5. Orr TG. Fracture of great toe sesamoid bones. Ann Surg 1918;67:609–12. 6. Petterklieber Wanivenhaus. The arterial supply of the sesamoid bones of the hallux: the course and source of the nutrient arteries as an anatomical basis for surgical approaches to the great toe. Foot Ankle 1992;13: 27–31. 7. Sobel M, Hashimoto J, Arnoczky S, et al. The microvasculature of the sesamoid complex: its clinical significance. Foot Ankle 1992;13:359–63. 8. Smith RW, Reynolds JC, Stewart MJ. Hallux valgus assessment: Report of Research Committee of American Orthopaedic Foot and Ankle Society. Foot Ankle 1984;5(2):92–103. 9. Dobas DC, Silvers MD. The frequency of the partite sesamoids of the first metatarsophalangeal joint. Am Podiatry Assoc 1977;67:880–2. 10. Jahss MS. In disorders of the foot & ankle:medial and surgical management, 2nd ed. Philadelphia: WB Saunders; 1991 pp 1062–1075. 11. Coughlin MJ, Roger MA., 7th ed. C.V Mosby: St. Louis; 1999 pp 437–499. 12. Apley AG. Open sesamoid: a reappraisal of the medical sesamoid of the hallux. Proc R Soc Med 1966;59:120.
R. Anwar et al. 13. Blundell CM, Nicholson P, Blackney MW. Percuaneous screw fixation for fractures of the sesamoid bones of the hallux. J Bone Jt Surg (Br) 2002;84B(8):1138–41. 14. O’Rahilly R. A survey of carpal and tarsal anomalies. J Bone Jt Surg 1953;35A:626–42. 15. Rosenmuller J. De mon nullis musculorum corpus humani varietatibus; vol. 8, Leipzig 1804. 16. Shepherd FJ. A hitherto undescribed fracture of the astralagus. J Anat Physiol 1883;17:79–81. 17. Wakely C, Johnson D, Watt I. The value of MR imaging in the diagnosis of the os trigonum syndrome. Skeletal Radiol 1996;25:133–6. 18. Blake R, Lallas P, Furguson H. The os trigonum syndrome: a literature review. J Am Podiatr Med Assoc 1992;82: 154–61. 19. Hedrick M, Mc bride A. Posterior ankle impingement. Foot Ankle 1994;15:2–8. 20. Wredmark T, Carlstedt C, Bauer H, et al. Os trigonum syndrome: a clinical entity in ballet dancers. Foot Ankle 1991;11:404–6. 21. Geist ES. Supernumerary bones of the foot-a roentgenstudy of the feet of one hundred normal individuals. Am J Orthop Surg 1914;12:403–14. 22. Sella E, Lawson J. Biomechanics of the accessory navicular synchondrosis. Foot Ankle 1987;8:156–63. 23. Grogan D, Gasser S, Ogden J. The painful accessory navicular: a clinical and histopathological study. Foot Ankle 1989;10:164–9. 24. Kidner FC. The prehallux (accessory scaphoid) in its relation to flat foot. J Bone Jt surg 1929;11:831–7. 25. Henderson RS. Os Intermetarseum and a possible relationship to hallux valgus. J Bone Jt surg 1963;45B:117–21. 26. Harris RI, Beath T. Etiology of peroneal spastic flat foot. J Bone Jt Surg 1948;30B:624–34.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 49–58
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TRAUMA
Acute injuries of the extensor mechanism of the knee `, Aleksandar Lesˇic ` Marko Bumbasˇirevic Institute for Orthopaedic Surgery and Traumatology, Clinical Centre, Visegradska 26, Belgrade 11000, Yugoslavia
KEYWORDS Extensor mechanism injuries; Patellar tendon; Quadriceps tendon; Injuries; Patella fractures
Summary Injuries of the extensor mechanism are still a challenge for orthopaedic surgeons. Early accurate diagnosis is important, as the method of treatment and the outcome depend on this. However, other factors include the time since injury, as those treated acutely have a more favourable outcome. Numerous techniques have been described for treating disruption of the quadriceps and patellar tendon. The best results have been obtained by anatomical reconstruction of fresh disruption. For patellar fractures, the best results are reported after anatomical reduction and internal fixation with a tension band, while the worst choice is total patellectomy. & 2005 Elsevier Ltd. All rights reserved.
Introduction Active knee extension is necessary for both standing and walking. However, during these activities, high energy is generated at the knee and the patellofemoral joint, especially during running, jumping and climbing.
Anatomy The extensor mechanism of the knee consists of the quadriceps muscle and tendon, patella and patellar tendon. The quadriceps muscle originates from the pelvic bones (m. rectus femoris from the anterior inferior iliac spine), the anterior surface of the Corresponding author. Fax: +38111 436 388.
E-mail address:
[email protected] (A. Lesˇic`).
femur and the intermuscular septa (m.vastus intermedius, vastus medialis and lateralis) inserting into the patella, with a 2 cm length of quadriceps tendon.1 The patellar tendon is shorter and connects the lower pole of the patella to the tibial tubercle. At maximum flexion, the patella lies deep in the trochlear sulcus (between the femoral condyles). The knee extensor mechanism also consists of the medial and lateral patellar retinaculi, which are reinforced by the fascia lata extension which thickens to form the iliotibial band.1
Mechanism of the injury Since the patella is a subcutaneous bone, without subcutaneous soft tissue, it is susceptible to injury by a direct blow. Other than this, injuries of the
0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2005.01.004
ARTICLE IN PRESS 50 extensor mechanism are caused by an excessively forceful quadriceps tendon contraction. In young healthy individuals it is less likely for a disruption to occur, while it is more probable and common in the old, or in persons with predisposing factors such as renal failure, secondary hyperparathyroidism, diabetes mellitus, rheumatoid arthritis, gout and other metabolic diseases. It may be caused by large doses of corticosteroids or direct steroid injections.2 There have been reports of patellar tendon failure after anterior cruciate ligament (ACL) reconstruction with a patella tendon bone (PTB) graft, when the middle third of the patella has been taken and devascularisation of the remaining patellar tendon occurs.3,4 A patellar fracture can even occur during ACL reconstruction with a PTB graft.5,6 Patellar dislocations can result in patellar osteochondral fractures.7
Fractures of the patella Fractures of the patella occur most frequently in patients between 40 and 50 years of age and they comprise 1% of all fractures.1,8,9 The patella, except on its distal pole, articulates with the femoral trochlea, and during a direct fall on the knee or in dashboard injuries compression forces are generated. Usually, there is a transverse fracture, but longitudinal, as well as avulsion and stress fractures can occur producing a stellate pattern (Fig. 1). The fracture pattern indicates the kind of treatment required.
M. Bumbasˇirevic`, A. Lesˇic` The aim of treatment is to restore anatomically the articular congruity and extension efficency, as well as to permit early knee motion and weight bearing. In the case of gross comminution, the patella must be sacrificed, and a partial or even total patellectomy is performed. In the latter situation, one must be aware of a significant loss of extension strength and anterior knee protection that results.
Clinical findings According to Scuderi, fractures of the patella can easily be overlooked.10 Usually, there is swelling of the soft tissue, while a skin abrasion is present in up to 25% of cases and this can interfere with the timing of surgery and the line of incision.7 If the parapatellar retinacula (medial and lateral) are preserved, there is minimal displacement of patellar fragments and the patient can raise the extended leg (straight leg-raise), indicating the possibility of non-operative treatment. However, in most cases there is disruption of the extensor retinaculum and mild-to-large displacement of fragments exists with a palpable gap and the patient is unable to raise the leg.11 In the presence of a large hematoma, the integrity of the knee joint ligaments must be confirmed (ACL-PCL), since a PCL injury is present in 3% of cases.7 Also a hip examination is necessary, since concomitant fractures of the acetabulum with dislocation of the hip are possible, due to a blow on to the patella with the hip flexed with axial transmission of the forces to the hip joint.
X-ray findings
Figure 1 Scheme for classification of patellar fractures according to the fracture line pattern: (a) transverse, (b) vertical, (c) marginal, (d) comminuted, (e) osteochondral, and (f) sleeve.
Standard conventional antero-posterior and lateral radiographs are mandatory in the evaluation of both patellar fractures and disruptions of the quadriceps or patellar tendon. When there is doubt about the existence of patella bipartita or a tendon disruption, a radiograph of the opposite knee joint is helpful. The accessory ossicle of the bipartite patella is always on the superolateral corner of both patellae. If there is a symmetrical high or low position of the patella, this may just be a patella alta or patella baja. An assymetrical patellar position suggests a tendon injury lesion. CT and/or MRI imaging is useful in the evaluation of chondral and tendon injuries.12,13
ARTICLE IN PRESS Acute injuries of the extensor mechanism of the knee
Classification Fractures with a displacement less than 2–3 mm step-off are considered non-displaced.11 The pattern of the fracture on plain and lateral views, enables a classification, i.e. transverse, vertical, superior or inferior pole and comminution. Besides the AO classification, Insall and Duparc1,5 classified patellar fractures into three groups: Type I—single transverse fracture, type II—comminution of the inferior pole and type III—global comminution or stellate fractures. Types I and III account for 70% of all patellar fractures.1,14
Treatment Non-displaced fractures with an intact, undamaged extensor retinaculum, can be treated non-operatively, with a plaster cast above the knee or a knee brace for a period of 4–6 weeks. Isometric quadriceps contraction exercises are instituted immediately, followed by straight leg raising. Weight bearing is allowed. After 6 weeks in a brace, the knee immobiliser can be unlocked to allow an increasing range-of-motion.10 In displaced patellar fractures surgical treatment is indicated.9,15–18 The necessary surgical technique is determined both by the X-ray picture and the intraoperative finding, i.e. sometimes only during surgery can the degree of comminution or number of osteochondral fragments be determined. This can change the initial plan for the internal fixation of the patellar fracture. There are numerous fixation methods: tension banding,15,19,20 tension band with cerclage,21 fixation of patellar fracture with absorbable sutures in children22 or nonabsorbable sutures in adults,23,24 simple compression by metal wire or hooping, screw fixation, percutaneous cannulated screw fixation assisted by arthroscopy,25,26 external fixation and partial or total patellectomy.7,27 Transverse patellar fractures are fixed internally with a modified tension band, developed by the AO group (Figs. 2a–d). Thus, the modified tension band method of fixation relies on an anteriorly placed tension band (18-gauge wire) that is anchored by two Kirschner (K) wires placed longitudinally and in parallel to align the patellar fracture. The K wires are best introduced into the bone in the retrograde manner through the proximal fragment and after repositioning they should be driven progradely into the distal fragment of the patella. During reposition and internal fixation the knee is placed in 10 degrees of flexion. Once the tension band is placed around and in the front of patella, further knee
51 flexion produces further impaction of the fragments and, according to Wolf’s law, this induces osteogenesis. Prior to closure of the retinacula, it is wise to palpate the articular surface of the patella in order to check whether accurate reduction has been obtained. Also, the knee should be flexed during the operation and the fracture site checked for stability. Both retinaculae are reconstructed and the knee immobilised postoperatively in 20–25 degrees of flexion for a short period. Partial weight bearing is allowed after 4 weeks.11 Ecker modified Magnusson’s technique by adding an anterior tension band.14,15 Lotke and Ecker’s tension band for transverse patellar fracture fixation is recommended by Aglietty and Buzzi.1 Cerclage alone is the only choice when comminution of the patella exists and when patellectomy should be avoided (Figs. 3a–c). In the presence of large fragments, fixation can be done with a cannulated screw. Fixation with screws is also performed when the number of fragments should be reduced, prior to the placement of the tension band. Small fragments, which should not be excised, can be fixed with small K wires, which are cut at the surface level. In cases with patellar comminution, fragments can be put together concentrically by hooping with metal wire. External fixation may be indicated in open patellar fractures.7 Partial or total patellectomy is performed when there is no possibility for reconstruction of the patella. Partial patellectomy is preferable to total excision, with preservation of any kind of bone-tobone contact. In the case of comminution of the proximal or distal pole, the quadriceps or patellar tendon is reattached to the remaining patella bone tissue by per osseous sutures.7,27 The expected outcome of partial patellectomy is increased pressure on the decreased articular surface area. To prevent this, anteriorisation of the patella is preferable, which includes an additionally placed suture secured by a wire (Figs. 4a–d). Also, augmentation and reinforcement with a semitendinosus graft could be performed.7 Favourable to excellent results have been reported in 78–86% of the patients with partial patellectomy.11 Primary total patellectomy is now rarely done, because total patellectomy is a mutilating operation and should be avoided whenever possible. In cases where there is severe patello-femoral arthrosis with pain after internal fixation of a patellar fracture, it is never too late to do the patellectomy. The final result is poor.11,28–31 The aim of total patellectomy is to restore the extensor mechanism without tension. If there is tension on the previous site of the patella, the defect can be closed by a
ARTICLE IN PRESS 52
M. Bumbasˇirevic`, A. Lesˇic`
Figure 2 X-ray picture of a patellar fracture (a,b) and X-ray after internal fixation with two Kirschner wires and a tension band (c,d).
flap from the rectus femoris muscle fascia or, alternatively, the quadriceps tendon can be turned down. Postoperatively, the limb is immobilised in a cylindrical cast for 6 weeks and a prolonged period (up to 2 years) of rehabilitation is mandatory.11 After the patellectomy the pain and discomfort may persist.31 External fixation is recommended for open fractures.7
Complications Complications after patellar fractures include: stiffness of the knee, patella infera, non-unions, malunions, patello-femoral arthrosis.7,11 According
to Aglietti and Buzzi, after the operative treatment of patellar fractures infection occurs in 5% of cases, aseptic pseudarthrosis also in 5%, loss of reduction and deep venous thrombosis in 2.5%, but after total patellectomy the complication rate increases and infection or deep venous thrombosis are recorded in 11% of cases.1 Open fractures of the patella are usually the result of a high-energy trauma and they are associated with gross comminution. After thorough debridement and irrigation, the treatment should include internal fixation or partial patellectomy. Scuderi recommended internal fixation to preserve as much of the patella as possible.10 Other distinct types of patellar fracture are avulsion and stress fractures of the patella,
ARTICLE IN PRESS Acute injuries of the extensor mechanism of the knee
53
Figure 3 X-ray picture of a comminuted patellar fracture (a), treated by hooping with two Kirschner wires and a wire loop (b,c).
especially in children. This can often be inadvertently overlooked. Avulsion patellar fractures are divided into: superior, inferior, medial or lateral avulsion patellar fractures. The superolateral fracture must be distinguished from the patella bipartita, and the inferior one from Sinding–Larsen–Johansson disease, which is common in jumpers.10 Medial and lateral avulsion patellar fractures are osteochondral, and they occur during dislocation of the patella. In the superior pole avulsion fracture, the chondral fragment should be left in place or fixed and not extirpated.10
On the other hand, stress fractures occur mostly in jumpers and running athletes7,32 and they are usually transverse, but vertical ones have also been reported. During knee flexion and quadriceps contraction high forces are generated, which, accompanied by cyclic loading and diminishing of bone strength, results in a stress fracture. Undisplaced stress fractures of the patella can be treated by 4–6 weeks immobilisation, but displaced fractures should be fixed.32 One must keep in mind that stress fractures heal more slowly than acute traumatic ones, and that they can be associated with patellar avascular necrosis.
ARTICLE IN PRESS 54
M. Bumbasˇirevic`, A. Lesˇic`
Figure 4 X-ray picture of comminution of the distal pole of the patella (a,b), treated by partial patellectomy (c,d).
Disruption of the quadriceps tendon Besides patellar fractures, another cause of extensor mechanism dysfunction due to trauma is disruption of the quadriceps or patellar tendon. These are less common than fractures of the patella. In addition to disruption of the tendon adjacent to the patella, disruption can also occur at the musculo-tendinous junction or inside the quadriceps muscle belly itself. Avulsion of m.rectus femoris from the anterior inferior iliac spine is seen on pelvic radiograms. This is not a common injury and it can be treated by rest and analgesics. Surgery is indicated only for competitive sportsmen.
Distally, injuries of the quadriceps muscle belly can occur in the midsubstance. These are commonly misdiagnosed as quadriceps muscle contusions. Actually, the rupture usually occurs in m.rectus femoris and m.vastus medialis.10 Since direct suture of a muscle is quite impossible, during the first 5 days the defect is filled by a sutured iliotibial band or Dacron prosthesis. Rupture of the quadriceps tendon is infrequent and occurs mainly in persons over 40 years old,2,33 while patellar tendon disruptions occur in patients under the the age of 40 years. Ruptures of the quadriceps tendon proximal to the insertion at the proximal patellar pole are palpable, and extension of the knee is impossible. CT, MRI and ultrasound
ARTICLE IN PRESS Acute injuries of the extensor mechanism of the knee are indicated, especially in chronic cases, in order to show any degeneration in the tendon.2,13 Surgery is indicated in most cases of acute and chronic quadriceps tendon ruptures. The history of surgical treatment of extensor mechanism disruptions dates from the time of Gallie. In 1927, Gallie and Le Mesurier10 surgically repaired the quadriceps tendon with a fascia lata graft. Numerous techniques have been described for quadriceps tendon ruptures33,34 ranging from simple sutures with silk, to wire reinforced repairs, autografts, xenografts, allografts and the use of synthetic materials. Even a kangaroo tendon was used for repairs.10,35 McLaughlin proposed two-stage procedures for old ruptures. In acute ruptures, repair can be obtained by an end-to-end heavy suture,2 augmented by sutures passed through drill holes in the patella. A protecting wire which passes through the quadriceps tendon proximally and the tibial tubercle distally according to Muller et al. reinforces the construct13 (Figs. 5a–c). The sutures must be strong enough to permit knee flexion to 90–1201 (checked during the operation), but postoperatively a plaster cast or brace is applied above the knee, with tolerated weight bearing. In chronic disruption of the quadriceps tendon, there is retraction of the tendon tissue by a few centimeters.36 The quadriceps tendon can be lengthened by the Codovilla technique which is a V–Y advancement flap2 (Fig. 6a). If mobilisation of the proximal tissue is insufficient, then the Scuderi technique33 or a tendon graft is employed (Fig. 7). The Scuderi technique can be used to reinforce the suture site both in the tendon allograft and Codovilla flap. Alternatively, reinforcement can be obtained with a protective wire. Postoperatively, the knee is also immobilised in a brace or plaster cast for at least 8 weeks.
Patellar tendon ruptures Patellar tendon ruptures are at the most distal localisation of the extensor mechanism and occur, as mentioned above, in people younger than 40 years. Patellar tendon rupture is a last stage of tendinopathy, because healthy tendons rarely rupture.37 Predisposing factors such as rheumatoid arthritis, diabetes mellitus, chronic renal failure and/or systemic lupus erythematosus, as well as steroid medication are often recorded. The disruption usually occurs at the junction with the lower pole of the patella, and less commonly in the tendon midsubstance. Diagnosis is based on proper
55
Figure 5 Scheme for operative treatment of acute quadriceps tendon rupture (a,b) and a case with wire reinforcement (c).
clinical examination and in particular the patient is unable to raise the extended leg. The patella may be retracted proximally, but when the retinacula are intact, the patella can be undisplaced. Clinical palpation, ultrasound and MRI examinations are sometimes necessary for the correct diagnosis of patellar tendon rupture in order to exclude bone fragments and intra-articular pathology.37 The most useful classification of patellar tendon rupture is that of Siwek, because it recognises immediate versus the delayed diagnosis of rupture.33 In most cases, surgical treatment is indicated, particularly when proximal migration of the patella is evident on lateral radiographs.38
ARTICLE IN PRESS 56
Figure 6 Scheme for operative treatment of chronic quadriceps tendon rupture where distalisation is obtained by a V–Y flap (a,b).
M. Bumbasˇirevic`, A. Lesˇic`
Figure 8 Scheme for operative treatment of patellar tendon rupture: patellar tendon substitution by semitendinosus and gracilis tendon graft—Ecker technique.
Figure 9 Scheme for operative treatment of patellar tendon rupture: patellar tendon substitution by semitendinosus graft—Kelikian technique.
Figure 7 Scheme for operative treatment of chronic quadriceps tendon rupture where the suture site is augmented by a tendon allograft.
Acute patellar tendon ruptures can be treated by end-to-end sutures. Early surgery gives the best results.39–41 The recommended technique is a modification of McLaughlin’s procedure.38 If the tendon tissue is inadequate, then the pull-out technique (through drill holes) through the inferior pole of the patella or tibial tubercle is performed. The suture site can be protected by a wire or PDS, in a similar manner to the quadriceps tendon reconstruction.42
For chronic cases (delayed diagnosis) with proximal migration of the patella, both distal mobilisation of the patella (by Steinam pin placed through the patella, or by V–Y lengthening of the quadriceps tendon) and augmentation or tendon substitution are carried out. The results of the delayed repair are inferior to those of acute repair.37 With a long delay between injury and surgery, the occurrence of quadriceps contracture and proximal patellar migration with fibrosis between the patella and underlying tissue is most likely.37 The patellar tendon can be substituted with semitendinosus and gracilis grafts, according to Ecker43 (Fig. 8), or by a semitendinosus graft only, according to Kelikian and coworkers44 (Fig. 9). In both techniques the graft is pulled through the hole in the distal pole of the patella and through the
ARTICLE IN PRESS Acute injuries of the extensor mechanism of the knee tibial tubercle. As well as traction with a Steinman pin, distal mobilisation of the patella in an old, neglected patellar tendon rupture can be obtained using an external ring fixator.45 In such cases the patella can be mobilised distally by a Z plasty procedure, as recommended by Scuderi. Internal protection of the suture site can be also obtained with LAD, Dacron or PDS-resorbable material.38,42 The timing of patellar tendon repair is the only factor that correlates with the final outcome. Namely, early surgery is the best choice, while rehabilitation in delayed repair is longer and more conservative.37 Complications include shortening, flexion limitations, decreased quadriceps strength, as well as secondary ruptures and wound infection.37 Finally, the extensor mechanism can be disrupted at the distal tubercle level, an avulsion fracture of the tibial tuberosity. This type of injury may be associated with pre-existing Osgood Schlatter disease. Avulsion of the tibial tubercle is most commonly seen in adolescents (ages 12–17)10 and in 50% of cases the patients are jumpers. The avulsion can be palpated under the skin and a peak can be seen on the lateral radiograms. Operative treatment is suggested for types 2 and 3 of displaced tibial tubercle fractures according to their classification (Ogden type 1,2,3).10
References 1. Aglietty P, Buzzi R. Fractures of the patella. In: Insall JN, Windsor RE, Scott NH, Kelly MA, Aglietty P, editors. Surgery of the knee. New York, Edinburgh, London: Churchill Livingstone; 1993. p. 1085–102. 2. Lobenhoffer P, Thermann H. Rupture of quadriceps tendon. Duparc J, editor. Surgical techniques in orthopaedics and traumatology, vol. 8. Paris, Amsterdam, New York, Oxford: Elsevier; 2002 55-500-C-10. 3. Bonatus TJ, Alexander AH. Patellar fracture and avulsion of the patellar ligament complication arthroscopic anterior cruciate ligament reconstruction. Orthop Rev 1991;20: 770–4. 4. DeLee JC, Craviotto DF. Rupture of the quadriceps tendon after the central third patellar tendon anterior cruciate ligament reconstruction. Am J Sports Med 1991;19:415–6. 5. Miller MD, Nichols T, Butler CA. Patella fracture and proximal patellar tendon rupture following arthroscopic anterior cruciate ligament reconstruction. Arthroscopy 1999;15(6): 640–3. 6. DuMontier TA, Metcalf MH, Simonian PT, Larson RV. Patella fracture after anterior cruciate ligament reconstruction with the patella tendon: a comparison between different shaped bone block excisions. Am J Knee Surg 2001;1481: 9–15. 7. Neyret P, Ait Si Slmi T, Rongieras F. Fractures of the patella. Duparc J, editor. Surgical techniques in orthopaedics and traumatology, vol. 8. Paris, Amsterdam, New York, Oxford: Elsevier; 2002 55-500-D-10.
57 8. Ray JM, Hendrik J. Incidence, mechanism of injury and treatment of fractures of patella in children. J Trauma 1992; 32:464–7. 9. Bostrom A. Fractures of the patella. Acta Orthop Scand 1972;143(suppl):1–80. 10. Scuderi GR. The patella. New York, Berlin, Heidelberg, London, Paris, Tokyo, Hong Kong, Barcelona, Budapest: Springer; 1995. 11. Cramer KE, Moed BR. Patellar fractures: contemporary approach to treatment. J Am Acad Surg 1997;6(6):323–31. 12. Apple JS, Martinez S, Allan NB. Occult fractures of the knee—tomographic evaluation. Radiology 1983;148:383–7. 13. Kuvila TE, Brems JJ. Diagnosis of acute rupture of the quadriceps tendon by magnetic resonance imaging. A case report. Clin Orthop 1991;262:236–41. 14. Lotke PA, Ecker ML. Transverse fractures of the patella. Clin Orthop 1981;158:180–4. 15. Muller ME, Allgower M, Schneider R, Willenneger H. Manual of internal fixation, 3rd ed. Berlin: Springer; 1991. p. 564–567. 16. Lhowe DW. Fractures of the patella. In: Siliski JM, editor. Traumatic disorders of the knee. New York, Berlin: Springer; 1994. p. 159–68. 17. Weber MJ, Janecki CJ, McLeod P, Nelson CL, Thompson JA. The effect of various forms of internal fixation in patella fractures. J Bone Jt Surg 1980;62A:215–20. 18. Carpenter JE, Kasman R, Matthews LS. Fractures of the patella. J Bone Jt Surg 1993;75A:1550–62. 19. Mehdi M, Husson JL, Polard JL, Ouahmed A, Poncer R, Lombard J. Treatment results of fractures of the patella using pre-patellar tension wiring. Analysis of series of 203 cases. Acta Orthop Belg 1999;65(2):188–96. 20. Wu CC, Tai CL, Chen WJ. Patellar tension band wiring: a revised technique. Arch Orthop Traum Surg 2001;121(1–2): 12–6. 21. Fortis AP, Milis Z, Kostopoulos V, Tsantzalis S, Kormas P, Tzinieris M, Boudouris T. Experimental investigation of the tension band in fractures of the patella. Injury 2000; 33(6):489–93. 22. Sturdee SW, Templeton PA, Oxborrow NJ. Internal fixation of a patella fracture using an absorble suture. J Orthop Trauma 2002;16(4):272–3. 23. Gosal HS, Singh P, Field RE. Clinical experience of patellar fracture fixation using metal wire or non-absorbable polyester—a study of 37 cases. Injury 2001;32(2):129–35. 24. Patel VR, Parks BG, Wang Y, Ebert FR, Jinnah RH. Fixation of patella with braided polyester suturey: a biomechanical study. Injury 2000;31(1):1–6. 25. Makino A, Aponte-Tinao L, Muscolo DL, Puigdevall M, CostaPaz M. Arthroscopic-assisted surgical technique for treating patella fractures. Arthroscopy 2002;18(6):671–5. 26. Tandogan RN, Demirors H, Tuncay CI, Cesur N, Hersekli M. Arthroscopic—assisted percutaneous screw fixation of select patellar fractures. Arthroscopy 2002;18(2):156–62. 27. Andrews JR, Hughston JC. Treatment of the patella fractures by partial patellectomy. South Med J 1977;70:809–13. 28. Sutton FS, Thompson CH, Lipke J, Kettlekamp D. The effects of patellectomy on knee function. J Bone Jt Surg 1976;58A: 537–40. 29. Einola S, Aho AJ, Kallio P. Patellectomy after fracture. Longterm follow-up results with specific al reference to functional disability. Acta Orthop Scand 1976;47:441–7. 30. Jakobsen J, Christinsen KS. Rasmussen OS. Patellectomy. A 20-year follow-up. Acta Orthop Scand 1985;56:430–2. 31. Peeples RE, Margo MK. Function after patellectomy. Clin Orthop 1978;132:180–6.
ARTICLE IN PRESS 58 32. Teitz CC, Harrington RM. Patellar stress fracture. Am J Sports Med 1992;20(6):761–5. 33. Siwek CW, Rao JP. Ruptures of the extensor mechanism of the knee joint. J Bone Jt Surg 1981;63A:932–7. 34. Kelly DW, Carter VS, Jobe FW. Patella and quadriceps tendon ruptures—jumper’s knee. Am J Sports Med 1984;12:375–80. 35. Larsen L, Lnd PM. Ruptures of the extensor mechanism of the knee joint. Clin Orthop 1986;213:150–3. 36. Lobenhoffer P, Thermann H. Quadriceps and patellar tendon ruptures. Orthopade 2000;29(3):228–34. 37. Matava MJ. Patellar tendon ruptures. J Am Acad Surg 1997;4(6):287–96. 38. Hertel P. Rupture of the patellar tendon. Duparc J, editor. Surgical techniques in orthopaedics and traumatology, vol. 8. Paris, Amsterdam, New York, Oxford: Elsevier; 2002 55500-E-10. 39. Enad JG. Patellar tendon ruptures. South Med J 1999;92(6): 563–6.
M. Bumbasˇirevic`, A. Lesˇic` 40. Marder RA, Timmerman LA. Primary repair of patellar tendon rupture without augmentation. Am J Sports Med 1999;27(3):304–7. 41. Ong BC, Sherman O. Acute patellar tendon rupture: a new surgical technique. Arthroscopy 2000;16(8):869–70. 42. Kasten P, Schewe B, Maurer F, Gosling T, Krettek C, Weise K. Rupture of the patellar tendon. A review of 68 cases and a retrospective study of 29 ruptures comparing two methods of augmentation. Arch Orthop Trauma Surg 2001;121(10): 578–82. 43. Ecker ML, Lotke PA, Glazer RM. Late reconstruction of the patellar tendon. J Bone Jt Surg 1979;61A:884–6. 44. Kelikian H, Riashi E, Gleason J. Restoration of quadriceps function in neglected tear of patellar tendon. Surg Gynec Obstret 1957;104:200–4. 45. Lhowe DW. Extensor mechanism disruption. In: Traumatic disorders of the knee. New York, Berlin: Springer; 1994. p. 169–174.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 59–67
www.elsevier.com/locate/cuor
ARTHROPLASTY
The outcome of total hip and knee arthroplasty in diabetics Peter K.H. Chan, Ivan J Brenkel, Joseph Aderinto Department of Orthopaedics, Queen Margaret Hospital, Whitefield Road, Dunfermline, Fife KY12 0SU, UK
KEYWORDS Hip arthroplasty; Knee arthroplasty; Diabetes; Outcome; Infection
Summary Patients with diabetes have a higher rate of deep infection.22–26 The routine use of prophylactic antibiotics, antibiotic loaded cement and a modern operating environment, however (laminar air flow with or without clean air) should make the risk less significant.27 In addition extra care should be taken on handling of the skin (especially around the knee) and the appropriate sutures and suturing technique adopted. The rate of aseptic loosening is higher in diabetic patients and is most likely due to the neuropathy in these patients. The patients and surgeon should be aware of this increased risk. & 2005 Elsevier Ltd. All rights reserved.
Introduction Total hip arthroplasty (THA) and total knee arthroplasty (TKA) are among the most common major operations performed by the United Kingdom (UK) National Health Service (NHS). The numbers, both in the NHS and private healthcare sector, have soared over the last 10 years and are expected to continue rising over the next 25 years.1 One of the key reasons is due to an increasing aged population. The prevalence of diabetes mellitus is also rising. It is estimated that currently 1.4 million in the UK suffer from diabetes with a further 1 million undiagnosed, ‘the missing million’2 i.e. approximately 4% of the population. This is expected to Corresponding author.
E-mail address:
[email protected] (P.K.H. Chan).
rise over the next decade. Worldwide over 150 million have diabetes, expected to rise to 300 million by 2025.3 The majority of this increase will be in the developed nations including the United Kingdom. This reflects unhealthy diet, obesity, sedentary lifestyle and the population ageing.2 Overall diabetes is a global health problem that is expected to present one of the 21st century’s biggest medical challenges.3 It follows from these figures that the number of THAs and TKAs performed in diabetics will also increase substantially but as yet very little has been reported about the outcomes and complication rates of THAs and TKAs performed on this particular subset of arthroplasty patients. In this paper we shall discuss briefly trends in total hip and knee arthroplasty and the epidemiology and pathophysiology of diabetes before reviewing the literature
0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2005.02.010
ARTICLE IN PRESS 60 on the outcome of diabetics undergoing THA or TKA with particular reference to infection.
P.K.H. Chan et al.
Risk factors for the development of diabetes
Trends in total knee and hip arthroplasty
THA and TKA are cost effective treatments for disability secondary to joint arthroses, reducing pain, increasing mobility and improving quality of life. In the NHS alone more than 43,000 primary THAs4 were performed last year. This figure has risen from 32,000 in 20004 and that figure is expected to rise by a further 22% to 53,000 by 2010. TKA is also on the increase. Between 1991 and 2000 the incidence of primary TKA has more than doubled and that figure is expected to increase from the 2003 figure of 35,000 primary TKAs by 60% to 56,000 by 20105 overtaking hip replacements as the most common primary arthroplasty operation. Similar trends have been reported in Australia, USA and Scandinavia.5–9 The greatest increase in rates of primary THAs and TKAs have been in those aged 55–64 and in those over 80 with a growing number in the over 85s.1 Undoubtedly, as surgical and anaesthetic techniques and outcomes improve, even more elderly people will undergo THA and TKA. Increasing age is a risk factor for the development of diabetes and thus this group of elderly patients (over 85s) will have a higher prevalence of diabetes than the population in general. Risk of adverse outcomes of THAs or TKAs in the diabetic population may be amplified in a fragile group of patients.
Epidemiology and pathophysiology of diabetes Diabetes is already a global health problem likely to increase markedly over the next 25 years. In 1985, an estimated 30 million worldwide had diabetes. That figure today is over 150 million with the projected number to be over 330 million in 2025. Prevalence is higher in developed countries, but is projected to rise in both developed and developing countries.3 In the UK the number of people diagnosed with diabetes is around 1.4 million with a further 1 million thought to have undiagnosed diabetes.2 It is characterized by abnormal glycaemic control either as a result of insulin deficiency (Type 1) or insulin resistance of the peripheral tissues (Type 2). By far the most common is Type 2 diabetes, which account for 85–95% of all diabetics.
Age: Prevalence of diabetes increases with age, with an average age of diagnosis at 51 years.2 Obesity: As a nation, the UK is increasingly overweight and less active, which is associated with an increase in diabetes. Familial: Type 2 diabetes tends to run in families. One study2 showed that in newly diagnosed with Type 2 diabetes between the ages of 25 and 65, almost half (41%) had a close relative with diabetes. Ethnic: Diabetes is 3–5 times more common among people of African-Caribbean and Asian origin living in the UK.
Complications of diabetes Most of the common complications of diabetes (retinopathy, nephropathy, coronary heart disease, peripheral vascular disease, foot disease and peripheral neuropathy) are mediated by changes to the structure of small to medium blood vessels. Experimental studies have shown defects in the host-defense mechanisms of diabetics including impaired leucocyte function specifically phagocytosis.10 The adverse affects of hyperglycaemia on fracture healing and bone remodeling have also been well demonstrated in experimental and clinical studies.11–13 More recently it has been recognized that diabetes causes changes in collagen metabolism with the net result of increased collagen cross-linking, changing the chemical and mechanical behaviour of this tissue.14 All these factors may be implicated in the recognized higher rate of surgical wound complications reported in diabetics. The ratio of HbA1c (glycosylated haemoglobin), expressed as a percentage, relative to the normal (unglycosylated) haemoglobin should be less than 5 in normal individuals. This ratio used as a measure of glycaemic control. Although a useful measurement to estimate glycaemic control over a period of time, there is no evidence in the literature to our knowledge that correlates poor diabetic control with poorer outcomes after THAs and TKAs. The duration of diabetes from onset is the single most important factor related to the development diabetic complications and it is these complications that may affect outcome from this type of surgery.
ARTICLE IN PRESS The outcome of total hip and knee arthroplasty in diabetics
Total hip and knee arthroplasty in diabetics When undertaking total hip and knee arthroplasty in diabetics it is important that patients are carefully managed. We have established guidelines and summarize the key points from the protocol used in our hospital below. The aims of diabetic care in patients undergoing surgery are to avoid hypoglycaemia and ketoacidosis. At the pre-assessment stage, in addition to the normal tests and examinations, we document whether non insulin or insulin-dependant diabetes mellitus (NIDDM or IDDM) and ascertain recent glycaemic control by measuring HbA1c. IDDM and patients with poor glycaemic control may well need more intensive monitoring during the perioperative phase. Patients should be admitted a day before surgery and all routine blood investigations repeated. An insulin sliding scale is commenced 2 h before surgery, the patient should be operated first on the list and the sliding scale continued until the patient is alert and able to eat, or glucose levels are stable, after surgery. Otherwise postoperative care is the same as for any other patient undergoing this form of major surgery.
Total hip arthroplasty in diabetics The literature suggests the diabetic patients undergoing THA have an increased risk of infection.15,16 However most authors reviewed overall risk factors in patients undergoing THA and, to the authors knowledge, only two papers have looked at the outcome of THA in diabetics.17,18 In a retrospective review of 44 patients who between them underwent 66 Charnley low-friction arthroplasties (LFA) from 1967 to 1980, Menon et al.17 showed that diabetics had a higher rate of wound complications and deep infection. It must be stressed that even though the Charnley clean-air enclosure was used, prophylactic antibiotics were not. Prophylactic antibiotics are now established practice during THAs and have been shown to significantly reduce the rate of deep infection. This may explain the higher reported rate of deep infection in this study. Moeckel et al.16 reported a retrospective analysis of 81 THAs in 69 patients. Patients with rheumatoid arthritis and other inflammatory arthritis (1 hip) were excluded to better assess the outcome in those diabetic patients with diagnoses of osteoarthritis. They used the Hospital for Special Surgery Hip Rating System19 and radiographically (by
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Johnston et al.19). Revision for whatever reason was considered a failure, and the clinical results were classed as poor. The mean follow up period was 4.1 years, (range 2–6.5 years). The mean preoperative HSS hip score was 16 while the mean postoperative HSS hip score was 35. Sixty-three THAs were rated as excellent, 15 as good and 3 as poor. All 3 poor hips were revised (revision rate of 3.7%). There were no cases of deep or superficial infection. Three revisions were performed for aseptic loosening or recurrent dislocation. Radiolucencies were documented around 3 stems (3.7%) and 18 cups (22.2%). Only one stem and one cup were revised for aseptic loosening. As with other studies they reported a high rate of perioperative complications including UTI (10 patients), MI (5 patients), DVT (2 patients) giving an overall incidence of 24.3% for medical complications. We looked at 1247 non-diabetics and 82 diabetics prospectively over 6 years20 with at least 3 years follow up, average 3.6 years. At a pre assessment clinic 7–10 days preoperatively, height, weight, body mass index (BMI), medical history, SF 36 and Harris hip scores were recorded. All patients were treated in the Victoria Hospital, Kirkcaldy, Fife in an operating theatre equipped with vertical laminar flow with ultra clean-air. All patients had 1 g cetriaxzone on induction of anaesthesia or gentamicin if allergic and had a cemented prosthesis implanted using gentamicinloaded cement (Palacos). Low molecular weight heparin (Dalteparin 5000 U) was continued until discharge. Patients were reviewed at a dedicated hip clinic by an audit nurse at 6,18 and 36 months post operatively. Data was collected on the rate of deep and superficial infection. Superficial infection was defined as either clinical erythema and/or oedema of wound and/or persistent wound drainage with or without a positive swab result. Deep infection was defined as either a positive aspirate from the hip, or where a second procedure has been performed which clinically indicated infection. Deep infection was further subdivided into early deep infection (within 3 months of operation) or late (after 3 months). Other complications such as dislocation and loosening were noted. There was no significant difference with respect to age, sex and diagnosis between the two groups but diabetic patients did have a significantly higher BMI (30.2 vs 27.7, Po0.001) and higher incidence of coronary artery disease (31% vs 15%, Po0.001 (Table 4). There was no increase in the rate of deep periprosthetic infection, superficial infection, dislocation, blood loss and DVT between diabetics and
ARTICLE IN PRESS 62
P.K.H. Chan et al.
non-diabetics even after adjusting for potential confounders of age, sex, diagnosis, BMI and the presence of coronary artery disease and there was no difference in the outcome in IDDM and NIDDM. However diabetic patients had a longer in patient stay following THA, (10.7 days vs 9.6 days). This is similar to the findings of Forrest et al.21
common sense approach of treating any superficial infection aggressively should be adopted. Other factors are also important. Meticulous skin handling, minimizing trauma to the tissues, using mono filament nylon and interrupted sutures also plays an important role in reducing the rate of wound complications in all patients undergoing TKA.34
Conclusions While a number of publications have shown an increased risk of infection in diabetic patients undergoing THA,16,18 they did not look specifically at diabetic patients.19 There is only one recent publication looking specifically at diabetic patients.19 Taken together these papers suggest that with modern techniques, there is no increased risk of infection. Our findings20 confirm this view. However, Moeckel et al.19 did show a high radiographic loosening rate. This may suggest that diabetic patients may be prone to early loosening. More research is needed in this area, in particular longer follow up studies. We plan to continue monitoring our cohort of diabetic patients.
Deep infection There are many factors that may influence the development of deep infection including bacterial virulence, the host’s ability to eliminate infection and the wound environment. The use of prophylactic antibiotics in reducing the rate of deep infection is well established,34 but laminar flow, ultraclean air and body exhaust suits and their relative risk reduction in decreasing the rate of infection when used in conjunction with prophylactic antibiotics remains controversial.34 Despite this, in view of the reported increased rate of deep infection of TKAs in diabetics it would seem reasonable that as many precautions are taken as practicable. Thus, preoperatively, skin ulcers etc which are more common in diabetics and are a source of potential metastatic infection should be treated. We would advocate the use of a broad spectrum antibiotic given ideally 30 min before surgery and 10 min before inflation of a tourniquet34 and the use of an antibiotic-loaded cement (either pre-loaded or mixed at time of surgery), as a minimum during the perioperative phase. The overall rate of deep infection reported in the literature for TKA is 0.7–2%.17–30 In the diabetic population the mean rate of deep infection reported is 4.5%22–27 ranging from 1.2%27 to 13.5%.22 The latter was reported by Chiu et al.22 which is the only randomised prospective trial looking at rate of infection of TKA within the diabetic population comparing the use of cefuroxime-loaded cement and plain cement. Five out of 41 (13.5%) patients developed deep infection in the group who received plain cement, while none of 41 patients with cefuroxime-loaded cement developed infection. The overall infection rate for the whole group was 5 out of 78 (6.4%). The place of antibiotic-loaded cement in diabetic patients is unclear; one study has reported that intravenous cefuroxime is just as effective as cefuroxime added to the cement.35 Meding et al.27 found a slightly higher infection rate in their diabetic group (1.2% vs 0.7%), but the difference was not significant. All 4 patients who developed deep infection had cefuroxime-impregnated cement, while only 74% of the non-diabetic infected patients had antibiotic-loaded cement. Yang et al.23 reported using gentamicin-loaded
Total knee arthroplasty in diabetics To date, there have been relatively few studies reporting on the outcome of TKA in diabetics (Table 1). Most have been retrospective and the numbers have been small, but the most recent study by Meding et al.27 was by far the largest and included 329 TKAs performed on diabetic patients. Wound complications The combination of impaired host defenses, thin capsule and subcutaneous tissue and variability of the blood supply to the skin around the knee, suggest wound complications should be higher in diabetics with a theoretical higher risk of developing into a deep infection. However, there has been no correlation shown between postoperative wound complications and the development of deep infection in any of the published studies. The rate of reported superficial wound complications in diabetics after THA varied from 1.2% to 12% 1,14,17,22–30 (Table 1) which is comparable to TKAs performed on non-diabetics which have been reported as high as 10–20%.31–33 Meding et al.27 reported twice as many wound complications in IDDM but concluded that the numbers were so small to preclude statistical analysis. No other studies have mentioned a difference in rate of wound complications between diabetics and non-diabetics. With the close proximity of the skin and thin subcutaneous tissue to the knee joint itself, a
Publications on total knee replacements in diabetic patients.
Patients IDDM NIDDM Age Follow up (Years) Numbers of TKAs Superficial infection Deep infection
Revision rate
Yang et al.23
Pagagelopoulos et al.24
Serna et al.25
England et al.26
Meding et al.27
67 7 (10%) 60 (90%) 71 4.2 78 2.6%
86 7 (8%) 79 (92%) 69 3.6 109 7.3%
51 12 (24%) 39 (76%) Not reported 8 68 2.5%
48 8 (17%) 40 (83%) 67 4.5 53 5.7%
46 6 (13%) 40 (87%) 68 4.3 59 12%
291 118 (36%) 211 (64%) 70 4.3 329 1.4%
6% 4 NIDDM 1 IDDM 0
5.5% 6 NIDDM 0 IDDM 2%
1.5% 1 NIDDM 0 IDDM 7%
5.7% 3 NIDDM 0 IDDM 2%
6.8% 3 NIDDM 1 IDDM 3%
1.2% 0 NIDDM 4 IDDM 3.6%
Not reported
D ND 53 — 77 83 D ND 37 — 77 — D ND 43 55 57 69 Retrospective (Matched Control Group) 7.4%
D 50 85 Not reported
D 50 80 D 50y 86 D 50y 73 Retrospective
Not reported
D 47 80 D 41 70 Retrospective
10%
3.6%
C+A 51 91 Not reported
C 48 86
Prospective Randomized Trialz
D 37 79 D 44 64 Retrospective
Not reported
9.2%
Not reported
ND — 92
Not reported
Retrospective (Matched Control Group) 6.3%
ND 39 75 ND 49 80
D, diabetics; ND, non diabetics. All the reports that have been listed in Table 1 were given prophylactic antibiotics but postoperative regime, type of prosthesis (whether cemented or uncemented), and surgical and operating environment did vary. 13.5% infection occurred in the group who did not receive cefuroxime-impregnated cement. y Average preoperative KSS score of both D and ND. z A randomised single-blinded trial evaluating the role of cefuroxime-impregnated cement in diabetic patients undergoing TKA.
ARTICLE IN PRESS
Aseptic loosening HSS Pre op Post op KSS knee/pain Pre op Post op KSS function Pre op Post op Type of study
Chiu et al.22
The outcome of total hip and knee arthroplasty in diabetics
Table 1
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ARTICLE IN PRESS 64
P.K.H. Chan et al. Table 2
The hospital for special surgery (HSS) knee scoring system.
Score (Total 104)
Pain
Function
Range of motion
Muscle strength
Instability
Flexion deformity
Max 30
Max 22
Max 22
Max 10
Max 10
Max 10
In addition there are subtractions for use of walking aids, extensor lag and residual deformity (Max penalty being 5 points).
The maximum amount that can be awarded is 100 points.
Table 3
The knee society scoring (KSS) system. Knee score Pain
Score (max) Total (max) Deductions
Function score Range of motion
Stability
50 25 Max 25 100 Flexion contracture, extension lag & malalignment
Walking
Stairs
50 100 Walking aids
50
In addition the patients are divided into 3 separate categories. Patient Category: A. Unilateral symptoms (including other side successfully replaced). B. Bilateral knee symptoms. C. Multiple joints affected or medical infirmity. If total is a minus score, score is 0.
cement in only 12% of patients. Other studies did not report whether or not they used antibiotics in their cement.24–26. That said, most studies have shown an increased deep infection rate,22,23,25–27 so it is important to take all necessary precautions, including the routine use of prophylactic intravenous antibiotics, clean air theatres, good surgical technique and antibiotic-loaded cement, to minimize the risk in this group of patients. Looking at the five studies of knee replacement in diabetics22–27 together, there were 627 patients. Of these 469 (75%) patients were NIDDM while 158 (25%) were IDDM. Deep infections occurred in both groups. There were a total of 23 deep infections, 17 NIDDM (73.9%) and 6 IDDM (26.1%). No correlation between deep infection and diabetic subtype has been reported so far (Table 1). Outcome scores The Hospital for Special Surgery (HSS) knee score36 and the Knee Society score (KSS)37 are commonly used to measure outcome of TKA (Tables 2 and 3). A HSS score of 85–100 points represents an excellent result, 70–84 points a good result, 60–69 points a fair result and o60 points a poor result. The KSS goes further, stratifying patients into 1 of 3 categories depending on their overall musculoskeletal status. Patients in group A have unilateral knee symptoms or the other knee successfully replaced, group B patients have bilateral symptoms and group C have multiple joints affected or
medical infirmity. Separate scores are obtained for pain and function to permit better assessment of both specific prosthetic knee function and overall functional status of the patient. England et al.26 Introduced an arbitrary score of 50 for pain and 40 for function in those TKAs that failed (for whatever reason) and these patients were still placed in their most appropriate categories. This allows for failed knees to be penalized at time of assessment but at the same time does not have the disproportionate downward effect on average scores (especially if assessing a small number of knees). He argued that failed knees could be minimally painful and have adequate residual function. In the studies that reported HSS scores22,24–26 there were significant improvements in the HSS score postoperatively. Averaging the four studies the preoperative HSS score was 51 points and postoperative HSS score 83 points. Of those studies which reported percentages of their patients in the relative groups24–26 81% of the TKAs were rated excellent or good, 9% rate-fair and 10% rated poor (Serna et al.25 scored his knees at 90–100 points as excellent, 80–89 as good, 70–79 as fair and o70 as poor which may explain why they had a higher percentage of poor outcomes). The postoperative HSS scores in diabetics were found to be significantly lower in 2 studies: Pagagelopoulos et al.24 reported a postoperative KSS score of 77 in diabetics and 86 in the matched
ARTICLE IN PRESS The outcome of total hip and knee arthroplasty in diabetics control (Po0.05); Serna et al.25 reported an average postoperative HSS score of 85 in diabetics and 92 in the matched control group which was significant (Po0.01). There were no statistically significant differences in the HSS scores with regard to various diagnoses, cement vs uncemented fixation, preoperative deformity and number of prior surgical procedures, in the same study.25 In the studies that reported KSS there were similar improvements.22–24,26,27 The average preoperative knee scores from the 5 studies improved from 43 points to an average postoperative score of 82 points. Meding et al.27 found that the diabetic patients had a higher preoperative knee score, possibly due to diabetic patients having a subclinical or clinical neuropathy with a loss of pain perception. The postoperative improvement in the knee scores was similar for their diabetic and nondiabetic patients (Table 1). As expected knee function scores were lower in diabetic patients both pre and postoperatively. Scores were even lower in patients with insulin-dependent diabeties (Table 1). Despite this, however, the average preoperative function scores improved form 43 points to an average postoperative function score of 66 points.
Stiff knees Meding et al.27 showed no difference in the manipulation under anaesthetic rates in their diabetics and non-diabetic groups (91.2% in both groups).
Aseptic loosening In diabetes mellitus, sensory and autonomic neuropathy may occur even at subclinical levels.38 Loss of sensation, proprioception and pain perception could lead to increased risk of aseptic loosening. Revision for aseptic loosening of TKAs does seem to be higher in diabetics. The three studies that included matched control groups24,25,27 all reported higher rates of revision, although only two reported this to be significant.25,27 Meding et al.27 reported revision rates for aseptic loosening, of 3.6% in diabetics vs 0.4% in the matched control group (Po0.05). Similarly Serna et al.25 reported a revision rate of 7% in diabetics and 1.9% in the matched control group (Po0.001). Pagagelopoulos et al.24 also reported an increase of progressive radiolucencies and aseptic loosening on radiographic evaluation compared to the matched control group (7.4% vs 3%) but this difference was reported as not significant.
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Survivorship Two studies addressed the long-term survivorship of the prosthesis using the Kaplan–Meier survivorship analysis. Patients who underwent revision surgery or those advised to have revision were considered implant failures. Pagagelopoulos et al.24 reported that the probability of implant survival was 95% at 5 years and 91% at 10 years. There was no significant difference between the diabetics and the matched control. Similarly Meding et al.27 reported a figure of 98% at 7 years with no significant difference between diabetics and non-diabetics. Furthermore when IDDM and NIDDM patients were compared, again there was no significant difference reported. They also were unable to establish an association between implant survival and patient age at surgery, type of diabetes presence of systemic complications of diabetes, bilateral arthroplasty or underlying diagnoses. Men had a reduced probability of implant survival at 10 years (84%) than women (97%). Increased weight and previous operations were the only other risk factors for a decreased probability of implant survival with figures of 64% (compared with 98%) and 85% (compared to 97%) at 10 years, respectively. Uncemented TKR Only one study looked at the uncemented TKA in diabetic patients.24 It found no difference in the appearance of radiolucencies or rate of aseptic loosening within this subgroup, which comprised 57% of the study population. Studies have demonstrated defects in fracture healing in experimental diabetes (related to bone ingrowth), which gives a theoretical increased risk of early failure in uncemented total knee arthroplasty. Despite no reported increase in the rate of aseptic loosening in this series, we would be cautious in advising the use of uncemented TKAs in diabetics when cemented TKAs have proven long term results. Medical complications Urinary tract infection (UTI). Reported rates of UTI in diabetics during the perioperative phase after TKA range from 1.2% to 15%.23–25,27 Yang et al.23 reported a significant correlation between development of symptomatic UTI between catheterized and non-catheterized patients, the risk of UTI being 35% and 9%, respectively. The risk of UTI also increased with duration of catheterization. Only one patient in this study with a UTI went on to develop a deep infection in the knee joint, thought to be unrelated. In a separate study looking at urinary complications in non-diabetic elderly females undergoing THA, Carpiniello et al.39 reported that routine
ARTICLE IN PRESS 66 perioperative catheterization can reduce the risk of UTI form 16% to 4%. Although it is obviously desirable to try and minimize the risk of UTI, no study to date has established a relationship between symptomatic UTI and the development of deep joint infection. A pragmatic approach should be taken, and the threshold for elective catheterization at time of surgery should be low especially if there has been a previous history of urinary tract problems or anticipated longer immobility post surgery and removed as soon as it is feasible. Deep vein thrombosis (DVT). Reported rates of DVT varied from 0% to 54%.23,24,26 There were no reported cases of pulmonary embolus. Pagagelopoulos et al. had reported no cases of DVT and Yang et al. reported only 1 case of DVT (1%) but routine ultrasonography or venography was not performed in these studies. Only those suspected clinically of DVT were investigated using ultrasonography. In contrast England et al. was the only study to routinely perform venograms on all their patients (on the 5th postoperative day) and found a DVT rate of 54% with no reported cases of PE using only postoperative aspirin as prophylaxis. They did not report any difference in rate of DVT between IDDM and NIDDM. This rate of DVT is comparable to other TKA studies.31,40,41. Neuropathy. Meding et al.27 found a significantly higher neuropathy rate in the diabetic group. Serna et al.25 also found 9% of there cases had a post operative neuropathy. Cardiovascular and gastro-intestinal. Meding et al.27 showed that the stoke rate, myocardial infarction rate and the gastrointestinal complications were no different in their diabetic group compared to the non diabetic patients.
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(7):825–30. 2. Diabetes UK: Fact sheet; no 2. 2004. www.diabetes.org.uk/ fact/fact2.htm accessed 14/07/2004. 3. International Diabetes Federation 2004: Facts and figures; prevalence www.idf.org/home/index.cfm?node=264 accessed 28/06/2004. 4. Report by the controller and auditor general. Hip replacements: an update, July 2003. HC956: Session 2002–2003. 5. Robertsson O, Dunbar MJ, Knutson K, Lidgren L. Past incidence and future demand for knee arthroplasty: a report from the Swedish Knee Arthroplasty Register regarding the effect of past and future population changes on the number of arthroplasties performed. Acta Orthop Scand 2000;71(4):376–80.
P.K.H. Chan et al. 6. Lucht LI. The Danish Arthroplasty Register: 11 years and 73,000 arthroplasties. Acta Orthop Scand 2000;71(5): 433–9. 7. Havelin LI, Engesaeter LB, Espehaug B, Furnes O, Lie SA, Vollset SE. The Norwegian Arthroplasty Register: 11 years and 73,000 arthroplasties. Acta Orthop Scand 2000;71(4): 337–53. 8. Wells VM, Hearn TC, McCaul KA, Anderton SM, Wigg AE, Graves SE. Changing incidence of primary total hip arthroplasty and total knee arthroplasty for primary osteoarthritis. J Arthroplasty 2002;17(3):267–73. 9. American Academy of Orthopaedic surgeons. Orthopaedicrelated Statistics. http://www.aaos.org/wordhtml/research/stats/stats_3.ntm accessed 16/05/2003. 10. Robertson HD, Polk HC. The mechanism of infection in patients with diabetes mellitus: a review of leucocyte malfunction. Surgery 1974;75:123–8. 11. Einhorn TA, Boskey AL, Gundberg CM, Vigorita VJ, Devlin VJ, Beyer MM. The mineral and mechanical properties of bone in chronic experimental diabetes. J Orthop Res 1988;6(3): 317–23. 12. Herbsman H, Kwon K, Shaftan GW, Gordon B, Fox LM, Enquist IF. The influence of systemic factors on fracture healing. J Trauma 1966;6(1):75–85. 13. Loder RT. The influence of diabetes mellitus on the healing of closed fractures. Clin Orthop 1988;232:210–6. 14. Kennedy L, Baynes JW. Non-enzymatic glycosylation and the chronic complications of diabetes. Diabetologia 1984;26:93–8. 15. Wymenga AB, van Horn JR, Theeuwes A, Muytjens HL, Slooff TJ. Perioperative factors associated with septic arthritis after arthroplasty. Prospective multicenter study of 362 and 2,651 hip operation. Acta Orthop Scand 1992;63(6): 665–71. 16. Kaandorp CJ, Van Schaardenburg D, Krijnen P, Habbema JD, van de Laar MA. Risk factors for septic arthritis in patients with joint disease. Arthritis Rheum 1995;38(12):19–25. 17. Menon TJ, Thjellesen D, Wroblewski BM. Charnley low friction arthroplasty in diabetic patients. J Bone Joint Surg 1983;65-B:580–1. 18. Moeckel B, Huo MH, Salvati EA, Pellicci PM. Total hip arthroplasty in patients with diabetes mellitus. J Arthroplasty 1993;8(3):279–84. 19. Johnston RC, Fitzgerald RH, Harris WH, Poss R, Muller HE, Sledge CB. Clinical and radiological evaluation of total hip replacement: a standard system of terminology for reporting results. J Bone Joint Surg 1990;72-A(2):161–8. 20. Chan P, Brenkel IJ, Aderinto J. The outcome of total hip arthroplasty in diabetes mellitus. Br J Diabetes Vascular Diseases, submitted; September 2004. 21. Forrest G, Fuchs M, Gutierrez A, Girardy J. Factors affecting length of stay and need for rehabilitation after hip arthroplasty. J Arthroplasty 1998;13(2):186–90. 22. Chiu FY, Lin CFJ, Chen CM, Lo WH, Chaung TY. Cefuroxime impregnated cement at primary total knee arthroplasty in diabetes mellitus. J Bone Joint Surg 2001;83-B(5):691–5. 23. Yang K, Yeo SJ, Lee BPH, Lo NN. Total knee arthroplasty in diabetic patients: a study of 109 consecutive cases. J Arthroplasty 2001;16(1):102–6. 24. Pagagelopoulos PJ, Idusuyi OB, Wallrichs SL, Morrey BF. Long term outcome and survivorship analysis of primary total knee arthroplasty in patients with diabetes mellitus. Clin Orthop 1996;330(1):124–32. 25. Serna F, Mont MA, Krackow KA, Hungerford DS. Total knee arthroplasty in diabetic patients; comparison to a matched control. J Arthroplasty 1994;9(4):375–9.
ARTICLE IN PRESS The outcome of total hip and knee arthroplasty in diabetics 26. England SP, Stern SH, Insall JN, Windsor RE. Total knee arthroplasty in diabetes mellitus. Clin Orthop 1990;260:130–4. 27. Meding JB, Reddleman K, Keating ME, et al. Total knee replacement in diabetes mellitus. Clin Orthop 2003;416: 208–16. 28. Morrey BF, Westholm F, Schoifet S, Rand JA, Bryan RS. Long term results of various treatment options for infected total knee arthroplasty. Clin Orthop 1989;248:120–8. 29. Scuderi GR, Insall JR, Windsor RE, Moran MC. Survivorship of cemented knee replacements. J Bone Joint Surg 1989; 71-B(5):798–803. 30. Wilson MG, Kelly K, Thornhill TS. Infection as a complication of total knee arthroplasty: risk factors and treatment in sixty-seven cases. J Bone Joint Surg 1990;72-A:878–83. 31. Ecker ML, Lotke PA. Postoperative care of the total knee patient. Orthop Clin Am 1989;20:55–62. 32. Goldberg VM, Figgie MP, Figgie 3rd HE, Heiple KG, Sobel M. Use of the total condylar knee prosthesis for treatment of osteoarthritis and rheumatoid arthritis: long-term result. J Bone Joint Surg 1988;70-A(6):226–34. 33. Insall JN, Lachiewicz PF, Burstein AH, et al. The posterior stabilized prosthesis: A modification of the total condylar design: two to four clinical experience. J Bone Joint Surg 1982;64-A:1317–23.
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34. Hanssen AD, Osmon DR, Nelson CL. Prevention of deep periprosthetic joint infection. J Bone Joint Surg 1996;78A(3):458–71. 35. McQueen MM, Hughes SPF, May P, Verity L. Cefuroxime in total joint arthroplasty. J Arthroplasty 1990;5(2): 169–72. 36. Insall JN, Ranawat CS, Aglietti P, Shine J. A comparison of four models of total knee-replacement prosthesis. J Bone Joint Surg 1976;58-A(6):754–65. 37. Insall JN, Dorr LD, Scott RD, Scott WN. Rationale of knee society clinical rating system. Clin Orthop 1989;248: 13–4. 38. Horowitz SH. Diabetic neuropathy. Clin Orthop 1993;269: 78–85. 39. Carpiniello VL, Cendron M, Altman HG, Malloy TR, Booth R. Treatment of urinary complications after total joint replacement in elderly females. Urology 1988;32(3):186–8. 40. Lynch AF, Bourne RB, Rorabeck CH, Rankin RN, Donald A. Deep vein thrombosis and continuous passive motion after total knee arthroplasty. J Bone Joint Surg 1988;70-A(1): 11–4. 41. Stulberg BN, Insall JN, Williams GW, Ghelman B. Deep vein thrombosis following total knee replacement: an analysis of six hundred and thirty-eight arthroplasties. J Bone Joint Surg 1984;66-A(2):194–201.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 68–77
www.elsevier.com/locate/cuor
TUMOURS
Sarcomatous degeneration in Paget’s disease of bone H. Sharmaa,, M.J. Janeb a
44 Abercorn Road, Newton Mearns, Glasgow, Scotland G77 6NA, UK Scottish Bone Tumour and Sarcoma Service, Western Infirmary, Glasgow G11 6NT, UK
b
KEYWORDS Paget’s disease; Sarcomatous degeneration; Bone; Osteosarcoma; Survival
Summary Sarcomatous degeneration is a rare but serious complication of Paget’s disease of bone with an incidence of 0.1–1%. The true aetiology of Paget’s sarcoma remains unclear. The most common sites for Paget’s sarcoma are femur, humerus, pelvis, skull and tibia. Sarcomatous degeneration rarely occurs before the age of 50 years affecting men twice as often as women usually in patients with diffuse, polyostotic Paget’s disease. Progressively increasing pain or new pain is the main presenting symptom. Pathological fractures occur in almost a third of long bone cases. The radiographic presentation is most commonly lytic. Histologically, approximately 50% of the lesions represent osteosarcomas. Patients with Paget’s sarcoma have a worse prognosis than primary osteosarcoma in spite of recent advancements in therapeutic strategies including surgery, radiation therapy and chemotherapy. & 2005 Elsevier Ltd. All rights reserved.
Introduction Paget’s disease of bone in the geriatric population is the second most common bone disorder after osteoporosis.1 It is a disorder characterised by a disturbance in the rate of bone turnover, initiated by an early increase in osteoclastic bone resorption followed by excessive and pathological osteoblastic bone formation, resulting in distorted bones with thickened cortices, coarse trabeculations and an Corresponding author. Tel.:+44 141 6393 697; fax:+44 141 211 1920. E-mail addresses:
[email protected] (H. Sharma),
[email protected] (M.J. Jane).
immature woven appearance.2 The most serious complication of Paget’s disease of bone is sarcomatous change. The occurrence of sarcomatous degeneration in approximately 1% of Paget’s patients contributes significantly to the mortality and morbidity. Twenty per cent of the patients with osteosarcoma who are older than 40 years of age and as high as 50% of the patients with osteosarcoma over the age of 60 have Paget’s disease as a predisposing condition, making this a significant geriatric health risk.3–5 As a rule, Paget’s sarcoma is rapidly progressive and fatal. The increasing use of antipagetoid disease-modifying medications is associated with a significant reduction in the overall incidence of Paget’s
0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2005.01.005
ARTICLE IN PRESS Sarcomatous degeneration in Paget’s disease of bone sarcoma in the last decade. This article is an overview of the natural history, clinical manifestations, radiological evaluation, histopathological interpretation, prognostic prediction and management strategy of patients with Paget’s sarcoma.
Historical perspective Sir James Paget observed sarcomas arising in five of his original 23 patients.6 In 1933, Jaffe suggested that the markedly increased proliferative capacity of the osseous tissue involved in Paget’s disease might be the basic stimulus for tumour formation.7 The available evidence is in the form of various clinico-pathological reviews on malignant transformation in Paget’s disease, describing its clinicoradiographic presentation and prognosis. The Mayo Clinic reported 50 years experience with 38 cases, the Memorial Sloan Kettering Cancer centre documented 85 cases in 55 years and the Bristol-Leeds combined series (only big series from the UK) had 80 confirmed cases of Pagets’s sarcoma in 31 years.3,8,9
Epidemiology Incidence In symptomatic patients with Paget’s disease, the incidence is about 2–4%; however, when all patients who have Paget’s disease of bone are included, the incidence is usually about 0.1%. This increase in risk is several 1000-fold higher than that of the general population.10 Although the incidence is relatively low, it is a major factor contributing to the higher morbidity and mortality in the natural course of the disease because of the high incidence of Paget’s disease in the general population.11
69 destructive lesion. The most common sites reported in the literature appear (in decreasing order of frequency) in the femur, humerus, pelvis, skull and tibia.16 Some reports describe simultaneous occurrence of a multifocal Paget’s sarcoma.17 Interestingly, approximately 50% of the patients with Paget’s disease show involvement of the spine; however, the spine and sacrum are rarely involved by the Paget’s sarcoma. On the contrary, the humerus is an uncommon site of Paget’s disease, whereas it is a common site of sarcomatous degeneration.18
Geographical distribution Epidemiologic studies have showed that Paget’s disease is most common in Western Europe, excluding Scandinavia, with the highest prevalence reported in the United Kingdom, particularly in the Lancashire area. Merkow and Lane observed the incidence in Northern Europe from 3% to 4% in middle-aged patients to 10% to 15% in elderly patients.19,20 These numbers are based on the pioneering autopsy series of Schmorl21 and the British radiographic survey by Pygott.22 It is seen with relative frequency in North America, Australia, and New Zealand, the New World settled by Western Europeans. Paget’s disease is considered rare in Africa, South America and Asia. The exact incidence of Paget’s sarcoma is unknown.
Type of Paget’s disease Paget’s disease may be monostotic or polyostotic, and it may or may not be symptomatic. The prevalence of polyostotic disease in Paget’s sarcoma ranges from 57 to 100%.3,4,13 According to the 238 reports in the literature, 79% had polyostotic and 21% had monostotic Paget’s disease.16
Age, sex and side Most patients are 55–80 years old. The mean age is reported to be between 60 and 65 years by most of the studies.3,4,8,9,12–15 Men are affected twice as common as women, similar to that of Paget’s disease. There are no convincing evidences for predilection to laterality.
Anatomical distribution Sarcomas can develop in any part of any bone affected by Paget’s disease, but are more likely to occur with advanced disease and to present with a
Aetiology Sir James Paget was the first to describe the disease that bears his name, which he termed osteitis deformans in 1877. His first patient, was from the north of England, had multiple long bones involved, increasing cranium size and signs of heart failure, ultimately succumbing to a secondary sarcoma arising in the diseased humerus. Paget recognised this clinical entity of bone deformity and pain to be caused by a primary disturbance of bone resorption, which he thought to be a manifestation of chronic inflammation.6
ARTICLE IN PRESS 70 It has been suggested that there is a genetic predisposition to pagetic osteosarcoma, since the majority of Paget’s disease patients who develop osteosarcoma have polyostotic Paget’s disease. Furthermore, they have found that both pagetic and sporadic osteosarcomas showed a loss of heterozygosity of chromosome 18, which involves the same locus seen affected in familial Paget’s disease.5 The viral aetiopathogenesis is postulated with the paramyxovirus group as the main culprit, although the sarcomatous triggering mechanism remains unclear. It has been stated that hypervascularity of the pagetic bones increases the risk of early spread of metastases. Dysfunctional immunological response could be a contributory factor. The occurrence of pathological fractures and higher alkaline phosphatase levels are non-specific and are not reliable indicators. The exact aetiology of a multifocal sarcomatous degeneration is unknown and controversies on whether it is due to multicentric or metastatic origin remain unclear.4,12
Clinical presentation Progressive pain, mass with or without pain, pathological fracture and/or abnormal neurological features constitute a wide variety of symptom constellation in patients with Paget’s sarcoma. Most patients present with a history of an acute onset of pain or an increase in the intensity of chronic pain. The pain typically is of short duration, approximately 4–5 months. Swelling or associated
H. Sharma, M.J. Jane soft-tissue masses are present in approximately half of the cases. Not all swelling, however, results from malignant transformation.10 The predominantly destructive nature of the bone lesions explains the frequency of pathologic fractures (approximately 13). It is not unusual for a spontaneous fracture to be the presenting manifestation.23 Pain is the most reliable indicator of malignant transformation in Paget’s disease. Any patient with Paget’s disease who develops new pain in a previously pain-free area of Paget’s disease, or worsening of pain, or a lytic area in sclerotic Paget’s bone should be evaluated for possible sarcomatous degeneration. If one Paget’s sarcoma is found, the entire body should be surveyed as the tumour can arise in more than one site (multifocal Paget’s sarcoma).
Biochemistry The level of alkaline phosphatase is not a reliable tumour marker. An abrupt elevation of alkaline phosphatase should alert the clinician to the possibility of malignant transformation of a pagetic lesion; however, the degree of elevation (on top of an already elevated level) is variable.3
Radiological findings Plain X-rays Cortical thickening, loss of cortico-cancellous differentiation and enlargement of the bone are
Figure 1 Radiograph revealing tumour destroying the right ilium and soft-tissue calcified mass hanging from right iliac blade.
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Figure 2 Radiograph revealing pelvifemoral Paget’s disease with disappearing sacrum.
Figure 3 Radiograph revealing widespread Paget’s disease throughout right proximal femur and the pelvis with a pathological subcapital femoral neck fracture.
classic findings of typical Paget’s disease. Cortical destruction, soft-tissue extension and tumour mass calcification are typical radiological signs of sarcomatous change in the Paget’s disease.2 Several patterns, such as predominantly osteolysis, predominantly osteosclerosis or mixed pattern can be
seen on radiographs; however, osteolysis is the major characteristic feature (Figs. 1–10). The classic periosteal reaction is conspicuous by its absence. Multiple, small radiolucencies are less suggestive than a single, large area. The lucencies must be clearly destructive and progressive to
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Figure 5 Radiograph disclosing Paget’s sarcoma presenting with an upper tibial pathological fracture.
Figure 4 Radiograph shows extensive Paget’s disease in the femoral shaft with sarcomatous destruction in the distal third.
reliably indicate malignant transformation. It can be difficult to see at the onset in involvement of the skull or pelvis.
Bone scan Isotope 99m Technetium polyphosphate scan is sensitive but non-specific. It is very difficult to distinguish between the increased uptake seen in the sarcomatous lesion and that seen in Paget’s disease of bone itself.
CT scan Development of a soft-tissue mass is best seen on CT scan, particularly when it is ossified. The softtissue component enhances with the use of contrast. CT scan seems to be as accurate as MRI to observe tumour development and assess tumour spread.24 CT scans of the chest and abdomen should be carried out in order to establish
Figure 6 Radiograph revealing union obtained by conservative mode of treatment in a tibial pathological fracture.
whether metastases are present. A representative spinal Paget’s sarcomatous destruction is shown in Fig. 11.
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Figure 7 Radiograph with scapular paget’s sarcoma. Note the unusual sclerotic pattern.
show a low signal abnormality on the T1-weighted sequence corresponding to osteolysis on the radiograph found to have malignant degeneration. Some patients with osteolytic lesions on T1-weighted MRI can show preservation of fat signal in the areas of osteolysis.25
Histological findings
Figure 8 Radiograph revealing humeral Paget’s disease with sarcomatous change.
MRI scan MRI is valuable in the evaluation of local and focal tumour spread. Skip lesions within the medullary canal can be seen with MRI. It demonstrates softtissue extension of tumour in 90% of the cases, often to a much more dramatic extent than is apparent on plain roentgenograms.23 MR images
The exact pathology of lesions arising from Paget’s disease needs to be confirmed by biopsy. Adequate and representative biopsy material is essential to elicit the type of sarcoma, grade, microvasular invasion, soft-tissue extension and adjacent bone infiltration in the presence of typical Pagetic bone features. The gross appearance and microscopic characteristics of Paget’s sarcoma are no different from those of primary osteogenic sarcoma. Osteosarcoma is the most common type of Paget’s sarcoma present in approximately 60% of the lesions (Fig. 12) followed by malignant fibrous histiocytoma, fibrosarcoma, chondrosarcoma and giant-cell sarcoma.3,9,12 Periosteal and juxtacortical sarcomas do not arise from Paget’s disease. Osteogenic sarcoma is characterised by the malignant spindle cell stroma forming osteoid or primitive bone. The tumour can have different appearances depending on the matrix produced: bone (osteoblastic), fibrous (fibroblastic), cartilage (chondroblastic) or blood vessels (telangiectatic).
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Figure 9 Radiograph revealing lateral epicondylar destruction by the Paget’s sarcomatous lesion. This patient was referred as a case of possible tennis elbow.
Differential diagnosis Radiation and pagetic osteogenic sarcomas should be distinguished from classical osteogenic sarcoma.18 Both occur in older patients with significantly greater comorbidity. Roentgenographically, radiation osteogenic sarcoma is typically sclerotic, whereas pagetic osteogenic sarcoma is lytic and associated with pathologic fracture. Radical resection gives the best result, local control and survival. Chemotherapy has not proven effective to date. Improvements in tumour imaging and more intensive chemotherapy regimens may permit limbsparing surgery. Overall results remain poor, with approximately 15% 5-year survival.
Treatment The management depends upon a multidisciplinary team approach and requires full planning and workup in the form of thorough clinical evaluation, detailed radiological studies and a comprehensive histo-pathological assessment. Clinical correlation is important wherever a dilemma is observed. The decision on limb salvage versus limb ablation and on surgical treatment alone versus surgery with
adjuvant therapy is crucial and should be taken in a multidisciplinary bone tumour meeting. Treatment for Paget’s sarcoma depends on the stage of the tumour, general status of the patient and whether it is axial or appendicular in location. It can vary from wide resection and chemotherapy, and limb ablation surgery to palliative radiation for pain control.
Surgery When contemplating surgery or the deciding on the approach towards limb-saving surgeries versus limb-sacrificing surgeries, patient-related factors must be considered. The aim of the surgery is to remove all the tumour tissues with wide margins. Radical margins, usually amputation, are required for reliable, local control. The prognosis, even with local control, is dismal. Super-major surgeries like a radical hemipelvectomy, hindquarter and forequarter amputation give no added benefit to a better survival. Late presentation, diagnostic delay and delay in instituting therapeutic modality are possible factors responsible for achieving poor local control. More effective treatment is clearly needed, and is an open researching domain.
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Chemotherapy Conventional chemotherapy regimens for non-pagetic osteosarcomas are ineffective for almost all of the pagetic sarcomas.23 When dealing with osteosarcoma in Paget’s disease, the response to chemotherapy is generally much less positive than with classic osteosarcoma. It seldom provides meaningful alteration in the rapid, downhill course and is often devastating to the remaining lifestyle in this age group.
Radiotherapy Paget’s sarcoma is relatively resistant to radiation therapy and there is no curative role of radiotherapy. It can be prescribed as a neoadjuvant or as an adjuvant therapy along with operative intervention. Short-term palliation is usually achieved with large doses of radiotherapy.
Prognosis
Figure 10 Radiograph of the right forearm revealing a mixed pattern (both sclerotic and lytic appearance) in the diaphyseal portion of the radius with an extensive, destructive soft-tissue mass.
Figure 11 CT scan revealing involvement of a lumbar vertebra with predominantly lytic Paget’s sarcoma.
Poor prognostic predictors are enumerated in Table 1. The prognosis is poor in Paget’s sarcoma in comparison to the de novo sarcomas. Advanced age of the patients, advanced stage of the disease, pathological fracture occurring at the site of sarcoma, high-grade anaplastic tumour, poor general health, surgically inaccessible sites and metastasis at initial diagnosis rapidly influences the survivorship between the two groups. Sarcomatous transformation is a rare phenomenon commonly with a fatal outcome. The original description of 23 patients with osteoitis deformans by Sir James Paget included five sarcomas with a fatal outcome.6 In a retrospective review of patients over the age of 40 years with osteosarcoma, 42 out of 481 patients from 12 centres had osteosarcoma arising in Paget’s disease with a median survival of 9 months.26 At the Memorial Sloan Kettering cancer centre, there were no survivors for axial tumours (in comparison to 23% 5-year survivorship for the appendicular tumours).3 Smith et al. (1984) found 7.5% and 11% 5-year survival rate for axial and appendicular tumours, respectively.8 The mean survival was 7.5 months for a series of 89 cases from the Scottish bone tumour registry (unpublished data). The 5-year survival rate was 7.9%, with a mortality rate of 86.8% 36 months after diagnosis. There are but a few isolated cases of long-term survival reported. Analysis of these long-term survivors from the previously published series did not reveal any
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Figure 12 Cross-section of the amputation specimen showing a diaphyseal radial lesion with soft-tissue mass-sparing ulna. Microscopy showing a high-grade chondroblastic osteosarcoma with areas of malignant cartilage. There was evidence of vascular invasion. The lesion also confirming the presence of Paget’s bone.
Table 1 Summarising poor prognostic factors associated with Paget’s sarcoma.
Age over 70 Male gender Pelvic and spine Paget’s sarcoma Presence of pathological fractures Presence of neurological complications Pleomorphic sarcoma Metastasis at diagnosis
Acknowledgements We would like to thank medical illustration department and Scottish Bone Tumour Registry (Dr. Robin Reid and Jean Campbell) for photograph ic assistance in this review article.
Practice points
significantly different prognostic predictors to help us in elucidating better treatment strategy.3 The prognosis is generally fatal at a very rapid rate. The prognosis for Paget’s sarcoma remains poor despite radical surgery, adjuvant or neo-adjuvant chemotherapy/radiotherapy. There are no significant survival differences between patients treated with surgery alone or after instituting adjuvant and neoadjuvant chemotherapy along with surgery.
Conclusions In conclusion, sarcomatous degeneration is a rare and dismal complication of Paget’s disease of bone. Patients with Paget’s sarcoma tend to show no significant results to improvements in therapy strategies including surgery, radiation therapy and chemotherapy. We emphasise the need for more research by a combined genetic, molecular biological, oncological, surgical, radiological and histological approach in the management of Paget’s sarcoma to improve the overall prognosis.
The true incidence of Paget’s sarcoma is falling recently probably due to the use of disease-modifying antipagetic medications. Osteogenic sarcoma is the most common histological type of sarcoma. Late presentation, diagnostic delay and delay in instituting therapeutic modality are possible factors responsible for achieving poor local control. Patients with Paget’s sarcoma tend to have a very poor prognosis despite radical surgery, radiotherapy and chemotherapy.
Research directions
To combine all the tumour registry of the UK to a centralised tumour registry database to elucidate the incidence and prevalence of Paget’s sarcoma. Further research is needed to determine the aetiopathogenesis. A prospective determination of the factors responsible for reduction in the incidence of Paget’s sarcoma. More research efforts for primary prevention of the disease.
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References 1. Hamdy RC. Paget’s disease of bone: assessment and management. London: Praeger Publishers; 1981. p. 2. 2. Chapman MW, editor. Chapman’s orthopaedic surgery. 3rd ed. Philadelphia, PA: Lippincott, Williams & Wilkins; 2001. 3. Wick MR, Siegal GP, Unni KK, McLeod RA, Greditzer III HG. Sarcomas of bone complicating osteitis deformans (Paget’s disease): fifty years’ experience. Am J Surg Pathol 1981; 5(1):47–59. 4. Huvos AG, Butler A, Bretsky SS. Osteogenic sarcoma associated with Paget’s disease of bone. A clinicopathologic study of 65 patients. Cancer 1983;52(8):1489–95. 5. Hansen MF, Nellissery MJ, Bhatia P. Common mechanisms of osteosarcoma and Paget’s disease. J Bone Miner Res 1999; 14:39–44. 6. Paget J. On a form of chronic inflammation of bones. Med Chir Trans 1877;60:37–63. 7. Jaffe HL. Paget’s disease of bone. Arch Pathol 1933;15: 83–131. 8. Smith J, Botet JF, Yeh SD. Bone sarcomas in Paget disease: a study of 85 patients. Radiology 1984;152(3):583–90. 9. Price CH, Goldie W. Paget’s sarcoma of bone. A study of eighty cases from the Bristol and the Leeds bone tumour registries. J Bone Joint Surg Br 1969;51(2):205–24. 10. Hadjipavlou A, Lander P, Srolovitz H, Enker IP. Malignant transformation in Paget disease of bone. Cancer 1992;70: 2802–8. 11. Polednak AP. Rates of Paget’s disease of bone among hospital discharges, by age and sex. J Am Geriatr Soc 1987; 35(6):550–3. 12. Schajowicz F, Santini Araujo E, Berenstein M. Sarcoma complicating Paget’s disease of bone. A clinicopathological study of 62 cases. J Bone Joint Surg Br 1983;65(3):299–307. 13. Haibach H, Farrell C, Dittrich FJ. Neoplasms arising in Paget’s disease of bone: a study of 82 cases. Am J Clin Pathol 1985;83(5):594–600. 14. Huvos AG. Osteogenic sarcoma of bones and soft tissues in older persons. A clinicopathologic analysis of
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117 patients older than 60 years. Cancer 1986;57(7): 1442–9. Moore TE, King AR, Kathol MH, el-Khoury GY, Palmer R, Downey PR. Sarcoma in Paget disease of bone: clinical, radiologic, and pathologic features in 22 cases. Am J Roentgenol 1991;156(6):1199–203. Jattiot F, Goupille P, Azais I, Roulot B, Alcalay M, Jeannou J, Bontoux D, Valat JP. Fourteen cases of sarcomatous degeneration in Paget’s disease. J Rheumatol 1999;26(1): 150–5. Choquette D, Haraoui B, Altman RD, Pelletier JP. Simultaneous multifocal sarcomatous degeneration of Paget’s disease of bone. A hypothesis. Clin Orthop 1983;179: 308–11. Frassica FJ, Sim FH, Frassica DA, Wold LE. Survival and management considerations in postirradiation osteosarcoma and Paget’s osteosarcoma. Clin Orthop 1991(270): 120–7. Merkow RL, Lane JM. Current concepts of Paget’s disease of bone. Orthop Clin North Am 1984;15(4):747–63. Merkow RL, Lane JM. Paget’s disease of bone. Orthop Clin North Am 1990;21(1):171–89. Schmorl G. Uber Osteitis deformans Paget. Virchow’ Arch (Pathol Anat) 1932;283:694–751. Pygott F. Paget’s disease of bone; the radiological incidence. Lancet 1957;272(6980):1170–1. Harrington KD. Surgical management of neoplastic complications of Paget’s disease. J Bone Miner Res 1999;14:45–8. Roberts MC, Kressel HY, Fallon MD, Zlatkin MB, Dalinka MK. Paget disease: MR imaging findings. Radiology 1989;173: 341–5. Sundaram M, Khanna G, El-Khoury GY. T1-weighted MR imaging for distinguishing large osteolysis of Paget’s disease from sarcomatous degeneration. Skeletal Radiol 2001;30(7): 378–83. Grimer RJ, Cannon SR, Taminiau AM, Bielack S, KempfBielack B, Windhager R, Dominkus M, Saeter G, Bauer H, Meller I, Szendroi M, Folleras G, San-Julian M, van der Eijken J. Osteosarcoma over the age of forty. Eur J Cancer 2003; 39(2):157–63.
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CME SECTION
Three external CME points available The following series of questions are based on the CME designated article for this issue—‘Ionising radiation and orthopaedics’ by P. Dewey, S. George and A. Gray. Please read the article carefully and then complete the self-assessment questionnaire by filling in the square corresponding to your response to each multiple-choice question. For true or false questions, please fill in one square only. After completing the questionnaire, either post or fax the answer page back to the Current Orthopaedics Editorial Office at the address at the bottom of the RESPONSE sheet. Please photocopy this page if you wish to keep your copy of Current Orthopaedics intact. Replies received before the next issue of Current Orthopaedics is published will be marked and those reaching an adequate standard will qualify for three external CME points. You will be notified of your marks and a CME certificate will be despatched for your records.
Questions 1. Which of the following malignancies has been shown to cluster in orthopaedic surgeons?
A. B. C. D. E.
Ocular melanoma Squamous cancer of the skin Thyroid cancer Acute lymphoblastic leukaemia Acute myeloblastic leukaemia
2. What is the fundamental source of energy that produces X-rays in an X-ray tube?
A. Electrons moving from an outer shell to an inner shell and releasing energy under the influence of an applied potential difference B. Electrons slowing down rapidly as they approach a positively charged target C. Electrons rebounding from collision with negatively charged electron clouds in the atoms of a cathode D. Nuclear degeneration of a heavy metal isotope E. Nuclear collisions releasing alpha and beta particles doi:10.1016/j.cuor.2005.02.005
3. If image quality is suboptimal and an X-ray has to be repeated, what is the preferred mechanism for achieving better exposure?
A. B. C. D. E.
Increase the current Increase the voltage Increase the exposure time Remove filtration Use a more sensitive film
4. If a surgeon moves from 1 m away from an Xray source to 4 m away, what is the effect on the dose of radiation to which he is exposed?
A. B. C. D. E.
No effect It falls to a third It falls to a quarter It falls to a ninth It falls to one-sixteenth
5. What is the magnitude of difference between the allowed whole body annual exposure to radiation for an occupationally exposed individual when compared to a member of the general public, as
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defined by the International Commission on Radiation Protection?
9. Which of the following exposes an individual to the greatest dose equivalent of radiation?
A. The occupationally exposed should receive no greater annual dose equivalent than the general public B. The occupationally exposed should receive an annual dose equivalent no more than twice that which is acceptable for the general public C. The occupationally exposed should receive no more than 10 times the acceptable limit for the general public D. The occupationally exposed should receive no more than 20 times the acceptable limit for the general public E. The occupationally exposed should receive no more than 100 times the acceptable limit for the general public
A. B. C. D. E.
6. What interaction is responsible for most longterm effects of radiation on an organism? A. B. C. D. E.
Direct disruption of cell membranes Scission of DNA molecules Oxidation of carbon chains Ionisation of water Death of rapidly dividing epithelial cells
7. What is the probability of an individual developing a fatal cancer as a consequence of acute uniform exposure to 1 Sievert of radiation? A. B. C. D. E.
Even chance 1 in 5 1 in 10 1 in 20 1 in 100
8. The development of which of the following is a stochastic effect of radiation exposure? A. B. C. D. E.
Impaired fertility Bone marrow dysplasia Non malignant skin changes Malignant melanoma Cataract formation
A CT scan of the head An X-ray of the lumbar spine A hip X-ray A single flight from Europe to Australia A years exposure to average background radiation
10. What is the recommended lead equivalence for materials used to manufacture lead gowns to be worn in operating theatres? A. B. C. D. E.
0.2 mm 0.5 mm 1 mm 2 mm 5 mm
11. Approximately what proportion of the radiation striking a protective lead gown passes through to the wearer? A. B. C. D. E.
0.1% 0.5% 1% 5% 10%
12. What is the estimated risk of fatal cancer arising from a single plain X-ray examination of the lumbar spine? A. B. C. D. E.
1 1 1 1 1
in in in in in
1300 13000 130000 1.3 million 13 million
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CME SECTION
Answers to CME questions in Vol. 18, issue 5 Please find below the answers to the Current Orthopaedics CME questions from Vol. 18, issue 5 which were based on the article—‘Surgery in Infectious Diseases’ by Prof. D. I. Rowley from the same issue. 1
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BOOK REVIEWS Linda J. Sandell, Alan J. Grodzinsky, Tissue Engineering in Musculoskeletal Clinical Practice, American Academy of Orthopaedic Surgeons, ISBN 0892033290, 2004 (400pp., £84). This is a book produced by the American Academy of Orthopaedic Surgeons and edited by two eminent scientists. It is a very useful compendium of this rapidly changing field. The faculty is a distinguished one although the contributions vary in their detail and depth in their attempt to maintain clinical as well as a scientific focus. There are considerable advances in practical application of tissue engineering in articular cell implantation in the knee and the potential for
other methods of chondral repair make good reading. Also the cutting edge work on stem cells and their potential for clinical application. As yet clinical applications relate mainly to cartilage cell transplantation and of course follow-up of other approaches are essentially limited at this stage. All those interested in the future development of orthopaedics would benefit from perusal of this text which has a very optimistic theme throughout. Time will show which of the many exciting initiatives will prove to be valuable in clinical practice. George Bentley
doi:10.1016/j.cuor.2005.02.001
Richard Berger, Arnold Peter Weiss, Hand Surgery, Lippincott, Philadelphia, PA, ISBN 0-78172874-6, 2003 (2800 pp., US$ 350). Book reviews can be a chore, with the dubious reward of keeping the book. Not so this time. This is a fantastic book. I am delighted to keep it. It is actually 2 books; 2 volumes of about 1000 pages in each volume. It is a comprehensive (well, almost comprehensive, see below) textbook on all aspects of Hand Surgery, covering not only the operative descriptions but also the background pathophysiology and clinical assessment. In most of the topics, a number of alternative treatments are described and algorithms are presented to help the reader select the appropriate one. The text is supplemented with many clear diagrams and photographs. Most of these are black and white, but where particular emphasis is required, colour photographs and diagrams are used to good effect. The first volume begins with a review of basic sciences related to hand surgery and includes chapters on hand therapy and radiographic imaging of the hand. There follows a series of excellent chapters on fractures and ligament injuries to the
hand and forearm. This is followed by chapters on arthroscopic treatment. Thereafter, the first volume deals with tendon injuries, nerve injuries and compressive neuropathies. The second volume deals with all the rest: brachial plexus injuries, the spastic hand, burns, Dupuytren’s disease, arthritic conditions, congenital hand surgery, vascular conditions, tumours and pain management. There are also chapters on reconstruction of specific anatomical areas such as the thumb and forearm. For anyone who finds wrist instability difficult to understand, read chapter 24. This is a masterpiece by Dobbins and Linscheid entitled ‘‘A fifty year overview of wrist instability’’. The chapter comprehensively covers the biomechanics of these injuries. It also translates and explains the gobbledygook that has arisen around the terminology describing the instability patterns. Clinical evaluation, indications for surgery and surgical principles are all covered. Mandatory reading for senior trainees prior to their exams. Inevitably, with a work of this breadth, there will be omissions. And so there is in this book. For example, there is no description of the treatment of compressive neuropathies of the radial and posterior interrosseus nerves.
ARTICLE IN PRESS Book Reviews However, the criticisms are minor. For the budding hand surgeon: buy, beg or steal a copy of this book. For the general orthopaedic trainee the chapters in the first volume will be the most useful and the algorithms for treating conditions such as
83 scaphoid non-unions are particularly helpful. This is a very good book and deserves to be widely read.
S.L. Knight
doi:10.1016/j.cuor.2005.02.002
Lawrence R. Menendez (Ed.), Orthopaedic Knowledge Update: Musculoskeletal Tumors, American Academy of Orthopaedic Surgeons, ISBN 0-89203-257-X ($129. 395pp. plus accompanying CD-ROM). The American Academy of Orthopaedic Surgeons has published update books regularly since 1994. The latest of the OKU series, Musculoskeletal Tumors, consists of 41 chapters divided into five sections: General Considerations, Benign Bone Tumours, Malignant Bone Tumours, Soft-Tissue Tumours, and Carcinoma Metastatic to Bone. As is ideal for an orthopaedic oncology book, it is endorsed by the Musculoskeletal Tumour Society. The majority of the 55 authors are North American, but there is European and Australian input. The book has the feel of a who’s who of Orthopaedic Oncology. Each chapter has an easy to read layout with appropriate subdivisions and an annotated bibliography of recent articles and a classic bibliography. The classic bibliography should inspire further reading! The text is up to date as well as covering classic thinking.
The accompanying CD-ROM contains additional annotated images not included in the text. It is easy to operate and navigate, but it is a little disappointing that only 13 of the 41 chapters are covered. It would provide the ideal opportunity for expansion of all the chapters. The book is well laid out and easy to read. The illustrations are of a high quality. OKU Musculoskeletal Tumors provides a very detailed review of classic and current thinking on the management of primary and metastatic bone tumours. The book is too detailed for the candidate for the FRCS (Tr. & Orth.), but it will serve as a useful addition to the library for the senior trainee with a subspecialty interest and for those orthopaedic surgeons with an interest in bone tumour management. More importantly it will act as a source of reference for those who see bone tumours infrequently, who need rapid access to information.
Robert U. Ashford
doi:10.1016/j.cuor.2005.02.003
William M. Ricci (Ed.), Complications in Orthopaedics Tibial Shaft Fractures, American Academy of Orthopaedic Surgeons. This volume of a series deals with the up to date development of complications in tibial shaft fractures. It has been set at a level that reflects the knowledge in the field that reasonably should be expected of a general orthopaedic trainee approaching their intercollegiate examination and certainly an expected level of knowledge of a trainee commencing a fellowship in Trauma and Orthopaedics. There is a consistency in organization and writing of each chapter based on a structure that leads the reader to the development of a judgmental doi:10.1016/j.cuor.2005.02.004
incorporation of the presented opinions and treatment strategies. The result is a well balanced and unbiased review of the latest scientific information, with chapters that are stimulating and thought provoking. The chapters divided into three main sections completely fulfill author’s aim, leading to a personal yet well documented and scientifically proven treatment strategy. With this publication the American Academy continues its reputation for producing authoritative texts.
P. Gannoudis
Aims and Scope Current Orthopaedics presents a unique collection of international review articles summarizing the current state of knowledge and research in orthopaedics. Each issue focuses on a specific topic, discussed in depth in a mini-symposium; other articles cover the areas of basic science, medicine, children/adults, trauma, imaging and historical review. There is also an annotation, self-assessment questions and an exam section. In this way, the entire postgraduate syllabus will be covered in a 4-year cycle. The Journal is cited in: Cochrane Center, EMBASE/ Excerpta Medica, Infomed, Reference Update and UMI Microfilms.
Editor Professor R. A. Dickson MA, ChM, FRCS, DSc St James’s University Hospital Trust, Leeds, UK
Editorial Committee President of BOTA, M. A. Farquharson-Roberts (Gosport, UK), I. Leslie (Bristol, UK), D. Limb (Leeds, UK), M. Macnicol (Edinburgh, UK), I. McDermott (Ruislip, UK), J. Rankine (Leeds, UK)
Editorial Advisory Board L. de Almeida (Portugal) G. P. Songcharoen (Thailand) R. W. Bucholz (USA) J. W. Frymoyer (USA) R. W. Gaines (USA) S. L. Weinstein (USA) M. Bumbasirevic (former Yugoslavia)
A. K. Mukherjee (India) A. Kusakabe (Japan) A. Uchida (Japan) M.-S. Moon (Korea) R. Castelein (The Netherlands) R. K. Marti (The Netherlands) G. Hooper (New Zealand) A. Thurston (New Zealand) E. G. Pasion (Philippines)
D. C. Davidson (Australia) J. Harris (Australia) S. Nade (Australia) G. R. Velloso (Brazil) J. H. Wedge (Canada) S. Santavirta (Finland) P. N. Soucacos (Greece) M. Torrens (Greece) J. C. Y. Leong (Hong Kong)
Available online at www.sciencedirect.com
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ARTICLE IN PRESS Current Orthopaedics (2005) 19, 85–93
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MINI-SYMPOSIUM: THE FOOT
(i) The structure and function of the foot in relation to injury Peter J. Briggs Freeman Hospital, 34 Chollerford Close, Gosforth, Newcastle upon Tyne, NE7 7DN, UK
KEYWORDS Foot; Fracture; Dislocation; Plantar aponeurosis; Os calcis; Talus; Navicular; Cuboid; Cuneiform; Metatarsal; Subtalar; Talonavicular; Calcaneocuboid; Tarsometatarsal; Metatarsophalangeal
Summary The supportive function of the foot is provided by the bones, joints and ligaments of the midfoot, the central tarsometatarsal joints, and the midtarsal joint. Subtalar, talonavicular, and medial and lateral tarsometatarsal flexibility allows the foot to adjust to uneven ground and for the changing shape of the foot during heel elevation and propulsion. The plantar aponeurosis and deep transverse intermetatarsal ligaments support the foot and also have dynamic functions in stabilisation and movements. The foot is subject to a wide spectrum of injury severity from different injury mechanisms, producing various patterns of injury. The goals of management are to provide pain relief and restore function where possible. Understanding the structure and function of the foot helps us understand how these injuries can occur, how its function will be affected as a consequence, and enables us to define basic principles of management. & 2005 Elsevier Ltd. All rights reserved.
Introduction Our feet need to be stable and supportive, flexible, and energy efficient to be able to support body weight, withstand the forces generated by contact with the ground, propel us forward, and cope with uneven surfaces and various types of footwear. To achieve this they must be stable and supportive, flexible, and energy efficient. Tel.: +44 191 213 7330; fax: +44 191 223 1238.
E-mail address:
[email protected] (P.J. Briggs).
Injuries to the foot are common, and many of them resolve with little need for active management. Unfortunately, some apparently innocuous injuries lead to persistent symptoms and disability if left untreated. Conversely severe injuries can present difficulties in determining the extent of injury and priorities in treatment. My aims are to describe the basic structure and function of the foot, concentrating on the bones, joints and ligament mechanisms. From this we can see how injury can occur, how function may be affected as a consequence, and define principles in the management of skeletal injury in the foot.
0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2004.12.007
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Structure The foot is considered as having three main parts (Fig. 1). The hindfoot articulates with the midfoot through the talonavicular and calcaneocuboid (midtarsal) joints, and the forefoot with the midfoot through the tarsometatarsal joints.
Hindfoot In the hindfoot there are three distinct articular facets between the talus and os calcis, the anterior, middle and posterior. Functionally they act as a highly congruent subtalar joint providing supination and pronation of the heel. The joint is supported by a number of ligaments, the most important of which are the interosseous ligament in the sinus tarsi canal and the medial ligament, which forms the deepest part of the deltoid ligament (Fig. 2). The os calcis also provides attachment for important structures such as the tendo Achillis and plantar aponeurosis.
Figure 2 Coronal MRI scan through the subtalar joint showing the medial and interosseous ligaments.
Midfoot The bones of the midfoot, the navicular, cuneiforms and cuboid, are all firmly attached to each other. The joint between the cuboid and navicular is usually a fibrous joint, but all others are flat synovial joints. The ligamentous attachments, particularly the plantar and interosseous ligaments, are strong and allow little movement between individual bones. The two joints of the midtarsal joint are quite different, but work together with the subtalar joint to allow movement between the hindfoot and midfoot. The talar head is slightly egg shaped but the talonavicular joint behaves as a ball and socket joint with no unique axis of motion.1 The capsular ligaments between the talus and navicular are relatively weak. The talar head is instead stabilised in a deep socket comprising the corresponding articular surface of the navicular, the anterior articular facet of the os calcis, and the intervening calcaneonavicular ligaments,2 including the navicular band of the bifurcate ligament (Fig. 3). The navicular is firmly attached to the os calcis and so
Figure 3 ‘‘Socket’’ of the talonavicular joint comprising the navicular (N), anterior (A) and middle (M) facets of the os calcis, the two inferior (ICN) and superomedial (SMCN) calcaneonavicular ligaments, and the navicular component of the bifurcate ligament (B). The interosseous ligament (I) is shown.
Figure 1 Regions of the foot.
the interosseous and medial ligaments of the subtalar joint also function to hold the talar head in relation to it. Rotation essentially occurs about a centre within the talar head, restricted by the constraints of the calcaneocuboid and subtalar joints. Tibialis posterior is the only significant
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Figure 5 Ligaments of the tarsometatarsal joints. The Lisfranc ligament (L) lies between the base of the 2nd metatarsal and the medial cuneiform. Figure 4 Sagittal MRI scan showing the saddle shaped calcaneocuboid joint and the short plantar ligament (SP).
muscle attached to the midfoot through the tuberosity of the navicular. The calcaneocuboid joint is a saddle shaped joint with a dorsal lip from the anterior process of the os calcis. The joint allows some sliding motion and abducts and adducts with subtalar movement in the weightbearing foot. Stability of the joint is provided by the shape of the articular surfaces, and the strong long and short plantar ligaments (Fig. 4) attached to the underside of the os calcis which extend to the underside of the cuboid and the central three metatarsals.
Figure 6 The plantar aspect of the forefoot showing the plantar plates (PP), the plantar aponeurosis (PA), and the deep transverse intermetatarsal ligaments (DTI).
Forefoot The metatarsals articulate with the midfoot by a row of joints across the foot. The 2nd, and to a lesser degree the 3rd, are firmly attached to their respective cuneiforms with strong ligaments. The base of the 2nd metatarsal, wedged between the medial and lateral cuneiforms, also has strong ligamentous attachments to each of these.3 The plantar ligaments, and in particular the Lisfranc ligament between the medial cuneiform and 2nd metatarsal are particularly important in stabilising the tarsometatarsal joints (Fig. 5). The 1st, 4th, and 5th metatarsals are more mobile, capable of some flexion and extension, as well as abduction on the medial and lateral sides of the forefoot.4 Tibialis anterior and the peroneal tendons are attached to metatarsals and may act to move the tarsometatarsal joints, but like all long tendons will also have effects at the midtarsal and hindfoot joints. The intrinsic muscles, arising in part from
the midfoot and hindfoot as well as the forefoot, are of minor importance in terms of strength in the normal foot, but are of major significance in terms of swelling and compartment syndrome in the injured foot. The metatarsophalangeal joints are sloppy hinge joints providing flexion/extension movement as well as a small amount of abduction/adduction. They are supported by collateral ligaments. The plantar capsule of each joint is thickened to form the plantar plates and these are all connected to each other by the broad deep transverse intermetatarsal ligaments (Fig. 6). The medial and lateral ends of this transverse structure merge with the collateral ligaments of, respectively, the 1st and 5th MTP joints, which helps to prevent splaying of the metatarsals.5 The plantar plates also provide distal attachment for the plantar aponeurosis, important in stabilising the longitudinal arch and in the function of the foot.
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Function
Flexibility in the foot
The foot as a support
As well as being a firm supportive structure the foot needs to be flexible in order to cope with irregular walking surfaces and again for propulsion. Joints move and the foot changes shape as we walk. The heels pronate slightly on heel strike, motion being limited by the supporting ligaments of the subtalar joint. Pronation of the subtalar joint is also limited by the shape of the forefoot as it contacts the ground and the stability of the midtarsal joint. As heel elevation begins, primarily under the influence of the gastrocnemius–soleus complex, the subtalar joint starts to supinate, and this steadily increases as the heel elevates. This pronation and supination of the subtalar joint is dependent on the congruity of the joint and motion at the midtarsal joint, in particular the talonavicular joint. Tibialis posterior is the most effective active supinator of the hindfoot assisted by the gastrocnemius–soleus and long flexors. The plantar aponeurosis also contributes to this heel supination as a consequence of the windlass mechanism.8
The foot is clearly a complex structure with flexible and non-flexible parts whose functions are interdependent. In order to provide support for standing and a lever for propulsion the foot needs to be firm and stable. The bones of the midfoot, all firmly attached to each other, are central to this supportive function through the midtarsal and tarsometatarsal joints. The midtarsal joint provides stability between the hindfoot and midfoot. How this occurs is poorly understood. The concept of parallel and crossing joint axes, that is widely promoted,6 (for which there is no published supporting scientific evidence) has been discounted by van Langelaan.1 Stability is probably primarily a function of the calcaneocuboid joint. The shape of the articulating surfaces and the plantar ligaments, such as the long and short plantar ligaments and plantar aponeurosis which are under tension on weight bearing, are likely to be important in stabilising this joint.4,7 Once the midtarsal joint is stabilised on weight bearing the foot becomes a firm supportive structure from the heel to the central metatarsal heads owing to the relative immobility of the joints in the midfoot and 2nd and 3rd tarsometatarsal joints (Fig. 7).
Figure 7 Plantar view of the foot. The shaded bones provide structural support on weight bearing through the strong plantar ligaments such as the long and short plantar ligaments. The un-shaded bones remain mobile at their articulations.
Extra-articular ligament mechanisms The main extra-articular ligaments are the plantar aponeurosis and the deep transverse intermetatarsal ligaments in the forefoot. They support the arch of the foot and prevent splaying of the forefoot. In addition to these static functions they have important dynamic functions in the foot. When the toes are extended at the MTP joints the arch of the foot elevates and the heel supinates. This is a consequence of the plantar aponeurosis being pulled around the metatarsal heads (Fig. 8). The metatarsal heads must, therefore, move closer to the heel. This is known as the windlass mechanism.9 When the toes are extended during heel elevation in gait the same change in shape of the foot occurs, and the windlass mechanism contributes to the supination of the heel.
Figure 8 Diagram illustrating the windlass mechanism. When the toe is extended the foot shortens and the arch rises.
ARTICLE IN PRESS The structure and function of the foot in relation to injury
Figure 9 Diagram illustrating the reversed windlass mechanism. When the foot bears weight tension is generated in the plantar aponeurosis causing flexion of the toes.
When the forefoot is bearing weight tension is generated in plantar ligaments including the plantar aponeurosis, and is probably important in stabilising the midtarsal joint. As the plantar aponeurosis is attached to the proximal phalanges, flexion occurs at the MTP joints, keeping the toes on the ground (Fig. 9). This is known as the reversed windlass mechanism,9 which is probably the strongest flexor of the MTP joints. Tension increases as the heel rises and is released at toe off, assisting propulsion. The primary stabiliser of the first metatarsal is the deep transverse intermetatarsal ligament, controlling sagittal as well as transverse plane movements. The plantar aponeurosis also reduces the sagittal plane movement of the 1st metatarsal. This stabilising effect increases as the hallux is extended, and abolished by plantar aponeurosis division.10 After heel elevation, when only the metatarsal heads and toes are in contact with the ground, the importance of stability of the 1st metatarsal, along with the 2nd and 3rd, increases as heel elevation increases, until final push-off. These dynamic functions of the plantar aponeurosis are dependent on the flexibility of the MTP joints and the length of the skeleton of the foot.
Injury to the foot The foot may suffer acute injury or overuse type injuries such as stress fractures and ligament and tendon damage. Twisting and bending forces in various directions produce different injury patterns. Compression or crushing forces tend to cause more severe injuries with a greater soft tissue component. Compression forces can be combined with twisting or bending and may cause more
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significant damage. The severity of injury is also clearly related to the energy of injury ranging from simple falls to falls from a height and motor vehicle accidents. Pronation and supination forces most commonly cause injury around the ankle, but damage can occur in the foot. Avulsion fractures at the base of the 5th metatarsal are common. Less common are fractures of the anterior process of the os calcis or the lateral process of the talus and unfortunately frequently missed. These are probably ligament avulsion fractures. Although the precise mechanism for lateral process fractures of the talus is uncertain it is usually associated with injury to the lateral ligament complex of the ankle. These fractures give rise to persisting symptoms, which may be related to impingement, joint surface damage or alteration in joint stability.
Tarsometatarsal joint Plantarflexion injuries of the foot occur from longitudinal loading of the foot in a plantarflexed position. This can occur when weight bearing on the extreme plantarflexed foot, or if a force is directed against the back of the heel when the heel is elevated and the forefoot is in contact with the ground as may occur in sport (Fig. 10). Injury tends to occur at the tarsometatarsal joints where there is rupture of the weaker dorsal ligaments causing the metatarsals to plantarflex and displace dorsally. Abduction or adduction stress as a consequence of the limb or body moving about an immobilised forefoot, such as in a stirrup, can also injury the tarsometatarsal joint. Various patterns of injury are seen including partial or complete injuries and divergent injuries.11 The dorsal intermetatarsal ligaments between the bases of the 2–5th metatarsals tend to keep the lateral four metatarsals together so that the 1st ray may not be injured or be displaced in a different direction. Although tarsometatarsal joint injuries are often considered to be high-energy injuries, this is not necessarily the case. It is becoming increasingly recognised that low energy trauma, causing minimally displaced injuries, and those where instability can only be demonstrated on stress radiographs from rupture of Lisfranc’s ligament, can give rise to chronic symptoms. Anatomic reduction and fixation has been shown to improve the outcome of these injuries,12 but the most important factor is probably restoration of stability between the bases of the 2nd and 3rd metatarsals and the cuneiforms to reconstruct the supportive function of the foot.
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Figure 10 Lisfranc injury mechanisms. A force directed at the back of the heel when the forefoot is in contact with the ground may disrupt the weaker dorsal ligaments of the tarsometatarsal joints. The ligaments may also be injured when weight bearing on the hyperplantarflexed foot. Plantar ligaments will tend to be protected by tension in the plantar aponeurosis from toe extension.
Midtarsal joint Midtarsal joint injuries are less common than tarsometatarsal injuries. Minor avulsion fractures may be seen around the talonavicular joint or lateral aspect of the cuboid and these heal readily with functional treatment. Significant injury to the midtarsal joint generally requires high-energy trauma. The most frequent mechanism appears to be medially directed bending stress with or without some degree of longitudinal compression.13,14 Lateral or plantar bending, or crushing can also cause midtarsal joint injury. Injury usually results in fracture of articulating bones and the navicular is most frequently damaged as a result of compression against the talar head. Split and comminuted fractures occur. Comminution usually affects the plantar lateral aspect of the bone in the region of the attachment of the plantar calcaneonavicular ligament and the navicular component of the bifurcate ligament. With loss of these plantar ligament attachments the dorsomedial fragment is often displaced by the intact tibialis posterior (Fig. 11). The disruption and loss of thickness of the navicular may lead to adduction of the forefoot or loss of arch height. It is important to try to restore the stability and function of the talonavicular joint by reduction and fixation of the navicular, with bone grafting if necessary, in order to restore stability and flexibility at the subtalar and midtarsal joints. With comminuted fractures this may
Figure 11 The dorsomedial fragment in navicular fractures tends to be displaced by the pull from tibialis posterior as it is no longer attached to the strong inferior calcaneonavicular ligaments.
be difficult, but the rigidity of the midfoot can sometimes be utilised to enhance fixation by using buttress plates bridging the naviculocuneiform joints to secure congruity of the talonavicular joint (Fig. 12).
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Injury to the midtarsal joint by lateral bending causes compression fractures of the cuboid or anterior process of the os calcis, and are often associated with avulsion fractures of the tuberosity of the navicular. Bone grafting and fixation are often required to restore the length of the lateral side, alignment of the foot, and stability of the calcaneocuboid joint, important for midtarsal stability on weight bearing and heel elevation.
Injuries to the hindfoot Talus fracture Dorsiflexion forces may cause injury around the ankle or hindfoot. The strength of the plantar ligamentous structures probably protects the mid-
Figure 12 The dorsomedial fragment of the navicular has been reduced and held with a dorsal buttress plate fixed to the intermediate cuneiform, restoring congruity to the talonavicular joint. The small comminuted plantar fragments of the navicular were unsuitable for direct fixation of the fracture.
Figure 13 With the talus compressed against the tibia a dorsiflexion force to the forefoot can cause a fracture of the talar neck or body by impingement against the anterior tibia.
Figure 14 Sagittal and coronal primary fracture lines that typically occur in fractures of the os calcis. Additional fracture lines occur to produce the joint depression or tongue type fracture patterns.
foot and forefoot from acute injury. High-energy trauma can result in fracture of the neck or body of the talus. The mechanism involves impingement of the anterior tibia against the anterior talus, but in the experimental situation compression under the heel is also required to generate these fracture patterns (Fig. 13).15 More severe fracture patterns are seen if there is a supination component to the trauma. One of the main concerns following such fractures is damage to the vulnerable vascularity of the body of the talus.
Os calcis fracture Crushing or compression can cause major injuries to the foot. The forefoot is most frequently damaged by external compression forces, but axial loading under the heel can cause significant injury to the hindfoot and to the os calcis itself. Os calcis fractures are frequently comminuted, displaced and involve the subtalar and sometimes the calcaneocuboid joint. The pattern of fracture is a consequence of the anatomy of the bones and the subtalar joint. The strongest ligamentous attachments between the talus and os calcis, the medial ligament and interosseous ligament, are both medial to the main load-bearing posterior facet of the subtalar joint. Under axial loading a sagittal split, or primary fracture line, occurs separating the medial sustentacular fragment from the lateral articular fragment (Fig. 14). The lateral process of the talus impinges in the angle of Gissane to produce a second primary fracture line separating the anterior and posterior parts of the os calcis.16 The articular fragment becomes impacted in the tuberosity fragment which in turn comes to lie between the sustentacular and articular fragments and must be distracted from this position if the articular fragment is to be reduced. The sustentacular fragment remains in its anatomical
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relationship with the talus by virtue of the medial and interosseous ligaments. Subtalar joint Subtalar dislocation, in reality a combined subtalar and talonavicular dislocation, occurs as a result of high-energy trauma. Displacement in these injuries is usually in a medial direction due to the greater capacity for inversion at the subtalar joint and the relative strength of the medial ligament. Once the interosseous ligament of the subtalar joint ruptures the talar head can be dislocated from its osseoligamentous socket. The navicular remains attached to the hindfoot because of the strength of the calcaneonavicular ligaments. Fracture of the talar neck or body, subtalar dislocation, and intra-articular os calcis fracture all affect the subtalar joint. Reduction of subtalar dislocation is clearly important, and this may need to be an open procedure to relocate any tendon entrapment. The urge to achieve early movement in the joint must be countered against the risk of hindfoot instability and so the current recommendation is for 4–6 weeks immobilisation. By contrast instability of the subtalar joint after os calcis fracture is a consequence of persisting depression of the articular fragment, because the interosseous and medial ligaments usually remain intact. The primary aim of surgical reconstruction of these fractures is to restore congruity to the joint to avoid instability and allow normal movement. As the joint is a highly congruent multifaceted articulation it seems that a highly accurate reduction is required in order to achieve this, and the margin for error may be less than 1 mm.17 Other aims of surgery are to restore the height and alignment of the heel to restore normal function to the tendo Achillis and theoretically also to the plantar aponeurosis, as well as to reduce lateral impingement and improve shoe fitting.
Crush injury The rigidity of the midfoot protects it from twisting and bending forces with damage occurring either at the more mobile midtarsal joint or the tarsometatarsal joints. It can, however, be damaged by crushing injuries producing complex and varied fractures and dislocations through the midfoot bones. Such injuries usually also involve either the midtarsal or tarsometatarsal joints. Reduction and fixation of these injuries is important for restoring the supportive function of the foot, but the timing of this must be determined with regard to the soft tissue injury.
Figure 15 Fractures of the metatarsal necks tend to plantarflex under the influence of the plantar aponeurosis. This may be exacerbated by swelling and bleeding in the muscle compartments of the foot.
Fractures of the metatarsals are common and may be the result of crush injury or overuse. Crushing is associated with greater degrees of soft tissue injury with the risk of compartment syndrome, multiple fractures, and displacement. The more distal the fracture the greater the risk of displacement and there is a tendency for plantar displacement and shortening because of tension in the plantar structures including the plantar aponeurosis, which is likely to be exacerbated by soft tissue swelling (Fig. 15). Displaced fractures can cause significant problems, not only from irregularity of the height of metatarsal heads causing metatarsalgia, but from shortening which may compromise the function of the plantar aponeurosis. This may be a contributory factor in the development of secondary claw toe deformity from loss of the reversed windlass mechanism. The supporting and dynamic functions of the plantar aponeurosis at the midfoot and hindfoot may also be impaired. Displacement of more than 3–4 mm or angulation greater than 101 should be reduced.18
Conclusions In managing the injured foot our aims should be to relieve pain, and restore stability and flexibility to bones and joints. Joints should be reduced and stabilised—non-flexible ones so that their supportive function can be restored; flexible ones so that they are congruent, allowing restoration of motion without instability. The length and alignment of bones should be restored and maintained for the proper functioning of the extra-articular ligamentous systems—the plantar aponeurosis and deep transverse intermetatarsal ligament complex. Where normal function of part of the foot cannot be restored this should be done with an understanding of how this will affect the function of the foot as a whole. Arthrodesis of a non-flexible joint will have minimal impact on foot function, but
ARTICLE IN PRESS The structure and function of the foot in relation to injury arthrodesis of a normally flexible joint, although it may be necessary in order to provide pain relief and stability, will have some effect on foot function. Stability can be achieved with appropriate reduction and fixation techniques, but stiffness remains a common sequel to the badly injured foot and may be aggravated by surgery and immobilisation. The merits of surgical fixation of fractures and dislocations in the foot must be weighed against the risks of surgery and further soft tissue disruption. With a proper understanding of the structure and function of the foot a balanced judgement can be made regarding surgery and the techniques that might be used.
4. 5.
6.
7. 8.
9.
Practice points
10.
11.
Restore structural stability to the calcaneocuboid, midfoot, and tarsometatarsal joints. Restore stability and flexibility to the subtalar, talonavicular, and metatarsophalangeal joints. Restore skeletal length and alignment to preserve the supportive and dynamic functions of the plantar aponeurosis.
12.
13. 14.
15.
References 1. van Langelaan EJ. A kinetical analysis of the tarsal joints. An X-ray photogrammetric study. Acta Orthop Scand Suppl 1983;54:1–269. 2. Taniguchi A, Tanaka Y, Takakura Y, Kadono K, Maeda M, Yamamoto H. Anatomy of the spring ligament. J Bone Joint Surg [Am] 2003;85-A:2174–8. 3. Solan MC, Moorman CT, Miyamoto RG, Jasper LE, Belkoff SM. Ligamentous restraints of the second tarsometatarsal
16.
17.
18.
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joint: a biomechanical evaluation. Foot Ankle Int 2001;22: 637–41. De Doncker E, Kowalski C. Le pied normal et pathologique. Acta Orthop Belgica 1970;36:386–559. Stainsby GD. Pathological anatomy and dynamic effect of the displaced plantar plate and the importance of the integrity of the plantar plate—deep transverse metatarsal ligament tie-bar. Ann Roy Coll Surg Engl 1997;79:58–68. Mann RA. Biomechanics of the foot and ankle. In: Coughlin MJ, Mann RA, editors. Surgery of the foot and ankle. 7th ed. St. Louis: Mosby; 1999. p. 2–35. Hicks JH. The foot as a support. Acta Anatomica 1955;25: 34–45. Tansey PA, Briggs PJ. Active and passive mechanisms involved in the control of heel supination. Foot Ankle Surgery 2001;7:131–6. Hicks JH. The mechanics of the foot II. The plantar aponeurosis. J Anat 1954;88:25–31. Khaw F-M, Mak P, Johnson GR, Briggs PJ. Distal ligamentous restraints of the first metatarsal. An in vitro biomechanical study. Clin Biomech 2004; in press. Hardcastle PH, Reschauer R, Kutscha-Lissberg E, Schoffmann W. Injuries to the tarsometatarsal joint. Incidence, classification and treatment. J Bone Joint Surg [Br] 1982;64-B:349–56. Myerson MS. The diagnosis and treatment of injury to the tarsometatarsal joint complex. J Bone Joint Surg [Am] 1999;81-B:756–63. Main BJ, Jowett RL. Injuries of the midtarsal joint. J Bone Joint Surg [Br] 1975;57-B:89–97. Sangeorzan BJ, Benirschke SK, Mosca V, Mayo KA, Hansen ST. Displaced intra-articular fractures of the tarsal navicular. J Bone Joint Surg [Am] 1989;71-A:1504–10. Peterson L, Romanus B, Dahlberg E. Fracture of the collum tali: an experimental study. J Biomech 1976;9:277–9. Essex-Lopresti P. The mechanism, reduction technique, and results in fractures of the os calcis. Br J Surg 1952;39: 395–419. Buckley RE, Meek RN. Comparison of open versus closed reduction of intraarticular calcaneal fractures: a matched cohort in workmen. J Orthop Trauma 1992;6:216–22. Granberry WM, Shereff MJ. Treatment of complex forefoot injuries. In: Adelaar RS, editor. Complex foot and ankle trauma. Philadelphia, New York: Lippincott-Raven; 1999. p. 205–16.
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MINI-SYMPOSIUM: THE FOOT
(ii) The hindfoot: Calcaneal and talar fractures and dislocations—Part I: Fractures of the calcaneum Donald J Mcbridea,, C. Ramamurthya, Patrick Laingb a
University Hospital of North Staffordshire, Princes Road, Stoke-On-Trent ST4 7LN, UK Wrexham Maelor Hospital,Wrexham LLI3 7TD, UK
b
KEYWORDS Hindfoot fractures; Hindfoot dislocations; Calcaneal fractures; Os calcis fractures; Talus fractures; Management; Complications
Summary While extra-articular calcaneal fractures are usually treated simply with good results, the management of intra-articular calcaneal fractures remains controversial. Despite advances in surgical techniques and a good understanding of possible complications making operative treatment relatively ‘safe’, doubts remain about the efficacy of surgery in reducing the two main problems of persistent pain and subtalar osteoarthritis. Further randomised controlled trials may be required to confirm or refute the potential benefits of surgery. & 2005 Published by Elsevier Ltd.
Introduction The calcaneum is the most frequently injured tarsal bone comprising 1–2% of all fractures and about 75% of those affecting the foot. The management of calcaneal intra-articular fractures and dislocations, particularly surgical, remains highly controversial. There have been significant advances in relation to understanding the fracture mechanism,1 classification,2 surgical approaches,3 operative techniques and the management of the soft tissues before, during and after surgery.4 A recent study has given some support to surgery5 particularly in Sanders
grade II and, to a lesser extent, grade III fractures, but some reservations have been expressed.
Fracture patterns and mechanism Calcaneal fractures may be either extra-articular (25%) or intra-articular (75%). The fracture pattern is dependent on:
the direction and amount of force applied, the position of the foot relative to the ankle, the neuromuscular system, the bone quality, which may be affected by the patient’s age.
DOI of original article: 10.1016/j.cuor.2005.03.005
Corresponding author. Tel.: +01782 554452;
fax: +01782 630270. E-mail addresses:
[email protected] (D.J. Mcbride),
[email protected] (C. Ramamurthy),
[email protected] (P. Laing). 0268-0890/$ - see front matter & 2005 Published by Elsevier Ltd. doi:10.1016/j.cuor.2005.03.004
Extra-articular fractures These usually affect the anterior process, the calcaneal tuberosity, the body of the calcaneum
ARTICLE IN PRESS The hindfoot: Calcaneal and talar fractures and dislocations—Part I: Fractures of the calcaneum (not involving the subtalar joint) or, rarely the sustentaculum tali. They are generally simple injuries which may be treated conservatively but some may require further investigation and surgery.
Anterior process fractures There are two principle types of anterior process fracture:
affecting the upper and lateral part of the lateral process with simple avulsion of the bifurcate ligament. Conservative treatment is usually appropriate. a larger intra-articular fracture affecting the calcaneocuboid joint due to forced abduction of the forefoot or eversion in dorsiflexion resulting in compression.6 This may be associated with intra-articular fractures of the subtalar joint and should be investigated by CT scan with a view to operative treatment. These are easily missed and may cause long-term discomfort.
Fractures of the body These are generally simple fractures involving the posterior and inferior parts of the body lying behind the posterior facet of the subtalar joint. They are normally conservatively treated and have a good prognosis, but occasionally the heel pad is affected, which may give rise to more protracted symptoms and require further treatment.
Fractures of the calcaneal tuberosity The foot is in plantarflexion at the time of the injury with the force going directly upwards through the tuberosity, resulting in avulsion of the tendo Achilles or a fracture of the medial process. The fracture line runs from a point inferior to the posterior facet of the subtalar joint a variable distance into the body. Undisplaced fractures are satisfactorily treated in an equinus below knee cast, an anterior equinus slab or a functional brace but displaced fractures require open reduction and internal fixation. This can be quite difficult in the occasional case presenting late.
perspective, the aims should be:
adequate pain relief both immediately and in the longer term, adequate restoration of subtalar joint function, early return to work, reduction of the risk of long-term subtalar osteoarthritis.
History and examination Such fractures usually follow falls from a height greater than 2 m and are most commonly unilateral.7 They may be associated with more proximal injuries, particularly lumbar fractures and are sometimes seen in polytrauma patients, often with associated talar fractures or dislocations.8 With compression, the longitudinal arch may be reduced or abolished with broadening of the hindfoot. Bruising laterally or on the plantar surface of the foot after 24–48 h (Fig. 1) may be associated with the development of blisters and occasionally compartment syndrome. Open fractures, with or without dislocation, are rare.
Radiography Properly performed plain radiographs can yield as much information as more complex investigations. They should include an AP view of the foot and ankle, a lateral views of the ankle and calcaneum and an axial view. Brodens views taken either preoperatively or intraoperatively with the foot internally rotated 451 and inclined 101, 201, 301 and 401 to the posterior facet give an excellent view of the subtalar joint. Bohler’s angle, formed by the intersection of lines drawn from the posterior tuberosity and anterior process should be measured. It is normally 25–401 (Fig. 2). Gissane’s angle should also be
Intra-articular fractures These form the vast majority of calcaneal fractures and are a significant challenge. From the patient’s
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Figure 1 Skin bruising.
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Figure 2 Bohler’s and Gissane’s angles.
measured; the angle of inclination of the subtalar joint intersecting with a line drawn from the superior process of the calcaneum (Fig. 2). CT scanning has become the investigation of choice for preoperative planning and occasionally intraoperative assessment.9
Classification The Sanders classification2 is widely accepted (Fig. 3) but not universally.10 Problems usually arise because of incorrectly or inadequately performed CT scans and the most useful ‘cuts’ are taken in the coronal plane inclined 251 through the sustentaculum tali (Fig. 4) which may be occasionally fractured in isolation (Fig. 5). 3D reconstructions may be useful, particularly when the talus or cuboid is subtracted. Joint assessment with a radiologist often yields the greatest information.
Management of intra-articular calcaneal fractures This is either conservative or operative. A variety of ‘semi-conservative’ techniques have been described which are of historical interest.11,12 More recently minimally invasive techniques have been developed using either intraoperative X-ray or CT scan guidance9 but their position in management awaits clarification. Conservative This should not be considered as the easy option. All patients with intra-articular fractures should be admitted to hospital and, while awaiting investigation, have the limb rested, with ice packs applied with or without compression (eg. ‘Flowtron’ boots), and with elevation preferably on a Braun frame.
Figure 3 Sanders classification.
The following may be considered for conservative treatment:
Sanders grade I fractures with insignificant displacement of the fracture fragments i.e. less than 2 mm. Those with contra-indications for surgical treatment such as poorly controlled diabetes, peripheral vascular disease, heavy smokers,13 ethanol and drug addiction and patients who may be potentially unreliable or poorly compliant with treatment. Age is a relative contraindication but it is unusual to offer surgery to those over 60.
When the swelling and pain have settled, the fracture is managed in a below knee lightweight cast or, preferably a functional brace for a 4–6
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week period, non-weight bearing for a further 2 weeks dependent on radiographic appearance with physiotherapy mobilising the subtalar, ankle and other adjacent joints.
Figure 4 CT coronal view of calcaneal fracture.
Operative Why is surgical treatment of these injuries so controversial?14 They are intra-articular, occur in a major weight-bearing joint, and have important effects on hindoot mechanics, significantly altering the relationship between the ankle and subtalar joints and the midfoot and forefoot. They result in effective Achilles tendon shortening and variable lateral impingement, principally affecting the peroneal tendons. The controversy arises from historical concern regarding complications of surgical treatment. However, with sensible preoperative planning (including timing), careful management of soft tissues and bony structures intraoperatively, early active and passive mobilisation of the joints postoperatively and careful patient selection, complications can be minimised. The decision to offer surgery to individual patients depends on the Sanders classification of the fracture.2 However, the plain radiographs and CT scans, including the 3D reconstructions, help clarify the primary and secondary fracture lines (Fig. 6) for each individual injury. In general terms, grade II and III fractures should undergo open reduction and internal fixation (ORIF) and grade IV fractures may alternatively undergo calcaneal body reconstruction with a primary subtalar fusion.15,16 The aims of surgery are:
Figure 5 CT scan coronal view showing sustentaculum tali fracture.
reconstruction of the subtalar joint, particularly the posterior facet, restoration of calcaneal height, restoration of calcaneal width, if necessary, reconstruction of the calcaneocuboid joint, if necessary primary subtalar fusion (selected grade IV cases).
Surgery is carried out when the swelling has subsided and the ‘wrinkle sign’ is present (Fig. 7), usually between 5 and 14 days after the injury. After 3 weeks, partial bone healing has often occurred making reduction more difficult with an increased risk of wound complications. The operation is performed under general or regional anaesthetic with the patient in the lateral (unilateral fracture) or prone (bilateral) position with a thigh tourniquet. An extended lateral approach with an L-shaped incision as described by Sanders2 and Eastwood et a1.3 is currently the preferred technique. A medial approach is seldom
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Figure 8 Extended lateral approach.
Figure 6 Fracture lines.
Figure 7 ‘Wrinkle sign’.
required. The skin incision starts about 3–4 cm above the level of the ankle between the distal fibula and the Achilles tendon and curves at about 901 passing down the lateral border of the foot to about 1 cm short of the fifth metatarsal base taking care to avoid the local ‘bruised area’ (Fig. 8). The sural nerve is at risk at both the proximal and distal parts of the incision. A complete flap is elevated down to the periosteum until the peroneal tendons are identified and retracted. Three stout K-wires are inserted in the distal fibula, the talus and the
cuboid as retractors to expose the whole of the calcaneum. The subtalar joint is opened by dividing the calcaneo-fibular ligament and by removing local soft tissue. The lateral component of the articular surface is usually rotated inferiorly and lies deep to the lateral wall of the os calcis. Opening the lateral wall allows visualisation of this fragment and its reduction to the main medial fragment (Sanders II) or fragments (Sanders 111/ 1 V). This part of the calcaneum should be temporarily fixed with two or more K-wires. Frequently the main body fragment needs to be depressed and shifted medially to allow room for the reduction of the lateral articular fragment(s) and wall. Then the distal part of the calcaneum extending down to the calcaneo-cuboid joint is approached. This fragment(s) is normally rotated away from the operator vertically by the local strong ligaments and may also be vertically split. The superior soft tissue has to be released carefully to derotate the fragment(s) prior to the insertion of two or more K-wires. Once this has been achieved, there are usually proximal and distal segments with the wires being utilised like the joysticks of an aeroplane to restore the angle of Gissane. Check radiographs using an image intensifier, in particular Brodens views, confirm the adequacy of the reduction. The plate and screws of choice may be applied and may include a Y reconstruction plate, a calcaneal plate either with or without locking screws (Fig. 9). In grades II and III, a bone graft is rarely required but with grade IV fractures, screws are inserted across the subtalar joint after removing the articular cartilage and inserting a corticocancellous autologous bone graft. Further check radiographs are taken at this stage. The peroneal tendons are relocated and the wound closed over a single drain with sutures of choice that should be retained for 3 weeks. A backshell cast may be applied for comfort for 48 h during which time the
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screws or plate and may occasionally cause peroneal tendon impingement, which may require removal. Subtalar osteoarthritis: This occurs in conservatively or operatively treated fractures. The principle reason for surgery is to try and reduce its incidence and there is a trend towards support for this from the current literature.5 Each case should be treated on its individual merits.
Practice points and research directions
Figure 9 Internal fixation of os calcis fracture.
limb is elevated. The drain is then removed and the patient mobilised non-weight bearing for 6–8 weeks with crutches when radiographs are performed to assess whether full weight bearing may commence. Early active and passive motion of the ankle, subtalar, and adjacent joints should be encouraged by the physiotherapist. Surgical complications have been well covered in a recent article.13 They include:
Wound complications including infection, haematoma and dehiscence: Superficial infection occurs in up to 27% with deep infection and osteomyelitis in up to 2.5%. The latter is more commonly seen following open fractures. Haematoma occurs more frequently when drains are not utilised. Wound dehiscence usually starts at the angle of the incision. These may be reduced by careful timing of surgery and with careful handling of the soft tissues. Additional risk factors include diabetes, peripheral vascular disease and smoking. Compartment syndrome: This may occur after conservative or operative treatment. The incidence varies from 10% to 50%.17 Early recognition and surgical treatment by fasciotomy is essential to prevent serious long-term complications including contractures and pain. Neurological injury: The sural nerve is at greatest risk but the medial and lateral plantar nerves may be damaged when drilling or inserting screws or wires from the lateral side or when using a medial approach. Malunion with or without adequate subtalar reduction: This, of course, is much commoner after conservative treatment. The types of malunion have been classified by Stephens and Sanders.18 Metalwork problems: These are relatively uncommon but may present as prominence of the
Calcaneal fractures are the commonest injuries of the tarsal bones. Sanders CT scan classification is a useful method of assessing the fracture pattern and deciding on management. Despite rapid and excellent advances in surgical treatment there remains no convincing evidence that this should be the treatment of choice. The strongly held belief by many surgeons of the advantages of surgical treatment can only be confirmed or refuted by properly evaluated randomised controlled trial.
References 1. Carr JB. Mechanism and pathoanatomy of the intraarticular calcaneal fracture. Clin Orthop 1993;290:36–40. 2. Sanders R, Fortin P, Dipasquale T, Walling A. Operative treatment in 120 displaced intraarticular calcaneal fractures. Results using a prognostic computed tomography scan classification. Clin Orthop 1993;290:87–95. 3. Eastwood DM, Langkamer VG, Atkins RM. Intra-articular fractures of the calcaneum. Part II: Open reduction and internal fixation by the extended lateral transcalcaneal approach. J Bone Joint Surg 1993;75-B(2): 189–95. 4. Levin LS, Nunley JA. The management of soft-tissue problems associated with calcaneal fractures. Clin Orthop 1993;290:151–6. 5. Buckley R, Tough 5, McCormack R, Pate G, Leighton R, Petrie D, Galpin R. Operative compared with nonoperative treatment of displaced intra-articular calcaneal fractures: a prospective, randomized, controlled multicenter trial. J Bone Joint Surg Am 2002;84-A(10):1733–44. 6. Ebraheim NA, Biyani A, Padanilam T, Christiensen G. Calcaneocuboid joint involvement in calcaneal fractures. Foot Ankle Int 1996;17:563–5. 7. Dooley P, Buckley R, Tough S, McCormack B, Pate G, Leighton R, Petrie D, Galpin B. Bilateral calcaneal fractures: operative versus nonoperative treatment. Foot Ankle Int 2004;25(2):47–52. 8. Gregory P, DiPasquale T, Herscovici D, Sanders R. Ipsilateral fractures of the talus and calcaneus. Foot Ankle Int 1996;17:701–5.
ARTICLE IN PRESS 100 9. Rammelt 5, Amlang M, Barthel S, Zwipp H. Minimally invasive treatment of calcaneal fractures. Injury 2004;35(Suppl 2):5B55–63. 10. Bhattacharya R, Vassan UT, Finn P, Port A. Sanders classification of fractures of the os calcis. An analysis of inter- and intra-observer variability. J Bone Joint Surg Br 2005;87(2):205–8. 11. Essex-Lopresti P. The mechanism, reduction, technique, and results in fractures of the os calcis. Br J Surg 1952;39:395–419. 12. Pozo JL, Kirwan EO’G, Jackson AM. The long-term results of conservative management of severely displaced fractures of the calcaneus. J Bone Joint Surg 1984;66-B(3):386–90. 13. Lim EVA, Leung JPF. MD complications of intraarticular calcaneal fractures. Clin Orthop Relat Res 2001(391):7–16.
D.J. Mcbride et al. 14. Randle JA, Kreder HJ, Stephen D, Williams J, Jaglal 5, Flu R. Should calcaneal fractures be treated surgically? A metaanalysis. Clin Orthop 2000;377:217–27. 15. Sanders R. Displaced intra-articular fractures of the calcaneus. J Bone Joint Surg Am 2000;82:225–50. 16. Huefner T, Thermann H, Geerling J, Pape HC, Pohlemann T. Primary subtalar arthrodesis of calcaneal fractures. Foot Ankle Int 2001;22(1):9–14. 17. Myerson M, Manoli A. Compartment syndromes of the foot after calcaneal fractures. Clin Orthop 1993;290: 142–50. 18. Stephens HM, Sanders R. Calcaneal malunions: results of a prognostic computed tomography classification system. Foot Ankle Int 1996;17:395–401.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 101–107
www.elsevier.com/locate/cuor
MINI-SYMPOSIUM: THE FOOT
(ii) The hindfoot: Calcaneal and talar fractures and dislocations—Part II: Fracture and dislocations of the talus Donald J Mcbridea,, C. Ramamurthya, Patrick Laingb a
University Hospital of North Staffordshire, Princes Road, Stoke-On-Trent ST4 7LN, UK Wrexham Maelor Hospital, Wrexham LLI3 7TD, UK
b
KEYWORDS Hindfoot fractures; Hindfoot dislocations; Calcaneal fractures; Os Calcis fractures; Talus fractures; Management; Complications
Summary Talar fractures and dislocations are uncommon but even initially apparently simple fractures may be more complex after adequate investigation. Talar neck fractures and the less common talar body fractures remain a surgical challenge with high complication rates, which have been shown to be reduced by early intervention with anatomical reduction and fixation. & 2005 Published by Elsevier Ltd.
Introduction
Anatomy and blood supply
While fractures and dislocations of the talus are rare they can have devastating effects leading to significant disability due to the unique anatomy and blood supply of the talus. Patients must be informed of this risk from the outset.
It is essential to understand the special anatomy and blood supply of the talus (Fig. 1). The talus has three parts, the head, neck and the body. It transmits body weight between the ankle and subtalar joints and articulates with the navicular distally and medially. The trochlea is wider at the front and, therefore, dorsiflexion of the ankle provides a more stable configuration. In addition its unique shape accommodates plantar-flexion and rotation at the ankle, inversion and eversion at the sub-talar joint with rotation and translation at the talo-navicular joint. About 70% is covered with articular cartilage and only the extensor digitorum brevis takes origin from
DOI of original article: 10.1016/j.cuor.2005.03.004
Corresponding author. Tel.: +01782 554452;
fax: +01782 630270. E-mail addresses:
[email protected] (D.J. Mcbride),
[email protected] (C. Ramamurthy), denise.
[email protected] (P. Laing). 0268-0890/$ - see front matter & 2005 Published by Elsevier Ltd. doi:10.1016/j.cuor.2005.03.005
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D.J. Mcbride et al. compression fracture (sometimes with an associated navicular injury) and a longitudinal or oblique fracture. These rarely require treatment of themselves but a talar head fracture may be associated with other midfoot injuries including fracture dislocations, which will require separate management.
Fractures of the talar neck with or without dislocation
Figure 1 Blood supply of the talus.
its surface. The extraosseous blood supply arises from the three main arteries in the distal leg; the posterior and anterior tibial and the peroneal. The artery of the tarsal canal (posterior tibial) delivers most of the blood supply to the talar body and the artery of the tarsal sinus (anterior tibial and peroneal) provides the main contribution to the talar head and neck. These latter two vessels form an arterial ring around the sinus tarsi and talar neck. Additional blood supply to the talar body is derived from the deltoid artery in the deep portion of the deltoid ligament (Fig. 1). It is vulnerable to avascular necrosis as arterial continuity across the talus only occurs in about 60%.1,2
These constitute about 50% of all talar fractures, 3–4% of fractures affecting the foot and 0.5% of all fractures. Nowadays, they most frequently result from road traffic accidents but they were classically described in pilots as ‘aviators astragalus’.4 Approximately, one-fifth to one-third will have associated foot or ankle fractures, particularly the medial malleolus, and two-thirds will have other bone or soft tissue injuries. The fractures may be open and part or all of the body may be extruded through the skin.
Mechanism The fracture is caused by forced dorsi-flexion of the ankle against a fixed distal tibia with the talar neck impacting against its anterior margin. Wilson5 considered this in some detail, reviewing the literature and suggesting the following:
Talar injuries
A high injury injury is required e.g. RTA or airplane crash. The victim is braced for an emergency i.e. has a rigidly extended limb with the joints fixed by muscular action. The arch of the foot is poised on a small impact body e.g. The pedal of a car or the rudder bar of an older type of aircraft.
A variety of injuries may occur to this relatively small bone. They may be described as central or peripheral3,4 or in anatomical terms:
Subsequently, with further force, rotation either occurs into inversion (commonest) with dislocation of the sub-talar, ankle or talo-navicular joints. The talar body may extrude through the skin postero-medially and may damage the local neurovascular bundle. Rarely, rotation occurs into eversion with the foot and talar head subluxating or dislocating laterally.
Fractures of the talar head. Fractures of the talar neck with or without dislocation. Fractures of the talar dome. Fractures of the posterior process. Fractures of the lateral process. Osteochondral fractures affecting the talar dome. Minor avulsion fractures usually associated with ligament injuries of the ankle.
Classification Hawkins6 described three fracture types in 1970 with Canale and Kelly7 adding a fourth. These are:
Fractures of the talar head
These are rare, only accounting for about 5–10% of talar fractures. There are two main types; a
Type I: Undisplaced fracture of the talar neck which only disrupts the blood supply to the dorsolateral neck.
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Type II: Displaced fracture of the talar neck with sub-talar joint subluxation or dislocation. This affects the blood supply to the dorsolateral neck but also from the sinus tarsi and tarsal canal. Type III: Displaced fracture of the talar neck with dislocation of the sub-talar and ankle joints. The talar body blood supply is completely disrupted except for the deltoid branches, which may be twisted. Type IV Displaced fracture of the talar neck with dislocation of the sub-talar and ankle joints and subluxation or dislocation of the talo-navicular joint. This additionally affects the blood supply to the talar head.
Management
Figure 2 Type I neck of talus fracture.
Type I (Fig. 2) These are usually treated conservatively with immobilisation in a lightweight below knee cast for 6–12 weeks non-weight bearing. Radiographs should be obtained regularly over the first few weeks. There is some controversy about the position of the cast with some advocating partial or full equinus to reduce the risk of displacement and others proposing ORIF of these fractures to ablate this risk. An equinus cast may lead to an equinus deformity and, therefore, there should be a low threshold for fixation. Clearly if the fracture does displace it automatically becomes a type II.
Type II This is essentially a displaced unstable fracture with a variable soft tissue injury. The minimum initial treatment should be an immediate closed reduction to relieve soft tissue tension. A cast may be applied, usually in plantar-flexion, but if a perfect anatomical reduction cannot be achieved then surgical intervention should not be delayed. Alternatively if the position is satisfactory a CT scan may be requested prior to surgery. The ideal situation, however, is closed reduction, followed by a CT scan then surgery. The aims of the operation are the same as in any fracture involving a weight-bearing joint; stable anatomical reduction and internal fixation. Closed percutaneous screw fixation is an occasional option but does not allow for adequate visualisation of qthe reduction. Most therefore advise open reduction and internal fixation, using anteromedial, anterolateral or posterolateral approaches with or
Figure 3 Internal fixation of talar fracture.
without a medial malleolar osteotomy. Two or more screws are generally used to provide stable fixation (Fig. 3) and are best inserted from posterior to anterior, as this is more biomechanically sound. The position is confirmed using an image intensifier.
Type III (Fig. 4) These injuries require immediate surgical treatment. Closed reduction is seldom possible and even open reduction may be anything but straightforward. Reduction is aided by maximum muscle relaxation and the use of a calcaneal pin or a reduction device on a frame. Similar approaches
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Post-operative care For grade II, III and IV fractures the post-surgical care is similar. An initial plaster backshell is applied for comfort to allow the soft tissues to heal and the swelling to settle followed by a below knee cast for 8–12 weeks to allow fracture healing, as assessed by serial radiographs. Following plaster removal weight bearing is allowed with physiotherapy to encourage early mobilisation of the affected joints. Follow-up should be for a minimum period of 2–3 years.
Dislocations
Figure 4 Type III talar fracture.
are utilised as with type II fractures but there is a high incidence of associated medial malleolar fracture that may facilitate reduction. The fracture itself is often comminuted especially in the medial neck and care has to be taken with reduction and fixation to prevent varus deformity of the neck. The anterolateral approach allows accurate reduction of the lateral neck and visualisation of the sub-talar joint. Bone graft may be used medially if required.
Isolated dislocations of the sub-talar joint (Fig. 5) are rare8 with 80% occurring medially but they may be lateral, anterior or posterior, the latter two being extremely rare. In order to occur there has to be an associated dislocation of the talo-navicular joint. The injury may initially be misdiagnosed but prompt closed reduction is necessary and can usually be achieved. Once reduced the position is often stable with a good range of movement. Occasionally, open reduction is required most
Type IV These are similar to type III fractures with supplementary stabilisation of the talonavicular joint, usually with K-wires, which are removed at 6–8 weeks.
Open fractures Type II, III and IV fractures are frequently associated with significant open wounds, which should be treated in a standard manner with lavage, surgical debridement, fixation to protect the healing tissue, antibiotics and, usually, secondary closure. Minor wounds will usually heal uneventfully but occasionally more major soft tissue loss may require the attention of a plastic surgeon, who should be involved early.
Figure 5 Subtalar dislocation.
ARTICLE IN PRESS The hindfoot: Calcaneal and talar fractures and dislocations—Part II: Fracture and dislocations of the talus commonly because of interposed anterior soft tissues. Associated fractures are common and may be diagnosed on CT scans. They are treated on their own merits. A below knee cast is applied for 4–6 weeks followed by physiotherapy.
Complications The frequency and severity of complications is usually proportional to the degree of displacement, in particular (Table 1):
mented with bone graft and with care to maintain a plantigrade foot. In selected cases with minimal collapse a combined sub-talar fusion with an ankle replacement may be appropriate. Ankle and sub-talar osteoarthritis tend to increase with the Hawkins grading and should be treated on their own merits. They usually develop within 2 years of the injury but it may be difficult to isolate the exact site of the patient’s discomfort clinically. CT scans and diagnostic injections may be useful.
Fractures of the talar dome
delayed union, malunion, avascular necrosis.
Delayed union and non-union occur with increasing frequency with the greater severity of the injury. Non-union is usually defined as no evidence of healing at 6 months. Treatment is difficult but may include revision fixation with bone grafting. Varus mal-union is common in conservatively treated cases but should be minimised by prompt and adequate surgical intervention. Late treatment is difficult although corrective osteotomies have been suggested.9 Avascular necrosis (osteonecrosis) of the talar body10 occurs more frequently with increasing severity of the injury. Symptoms arising from this are variable and not always disabling, in fact, 25% do well with no treatment. The main problem arises when the talus revascularises and becomes quite soft, the whole process taking 2–3 years. Hawkins5 described a sign that may be an early indicator of adequate blood supply to the talar body. It is usually present by 6–8 weeks and appears as a subchondral linear radiolucency of the talar dome on AP radiographs of the ankle, usually on the medial side. However, absence of this sign does not necessarily indicate that avascular necrosis will not develop. Conservative treatment with partial or non-weight bearing, or with a patellar tendon bearing brace, for 2 years is poorly tolerated. In symptomatic cases a trans-calcaneal-talar-tibial arthrodesis may be appropriate, usually suppleTable 1
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These injuries are less common than talar neck fractures but tend to have a poorer prognosis with avascular necrosis occurring more frequently the more posterior the injury. The fracture usually exits the talus posteriorly and frequently involves the ankle and sub-talar joints (Fig. 6). Unfortunately, this frequently leads to secondary osteoarthritis. While undisplaced fractures confirmed on CT scan can be treated conservatively there should be a low threshold for open reduction and internal fixation, which should be undertaken for all displaced fractures.11 The fracture(s) may be approached via a medial malleolar or fibular osteotomy, or both, with anatomical reduction and rigid internal fixation. Occasionally a posterior fracture may be held with closed percutaneous screw fixation (Fig. 7). Post-operative treatment is the same as with other talar fractures.
Fractures of the posterior process These fractures usually involve the lateral posterior process (Stieda), and less frequently the medial posterior process. They are frequently confused with a large os trigonum. The diagnosis may be made more accurately with a CT scan. Small undisplaced fractures can be treated conservatively, but larger displaced fractures should be treated by open reduction and internal fixation using a posterolateral or posteromedial approach as required. Occasionally, these fractures affect the
Complications of talar fractures.
Hawkins type
Type I (%)
Type II (%)
Type III (%)
Delayed/nonunion AVN AnkleOA Sub-talar OA Good results
1.5 3 15 24 72
7 31 36 66 37.5
11 77 69 63 24
NB: there are no reliable figures for type IV fractures in the literature.
ARTICLE IN PRESS 106
D.J. Mcbride et al. Small undisplaced fractures may be treated conservatively but larger displaced fractures require open reduction and internal fixation to reduce the risk to the ankle and sub-talar joints. However, these fractures tend to do badly even when the fixation is adequate.
Osteochondral fractures affecting the talar dome These are mainly associated with trauma but occasionally are idiopathic. They frequently occur with acute ankle sprains but are commoner in chronic lateral ligament instability. They are usually medial or lateral and may present with pain, instability, locking and a history of injury. Plain radiographs may make the diagnosis but CT and MRI scans often will reveal unrecognised Figure 6 Talar body fracture.
Figure 7 Internal fixation of talar body fracture.
function of flexor hallucis longus if not treated and ununited fractures presenting late may require removal.
Fractures of the lateral process These injuries account for about 25% of all talar fractures and occur with axial compression with dorsiflexion and external rotation. They frequently occur in snowboarders.12 A high index of suspicion is required to diagnose as they are frequently missed on plain X-rays, necessitating CT scan (Fig. 8). They may extend into the talo-fibular articulation and the posterior facet of the sub-talar joint.
Figure 8 Lateral process fracture of talus (Snowboarder’s fracture).
ARTICLE IN PRESS The hindfoot: Calcaneal and talar fractures and dislocations—Part II: Fracture and dislocations of the talus associated lesions. There are various classifications depending on the severity of the lesion.13 An arthroscopic assessment aids diagnosis and treatment that may include debridement, drilling, micro-fracture or autlogous chondrocyte implantation usually harvested from the knee, but more recently from the ankle.14 Practice points and research directions
Fractures and dislocations of the talus are rare but can cause significant problems. Certain injuries, in particular posterior and lateral process fractures or osteochondral defects, may be difficult to accurately diagnose with potential significant implications. However, minor avulsion fractures do occur which may be treated simply. Talar neck fractures are the commonest injuries and are classified according to Hawkins as grades I-Ill and Canale and Kelly grade IV. This grading correlates well with the potential for complications, in particular, avascular necrosis and osteoarthritis. Talar body fractures tend to have a poorer prognosis. Patients should be warned from the outset about the potential risks including those associated with treatment. Further studies to determine the exact mechanism of injury and to clarify the short and long term effects of surgical intervention are required.
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References 1. Haliburton RA, Sullivan CR, Kelly PJ, Peterson LFA. The extra-osseous and intraosseous blood supply of the talus. J Bone Joint Surg Am 1958;40:1115–20. 2. Mulfinger GL, Trueta J. The blood supply of the talus. J Bone Joint Surg Br 1970;52:160–7. 3. Boack DH, Manegold S. Peripheral talar fractures. Injury 2004;35(Suppl. 2):SB23–35. 4. Cronier P, Talha A, Massin P. Central talar fractures—therapeutic considerations. Injury 2004;35(Suppl. 2):SB10–22. 5. Wilson DW. Fractures of the foot. In: Klenerman L, editor. The foot and its disorders. 3rd ed. Oxford: Blackwell Scientific Publications; 1991. p. 161–244. 6. Hawkins LG. Fractures of the neck of the talus. J Bone Joint Surg Am 1970;52:991–1002. 7. Canale ST, Kelly Jr FB. Fractures of the neck of the talus. Long-term evaluation of seventy-one cases. J Bone Joint Surg Am 1978;60:143–56. 8. Bibbo C, Anderson RB, Davis WH. Injury characteristics and the clinical outcome of subtalar dislocations: a clinical and radiographic analysis of 25 cases. Foot Ankle Int 2003;24(2): 158–63. 9. Monroe MT, Manoli A. Osteotomy for malunion of a talar neck fracture: a case report. Foot Ankle Int 1999;20(3):192–5. 10. Adelaar RS, Madrian JR. Avascular necrosis of the talus. Orthop Clin North Am 2004;35(3):383–95. 11. Vallier HA, Nork SE, Benirschke SK, Sangeorzan BJ. Surgical treatment of talar body fractures. J Bone Joint Surg Am 2003;85:1716–24. 12. Kirkpatrick DP, Hunter RE, Janes PC, Mastrangelo J, Nicholas RA. The snowboarder’s foot and ankle. Am J Sports Med 1998;26(2):271–7. 13. Hepple 5, Winson IG, Glew D. Osteochondral lesions of the talus: a revised classification. Foot Ankle Int 1999;20(12): 789–93. 14. Hangody L, Kish G, Modis L, Szerb I, Gaspar L, Dioszegi Z, Kendik Z. Mosaicplasty for the treatment of osteochondritis dissecans of the talus: two to seven year results in 36 patients. Foot Ankle Int 2001;22(7):552–8.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 108–118
www.elsevier.com/locate/cuor
MINI-SYMPOSIUM: THE FOOT
(iii) Tarsometatarsal injuries—Lisfranc injuries Nilesh K. Makwanaa,b, a
Wrexham Maelor Hospital, Croesnewydd Road, Wrexham LL13 7TD, UK The Robert Jones and Agnes Hunt Hospital, Oswestry, Shropshire SY10 7AG, UK
b
KEYWORDS Tarsometatarsal injury; Lisfranc; Fracture— dislocation
Summary Lisfranc injuries are relatively uncommon injuries but with increasing motor vehicle use their incidence may be increasing. Missed injuries can lead to chronic pain, deformity and disability and this can be avoided by having a high index of suspicion. Subtle injuries are difficult to diagnose and special imaging or stress Xrays are useful in diagnosis. The classification proposed by Hardcastle et al. (J Bone Joint Surg 64-B (1982) 349) is used most commonly and the aim of treatment must be to obtain an anatomical reduction and stable fixation as soon as possible. Treatment after 6 weeks yields poor results and salvage arthrodesis is inferior to primary reduction and stabilisation. Reduction may be by closed or open methods and fixation by K wires, screws or bioabsorbable screws. Complications occur frequently and need to be detected and managed appropriately. & 2005 Elsevier Ltd. All rights reserved.
History and introduction Jacques Lisfranc de St. Martin (1790–1847) was a French gynaecologist and surgeon. He served in the Napoleonic army and described amputation through the tarsometatarsal (TMT) joint. During the Napoleonic era cavalry troops frequently sustained a Lisfranc dislocation when the foot became trapped in the stirrup. This often led to a profound vascular insult resulting in a Lisfranc amputation. The amputation was described by the French surgeon and it should be noted that he did not describe the fracture dislocation himself.1 Eponyms now associated with Lisfranc include Lisfranc amputation, Wrexham Maelor Hospital, Croesnewydd Road, Wrexham LL13
7TD, UK. Tel.: +44 01978 725191; fax: +44 01978 725391. E-mail address:
[email protected] (N.K. Makwana).
Lisfranc dislocation, Lisfranc joints, Lisfranc ligament and Lisfranc fracture. TMT injuries are rare and can be easily overlooked leading to long term pain and disability.2–6 Early diagnosis and prompt accurate reduction and stabilisation will minimise long-term disability. Controversies exist as to the best method of treatment for these injuries including open or closed reduction, use of screws or Kirshner wires, the timing of treatment and duration of immobilisation. However, in general, a consensus exists that precise anatomical reduction and stabilisation should be achieved as soon as is possible. Lisfranc injuries account for 0.2% of all fractures4,7 and are more common in males. The incidence of Lisfranc injuries is low with 1 case per year in 55,000 fractures treated annually at the Boston City hospital.8 English9 found that only 24 or
0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2004.12.008
ARTICLE IN PRESS Tarsometatarsal injuries—Lisfranc injuries 0.2% of 11,000 patients treated at the Royal Infirmary in Edinburgh had fracture dislocations or multiple fractures involving the metatarsal bones. Vuori and Aro (1993)10 noted an increasing annual incidence of Lisfranc injuries from 7% during 1980–1984 to 12% from 1985 to 1989. That is a 70% increase over the two periods. This may represent a true increase with increasing numbers of high-energy vehicle accidents or better detection of these injuries. Between 20% to 39% of these injuries can be missed10,11 This is especially so in the patient with polytrauma who has concomitant head and chest trauma. The long bone fractures and major injuries are often given precedence with the foot injury given less attention. This combined with poor quality X-rays accounts for the missed or delay in diagnosis.
Anatomy The TMT complex consist of the metatarsals, cuneiforms and cuboid bones with the stability provided by the osseous, capsule and ligamentous attachments.12
Osseous stability The bases of the metatarsals form a transverse arch, high medially and low laterally. In the frontal plane, the lateral aspect of the arch is 20 mm posterior to the medial side.13 The apex corresponds to the second metatarsal or middle cuneiform (Fig. 1). Additional bone stability is provided by the recessed nature of the second metatarsal between the medial and lateral cuneiform. The second metatarsal is often considered the ‘‘keystone’’ as in a Roman arch and is important in
Figure 1 Coronal CT scan at base of metatarsal. Second metatarsal forms the ‘‘apex’’ of the Roman arch. Note fractures of the base of 2nd and 3rd metatarsal.
109 maintaining the arch. The medial cuneiform protrudes 8 mm and the lateral cuneiform 4 mm relative to the second metatarsal, thus creating a cuneiform mortise, which receives its tenon, the 2nd metatarsal base. An interlocking mechanism also exists with the lateral cuneiform being recessed between the second and fourth metatarsal. As a result of the complex interlocking mechanism disruption of the TMT complex is often associated with a metatarsal fracture, usually the second.
Capsular stability The articular capsule consists of a fibrous membrane lined by synovium. The joint capsule divides the TMT complex into columns and this has been proposed as a basis for the classification of these injuries14 The medial column includes the first TMT joint, the central column includes the second and third TMT joints and the lateral column includes the fourth and fifth TMT joints. The medial and lateral column capsule and synovial membrane do not communicate. The normal sagittal motion of the first TMT joint is 3.5 mm, the lateral column is more flexible with a sagittal motion of 13 mm and the central column the least flexible with only 0.6 mm motion. It is held virtually rigid in the recess.12
Ligamentous stability The ligaments of the Lisfranc complex are variable both in course, number and insertion. They are classified into dorsal, plantar and interosseus ligaments. Each has longitudinal and transverse elements. The longitudinal elements connect the TMT joint and the transverse the intermetarsal and intercuneiform bones. There is no intermetatarsal ligament between the 1st and 2nd metatarsal. The dorsal ligaments are short flat ribboned structures numbering 6–8. They are weaker than the plantar and interosseus ligaments; hence, dorsal disruptions or dislocations are more common. The interosseus ligaments are strong and correspond to the first, second and third cuneiformmetatarsal space. The largest is the Lisfranc ligament, which is 8–10 mm long and 5–6 mm thick. It originates on the lateral side of the first medial cuneiform and inserts on the medial side of the base of the 2nd metatarsal. In 22% of cases the ligament is formed by two bands.12 Biomechanical studies of the Lisfranc ligament in cadavers has shown the strength of the ligament to be approximately 449N758.15 No interosseus
ARTICLE IN PRESS 110 ligaments exist in the fourth space. Following injury an avulsion of the Lisfranc ligament can occur and this is seen radiologically as a flake fragment in the first intermetatarsal space. This may be an avulsion from the metatarsal or the cuneiform. The plantar cuneiform-metatarsal ligaments are well defined medially but variable laterally. They are variable in number. The first cuneiform metatarsal ligament is broad and there is no cuneiformmetatarsal ligament from the middle cuneiform to the second metatatarsal. An oblique ligament connects the medial cuneiform to the base of the second and third metatarsal and is the strongest. In addition to the ligaments, soft tissue structures reinforce the plantar aspect making plantar dislocations unlikely. These include muscle, tendons such as the peroneus longus and also the plantar fascia. Biomechanically the dorsal ligaments are weaker than the plantar and interosseus ligaments and as a result, in indirect injuries, the dorsal ligaments fail in tension before the plantar ligaments, hence dorsal dislocation being more common.
N.K. Makwana Divergent: These can be partially or totally incongruent. The first metatarsal displaces medially and the lateral four, single or in combination, displace laterally. This classification allows treatment to be planned and is also useful for prognosis. Myerson14 has proposed a columnar classification based on the anatomical division of the TMT complex into medial, central and lateral columns. Although the classification is simple it has not yet been validated. A further classification was proposed by Nunley17 to include subtle injuries in athletes where low energy injury often leads to midfoot sprains. Nunley categorised these into three stages. Stage 1 injuries are undisplaced injuries of the TMT complex with pain, local tenderness and a positive bone scan with normal weight-bearing X-ray. Stages 2 and 3 are displaced injuries seen on X-ray. Treatment of stage 1 is with a plaster cast for 6 weeks initially and a further 4 weeks if tenderness persists. Stages 2 and 3 are treated as displaced Lisfranc injuries outlined below.
Mechanism of injury Classification Early classifications of the Lisfranc joint were based on the mechanism of injury, which is often complex and variable. Direct force crushes the metatarsal plantarwards with secondary medial or lateral displacment. In indirect injuries rotational forces occur with the foot in a plantarflexed position. A dorsal dislocation results with additional displacement. These classifications help define the deforming force but do not provide information that would guide management. Que´nu and Ku ¨ss16 were the first to classify these fractures into a simple system based on the direction of metatarsal displacement. They classified the injuries into three groups, homolateral, isolated and divergent. It does not include every type of displacement and based on 119 TMT injuries was modified by Hardcastle (1982)4 into the current accepted classification (Fig. 2). Type A: Total injury: there is incongruity of the entire TMT joint. Displacement may be sagittal, coronal or both. Type B-Partial: there is partial incongruity. The displaced segment is in one plane. These injuries are further subdivided. Medial displacements affect the first metatarsal either in isolation or combined with displacement of second, third or fourth metatarsal. Lateral displacement affects the 2–5th metatarsal, not the first. Type C
During the Napoleonic era Lisfranc injuries were commonly sustained following a fall off a horse with the foot trapped in the stirrup. This mechanism is now rare and most injuries occur following road traffic accidents, a crush injuries e.g. industrial, following a fall or are sports related.4 Minor trauma such as a simple twist can also lead to a Lisfranc injury especially in elderly patients and athletes.17,18 The exact mechanism of the injury is not known because of the intricate nature of the TMT complex and the variable nature of the forces inflicted on it. Early studies showed that a violent force resulted in various injury patterns.4,8 Jeffreys19 found in cadaveric experiments that pronation (eversion) of the hindfoot with the forefoot fixed resulted in a type A injury. Supination (inversion) of the hindfoot with the forefoot fixed resulted in a type B partial injury. A general consensus exists that the basic mechanism can be classified into direct and indirect injuries.4,5,8,11,14,18,19 Direct injuries as a result of crushing are often associated with significant trauma to surrounding tissues and may be associated with an open injury, compartment syndrome or ischaemia.18 Gissane20 highlighted the fact that amputation may result if reduction is delayed in injuries where there is vascular compromise. The metatarsals are often displaced plantarwards (Fig. 3a and b) but Myerson5 showed that in his series 43% of Lisfranc injuries
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Figure 2 Classification of Lisfranc injuries. (Reproduced with permission and copyright& of the British Editorial Society of Bone and Joint surgery. Hardcastle PH, Reschauer R, Schoffmann W. Injuries to the tarsometatarsal jointy J Bone Joint Surg. 1982, 64-B. 349–356.)
caused by crushing had dorsal displacement of the metatarsal. The position of the metatarsal depends on the point of forces applied to the foot during the crushing injury. Indirect injuries occur as a result of longitudinal forces applied with both the foot and ankle in a plantarflexed position. The dorsal ligaments fail in tension and the TMT joint is displaced dorsally primarily and secondary displacement either medial or lateral can occur.21 Such injuries can occur from a fall in the ‘‘toe dancer’’ position (Fig. 4) or more commonly in road traffic accidents when the
forefoot is forced against the bulkhead on impact. Indirect injuries are more common than direct injuries. Type C injuries are more difficult to explain and the exact mechanism for these has not been established.
Associated injuries Fractures of the tarsal and metatarsal bones frequently occur in association with Lisfranc injuries. They are often associated with high-energy
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N.K. Makwana frequently associated with Lisfranc injuries. Wilppula22 reported 18 out of 26 patients had associated fractures (69%) of the foot. Myerson5 found 32% of patients had an ipsilateral foot and ankle concomitant fracture. Metatarso-phalangeal dislocations can also occur and may occur in isolation to give rise to a single floating metatarsal.23–25 Direct crush injuries can result in significant soft tissue injury and may cause ischaemia or compartment syndrome. Prompt early reduction may prevent further vascular compromise and avoid the need for amputation.20 If compartment syndrome is suspected then the compartment pressures may be monitored and an urgent fasciotomy performed.
Clinical symptoms and signs The symptoms and signs following a Lisfranc injury are variable. Subtle injuries with only mild tenderness and minimal swelling of the midfoot may occur in athletes or elderly. In patients with high-energy trauma significant pain, swelling and deformity occur. Open crush injuries are common and will require prompt debridement and stabilisation. Spontaneous reduction of the TMT joint can occur, masking the extent of injury and leading to a delay in diagnosis. Bruising on the plantar aspect may also be a clinical indicator of a Lisfranc injury. Figure 3 AP (a) and lateral (b) X-ray of a crush injury with a type B medial plantar dislocation of the first metatarsal.
Figure 4 Indirect injury may occur from a fall with the foot and ankle plantar flexed.
injuries and may involve the cuboid, calcaneus, talus and malleoli. Aitken and Poulson8 reported that fractures of the base of the second metatarsal and crush injuries of the cuboid were most
Investigations For all Lisfranc injuries standard AP, lateral and 301 internal oblique views should be obtained both initially and after reduction. On the AP view the first and second TMT joints are visualised and in the oblique view the lateral 3–5th TMT joints seen. Normal consistent parameters have been established which can help with diagnosis (Table 1).26 On the lateral view the relationship of the medial cuneiform to the fifth metatarsal base can be used to identify significant injuries with flattening of the medial arch. The normal relationship with the medial cuneiform being higher than the fifth metatarsal is reversed.27 A high index of suspicion should be maintained as up to 39% of injuries can be missed especially in subtle injuries and where the fracture dislocation has reduced spontaneously. In patients with polytrauma other injuries distract from the foot injury and this combined with poor quality X-rays often leads to a delay in diagnosis. If any doubt exists, then the other foot can be X-rayed for comparison and weight-bearing views obtained (Fig. 5).28 If pain and tenderness prevent
ARTICLE IN PRESS Tarsometatarsal injuries—Lisfranc injuries full weight bearing then this may be performed under regional ankle block or once pain and swelling have subsided. Avulsion fracture at the base of the first metatarsal or cuboid should also raise suspicion. The Fleck sign may be seen which represents an avulsion of the Lisfranc ligament (Fig. 6). Subtle injuries in athletes and elderly may be difficult to diagnose. In these cases, stress views under regional or general anaesthetic may be performed with abduction and pronation stressing of the TMT joint18 with the hindfoot stabilised or compression and distraction of the second TMT joint.14 Any obvious instability is detected and the injured and non-injured side can be compared. CT scanning is indicated if plain X-rays are normal and suspicion exists of a Lisfranc injury. Fractures of the base of the metatarsal and cuneiforms are easily identified and joint congruity assessed. Any soft tissue interposition can also be detected as well as small flake fragments. The disadvantage of CT scans are that they are static images and may not be as useful in pure ligamentous injuries which need dynamic imaging.14 In one cadaveric study CT scan detected all injuries with 1 mm and one third of all 2 mm displacements compared to none detected by plain X-ray.29 Although CT scans are sensitive, their role is limited for the evaluation of complex comminuted fractures where surgical treatment may be modified if severe comminution exists precluding internal fixation. MRI has been used to identify subtle and pure ligamentous injuries to the TMT joint. Priedler30 was the first to show that MRI can accurately detect ligament injuries, fractures and displacement of the TMT joint. MRI also allowed the Lisfranc ligament to be visualised and any disruption detected (Fig. 7). The Lisfranc ligament is seen as a hypointense band-like structure between the medial cuneiform and the second metatarsal base. In a subsequent study Preidler31 showed the superiority of MRI scan compared to plain X-rays in 49 patients with hyperflexion injuries of the foot. Plain X-rays missed 50% of the TMT injuries.
Table 1 1 2 3 4 5 6
113
Principles of treatment The major advance in the last decade has been the emphasis on early stable anatomical reduction and stabilisation of these injuries. In displaced
Figure 5 Standing AP views of both feet. Note diastasis between first and second metatarsal on the left side.
Figure 6 The Fleck sign (circled).
Normal X-ray parameters used for identifying Lisfranc injury. The first metatarsal lines up medially and laterally with the medial cuneiform The first intermetatarsal and intertarsal space have equal widths Medial border of the 2nd metatarsal aligns itself with medial border of middle cuneiform Lateral border of 3rd metatarsal aligns itself with lateral border of lateral cuneiform The medial border of 4th metatarsal aligns itself with medial border of cuboid Dorsal or plantar displacement on lateral views
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fractures and dislocations non-operative management has a limited role. Only two studies have reported satisfactory results with non-anatomic reduction8,32 Brunet32 reviewed 33 patients after an average 15 years and found neither the initial fracture type, nor the type of treatment had any affect on outcome. Myerson18 advised that there is no place for closed reduction and plaster cast application as once the soft tissue swelling subsides redisplacement is very likely. In addition the strong plantar muscle and tendon tend to bowstring the TMT joint and maintain displacement. Of 15 patients undergoing this treatment no excellent results were achieved. The vast majority of evidence supports early anatomical reduction and stable fixation.4–5,14,22,34 Arntz33 concluded that there was a direct correlation between achieving an accurate reduction and a satisfactory clinical outcome. This was confirmed by Myerson5 who reviewed 60 patients after an average 4.2 years follow up and found a correlation between the quality of initial reduction and the outcome (Fig. 8). Although perfect anatomical alignment does not guarantee a good clinical outcome the outcome is more favourable. Although most studies have shown that early anatomical reduction and stable fixation leads to the best outcome, no consensus exists on how to achieve this. Reduction may be by closed or open methods, fixation by K wires or screws and the duration of immobilisation is variable. An algorithm
showing the principles of management is shown in Fig. 9.
Closed reduction and Kirschner-wire(K-wire) stabilisation Closed reduction can be achieved with longitudinal traction, which may be aided by Chinese finger traps. Once reduction is achieved then the TMT joints should be stabilised. Hardcastle4 found the main reason for unsatisfactory results was redisplacement if the Lisfranc injury was not stabilised with a K-wire. He advised that Type A injury is treated with a K-wire across the first TMT joint and a second laterally into the fifth TMT joint. For type B injuries a single lateral K-wire for lateral segment injuries and two K-wires into the first TMT for medial injuries should be used. In type C injuries two medial and one lateral can be used. The K-wires are removed at 6–8 weeks. Some of the disadvantages with a K-wire include migration, breakage, infection and loss of reduction.33 In pure ligamentous injuries 6–8 weeks of immobilisation may not be sufficient for the ligaments to heal and prolonged use increases the risk of infection. However, studies have shown good outcomes with closed reduction and K-wire stabilisation. The main determinant of outcome appears to be early anatomical reduction and stabilisation.4,14,34 Post operatively the foot is protected in a below knee plaster cast with non-weight bearing for 6 weeks. The wires can then
Figure 7 MRI scan showing Lisfranc ligament (arrowed).
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Figure 8 Correlation of clinical outcome with quality of reduction. (Copyright&1986 by the American Orthopaedic Foot and Ankle Society, Inc., originally published in Foot and Ankle International 6(5):225–242 and reproduced here with permission).
be removed at 6–8 weeks and an orthosis to support the medial arch given for 3–6 months.
History midfoot injury Local pain and tenderness
Open reduction and stabilisation X-ray AP/lateral and oblique. (weight bearing)
Lisfranc Injury
Closed reduction and percutaneous fixation Open reduction and internal fixation
Stable injury . Undisplaced
POP 6-8 weeks
Suspect Lisfranc Injury ?
X-ray other foot. Stress views CT / MRI
Unstable displaced.
Treat as Lisfranc injury
Figure 9 Algorithm for the management of TMT injury.
Failure to reduce a Lisfranc injury may be due to a fracture fragment, soft tissue or tendon interposition such as the tibialis anterior tendon between the medial cuneiform and first metatarsal.4,18 The aim should be reduce the TMT joint anatomically. Any residual displacement of 2 mm or more between the medial and intermediate cuneiform, a talometatarsal angle greater than 151 or any coronal displacement results in a poor outcome.5 The surgical approach depends on the type of the fracture. A dorsal incision over the second metatarsal allows adequate exposure of the first and second TMT joint. The neurovascular bundle deep to extensor digitorum brevis is carefully protected. The second lateral incision should leave a sufficient bridge to prevent skin necrosis and is usually centred on the fourth metatarsal. The branches of the superficial peroneal nerve should be identified and protected to prevent damage and neuroma formation. Several studies have shown that stabilisation using screws can avoid the complication of K-wires and maintain a stable reduction. Closed reduction and percutaneous use of cannulated screws has been described with good clinical results
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Figure 10 Percuataneous and cannulated screw fixation of a type B lateral TMT injury.
(Fig. 10).5,33 Primary stabilisation of the medial cuneiform to the base of the second metatarsal is first performed. The first TMT joint is stabilised next with a 3.5 or 4 mm cannulated screw, then the lateral TMT joints are reduced and stabilised. The lateral TMT joints often reduce spontaneously once the first and second are stabilised. Occasionally, the cuboid may require distraction and stabilisation if crushed. The lateral 3–5th TMT joints are normally stabilised with a K-wire. Partial weight bearing can be commenced immediately in a below knee cast and full weight bearing allowed at six weeks. The screws are removed at 4 months but occasionally can be left longer. There is no evidence that partial or fully threaded screws have any difference in the rate of osteoarthritis in the TMT joint.28 Damage to the TMT at the time of the initial injury probably determines the rate of osteoarthritis. In diabetic patients, who form a special subgroup, large 6.5 mm screws may be required if bone quality is poor. Screw breakages can occur and in one study this complication occurred in 25% of cases where screws were only removed for symptoms or signs.35 Thordarson36 reported on the use of polylactide (PLA) bioabsorbable screws with good clinical results. Fourteen patients with a Lisfranc injury underwent open reduction with stabilisation using
PLA screws. No soft tissue reaction, osteolysis or loss of reduction was reported. The need for subsequent surgery to remove metalwork was avoided. Cuboid crush injuries should be treated to restore the lateral column length with distraction, bone grafting and stabilisation either with a cervical H plate or K-wires.14 In severe compound injuries precluding internal fixation, stabilisation can be achieved with external fixators and definitive surgery performed once the soft tissue injury has healed and the swelling reduced.
Timing of surgery The aim of treatment should be early anatomical reduction and stable fixation within 24 h.28 Early reduction reduces the risk of vascular compromise, skin problems and facilitates anatomical reduction. If significant swelling exists then surgery can be delayed until the swelling has reduced. Dislocation without a fracture may be treated up to three months after which salvage arthrodesis is advised.28 Hardcastle4 reported poor results if reduction was performed after 6 weeks and this may be due to joint incongruity and damage, and difficulty with reduction due to soft tissue interposition.
ARTICLE IN PRESS Tarsometatarsal injuries—Lisfranc injuries
Complications Early complications The early complications include vascular injury, compartment syndrome, redislocation, complex regional pain syndrome and skin necrosis. Gisssane20 reported 3 patients who underwent below knee amputation for vascular compromise and advised that reduction should not be delayed. Hardcastle4 reported 2 patients out of 22 with type A injuries who underwent amputation for ischaemia. Myerson reported a 13% amputation rate in patients with predominately high-energy injuries with polytrauma.5 Compartment syndrome might develop especially in crush injuries. The reported incidence is 4–7%.33,35 A high index of suspicion should be maintained and early fasciotomy performed. Redislocation can occur early especially if stabilisation has not been performed.4 However, late dislocation has been reported despite internal fixation for a minimum period of 4 months.36
Late complications Late complications include osteoarthritis of the TMT joints, deformity (pes planus, cavus or planovalgus), chronic pain, prominent exostoses, non-union and abnormal gait. As a result of the mechanism of injury and energy transferred osteoarthritis occurs in many patients despite adequate reduction. Myerson reported a 15% incidence of osteoarthritis in patients with good or excellent quality of reduction.5 The incidence is higher if reduction was non-anatomical33–35and it may also be higher in pure ligamentous injuries.35 The presence of osteoarthritis radiologically does not correlate with the clinical outcome.5,28 Any salvage procedure for osteoarthritis should be delayed for at least 12 months as the symptoms or signs can improve for an average 1.3 years.36
Outcome In general, most studies have consistently shown that the clinical and functional outcome following Lisfranc injuries are better if early anatomical reduction and stable fixation is performed. Although anatomical reduction and fixation does not guarantee an excellent outcome the studies have shown that non-anatomical reduction leads to poor results. Stenstro ¨m38 reviewed 40 patients at 5 years and found no patient with an excellent result if reduction was non-anatomical and half of these
117 were on a full pension. In those patients with an anatomical reduction 50% had good or excellent result and only 25% of them were on a full pension.38 Following anatomical reduction Teng et al.39 found that after an average of 41 months the objective gait analysis was restored to normal but subjectively patients were less satisfied due to stiffness and discomfort. Primary arthrodesis has been advocated by Granberry and Lipscomb40 and may be indicated if severe comminution of the TMT joint exists preventing stable reduction. Most studies do not support this and have found this not necessary.34 Persisting pain and discomfort with or without deformity can be treated with functional foot orthoses initially. If this does not alleviate the symptoms then an arthrodesis is indicated. Identification of the painful joint may require further investigations with a bone scan, selective local anaesthetic injections and CT scanning. Arthrodesis for painful osteoarthritis of the TMT may be performed in-situ where there is minimal deformity or a realignment arthrodesis with or without bone grafting may be necessary. Johnson and Johnson41 used a dowel technique in 15 patients with an in situ technique. Good or excellent results were seen in 70% with only 2 non-unions. Sangeorzan37 reported 69% good or excellent results in 20 patients who underwent a realignment arthrodesis with structural iliac bone graft. Four of these patients returned to their preinjury occupation. On average 3 joints were fused. The results of salvage arthrodesis are not as good as primary anatomical reduction and stable fixation. Myerson5 showed no good or excellent results in those cases where an arthrodesis was performed.
Conclusion Lisfranc injuries are relatively uncommon injuries but with increasing motor vehicle use their incidence may be increasing. Missed injuries can lead to chronic pain, deformity and disability and this can be avoided by having a high index of suspicion for these injuries. Subtle injuries are difficult to diagnose and special imaging or stress X-rays are useful in diagnosis. The classification proposed by Hardcastle et al.4 is used most commonly and the aim of treatment must be to obtain an anatomical reduction and stable fixation as soon as possible. Treatment after 6 weeks yields poor results and the results of salvage arthrodesis are not as good as primary reduction and stabilisation. Reduction may be by closed or open methods and fixation by
ARTICLE IN PRESS 118 K-wires, screws or bioabsorbable screws. Complications occur frequently and need to be observed and treated appropriately.
References 1. Cassebaum WH. Lisfranc fracture dislocations. Clin Orthop 1963;30:116. 2. Arntz CT, Hansen ST. Dislocations and fracture dislocations of the tarsometatarsal joints. Orthop Clin North Am 1987;18:105–14. 3. Brunet JA, Wiley JJ. The late results of tarsometatarsal joint injuries. J Bone Joint Surg 1987;69-B:347–440. 4. Hardcastle PH, Reschauer R, Schoffmann W. Injuries to the tarsometatarsal joint. J Bone Joint Surg 1982;64-B:349–56. 5. Myerson MS, Fisher RT, Burgess AR, Kenzora JE. Fracture dislocations of the tarsometatarsal joints. End results correlated with pathology and treatment. Foot Ankle 1986;6:225–42. 6. Resch S, Stenstrom A. The treatment of tarsometatarsal injuries. Foot Ankle 1990;11:117–23. 7. Buzzard BM, Briggs PJ. Surgical management of acute tarsometatarsal fracture dislocation in the adult. Clin Orthop 1998;353:125–33. 8. Aitken AP, Poulson D. Dislocations of the tarsometatarsal joints. J Bone Joint Surg 1963;45A:246–60. 9. English TA. Dislocation of the metatarsal bone and adjacent toe. J Bone Joint Surg 1964;46B:700. 10. Vuori JP, Hannu TA. Lisfranc joint injuries: trauma mechanisms and associated injuries. J Trauma 1993;35(1):40–5. 11. Goosens M, DeStoop N. Lisfrancs fracture dislocation: etiology, radiology and results of treatment. Clin Orthop Rel Res 1983;176:154–62. 12. Sarrafian SK. Anatomy of the Foot and Ankle. Descriptive topographic functional. 2nd ed. JB Lippincott; 1993. 13. De Palma L, Santucci A, Sabetta SP, Rapali S. Anatomy of the Lisfranc joint Complex. Foot Ankle Int 1997;18(6):356–64. 14. Chiodo C, Myerson MS. Developments and advances in the diagnosis and treatment of injuries to the Tarsometatarsal joint. Orth Clin North Am 2001;32(1):11–20. 15. Solan MC, Claude TM, et al. Ligamentous restraints of the second tarsometatarsal joint: a biomechanical evaluation. Foot Ank Int 2001;22(8):637–41. 16. Que ´nu E, Ku ¨ss G. Etude sur les luxations du metatarse. Reb Chir 1909;39:281. 17. Nunley JA, Vertullo CJ. Classification, investigation and management of midfoot sprains. Lisfranc injuries in the athlete. Am J Sport Med 2002;30(6):871–8. 18. Myerson M. The diagnosis and treatment of injuries to the Lisfranc joint complex. Orth Clin North Am 1989;20(4): 655–64. 19. Jeffreys TE. Lisfranc’s fracture—dislocation. A clinical and experimental study of tarsometatarsal dislocations and fracture—dislocations. J Bone Joint Surg 1963; 45B: 456–551.
N.K. Makwana 20. Gissane WA. Dangerous type of fracture of the foot. J Bone Joint Surg 1951;33B:535–8. 21. Anderson LD. Injuries of the foot. Clin Orthop Rel Res 1977;122:18–27. 22. Wilppula E. Tarsometatarsal fracture—dislocation. Late results in 26 patients. Acta Orthop Scan 1973;44: 335–45. 23. Milankov M, Miljkovi N, Popovic N. Concomitant plantar tarsometatarsal (Lisfranc) and metatarsophalangeal joint dislocations. Arch Orthop Trauma 2003;123:95–7. 24. Kasmaoui EH, et al. The floating metatarsal. A rare traumatic injury. Acta Orthop Belgica 2003;69(3):295–7. 25. Espierrez JC, et al. The floating metatarsal: first metatarsophalangeal joint dislocations with associated Lisfranc dislocation. J Foot Ankle Surg 2003;42(5):309–11. 26. Stein RE. Radiological aspects of the tarsometatarsal joints. Foot Ankle 1983;3:286. 27. Faciszewski T, Burks RT, Manaster BJ. Subtle injuries of the Lisfranc joint. J Bone Joint Surg 1990;72:79–83. 28. Trevino SG, Kodros S. Controversies in tarsometatarsal injuries. Orthop Clin North Am 1995;26:229–38. 29. Lu J, Ebraheim NA, Skie M, et al. Radiographic and computed tomographic evaluation of Lisfranc dislocation: a cadever study. Foot Ank Int 1997;18:351–5. 30. Preidler KW, Brossmann J, Daenen B, et al. MR Imaging of the tarsometatarsal joint. AJR 1996;167:1217–22. 31. Preidler KW, Peicha G, Lajtai G, et al. Conventional radiography, CT and MR imaging in patients with hyperflexion injuries of the foot: diagnostic accuracy in the detection of bony and ligamentous changes. AJR 1999;173:1673–7. 32. Brunet JA, Wiley JJ. The late results of tarsometatarsal joint injuries. J Bone Joint Surg 1987;69B:437–40. 33. Hansen ST, Arntz CT. Fractures and fracture—dislocations of the tarsometatarsal joint. J Bone Joint Surg 1988;70A(2): 173–81. 34. Mulier T, Reynders P, Sioen W, et al. The treatment of Lisfranc injuries. Acta Orthop Belgica 1997;63(2):82–9. 35. Kuo RS, Tejwani NC, Digiovanni CW, et al. Outcome after open reduction and internal fixation of Lisfranc joint injuries. J Bone Joint Surg 2000;82A(11):1609–18. 36. Thordarson DB, Hurvitz G. PLA screw fixation of Lisfranc injuries. Foot Ank Int 2002;23(11):1003–7. 37. Sangeorzan B, Veith R, Hansen ST. Salvage of Lisfranc‘s tarsometatarsal joint by arthrodesis. Foot Ankle 1990; 10(4):193–9. 38. Resch S, Stenstro ¨m A. The treatment of tarsometatarsal injuries. Foot Ank 1990;11(3):117–23. 39. Teng LA, Pinzur MS, Lomasney L, et al. Functional outcome following anatomic restoration of tarsometarsal fracture dislocation. Foot Ank Int 2002; 23(10): 922–6. 40. Granberry WM, Lipscomb PR. Dislocation of the tarsometatarsal joint. Surg Gynec Obstet 1962;114:467–9. 41. Johnson J, Johnson K. Arthrodesis for degenerative arthritis of the tarsometarsal joints. Foot Ankle 1986;6(5): 243–53.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 119–126
www.elsevier.com/locate/cuor
TUMOURS
The role of chemotherapy in the treatment of bone and soft tissue sarcomas Alessandra Longhi, Elisabetta Setola, Michela Versari, Gaetano Bacci Chemotherapy at the Dept of Musculoskeletal Oncology, Istituti Ortopedici Rizzoli, Via GC, Pupilli 1, Bologna 40136, Italy
KEYWORDS Sarcomas; Bone; Soft tissue; Chemotherapy
Summary While surgery remains the cornerstone of treatment of bone and soft tissue sarcomas, chemotherapy has improved the 5-year overall survival in osteosarcoma and Ewing’s sarcoma from 10% to 70% in localized disease. Patients with metastases at presentation treated with surgery combined with chemotherapy have a 3-year survival of 30–50%, but cure is still rare. The role of adjuvant chemotherapy in soft tissue sarcoma has yet to be determined, but it is likely that some patients will benefit. As some bone sarcomas do not respond to chemotherapy, surgery remains the only effective treatment, and there are no effective drugs to treat relapsing patients. Radiotherapy has both a curative role in combination with chemotherapy in soft tissue and Ewing’s sarcoma and a palliative role in the other sarcomas. & 2005 Elsevier Ltd. All rights reserved.
Bone sarcomas Primary malignant bone tumours represent 0.2% of newly presenting cancers. The different histotypes are related to the original cell (Table 1). The most common bone sarcomas are: osteosarcoma 45%, chondrosarcoma 22%, and Ewing’s sarcoma 15%. Osteosarcoma and Ewing’s sarcoma have shown dramatically improved cure rates since the introduction of adjuvant (postoperative) and neo-
adjuvant (preoperative) chemotherapy. Chondrosarcoma and chordoma do not respond to chemotherapy.
Osteosarcoma (OS) Osteosarcoma is classified:
Corresponding author. Tel.: +39 051 6366199;
fax: +39 051 6366277. E-mail addresses:
[email protected] (A. Longhi),
[email protected] (M. Versari),
[email protected] (G. Bacci).
0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2005.02.009
High Grade Central OS o Fibroblastic o Osteoblastic o Chondroblastic o Telangiectatic Low Grade central o Grade 1 o Grade 2
ARTICLE IN PRESS 120 Table 1
A. Longhi et al. Different histotypes of bone sarcomas and treatment-sensitivity.
Histologic type
Malignant bone tumor
Chemo-sensitive
RT-sensitive
Osteogenic
Classic osteosarcoma Small cell osteosarcoma Multifocal osteosarcoma
Yes Yes Yes
No Yes Yes
Chondrogenic
High grade chondrosarcoma Dedifferentiated chondrosarcoma Mesenchymal chondrosarcoma
No Y/N Yes
No No No
Nervous
Ewing’s sarcomas Primary neurectodermal tumours
Yes No
Yes No
Histiocytic
Malignant fibrous histiocytoma
Yes
No
Fibrous
Fibrosarcoma
No
No
Smooth muscular
Leiomyosarcoma
No
No
Notocordal
Chordoma
No
No
Vascular
Hemangioendothelioma Hemangiopericytoma
No No
No No
Lipogenic
Liposarcoma
No
No
Mixed
Malignant mesenchymoma
No
No
Hematopoetic
Multiple myeloma Lymphoma
Yes Yes
Yes No
Parosteal/periosteal (low malignancy) Secondary OS (to Paget’s disease, irradiated bones).
It is a high grade malignant spindle cell tumour arising within bone and histologically characterized by production of ‘tumour’ ‘osteoid’ or immature bone directly from the malignant spindle cell stroma. It is the most frequent type of malignant bone tumour, with an annual incidence of about 3 new cases per million. It occurs mainly in childhood and adolescence with a median age of 16. When it occurs over 40 years of age, it is usually associated with pre-existing bone diseases. Ten percent of cases occur in patients over 60. Males are affected more commonly than females, ratio 1.6:1.0. At presentation osteosarcoma is localized in 80% of cases while metastases are present in about 20%.1 75% are in the appendicular skeleton, arising in the metaphysis of long bones. Lung is the most common metastatic site, followed by bone. Unfavourable prognostic indicators are:
male gender primary tumour in the pelvis or axial skeleton poor tumour necrosis (o90%) after preoperative chemotherapy
tumour volume elevated serum alkaline phosphatase inadequate surgical margins metastatic disease.
Metastatic disease at presentation is the most important unfavourable prognostic factor. Disease Free Survival (DFS) is 70% in localized disease, but falls to 20–30% in cases of metastatic disease even after combined treatment. Thus low grade (1–2), periosteal and parosteal osteosarcoma that metastasise slowly have an overall survival of 75–85% with surgery alone. To understand current best practice, it is necessary to understand how current treatments developed. Until the 70’s osteosarcoma was treated by amputation alone. Despite good local control, most patients died due to pulmonary metastases. The 5-year DFS was 12%, and 3 out of 4 patients died within 2 years of diagnosis. In the early 70’s adjuvant chemotherapy following surgery was introduced, the aim being to kill micrometastases that had already spread at diagnosis, even in Around this time, UK practice was immediate irradiation
followed by amputation if metastasis free at about 6 months, the ‘Cade regime’.
ARTICLE IN PRESS The role of chemotherapy in the treatment of bone and soft tissue sarcomas apparently localised disease. The first protocols included high doses of methotrexate (MTX) or Doxorubicine (DOX) or the two combined. The 5year DFS rose to between 40% and 60%. Other chemotherapeutic agents were added (Vincristine, Bleomicine, and Dactinomycin) but abandoned due to poor effectiveness. However the subsequent addition of Cisplatin (CDP) and Ifosfamide (IFO) to DOX and MTX led to further improvement in the 5-year DFS (70%). After 1983, neoadjuvant (preoperative) chemotherapy was introduced and the DFS reached a 70–75%. Neoadjuvant chemotherapy, in addition to eradicating micro-metastases, was intended to destroy the primary tumour cell. Reduction of the tumour bulk would permit more limb sparing surgery, from 10% to 95%. An additional benefit of neoadjuvant chemotherapy was a prognostic evaluation based on tumour necrotic response to chemotherapy permitting identification of postoperative chemotherapies. Currently neoadjuvant treatment protocols for osteosarcoma aim to:
increase the percentage of healing further reduce mutilating surgery reduce toxicity.
Drugs Currently MTX, DOX, CDP and IFO remain the mainstays of treatment. It must not be forgotten that in almost all adjuvant and neoadjuvant chemotherapy protocols for osteosarcoma, there have been deaths due to drug toxicity. Methotrexate. MTX is only effective when used in high doses.2,3 However there is great individual variation in the metabolism of MTX, and recent neoadjuvant protocols tailor the dosage of MTX to each patient, based on blood levels after the first cycle with 12 g/m2. Doxorubicin. DOX if used as a single agent in OS has a response rate of about 30%. Cardiotoxicity is its main side effect and cardiomyopathy can be manifest many years after treatment.4,5 Nonetheless, as significant benefits accrue from an early use of this drug and as the risk of DOX cardiotoxicity correlates with the cumulative dose of the drug, more recent protocols use reduced dosages by 24 h infusion rather than single bolus. Cisplatin. In current preoperative protocol with 4 drugs (MTX, CDP, DOX, IFO), intra-arterial administration of CDP does not offer any advantages. Intravenous infusion over 48 or 72 h rather than over 5 h has the same effect with less neurologic and renal toxicity.
121
Ifosphamide. IFO is the latest drug used to treat osteosarcoma. Recent protocols include high dose IFO together with the other drugs. Currently we use IFO (15 g/m2) over 5 days for patients who relapse. Adjuvant or neoadjuvant chemotherapy? Is neoadjuvant chemotherapy for OS, used for many years, still appropriate? As reconstructive endoprostheses are readily available, and chemotherapy can be started 4–5 days after surgery, delay before surgery is not necessary. Neo-adjuvant chemotherapy given for several weeks before surgery runs the risk of leaving un-operated a drug resistant tumour, with subsequent selection of chemo-resistant clones that can metastasize. The only relevant controlled study was by the Pediatric Oncology Group between 1986 and 1993.6 Patients were randomized to adjuvant or neoadjuvant groups, receiving the same chemotherapy regimen with MTX-CDP-DOX-BCD. The number of amputations, DFS, and overall survival were the same in the two groups. We believe that treatment should be individually tailored. There is advantage to be gained from neoadjuvant chemotherapy for an easily resectable lesion (e.g. of the fibula), but a large OS of the humerus, at limit of resectability, could greatly benefit from neoadjuvant chemotherapy as lesions preoperatively treated with chemotherapy are more easily operable than untreated tumours. Current neoadjuvant protocols have a 5-year DFS range between 61% and 76%. Two problems remain, what is the best treatment for patients with distant metastases at presentation, and what is the best treatment for patients who relapse? Primary metastatic osteosarcoma About 20% of all osteosarcomas are metastatic at presentation. Current practice is aggressive treatment with chemotherapy and surgery of the primary tumour and all metastases. In our series,7 none of the patients with both bone and lung metastases achieved remission. The number of lung metastases was a significant prognostic factor: all patients with less than 5 nodules were disease free after treatment, but only 40% of those with more than 5 lung nodules. At a mean follow up of 4 years (2–7) only 7 (20%) of the 36% pts who achieved remission remained disease free. The 2-year DFS for the group of 36 pts who reached a disease-free status after treatment was 38% (28% in those with only lung metastases, 0% otherwise). The COSS study,8 reported similar results. Despite aggressive treatment, the prognosis of osteosarcoma metastatic at presentation is still poor. Survival is related to the number and location of metastases
ARTICLE IN PRESS 122 and completeness of surgical resections of all tumour sites. Also patients with multifocal bone disease at presentation have an extremely poor prognosis, but systemic chemotherapy and aggressive surgical resection may achieve significant prolongation of life.9 Treatment of metastatic relapsed osteosarcoma Despite chemotherapy and surgical resection, 30–40% of patients with local osteosarcoma of extremities relapse. Recurrence is most common in the lungs. Complete resection of recurrent disease is the most important prognostic factor at first relapse with a 3/5-year survival rate of 20–40% following resection of metastatic pulmonary tumours.10 Prognosis is better with less than 4 nodules, and with a longer disease free interval. The prognosis for patients who develop bone metastases or local recurrence is even worse. Surgery for metastases is still the best accepted strategy, while the role of second-line chemotherapy is not well defined yet, because all the most effective drugs are used in neo-adjuvant chemotherapy. New experimental drugs Peripheral blood stem cell transplant utilizing high dose chemotherapy does not seem to improve outcome.11 High dose samarimn-153-EDTMP may provide significant pain control in patients with bone metastases. Other drugs undergoing trial include Gemcitabine with Docetaxel. Correlation of HER2 expression with unfavourable prognosis has led to a trial of Herceptin. Ecteinascidin-743 in combination with other drugs is subject to an ongoing trial. Encouraging results were reported in localized osteosarcoma with a combination of Muramyltripeptide, (derivative of the BCG cell wall, with immunostimulation activity) together with IFO and standard therapy. CDP, MTX and DOX.
Ewing’s sarcoma Ewing’s sarcoma (ES) is the second, most common, primitive malignant tumour of bone after osteosarcoma. It represents the 3% of all malignant paediatric tumours; 90% of patients are aged less than 20 years with a peak incidence at 14 years. Histologically, ES comprises a group of small round cell tumours of neuro-ectodermal origin. It arises in bone marrow or soft tissue (when in the chest wall it is called Askin tumor). ES can be distinguished immuno-histochemically from other
A. Longhi et al. paediatric ‘blue tumors’ by expression of MIC2 gene. ES is an aggressive disease with a high mortality. About 25% of patients have clinically apparent metastases at presentation. Lung is the most common site of metastases followed by bone and bone marrow. However, 20–30% of those with apparently localized disease have a micro-metastatic disease in bone marrow, detectable by molecular techniques such as PCR. This correlates with poor outcome. Unfavourable prognostic factors are:
metastatic disease (patients with bone metastases have worst overall survival) elevated serum LDH level at presentation poor histologic response to induction chemotherapy tumour in axial skeleton.
Overall survival at 5 years has improved from 10– 15% to 60–70% with chemotherapy combined with local treatment (surgery and/or radiotherapy). Treatment for localized disease Standard therapy for localized ES includes preoperative induction chemotherapy (4–5 cycles), and local treatment with surgery and/or radiotherapy. ES is very radiosensitive; radiotherapy alone is used for large tumours where surgery is not feasible (e.g. vertebra, pelvis) and may be used post-operatively if surgical margins are inadequate. Subsequently, 10–22 weeks of chemotherapy are given for consolidation. The aim is local control and the eradication of micro-metastases. Drugs used in the 1970s were DOX, Cyclophosphamide (CIFO) and Vincristine (VCR) +/ Dactinomycin (DAC), combined (VACD). With these 4 drugs, the 5-year DFS was 30–60%. Latterly, IFO and Etoposide (ET) have been added to most protocols as they show synergistic activity and increased DFS to 60–70% and OS to 80%. The introduction of granulocyte colony-stimulating factors (GCSF) has allowed increased drug dosage without toxicity. Increased dosage may increase DFS and OS, but tailoring treatments to histologic response, tumour volume and site is essential. Surgery gives better DFS than radiotherapy alone, but radiotherapy is often the choice for large volume axial bone tumours with a worse prognosis anyway. We compared12 the role of surgery and radiotherapy in 268 patients with non-metastatic Ewing’s sarcoma localized to an extremity. The results, supported by other studies, suggest that surgery is the best option, at least for
ARTICLE IN PRESS The role of chemotherapy in the treatment of bone and soft tissue sarcomas limb ES. Postoperative radiation therapy must be added in case of inadequate margins. Treatment of metastatic disease and relapses The prognosis of metastatic disease is still poor especially for bone metastases but as many as one third with only lung metastases achieve remission with conventional combined multimodal treatment (chemotherapy, surgery, radiotherapy). Most protocols use the same drugs (VCR, DOX, IFO, CIFO, ET, DAC) used in localized disease but at higher doses with GCSF support or PBSC Rescue as increased dose was thought to improve the fraction of tumour cells killed, but results were not good. This regime often includes a myeloablative consolidation treatment with megatherapy with or without total body irradiation. The rationale for total body irradiation is the eradication of micrometastases, and it has been used in high-risk patients as a part of a multimodal treatment with systemic chemotherapy, but in the majority of studies it did not increase survival and it increased toxicity. Myeloablative megatherapy with alkylators such as Melphalan and Busulphan in patients with bone or bone marrow metastases have shown good results.13,14 Lung radiotherapy is indicated for patients with lung metastases, in remission after chemotherapy, with consolidation purpose. New experimental drugs Topoisomerase I inhibitors are a new class of anticancer drugs. Early experience showed modest activity when used alone, but better when used in combination with alkylators. Irinotecan+Temozolamide showed some activity in heavily pretreated pediatric solid tumors.
Other bone tumors Small cell osteosarcoma: A rare variant of osteosarcoma resembling Ewing’s sarcoma, but with a worse prognosis. Treatment is as for osteosarcoma. Radioinduced osteosarcoma: A late complication of radiotherapy treatment arising in previously irradiated fields. It is associated with higher doses of radiotherapy (440 cGy) and with a latency of 5–20 years. Treatment is the same as classic osteosarcoma. Chondrosarcoma: The second most common primary malignant tumour of bone. There are five types of chondrosarcoma:
central peripheral
123
mesenchymal dedifferentiated clear cell
The 10-year survival with peripheral is 77% vs 32% for central lesions. Chondrosarcomas are not chemosensitive and surgery is the main therapy. An exception is mesenchymal chondrosarcoma which is highly aggressive with a 10-year survival of less than 30% so adjuvant chemotherapy is recommended. 10% of chondrosarcomas dedifferentiate into osteosarcoma or fibrosarcoma requiring chemotherapy. Malignant fibrous histiocytoma: Chemosensitive and can benefit from adjuvant chemotherapy.
Soft-tissue sarcomas Adult soft-tissue sarcomas account for 0.7% of all cancers. They arise from primitive mesoderm and in any extra-skeletal connective tissue, in the extremities (50–60%), trunk and retroperitoneum (30–40%), or head and neck (10%). A small percentage arise in the gastrointestinal tract—gastrointestinal stromal tumors.15 They are classified histologically, but each type can behave as benign to local recurring or highly malignant. The current staging system is based on the main prognostic factors: histologic grade, size, and depth of the tumour (relative to the superficial fascia).16 They have an intermediate chemosensitivity. Hence a surgically based multi-disciplinary treatment is necessary for optimum results. Where surgery is difficult or not feasible (e.g. retroperitoneal or trunk tumours) results are poor. Latterly there have been attempts to improve local control. The role of chemotherapy in metastatic disease is unclear. Patients with high-risk lesions seem to benefit from adjuvant or neoadjuvant chemotherapy. For metastatic disease, various drugs have been tested as single agent or combination regimes, but results in terms of response rate and overall survival are often contradictory. Newer drugs and improved knowledge of the biology of these tumours could help in the definition of more targeted therapies for this heterogeneous group of diseases.17,18
Adjuvant chemotherapy It is difficult to assess the role of adjuvant chemotherapy because the first generation of
ARTICLE IN PRESS 124
A. Longhi et al.
clinical trials included small numbers of patients, with different tumor histologies, grade and location, treated with different drugs at different doses. The Sarcoma Meta-Analysis Collaboration Group (SMAC) 19 collected the data from 14 randomized clinical trials and showed a small survival benefit of 4% overall at 10 years for the treatment group (not significant, P ¼ 0:12), increasing to 7% (P ¼ 0:029) for extremity lesions. The absolute benefits in local relapse-free interval, distant relapse-free interval, and overall recurrence-free survival where respectively 6%, 10%, and 10% in favor of chemotherapy.19 Later trials (after 1990), indicated that DOX and IFO are the most active agents in soft tissue sarcomas. The study from the Italian Sarcoma Group compared local treatment alone with local treatment plus five cycles of epirubicin and IFO the absolute benefit deriving from chemotherapy was
Table 2
13% at 2 years and increased to 19% at 4 years (P ¼ 0:04).20
Neo-adjuvant chemotherapy As with bone tumours, neo-adjuvant therapy offers many advantages, particularly shrinkage of tumour mass, improving the chances of limb/organ salvage, and may permit radical surgery in initially inoperable tumours. It also allows assessment of the tumour to chemotherapy. Despite the theoretical advantages, there is no evidence that neoadjuvant chemotherapy is better than an adjuvant approach in terms of DFS, and overall survival but response to neoadjuvant treatment is a prognostic factor for local disease control. This is true for radiographic response and for histologic response as well.21
Combination chemotherapy in metastatic STS.
Institute/study
No pts
Type pts
Gottlieb23 Borden et al.
24
Elias et al.25 Yap et al.26 Schoenfeld et al.
27
Dose (mg/m2)
RR (CR)
A+D
60
47%
275
advanced
A+D A A
A 60+D 1250 A 70 A 75
30% 16% 18%
105
advanced untreated
MAID
A 69, I 7500, D 900
47% (10%)
140
advanced
CyVADIC
200
ECOG Antman et al.
Drug
A
A 70
27%
VAdriC VAC
V 1.4, A 70, Cy 50 V 1.4, Act 0.4, Cy 50
19% 11%
untreated
A+D
17%
metastatic/unresectable
ADI
32%
262
advanced
A MAI MAP
A 80 A 60, I 7500 Mito 8/A 60/P60
20% 34% 32%
Santoro et al.30
663
y
A CyVADIC A+I
75 cy500/A50/V1.5/DTIC 750 A50/I5
23.3% 28.4% 28.1%
Steward31
104
A+I+GM-CSF
75/5g
45% (10%)
Le Cesne32
294
A+I A+I+GMCSF
50/5 75/5+GM-CSF
Intergroup
340
50% (17%)
28
Edmonson et al.
29
21% 23.3%
A ¼ Doxorubicine, D ¼ Dacarbazine, I ¼ Ifosfamide, Cy ¼ Cyclofosfamide, V ¼ Vincristine, Act ¼ Actinomycin-D, MAID ¼ mesna, doxorubicine, ifosfamide, dacarbazine, ADI ¼ MAID, MAI ¼ mesna, doxorubicine, Ifosfamide, MAP ¼ mitimycin-C, doxorubicine, cisplatin, CyVADIC ¼ Cyclofosfamide, vincristine, doxorubicine, dacarbazine.
ARTICLE IN PRESS The role of chemotherapy in the treatment of bone and soft tissue sarcomas
125
Recurrent and metastatic disease
Conclusions
Relapse is common within two to three years from diagnosis. Retro-peritoneal sarcomas tend to have local recurrence at higher rates. Distant relapse is more frequent to the lungs (20% of patients), less to bone (7%), liver (4%), and lymph nodes (less than 4%). Myxoid liposarcoma of the extremity tends to metastasize to the abdomen and pelvis. If possible, salvage treatment both for local and distant recurrence is radical re-excision with or without radiotherapy. In patients with less than four lung metastases and no endobronchial invasion, and after a long disease free interval, complete pulmonary resection can give long-term survival in 15–40%. While chemotherapy remains an option for inoperable patients with metastatic or recurrent disease, the response rates in Stage IV soft tissue sarcoma have been low.
Adjuvant or neoadjuvant chemotherapy, with Doxorubicine+Ifosfamide regimens in conjunction with radiotherapy is recommended for patients presenting with large (45 cm), intermediate- or highgrade tumours. For untreated metastatic patients a combination of surgery (always recommended when feasible) and DOX-IFO based chemotherapy can be used for palliative purposes and is able to prolong survival.
Drugs Doxorubicine: The first drug that showed activity in metastatic soft tissue sarcoma with a response rate of 20–30% when administered as single agent. Cyclophosphamide: It is inactive as a single agent and after a randomized controlled trial 22 has been replaced by ifosfamide. The studies on combination chemotherapy in metastatic soft tissue sarcoma are shown in Table 2.
New agents Gemcitabine has shown activity in several types of tumours including soft tissue sarcomas. Other newer agents include docetaxel and paclitaxel. Liposomal DOX is a new form of DOX in which the drug is encapsulated in liposomes aiming to reduce toxicity, in particular cardiotoxicity and myelosuppression. It has equivalent activity to standard DOX, and should be considered for those patients who are at risk of greater cardiotoxicity. Ecteinascidin-743 (ET-743): A novel marine-derived antineoplastic agent. Preclinical and initial clinical data have shown an activity of the compound, alone or in combination with cisplatin, paclitaxel and DOX, in some type of tumours, such as breast and ovarian cancer, and soft tissue sarcomas. No responses have been reported for GISTs, while best responses were seen in patients with leiomyosarcoma and liposarcoma.
References 1. De Vita VT. Cancer: practice and principles of oncology. Philadelphia: Lippincott Williams & Wilkins; 1997. p. 1816–1838. 2. Bacci G, Ferrari S, Picci P, et al. Methotrexate serum concentration and histological response to multiagent primary chemotherapy for osteosarcoma of the limbs. J Chemother 1996;8:472–8. 3. Graf N, Winkler K, Betlemovic M, Fuchs N, Bode U. Methotrexate pharmacokinetics and prognosis in osteosarcoma. J Clin Oncol 1994;12:1443–51. 4. Winkler K, Beron G, Kotz R, et al. Neoadjuvant chemotherapy for osteogenic sarcoma: results of a Cooperative German/Austrian study. J Clin Oncol 1984;2:617–24. 5. Bacci G, Picci P, Ferrari S, et al. Primary chemotherapy and delayed surgery for nonmetastatic osteosarcoma of the extremities. Results in 164 patients preoperatively treated with high doses of methotrexate followed by cisplatin and doxorubicin. Cancer 1993;72:3227–38. 6. Goorin AM, Schwartzentruber DJ, Devidas M, et al. Presurgical chemotherapy compared with immediate surgery and adjuvant chemotherapy for nonmetastatic osteosarcoma: pediatric Oncology Group Study POG-8651. J Clin Oncol 2003;21(8):1574–80. 7. Bacci G, Briccoli A, Rocca M, et al. Neoadjuvant chemotherapy for osteosarcoma of the extremities with metastases at presentation: recent experience at the Rizzoli Institute in 57 patients treated with cisplatin, doxorubicin, and a high dose of methotrexate and ifosfamide. Ann Oncol 2003;14: 1126–34. 8. Kager L, Zoubek A, Potschger U, et al. Primary metastatic osteosarcoma: presentation and outcome of patients treated on neoadjuvant Cooperative Osteosarcoma Study Group protocols. J Clin Oncol 2003;21:2011–8. 9. Longhi A, Fabbri N, Donati D, et al. Neoadjuvant chemotherapy for patients with synchronous multifocal osteosarcoma: results in eleven cases. J Chemother 2001;13:324–30. 10. Ferrari S, Briccoli A, Mercuri M, et al. Postrelapse survival in osteosarcoma of the extremities: prognostic factors for long-term survival. J Clin Oncol 2003;21:710–5. 11. Fagioli F, Aglietta M, Tienghi A, et al. High-dose chemotherapy in the treatment of relapsed osteosarcoma: an Italian sarcoma group study. J Clin Oncol 2002;20:2150–6. 12. Bacci G, Ferrari S, Longhi A, et al. Role of surgery in local treatment of Ewing’s sarcoma of the extremities in patients undergoing adjuvant and neoadjuvant chemotherapy. Oncol Rep 2004;11:111–20. 13. Ladenstein R, Hartmann O, Pinkerton, et al. A multivariate and matched pair analysis on high-risk Ewing tumor (ET)
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patients treated by megatherapy (MGT) and stem cell reinfusion (SCR) in Europe. Proceedings of the ASCO; 1999. p. 2144. Hawkins DS, Barker L, Sanders JE, et al. Outcome of patients with recurrent Ewing’s sarcoma family of tumors (ESFT). Proceedings of the ASCO; 2004. p. 8517. Brennan MF, Casper ES, Harrison LB. Soft tissue sarcoma. In: Devita VT, Hellman S, Rosenberg SA, editors. Cancer: Principle and Practise of Oncology. 6th ed. Philadelphia: Lippincott Raven Publishers; 2002. p. 1738–887. American Joint Committee on Cancer. Cancer staging manual, 6th ed. Philadelphia: Lippincott Raven; 2002. p. 221–8. Connier JN, Pollok RE. Soft tissue sarcomas. CA Cancer J Clin 2004;54:94–109. Spira AI, Ettinger DS. The use of chemotherapy in soft-tissue sarcomas. The Oncologist 2002;7:348–59. Tierney JF. Adjuvant chemotherapy for localised resectable soft-tissue sarcoma of adults: meta-analysis of individual data. Sarcoma Meta-analysis Collaboration. Lancet 1997; 350:1647–54. Frustaci S, Gherlinzoni F, De Paoli A, et al. Adjuvant chemotherapy for adult soft tissue sarcomas of the extremities and girdles: results of the Italian randomized cooperative trial. J Clin Oncol 2001;19:1238–47. Eilber FC, Rosen G, Eckardt J, et al. Treatment-induced pathologic necrosis: a predictor of local recurrence and survival in patients receiving neoadjuvant therapy for highgrade extremity soft tissue sarcomas. J Clin Oncol 2001; 19:3203–9. Stuart-Harris RC, Harper PG, Parsons CA, et al. High-dose alkylation therapy using ifosfamide infusion with mesna in the treatment of adult advanced soft-tissue sarcoma. Cancer Chemother Pharmacol 1983;11:69–72. Gottlieb JA, Baker LH, Quagliana JM, et al. Chemotherapy of sarcomas with a combination of adriamycin and dimethyl triazeno imidazole carboxamide. Cancer 1972;30:1632–8. Borden EC, Amato DA, Rosenbaum C, et al. Randomized comparison of three adriamycin regimens for metastatic soft tissue sarcomas. J Clin Oncol 1987;5:840–50. Ellis A, Ryan L, Sulkes A, et al. Response to mesna, doxorubicin, ifosfamide, and dacarbazine in 108 patients
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with metastatic or unresectable sarcoma and no prior chemotherapy. J Clin Oncol 1989;7:1208–16. Yap BS, Baker LH, Sinkovics JG, et al. Cyclophosphamide, vincristine, adriamycin, and DTIC (CYVADIC) combination chemotherapy for the treatment of advanced sarcomas. Cancer Treat Rep 1980;64:93–8. Schoenfeld DA, Rosenbaum C, Horton J, et al. A comparison of adriamycin versus vincristine and adriamycin, and cyclophosphamide versus vincristine, actinomycin-D, and cyclophosphamide for advanced sarcoma. Cancer 1982; 50:2757–62. Antman K, Crowley J, Balcerzak SP, et al. An intergroup phase III randomized study of doxorubicin and dacarbazine with or without ifosfamide and mesna in advanced soft tissue and bone sarcomas. J Clin Oncol 1993;11: 1276–85. Edmonson JH, Ryan LM, Blum LH, et al. Randomized comparison of doxorubicine alone versus ifosfamide plus doxorubicin or mitomycin, doxorubicin and cisplatin against advanced soft tissue sarcomas. J Clin Oncol 1993; 11(7):1269–75. Santoro A, Tursz T, Mouridsen H, et al. Doxorubicin versus CYVADIC versus doxorubicin plus ifosfamide in first-line treatment of advanced soft tissue sarcomas: a randomized study of the European Organization for Research and Treatment of Cancer Soft Tissue and Bone Sarcoma Group. J Clin Oncol 1995;13:1537–45. Steward WP, Verweij J, Somers R, et al. Granulocytemacrophage colony-stimulating factor allows safe escalation of dose-intensity of chemotherapy in metastatic adult soft tissue sarcomas: a study of the European Organization for Research and Treatment of Cancer Soft Tissue and Bone Sarcoma Group. J Clin Oncol 1993;11:15–21. Le Cesne A, Judson I, Crowther D, et al. Randomized phase III study comparing conventional-dose doxorubicine plus ifosfamide versus high-dose doxorubicin plus ifosfamide plus recombinant human granulocyte-macrofage colony-stimulating factor in advanced soft tissue sarcomas: a trial of the European Organization for Research and Treatment of Cancer/Soft Tissue and Bone Sarcoma Group. J Clin Oncol 2000;18:2676–84.
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SPINE
Cervical spondylosis. Part III: Cervical arthroplasty Michael J. Torrens Departments of Neurosurgery, Hygeia Hospital, Erythrou Stavrou 4, Maroussi 15 123, Athens, Greece and Frenchay Hospital, Bristol, UK
KEYWORDS Cervical spondylosis; Cervical arthroplasty; Artificial discs; Disc prostheses; Total disc replacement
Summary An appreciation of the frequency with which cervical fusion accelerates adjacent disc disease has led to the development of mobile artificial disc prostheses. At least six models are well advanced in clinical trials. Initial results show that such discs are as effective as current surgical techniques involving fusion, that they have few complications and that they preserve the range of movement of the relevant intervertebral joint. The question as to whether they will endure and prevent accelerated disc disease will only be answered by very long-term studies (10–20 years). Meanwhile, the results are encouraging and cervical arthroplasty may well be indicated in the majority of cervical disc problems requiring surgery, provided they are not associated with other local spinal disease or instability. & 2005 Elsevier Ltd. All rights reserved.
Introduction In 2002, at the end of a previous paper in this series,1 I predicted that there would be slow progress towards non-fusion, arthroplasty techniques in the management of cervical disc disease and accompanying spondylosis. I was very enthusiastic at that time but did not for a moment imagine the explosion of interest in implantable, mobile, cervical disc joints that is occurring currently. This may be premature but there is no evidence that it is misdirected or dangerous. An enormous clinical effort and commercial investment is driving it forward. Several recent meetings have been devoted to the subject and at least two dedicated journal supplements have been Tel.: +30210 6867107; fax: +30210 6801655.
E-mail address:
[email protected].
published in 2004.2,3 Cervical arthroplasty appears to have arrived, no disasters have blunted enthusiasm as yet, and the subject deserves serious appraisal.
Historical evolution of anterior discectomy Anterior cervical discectomy and fusion was first described in 19584,5 and has since become one of the most effective and reliable of spinal surgical procedures. The early operations used iliac crest autograft to replace the removed disc and encourage fusion, but an unacceptable rate of graft collapse and protrusion led to the first modifications. Some surgeons employed plating for support; others performed only simple discectomy without
0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2005.03.002
ARTICLE IN PRESS 128 grafting and with vertebral end plate preservation. The latter has proved reliable but the consequent disc space narrowing may entrap nerve roots in the foramina and also fusion is less certain. Some patients with failed fusion complain of increased local neck pain. However, it was also observed that complete success was possible in the absence of fusion. Disc space narrowing and graft donor site complications (pain and infection) resulted in the increased use of allograft. This was later rejected because of frequent graft failure and the risk of disease transmission. The next development was of metal spacers and cages, supplemented by artificial bone substitute and bone morphogenetic protein (BMP). Metal has a tendency to fracture the vertebral end plate and this has led to the development of plastic synthetics, such as polyetheretherketone (PEEK), which have a hardness similar to bone. By combining PEEK and BMP with the use of a cervical plate, a 100% fusion rate has been reported,6 but this requires multiple (and expensive) implants. A high fusion rate and long follow-up has led to an appreciation of the significant complications of fusion. Accelerated degenerative disease adjacent to congenital cervical fusion is well known. Iatrogenic fusion produces the same effect. Longterm follow-up has shown 50–92% of patients undergoing fusion may develop radiographically confirmed adjacent level degeneration.7,8 Twentyfive percent of operated cases will develop radiculopathy or myelopathy due to such degeneration9 and 16–19% will require a further operation.7,10 These observations have led a significant number of spinal surgeons to believe that the future of cervical disc surgery lies with arthroplastic techniques that maintain the mobility of the disc joint. In addition to ‘knock on’ discopathy, as described above, multiple fusions lead to restricted neck movement that can be socially disabling and even potentially dangerous, as when it precludes emergency endotracheal intubation.
The development of cervical arthroplasty One pioneering attempt to replace cervical discs occurred in the 1960s when Fernstrom11 inserted a spherical metal device into the intervertebral space, but this failed very frequently because it either fractured the end plate or caused hypermobility. Though developments occurred in lumbar arthroplasty in the 1980s, the next significant
M.J. Torrens progress in the cervical area was at Frenchay Hospital, Bristol in the early 1990s. Brian Cummins and his colleagues devised a metal on metal, ball and socket joint secured by screws.12 A number of practical problems stimulated design revision and eventually the system was acquired and further developed by Medtronic as the Prestige range of prostheses (Fig. 1). Using the first modified Prestige prosthesis, a prospective trial was started in 2000. The preliminary results in 15 patients showed 100% success in preserving movement.13 Minor technical problems (screw breakage) had no clinical repercussions. At much the same time, clinical trials of other metallic designs began. These include the Bryan disc (Medtronic), the PCM disc (Cervitech), the ProDisc-C (Synthes) and the CerviCore disc (SpineCore). The Bryan disc consists of a saline-lubricated polyurethane core between two titanium plates which adhere to the vertebra by bony ingrowth into the porous titanium surface thus avoiding screws and allowing a very low projection profile (Fig. 2). It also has some shock absorbing potential. Over 2000 such discs have been implanted, mainly in Europe and Australia, but few have been prospectively evaluated. A series of 26 patients with one or two level implants reported from Canada has shown preservation of movement in all patients evaluated radiologically,14 with a mean range of segmental movement (ROM) of 7.81 which was not significantly different from the preoperative ROM of 10.11. The overall spinal mobility (C2–C7) increased by 10.51, presumably because pain was reduced. The PCM disc (Fig. 3) combines TiCaP-coated cobalt–chromium with ultra-high molecular weight polyethylene, a familiar, tried and tested combination. Trials are less well advanced but again the first anecdotal reports are of successful movement preservation.15 The ProDisc-C (Fig. 4) copies a design used successfully in the lumbar region. It consists of two cobalt–chromium–molybdenum endplates with a polyethylene insert. Immediate stability is provided by a central keel, which slides into a prepared groove in the vertebral body. The CerviCore disc is a metal on metal design very similar to Prestige. A recent and very interesting development has been the production of a non-metallic disc (Neodisc) by a British company, Pearsall’s. This consists of a woven (embroidered) polyester ‘ligament’ enclosing an artificial disc nucleus made of medical grade silicone (Fig. 5). Independent analysis of explanted discs in animal studies has shown biointegration of This paper is dedicated, posthumously, to Brian Cummins
whose enthusiasm for life and neurosurgery will never be forgotten by his friends.
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Figure 1 The evolution of the Cummins/Frenchay/Medtronic cervical disc: (A) the round, ball and socket, screw-fixed prototype, (B) the ovoid form of the first Medtronic Prestige disc and (C) the likely form of the revised Prestige disc with screwless fixation. (Reproduced with permission.)
the polyester ligament with fibrous tissue ingrowth. At present, the ligaments require to be attached by metal screws but other non-metallic fixation systems are under review and implantation in human subjects has started. The average postoperative ROM has been recorded as 6.11.16
Contraindications Since the indications for cervical arthroplasty are (or will soon become) almost every case of cervical
disc disease that requires surgical treatment it is easier to list the contraindications: 1. Disease requiring discectomy at more than two levels. Three level arthroplasty will probably prove to be stable but the studies are not yet adequate. 2. Very young patients. The prostheses may not last 50 years or more. 3. Osteoporosis. 4. Instability or disease involving posterior elements. 5. Previous laminectomy.
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Figure 2 The Medtronic Bryan disc prosthesis. (Reproduced with permission.)
M.J. Torrens
Figure 4 The Synthes ProDisc-C. (Reproduced with permission.)
there are certain situations where preservation of mobility is especially indicated: 1. A second operation after a previous fusion. 2. At a level next to early disc degeneration which would be accelerated by fusion. 3. An operation between fused levels.
A typical implantation procedure
Figure 3 The Cervitech PCM artificial disc. (Reproduced with permission.)
6. Intercurrent disease such as active infection. 7. Kyphosis requiring correction. 8. Spinal stenosis due to ossification of the posterior longitudinal ligament or multiple compressions due to hypertrophied interlaminar ligaments. 9. Disc space not visible on lateral X-ray with the patient lying (disc too low for operative approach?).
Special indications Although, as already stated, most cervical discectomy operations should be followed by arthroplasty,
The operation consists of two separate procedures. Discectomy/decompression must be performed in the traditional way. Subsequently, the mobile disc prosthesis is inserted. However, the disc prosthesis may require the creation of a wider interspace than is necessary for a traditional, end-plate sparing discectomy. It is advisable to take advantage of this width for better visibility during decompression and this will affect the order of operative procedures. A typical operation may consist of the following stages: 1. Careful positioning of the image intensifier and the patient with immobilisation of the head and neck to prevent movement (Fig. 6). For accuracy, constant videoscopic control is needed and fixed centering and angle measurements may be required. 2. Routine anterior approach with all the usual precautions, including an obsessionally correct identification of the affected disc level. 3. Preparation of the interspace and endplates as appropriate for the chosen prosthesis.
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Figure 6 The position for operation with the head fixed by strapping, the neck supported by a rolled towel and the image intensifier in place.
Figure 5 The Neodisc developed by A. Jackowski and manufactured by Pearsalls: (A) anterolateral view showing interlocking ligaments and screw fixation and (B) sagittal section revealing the silicone ‘nucleus’.
4. Performance of discectomy /decompression. 5. Insertion of prosthesis. 6. Routine closure. Probably, the most frequently used prosthesis is the Bryan disc and this will be used as an example to explain the operation further. The size of the prosthesis must be exactly that of the end plate and is better chosen from measure-
ment of CT than MRI because of possible MRI distortion especially when previous implants have been inserted. The prosthesis needs to be exactly and correctly positioned. The measurements for this are made in relation to an external frame, which is leveled and checked against the image intensifier to assess the angle of the relevant disc (Fig. 7). After the spine has been exposed and a preliminary discectomy has been performed, the midline is calculated exactly and a drilling jig screwed in place appropriately centered and angled (Fig. 8). Depth of drilling is checked both visually and by X-ray using a probe (Fig. 9). The drills and milling discs then prepare an exact surface contour to receive the prosthesis. The position of the prosthesis is checked by a temporary phantom (Fig. 10) which also keeps the disc space open while the drilling jig is removed and a vertebral retractor inserted. The preparation of the interspace leaves an excellent visual access for further discectomy and decompression using the operating microscope for assisted vision. After completing the decompression, with removal of the disc, posterior longitudinal ligament and osteophytes as required to open the spinal canal and foramina, the prosthesis is simply pressed gently into place in the same way that a cage would be inserted. It is essential that all bone dust and other loose fragments of tissue should be carefully washed out.
Results It will take many years to confirm the hypothesis that movement preservation has a significant effect
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Figure 7 A pendulum is fixed to the image intensifier to mark vertical. The angle of implantation of the disc prosthesis is calculated by drawing a line along the back of the vertebral bodies. The disc implant is at right angles to this.
Figure 8 A centrally aligned wedge is hammered into the disc space after preliminary discectomy. This wedge guides the insertion and fixation of the milling jig for preparation of the end plate/vertebral surfaces.
in preventing adjacent disc degeneration. It is rather disappointing that few randomised controlled trials have been set up to compare arthroplasty with fusion; however, the rate of change of disc design means that the prostheses evaluated now will be obsolete long before the trials are finished. The initial randomised comparisons of arthroplasty and fusion17,18 have shown no significant difference in early results between the two methods. There is a general impression that post-
M.J. Torrens
Figure 9 Depth of drilling must be carefully checked both by video and by measurement at every stage of the procedure.
Figure 10 After the preparation of the bone surfaces, a disc phantom/distractor is placed in the interspace. Distraction is then maintained by a distractor attached to the screws in the vertebrae while the final decompressive surgery is undertaken.
operative pain and length of hospital stay are both less with arthroplasty but this has yet to be demonstrated objectively. Motion preservation, as noted in an earlier paragraph, has been successful (Fig. 11). Radiological studies following arthroplasty confirm a sagittal ROM of 5.9–7.81 compared to preoperative ROM of 5.9–10.11.14,17 The mean ROM may reduce with time. A reduction of half a degree has been noted between 3 months and 12 months
ARTICLE IN PRESS Cervical spondylosis. Part III: Cervical arthroplasty
133 evaluations, particularly concerning screws breaking or pulling out. The prostheses have been redesigned to avoid screw fixation, which also tended to cause dysphagia. There have been occasional reports of malpositioning and displacement of prostheses. At least one misplaced disc has had to be removed.17 A further complication has been local pain, movement restriction and early paradiscal calcification some weeks after surgery. This seems to be related to bone dust left behind after the drilling procedures and requires treatment with antiinflammatory drugs and mobilisation exercises, otherwise it my lead to fusion around the prosthesis. All these problems can be minimised by more careful attention to operative technique.
Discussion
Figure 11 The mobility demonstrated by a Bryan disc postoperatively: (A) flexion and (B) extension. Note also the antero-posterior translational movement allowed by the Bryan type of disc.
postoperatively.17 Movement is maintained at 48 months follow-up.19
Complications and adverse events All the typical, though fortunately rare, complications of the anterior cervical approach occur with the usual frequency. These include operating on the wrong level, dysphonia, dysphagia, oesophageal injury, respiratory obstruction due to oedema or haematoma and local neurological injury. Adverse events associated with the mobile disc prostheses were mainly recorded during the early
An enthusiasm among surgeons for instrumentation in the cervical spine was mentioned previously.1 On the crest of this wave, several companies have introduced mobile disc prostheses onto the market and more are being developed. By the time this paper is published, it is likely that the first FDA approvals will have been given. One might have wished for a more exhaustive evaluation but, for reasons stated above, this was never and will never be really practical. The ‘trial by ordeal’ has already taken place and the concept has survived. The early results are the same or better than those of established techniques.17,18 Most technical problems have been overcome and design details are certain to improve still further and rapidly. The outstanding questions are related to the long term. Are the late problems of device failure more or less significant than the benefit of preserving mobility and avoiding the up to 19% rate of further surgery that has been reported after fusion?7,10 We can only guess. Potential problems are those related to the durability of the prosthesis and its interface with bone. Orthopaedic surgeons in particular will be familiar with such problems in relation to hip and knee prostheses. However, designers of mobile disc prostheses have two particular advantages. All the technology accrued from other prosthetic designs is available and, also, the relative stress factors in the neck are much less than at the hip or knee. In vitro material wear analyses have shown a rate of wear of 0.093 mm3/million cycles20 for disc implants which is two orders of magnitude less than equivalent figures for hip arthroplasty. Despite optimistic predictions, the possibility of implant failure must be considered very seriously. Disc
ARTICLE IN PRESS 134 prostheses will be inserted at a much earlier age than hip and knee prostheses, requiring predictable reliability for perhaps three times longer. Also the process of surgical revision is likely to be fraught with difficulty and will most likely require fusion subsequent to prosthesis removal. So will cervical arthroplasty be a success? Surgical intuition says yes. Regulatory institutions may delay the progress for a while, especially in the UK, but the combined force of public demand, surgical enthusiasm and commercial pressure will overcome in the end. I believe that arthroplasty in the cervical region will be more successful than in the lumbar region because it uses a surgical approach already familiar and because the incidence of facet disease is relatively much less in the neck making the indication for use almost universal. The most successful prostheses will be those that combine reliability with ease of insertion. When reliability has been conclusively demonstrated, their implantation will become more frequent and earlier, including use to prevent spondylotic changes such as facet osteoarthritis and stenosis. In this context, lumbar arthroplasty may burgeon—imagine preventing the morbidity of chronic lumbar spondylosis! Perhaps, in another generation, genetically engineered discs may become available but we have many years of cervical arthroplasty ahead.
References 1. Torrens M, Miliaras G. Cervical spondylosis. Part II, surgical management. Curr Orthop 2002;16:300–10. 2. Haid R, Traynelis V, editor. Cervical arthroplasty. Neurosurgical Focus 2004; 17(3). 3. Albert TJ, Kostuik JP, editor. Disc replacement special edition. Spine J 2004; 4(6) Suppl 1: 143–354. 4. Smith G, Robinson R. The treatment of certain cervical spine disorders by anterior removal of the intervertebral disc and interbody fusion. J Bone Joint Surg Am 1958; 49:607–22.
M.J. Torrens 5. Cloward RB. The anterior approach for the removal of cervical disks. J Neurosurg 1958;10:602–17. 6. Mummaneni PV, Haid RV. The future in the care of the cervical spine: interbody fusion and arthroplasty. J Neurosurg (Spine 1) 2004;2:155–9. 7. Katsuura A, Hakuda S, Sarohashi Y, et al. Kyphotic malalignment after anterior cervical fusion is one of the factors promoting the degenerative process in adjacent vertebral levels. Eur Spine J 2001;10:320–4. 8. Goffin J, van Loon J, Van Calenbergh F, et al. Long-term results after anterior cervical fusion and osteosynthetic stabilization for fractures and/or dislocations of the cervical spine. J Spinal Disord 1995;8:499–508. 9. Hilibrand AS, Carlson GD, Palumbo MA, et al. Radiculopathy and myelopathy at segments adjacent to the site of a previous anterior cervical arthrodesis. J Bone Joint Surg Am 1999;81:519–28. 10. Gore DR, Sepic SB. Anterior discectomy and fusion for painful cervical disc disease. A report of 50 patients with an average follow up of 21-years. Spine 1998;23:2047–51. 11. Fernstrom U. Arthroplasty with intercorporal endoprosthesis in herniated disc and painful disc. Acta Chir Scand 1966(Suppl 357):154–9. 12. Cummins BH, Robertson JT, Gill SS. Surgical experience with an implanted artificial cervical joint. J Neurosurg 1998; 88:943–8. 13. Wigfield CC, Gill SS, Nelson RJ, et al. The new Frenchay artificial cervical joint: results from a two-year pilot study. Spine 2002;27:2446–52. 14. Dugal N, Pickett GE, Mitsis DK, Keller JL. Early clinical and biomechanical results following cervical arthroplasty. Neurosurg Focus 2004;17(3):62–8. 15. Le H, Thongtrangan I, Kim DH. Historical review of cervical arthroplasty. Neurosurg Focus 2004;17(3):1–9. 16. Jackowski A. Personal communication. 17. Porchet F, Metcalf NH. Clinical outcomes with the Prestige II cervical disc: preliminary results from a prospective randomized clinical trial. Neurosurg Focus 2004; 17(3):36–43. 18. Wigfield CC, Gill SS, Nelson RJ, et al. Influence of an artificial cervical joint compared with fusion on adjacentlevel motion in the treatment of degenerative cervical disc disease. J Neurosurg (Spine 1) 2002;96:17–21. 19. Robertson JT, Metcalf NH. Long term outcome after implantation of the prestige I disc in an end stage indication: 4 year results from a pilot study. Neurosurg Focus 2004;17(3):6–71. 20. Hellier WG, Hedman TP, Kostuik JP. Wear studies for development of an intervertebral disc prosthesis. Spine 1992(Suppl 6):86–96.
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ORTHOPAEDIC INFORMATICS
Personal digital assistants in orthopaedic surgery K. Barbosa, L. Funk Hope Hospital, Eccles Old Road, Salford M6 8HD, UK
KEYWORDS Personal digital assistants; Classification; Features
Summary Personal digital assistants (PDAs) have become a constant companion to most professional people. The increase in processing power and wireless connectivity have made these devices useful tools for data collection, quick reference and diary-keeping. In this article we discuss the specific features and benefits for orthopaedic surgeons and trainees, with a view to future developments. & 2005 Elsevier Ltd. All rights reserved.
Introduction In the near future it is possible that doctors will routinely carry a small handheld diagnostic device resembling the current personal digital assistant (PDA). Its present use may not be as sophisticated as that used by Dr. Spock on ‘the Starship Enterprise’ but recent innovations open the door for the use of these devices as medical tools. For the present, PDAs are regularly used by a small number of enthusiasts for patient management, information storage and connectivity.
What is a PDA? PDAs are computers that are miniaturised for portability, and thus are readily accessible at all times. Early machines performed functions such as address book, calculator, clock, date, diary and basic word processor. They are now capable of even Corresponding author.
E-mail address:
[email protected] (L. Funk).
advanced data management and digital imaging. Most devices have internet connectivity and wireless communication more advanced than plain infrared transmission, such as Bluetooth and Wi-Fi.
Classification of devices With so many machines available on the market, a beginner may find it difficult to buy the right one. The best way to start is by classifying PDAs according to the operating system. 1. Palm operating systems are produced by Palm, Sony, Acer and Visor. 2. Pocket PC (Windows CE) is used by Toshiba, HP, Compaq and Dell. 3. Psion devices, which used Epoc operating systems, are now extinct. However the system has been developed by the Symbian alliance (see below). 4. Linux based systems, e.g. Yopy. 5. Symbian, which has been developed jointly by Psion, Ericsson, Nokia, Motorola and Panasonic
0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2005.02.012
ARTICLE IN PRESS 136 and used by mobile phones that have PDA functions, e.g. Nokia 9210. Palm and Pocket PC devices dominate the current market. All systems perform similar tasks, but have some advantages in certain applications and connectivity. Having classified the devices the following factors need to be considered.
General features of PDA (a) Palm models are generally smaller in size. The difference may have practical implications for some. The swivelling panel of a Sony affords protection to the screen without a jacket. Jackets add to the bulk of the device. But sometimes jackets perform more than protective functions and may contain expansion slots for memory cards and modem cards. Some expansion packs allow connection to the local net or internet via LAN or GSM networks. Other devices owe their size to the onboard keyboards, e.g. The HP 728. (b) While Pocket PCs have always had colour screens and traditionally Palm devices were monochrome, all the recent editions of Palm have been produced with colour displays. However, colour displays are a significant drag on battery power. (c) Pocket PC devices tend to have bigger built in storage memory with 64 and 128 Mb being supplied. Palm devices are now available with up to 32 Mb memory. However, Palm software and documents tend to be more compact and require less space, so the same amount of memory may not be necessary for Palm devices. (d) Palm devices tend to be a bit cheaper and often smaller.
Operating systems (a) If you are used to the Microsoft Windows operating system, the Pocket PC interface will be familiar, but the Palm interface is probably more intuitive. While Microsoft has greatly improved the Windows CE interface with the introduction of the Pocket PC 2002, it is a little cousin to Windows, which means while it is quite powerful, it also has a bit more of a learning curve. (b) Epoc based machines provide very useful and adaptable programmes like spreadsheets with advanced statistical functions and a contact
K. Barbosa, L. Funk manager which can be reprogrammed into a database. Epoc was designed specifically for hand held devices (the Psion series of hand held), thus it is quick, small and reliable. However, it is not well supported by third party software manufacturers. (c) Windows based software require more processing power and have hence lower battery life (2–3 days compared to 1–2 weeks for Palm devices).
Basic functions supplied with the minimum specification machines These include an Address book, Contacts Manager, Calendar/Diary, To Do List, Jotter, Email Application, Phone Manager, word processor, spreadsheet application, World Time Clock, Clock/Alarm, Calculator, Media Player and Dictaphone. The above diary functions can synchronise with Microsoft Outlook. Phone devices in addition support dual band network connectivity and Fax.
Special features Synchronisation All devices will synchronise with your computer, be it Windows or Apple Macintosh. Special software may be required for certain programmes, especially for Palm devices. Pocket PCs integrate better with Microsoft Word and Excel (Microsoft makes all those products, after all). If you need to integrate with Outlook, the Pocket PC does it out of the box, while Palm products need additional software.
Data input Palm uses the Graffiti method. Graffiti is a handwriting system developed for Palm devices. The user needs to learn specific writing methods to input data rapidly. This is quite quick and easy to learn. Microsoft has gone down the road of trying to recognise the user’s own handwriting, which is currently still less accurate than Graffiti but improving rapidly. Both have on-screen keyboards which limit the size of the display. Full size keyboards are also available as accessories with most brands, which can be carried folded to the size of a card.
Expandability With the ability to increase memory, one can store a lot of programmes and data outside the memory of the
ARTICLE IN PRESS Personal digital assistants in orthopaedic surgery machine. Palm devices use memory cards while Sony uses the propriety ‘Memory stick’ which can be used in their other devices. Pocket PC also have facilities for expansion with memory cards from 32 Mb to 1 Gb.
Internet connectivity Standard PDAs all can connect to the internet via a linked computer. Some devices have inbuilt modems for direct connection or expansion modem packs allow PDAs to connect to the net via ordinary phone lines. Wireless connection to mobile phones allow access to email and internet away from a fixed phone line, but the connection speed is slow (and expensive). GSM and G3 networks provide faster access, but are not widely used. If you are still confused, do not worry as PDAs are at a stage of very rapid evolution with miniature electronics, wireless developments, and evolving software. When purchasing a PDA it is essential that you identify your specific requirements and then buy the device that best suits your personal needs.
PDAs and the NHS The NHS Information Authority is a specific body established for the development of information management and usage in the NHS. One of its major objectives is enabling the NHS to use information to improve the quality of patient care. Most hospitals in the UK (and in most first world countries) use varying levels of computerised information technology. Hand held devices are part of most IT strategies, as they allow for access to medical information away from main terminals and whilst on the move. Clinicians and staff generally are mobile workers and would benefit from having access to patient information when required without being restricted by the position of the computers. A number of hospitals are trialing the use of hand held devices linked via wireless networks to the main hospital IT network. These are kept on each ward. Nursing assessments and interventions are generally inputted. This can be done at the bedside. The staff also have rapid access to investigation results at the bedside. However, most hospitals do not have the infrastructure at present to support this technology and the use of PDAs as part of the hospital network is still a long way off.
Current benefits of PDAs to Orthopaedic surgery From our own data orthopaedic surgeons seem to have embraced PDA technology more than most
137 other medical specialties. A small poll at a typical UK District General Hospital in July 2003 showed that 60% of the orthopaedic surgeons (junior and senior grades) owned and used a PDA. The only bigger user group was the anaesthetists, with 90% of anaesthetists using PDAs. Palm devices were more popular than Pocket PC machines. Interestingly, 30% of those clinicians who owned a PDA did not find any medical use for the device other than for log book purposes.
General uses Clinicians are using PDAs professionally already, although their use is variable and limited to the technophiles at present. The current medical use of PDAs are: 1. Surgical Log Book: This is perhaps the most common use of a PDA by surgical personnel. The Royal College of Anaesthetists have a PDA compatible log book and similar log books are available from other programmers. You can use an Excel, Word or third party software like HandBase to create your own log book. It is a requirement for orthopeadic trainees to use the web-based logbook administered by the Royal College of Surgeons of Edinburgh, which is available in palm and pocket PC formats. 2. Textbooks: Various textbooks are available for download on to the PDA. They can take a lot of the memory so it is probably best stored in the accessory memory. Campbells Operative Orthopaedics, anatomy reference software and numerous medical books and dictionaries are available. The advantage of having a massive tome like Campbells available in your shirt pocket can make ownership of a PDA worthwhile alone. 3. Quick reference: The textbooks are useful for rapid reference, clinical decision-making and practical guidelines. With the advent of increasing patient expectations, rapid medical developments and information overload it is advantageous to have access to the latest information. With mobile access to the internet it is possible to search the Medical Reference databases, such as PubMed. This is made even easier with special reference management software packages which automatically organise your references for you on your PDA. 4. Patient tracking: Software is available to store basic patient demographics, patient assessments, investigation results and recording ward rounds. Duties such as patient hand-over, transfer
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Figure 1
and discharge can be eased. Some of the comprehensive packages available are HandBase clerking template, Patient keeper, Ward watch and Patient Tracker. Security and the time taken to input data are issues which prevent broader use of this at the present time and limiting use to the technophiles. However, with connectivity to hospital electronic records and offline storage of data this will become less of a problem. 5. Medical calculations: PDAs are very useful for paediatric dose calculations, drug doses according to surface areas and physiological calculations. Many anaesthetic colleagues use it for calculating intravenous fluid and electrolyte replacement. There are also programmes for medical statistics. Examples are DoseCalc, EnteralCalc, Medmath and Medcalc. 6. Drug formulary and prescribing: Besides drug information books, packages are available for prescribing that will print accurate and legible prescription and transmit it electronically to the hospital pharmacy. Intuitive software aims to reduce the human errors by checking for correct dosages and interactions between the prescribed drugs. Recent advances and newer developments include voice interactivity. This will allow real time transla-
tion and dictation of ward rounds and the dictation of prescriptions. Recent advances in software and by attaching the appropriate peripheral devices allow the use of PDAs as an intelligent stethoscope or even a sophisticated mobile ultrasound machine. With government targets of computerising all patient records and processes within the NHS by the year 2005, some clinicians are already arming themselves with their own mobile personal computer and using them in their daily practice. Below is our vision of the anticipated role of PDAs and hand held devices in the future for Orthopaedic Surgeons (Fig. 1).
Web resources for orthopaedic surgeons General information sites and useful links: If you are a beginner best to start at one of these sites that give general information and useful links to other general sites and importantly sites for downloading and buying software and hardware. Most of these sites are maintained by medical staff and are constantly updated. 1. www.ncht.org.uk: besides general information Craig Webster gives information about applications of PDA currently being used at his hospital.
ARTICLE IN PRESS Personal digital assistants in orthopaedic surgery 2. www.handheldfordoctors.com: This is a useful site fore learning basics of PDA use. Dr. Mohammed Al-Ubaydli has written a book on the use of a PDA. 3. www.pdamd.com: Besides a learning centre for beginners, this is a site for discussion forums on various programmes and hardware. There is also a news site for information about recent releases. 4. www.sghms.ac.uk: Maintained by staff from St. Georges Hospital, London. 5. www.epocrates.com: Useful database of drug information. 6. www.avantgo.com: Avantgo software allows download of useful websites and information. From the net.
Pocket PC users
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2.
3.
4.
1. www.pocketpccity.com 2. www.handango.com Palm users 5. 1. www.palmgear.com very useful for information, updates, and software and hardware buys. 2. www.palmaris.com useful site for obtaining software. 3. www.healthypalmpilot.com: One of the sites where a lot of material is available for download specifically related to orthopaedics. There is also a section for frequently asked questions and a message box where users have given their opinion on various programmes. Psion/EPOC users 1. www.stavex.doctors.org.uk: This is a recommended site for orthopaedic surgeons still owning Psion computers. Being run by an orthopaedic surgeon who uses an Epoc based system in everyday practice there is reliable information of programmes for orthopaedic practitioners.
Programmes and electronic books for orthopaedics 1. Brief Op Note Orthopaedic Edition: This is a word based programme for facilitation of operative note writing. It is a 3 page note: the first keeps patient and surgeon details and name of
6.
7. 8. 9.
operation. The second takes detailed note and the third is the orthopaedic power page with orthopaedic implant, trauma equipment, arthroscopic techniques and other categories. Fracture 1.0. This is a programme that has various systems of fracture and orthopaedic classifications and outcome scoring measures. It is an Epoc based programme available for download at the palmaris site. Earlier versions of the programme are available for download at the developers site at www.stavex.doctors. org.uk. PDA The Knee, PDA Anterior Cruciate Reconstruction Notes and PDA views of Reconstruction of Posterior Cruciate are various files showing views of the knee and diagrams of reconstruction of the respective ligaments available for download on your PDA. This is a file showing three views of the knee. PDA Orthopaedic Surgery notes: Available for Epoc users this orthopaedic textbook has had very good reviews by all users. At 360 kb it fits well in a PDA and has comprehensive information on diagnostic and patho-physiology of many conditions related to musculo-skeletal system. The 5 min Orthopaedic Consult by Sponseller. Another volume from the series of 5 min consults for orthopaedic practice. PDA disaster Trauma Handbook. Developed following the September attack it gives current text on Terrorism. Trauma and Biochemical warfare and free access to extensive online information. Handbook of Fractures PDA Cdrom by Kovaal. The 5 min Sports Medicine Consult by Bracker. Techniques in Operative Orthopaedics: A series of 7 volumes of operative techniques based on Campbell’s Operative Orthopaedics. 75–100 procedures described in a bulleted step-by-step fashion. Serves for a quick preoperative read.
Summary PDAs are and will continue to be a useful tool for orthopaedic surgeons. Since orthopaedic surgeons have embraced the technology more so than most other specialties, programmes and applications will continue to be developed specifically for Orthopaedics. With the advancement in wireless technology and digital imaging rapid access to information and rapid transfer of data and images from the convenience of a small handheld device may become routine practice.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 140–154
www.elsevier.com/locate/cuor
TRAUMA
Acetabular fractures J. McMaster, J. Powell Department of Surgery, University of Calgary, AC144C 1403-29th Street NW, Calgary, Alta., Canada
KEYWORDS Acetabular fractures; Classification; Assessment; Non-operative treatment; Operative treatment; Surgical approaches; Surgical technique; Complications; Outcome
Summary The relative infrequency and complexity of acetabular fractures provide a challenge for trauma surgeons. In young patients, the management may be complicated by other injuries. The aim of treatment is to maintain a stable congruent joint. Although there is a role for non-operative treatment the hip joint tolerates instability and incongruity poorly. Operative treatment is complex due to the limitations of the surgical approaches, and the complex three-dimensional anatomy. The relative merit of each surgical option must be considered, and the decision is often a compromise of exposure vs. complications. In the older patients, achieving a stable congruent hip, with open reduction and internal fixation, may not be possible due to poor bone quality. Total hip replacement may be considered a better option. Outcome of acetabular fractures is dependent on the quality of surgical reduction and fixation, in turn this has been related to the experience of the surgeon. & 2005 Elsevier Ltd. All rights reserved.
Introduction Treatment of fractures of the acetabulum is a challenge for orthopaedic surgeons for several reasons:
There are two distinct groups that make up the majority of acetabular fracture patients. J High energy trauma in young active patients, frequently associated with poly-trauma. J Older patients with poor bone stock who frequently present with complex fracture patterns.
Corresponding author. Tel: +1 403 270 2015; fax: +1 403 270 8004. E-mail addresses:
[email protected] (J. McMaster),
[email protected] (J. Powell).
Irreversible damage to the articular surface. Comprehension of fracture patterns requires a detailed understanding of complex three-dimensional pathoanatomy. Difficult surgical access. Prolonged rehabilitation. Significant potential post-operative complications.
Anatomy and biomechanics The acetabulum is formed by the ilium, pubis and ischium and during development they are linked together to form the triradiate cartilage. The triradiate cartilage has its apex in the floor of the acetabulum and fuses between 18 and 23 years of age. For the purposes of fracture description the
0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2005.03.001
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nomenclature described by Letournel and Judet1 is most commonly used. The anterior column (Fig. 1) includes the anterior iliac crest, anterior acetabulum and superior pubic ramus. The posterior column extends from the sciatic notch to the ischial tuberosity and includes the posterior wall of the acetabulum. Fractures involving the anterior and posterior columns characteristically pass through relatively weak areas. The columns are attached to the sacrum through a strut of dense bone called the sciatic buttress. This transmits load between the torso (via the sacrum) and the lower extremity (via the columns). The main weight bearing surface of the acetabulum is cradled between the anterior and posterior columns and is referred to as the dome or roof. Fractures may also involve the anterior and posterior walls of the acetabulum in isolation or in combination with column fractures. The cortical bone overlying the acetabulum within the inner wall of the true pelvis is called the quadrilateral plate. Key to the management of acetabular fractures is the nerves and blood vessels that supply the muscles around the hip and the blood supply of the femoral head and acetabulum (Fig. 2). The superior and inferior gluteal neurovascular bundles supply the gluteus medius/minimus and gluteus maximus, respectively. These structures can be damaged at the time of injury or intraoperatively. The deep branch of the medial femoral circumflex artery (MFCA) is the primary blood supply to the femoral head and must be protected to ensure viability of the femoral head. This vessel has a constant extracapsular course2 that runs along the inferior border of obturator externus and then superiorly over the anterior surface of the inferior
gemellus, obturator internus and superior gemellus close to their common femoral insertion. Terminal branches then perforate the joint capsule, 2–4 mm lateral to the bone cartilage junction, at the level of the superior gemellus. An anastomosis between the inferior gluteal artery and the deep branch of the MCFA runs along the inferior border of the piriformis. The acetabulum and hemi-pelvis are abundantly supplied as a result of its muscular attachments. However, problems can arise when the soft tissue approach involves extensive stripping from both the inner and outer table of the pelvis.
Classification Acetabular fractures are commonly classified using the Letournel–Judet system.1 This classification system describes the fracture in terms of elementary fractures and associated fractures (Fig. 3), and has been assimilated into the AO comprehensive classification system. A column fracture describes a fracture that has separated all or part of the column from the axial skeleton. T-shaped and transverse fractures involve fracture lines extending through the acetabular part of both columns; however, the superior part of the columns remains in continuity with the axial skeleton. A T-shaped fracture differs from a transverse fracture as it also has an extension which runs through the inferior part of the acetabulum and splits the rami. A both columns fracture can be considered a ‘high’ T-shaped fracture where both columns have been separated from the sciatic buttress.3 A fracture is described as
Figure 1 Descriptive anatomy.1
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Figure 2 Nerve and blood supply of the femoral head and gluteal muscles. G Max—gluteus maximus origin; G Med—gluteus medius origin; G Min—gluteus minimus origin; Ob Int—obturator internus; Ob Ex—obturator externus; QF—quadratus femoris.
Figure 3 Elementary and associated fracture patterns.1
ARTICLE IN PRESS Acetabular fractures a wall fracture if it is limited to the acetabular wall. It is accepted, however, that with this system there is the potential for overlap between a large wall fracture and a column fracture. However, isolated wall fractures do not tend to extend into the sciatic notch, involve the quadrilateral plate or extend into the obturator ring.4 Approximately 50% of acetabular fractures are either posterior wall or both columns.
Pathology Motor vehicle accidents are the most common cause of acetabular fractures and the type of fracture has been shown to correlate with direction of impact. In the majority of cases, the acetabular fracture will result from impact transmitted to the acetabulum through the femoral shaft or greater trochanter.1 The type of fracture will also be dependent on the hip position at the time of impact. Frontal collision with an impact applied through the axis of the femur results in fractures of the posterior wall and column. An adducted leg position predisposes the occupant to a posterior wall fracture and an abducted hip a posterior column fracture. Loading through the greater trochanter (e.g., side impact) is postulated to cause anterior wall and column fractures, transverse, T-shaped and both column fractures.
143 from sciatic nerve injury is variable. In contrast, femoral nerve injury is very rare, and the recovery good. Preoperative assessment of femoral nerve function is important as injury is more frequently associated with intraoperative trauma. Acetabular fractures in isolation rarely cause haemodynamic instability but this may be a feature of an associated pelvic fracture. Open fractures are reported with an incidence of p1%.5,7 Closed degloving injuries (Morel-Lavallee lesion) occur in up to 16% of patients.7 The injury is the result of the soft tissue being stripped away from the fascia and is associated with haematoma, fat necrosis and ischaemic skin flaps. Microbiology cultures taken from these areas have demonstrated high rates of bacterial colonisation (46%)8 despite the closed nature of the injury. Surgical skin incisions may also further compromise skin viability. It has been recommended that the injury should be surgically debrided, before or during acetabular surgery, through an incision centred on the lesion. In most cases, the de-gloved area should be left open and allowed to heal by secondary intention.8 Labral tears and avulsions are a constant feature of some fractures. This problem is seen particularly with transverse fractures and it has been recommended that these lesions may require resection or repair.
Investigations Assessment
X-ray
General
The X-ray assessment of acetabular fractures is well described using the AP and Judet views (iliac and obturator obliques). Each view allows an optimum view of different aspects of the anatomy relevant to acetabular fractures. On the AP view the ilio-pectineal and ilio-ischial lines represent outlines of the anterior and posterior columns, respectively (Fig. 4). The obturator oblique demonstrates the obturator ring, posterior wall and lower portion of anterior column. This is the best view to observe the ‘spur’ sign which is frequently seen in both column fractures. The spur is formed by the inferior apex of the intact ilium which is formed when both columns are split from the sciatic buttress. The iliac oblique demonstrates the iliac wing, greater sciatic notch, posterior column and edge of anterior wall. It is important to appreciate that these views are obtained by tilting the patient 451 on each side with the X-ray tube and film vertically aligned. Views obtained by tilting the machine result in significant distortion. Disruption
All acetabular fractures should be assessed in accordance with ATLSs protocols. In one large series reported from a tertiary referral centre,5 56% of acetabular fractures had at least one additional injury (19% head injury, 8% abdominal injury, 18% chest injury, 6% genito-urinary, 35% extremity injury, 4% spinal injury).
Specific Dislocation of the femoral head is reported in 32–39%5,6 of acetabular fractures. Anterior dislocations in association with acetabular fractures are very rare. Damage to the femoral head is commonly seen. Preoperative sciatic nerve injury was reported in 12% of Letournel and Judet’s series of 940 patients. Sciatic nerve palsies are frequently seen in association with posterior dislocation and most commonly involve the peroneal branch. Recovery
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Figure 4 Radiological assessment: A—AP pelvis; B—iliac oblique; C—obturator oblique. AW—anterior wall; AC—anterior column; PC—posterior column; PW—posterior wall; OR—obturator ring.
of the various landmarks described will allow the fracture pattern to be interpreted. To interpret the AP and Judet views a systematic approach should be used.4 In addition to looking for ilio-ischial and ilio-pectineal line disruption, for posterior and anterior column fractures, respectively, it is recommended that an assessment be made of the iliac wing and obturator ring using the appropriate oblique views. A fracture extending into the obturator ring is representative of a T-shaped or both column fractures. If the fracture extends into the iliac wing above the acetabulum, then an anterior column fracture must be present. AP and Judet views also allow the roof arcs, as described by Matta and Merritt,9 to be determined. On each of the three views, two lines are drawn from the geometric centre of the femoral head: one line vertical and the other to the fracture. The angle between these two limbs is recorded. Medial, anterior and posterior roof arc measurements are recorded from the AP, obturator oblique and iliac oblique, respectively. These measurements allow the amount of superior intact acetabular dome to be described.
CT CT allows the fracture pattern to be assessed in more detail and provides valuable information with regard to comminution, marginal impaction (in wall fractures) and intra-articular fragments. Clues to the fracture pattern can be determined by observing the direction of the fracture lines on the CT. On the axial views, splits in the coronal plane often represent column fractures. Sagittal splits, in the roof of the acetabulum, are seen commonly with transverse or T-shaped fractures. Oblique fractures that do not extend into the quadrilateral plate are seen with wall fractures.
CT scans can help differentiate multi-fragmentary T-shaped from both column fractures. Tshaped fractures have at least one part of the acetabulum attached to the sacrum via the sciatic buttress.
Initial treatment Reduction Acetabular fractures are frequently associated with dislocation. It is important to perform and maintain a reduction as soon as possible. Persistent dislocation has the potential to influence long-term outcome. A dislocated femoral head is susceptible to cartilage necrosis secondary to point loading, and avascular necrosis (AVN) as the result of a compromised blood supply. Overlying neurovascular bundles may also be compromised; the sciatic nerve is particularly at risk with posterior dislocation. Reduction will require conscious sedation or general anaesthetic. The use of muscle relaxants is preferable to facilitate an atraumatic reduction. Following reduction a dynamic assessment of stability should be made as this may influence management if non-operative treatment is being considered.10 Reduction can be maintained with skin or skeletal traction. Traction also helps to prevent shortening and minimise difficulty in reduction, especially when reduction is delayed. Careful radiological assessment must be made to ensure a congruent reduction. If there is an incongruent reduction on the AP pelvis X-ray, or the patient is being considered for non-operative treatment then a fine cut (p3 mm) CT scan should be performed to detect intra-articular fragments.
ARTICLE IN PRESS Acetabular fractures
Venous thrombo-embolism prophylaxis Pelvic and acetabular fractures are both associated with significant risk of venous thrombo-embolism (VTE). There remains significant controversy over appropriate VTE prophylaxis. Chemical prophylaxis should not be considered until the patient has been shown to be haemodynamically stable. It is believed mechanical prophylaxis has some benefit, and can be considered immediately. Patients who experience a significant delay in operative treatment or who have not received optimal prophylaxis should be considered for further investigation and, where proximal clot is identified, an inferior vena caval (IVC) filter. Venography remains the gold standard technique as newer techniques, MRI and CT venography, have demonstrated high false positive rates and unnecessary use of IVC filters should be avoided. A recent survey11 of trauma surgeons dealing with pelvic and acetabular fractures reported that routine preoperative screening was performed by 48% of surgeons, with the majority using ultrasound. Approximately 34 used chemical prophylaxis, 34 used mechanical prophylaxis and 12 used at least one method.
Non-operative treatment Indications For non-operative treatment to be considered, the hip has to be stable, and the femoral head contained within sufficient congruent weight bearing acetabulum. Displaced fractures involving the columns or walls have the potential to cause loss of congruence between the femoral head and acetabulum. If the fracture occurs within the superior part of the acetabulum it will both reduce the surface area involved in weight bearing and cause instability. In single column fractures, significant displacement within the weight bearing dome will always result in incongruity as the intact column remains attached to the axial skeleton. Wall fractures do not usually significantly affect the weight bearing surface area but can cause instability. Both instability and reduced weight bearing surface area are poorly tolerated by the hip and predispose to early degenerative change. When considering column fractures there has been some debate over the criteria used for consideration of non-operative management. Matta and Merritt9 and Olson and Matta12 produced radiological criteria derived from their clinical experience. Measurements
145 were proposed based on roof arc angles (see X-ray section). Roof arc angles were measured on the AP and both Judet views9 and felt to be acceptable if the hip was congruent and all three roof arc measurements were X451. This corresponds to an intact superior 10 mm of acetabulum on the CT scan.12 These assessments must be performed out of traction. Tornetta10 performed dynamic stress views using fluoroscopy and found 7% of patients with roof arcs X451 to be unstable. Vrahas et al.13 performed a biomechanical study and considered medial, anterior and posterior roof arcs of p451, 251 and 701, respectively, to be indications for operative intervention. In both column fractures, the columns are detached from the axial skeleton but are constrained by the remaining soft tissue attachments. The soft tissue has the potential to hold the fracture fragments and maintain congruity despite displacement within the weight bearing dome. This situation is described as secondary congruence and has the potential to be treated nonoperatively. Fractures of the acetabular walls should be considered separately. Olson and Matta12 felt that involvement of 450% of the posterior wall was unsuitable for non-operative treatment. A biomechanical study14 determined that p20% involvement of the posterior wall is likely to be stable, X40% is likely to be unstable. It would therefore be acceptable to make a radiological assessment (plain X-rays and CT) of stability using the described roof angles as a guide. In those patients that are considered appropriate candidates for non-operative treatment an EUA should be considered to allow confirmation. In summary, non-operative management should be considered in the following circumstances:
Co-morbities limiting physiological reserve. Insufficient bone stock to allow adequate fixation. A hip joint that is congruent within a sufficient superior acetabular dome to allow it to be stable under physiological loads. o Undisplaced column fractures. o Displaced column fractures that involve the inferior part of the acetabulum. o Wall fractures with sufficient intact wall to maintain hip stability. Congruent both column fractures.
Treatment If non-operative management is chosen then the patient must be kept non-weight bearing for 4–8
ARTICLE IN PRESS 146 weeks. Traction through a tibial pin may be appropriate to prevent further displacement. When implemented appropriately, good results are achievable.
Open reduction and internal fixation ORIF is the treatment of choice in those fractures that fail to fulfil criteria for non-operative treatment in patients who have sufficient physiological reserve. The timing for operative intervention has been shown to be important with several studies reporting poorer results when ORIF is attempted at greater than 3 weeks post-injury. With progressive delays reduction becomes harder to achieve. When possible, ORIF should take place at 2–5 days to avoid the increased bleeding seen in the first 48 h. Reduction has been shown to correlate directly with outcome5 and the clinical results of delayed reconstruction (421 days) is poor in comparison with earlier intervention.15 Delay is also associated with an increase in VTE and skin problems. Urgent ORIF may be necessary in the following circumstances:
Reduction of an associated dislocation of the femoral head cannot be maintained. Retained intra-articular fragments. Closed reduction has not been possible. Closed reduction has resulted in a new onset neurological deficit. Open fracture.
Preoperative preparation As for all trauma surgery every attempt should be made to optimise the patient medically. The patient should be cross matched for 6 units of blood as blood loss of 1–2 l, but potentially up to 6 l, is not unusual.5 For this reason a cell saver is also beneficial. Surgical preparation is also necessary as the surgery is complex and intensive for equipment and manpower. A preoperative plan using all available imaging will allow most problems to be anticipated and allow the correct equipment to be available. The appropriate pelvic instrumentation with specialised reduction aids are required in addition to a radiolucent table and image intensifier. Some fractures will benefit from intraoperative traction either using the table attachments or a femoral distractor. Intraoperative nerve monitoring has
J. McMaster, J. Powell been described but is not routinely used in most centres.11 Assistance is mandatory and experienced assistance is invaluable. The patient should then be positioned on a radiolucent operating table, and the image intensifier is then used to check that satisfactory AP, Judet’s, inlet and outlet pelvic views can be achieved. These views can be obscured by bowel gas or contrast within the GI tract. Prior to surgery the patient will require prophylactic antibiotics. The anaesthetist must be made aware that muscle relaxants may be required and that the use of nitrous oxide should be avoided to minimise bowel gas.
Approaches The primary aim is to achieve reduction and usually the approach that allows reduction will also be sufficient to place adequate fixation. The surgical approach is usually based on the pattern of displacement. The surgical approach used should allow adequate visualisation for direct reduction and fixation techniques. A useful feature of any approach is the indirect access that can be achieved through palpation. This allows an assessment of reduction and facilitates indirect techniques. There are three main approaches which are used in the majority of acetabular fractures (Kocher-Langenbeck, ilio-inguinal and extended ilio-femoral, EIF) and numerous reported modifications. In Matta’s5 large series, 98% of the cases were treated using one of these operative approaches. The remaining 2% had a double Kocher-Langenbeck and ilio-inguinal approach. The benefits of each approach have to be carefully balanced with the relative risks. The bigger the approach, the bigger the complications but the smaller the approach the greater the potential difficulty and the greater risk of malreduction. Kocher-Langenbeck This standard approach involves and incision centred on the greater trochanter with a distal limb along the axis of the femur and a proximal limb directed towards the posterior superior iliac spine (PSIS) (Fig. 5). Fascia lata and gluteus medius are split and reflection of piriformis, obturator internus and the gemelli allows access to the posterior wall and column. All of the standard approaches that allow access to the outer table of the pelvis have the potential to allow visualisation, to a varying degree, of the acetabular surface using a capsulotomy and
ARTICLE IN PRESS Acetabular fractures
147 Approach
Access
Kocher Langenbeck
Suitable Fracture Configurations: Posterior wall; Posterior column; Transverse; Posterior wall plus posterior column; (Posterior wall with transverse and T-shaped – if simple otherwise consider extended iliofemoral).
Extension 1: Surgical hip dislocation
Suitable Fracture Configurations: As above + suitable for high multifragmentary transverse fractures and associated fractures of the femoral head.
Extension 2: Triradiate
Suitable Fracture Configurations: Allows greater access to iliac crest for the treatment of both column fractures with significant posterior displacement.
Figure 5 Kocher-Langenbeck incision, extensions and indications.
ARTICLE IN PRESS 148 dislocation or distraction of the femoral head. A surgical hip dislocation can be performed as part of the Kocher-Langenbeck and allows direct access to the entire articular surface of the femur and acetabulum. This is particularly useful when addressing large femoral head fractures. This approach preserves the deep branch of the MCFA and involves a trochanteric flip osteotomy that includes the insertion of gluteus medius and the origin of vastus lateralis. The trochanter is retracted anteriorly, a capsulotomy is performed and the hip is dislocated. The blood supply to the femoral head via the deep branch of the medial femoral circumflex is at risk. Care must be taken when releasing the short external rotators. A cuff of 1.5 cm should be left at the trochanteric insertion. An alternative osteotomy involves a standard trochanteric osteotomy with reflection of the abductors superiorly off the pelvis, maintaining the superior gluteal vascular pedicle. This procedure is usually accompanied by an additional skin incision directed anteriorly from the greater trochanter towards the anterior superior iliac spine (ASIS). This is described as the triradiate approach. Ilio-inguinal The inner table of the anterior column is accessed through an approach which detaches the abdominal wall from the iliac crest and opens the inguinal canal. Iliacus is then stripped from the inner table of the acetabulum. It requires the mobilisation of the contents of the inguinal canal and the femoral neurovascular bundle (Fig. 6). Many modifications have been described for this approach. Most of these approaches aim to allow additional access to the outer table of the anterior column. One approach involves a longitudinal extension of the ilio-inguinal incision based on the ASIS. Extended ilio-femoral This approach is derived from the ilio-femoral approach described by Smith Peterson and extends posteriorly along the iliac crest (Fig. 7). The abductors are reflected off the outer table of the pelvis on the superior gluteal neurovascular pedicle. Surgical tactic In general, extensile approaches (EIF and triradiate) are avoided and a single column approach (Kocher-Langenbeck or ilio-inguinal) is used when possible. If a single column approach is used it is usually directed at the column with the greatest displacement. If both columns are involved reduction of the least displaced fracture can often be
J. McMaster, J. Powell performed indirectly. If this is not possible it may be possible to extend the standard approach using one of the numerous modifications. Double incision approaches (Kocher-Langenbeck and ilio-inguinal), either simultaneous or staged, have been described to allow direct access to both columns. The decision on the approach used will depend on experience and training. Helfet and Schmeling16 reported on 84 complex acetabular fractures treated using a non-extensile approach (KocherLangenbeck or ilio-inguinal) and achieved an overall acceptable reduction (o2 mm step-off and o3 mm intra-articular gap) rate of 90.5%. It will also depend on patient factors such as age, level of function and soft tissues.
Reduction techniques Indirect Traction can be applied through the leg or directly to the pelvis and femur. This will allow reduction in those situations where soft tissue connection has been maintained. In certain fractures, there is a significant rotational component to the fracture displacement. In these situations, Schantz pins can be placed directly or under image intensifier control and can be used as joysticks to manipulate the fracture fragments. Direct Many direct techniques are used to achieve reduction of these complex fractures. Specific fracture reduction forceps are invaluable. The reduction clamps are varied in their size, angle and offset to accommodate the wide variety of fracture patterns. Temporary screws can be used in conjunction with three hole plates or forceps to help temporarily manipulate and stabilise the fracture.
Internal fixation techniques Posterior wall These fractures are often associated with impaction (Fig. 8). Open reduction is necessary with elevation of the depressed articular fragments with the underlying subchondral bone. The resultant defect is packed with bone graft or bone substitute. The fracture is reconstructed and stabilised where possible with lag screws augmented by a buttress plate. In those situations where comminution prevents lag screw fixation, spring plates fashioned from 13 tubular plates can be used in the buttress mode. These fixation constructs have been shown to be biomechanically superior to fixation with screws used in isolation.
ARTICLE IN PRESS Acetabular fractures
149
Approach
Access
Ilioinguinal
Suitable Fracture Configurations: Anterior wall; Anterior column; Transverse (occasional); Anterior column/wall with posterior hemitransverse; Both column (unless multi-fragmentary posterior column); T-shaped (rare).
Extension 1: + Iliofemoral
Suitable Fracture Configurations: As above + allows greater access to anterior hip joint and outer table of iliac crest.
Figure 6 Ilioinguinal incision, extensions and indications.
Column fractures The same principles are used as for intra-articular fractures elsewhere in the body. The aim is to achieve a stable anatomical reduction, with compression, that allows early mobilisation. This is best achieved with lag screw fixation and a plate in the neutralisation or buttress mode (Fig. 8). Lag screws
can be placed between columns either through the plate or separately positioned. Biomechanical tests have shown that when plating a column fracture the construct is stiffest with two screws on each side with screws placed as close to the fracture line as possible and at the ends of the plates. As an adjunct to reduction and fixation, cerclage wires
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J. McMaster, J. Powell Approach
Access
Extended Iliofemoral
Suitable Fracture Configurations: This approach is used occasionally for transverse fractures and all of the associated fracture configurations that cannot be dealt with using a one column approach.
Figure 7 Extended iliofemoral (EIF) incision, extensions and indications.
Figure 8 Pre- and post-fixation of a posterior wall fracture associated with impaction: A—axial CT demonstrating fracture and marginal impaction; B—post-operative axial CT with reconstructed wall; C—post-operative X-ray with lag screw and buttress plate.
can be placed around the ilium, through the greater sciatic notch at the level of the anterior inferior iliac spine. Using safe corridors within the pelvis, column screws can be placed. They can be placed both antegrade and retrograde and are used in both open and percutaneous techniques (Fig. 9). Transverse fractures If possible these fractures are fixed through a single column approach that allows sufficient access to
lag and plate one column. As long as reduction is achieved the other column can be stabilised, indirectly, with a column screw (Fig. 10). This has been found to be a stable construct on biomechanical testing.
Displaced fractures of the quadrilateral plate These fractures are difficult to treat as visualisation and access for instrumentation is limited. One useful technique is to use a spring/buttress plate
ARTICLE IN PRESS Acetabular fractures
151
Figure 9 Both column fractures treated through ilio-inguinal approach. A—preoperative AP; B—preoperative iliac oblique; C—preoperative obturator oblique; D—preoperative axial CT. Anterior column plate with lag screws placed from the anterior to posterior column. Additional plate spanning anterior column fracture through iliac crest. A screw was used for the re-attachment of the anterior superior iliac spine. E—post-operative AP; F—post-operative iliac oblique; G—post-operative obturator oblique.
Figure 10 Transverse fracture treated through Kocher-Langenbeck approach with posterior plate and anterior column screw. Despite the heterotopic ossification this gentleman had excellent function and ROM. Note the vascular clips, at the sciatic notch, used to control bleeding from the superior gluteal vessels.
that prevents the fracture displacing and does not rely on direct fixation.
considered. Total hip replacement in the acute setting can be associated with significant complications. However, in older patients, it can provide a satisfactory alternative to definitive ORIF.3
Total hip replacement ORIF is not recommended in older patients, especially if there is evidence of impaction or osteoporosis. In these circumstances, a limited reconstruction and total hip replacement can be
Rehabilitation A knee immobiliser during the immediate postoperative period is useful to protect fixation of the
ARTICLE IN PRESS 152 posterior column and wall by preventing hip flexion during recovery. The neurological and vascular status of the limb should be checked and recorded frequently in the initial post-operative period. The patient should receive a short course of prophylactic intravenous antibiotics. Immediate weight bearing of 20–30 lb before commencing full weight bearing at 8–12 weeks5,7 is thought to be acceptable, except in those cases where fixation is tenuous and initial protection with traction is beneficial. Limitation of hip flexion to 601 is important to protect posterior wall and posterior column fixation. It is important to review the patient clinically and radiologically at 2 weeks to assess for loss of fixation. If displacement occurs this is best dealt with within the first 3 weeks.17
Complications Heterotopic ossification It is well established that there is a high incidence of heterotopic ossification (HO) following acetabular surgery. Although patient factors are relevant, this complication is particularly related to the approach. Stripping and trauma to the gluteal muscles predisposes to HO formation. Consequently, EIF and triradiate approaches have a high reported incidence, 35–57% and 86%, respectively,1,6,7 whereas there is a low incidence in patients treated with the ilio-inguinal approach 4.8%1,5 and a moderate risk, 19–26%,1,7,18 with the Kocher-Langenbeck. There is ongoing controversy in the literature with regard to the efficacy of prophylaxis against HO. Indomethacin and radiation have both been used for prophylaxis and both have been reported as providing benefit. In comparative prospective randomised trials, radiation has been shown to be equivalent to indomethacin as a method of HO prophylaxis.19 The most recent study looking at the effect of indomethacin on HO formation, a prospective randomised trial involving 107 patients,20 did demonstrate that indomethacin had a lower HO rate when assessed by Brooker grade and CT volumetric analysis. However, this was not statistically significant and the authors concluded that indomethacin provided no advantage. A potential limitation of this study is the lack of data on patient compliance. An additional consideration is the established detrimental effect of indomethacin on long bone healing in poly-trauma.21
J. McMaster, J. Powell Single dose or fractionated radiation administered within 72 h post-operation has been used and in some studies that have reported low HO rates. A trial using a combination of indomethacin and radiation in patients treated with a posterior or EIF approach reported an overall incidence of 19% of which all were Brooker I.22 Radiation prophylaxis is expensive and there are theoretical concerns about malignancy and the effect on reproductive cells. In addition, there are logistical difficulties performing the treatment in the required time frame as many patients will be requiring high levels of nursing and medical support. Not all patients with radiologically determined HO have functional limitation.18 Matta5 reported a 9% functionally significant (X20% loss in range of motion (ROM)) HO rate in a group that received no prophylaxis (2% of ilio-inguinal, 20% of EIF, 8% of Kocher-Langenbeck). The requirement for excision of HO is reported in only 2–5%.7,18 At present there are no good guidelines for HO prophylaxis. The argument for using prophylaxis is stronger in the presence of certain risk factors: an extensile approach,6,15 significant muscle trauma,15 head injury,15 male gender20 and delayed treatment (421 days).15 Within our unit the presence of two risk factors is used as an indication to treat with HO prophylaxis.
Venous thrombo-embolism The incidence of distal deep venous thrombosis (DVT) is poorly documented in the large studies but an incidence of 3–6%1,16 is reported. The incidence of pulmonary embolus (PE) is reported as 2–4%1,16 and is believed to be the biggest cause of death following acetabular fractures. Peri-operative death from all causes is reported with a frequency of 0–2.5%.1,5,7
Infection In centres involved with treating large numbers of acetabular fractures, the overall infection rate is reported at 3–5%.1,5,7,23 Deep infection has been reported with an incidence of 3%.5 Several authors have reported significantly higher infection rates early in their series, related to inexperience and longer operation times. Infection rates also vary depending on the approach. Extensile approaches have been associated with infection rates of 8.5%6 whereas the ilio-inguinal approach has been reported as having a 3% infection rate.24 Obesity is a major risk factor.
ARTICLE IN PRESS Acetabular fractures
Nerve injury The most significant iatrogenic nerve injury following treatment of acetabular fractures involves the sciatic nerve, 3–11%.1,5,7,16 Care must be taken with retractor placement and maintaining a flexed knee and extended hip when performing posterior approaches. Sciatic nerve injuries also occur with ilio-inguinal approaches and this has been attributed to reduction techniques involving flexion of the hip and placing the nerve under tension. To reduce tension in the nerve the knee is kept flexed and the hip extended. Femoral nerve injury has been reported rarely (1%) following the ilio-inguinal approach.5 A 1% obturator nerve injury has been reported.7 Hip abductor weakness has been noted to be a significant problem in posterior approaches, and this has been partly attributed to damage to the gluteal nerves during retraction. The femoral cutaneous nerve of thigh is frequently damaged during ilio-inguinal and EIF approaches but is associated with little significant morbidity.
153 be taken to avoid this complication by ensuring good intraoperative imaging. The spherical shape of the acetabulum means that each screw only needs to be identified as being out of the joint on one view to confirm its extra-articular position. A useful technique in this situation is to use the image intensifier to look down the long axis of the screw. Post-operative CT can confirm screw position
Failure of fixation In the large reported series, failure of fixation is reported with a frequency of 1–3%.1,5,16 The results of revision surgery are less satisfactory than with primary fixation5 and if revision is required there is benefit in this being performed early.15
Non-union Very low rates of non-union have been reported3 but when it occurs it is seen most frequently in transverse fractures with unstable fixation.25 The use of indomethacin prophylaxis is also believed to contribute to non-union.
Vascular injury Osteoarthritis Femoral vessel injury is reported in 0.8–2% of ilioinguinal exposures.1,7 In addition, during this approach the surgeon should be aware of a very high incidence of retro-pubic anastomoses between the femoral and obturator vessels. These vessels need to be ligated prior to division as they have significant capacity to bleed and control may be difficult. The superior gluteal artery can be damaged with the consequence of significant bleeding and the potential for gluteal muscle necrosis. This complication has not been demonstrated clinically. AVN is most commonly seen in fractures associated with dislocation. The incidence varies between studies, 3–10%.5,16,18 Although damage of the blood supply to the femoral head occurs at the time of the injury it can also be damaged intraoperatively. Ganz’s research group have highlighted the significance of the deep branch of the MFCA and proposed that iatrogenic injury of this vessel may explain the perceived discrepancy between reported AVN rates in uncomplicated dislocations treated with closed reduction and fracture dislocations that require ORIF.2
Intra-articular screw penetration This problem is reported infrequently but can result in post-traumatic arthrosis and every effort should
This is reported by most outcome studies and is attributed to cartilage necrosis, articular incongruity and instability. Cartilage necrosis can be related to irreversible damage to the articular surface at the time of injury. Femoral head damage identified intraoperatively has been shown to be predictive of a worse prognosis. This may explain why one study5 reported a poor outcome in 32% of their anatomically reduced posterior wall fractures. However, evidence of femoral head damage does not guarantee a poor result. Articular incongruity (secondary to intra-articular metal work and mal-reduction) and instability both predispose to osteoarthritis as a result of abnormal loading of the articular surface.
Functional outcome Studies published from large centres with experience in acetabular trauma report good to excellent results in approximately 80% of cases.1,5,7 Most of the historical data on acetabular fractures was compiled using the d’Aubigne-Postel scale.1 This scoring system is limited in its application as the highest score does not correlate with a return to normal activities. A ‘good’ score can be achieved
ARTICLE IN PRESS 154 with a patient complaining of a slight or intermittent pain with normal activity; hip flexion limited to 701 and a slight limp. Despite the potential limitations of the scoring systems used, several factors have been identified which correlate with outcome. It has been established that the surgeon has a large influence on outcome. The most frequently associated factor with outcome is the quality of the reduction.1,5,7,16 Anatomical reduction has been seen to be highly significant for excellent or good results and any mal-reduction was associated with a worse outcome.5 As a result the experience of the surgeon plays an important part in the ability to achieve an anatomic reduction. Several large studies report a significant learning curve. This is demonstrated by several surgeons reporting poorer results at the start of their series.1,16 The timing of surgery is also important with delay 43 weeks associated with poorer functional outcome and a high incidence of AVN, OA, HO and sciatic nerve injury.15 Approximately 10% of hips will be expected to fail within 2 years.3 THR performed in this group is seen to perform less well than in a matched cohort of THR for OA. In addition, acetabular fractures initially treated non-operatively, performed better than those treated initially with ORIF. The timing and role of THR in acetabular fractures is still being established.
References 1. Letournel E, Judet R, editors. Fractures of the acetabulum. 2nd ed. Berlin: Springer; 1993. 2. Gautier E, Ganz K, Krugel N, Gill T, Ganz R. Anatomy of the medial femoral circumflex artery and its surgical implications. J Bone Jt Surg—Br Vol 2000;82(5):679–83. 3. Tile M, Helfet D, Kellam J, editors. Fractures of the pelvis and acetabulum. 3rd ed. Lippincott Williams and Wilkins; 2004. p. 830. 4. Brandser EA, El-Khoury GY, Marsh JL. Acetabular fractures: a systematic approach to classification. Emerg Radiol 1995;2(1):18–28. 5. Matta JM. Fractures of the acetabulum: accuracy of reduction and clinical results in patients managed operatively within three weeks after the injury. J Bone Jt Surg—Am Vol 1996;78(11):1632–45. 6. Alonso JE, Davila R, Bradley E. Extended iliofemoral versus triradiate approaches in management of associated acetabular fractures. Clin Orthop Relat Res 1994;305:81–7. 7. Mayo KA. Open reduction and internal fixation of fractures of the acetabulum. Results in 163 fractures. Clin Orthop Relat Res 1994;305:31–7.
J. McMaster, J. Powell 8. Hak DJ, Olson SA, Matta JM. Diagnosis and management of closed internal degloving injuries associated with pelvic and acetabular fractures: the Morel-Lavallee lesion. J Trauma—Injury Infect Crit Care 1997;42(6):1046–51. 9. Matta JM, Merritt PO. Displaced acetabular fractures. Clin Orthop Relat Res 1988;230:83–97. 10. Tornetta 3rd. P. Non-operative management of acetabular fractures. The use of dynamic stress views. J Bone Jt Surg—Br Vol 1999;81(1):67–70. 11. Morgan SJ, Jeray KJ, Phieffer LS, Grigsby JH, Bosse MJ, Kellam JF. Attitudes of orthopaedic trauma surgeons regarding current controversies in the management of pelvic and acetabular fractures. J Orthop Trauma 2001;15(7):526–32. 12. Olson SA, Matta JM. The computerized tomography subchondral arc: a new method of assessing acetabular articular continuity after fracture (a preliminary report). J Orthop Trauma 1993;7(5):402–13. 13. Vrahas MS, Widding KK, Thomas KA. The effects of simulated transverse, anterior column, and posterior column fractures of the acetabulum on the stability of the hip joint. J Bone Jt Surg—Am Vol 1999;81(7):966–74. 14. Keith J, Brashear H, Guilford B. Stability of posterior fracture—dislocations of the hip. J Bone Jt Surg—Am Vol 1988;70(A):711–4. 15. Johnson EE, Matta JM, Mast JW, Letournel E. Delayed reconstruction of acetabular fractures 21–120 days following injury. Clin Orthop Relat Res 1994;305:20–30. 16. Helfet DL, Schmeling GJ. Management of complex acetabular fractures through single nonextensile exposures. Clin Orthop Relat Res 1994;305:58–68. 17. Mayo KA, Letournel E, Matta JM, Mast JW, Johnson EE, Martimbeau CL. Surgical revision of malreduced acetabular fractures. Clin Orthop Relat Res 1994;305:47–52. 18. Oransky M, Sanguinetti C. Surgical treatment of displaced acetabular fractures: results of 50 consecutive cases. J Orthop Trauma 1993;7(1):28–32. 19. Burd TA, Lowry KJ, Anglen JO. Indomethacin compared with localized irradiation for the prevention of heterotopic ossification following surgical treatment of acetabular fractures. J Bone Jt Surg—Am Vol 2001;83A(12): 1783–8 [erratum appears in J Bone Jt Surg—Am Vol 2002;84A(1):100]. 20. Matta JM, Siebenrock KA. Does indomethacin reduce heterotopic bone formation after operations for acetabular fractures? A prospective randomised study. J Bone Jt Surg—Br Vol 1997;79(6):959–63. 21. Burd TA, Hughes MS, Anglen JO. Heterotopic ossification prophylaxis with indomethacin increases the risk of longbone nonunion. J Bone Jt Surg—Br Vol 2003;85(5):700–5. 22. Moed BR, Letournel E. Low-dose irradiation and indomethacin prevent heterotopic ossification after acetabular fracture surgery. J Bone Jt Surg—Br Vol 1994;76(6):895–900. 23. Routt Jr ML, Swiontkowski MF. Operative treatment of complex acetabular fractures. Combined anterior and posterior exposures during the same procedure. J Bone Jt Surg—Am Vol 1990;72(6):897–904. 24. Matta JM. Operative treatment of acetabular fractures through the ilio-inguinal approach. A 10-year perspective. Clin Orthop Relat Res 1994;305:10–9. 25. Mohanty K, Taha W, Powell JN. Non-union of acetabular fractures. Injury 2004;35(8):787–90.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 155–165
www.elsevier.com/locate/cuor
PAIN
Complex regional pain syndrome Andrew McBride, Roger Atkins University Department of Trauma & Orthopaedic Surgery, Bristol Royal Infirmary, Marlborough Street, Bristol, BS2 8HW, UK
KEYWORDS Complex regional pain syndrome; Reflex sympathetic dystrophy; Causalgia
Summary Complex regional pain syndrome (CRPS) is a disabling chronic pain condition of unknown aetiology. Traditionally it has been thought to be a rare complication following trauma; however prospective studies demonstrate it to be a common disabling complication of both trauma and operative procedures involving the upper and lower limbs. The condition is usually self-limiting, causing significant disability for up to a year. Unfortunately in a minority of patients CRPS does not resolve, causing life-long misery. Modern research is aimed at understanding the interactions of processes occurring locally at the site of injury with changes observed in the peripheral and central nervous systems, as well as future preventative measures and treatments. A bewildering array of proposed treatment modalities, both tested and experimental, have been proposed. Despite differences between researchers and the specialities involved in the management of CRPS, early recognition with sympathetic yet aggressive treatment is agreed to be vital to expedite optimal outcome. & 2005 Elsevier Ltd. All rights reserved.
Introduction Complex regional pain syndrome (CRPS) is a disabling chronic pain condition of unknown aetiology. It is most commonly encountered following trauma to a limb and is diagnosed clinically by the presence of abnormal pain, sensory changes, swelling, vasomotor instability (VMI), joint stiffness, motor dysfunction, trophic changes and increased sudomotor activity. Research work over the last 20 years has demonstrated that CRPS is not a rare sympathetically mediated condition seen Corresponding author. Tel.: +44 117 928 2878;
fax: +44 117 928 4206. E-mail addresses:
[email protected] (A. McBride),
[email protected] (R. Atkins).
only in psychologically abnormal patients, rather it is a common and probably inevitable sequel of trauma, including surgery. Understanding of the condition has been progressed by the establishment of internationally agreed diagnostic criteria combined with progress in clinical and basic science research. This article will summarise current understanding within an orthopaedic context.
Terminology The origins of CRPS can be traced to the American Civil War; soldiers who had sustained nerve injuries were reported on by Mitchell and colleagues who observed a post-injury burning pain they termed
0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2005.02.011
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The diagnosis of CRPS is a clinical one and there is no single diagnostic test. Despite the IASP diagnostic criteria agreed on nearly a decade ago (Table 2) a lack of consensus remains. Validation studies have lead to refinement of these criteria in
Table 1
Previous terms for CRPS.
CRPS type 1 (no discernable nerve injury)
CRPS type 2 (discernable nerve injury)
Reflex sympathetic dystrophy (RSD) Su ¨deck’s atrophy Algodystrophy
Causalgia Major causalgia Mitchell’s causalgia
Shoulder hand syndrome Painful post traumatic osteoporosis Minor causalgia Algoneurodystrophy Post traumatic pain syndrome Painful post traumatic dystrophy Transient migratory osteoporosis
Table 2
Clinical features Signs and symptoms CRPS is a biphasic condition that begins up to a month after the precipitating event. In the acute stage of the condition, the symptoms and signs of regional inflammation affecting an area larger than the site of injury are characteristic (Fig. 1). Later this inflammatory picture is replaced by atrophy and contracture (Fig. 2). Throughout the course of CRPS, the pain experienced is neuropathic. Spontaneous or burning pain, hyperalgesia, allodynia and hyperpathia (Table 5) are common but not universal.4 Pain is unremitting, worsening and radiating with time, although sleep is often unaffected. It is disproportionate to the to the precipitating insult. The distribution of pain tends to be distal to the site of injury. It is often diffuse and not limited to the territory of a single peripheral nerve. The salient features of an inflammatory process in the early stage of the condition are due to VMI. These include skin colour changes (pink or red), swelling, altered skin temperature and changes in sudomotor function (Fig. 3). These symptoms maybe variable and can be related to exercise, painful stimuli and changes in environment. Some clinicians and researchers subdivide the acute stage into two distinct groups depending on the temperature difference findings; therefore the terms hot’’ and cold’’ CRPS are coined. Motor symptoms are present in the majority of cases and can include tremor, weakness, exaggerated tendon reflexes, dystonia and myoclonic jerks.5,6 Limited active range of movement is due to pain and oedema initially, with contractures contributing later on in the condition (Fig. 4). ’’
Diagnosis
an attempt to reduce the effect of over-diagnosis (Table 3).2 A different approach may be more relevant for the orthopaedic surgeon (Table 4).3
’’
causalgia. Since then the condition has been described under a number of different guises each one having been popularised depending on the precipitating factor, the country concerned or by the speciality treating the patient (Table 1). To avoid a term suggesting aetiology or site the International Association for the Study of Pain (IASP), in 1994, agreed on the new nomenclature of CRPS.1 Two types of CRPS are currently recognised: type 1, where there is no discernable nerve damage present (formerly termed Reflex Sympathetic Dystrophy) and type 2, where there is a discernable nerve injury (formerly termed causalgia).
IASP diagnostic criteria for CRPS.
(1) The presence of an initiating noxious event, or a cause of immobilisation. (2) Continuing pain, allodynia, or hyperalgesia with which the pain is disproportionate to any inciting event. (3) Evidence at some time of oedema, changes in skin blood flow, or abnormal sudomotor activity in the region of
the pain. (4) This diagnosis is excluded by the existence of conditions that would otherwise account for the degree of pain
and dysfunction.
ARTICLE IN PRESS Complex regional pain syndrome Table 3
157
Modified IASP diagnostic criteria for CRPS.
(1) Continuing pain that is disproportionate to any inciting event. (2) Must report at least one symptom in each of the following categories:
(3)
Sensory: Reports of hyperaesthesia. Vasomotor: Reports of temperature asymmetry and/or skin colour changes and/or skin colour asymmetry. Sudomotor/Oedema: Reports of oedema and/or sweating changes and/or sweating asymmetry. Motor/trophic: Reports of decreased range of movement and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nails, skin). Must display at least one sign in two or more of the following categories: Sensory: Evidence of hyperalgesia and/or allodynia. Vasomotor: Evidence of temperature asymmetry and or skin colour changes and/or asymmetry. Sudomotor/Oedema: Evidence of oedema and/or sweating changes and/or sweating asymmetry. Motor/Trophic: Evidence of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nails, skin).
Table 4
Suggested criteria for the diagnosis of CRPS within an orthopaedic setting.
The diagnosis is made clinically by the finding of the following abnormalities, which should not be readily explained by the underlying orthopaedic condition. (1) Neuropathic pain: Non-dermatomal, without cause, burning, with associated allodynia and hyperpathia. (2) Vasomotor instability and abnormalities of sweating: Warm red and dry, cool blue and clammy or an increase in temperature sensitivity. Associated with an abnormal temperature difference between the limbs. (3) Swelling. (4) Loss of joint mobility: (5) Joint and soft tissue contracture. These clinical findings are backed up by: (1) Radiographic evidence of osteoporosis after three months. (2) Increased uptake on bone scintigraphy early in CRPS.
Figure 1 Early CRPS affecting the right hand, following distal radial fracture. Note the discolouration and finger swelling.
The atrophic stage of the condition commences as the VMI and oedema resolves but marked motor and trophic changes occur. The skin is thin with
joint creases and subcutaneous fat disappearing. brown-grey scaly pigmentation develops in a high proportion of patients. Hairs become fragile,
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uneven and curled while nails are pitted, ridged, brittle and discoloured brown. Palmar and plantar fascias can thicken and contract manifesting as Dupuytren’s disease (Fig. 5).7 Tendon sheaths constrict with triggering and increased resistance to movement. Muscle contracture combined with tendon adherence leads to reduced tendon excursion. Joint capsules and collateral ligaments become shortened, thickened and adherent, causing
joint contracture. Bone loss and patchy osteoporosis occurs,8 but despite these changes osteoporotic fracture is uncommon.
Figure 2 (a, b) Late CRPS affecting the left hand. Note the muscle atrophy and finger contractures.
Figure 3 Increased sudomotor function in a foot affected by CRPS.
Table 5
Regions affected The upper limb is more commonly affected than the lower. Distal involvement tends to predominate probably due to the relatively higher occurrence of injuries at the wrist in the general population. When the entire arm is affected the elbow tends to be spared. Patients with distal upper limb CRPS have a significant incidence of associated shoulder complaints (the so-called shoulder-hand syndrome). In most this is due to a biceps tendonitis.9 It is probable that a significant proportion of frozen shoulders can be considered a form of CRPS.10 The clinical similarities between the two are supported by changes observed on bone scans and plain radiographs.11 CRPS can occur following surgical procedures in the upper limb such as carpal tunnel
IASP Pain definitions.
Pain: An unpleasant sensory and emotional experience that we primarily associate with tissue damage or
describe in terms of tissue damage or both. Allodynia: Pain due to a stimulus that does not normally provoke pain. Hyperaesthesia: Increased sensitivity to stimulation, excluding special senses. Hyperalgesia: An increased response to a stimulus that is normally painful. Hyperpathia: Pain characterised by an increased reaction to a stimulus, especially a repetitive one, as well as an increased threshold.
ARTICLE IN PRESS Complex regional pain syndrome
159 tures.15 Following total knee replacement an incidence of 41% at 3 months and 19% at 6 months following surgery has been reported.16 CRPS may occur at any age but it is more common in middle-aged adults. It affects both sexes and all races, but is more common in females.
Causation
Figure 4 Joint stiffness affecting the right hand in early CRPS.
Trauma is the commonest precipitating event, accounting for 30–77% of cases, the majority following minor insults to an extremity. A major difficulty in the understanding of this condition has been why one fracture or traumatic insult should give rise to CRPS while an identical fracture or insult in another patient or even in a different limb in the same patient does not. In up to 25% of cases no precipitant insult can be identified. Whilst trauma is the commonest precipitant, CRPS is also reported following a wide range of disease processes including: cerebral vascular events, myocardial ischaemia and herpes zoster infection.
Natural history
Figure 5 Early Dupuytren’s disease affecting the righthand associated with the onset of CRPS following distal radial fracture.
decompression (whether performed endoscopically or as an open procedure), and Dupuytren’s release. CRPS affecting the lower limb is recognised following both trauma and surgery. These include tibial fractures, amputations and crush injuries to the foot. As well as the periphery of the lower limb, the CRPS and its association with insults to the knee have also been extensively reported on.12 In pregnancy the hip can be affected. In other specialities CRPS affecting the face and thoracic wall have been described.
The exact onset of CRPS following a precipitating insult is difficult to ascertain. The acute stages of the condition mimic those of acute inflammation, an expected finding in the immediate time period following either trauma or surgery. It is probable that the majority of cases begin within a month after the initial insult; some researchers report the onset of some cases are delayed by up to several months. These, however, are a minority and certainly question the relevance of the reported initial insult. The clinical course and severity following onset is varied, reflected by the reported lower incidence following trauma in studies involving established cases. Although most cases resolve within a year,17 some features, particularly stiffness, remain suggesting CRPS may be responsible for significant long-term morbidity even when mild.18
Pathogenesis Incidence The full-blown, severe form of CRPS is fortunately rare, reflected by the low prevalence in retrospective studies.13 However prospective studies show that a mild form of the condition occurs commonly following trauma or surgical insult. An incidence of up to 37% is seen following distal radial fractures14 and 30% following tibial shaft frac-
The development of CRPS probably involves at least two linked pathophysiological processes, one occurring at the site of the injury, involving local soft tissues and the peripheral nervous system, and the second occurring in the central nervous system leading to altered reflexes and neuronal pathways. A number of theories have been investigated and discussed (Fig. 6):
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• Psychological
• Central sensitisation • Sympathetic nervous
factors
system
-Sympathetic mediated pain
• Genetic
predisposition
• Immobilisation
• Exaggerated
inflammatory response • Free radical damage OH O2-
• Neurogenic • Peripheral
inflammation sensitisation
Figure 6 Proposed mechanisms involved in the development of CRPS.
Genetic predisposition Evidence for an inherited component to the development of neuropathic pain has been described in both animal and human studies.19–21 CRPS has been linked to certain variations (polymorphisms) of genes encoding angiotensin-converting enzyme (ACE) and human leucocyte antigen (HLA) class I and II molecules. These genes have a high amount of variation and, as they are inherited
in a Mendelian fashion, can be useful as genetic markers of disease.
Exaggerated inflammatory response In the acute stages of CRPS the condition demonstrates all the classical symptoms and signs of inflammation: rubor, calor, dolor, tumour and functio laesa.6 Sudeck first postulated that an
ARTICLE IN PRESS Complex regional pain syndrome exaggerated inflammatory response could contribute to the aetiology of the condition he described in 1900. Over the last decade this theory has been revisited and investigated. CRPS type 1 is associated with macromolecule extravasation, reduced oxygen extraction and consumption and tissue acidosis.22–24 Plasma markers of cellular inflammation as well as histological studies are normal; however an increase in inflammatory mediators and mast cell activity have been demonstrated in the skin of affected limbs of CRPS patients.25 It has been known for some time that tissue damage following acute inflammatory processes is caused in part by free radical deposition.26,27 Evidence for the involvement of free radicals in the development of the CRPS has been reported by a number of researchers. An animal model has demonstrated a CRPS-like limb following free radical donor infusion directly into the limb.28 Amputated human specimens affected by CRPS show basement membrane thickening consistent with overexposure to free radicals.29 Treatment of CRPS patients with topical free radical scavengers appears to provide some relief.30
Neurogenic inflammation Stimulation by increased cytokine activity maintains nociceptor reaction to an injury by a process called neurogenic inflammation. During this process neuropeptides including substance P, calcitonin generelated peptide (CGRP) and somatostatin are released. Peripherally these neuropeptides contribute to changes in vascular permeability whilst centrally they have an excitatory affect.31 Infusion of exogenous substance P into the painful extremity potentiates the symptoms of CRPS,32 whilst in an animal model of CRPS a substance P receptor antagonist reverses the extravasation, warmth and oedema seen following sciatic nerve transection.33
Sympathetic nervous system abnormalities The diagnosis of CRPS is dependent on the presence of the symptoms and signs of VMI and trophic changes suggesting sympathetic nervous system (SNS) dysfunction. Although the SNS is not normally active in the processing and transmission of noxious stimuli in some cases of CRPS the phenomenon of sympathetically maintained pain (SMP) is now recognised.1 SMP maybe relieved by stellate ganglion block to the affected limb34 and then restored by noradrenalin injection.35 Increasing sympathetic activity worsens spontaneous pain and mechanical
161 allodynia.36 Pain can be enhanced or provoked, after sympathectomy, by injection of adrenergic agonists into the skin of the symptomatic limb.37 However intravenous regional sympathetic blockade with guanethidine, traditionally a mainstay of treatment in resistant cases, does not improve the symptoms or alter the natural history of CRPS.38 The mechanism by which the SNS may be involved in CRPS pain is not clear. Adrenergic supersensitivity in the affected limb may explain this in a number of ways. The density of a1 adrenoceptors is increased in the non-vascular epidermal tissue of symptomatic limbs. Following partial nerve injury, when both injured and uninjured somatic axons start to express a1 adrenoceptors.39 Cutaneous vasculature shows increased responsiveness to noradrenalin in limbs of CRPS patients. Thus adrenergic supersensitivity could lead to sympathetic over-activity causing the sensitisation of the somatic sensory nervous system to circulating catecholamines and noradrenalin released from post-ganglionic sympathetic terminals. Adrenergic supersensitivity may cause vasoconstriction, aggravating tissue inflammation, causing a build up of nociceptive mediators produced during the inflammatory process. Alternatively adrenergic supersensitivity might interfere with the normal production of mediators such as nerve growth factor (NGF). a1 adrenergic activity increases the secretion of NGF, an inflammatory mediator known to stimulate the growth of nociceptive afferents and to cause the release of nociceptive mediators from mast cells, sympathetic neurones and macrophages.40 Increased a2 adrenergic activity in the SNS stimulates the synthesis of prostaglandins E and I both potent in increasing the excitability of nociceptive afferent nerve fibres.41
Peripheral sensitisation Changes in normal neuronal functioning, leading to pain hypersensitivity, including allodynia have been attributed to neuronal plasticity. This physiological process is an ongoing phenomenon that reflects changes in neuronal environment and activity.42 The experience of pain occurs when small fibre nociceptors (C and Ad fibres in the skin) are stimulated. These fibres normally require significant energy and hence a stimulus that is tissue threatening or damaging for a pain to be felt. These fibres are however activity dependent and if stimulated at low intensity the perception is crude touch. If the stimulus is repetitive and potentially threatening these nociceptors can become sensitised, decreasing their threshold to fire. This is a
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Central processing changes The unexplained pain of CRPS has been linked to central sensitisation. Following nerve injury, both injured and non-injured sensory afferents can fire spontaneously. Prolonged input to the dorsal horn as a result of spontaneous firing in C fibre nociceptors sensitises dorsal horn neurons so that they abnormally respond to innocuous inputs. This may lead to an exaggerated dorsal horn response to A-fibre input and thus allodynia. Peripheral nerve injury may also reduce the affect of central descending inhibitory pathways. The spread of pain beyond the territory of an affected nerve can be reversed by certain receptor antagonists implicated in central sensitisation.43
Fracture management The incidence of CRPS following tibial shaft fracture is not affected by the method of fracture management employed.15 Equally both the severity of the fracture and the quality of reduction following distal radial fracture are not influential.14 Undue immobilisation has been proposed as a cause of CRPS and CRPS features, except pain, are seen after cast immobilisation.44 Excessive plaster of paris cast tightness has been linked to the development of CRPS following distal radial fracture.45 Immobilisation has been proposed to cause a neglect-like’’ phenomenon in which the patients find difficulty in initiating movement or accurately directing it.46 Learned pain avoidance behaviour in response to allodynia may exacerbate changes of disuse since normal tactile and proprioceptive input are necessary for correct central nerve signal processing. Indeed, it has been suggested that abnormal mobility is the entire cause, due to loss of integration between sensory input and motor output, in a manner akin to seasickness.47,48
Psychological factors Some physicians may feel that the complex array of symptoms, the seemly innocuous minor trauma’’ preceding the onset (or in deed lack of trauma) and the lack of conclusive diagnostic tests or imaging points to CRPS being primarily of psychological origin. This concept, however, is unsupported.49 Although several studies have linked certain psychological factors with CRPS including emotional lability, low pain threshold, hysteria, depression and antecedent psychological stress, most CRPS patients are normal. One proposed theory is that of a complex interaction between the, now apparent, pathophysiological models for the disease and certain psychological processes to explain the progression and longevity seen in certain patients.50 ’’
normal adaptive physiological response to injury. Unfortunately this response can become harmful when the threatening environment recedes but the nociceptors remain sensitised. This pathophysiological state is further compounded by the fact that these small fibres proliferate in response to the pro-inflammatory soup of cytokines, neurotransmitters and growth factors that are released locally during the initial injury phase. A combination of activity dependent firing, an adaptive response to a repeated stimulus and proliferation in response to an injury environment leads to a vicious circle of continuing pain without a noxious stimulus present.
A. McBride, R. Atkins
Investigations and differential diagnosis Fortunately the severe and therefore obvious cases of CRPS are rare following trauma. The more common marginal case however does present a diagnostic dilemma. The differential diagnosis of the painful, swollen, hot limb in the orthopaedic setting includes the direct effects of the original trauma, undiagnosed fracture, cellulitis, arthritis and malignancy. A carefully taken history and initial investigations in these marginal cases should be directed to their exclusion. CRPS does not cause elevation of the blood and serum markers of inflammation. All other routine biochemical indices are also unchanged. Plain radiography demonstrates features of rapid bone loss: visible demineralisation with patchy, subchondral or sub-periosteal osteoporosis, metaphyseal banding and profound bone loss (Fig. 7).51 Bone involvement is universal with increased uptake on bone scanning in early CRPS (Fig. 8). This was originally thought to be peri-articular, suggesting arthralgia.52,53 However CRPS does not cause arthritis and recent studies have shown generalised hyperfixation.54 Later the bone scan returns to normal. A normal bone scan without radiographic osteoporosis virtually excludes adult CRPS. MRI can be helpful to exclude other pathologies and in CRPS may demonstrate early bone and soft tissue oedema, joint effusions and late atrophy with fibrosis but is not diagnostic. Temperature difference between the limbs is greater in CRPS than other pain syndromes but this is not usually applied in an orthopaedic context.55,56
’’
ARTICLE IN PRESS Complex regional pain syndrome
Figure 7 Patchy osteopenia associated with CRPS affecting the foot.
Figure 8 Bone scan changes affecting the left-hand seen in early CRPS.
Management Early recognition of CRPS is the key to achieving the best results. Aggressive, sympathetic multi-disciplinary treatment is necessary. For those patients with concomitant psychosocial factors an especially vigorous approach is required. Reassurance of the self-limiting natural history of the condition should be emphasised. Increased function of the affected limb should be sought using a combination of simple analgesia and supervised physiotherapy to break the vicious cycle of disuse.57 Non-steroidal antiinflammatory drugs appear to give better pain relief than opiates. Immobilisation and prolonged splintage should be avoided where possible. Limb inactivity will not only slow the recovery but can produce permanent disability through contractures; therefore if used, splintage must be in the
163 safe position. For most orthopaedic patients who develop CRPS this approach will provide a good outcome. If these simple measures do not result in rapid resolution, involvement of pain specialists is crucial. Numerous second line measures have been proposed but properly constructed scientific studies are lacking58 and these treatments are often unsuccessful so that patients are left with pain and disability. Further treatments include centrally acting analgesic medications such as amitriptyline, gabapentin or carbamazepine; regional anaesthesia; the use of membrane stabilising drugs such as mexilitene; sympathetic blockade; desensitisation of peripheral nerve receptors with capsaicin; transcutaneous nerve stimulation or an implanted dorsal column stimulator. Where the knee is affected, epidural anaesthesia and continuous passive motion may be appropriate. The role of surgery is limited. Where CRPS is caused by a surgically correctable nerve lesion, such as median nerve compression at the wrist, surgical intervention may provide relief, but this should be undertaken cautiously in the presence of active disease. Surgery is rarely indicated to treat fixed contractures, which usually involve all of the soft tissues. Surgical release must therefore be radical and expectations limited. Surgery for contracture should be delayed until the active phase of CRPS has completely passed and ideally there should be a gap of at least a year since the patient last experienced pain and swelling. Amputation of a limb affected by severe CRPS should be approached with great caution. In a series of 28 patients who underwent 34 amputations in 31 limbs, surgery was usually performed for recurrent infection or to improve residual function. Pain relief was rare and unpredictable and neither was infection always cured nor function universally improved. CRPS often recurred in the stump, especially if the amputation level was symptomatic at the time of surgery.59 Generally, surgery represents a painful stimulus, which may exacerbate CRPS or precipitate a new attack. This risk must be balanced carefully against the proposed benefit. The risk of surgically precipitated recurrence is greatest when the same site is operated upon in a patient with abnormal psychology in the presence of active disease and lowest when these conditions do not apply. Surgery must be performed carefully with minimal trauma with excellent post-operative analgesia. Ideally the anaesthetist will have a particular interest in the treatment of CRPS.
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CRPS in children The condition in this age group differs from adults both in severity of symptoms and in response to treatment. For these reasons it has long been under reported. In a series of 70 cases, neither severe disabling pain nor trophic changes were common.60 The characteristic radiographic changes seen in the advanced form of the disease in adults does not occur. Psychological factors have been implicated. Symptom severity and the reaction of the family to the symptoms of CRPS can be amplified by the pressures of academics or organised sports and by substantial family stress such as parental conflict, and sibling rivalry. Good response to physical therapy makes this the mainstay of treatment with an emphasis on functional goals as well as reduction of pain.
Research directions
Further understanding of the pathophysiological processes occurring Exploring links with other chronic pain states. Is there a common localised initiating pathological process occurring? Epidemiological studies to identify risk factors for progression to long-term disability Validation of current proposed therapeutic and physical therapies through well designed randomised control trials
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ARTICLE IN PRESS Complex regional pain syndrome 28. van der Lann L, Kapitein P, Verhofstad A, Hendriks T, Goris RJA. Clinical signs and symptoms of acute reflex dystrophy in the hind limb of the rat, induced by infusion of a free-radical donor. Acta Orthop Belg 1998;64:210–7. 29. van der Laan L, Laak ter HJ, Gabreels-Festen A, Gabreels F, Goris RJA. Complex regional pain syndrome I (RSD): pathology of skeletal muscle and peripheral nerve. Neurology 1998;51:20–5. 30. Perez R, Zuurmond W, Bezemer P, et al. The treatment of complex regional pain syndrome type 1 with free radical scavengers: a randomised control study. Pain 2003;102: 297–307. 31. Huygen F, de Bruijn A, Klein J, Zijlstra F. Neuroimmune alterations in the complex regional pain syndrome. Eur J Pharmacol 2001;429:101–11. 32. Weber M, Birklein F, Neundorfer B, Schmelz M. Facilitated neurogenic inflammation in complex regional pain syndrome. Pain 2001;91:251–7. 33. Kingery W, Davies M, Clark J. A substance P receptor (NK1) antagonist can reverse vascular and nociceptive abnormalities in a rat model of complex regional pain syndrome type II. Pain 2003;104:75–84. 34. Price DD, Long S, Wilsey B, Rafii A. Analysis of peak magnitude and duration of analgesia produced by local anesthetics injected into sympathetic ganglia of complex regional pain syndrome patients. Clin J Pain 1998;14: 216–26. 35. Torebjork E, Wahren L, Wallin G, Hallin R, Koltzenburg M. Noradrenaline-evoked pain in neuralgia. Pain 1995;63: 11–20. 36. Janig W. CRPS 1 and CRPS 2: a strategic view. Harden RN, Baron R, Ja ¨nig W, editors. Complex regional pain syndrome: progress in pain research and management, vol. 22. Seattle: IASP Press; 2001. p. 3–15. 37. Ali Z, Raja SN, Wesselmann U, Fuchs PN, Meyer RA, Campbell JN. Intradermal injection of norepinephrine evokes pain in patients with sympathetically maintained pain. Pain 2000;88:161–8. 38. Livingstone JA, Atkins RM. Intravenous regional guanethidine blockade in the treatment of post-traumatic complex regional pain syndrome type 1 (algodystrophy) of the hand. J Bone Joint Surg Br 2002;84B:380–6. 39. Campbell J, Raga S, Meyer R. Painful sequelae of nerve injury. In: Dubner R, Gebhart G, Bond M, editors. Proceedings of the fifth world congress on pain. Amsterdam: Elsevier Science Publishers; 1988. p. 135–43. 40. Tuttle JB, Etheridge R, Creedon DJ. Receptor-mediated stimulation and inhibition of nerve growth factor secretion by vascular smooth muscle. Exp Cell Res 1993; 208:350–61. 41. Gonzales R, Sherbourne CD, Goldyne ME, Levine JD. Noradrenaline-induced prostaglandin production by sympathetic postganglionic neurons is mediated by a2-adrenergic receptors. J Neurochem 1991;57:1145–50. 42. Woolf CJ, Salter MW. Neuronal plasticity: increasing the gain in pain. Science 2000;288:1765–8. 43. Woolf CJ, Mannion RJ. Neuropathic pain: aetiology, symptoms, mechanisms, and management. Lancet 1999;353: 1959–64.
165 44. Butler SH. Disuse and CRPS. Harden RN, Baron R, Ja ¨nig W, editors. Complex regional pain syndrome: progress in pain research and management, vol. 22. Seattle: IASP Press; 2001. p. 141–50. 45. Field J, Protheroe DL, Atkins RM. Algodystrophy following Colles’ fracture is associated with secondary tightness of casts. J Bone Joint Surg Br 1994;76B:901–5. 46. Galer BS, Harden N. Motor abnormalities in CRPS: a neglected but key component. Harden RN, Baron R, Ja ¨nig W, editors. Complex regional pain syndrome: progress in pain research and management, vol. 22. Seattle: IASP Press; 2001. p. 135–40. 47. Harris AJ. Cortical origin of pathological pain. Lancet 1999;354:1464–6. 48. McCabe CS, Haigh RC, Ring EF, Halligan PW, Wall PD, Blake DR. A controlled pilot study of the utility of mirror visual feedback in the treatment of complex regional pain syndrome (type 1). Rheumatology (Oxford) 2003;42:97–101. 49. Bruehl S, Husfeldt B, Lubenow TR, Nath H, Ivankovich AD. Psychological differences between reflex sympathetic dystrophy and non-RSD chronic pain patients. Pain 1996;67: 107–14. 50. Bruehl S. Do psychological factors play a role in the onset and maintenance of CRPS-I?. Harden RN, Baron R, Ja ¨nig W, editors. Complex regional pain syndrome: progress in pain research and management, vol. 22. Seattle: IASP Press; 2001. p. 279–90. 51. Kozin F, Genant HK, Bekerman C, McCarty DJ. The reflex sympathetic dystrophy syndrome. II. Roentgenographic and scintigraphic evidence of bilaterality and of periarticular accentuation. Am J Med 1976;60:332–8. 52. Mackinnon SE, Holder LE. The use of three-phase radionuclide bone scanning in the diagnosis of reflex sympathetic dystrophy. J Hand Surg [Am] 1984;9A:556–63. 53. Atkins RM, Tindale W, Bickerstaff D, Kanis JA. Quantitative bone scintigraphy in reflex sympathetic dystrophy. Br J Rheumatol 1993;32:41–5. 54. Bickerstaff DR, Charlesworth D, Kanis JA. Changes in cortical and trabecular bone in algodystrophy. Br J Rheumatol 1993; 32–1:46–51. 55. Perelman RB, Adler D, Humphreys M. Reflex sympathetic dystrophy: electronic thermography as an aid in diagnosis. Orthop Rev 1987;16–8:561–6. 56. Wasner G, Schattschneider J, Baron R. Skin temperature side differences—a diagnostic tool for CRPS? Pain 2002; 98–1–2:19–26. 57. Stanton-Hicks M, Baron R, Boas R, et al. Complex regional pain syndromes: guidelines for therapy. Clin J Pain 1998;14: 155–66. 58. Kingery WS. A critical review of controlled clinical trials for peripheral neuropathic pain and complex regional pain syndromes. Pain 1997;73:123–39. 59. Dielissen PW, Claassen AT, Veldman PH, Goris RJ. Amputation for reflex sympathetic dystrophy. J Bone Joint Surg Br 1995;77B:270–3. 60. Wilder RT, Berde CB, Wolohan M, Vieyra MA, Masek BJ, Micheli LJ. Reflex sympathetic dystrophy in children. Clinical characteristics and follow-up of seventy patients. J Bone Joint Surg Am 1992;74A:910–9.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 166–168
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CME SECTION
Three external CME points available The following series of questions are based on the CME designated article for this issue—‘Acetabular Fractures’ by J. McMaster and J. Powell. Please read the article carefully and then complete the self-assessment questionnaire by filling in the square corresponding to your response to each multiple-choice question. For true or false questions, please fill in one square only. After completing the questionnaire, either post or fax the answer page back to the Current Orthopaedics Editorial Office at the address at the bottom of the RESPONSE sheet. Please photocopy this page if you wish to keep your copy of Current Orthopaedics intact. Replies received before the next issue of Current Orthopaedics is published will be marked and those reaching an adequate standard will qualify for three external CME points. You will be notified of your marks and a CME certificate will be despatched for your records.
Questions 1. At what age does the triradiate cartilage fuse? A. B. C. D. E.
5–7 years 8–10 years 11–13 years 14–17 years 18–23 years
2. Which of the following is not an elementary fracture pattern according to Letournel and Judet? A. B. C. D. E.
Posterior wall T Shaped Anterior column Transverse Posterior column
3. If a force is applied axially along the femur to produce an acetabular fracture, and the femur is in a position of abduction, what pattern of fracture is predisposed? A. B. C. D. E.
T shaped Transverse Both columns Posterior wall Posterior column
0268-0890/$ - see front matter doi:10.1016/j.cuor.2005.04.004
4. Which of the following statements about nerve injury in association with acetabular fractures is incorrect? a. The rate of sciatic nerve injury associated with acetabular fractures is approximately 12% b. Femoral nerve injury is rare in association with acetabular fractures, and the prognosis is poor c. Sciatic nerve injuries associated with acetabular fractures most commonly involve the peroneal branch d. Sciatic nerve injuries are commoner in association with posterior dislocation e. Assessment of femoral nerve function is important before surgery for acetabular fractures, as intraoperative injury is an important complication 5. What fracture pattern is associated with the spur sign? a. b. c. d. e.
Both columns Transverse Anterior column Posterior column Posterior column with posterior wall
6. If a fracture line extends into the iliac wing above the acetabulum on plain films, what fracture pattern must be present?
ARTICLE IN PRESS CME SECTION a. b. c. d. e.
Posterior column Posterior wall Anterior Column Anterior wall T shaped
7. Which of the following statements about the CT scan interpretation of acetabular fractures is incorrect? a. On axial views, splits in the coronal plane often represent column fractures b. On axial views, sagittal splits in the roof of the acetabulum are seen commonly with transverse fractures c. Oblique fractures that do not extend into the quadrilateral plate are seen with wall fractures d. No part of the acetabulum is connected to the scarum via the sciatic buttress in T shaped fractures e. CT scans can help differentiate T shaped from both column fractures 8. If all three roof arc angles are 45 degrees or more on plain X-rays, what is the minimum distance between the first CT scan slice that catches the apex of the acetabulum and the first slice that records a fracture line within the hip joint? A. B. C. D. E.
2 mm 5 mm 10 mm 15 mm 20 mm
9. Which of the following best describes a series of assessments that reveal a fracture that is suitable for nonoperative management? A. All three roof arcs o45 degrees B. o50% of posterior wall involved C. Fracture is stable on EUA
167 D. 50% posterior wall involvement but stable on EUA E. Medial and anterior roof arcs 25 degrees, posterior roof arc 60 degrees, stable on EUA
10. Which of the following is not an indication for urgent open reduction and internal fixation, carried out sooner than the accepted optimum time for surgery? a. Closed reduction of an associated hip dislocation did not improve an existing neurological deficit b. Closed reduction of an associated hip dislocation was followed by the onset of a new neurological deficit c. Intraarticular fragments on CT scan after closed reduction d. Reduction of associated femoral head dislocation cannot be maintained e. Open fracture
11. Which of the following fracture patterns can be adequately treated via ilioinguinal approach? a. b. c. d. e.
Posterior column Anterior column with posterior hemitransverse Multifragmentary both column Posterior wall with T shaped fracture Transverse with femoral head fracture
12. What is the approximate incidence of heterotopic ossification complicating fixation of acetabular fractures through a triradiate approach? a. b. c. d. e.
o10% 10–19% 20–49% 50–74% 475
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ARTICLE IN PRESS Current Orthopaedics (2005) 19, 169
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CME SECTION
Answers to CME questions in Vol. 18, issue 6 Please find below the answers to the Current Orthopaedics CME questions from Vol. 18, issue 6 which were based on the article—‘Acute compartment syndrome’ by S. Singh, P. Trikha and J. Lewis from the same issue. 1
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doi:10.1016/j.cuor.2004.12.010
Aims and Scope Current Orthopaedics presents a unique collection of international review articles summarizing the current state of knowledge and research in orthopaedics. Each issue focuses on a specific topic, discussed in depth in a mini-symposium; other articles cover the areas of basic science, medicine, children/adults, trauma, imaging and historical review. There is also an annotation, self-assessment questions and an exam section. In this way, the entire postgraduate syllabus will be covered in a 4-year cycle. The Journal is cited in: Cochrane Center, EMBASE/ Excerpta Medica, Infomed, Reference Update and UMI Microfilms.
Editor Professor R. A. Dickson MA, ChM, FRCS, DSc St James’s University Hospital Trust, Leeds, UK
Editorial Committee President of BOTA, M. A. Farquharson-Roberts (Gosport, UK), I. Leslie (Bristol, UK), D. Limb (Leeds, UK), M. Macnicol (Edinburgh, UK), J. Rankine (Leeds, UK)
Editorial Advisory Board E. G. Pasion (Philippines) L. de Almeida (Portugal) G. P. Songcharoen (Thailand) R. W. Bucholz (USA) J. W. Frymoyer (USA) R. W. Gaines (USA) S. L. Weinstein (USA) M. Bumbasirevic (former Yugoslavia)
J. C. Y. Leong (Hong Kong) A. K. Mukherjee (India) A. Kusakabe (Japan) A. Uchida (Japan) M.-S. Moon (Korea) R. Castelein (The Netherlands) R. K. Marti (The Netherlands) G. Hooper (New Zealand) A. Thurston (New Zealand)
D. C. Davidson (Australia) J. Harris (Australia) S. Nade (Australia) G. R. Velloso (Brazil) J. H. Wedge (Canada) S. Santavirta (Finland) P. N. Smyrnis (Greece) P. N. Soucacos (Greece) M. Torrens (Greece)
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ARTICLE IN PRESS Current Orthopaedics (2005) 19, 171–179
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MINI-SYMPOSIUM: THE WRIST
(i) Examination of the wrist—surface anatomy of the carpal bones R. Srinivas Reddy, J. Compson Upper Limb Unit, Department of Orthopaedics, King’s College Hospital, London SE5 9RS, UK
KEYWORDS Wrist examination; Carpal bones; Surface anatomy
Summary An accurate clinical examination is vital in the diagnosis of wrist injuries. Though various investigations including special X-ray views, computer tomography, and isotope bone scans are used to confirm the diagnosis of carpal bone fractures and wrist ligament injuries, initial diagnosis and localisation is by clinical examination. The fundamental basis of both inspection and palpation is knowledge of surface anatomy. This paper gives a brief overview of carpal osteology and then a method of examination of the carpus which we hope will be used to improve basic examination of the wrist. & 2005 Elsevier Ltd. All rights reserved.
Introduction Despite the improvement in imaging techniques and the use of arthroscopy, clinical examination remains the most important step in the diagnosis of wrist injuries. Several common carpal fractures (Table 1) require either special X-ray views, computer tomography or isotope bone scans to confirm the diagnosis. However the initial localisation and recognition of the severity of the injury is by clinical examination. Without this, appropriate use of imaging is impossible and can lead, at best, to unnecessary investigations and, at worse, to a missed diagnosis. This is best illustrated by fractures of the hook of hamate which are rarely Corresponding author. 5, Derwent close, Gamston, Nottingham NG2 6NF, UK. Tel.:+44 7818 418350. E-mail addresses:
[email protected] (R. Srinivas Reddy),
[email protected] (J. Compson).
seen on standard X-ray views. The fracture however is easily suspected clinically if one knows the surface anatomy of the hamate though in reality it is often missed. The diagnosis can be confirmed by special oblique views, carpal tunnel views or by isotope bone scanning. However the definitive test which not only diagnoses the fracture but also shows displacement and the state of healing is a CT scan. For similar reasons, as well as being a commonly missed injury, the scaphoid can fracture at three levels and one needs to know how to palpate the tubercle, waist and proximal pole individually to thoroughly examine the bone and pick up all possible fracture types. Of equal importance some significant ligament injuries, especially when there is no associated dislocation can look surprisingly normal on X-ray (Table 2) and their diagnosis also requires clinical acumen.
0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2005.02.008
ARTICLE IN PRESS 172 Table 1
R. Srinivas Reddy, J. Compson Clinically diagnosed carpal fractures and confirmation techniques.
Carpal bone fracture
Investigations
Scaphoid fractures Hook of hamate fractures Pisiform fractures Trapezium ridge fractures Dorsal flake fractures of the triquetrum
Special X-ray views, isotope bone scans, MRI scans Special X-ray views and CT scans Special X-ray views CT scans Bone scans
Table 2 Significant ligamentous injuries with ‘normal’ X-rays. Ligament injuries
X-ray findings
Acute scapholunate dissociation Acute lunotriquetral dissociation Thumb carpometacarpal ‘Beak’ ligament tear
Normal Normal Normal
The basic tenets of examination are look, feel and move. However a vital component in both looking and feeling is knowledge of surface anatomy. Without this the important localisation of carpal injuries is impossible. In a recent study we asked orthopaedic and casualty doctors of all grades to demonstrate the palpation of seven, commonly injured bony landmarks in the carpus. Only two got them all right and none of these was a consultant! Because of this we have written a series of articles on examination of the wrist, which though superficially simplistic we believe are important for both clinical practice as well as examination purposes, especially for those too embarrassed (mainly consultants) to admit they lack the basic knowledge! We have started with surface anatomy since we believe this to be the fundamental basis of examination.
Osteology of the carpus The carpus contains eight bones in two rows, proximal and distal. The proximal row consists of three bones the scaphoid, lunate, and triquetrum which are attached to each other by intrinsic intercarpal ligaments, the scapholunate and lunotriquetral. They form an arch which is convex proximally and articulates with the radius and the articular disc of the triangular fibro-cartilage complex (TFCC) to form the radio-carpal (wrist) joint. The pisiform, though overlying the triquetrum and articulating with its volar surface, is not
functionally a proximal row bone but is separate and lies in the tendon of flexor carpi ulnaris. The distal row of bones, made up of the trapezium, trapezoid, capitate and hamate, are firmly attached to each other by strong intercarpal ligaments. The distal row articulates with the proximal row to form the midcarpal joint and also articulates with the bases of the metacarpal bones. The distal is more arched than the proximal row with a deep concave volar surface which makes the trapezium lie more palmar than expected compared to the capitate. The ulnar side is deepened by the hook of hamate which produces a deep carpal groove, which accommodates the flexor tendons and the median nerve as they pass into the hand through the carpal tunnel.1,2 Each carpal bone is considered individually.1,2
Scaphoid (Figs. 1A and B—c–e) The scaphoid has the oddest shape and orientation of all the carpal bones. It lies at about 451 to the long axis of the wrist in both radial and palmar directions. Its proximal end or pole is therefore on the dorsum of the carpus and its distal end, the tubercle, is subcutaneous on the palmar surface. It is a bone of two halves; the proximal is similar to the adjacent lunate with a deep crescentic shape lying tightly in the curve of the scaphoid fossa of the radius and distally, with the lunate, forming a socket holding the head of the capitate. The distal end has a tubercle which is offset and gives an overall twist to the bone which also has a gentle curve in its long axis allowing it to lie between the concave scaphoid fossa of the radius and the convex head of capitate. The waist and distal pole of the scaphoid are not firmly held by adjacent bones and act as a strut transmitting distal row movements to the proximal bones.
Lunate (Figs. 1A and B—f) The lunate is semilunar and has a convex proximal surface that articulates with the radius and TFCC
ARTICLE IN PRESS Examination of the wrist—surface anatomy of the carpal bones and its distal surface is deeply concave to fit the ulnar side of the head of the capitate. The articulation between the three bones, capitate, scaphoid and lunate, forms a ball and socket in the middle of the mid-carpal joint. Most of the bone, like the proximal pole of the scaphoid, when the wrist is in a neutral position, lies under the cover of the dorsal rim of the radius and cannot be palpated. It is uncovered by flexion of the wrist.
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carpal bone. It articulates proximally with the scaphoid, distally with the thumb and index metacarpals and medially with the trapezoid. There is a prominent ridge and tubercle with a groove lying obliquely on the palmar surface. The ridge is part of the fibro-osseous sheath of flexor carpi radialis and can be fractured after a fall on the outstretched hand since it is the first part of the carpus to hit the ground.
Triquetrum (Figs. 1A and B—g) Trapezoid (Figs. 1A and B—l) The triquetrum is somewhat pyramidal and bears an oval facet on its palmar surface for articulation with the pisiform. It articulates laterally with the lunate and distally with the hamate. The bone lies more distally and obliquely than expected and moves by sliding on its flat articular surfaces. It has a dorsal tubercle which is commonly fractured.
The trapezoid articulates distally mainly with the metacarpal base of the index finger and proximally with the scaphoid. Laterally it articulates with the trapezium and medially with the capitate and is difficult to palpate.
Pisiform (Figs. 1A and B—h)
Capitate (Figs. 1A and B—k)
The pisiform is like a small patella lying in the tendon of flexor carpi ulnaris. It increases the distance of the FCU from the centre of rotation of the wrist and thus improves the lever arm and therefore the strength of the muscle. This is the same function the patella has in the knee and the pisiform has all the pathologies found in its larger brother.
The capitate is the largest carpal bone and articulates distally mainly with the middle metacarpal base and proximally with the scaphoid and lunate. Laterally it articulates with the trapezoid and medially with the hamate. The proximal end is ball shaped and is difficult to palpate individually.
Hamate (Figs. 1A and B—i and j) Trapezium (Figs. 1A and B—m and n) The trapezium is larger than is normally assumed, which is why trapeziectomies seem to keep going on forever! It also lies more volar than any other
The most important part of the hamate to examine is the hook projecting from the distal part of its palmar surface. It is much larger than one would assume from palpation or X-rays.
Figure 1 Palmar (A) and dorsal view (B) of the carpus describing the osteology. Landmarks on the 3D CT reconstruction are—(a) radial styloid, (b) ulnar styloid, (c) scaphoid tubercle, (d) waist of scaphoid, (e) proximal pole of scaphoid, (f) lunate, (g) triquetrum, (h) pisiform, (i) hook of hamate, (j) hamate, (k) capitate, (l) trapezoid, (m) tubercle of trapezium, (n) trapezium.
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Surface anatomy landmarks The following routine is used by the senior author to teach and demonstrate the surface anatomy of the carpal bones. We believe it is worth going through each step examining the right wrist with the left hand. To simplify orientation all the illustrations are of the right wrist. The various landmarks are numbered in the adjoining figures and the best way to understand is to closely correlate the figures with the text descriptions.
Dorsal view of the carpus and the wrist (Figs. 2A and B) The starting point is Lister’s tubercle (1) which lies on the dorsal surface of the distal radius in line with the web space between the index and middle
R. Srinivas Reddy, J. Compson fingers. It is normally easily palpable using the pulp of the thumb; however if one has problems feeling it, if one extends the wrist it is normally at the level of the most proximal extensor skin crease. It is felt as a small longitudinal ridge in the long axis of the forearm. It can also be found by extending proximally by about 2 cm the line of extensor pollicis longus on the back of the hand and is felt just radially to where the tendon lies.3,4 The next move is to slide the thumb about 1–2 cm distally towards the fingers. The tip of the thumb should fall into a soft depression just distal to the dorsal rim of the radius (Figs. 3A and B). This has been called the crucifixion fossa (2).5,6 This fossa can also be located by following the line of the web space between the index and middle fingers proximally until it falls into the same depression just distal to the radius. We are not sure of the origins of the name, crucifixion fossa; however it was first heard by
Figure 2 Dorsal view of the carpus and wrist as 3D CT reconstruction (A) and clinical photograph (B). Landmarks in both figures are—(1) Lister’s tubercle, (2) crucifixion fossa at the level of the scapholunate junction, (3) radial styloid process, (11) head of ulna, (12) ulnar styloid process, (13) triquetrum.
Figure 3 (A) Palpation of the Lister’s tubercle, (B) palpation of the lunate and scapholunate junction with the wrist in flexion. Landmarks are—(1) Lister’s tubercle, (2) crucifixion fossa at the level of scapholunate junction.
ARTICLE IN PRESS Examination of the wrist—surface anatomy of the carpal bones
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Figure 4 X-rays of lateral views of the wrist in neutral (A) and in palmar flexion (B). The asterisk (*) symbol in both the views indicates the position of the lunate and the proximal pole of scaphoid with the scapholunate junction in between them, and they are more prominent with the wrist in flexion.
Figure 5 Lateral (radial) view of the carpus and wrist as 3D CT reconstruction (A) and clinical photograph (B). Landmarks in both figures are—(3) radial styloid, (4) waist of scaphoid, (5) trapezium, (6) base of the first metacarpal, EPL: extensor pollicis longus, APL: abductor pollicis longus and extensor pollicis brevis.
one of the authors in a talk by Professor John Stanley. It is probably named such since it lies almost directly over the scapholunate joint and a nail introduced here will produce a clinically significant scapholunate dissociation which would not cut out with load. The capitate and the rest of the strongly joined distal carpal row would prevent this. The Romans probably knew their anatomy better than we do! The tip of the thumb is now at about the level of the mid-carpal joint since the proximal row is under the rim of the radius. If the wrist is now flexed with the tip of the thumb still in the crucifixion fossa one will feel a hard lump coming up into the recess. This is the proximal row and the thumb is now over the area of the scapholunate joint. Ulnarwards, the adjacent radial side of the lunate and radially the proximal pole of the scaphoid can be felt, depending on the degree of ulnar or radial deviation (Figs. 4A and B).7,8
Lateral (radial) view of the carpus and the wrist (Figs. 5A and B) Moving the thumb radially along the dorsal rim of the radius one crosses the sheath of extensor pollicis longus until it eventually comes to the radial styloid (3). You will have noted that it lies volar to the long axis of the radius. This means that
a K-wire driven through its tip into the radius is likely to come out of the back of the bone. This is worth noting the next time one wires a distal radial fracture. Moving the thumb distally, one enters the soft recess of the anatomical snuffbox. The radial rim is the base of a triangle and one can easily palpate its radial (anterolateral) border which is formed by the abductor pollicis longus and extensor pollicis brevis and its ulnar (posteromedial) border which is formed by the extensor pollicis longus. The floor of the snuffbox is formed by (proximal to distal) the radial styloid process, the waist of the scaphoid (4), the trapezium (5) and the base (6) of the thumb metacarpal. With the wrist in a neutral position it is difficult to feel the scaphoid or trapezium. If one places the thumb tip into the snuffbox and then ulnar deviates the wrist, bone can be felt filling the recess. This is mainly the waist and the non-articular dorsal ridge of the scaphoid, though one can also feel part of the trapezium (Figs. 6A and B).3–5
Palmar view of the carpus and the wrist (Figs. 7A and B) Moving to the palmar side of the wrist the thumb tip crosses the first dorsal compartment
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Figure 6 Anatomical snuffbox is revealed better with the wrist in ulnar deviation. (A) X-ray of wrist in ulnar deviation, (B) clinical photograph of wrist in ulnar deviation. Landmarks are—(3) radial styloid, (4) waist of scaphoid, (5) trapezium, (6) base of the first metacarpal.
Figure 7 Palmar view of the carpus and wrist as 3D CT reconstruction (A) and clinical photograph (B). Landmarks in both figures are—(7) tubercle of the scaphoid, (8) tubercle of trapezium, (9) pisiform, (10) hook of hamate.
[De Quervain’s tendons] until it feels the radial pulse. Moving distally the thumb again falls into a soft recess bordered ulnarwards by the tendon of flexor carpi radialis. Moving more distally and at the level of the distal flexor crease lies a bony prominence. This is the tubercle of the scaphoid (7) which can be more easily palpated by extending the wrist. If one now places the left index finger tip on the tubercle and also one’s thumb in the crucifixion
fossa on the back of the wrist which is over the proximal pole of the scaphoid you will be holding both ends of the scaphoid. One will note how it lies at 451 to the long axis of the wrist in both a palmar and radial direction. If one then radially deviates the wrist and keeps the thumb and finger in the same place on the bone one can see and feel how the scaphoid flexes. If one then ulnar deviates the wrist it does the opposite and the scaphoid can be
ARTICLE IN PRESS Examination of the wrist—surface anatomy of the carpal bones felt lying in a more extended position. If one now again places the thumb on the tubercle of the scaphoid and moves distally under the cover of the thenar muscles one can feel the tubercle and ridge of the trapezium (8), facilitated by deviating the wrist ulnarwards.2–5 Keeping on the palmar side of the wrist but moving across the carpal tunnel to the ulnar side one can easily palpate the pisiform bone (9). This was the most consistently demonstrated bone in our study. The pisiform forms an elevation, which can be seen and felt on the palmar aspect of the wrist at the base of the hypothenar eminence (Figs. 8A and B). It lies just distal to the most medial end of the distal wrist crease at the ulnar border. The next manoeuvre is to place one’s thumb over the pisiform and move it distally by about 2 cm and then towards the mid-line by about a centimetre. Your thumb should be in the line of the ring finger. Deeply under the hypothenar muscles one can feel a large and solid bony lump which is the clinically important hook of hamate (10). It is not easy to feel and may require firm pressure to do so but anyone treating carpal injuries should be able to palpate this part of the bone.2–5
Medial (ulnar) view of the carpus and wrist (Figs. 8A and B, 9A and B) Moving back to the dorsum of the wrist but this time on the ulnar side and palpating with the index finger. Start with the head of the ulna (11) which is easily visible and forms an elevation on the dorsal and medial aspect of the wrist especially when the wrist is pronated. With the wrist in pronation move the finger tip ulnarwards across the ulnar head until you can feel the tendon of extensor carpi ulnaris overlying the bony prominence of the ulnar styloid (12). Keeping the finger on the tendon and supinating and pronating the wrist the tendon can be felt rolling around the ulnar head and appreciate how the
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ulnar styloid becomes more dorsal on supination and volar on pronation. Moving the finger tip distally from the ulnar styloid one again enters a soft recess ‘The Ulnar Snuffbox’. This is more difficult to palpate than the anatomical snuffbox but the sides can be felt better by ulnar deviating the wrist. Dorsally one can feel the tendon of extensor carpi ulnaris (14) and volarwards the flexor carpi ulnaris (15). The triquetrum (13) is in the base of the fossa and can be found distal to the ulnar styloid process: it is felt more easily by first deviating the wrist (Fig. 9B) ulnarwards, placing the fingertip into the soft recess distal to the ulnar styloid then moving the wrist into radial deviation. The triquetrum is felt moving under the finger.4–6 Moving the fingertip onto the dorsum of the wrist at the same level, one can palpate the dorsum of the triquetrum (Fig. 9A). Here lies a small tubercle which is not easily felt but is commonly knocked off in hyperextension injuries and appears as a flake on lateral X-rays. Localisation however requires clinical examination. The volar surface of the triquetrum cannot be directly palpated due to the overlying pisiform; however it can be tested for tenderness by indirect force through the pisiform. It is important to exclude pisiform tenderness which can be elicited by pushing the pisiform from the ulnar side. This covers all the bones in the proximal row except for the lunate which is difficult to palpate due to the overhang of the radial rim and the overlying extensor tendons, even when the wrist is flexed.
Distal row The last part of the examination is to palpate the distal row. Apart from the tubercle of the trapezium and the hook of hamate this needs to be done from the dorsum. Though one has difficulty in exactly differentiating each bone precisely their positions can be worked out by following the
Figure 8 Medial (ulnar view) of the carpus and wrist as 3D CT reconstruction (A) and clinical photograph (B). Landmarks in both figures are—(12) ulnar styloid, (13) triquetrum, (14) extensor carpi ulnaris, (15) flexor carpi ulnaris.
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Figure 9 (A) Palpation of the dorsal aspect of triquetrum with the wrist in neutral position, (B) Palpation of the triquetrum in the ulnar snuff box with the wrist in radial deviation. Landmarks in both figures are—(11) head of ulna, (12) ulnar styloid process, (13) triquetrum.
Figure 10 Dorsal view of the wrist and carpus as 3D CT reconstruction (A) and clinical photograph (B), following the metacarpals to their bases towards the carpometacarpal joints. Landmarks in both the figures are—(a) thumb (1st) metacarpal, (b) index finger (2nd) metacarpal, (c) middle finger (3rd) metacarpal, (d) ring finger (4th) metacarpal, (e) little finger (5th) metacarpal, (f) hamate, (g) capitate, (h) trapezoid, (i) trapezium.
associated metacarpal shafts proximally to the base and then on to the adjacent carpal bone (Figs. 10A and B). If the wrist and digits are placed in flexion, it may be easier to palpate the carpal bone having eliminated the overhang of the metacarpal base. At the base of the thumb metacarpal is the trapezium. At the base of the index metacarpal is the trapezoid; the capitate is found at the base of the middle finger. The hamate can be located by following both the ring and little finger metacarpals to their bases since they both articulate with the hamate in a single joint.
References 1. Sinnatamby SC. Osteology of the upper limb. In: Sinnatamby SC, editor. Last’s anatomy. Edinburgh: Churchill Livingstone; 1999. p. 103–4. 2. Soames WR. Skeletal system; Ellis H, Dussek EJ. Surface anatomy. In: Williams LP, editor. Gray’s anatomy. New York: Churchill Livingstone; 1995. p. 646–649, 1926–1928. 3. Borley NR. Upper limb. In: Borley NR, editor. Clinical surface anatomy. London: Manson Publishing Ltd; 1997. p. 50–6. 4. Keogh B, Ebbs S. The upper limb. In: Keogh B, Ebbs S, editors. Normal surface anatomy. London: William Heinemann Medical Books Ltd; 1984. p. 114–5.
ARTICLE IN PRESS Examination of the wrist—surface anatomy of the carpal bones 5. Saffar P. Clinical examination of the wrist. In: Saffar P, editor. Carpal Injuries, anatomy, radiology, current treatment. Paris: Springer; 1990. p. 11–6. 6. Ritchie JV, Munter DW. Emergency department evaluation and treatment of wrist Injuries. Emerg Med Clin North Am 1999;17(4):823–42.
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7. Weinzweig J, Watson KH. Examination of the wrist. In: Weinzweig J, Watson KH, editors. The wrist. Philadelphia: Lippincott Williams & Wilkins; 2001. p. 48–59. 8. Rex C. Examination of wrist. In: Rex C, editor. Clinical assessment and examination in orthopaedics. New Delhi: Jaypee Brothers Medical Publishers (P) Ltd; 2002. p. 47–55.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 180–189
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MINI-SYMPOSIUM: THE WRIST
(i) Examination of the wrist—soft tissue, joints and special tests R. Srinivas Reddy, J. Compson Upper Limb Unit, Department of Orthopaedics, King’s College Hospital, London SE5 9RS, UK
KEYWORDS Wrist examination; Carpal bones; Distal radio-ulnar joint; Triangular fibrocartilage complex; Radio-carpal joint; Midcarpal joint
Abstract Despite the advances in imaging, clinical examination remains the most important means of diagnosis in the wrist. This is especially important in soft tissue injuries after which the radiological changes are subtle and the pathology is dynamic and cannot be appreciated on static images. The wrist joint, however, is complex involving four joints, eight bones, over 20 articulations and numerous ligaments, so a meticulous examination and attention to detail is important in arriving at an accurate diagnosis. We describe a sequence of examination of the wrist, which we routinely use and have found both easy to perform and remember. & 2005 Elsevier Ltd. All rights reserved.
Introduction In a previous article we described the use of clinical examination in the diagnosis of carpal fractures and the surface anatomy of the carpal bones. Clinical acumen is even more important in diagnosing injuries involving the soft tissues of the wrist, for instance in tears of the carpal ligaments after which X-rays and more advanced techniques like MRI can look virtually normal. This is particularly relevant in injuries where there is little or no static dislocation or displacement of the carpal bones for instance in tears of the scapholunate or lunotriquetral ligaments. Corresponding author. 5, Derwent Close, Gamston, Nottingham NG2 6NF, UK. Tel.: +44 7818 418350. E-mail addresses:
[email protected] (R.S. Reddy),
[email protected] (J. Compson).
Equally, non-traumatic pathology can affect all or only a part of the carpus and localising the source of the pain or instability requires a reasonable knowledge of the anatomy and how to examine each area. Unfortunately the anatomy of the carpus is complex. The wrist joint is formed by at least four joints, the radio-carpal, the midcarpal, the pisotriquetral and the distal radio-ulnar, even if one doesn’t include the five adjacent carpo-metacarpal joints. Though there are only eight carpal bones there are at least 20 articulations between the bones as well as the adjacent radius, ulna and metacarpals. In addition to the above, there are intraarticular soft tissue structures including the intrinsic intercarpal ligaments and the triangular fibrocartilage (TFC) complex (TFCC). Also running through the capsule are another set of ligaments known as extrinsic ligaments, which are important stabilisers of the
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ARTICLE IN PRESS Examination of the wrist—soft tissue, joints and special tests carpal bones. Overlying these are the tendons and their sheaths that cross the carpus to insert distally and either directly or indirectly move the wrist. These include twelve tendons in six separate extensor compartments on the dorsum of the wrist as well as eleven on the volar side.1 When it comes to examination, though, it would be ideal to know exactly the anatomy of the wrist. Unfortunately even so-called experts still argue on the ligamentous anatomy. Practically, a reasonable knowledge of where the bones and hence the joints are, as well as the overlying tendons, should suffice for examination of most conditions. A little knowledge of the ligaments is a dangerous thing, since it confuses rather than helps. If one is keen to go against this advice we would recommend one should only look at ligament anatomy as described in the last few years. One of the recent textbooks on wrist surgery is a good starting point rather than the more classical anatomical texts. The latter, however, are ideal for the rest of the structures. We would recommend before reading this article that one should have read our previous article on examination of the carpal bones and the surface anatomy of the wrist. It is also important that one’s knowledge of the overlying tendons is not too rusty and may need refreshing. Classically examination has been taught using the steps, Look, Feel and Move. We believe that for the wrist (and in other joints used as short cases in exams) a different sequence is useful. We recommend one should, 1. Ask patients to point to (with a single digit) the most painful area. 2. Look. (And describe in exams.) 3. Test movements. (a) Ask the patient to do the passive movements that he/she can demonstrate themselves. (Giving clues to pain without causing consternation of examiners by hurting the patient.) (b) Ask patients to actively move joint in all directions. (c) Demonstrate passive movements not previously tested. 4. Feel and do special tests and manoeuvres. (In logical sequence of anatomy.) Special tests for clinical examination of the wrist have been considerably expanded in recent years and a careful examination usually suggests the diagnosis of the lesion provided time is taken to seek out the signs.2 The examination must always be made in comparison with the other side, looking for deformity but also, especially in the wrist,
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Figure. 1 Doctor sitting in front of the patient and inspecting the wrists.
looking for laxity since there is a large degree of normal variability in the joint. It goes without saying that the limbs are exposed to the elbow so that these too can be examined. The correct positioning is with the examiner seated opposite and quite close to the patient (Fig. 1). The patient must be able to rest forearms and elbows on the corner of the desk or on the arms of a chair with the shoulder and rest of the body relaxed. Since we have described palpation of the wrist in our previous article we will emphasise the three other main components of the examination process. Look, Move and Special Tests.
Inspection It is worthwhile asking, as the first step in examination, for the patient to indicate, using one finger, the exact location of maximum pain. This is often very accurate, particularly in chronic mechanical disruptions. It is not so good in acute injuries, when the haemarthrosis spreads the pain across the wrist, or in chronic inflammatory conditions. The senior author finds it helps in distinguishing mechanical problems, which may be amenable to surgery, from the chronic pain syndromes in which the patient fails to localise the pain. In these cases the authors suggest a lot of care when advising surgical treatment. It is also useful to warn a nervous examination candidate where not to grab and thus annoy the examiner! Inspection is best undertaken with the patient sitting opposite the examiner. It is worth holding the hands gently so one can turn the hands over to inspect both sides (Fig. 1). As with all joints one should look for universal changes such as scars and skin changes; however, there are some
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particular aspects unique to the wrist.3 Alignment and attitude are important. Radial deviation of the wrist can, for instance, indicate radial shortening or loss of radial slope following malunion of fractures. It can also indicate scapholunate dissociation in which the flexed scaphoid shortens the radial side of the carpus. Radial deviation of the carpus is also common in inflammatory arthropathies. Ulnar deviation is uncommon but prominence of the ulnar head is an important indicator of distal radio-ulnar joint (DRUJ) or ulnar-sided carpal pathology. The prominent ulnar head can be due to dorsal dislocation of the DRUJ but more commonly it indicates a normally placed ulnar head with a subluxed ulnar side and pronation of the carpus. In the rheumatoid wrist this latter situation is known as the Ulnar Caput Syndrome but similar deformity can be seen in TFCC tears. The overlying extensor carpi ulnaris (ECU) tendon is often more pronounced in this situation though even in the normally shaped wrist it is worth looking for this tendon since it is a common site of pathology. Looking at the wrist from the side, it is worth noting if there is either a dinner fork or reverse dinner fork deformity. Though this obviously can indicate malunion of distal radial fractures it can also indicate either a dorsal or volar intercalated segmental instability with carpal collapse or the subluxation found in inflammatory arthropathies. Some lumps are more common in the wrist than other joints, for instance ganglions and rheumatoid synovitis, which can be quite visible dorsally. Other lumps are less common but worth a search for. These include metacarpal bosses, which are bone prominences overlying most commonly the 2nd and 3rd carpo-metacarpal joints and the prominent proximal pole of the scaphoid seen in scapholunate dissociation, which is more prominent with the wrist flexed.
observe movement next. Passive extension and flexion is first assessed by sitting opposite the patient and asking them to follow the demonstrated actions. These demonstrated movements are tested by asking the patient to place his or her palms together and pushing, thus extending the wrists (Fig. 2A). This is repeated placing the back of the hands together and testing flexion (Fig. 2B). By doing this one can observe not only movement but also the limit due to pain and directly compare both sides. Next active movement is tested by again asking the patient to follow the demonstrated actions. Both wrists are assessed simultaneously and if necessary measured with a goniometer, though in most situations comparative movement is all that is needed. All movements are tested with the elbows flexed to about 901 and should include flexion/ extension, ulnar/radial deviation and pronation/ supination (Figs. 3A–3F). Extension should be observed with the metacarpo-phalangeal (MCP) joints flexed at 901 to negate the tenodesis effect of the flexor tendons. Likewise flexion should be tested with the MCP joints in extension to relax the long extensors. Radial and ulnar deviation are tested with the forearms placed in full supination and the hands rested on the table. Pronation and supination are tested with the elbows at right angles and tight into the patient’s side. Having tested these motions actively the passive range is assessed. It is sometimes useful to observe the patient making a fist and also circumducting the wrist,
Practice points: inspection
Ask patient to point at the most painful point. Observe alignment. Observe general conditions, scars, etc. Observe and describe lumps.
Movements Following inspection of the wrist the authors believe that with the wrist it is best practice to
Figure. 2 Passive movements: (A) extension and (B) flexion.
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Figure. 3 Active movements: (A) extension, (B) flexion, (C) radial deviation, (D) ulnar deviation, (E) pronation and (F) supination.
watching for ease of movement and listening for clicks.
Palpation and special tests Palpation and special tests in the wrist are probably best done at the same time. It is important to do the examination in a logical and repeatable sequence so as not to miss any part of the joint. Though in principle it is recommended to start with the pain-free regions, we believe that it is best to stay to the same tried and tested order. The authors recommend the following:
Distal radio-ulnar joint (DRUJ) and extensor carpi ulnaris (ECU) tendon Examination of the DRUJ involves testing for range of movement, pain, tenderness, instability and crepitus. The DRUJ is most lax in the mid range of pronation and supination.This is best elicited with the arm in the position as shown in Fig. 4A. The radius and the carpus are stabilised in mid rotation with the elbow on the desk and the distal ulna is
held between thumb and forefinger. Ballottement elicits laxity, crepitus and pain. It must be compared with the other side since there is a wide range of normality.1,3 Rotating the wrist into full pronation and supination results in tightening either of the volar or dorsal components of the TFC, respectively. This stabilises the DRUJ. Laxity on ballottement (Fig. 4B and 4C) in full rotation is abnormal and indicates loss of the stabilisers of the distal ulna.4 Practice points: stabilisers of the distal ulna The main soft tissue components necessary for stability are: 1. TFCC. 2. DRUJ capsule. Other extrinsic components that play a lesser role in stability include: 3. ECU tendon and its sheath. 4. Interosseous membrane. 5. Extensor retinaculum. 6. Pronator quadratus.
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Practice points: extensor tendon compartments Fibrous septae pass from the deep surface of the extensor retinaculum to the bones of the carpus, dividing the extensor tunnel into six compartments. From the radial (lateral) to the ulnar (medial) aspect, the compartments contain the following: 1. Abductor pollicis longus and extensor pollicis brevis. These tendons lie over the lateral aspect of the radius. 2. Extensor carpi radialis longus and extensor carpi radialis brevis. These tendons run on the radial aspect of the lister’s tubercle. 3. Extensor pollicis longus. This tendon passes ulnar to the lister’s tubercle. 4. Extensor digitorum communis and extensor indicis. 5. Extensor digiti minimi. This tendon overlies the DRUJ. 6. ECU. This tendon passes near the base of the ulnar styloid process.
The ECU is an unusual tendon in that it not only moves longitudinally but also sideways over the ulnar styloid when the forearm rotates. It is a common site of pain especially when there is a prominent ulnar head due to a subluxed carpus. One should palpate and feel it move with ones fingertip by asking the patient to rotate the wrist. Tenderness, swelling, instability and snapping can be observed.
Figure. 4 Examination of the distal radio-ulnar joint (DRUJ test) with forearm in different positions: (A) forearm in mid prone position, (B) forearm in full pronation and (C) forearm in full supination.
In many patients, however, instability is difficult to reproduce clinically. One often finds lack of rotation because further movement would produce pain and is resisted. This is similar to the provocation tests one sees in shoulder instabilities. The true extent of the instability may not be apparent until the patients are anaesthetised. When testing the DRUJ one should palpate the ECU tendon running in the sixth extensor compartment.5
Flexor carpi ulnaris, the pisiform bone and piso-triquetral joint The next part of the wrist to be examined is the ulnar-sided flexor mechanism which includes the flexor carpi ulnaris (FCU), the pisiform and the piso-triquetral joint. The piso-triquetral joint is a site of pathology, which is often missed and readily treatable. One also has to exclude pain in this joint before testing the lunotriquetral joint since both joints are stressed when testing the latter. The pisiform is similar to and has all the pathologies of the patella. These include fractures, chondromalacia osteoarthritis and instability. The bone lies within the tendon of flexor carpi ulnaris. The tendon is easily felt with the tip of the finger, which moves distally, testing for tenderness until the pisiform is encountered. The easiest position in
ARTICLE IN PRESS Examination of the wrist—soft tissue, joints and special tests which to do this is by holding the patients hand palm down and feeling the tendon and pisiform with the tip of the index finger (Fig. 5A). Pushing the ulnar border of the pisiform towards the mid line can test the piso-triquetral joint. This is helped by slightly flexing the wrist to increase the mobility of the joint. Equally feeling the tendon and asking the patient to push against resisted flexion and ulnar deviation the FCU tendon can be tested. The pisiform can also be palpated with the palm up and using the thumb and forefinger. The pisiform lies just distal to the ulnar end of the distal wrist crease. Examination (Fig. 5B) is performed by applying gentle thumb pressure on the pisiform towards the mid line or by grasping the bone between thumb and forefinger and moving it transversely both ways.1 Lunotriquetral joint: Having tested the pisotriquetral joint, the next site of examination is the lunotriquetral joint which is tested for pain, tenderness and instability. This is assessed by using Masquelet’s Ballottement test (Fig. 6). In this test the examiner’s thumbs are used to apply dorsal pressure on the lunate and the triquetrum while counter pressure is applied to these bones on the volar aspect by the examiner’s index fingers. The
Figure. 5 (A) and (B) Examination of the pisiform bone and the piso-triquetral joint.
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Figure. 6 Masquelet’s Ballottement test for the lunotriquetral joint.
index finger below the triquetrum will be on the pisiform so both bones are held in one hand and balloted against the lunate. A shear force is applied across the joint. Painful shearing or instability demonstrates ligamentous injury.1,3 Ulnar abutment: At this point it is worth testing for ulnar abutment. In this syndrome the distal ulnar head, impinges on the proximal and ulnar corner of the lunate in ulnar deviation. This is tested by forced ulnar deviation of the wrist producing pain in this area. The syndrome normally includes a central tear of the TFC, which is caught between the two bones. The abutment is tested in various degrees of flexion and extension. A visibly prominent ulnar head often does not cause abutment since it actually overrides rather than impinges on the carpal bones. It tends to occur in wrists where there is radial shortening but no tilt and occurs most commonly after trauma though it is also common in the congenital ulnar plus wrist. Triangular fibrocartilage complex (TFCC): Tears of the TFC are common but are often not painful. They can produce either pain due to catching of the cartilage or lesions of the entire complex may cause instability of the ulnar side of the wrist. Examination of the TFC structure has already been alluded to earlier in this article. If one sees a prominent ulna head this could be due to a TFC tear, which has resulted in subluxation of the ulnar side of the wrist. Likewise ballottement of the DRUJ can produce a painful click, which can be from a torn TFC. Unfortunately one cannot directly palpate the TFC due to the overhang of the distal ulna so all testing needs to be indirect. The TFC is examined (Fig. 7A) by resting the elbow on the table and one hand of the examiner supporting the patient’s forearm at the level of the distal radius and ulna. This hand clamps across both
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Figure. 7 (A) Examination of the triangular fibrocartilage complex and (B) scapholunate shear test.
radius and ulna allowing no movement at the DRUJ. The examiner performs a grinding test on the TFC. The other hand applies axial loading on the patient’s hand, keeping it in ulnar deviation i.e. compressing the TFC. The carpus is then pronated and supinated, and the TFC assessed for pain, clicking or both. If there is subluxation of the carpus reduction by lifting the carpus dorsally can produce pain or clicking from a torn TFC.1,3
The lunate After examining the TFC, one should palpate the lunate to exclude fractures or Kienbocks disease. As described in our first article, the lunate lies under the 4th extensor compartment and is much better palpated with the wrist in flexion, which brings the bone out from under the overhang of the distal radius. The scapholunate join: The next structure examined is the scapholunate joint. Palpation is performed by placing the tip of ones thumb in the crucifixion fossa. This recess lies about a centimetre distal to Lister’s tubercle. It is best located by holding the patients hand palm down and feeling
R.S. Reddy, J. Compson the tubercle with the thumb and then moving the tip distally until it falls into a soft recess, the crucifixion fossa. Flexion of the wrist produces the loss of the recess as the scapholunate joint and adjacent lunate and proximal pole of the scaphoid come out from under the overhang of the radius. Tenderness in this area indicates synovitis associated with either scapholunate joint laxity or disruption, or a proximal scaphoid fracture or nonunion. If the crucifixion fossa is difficult to palpate or there is already a hard lump present, this could be either a ganglion or the proximal pole of the scaphoid that is sitting high due to scapholunate dissociation. It must be remembered that small ganglions are the ones most likely to cause pain as they are imprisoned under the extensor retinaculum. Unfortunately both these and scapholunate dissociation are most painful in extension and radial deviation. Scapholunate pain and instability can be tested in several ways. The shear test (Fig. 7B) is done with one hand of the examiner holding the scaphoid at both ends, distally with the index finger over the scaphoid tuberosity, which is the most prominent lump on the volar and radial side of the wrist, and proximally the thumb over the proximal pole of the scaphoid in the crucifixion fossa. The other thumb is placed over the lunate dorsally and a shear force is applied to detect scapholunate instability.1,3 A grinding test can be used feeling for crepitus or a click and eliciting pain if present. As with any wrist examination the laxity needs to be compared with the normal side. Another method is Kirk Watson’s test, the scaphoid shift manoeuvre. This is used to test for scapholunate interosseous ligament injury. The patient is seated with the elbow rested on a table surface with the hand placed in full ulnar deviation and stabilised by the examiner holding the metacarpals (Fig. 8A). The examiner’s other thumb is placed firmly on the tubercle of the scaphoid and the wrist is moved into radial deviation (Fig. 8B). The scaphoid cannot flex because of firm pressure; however, this is overcome in the normal wrist by the scapholunate ligament which pulls the proximal pole of the scaphoid smoothly into the scaphoid fossa of the radius. If the ligament is disrupted, the proximal pole remains on the dorsal rim of the radius until it suddenly pops back into place.1,3 The scaphoid. The next part of the examination is to palpate the scaphoid as described in our previous article. This should include the proximal pole already palpated in the crucifixion fossa, the waist in the anatomical snuffbox (more easily felt in ulnar deviation) and the tubercle (Fig. 9A). Painful non-union of the scaphoid can also be
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Figure. 8 Sequence of the Kirk Watson’s test: (A) wrist in ulnar deviation and (B) wrist is moved into radial deviation with continued pressure on the scaphoid.
Figure. 9 Examination for scaphoid pathology: (A) palpating in the anatomical snuffbox and (B) grinding test—axial pressure along the 1st metacarpal with wrist in radial deviation.
tested by the grinding test, which is the axial loading of the first metacarpal and then twisting it but allowing the wrist to go into radial deviation (Fig. 9B).1,3 By stabilising the carpus the grinding test is also used to test for the 1st metacarpo-trapezial joint pathology. Crepitus can be felt in osteoarthritis of the carpo-metacarpal (CMC) joint of the thumb but infrequently in scaphoid non-union. The trapezium. Having tested the scaphoid the trapezium is palpated including the tubercle and ridge as described in our previous article. Carpo-metacarpal joints (CMC). Once the trapezium has been palpated the CMC joints of all the digits are examined. One should palpate them for subluxation and lumps (bony or ganglions) and test them for movement, pain and in the thumb for instability. The dorsum of the first metacarpal is followed proximally until the overhang at the level of the CMC joint is noted. The joint itself is better identified by opposing the patient’s thumb. Subluxation is noted. If a longitudinal force is now passed through the shaft of the metacarpal, instability may be detected. This can sometimes
be enhanced by translation. Testing for instability due to rupture of the Beak ligament is difficult and both sides need to be compared. To test for wear in the joint, a grind test is performed in which the trapezium is stabilised with one hand and the metacarpal is moved transversely and rotated (Fig. 10A), feeling for crepitus.1,3 In a similar fashion the joints between the 2nd metacarpal and trapezoid, the 3rd metacarpal and capitate and the 4th and 5th metacarpals and the hamate are tested for pathology. Unique to the 2nd and 3rd metacarpals are bosses found overhanging the CMC joints. Theses are either just pure bony lumps or have associated ganglions. Though not tender, pain can be elicited from them by extending the relevant metacarpals or by asking the patient to sublux one of their extensor tendons over the lump. Movement of the CMC joints increases from the index to the little finger as does the ability to note crepitus or stability. Hook of hamate: Even in chronic pain, one should always test for tenderness of the hook of hamate especially if the patient complains of pain in the palm. Pain secondary to an acute fracture or
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Figure. 10 (A) Examination of the first carpo-metacarpal joint and (B) examination of the hook of hamate.
The modified Fisk’s forward shift test (Pseudostability test): This test (Fig. 11) is devised to show non-specific pathology in the wrist. The patient must be very relaxed with the wrist in neutral position. Assess the laxity by comparing with the normal side. The examiner firmly grips on the distal forearm and with the other hand grasps the CMC joints. The hand is then pressed firmly palmarwards. Normally there must be palmar translation of about a centimetre and if there is any acute pathology in the wrist, this normal translation will not happen due to spasm of the muscles. The presence of pseudostability is important and is an equivalent to the apprehension sign as seen in patellofemoral instability or in shoulder instability.3 Midcarpal joint stability tests: The last tests performed on the wrist are tests for midcarpal instability. These must always be done in comparison with the normal side and in some cases also looks for general joint instability. The difficulty is that many wrists are naturally very lax and click and thus interpretation is difficult especially in non-traumatic cases. This one is best left to the experts! The tests include: The anteroposterior drawer test: One of the examiner’s hands holds the patient’s hand and applies axial traction (Fig. 12) while the other hand stabilises the patient’s forearm. An anteroposterior force is applied and a reduction is elicited at the radio-carpal and the midcarpal joint. Pivot Shift test: This test consists of supinating and volar subluxing the distal row of carpus (Fig. 13A and B). The patient’s elbow is flexed to 901, hand is fully supinated and the distal forearm is held firmly maintaining the wrist in neutral position. The hand is initially moved into full radial deviation and the ulnar side of the carpus is forced
Figure. 11 Modified Fisk’s forward shift test.
non-union of the hook of hamate can be an elusive cause of wrist pain. It can be examined (Fig. 10B) by placing the thumb on the pisiform and then moving approximately 1–2 cm distally and radially along a line joining the pisiform to the neck of the 2nd metacarpal. Simultaneous pressure is applied on the dorsal and ulnar aspect of this bone with the index and middle fingers.1
Figure. 12 Anteroposterior drawer tests for radio-carpal and midcarpal joint instability.
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Practice points: order for palpation and special tests
Figure. 13 Pivot shift test for midcarpal joint instability: (A) hand is moved into full radial deviation and ulnar side of the carpus is forced into further supination and volar subluxed position and (B) the hand is now moved from radial deviation into ulnar deviation.
into further supination and volar subluxed position. The hand is now moved from radial to ulnar deviation, the distal row snaps back painfully into position. Midcarpal instability secondary to excessive ligamentous laxity will allow the capitate to volarly sublux from the lunocapitate fossa and this snaps back painfully into position during this manoeuver.1,3
Examine DRUJ and ECU. Examine and palpate flexor carpi ulnaris, pisiform bone and piso-triquetral joint. Palpate triquetrum Perform ballottement test for lunotriquetral joint Test for ulnar abutment. Examine TFCC. Palpate for lunate tenderness. Palpate scapholunate joint and perform tests for instability. Palpate scaphoid. Palpate trapezium. Examine CMC joints in order. Palpate the hook of hamate. Fisk’s forward shift test. Perform midcarpal instability tests.
References 1. Weinzweig J, Watson KH. Examination of the wrist. In: Weinzweig J, Watson KH, editors. The wrist. Philadelphia: Lippincott Williams & Wilkins; 2001. p. 48–59. 2. Saffar P. Clinical examination of the wrist. In: Saffar P, editor. Carpal injuries, anatomy, radiology, current treatment. Paris: Springer; 1990. p. 11–6. 3. Rex C. Examination of wrist. In: Rex C, editor. Clinical assessment and examination in orthopaedics. New Delhi: Jaypee Brothers Medical Publishers (P) Ltd.; 2002. p. 47–55. 4. Imbriglia JE, Clifford JW. Management of the painful distal radioulnar joint. In: Weinzweig J, Watson KH, editors. The wrist. Philadelphia: Lippincott Williams & Wilkins; 2001. p. 369–74. 5. Hoppenfeld S, DeBoer P. The Wrist and hand. In: Hoppenfeld S, DeBoer P, editors. Surgical exposures in orthopaedics: the anatomic approach. Philadelphia: Lippincott Williams & Wilkins; 2003. p. 182.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 190–195
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MINI-SYMPOSIUM: THE WRIST
(ii) Management of Peri-Trapezial Osteoarthritis J.W.K. Harrison, N.R.M. Fahmy Department of Orthopaedics, Hand Surgery Unit, Stepping Hill Hospital, Poplar Grove, Stockport SK2 7JE, UK
KEYWORDS Peri-traperial arthritis; Clinical features; Classification; Treatment
Summary The trapeziometacarpal joint or first carpometacarpal joint (CMCJ) is the commonest site of osteoarthritis in the hand causing considerable pain and disability. It most commonly affects post-menopausal females. One in four females over 40 may have radiographic evidence of changes to the trapeziometacarpal joint although most are asymptomatic. Careful clinical examination and radiographic studies will diagnose both the arthritis and the affected joint. The various surgical options generally produce satisfactory results. Therefore, other factors such as the length of the surgery and time for recovery may be important. & 2005 Elsevier Ltd. All rights reserved.
Anatomy The articulation of the trapezium includes the trapeziometacarpal, triscaphoid (scaphotrapezial, scaphotrapezoid and trapeziotrapezoid) and trapezial-second metacarpal base joints (Fig. 1). The trapeziometacarpal joint has been mainly studied. It is saddle-shaped (biconcavoconvex) allowing flexion, extension, abduction, adduction, opposition and retropulsion. During pinch grip there is combined flexion, adduction and pronation. There is minimal bony constraint of the joint and static stability is dependent on ligaments. The beak ligament (volar oblique or anterior oblique ligament) is the primary static stabiliser preventing dorsal subluxation of the metacarpal in pinch grip and allows rotational motion.1 It is intracapsular Corresponding author. Hand Surgery Unit, Stepping Hill
Hospital, Poplar Grove, Stockport SK2 7JE,UK. E-mail address:
[email protected] (J.W.K. Harrison).
and originates from the volar–ulnar corner of the trapezium and attaches to the volar beak of the base of the thumb metacarpal. It is important in the mechanism of the Bennett’s fracture-dislocation where there is avulsion of a fragment of bone from the volar–ulnar corner of the metacarpal base with subsequent dorso-radial displacement of the metacarpal. Due to the strength of the beak ligament a pure dislocation is very unusual. The dorsal ligament is thin and reinforced by the abductor pollicis longus. The lateral ligament is a broad band running from radial surface of trapezium to the thumb metacarpal base.
Pathophysiology Primary arthritis in post-menopausal women is the most common cause of degenerative disease of the trapeziometacarpal joint. A study has shown
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Figure 1 (a) Trapeziometacarpal joint OA and (b) Pan-Trapezial OA.
radiological evidence of osteoarthritis of the trapeziometacarpal joint in 25% of post-menopausal women and of the triscaphoid joint in 2% although only 28% of these were symptomatic.2 It is thought that attritional changes in the beak ligament lead to ligament laxity and destabilisation of the joint. This is supported by the demonstration of a decrease in strength of the ligament with age.3 Hypermobility and instability of the trapeziometacarpal joint are a common finding in young women and this finding has been linked to the development of arthritis although mainly by circumstantial evidence.4 Other factors include secondary degeneration following trauma such as with Bennett’s or Rolando fractures and obesity.5 It is thought that laxity of the trapeziometacarpal joint leads to abnormal shear forces across the articular surface causing cartilage wear and degenerative changes. The trapeziometacarpal joint is incongruent with contact mainly occurring on the volar surface during flexion–adduction activities of the thumb.6 Studies have suggested degeneration is initiated on the volar surfaces of the joint and progresses dorsally with more advanced disease.7 A more recent cadaveric study looking at the pattern of articular cartilage wear has suggested wear is initiated on the radial quadrants of the metacarpal articular surface and progresses to the volar quadrants with advancing disease, while wear is initiated on the dorsal–radial quadrant of the trapezium and progresses to the volar quadrants in late-stage osteoarthritis.8 The area of wear is greater on the trapezium than the metacarpal base suggesting translation occurs during movement of
the joint. In more advanced disease eburnation affects the whole joint surface and rim osteophytes develop. Carpal tunnel syndrome commonly occurs with peri-trapezial osteoarthritis due to effusion from the degenerate joints on the volar aspect of the carpus causing compression in the tunnel.
Clinical features Patients typically present with pain at the base of the thumb. Commonly there may have been a history of minor trauma causing continuing pain. They may complain of weakness on power grip and pinch grip, as well as stiffness. On examination there is prominence of the base of the thumb metacarpal due to adduction of the trapeziometacarpal joint and osteophytes. True subluxation of the joint is rare due to the strength of the beak ligament and if present occurs late in the disease with attrition of the ligament. The adduction deformity of the thumb metacarpal leads to a contracture of the first web space and compensatory hyperextension of the thumb metacarpophalangeal joint. There may be tenderness to the volar aspect of the base of the thumb. Tenderness over the dorso-radial aspect of the wrist suggests arthritis in the triscaphoid joint. The range of movement of the thumb metacarpal should be recorded and painful laxity sought by attempting to sublux the joint in the dorso-volar and radio-ulnar planes. Provocation tests may
ARTICLE IN PRESS 192 cause pain and crepitus. These include the grinding test with axial loading and circumduction of the thumb, and the crank test with axial loading during flexion and extension at the CMCJ. These should be compared with the opposite side. The distraction test is used to assess for painful ligament laxity. The examiner pulls on the thumb distracting and rotating the trapeziometacarpal joint. The triscaphoid joint is involved with movements of the wrist, specifically flexion and extension of the scaphoid during volar and radial deviation of the wrist. Therefore pain during these movements with a negative grinding test would suggest triscaphoid arthritis whereas a positive grinding test and pain on wrist movements would suggest pan-trapezial arthritis. The condition should be differentiated from De Quervain’s tenosynovitis which causes tenderness and crepitus of the extensor pollicis brevis and abductor pollicis longus tendons in the first extensor compartment although both conditions have a positive Finklestein’s test. Antero-posterior and lateral radiographs may show narrowing of the joint space, subchondral sclerosis, osteophytes and subluxation of the joint. A Robert’s view may be taken with full pronation of the forearm and internal rotation of the shoulder. Eaton and Littler static loading views may be obtained in difficult cases to show joint space narrowing and where instability is suspected. A PA view is taken with the thumb tip pinching on the tip of the index finger. There may be a role for ultrasonography in early cases to show a joint effusion before radiographic changes are present.9 MR scanning may be useful in younger patients in assessing injury to the ligaments.
Classification The condition has been classified into 4 stages.10 This is a radiographic classification although the severity of the disease may not correlate with the radiographic appearance. (I) Mild joint narrowing or subchondral sclerosis with joint hyperlaxity. (II) Joint narrowing with subchondral sclerosis and mild subluxation which is passively correctable. (III) Loss of joint space with osteophyte formation to the ulnar side of trapezium and cystic changes. Unable to reduce subluxation of joint and hyperextension deformity to MCPJ. (IV) As stage III with destruction of scaphotrapezial joint.
J.W.K. Harrison, N.R.M. Fahmy
Treatment There are few large randomised, controlled studies comparing the different treatments for osteoarthritis of the thumb. However surgical treatment when appropriate generally produces excellent results with pain relief and near normal function so other factors such as length of the surgery and speed of recovery may be important. Conservative treatment is indicated for patients with few limitations to activities of daily living (cooking, dressing and writing). In early disease (Stage I/II) non-steroidal anti-inflammatory drugs may be used. These are combined with physiotherapy and splinting to maintain the first web space. This aims to strengthen the thenar muscles and to modify activities to avoid positions leading to thumb metacarpal adduction and possibly subluxation of the joint. However in practice few patients are able to tolerate splinting and there will be limited compliance. The joints are subcutaneous and are easy to inject. However a steroid injection should be performed under image intensifier control to confirm correct placement. The long-term effectiveness of this is unpredictable with some patients deriving only a few hours of relief and some several years. In patients with painful laxity but no arthritic changes who do not settle with conservative treatment, ligament reconstruction may be used. This involves the use of flexor carpi radialis, abductor pollicis longus or extensor carpi radialis longus tendons to reinforce the beak ligament. Part of the tendon is generally split from its insertion and passed through a hole drilled through the base of the thumb metacarpal. Studies have shown 97% good or excellent results at average 5.2 years follow-up.11 An alternative option is a radially orientated closing wedge basal osteotomy of the thumb metacarpal bringing the thumb into abduction. This aims to concentrate loading of the trapeziometacarpal joint more dorsally and has had good results reported with complete pain relief in 50% of cases in one study and a successful result in 11 of 12 cases in another.12,13 In patients with osteoarthritis of the base of thumb joint (Stages II–IV) conservative treatments may again produce relief of symptoms. However if pain is disabling and conservative measures fail surgery should be considered. Trapeziectomy alone has produced excellent results with pain relief and improved grip and pinch strength.14,15 The capsule/ periosteal sleeve should be carefully dissected off the trapezium to allow repair of the capsule at the end of the procedure and attention should be
ARTICLE IN PRESS Management of peri-trapezial osteoarthritis directed to completely excising the trapezium especially between the thumb and second metacarpal bases. There is concern that simple trapeziectomy may cause dorsal subluxation of the metacarpal and loss of trapezial height leading to weakness of grip, pain and adduction deformity. This has lead to the development of procedures to prevent this subluxation and to maintain the trapezial space. Despite this there are no good studies showing improved results of more complicated procedures over trapeziectomy.16 Furthermore a study comparing trapeziectomy, tissue interposition and ligament reconstruction has shown no difference in trapezial height and that the resultant trapezial height is related to the pinch strength at a follow-up of 1 year.17 It should be noted in the above study a k-wire was passed from the thumb metacarpal to the scaphoid to maintain temporary distraction with all three procedures. Attempts to maintain the trapezial height lead to the use of interposition arthroplasty using a silicone implant. This produced excellent short-term results. However concerns regarding high rates of synovitis and radiological signs of loosening have led to a decreased use of the procedure although studies suggest most patients with signs of loosening were asymptomatic.18 Trapezial excision with ligament reconstruction and tendon interposition (LRTI) has produced
193 excellent results using either the flexor carpi radialis (FCR) or adductor pollicis longus (APL) tendons.19,20 A strip of the APL tendon from the insertion into the metacarpal base is used, or the whole or a strip of FCR. A suspensory ligament reconstruction is performed to reinforce the intermetacarpal ligament and prevent subluxation of the thumb metacarpal base. The tendon interposition is then performed by rolling up the remaining tendon and inserting this into the trapezial space to act as a spacer (Fig. 2). However two randomised studies have shown no difference in outcome with or without tendon interposition following trapeziectomy and ligament reconstruction.21,22 This is a time-consuming procedure and there is not yet any compelling evidence that ligament reconstruction produces better results than simple trapeziectomy or arthrodesis. The complexity of LRTI with no convincing evidence of improved results has lead to the use of simpler techniques. Trapeziectomy and k-wire distraction is quick to perform and has shown excellent results with 92% pain free at 24 months.23 The trapezium is excised piecemeal and a k-wire passed between the distracted first metacarpal base and the second metacarpal. This provides decompression of the joint and allows healing between the metacarpal bases for the 5 weeks before wire removal. At 24 months follow-up the trapezial height was less than for ligament
Figure 2 (a) Trapeziectomy (b) trapeziectomy with ligament reconstruction and tendon interposition using FCR.
ARTICLE IN PRESS 194 reconstruction studies but greater than for trapeziectomy alone. Our chosen technique is a further modification of the distraction technique. The trapezium is carefully dissected from its capsule and excised whole. Approximately a third of the excised trapezium is wrapped in Spongostans (Johnson & Johnson, Skipton, UK) and reinserted into the trapezial space. The capsule is carefully repaired and the thumb metacarpal is distracted and held in abduction with two 1.6 mm k-wires passed between the thumb and second metacarpals (Fig. 3). The advantages are maintenance of trapezial height to allow good pinch strength and rapid recovery of function following removal of kwires at 6 weeks. A review of the 51 patients treated by this method at mean follow-up of 15 months (range 4–44 months) has shown excellent results in 89% of cases. There have been no episodes of deep infection from necrosis of the bone nucleus which has not been shown to be resorbed. In younger higher demand patients trapeziometacarpal arthrodesis has been suggested to maintain good pinch grip strength. The trapeziometacarpal joint alone must be involved as preexisting osteoarthritis of the triscaphoid joint may lead to continuing pain. Furthermore, there is concern that the increased strain on adjacent joints may lead to the development of pantrapezial osteoarthritis.24 Studies have shown excellent results for trapeziometacarpal arthrodesis with complete pain relief in 70% of 48 patients at mean follow-up of 90 months.25 However there was a non-union rate of 30% and increased incidence of
J.W.K. Harrison, N.R.M. Fahmy scaphotrapezial OA and this study was not in favour of arthrodesis. Another study showed similar results comparing arthrodesis to trapeziectomy and ligament reconstruction. However there was an increased complication rate with arthrodesis but this did not seem to affect outcome.26 A total carpometacarpal joint replacement arthroplasty generally consists of cemented trapezial and stemmed metacarpal components. These have shown excellent short-term results. However high rates of loosening and dislocation have been reported in the longer term.27
Triscaphoid and pantrapezial arthritis Any arthroplasty of the base of the thumb for pantrapezial arthritis will require trapezial excision otherwise symptoms will continue and may even worsen due to the increased forces on surrounding joints with certain procedures. A limited fusion of the triscaphoid joint for arthritis is not advisable due the restriction to wrist movements this would cause.
Complications of surgery With accurate pre-operative diagnosis the vast majority of patients improve following surgery. Injury to the superficial branch of the radial nerve can result in a painful neuroma and an area of paraesthesia. Complex regional pain syndrome
Figure 3 (a) Post-operative radiograph of trapeziectomy with k-wire distraction and reinsertion of bone nucleus showing good distraction and (b) at 6 weeks following removal of wires.
ARTICLE IN PRESS Management of peri-trapezial osteoarthritis (Type I) can occur following surgery and requires urgent physiotherapy. Correction of the adduction deformity of the thumb metacarpal following surgery will generally correct any hyperextension of the thumb metacarpophalangeal joint due to effective lengthening of the flexor pollicis longus. However continuing hyperextension requires surgical correction. The simplest option is a stabilisation of the joint in slight flexion. Alternatively a volar plate advancement can be performed or fusion of the radial sesamoid of the flexor pollicis brevis to the base of the thumb metacarpal.
References 1. Pellegrini Jr. VD, Olcott CW, Hollenberg G. Contact patterns in the trapeziometacarpal joint: the role of the palmar beak ligament. J Hand Surg [Am] 1993;18(2):238–44. 2. Armstrong AL, Hunter JB, Davis TR. The prevalence of degenerative arthritis of the base of the thumb in postmenopausal women. J Hand Surg [Br] 1994;19(3):340–1. 3. Najima H, Oberlin C, Alnot JY, Cadot B. Anatomical and biomechanical studies of the pathogenesis of trapeziometacarpal degenerative arthritis. J Hand Surg [Br] 1997;22(2): 183–8. 4. Eaton RG, Littler JW. Ligament reconstruction for the painful thumb carpometacarpal joint. J Bone Joint Surg [Am] 1973;55(8):1655–66. 5. Haara MM, Heliovaara M, Kroger H, Arokoski JP, Manninen P, Karkkainen A, Knekt P, Impivaara O, Aromaa A. Osteoarthritis in the carpometacarpal joint of the thumb. Prevalence and associations with disability and mortality. J Bone Joint Surg [Am] 2004;86-A:1452–7. 6. Ateshian GA, Ark JW, Rosenwasser MP, Pawluk RJ, Soslowsky LJ, Mow VC. Contact areas in the thumb carpometacarpal joint. J Orthop Res 1995;13(3):450–8. 7. Pelligrini Jr. VD. Osteoarthritis of the trapeziometacarpal joint: the pathophysiology of articular cartilage degeneration. II. Articular wear patterns in the osteoarthritic joint. J Hand Surg [Am] 1991;16(6):975–82. 8. Koff MF, Ugwonali OF, Strauch RJ, Rosenwasser MP, Ateshian GA, Mow VC. Sequential wear patterns of the articular cartilage of the thumb carpometacarpal joint in osteoarthritis. J Hand Surg [Am] 2003;28(4):597–604. 9. Iagnocco A, Coari G. Usefulness of high resolution US in the evaluation of effusion in osteoarthritic first carpometacarpal joint. Scand J Rheumatol 2000;29(3):170–3. 10. Eaton RG, Glickel SZ. Trapeziometacarpal osteoarthritis: staging as a rationale for treatment. Hand Clin 1987;3:455. 11. Lane LB, Eaton RG. Ligament reconstruction for the painful prearthritic’’ thumb carpometacarpal joint. Clin Orthop 1987;220:52–7.
195 12. Molitor PJ, Emery RJ, Meggitt BF. First metacarpal osteotomy for carpo-metacarpal osteoarthritis. J Hand Surg [Br] 1991;16(4):424–7. 13. Tomaino MM. Treatment of Eaton stage I trapeziometacarpal disease. Ligament reconstruction or thumb metacarpal extension osteotomy? Hand Clin 2001;17(2):197–205. 14. Dhar S, Gray IC, Jones WA, Beddow FH. Simple excision of the trapezium for osteoarthritis of the carpometacarpal joint of the thumb. J Hand Surg [Br] 1994;19(4):485–8. 15. Vandenbroucke J, De Schrijver F, De Smet L, Fabry G. Simple trapeziectomy for treatment of trapeziometacarpal osteoarthritis of the thumb. Clin Rheumatol 1997;16(3): 239–42. 16. Davis TR, Brady O, Dias JJ. Excision of the trapezium for osteoarthritis of the trapeziometacarpal joint: a study of the benefit of ligament reconstruction or tendon interposition. J Hand Surg [Am] 2004;29(6):1069–77. 17. Downing ND, Davis TR. Trapezial space height after trapeziectomy: mechanism of formation and benefits. J Hand Surg [Am] 2001;26(5):862–8. 18. Lanzetta M, Foucher G. A comparison of different surgical techniques in treating degenerative arthrosis of the carpometacarpal joint of the thumb. A retrospective study of 98 cases. J Hand Surg [Br] 1995;20(1):105–10. 19. Kaarela O, Raatikainen T. Abductor pollicis longus tendon interposition arthroplasty for carpometacarpal osteoarthritis of the thumb. J Hand Surg [Am] 1999;24(3):469–75. 20. Tomaino MM, Coleman K. Use of the entire width of the flexor carpi radialis tendon for the ligament reconstruction tendon interposition arthroplasty does not impair wrist function. Am J Ortho 2000;29(4):283–4. 21. Gerwin M, Griffith A, Weiland AJ, Hotchkiss RN, McCormack RR. Ligament reconstruction basal joint arthroplasty without tendon interposition. Clin Orthop 1997;342:42–5. 22. Kriegs-Au G, Petje G, Fojtl E, Ganger R, Zachs I. Ligament reconstruction with or without tendon interposition to treat primary thumb carpometacarpal osteoarthritis. A prospective randomized study. J Bone Joint Surg [Am] 2004;86: 209–18. 23. Kuhns CA, Emerson ET, Meals RA. Hematoma and distraction arthroplasty for thumb basal joint osteoarthritis: a prospective, single-surgeon study including outcomes measures. J Hand Surg 2003;28(3):381–9. 24. Carroll RE. Arthrodesis of the carpometacarpal joint of the thumb. A review of patients with a long postoperative period. Clin Orthop 1987;220:106–10. 25. Damen A, Dijkstra T, van der Lei B, den Dunnen WF, Robinson PH. Long-term results of arthrodesis of the carpometacarpal joint of the thumb. Scand J Plast Reconstr Surg Hand Surg 2001;35(4):407–13. 26. Hartigan BJ, Stern PJ, Kiefhaber TR. Thumb carpometacarpal osteoarthritis: arthrodesis compared with ligament reconstruction and tendon interposition. J Bone Joint Surg [Am] 2001;83:1470–8. 27. De Smet L, Sioen W, Spaepen D, Van Ransbeeck H. Total joint arthroplasty for osteoarthritis of the thumb basal joint. Acta Orthop Belg 2004;70(1):19–24.
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ARTICLE IN PRESS Current Orthopaedics (2005) 19, 196–208
www.elsevier.com/locate/cuor
MINI-SYMPOSIUM: THE WRIST
(iii) MR imaging of the wrist Philip Robinson Chancellor Wing X-ray, St. James University Hospital, Beckett Street, Leeds LS9 7TF, UK
KEYWORDS MR Imaging; MR Arthrography; Ultrasound; Wrist; Ligaments
Summary MR imaging is well established for the assessment of many areas of musculoskeletal disease however its accuracy for some wrist disorders is variable. The use and interpretation of MR imaging of the wrist must be performed with the knowledge of the technique’s relative strengths and limitations. MR imaging is an accurate and effective imaging tool for the diagnosis and grading of osseous and extracapsular soft tissue abnormalities of the wrist. Evaluation of intrinsic ligament abnormality of the wrist is difficult given the small size of these structures as well as the wide normal variance and incidence of asymptomatic defects. At present MR arthrography offers a more accurate imaging evaluation of the main intrinsic ligament complexes and cartilage of the carpus. & 2005 Elsevier Ltd. All rights reserved.
Introduction
MR techniques
MR imaging is well established for the assessment of many areas of musculoskeletal disease; however, its accuracy for some wrist disorders is variable.1–3 The use and interpretation of MR imaging of the wrist must be performed with knowledge of the technique’s relative strengths and limitations. This article will provide a pictorial review of wrist pathologies which often require MR imaging for diagnosis and staging. The procedures and techniques for optimal conventional MR imaging and MR arthrography will also be discussed.
Conventional MR imaging
Tel.: +44 113 206 4807; fax: +44 113 206 4587.
E-mail address:
[email protected].
In this context conventional means MR imaging performed without arthrographic injection although the patient may still receive intravenous contrast. There are a number of technical factors that result in difficulties for current MR imaging systems evaluating all wrist disorders to a high degree of accuracy. At the periphery of the bore of the MR scanner it is difficult to maintain a homogenous magnetic field. If the wrist is placed at the side of the body it is at the periphery of the magnetic field which in practical terms means that signal from the wrist can be distorted resulting in lower quality images. In MR imaging fat suppression techniques are often
0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2005.03.003
ARTICLE IN PRESS MR imaging of the wrist used to reduce fat signal and thus highlight pathological signal. However, if the wrist is by the patients side the magnetic field inhomogenicity results in patchy or complete loss of fat suppression making interpretation difficult. The main advantage of placing the hand at the side of the body is that motion artefact is reduced because this is usually a comfortable position for the patient. Alternative postures such as the ‘Superman’ position where the hand is held directly above the head mean that the wrist is now positioned in the centre and most homogenous area of the magnetic field. However, this position is not as comfortable and image quality can be considerably degraded by motion artefact negating any of the other perceived advantages. In my practice the hand is typically placed beside the patient to maintain comfort as each examination takes at least 25 min. Specialised sequences are used to try and combat inhomogenicity, for example, STIR sequences are less affected than other fat suppression techniques by magnetic field variance. Motion artefact can also be reduced by employing fast spin echo techniques instead of conventional spin echo sequences resulting in most examinations taking less than 25–30 min. Radiofrequency coils are used in MR imaging to place over and enhance signal from anatomical areas of interest. Again, this is a potential limitation for wrist imaging as few centres have a dedicated wrist coil leading to further compromises and modifications of other coils.4,5 The good news is that the new MR imaging systems have larger bores with homogenicity maintained throughout the entire magnet. Additionally, new sequences and multipurpose coils are now becoming available which enhance the signal and decrease the time of examination further so that in the immediate future the above limitations should become less relevant. A routine wrist MR examination should include scanning in the sagittal, axial and coronal planes. T1 weighted sequences can demonstrate normal osseous anatomy but it is the proton density and T2 weighted sequences (usually with fat suppression) which provide details of abnormality involving bone marrow, ligaments, cartilage and surrounding soft tissues.6,7
Figure 1 Painfull wrist after fall with a clinically suspected scaphoid fracture. (a) Plain radiograph appears normal. (b) Coronal T2w fat suppressed MR image shows bone marrow oedema in the capitate. (c) Coronal T1w MR image confirms the low signal fracture margins.
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Figure 2 Coronal T1w MR image shows carpal and radial styloid cortical erosions (black arrowheads). The ulnar styloid is markedly thinned (arrow) with a thickened and degenerate articular disc (white arrowhead) of the TFCC.
Conventional MR imaging is excellent at depicting bone marrow, muscle and tendon abnormality.3,7,8 Therefore this is the investigation of choice for radiologically occult fractures (Fig. 1) and sequelae (osteonecrosis) as well as globally evaluating the wrist and hand for inflammatory rheumatological disorders (Fig. 2). In my practice musculoskeletal ultrasound is the first investigation for the evaluation of wrist muscle and tendon abnormalities as well as soft tissue masses. If a mass is confirmed as a ganglion no further investigation is performed but if the mass appears complex on ultrasound then MR imaging can detail the exact position and surrounding anatomy prior to biopsy or resection. Intravenous gadolinium injection can yield additional information on the tissue characteristics of a mass or area of inflammation as well as producing angiographic detail without the need for intra-arterial catheterisation (Fig. 3).6,7 Currently, conventional MR imaging reaches its limits when evaluating the intrinsic ligaments and cartilage of the wrist.1,2,9 There are a number of reasons for this including the technical factors already described. The intrinsic carpal ligaments are extremely small (less than 2–3 mm) and the articular surfaces are markedly curved which makes precise and reproducible visualisation of
Figure 3 Reconstructed MR angiographic image showing the vessels of the wrist and hand with an arteriovenous malformation in the distal little finger (arrowheads).
normal structures difficult.1,9 It is because of these difficulties that arthrography in the form of MR arthrography is widely used in the assessment of ligament abnormalities.10
MR arthrography of the wrist There are two techniques for producing an arthrographic effect within the joint on MR imaging, namely direct and indirect MR arthrography.
Direct arthrography Direct MR arthrography involves direct injection of contrast into the joint and has largely developed
ARTICLE IN PRESS MR imaging of the wrist
Figure 4 Fluoroscopically guided injection (using a 23 gauge needle) into the radiocarpal joint prior to injection of gadolinium solution for MR arthrogram.
over the last decade offering a number of advantages over conventional MR imaging. The technique assesses complex anatomy through distension of the joint, bathing of internal structures with contrast and leakage into abnormal clefts or tears.10 Proposed disadvantages of intra-articular injection include that it is invasive with the potential complication of iatrogenic infection. In comparison to conventional MR imaging there is added time and expense with associated radiation exposure required to perform the injection (Fig. 4). However, ultrasound can now be used to guide needle placement, which greatly increases the speed of the procedure and removes the necessity for radiation exposure. In reality, with good technique the risk of infection is very low and the additional time and expense can be outweighed by the increased diagnostic accuracy, which can potentially remove the need for surgery or arthroscopy.
Figure 5 Rugby player with wrist pain and clinically suspected scapholunate ligament (SLL) tear. (a) Screening image during arthrography prior to MR imaging shows low attenuation contrast in the proximal carpal joint (arrow) but also flowing between the scaphoid and lunate (arrowhead) indicating a SLL tear. (b) Reconstructed coronal gradient echo MR arthrogram image shows high signal contrast outlining a normal lunotriquetral ligament (arrow) and defect of the SLL (arrowhead). (c) Axial T1w fat suppressed MR image at the level of the scaphoid (S) and lunate (L) shows an intact dorsal component of SLL (arrowheads) but an irregular and torn volar component (arrow). The player was treated conservatively.
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ARTICLE IN PRESS 200 Although saline has been used as a MR arthrographic contrast agent its main disadvantage is not being able to differentiate increased peri-articular signal due to saline leakage from extra-capsular soft tissue oedema.10 Therefore, it is generally accepted that intra-articular injection of gadolinium solution is the optimal contrast agent for joint assessment. Intra-articular injection of pure gadolinium causes marked signal loss and therefore a dilute solution (with saline) is necessary to produce optimal signal characteristics. At present, I prefer fluoroscopic guidance and iodinated contrast to confirm intra-articular position because the wrist can then be screened dynamically at injection which potentially adds to the information obtained from the subsequent MR arthrogram. MR imaging should usually begin within 30 min after intra-articular injection and the patient should not exercise the joint, as this will increase absorption of the gadolinium solution and decrease the amount of distension. Sequences typically performed include T1 weighted fat suppressed sequences, which emphasise the high signal gadolinium solution against the relatively low signal cartilage and ligamentous structures (Fig. 5). A T2 weighted sequence is always performed to assess for any soft tissue or bone marrow oedema. Volume acquisitions can also be performed so that very thin high-resolution slices (0.5–1 mm compared to 2–3 mm) can be reconstructed to view the components of the intrinsic ligaments (see below) (Fig. 5).7,10
Figure 6 Coronal T1w fat suppressed MR image post intravenous gadolinium shows an intact SLL (arrow) and TFCC (arrowheads). Note subchondral osseous bone marrow enhancement (*) of the lunate.
P. Robinson
Indirect arthrography Indirect MR arthrography is not widely practised in Europe and has largely been evaluated in North America.9 The technique involves intravenous injection of gadolinium and relies on the principle that gadolinium is weakly plasma protein bound. This property allows the contrast to diffuse from the blood vessels within the synovium into the actual joint space producing an arthrographic effect (Fig. 6). The ability for gadolinium to flow into the joint is decreased if there is already an effusion present, if the patient undergoes active exercise of that joint or if there is active synovitis. However, flow of gadolinium into the joint is increased if the joint undergoes passive exercise for 5–10 min before scanning commences.11
Figure 7 (a) Reconstructed coronal gradient echo and (b) axial T1w fat suppressed MR arthrogram images show the radiolunate ligament (arrowheads) between the lunate (L) and radial styloid (R).
ARTICLE IN PRESS MR imaging of the wrist In comparison to direct MR arthrography this technique’s ability to produce an arthrographic effect is less dependable and there is no significant distension of the joint (Fig. 6). It is also difficult to differentiate leakage of contrast from peri-articular enhancement because the contrast has been given intravenously. However, supporters of this technique argue that assessment of peri-articular contrast enhancement is an advantage and overall the technique is less invasive and considerably cheaper than direct arthrography. The decreased radiologist input is also thought to increase efficiency for the radiologist and MR scanner throughput.
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Ligament injuries The ligaments of the wrist can be classified as extrinsic (capsular) or intrinsic (inter-ossesous) with clinical and imaging investigations focussing on intrinsic ligaments abnormalities as a source of pain and instability. The exact contribution of specific extrinsic ligament abnormalities to wrist instability and pain is more controversial. One imaging study has defined the appearance of the extrinsic ligaments in cadavers using MR arthrography (Fig. 7).12 However, there are no reliable data detailing extrinsic ligament abnormalities or their significance, therefore I will focus on evaluating the intrinsic ligaments.7,13
Figure 8 (a) Coronal T1w fat suppressed MR arthrogram image shows a radial capsule tear and stranding (arrowheads). The SLL was normal. (b) Reconstructed coronal gradient echo MR arthrogram image shows a flap defect (arrow) of the radial articular cartilage. (c) Axial and (d) sagittal T1w fat suppressed MR images post intravenous gadolinium show extensive nodular dorsal synovitis (arrowheads).
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Scapholunate ligament The scapholunate ligament is the intrinsic intraosseous ligament that provides stability for the scapholunate articulation which in turn provides a large proportion of the stability of the wrist. There are three main components to the ligament with dorsal, volar and central portions.14 The dorsal component consists of collagen and fibrocartilage while the volar component consists of relatively looser connective tissue. The dorsal component is the strongest part and therefore damage to the volar or central portions in isolation can sometimes be treated conservatively (Fig. 5). A limitation of fluoroscopic arthrography is that any defect including a complete tear, partial tear or degenerative perforation allows iodinated contrast to flow between the scaphoid and lunate (Fig. 5). This is where MR imaging (usually MR arthrography) can refine the diagnosis by identifying these individual components in clinically suspected injury. MR arthrography can confirm an intact ligament complex or partial tear influencing the type of conservative treatment or surgical procedure performed (Fig. 5).10,15 MR arthrography can also identify alternative or concomitant sources of pain such as capsular ligament tears, synovitis and osteochondral injuries (Fig. 8).10,16 The interpretation of such ligament defects relies heavily on the clinical context as asymptomatic perforations or degenerative tears are common.1,17,18 It is always dangerous to routinely perform a MR imaging investigation hopefully searching for abnormality or with a clinical request
Figure 10 Reconstructed coronal gradient echo MR image shows the high signal radial cartilage undercutting the attachment (arrow) of the TFCC articular disc. Note also the high signal from the intact loose connective tissue (arrowhead) at the ulnar attachment.
of ‘wrist pain’. Interaction practitioner should result in examination to confirm or suspected injury and identify concomitant injuries.
with a specialised tailoring of the MR grade a clinically any other significant
Lunotriquetral ligament The lunotriquetral intra-osseous ligament, between the lunate and triquetrum, also contributes to proximal carpal stability. Like the scapholunate ligament it has three components with the dorsal component also slightly stronger than the volar component.19 The MRI appearances of the normal and abnormal lunotriquetral ligament complex are much more variable than with the scapholunate ligament.9,16,19,20 MRI studies report a wide range of accuracy for diagnosing abnormality in this region (Fig. 9).9,19 However, imaging of this structure alone is rarely performed because if suspected clinically the management consists of non surgical treatment with intervention reserved for chronic cases.
Triangular fibrocartilage complex (TFCC) Figure 9 Reconstructed coronal gradient echo MR arthrogram image shows an intact SLL (arrow) and torn lunotriquetral ligament (arrowhead).
The TFCC is a complex and dynamic anatomical structure consisting of an articular disc, radioulnar
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ligaments, meniscal homologue, extensor carpi ulnaris (ECU) tendon sheath, ulnolunate and ulnotriquetral ligaments. The structure is the primary stabiliser of the distal radioulnar joint and transmits 18% of all forces applied across the wrist. MR
Figure 12 Coronal T1w fat suppressed MR image post intravenous gadolinium shows synovitis of the distal radioulnar joint (arrowheads) underlying an intact TFCC (arrows).
imaging can accurately evaluate the articular disc, radioulnar ligaments and ECU sheath with variable visualisation of the meniscal homologue, ulnolunate and ulnotriquetral ligaments. 2,7,21,22 There are a number of imaging pitfalls in assessing this region most notably misdiagnosing the high signal undercutting of the radial attachment by articular cartilage or the loose connective tissue at the ulnar attachments as tears (Fig. 10).2,7 However, there are further pitfalls as central degenerative perforations are not uncommon over the age of 30.21,23,24 Use of these imaging techniques to answer a specific clinical query is again ideal (Fig. 11). Clinical series have also reported other significant causes of ulnar sided wrist pain including synovitis and cartilage damage (Fig. 12).
Figure 11 (a) Reconstructed coronal gradient echo MR arthrogram image shows scar tissue (*) replacing the TFCC with an old ulnar styloid fracture fragment (arrowhead). (b) Reconstructed coronal gradient echo MR arthrogram image shows a clinically asymptomatic scarred SLL (arrow). There is an intact articular disc (white arrowhead) but complete disruption of the ulnar attachment (black arrowhead) of the TFCC. (c) Coronal T1w fat suppressed MR arthrogram image shows a large tear of the articular disc (arrow) from the radial attachment (arrowhead) allowing contrast to flow into the distal radioulnar joint (*).
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Figure 13 Ulnar impaction syndrome. Coronal T2w MR image shows a central defect (arrowhead) between the radial attachment and main disc (large arrows). Note the lunate subchondral defects (small arrows).
Ulnar impaction This is a complex of abnormalities which result in chronic ulnar sided pain. Imaging features include positive ulnar variance, TFCC tear (usually central disc), lunotriquetral ligament defect and articular cartilage damage (Fig. 13).3 Identification is important as an ulnar osteotomy can correct the mechanical impairment and symptoms.
Osseous injury Conventional MR imaging provides an excellent assessment for fractures of the wrist not visible on plain radiographs.1,3,7 This most commonly relates to scaphoid fractures but also radiographically occult fractures of the capitate and hamate (Fig. 1).8 However, the current limited availability of MR imaging in the UK results in isotope bone scans usually being performed in clinically equivocal scaphoid fractures at 14 days.25 This is despite a number of studies establishing a financial benefit in reduced treatment costs and days missed from work for immediate MR imaging in radiograph negative cases.25 Bone scans are sensitive for fractures but can be non-specific (false positive 6–16%) showing increased activity with adjacent
Figure 14 Persisting pain after scaphoid fracture. (a) Coronal T1w MR image shows the fracture line (arrowheads) indicating non-union. There is low signal (*) from the adjacent bone marrow of the proximal pole. (b) Coronal T2w fat suppressed MR image shows the fracture line (arrowheads) but high signal (black *) from the marginal bone marrow. The bone marrow signal of the proximal aspect of the proximal pole is normal (white *).
soft tissue injuries. A limited MR examination can quickly establish the presence of a fracture but can also identify other soft tissue injuries without involving radiation. These associated injuries can include capsular tears, associated ligament or cartilage damage (Fig. 8). MR imaging is also sensitive for diagnosing and grading post traumatic complications such as nonunion and avascular necrosis.26,27 Most commonly,
ARTICLE IN PRESS MR imaging of the wrist
205 necrosis indicating the need for more aggressive surgical intervention. Physeal injury can occur in skeletally immature athletes particularly gymnasts. Chronic repetitive
Figure 15 Coronal T1w fat suppressed MR arthrogram image shows collapse of the lunate with contrast passing through an oblique cleft.
this relates to the proximal pole of the scaphoid after fracture and osteonecrosis of the lunate (Keinbocks disease) (Figs. 14 and 15). In the early stages of avascular necrosis radiographs are usually normal while isotope bone scans can be nonspecific remaining positive in the early and late stages of osteonecrosis. MR imaging has improved spatial resolution compared to isotope bone scanning and can evaluate early cystic change and fragmentation (Fig. 16).7,28 The presence of marrow oedema implies continued vascularity while low signal on all sequences implies complete osteonecrosis.7 Some studies have evaluated the use of intravenous gadolinium and subsequent enhancement characteristics of bone to try and further grade potential osteonecrosis. 27,29 Absence of enhancement or markedly decreased enhancement in the proximal pole compared to the distal pole of the scaphoid would suggest avascular
Figure 16 Dynamic intravenous gadolinium MR images of the scaphoid. (a) Precontrast MR image shows diffuse low signal bone marrow throughout the scaphoid with a central cyst (arrow). (b) Subsequent image shows contrast entering a wrist vein (arrows). (c) Subsequent image shows some minor subcortical (arrowheads) and cyst enhancement. However, the majority of the proximal (arrow) and distal (*) pole bone marrow does not enhance indicating necrosis.
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Figure 18 Ulnar sided symptoms. (a) Coronal T2w gradient echo and (b) axial T2w fat suppressed images show a cystic ganglion (*) arising from between the hamate (H) and lunate (arrow) decompressing into the distal palm.
Soft tissue masses Figure 17 Gymnast with wrist pain. Coronal (a) T2w fat suppressed and (b) T1w MR images show widening (*) of the radial physis and surrounding oedema (arrows) indicating physeal stress reaction.
loading of the wrist can lead to microfractures with the potential complication of premature fusion of the physeal plate.30 MRI can detect abnormality in this area when radiographs still appear normal (Fig. 17).30 Isotope bone scans were previously used to evaluate this condition but there is often increased uptake at the normal physis and a normal contralateral side for comparison cannot be depended on. However, the main disadvantage of isotope bone scanning for this condition is the considerable radiation dose involved.
Soft tissue masses around the wrist are most frequently ganglia arising from capsular defects in the extrinsic ligaments (Fig. 18). Ultrasound can often confirm the diagnosis and origin in the majority of clinically equivocal cases. However, if ultrasound confirms a solid mass this could still represent a complex ganglion but a more sinister soft tissue mass needs to be excluded (Fig. 19). In this situation MR imaging can help in further characterising the mass and the surrounding anatomy prior to biopsy or surgery. Specific sequences can identify the presence of fat, fluid, vessels or oedematous tissues within a mass (Figs. 3, 20 and 21). Intravenous gadolinium can also help to further characterise abnormality with non-enhancement occurring with fluid or avascular debris that can occur in complex ganglia or inflammatory masses
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Figure 20 Haemangioma of the wrist. (a) Coronal T1w MR image shows a soft tissue mass (arrows) containing high signal fat and low signal vessels. (b) Axial T2w fat suppressed MR image shows the vascular mass (arrow) abutting the first extensor compartment tendons (arrowheads) and radius (R, ulnar ¼ U).
(Fig. 19). Soft tissue tumours can have patchy areas of non-enhancement indicating areas of necrosis; however, the majority of the lesion still enhances markedly. For aggressive sarcomas the MRI appearances are usually non-specifc for histological type with heterogenous oedema and enhancement often present. Occasionally, tumours can be completely characterised, for example, lipomas, haemangiomas and giant cell tendon sheath tumours (GCTTS) (Figs. 20 and 21).
Figure 19 Complex mass on ultrasound. (a) Coronal T1w MR image shows an intermediate signal mass (*) arising from around the TFCC (arrowhead). (b) Coronal T2w and (c) T1w fat suppressed post IV gadolinium MR images show the contents as non-oedematous (arrows) and avascular debris (arrowheads) within a complex ganglion.
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Figure 21 Axial T1w MR image shows soft tissue enlargement of the median nerve (arrow) containing high signal fat consistent with a fibrolipohamartoma of the median nerve.
Conclusion MR imaging is an accurate and effective imaging tool for the diagnosis and grading of osseous and extra-capsular soft tissue abnormalities of the wrist. Evaluation of intrinsic ligament abnormality of the wrist is difficult given the small size of these structures as well as the wide normal variance and incidence of asymptomatic defects. At present, MR arthrography offers a more accurate imaging evaluation of the main intrinsic ligament complexes and cartilage of the carpus.
References 1. Miller RJ. Wrist MRI and carpal instability: what the surgeon needs to know, and the case for dynamic imaging. Semin Musculoskelet Radiol 2001;5(3):235–40. 2. Haims AH, et al. Limitations of MR imaging in the diagnosis of peripheral tears of the triangular fibrocartilage of the wrist. Am J Roentgenol 2002;178(2):419–22. 3. Oneson SR, et al. MR imaging of the painful wrist. Radiographics 1996;16(5):997–1008. 4. Totterman SM, et al. Two-piece wrist surface coil. Am J Roentgenol 1991;156(2):343–4. 5. Morley J, Bidwell J, Bransby-Zachary M. A comparison of the findings of wrist arthroscopy and magnetic resonance imaging in the investigation of wrist pain. J Hand Surg [Br] 2001;26(6):544–6. 6. Haims AH, et al. MRI in the diagnosis of cartilage injury in the wrist. Am J Roentgenol 2004;182(5):1267–70. 7. Sofka CM, Potter HG. Magnetic resonance imaging of the wrist. Semin Musculoskelet Radiol 2001;5(3):217–26. 8. Breitenseher MJ, et al. Radiographically occult scaphoid fractures: value of MR imaging in detection. Radiology 1997;203(1):245–50. 9. Haims AH, et al. Internal derangement of the wrist: indirect MR arthrography versus unenhanced MR imaging. Radiology 2003;227(3):701–7.
P. Robinson 10. Steinbach LS, Palmer WE, Schweitzer ME. Special focus session. MR arthrography. Radiographics 2002;22(5): 1223–46. 11. Schweitzer ME, et al. Indirect wrist MR arthrography: the effects of passive motion versus active exercise. Skelet Radiol 2000;29(1):10–4. 12. Theumann NH, et al. Extrinsic carpal ligaments: normal MR arthrographic appearance in cadavers. Radiology 2003; 226(1):171–9. 13. Totterman SM, et al. Intrinsic and extrinsic carpal ligaments: evaluation by three-dimensional Fourier transform MR imaging. Am J Roentgenol 1993;160(1):117–23. 14. Berger RA, Blair WF. The radioscapholunate ligament: a gross and histologic description. Anat Rec 1984;210(2): 393–405. 15. Scheck RJ, et al. The scapholunate interosseous ligament in MR arthrography of the wrist: correlation with non-enhanced MRI and wrist arthroscopy. Skelet Radiol 1997;26(5): 263–71. 16. Scheck RJ, et al. The carpal ligaments in MR arthrography of the wrist: correlation with standard MRI and wrist arthroscopy. J Magn Reson Imag 1999;9(3):468–74. 17. Linkous MD, Pierce SD, Gilula LA. Scapholunate ligamentous communicating defects in symptomatic and asymptomatic wrists: characteristics. Radiology 2000;216(3): 846–50. 18. Timins ME, et al. MR imaging of the wrist: normal findings that may simulate disease. Radiographics 1996;16(5): 987–95. 19. Smith DK, Snearly WN. Lunotriquetral interosseous ligament of the wrist: MR appearances in asymptomatic volunteers and arthrographically normal wrists. Radiology 1994;191(1): 199–202. 20. Smith DK. MR imaging of normal and injured wrist ligaments. Magn Reson Imag Clin N Am 1995;3(2):229–48. 21. Miller RJ, Totterman SM. Triangular fibrocartilage in asymptomatic subjects: investigation of abnormal MR signal intensity. Radiology 1995;196(1):22–3. 22. Oneson SR, et al. MR imaging diagnosis of triangular fibrocartilage pathology with arthroscopic correlation. Am J Roentgenol 1997;168(6):1513–8. 23. Metz VM, et al. Age-associated changes of the triangular fibrocartilage of the wrist: evaluation of the diagnostic performance of MR imaging. Radiology 1992;184(1): 217–20. 24. Zanetti M, et al. Characteristics of triangular fibrocartilage defects in symptomatic and contralateral asymptomatic wrists. Radiology 2000;216(3):840–5. 25. Raby N. Magnetic resonance imaging of suspected scaphoid fractures using a low field dedicated extremity MR system. Clin Radiol 2001;56(4):316–20. 26. Munk PL, Lee MJ. Gadolinium-enhanced MR imaging of scaphoid nonunions. Am J Roentgenol 2000;175(4): 1184–5. 27. Munk PL, et al. Gadolinium-enhanced dynamic MRI of the fractured carpal scaphoid: preliminary results. Australas Radiol 1998;42(1):10–5. 28. Steinbach LS, Smith DK. MRI of the wrist. Clin Imag 2000; 24(5):298–322. 29. Cerezal L, et al. Usefulness of gadolinium-enhanced MR imaging in the evaluation of the vascularity of scaphoid nonunions. Am J Roentgenol 2000;174(1):141–9. 30. Shih C, et al. Chronically stressed wrists in adolescent gymnasts: MR imaging appearance. Radiology 1995;195(3): 855–9.
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ORTHOPAEDIC INFORMATION
Digital imaging for orthopaedic surgeons Lennard Funk Hope Hospital, Eccles Old Road, Salford M6 8HD, UK
KEYWORDS Digital photography; Pixels; Storage media; Image processing
Summary The age of digital photography and video is well upon us now. Most surgeons use digital cameras, DVDs and digital camcorders in their personal lives. Most surgeons have also tried to apply digital photography in their clinical practice for recording interesting cases, teaching purposes and as part of clinical records. However, this technology is still fairly new and advancing at rapid pace. The particular requirements for Orthopaedics, such as photographing radiographs and operative images, are not usually addressed by the automatic settings of digital cameras. This paper is aimed at those surgeons with digital cameras and imaging equipment, who want to maximise and improve their technique in digital photography in the setting of Orthopaedic and Trauma surgery. I am no expert in photography (digital or otherwise). Nor do I put forth this content as fully verified and error-free, although I try very hard to make it so. My goal here is simple—to share what I have learned through experience and cross-checked reading in a rapidly growing and developing field, still rather poorly documented by the vendors and mainstream publications. & 2005 Elsevier Ltd. All rights reserved.
Introduction This paper deals with the following common difficulties: 1. Why do I need digital photographs? 2. Which camera should I buy? 3. How do I best photograph Operations and Clinical subjects? 4. How do I best photograph X-rays? 5. How do I e-mail, print and publish Images? 6. How should I Store & Manage images?
E-mail address:
[email protected].
Before proceeding there are a few terms requiring clarification 1. Exposure: Relates to the brightness of an image. It represents the length of time the camera film or CCD (charge coupled device, which recovers the image in digital camera) is ‘exposed’ to light. The darker the environment you are photographing, the longer you need to expose the film to the ambient light to get a good image. 2. Exposure Compensation: The amount you increase or decrease the exposure is specified in ‘‘stops.’’ One ‘‘stop’’ increase represents a
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doubling of the amount of light reaching the film. You specify +1 to open the aperture or slow down the shutter speed and –1 to achieve the converse. It is easy to use exposure compensation because you can preview your changes on the LCD camera’s monitor. I would recommend an EC (exposure compensation) of 2 for Xrays, where an extremely dark background occupies a very large part of the image and you want to retain detail in the brighter parts of the scene. You can alter this according to your camera and requirements. 3. ISO Equivalent: ISO is the sensitivity of traditional films to light. A high ISO film (or ISO equivalent in digital cameras) is more suitable for low light conditions, but the image becomes more ‘grainy’. Therefore one should have the option of different ISO Equivalents in a digital camera. 4. Spot metering: Metering is the determination of the amount of light entering the camera, which is used to determine focus and exposure settings. This can be an average reading of the entire image or a reading of a small section of the image, within the central portion-so-called ‘‘spot metering’’.
How do I best photograph operations/ clinical subjects?
Why do I need digital photographs?
Orthopaedics is a very visual specialty and every aspect of our work requires some form of imaging. This includes clinical care, education, research and medicolegal work. The inclusion of a visual record is of great benefit to all concerned in a patient’s care—a picture is worth a 1000 words.
These are a few tips gleaned from medical photographers and bitter experience.
Which camera should I buy? The best you can afford is the simple answer, though there are some specific features you require when using a Digital Camera for Orthopaedic purposes. These include
At least 3 Megapixels image capacity—the current minimum requirement for publication (see below). Macro facility of about 8 cm—for clinical photographs and X-rays. Attachment for Tripod—improves the sharpness when photographing radiographs Manual override—for manual focus, manual exposure control is particularly useful for radiographs and operative photographs.
Preview image facility—on an LCD screen allows you to immediately assess the quality of the photographed subject and then readjust the settings appropriately for subsequent shots. Flash control—flash intensity often has to be reduced for operative photographs. An external hand-held flash or option for a ring flash is ideal for operative photographs, allowing light to wash the subject without unwanted shadows.
Move the operating lights lights off the subject, so as to use flash only. Clear away blood and any metal glare—glare is accentuated in most digital images. Change bloody swabs for clean ones—this will reduce glare and improve exposure control. Compose the shot carefully to ensure that what you want to demonstrate is shown. You may never get the opportunity again. Shoot a perspective shot, showing the entire limb or surgical area. Often when looking at a close-up of a surgical site later the orientation can be lost without a perspective view. Shoot from different angles. Hold camera with two hands. Shove the surgeon out of the way! Optimising exposure for clinical and operative images J Slow ‘film speed’—low ISO Equivalent (ISO 100)—this improves the sharpness and brightness of an often shadowy image. J Use a flash—Handheld preferable. J Alter flash strength—the automatic settings are often too bright. Look for a camera that will allow you to do this. J Spot meter on mid-tone area or meter off the palm of your hand. If in doubt expose for the highlights, to avoid white-outs, and plan to bring up the shadows in post-processing as needed. Focus J Manual focus is preferable. This is especially useful when photographing in a deep wound, such as in shoulder surgery. J Focus and compose: If you do not have manual focus then focus on the part of the image you want sharp, hold the shutter
ARTICLE IN PRESS Digital imaging for orthopaedic surgeons button half-way down, then move the camera to compose a good image, and then push the shutter button all the way down. Most cameras allow this technique.
211 One should appreciate the advantages of common file formats, which can be utilised to aid these processes. Below is a table summarising the qualities we need to be aware of. Common File Formats
Tips for photos using the Operating light and no flash
Uncompressed
Compressed
BMP
JPEG
Native format
Lowest ISO equivalent film. White balance adjusted. Macro 8 cm. Spot metering. Inbuilt flash. J Flash intensity ¼ 3 6
TIFF
Scanned Photographs images Publication True colour images Print & Print & Web & e-mail publication publication
GIF Line diagrams 256 colour images Animations; transparency
How do I best photograph X-rays? Exposure
Avoid reflections—do not use a flash. Photograph in a dark room with no windows reflected on film. Spot meter off a mid-range grey tone. Reduce exposure compensation 2 stops (2)—see below. Alter white balance. Do not alter brightness and contrast. Do not use Black and White (B&W) mode— record in colour and convert to B&W in postprocessing. You will get more conversion options, better results and a colour version of your photo.
Focus
Place camera on tripod. Macro mode. Autofocus. 55 mm macro lens. Shutter speed ¼ 1/2 s( ¼ aperture f 5.6).
How do I best e-mail, print and publish images?
E-mailing photos Small file sizes are the key here, as speed of transfer is more important than print quality (usually). Of course, the purposes of the image and the connection speeds influence the file size requirements, but generally aim for a file size of less than 200 Kb. I recommend converting images to JPEG format at 50% compression. Send one image per e-mail message. Many photo editing packages will convert file formats. Simply save a copy of the file in a different format. However, remember to keep the original uncompressed file also.
Photos for publication Publishers will generally specify the image format and print resolution required. The most common format is TIFF. Remember when converting from a JPEG to a TIFF, there will be no increase in resolution. The most commonly requested print resolution is 300dpi (dpi ¼ dots per inch). Print resolution is not equal to screen resolution. Below is the formula you may require to determine the required print or screen resolution.
Each of these processes demands specific image requirements for optimal useage and results. File size is a priority for sending by email, whilst image quality is more important for printing and publishing images. Publishers also demand specific image resolutions for their publications and this may differ between publishers. This is quite confusing for surgeons.
Print resolution (dpi) ¼ (pixels of length)/ (inches of length).
For example, if we have an image of 1000 pixels across and want to print an image size of 10 in across (length) then the printed resolution required is 100 dpi. We can provide this information to the image software package prior to printing the image.
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How should I store and manage images? As you begin to develop a strategy for culling, editing, storing and organising the mountain of images you face, keep in mind that the goal is to end up with an effective retrieval system, not just a storage system. Never, ever edit your original images. Always work on copies. Archive the originals for safe keeping, usually on an external hard drive. Repeatedly saving JPEG images in JPEG format results in a slow but sure accumulation of JPEG artifacts. If you modify an image and think you may edit it again later, save a copy in a lossless format like PNG, TIFF or your editor’s proprietary format. Most digital photographs deserve at least a trial pass through your photo editor’s ‘‘autobalance’’, ‘‘instant fix’’ or ‘‘general enhancement’’ feature. If you are new to post-processing, you can begin to get a feel for what works and what does not by noting what adjustments were made to achieve the good, the bad and the ugly results. Even a suboptimal auto-balance result can be a good starting point for your manual adjustments. This is the stage to convert your X-ray photogrephs to grayscale images, but remember to keep the unaltered original as well.
Principles 1. Stable Storage Media—I prefer an external hard disc drive, but removable storage media, such as CD-R, DVD-R, Zip drives, etc. are perfectly adequate. 2. Inexpensive—the cheapest £/Mb is advisable. 3. Rational folder structure—rational file-naming system. 4. Fast access. 5. Versatile.
Folder structures Arrange the folders on your computer in a way that is logical and allows you to easily find an image. Put a lot of thought into this. An example of the hierarchical system I use is given below C:/My Documents /Orthopaedics /Shoulder /Arthroplasty /History /History_Images. So if I wanted an image of a historical shoulder prosthesis, I know exactly where to look. You
L. Funk should develop a system that is logical to you and suits your personal way of working. Thumbnail image management software does help significantly in this process, but you still need a good folder structure. Some common, good image management software programmes include ThumbsPlus—www.cerious.com (my personal favourite); ACDSee—www.acdsystems.com -(easy & quick); Axialis—www.axialis.com (good for video & multimedia). For those familiar with Microsoft Access or Excel, these can also be used as an image management databases, by utilising the hyperlink field property. An example of this can be seen at: http://www.northernjourney.com/photo/articles/ Two useful image management software solutions, specifically written for Orthopaedic Surgery are PhotoIntern—www.desktopmedical.com Endocom, by Contec Medical—www.contecmedical.com
File naming tips Dates ¼ ‘0020816’, not ‘16082002’ Alphanumeric ¼ use ‘001’, not 1’ Long file names—suggestions: sd00475_murrayj_humerus_prox_3part_malunion_ 001a 11/cl.l_sd00475_20020317_plantan_malunion_ 001a Picture information extractor (PIE) shareware— www.picmeta.com—this utility deftly manages camera-to-PC image transfers with on-the-fly file renaming to insure a unique file name for every image. For instance, the PIE filename 0001011541-I4.jpg refers to an image taken at 3:41:14 PM on 1/1/2000. You can easily customize the filename mask PIE uses to rename downloaded images to suit your own filing scheme. For more information see: www.shortcourses.com
Consent for patient images As it becomes easier and more commonplace for clinicians to take photographs of their patients, issues of confidentiality and consent have become more important. Liability issues need to be considered. Not only is it good practice to obtain consent for images from a patient, but it is required by most NHS Trusts and laid out in the GMC Guideline document ‘Making and Using Visual
ARTICLE IN PRESS Digital imaging for orthopaedic surgeons and Audio Recordings of Patients’ published in 1997. Most NHS Trusts have a Consent From for Photography and Video, However, this may not include consent for education, research and publication. You may need to add these to the consent forms if you plan to use the images for these purposes. The American Health Information Management Association recommendations for photographing or video of patients are as follows:
Clinicians should have written policies addressing (1) circumstances under which patient photography is permitted, (2) patient consent, (3) ownership, storage, and retention of the images, and (4) patient authorisation for the release and/or use of images outside the organisation. Generally, the patient or his or her legal representative should give written consent before photography is done by anyone other than a friend or family member of the patient. Photographs, videotapes, and other images should be clearly identified with the patient’s name, identification number, and date, and stored securely to protect their confidentiality. If used to document patient care, they should be kept for the same time period law requires medical records to be kept.
Useful websites
213
It is worthwhile bearing this in mind when developing a library of patient images and establishing a procedure of consent.
Useful websites
Diploma in Medical Informatics—http://www. diploma.rcsed.ac.uk/ A Short Course in Digital Photography—http:// www.shortcourses.com/book01/contents.htm Digital Photography Tutorials—Basics—http:// www.huntfor.com/photography/tutorials/ digitbasics.htm Digital Photography for What It’s Worth (dpFWIW)—http://www.cliffshade.com/dpfwiw/ Digital PhotoCorner—Digital Terms—http:// www.dpcorner.com/al_about/terms.shtml Camera Basics—http://www.azuswebworks.com/ photography/ph_cam.html Digital Camera Resource Page—http://www. dcresource.com/ Digital Cameras & Imaging—http://www. photoworld.com/digital/digital.htm Gross Specimen Photography—http://www. neosoft.com/uthman/gross_photo.html Macro Photography—http://www.photo.net/ photo/macro
KODAK Flash Photography—Introduction— http://www.kodak.com/global/en/consumer/ pictureTaking/fIash/flashPhoMain.shtml CNET Help.com How-Tos and Tips—http:// www.help.com/cat/5/39/ht/index.html Advice for first-time digital camera users—http:// www.cliffshade.com/dpfwiw/advice.htm Exposure—http://www.88.com/exposure/ Written authorisation from the patient or his or her legal representative should be obtained before photographs, videotapes, or other images are released to outside requestors.
Diploma in Medical Informatics—http://www. diploma.rcsed.ac.uk/ A Short Course in Digital Photography—http:// www.shortcourses.com/book01/contents.htm Digital Photography Tutorials—Basics—http:// www.huntfor.com/photography/tutorials/ digitbasics.htm Digital Photography For What Its Worth (dpFWIW)—http://www.cliffshade.com/dpfwiw/ Digital PhotoComer—digital terms—http:// www.dpcorner.com/alLabout/terms.shtml Camera Basics—http://www.azuswebworks. com/photography/ph_cam.html Digital Camera Resource Page—http://www. dcresource.com/ Digital Cameras & Imaging—http://www. photoworld.com/digital/digital.htm Gross Specimen Photography—http://www. neosoft.com/uthman/gross_photo.html Macro Photography—http://www.photo.net/ photo/macro KODAK Flash Photography—Introduction— http://www.kodak.com/global/en/consumer/ pictureTaking/flash/flashPhoMain.shtml CNET Help.com How-Tos and Tips—http:// www.help.com/cat/5/39/ht/index.html Advice for first-time digital camera users— http://www.cliffshade.com/dpfwiw/advice.htm Exposure—http://www.88.com/exposure/
Summary As more surgeons and clinicians routinely photograph their radiographs and patients, a whole new
ARTICLE IN PRESS 214 world of imaging and image management skills need to be learnt. Publications are demanding digital images and presentations are now almost universally digital. I have briefly covered most of the basics you may require when embarking on
L. Funk digital imaging. No doubt, many will have their own preferred equipment, software and techniques. Digital imaging adds a useful dimension to a surgical practice, but one must be aware of consent and liability issues.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 215–222
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TUMOURS
Pigmented villonodular synovitis: Diagnostic pitfalls and management strategy Himanshu Sharmaa,, M.J. Janeb, R. Reidc a
44 Abercorn Road, Newton Mearns, Glasgow G77 6NA, UK Scottish Endoprosthetic Bone Tumour Service, Scottish Bone Tumour and Sarcoma Service, Western Infirmary, Glasgow G11 6NT, UK c Scottish Bone Tumour Registry, Western Infirmary, Glasgow G11 6NT, UK b
KEYWORDS Pigmented villonodular synovitis; Giant cell tumour of the tendon sheath; Synovectomy; Recurrence; Radiotherapy
Summary Pigmented villonodular synovitis (PVNS) is a locally aggressive synovial proliferative disorder of unknown aetiology affecting the linings of joints, tendon sheaths and bursae. The prevalence of PVNS is 1.8 patients per million population, equally affecting both genders in the third and fourth decade of life. The most commonly occurring sites are the knee, hand, hip, ankle and shoulder. PVNS represents a part of a disease spectrum that includes a localised form (giant cell tumour of the tendon sheath, GCTTS) and the more diffuse intra-articular form that is referred to as PVNS. A high index of suspicion for PVNS should be observed in cases presenting with a painless or painful swelling in the large joints of chronic duration with or without a history of trauma. Diagnostic dilemma can occur in PVNS, not only at the clinical and radiological level, but also while interpreting the histopathological findings. Complete recovery can be achieved in the majority of cases with localised disease by complete excision. Long-term follow-up is recommended for the diffuse variety because of difficulty in achieving complete excision and a high recurrence rate. External beam radiation therapy and intra-articular instillation of radioactive colloids have been described for local relapsed and residual PVNS after surgical treatment and in the very large diffuse form of PVNS where the primary operative intervention alone may leave some residual disease. & 2005 Elsevier Ltd. All rights reserved.
Introduction Corresponding author. Tel.: +44 141 639 3697;
fax: +44 141 201 5082. E-mail addresses:
[email protected] (H. Sharma),
[email protected] (M.J. Jane),
[email protected] (R. Reid).
Pigmented villonodular synovitis (PVNS) is a locally aggressive synovial proliferative disorder of unknown aetiology affecting the linings of joints, tendon sheaths and bursae. It was first described by Chassignac1 and later on coined by Jaffe et al.2 The
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ARTICLE IN PRESS 216 most commonly occurring sites are the knee, flexor tendon sheaths of the hand and hip joint, followed by the ankle and shoulder.2–4 There are numerous factors causing diagnostic difficulties not only at clinical and radiological levels, but also histologically in the course of PVNS. The management strategy depends on the type, site and aggressiveness of the PVNS lesion. This article is an overview of the aetiopathogenesis, diagnostic pitfalls in the clinical manifestations, radiological evaluation and histopathological interpretation, factors influencing recurrence and appropriate management strategy of patients with PVNS.
H. Sharma et al. and presenting most commonly with mechanical symptoms. (c) Diffuse pigmented villonodular synovitis (DPVS), presenting with chronic oedema and pain, most commonly in the knee, hip and ankle. It has been reported that the diffuse form is four times more common than the localised form in the knee. All three categories display similar histology including villous synovial proliferation with microscopic villi, histiocytes, foam cells and multinucleated giant cells.8 However, in the localised form, the synovial tissue does not display a reactive hyperplasia as seen in the diffuse variant.3,4
Epidemiology Prevalence The prevalence of PVNS is approximately 1.8 patients per million population.3
Age, sex and side PVNS most commonly affects adult patients in the third or fourth decade. There is a slight female preponderance in GCTTS, but equal sex incidence in PVNS. This condition is relatively rare in children. There is no predilection for any laterality.3–6
Anatomical distribution The condition occurs in the form of unilateral monarticular arthritis, although, can rarely be polyarticular. Almost all joints have been reported to be affected. It is most common in the knee joint. The most commonly occurring sites after the knee joint are flexor tendon sheaths of the hand, the hip joint followed by the ankle and shoulder.2–4
Types of PVNS PVNS represents a part of a disease spectrum that includes diffuse and localised forms of GCTTS, to the more diffuse intra-articular form that is referred to as PVNS.7 Granowitz and Mankin classified the entity into three categories on the basis of clinical presentation.8 (a) Isolated, discrete lesion occurring within a tendon sheath, most often seen in the hand. (b) Localised pigmented villonodular synovitis (LPVS), occurring most commonly in the knee
Aetiopathogenesis The aetiopathogenesis still remains uncertain. Inflammatory synovial hyperplasia, benign neoplasia of unknown aetiology, abnormality of local lipid metabolism, repetitive trauma and haemorhage are the various hypotheses put forward to explain the possible aetiology of PVNS. The main aetiology of PVNS has been proposed to be precipitated by trauma. In 1941, Jaffe et al. originally described the lesion histologically and showed that PVNS lacked neoplastic cells. He proposed a hypervascular cellular phase subsequent to trauma produced hyalinisation and fibrosis.2 More recently, cytogenetic abnormality in the form of monoclonality and chromosomal abnormality has been described.9 The mechanism of bone involvement in PVNS is controversial. Increased joint pressure attributable to synovial overgrowth, external compression by the tumour, erosion by lysosomal enzymes released from synovial histiocytic cells or invasion of granulation tissue through the vascular foramina are some of the proposed hypotheses put forward to explain the bony invasion in PVNS (Figs. 1–3).10,11
Clinical presentation It is insidious in onset. The patient usually presents with local discomfort and swelling of chronic duration. Patients may have mechanical symptoms in the form of locking, catching, stiffness or instability. The atypical clinical course consists of areas of erythema, stiffness and a palpable big mass. A previous history of trauma to the affected region can be found in less than 50% of patients.3,11
ARTICLE IN PRESS Pigmented villonodular synovitis: Diagnostic pitfalls and management strategy GCTTS and LPVS usually present with a slow growing nodular soft tissue mass related to a tendon sheath or joint capsule. Lesions in the hand are usually painless, while lesions in the foot and ankle may be painful due to pressure effects of footwear. The factors causing diagnostic dilemma in PVNS are summarised in Table 1.
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Radiological findings Plain X-rays Plain radiographs are usually normal in early PVNS. Additionally, the patients with radiographic changes are those with more extensive disease involving bone and at a late stage of the disease. Plain X-rays typically show a soft tissue mass or joint effusion in the early stage, whereas erosions with a sclerotic rim and subchondral lucencies in the advanced cases. Well-defined erosions with relative preservation of the joint space are noted early in the disease.12 With disease progression, joint space loss may become severe and concentric, particularly when involving joints with a limited volume capacity such as the hip.13 In the localised form of PVNS (GCT of tendon sheath) 15–25% of the patients can have erosive bony lesions, while in the diffuse PVNS, bone erosions are present in as many as 33–56% of cases.14–17
Bone scan Isotope 99m Technetium polyphosphate scan is sensitive but non-specific. It is very difficult to distinguish between the increased uptake seen in the PVNS and other generic causes like infection, trauma and tumours. Recently, Mackie18 confirmed that increased Thallium-201 uptake was found in all cases of PVNS on early and delayed phases.
CT scan
Figure 1 Lateral radiograph of the ankle revealing erosion of the anterior subtalar joint.
CT scanning seems to be less accurate than MRI to observe soft tissue extension and to assess the recurrence of the lesion after excision. A soft tissue mass of high density in relation to surrounding muscle is usually seen on CT due to a high
Figure 2 Oblique radiograph of the foot revealing erosion of the cuboid bone.
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Figure 3 Lateral and anteroposterior views of the ankle showing multiple small lytic lesions affecting talus.
Table 1 Summary of the factors causing diagnostic dilemma in pigmented villonodular synovitis.
History of trauma may or may not be present. Late presentation is quite common. More commonly painless, sometimes painful
lump in the tendons or swelling of the joints of chronic duration. Plain films may be normal. MRI may be non-specific, cannot reliably distinguish between benign and malignant lesions. Histology may be non-specific. Aetiology remains unclear.
haemosiderin content. Underlying bone erosions or cysts can be well appreciated in the CT scan.
MRI scan MRI is a useful non-invasive means of diagnosis and the current investigation of choice. The MR imaging appearance of PVNS consists of multiple synovial lesions with low or intermediate signal intensity on T1-weighted and low signal intensity on T2weighted and gradient-echo images.4,7,14 Findings on MRI are mainly attributable to the haemosiderin deposition in the affected tissues due to its magnetic susceptibility properties. In addition to the deposits of haemosiderin, the signal characteristics also reflect the histological composition of the tissue, particularly lipids and inflammatory fibrosis (Figs. 4–6).
Figure 4 MRI scan (T1-weighted image) showing a lowsignal lobulated soft tissue lesion (diffuse PVNS) affecting the ankle joint as well as the tendon sheaths of the plantar flexors.
The utility of MRI in determining the distribution of abnormal tissue is crucial in the subsequent surgical planning and decision making process.7,14,19–22 Magnetic resonance imaging is also useful for postoperative surveillance of the patients. Although very sensitive in diagnosing these lesions, the MRI appearance is non-specific, and is often confused with rheumatoid pannus or soft tissue sarcoma. The uncommon diffuse variant of GCTTS has an ill-defined appearance that may be indistinguishable from soft tissue sarcomas or the rare malignant GCTTS. Recurrent GCTTS can also
ARTICLE IN PRESS Pigmented villonodular synovitis: Diagnostic pitfalls and management strategy
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Figure 6 Sagittal T1-weighted image of knee shows an oval posterior synovial mass of low signal intensity stretching the posterior joint capsule.
mimic soft tissue sarcoma clinically and on imaging studies.
Histological findings Aspiration can be attempted in large joints with effusion. Joint aspiration usually reveals 75% blood and 25% yellow fluid.15 Arthroscopic or CT guided biopsy may be undertaken to obtain preoperative diagnosis and is likely to yield positive histology. Grossly, PVNS may be nodular or globular yellowish villous growths associated with synovial membranes. Microscopic findings include haemosiderin deposits both intracellular and intracellular, foamy histiocytes, giant cells and large synovial cells.4,21 Osteoids and few mitotic figures can be seen. Malignant transformation, fortunately rare, has also been described in the literature.23
’’
Figure 5 Lateral view of the knee shows normal appearance.
to affect multiple joints. Contrary to PVNS, ganglion cyst, sebaceous/inclusion cyst, lipoma, posttraumatic loose body in the large joints, haemangioma, nerve sheath tumour, foreign body granuloma and the majority of synovial sarcomas typically display high intensity signals on MRI. Some soft tissue sarcomas like malignant fibrous histiocytoma, fibromatosis, xanthoma, Morton’s neuroma, burnt out’’ rheumatoid pannus, amyloidosis, tophaceous gout and synovial osteochondromatosis can have similar low/intermediate intensity signals on MRI as seen in PVNS.10,14 Appropriate histological assessment is crucial in differentiating these lesions from PVNS. Haemophilia, haemochromatosis, haemosiderosis and haemorrhagic synovitis also demonstrate haemosiderin deposits on histological sections; however, the pigment is largely confined to the synovial cells and macrophages in all of these conditions, whereas the distribution in PVNS is more diffuse (both intra- and extra-cellular). Giant cells and histiocytes seen in PVNS are not classically seen in the other three conditions.
Treatment Differential diagnosis The main differential diagnosis is rheumatoid arthritis. Unlike PVNS, rheumatoid arthritis tends
A combination of clinical, radiographic and histological correlation is necessary to make the diagnosis with certainty. Clinical correlation in these cases is utilised to differentiate between
ARTICLE IN PRESS 220 these different pathologic disease processes. Aggressive forms of the disease should be closely observed, and managed by appropriate investigations and treatment planning to obtain optimal outcome. Total synovectomy (open or arthroscopic) is required for the diffuse form (recurrence common), local excision for the nodular form (recurrence rare) and radiotherapy has been used in the management of recurrent and residual lesions with varying success.
Surgery Surgical excision is the treatment of choice for localised GCTTS and diffuse PVNS. In localised disease, wide excision usually minimises the chances of local recurrence but recurrence is common if excision is inadequate. In diffuse disease, total synovectomy has a much lower recurrence rate than partial synovectomy and is the preferred treatment of choice.24 To ensure complete excision of the abnormal mass and the affected surrounding tissues, an open procedure on both sides of the joint should be performed. Aggressive control of the disease should be contemplated as early as possible. Complete excision may sometimes be limited by the proximity of the neurovascular bundle. Arthroscopy is an effective tool for both diagnosis and treatment of PVNS. Arthroscopy is the treatment of choice for localised forms. Arthroscopic synovectomy may be indicated for the inactive form of diffuse disease. Open complete synovectomy is the preferred treatment for diffuse forms of PVNS. Incomplete removal most likely results in recurrence of the lesion.11 Subsequent consideration for arthrodesis or arthroplasty of the affected joint for secondary osteoarthritis should be well explained to the patients during the consenting process. The bone destruction caused by PVNS may be extensive and this can necessitate joint reconstruction (particularly when the hip or the knee is involved). If PVNS is seen as an incidental finding, it should not affect the decision to proceed with a preplanned reconstructive procedure.
H. Sharma et al. PVNS where the primary operative intervention alone may leave some residual disease. Synoviorthesis with Yttrium-90 seems to be a good adjuvant for the treatment of recurrent PVNS.25 The risk of periarticular fibrosis and more sinister complication in the form of radiation-induced sarcoma after radiotherapy has been reported in the literature.9 In addition, growth arrest may occur in skeletally immature patients. Blanco et al. presented the results of combined partial arthroscopic synovectomy and low-dose radiation therapy in the treatment of diffuse PVNS of the knee.26 The authors conducted a prospective study of the treatment of 22 patients with clinical, ultrasonic and histologically confirmed findings of diffuse PVNS of the knee. They found that combination therapy was effective in reducing symptoms of pain and oedema, and in improving overall function of patients. Three had clinically and ultrasonically confirmed recurrence of disease and were treated with repeat arthroscopic synovectomy without harmful effects from radiotherapy.26
Recurrence Recurrent tumours are more tissue destructive and more invasive. Recurrence is documented as high as 30% in the previously published literature.4,27 Recurrence is more common in diffuse variants treated with intralesional primary treatment with incomplete synovectomy. Delay in diagnosis, delay in instituting treatment, intralesional primary treatment and intraoperative hesitation in thoroughly debriding the lytic lesions from the articular surface can lead to recurrence. Recurrences may be re-excised or may be treated with radiotherapy alone or combined radiotherapy and surgery. Amputation has been suggested for widespread recurrent ‘hard to control’ disease.28 Joint arthrodesis may be considered when there are associated degenerative bone changes.29 At followup, clinical examination with plain X-rays should suffice, although MRI scan is helpful and recommended in symptomatic postoperative patients. Table 2 summarises the factors influencing recurrence of PVNS.
Radiotherapy Two types of radiotherapy in the form of external beam radiation therapy and intra-articular instillation of radioactive colloids have been described in the literature. The radiation therapy is indicated for local relapsed and residual PVNS after surgical treatment and in the very large diffuse form of
Conclusion In conclusion, a high index of suspicion for PVNS is required for cases presenting with a painless or painful mass in the large joints of chronic duration. Complete recovery can be achieved in the majority
ARTICLE IN PRESS Pigmented villonodular synovitis: Diagnostic pitfalls and management strategy Table 2 Summary of the factors influencing recurrence of the pigmented villonodular synovitis.
Delay in diagnosis Delay in instituting treatment Intralesional primary treatment Intraoperative hesitation in thoroughly debriding the lytic lesions from the articular surface. Arthroscopic treatment for diffuse form of PVNS affecting large joints.
Research directions
of cases with localised disease by complete excision of the lesion. Delay in diagnosis, delay in instituting treatment, intralesional primary treatment and intraoperative hesitation in thoroughly debriding the lytic lesions from the articular surface can lead to residual disease and possibly recurrence later on. Diffuse intra-articular disease in young people remains a difficult problem.
Acknowledgements We would like to thank medical illustration department and Jean Campbell, secretary, Scottish Bone Tumour Registry for their kind assistance in the preparation of this review article. Practice points
Monarticular synovial swelling, most common site is the knee, but other joints affected include hip, ankle and shoulder Most commonly in the third and fourth decades with no sex predilection Intra-articular PVNS tends to be of the diffuse form, while tendon sheath PVNS is the nodular form MRI is the current imaging technique of choice Aspiration of the joint will characteristically reveal a blood tinged/haemorrhagic, dark brown aspirate. Synovial biopsy should be performed if there is any doubt Microscopic findings include haemosiderin deposits, foamy histiocytes, giant cells and large synovial cells A combination of clinical, radiological and histological correlation is necessary to make the diagnosis with certainty Early diagnosis and aggressive surgical treatment is recommended
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A prospective determination of the factors responsible for recurrence in the diffuse variety of PVNS Further research is needed to determine the aetiopathogenesis of aggressive forms of PVNS More research efforts are needed for primary prevention of the disease
References 1. Chassignac M. Cancer de la gaine des tendons [cancer of the tendon sheath]. Gaz Hop Civ Milit 1852;47:185–6. 2. Jaffe H, Lichtenstein L, Sutro C. Pigmented villonodular synovitis, bursitis and tenosynovitis: a discussion of the synovial and bursal equivalents of the tenosynovial lesion commonly denoted as xanthoma, xanthogranuloma, giant cell tumor or myelopaxoma of the tendon sheath, with some considerations of the tendon sheath lesion itself. Arch Pathol 1941;3l:731–65. 3. Myers BW, Masi AT. Pigmented villonodular synovitis and tenosynovitis: a clinical epidemiologic study of 166 cases and literature review. Medicine (Baltimore) 1980;59(3): 223–38. 4. Rao AS, Vigorita VJ. Pigmented villonodular synovitis (giantcell tumor of the tendon sheath and synovial membrane). A review of eighty-one cases. J Bone Joint Surg Am 1984; 66(1):76–94. 5. Gonzalez Della Valle A, Piccaluga F, Potter HG, Salvati EA, Pusso R. Pigmented villonodular synovitis of the hip: 2- to 23-year followup study. Clin Orthop 2001(388):187–99. 6. Durr HR, Stabler A, Maier M, Refior HJ. Pigmented villonodular synovitis. Review of 20 cases. J Rheumatol 2001;28(7):1620–30. 7. Llauger J, Palmer J, Monill JM, Franquet T, Bague S, Roson N. MR imaging of benign soft-tissue masses of the foot and ankle. Radiographics 1998;18(6):1481–98. 8. Granowitz SP, Mankin HJ. Localised pigmented villonodular synovitis of the knee. Report of five cases. J Bone Joint Surg Am 1967;49(1):122–8. 9. O’Sullivan B, Cummings B, Catton C, et al. Outcome following radiation treatment for high-risk pigmented villonodular synovitis. Int J Radiat Oncol Biol Phys 1995;32: 777–86. 10. Ugai K, Morimoto K. Magnetic resonance imaging of pigmented villonodular synovitis in subtalar joint. Report of a case. Clin Orthop 1992(283):281–4. 11. Flandry F, Hughston JC. Pigmented villonodular synovitis. J Bone Joint Surg Am 1987;69(6):942–9. 12. Lin J, Jacobson JA, Jamadar DA, Ellis JH. Pigmented villonodular synovitis and related lesions: the spectrum of imaging findings. Am J Roentgenol 1999;172(1):191–7. 13. Cotton A, Flipo RM, Chastanet P, Desvigne-Noulet MC, Duquesnoy B, Delcambre B. Pigmented villonodular synovitis of the hip: review of radiographic features in 58 patients. Skeletal Radiol 1995;24(1):1–6. 14. Harris O, Ritchie DA, Maginnis R, Lamb GR, Helliwell T, Jane M, Davies AM. MRI of giant cell tumour of tendon sheath and
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nodular synovitis of the foot and ankle. Foot 2003; 13(1):19–29. Bravo SM, Winalski CS, Weissman BN. Pigmented villonodular synovitis. Radiol Clin North Am 1996;34:311–26. Ushijima M, Hashimoto H, Tsunoyoshi M, Enjoji M. Giant cell tumor of the tendon sheath (nodular tenosynovitis). A study of 207 cases to compare the large joint group with the common digit group. Cancer 1986;57:875–84. Dorwart RH, Genant HK, Johnston WH, Morris JM. Pigmented villonodular synovitis of synovial joints: clinical, pathologic, and radiologic features. Am J Roentgenol 1984;143(4): 877–85. Mackie GC. Pigmented villonodular synovitis and giant cell tumor of the tendon sheath: scintigraphic findings in 10 cases. Clin Nucl Med 2003;28(11):881–5. Kransdorf MJ. Benign soft tissue tumors in a large referral population: distribution of diagnoses by age, sex and location. Am J Roentgenol 1995;164:395–402. Jelinek JS, Kransdorf MJ, Shmookler BM, Aboulafia AA, Malawer MM. Giant cell tumour of tendon sheath: MR imaging findings in nine cases. Am J Roentgenol 1994;162: 919–22. Iovane A, Midiri M, Bartolotta TV, Candela F, Carcione A, Lagalla R, Cardinale AE. Pigmented villonodular synovitis of the foot: MR findings. Radiol Med (Torino) 2003;106(1–2): 66–73. Cheng XG, You YH, Liu W, Zhao T, Qu H. MRI features of pigmented villonodular synovitis (PVNS). Clin Rheumatol 2004;23(1):31–4.
H. Sharma et al. 23. Bertoni F, Unni KK, Beabout JW, Sim FH. Malignant giant cell tumor of the tendon sheaths and joints (malignant pigmented villo-nodular synovitis). Am J Surg Pathol 1997;21: 153–63. 24. Ogilvie-Harris DJ, McLean J, Zarnett ME. Pigmented villonodular synovitis of the knee. The results of total arthroscopic synovectomy, partial, arthroscopic synovectomy, and arthroscopic local excision. J Bone Joint Surg Am 1992; 74:119–23. 25. Shabat S, Kollender Y, Merimsky O, Isakov J, Flusser G, Nyska M, Meller I. The use of surgery and yttrium 90 in the management of extensive and diffuse pigmented villonodular synovitis of large joints. Rheumatology (Oxford) 2002;41(10):1113–8. 26. Blanco CE, Leon HO, Guthrie TB. Combined partial arthroscopic synovectomy and radiation therapy for diffuse pigmented villonodular synovitis of the knee. Arthroscopy 2001;17(5):527–31. 27. Schwartz HS, Unni KK, Pritchard DJ. Pigmented villonodular synovitis. A retrospective review of affected large joints. Clin Orthop 1989(247):243–55. 28. Ghert MA, Scully SP, Harrelson JM. Pigmented villonodular synovitis of the foot and ankle: a review of six cases. Foot Ankle Int 1999;20(5):326–30. 29. Rochwerger A, Groulier P, Curvale G, Launay F. Pigmented villonodular synovitis of the foot and ankle: a report of eight cases. Foot Ankle Int 1999;20(9):587–90.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 223–230
www.elsevier.com/locate/cuor
CHILDREN
Developmental dysplasia of the hip (DDH) James J. McCarthy, Peter V. Scoles, G. Dean MacEwen Shriners Hospital for Children, Philadelphia, USA
KEYWORDS Hip; Pavlik harness; Dysplasia; Dislocation; Developmental; Instability
Summary Developmental dysplasia of the hip (DDH) is common, ranging from mild dysplasia to frank dislocation. The diagnosis can be difficult, even in experienced hands, particularly when there are bilateral dislocations. All infants should be screened clinically, but the value of other screening methods, such as ultrasound is still debated. Initial treatment in the infant is with a Pavlik harness. If this is ineffective or if the child presents later, more aggressive treatment, such as a closed reduction, or even surgical reduction may be indicated. All hips must be carefully followed until maturity. If diagnosed and treated promptly excellent results can be obtained, but long-term sequelae occur even in patients given optimal treatment. & 2005 Elsevier Ltd. All rights reserved.
Introduction Developmental dysplasia of the hip (DDH) has been recognized from the time of Hippocrates. It is a common condition which remains controversial and confusing despite diagnostic and treatment advances. The terminology can be unclear and inconsistent, diagnosis can be subtle and there can be long-term sequelae even in patients given optimal treatment. For example, despite DDH having been documented to occur in patients who did not have dysplasia a birth, there is still an erroneous belief that all cases of DDH are present at birth and, if diagnosed later, represent a Corresponding author. Tel.: +1 215 430 4032;
fax: +1 215 430 4079. E-mail addresses:
[email protected] (J.J. McCarthy),
[email protected] (P.V. Scoles),
[email protected] (G.D. MacEwen).
‘‘missed’’ diagnosis. The value of screening methods is still commonly debated. Thus it is unsurprising that DDH is commonly associated with malpractice suits, even though results of treatment are generally quite good. The aim of this article is to present a basic outline of the disorder, reflect upon some of the controversies, and provide an algorithm for the treatment of the child with DDH.
Terminology Discussions of congenital or developmental disorders of the infant hip are made more difficult by conflicting terminology. This condition has been called: hip dysplasia, congenital dislocation of the hip (CDH), developmental dysplasia of the hip (DDH).
0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2005.05.007
ARTICLE IN PRESS 224 In part this is due to attempts to reflect the aetiology, which is still unclear, or at least unpredictable. Thus in 1991, the Pediatric Orthopaedic Society of North America and the American Academy of Orthopaedic Surgeons endorsed the term ‘‘DDH’’ in an effort to emphasize the developmental nature of the hip disorder. As The American Heritage College Dictionary defines ‘‘dysplasia’’ as ‘‘abnormal development or growth’’ ‘‘DDH’’ is somewhat redundant! Most commonly, DDH is used when referring to instability, dislocation or acetabular dysplasia of the hip. The abnormal development of the hip includes the osseous structures, such as the acetabulum and the proximal femur, as well as the labrum, capsule, and other soft tissues. However internationally, this disorder is often still referred to as ‘‘CDH,’’ but DDH is the term used in this article. More specific terms are often used to better describe the condition. A natural tendency to use phrases that refer to physical examination findings (instability), or anatomic abnormalities (subluxation or dislocation) in an aetiologic or pathophysiologic sense, complicates interpretation of existing literature. We have attempted to define these terms as follows: Instability: A clinical diagnosis made on examination where passive manipulation subluxates or dislocates the hip. Subluxation: An anatomic diagnosis, usually made from imaging studies, in which there is incomplete contact between the articular surfaces of the femoral head and acetabulum. Dislocation: An anatomic diagnosis, usually made from imaging studies, in which there is complete loss of contact between the articular surface of the femoral head and acetabulum. Teratologic: A diagnosis in which physical exam and/or imaging studies show a dislocated hip prior to birth.
Incidence The overall frequency is usually quoted as approximately 1 in 1000. This figure depends on how DDH is defined as demonstrated by Barlow’s classic study,1 in which he reported that the incidence of hip instability in the newborn examination was as high as 1 in 60. However, over 60% of these hips became stable by 1 week and 88% by 2 months. Extrapolation of these findings suggests an incidence of 1/ 500 (12% of the 1 in 60, or 0.2%) with residual hip instability, as compared to the usually cited figure of 1 in 1000.
J.J. McCarthy et al.
Anatomy/aetiology The normal growth of the acetabulum is dependent on normal epiphyseal growth of the triradiate cartilage and the three ossification centres of the acetabular portion of the pubis (os acetabulum), ilium (acetabular epiphysis), and ischium. Normal growth is also dependent on normal interstitial appositional growth within the acetabulum2; the presence of the spherical femoral head within the acetabulum appears to be critical for stimulating normal development of the acetabulum. Many factors may contribute to DDH. The high incidence of DDH among Native Americans and Laplanders (nearly 25–50 per 1000) and low incidence among the southern Chinese and African-American populations, as well as increased incidence among children whose parents have DDH, suggests underlying genetic influences. Otherwise normal neonates with findings of hip instability and ligamentous laxity on physical examination may subsequently develop radiographic evidence of hip dysplasia. This has led many to conclude that ligamentous laxity is a significant aetiologic factor. However, DDH is not characteristic of collagen abnormalities with significant ligamentous laxity, such as Ehlers–Danlos syndrome or Marfan’s syndrome. Barlow1 noted that most neonates with instability have normal hip development without treatment. It may therefore require more than just ligamentous laxity for DDH to result. At birth, Caucasian children (who have a higher incidence of DDH) tend to have a shallower acetabulum, as compared to children of other races.3 Therefore, there may be a susceptible period at birth in which abnormal positioning or a brief period of ligamentous laxity combined with a shallow acetabulum may result in hip instability. Other factors related to DDH include intrauterine positioning and gender, and some of these are interrelated. Female gender and breech positioning are all associated with an increased incidence of DDH. Eighty percent of those with DDH are female, and the incidence of breech positioning in children with DDH is approximately 20% (compared with 2–4% in the general population.)4 The incidence of DDH in females born breech is as high as 1 in 15.5 Other musculoskeletal disorders of intrauterine malpositioning or crowding, such as metatarsus adductus and torticollis, have been reported to be associated with DDH.6,7 Oligohydramnios is also reported to be associated with an increased incidence of DDH. The left hip is more commonly affected by DDH, and this may be related to the common intrauterine position of the left hip against the mother’s sacrum, placing it into an adducted
ARTICLE IN PRESS Developmental dysplasia of the hip (DDH) position. Children in cultures where the mother swaddles the baby, keeping the hips adducted, also have a higher rate of hip dysplasia. Abnormal development of the hip also occurs in children with underlying neuromuscular disorders, such as cerebral palsy, myelomeningocele, arthrogryposis, and Larsen’s syndrome, although hip dysplasia in these children is not usually classified as DDH.
Clinical presentation Careful examination of the hip in the newborn period will identify the majority of the infants with DDH, but not all children with DDH have clinical signs at birth, even when examined by physicians with specialty training or when augmented by other imaging modalities.8 This may be due to the difficulty of making the diagnosis, or the hip may not have been unstable or dislocated at birth. Ortolani9 and Barlow1 designed physical diagnostic tests to detect unstable hips in infancy. The Ortolani test is performed by placing the thumb over the inner thigh and the index finger on the greater trochanter. The hip is abducted and gentle pressure is placed over the greater trochanter. A ‘‘clunk’’, like turning a light switch on or off, is felt when the hip is reduced. This should be done gently, such that the fingertips do not blanch. Ortolani felt that a positive test was associated with reduction of the hip into the acetabulum, but it may also be caused by passage of the femoral head over a biconcave ridge in the acetabulum.2 The Barlow test is performed with the hips in an adducted position and slight gentle posterior pressure applied to the hips. A clunk should be felt
225 as the hip subluxes out of the acetabulum. A highpitched ‘click’ (as opposed to a ‘clunk’) in all likelihood has little association with acetabular pathology.10 To perform these maneuvers correctly, the patient must be relaxed, and only one hip should be examined at a time. Clinical examination when the child is 3–6 months of age is quite different. At this age, findings with the Ortolani and Barlow exams are more difficult to discern. The Galeazzi sign (or Allis sign) is a classic identifying sign for unilateral hip dislocation. This is performed with the patient lying supine and the hips and knees flexed (Fig. 1). Examination should demonstrate that one leg appears shorter than the other. Although this is usually due to hip dislocation, it is important to realize that any limb length discrepancy will result in a positive Galeazzi sign. Additional physical examination findings for late dislocation include asymmetry of the gluteal thigh or labral skin folds, although thigh folds have been reported to be abnormal in as many as 20% of all newborn children. Limited abduction of the affected hip is also a common finding in children with unilateral DDH. Children commonly stand or walk with external rotation, and this is most likely due to contractures of the external rotators, but it can also be a sign of a dislocated hip, especially if it persists beyond early walking age. Bilateral dislocation of the hip, especially at a later age, can be quite difficult to diagnose. This often presents as a waddling gait with hyperlordosis. Many of the above-mentioned clues for a unilateral dislocated hip will not be present, such as Galeazzi sign, asymmetrical thigh and skin folds, or asymmetrically decreased abduction. Careful examination is essential and a high level of suspicion is important.
Imaging studies
Fig. 1 Galeazzi sign.
Ultrasound plays an important role in both the diagnosis and treatment of DDH. Most authors agree that it is an excellent tool for the assessment of children with suspected hip instability (i.e. when clinical examination is equivocal) and is useful as an adjunct in the treatment of children with hip dysplasia, especially in monitoring reduction by closed methods.11 However, routine ultrasound evaluation of newborns is more controversial; the primary concern is the over-diagnosis (increased false-positive results) of hip dysplasia. In addition, the routine use of ultrasound for children, even those with risk factors, has not yet been shown to
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reduce the prevalence of late diagnosis of hip dysplasia.12 After the femoral head begins to ossify (at 6–12 months of age), the usefulness of ultrasound diminishes. Therefore, the use of ultrasound for routine screening children is not currently recommended. Radiographic evaluation of the pelvis can be used to assess the hips, although early radiographs (within the first 6–12 weeks) may be misleading. Numerous radiographic measurements have been used to assist in the evaluation of DDH (Fig. 2). The most commonly used are: Hilgenreiner’s line: Drawn from an anteroposterior radiograph of the hips, a horizontal line is drawn between the triradiate epiphyses. Perkin’s line: Drawn perpendicular to Hilgenreiner’s line through the superolateral edge of the acetabulum, dividing the hip into four quadrants. The proximal medial femur should be in the lower medial quadrant or if the ossific nucleus of the femoral head, if present (usually seen between 4 and 7 months), should be in the lower medial quadrant. Acetabular index: The angle between Hilgenreiner’s line and a line drawn from the triradiate epiphysis to the lateral edge of the acetabulum. Classically, this decreases with age and should measure less than 201 by 2 years of age. Shenton’s line: A line drawn from the medical aspect of the femoral neck to the inferior border of the pubic rami. It should create a smooth arc that is not disrupted. If disrupted, it indicates some degree of hip subluxation. This measurement may be unreliable in infants. Dozens of other radiographic measurements have been proposed to assist with the radiographic evaluation of DDH in infants, children, and young adults, which can be confusing. For example, the acetabular index is used to assess the acetabular depth in infants and children and is often measured in an attempt to assess the effect of treatment.
The acetabular angle of Sharp is primarily used to assess residual dysplasia in patients after the closure of the tri-radiate cartilage. It is important to understand the indications and limitations of these measurements. As well as the radiographic measurements, there are a number of radiographic descriptions used to assess the degree of dysplasia and the effects of reduction. The acetabular teardrop is formed by the cortical surfaces of the acetabular fossa (laterally), the pelvic wall (medially) and the cotyloid notch (inferiorly). If the ‘‘teardrop’’ takes on a ‘‘V-shape’’ with widening of the superior width, the prognosis is poorer.13 The shape of the ‘‘sourcil,’’ or eyebrow, of the acetabulum can also be a gauge to the degree of acetabular dysplasia. An evenly distributed sourcil with the lateral edge horizontal or curved downward is an indication of a normally developing acetabular roof, whereas a sourcil that has a lateral triangular shape or is curved upward is more consistent with a dysplastic acetabulum. More recently, the presence of the acetabular notch (a scooped deformity on the superolateral aspect of the acetabular edge) has been associated with dysplasia.14 It can be difficult to delineate radiographically acetabular dysplasia in the young adult that is severe enough to lead to early osteoarthrosis. A centre edge (CE) angle of less than 161 has often been used to predict early osteoarthrosis, but other authors have found this measurement to be less reliable. Subluxation, defined as a break in Shenton’s line, has been shown to be associated with osteoarthrosis and decreased function. Arthrograms are dynamic studies performed by injecting dye into the hip joint and examining the patient with aid of fluoroscopy, usually with the patient under anesthesia. Although this can be performed independently, it is routinely performed in conjunction with a closed reduction. Arthrography can be helpful in determining the underlying cartilaginous profile and dynamic stability of the hip.15
Treatment Early diagnosis aids in the successful treatment of DDH. Prompt recognition and appropriate treatment provides the child with the greatest opportunity for a good outcome. An algorithm is outlined in Table 1.
Pavlik harness Fig. 2 Radiographic measurements.
The Pavlik harness is the treatment of choice for neonates with hip instability. It is designed to hold
ARTICLE IN PRESS Developmental dysplasia of the hip (DDH)
227 excellent means of documenting stability and reduction of the hip in the Pavlik harness and should be performed early in the course of treatment. If the hip is not reduced, then the Pavlik harness should be discontinued. Risk factors for failure of the Pavlik harness include: bilateral dislocations, older age at time of initial treatment, inability to reduce the hip with manipulation, and initial coverage less than 20% as determined by ultrasound.16,17 There is little consensus as to the overall time the Pavlik should be worn, although a minimum of 3 months seems to be reasonable. If the hip is satisfactorily reduced in the harness, we maintain this treatment at least until the hip is stable clinically and by ultrasound out of the brace. Abduction splinting is maintained thereafter, until there is no radiographic evidence of residual dysplasia. The use of an abduction brace if there is a failure of the Pavlik harness treatment has been suggested to be successful in over 80% of patients. The Pavlik harness is not appropriate for use in infants in whom diagnosis is made later than 6
the hips in a position that encourages normal growth and development while permitting motion within a safe range. To ensure that the Pavlik harness is fitted properly to hold the hip in a reduced position, close supervision and frequent adjustments are essential.16 It should be placed such that the chest strap is at the nipple line with two finger breadths of space between the chest and strap. The anterior strap should be positioned at the mid-axillary line with the hips flexed to no more than 100–1101 as excessive hip flexion can lead to femoral nerve compression and inferior dislocations. The posterior abduction strap should be at the level of the child’s scapula and adjusted to allow for comfortable abduction, thus preventing the hips from adducting to the extent that the hips dislocate. Excessive abduction should be avoided because of concern regarding the development of avascular necrosis. It is important to carefully monitor the patient to insure that the harness fits and the hips are reduced. Fitting should be checked clinically within the first week and then weekly thereafter, and quadriceps function should be assessed at all clinic visits. Ultrasound is an
Table 1
A suggested algorithm for treatment of DDH.
Diagnosis of DDH
Patient < 6 months
Yes
Pavlik harness No
Hip reduced in harness? (ultrasound)
Yes
Hip reduced in spica? (X-ray + CT)
Yes
Continue until stable
No
Patient 6-24 months
Yes
Closed reduction +/-Traction No
No Patient > 24 months
Yes
Continue casting for 6-12 weeks (longer for closed reduction)
Open reduction +/- femoral shortening +/pelvic osteotomy
Abduction bracing
Monitor until skeletal maturity
Consider pelvic osteotomy
No
Yes
Acetabular remodeling (AI < 20°)
ARTICLE IN PRESS 228 months of age. In these patients, contractures of the hip capsule and supporting ligaments prevent gentle reduction of the hip. Interposition of the limbus or the tendon of the iliopsoas tendon may block the femoral head from entering the acetabulum.2
Closed reduction Patients presenting between 6 months and 2 years of age are best managed by a period of skin traction followed by careful reduction under anesthesia. Closed reduction is performed with the aid of arthrography, used to determine the adequacy of the reduction. Arthrography is especially useful in determining the adequacy of closed reduction of the hip. A medial dye pool and/or an interposing limbus is associated with a poor prognosis. If, on the other hand, there is a sharp or even a blunted limbus and no medial dye pooling, prognosis is good. The safe zone of Ramsey, the angle between maximum abduction and minimum abduction in which the hip remains reduced, should also be measured. This should be at least 251 and can be increased with release of the adductor longus. The cone of stability is a cone that involves hip flexion, abduction and internal/external rotation. If this cone measures greater than 301, it is considered satisfactory. Then a spica cast is applied, with care taken in molding over the posterior aspect of the greater trochanter of the ipsilateral limb. Then a postoperative CT scan is taken to ensure there is no evidence of posterior subluxation. The cast should be worn for 6–12 weeks, when the hip is reexamined and, if found to be stable, the patient is placed in an abduction brace. If still unstable, a further period in a spica cast is necessary.
Operative treatment Indications for surgery are met if the expected results of the surgery are better than those of the natural history. The natural history of untreated hip dislocations depends, in part, on the severity of the disease, bilaterality, and whether or not a false acetabulum is formed. Unilateral dislocations result in significant leg length inequality, with a gait disturbance and possibly associated hip and knee pain. The development of a false acetabulum is associated with a poor outcome in approximately 75% of patients. Bilateral hip dislocation in a patient without false acetabuli will have a better
J.J. McCarthy et al. overall prognosis. In fact, Milgram reported a case of a 74-year-old man with no history of hip or thigh pain whose dislocated hips were only discovered shortly before his death. Relative contraindications to surgery include age over 8 years for a unilateral hip dislocation, or over 4–6 years for bilateral hip dislocation, especially if there is no false acetabulum.
Open reduction Open reduction is the treatment of choice for the child presenting older than 2 years of age or for the younger child after failed closed reduction. There are two surgical approaches for open reduction of the hip: the medial approach and the anterior approach. The advantages of the medial approach are:
if bilateral both hips can be reduced at the same time, obstacles to reduction e.g. psoas tendon are easily identified, the adductor longus can be sectioned through the same incision, the hip abductor muscles and iliac apophysis are avoided, the resultant scar is relatively inconspicuous. Problems with this approach include:
increased risk avascular necrosis, the potential lack of familiarity of surgeons with this approach, the inability to perform capsular plication or a pelvic procedure through this incision.
If a medial approach is used, the post-operative cast plays a much more important role than the more commonly used anterolateral approach. This can, if necessary, be combined with a capsule plication, and/or an acetabular procedure. Between the ages of 2 and 3 years, either traction or femoral shortening can be considered, but in a child older than 3 years of age, femoral shortening is typically performed instead of traction18 (Fig. 3). Proximal femoral dysplasia, such as that seen with significant anteversion or coxa valga, can also be corrected at the same procedure. After open reduction, a spica cast is worn for 6–12 weeks. As with a closed reduction, a CT scan may be necessary to confirm reduction. The patient is then placed in an abduction orthosis. The length of time in a hip orthosis remains controversial and depends on the treating physician’s experience and the individual
ARTICLE IN PRESS Developmental dysplasia of the hip (DDH)
229
Fig. 3 Open reduction, femoral shortening and pelvic osteotomy in a 6-year-old female. Preoperative and 6 months postoperative radiographs.
patient. The authors’ practice is for full-time orthosis wearing for 3 months after cast removal, and wean to night-time splinting when there is radiographic evidence of acetabular remodeling and no recurrent subluxation.
Pelvic osteotomies A pelvic osteotomy for residual hip dysplasia may be necessary. A pelvic osteotomy can be performed at the time of open reduction, and is indicated if there is persistent instability after open reduction. As acetabular remodeling may occur after open reduction, some surgeons feel at least 12–18 months of acetabular remodeling should be allowed before an acetabular procedure is undertaken. In children over 4 years of age with significant hip dysplasia, an acetabular procedure should be considered at the time of open reduction due to the decrease in remodeling potential.
Complications Complications include
Redislocation, stiffness of the hip, infection, blood loss, the most devastating, avascular necrosis (AVN) of the femoral head.
The incidence of AVN varies significantly, depending on the study, from 0 to 73%20 and may be evident years after the surgery. Numerous studies show that extreme abduction, especially combined with extension and internal rotation, results in a higher incidence of AVN. All reductions (open or closed) have a risk of AVN, and all patients must be followed to skeletal maturity.
Results Overall, the prognosis of children treated for hip dysplasia is good. In one study of children between the ages of 1 and 3 years, 83% had a good or excellent results (Severin class I or II).19
Conclusion Developmental dysplasia of the hip (DDH) is a common disorder. Clinical screening exams should be performed in all infants, and repeated at each evaluation until walking with a normal gait. Special attention should be directed towards children with underlying risk factors. Additional evaluation methods, such as ultrasound or radiographs may be needed. The diagnosis can be difficult, even in experienced hands, and a late diagnosis does not necessarily imply a missed diagnosis. Treatment depends on the age of initial diagnosis and success
ARTICLE IN PRESS 230 of previous treatment. Earlier treatment usually requires less aggressive methods. Follow up should be continued to skeletal maturity, and both hips should be carefully evaluated. Although outcomes are usually very good, long-term sequelae occur even in patients who receive optimal treatment.
References 1. Barlow TG. Early diagnosis and treatment of congenital dislocation of the hip. J Bone Joint Surg Br 1962;44:292. 2. Ponseti IV. Growth and development of the acetabulum in the normal child: anatomical, histological, and roentgenographic studies. J Bone Joint Surg Am 1978;60:575. 3. Ralis A, McKibbin B. Changes in shape of the human hip joint during its development and their relation to its stability. J Bone Joint Surg Br 1973;55:780. 4. Salter R. Aetiology, pathogenesis, and possible prevention of congenital dislocation of the hip. Can Med Assoc J 1968;98:933. 5. 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;58:1000–4. 6. Kumar SJ, MacEwen GD. The incidence of hip dysplasia with metatarsus adductus. Clin Orthop 1982;164:234. 7. Weiner DS. Congenital dislocation of the hip associated with congenital muscular torticollis. Clin Orthop 1976; 121:163. 8. Ilfeld FW, Westin GW, Makin M. Missed or developmental dislocation of the hip. Clin Orthop 1986;203:207. 9. Ortolani M. Congenital hip dysplasia in the light of early and very early diagnosis. Clin Orthop 1976;119:6.
J.J. McCarthy et al. 10. Darmonov A. Clinical screening for congenital dislocation of the hip. J Bone Joint Surg Am 1996;78:383. 11. Harcke HT, Kumar SJ. The role of ultrasound in the diagnosis and management of congenital dislocation and dysplasia of the hip. J Bone Joint Surg Am 1991;73:622. 12. Clarke NMP, Clegg J, Al-Chalabi AN. Ultrasound screening of hips at risk for CDH: failure to reduce the incidence of late cases. J Bone Joint Surg Br 1989;71:9. 13. Albinana J, Morcuende JA, Weinstein SL. The teardrop in congenital dislocation of the hip diagnosed late. J Bone Joint Surg Am 1996;78:1048. 14. Portinaro NM, Matthew SJE, Benson MK. The acetabular notch in hip dysplasia. J Bone Joint Surg Br 1994;76: 271. 15. O’Sullivan ME, O’Brien T. Acetabular dysplasia presenting as developmental dysplasia of the hip. J Pediatr Orthop 1994;14:13. 16. Viere RG, Birch JG, Herring JA, et al. Use of the Pavlik harness in congenital dislocation of the hip: an analysis of failures of treatment. J Bone Joint Surg Am 1990;72: 238. 17. Lerman JA, Emans JB, Millis MB, Share J, Zurakowski D, Kasser JR. Early failure of Pavlik harness treatment for developmental hip dysplasia: clinical and ultrasound predictors. J Pediatr Orthop 2001;21:348. 18. Schoenecker PL, Strecker WB. Congenital dislocation of the hip in children: comparison of the effects of femoral shortening and of skeletal traction in treatment. J Bone Joint Surg Am 1984;66:21. 19. Zionts LE, MacEwen GD. Treatment of congenital dislocation of the hip in children between the ages of one and three years. J Bone Joint Surg Am 1986;68:829. 20. Keret D, MacEwen GD. Growth disturbance of the proximal part of the femur after treatment for congenital dislocation of the hip. J Bone Joint Surg Am 1991;73:410.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 231–242
www.elsevier.com/locate/cuor
TRAUMA
Injuries of the midfoot Nilesh K. Makwanaa,, Marck R. van Lieflandb a
Wrexham Maelor Hospital, Croesnewydd Road, Wrexham, LL13 7TD, UK Nutkin, Church Lane, Selattyn, SY10 7DN, Shropshire, UK
b
KEYWORDS Midfoot fracture; Fracture; Tarsal fracture; Stress fracture
Summary Injuries of the midfoot are relatively rare but they can lead to significant morbidity if missed. Serious injuries may present in a subtle manner and are often misdiagnosed as a sprain. Small avulsion fractures of the navicular and cuboid may be misdiagnosed as a simple avulsion when in fact they represent a more severe midfoot injury. A high index of suspicion is required. Good quality X-rays with three views must be obtained and if suspicion exists further imaging with a bone scan, CT or MRI is necessary. Prompt diagnosis and early treatment will prevent long-term disability and morbidity. Salvage procedures following these injuries often involve arthrodesis that limit mobility and frequently lead to an unsatisfactory outcome. & 2005 Elsevier Ltd. All rights reserved.
Introduction Injuries of the midfoot are relatively rare. If these injuries are missed, however, they can lead to significant morbidity and disability. Early recognition of these injuries and prompt accurate treatment may minimise the long-term morbidity. Accurate diagnosis using standard three views X-rays and if necessary followed by CT, MRI or bone scans should identify most injuries and aid in the management. Salvage procedures often include arthrodesis of the affected joints and the results of this are rarely good. This review will describe Corresponding author. Tel.: +44 1978 725191;
fax: +44 1878 725391. E-mail addresses:
[email protected] (N.K. Makwana),
[email protected] (M.R. van Liefland).
the common injuries of the midfoot including their classification, investigations, treatment and outcome.
Anatomy of the midfoot The midfoot is a relatively rigid structure in comparison to the hindfoot and forefoot and as such it provides a stable structure to transmit load. The bones comprising the midfoot include the cuboid, navicular and the three cuneiforms. The cuboid supports the lateral column and is positioned between the calcaneum and the base of fourth and fifth metatarsals. The calcaneocuboid joint is saddle shaped. The dorsal surface is traversed by extensor digitorum brevis and peroneus tertius. Ligaments from the dorsum attach
0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2005.05.002
ARTICLE IN PRESS 232 widely to the navicular, lateral cuneiform and fourth and fifth metatarsals. On the plantar aspect the cuboid has a groove for the peroneus longus tendon. Ligaments on the plantar surface spread to the fourth and fifth metatarsals and calcaneum as well as to the navicular and lateral cuneiform. The cuboid articulates with the navicular and a facet for the navicular bone exists in 45.5–54.5% of feet.1 The navicular (scaphoid) is interposed between the cuneiforms and talus. The joint surface is concave proximally and convex distally with facets for the cuneiforms. Similar to the talus most of its joint surface is covered with cartilage. The calcaneonavicular, talonavicular and navicular-cuneiform ligaments attach dorsally. The anterior, tibionavicular, part of the deltoid ligament also supports the anteromedial aspect of the joint. The tibialis posterior tendon inserts into the medial tuberosity. A separate tuberosity from the main navicular is known as the naviculare secundarium. The head of the talus lies in a deep socket or acetabulum pedis formed by the navicular, anterior calcaneum, the bifurcate ligament and calcaneonavicular ligaments. The superomedial calcaneonavicular ligament originates from the sustentaculum tali and inserts on to the navicular. The articular surface is smooth and fibrocartilaginous on the volar aspect. The spring ligament (inferior calcaneonavicular ligament) originates from the coronoid cavity of the calcaneus anteriorly and inserts into the volar aspect of the navicular. The bifurcate ligament (ligament of Chopart) is formed by the lateral calcaneonavicular and medial calcaneocuboid ligament. The blood supply of the navicular is derived from a branch of the dorsalis pedis artery dorsally and from a branch of the medial plantar artery volarly. The tuberosity receives branches from an anastomosis of these two. A rich anastomosis exists around the circumference of the navicular and a paucity of vessels supplying the central one-third occurs in adults. Torg et al.2 showed with microangiographic studies that the lateral and medial third were vascular and the central one-third avascular. This probably accounts for the increased rate of non-union and avascular necrosis seen following fracture. The three cuneiforms are positioned between the navicular and the first three metatarsals. They form a transverse arch with the cuboid. The medial cuneiform has a plantar-based wedge, whereas the intermediate and lateral cuneiform have a dorsally based wedge. The middle cuneiform is recessed 8 mm relative to the medial and 4 mm relative to the lateral cuneiform, which creates the mortise
N.K. Makwana, M.R. van Liefland for the second metatarsal base, rather like a tenon in a tenon joint. Numerous accessory bones exist around the midfoot and they are thought to be developmental anomalies. The os tibiale (naviculare secundarium) is located on the posteromedial aspect of the navicular and incorporated in the tibialis posterior tendon. It is seen in 3–12% of feet and may have a fibrous, fibrocartilaginous or bony connection. The os supranaviculare (Pirie’s bone) is located dorsally to the talonavicular joint and the os vesalianum lies just proximal to the fifth metatarsal tuberosity base. The os peroneum lies in the tendon of peroneus longus under the cuboid. Tendon ruptures often occur in the region and may be misdiagnosed as an avulsion fracture of the fifth metatarsal or cuboid. Awareness of these accessory bones is important to avoid misdiagnosing fractures. The midfoot joints consist of the Chopart’s joints i.e. the talonavicular and calcaneocuboid, and the lesser tarsal bones, the navicular, cuboid and cuneiforms. The cuboid and navicular act as an amphiarthrosis and move together on the anterior calcaneum and talar head. A longitudinal and transverse axis exist. The longitudinal axis is 15 upwards to horizontal and 9 medial.3 The movement around this axis is supination and pronation and also helical with a screwlike action. The second transverse axis is steeper and oblique with dorsiflexion-abduction or plantarflexion-adduction with the calcaneus and talus fixed. With the hindfoot in varus the axis of the midtarsal joints are no longer congruent and motion in the midfoot is reduced. This allows the midfoot to become a rigid lever arm through which propulsion can occur during gait. With hindfoot valgus the axes are parallel and the midfoot becomes flexible. This allows the foot to adapt to different surfaces and also allows energy absorption during heel strike, which decreases stresses in the midfoot joints. The medial column, i.e. the talonavicular, naviculocuneiform and first and second tarsometatarsal joint, is relatively rigid compared to the lateral column, i.e. calcaneocuboid, cuboid, fourth and fifth metatarsal joint. Therefore, patients tolerate arthrodesis in the medial column better than in the lateral column.
Midtarsal joint injuries Injuries of the midtarsal joints are rare and frequently overlooked. They often occur in young patients4 and have important economic consequences. In one review high energy road traffic
ARTICLE IN PRESS Injuries of the midfoot accidents accounted for 72% of these injuries and 33% of injuries involved the Chopart and/or Lisfranc joints.4 Associated fractures occurred in 74% of cases. However, these injuries can occur with low energy force as a simple fall or twist.5,6 Delayed or inadequate treatment can lead to permanent disability.7 The largest series was that reported by Main and Jowett7 who reviewed 71 midtarsal joint injuries. In their series a delay in the diagnosis was seen in 41% of cases. The injuries were classified based on the direction of force and the resulting displacement. Five groups were identified and these form the basis of the current classification:
longitudinal, medial, lateral, plantar, crush injuries.
Longitudinal injuries These accounted for 41% of injuries. The mechanism of injury is a force transmitted along the metatarsals in the plantarflexed foot that leads to compression of the navicular between the talar head and cuneiform. The navicular splits and a medial fragment is displaced medially. With more severe injuries an impaction fracture of the talus can occur. With less plantarflexion of the foot the navicular can displace dorsally with impaction of the lower pole. Undisplaced fractures are treated with a below knee walking cast. Displaced fractures will require closed or open reduction and internal fixation. In Main and Jewett’s series five out of 15 patients with pure longitudinal injuries without bony displacement medially had a poor result, compared to two out of 14 when medial displacement was present. In addition undisplaced injuries had a better outcome compared to displaced.
Medial injuries In 30% of injuries forces from the lateral to medial side of the foot lead to medial injuries. There are three resulting fracture patterns:
fracture sprain, fracture subluxation/dislocation, swivel dislocation.
Fracture sprains are caused by an inversion strain and X-rays show a flake fracture of the talus or navicular medially and a flake fracture of the
233 calcaneus and cuboid laterally. In a subluxation/ dislocation injury the whole foot displaces medially at the talonavicular and calcaneocuboid joint. A swivel dislocation is an unusual injury where the talonavicular joint is disrupted and the calcaneocuboid joint remains intact. The foot does not invert or evert but rotates, swivelling on the interosseus talocalcaneal ligament. High falls accounted for the majority of cases. Fracture sprains are stable and can be treated by a short period in a below knee walking cast and thereafter protected with a medial arch support and a hard soled shoe. They can displace if initially left unprotected. A fracture subluxation/dislocation requires prompt reduction either closed or open. The fracture is stabilised with a K-wire or screws. K-wires are removed at 6 weeks and nonweight bearing is maintained for a further 6 weeks. If screws are used protection in a below non-weight bearing-knee cast for 6 weeks is followed by partial to full weight bearing in a cast or fracture boot for a further 6 weeks. They are removed at 12 weeks. A medial arch support is prescribed for 9–12 months in both cases.
Lateral injuries These accounted for 17% of injuries. Again the patterns include a fracture sprain, fracture subluxation/dislocation and a swivel type injury. In fracture sprains an abduction force causes an avulsion of the navicular tuberosity or flake fragment medially with an impaction injury on the lateral side (Fig. 1). This fracture pattern has also been termed the nutcracker fracture.8–10 These injuries usually occur following a fall. A lateral subluxation/dislocation at the talonavicular and calcaneocuboid joint usually occurs following a high fall or road traffic accident. Treatment is similar to medial injuries. The outcome is better with sprains. The nutcracker injuries can be treated by restoring the lateral column length and fusing the calcaneocuboid joint or, in younger patients, by bone grafting and temporary stabilisation of the calcaneocuboid joint.10 Dewar and Evan6 recommended reattaching the avulsed navicular fragment and fusing the calcaneocuboid joint because of better results than achieved with a plaster cast.
Plantar forces These accounted for only 7% of injuries seen in Mann and Jowett’s series. These often follow high energy injuries like road traffic accidents. Injuries
ARTICLE IN PRESS 234
N.K. Makwana, M.R. van Liefland Crush injuries to the midfoot are rare and often reported as isolated case reports.12,13 Larger series have reported a variety of treatment techniques including lag screw fixation across the navicular fragments.14 Main and Jowett used either open or closed reduction and plaster cast, debridement or excision of the bone in four patients, resulting in three fair and one poor result.
Associated problems
Figure 1 A 52-year old woman sustained an abduction injury to her midfoot, resulting in a lateral fracture sprain. Black arrow—impaction fracture cuboid. White arrow—avulsion fracture navicular. Note also the os naviculare secundarium (os tibiale).
can vary from a sprain to fracture subluxation/ dislocation and swivel injuries.
Crush injuries These were the least common injuries seen and accounted for only 6% of cases. Only crush injuries were associated with a compound injury. No constant pattern of injury is seen and the outcome in Mann and Jowett’s series was only fair in 75% of cases. Soft tissue injury is common and insuring an adequate soft tissue envelope for the foot becomes a primary goal. The principle of management of the osseous structure is maintaining adequate medial and lateral column length to avoid cavus or planus deformities, respectively. The aim is to obtain a plantigrade foot and to preserve motion in the Chopart joints by using stable internal fixation or arthrodesis to maintain anatomical alignment.11 If stable fixation of a comminuted navicular is not possible, a bridging plate from the talus to the first metatarsal can be used and removed at 3 months. Sangeorzan et al.11 used this technique in seven patients and all fractures healed without loss of position. Compound injuries are treated in a standard fashion with early debridement and fracture stabilisation followed by secondary soft tissue closure. Compartment syndromes can occur and should be treated appropriately.
Midfoot injuries are rare and can be easily missed or misdiagnosed as an ankle sprain.6 A high index of suspicion should be maintained and simple avulsions of the navicular tuberosity should not be considered in isolation. Howie et al.5 found that of 14 patients with a navicular tuberosity fracture seven had damage to the anterior process of the calcaneus which may have represented an occult subluxation of the midtarsal joint. All seven patients had prolonged symptoms and three had persistent but not disabling pain 3 years after injury.5 These injuries were seen in middle aged women falling a short distance. Occasionally ecchymoses on both sides of the foot may be seen and can indicate an occult injury.6 Good quality X-rays including an AP, lateral and oblique should be obtained and if necessary a CT scan should be requested. Prompt reduction and immobilisation may prevent longterm disability. High energy injuries may be associated with compound injuries and compartment syndrome and these should be treated promptly. A below knee amputation was necessary in 1.9% of cases in a study by Thermann et al.15 In the same study 11.6% of cases required a fasciotomy for compartment syndrome. The outcome of longitudinal injuries is correlated with the severity of injury and displacement.7 Reduction may improve outcome but this is not guaranteed as cartilage damage may already be present at injury. Considerable impairment was seen at an average follow-up of 9 years in the study reported by Thermann et al.15 In cases where severe joint destruction is seen a primary arthrodesis may be indicated. The outcome of lateral injuries is not as good as medial injures and salvage procedures often include a triple arthrodesis. Main and Jowett demonstrated that the outcome following these injuries depends on the stability of the medial column.7
Fractures of the navicular The navicular bone is termed the keystone for the vertical stress on the medial arch.16 Following
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Figure 2 Post-traumatic avascular necrosis and osteoarthritis 2 years after an undiagnosed navicular injury.
trauma it is essential to restore the anatomy to avoid deformity and later disability. The tenuous central blood supply has been described and it is hence more likely to develop avascular necrosis or a non-union compared to other midfoot structures (Fig. 2). The diagnosis of navicular fractures has been described as ‘sometimes obvious, frequently difficult and occasionally elusive’.16 Fractures of the navicular are rare but more common than fractures of the cuboid or cuneiforms.17 Pain and tenderness over the navicular region should be investigated with AP, lateral and oblique X-ray views. Normal X-rays with persistent pain warrant further investigation with a bone scan, CT scan or MRI to rule out occult fractures. Watson-Jones18 first described these injuries as a fracture of the tuberosity, fracture of the dorsal lip and a transverse or horizontal fracture of the body. DeLee19 classified these into four groups, which is currently the adopted classification. These are the cortical avulsion fracture also known as the ‘chip’ fracture, tuberosity fracture, fractures of the body, and stress fractures.
Dorsal cortical avulsion fracture The mechanism is usually a twisting injury with inversion and plantar flexion or eversion of the foot. The dorsal talonavicular ligaments and capsule or the anterior part of deltoid is under tension leading to an avulsion fracture. These fractures are the most common and accounted for 47% of
fractures in the largest series reported by Eichenholtz and Levine16. Giannestras and Sammarco20 noted the association with lateral sprains of the ankle. Careful examination will distinguish between the two. An occult injury of the Chopart joints should be suspected. Treatment of this injury is conservative with a short period of immobilisation with a simple support bandage. Persistent symptoms can be treated by excision of the fragment. Large fragments which involve more than 25% of the joint surface should be treated by ORIF to minimise discomfort, reduce the risk of osteoarthritis and prevent subsequent midtarsal subluxation.
Tuberosity fracture These injuries result from twisting with eversion or valgus of the hindfoot. The tibialis posterior tendon and anterior part of the deltoid ligament are under tension resulting in an avulsion of the navicular tuberosity (Figs. 3 and 4). These injuries may be associated with a compression injury of the lateral column, which represents a more serious midfoot injury, which requires treatment as outlined above. These fractures should not be confused with an accessory navicular (os tibiale externum), which has a smoother outline. If doubt exists the other foot can be X-rayed as accessory ossicles are often bilateral. For simple avulsion injuries symptomatic treatment with a supportive bandage is all that is required. For severe discomfort a period in a
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N.K. Makwana, M.R. van Liefland
Figure 3 Navicular avulsion fracture. Note also accessory navicular!
walking cast may be required. Non-union is often asymptomatic but excision of the fragment may be indicated when painful. A large fragment or diastasis of more than 5 mm may be an indication for ORIF followed by a non-weight-bearing cast for 8 weeks.21
Navicular body fractures Fractures of the body are rare. They usually result from a direct axial load secondary to a fall or by indirect force. A vertical fracture is thought to result from forcible plantar flexion and abduction of the midfoot. Main and Jowett considered these fractures as part of the longitudinal midtarsal joint injuries. These fractures occur with high energy trauma and may be associated with soft tissue injury and compartment syndrome. Good quality X-rays should be obtained including an AP, lateral and oblique and if necessary a CT scan. Pinney and Sangeorzan et al.14 classified these fractures into three types (Fig. 5). In type 1 fractures the fracture line is transverse in the coronal plane with a dorsal fragment that is less than 50% of the body (Fig. 6). AP X-ray may show a normal medial border. The most common is type 2 when the fracture line passes from dorsolateral to plantarmedial with the main large fragment being dorsomedial. In type 3 fractures there is central or lateral comminution and there may be disruption of the medial column of the foot and lateral displacement of the foot (Fig. 7). In addition disruption of the calcaneocuboid joint may be seen. Sanders and Hansen noted
Figure 4 Navicular avulsion fracture treated with ORIF and restoration of joint congruency.
that with the medial fragment intact the foot may displace medially with varus of the hindfoot.22 Non-displaced fractures can be treated by a nonweight-bearing cast for 8–10 weeks until union. In displaced fractures closed reduction is unlikely to be maintained and ORIF is recommended. A dual incision may be necessary using a dorsomedial and dorsolateral approach. Care is taken to protect the neurovascular structures that lie in the first web space to avoid devascularisation of the remaining bone fragments. An extra-articular distractor may aid with reduction. Bone graft from the distal or proximal tibia may be necessary to fill any defects. Type 1 fractures can be treated using a 3.5 or 4 mm lag screw perpendicular to the fracture line. In type
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Figure 5 Sangeorzan’s classification of navicular fractures. Type 1 with dorsal fragment, type 2 with dorsomedial fragment, type 3 with central comminution.
Figure 6 Navicular fracture, Sangeorzan type 1 with dorsal displacement. Treated by ORIF.
2 fractures comminution of the plantarlateral fragment and subluxation of the dorsomedial fragment makes reduction difficult. An external
distractor such as an external fixator from the talus to the first metatarsal may aid visualisation and reduction. If there is minimal comminution and
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N.K. Makwana, M.R. van Liefland The talonavicular joint should be preserved as fusion limits subtalar movement. The medial column rarely requires a structural iliac bone graft to restore its length. Postoperatively non-weight bearing is advised for 10–12 weeks and K-wires are removed at 6 weeks. Transfixation screws should be removed at 6 months to prevent breakage. A medial arch support should be used for an additional 6–12 months. Eichenholtz and Levine16 reviewed the largest series of 67 navicular fractures of which 19 were body fractures. Most were managed conservatively. Five patients subsequently required a talonavicular fusion or triple arthrodesis, resulting in one excellent, three good and one fair result.16 Pinney et al.14 reported on their results in 21 navicular fractures. Reduction was satisfactory in all type 1, 67% type 2 and 50% of type 3. Of 15 satisfactory reductions 14 had good results and one fair. Avascular necrosis was seen in two cases and partial avascular necrosis in four. Final outcome was determined by the quality of reduction and by the type of fracture.
Stress fractures of the navicular
Figure 7 23-year old man with a Sangeorzan type 3 navicular fracture, treated by ORIF, obtaining good restoration of joint surface.
good preservation of the joint surface a lag screw from the dorsomedial aspect to the plantarlateral fragment is inserted. If the plantarlateral fragment is too comminuted then transfixing the dorsomedial fragment to the second or third cuneiforms or cuboid with screws is recommended. If fixation is not possible, the aim is an ankylosis between the dorsomedial fragment to the cuboid or lateral cuneiform. Persistent subluxation of the talonavicular joint is addressed by placing a temporary K-wire across this joint. In type 3 fractures an attempt should be made to restore normal anatomy if possible and the fragments held by transfixation to the cuneiforms. The outcome following these injuries is poor with only one good result out of four in the series by Pinney et al.14 If significant joint damage exists then consideration should be given to fuse the navicular cuneiform joints primarily.23
Towne et al.24 first described stress fractures of the navicular in two boys and noted that they ‘may require special roentgenographic views and laminography for detection’. Stress fractures of the navicular were considered to be rare with an incidence of 0.7% of stress fractures in one series.25 Over 150 cases have been reported and Hunter26 stressed that these injuries were probably more common than recognised and this was supported by Khan et al.27 Stress fractures of the navicular are more common in men than women with an average age of 20 (range 14–45). Most occur following sports, particularly track and field events (Fig. 8). An increase in athletic activity in an unfit person who takes up jogging or in an athlete before an important event can lead to a sudden increased stress in the navicular giving rise to a stress fracture. Delay in diagnosis is common with an average of 7.2 months in one study.2 Patients usually present with insidious medial foot pain or a cramp like sensation. Hunter26 noted that standing on tip toes reproduces pain over the navicular. There is little swelling but usually tenderness on palpation. Pain often resolves with rest and most patients can jog but avoid forefoot strike. Failure to recognise these early symptoms and a delayed diagnosis may result in fracture propagation and displacement.2,26,27 Torg et al.2 found that predisposing features included a short
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Figure 8 17-year old female cross country runner with a navicular stress fracture, treated by ORIF and autologous bone grafting.
first metatarsal, metatarsus adductus and hyperostosis or stress fractures of the second, third or fourth metatarsal. If a stress fracture is suspected standing AP, lateral and oblique X-rays should be performed. It should be borne in mind that the X-ray features lag symptoms by 2–3 weeks and serial X-rays may be indicated.28 A coned down view may be necessary and if X-rays are negative then a bone scan will show increased uptake. A CT scan will clarify the fracture pattern and whether it is partial or complete. The fracture often lies in the central one-third in the sagittal plane. An MRI scan will show a characteristic intraosseous band of low signal that is continuous with the cortex and surrounding areas of decreased signal intensity on T1 images. T2 images show high signal changes around the fracture (Fig. 8). Stress fractures are treated by non-weight bearing for 6–8 weeks. Torg et al.2 treated 10 uncomplicated fractures (five partial and five complete non-displaced) by non-weight bearing for 6–8 weeks and all fractures healed and patients returned to full activity by 3.8 months (3–6
months). Fitch et al.29 found that 14 out of 37 treated by non-weight bearing in a cast or rest resumed sports by 10 months. Khan et al.27 found that 86% of cases ð19 22Þ resumed sports after treat9 ment with non-weight bearing compared to 26% ð34 Þ treated with weight-bearing. In seven out of nine cases which were treated by weight-bearing rest or walking cast a delayed or non-union resulted. If a stress fracture fails to heal after a period of weight bearing then non-weight bearing is advised for a further 6–10 weeks with 90% success. Displaced, complete, delayed unions and non-unions should be treated by ORIF and bone grafting followed by nonweight bearing until union. Fitch et al.29 showed that not all stress fractures heal by non-weight bearing and radiographs may reveal a complete fracture, extension of a fracture, delayed union or a medullary cyst. En bloc resection of the fracture and bone grafting without internal fixation if the fracture was stable was performed resulting in 15 out of 18 cases (80%) becoming asymptomatic and returning to pre-injury sport levels at an average of 8 months. CT scanning is usually needed to monitor healing.
ARTICLE IN PRESS 240 New modalities of treatment include external electromagnetic or ultrasonic therapy or implantable electrodes. The long-term efficacy is not yet known. Untreated stress fractures may progress to a complete non-union with subsequent deformity. A talonavicular or triple arthrodesis with structural bone grafting can be used as a salvage procedure.
Cuboid fractures The cuboid is an important bone as it maintains the lateral column of the foot and articulates with both the calcaneus, fourth and fifth metatarsal and in some cases the navicular. The position of the cuboid is such that isolated fractures of the cuboid are rare. Avulsion of ligament and capsule is the most common cause of cuboid fractures, with fracture dislocation, compression, stress fracture, and toddler’s fractures also seen.28,29 Avulsion fracture and compression ‘nutcracker’ fracture result from indirect forces which may be associated with a midfoot injury.8–10 These injuries need to be recognised and treated as described before. Fractures are commonly seen following a road traffic accident or a fall. Isolated fractures of the cuboid are rare but mal-union is likely to lead to restricted movement.30,31 Clinically the patients present following an injury which may be a direct force to the lateral border of the foot or following a fall with a twisting element. Pain is localised over the cuboid and careful examination should exclude a medial Chopart injury. Undisplaced fractures can be treated in a below knee walking cast for 6–8 weeks. The treatment of displaced cuboid fractures is controversial. Hermel and Gerson-Cohen32 recommended that early arthrodesis in a comminuted fracture would decrease the period of morbidity. In contrast others have recommended accurate anatomical reduction and fixation to maintain the lateral column length and mobility.30 Cuboid fractures treated by conservative methods resulted in only fair or poor results in the series by Main and Jowett7 and all required a triple arthrodesis later. Despite comminution of the joint articular surface the anatomy can be restored and if necessary bone graft used with satisfactory results obtained.30 The surgical incision should spare the stabilising ligaments of the calcaneocuboid joint and the distal tarsometatarsal ligaments. A small distractor may aid exposure of the joint to assist reduction and a buttress or H-plate applied to maintain reduction. Occasionally with marked comminution a plate can extend from the calca-
N.K. Makwana, M.R. van Liefland neus to the fifth metatarsal and allow an ankylosis to form with preservation of lateral column length. Postoperatively the foot is kept non-weight bearing until union. The plate is removed at 6 months. Late symptoms or signs with degenerative changes can be treated with an arthrodesis. Stress fractures of the cuboid are rare. Stress fractures in the foot usually involve the navicular (see above), calcaneus and metatarsals. The mechanism of stress fracture of the cuboid is not known with any certainty as it forms part of the lateral column which is flexible compared to the medial column and therefore protected from repetitive stresses. Beaman and Saltzman et al.33 reported on two cases in college athletes who were treated by immobilisation and activity modification. This led to the resolution of symptoms in both cases.
Cuneiform fractures As with injuries to the cuboid, fractures of the cuneiforms are rare. The mechanism of injury is usually direct trauma and displacement is uncommon. Indirect force may result in a cuneiform fracture but these are often associated with a Chopart and/or Lisfranc injury and are treated as such. Isolated fractures of the cuneiform are rare. Patterson34 reported on an isolated fracture of the medial cuneiform following a motorcycle accident. The patient was asymptomatic at 3 months following anatomical reduction and fixation. Cuneiform fracture-dislocations have been reported and are relatively uncommon. Closed-reduction of the medial cuneiform may be prevented by interposition of the tibialis anterior tendon and will then require an open reduction.35 Small avulsion injuries can be treated conservatively in a wooden sole shoe or walking cast. Displaced fractures will require good quality X-rays or a CT scan to exclude a Chopart or Lisfranc injury. Displaced fractures will require anatomical reduction and internal fixation followed by a period of non-weight bearing in a plaster cast for 6 weeks (Fig. 9). If associated ligament injury is present then protection for a further 4–6 weeks is recommended. In comminuted fractures stabilisation with K-wires may be necessary and these can be removed at 6 weeks.
Key points
Midfoot injuries are rare and often subtle They often present as small avulsion fractures
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Figure 9 23-year old woman, sustained cuneiform fractures in an RTA. Treated by ORIF and NWB 8 weeks.
A more complex ligamentous injury should be suspected Appropriate treatment can prevent long term disability Salvage procedures often result in an unsatisfactory outcome.
References 1. Sarrafian SK. In: Anatomy of the foot and ankle. Descriptive topographic functional. 2nd ed. Philadelphia: JB Lippincott Company; 1993. 2. Torg JS, Pavlov H, Cooley LH, et al. Stress fractures of the tarsal navicular. J Bone Joint Surg 1982;64A:700–12. 3. Manter JT. Movements of the subtalar and transverse tarsal joints. Anat Rec 1941;80:407. 4. Richter M, Wippermann B, Krettek C, Schratt H, Hufner T, Thermann H. Fractures and fracture dislocations of the midfoot: occurrence, causes and long term results. Foot Ankle Int 2001;22(5):392–8. 5. Howie CR, Hooper G, Hughes SPF. Occult midtarsal subluxation. Clin Orthop Rel Res 1986;209:206–9.
6. Dewar FP, Evans DC. Occult fracture-subluxation of the midtarsal joint. J Bone Joint Surg 1968;50-B(2):386–8. 7. Main BJ, Jowett RL. Injuries of the midtarsal joint. J Bone J Surg 1975;57-B(1):89–97. 8. Herel MB, Gershon-Cohen J. The nutcracker fracture of the cuboid by indirect violence. Radiology 1953;60:850–4. 9. Hunter JC, Sangeorzan BJ. A nutcracker fracture: cuboid fracture with an associated avulsion fracture of the tarsal navicular. AJR 1996;166:888. 10. Hsu JC, Chang JH, Wang SJ, Wu SS. The nutcracker fracture of the cuboid in children: a case report. Foot Ankle Int 2004;25(6):423–5. 11. Schildhauer TA, Nork SE, Sangeorzan BJ. Technical trick. Temporary bridging plating of the medial column in severe midfoot injuries. J Orthop Trauma 2003;17(7):513–20. 12. Dhillon MS, Gupta R, Nagi ON. Inferomedial (sustentacular) dislocation of the navicular: a case report. Foot Ankle Int 1999;20:196–200. 13. Dixon JH. Isolated dislocation of the tarsal navicular [letter]. Injury 1979;10:251. 14. Pinney SJ, Sangeorzan BJ, Benirschke SK, Mosc V, et al. Displaced intra-articular fractures of the tarsal navicular. J Bone Joint Surg 1989;71A:1504–10. 15. Richter M, Wippermann B, Krettek C, Thermann H, et al. Fractures and fracture dislocations of the midfoot:
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16. 17. 18. 19.
20.
21.
22. 23.
24. 25.
occurrence, causes and long-term results. J Bone Joint Surg 2000;82A(11):1609–18. Eichenholtz SN, Levine DB. Fractures of the tarsal navicular bone. Clin Orthop 1964;34:142–57. Wilson PD. Fractures and dislocations of the tarsal bones. South Med J 1933;26:833–45. Watson-Jones R. Fractures and joint injuries, vol. II, 4th ed. Baltimore: The Williams and Wilkins Co; 1955. DeLee JC. Fractures and dislocations of the foot. In: Mann RA, Coughlin MJ, editors. Surgery of the foot and ankle, vol. 2, 6th ed. St Louis: Mosby—Year book; 1993. p. 1465–703. Giannestras N, Sammarco GJ. Fractures and dislocations of the foot. Rockwood CA, Green DP, editors. Fractures, vol. 2. Philadelphia: JB Lippincot; 1987. p. 1400–95. Sanders R. Fractures of the midfoot and forefoot. In: Mann RA, Coughlin MJ, editors. Surgery of the foot and ankle, vol. 2, 7th ed. St. Louis: Mosby; 1999. p. 1574–605. Sanders R, Hansen Jr ST. Progressive talonavicular dissociation. Orthop Trans 1989;13:572. Johnstone AJ, Maffulli N. Primary fusion of the talonavicular joint after fracture dislocation of the navicular bone. J Trauma 1998;45:1100–2. Towne LC, Blazina ME, Cozen LN. Fatigue fracture of the tarsal navicular. J Bone and Joint Surg 1970;52-A(3):376–8. Orava S, Puranen J, Ala-Ketola L. Stress fractures caused by physical exercise. Acta Orthop Scand 1978;49:19–27.
N.K. Makwana, M.R. van Liefland 26. Hunter LY. Stress fracture of the tarsal navicular: more important than we realize? Am J Sports Med 1981;9: 217–9. 27. Khan KM, Bruckner PD, Kearney C, Fuler PJ, et al. Tarsal navicular stress fractures in athletes. Sports Med 1994;17: 65–76. 28. Geslien GE, Thrall JH, Espinosa JL, Older RA. Early detection of stress fractures using 99m Tc-polyphosphate. Radiology 1976;121:683–7. 29. Fitch KD, Blackwell JB, Gilmour WN. Operation for nonunion of stress fractures of the tarsal navicular. J Bone Joint Surg 1989;71-B:105–10. 30. Sangeorzan BJ, Swiontkowski MF. Displaced fractures of the cuboid. J Bone Joint Surg 1990;72-B:376–8. 31. Simonian PT, Vahey JW, Rosenbaum DM, Mosca VS, Staheli LT. Fracture of the cuboid in children. J Bone Joint Surg 1995;77-B:104–6. 32. Hermel MB, Gershon-Cohen J. Nutcracker fracture of the cuboid by indirect violence. Radiology 1953;60:850–4. 33. Beaman DN, Roeser WM, Holmes JR, Saltzman CL. Cuboid stress fractures: a report of two cases. Foot Ankle Int 1993;14:525–8. 34. Patterson RH, Petersen D, Cunningham R. Isolated fracture of the medial cuneiform. J Orthop Trauma 1993;7:94–5. 35. Compson MP. An irreducible medial cuneiform fracture– dislocation. Injury 1992;23(7):501–2.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 243–245
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CME SECTION
Three external CME points available The following series of questions are based on the CME designated article for this issue—‘‘Examination of the wrist: Parts I and II’’ by R. Srinivas Reddy and J. Compson. Please read the article carefully and then complete the self assessment questionnaire by filling in the square corresponding to your response to each multiple-choice question. For true or false questions, please fill in one square only. After completing the questionnaire, either post or fax the answer page back to the Current Orthopaedics Editorial Office at the address at the bottom of the RESPONSE sheet. Please photocopy this page if you wish to keep your copy of Current Orthopaedics intact. Replies received before the next issue of Current Orthopaedics is published will be marked and those reaching an adequate standard will qualify for three external CME points. You will be notified of your marks and a CME certificate will be despatched for your records
Questions
4. How far can the pisiform be moved by manual pressure when examining the normal wrist?
1.In which tendon is the Pisiform bone situated? A. B. C. D. E.
Abductor digiti minimi Extensor carpi ulnaris Flexor carpi ulnaris Flexor digiti minimi 3rd palmar interosseus
2. Which of the following is not part of the distal row of the carpus? A. B. C. D. E.
Triquetrum Hamate Capitate Trapezoid Trapezium
A. B. C. D. E.
Not at all No more than 5 mm in any direction 1 cm distally and 5 mm towards the midline 2 cm distally and 1 cm towards the midline 1 cm distally and 5 mm away from the midline
5. Which bone lies in the base of the ‘ulnar snuffbox’? A. B. C. D. E.
Pisiform Triquetrum Hamate Base of 5th metacarpal Ulnar styloid process
3. Which of the following does not form a boundary for the anatomical snuff box?
6. Which of the following does not cause radial deviation of the carpus?
A. B. C. D. E.
A. B. C. D. E.
Abducto pollicis longus Extensor pollicis longus Extensor pollicis brevis Waist of scaphoid Radial artery
doi:10.1016/j.cuor.2005.06.001
Ulnar caput syndrome Radial shortening due to fracture Inflammatory arthropathy Scapholunate dissociation Fracture malunion with loss of radial slope
ARTICLE IN PRESS 244 7. Which of the following is not one of the stabilisers of the distal ulna? A. B. C. D. E.
Triangular fibrocartilage complex Extensor carpi ulnaris sheath Extensor retinaculaum Flexor carpi ulnaris and pisiform Pronator quadratus
8. Which of the following correctly associates a numbered extensor compartment and its contents? A. First — extensor pollicis longus and extensor pollicis brevis B. Second — extensor carpi radialis longus and extensor carpi radialis brevis C. Third — extensor pollicis longus and extensor indicis D. Fourth — extensor digitorum communis E. Fifth — extensor carpi ulnaris 9. Which bone lies under the fourth extensor compartment? A. B. C. D. E.
Scaphoid Lunate Triquetrum Trapezium Trapezoid
CME SECTION 10. With an acute painful wrist ligament injury, how much translation is observed on performing the modified Fisk’s forward shift test (pseudostability test)? A. B. C. D. E.
More than 2 cm 1.6 – 2 cm 1.1 – 1.5 cm 0.6 – 1 cm Less than 0.5 mm
11. In the wrist, what does the pivot shift test detect? A. B. C. D. E.
Ulnar collateral ligament injury in the thumb Scaphoid nonunion Scapholunate ligament rupture Midcarpal instability Distal radioulnar joint instability
12. In which of the following circumstances is ulnar abutment least likely? A. B. C. D.
Visibly prominent ulnar head Radial shortening with no tilt after fracture Congenital ulnar plus wrist Pain elicited clinically on ulnar side by forced ulnar deviation of wrist E. Torn TFCC observed on arthroscopy for ulnar sided wrist pain
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Your details (Print clearly) NAME. . . . . . . . . . . . . . . . . . . . . ADDRESS. . . . . . . . . . . . . . . . . . . . FAX NO. . . . . . . . . . . . . . . . . . . . . EMAIL. . . . . . . . . . . . . . . . . . . . . RETURN THE COMPLETED RESPONSE FORM by fax to +44-113-206-6791, or by post to CME, Current Orthopaedics, Orthopaedic Surgery, Clinical Sciences Building, St. James’s University Hospital, Beckett Street, Leeds LS9 7TF, UK.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 246
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CME SECTION
Answers to CME questions in Vol. 19, issue 1 Please find below the answers to the Current Orthopaedics CME questions from Vol. 19, issue 1 which were based on the article—‘Ionising radiation and orthopaedics’ by P. Dewey, S. George and A. Gray from the same issue. 1 2 3 4 5 6 7 8 9 10 11 12
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Aims and Scope Current Orthopaedics presents a unique collection of international review articles summarizing the current state of knowledge and research in orthopaedics. Each issue focuses on a specific topic, discussed in depth in a mini-symposium; other articles cover the areas of basic science, medicine, children/adults, trauma, imaging and historical review. There is also an annotation, self-assessment questions and an exam section. In this way, the entire postgraduate syllabus will be covered in a 4-year cycle. The Journal is cited in: Cochrane Center, EMBASE/ Excerpta Medica, Infomed, Reference Update and UMI Microfilms.
Editor Professor R. A. Dickson MA, ChM, FRCS, DSc St James’s University Hospital Trust, Leeds, UK
Editorial Committee President of BOTA, M. A. Farquharson-Roberts (Gosport, UK), I. Leslie (Bristol, UK), D. Limb (Leeds, UK), M. Macnicol (Edinburgh, UK), J. Rankine (Leeds, UK)
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D. C. Davidson (Australia) J. Harris (Australia) S. Nade (Australia) G. R. Velloso (Brazil) J. H. Wedge (Canada) S. Santavirta (Finland) P. N. Smyrnis (Greece) P. N. Soucacos (Greece) M. Torrens (Greece)
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ARTICLE IN PRESS Current Orthopaedics (2005) 19, 247–254
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MINI-SYMPOSIUM: HIP REPLACEMENT
(i) A review of minimally invasive hip replacement surgery—current practice and the way forward N.A. Siddiqui, P. Mohandas, S. Muirhead-Allwood, T. Nuthall The London Hip Unit, 30 Devonshire Street, London, W1G 6PU, UK
KEYWORDS Hip; Total hip replacement; Minimally invasive surgery
Summary Advances in surgical techniques and greater understanding of the anatomy of the hip now permit minimally invasive hip replacement. Benefits include shorter hospitalization and faster rehabilitation. & 2005 Elsevier Ltd. All rights reserved.
Introduction Around 37,800 primary total hip replacements (THRs) are carried out in England and Wales every year.1 It is an extremely successful procedure, which has evolved through a series of implants and operative techniques. There are many surgical approaches to the hip joint for THR, each having its own advantages and disadvantages. The most commonly used are the anterior and posterior approaches. Around 50% of all primary THRs are performed using the anterior or antero-lateral approach, as this is thought to give an overall superior view of the acetabulum and reduced dislocation rates compared with the posterior approach in particular. Whichever approach is used the incision tends to be relatively long, current practice is to use a single incision up to 30 cm long to approach the hip joint, with considerable cutting of muscle and other soft Corresponding author.
tissues. Trauma inevitably causes a significant inflammatory response, which delays healing. Current surgical practice has benefited greatly from techniques which minimize surgical exposure and dissection, ranging from arthroscopy, through the wide variety of abdominal and pelvic laparoscopic procedures, thoracic surgery, to laparoscopic hernia repair. Minimally invasive surgery (MIS) of the hip joint, utilising a smaller incision with reduced tissue damage is a logical progression. The advantages of the MIS technique arise from the reduction in trauma to the soft tissues with dissection. This reduces postoperative pain, allows greater mobility, reduces the length of hospital stay, gives a smaller scar (Fig. 1), and reduces the need for blood transfusion. It follows that performing the operation using a much smaller approach will cause much less trauma to the underlying tissues. There are a variety of approaches to the hip joint which are termed MIS. These range from new paths to the hip joint which have been developed that involve little or no cutting of tissues, relying instead on retraction to
0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2005.06.004
ARTICLE IN PRESS 248
N.A. Siddiqui et al.
Figure 2 Angled acetabular reamer compared to standard straight introducer.
Figure 1 Example of a mini-posterior approach scar at 6 weeks postoperatively.
give a good operative field, to performing the same operation as a standard approach through either one or two smaller incisions. To facilitate good exposure through a smaller incision, there is now a wide range of specially adapted instruments available. Some approaches require intraoperative X-ray screening to ensure correct placement of the prosthetic components as small incisions may not permit sufficient direct visualization. Techniques are being developed which rely on an electromagnetic map being made of the hip joint using small implants in the bone so that the orientation can be demonstrated without having to have exposure to harmful X-rays for every procedure. Prostheses are also being introduced which cater specifically for MIS to allow easier implantation through much smaller incisions. Femoral stems in particular can be difficult to orientate and insert correctly through a small incision, and the soft tissues and skin can prevent easy insertion.
History of MIS Despite MIS having been used as a technique since 19932 via the anterior approach, there is no clear
Figure 3 Variety of MIS retractors.
definition of what constitutes a minimal invasive surgical procedure. Some see it as just using a smaller incision, up to 10 cm long3, others as a new approach to hip surgery involving different anatomical pathways to facilitate better access through a smaller incision. Others would argue that MIS should incorporate a different technique involving less muscle cutting and therefore less soft tissue trauma, thereby enabling better recovery not just because the skin incision is small but because the trauma to the deeper soft tissues is also minimized. The traditional approach to the hip uses instruments unsuitable for MIS, which has led to a huge number of new instruments being designed for MIS. These include specially designed retractors, some with light attachments, angled reamers to gain access to the acetabulum for reaming without needing excessive retraction, and prosthesis introducers with longer shafts or different angles. Some examples are shown in Figs. 2–4:
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incision. The outcomes of a study into the twoincision technique found a greater number of complications if the patient’s BMI was over 30 kg/m2.
Surgical technique The approaches to the hip are broadly classified into:
Single-incision approach Two-incision approach
Single incision approach Figure 4 Angled acetabular component introducers.
Anatomical studies The search for radically different approaches to the hip has led to re-assessment of the anatomy of the hip.4 These minimize tissue trauma utilising intermuscular access, where tissues are retracted and spread open rather than being cut, as well as identifying neurovascular hazards to further minimize complications. An added benefit is that with less soft tissue disruption, the risk of dislocation will be minimized.
The single incision technique is currently the most commonly used MIS technique, but there is some confusion regarding correct nomenclature of the differing techniques:
Anterior (modified Smith–Peterson) Anterolateral (modified Watson–Jones also referred to as the OCM technique) Direct lateral approach6 (modified Hardinge) Posterior approach (modified Moore7)
The anterior approach The anterior approach has many variations, mostly passing through the internervous line between the sartorius (supplied by the femoral nerve) and tensor fascia lata muscles (supplied by the superior gluteal nerve), as illustrated by Siguier et al.2
Indications The MIS technique is, at present, only suitable for primary THR.5 It may be used for cemented or uncemented prostheses. It is contra-indicated for difficult primary THR, e.g. where there is significantly abnormal anatomy, complete hip dislocation, or where it may be necessary to perform additional procedures. A standard incision is recommended for such procedures at present. It is not suitable for procedures such as hip resurfacing where the femoral head is preserved because exposure of the acetabulum is limited. MIS technique is unsuitable for revision hip surgery, as this usually requires much wider exposure to remove the existing prosthesis and cement if present. There is also a higher incidence of femoral fracture during revision hip surgery which would need adequate exposure to stabilize. Patient size may also be a limiting factor. In an obese or well muscled patient, it can be very difficult to reach the deeper structures through a small
The anterolateral approach A technique developed by Heinz Rottinger8 (Orthopaedica Chirurgica Munich—OCM) uses an intermuscular approach anterolaterally, a modification of the Watson–Jones approach. This has been used by Bertin and Rottinger for over 300 patients. The incision starts at the anterior tubercle of the greater trochanter and extends 7 cm towards the anterior superior iliac spine. A plane is developed by blunt dissection between the tensor fascia lata posteriorly and the gluteus medius and minimus anteriorly to expose the anterior capsule which is then opened via a U-shaped capsulotomy. Using this technique no muscles or tendons need to be incised or split, which is thought to lead to better return to function of the abductor musculature. Abductor function is also preserved by avoiding the division of the anterior portions of the abductors and damage to the superior gluteal nerve is avoided. Denervation of the posterior portion of vastus lateralis is also prevented because this muscle does not need to be split.
ARTICLE IN PRESS 250 The direct lateral approach The mini-incision direct lateral approach, which is also sometimes confusingly referred to as the modified Hardinge approach, has been described by Ilizaliturri et al.,6 who used standard instruments to perform the procedures in 40 patients, rather than the specialized MIS instruments used by most other surgeons for different approaches. The greater trochanter is again the bony landmark, and an incision is made starting 2 cm proximal to the tip of the greater trochanter in its midline, extending 5–8 cm distally parallel to the long axis of the femur. The iliotibial band is incised, and the trochanteric bursa is resected. A ‘hockey stick’ incision is made through the gluteus medius muscle fibres, and gluteus minimus and rectus femoris fibres are detached from the hip capsule and greater trochanter to gain exposure to the hip capsule. After capsulotomy the hip can be dislocated in external rotation or the femoral head resected in situ with a high neck cut and then dislocated to expose the acetabulum and femur. The posterior approach In the posterior mini-incision approach the patient is positioned in the lateral decubitus position. The 6–10 cm incision is made over the posterior third of the greater trochanter in line with the femur, with one third of the incision extending proximal to the tip of the greater trochanter. The incision may be curved slightly posteriorly (Fig. 5). This gives the added flexibility of extending the incision in either direction as for a normal THR if further exposure is needed. The tensor fascia lata and gluteus maximus fascia are incised longitudinally and the muscle is split. The short external rotators are exposed and electrocautery used to detach piriformis and the short external rotators from the posterior aspect of the greater trochanter. These can be repaired at the end of the procedure with sutures passed
Figure 5 Posterior-mini approach incision position.
N.A. Siddiqui et al. through drill-holes made in the trochanter. After dislocating the hip the femoral head and neck are resected to expose the acetabulum. The acetabulum is reamed and the prosthesis inserted before the leg is flexed and internally rotated to deliver the proximal femur into the wound for reaming and prosthesis insertion, with the aid of further retractors to hold the proximal femur exposed. One of the main potential risks associated with this approach in particular is the risk of sciatic neuropraxia as a result of vigorous retraction to gain a better posterior view. If the view is inadequate then it is safer to extend the incision and have a longer scar than to risk sciatic injury.3
Two-incision approach The two-incision approach was described by Berger,5 and was developed and patented by the team of Dana Mears4 using the facilities of an anatomy laboratory to plan an approach to the hip with minimal trauma to vessels and nerves. Poor direct visualization means that intraoperative fluoroscopy is essential. The incisions are shown in Fig. 6. The patient is positioned supine on the operating table. The anterior of the two incisions is oblique, 4–6 cm in length, and made directly overlying the femoral neck, using fluoroscopy to accurately place the incision. The approach is between the tensor fascia lata muscle and the sartorius muscle superficially and then the tensor fascia lata muscle and rectus femoris muscle. No muscle fibres are cut gaining access to the capsule of the hip and incising it. The femoral head is removed in situ, enabling preparation of the acetabulum and insertion of the acetabular prosthesis. Fluoroscopy may be used for accurate reaming and placement of the prosthesis. The more posterior/lateral incision is made as if approaching the hip to place an intramedullary nail. An awl is used to enter the femoral canal, followed by reaming and insertion of the prosthesis. Again, fluoroscopy may be used to assist in correct positioning of the reamer/rasp and prosthesis. The abductors are not cut or traumatized to any great extent during this approach. Early complications from a multi-centre trial which started in 2001 included a 2.8% risk of proximal femoral fracture and injuries to the lateral femoral cutaneous nerve which were partial and temporary. This is acknowledged to be a more technically demanding technique than the single-incision anterior or posterior approaches, but the team developing it believe it allows much earlier discharge from hospital.4 However,
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Figure 6 Scar positions for the two-incision approach.
there is currently a lack of comparative trials to back up this view.
Guided prosthesis insertion With a mini-incision, particularly in the twoincision approach, visualization of the bony landmarks may be difficult, particularly the acetabulum. When inserting the acetabular component assisted visualization can be helpful. While most prostheses can be implanted to a reasonable degree of accuracy using just bony landmarks, navigational techniques can minimize implant misalignment, using intraoperative fiuoroscopy. This means it is less important to gain full direct visualization of the bony landmarks. Indeed, some studies suggest that the orientation of the prostheses may actually be better than direct visualization as the position is being checked fluoroscopically continuously during insertion. The length of time fiuoroscopy is needed during a procedure diminishes as the surgeon gains experience.9 In this study, time fiuoroscopy was used decreased from an average of 150 s for the first case to 100 s by the tenth case. Newer techniques, using technology which is already used in neurosurgery, where stereotactic information is provided using a three-dimensional image are becoming available. They require careful
preoperative planning with scans of the pelvic anatomy, imaging equipment to process this data, and a handheld probe with various cameras around the operating theatre to judge the position of the probe in three dimensions. No intraoperative exposure to X-rays is needed, but there is a need for detailed anatomical mapping using a preoperative CT scan. It does require significant experience for the surgeon to become accustomed to this new technique.10 The mini-incision technique with navigation via a posterior approach was first used in October 1998 for primary THR.10 Only the acetabular component was placed with navigational tools in the early series involving 33 patients. The HipNav system (Robotics Institute, Carnegie Mellon University) can be utilized for both cup and stem placement. It uses the patients’ CT scan for preoperative planning and an optical tracking system for intraoperative guidance. The surgeon selects the size and type of components and places them in an initial orientation on the pelvic and femoral models generated on the preoperative planner from the patients’ CT scan. Intraoperatively an infrared localizer determines the spatial location of markers rigidly attached to surgical tools and bony landmarks. Any acetabular component introducer handle can be equipped with tracking markers that allow active, continuous and precise tracking of the guide’s orientation relative to the pelvis. By introducing femoral tracking and navigation the
ARTICLE IN PRESS 252 system allows intraoperative control of stem placement and information regarding range of motion, offset and leg length in real time. The increased cost and exposure to radiation must be weighed against the advantages offered by computer navigation. Sherry et al.11 describe a technique called the NILNAV system whereby there is no need for either a navigation system or intraoperative X-rays. They have used a CFP stem (LINK Waldemar, Germany) with various attachments to the jig and other designed instruments such as ‘‘lollipop’’ spacers to orientate the acetabular cup to the stem. Early reports on 14 patients show good results with regard to hospital discharge as well as pain and quality of life. However, this is not a universally adaptable system, and cannot be used with all types of prosthesis.
Results and benefits of MIS Implant positioning One of the difficulties anticipated was concern relating to accurate placement of prosthetic components. Results of 105 patients receiving uncemented implants in one study by Dorr4 using the posterior mini-incision approach showed good cup positioning in both anteversion (15–301 acceptable) in 92% of patients, and inclination (25–451 acceptable) in 89% of patients. Femoral placement was also good, with 90% being within 31 of neutral positioning. Wenz12 used a wider range of positions for the acetabulum to define normal as 35–551 inclination, and showed that acetabular positioning was good in 94% of patients. He also defined neutral alignment of the stem as being 751, and achieved this in all cases. In a series of 142 patients operated on using the two-incision technique by Irving,7 fluoroscopy or other intraoperative imaging was not used at all. Postoperative radiographic analysis showed that the acetabular component was well positioned in 99% of these patients.
Postoperative morbidity All patients experience pain after THR to varying degrees. Some of this pain will be a result of invasion of the bone by reaming and insertion of prostheses, cement, screws, etc. The other main source of the pain will be originating from the soft tissues. The idea is that the less soft tissues are traumatized the less this aspect of pain should be.
N.A. Siddiqui et al. As well as causing the patient discomfort, pain is one of the main causes for poor mobility immediately postoperatively. By reducing their pain their mobility should be expected to be improved quite significantly. Additionally as the deeper soft tissues, and muscles in particular, have been cut much less or not at all, mobility should be improved. Earlier mobilization should also reduce morbidity from such causes as pneumonia and basal atelectasis, deep venous thrombosis and pulmonary embolism. The reduction in tissue trauma and the smaller skin incision, should reduce the need for blood transfusion procedures13 and the associated morbidity and cost. Sculco7 describes several small studies at his institution showing reduced blood loss (378 vs. 504 ml) in the groups of patients who had the single-incision technique as compared to a similar group having a standard incision, as well as slightly reduced surgical time and length of stay. A faster return to normal gait pattern was also seen with this group. In a prospective study of 42 patients at the same institute having a mini-posterior approach compared to 42 patients having a standard incision, although there was no significant difference in the operative time, estimated blood loss, or length of hospital stay, there was a slightly better Harris Hip Score in the mini-incision group, and all the patients in the mini-incision group expressed greater satisfaction with their scar’s cosmetic appearance. Earlier mobility and fewer complications results in a shorter hospital stay, with significant social and financial benefits. Mears’ study of patients having the two-incision technique showed over 90% of their patients left hospital within 24 h of surgery.4 A further study of 100 patients by Duwelkius et al.,4 using the two-incision method, showed 90% leaving hospital within 24 h of their THR, with the remainder leaving on the second postoperative day. However, the patients selected all weighed under 100 kg, were under 75 years old, and were less muscular than those having a standard approach hip replacement by the same surgeon. One hundred patients in a study by Berger4 were operated on using the two-incision technique. As experience of the technique increased, patients were selected less according to their physical characteristics and became more representative of the usual patient group operated on in his practice. Of the last 88 patients in the study 75 (85%) were discharged home the same day as surgery. It is to be expected that the overall rehabilitation period will be shorter as well, although there are no published studies to support this as yet.
ARTICLE IN PRESS A review of minimally invasive hip replacement surgery—current practice and the way forward Patients report much greater satisfaction with the appearance of a scar which is much smaller than a traditional incision. This has led to many of our patients specifically requesting a minimally invasive procedure.
Long-term outcomes Most published data relates to the two-incision technique; there is a relative paucity of published data relating to the single-incision technique, using any of the myriad of approaches. The techniques are too new for there to be long-term follow up and/or large series to permit comparison with longterm outcome studies looking at conventional THR. The main criticism of most published studies is that they focus on operative time, hospital stay, and radiographic analysis, rather than functional outcome and patient satisfaction. Duwelius14 does, however, note an average Harris Hip Score improvement from 52 points preoperatively to 90 points at 1 year (maximum 100 points). Many surgeons who perform smaller numbers of THRs may not benefit from this technique, as more experience is needed to achieve optimum results requiring a surgeon to be performing at least 50 arthroplasties per year.3 This will limit the number of centres where this procedure may be carried out, and thus limit the availability of data on outcomes. Patient selection may currently be causing bias in some studies reporting discharge times of around 24 h after the procedure. These may be younger and more active patients preoperatively, as it is clear that the older and more frail patient who already struggles with mobility due to multiple problems may not walk out of hospital so soon after having the procedure.
Future developments Currently both the one incision and two incision approaches are being reviewed by the United Kingdom National Institute for Clinical Excellence. The lack of powerful studies and the relatively new and innovative nature of the MIS technique has meant that this review is taking some time to complete. The report on the two-incision technique is expected in late 2005, with the report on the one-incision technique expected the following year. There have been no randomized trials, indeed some patients entered into early trials had heard of the two-incision technique and asked for it by
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name,15 and might therefore be expected to perform better as their expectations were much higher. In the same study all patients with major complications in the previous year (e.g. myocardial infarction) were excluded, as were those with three or more poorly controlled medical comorbidities. Similarly a common theme in many of the published trials seems to be a well thought out and implemented pain management protocol which also addresses nausea and vomiting as well as dizziness. Part of this regimen involves performing surgery under an epidural, not general anaesthetic. The incidence of postoperative nausea and vomiting is thought to be reduced significantly this way, as well as ensuring adequate hydration15 and patients may be sedated or rendered unconscious during the procedure using agents such as propofol, rather than any anaesthetic agents.4 Patients in one study would attend classes preoperatively and be taught by a specialist nurse what to expect from the operation, immediate postoperative phase and recovery process. They were also told that they would be able to walk independently on the day of their operation.15 This was reinforced by intensive physiotherapy and occupational therapy, which were started as early as 5 h postoperatively. Hence if patients’ expectations of their operation are that they will have a tremendous improvement in function immediately postoperatively, compared to the general perception of having severe pain and immobility after a THR, then they are more likely to have a better immediate outcome. Thus, what proportion of this rapid recovery is due to careful preoperative preparation of patients, patient selection, postoperative pain and nausea regimens, and early intensive physiotherapy, and how much is due entirely to the operative technique remain unclear. Therefore large studies are needed with traditional techniques being compared directly with MIS approaches. This must include patient selection, preoperative explanation and counselling, anaesthetic techniques, postoperative analgesic and physiotherapy regimens, as well as functional and radiological analysis in the long term and not just concentrating on the operative data. Only then will the true value of the MIS technique be known.
References 1. NICE Technology Appraisal Guidance No. 2. Guidance on the selection of prostheses for primary total hip replacement; April 2003.
ARTICLE IN PRESS 254 2. Siguier T, et al. Mini-incision anterior approach does not increase dislocation rate: a study of 1037 total hip replacements. Clin Orthop Relat Res 2004;426: 164–73. 3. Sculco TP. Minimally invasive total hip arthroplasty, in the affirmative. J Arthroplasty 2004;19(4 Suppl. 1):78–80. 4. Berry DJ, Berger RA, Callaghan JJ, et al. Minimally invasive total hip arthroplasty symposium. J Bone Joint Surg-Am 2003;85-A(ll):2235–46. 5. Berger RA. The technique of minimally invasive total hip arthroplasty using the two-incision approach. AAOS instructional course lectures, vol. 53; 2004. p. 149–55. 6. Ilizaliturri VM, et al. Small incision total hip replacement by the lateral approach using standard instruments. Orthopedics 2004;27(4):377–81. 7. Sculco TP, Jordan LC. The mini-incision approach to total hip arthroplasty. AAOS instructional course lectures, vol. 53; 2004. p.141–7. 8. Bertin KC, Rottinger H. Anterolateral mini-incision hip replacement surgery: a modified Watson–Jones approach. Clin Orthop Relat Res 2004;429:248–55.
N.A. Siddiqui et al. 9. Archibeck MD, White MD. Learning curve for the two-incision total hip replacement. Clin Orthop Relat Res 2004;429:232–8. 10. DiGioia AM 3rd, Blendea S, Jaramaz B, Levison TJ. Less invasive total hip arthroplasty using navigational tools. AAOS instructional course lectures, vol. 53; 2004. p. 157–64. 11. Sherry E, Egan M, Warnke PH, et al. Minimal invasive surgery for hip replacement: a new technique using the NILNAV hip system. ANZ J Surg 2003;73(3):157–61. 12. Wenz JF, et al. Mini-incision total hip arthroplasty : a comparative assessment of perioperative outcomes. Orthopedics 2002;25(10):1031–43. 13. Harwin SF. Blood conservation in total joint arthroplasty: blood as a drug. Issue Series Title: Orthopedics 2004;27(3): 276–7. 14. Berger RA, Duwelius PJ. Two-incision minimally invasive total hip arthroplasty: operative technique and early results from four centres. J Bone Joint Surg-Am 2003;85: 2240–2. 15. Duwelius PJ, Berger RA, Hartzband MA, Mears DC. Rapid rehabilitation and recovery with minimally invasive total hip arthroplasty. Clin Orthop Relat Res 2004;429:239–47.
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www.elsevier.com/locate/cuor
MINI-SYMPOSIUM: HIP REPLACEMENT
(ii) Conservative hip implants Ian D. Learmonth University of Bristol, Bristol Royal Infirmary, Bristol, BS2 8HW, UK
Summary Arthritis of the hip primarily involves the articulation between the femoral head and the acetabulum. The primary surgical objective is to replace these articular surfaces. In achieving this it is desirable to attempt to obtain a homogeneous transfer of forces to the proximal femur. This is best provided by retention of the femoral neck. Survivorship of the implant is determined by the durability of fixation and of the articular interface. Early attempts to achieve a conservative hip replacement were betrayed by poor materials, inadequate fixation and failure of the articulation. This paper explores how these shortcomings were addressed during the evolution of total hip arthroplasty to produce the contemporary designs of conservative hip implants. & 2005 Elsevier Ltd. All rights reserved.
Introduction Arthritis of the hip affects predominantly the joint itself. Early attempts at surgical treatment of hip arthritis were directed at replacing the joint surfaces—either by interpositional or resurfacing arthroplasty (RA). While there were a few good long-term outcomes, material and design deficiencies generally led to poor results. However, improved materials, better fixation and a greater understanding of the tribological imperatives have generated a resurgence of interest in metal-onmetal resurfacing arthroplasty (Fig. 1). Encouraging early results have been reported.1 The limits of the clinical application are yet to be defined. However, resurfacing arthroplasty does not fall within the scope of this article. Tel.: +44 0 117 928 2658; fax: +44 0 117 929 4217.
E-mail address:
[email protected].
In 1987 Jones and Hungerford2 coined the term cement disease’’ to describe osteolysis. While this proved to be a misnomer, it added impetus to the swing towards cementless fixation. Long-term success of hip implants is determined by both durability of fixation and articulation. Early cementless implants obtained reproducible fixation distally. However this was associated with thigh pain,3 and the distal off-loading predisposed to stress shielding with loss of proximal bone stock.4,5 Indeed, when considering the efficacy of porouscoated cementless fixation, Amstutz noted The incidence of thigh pain, radiographic stress shielding and removal problems must still be solvedy’’.6 All these issues are addressed by conservative implants. Patients today are better informed than ever before. They are politically empowered to demand early surgical intervention to restore quality of life. Ever younger cohorts are presenting for total hip
0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2005.04.002
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Hip arthritis; Surgery; Conservative arthroplasty; Femoral component
’’
KEYWORDS
ARTICLE IN PRESS 256 arthroplasty.7 The high probability of revision in these younger more active patients has been one of the main factors driving the quest for more bonesparing conservative options at total hip replacement (THR). More bone would then be available in
I.D. Learmonth the proximal femur for any subsequent revision surgery. Conservative implants also appeal to those surgeons embracing the increasingly popular concept of minimally invasive surgery with accelerated rehabilitation regimens.8 This paper will review the development of conservative implants over the years.
Conservative implants
Figure 1 Radiograph of a metal-on-metal resurfacing arthroplasty.
There are a variety of short-stemmed prostheses that obtain proximal fixation, such as the CFP (Waldemar-Link), Stellcor (Sulzer) and SHO (Biomechanica). However this paper will principally consider only those implants that are virtually confined to the metaphysis. Huggler and Jacobs designed the thrust plate prosthesis (TPP), which was first implanted in 1978.9 They reviewed their results in 1993.10 The implant (Fig. 2a) is designed to load the medial cortex of the femoral neck as physiologically as possible. The TPP has evolved through three generations. The latest version has an oval thrust plate attached to the mandrel. A central bolt passes through the lateral plate just below the greater trochanter and engages with a screw thread
Figure 2 (a) Radiograph showing replacement of the femoral head using a thrust plate prosthesis. (b) Radiograph of the femoral prosthesis used by Wiles in 1937. Note the similarity to the thrust plate.
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contained within the mandrel thrust plate unit. It is of interest how closely this implant resembles the implant designed by Philip Wiles first inserted in 1938 (Fig. 2b). In seeking a conservative’’ uncemented implant with proximal fixation, surgeons at the Mayo Clinic recognised that a wedge-shaped device which tapered in both the sagittal and coronal planes should give stability when inserted into an irregularly shaped cavity by providing multiple point contact. In 1982 these features were incorporated into a short double-tapered titanium alloy proximal femoral replacement—the Mayo Conservative Hip (Fig. 3). The distal end of the implant was curved inferiorly to provide a flat surface to contact the lateral cortex. The rigidity of mechanical fixation in all planes was found to be similar to that of a conventional cementless implant. The ESKA femoral neck endoprosthesis (CUT) is a mini-prosthesis which is anchored in the metaphysis and provides proximal physiological stress trans’’
Figure 4 The ESKA femoral neck endoprosthesis.
Figure 3 The Mayo conservative femoral prosthesis (illustration kindly provided by Dr. B Morrey).
mission, thus avoiding stress shielding (Fig. 4). It lends itself to minimal access surgery and is itself minimally invasive as only the femoral head is removed. It has been recommended for young arthritic patients with good bone quality.11 The IPS (DePuy) femoral stem (Fig. 5a) was developed approximately 10 years ago. This anatomic stem was designed to provide pure proximal loading, thus optimising load transfer in the metaphyseal region and reducing stress shielding. The stem was used principally for alignment and was designed to have no contact in the diaphysis, thus avoiding distal off-loading. In 1999 Walker et al.12 noted that a lateral flare which loaded the lower region of the greater trochanter would assist in transmitting loads to the proximal femur. They also suggested that stems with a lateral flare could be made shorter than designs not incorporating a lateral flare. In 1995 Santori designed a customised shortstemmed implant with the team at Stanmore Customs. This stem provided an anatomic fit in
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I.D. Learmonth
Figure 5 (a) The proximally fixed IPS. Note that the stem makes no contact with the diaphyseal cortex, thus loading the metaphysis. (b) Radiograph of the Santori customised femoral implant. (c) Combining the design features of the IPS and the Santori stem—the Proxima, a conservative metaphyseal implant.
the metaphysis with longitudinal slots for rotational stability, a pronounced lateral flare and no distal stem. The design and manufacture of this implant was taken over by DePuy International in 2002 (Fig. 5b). The similarity of the design of the metaphyseal region between the IPS and the Santori stem was recognised and the Proxima stem was evolved as a result of the combination of these philosophies.
The Proxima is a stemless, proximally fixed anatomic implant (Fig. 5c). Appropriate sizing and the anatomic shape provide rotational and axial stability. DePuy have also developed a wedge-shaped cylindrical implant—the Silent Hip—which has a textured surface and is impacted into the neck to provide initial stability (Fig. 6). Long-term stability is provided by bone ingrowth. This is a very
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Figure 6 (a, b) The Silent femoral neck prosthesis.
’’
Results Buergi et al.13 reported on the radiological and clinical outcome of 102 consecutive THRs in which the third generation of thrust plate was used.12 The mean follow-up was 58 months (range 26–100).
Eighty per cent of patients were younger than 60 years of age. Four implants were revised—two for infection and two for aseptic loosening. They noted that in 85% of cases load transmission occurred through the most proximal part of the medial cortex. Huggler et al. reviewed their long-term’’ results in 1993 and noted that the basic feature of the thrust plate is direct load transfer to the medial cortical bone of the femoral neck. They reported that histological examination of an implant removed at 8 years confirmed that newly formed ’’
conservative implant and is not dissimilar to the ESKA cigar’’ prosthesis.
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bone is in direct contact with the thrust plate with no interposed fibrous tissue. Ishaqui et al.14 reviewed 170 thrust plate prostheses clinically and radiologically at a mean follow-up of 5–8 years. Kaplan–Meier survivorship at 8 years was 90.5%. However they noted that good to excellent clinical results were achieved after revising the thrust plate. Morrey et al.15 reported on 162 total hip replacements in which the Mayo conservative uncemented femoral component was used. The mean age of the patients was 50.8 years and the mean follow-up 6.2 years (range 2–13). Survival without mechanical loosening was 98.2% at both 5 and 10 years, while survival without osteolysis was 99% at 5 and 91% at 10 years. While recognising the problem of osteolysis associated with wear debris, the authors note that its reliable mechanical stability makes this implant an attractive design, particularly for use in younger patients. They also observed a statistically significant reduction in the amount of blood loss compared with a control group of uncemented implants and ascribe this to the absence of reaming of the femoral canal. In addition they frequently saw increased bone density in zones 3 and 6. Kim16 prospectively followed up a consecutive series of 60 hips (50 patients) for a minimum of 6 years in which a close proximal fit and short tapered distal stem’’ prosthesis (IPS) was used. The mean age was 46.6 years with a mean follow-up of 6.3 years. Transitory thigh pain was present in 2% of cases. No component had been revised and there was no radiological evidence of aseptic loosening. However, a metal-on-polyethylene couple was used in all hips and a higher rate of polyethylene wear was noted in these younger patients. We have reviewed 81 consecutive IPS stems followed up for a mean of 3 years 9 months (range 2–6 years). One hip was revised for deep infection. There have been no other revisions and there was no radiological evidence of aseptic loosening. Indeed good buttressing of the bone was routinely encountered in the metaphyseal region. No patient complained of thigh pain. This review is due to be presented at the 7th EFORT Congress in Lisbon in June 2005. The author reviewed 106 Santori customised femoral stems. The mean age of the patients was 55 years. There were no revisions at a mean followup of 2 years (range 1–9 years). Good condensation of bone was noted circumferentially around those implants that were confined to the metaphysis with no stem. There was no evidence of bone resorption in any zone in these implants. Early results are encouraging.
Discussion There has been a recent tremendous resurgence of interest in resurfacing arthroplasty. This is the only surgical treatment for arthritis of the hip which preserves the femoral head. However, RA does not lend itself to minimal access surgery and clinical concerns remain regarding the vascularity of the femoral head and the incidence of femoral neck fracture—both in the short and the longer term. In addition there are well-identified contra-indications for RA. These can be broadly defined as follows:
Anatomical: excessive anteversion, severe slip of the femoral epiphysis, etc. Biomechanical: inability to restore offset and limb length (valgus neck, coxa breva, coxa plana, etc.). Pathological: poor supporting bone (osteonecrosis, multiple large cysts, etc.).
There is therefore a need for alternative conservative prostheses. There are two major contemporary issues that are driving the development of conservative implants. Firstly the increasing popularity of minimally invasive surgery and secondly the desire to optimise the loading of the proximal femur and to preserve bone stock. Ever younger cohorts of patients are presenting for total hip replacement. These patients demand restoration of their quality of life, which is reflected by their ability to pursue their recreational activities such as golf, tennis, skiing, etc. Implants inserted in these patients will not only have to last longer, they will also be exposed to an increased level of activity. Minimally invasive surgery should be associated with reduced soft tissue damage, shorter hospitalisation and an accelerated programme of rehabilitation and recovery. Minimally invasive should also relate to conservation of bone stock—although this is seldom the practice of surgeons carrying out this surgical technique. A concept relating to both the soft tissue and the bone is to be applauded, but should be embraced with caution. Few mid-term and long-term results are available for the conservative implants. In addition the mini-incision may be associated with an increased risk of complications. Woolson et al.17 compared THRs performed with a standard or a mini-incision and found that the mini-incision group had a significantly higher risk of wound complications, acetabular component malposition and poor fit and fill of cementless femoral components.
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Conclusion ’’
Wroblewski et al.18 noted that the successful long-term clinical results with the Charnley low friction torque arthroplasty identified proximal femoral shielding as a long-term problem. They ascribed this problem to distal load transfer in a stiffer stem that no longer fractured. Wroblewski introduced the triple taper polished cemented stem to address this problem.18 Proximal stress protection is encountered earlier with cementless stems, particularly those which gain fixation in the diaphysis. Many surgeons have therefore sought a more bone preserving, bone conserving option for younger more active patients. It has been shown that forces developed on weightbearing are more evenly distributed to the proximo-medial femur if the femoral neck is preserved. This also allows for anatomical reconstruction of the proximal femur and provides enhanced rotational stability. However a disadvantage of these femoral neck implants is that they cannot adjust for or accommodate anatomic abnormalities of the proximal femur (e.g. excessive anteversion, etc.). Achieving initial stability may also present a problem and this initial stability is essential for osseointegration and subsequent durable fixation. This led Santori19 to develop the twostep solution’’ in which a titanium femoral neck prosthesis was initially inserted through the lateral cortex. At 3 months, having achieved secure bony fixation, the femoral head is removed, the acetabulum is replaced and a prosthetic femoral head is applied. While this highlights the potential problem of achieving adequate initial stability in those cigar-shaped prostheses that rely on impaction into the femoral neck for fixation, I doubt if this two-stage solution would find wide acceptance. Significant cortical bone mass has been demonstrated at the proximo-lateral flare of the femur.20 Experiments have shown that if a femoral stem has a medial and lateral flare proximally, the loads are transferred to the proximal femur and stress protection in this area is avoided. This is particularly true if there is no stem contact distally, which could promote distal off-loading. Indeed, the results suggest that a stem below the lesser trochanter is unnecessary.12 Another important benefit of a bone-sparing and preserving proximal femoral implant is the relative ease with which this can be converted to a conservative’’ revision prosthesis, which need only invade the proximal diaphysis. This provides one extra step in the revision programme of a younger patient.
There is an old surgical aphorism the ability to perform an operation is not an indication to do it’’. Similarly the mere ability to manufacture and to insert a conservative femoral implant is not necessarily an indication to use it. If the surgeon is confident that the implant that he routinely uses will outlast the patient—then he should use it. Otherwise he should think about the next operation and consider a bone-sparing option. Conservative proximal femoral implants offer such an option.
Acknowledgements I would like to thank Alison Foxwell and Martha van der Lem for their assistance in the preparation of this manuscript.
References 1. McMinn DJW, Pynsent PB, De Cock CAEM, Isbister ES, Treacy RBC. Results of metal on metal hip resurfacing. J Bone Joint Surg Br 2000;82(B Supp II):125. 2. Jones LC, Hungerford DS. Cement disease. Clin Orthop 1987;225(Dec):192–206. 3. Callaghan JJ, Dysart SH, Savory CG. The uncemented porous-coated anatomic total hip prosthesis. Two-year results of a prospective consecutive series. J Bone Joint Surg Am 1988;70-A:337–46. 4. Engh CA, Bobyn JD, Glassman AH. Porous coated hip replacement. The factors governing bone ingrowth, stress shielding and clinical results. J Bone Joint Surg Br 1987; 69-B:44–55. 5. Malchau H, Herberts P, Wang YX, Karrholm J, Romanus B. Long-term clinical and radiological results of the Lord total hip prosthesis. A prospective study. J Bone Joint Surg Br 1996;78-B:884–91. 6. Amstutz HC, Namba R. Cementless femoral fixation using porous ingrowth fixation. In: Amstutz HC, editor. Hip arthroplasty. New York: Churchill Livingstone; 1991. p. 285–293. 7. Tennent TD, Goddard NJ. Current attitudes to total hip replacement in the younger patient: results of a national survey. Ann R Coll Surg Engl 2000;82:33–8. 8. Irving JF. Direct two-incision total hip replacement without fluoroscopy. Orthop Clin North Am 2004;35:173–81. 9. Huggler AH, Jacob HA. A new approach towards hip prosthesis design. Arch Orthop Trauma Surg 1980;97:141–4. 10. Huggler AH, Jacob HA, Bereiter H, Haferkom M, Ryf C, Schenk R. Long-term results with the uncemented thrust plate prosthesis (TTP). Acta Orthop Belg 1993;59 (Supp 1):215–23. 11. Thomas W, Lucente L, Mantegna N, Grundei H. ESKA (CUT) endoprosthesis. Orthopaedics 2004;33:1243–8. 12. Walker PS, Culligan SG, Hua J, Muirhead-Allwood SK, Bentley G. The effect of a lateral flare feature on uncemented hip stems. Hip Int 1999;9:71–80. 13. Buergi ML, Stoffel KK, Jacob HA, Bereiter HH. Radiological findings and clinical results of 102 thrust plate femoral hip
’’
’’
ARTICLE IN PRESS 262 prostheses. A follow-up of 2–8 years. J Arthroplasty 2005;20:108–17. 14. Ishaque BA, Wienbeck S, Sturz H. Midterm results and revisions of the thrust plate prosthesis (TPP). Z Orthop Ihre Grenzgeb 2004;142:25–32. 15. Morrey BF, Adams RA, Kessler M. A conservative femoral replacement for total hip arthroplasty. A prospective study. J Bone Joint Surg Br 2000;82-B: 952–8. 16. Kim YH. Cementless total hip arthroplasty with a close proximal fit and short tapered distal stem (third-generation) prosthesis. J Arthroplasty 2002;17:841–50.
I.D. Learmonth 17. Woolson ST, Mow CS, Syquia JF, Lannin JV, Schurman DJ. Comparison of primary hip replacements performed with a standard incision or a mini-incision. J Bone Joint Surg Am 2004;86-A:1353–8. 18. Wroblewski BM, Siney PD, Fleming PA. Triple taper polished stem in total hip arthroplasty: rationale for the design, surgical technique and seven years of clinical experience. J Arthroplasty 2001;16(Supp 1):37–41. 19. Santori F. Personal communication; 2004. 20. Fetto JF, Bettinger P, Austin K. Reexamination of hip biomechanics during unilateral stance. Am J Orthop 1995(Aug):605–12.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 263–279
www.elsevier.com/locate/cuor
MINI-SYMPOSIUM: HIP REPLACEMENT
(iii) Resurfacing arthroplasty of the hip Paul Robertsa,, Peter Grigorisb,c, Hendrik Boschd, Nilesh Talwakere a
Royal Gwent Hospital, Cardiff Road, Newport, NP9 2UB, UK Department of Medical Engineering, School of Engineering, Design and Technology, University of Bradford, Richmond Road, Bradford, West Yorkshire BD7 1DP, UK c 2nd Orthopaedic Department, University of Athens, Ag. Olga Hospital, 142 33 N. Ionia, Athens, Greece d Department of Orthopaedics and Trauma, Royal Gwent Hospital, Cardiff Road, Newport, NP9 2UB, UK e Department of Orthopaedics and Trauma, Royal Gwent Hospital, Cardiff Road, Newport, NP9 2UB, UK b
KEYWORDS Hip arthroplasty; Hip resurfacing; Metal-on-metal; Tribology
Summary Hip resurfacing is an attractive concept as it preserves proximal femoral bone stock, optimises stress transfer to the proximal femur and offers inherent stability and optimal range of movement. The results of hip resurfacing in the 1970s and 1980s were disappointing and the procedure was largely abandoned by the mid1980s. The expectation that these prostheses would be easy to revise was not often fulfilled. The large diameter of the articulation combined with thin polyethylene cups or liners, led to accelerated wear and the production of large volumes of biologically active particulate debris, leading to osteolysis and implant loosening. The renaissance of modern metal-on-metal articulations for total hip arthroplasty enabled the introduction of a new generation of hip resurfacings and the majority of the main implant manufacturers have already introduced such systems. Early results are encouraging and complications commonly seen in the 1970s and 1980s, such as early implant loosening and femoral neck fracture, now appear to be rare. & 2005 Elsevier Ltd. All rights reserved.
Introduction Total hip replacement in its current form has proven very effective in late middle aged and elderly patients, with implant survival rates in excess of 90% at 10 years.1 However, when younger Corresponding author. Tel.: +01633 238917; fax: +01633 656293. E-mail address:
[email protected] (P. Roberts).
patients are reviewed, especially males under 55 years of age, this survival figure drops to 80% at 10 years. By 16 years postoperatively reported survival figures are as low as 33%. Hip resurfacing is being advocated as an alternative treatment for young and active patients with hip arthritis. Resurfacing is an attractive concept, as it preserves proximal femoral bone stock, optimises stress transfer to the proximal femur and, due to the large diameter of the articulation, offers inherent stability and optimal range of movement.
0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2005.05.004
ARTICLE IN PRESS 264
History The concept of hip resurfacing is not new. Contemporary designs have evolved directly from the original mould arthroplasty introduced by Smith Petersen in 1948.2 Despite this being a hemiarthroplasty with no means of stable fixation to the femoral head, some survived for many years, although the outcomes were unpredictable. The first total resurfacing arthroplasty was developed by Charnley in the early 1950s utilising a Teflon-onTeflon bearing.3,4 This implant was associated with early failure, which Charnley ascribed to avascular necrosis of the femoral head. He subsequently recognised the poor wear characteristics of Teflon when he used it as the bearing material in total hip replacement. In 1967, Maurice Muller designed a metal-onmetal articulation. He implanted 18 surface replacements in young patients, in addition to 35 stemmed prostheses (Fig. 1). Despite excellent early clinical results, Muller abandoned the use of the metal-on-metal articulation in favour of metalon-polyethylene. Six of these all metal articulations were revised after functioning for up to 25 years.5,6 Cemented hip resurfacings utilising polyethylene (PE) acetabular components and metal femoral components were implanted in 1971 by Paltrinieri and Trentani in Italy7 and in 1974 by Freeman in the UK.8,9 Freeman had earlier used a PE femoral component and a metal acetabular component, but
P. Roberts et al. this was associated with rapid wear of the convex surface. In the same year, Wagner in Germany introduced a hip resurfacing (Fig. 2) which became widely used in Europe.10 The PE acetabular components had a thickness of only 4 mm. Both Co–Cr and ceramic femoral components were available, but the technique of femoral head preparation was crude. From 1976 a cementless alumina ceramic-on-ceramic resurfacing was used by Salzer in Vienna, but it was soon abandoned because of high rates of early loosening.11 In 1975, Amstutz introduced the total hip articular replacement using internal eccentric shells (THARIES) at UCLA.12,13 The original prosthesis was cemented and consisted of a Co–Cr femoral component and an all-PE acetabular
Figure 2 Cemented metal-on-polyethylene resurfacing system, introduced by H. Wagner in 1974.
Figure 1 Metal-on-metal hip prostheses introduced by M. Mueller and A. Huggler in 1967. On the right, a cementless hip resurfacing.
ARTICLE IN PRESS Resurfacing arthroplasty of the hip component. Subsequently, an uncemented system was introduced. In 1989, Buechel and Pappas introduced a cementless resurfacing system with a modular PE acetabular component and a titanium-nitridecoated titanium alloy femoral component.14
Modes of failure of first generation resurfacings The results of hip resurfacing in the 1970s and 1980s were disappointing and the procedure was largely abandoned by the mid-1980s except in a small number of centres. The expectation that these prostheses would be easy to revise was not often fulfilled. Although proximal femoral bone stock was well maintained, there was frequently extensive destruction of the acetabulum. This was partly a consequence of excessive removal of bone to accommodate the acetabular component and its cement mantle, but was mainly due to periprosthetic osteolysis. With our present knowledge, the first generation of metal-on-polyethylene resurfacings represented an excellent model of a high wear producing bearing. The large diameter of the articulation combined with thin PE cups or liners led to accelerated wear and the production of large volumes of biologically active particulate debris, leading to osteolysis and implant loosening (Fig. 3). However, as the implications of wear debris induced osteolysis were not fully appreciated at the time, failure was attributed to other factors,
Figure 3 Extensive osteolysis around a Porous Surface Replacement system introduced by H. Amstutz in 1983. The modular acetabular cup consisted of a chamfered Titanium alloy shell and a thin polyethylene liner.
265 including avascular necrosis of the femoral head and acetabular component loosening due to high frictional torque. The high incidence of femoral neck fracture was also an issue. The concern that resurfacing of the femoral head leads to avascular necrosis has not been confirmed by retrieval studies. Howie et al.15 examined 72 failed Wagner resurfacings. They concluded that there was viable bone in the femoral head and neck in the majority of cases. The bone destruction was consistent with wear particle induced osteolysis, not avascular necrosis. Similar findings have been reported by other investigators.16 Freeman has argued that the major blood supply to the arthritic femoral head is through intraosseous vessels, not through the subsynovial anastomoses.17 Such intraosseous vessels would not be disrupted during the exposure and preparation of the femoral head. This may explain why avascular necrosis has not been proven to be a significant complication following hip resurfacing. However, the debate concerning the effect that resurfacing has on the blood supply of the femoral head continues. The influence of the increased frictional torque, which is a consequence of the large diameter of the articulation, has been addressed by Mai et al.18 A relatively homogeneous group of 170 osteoarthritic patients who underwent a cemented THARIES resurfacing arthroplasty was studied. Hips were divided into three groups according to the diameter of the articulation. The authors showed that the larger-diameter prostheses survived significantly longer than the smaller ones, indicating that frictional torque was not the main factor causing acetabular component loosening. The experience of surface hemiarthroplasty for AVN of the femoral head using cemented components articulating against the host acetabulum, has clarified further the role of PE wear debris in the failure of hip resurfacing.19,20 In the absence of a PE bearing, no loosening or osteolysis was observed and the hips that required reoperation were revised for groin pain related to wear of the acetabular articular cartilage. Histological examination of the retrieved femoral head remnants showed a thin soft-tissue membrane interposed between the bone and the cement. The cement mantle was intact and the adjacent bone was viable. Contact radiographs of the slab sections showed the normal appearance of trabecular bone and no osteolytic lesions. The femoral neck fractures seen in the first generation of hip resurfacings were, with the benefit of hindsight, due to a combination of osteolysis of the femoral neck and the surgical technique advocated at the time. Intraoperative
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P. Roberts et al.
neck notching was often a consequence of extreme valgus positioning of the implant, which was recommended to reduce the tension and shear stresses across the head–neck junction.17 Undersizing of the implants in order to minimise frictional torque also resulted in notching. Trochanteric osteotomy, which was commonly used, could also compromise the femoral neck if it was too extensive.
The renaissance of hip resurfacing The reintroduction of metal-on-metal articulations for total hip arthroplasty (THR) began in 1988. Bernard Weber in collaboration with Sulzer developed the Metasul bearing; a precisely engineered, high-carbon-containing wrought-forged cobalt–chrome alloy with excellent wear characteristics.21 Large numbers of these bearings were used in Europe with good early results. The availability of a durable, low wear bearing which could be used in a large-diameter articulation enabled Heinz Wagner in Germany to introduce a second-generation hip resurfacing in 1991.22 This was a cementless system (Fig. 4). The acetabular component was a titanium alloy shell with a Metasul inlay. The thickness of the construct and the extensive macro-features on its external surface made it difficult to implant. There were only four sizes available and the instruments for the preparation of the femoral head were crude. Only small numbers of the Wagner metal-on-metal resurfacings were used and no long-term results are available. In the same year, in the UK, Derek McMinn in collaboration with Corin introduced a hip resurfacing based on a cast Co–Cr alloy.23 The initial design was smooth surfaced, press-fit on both sides (Fig. 5). The acetabular component was a modification of the Freeman finned cup. This design was associated with a high incidence of early failure due to aseptic loosening of both components. The following year the components were coated with hydroxyapatite (HA), but only a small number of these implants were inserted. In the same year, McMinn introduced a system in which both components were cemented. The original acetabular component was modified by removing the central peg and peripheral fins. The femoral component was not modified for cementing. This system had a high incidence of early acetabular loosening due to cement-cup debonding. This led to the introduction of a hybrid system in 1994, with a cementless HA-coated acetabulum. This implant was with-
Figure 4 The Wagner cementless metal-on-metal resurfacing. Both components consisted of two layers; a titanium alloy metal backing and a MetasulTM articulation.
Figure 5 The McMinn Mark I cementless metal-on-metal resurfacing system. The smooth surfaced components were made of cast Co–Cr alloy.
drawn in 1996, apparently because of problems with the manufacturing of the bearing. Subsequently, two different resurfacing systems evolved,
Design differences of contemporary hip resurfacings. Bearing
Acetabulum
Femur
Heat treatment
Size increments (mm)
Shape
Surface
Size increments (mm)
Cement mantle (mm)
Stem
Conserve plus 1996 Wright Medical
Cast
HIP* and SHTy
2
Truncated hemisphere
2
1
7Load bearing
Birmingham Smith and Nephew
1997
Cast
None
2
Hemisphere
Co–Cr beads Sintered 7HAz Co–Cr beads Cast-in
4
0
Not defined
Cormet Corin Durom
1997
Cast
HIP and SHT
2
4
0
Not defined
2001
Wroughtforged
Not applicable
2
Equatorial expansion Truncated hemisphere
2
1
Non-load bearing
2004
Cast
None
2
Hemisphere
2
0.5
Not defined
2004
Cast
HIP
2
Truncated hemisphere
2
‘‘Thin’’
Non-load bearing
Zimmer ReCap Biomet ASR DePuy
+HA Ti-VPSy +HA Ti-VPS
Ti-VPS 7HA Co–Cr beads
ARTICLE IN PRESS
Process
Introduced
Resurfacing arthroplasty of the hip
Table 1
Sintered +HA
*HIP hot isostatically pressed.ySHT solution heat treated.zHA hydroxyapatite.yTi-VPS Titanium vacuum plasma spray.
267
ARTICLE IN PRESS 268 one developed by Corin and the other by Midland Medical Technologies.
Contemporary hip resurfacing By the end of 2004, the majority of the main implant manufacturers had introduced metal-onmetal hip resurfacing systems (Table 1). All these systems have a number of features in common including: (i) a bearing made from high carbon containing Co–Cr alloy, (ii) cementless fixation of the acetabular component, (iii) cemented fixation of the femoral component. However, there are important differences between these implants, particularly relating to the metallurgy and geometry of the bearing and to aspects of the fixation of the acetabular and femoral components.
The bearing The factors that influence the tribological behaviour of metal-on-metal bearings include:
the type of alloy, the manufacturing process, the clearance of the articulation (diametrical mismatch), the sphericity of the components, the roughness of the articulating surfaces, the diameter of the articulation.
Metallurgy Perhaps the most controversial issue in contemporary metal-on-metal hip resurfacing is the metallurgy of the bearing. Whilst all manufacturers now use high carbon containing Co–Cr alloy, the processing of the alloy differs. The alloy can either be wrought-forged or cast. If cast, the components may undergo post-casting heat treatments such as hot isostatic pressing and/or solution heat treatment. Wrought Co–Cr alloy offers theoretical advantages over cast Co–Cr alloy as a bearing surface. Wrought Co–Cr is harder than cast Co–Cr (430 HV vs. 365 HV), enhancing wear resistance.24 The wrought alloy can also be highly polished, reducing surface roughness and enhancing lubrication. However, the results of hip simulator studies are conflicting: St. John et al.25 reported that cast
P. Roberts et al. alloys had greater wear resistance than wrought alloys. In contrast, Streicher et al.26 showed that wrought Co–Cr alloy had better wear characteristics than cast. The importance of heat treatments on cast Co–Cr alloy has been particularly hotly debated over the last 6 years. The annealing process results in depletion of the surface carbides, but the results from hip simulator studies demonstrate no significant difference in the wear behaviour between cast and heat-treated alloys.27 Until long-term clinical outcomes and/or reliable retrieval studies become available, it will not be possible to determine the relevance of the differences in the metallurgy of the currently available hip resurfacings. Bearing geometry Whilst metallurgical differences may be important, the control of bearing geometry is critical in determining the behaviour of large-diameter metal-on-metal bearings. In particular, the clearance, sphericity and surface roughness, all of which are dependant on the quality of the manufacturing process, greatly influence both the initial runningin wear and the steady state wear of the bearing.28 If other factors are equal, a low clearance increases the potential for fluid film lubrication, with full separation of the bearing surfaces.29 This lubrication regimen is associated with very low wear and very low friction (theoretically nil). However, a clearance that is too low could result in clamping of the articulation if there is deformation of the acetabular component under load, a significant risk with thin-walled, large-diameter cups. In contrast, an excessively large clearance will not generate full fluid film lubrication and will result in a low contact area and therefore high contact stresses, with associated high wear. A clearance of 100–150 mm appears to be the optimal compromise for large-diameter metal-on-metal articulations.30 Surface roughness is also an important factor in influencing the lubrication of metal-on-metal bearings. The lambda coefficient (film thickness ratio) indicates the lubrication mode occurring in total hip prostheses, with lambda values greater than 3 indicating full fluid film lubrication, and values less than 3 indicating mixed film lubrication. The value of lambda is inversely related to the mean roughness of the articulating surfaces. A 50% reduction in the average roughness would lead to doubling of the lambda coefficient, and thereby enhanced lubrication. Wrought Co–Cr alloy can now be polished to achieve a surface roughness of only 5 nm, greatly improving the potential for full fluid
ARTICLE IN PRESS Resurfacing arthroplasty of the hip film lubrication compared to alloys with higher surface roughness. For hard-on-soft articulations in general, the greater the diameter of the articulation the higher the volumetric wear, primarily because of the increased sliding distance. This relationship does not hold true for large-diameter metal-on-metal articulations. Smith et al.31 reported significantly lower steady-state wear rates for 36 mm diameter metal-on-metal bearings compared to 28 mm bearings under the same test conditions. Our own hip simulator studies of the bearing of the DuromTM hip resurfacing have confirmed this observation.30 It appears that for metal-on-metal bearings a large diameter is an advantage, probably because of the greater propensity for generating continuous fluid film lubrication.32
Acetabular fixation The main difference between the various contemporary resurfacing acetabular components is the surface used for bone in-growth. Titanium vacuum plasma sprays and Co–Cr beads are currently in use, with or without HA. Both surfaces have been shown to have satisfactory performance when used for conventional total hip replacements, although Titanium is considered to be more biocompatible than Co–Cr. However, concern has been raised that the extreme temperature involved in the sintering process of Co–Cr beads may alter the metallurgy of the monobloc component, which could in turn have a deleterious effect on the bearing surface.
Femoral fixation The major issue relates to the optimal cement mantle thickness and the degree of cement pressurisation.
Table 2
269 The thickness of the cement mantle is determined by the diametrical difference between the implant and the corresponding reamer. Systems which produce very thin or incomplete cement mantles, and which do not allow escape of cement during femoral component insertion, can result in excessive penetration of cement into the cancellous bone of the femoral head, jeopardising bone viability. In addition, the force required to fully seat such implants can result in fracture of the femoral neck. Our finite element studies have demonstrated that a cement mantle less than 1 mm is prone to fatigue fracture under cyclical loading.33 A thicker mantle reduces the risk of cement fracture but would result in increased removal of femoral head bone and could be associated with neck notching. The optimal compromise is a cement mantle of approximately 1 mm. The role of the short stem of these implants can be for alignment alone, or alignment and force transmission. Force can be transmitted by cementation of the stem, by bony in-growth or by frictionfit. Whether it is advantageous for the stem to transmit force remains controversial. A stem which transmits force may protect a deficient femoral head, but could result in stress shielding, leading to loss of bony support in the long term.33
Indications and contra-indications Before defining the indications and contra-indications for hip resurfacing, it is appropriate to consider the theoretical advantages and disadvantages of the procedure compared to conventional THR (Table 2). To date, the follow-up is too short to confirm all the potential advantages of metal-on-metal hip
Potential advantages and disadvantages of hip resurfacing.
Advantages
Disadvantages
Initial preservation of proximal femoral bone stock More normal loading of femur eliminating proximal femoral stress shielding Easier and more durable revision of femoral component if required Reduced risk of leg lengthening/shortening
No long-term outcome data No published controlled studies
Reduced risk of dislocation Improved range of movement Improved function/activity level Low wear bearing reducing risk of peri-prosthetic osteolysis
Technically more demanding New modes of failure—femoral head collapse, femoral neck fracture
ARTICLE IN PRESS 270 resurfacing. The procedure is self-evidently conservative of proximal femoral bone stock at the time of surgery and Kishida et al.34 have reported better preservation of periprosthetic bone mineral density 2 years after surgery in a group of patients who had undergone resurfacing arthroplasty of the hip compared to a similar group who had undergone a conventional uncemented THR (case control study). There is however no published report documenting better outcomes for revision of hip resurfacings compared to revision of stemmed hip replacements, although such a study would take many years to complete. The results from the first generation of hip resurfacings indicate that there is a reduced rate of dislocation, though controlled trials will be required to determine if hip resurfacing offers a reduced risk of leg length discrepancy, an improved range of movement and improved activity level compared to conventional THR. Such studies are currently ongoing (Personal Communication, M Lavigne, P Venditolli, Hopital Maisoneuve-Rosemont, Montreal).
Indications The general indications for surface arthroplasty of the hip are essentially the same as for conventional THR. Based on current evidence it appears reasonable to offer hip resurfacing to fit and active patients who wish to regain an active lifestyle after surgery and who would most probably outlive a conventional hip replacement and therefore face the possibility of multiple revision procedures during their lifetime. In the UK, the National Institute for Clinical Excellence (NICE) have documented the lack of long-term outcome data on hip resurfacing and the lack of randomised controlled trials comparing metal-on-metal resurfacing arthroplasty of the hip with conventional THR.35 Nevertheless, they concluded that: ‘‘patients who are likely to outlive conventional primary hip replacements should have the choice of receiving metal-on-metal hip resurfacing arthroplasty’’.35 They also stated that: ‘‘the suitability of hip resurfacing should be based on patient’s activity levels rather than age alone’’. A further review is due this year. The NICE guidelines could be reasonably extended for patients with deformity of the proximal femur which would make stemmed conventional THR difficult or impossible (Fig. 6). Hip resurfacing, or some other form of hip reconstruction using a large-diameter articulation, may also be appropriate for patients with a high risk of dislocation, such as those with neuromuscular conditions.
P. Roberts et al.
General contra-indications The contra-indications for hip resurfacing relate primarily to the bone stock and bone quality of the femoral head and femoral neck (Table 3) (Fig. 7). The most common reported modes of failure of contemporary hip resurfacing are aseptic loosening of the femoral component and fracture of the femoral neck. Whilst early femoral neck fracture is usually related to a technical problem at the time of surgery, such as neck notching or forceful impaction of the femoral component, the causes of femoral component loosening and late femoral neck fracture are more complex, but the bone stock and bone quality of the femoral head appear to be critical. The problem is determining what extent of femoral head deficiency or what degree of femoral head/neck osteoporosis is incompatible with the long-term survival of a cemented resurfacing femoral component. Beaule´ et al.36 have developed a ‘‘Surface Arthroplasty Risk Index’’ (SARI) in an attempt to identify preoperatively patients unsuitable for surface arthroplasty (Table 4). They studied 119 patients under the age of 40 undergoing metal-on-metal surface arthroplasty of the hip. In patients with a SARI score of greater than 3, the relative risk of early problems was 12 times greater than if the SARI score was equal to or less than 3. However, the SARI score does not take into account the position of the cysts within the femoral head, particularly cysts extending across the head–neck junction. Although a potentially useful tool, the validity of the SARI score needs to be verified with long-term outcome data. The relevance of osteoporosis of the femoral head and neck to loss of femoral component fixation is yet to be defined. This is of particular importance if hip resurfacing is carried out on postmenopausal women and young patients with inflammatory arthritis.
Specific contra-indications Renal failure Blood, serum and urine levels of cobalt and chromium ions are higher in all patients with metal-on-metal bearings in situ, compared to the ‘‘normal’’ population. The levels continue to increase during the initial running in period of the bearing and then stabilise at around 18–24 months. Both chromium and cobalt ions are excreted in the kidney by glomerular filtration. There is no active excretory pathway. The blood and serum levels are consequently dependent on the rate of production/
ARTICLE IN PRESS Resurfacing arthroplasty of the hip
271
Figure 6 (a,b) Osteoarthritic hip above a deformed femoral shaft. The deformity can be ignored by using a surface replacement.
Table 3
Contra-indications for hip resurfacing.
Bone stock
Femoral cysts AVN Acetabular rim deficiencies
Bone quality
Osteoporosis Inflammatory arthritis
Systemic
Renal failure Metal allergy
ingestion and the glomerular filtration rate. The serum level will therefore mirror the serum creatinine level and will be particularly elevated
in patients with renal failure. Until the effects (if any) of the long-term elevation of chromium and cobalt ions are understood, it is prudent to avoid the use of metal-on-metal bearings in patients with renal disease. Metal allergy The relevance of cutaneous metal sensitivity to implant failure remains controversial. Helab et al.37 reported that preoperative skin testing in patients undergoing joint replacements is unreliable for predicting the response to the metallic components. Doubt remains as to whether noncutaneous metal allergy is a clinically relevant problem. The issue of aseptic lymphocytic vasculitic
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P. Roberts et al.
Figure 7 Contra-indications to hip resurfacing. (a(i)–a(iii)) large cyst crossing head–neck junction; (b) extensive avascular necrosis; (c) superior rim deficiency.
ARTICLE IN PRESS Resurfacing arthroplasty of the hip
273
associated lesions (ALVAL) will be discussed later in this article. Developmental dysplasia of the hip (DDH) Patients with osteoarthritis secondary to minor DDH (Crowe type I) can be treated satisfactorily with hip resurfacing (Fig. 8). However, the deformities associated with more severe forms of DDH (Crowe types II, III and IV) are difficult to address with surface arthroplasty. In particular, it is not possible to correct the often-marked anteversion of the proximal femur or address the issues relating to leg length (Fig. 9). Although combined hip resurfacing Table 4
Surface Arthroplasty Risk Index.
Femoral cysts41 cm Weight482 kg Activity level UCLA activity score46 Previous surgery to hip
2 2 1 1
points points point point
and subtrochanteric de-rotational osteotomy has been advocated in such cases, the senior authors (PR and PG) consider conventional THR to be more appropriate in patients with osteoarthritis secondary to severe DDH. The problem of addressing leg length inequality also applies to the post-Perthes’ hip, with a coxa magna and a short femoral neck. Women of childbearing age The issue of the use of metal-on-metal bearings in women of childbearing age has been addressed by Brodner et al.38 They investigated pregnant women who had metal-on-metal bearings in situ. They measured the metal ion concentrations in the maternal blood and the cord blood. They found, as expected, that the concentrations of chromium and cobalt in the maternal blood were elevated. However, there was no elevation of metal ion concentrations in the cord blood, indicating that
Figure 8 (a,b) Secondary osteoarthritis in Crowe type I DDH treated by hip resurfacing.
ARTICLE IN PRESS 274
P. Roberts et al. will be critical. Because there is a fixed relationship between the diameter of the acetabular and the femoral components, acetabular bone stock can be compromised if the femoral component is oversized in an attempt to avoid neck notching. Preservation of acetabular bone stock is therefore dependent on accurate preparation of the femoral head.
Exposure
Figure 9 Crowe type IV DDH unsuitable for hip resurfacing.
metal ions do not cross the placental barrier. Based on this work, it appears that there will be no deleterious effects on the foetus if a pregnant woman has a metal-on-metal bearing in situ.
Operative technique There are significant differences between the operative technique for hip resurfacing compared to conventional THR. The differences relate particularly to the exposure, the implantation of the acetabular component and the preparation of the femoral head. Many surgeons have reported a significant learning curve, with an increased incidence of complications in the early cases. It is therefore highly recommended that appropriate training is undertaken before embarking on hip resurfacing. NICE have stated: ‘‘metal-on-metal hip resurfacing arthroplasty should be performed only by surgeons who have received training specifically in this technique’’. The essential objectives during a hip resurfacing procedure are to maintain or restore the anatomy of the femoral head and neck (head height, orientation, and neck offset) and to preserve the acetabular bone stock. Should revision of a resurfacing be required, it is the acetabular bone stock rather than the femoral bone stock that
Hip resurfacing can be carried out through a posterior or a direct lateral approach, although the posterior approach is currently favoured by most surgeons. The Ganz approach to the hip has also been advocated as a way of preserving the deep branch of the medial femoral circumflex artery, which may be important in supplying the anterior-superior quadrant of the femoral head.39 The direct lateral approach has been less favoured than the posterior approach because of the risk of abductor dysfunction if the abductor repair fails, particularly as the surgery is generally carried out in young patients who wish to regain an active lifestyle. Our own in-vitro strain gauge studies have also demonstrated that if the abductors are dysfunctioned after a hip resurfacing, the stress across the femoral neck is doubled compared to the state when the abductors are functioning normally.40 This may explain the historical observation that fractures of the femoral neck following hip resurfacing most commonly occur in patients with an abductor lurch.41 The senior authors (PR, PG) therefore recommend the posterior approach. Because the head and neck of the femur are preserved, exposure of the acetabulum can be difficult. The exposure can be facilitated by carrying out a circumferential capsulotomy and releasing the tendon of gluteus maximus from the linea aspera. When using a posterior approach, the femoral head should be translated superior to the acetabulum, under the gluteus minimus, so that it comes to lie on the wing of the ilium close to the lateral side of the anterior inferior iliac spine. Forceful retraction of the femoral head and neck should be avoided as this can result in femoral nerve palsy and/or fracture of the anterior wall of the acetabulum. In particularly difficult cases (muscular male, large femoral head, ankylosed hip), it can be advantageous to partially prepare the femoral head prior to acetabular exposure. The debulked femoral head is then a lesser obstacle to the exposure of the acetabulum.
ARTICLE IN PRESS Resurfacing arthroplasty of the hip In muscular males the bulk of the thigh muscles, together with the femoral head and neck, tend to push the acetabular reamer shaft and acetabular impactor shaft into excessive abduction and retroversion, resulting in malpositioning of the acetabular implant, which can be associated with instability. In such cases, the use of offset (dog leg) reamers and cup impactors can be beneficial. Hip resurfacing is inherently a form of ‘‘minimally invasive surgery’’, as the femoral head and neck are preserved and the femoral canal is not violated. However, it is a difficult procedure to carry out through a ‘‘mini incision’’ because of the problems associated with exposure of the acetabulum and the necessity for access to the femoral head and neck for precise femoral head preparation. There have been anecdotal reports of increased intraoperative complications, including nerve palsies and femoral neck notching, when mini incisions are used for hip resurfacing. The value of mini incision surgery for hip resurfacing remains to be defined.
Acetabular cup insertion The insertion of the uncemented acetabular component can be more difficult than in conventional THR because: (i) Primary stability must be achieved without the use of screws (unless a ‘‘dysplasia system’’ is being used). (ii) The lack of holes in the cup can make it difficult to determine when full seating has been achieved. (iii) The cup insertor fixes to the rim of the acetabular component. The cup insertor is therefore more bulky than a conventional insertor which fixes to the acetabular shell through a polar hole. (iv) The femoral head and neck and the bulk of the thigh muscles can push the cup impactor shaft into excessive abduction and retroversion (from a posterior approach). The keys to acetabular preparation and insertion are the recognition of the factors which can lead to component malpositioning and gaining adequate exposure to the whole of the acetabular rim.
275 to oversizing of the acetabulum and thereby unnecessary sacrifice of acetabular bone stock) and without notching the femoral neck, which is recognised to be a potent cause of femoral neck fracture. Femoral component positioning is complicated by two factors: (i) In general the femoral head is not centered on the femoral neck. The osteoarthritic process leads to the bulk of the head being more posterior and more inferior than the neck (Fig. 10). There is often little femoral head bone superior and anterior to the neck. This deformity can be extreme in cases of previous slipped upper femoral epiphysis. In order to avoid notching of the femoral neck, the preparation of the femoral head must be based on the anatomy of the femoral neck rather than the anatomy of femoral head. Consequently, the preparation of the femoral head invariably appears to be eccentric, with the bulk of the bone being removed from the posterior and inferior parts of the head. (ii) Osteophytes can distort the normal anatomy of the femoral neck and head–neck junction. Preservation of such osteophytes can lead to oversizing of the femoral component and/or reduction in the range of movement due to impingement. However, if the osteophytes are removed, particularly ‘‘mature’’ corticated neck osteophytes, then large areas of soft cancellous bone may be exposed, which is thought to be a risk factor for subsequent neck fracture. In general, soft osteophytes can be removed, but mature corticated osteophytes should be removed only if they will result in femoral component oversizing or significant impingement. Even in this situation, corticated osteophytes should only be partially debulked in order to avoid exposing cancellous bone of the neck (Fig. 11). Accurate, reliable and reproducible preparation of the femoral head can be facilitated by the use of sophisticated jigs which allow angular alignment and component positioning to be set independently. Computer guidance may be of value in femoral head preparation, but to date, there is no evidence that this technique is any more accurate or reproducible.
Femoral head preparation
Results of contemporary hip resurfacing Preparation of the femoral head is challenging. The head must be prepared to accept a femoral component without oversizing (which would lead
No randomised controlled trial comparing the outcome of hip resurfacing with conventional THR has
ARTICLE IN PRESS 276
P. Roberts et al.
Figure 10 (a,b) Eccentricity of the femoral head on the femoral neck. The remodelling commonly seen in osteoarthritis results in there being little femoral head bone superior or anterior to the neck.
been published. Likewise, there are no long-term (greater than 10 years) observational data on outcomes. However, short- and medium-term results of hip resurfacing are now becoming available. Daniel, Pinsent and McMinn reported on 446 patients under the age of 55 at the time of surgery, who had undergone hip resurfacing using either the McMinn resurfacing hip arthroplasty or the Birmingham Hip Resurfacing prosthesis.42 The minimum follow-up was 1.1 years, the maximum 8.2 years and the mean 3.3 years. Follow-up was by postal or telephone questionnaire. The results of radiological follow-up were not documented. There was only one failure; a case of avascular necrosis occurring at 8 months. The Kaplan–Meier cumulative survival rate was 99.78% at 8 years. Excellent Oxford hip scores and UCLA activity-level scores (modified) were achieved. However, 186 patients operated on by the senior author (D.J.W. McMinn) in 1996 were excluded from this study, apparently because a unique pattern of failure of the implants was observed (metal wear, metallosis and osteolysis), which the authors ascribed to problems with the manufacturing of the bearing. Amstutz et al.43 have reported on 400 Conserve Plus hip resurfacings carried out on patients
with a mean age of 48.2 years. The minimum follow-up was 2.2 years, the maximum 6.2 years and the mean 3.5 years. The vast majority of patients were assessed both clinically and radiologically. The Kaplan–Meier survival rate of the component at 4 years was 94.4%. There were 14 clinical failures requiring revision surgery: seven for femoral component loosening, three for femoral neck fracture, one for acute cup migration, one for recurrent subluxation, one for deep infection and one for component mismatch. In addition, in 16 cases there was extensive radiolucency around the short femoral stem. This was considered to be probably indicative of early femoral loosening, although only one such patient was symptomatic. The dislocation rate was 0.75% (three of 400 cases). Excellent functional results were achieved. Our early results of the first 200 consecutive hip resurfacings using the Durom system have also been encouraging. The patients average age was 48. At a mean follow-up of 2.2 years (minimum ¼ 1.1, maximum ¼ 4.6), there have been no failures and no cases of dislocation or deep infection.44 Similar good early results were reported by De Smet et al.45 for the Birmingham Hip Resurfacing, with
ARTICLE IN PRESS Resurfacing arthroplasty of the hip
277
Continuing concerns Cancer risk Concern has been raised about the biological effect of the elevated levels of metal ions and metal particles found in the blood, periprosthetic tissues and lympho-reticular system in patients with metal-on-metal bearings. However, it is not known at what levels chromium and cobalt ions released from implants are likely to be toxic. The latency period for the development of haemopoetic or musculo-skeletal malignancies is likely to be prolonged. However, to date, there is no evidence that patients with metal-on-metal bearings in situ are more likely to develop such malignancies when compared with the general population. Visuri analysed a large cohort of patients in Finland with McKee-Farrar metal-onmetal THR’s in situ. At 15 years, the total cancer risk in this study group did not deviate from that of the general population.46
Metal sensitivity
Figure 11 (a,b) The thick corticated inferior neck osteophyte has been only partially removed at the head–neck junction.
only one failure (a femoral neck fracture) in 200 patients at a mean of 1.1 years after surgery. In summary, the above papers and other papers in the literature indicate that contemporary hip resurfacing is associated with good early–mid-term results. The primary modes of failure are aseptic loosening of the femoral component and femoral neck fracture. Further work will be required to determine whether these complications are technique related, or whether they relate to biological problems of the femoral head inherent to the procedure of hip resurfacing. Long-term observational studies and controlled trials will be required to determine if the potential advantages of hip resurfacing compared to conventional THR are realised.
Recent reports have documented the presence of a marked perivascular infiltration of lymphocytes and plasma cells in the periprosthetic tissues around some metal-on-metal articulations (ALVAL).47,48 The pattern of inflammation is different to that seen in the tissues around metal-on-polyethylene implants. It has been postulated that the lymphocyte-rich infiltrate could represent some form of immunological response to the metal wear debris. The clinical relevance of this finding is as yet unclear, but the possibility exists that it might represent a novel mode of failure for some metalon-metal joint replacements.
Conclusion The failure of previous generations of hip resurfacings was essentially a consequence of the use of inappropriate materials, poor implant design and inadequate instrumentation. It was not an inherent problem with the procedure itself. The early results of contemporary hip resurfacings are encouraging. The complications commonly seen in the 1970s and 1980s, such as early implant loosening and femoral neck fracture, now appear to be rare. Whilst early results should be regarded with caution, the present generation of metal-on-metal surface replacements potentially offer the ultimate bone
ARTICLE IN PRESS 278 preservation and restoration of function in appropriately selected young patients. Resurfacing implants demand high manufacturing standards to produce consistently low wear bearings. Rigorous quality control by the implant manufactures is therefore essential. The background research and better understanding of implant failure suggests that hip resurfacing has now developed beyond that of an experimental procedure. Concerns remain with the long-term biological effects of the elevated metal ion levels found in all patients with metal-on-metal bearings in situ, although to date there is no evidence of any adverse clinical effect. Only long-term results and experience with this technology in the wider Orthopaedic community will give the answer as to whether the results will be durable, or if hip resurfacing will simply become a bone conserving intervention prior to conventional total hip replacement.
References 1. Malchau H, Herberts P, Eisler T, Garellick G, So ¨derman P. The Swedish total hip replacement register. J Bone Joint Surg 2002;84-A(Suppl. 2):2–20. 2. Smith-Petersen MN. Evolution of mould arthroplasty of the hip joint. J Bone Joint Surg 1948;30-B:59–75. 3. Charnley JC. Arthroplasty of the hip: a new operation. Lancet 1961;i:1129–32. 4. Charnley JC. Tissue reactions to polytetrafluoroethylene (Letter). Lancet 1963;ii:1379. 5. Muller ME. Lessons of 30 years of total hip arthroplasty. Clin Orthop 1992;274:12–21. 6. Muller ME. The benefits of metal-on-metal total hip replacements. Clin Orthop 1995;311:54–9. 7. Trentani C, Vaccarino F. The Paltrinieri–Trentani hip joint resurface arthroplasty. Clin Orthop 1978;134:36–40. 8. Freeman MAR, Swanson SAV, Cameron H, et al. ICLH cemented double cup total replacement of the hip. J Bone Joint Surg 1978;60-B:137–8. 9. Freeman MAR, Cameron HU, Brown GC. Cemented double cup arthroplasty of the hip. Clin Orthop 1978;134:45–52. 10. Wagner H. Surface replacement arthroplasty of the hip. Clin Orthop 1978;134:102–30. 11. Salzer M, Knahr K, Locke H, Stark N. Cement-free bioceramic double-cup endoprosthesis of the hip joint. Clin Orthop 1978;134:80–6. 12. Amstutz HC, Clarke IC, Cristie J, et al. Total hip articular replacement by internal eccentric shells. Clin Orthop 1977;128:261–84. 13. Amstutz HC, Graff-Radford A, Gruen TA, Clarke IC. THARIES surface replacements. Clin Orthop 1978;134:87–101. 14. Buechel FF. Resurfacing total hip replacement for avascular necrosis in young patients: Durability, revision options and future technology, Presented at the 6th annual current concepts in joint replacement symposium, Orlando, FL, 1990. 15. Howie DW, Cornish BL, Vernon-Roberts B. The viability of the femoral head after resurfacing hip arthroplasty in humans. Clin Orthop 1993;291:171–84.
P. Roberts et al. 16. Campbell P, Mirra J, Amstutz HC. Viability of femoral heads treated with resurfacing artrhroplasty. J Arthroplasty 2000;15(1):120–2. 17. Freeman MAR. Some anatomical and mechanical considerations relevant to the surface replacement of the femoral head. Clin Orthop 1978;134:19–24. 18. Mai MT, Schmalzreid TP, Dorey FJ, et al. The contribution of frictional torque to loosening at the cement–bone interface in THARIES hip replacements. J Bone Joint Surg 1996;78A:505–11. 19. Amstutz HC, Grigoris P, Safran MR, Grecula MJ, Campbell PA, Schmalzried TP. Precision-fit surface hemiarthroplasty for femoral head osteonecrosis: Long term results. J Bone Joint Surg 1994;76-B:423–7. 20. Grecula M, Grigoris P, Schmalzried TP, Dorey F, Campbell PA, Amstutz HC. Endoprostheses for osteonecrosis of the femoral head. A comparison of four models in young patients. International Orthopaedics 1995;19:137–43. 21. Weber BG. Experience with the Metasul total hip bearing system. Clin Orthop 1996;329S:S69–77. 22. Wagner M, Wagner H. Preliminary results of uncemented metal-on-metal stemmed and resurfacing hip replacement arthroplasty. Clin Orthop 1996;329S:S78–88. 23. McMinn D, Treacy R, Lin K, Pynsent P. Metal-on-metal surface replacement of the hip. Clin Orthop 1996;329S:S89–98. 24. Archard JF. Contact and rubbing of flat surfaces. J Appl Phys 1953;24:981–8. 25. St. John K, Poggie R, Zardiackas L, Afflitto R. Comparisons of two cobalt based alloys for use in metal-on-metal hip prostheses: evaluation of wear properties in a simulator. Disegi J, Kennedy R, Pillar R, editors. Cobalt-Base Alloys for Biomedical Applications, 1365. West Conshohocken, PA: American Society for Testing Materials STP; 1999. p. 145–55. 26. Streicher RM, Semlitsch M, Schon R, Weber H, Rieker C. Metal-on-metal articulation for artificial hip joints: laboratory study and clinical results. Proc Inst Mech Eng H 1996;210:223–32. 27. Bowsher JG, Nevelos J, Pickard J, Shelton JC. Do heat treatments influence the wear of large metal-on-metal hip joints? An in vitro study under normal and adverse conditions. Presented at the 49th annual meeting, Orthopaedic Research Society, New Orleans, LA, February 2003. 28. Chan FW, Bobyn JD, Medley JB, Krygier JJ. Wear and lubrication of metal-on-metal hip implants. Clin Orthop 1999;369:10–24. 29. Jin ZM. Analysis of mixed lubrication mechanism in metalon-metal hip joint replacement. Proc Inst Mech Eng H 2002;216:85–9. 30. Rieker CB, Schon R, Konrad R, Liebentritt G, Gnepf P, Shen M, Roberts P, Grigoris P. In-vitro tribology of large metal-onmetal implants—influence of the clearance. Orthop Clin North Am 2005 in press. 31. Smith SL, Dowson D, Goldsmith AA. The effect of femoral head diameter upon lubrication and wear of metal-on-metal total hip replacements. Proc Inst Mech Eng H 2001;215(2): 161–70. 32. Udofia IJ, Jin ZM. Elastohydrodynamic lubrication analysis of metal-on-metal hip-resurfacing prostheses. J Biomech 2003; 36(4):537–44. 33. Soulhat J, Hertig D, Ploeg H, O’Keane M, Roberts P, Grigoris P. Finite element analysis of a cemented hip resurfacing. J Bone Joint Surg 2003;85-B(Supp I):7. 34. Kishida Y, Sugano N, Nishii T, Miki H, Yamaguchi K, Yoshikawa H. Preservation of the bone mineral density of the femur after surface replacement of the hip. J Bone Joint Surg 2004;86-B(2):185–9.
ARTICLE IN PRESS Resurfacing arthroplasty of the hip 35. National Institute for Clinical Excellence. Guidance on the use of metal on metal hip resurfacing arthroplasty. Technology Appraisal Guidance No. 44, June 2002. 36. 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 2004(418):87–93. 37. Hallab NJ, Mikecz K, Jacobs JJ. A triple assay technique for the evaluation of metal-induced, delayed type hypersensitivity responses in patients with or receiving total joint arthroplasty. J Biomed Mater Res 2000;53:480–9. 38. Brodner W, Grohs JG, Bancher-Todesca D, Dorotka R, Meisinger V, Gottsauner-Wolf F, Kotz R. Does the placenta inhibit the passage of chromium and cobalt after metal-onmetal total hip arthroplasty? J Arthroplasty 2004;19(8, Suppl. 3):102–6. 39. Ganz R, Gill TJ, Gautier E, Ganz K, Krugel N, Berlemann U. Surgical dislocation of the adult hip a technique with full access to the femoral head and acetabulum without the risk of avascular necrosis. J Bone Joint Surg 2001;83-B(8):1119–24. 40. Ganapathi M, Evans SL, Roberts P. Strain Pattern Following Surface Replacement of the Hip. Sheffield: Presented at British Hip Society; 2004. 41. Capello WN, Ireland PH, Trammel TR, Eicher P. Conservative total hip arthroplasty: a procedure to conserve bone stock. Clin Orthop 1978;134:59–74.
279 42. 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 2004;86-B(2):177–84. 43. 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;86A(1):28–39. 44. Grigoris P, Roberts P, Panousis K, Bosch H. The evolution of hip resurfacing arthroplasty. Orthop Clin North Am 2005 in press. 45. De Smet, Pattyn C, Verdonk R. Early results of primary Birmingham hip resurfacing using a hybrid metal on metal couple 211. Hip Int 2002;12(2):158–62. 46. Visuri T, Pukkala E, Paavolainen P, Pulkkinen P, Riska E. Cancer risk after metal on metal and polyethylene on metal total hip arthroplasty. Clin Orthop 1996;329S:S280–9. 47. 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 2005;87-A(1):18–27. 48. Willert HG, Buchhorn GH, Dipl-Ing Fayyazi A, Flury R, Windler M, Koster G, Lohmann CH. Metal-on-metal bearings and hypersensitivity in patients with artificial hip joints. A clinical and histomorphological study. J Bone Joint Surg 2005;87-A(1):28–36.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 280–287
www.elsevier.com/locate/cuor
MINI-SYMPOSIUM: HIP REPLACEMENT
(iv) The science of metal-on-metal articulation J.L. Tippera,, E. Inghama, Z.M. Jinb, J. Fisherb a
Institute of Medical and Biological Engineering, School of Biochemistry and Microbiology, University of Leeds, Leeds, LS2 9JT, UK b Institute of Medical and Biological Engineering, School of Mechanical Engineering, University of Leeds, Leeds, LS2 9JT, UK
KEYWORDS Metal-on-metal; Lubrication; Head diameter; Clearance; Kinematics; Wear particles
Summary In recent years there has been renewed interest in metal-on-metal (MOM) bearings for both total hip replacement and surface replacement hip arthroplasty. Short-term clinical results have been encouraging; with low wear rates and few prostheses requiring revision. This review concentrates on the factors that affect the wear of all metal devices such as specification of the alloy, processing techniques, head diameter, clearance between the components, lubrication regime, loading and surface finish. The concerns associated with MOM bearings are also discussed. These include wear particle release and dissemination, and elevated metal ion levels, which may lead to cytotoxicity, hypersensitivity and genotoxicity. & 2005 Elsevier Ltd. All rights reserved.
Introduction The majority of the 800,000 total joint replacements (TJRs) performed worldwide each year are hip replacements and comprise a metal femoral head articulating on an ultra-high molecular weight polyethylene (UHMWPE) acetabular cup. The biological response to UHMWPE wear particles, generated at the articulating surfaces, leads to the production of inflammatory cytokines, bone resorption and eventual osteolysis. A revision operation is then required, which has implications for both the Corresponding author. Tel.: +44 113 3435611;
fax: +44 113 3435638. E-mail addresses:
[email protected] (J.L. Tipper),
[email protected] (E. Ingham),
[email protected] (Z.M. Jin),
[email protected] (J. Fisher).
patient and the healthcare provider whilst the ageing population becomes more active and lives longer, an increasing number of prostheses are being implanted into younger patients. Consequently, implant longevity has become more important. The management of an arthritic hip in young active patients represents a challenge to the orthopaedic surgeon. Average survivor rates for males under 55 years fall as low as 70% at 10 years for conventional hip arthroplasty. Metal-on-metal (MOM) articulations have been seen as one potential solution to the problems associated with UHMWPE-induced osteolysis. The observation that a small number of patients with first-generation MOM prostheses exhibited good clinical and radiographical results after 20 years in vivo led to the development of second-generation MOM hip prostheses, and in 1988 the Metasul prosthesis was
0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2005.08.002
ARTICLE IN PRESS The science of metal-on-metal articulation introduced into clinical practice. This comprised of a cobalt chrome alloy femoral head articulating on a cobalt chrome alloy acetabular cup. Over 200,000 Metasul combinations have been implanted to date. Short-term clinical performance has been encouraging; with low wear rates, and few prostheses requiring revision. However, long-term clinical performance is as yet unknown. Hip resurfacing offers an alternative for younger more active patients, as it has many theoretical advantages over conventional THR, including femoral bone preservation, reduced risk of dislocation and increased range of movement that can benefit this particular group of patients. The results of the early hip resurfacing prototypes using nonMOM articulations did not meet expectations and early failures were seen as a result of cup loosening and femoral collapse. Recently, several MOM hip resurfacing prostheses have been reintroduced with improved design and manufacturing. The early clinical results of these new MOM resurfacing prostheses are encouraging, and as a result this type of prosthesis is gaining popularity with patients.1
Wear performance A low wear rate is believed to be critical for extending the implant life of a prosthetic joint, and wear volumes produced by MOM articulations have been estimated to be 40–100 times lower than metal-on-polyethylene bearings.2 The wear of MOM prostheses is known to be highly dependent upon the materials, tribological design and finishing technique. Clinical studies of retrieved first and second-generation MOM hip prostheses have shown linear penetrations of approximately 5 mm/year.1 This is equivalent to a wear volume of approximately 1 mm3/year, two orders of magnitude lower than conventional polyethylene acetabular cups. The wear of hard-on-hard bearings such as MOM hip prostheses has two distinct phases. An initial elevated bedding in wear period occurs during the first million cycles or first year in vivo. This is followed by a lower steady-state wear period once the bearing surfaces have been subjected to the self-polishing action of the metal wear particles, which may act as a solid-phase lubricant.3 Hip-joint simulators have generally shown steady-state wear rates to be lower than those reported in vivo.4,5 Wear simulators represent ideal articulation conditions during the walking cycle. The reality in vivo may differ markedly in terms of surface finish, fluctuations in load, and range of motion. The
281 difference between low in vitro wear in simulators and in vivo wear has been investigated through studies with elevated loads, stop/start motion,5,6 and different kinematics.7,8 These studies have shown that changes in tribological conditions resulted in an increase in wear rates. These factors together with the effect that head diameter and diametral clearance have on the wear of MOM hip prostheses will be discussed in more detail below.
Tribology of metal-on-metal bearings The tribology of MOM bearings is dependent on many factors including metallurgy, the design of the prosthesis and its geometry, the lubrication of the surfaces, the loading regime and the kinematics that the prosthesis is subjected to.
Metallurgy It has long been recognised that cobalt chromium molybdenum (CoCrMo) alloy represents the preferred material for MOM hip prostheses. However, the use of wrought or cast materials, with or without heat treatment, and low (o0.05% w/w) or high (40.2% w/w) carbon content alloys have been fiercely debated. The effects that these variations in material have on the wear rate and hence the production of wear particles and release of metal ions, have been widely studied. Both processing method and carbon content have an effect on the micro-structure of the CoCrMo alloy. The distribution of the carbides in low and high carbon content CoCrMo alloys differs, with the high carbon content alloys demonstrating a biphasic structure, which is comprised of small grains of CoCrMo surrounded by embedded hard, scratch-resistant carbides which restrict the grain size.3 The low carbon content alloys comprise a single-phase structure with larger grains than the high carbon alloys, probably due to the absence of carbides. The low carbon content alloys have decreased hardness due to the lack of carbides. Wrought high carbon content CoCrMo alloys have a fine distribution of small carbides. High carbon content cast alloys exhibit large blocky carbides. Low carbon content alloys produce significantly higher wear rates than high carbon content alloys in both simple configuration wear tests and hip-joint wear simulator tests.3,4,9 Hence, the pairing of low carbon cups with low carbon femoral heads is not recommended. High carbon/ high carbon pairings show the lowest wear rates in hip-joint simulator tests.4,9 Dowson et al.10 compared the wear rates of cast and wrought CoCrMo
ARTICLE IN PRESS 282 alloys with and without various heat treatments. These authors reported no significant differences between the wear volumes of the wrought and cast high carbon CoCrMo materials. However, the wrought material exhibited a slight, non-significant advantage over the as cast material. Heat treatments and hot isostatic pressing have been shown to have little effect on the wear rate of MOM hip prostheses.10
Design and geometry The effect of head diameter and diametral clearance will be considered here. Head diameter is becoming increasingly important as MOM resurfacing prostheses gain popularity with surgeons and younger patients. This type of prosthesis has the advantage of conserving bone on the femoral side, is less invasive and may ‘buy time’ until a total hip arthroplasty is necessary. Resurfacing prostheses cover the femoral head and therefore have large diameter femoral components, the average being in the region of 54 mm. Smith et al.11 considered the effect of increasing head diameter on the wear of MOM hip prostheses. These authors tested 16, 22.225 and 28 mm diameter CoCrMo alloy femoral heads against CoCrMo alloy acetabular cups in a hip-joint simulator and found that with increasing head diameter, volumetric wear rate increased firstly and then decreased. Wear volumes were highest for the smallest diameter heads, at 4.85 and 6.30 mm3/106 cycles, respectively, for the 16 and 22.225 mm diameter heads. There was a marked decrease in wear exhibited by the 28 mm diameter heads, with bedding in wear of 1.60 mm3/ 106 cycles and a steady-state wear of 0.54 mm3/106 cycles. Dowson et al.12 also investigated the effect of increasing head diameter on the wear of MOM bearings, testing 36 mm conventional hip prostheses, and 54 mm diameter resurfacing prostheses in a hip-joint simulator. Stable run-in surfaces were established quickly as the head diameter increased from 28 to 36 mm and then to 54 mm. In agreement with previous studies,11 as head diameter increased wear volume decreased markedly, with steadystate values of 0.17 mm3/106 cycles for the 54 mm diameter bearings.12 The bedding in wear rates for all prostheses were substantially higher at 3.23 mm3/106 cycles for the 54 mm bearings. These results are in contrast to those reported for conventional UHMWPE-on-metal hip prostheses, where the wear of the UHMWPE acetabular cups was shown to be proportional to the sliding distance, as predicted by basic engineering principles. Therefore, reducing the femoral head
J.L. Tipper et al. diameter should lead to a reduction in wear volume and extension of prosthesis life. Charnley demonstrated the validity of this relationship and showed that maximum wear life of hip replacements could be achieved by making the head diameter half that of the socket diameter.13 Important additional factors must be considered such as rim impingement and neck strength, and it has been shown that optimal head diameter falls between 20 and 24 mm. The Charnley low friction arthroplasty, appropriately regarded as the ‘gold standard’ falls within this range at 22.225 mm. Dowson et al.12 also considered the effect of diametral clearance. The diametral clearance is defined as the diameter of the acetabular cup minus the diameter of the femoral head (Fig. 1). There is a direct relationship between clearance and lubrication, and as MOM bearings are lubrication sensitive, clearance has a direct effect on wear. Dowson et al.12 reported that for both 36 and 54 mm bearings as diametral clearance increased, bedding in wear of the MOM components increased significantly. For the resurfacing components, those couples with smaller diametral clearances (83–129 mm; with a head diameter of 54.5 mm, n ¼ 5) exhibited running in wear rates that were four-fold lower and steady-state wear rates that were two-fold lower, than those components with larger clearances (254–307 mm; with a head diameter of 54 mm, n ¼ 3). However, there does appear to be an optimum band of clearance, which produces favourable wear rates. Farrar et al.14 were the first to show reducing wear rates with reducing clearance down to approximately 80 mm with 28 mm MOM hip prostheses. However, reduction of clearances to below 30 mm caused wear to increase substantially. This was thought to be due Initial Bedding in Wear Cup radius R2 Head radius R1 Radial clearance = R2-R1
Steady State
Bedding in wear volume is dependent on radial clearance R2-R1
Figure 1 The effect of radial clearance on bedding in and steady-state wear.
ARTICLE IN PRESS The science of metal-on-metal articulation to geometrical errors, which are inevitable with any manufactured part. Where small clearances approached the order of the cumulative geometrical errors, contacts may develop much closer to the equator and the possibility of a local negative clearance exists. These authors found that it was possible to simulate the wear of equatorial bearing devices, such as those described for the pre-1970 McKee Farrar and Ring prostheses, with modern MOM prostheses in a hip simulator by having negative or very low clearances. During testing these devices with low clearances reached approximately 20,000 cycles, and exhibited extremely high wear, before seizing completely.
Lubrication MOM hip prostheses can be lubricated in three ways; boundary lubrication, mixed lubrication and full fluid-film lubrication, either alone or in combination. Lubrication is generally related to friction and wear and hence can play an important role in wear of particle generation in MOM bearings. Lubrication is dependent upon the viscosity of the lubricant, the sliding speed, the radius of the femoral head, clearance and surface roughness of the components.15 The lubrication analysis carried out by Jin et al. in 1997 first highlighted the importance of both head diameter and radial clearance on the lubrication of MOM hips. One of the experimental methods of studying lubrication qis through measuring friction. The coefficient of friction is commonly plotted against the Sommerfeld parameter, which is the product of the velocity, viscosity of the lubricant and the radius of the femoral head, divided by the load. This type of plot is called a Stribeck curve and an idealised form is depicted in Fig. 2. The trend of the curve
Coefficient of Friction
Boundary lubrication
Mixed lubrication
Full fluid film lubrication
0.1
0.01
0.001
viscosity × sliding speed × radius load
Figure 2 Stribeck curve indicating modes of lubrication.
283 indicates the modes of lubrication. The initial flat section of the curve indicates boundary lubrication and substantial contact between the surfaces of the hip prostheses. The falling trend in the Stribeck curve indicates mixed lubrication in which the load is carried partly by contact between asperities on the joint surfaces, and partly by the lubricating fluid. The rising trend of the curve indicates full fluid-film lubrication in which the load is fully supported by the lubricant and surface asperity contact is minimal. Theoretical analysis of the mode of lubrication can be made by calculating the ratio of effective lubricating film thickness in hip prostheses to composite surface roughness of the femoral head and acetabular cup.15 This is known as the lambda ratio, l. A l value greater than three indicates that full fluid-film lubrication is likely to be prevalent in the joint. Mixed lubrication is indicated when l is between one and three, and boundary lubrication when l is less than or equal to one. In general, as the l ratio increases wear decreases for MOM joints, with joints operating under boundary lubrication having the highest wear rates and joints operating under full fluid-film lubrication having the lowest. Smith et al.11 demonstrated this in their study on the effect of head diameter on lubrication, where head diameters of 16 and 22.225 mm were shown to have contact between the bearing surfaces at all times during the simulator tests, and hence a boundary lubrication regime was found to be prevalent. Alternatively, a mixed lubrication regime involving significant asperity contact may have prevailed. As head diameter increased to 28 mm a mixed lubrication regime was found to be prevalent; however, as only limited asperity contact occurred occasional fluid-film lubrication was indicated. As further increases in head diameter occur to 36 mm and beyond, the lubricating film alleviates metallic contact between the articulating surfaces and the volumetric running in wear12 and steady-state wear11 fall dramatically. As head diameter increases, the articulation is more likely to promote fluid-film lubrication and the benefits to the joints are subsequently seen in the wear characteristics. However, modern manufacturing and finishing techniques allow MOM bearings to be superpolished to achieve very low surface roughness Ra values. If surface asperities remain absent during articulation, the tendency towards higher l ratios and full fluid-film lubrication will increase. Diametral clearance also has an important effect on lubrication.15,16 It has been shown that the mean lubricant film thickness due to elastohydrodynamic action is strongly influenced by both increases in head diameter and decreases in
ARTICLE IN PRESS 284 5
λ ratio
4
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Full Fluid Film Lubrication λ = >3
3 ------------------------------------------------* Improved Design Mixed Lubrication ASR 2 * ASR 50 mm diameter * THR 1 28 mm diameter 0 0 0.05 0.1 0.15 0.2 0.25 Radial clearance (mm)
Figure 3 The effect of radial clearance (half of diametral clearance) upon lubrication and l ratio in metal-on-metal total hip implants and resurfacing prostheses (ASR, DePuy Int.).
clearance. Dowson et al.12 demonstrated that by increasing head diameter to 54 mm, decreased the volumetric wear of MOM articulations, but if clearance was optimised further reductions in wear could be achieved (Fig. 3). For the older designs of surface replacement prostheses the l ratio was between one and two, indicating a mixed lubrication regime. However, as prosthesis design was improved and clearances optimised, the l ratio approached three, indicating that full fluid-film lubrication was possible in these newer devices (Fig. 3). These studies clearly demonstrate the benefits of optimising the design of MOM hip prostheses, and that improvements in design such as optimising clearances for surface replacement prostheses and improving surface finishes of all components can have a significant effect on the wear of MOM devices.
Kinematics and load There has been a consistent trend for in vitro simulator wear rates to be lower than those reported in in vivo studies. The effects of kinematics and load have been studied by Firkins et al.9 and Williams et al.7, respectively. Firkins et al.9 compared the wear of MOM hip prostheses in two different hip simulators with different kinematic inputs. One simulator had three independent input motions, which produced an open elliptical wear path with a low level of eccentricity. The other simulator had two independent input motions, which produced an open elliptical wear path but with greater eccentricity. The two simulators had been shown to produce similar wear rates for UHMWPE acetabular cups.17 However, when MOM hip prostheses were tested the simulator, the wear path with greatest eccentricity produced a wear rate that was 10-fold greater than the simulator
with three independent motion inputs. In vitro simulations apply standard patterns of motion to the prostheses, whereas a more extensive range of activities and motions are applied in vivo. This was confirmed by Bowsher et al.8 who developed a severe simulator testing method for MOM hip prostheses that incorporated fast jogging cycles. These authors reported a nine-fold increase in steady-state wear rates for the simulator testing that incorporated these fast jogging cycles compared to normal walking gait simulations. The study by Firkins et al.9 applied different swing phase loads in two different simulators, and hence the differences in wear rates may have been due to the application of different loads rather than differences in kinematics alone. Williams et al.7 investigated the effect that swing phase load exerted on the wear of MOM hip prostheses. These authors investigated a number of different load conditions, including a low swing phase load (100 N), a swing phase load as recommended by ISO14242-1 (280 N), and a small (100 N) negative load applied during the swing phase, which caused separation of the head and insert. The latter is referred to as micro-separation, and simulates the effects of joint laxity that occurs after surgery. When micro-separation was introduced into the simulation testing of alumina ceramic-on-ceramic hip prostheses it was found to increase wear rates to clinically relevant levels, produce wear patterns similar to those observed in vivo, in the form of a wear stripe on the femoral head, and produce clinically relevant wear particles.18 It was found that increasing the swing phase load from 100 to 280 N in the same hip-joint simulator increased the wear of MOM hip prostheses by over 10-fold. Introducing micro-separation to the gait cycle of the simulation increased wear further, and a wear stripe was observed on the femoral heads, accompanied by rim damage on the acetabular cups. It was also found that increasing the swing phase load from 100 to 280 N led to higher coefficients of friction and the authors postulated that the significant increase in wear may be attributed to the dependence of MOM bearings on fluid-film lubrication conditions. During testing with low swing phase loads the fluid film will be allowed to replenish during the swing phase, resulting in lower friction and wear, but this effect will be smaller during testing with higher swing phase loads. This was consistent with the results of stop–start simulator testing,6 where the intermittent motion caused breakdown of the protective fluid film resulting in higher wear rates. During microseparation conditions, fluid-film replenishment would have been improved because of increased
ARTICLE IN PRESS The science of metal-on-metal articulation fluid entrainment during the swing phase; however, any benefit would soon be overwhelmed by the high stresses generated when the head contacted the insert rim at heel strike. There have been no reports of wear stripes on retrieved MOM explants; however, this may be due to the self-polishing mechanism of the metal components that occurs during gait. Williams et al.7 suggest that microseparation should not occur with every step as it does in the hip simulator and this may be sufficient to mask stripe wear in vivo. Factors that cause rim contact such as malpositioning of the acetabular cup or joint laxity producing micro-separation of components may elevate wear in vivo. Therefore, additional care may be required with the surgical techniques and fixation of MOM bearings compared to polyethylene-on-metal couples.
Concerns Although MOM hip prostheses produce significantly lower wear rates than conventional UHMWPE-onmetal couples, and 10-fold lower wear rates than highly crosslinked UHMWPE-on-metal hip prostheses, there are concerns associated with these bearings. Wear particles have been reported to be in the nanometer size range, an order of magnitude smaller than UHMWPE particles.4,19 Therefore, despite a lower wear volume than UHMWPE bearings the number of particles produced are estimated to be greater, possibly between one and ten million particles per step. These small particles have the potential to distribute throughout the body via the lymphatic system, with particles found in the lymph nodes, liver, spleen and bone marrow.20,21 As MOM hip prostheses are indicated for younger more active patients these particles will be present at these sites for a long periods of time, possibly 30–40 years. Whilst research has shown that high concentrations of nanometre-sized metal wear particles are cytotoxic to human fibroblasts and macrophages in vitro,22 there are also concerns about the release of metal ions from these small particles, and the potential effect that these ions have on cells and tissues. Elevated ion concentrations have been reported in both the blood and urine of patients with metallic implant components.23 In addition, contrary to what might be expected, there is no conclusive evidence that ion levels fall in vivo after the bedding in period of the MOM prostheses, during which wear of the prostheses are higher. Cobalt and chromium ions have high toxicity, and there are very real concerns about the effects of sub-lethal doses of metal ions,
285 which have been shown to cause DNA damage.24 This damage takes the form of chromosome aberrations and chromosome translocations. Over long periods of exposure the worry is that this will lead to the development of certain types of cancer, such as leukaemia and lymphoma. In animal models elevated levels of cobalt, chromium and nickel have been correlated with increased carcinoma rates.25 However, reports in the literature of malignancies developing after total hip or knee replacement surgery are exceedingly rare. Out of eight epidemiological studies on the relative risk of cancer after TJR, only one study looked specifically at MOM implants.26 This study did not find an increased risk of cancer development in the subjects receiving MOM hip prostheses compared to those receiving metal-on-polyethylene hip prostheses. However, all the studies to date have been substantially underpowered in terms of patient numbers required to show a difference between the two prosthesis types. Metal sensitivity is also a potential problem. Metal ions, whether produced secondary to wear debris or via corrosion can initiate a hypersensitivity response.27 A delayed cell-mediated response, or delayed-type hypersensitivity response can occur, in which cytokines are released by T-lymphocytes and increased activation of macrophages is seen, which may result in T-cell mediated periprosthetic osteolysis.27 Many metals can initiate a hypersensitivity response, the most common is nickel followed by cobalt and chromium. Therefore, with the well-documented elevation of cobalt and chromium ions in patients with MOM hip implants, there is a theoretical risk of developing hypersensitivity reactions. Recently, an immune response exclusively associated with second-generation MOM hip prostheses, has been described.28 Histomorphological changes suggest a type of hypersensitivity reaction to the all-metallic implants. The hypersensitivity hypothesis was further strengthened by the observation that these patients experienced early clinical failure at 11–60 months (mean 29 months), and the fact that patients who received a second MOM prosthesis did not experience any relief of symptoms. Conversely, patients who received either metal-onpolyethylene or ceramic-on-polyethylene couples reported that their symptoms completely disappeared. In a control group of patients with joint prostheses not containing cobalt, chromium or nickel these signs of an immunological reactions were absent. Reports of this type of reaction are becoming increasingly common, however, more research is needed in this area. It is not known whether these patients experience prosthesis
ARTICLE IN PRESS 286 failure because of a pre-existing metal sensitivity, or whether metal sensitivity develops because of a high wearing bearing and elevated metal ion levels. Theoretically, there would be an increased probability of developing hypersensitivity to elevated metal ion levels, and hence an increased risk of implant failure. Recently, Park et al.29 reported a 6% incidence of early onset osteolysis, which was associated with a delayed-type hypersensitivity response to metal in patients who received second-generation MOM hip prostheses. Interestingly, these authors reported that 8/9 patients with early osteolysis were hypersensitive to cobalt, with only two patients eliciting a hypersensitive reaction to nickel. It has previously been reported that nickel is a potent sensitiser, with crossreactivity to cobalt being common.30 This is the first report to link cobalt hypersensitivity with early failure of MOM hip prostheses. However, the study by Park et al.29 used patch testing to determine metal hypersensitivity, which has certain limitations when used as a method to determine deep-tissue hypersensitivity. Patch testing involves exposure to the allergen for short periods of time, whereas the patient experiences constant exposure to the orthopaedic implant. In addition, there is a lack of knowledge about, and availability of, appropriate metal challenge agents. No suitable standardised battery of relevant metals currently exists and there are also concerns that patch testing could induce hypersensitivity in a previously insensitive patient. To date, standardised effective testing methodology for the clinical determination of hypersensitivity reaction to metal implants has not been well established, since the methods are labour intensive and clinically unpopular. Hallab et al.31,32 described several methodologies for the diagnosis and detection of metal hypersensitivity in patients that have metal implants. These authors recommend a combined approach using three in vitro immunological assays to measure several components of lymphocyte activation in order to provide a technique better able to diagnose hypersensitivity responses to metals. Activated lymphocytes (CD4+ T helper cells) slow their rate of migration, begin to proliferate, and release various cytokines. The three assays include lymphocyte proliferation or lymphocyte transformation assays (LTA), lymphocyte migration inhibition assays and cytokine profiling of responding T cells. It is clear that there is a need for a prospective study in which a large group of patients with MOM bearings are evaluated with multiple in vitro hypersensitivity assays such as migration inhibition assays and proliferation assays, in order to investigate the relationship
J.L. Tipper et al. between metal hypersensitivity, osteolysis and prosthesis failure. The current generation of MOM implants have only early and mid-term results available, with no long-tern results published as yet. Therefore, although MOM bearings may be considered a viable alternative to either polyethylene or ceramic implants, outstanding and unresolved issues continue to exist with this prosthesis type, as they do with the alternatives.
References 1. Ebied A, Journeaux S. Metal-on-metal hip resurfacing. Curr Orthop 2002;16:420–5. 2. Amstutz HC, Grigoris P. Metal on metal bearings in hip arthroplasty. Clin Orthop 1996;329S:11–34. 3. Tipper JL, Firkins PJ, Ingham E, Stone MH, Farrar R, Fisher J. Quantitative analysis of wear and wear debris for high and low carbon content cobalt chrome alloys used in metal on metal hip replacements. J Mater Sci: Mater Med 1999;10: 353–62. 4. Firkins PJ, Tipper JL, Saadatzadeh MR, et al. Quantitative analysis of wear and wear debris from metal-on-metal hip prostheses tested in a physiological hip joint simulator. Biomed Mater Eng 2001;11:143–57. 5. Medley JB, Chan FW, Krygier JJ, Bobyn JD. Comparison of alloys and designs in a hip simulator study of metal on metal implants. Clin Orthop 1996;329S:148–59. 6. Roter G, Medley JB, Cheng N, Pare P, Krygier JJ, Bobyn JD. Intermittent motion: a clinically significant protocol for metal-metal hip simulator testing. Trans 48th Orthop Res Soc 2002:100. 7. Williams S, Stewart TD, Ingham E, Stone MH, Fisher J. Metalon-metal bearing wear with different swing phase loads. J Biomed Mater Res 2004;70B:233–9. 8. Bowsher J, Hussain A, Nevelos JE, Shelton JC. The development of severe simulator testing methods for metal-on-metal hip bearings. In: Proceedings of the ImechE—bearing surfaces for artificial hip joints. Leeds, December 2004. 9. Firkins PJ, Tipper JL, Ingham E, Stone MH, Farrar R, Fisher J. Influence of simulator kinematics on the wear of metal-onmetal hip prostheses. Proc Inst Mech Eng 2001;215H: 119–21. 10. Dowson D, Hardaker C, Flett M, Isaac GH. A hip joint simulator study of the performance of metal-on-metal joints. Part I: the role of materials. J Arthroplasty 2004;19: 118–23. 11. Smith SL, Dowson D, Goldsmith AAJ. The effect of femoral head diameter upon lubrication and wear of metal-on-metal total hip replacements. Proc Inst Mech Engr 2001;215H: 161–70. 12. Dowson D, Hardaker C, Flett M, Isaac GH. A hip joint simulator study of the performance of metal-on-metal joints. Part II: design. J Arthroplasty 2004;19:124–30. 13. Charnley J, Kamanger A, Longfield M. The optimum size of prosthetic heads in relation to the wear of plastic sockets in total replacement of the hip. Med Biol Eng 1969;7:31–8. 14. Farrar R, Schmidt MB. The effect of diametral clearance on wear between head and cup for metal on metal articulations. Trans 43rd Orthop Res Soc 1997:71.
ARTICLE IN PRESS The science of metal-on-metal articulation 15. Jin ZM, Dowson D, Fisher J. Analysis of fluid film lubrication in artificial hip joint replacements with surfaces of high elastic modulus. Proc Inst Mech Eng 1997;211H:247–56. 16. Jin ZM, Dowson D. A full numerical analysis of hydrodynamic lubrication in artificial hip joint replacements constructed from hard materials. Proc Inst Mech Eng 1999;213C:355–70. 17. Barbour PSM, Stone MH, Fisher J. A hip simulator using simplified loading and motion cycles generating physiological wear paths and rates. Proc Inst Mech Eng 1999;213H: 455–67. 18. Tipper JL, Hatton A, Nevelos JE, et al. Alum–alumina artificial hip joints. Part II: characterisation of the wear debris from in vitro hip joint simulations. Biomaterials 2002;23:3441–8. 19. Doorn PF, Campbell PA, Worrall J, Benya PD, McKellop HA, Amstutz HC. Metal wear particle characterisation from metal-on-metal total hip replacements: transmission electron microscopy study of periprosthetic tissues and isolated particles. J Biomed Mater Res 1998;42:103–11. 20. Langkamer VG, Case CP, Heap PF, et al. Systemic distribution of wear debris after hip replacement: a cause for concern? J Bone Joint Surg 1992;74B:831–9. 21. Case CP, Langkamer VG, James C, et al. Widespread dissemination of metal debris from implants. J Bone Joint Surg 1994;76B:701–12. 22. Germain MA, Hatton A, Williams S, et al. Comparison of the cytotoxicity of clinically relevant cobalt-chromium and alumina ceramic wear particles in vitro. Biomaterials 2003;24:469–79. 23. Jacobs JJ, Skipor AK, Patterson LM, et al. Metal release in patients who have had a primary total hip replacement. J Bone Joint Surg 1998;80A:1447–58. 24. Daley B, Doherty AT, Fairman B, Case CP. Wear debris from hip and knee replacements causes chromosomal damage in
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human cells in tissue culture. J Bone Joint Surg 2004;86B:598–606. Memoli VA, Urban RM, Alroy J, Galante JO. Malignant neoplasms associated with metal implant materials in rats. J Orthop Res 1986;4:346–55. 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;329S: 280–9. Hallab N, Merritt K, Jacobs JJ. Metal sensitivity in patients with orthopaedic implants. J Bone Joint Surg 2001;83A: 428–36. Willert H-G, Buchhorn GH, Fayyazi A. Hypersensitivity around metal/metal hips? In: Procedings of the international conference on metal–metal hip prostheses: past performance and future directions. Montreal, Canada, 2003. Willert H-G, Buchhorn GH, Fayyazi A. Hypersensitivity around metal/metal hips? In: Proceedings of the second international conference on metal–metal hip prostheses: past performance and future directions. Montreal, Canada, 2003. Park Y-S, Moon Y-W, Lim S-L, Yang J-M, Ahn G, Choi Y-L. Early osteolysis following second-generation metal-onmetal hip replacement. J Bone Joint Surg 2005;87A: 1515–21. Hallab NJ, Jacobs JJ, Black J. Hypersensitivity to metallic biomaterials: a review of leukocyte migration inhibition assays. Biomaterials 2000;21:1301–14. Hallab NJ, Mikecz K, Jacobs JJ. A triple assay technique for the evaluation of metal-induced, delayed type hypersensitivity responses in patients with or receiving total joint arthroplasty. J Biomed Mater Res (Appl Biomater) 2000; 53:480–9.
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www.elsevier.com/locate/cuor
MINI-SYMPOSIUM: HIP REPLACEMENT
(v) Silent osteolysis associated with an uncemented acetabular component: A monitoring and treatment algorithm J.H.M. Goosena, R.M. Casteleinb, C.C.P.M. Verheyena, a
Isala Clinics, Weezenlanden Hospital, P.O. Box 10500, 8011 JW Zwolle, The Netherlands University Medical Center Utrecht, P.O. Box 85500, 3508 GA Utrecht, The Netherlands
b
KEYWORDS Periacetabular osteolysis; Polyethylene wear; Total hip arthroplasty; Monitoring; Treatment
Summary The rate of polyethylene wear is correlated with the occurrence of osteolysis and the survival of joint prostheses. Several types of metal-backed uncemented acetabular components are associated with a rather high polyethylene wear rate. Silent, asymptomatic cavitational osteolysis can progress into segmental osteolysis that may become manifest and preclude revision procedures. Therefore close monitoring is recommended if silent osteolysis is suspected. A helical CT scan should be performed when signs of osteolysis or evident polyethylene wear are observed on conventional radiographs, or if it concerns a type of metal-backed acetabular component associated with a documented high wear rate. When a cavitational lesion is observed a helical CT scan should be performed yearly and treatment with bisphosphonates is to be considered. In case of segmental osteolysis or progression of a cavitational lesion, extensive debridement of the osteolytic cysts, bone grafting and replacement of the polyethylene liner is the treatment of choice. & 2005 Elsevier Ltd. All rights reserved.
Introduction Osteolysis, causing component loosening, is considered a main problem in hip arthroplasty.1 Exposure of particulate materials, including polyethylene and metal, to bone has been cited as an underlying cause of osteolysis in hip arthroplasty.2,3 Corresponding author. Tel.: +31 38 4244482; fax: +31 38 4243220. E-mail address:
[email protected] (C.C.P.M. Verheyen).
Wear particles migrate around the prosthesis or cement mantle and cause a local macrophage or sensitivity reaction, leading to the production of osteolytic mediators or local necrosis.4 The survival of joint prostheses depends to a large extend on factors that influence the rate of polyethylene wear.5 Another postulated cause of osteolysis is the exposure of periprosthetic bone to joint fluid and joint fluid pressure, causing death of exposed osteocytes.4 This can be due to early prosthesis migration and also to the shape or position of the acetabular or femoral component.6 Because metal
0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2005.02.014
ARTICLE IN PRESS Silent osteolysis associated with an uncemented acetabular on metal hip prostheses show significantly less wear and periprosthetic tissue reaction than metal–polyethylene hip prostheses, it is concluded that all second generation metal implants are to be considered in patients with a long life expectancy.4,7,8 Initially termed cement disease, it is generally accepted that, in most instances, osteolysis is a manifestation of an adverse cellular response to phagocytosable particulate wear and corrosion debris, possibly facilitated by local pressure-induced effects.9 Metal-backed acetabular components were introduced because of findings strongly suggesting a delay of cup loosening and migration by a more efficient stress transfer.10 Clinical studies, however, observed the opposite and concluded a higher wear rate for cemented metalbacked acetabular components than non-metalbacked components in cemented hip arthroplasty.11 Several authors have investigated the effect of implantation time on the wear rate with different results.11–16 Early periprosthetic osteolysis is rarely accompanied by pain or loss of function.17 Acetabular osteolytic defects can be classified as cavitational (a volumetric loss in the bony substance of the acetabulum but with the acetabular rim and medial wall of the hemispere remaining intact) or segmental (any loss of bone in the supporting rim or medial wall of the acetabulum).18 The dilemma of the way to diagnose and, if observed, how to treat and monitor silent osteolysis is the subject of further discussion.18–23
Monitoring and treatment Several studies indicated that radiographs largely understate the prevalence and location of osteolysis and CT scans are superior.19,20 Twenty-four per cent of cases of silent osteolysis were missed in 120 uncemented hip prostheses if only radiographs were used for detection compared with CT scans.20 Because the helical CT technique with metalartefact minimization does not converge, it is a more sensitive method than the conventional CT scan for identifying and quantifying osteolytic lesions.20,22 Puri et al.19 concluded that a CT scan is indicated to confirm the presence of substantial polyethylene wear or the observation of osteolysis on the regular radiographs (Fig. 1) and when a certain acetabular component is associated with excessive wear in the literature. The question if, how and when to treat silent osteolysis has been the subject of several studies.18,21–23 Patients with cavitational osteolysis
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may be considered candidates for treatment with bisphosphonates, which inhibit the TNF-alpha release by polyethylene particles causing osteolysis.20,24 Carlsson et al.22 determined the stability of the acetabular component in 100 revision operations and compared their findings with the preoperative radiologic obervations. Depending on the classification system, loosening of the acetabular component during the operation was demonstrated in only 6–31 per cent of the hips with radiolucent areas. The authors concluded that the radiographic evaluation of socket stability is troublesome. For treatment, the following strategies are to be considered: 1. Retention of a well-fixed shell, periacetabular bone grafting and revision of the liner: Retention of the socket with grafting of the periacetabular osteolytic lesion appears to be consistent with satisfactory socket longevity.25 Maloney et al.27 treated 35 patients with osteolytic cysts with bone grafting and replacement of the polyethylene insert. Intraoperatively, all acetabular shells where considered to be stable. After an average follow-up of 3 years all acetabular components seemed to be stable on conventional radiographs, 30 per cent of the osteolytic cysts disappeared radiologically and the other 70 per cent did not show progression. Beaule´ et al.25 treated 28 acetabular periprosthetic osteolytic cysts with bone grafting and replacement of the polyethylene insert during a revision operation because of aseptic loosing of the femoral component. Five of the 28 treated acetabular shells had to be replaced at a mean of 6.8 years after the index femoral revision. The authors concluded that revision of a stable uncemented acetabular shell solely because of periacetabular osteolysis is not indicated. Debridement of the osteolytic cysts, bone grafting and replacement of a polyethylene insert of improved quality while the metal shell remains in situ, proved to be a successfull treatment (Fig. 2). 2. Retention of a well-fixed shell with placement of a cemented liner: Beaule et al.26 placed 17 cemented polyethylene liners into a well-fixed uncemented shell and had favourable results after a follow-up of 5.1 years. This method is a good alternative for suitable candidates who have a well-fixed cementless socket with an inner diameter that is larger than the outer diameter of the liner. One of the limitations of this technique is the possible relative thinness of the replaced liner, which can interfere with the wear resistance of the polyethylene.26
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Figure 1 (a) A 74-year-old man with an uncemented total hip prosthesis. A hydroxyapatite coated metal shell with an air sterilized polyethylene liner is used. (b) Ten years postoperative an evident polyethylene wear (0.43 mm according to the method of Livermore34). And two osteolytic lesions can be observed (white arrows). (c) On the subsequent helical CT-scan, the lesions are seen in cross-section. (d) Helical CT-scan after bone grafting and liner replacement.
3. Revision of the acetabular shell: In case of loosening of the acetabular shell because of osteolysis, the acetabulum needs to be reconstructed with bone grafting. If 50 per cent or more of the surface of the acetabular shell contacts with the bone graft, a cemented acetabular component has to be placed. The placement of an uncemented acetabular component is indicated if the contact is less than 50 per cent.21 A proposed algorithm for surveillance and treatment of silent osteolysis is presented in Fig. 3. A wear rate of 0.20 mm per year seems to represent a critical threshold for the development of osteolysis.28 Puolakka et al.16 reviewed 107
metal-backed uncemented acetabular components on polyethylene wear after an average follow-up of 6 years. They observed an average polyethylene wear rate of 0.20 mm per year, which is rather high compared with studies on other polyethylene inserts in uncemented acetabular components.11–16 Because of an unacceptable survival percentage of 65 per cent after a 9-year follow-up the studied type of insert was withdrawn from the market.29 A metal shell containing screw holes correlates with a higher percentage of observed periacetabular osteolysis, while polyethylene particles, caused by back side wear of the polyethylene inserts, are exposed to the periacetabular bone through the screw holes.23 Huk et al.30 observed
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received a total hip arthroplasty bilaterally with liners of highly cross-linked polyethylene on one side and conventional polyethylene on the other. After a mean follow-up of 2 years the highly crosslinked polyethylene liners showed 31 per cent lower total penetration of the femoral head. The authors concluded that highly cross-linked showed a better wear performance and could increase the implant longevity. Longer follow-up is needed to establish if this new material is associated with less occurrence of osteolysis. It is to be expected that a better polyethylene quality will decrease the wear rate and the incidence of periprosthetic osteolysis.
Conclusion
Figure 2 Major osteolytic lesions with a stable shell. The treatment included debridement, bone grafting and liner replacement.
necrosis and granulomatous tissue reactions of the bone accompanied by polyethylene particles situated at the screw holes of the metal shell after an average implantation of 22 months. A reduction of wear rate by improving the quality of the polyethylene insert is expected to decrease the prevalence of osteolysis. Sterilization methods changed in the mid-1990s from gamma-irradiation in air to predominantly irradiation in inert gas or vacuum packaging. Mechanical in vivo degradation, which is based on an oxidative mechanism, is higher in air than in argon gamma-sterilized UHMWPE acetabular components after implantation because of radical formation in the polyethylene during sterilization in air.31 Kurtz et al.32 observed severe mechanical degradation caused by oxidation in 16 metal-backed air sterilized polyethylene liners after an average follow-up of 11.5 years. Head et al.33 performed a randomized trial of 200 patients in which argon sterilized cups were compared with cups sterilized in air with an average follow-up of 3 years. A wear reduction of 40 per cent was observed in the cups sterilized in argon. Highly cross-linked polyethylene shows an 80–90 per cent wear reduction in hip simulator testing.35 Digas et al.36 compared 32 patients who
A metal-backed acetabular component, poor rotational stability of the polyethylene insert and sterilization in air are factors that seem to correlate with a high polyethylene wear rate causing periprosthetic osteolysis. Early periprosthetic osteolysis is rarely accompanied by pain or loss of function. Timely treatment is indicated to prevent progression of the osteolytic lesions. As long as the metal shell is stable, extensive debridement of the osteolytic cysts, bone grafting and replacement of the polyethylene liner for a superior bearing material, is the treatment of choice for osteolytic lesions. In case of loosening of the acetabular shell, the acetabulum needs to be reconstructed with bone grafting, and an uncemented or cemented acetabular component has to be placed. Future studies need to concentrate on the improvement of the quality of arthroplasty components in order to minimize the prevalence of osteolysis. Patients treated with a metal-backed acetabular component associated with a high wear rate and a long-term follow-up should be monitored closely on linear wear rate, osteolysis and cup loosening. Practice points
A metal-backed acetabular component, poor rotational stability of the polyethylene insert and sterilization in air are factors that seem to correlate with a high polyethylene wear rate causing periprosthetic osteolysis. Timely treatment is indicated to prevent progression of the osteolytic lesions. In case of a stable metal shell the treatment of choice for osteolytic lesions is extensive
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Figure 3 Monitoring and treatment algorithm of acetabular silent osteolysis.
debridement of the osteolytic cysts, bone grafting and replacement of the polyethylene liner for a superior bearing material. In case of loosening of the acetabular shell, the acetabulum needs to be reconstructed with bone grafting and an uncemented or cemented acetabular component has to be placed.
Research directions
Future studies need to concentrate on the improvement of the quality of arthroplasty components in order to minimize the prevalence of osteolysis.
References 1. Harris WH. The problem is osteolysis. Clin Orthop 1995;311: 46–53. 2. Zicat B, Engh CA, Gokcen E. Patterns of osteolysis around total hip components inserted with and without cement. J Bone Jt Surg 1995;77:432–9. 3. Schmalzried TP, Kwong LM, Jasty M, Sedlacek RC, Haire TC, O’Connor DO, Bragdon CR, Kabo JM, Malcolm AJ, Harris WH. The mechanism of loosening of cemented acetabular components in total hip arthroplasty. Analysis of specimens retrieved at autopsy. Clin Orthop 1992;274:60–78. 4. Doorn PF. Wear and biological aspects of metal on metal total hip replacements. Thesis, 2000, p. 13 [Chapter 1]. 5. Willert HG, Buchhorn GH, Hess T. The significance of wear and material fatigue in loosening of hip prostheses. Orthopade 1989;18:350–69. 6. Aspenberg P, Van der Vis H. Fluid pressure may cause periprosthetic osteolysis. Particles are not the only thing. Acta Orthop Scand 1998;69:1–4.
ARTICLE IN PRESS Silent osteolysis associated with an uncemented acetabular 7. Jacobsson SA, Kjerf K, Wahlstrom O. Twenty-year results of McKee-Farrar versus Charnley prostheses. Clin Orthop 1996;329(Suppl):S60–8. 8. Schmalzried RP, Szuszczewicz ES, Akizuki KH, Petersen TD, Amstutz HC. Factor correlating with long term survival of McKee-Farrar to hip prostheses. Clin Orthop 1996; 329(Suppl):S48–59. 9. Jacobs JJ, Roebuck KA, Archibeck M, Hallab NJ, Giant TT. Osteolysis: basic science. Clin Orthop 2001;393:71–7. 10. Carter DR, Vasu R, Harris WH. Stress distributions in the acetabular region—II. Effects of cement thickness and metal backing of the total hip acetabular component. J Biomech 1982;15:165–70. 11. Cates HE, Faris PM, Keating EM, Ritter MA. Polyethylene wear in cemented metal-backed acetabular cup. J Bone Jt Surg [Br] 1993;75:249–53. 12. Devane PA, Bourne RB, Rorabeck CH, MacDonald S, Robinson EJ. Measuremetn of polyetylene wear in metal-backed acetabular cups. Clin Orthop 1995;319:317–26. 13. Hozack WJ, Rothman RH, Eng K, Mesa J. Primary cementless hip arthroplasty with a titanium plasma sprayed prosthesis. Clin Orthop 1996;333:217–25. 14. Kim YH, Kim JS, Cho SH. Primarty total hip arthroplasty with a cementless porous-coated anatomic total hip prosthesis. 10- to 12-year rsults of prospective and consecutive series. J Arthroplasty 1999;14:538–48. 15. Thanner J. The acetabular component in total hip arthroplasty. Evalution of different fixation principles. Thesis. Acta Orthop Scand (Suppl) 1999;286:70. 16. Puolakka TJS, Laine HJ, Moilanen TPS, Koivisto AM, Pajama ¨ki KJJ. Alarming wear of the first-generation polyethylene liner of the cementless porous-coated Biomet universal cup. Acta Orthop Scand 2001;72:1–7. 17. Lavernia CJ. Cost-effectiveness of early surgical intervention in silent osteolysis. J Arthroplasty 1998;13:277–9. 18. D’Antonio JA. Periprosthetic bone loss of the acetabulum. Classification and management. Orthop Clin N Am 1992;23: 279–90. 19. Puri L, Wixson RL, Stern SH, Kohli H, Hendrx RW, Stulberg SD. Use of helical computed tomography for the assessment of acetabular osteolysis after total hip arthroplasty. J Bone Jt Surg [Am] 2002;84:609–14. 20. Stulberg SD, Wixson RL, Adams AD, Hendrix RW, Bernfield JB. Monitoring pelvic osteolysis following total hip replacement surgery: an algorithm for surveillance. J Bone Jt Surg [Am] 2002;84:116–22. 21. Hozack WJ, Mesa JJ, Carey C, Rothman RH. Relationship between polyethylene wear, pelvic osteolysis and clinical symptomatology in patients with cementless acetabular components. A framework for decision making. J Arthroplasty 1996;11:769–72. 22. Carlsson AS, Gentz CF. Radiographic versus clinical loosening of the acetabular component in noninfected total hip arthroplasty. Clin Orthop 1984;185:145–50.
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23. Maloney WJ, Alto P, Peters P, Engh CA, Chandler H. Severe osteolysis of the pelvis in association with acetabular replacement without cement. J Bone Jt Surg [Am] 1993;75:1627–35. 24. Huk OL, Zukor KJ, Antoniou J, Petit A. Effect of pamidronate on the stimulation of macrophage TNF-alpha release by ultra-high-molecular-weight polyethylene particles: a role for apoptosis. J Orthop Res 2003;21:81–7. 25. Baule´ PE, LeDuff MJ, Dorey FJ, Amstutz HC. Fate of cementless acetabular components retained during revision total hip arthroplasty. J Bone Jt Surg [Am] 2003;85:2288–93. 26. Beaule PE, Ebramzadeh E, LeDuff M, Prasad R, Amstutz HC. Cementing a liner into a stable cementless acetabular shell: the double-socket technique. J Bone Jt Surg [Am] 2004;86: 929–34. 27. Maloney WJ, Herzwurm P, Paprosky W, Rubash HE, Engh CA. Treatment of pelvic osteolysis associated with a stable acetabular component inserted without cement as part of a total hip replacement. J Bone Jt Surg (Am) 1997;79: 1628–34. 28. Orishimo KF, Claus AM, Sychterz CJ, Engh CA. Relationship between polyethylene wear and osteolysis in hips with a second-generation porous-coated cementless cup after seven years of follow-up. J Bone Jt Surg [Am] 2003;85: 1095–9. 29. Puolakka TJS, Pajama ¨ki KJJ, Pulkkinen PO, Nevalainen JK. Poor survival of cementless Biomet total hip. A report on 1,047 hips from the Finnish Arthroplasty Register. Acta Orthop Scand 1999;70:425–9. 30. Huk OL, Bansal M, Betts F, Rimnac CM, Lieberman JR, Huo MH, Salvati EA. Polyethylene and metal debris generated by non-articulating surgaces of modular acetabular components. J Bone Jt Surg [Br] 1994;76:568–74. 31. Kurtz SM, Rimnac CM, Bartel DL. Degradation rate of ultra-high molecular weight polyetylene. J Orthop Res 1997;15:57–61. 32. Kurtz SM, Hozack W, Marcolongo M, Turner J, Rimnac C, Edidin A. Degradation of mechanical properties of UHMWPE acetabular liners following long-term implantation. J Arthroplasty 2003;18:68–78. 33. Head WC, Emerson RH, Millyard JM, Higgins L, Pindinson JL. Comparison of polyethylene wear in machined versus molded polyethylene liners in Ringloc acetabular cups. Plano, TX: Texas Center for Joint Replacement; 1999. 34. Livermore J, Ilstrup D, Morrey B. Effect of femoral head size on wear of the polyetylene acetabular component. J Bone Jt Surg [Am] 1990;72:518–28. 35. Bragdon CR, Jasty M, Muratoglu OK, O’Connor DO, Harris WH. Third-body wear of highly cross-linked polyethylene in a hip simulator. J Arthroplasty 2003;18:553–61. 36. Digas G, Karrholm J, Thanner J, Malchau H, Herberts P. Highly cross-linked polyethylene in total hip arthroplasty: randomized evaluation of penetration rate in cemented and uncemented sockets using radiosteriometric analysis. Clin Orthop 2004;429:6–16.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 294–304
www.elsevier.com/locate/cuor
TRAUMA
Humeral nails: When to choose what and how to use Christos Garnavos Orthopaedic Department of ‘‘Evangelismos’’, General Hospital, 8 Londou St, Glyfada 16675, Athens, Greece
KEYWORDS Intramedullary nailing; Diaphyseal humeral fracture; Humeral nails
Summary Intramedullary nailing of the humerus is controversial. This may be partly because of the complicated anatomy and the unique biomechanical characteristics of the arm, and also because the principles and nail designs used for the treatment of femoral and tibial fractures have been directly transposed to this location. Over the last few years there have been several reports on the indications for humeral nailing, timing of the procedure, surgical technique, and nail design. As a result, surgeons witnessed the appearance of a wide variety of humeral nails with different biomechanical properties and implantation techniques, reflecting the disputes concerning intramedullary nailing in the humerus. In this article it is proposed that humeral nails should be categorised into two distinct groups (fixed and bio), according to their main characteristics and their use must follow guidelines that will be outlined, paying respect to the fracture pattern and location. Other issues such as the timing of surgery and the role of reaming are also addressed in an effort to further improve the results of intramedullary nailing in the humerus. & 2005 Elsevier Ltd. All rights reserved.
Introduction Indications that are generally accepted for surgical treatment of an acute humeral fracture include multiple injuries, bilateral fractures, pathological fractures, floating elbow, brachial artery injury, brachial plexus palsy, open or segmental fractures and inability to maintain fracture alignment with functional bracing.1 However, over the last few years intramedullary nailing of humeral shaft Tel.: +302109628172.
E-mail address:
[email protected].
fractures has gained popularity amongst surgeons, particularly with the trend for developing treatment modalities that can be minimally invasive with low morbidity, providing simultaneously rapid recovery and prompt return to work and everyday life activities.2–13 Intramedullary nailing satisfies these criteria for diaphyseal femoral and tibial fractures but when we deal with humeral shaft fractures it seems that there is still confusion about the basic principles. Controversy exists as to why one should choose an intramedullary nail in preference to another implant, the timing of surgery, nail design selection, surgical technique
0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2005.06.003
ARTICLE IN PRESS Humeral nails: When to choose what and how to use (antegrade/retrograde–reamed/unreamed) and whether to bone graft or not. Being influenced by the success of intramedullary nailing in the femur and tibia, surgeons unsurprisingly transposed their knowledge and experience with the technique for treating humeral shaft fractures. However, in general, the unique anatomy and biomechanical characteristics of the humerus and its adjacent joints were overlooked.14 After numerous proposals concerning the design and capabilities of the ‘‘ideal’’ humeral nail and unconvincing debates about the ‘‘best’’ surgical technique, it seems that there is still doubt about ‘‘when to choose what and how to use it’’.
295 role (Fig. 2). Problems and complications that occur are mostly related to the complex anatomy and individual biomechanical characteristics of the humerus.35–37
During antegrade insertion With a fixed-nail, the deltoid and rotator cuff are injured by the surgeon’s knife, the penetrating awl,
Classifying humeral nails Despite many differences in design and intended surgical technique, humeral nails can be grouped generally into: (a) those offering strong mechanical fixation to the fracture (fixed-nails) and (b) those paying more attention to the biology and the anatomy of the arm (bio-nails), at the expense of rigidity of the fixation.
‘‘Fixed’’ humeral nails Nails in this category are made of either stainless steel or titanium, so their stiffness varies (Table 1). The common characteristic is that locking screws provide both proximal and distal interlocks and for that reason axial and rotational stability at the fracture site are good (Fig. 1).20,32–34 Because of the interlocking capabilities, location of the fracture within the diaphysis is not an important issue for the selection of surgical technique. In general, fixed-nails can be used with both antegrade and retrograde techniques (the decision mostly depends on the surgeon’s preference), without the location and type of fracture playing an important Table 1
Figure 1 A fixed humeral nail is locked proximally and distally with screws.
Examples of fixed humeral nails (listed alphabetically).
Name
Company
Insertion technique
Reamed/unreamed
References
ACE humeral nail Austofix humeral nail Flexible humeral nail Polarus nail (long version) Retrograde humeral nail Russell–Taylor humeral nail T2 Uniflex Unreamed humeral nail (UHN)
De Puy Austofix Synthes Acumed Biomet Smith and Nephew Stryker Biomet Synthes
Antegrade/retrograde Antegrade/retrograde Antegrade/retrograde Antegrade/retrograde Retrograde Antegrade Antegrade/retrograde Antegrade Antegrade/retrograde
Reamed Reamed/unreamed Reamed Reamed Reamed/unreamed Reamed Reamed/unreamed Reamed Unreamed
15,16 17,18 19 20 21,22 23–28
— 29 2,3,9–11,30,31
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Figure 2 Antegrade fixed-nailing of a distal humeral fracture.
the reamers (whenever used), and by the nail, the drills and locking screws.36–40 The inevitable penetration of the deltoid muscle for the insertion of the proximal locking screws adds to the injury in the area. Furthermore, drills and screws can injure the axillary nerve and the long head of biceps tendon.18,41–45 In addition, drilling and screw insertion for the distal interlock bears the significant risk of injuring the radial or the lateral cutaneus nerve of the forearm at the level of the elbow.6,9,18,29,35,42,43,46–49 During retrograde insertion With a fixed-nail, fractures at the supracondylar area have occurred as result of the eccentric insertion of the nail, the narrow humeral canal and the stiffness of the nail (Fig. 3).8–10,18,36,48,50 In addition, the axillary nerve is at risk by the locking screws used for locking the nail at the proximal end of the humerus.41 Both antegrade and retrograde techniques Fixed-nails share the problem of difficult and time consuming insertion of the locking screws at the tip of the nail. This is achieved with either the freehand technique, which in the humerus may be
Figure 3 Fracture at the supracondylar area is not a common complication of retrograde nailing.
particularly hazardous and sometimes difficult. This can be because of the inability to obtain an easy lateral view with the image intensifier or because of targeting devices that provide questionable reliability without eliminating the danger of injury to important vulnerable soft tissues (Fig. 4).6,9,18,29,35,36,41–43,47,49,51 Fixed-nails were used in the humerus, in the first instance, because of the excellent results produced by (fixed) intramedullary nailing of the femur and tibia. Problems related with their use in the arm were not foreseen. After the emergence of problems and complications directly related to the very techniques used to obtain stability (reamers, drills, locking screws), an important issue was raised: does the humerus need absolute stability (or at least as stable as is provided in the femur and tibia by a nail) or could a less stable environment suffice, thus offering the opportunity for avoidance
ARTICLE IN PRESS Humeral nails: When to choose what and how to use of some complications related to technique? In a recent article Perren (2002) states that the aim of modern fixation of long bone fractures is to ‘‘yproduce the best biological conditions for healing rather than absolute stability of fixation and this approach has been shown to give early solid union’’.52 If we bear in mind that functional bracing (still treatment of choice for acute humeral shaft fractures1) does not provide significant rotational or axial stability at the fracture site in the humerus, it becomes apparent that in the management of humeral shaft fractures absolute stability may not be necessary. Therefore, while the amount of stability required for uneventful healing of humeral shaft fractures remains to be defined, it could be stated that recent research and experience gained from the use of functional bracing have shown that humeral fractures can heal well with ‘‘adequate’’ or ‘‘relative’’ stability52,53. The appearance of bio-nails is based on this statement.
Figure 4 Failure of a targeting device to guide the distal screw properly.
Table 2 Name
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‘‘Bio’’ humeral nails Nails in this category are commonly made of either stainless steel or titanium (Table 2). Their shared characteristic is the avoidance of locking screws, at the tip of the nail. A unique, for each nail, feature or technique provides the ‘‘relative’’ stability needed for the fracture healing process. For example, the Marchetti nail consists of 4 or 5 spreading rods that abut firmly against the endosteum beyond the fracture and resist rotation (Fig. 5). Spreading wires are also used by the Halder nail. The Fixion nail expands and incarcerates within the humeral canal. The True-Flex nail is fluted (star shape cross-section) and, by selecting
Figure 5 Correct use of a retrograde bio-nail.
Examples of bio-humeral nails (listed alphabetically). Company
Insertion technique
Fixion nail Disc-O-Tech medical technologies Antegrade/retrograde Halder nail Corifix Retrograde Marchetti–Vicenzi nail Zimmer Retrograde True-flex nail Encore Antegrade
Reamed/unreamed References Reamed/unreamed Unreamed Semi-reamed Unreamed
4,54–56 5 11–13 57,58
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Figure 7 Avoidance of transverse-locking screws proximally during antegrade bio-nailing. The proximal interlock is provided by other means. Figure 6 Correct use of an antegrade bio-nail.
the appropriate nail size, the flutes resist rotation beyond the fracture (Fig. 6). Despite the different ways of achieving distal interlock, the common theme is avoidance of the use of locking screws. To eliminate the possibility of damage to the soft tissues around the shoulder joint, Marchetti-Vicenzi and Halder nails are inserted only with the retrograde technique. True-Flex nails inserted with the antegrade technique do not use transverse locking screws for the proximal interlock (Fig. 7). Problems and complications that have occurred with bio-nails are mostly related to their unique features but may also be the result of incorrect use of each nail. For example, the use of MarchettiVicenzi and Halder nails has been complicated by perforation of the humeral head by the expanding rods, while removal of the Marchetti-Vicenzi nail has been occasionally reported as difficult or impossible.5,11,50 Complications of other bio-nails include unacceptable alignment of the fracture and nail migration.14,36,56 Iatrogenic fracture or fracture extension and comminution at the supracon-
dylar area have been reported sporadically during retrograde bio-nailing.11,36,50 Union rates and functional outcomes after bio-nailing appear satisfactory and similar to those obtained after fixed nailing, as reported in independent, non-comparable studies.4,12,13,50,54,56–58 However, the lack of prospective comparable studies must be stressed.11 The quality of the fixation offered to the fracture site by bio-nails depends mainly on the features and design of each nail, as well as on the surgical technique and the fracture configuration and location. By definition, bio-nails offer an adequate interlock at the end closest to the insertion point whilst the tip interlock is achieved by nail design features and capabilities (shape, expansion, spreading rods, etc.). A general principle that should apply in bio-nailing, is that as much length of the nail as possible should be within the bone segment that is not the segment bearing the insertion site, to provide better stability. In this way, the spreading rods of the Marchetti nail have more room for expansion, and there is more contact surface with inflating or fluted nails, etc. Therefore, the advantages offered by the design of
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Figure 8 With bio-nailing the entry site of the nail must be nearer to the fracture site.
a bio-nail function better if the fixation is performed from the short to the long segment. This general rule has been recommended for fixed nailing but its application to bio-nailing is unequivocal (Figs. 8 and 9).7,8,59 Conclusively, a key point for humeral bio-nailing is that fractures of the proximal humeral diaphysis are better treated with antegrade technique while fractures of the distal humeral diaphysis are better treated with retrograde technique.7,8,14,59 However, because of their design, some bio-nails can be inserted with either the antegrade or the retrograde technique but not with both (e.g. Marchetti-Vicenzi retrograde, TrueFlex antegrade). This drawback may be responsible for some of the problems encountered with their use, such as inadequate fixation of proximal humeral fractures treated with the retrograde Marchetti-Vicenzi nail (where the rods do not have enough canal length to expand adequately) (Fig. 10) or unstable fixation of distal humeral fractures treated with the True-Flex nail (where there is not enough length of the humeral canal for the fins to engage and stabilise the distal segment) (Fig. 11). Fracture location has not been within the inclusion (or exclusion) criteria in any of the studies dealing with bio-nailing, which means that fracture location has not been, so far, a criterion for
Figure 9 With bio-nailing the entry site of the nail must be nearer to the fracture site.
determining either the use of a specific bio-nail or the performance of a specific operative technique (antegrade or retrograde), an issue that authors may need to address in future studies.
Reaming Reaming is recommended with several fixed and bio nails, copying the current practice used for intramedullary nailing of femoral and tibial fractures. However, the concept that use of a broader nail provides stronger and more stable fixation whilst allowing the use of wider stronger locking screws leading to safer/faster mobilisation, weight bearing, and fracture union may not hold true in the humerus, as we are dealing with a non-weight bearing bone.60,61
During antegrade nailing Reamers could add to the damage of the rotator cuff directly, as mentioned. It has been reported
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Figure 11 An antegrade bio-nail does not offer ‘‘adequate’’ rotational stability to a distal humeral fracture.
Figure 10 A retrograde bio-nail does not offer ‘‘adequate’’ rotational stability to a proximal humeral fracture.
that reaming of the humeral canal can cause heatinduced segmental necrosis with adverse consequences for fracture healing.38,62 Also, by-products of reaming could accumulate underneath the rotator cuff (as they are deposited during withdrawal of the reamers) and play a role in the pathogenesis of pain and post-operative stiffness of the shoulder joint.39 Unfortunately, there are no studies comparing the outcomes of reamed and unreamed antegrade humeral nails to support this hypothesis. Finally, reaming could damage the radial nerve directly if the fracture is not reduced accurately and is located at the spiral groove, where the nerve is close to the bone.36
During retrograde nailing Careful reaming does not appear to cause any additional problems, provided that thorough washing of the supracondylar area is performed at the end of the procedure. Contrary to what was said about antegrade nailing, reaming might be necessary during retrograde nailing, to enlarge the (usually narrow) distal humeral canal, thus facilitating nail insertion and reducing the possibility of iatrogenic fracture at the supracondylar area.63 However, although it has not been reported so far, similar complications that occur with insertion of a wide nail to a narrow humeral canal (e.g. supracondylar fracture) could happen with the use of too big reamers. Also weakening of the humeral canal with too much reaming could lead to subsequent stress fracture.
ARTICLE IN PRESS Humeral nails: When to choose what and how to use
Timing Over the last two decades intramedullary nailing has been established as the treatment of choice for diaphysial fractures of the femur and tibia, regardless of whether surgeons were dealing with recent or non-recent fractures.64 In the lower limb the method has gained acceptance because of (a) the optimal mechanical environment that is engendered for the healing bone (internal splintage of the fracture and weight shearing) (b) the early mobilisation and weight bearing that promotes fracture healing and early return to pre-fracture activities and (c) the complementary role of reaming, that facilitates insertion of stronger nails (with better mechanical properties thus permitting early weight bearing) and promotes fracture healing in non-acute fractures, delayed unions and pseudarthroses by internal debridement and creation of osteogenic byproducts around the fracture/pseudarthrosis site.35,64,65 None of these factors can be used in a similar manner in the humerus: the superior mechanical properties offered by intramedullary nails to fractured long bones of the leg are of little value in the arm, as the long bones of the upper limb do not bear the body weight. Reaming of the humeral canal cannot be recommended in the humerus for reasons that have been explained previously and dynamisation of the fracture site cannot effectively happen (non-weight bearing bone). However, fresh fracture haematoma, which is present after all recent fractures, plays an important role in the healing process and it may be the only biological factor assisting intramedullary nailing in the humerus.60,64 As a result, one could expect a better outcome from the use of intramedullary nails in fresh fractures and less favourable as time goes by. Consequently, in the humerus, better fracture healing and good functional results accompany early nailing and for that reason intramedullary splintage must be considered as a primary treatment option.14 In cases of delaying unions and pseudarthrosis intramedullary nailing can be a treatment alternative (alongside compression plating), but bearing in mind the analysis above, thorough debridement and bone grafting should be done to the fracture site.15,30,66 Compression of the ununited fracture by either interfragmentary wires or by the compression mechanism offered by some nails (AO, T2) could contribute to better results.10,30,66
Discussion In the surgical management of humeral shaft fractures intramedullary nailing could be the
301 treatment of choice, offering minimal morbidity and a low complication rate.4–9,12,55,58 However, nailing of the humerus must be distinguished from similar techniques used for the fixation of femoral and tibial diaphyseal fractures.14 The humerus has unique anatomical and biomechanical characteristics, so intramedullary nailing should be adapted and modified accordingly.14 The present study proposes a categorisation of humeral nails into fixed and bio. Knowledge of the differences between the two groups could help towards the selection of the most suitable nail for each fracture, according to fracture ‘‘personality’’, the required nail capabilities and the corresponding surgical technique. As a general rule fixed-nails can be used for the osteosynthesis of any diaphyseal humeral fracture and selection of the antegrade or retrograde technique is based upon the surgeon’s preference and experience. On the contrary, with bio-nailing antegrade or retrograde technique must be decided, taking account of fracture location, as the nail should be inserted from the shorter to the longer segment to offer better fracture stability. This proposed classification could define a framework for organising objective clinical and biomechanical studies in the future. In recent studies, ‘‘humeral nailing’’ is compared with other treatment modalities regardless of the nail used in the study.6,24,67,68 In this way, results (favourable or not) reflect on the specific humeral nail used in the study and not on other humeral nails with different design and identities Therefore, the term ‘‘humeral nailing’’ in a title, should not be used alone as, for example, the results of antegrade fixed-nailing may be different from results of retrograde bio-nailing for similar fractures.9,24,26,27,31,69 It is proposed that instead of saying or writing about ‘‘yplating V nailingy’’ or ‘‘ybracing V nailingy’’ we should be discussing ‘‘yplating V antegrade fixed-nailingy’’ or ‘‘ybracing V retrograde bio-nailingy’’ etc., Whenever a bio-nail is used in a study, location of the fracture should be clearly defined. Humeral nailing tends to be considered a homogeneous surgical method. For that reason there are hardly any studies comparing different types of nails in the treatment of similar humeral fractures.2,11 Scheerlinck and Handelberg (2002) published a comparison study between the retrograde Marchetti-Vicenzi nail and the Unreamed AO Humeral Nail inserted with the antegrade technique.11 Although this is a study in the right direction, comparing a fixed-nail (UHN) with a bio-nail (Marchetti-Vicenzi), the criteria for nail selection to treat each fracture ‘‘ywere based on
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the surgeon’s preference and group consensus’’. Nevertheless, the authors report that the retrograde Marchetti-Vicenzi nail was ‘‘preferably’’ used in more proximal fractures and the antegrade AO nail was used in more distal fractures, a statement that does not allow for reliable statistical comments. Furthermore, results from the use of the Marchetti-Vicenzi nail in proximal humeral fractures could be less satisfactory than if the same nail had been used in middle to distal humeral fractures (insertion from the short to the long segment), whilst with fixed-nailing the stability of the fracture site is less influenced by the insertion site.7,8,59 Furthermore biomechanical studies in vitro, that compare intramedullary nails with different characteristics (and mechanical properties) (fixednails V bio-nails), appear biased and scientifically doubtful.32–34 The stability offered by a fixed-nail is unquestionably superior to the stability offered by a bionail both in vivo and in vitro.32–34 However, what matters is the efficiency of an implant to offer a suitable environment for fracture healing in combination with low complication rates, low morbidity and rapid recovery parameters not examined in any of the biomechanical studies with cadaveric or plastic bones.52
Research Directions
Summary The expanding use of humeral nails and the development of new nail designs indicate that the future of humeral nailing in the treatment of humeral shaft fractures appears promising. Differentiating humeral from femoral and tibial nailing, along with creator understanding of the differences between types of humeral nails and insertion techniques will lead inevitably to better results. This will lead to expansion of the indications for the use of nails in the humerus. However, it seems that although humeral nailing is already challenging non-operative treatment there is still a long way to go to define its exact roles and indications in the treatment of humeral shaft fractures. Practice Points
Fixed-nails offer optimal stability and can be used for the osteosynthesis of any diaphyseal fracture. Although fixation from the short to the long segment has been recommended, both antegrade and retrograde techniques offer a good biomechani-
cal environment for prompt healing of any diaphyseal fracture. Drawbacks include the risks associated with the use of locking screws and occasionally difficult and timeconsuming distal interlocking. Bio-nails offer less stability to the fracture site, which may be adequate for prompt union, something that remains to be defined and confirmed with future studies. Insertion from short to long segment is generally recommended; therefore an antegrade or retrograde technique should be dependent upon fracture location rather than preference of the surgeon. Drawbacks are the lack of absolute stability and problems related to each specific implant design. Advantages are the reduction of the risk of neurovascular problems and reduced operating time. Humeral nailing should be performed earlier rather than later, as the humerus is not a weight bearing bone. Reaming is generally not recommended in the humerus, especially during antegrade nailing.
Clinical studies concerning humeral shaft fractures should be conducted by J defining—in the title—the type of implant used in the study, J comparing implants used for the fixation of similarly located fractures, J comparing different techniques in the fixation of similar fractures Biomechanical studies must compare implants with similar mechanical properties.
References 1. Gregory Jr PR. Fractures of the shaft of the humerus. In: Rockwood C, Green DP, Bucholz RW, Heckman JD, editors. Fractures in adults. 5th ed. Philadelphia: Lippincott Williams & Wilkins; 2002 Chapter 24. 2. Blum J, Janzing H, Gahr R, Langendorff HS, Rommens PM. Clinical performance of a new medullary humeral nail: antegrade versus retrograde insertion. J Orthop Trauma 2001;15:342–9. 3. Blum J, Rommens PM, Janzing H. The unreamed humeral nail—a biological osteosynthesis of the upper arm. Acta Chir Belg 1997;97:184–9. 4. Franck WM, Olivieri M, Jannasch O, Hennig FF. Expandable nail system for osteoporotic humeral shaft fractures: preliminary results. J Trauma 2003;54:1152–8.
ARTICLE IN PRESS Humeral nails: When to choose what and how to use 5. Halder SC, Chapman JA, Coudhury G, Wallace WA. Retrograde fixation of fractures of the neck and shaft of the humerus with the ‘‘Halder Humeral Nail’’. Injury 2001; 32:695–703. 6. Linn J. Treatment of humeral shaft fractures with humeral locked nail and comparison with plate fixation. J Trauma 1998;44:859–64. 7. Linn J, Hou SM. Antegrade locked nailing for humeral shaft fractures. Clin Orthop 1999;365:201–10. 8. Linn J, Hou SM, Hang YS, Chao EY. Treatment of humeral shaft fractures by retrograde locked nailing. Clin Orthop 1997;342:147–55. 9. Rommens PM, Blum J, Runkel M. Retrograde nailing of humeral shaft fractures. Clin Orthop 1998;350:26–39. 10. Rommens PM, Verbruggen J, Broos PL. Retrograde locked nailing of humeral shaft fractures. A review of 39 Patients. J Bone Jt Surg (Br) 1995;77(B):84–9. 11. Scheerlinck T, Handelberg F. Functional outcome after intramedullary nailing of humeral shaft fractures: comparison between retrograde Marchetti-Vicenzi and unreamed AO antergrade nailing. J Trauma 2002;52:60–71. 12. Tennant S, Thomas M, Murphy JP, Warren PJ. The MarchettiVincenzi humeral nail—a useful device in fresh fractures. Injury 2002;33:507–10. 13. Williams PR, Shewring D. Use of an elastic intramedullary nail in difficult humeral fractures. Injury 1998;29:661–70. 14. Garnavos C. Intramedullary nailing for humeral shaft fractures: the misunderstood poor relative. Current Orthop 2001;15(1):68–75. 15. Fontijne WP. Retrograde intramedullary nailing of distal humeral nonunions. Acta Orthop Scand 2002;73:706–8. 16. Mazirt N, Tobenas AC, Roussignol X, Duparc F, Dujardin FH. Experimental study of the primary stability of locked centromedullary nailing of the humeral diaphysis. Rev Chir Orthop Reparatrice Appar Mot 2000;86:781–6. 17. Bauze AJ, Clayer MT. Treatment of pathological fractures of the humerus with a locked intramedullary nail. J Orthop Surg 2003;11:34–7. 18. Ingman AM, Waters DA. Locked intramedullary nailing of humeral shaft fractures. J Bone Jt Surg (Br) 1994; 76-B:23–9. 19. Stannard JP, Harris HW, McGwin Jr. G, Volgas DA, Alonso JE. Intramedullary nailing of humeral shaft fractures with a locking flexible nail. J Bone Jt Surg 2003;85(A):2103–10. 20. Molster A, Gjerdet NR, Strand RM, Hole RM, Hove LM. Intramedullary nailing in humeral shaft fractures. Mechanical behavior in vitro after osteosynthesis with three different intramedullary nails. Arch Orthop Trauma Surg 2001;121:554–6. 21. Moran MC. Retrograde humeral nailing. Am J Orthop 1998; XXVIII(2S(Suppl)). 22. Todd LT, Gittins ME, Stutzman DJ. Retrograde humeral nailing: an anatomic study. Am J Orthop 1998;XXVIII (2S(Suppl)). 23. Ajmal M, O’Sullivan M, McCabe J, Curtin W. Antegrade locked nailing in humeral shaft fractures. Injury 2001; 32:692–4. 24. Chapman JR, Henley B, Agel J, Benca P. Randomized prospective study of humeral shaft fracture fixation: intarmedullary nails versus plates. J Orthop Trauma 2000; 14:162–6. 25. Cox MA, Dolan M, Synnott K, McElwain JP. Closed interlocking nailing of humeral shaft fractures with the Russell-Taylor nail. J Orthop Trauma 2000;14:349–53. 26. Crates J, Whittle AP. Antegrade interlocking nailing of acute humeral shaft fractures. Clin Orthop 1998(350):40–50.
303 27. Hems TE, Bhullar TP. Interlocking nailing of humeral shaft fractures: the Oxford experience 1991 to 1994. Injury 1996;27:485–9. 28. Ikpeme JO. Intramedullary interlocking nailing for humeral fractures: experiences with the Russell–Taylor humeral nail. Injury 1994;25:447–55. 29. Rupp RE, Chrissos MG, Ebraheim NA. The risk of neurovascular injury with distal locking screws of humeral intramedullary nails. Orthopedics 1996;19:593–5. 30. Martinez AA, Herrera A, Cuenca J. Good results with unreamed nail and bone grafting for humeral nonunion. Acta Orthop Scand 2002;73:273–6. 31. Sanzana ES, Duminer RE, Castro JP, Diaz EA. Intramedullary nailing of humeral shaft fractures. Int Orthop 2002;26: 211–3. 32. Blum J, Sternstein W, Hessmann MH, Karagul G, Hansen MM, Rommens PM. Self locking expandable intramedullary nails offer low rotational stability in biomechanical testing. Orthop Trauma Assoc Congress 2003 Poster. 33. Dalton JE, Salkeld SL, Satterwhite YE, Cook SD. A biofixedcomparison of intramedullary nailing systems for the humerus. J Orthop Trauma 1993;7(4):367–74. 34. Schopfer A, Hearn TC, Malisano L, Powell JN, Kellam JF. Comparison of torsional strength of humeral intramedullary nailing: a candaveric study. J Orthop Trauma 1994;8(5): 414–21. 35. Brumback RJ. The rationales of interlocking nailing of the femur, Tibia and Humerus: an overview. Clin Orthop 1996;324:292–320. 36. Farragos AF, Schemitsch EH, Mc Kee MD. Complications of intramedullary nailing for fractures of the humeral shaft: a review. J Orthop Trauma 1999;13:258–67. 37. Robinson MC, Bell MK, Court-Brown MC, McQueen MM. Locked nailing of humeral shaft fractures. J Bone Jt Surg (Br) 1992;74-B:558–62. 38. Remiger AR, Miclau T, Lindsey RW, Blatter G. Segmental avascularity of the humeral diaphysis after reamed intramedullary nailing. J Orthop Trauma 1997;11(4):308–11. 39. Schmidt AH, Templeman DC, Grabowski CM. Antegrade intramedullary nailing of the humerus complicated by heterotopic ossification of the deltoid: a case report. J Orthop Trauma 2001;15:69–73. 40. Stern JP, Mattingly AD, Pomeroy LR, Zenni JE, Kreig KJ. Intramedullary fixation of humeral shaft fractures. J Bone Jt Surg (Am) 1984;66-A:639–46. 41. Albriton MJ, Barnes CJ, Basamania CJ, Karas SG. Relationship of the axillary nerve to the proximal screws of a flexible humeral nail system: an anatomic study. J Orthop Trauma 2003;17(6):411–4. 42. Bono CM, Grossman MG, Hochwald N, Tornetta 3rd. P. Radial and axillary nerves. Anatomic considerations for humeral fixation. Clin Orthop. 2000(373):259–64. 43. Evans DP, Conboy LBV, Evans JE. The seidel humeral locking nail: an anatomical study of the complications from locking screws. Injury 1993;24:175–6. 44. Riemer BL, D’Ambrosia R. The risk of injury to the axillary nerve, Artery, and Vein from proximal locking screws of humeral interlocking nails. Orthopedics 1992;15: 697–9. 45. Riemer BL, D’Ambrosia R, Kelam JF, Butterfield SL, Burke III CJ. The Anterior acromial approach for antegrade intramedullary nailing of the humeral diaphysis. Orthopedics 1993;16:1219–23. 46. Blyth MJG, Macleod CMB, Asante DK, Kinninmonth AWG. Iatrogenic nerve injury with the Russell–Taylor humeral nail. Injury 2003;34:227–8.
ARTICLE IN PRESS 304 47. Kolonja A, Vecsei N, Mousani M, Marlovits S, Machold W, Vecsei V. Radial nerve injury after anterograde and retrograde locked intramedullary nailing of humerus. A clinical and anatomical study. Osteo Trauma Care 2002;10:192–6. 48. Linn J, Shen PW, Hou SM. Complications of locked nailing in humeral shaft fractures. J Trauma 2003;54:943–9. 49. Moran MC. Distal interlocking during intramedullary nailing of the humerus. Clin Orthop 1995;317:215–8. 50. Simon P, Jobard D, Bistour L, Babin SR. Complications of Marchetti locked nailing for humeral shaft fractures. Int Orthop 1999;23:320–4. 51. Garnavos C, Kanakaris N. Stress fracture due to unsuccessful targeting during intramedullary nailing. Eur J Trauma 2003; 29:105–7. 52. Perren SM. Evolution of the internal fixation of long bone fractures. The scientific basis of biological internal fixation: choosing a new balance between stability and biology. J Bone Jt Surg 2002;84(B):1093–110. 53. Sarmiento A, Zagorski JB, Zych GA, Latta LL, Capps CA. Functional bracing for the treatment of fractures of humeral diaphysis. J Bone Jt Surg 2000;82(A):478–86. 54. Capelli RM, Galmarini V, Molinari GP, De Amicis A. The fixion expansion nail in the surgical treatment of diaphyseal fractures of the humerus and Tibia. Our experience. Chir Organi Mov 2003;88:57–64. 55. Franck WM, Olivieri M, Jannasch O, Hennig FF. An expandable nailing system for the management of pathological humerus fractures. Arch Orthop Trauma Surg 2002;122: 400–5. 56. Lorich DG, Geller DS, Yacoubian SV, Leo AJ, Helfet DL. Intramedullary fixation of humeral shaft fractures using an inflatable nail. Orthopedics 2003;26:1011–4. 57. Garnavos C, Lunn GP. Preliminary clinical experience with a new fluted humeral nail. Injury 1994;25:241–5. 58. Garnavos C, Seaton J, Lunn PG. The treatment of selected fractures of the humeral shaft with the true-flex nail. Injury 1998;29:269–75.
C. Garnavos 59. Linn J, Inoue N, Valdevit A, Hang YS, Hou SM, Chao EYS. Biomechanical comparison of antegrade and retrograde nailing of humeral shaft fracture. Clin Orthop 1998;351: 203–13. 60. Chapman MW. The effect of reamed and nonreamed intramedullary nailing on fracture healing. Clin Orthop 1998;355(Suppl):S320–8. 61. Winquist RA. Locked femoral nailing. J Am Acad Orthop Surg 1993;1:95–105. 62. Ochsner PE, Baumgart F, Kohler G. Heat-induced segmental necrosis after reaming of one humeral and two tibial fractures with a narrow medullary canal. Injury 1998; 29(Suppl 2):B1–B10. 63. Marchetti PG, Vicenzi G. Intramedullary fixation system, Surgical Technique Humerus. Edited by Zimmer. 64. Chester S, Hallfeldt K, Perren S, Schweiberer L. The effects of reaming and intramedullary nailing on fracture healing. Clin Orthop 1986;212:18–25. 65. Starr AJ, Bucholz RW. Fractures of the shaft of the femur. In: Rockwood C, Green DP, Bucholz RW, Heckman JD, editors. Fractures in adults. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 2002 Chapter 41. 66. Lin J, Chiang H, Chang DS. Locked nailing with interfragmentary wiring for humeral nonunions. J Trauma 2002; 52:733–8. 67. McCormack RG, Brien D, Buckley RE, Mckee MD, Powell J, Schemitsch EH. Fixation of fractures of the shaft of the humerus by dynamic compression plate or intramedullary nail. J Bone Jt Surg 2000;82(B):336–9. 68. Wallny T, Sagebiel C, Westerman K, Wagner UA, Reimer M. Comparative results of bracing and interlocking nailing in the treatment of humeral shaft fractures. Int Orthop 1997;21:374–9. 69. Strothman D, Templeman DC, Varecka T, Bechtold J. Retrograde nailing of humeral shaft fractures: a biomechanical study of its effects on the strength of the distal humerus. J Orthop Trauma 2000;14:101–4.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 305–308
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TUMOURS
Management of lung metastases from musculoskeletal sarcomas Antonio Briccoli, Michele Rocca, Mariacristina Salone General Surgery of Istituto Ortopedico Rizzoli, University of Bologna, Italy
KEYWORDS Pulmonary metastases; Metastatic osteosarcoma; Metastatic soft tissue sarcoma
Summary Bone and soft tissue sarcomas metastasize to the lung in about onethird of patients. Surgery of lung metastases is possible in at least 35% of patients who have undergone primary surgery. Thoracotomy may be bilateral if necessary. Wedge resection is preferred; lobectomy or pneumonectomy is reserved for metastases in the hilum. The average overall survival following resection at 5-years is 37%. Results are influenced by the specific histotype of the primary tumour, by the interval between pulmonary metastases and treatment of the primary sarcoma, and by the number of metastases. & 2005 Elsevier Ltd. All rights reserved.
Introduction In bone and soft tissue sarcomas, surgery and adjuvant treatment can give good results in a large number of cases. Lung metastases are frequent at onset and during follow up. In bone sarcomas, the estimated frequency varies from 34% to 76%, while in the soft tissues sarcomas it is 11%.1 The presence of lung metastases greatly influences the prognosis following surgery.2 Autopsy studies have demonstrated that a single lung metastasis does not necessarily mean neoplastic diffusion: the lung can remain, for a variable time period, the only site of metastasis.
Patients with untreated metastases have a poor prognosis and die within 24 months from recognition of metastases. Surgery can modify this prognosis. Numerous series, some with long term follow up, show that one-third of these patients can be helped. The operative risk is relatively low, being less than 1%.3 During the past ten years alternative non-surgical treatments such as cryotherapy, radio frequency, ablation and alcholisation, have been proposed but none have obtained results similar to surgical metastasectomy.4 However treatment by isolated pulmonary perfusion deserves further clinical investigation.5
Indications Corresponding author. Tel.: +39 051 6366841;
fax: +39 051 331710. E-mail address:
[email protected] (A. Briccoli).
Selection criteria for lung metastasectomy are: (I) absence of extrathoracic metastases, (II) no robust
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ARTICLE IN PRESS 306 alternative therapies available, (III) good possibility of total removal of the pulmonary metastases, (IV) low surgical risk and (V) low risk of respiratory failure. Thus, a correct preoperative evaluation comprises: (I) exclusion of local recurrence from the sarcoma and extrathoracic sites of metastases using CT scan or P.E.T. (II) defining the site and number of lung metastases (chest CT scan) and assessment of respiratory and cardiac function. Modern technology in thoracic imaging has reduced false negative cases to 7–8%. And these are confined to small lesions, and those in difficult locations, e.g. adjacent to the diaphragm. False positive cases are more frequent (43%) when lung metastases are present at onset,6 but in patients with late lung metastases it is only 7–8%.
A. Briccoli et al. 90 80 70 60 50 40 30 20 10 EWING
OSTEO
SOFT TISSUE
0 12 mos
24 mos
36 mos
48 mos
60 mos
Figure 2 Results after metastasectomy in muscoloskeletal sarcomas.
Surgical treatment Metastases in the subpleural region are most frequent compared to hilar or parahilar sites. Thus, wedge resection is the most common surgical technique.7 This procedure, due to the haemometastatic genesis of lung metastases, allows sufficient resection, without significant pulmonary sacrifice. A good respiratory function is maintained in patients with more than one pulmonary resection as well as in synchronous bilateral excision. Lobectomy and pneumonectomy are performed for hilar metastases, adjacent or attached to pulmonary vessels (Fig. 1). Mini-invasive thoracotomy is preferable to the thoracoscopic approach. Thoracotomy allows an accurate manual investigation of the atelectatic lung, and can reveal metastases unseen on CT scan as a result of their
small size. In bilateral pulmonary resection or investigation, median sternotomy can be performed as an alternative to thoracotomy. For correct staging, overcoming the limits of CT scan, some authors recommend this approach in patients even with unilateral metastases8 although others believe this procedure is unnecessary.9 With sternotomy it is more difficult to remove lesions in the posterior segments, the risk of sepsis or nonharmonic pulmonary consolidation is higher and, above all, does not allow reoperation for pulmonary relapses. Results differ according to histogenesis of the lung metastases (Fig. 2) and their time of appearance.
Osteosarcoma On the basis of the time of appearance of lung metastases, three events can be distinguished. (1) metastases at the time of osteosarcoma diagnosis; (2) metastases during post-operative chemotherapy; (3) metastases at the end of post-operative chemotherapy.
Metastases at diagnosis Figure 1 A CT scan of chest shows a single metastasis suitable for surgical resection by lobectomy or pneumonectomy.
In patients with metastases at the time of histological diagnosis of the primary lesion,
ARTICLE IN PRESS Management of lung metastases from musculoskeletal sarcomas neoadjuvant chemotherapy is necessary, after 2 cycles, a repeat lung CT scan should be performed. If the suspected metastases have resolved further, surgery is unnecessary. If the CT scan remains changed, synchronous removal of the primary osteosarcoma and pulmonary metastases is recommended to allow further administration of post-operative chemotherapy in a shorter time lapse than if surgery was done sequentially. This is also more tolerable from the psychologic aspects. If the number and volume of metastases is found to have increased, thoracotomy is indicated only for the purpose of biopsy.
Metastases during post-operative chemotherapy When metastases appear during chemotherapy, treatment is ceased and an evaluation is done after 30 days. Surgery is recommended, even a synchronous bilateral procedure. After surgical recovery, the patient can complete the suspended chemotherapy.
307
Pulmonary recurrence after metastasectomy occurs in one-third of patients and when the initial indications for surgery are present. Re-operation is undertaken. Event free survival, at both 3 and 5 years is, 33%. The prognosis is influenced by the same factors which influenced the first operation.14
Ewing’s sarcoma Surgery of metastases from Ewing’s sarcoma is controversial. However there is some evidence to support resection. The rate of actuarial survival at 5 years in patients having operative treatment is 56–58%15,16 (Fig. 3). However, in these papers, the patients were selected from amongst those with a low number of metastases, and who had completed the preoperative non-surgical treatment as recommended by standard protocols. One area of concern is radiotherapy to the lungs for a therapeutic or a prophylactic purpose. Data present in literature are discordant.17 In our practice, 50% of patients who underwent metastasectomies received preoperatory pulmonary radiotherapy.
Metastases after chemotherapy Surgery is recommended also when diagnostically confirmed metastases appear after chemotherapy ceases. When relapse occurs 24 months from the onset of disease, no associated chemotherapy is administered; but if metastases appear within 24 months, high dose chemotherapy is necessary. Results obtained are favourable, with a 23–40% survival at 5 years from surgery.10,11 However, results are influenced by specific prognostic factors, in particular, by the diseasefree interval, i.e. the period of time from treatment of the osteosarcoma to pulmonary metastases.12,13 The survival rate at 5 years is 19–44% in patients with appearance of metastases within 24 months, and 61% in patients with metastases after 24 months. For metastatic resection undertaken at the time of primary osteosarcoma surgery, the disease-free survival at 2 years is 38%. The same prognostic significance applies to the number of metastases resected: survival is 48% for patients operated for one metastasis, 29% for 2–3 metastases, 24% for 4–5 metastases and 11% for more than 5 metastases. Bilateral metastases do not influence the prognostic significance, as does gender, age and site of the osteosarcoma or metastases.
Soft tissue sarcomas Surgical ablation of an isolated pulmonary metastasis or multiple lesions from a soft tissue sarcoma is the only useful treatment; other therapeutic procedures are considered palliative.18 Patients with good general status, who have resectable metastases, are potential candidates for
Figure 3 Overall survival in Ewing’s sarcoma:metastasectomy vs. no operation.
ARTICLE IN PRESS 308 surgery, using the same techniques described for other histotypes. Overall disease-free survival rate after metastasectomy at 5 years is 24%.19 The prognosis is governed by the disease-free interval, whilst age, gender, site and sarcoma volume, metastasis diameter and its localisation, uni- or bilateral, have no statistical relevance. Recently for patients with lung metastases, the use of post-operative chemotherapy is generally recommended. However, there are still insufficient results available.20
References 1. Chi SN, Conklin LS, Qin J, et al. The patterns of relapse in osteosarcoma: the Memorial Sloan-Kettering experience. Pediatr Blood Cancer 2004;42(1):46–51. 2. Nakano T, Tani M, Ishibashi Y, et al. Biological properties and gene expression associated with metastastic potential of human osteosarcoma. Clin Exp Metastasis 2003;20(7): 665–74. 3. Carter SR, Grimer RJ, Sneath RS, Matthews HR. Results of thoracotomy in osteogenic sarcoma with pulmonary metastases. Thorax 1991;46(10):727–31. 4. Abballa EK, Pisters PW. Metastasectomy for limited metastases from soft tissue sarcoma. Curr Treat Operations Oncol 2002;3(6):497–505. 5. Van Putte BP, Hendriks JM, Romijn S, Van Schil PE. Isolated lung perfusion for the treatment of pulmonary metastases current mini-review of work in progress. Surg Oncol 2003;12(3):187–93. 6. Picci P, Vanel D, Briccoli A, et al. Computer tomography of pulmonary metastases from osteosarcoma: the less poor technique: a study of 51 patients with histological correlation. Ann Oncol 2001;12(11):1601–4. 7. Torre W, Rodriguez-Spiteri N, Sierrasesumaga L. Current role for resection of thoracic metastases in children and young adults—do we need different strategies for this population? Thor Cardiovasc Surg 2004;52(2):90–5.
A. Briccoli et al. 8. Su WT, Chewning J, Abramson S, et al. Surgical management and outcome of osteosarcoma patients with unilateral pulmonary metastases. J Pediatr Surg 2004;39(3): 418–23. 9. Younes RN, Gross JL, Deheinzelin D. Surgical resection of unilateral lung metastases: is bilateral thoracotomy necessary? World J Surg 2002;26(9):1112–3. 10. Duffaud F, Digue L, Mercier C, et al. Recurrences following primary osteosarcoma in adolescents and adults previously treated with chemotherapy. Eur J Cancer 2003;39(14): 2050–7. 11. Briccoli A, Ferrari S, Picci P, Mercuri M, Bacci G, Guernelli N. Surgical treatment of pulmonary metastases of osteosarcoma. A propos of 206 operated cases. Ann Chir 1999;53(3): 207–14. 12. Tsuchiya H, Kanazawa Y, Abdel-Wanis ME, et al. Effect of timing of pulmonary metastase identification on prognosis of patients with osteosarcoma: the Japanese Musculoskeletal Oncology Group study. J Clin Oncol 2002;1520(16):3470–7. 13. Hirano J, Okamura S, Omoto K, et al. Prognosis for the cases after resection of pulmonary metastasis of osteosarcoma. Kyobu Geka 2003;56(1):4–8. 14. Karnak I, Emin Senocak M, Kutluk T, Tanyel FC, Buyukpamukcu N. Pulmonary metastases in children: an analysis of surgical spectrum. Eur J Pediatr Surg 2002;12(3):151–8. 15. Briccoli A, Rocca M, Ferrari S, Mercuri M, Ferrari C, Bacci G. Surgery for lung metastases in Ewing’s sarcoma of bone. Eur J Cancer 2004;30:63–7. 16. Paulussen M, Ahrens S, Craft AW, et al. Ewing’s tumors with primary lung metastases: survival analysis of 114 (European Intergroup) Cooperative Ewing’s sarcoma studies patients. J Clin Oncol 1998;16:3044–52. 17. Pinkerton CR, Bataillard A, Grillo S, Oberlin O, Fervere B, Philip T. Treatment strategies for metastatic Ewing’s sarcoma. Eur J Cancer 2001;37(11):1338–44. 18. Abballa EK, Pisters PW. Metastasectomy for limited metastases from soft tissue sarcoma. Curr Treat Opt Oncol 2002;3(6):497–505. 19. Belal A, Salah E, Hajjar W, et al. Pulmonary metastasectomy for soft tissue sarcoma: is it valuable? J Cardiovasc Surg (Torino) 2001;42(6):835–40. 20. Temple K, Brennan MF. The role of pulmonary metastasectomy in soft tissue sarcoma. Semin Thorac Cardiovasc Surg 2002;14(1):35–44.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 309–313
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SYNDROMES
Spondyloepiphyseal dysplasia Rouin Amirfeyza, Catriona Clarkb, Martin Garganc, a
Trauma and Orthopaedics, Frenchay Hospital, Bristol, UK Bristol University, Frenchay Hospital, Bristol, UK c Bristol Royal Hospital for Sick Children, Bristol, UK b
KEYWORDS Spondyloepiphyseal dysplasia; SED; SEDC; SEDT; Clinical features; Treatment
Summary Spondyloepiphyseal dysplasia (SED) includes a group of conditions affecting the vertebrae and epiphyses following a mutation in a collagen gene. These disorders are broadly categorised in to congenita and tarda subtypes. This article briefly reviews these two subtypes and summarises the latest evidence in the literature regarding their genetics, diagnosis and treatment. & 2005 Published by Elsevier Ltd.
Introduction Spondyloepiphyseal dysplasia (SED) is the name given to a group of disorders that cause deformation of vertebrae and abnormal growth at epiphyseal centres of peripheral bones. Severity and extent of symptoms vary widely and a range of radiographic features is seen. However, invariably spinal changes are seen as platyspondyly and the appearance of ossification centres, which are hypoplastic and irregular, is delayed. The main clinical outcomes are short stature (with a disproportionately short-trunk), chest malformations and early onset joint degeneration. The genetic abnormalities underlying SED are heterogeneous. SED is split into two main categories, SED congenita and SED tarda. Other rare forms of SED Corresponding author. Tel.: +44 117 342 8460.
0268-0890/$ - see front matter & 2005 Published by Elsevier Ltd. doi:10.1016/j.cuor.2005.06.007
with slightly different radiological and clinical features are reported. The two main forms are described below.
Spondyloepiphyseal dysplasia congenita (SEDC) Epidemiology and genetics SEDC is transmitted with an autosomal dominant inheritance pattern. SEDC has consistently been shown to correlate with defects in the gene COL2A1 on the long arm of chromosome 12, whose product is needed to form normal type II collagen.1 Type II collagen is found in cartilage, vitreous humour and the nucleus pulposus. Mutations of COL2A1 associated with SEDC have been found at multiple sites. The prevalence is approximately 3.4 per million population.5
ARTICLE IN PRESS 310 Clinical presentation The severity of symptoms and range of radiological changes are variable.2 SEDC presents at birth (antenatal testing is possible)3 with short stature and/or other clinical and radiological features. There is often exaggerated lumbar lordosis with associated hip flexion contractures and the abdomen protrudes. The neck is short and there may be pectus carinatum as well as a barrelshaped chest. Other associated features include a flat face, cleft palate and talipes equinovarus deformity. As development continues abnormal gait may become obvious due to coxa vara. Delayed ossification of capital femoral epiphyses can cause deformation and predispose to precocious OA. Thoracic scoliosis or kyphosis can develop in adolescence and may be rigid and severe. Atlantoaxial instability (and consequent spinal cord compression) is also common due to hypoplasia of the odontoid (or Os odontoideum) and can cause myelopathy, or occasionally sudden death.4 Associated ocular involvement, in the form of myopia, retinal detachment or cataracts, is common. SEDC has been divided into severe and mild variants.5 Severe disease causes very short stature, grossly affected hips, severe coxa vara and increased risk of myelopathy.6 Mild disease results in height just under the 3rd percentile and mild coxa vara. Both variants can be diagnosed at birth but cannot be differentiated until 3–4 years of age.5
R. Amirfeyz et al. Radiological features Radiological features of SEDC Chest Broad thorax Abnormal ribs Spine Children Delayed ossification centers Varying degrees of platyspondyly (Fig. 1) Posterior wedging of vertebral bodies Odontoid hypoplasia Adults Intervertebral disc spaces decrease Anteroposterior diameter of the vertebral bodies decreases Lordosis Progressive kyphoscoliosis The thoracolumbar junction shows the most marked abnormalities Hips Coxa vara is almost always present (Fig. 2) Femoral head flattened and irregular (Fig. 2) Distal femur flattened and irregular (Fig. 3) Knees Genu valgum (Fig. 3)
Treatment
Non-surgical J Includes input from ophthalmology and neurology and pulmonary function monitoring.
Figure 1 Radiographs of neck (lateral cervical spine view) and thoracolumbar area (anteroposterior view) showing platyspondyly in SED.
ARTICLE IN PRESS Spondyloepiphyseal dysplasia
311 of SED but of milder severity and later onset.9 Other case reports have diagnosed patients who have mild SED-type changes as having SEDT, and have described autosomal dominant and autosomal recessive inheritance.10 SEDT therefore is used in the literature to label different genetic diseases. Here, SEDT (X-linked) is discussed.
Figure 2 Typical coxa vara and flattened femoral heads. Evidence of early onset osteoarthritis on the left side.
Surgical (to relieve symptoms and improve function) J Spinal column – Treatment of scoliosis may start with bracing but some will need a spinal fusion. In young patients aged 3–10 years a distraction rod inserted with no spinal fusion can limit the condition until fusion is undertaken at spinal maturity. Often lumbar lordosis is improved upon surgical correction of hip flexion deformity. – For atlanto-axial instability or for patients with myelopathy, atlanto-axial fusion may help symptoms. Fusion to the occiput may be needed if the posterior ring of the atlas is too small.4 J In some cases of coxa vara, a valgus or valgusextension transtrochanteric osteotomy may help.7 J Varus supracondylar femoral osteotomy or a proximal tibial and fibular osteotomy can be useful if patients have symptomatic genu valgum.
The risk of any operation is increased due to atlano-axial instability, decreased pulmonary function resulting from an abnormal thorax and rigid spine deformities.8
Spondyloepiphysial dysplasia tarda (SEDT) The term SEDT was first used in 1957 by Maroteaux et al. to describe a condition that showed X-linked inheritance and presented with features characteristic
Epidemiology and genetics The prevalence of SEDT has been estimated as 1.7/ million in Britain.11 Only males are affected (Xlinked). The gene responsible for SEDT is SEDL (sedlin), and has been mapped to the short arm of the X chromosome (Xp22).12 The molecular basis for SEDT is unknown as the sedlin region produces a protein involved in intracellular transport rather than any connective tissue or cytoskeletal protein. Therefore, it is proposed that the mutated gene product is associated with the process of organising or regulating skeletal development resulting in abnormal endochondral bone formation.13 Clinical presentation Bannerman criteria for diagnosis of SEDT14
X-linked recessive inheritance Short stature first evident between 5 and 14 years of age Shortness due to impaired growth of spine Radiologically characteristic flattening of vertebrae with central humping Dysplastic changes of femoral heads and neck Minor changes in other bones
Appearance is often normal at birth, so the clinical presentation is of short stature that typically becomes obvious around the time of puberty, when the trunk seems to stop growing.15 Back pain is usually the first complaint and can be followed by decreased spinal mobility. Hip pain, scoliosis and barrel-shaped chest may develop. Premature osteoarthritis of large joints, in particular of the hip, follows. Some patients suffer from scoliosis and/or kyphosis. Radiological features Radiological features of SEDT16 Chest Increased thoracic anteroposterior and transverse diameters Shoulders Epiphyseal involvement (symmetrical) (Fig. 3) Pelvis Narrowing of the bony pelvis Spine (mainly in lower thoracic and lumbar region)
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Figure 3 Epiphyseal involvement in distal femora with flattening of the condyles and genu valgum as seen in SED. Left lateral, Right anteroposterior view.
Children (changes are progressive) Irregular generalised platyspondyly No ossification at the upper and lower anterior margins of the vertebral bodies ‘‘Humping’’ of the vertebrae (characteristic feature of SEDT): mounds of bone in the posterior and central parts of superior and inferior vertebral end-plates Adults Disc degeneration with narrowing of intervertebral spaces (height loss in adult life) Hips Deep acetabulae Short femoral necks Abnormal femoral heads which lead to mild but early degenerative changes Knees The distal femurs flattened Epiphyseal involvement (Symmetrical) Treatment
Surgical J Scoliosis should be managed as for adolescents with idiopathic scoliosis. If bracing is not successful posterior fusion may be needed. J Precocious osteoarthritis of the major weight bearing joints, especially the hips, is the main complication of SEDT, and if relief is not provided by valgus or valgus-extension intertrochanteric osteotomy, patients will often need arthroplasty.
References 1. Anderson IJ, Goldberg RB, Marion RW, Upholt WB, Tsipouras P. Spondyloepiphyseal dysplasia congenita: genetic linkage to type II collagen (COL2A1). Am J Human Genet 1990; 46:896–901. 2. Benetos IS, Kanellopoulos AD, Themistocleous GS, Gavras G, Korres DS. Spondyloepiphyseal dysplasia in three generations. Eur J Orthop Surg Traum 2005 http://springerlink.metapress.com/index/10.1007/s00590-004-0211-9. 3. Parilla BV, Leeth EA, Kambich MP, Chilis P, MacGregor SN. Antenatal detection of skeletal dysplasias. J Ultrasound Med 2003;22:255–8. 4. Miyoshi K, Nakamura K, Haga N, Mikami Y. Surgical treatment for atlantoaxial subluxation with myelopathy in spondyloepiphyseal dysplasia congenita. Spine 2004;29: E488–91. 5. Wynne-Davies R, Hall C. Two clinical variants of spondyloepiphysial dysplasia congenita. J Bone Jt Surg Br 1982;64: 435–41. 6. Nakamura K, Miyoshi K, Haga N, Kurokawa T. Risk factors of myelopathy at the atlantoaxial level in spondyloepiphyseal dysplasia congenita. Arch Orthop Trauma Surg 1998;117: 468–70. 7. Inoue T, Naito M, Shiota E, Nishino I, Ogata K. Transtrochanteric curved varus femoral osteotomy for spondyloepiphyseal dysplasia tarda. A case report. Fukuoka Igaku Zasshi 1999;90:329–32. 8. Saegusa M, Nakamura K, Matsushita T, Inokuchi K, Oda H. Intra-articular fracture of the knee with spondyloepiphyseal dysplasia congenita: successful result of open reduction and internal fixation. Arch Orthop Trauma Surg 2002;122:241–4. 9. Maroteaux P, Lamy M, Bernard J. La dysplasie spondyloepiphysaire tardive. Presse Med 1957;65:1205–8. 10. McKusick VA. Mendelian inheritance in man: a catalog of human genes and genetic disorders, 12th ed. Baltimore: Johns Hopkins University Press; 1998. 11. Wynne-Davies R, Gormley J. The prevalence of skeletal dysplasias. An estimate of their minimum frequency and the
ARTICLE IN PRESS Spondyloepiphyseal dysplasia number of patients requiring orthopaedic care. J Bone Jt Surg Br 1985;67:133–7. 12. Szpiro-Tapia S, Sefiani A, Guilloud-Bataille M, Heuertz S, Le Marec B, Frezal J, et al. Spondyloepiphyseal dysplasia tarda: linkage with genetic markers from the distal short arm of the X chromosome. Human Genet 1988;81:61–3. 13. Jang SB, Kim YG, Cho YS, Suh PG, Kim KH, Oh BH. Crystal structure of SEDL and its implications for a genetic disease spondyloepiphyseal dysplasia tarda. J Biol Chem 2002;277: 49863–9.
313 14. Bannerman RM, Ingall GB, Mohn JF. X-linked spondyloepiphyseal dysplasia tarda: clinical and linkage data. J Med Genet 1971;8:291–301. 15. Whyte MP, Gottesman GS, Eddy MC, McAlister WH. X-Linked recessive spondyloepiphyseal dysplasia tarda. Clinical and radiographic evolution in a 6-generation kindred and review of the literature. Medicine 1999;78:9–25. 16. Langer Jr LO. Spondyloepiphyseal dysplasia tarda. Hereditary chondrodysplasia with characteristic vertebral configuration in the adult. Radiology 1964;82:833–9.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 314–321
www.elsevier.com/locate/cuor
TRAUMA
Trauma-related sepsis and multiple organ failure: Current concepts in the diagnosis and management Vesna Bumbasirevic, Aleksandar Karamarkovic, Aleksandar Lesic, Marko Bumbasirevic Department of Anaesthesiology, Surgery and Orthopaedic Surgery, Clinical Centre, Belgrade, Yugoslavia
KEYWORDS Multiple organ failure; Sepsis; Trauma; Systemic inflammatory respone; Therapy
Summary Like other critical illnesses, severe traumatic injury is closely associated with the onset of a systemic inflammatory response, sepsis and progressive multiple organ dysfunction, which is the leading cause of death in intensive care units. Increased insight into the complex pathogenesis of this disease process has resulted in the development of a number of therapeutic interventions. This article outlines key mechanisms in the onset of sepsis and multiple organ dysfunction syndrome, as well as a more recent concept of treatment aimed at preventing the progress of those complications and decreasing mortality. & 2005 Elsevier Ltd. All rights reserved.
Introduction Traumatic injuries are the leading cause of death in persons aged under 30, and the third highest in the total population, following coronary and malignant diseases.1 Mortality of the traumatised has a tri-modal distribution,2 although this has recently been challenged. Thus, 45% of the injured die immediately in the first few minutes at the accident site. With the development of resuscitation procedures and the introduction of damage control operations that decrease the problems of hypothermia, acidosis and coagulopathy,3 mortality in the first 24 h has been decreased. However, mortality in the following days and weeks from the effects of sepsis and multiple Corresponding author. Fax: +38 111 436 388.
E-mail address:
[email protected] (A. Lesic).
organ insufficiency remains high (45%). There is a close relationship between trauma, hemorrhagic shock, Systemic Inflammatory Response Syndrome (SIRS), sepsis and Multiple Organ Dysfunction Syndrome (MODS). Despite better management of the traumatised and some understanding of the pathogenesis of sepsis and the etiology of MODS, mortality due to those latter complications is still high. In recent years, several therapeutic interventions have been shown to reduce mortality but population heterogeneity and the generalised definitions of inflammatory response and sepsis, which are currently under review,4 have constituted a major problem.
Pathophysiology Two patterns of MODS can emerge. A massive traumatic insult may lead to severe systemic
0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2005.05.006
ARTICLE IN PRESS Trauma-related sepsis and multiple organ failure: Current concepts in the diagnosis and management hyperinflammation and early MODS (one-hit model or primary MODS), or progressive MODS may follow sequential insults (two-hit model, secondary MODS).5 The second insult is presumed to be any untoward event or added stress that overwhelms the host’s capacity to generate an appropriate response. The exact mechanisms for dysfunction are unknown. Progressive dysfunction of increasing numbers of organs correlates with mortality by approximately 20% for each additional organ dysfunction.6 Two types of cell death have been identified—necrosis and apoptosis. Necrosis occurs in response to direct trauma and/or hypoperfusion/ reperfusion injury. The expression of apoptosis is altered in all critical illnesses. Apoptosis of lymphocytes and gut epithelial cells is increased,7 whereas that of neutrophils is delayed.8 Excessive apoptosis has been implicated as a cause of liver,9 kidney,10 and cardiac dysfunction. Much organ dysfunction in patients with sepsis can be explained by ‘‘cell hibernation’’ or ‘‘cell stunning’’.11 Sepsis is the most common cause of progression of MODS. In the post-resuscitation stage, patients with severe trauma go through phases of uncontrolled hyperinflammation and immunosuppression with dysregulation in relation to SIRS/Compensatory Anti-inflammatory Response Syndrome (CARS).12 The response type is determined by the intensity of the trauma and numerous other factors constituting predisposition: age, previous state and coexisting diseases, genetic factors, virulence of pathogenic organisms and inoculum size. In the hyperinflammation stage, proinflammatory mediators are released from activated monocytes and the complex of leukocytes and endothelial cells. The released cytokines (tumour necrosis factor-alfa (TNFa) and interleukins IL-2, IL-6, IL-8, coagulation factors and activated complement) stimulate the production of secondary mediators. The action of these mediators leads to a hyperdynamic, hypermetabolic state with diffuse micro-
Table 1
vascular lesions, formation of microthrombi and the loss of vasoregulation in microvascular vessels.13 Trauma patients are very susceptible to the development of infectious complications. This susceptibility is increased by the breached host defences and changes in host response from broken skin and mucosal surfaces (from devitalised tissue), splanchnic ischaemia and translocation of intestinal bacteria, indwelling catheters, drains, intravascular lines, endotracheal intubation, advanced age and co-morbidity (Table 1). In addition, trauma induces both an immunosuppressive and catabolic state that is unable to clear infection.12 Initially, sepsis may be characterised by increases in inflammatory mediators; but as sepsis persists, there is a shift towards an anti-inflammatory immunosuppressive state or anergy.14 Changes in the syndrome are possible at various stages of the disease and differ from patient to patient. The mechanism of immune suppression is a shift to antiinflammatory cytokines and CARS, due to reduced levels of Th1 cytokines (TNF-alfa, interferon gamma, and interleukin-2) but increased levels of the cytokines (interleukin-4 and interleukin-10) produced by type-2 helper T-cells (Th2). The other mechanism is anergy, a state of T-cell non-responsiveness to antigen, where both Th1 and Th2 subtypes exhibit decreased function and patients with trauma or burns have reduced levels of circulating T-cells.15 Apoptotic cell death may trigger anergy. One potential mechanism of lymphocyte apoptosis is stress-induced endogenous release of glucocorticoids.16 The type of cell death determines the immunological function of surviving immune cells. Apoptotic cells induce anergy or anti-inflammatory cytokines that impair the response to pathogens, whereas necrotic cells cause immune stimulation.17 Moreover, genetic factors and polymorphism in cytokine genes may influence whether a person has a marked hyperinflammatory
Susceptibility of trauma patients to infectious complications.
Breeched host defences
Broken skin and mucous membranes Devitalised tissue Indwelling catheters, drains, intravascular lines
Endotracheal intubation Nosocomial colonisation Mechanical ventilation
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Change in host response
Co-morbidity Advanced age Nutritional deficiency Splanchnic ischaemia and translocation of intestinal bacteria Long-term antibiotic prophylaxis Stress ulcer prophylaxis Immune anergy/CARS
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Table 2
Definition of systemic inflammatory response syndrome and sepsis.
The response is manifested by two or more of the following conditions
Temperature 438 or o36 1C Heart rate 490 beats/min Respiratory rate 420 breaths/min or PaCO2 o32 Torr (o4.3 kPa) WBC 412,000 cells/mm3, o4000 cells/mm3, or 410% immature (band) forms
Sepsis is the systemic response to infection American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference, Crit Care Med 1992; 20: 864–74.
Table 3
The PIRO concept for staging sepsis.4
Domain
Present
Future
Predisposition
Premorbid illness with reduced probability of short-term survival
Insult infection
Culture and sensitivity of infecting pathogens SIRS, other signs of sepsis, shock, CRP
Genetic polymorphisms in components of inflammatory response (e.g., TLR, TNF, IL-1, CD14) Assay of microbial products (LPS, mannan, bacterial DNA) Nonspecific markers of activated inflammation (e.g., PCT or IL-6) or impaired host responsivness; specific detection of target of therapy (e.g., protein C, TNF) Dynamic measures of cellular response to insult—apoptosis, cytopathic hypoxia, cell stress
Response
Organ dysfunction
Organ dysfunction as number of failing organs or composite score (e.g., MODS, SOFA)
TLR, Toll like receptor; TNF, tumor necrosis factor; IL, interleukin; LPS, lipopolysacharide; PCT, procalcitonin; SOFA, sepsis related organ failure assessment.
or hypoinflammatory response. Genetic testing and immunological monitoring could therefore identify early certain groups of patients who may benefit from targeted anti-inflammatory or immunostimulatory therapy.18 In these terms, a new classification system named Predisposition, Infection, Response, Organ dysfunction (PIRO) has been proposed4,18 (Tables 2 and 3).
A modern concept of intensive treatment Haemodynamic support The haemodynamic profile of a patient with SIRSsepsis progression is characterised by a hyperdynamic circulation with increased cardiac output and systemic vasodilation. Relative and absolute hypovolemia, biventricular dysfunction and microcirculatory abnormalities result in inadequate tissue perfusion. Signs of inadequate oxygen delivery (DO2) and oxygen debt are hypotension,
confusion, oliguria, lactic acidosis, a change in mixed venous oxygen saturation (SvO2) and gastric mucosal acidosis (as measured by gastric tonometry). Haemodynamic support is carried out by volume restitution, vasopressor and inotropic therapies. Various monitoring techniques are used to estimate the type of haemodynamic abnormalities and intensity of tissue hypoxia.19 Central venous pressure measurement in mechanically ventilated patients, as well as in those with increased intra-abdominal pressure, is insufficiently accurate. It is also well established that use of a pulmonary artery catheter (PAC) is frequently associated with inaccurate measurements.20 Moreover, PAC usage is not associated with a change in mortality rate.21 Central haemodynamic monitoring technology continues to advance and less invasive alternatives for the estimation of cardiac output are being made available.22 Lactates are not a precise parameter for detection of the intensity of tissue hypoxia in the early stage of progressive SIRS due to maintained
ARTICLE IN PRESS Trauma-related sepsis and multiple organ failure: Current concepts in the diagnosis and management neutralisation and recycling mechanisms, although increased lactate clearance has considerable significance in the estimation of a favourable outcome.23 Gastric and sublingual tonometries have not been widely used in clinical practice.24 The state of SIRS/sepsis is characterised by a pathological dependence on oxygen consumption (VO2) and on oxygen delivery, whereas the concept of a necessary supranormal DO2 increase has not been clinically confirmed in terms of mortality improvement.25 It is thought that these interventions occurred too late in the disease process. That the time is very important was shown by Rivers et al., who found it improved survival in patients with septic shock, while conducting a prospective randomised study investigating early goal-directed therapy within the emergency department.26 Monitoring included mean arterial pressure, central venous pressure and urine output and the endpoint was central SvO2 470%. It was also postulated that appropriate early aggressive resuscitation in trauma patients may reduce the incidence of trauma-induced SIRS and MOF.27 Fluid resuscitation may consist of natural or artificial colloids or crystalloids. There is no evidence-based support for one type of fluid over another. As the volume of distribution is much larger for crystalloids than for colloids, resuscitation with crystalloids requires more fluid to achieve the same endpoint and results in more oedema. Clearly, more studies are required in this area.28
Respiratory support Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are spectra of the same syndrome, which occurs upon damage to the alveolo-capillary membrane and is defined by the difference between the intensity of respiratory dysfunction and the intensity of PaO2/FiO2 ratio irregularity.29 The pathogenic substrate may act primarily, directly on the pulmonary epithelium (aspiration, inhalation injuries, pulmonary infection, pulmonary contusion) or secondarily, indirectly, through the pulmonary capillary vasculature (severe trauma with prolonged hypotension, sepsis, multiple transfusions, fat embolism, reperfusion injuriesy). Alveolar involvement in ALI/ARDS is heterogeneous, with normal and abnormal alveoli existing in juxtaposition. Compliance is reduced and airflow resistance increases. The increased work of breathing and muscular fatigue may lead to respiratory failure.30
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‘‘Protective strategy in mechanical ventilation’’ Mechanical ventilation has long been the main support to respiratory function in those states, but since the traditional method (tidal volumes 10–15 ml/kg body weight) may itself cause lung injury (ventilator-associated lung injury, ventilatorinduced lung injury, ventilator associated systemic inflammation),31,32 ventilation strategy in ARDS has recently become the subject of numerous randomised controlled studies. In the biggest study, a limited volume-pressure strategy led to a decrease in mortality by 9% with a forced expiration volume of 6 ml/kg predicted body weight and maintenance of end inspiratory plateau pressures below 30 cm H2O.33 Smaller randomised studies have shown permissive hypercapnia, aimed at maintaining a limited minute volume of ventilation, to be a safe method.34,35 Hypercarbia was limited in patients with already present metabolic acidosis but is contraindicated in patients with increased intracranial pressure. Raising end-expiratory pressure in ALI/ARDS maintains pulmonary units open and leads to an increase in partial oxygen pressure in arterial blood PaO2, whether applied through an endotracheal tube or a facial mask.36 Several minor studies, as well as one major one, have shown that a ‘‘prone’’ position can improve oxygenation in most ventilated patients with ALI/ ARDS.37,38 The big multi-centre trial did not prove this but post-hoc analysis detected improvement in patients with the most severe hypoxemia.39 The incidence of pneumonia during mechanical ventilation is decreased by 45% with elevation of the headrest.40 Sedation and analgesics decrease the intensity of stress and sympathetic stimulation; but mechanically ventilated patients with continuous daily sedation spend a significantly longer time with ventilation support and in special intensive care units.41 More effective treatment is carried out with intermittent administration of sedatives and/ or daily interruptions and proper titration of continuous sedative drips. This also decreases the necessity of tracheotomies. The use of intermediate and long-acting neuromuscular blockers contributes to prolonged weakness of the skeletal musculature.42 To avoid this risk, it is necessary to limit their use maximally. Other methods of respiratory support have also been tested: high-frequency ventilation, high-frequency oscillatory ventilation, non-invasive ventilation, extracorporeal membrane oxygenators, extracorporeal membrane removal of carbon dioxide, NO inhalation, surfactant and partial liquid ventilation. So far, there are no relevant data on their effectiveness. Further research on this is in progress.
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Infection-diagnosis and management Most often, it is difficult to distinguish between post-traumatic non-infective SIRS and the beginning of infection and sepsis.43,44 The probability of infection is increased with the advance of clinical symptoms contained in the definition of SIRS, as well as with progressive organ dysfunctions but the clinical signs may be very subtle initially. However, effective, aggressive therapy is very necessary.26 A delay in instituting appropriate sepsis therapy can result in an increased mortality rate.45 Nevertheless, the use of long-term prophylactic antibiotics following trauma is not recommended.46 Among the laboratory parameters, the level of Creactive protein (CRP) is most widely employed but the data clearly demonstrate that procalcitonin is a better marker of sepsis.47 Infection probability score is a simple score to predict infection and the variables can be obtained routinely.48 Many studies in the last few years have dealt with the relevance of cytokine profiles. Proinflammatory markers combined with anti-inflammatory cytokine profiles, may be an option for the future.49 They should be used in conjunction with other modalities rather than in isolation.50,51 Targeted clinical, imaging and bacteriological examinations aimed at foci detection as well as timely drainage and surgical procedures for the removal of abscesses, local infection foci and necrotic tissue are of great significance. When an infective complication of SIRS of unknown source is suspected, it is reasonable to replace the vascular catheters. Intravenous antibiotics should be administered from the very beginning, in the first few hours, immediately after diagnosing sepsis and taking specimens for microbiological analysis. The initial selection of an empirical antimicrobial regimen should be broad enough covering all likely pathogens, until the cause is determined. Then, further treatment is targeted depending on the antibiogram. This method of administration decreases the incidence of superinfections as well as bacterial resistance.52
Nutritional support Sepsis results in profound alteration in metabolism, a catabolic state, or ‘‘auto-cannibalism’’, with increased morbidity. What type of nutrition is required and by which route it should be given to critically ill patients are objects of debate.53 Parenterally administered nutrition is easier but the benefits of total parenteral nutrition (TPN) are
V. Bumbasirevic et al. undermined by complications related to central venous access and bowel inactivity, with its attendant translocation of gut bacteria and infections.54 Early administered enteral nutrition in trauma and other surgical patients maintains a better microcirculatory flow in the gastrointestinal region. Thus, meta-analysis of clinical tests has shown a decrease in the infection incidence and in the length of hospital treatment in comparison to TPN.55 However, a large multi-centre controlled study did not show many beneficial effects of early enteral immunonutrition (EN+L-arginine, omega-3 fatty acids, vitamin E, beta carotene, zinc, selenium) in patients with severe sepsis in comparison to TPN.56 Glutamine-enriched TPN decreases infective complications and endotoxaemia-induced intensification of inflammatory and coagulatory cascade processes, as well as the progress of MODS.57 Be it as it may, the concept of immunonutrition is still the subject of many studies both in terms of method of administration and in terms of favourable immunomodulatory effects of certain additives.
Low-dose corticosteroids Steroids have been used following trauma (spinal cord injury, head injury) for a number of years with mixed results.58 Corticosteroids have a range of anti-inflammatory actions and therefore might be expected to be of benefit to patients with sepsis. Despite favourable results obtained in experimental studies on animal models, clinical studies have remained without confirmation of a beneficial effect of short-course high-dose corticosteroids;59 whereas a meta-analysis indicated the possibility of increased mortality due to immunosuppression and nosocomial infection.60 The finding that patients in the progressive stage of sepsis have relative adrenal insufficiency has led to a new method of clinical examination. Thus, a significant reduction of mortality has been achieved with small doses of hydrocortisone (100 mg 2–3 times a day for 7 days) in patients who, in addition to restitution of intravascular volume, also need vasopressor therapy for maintenance of blood pressure.61 There is no proof that low-dose steroids improve the nonshock forms of sepsis.
Intensive insulin therapy Hyperglycaemia and insulin resistance are frequent in the states of critical illness. A large prospective clinical trial has demonstated the significant effect of proper glycaemic control in the prevention of
ARTICLE IN PRESS Trauma-related sepsis and multiple organ failure: Current concepts in the diagnosis and management progressive MODS in severe sepsis through administration of a continuous insulin drip. The best results were achieved in the group of patients with glycaemia values maintained at 80–110 mg/dl (4.4–6.1 mmol/l).62 Subsequent analysis showed that an improvement in survival was also obtained at 8.3 mmol/l and, by maintaining glycaemia at this value, the risk of hypoglycaemia was easier to avoid. Exogenous glucose is administered in parallel, with frequent determination of glycaemia (each hour or even more often at the beginning of insulin administration). Proper control of blood glucose concentration appears to be more important than the amount of insulin infused.63,64 The precise mechanisms involved in the prevention of MODS progress through satisfactory control of glycaemia are unknown. The phagocytic function of neutrophils is impaired in patients with hyperglycaemia, and correcting hyperglycaemia may improve bacterial phagocytosis.12 Another potential mechanism involves the antiapoptotic effect of insulin.65
Immunomodulating strategies Adjunctive therapy in sepsis is an attempt to interrupt or modify the systemic response. Recent studies investigating anti-inflammatory therapy as immunostimulatory have not shown a dramatically improved outcome.66 Major criticisms regarding incorrect hypotheses, errant study designs, inappropriate target groups and uncontrolled variables have arisen.67 However, further studies examining the use of combined and more targeted treatments are awaited.68–71 Coagulation modulating therapy The tight link between inflammation and coagulation is almost universal in patients with severe sepsis, which has led to the development of an anticoagulant strategy for treating patients in this condition.72–74 A multi-centre randomised controlled trial did not confirm the efficiency of recombinant tissue factor pathway inhibitor (TFPI), which is a physiological inhibitor of the extrinsic coagulation pathway.75 Antithrombin (AT) is a natural inhibitor of thrombin and other serine proteases. In patients with sepsis, AT levels are reduced and low levels have been correlated with a poor outcome.76 Administration of antithrombin III has not achieved any favourable effects in decreasing mortality, with the possible exception of a subgroup of patients who did not receive heparin.77 Protein C is a potent anticoagulant that inhibits factors Va and VIIa,
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activates fibrinolysis and inhibits thrombin production. This natural endogenous anticoagulant has additional anti-inflammatory effects in comparison to TFPI and AT III, including an anti-apoptotic action.78 Inactivation of thrombin generation during the deregulated inflammatory response decreases inflammation by inhibiting platelet activation, neutrophil recruitment, and mast cell degranulation but also inhibits cytokine production and leukocyte-endothelium adhesion. Another multi-centre, randomised controlled trial demonstrated that activated protein C could decrease mortality in patients with severe sepsis.79,80
Conclusions Progressive organ dysfunction syndrome of trauma patients is most often a consequence of septic complications. There has been an advance in diagnosis and treatment of such patients and it has been shown that simple but timely therapeutic procedures (early aggressive resuscitation, early enteral nutrition, infection control, tight glucose control), when used in combination, may prevent progressive complications and improve the outcome. In any case, sepsis is still a subject of extensive research.
References 1. MacKenzie EJ, Fowler CJ. Epidemiology. In: Matox KL, Feliciano DV, Moore EE, editors. Trauma. 4th ed. New York: McGraw-Hill; 2000. p. 21–36. 2. Baker CB, Oppenheimer L, Stephens B, et al. Epidemiology of trauma deaths. Am J Surg 1980;140:144–50. 3. Morley J, Kossygan K, Giannoudis PV. Damage control orthopaedics: a new concept in the management of the multiply injured patient. Curr Orthop 2002;16:362–7. 4. Levey MM, Fink MP, Marshall JC. 2001 SCCM/ESICM/ACCP/ ATS/SIS International sepsis definitions conference. Crit Care Med 2003;31(4):1250–6. 5. Rotstein OD. Modeling the two-hit hypothesis for evaluating strategies to prevent organ injury after shock/resuscitation. J Trauma 2003;54:S203–6. 6. Vincent JL, de Mendonca A, Cantraine F, et al. Use of SOSA score to assess the incidence of organ dysfunction/failure in intensive care units: results of a multicenter, prospective study. Working group on ‘‘sepsis-related problems’’ of European Society of Intensive Care Medicine. Crit Care Med 1998;26:1793–800. 7. Hotchkiss RS, Schmieg Jr RE, Swanson PE, et al. Rapid onset of intestinal epithelial and lymphocyte apoptotic cell death in patients with trauma and shock. Crit Care Med 2000;28:3207–17. 8. Chitnis D, Dickerson C, Munster AM, et al. Inhibition of apoptosis in polymorphonuclear neutophils from burn patients. J Leukocyte Biol 1996;59:835–9.
ARTICLE IN PRESS 320 9. Galle PR. Apoptosis in liver disease. J Hepatol 1997;27: 405–12. 10. Faraco PR, Ledgerwood EC, Smith KGC. Apoptosis and renal disease. Sepsis 1998;2:31–7. 11. Sawyer DB, Loscalzo J. Myocardial hibernation: restorative or preterminal sleep? Circulation 2002;105:1517–9. 12. Hotchkiss RS, Karl IE. The pathophysiology and treatment of sepsis. N Engl J Med 2003;348:138–50. 13. Marik PE, Varon J. Sepsis: state of the art. Dis Mon 2001;47:463–532. 14. Lederer JA, Rodrick ML, Mannick JA. The effects of injury on the adaptive immune response. Shock 1999;11:153–9. 15. Pellegrini JD, De AC, Kodys K, et al. Relationships between T lymphocyte apoptosis and anergy following trauma. J Surg Res 2000;88:200–6. 16. Fukuzuka K, Edwards III CK, Clare-Salzer M, et al. Glucocorticoid-induced, caspase dependent organ apoptosis early after burn injury. Am J Physiol Regul Integr Comp Physiol 2000;278:R1005–18. 17. Fadok VA, Bratton DL, Rose DM, et al. A receptor for phosphatidylserine-specific clearance of apoptotic cells. Nature 2000;405:85–90. 18. Vincent JL, Sun Q, Dubois M-J. Clinical trials of immunomodulatory therapies in severe sepsis and septic shock. Clin Infect Dis 2002;34:1084–93. 19. Task Force of American College of Critical Care Medicine, Society of Critical Care Medicine. Practice Parameters for haemodynamic support in adult patients in sepsis. Crit Care Med 1999;27:639–55. 20. Connors Jr AJ, Speroff T, Dawson NV, et al. The effectiveness of right heart catheterization in the initial care of critically ill patients. J Am Med Assoc 1996;276:889–97. 21. Yu DT, Platt R, Lanken PN, et al. Relationship of pulmonary artery catheter use to mortality and resource utilization in patients with severe sepsis. Crit Care Med 2003;31:2734–41. 22. Mehwald PS, Rusk RA, Mori Y, et al. A validation study of aortic stroke volume using dynamic 4-dimensional color Doppler: an in vivo study. Am J Soc Echocardiogr 2002;15: 1045–50. 23. Levraut J, Ichai C, Petit I, et al. Low exogenous lactate clearance as an early predictor of mortality in normolactatemic critically ill patients. Crit Care Med 2003;31:705–10. 24. Gutierrez G, Wulf-G EM, Reines DH. Monitoring oxygen and tissue oxygenation. Curr Opin Anaesthesiol 2004;17:107–17. 25. Gattinoni L, Brazzi L, Pelosi P. A trial of goal-orientated haemodynamic therapy in critically ill patients. Sv O2 collaborative group. N Engl J Med 1995;333:1025–32. 26. Rivers EP, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 2001;345:1368–77. 27. Lee CC, Marill KA, Carter WA, et al. A current concept of trauma induced multi-organ failure. Ann Emerg Med 2001;38:2. 28. Vincent J-L. Haemodynamic support in septic shock. Intensive Care Med 2001;27:S80–92. 29. Bernard GR, Artigas A, Brigham KL, et al. Report of the American–European Consensus conference on acute respiratory distress syndrome: definitions, mechanisms, relevant outcomes and clinical trial coordination. Consensus Committee. J Crit Care 1994;9:72–81. 30. Crimi E, Slutsky AS. Inflammation and acute respiratory distress syndrome. Best Pract Res Cli Anaesthesiol 2003;18:477–92. 31. Tremblay LN, Slutsky AS. Ventilator-induced lung injury: from barotrauma to biotrauma. Proc Assoc Am Physicians 1998;110:482–8.
V. Bumbasirevic et al. 32. International consensus conferences in intensive care medicine. Ventilator associated lung injury. Intensive Care Med 1999;25:1444–52. 33. Ventilation with lower tidal volumes compared with traditional volumes for acute lung injury and the acute respiratory distress syndrome. The acute respiratory distress syndrome network. New Engl J Med 2000;342:1301–8. 34. Hickling KG, Walsh J, Henderson S, et al. Low mortality rate in adult respiratory distress syndrome using low-volume, pressure-limited ventilation with permissive hypercapnia: a prospective study. Crit Care Med 1994;22:1568–78. 35. Bidani A, Tzouanakis AE, Cardenas VJ, et al. Permissive hypercapnia in acute respiratory failure. J Am Med Assoc 1999;272:957–62. 36. Marini JJ, Revenscraft SA. Mean airway pressure: physiologic determinants and clinical importance-Part I Physiologic determinants and measurements. Crit Care Med 1992;20: 1461–72. 37. Stocker R, Neff T, Stein S, et al. Prone positioning and lowvolume pressure-limited ventilation improve survival in patients with severe ARDS. Chest 1997;111:1008–17. 38. Jolliet P, Bulpa P, Chevrolet JC. Effects of prone position on gas exchange and haemodynamics in severe acute distress syndrome. Crit Care Med 1998;26:1977–85. 39. Gattinoni L, Tognoni G, Pesenti A, et al. Effect of prone positioning on the survival of patients with acute respiratory lung failure. N Engl J Med 2001;345:568–73. 40. Drakulovic M, Torres A, Bauer T, et al. Supine body position as a risk factor for nosocomial pneumonia in mechanically ventilated patients: a randomised trial. Lancet 1999;354: 1851–8. 41. Kollef MH, Levy NT, Ahrens TS, et al. The use of continuous IV sedation is associated with prolongation of mechanical ventilation. Chest 1998;114:541–8. 42. Rudis MI, Sikora CA, Angus E, et al. A prospective, randomized, controlled evaluation of peripheral nerve stimulation versus standard clinical dosing of neuromuscular blocking agents in critically ill patients. Crit Care Med 1997;25:25575–83. 43. Bochicchio GV, Napolitano LM, Joshi M. Persistent systemic inflammatory response is predictive of nosocomial infection in trauma. J Trauma 2002;53:245–51. 44. Meeran H, Messent M. The systemic inflammatory response syndrome. Trauma 2001;3:89–100. 45. Bochund P-V, Glauser MP, Calandra T. Antibiotics in sepsis. Intensive Care Med 2001;27:S33–48. 46. Hoth JJ, Franklin GA, Stassen NA, et al. Prophylactic antibiotics adversely affect nosocomial pneumonia in trauma patients. J Trauma 2003;55:249–54. 47. Luzzani A, Polati E, Dorizzi R. Comparation of procalcitonin and C-reactive protein as markers of sepsis. Crit Care Med 2003;31(6):1737–41. 48. Bota DP, Melot Ch, Ferreira FL, Vincent JL. Infection Probability Score (IPS): a method to help assess the probability of infection in critically ill patients. Crit Care Med 2003;31:2579–84. 49. Loisa P, Rinne T, Laine S, et al. Anti-inflammatory cytokine response and the development of multiple organ failure in severe sepsis. Acta Anaesthesiol Scand 2003;47:319–25. 50. Vincent J-L. Procalcitonin: the marker of sepsis? Crit Care Med 2000;28(4):1226–9. 51. Rivers EP. A landscape from the emergency department to the intensive care unit. Crit Care Med 2003;31(3):968–9. 52. Dellinger RP, Cerlet JM, Masur H, et al. Surviving Sepsis Campaign guidelines for management of severe sepsis and septic shock. Crit Care Med 2004;32(2):85873.
ARTICLE IN PRESS Trauma-related sepsis and multiple organ failure: Current concepts in the diagnosis and management 53. Preiser JC, Berre J, Carpentier Y, et al. Management of nutrition in European intensive care units: results of a questionnaire. Working Group on Metabolism and Nutrition of the European Society of Intensive Care Medicine. Intensive Care Med 1999;25:95–101. 54. Buchman AL, Moukarzel AA, Bhuta S, et al. Parenteral nutrition is associated with intestinal morphologic and functional changes in humans. J Parenter Enteral Nutr 1995;19:453–60. 55. Marik PE, Zaloga GP. Early enteral nutrition in actually ill patients: a systemic review. Crit Care Med 2001;29: 2264–70. 56. Bartolini G, Iapichino G, Radrizzani D, et al. Early enteral immunonutrition in patients with severe sepsis. Results of an interim analysis of a randomized multicentre clinical trial. Intensive Care Med 2003;29:834–40. 57. Ockenga J, Borchert K, Rifai K, et al. Effect of glutamineenriched total parenteral nutrition in patients with acute pancreatitis. Clin Nutr 2002;21(5):409–16. 58. Lockey DJ, Manara AR. The role of steroids following major trauma. Trauma 2001;3:53–61. 59. Veterans Administration Systemic Sepsis Cooperative Study Group. Effect of high-dose glucocorticoid therapy on mortality in patients with clinical signs of systemic sepsis. N Engl J Med 1987;317:659–65. 60. Lefering R, Neugebauer EA. Steroid controversy in sepsis and septic shock: a meta analysis. Crit Care Med 1995;23: 1294–303. 61. Annane D, Sebille V, Charpentier C, et al. Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock. J Am Med Assoc 2002;288:862–71. 62. Van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin therapy in the critically ill patient. N Engl J Med 2001;345:1359–67. 63. Finney SJ, Zekveld C, Elia A, et al. Glucose control and mortality in critically ill patients. J Am Med Assoc 2003;20:41–7. 64. Van den Berghe G, Wouters PJ, Bouillon R, et al. Outcome benefit of intensive insulin therapy in the critically ill:Insulin dose versus glycemic control. Crit Care Med 2003;31: 359–66. 65. Gao F, Gao E, Yue TL, et al. Nitric oxide mediates the antiapoptotic effect of insulin in myocardial ischemiareperfusion: the role of p-13 kinase, Akt, and endothelial nitric oxide synthase phosphorylation. Circulation 2002;105:1497–502.
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66. Vincent J-L, Sun Q, Dubois M-J. Clinical trials of immunomodulatory therapies in severe sepsis and septic shock. Clin Infect Dis 2002;34:1084–93. 67. Nasraeay SA. The problems and challenges of immunotherapy in sepsis. Chest 2003;123(suppl):451S–9S. 68. Bochud PY, Calandra Th. Pathogenesis of sepsis: new concepts and clinical implications for future treatment. Br Med J 2003;326:262–6. 69. Cohen J. Recent developments in the identification of novel therapeutic targets for the treatment of patients with sepsis and septic shock. Scand J Infect Dis 2003;35: 690–6. 70. Ward PA. The dark side of C5A in sepsis. Nature 2004;4:133–42. 71. Wadenbreck K, Goris A. Cytokine gene polymorphisms in multifactorial diseases: gateways to novel targets for immunotherapy? Pharmacol 2003;28:285–96. 72. Dellinger RP. Inflammation and coagulation: implications for the septic patient. Clin Infect Dis 2003;36:1259–65. 73. Demplfle C-E. Disseminated intravascular coagulation and coagulation disorders. Curr Opinion Anaesthesiol 2004;17: 125–9. 74. Marshall JC. Inflammation, coagulopathy, and the pathogenesis of multiple organ dysfunction syndrome. Crit Care Med 2001;29:99–106. 75. Abraham E, Reinhart K, Opal S, et al. Efficacy and safety of tifacogin (recombinant tissue factor pathway inhibitor) in severe sepsis: a randomized controlled trial. J Am Med Assoc 2003;290:238–47. 76. Fourrier F, Chopin C, Goudemand J, et al. Septic shock, multiple organ failure, and disseminated intravascular coagulation: compared patterns of antithrombin III, protein C, and protein S deficiencies. Chest 1992;101:816–23. 77. Waren BL, Eid A, Singer P, et al. Caring for the critically ill patients: high-dose antithrombin III in severe sepsis: a randomized controlled trial. J Am Med Assoc 2001;286: 1869–78. 78. Grey ST, Tsuchida A, Hau H, et al. Selective inhibitory effects of the anticoagulant activated protein C on the response of human mononuclear phagocytes to LPS, IFN-gamma, or phorbol ester. J Immunol 1994;153:3664–72. 79. Bernard GR. Drotregoin alfa (activated recombinant protein C) for the treatment of sepsis. Crit Care Med 2003;31(1): S85–93. 80. Bernard GR, Vincent JL, Laterre PF, et al. Efficacy and safety of recombinant human activated protein C for severe sepsis. N Engl J Med 2001;344:699–709.
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CME SECTION
Three external CME points available The following series of questions are based on the CME designated article for this issue—‘‘Resurfacing arthroplasty of the hip’’ by P. Roberts, P. Grigoris, H. Bosch and N. Talwaker. Please read the article carefully and then complete the self-assessment questionnaire by filling in the square corresponding to your response to each multiple-choice question. For true or false questions, please fill in one square only. After completing the questionnaire, either post or fax the answer page back to the Current Orthopaedics Editorial Office at the address at the bottom of the RESPONSE sheet. Please photocopy this page if you wish to keep your copy of Current Orthopaedics intact. Replies received before the next issue of Current Orthopaedics is published will be marked and those reaching an adequate standard will qualify for three external CME points. You will be notified of your marks and a CME certificate will be dispatched for your records.
Questions 1. Who developed the first total resurfacing arthroplasty? A. B. C. D. E.
McKee Salzer Charnley Muller Wagner
2. Which of the following was a major problem with first generation hip resurfacing implants? A. B. C. D.
Loss of femoral bone stock Loss of acetabular bone stock Avascular necrosis of the femoral head Obtaining adequate initial fixation of the acetabular component E. Tendency to place the femoral component in varus
3. Which of the following is not a common feature of currently available hip resurfacing systems? A. Bearing made from high carbon containing Co–Cr alloy B. Cementless fixation of the acetabular component doi:10.1016/j.cuor.2005.07.003
C. Cementless fixation of the femoral component D. Availability of acetabular components with 2 mm size increments E. Cement mantle in use of 1 mm or less 4. Which of the following has not yet been proved as fact? A. Wrought Co–Cr alloy is harder than cast Co–Cr alloy B. Wrought alloy can be polished to a smoother finish C. Annealing of Co–Cr alloy causes depletion of surface carbides D. Simulator studies have shown no difference in wear rates when comparing cast and heattreated alloys E. Simulator studies have shown that cast alloys have better wear resistance than wrought alloys 5. Two wrought Co–Cr alloy components are articulating in a test rig. They have been produced with a surface roughness of 5 nm and a clearance of 120 mm. What value for lambda (film thickness ratio) would you expect to be measured? A. 0.01 B. 0.1
ARTICLE IN PRESS CME SECTION C. 0.5 D. 1 E. 5 6. Which of the following statements about metal-on-metal bearings is not true? A. Low clearance is associated with a significant risk of clamping B. Fluid film lubrication can be achieved with a theoretical value for friction of zero C. Wrought Co–Cr is more readily produced with a surface roughness value that is conducive to fluid film lubrication than cast Co–Cr. D. Larger diameter components have higher volumetric wear rates E. Smaller diameter bearings are less likely to generate continuous fluid film lubrication 7. Which of the following is not a contra indication to resurfacing arthroplasty? A. Patients with neuromuscular disorders B. Patients with renal failure C. Patients with severe developmental dysplasia of the hip D. Patients with Rheumatoid disease E. Avascular necrosis of the femoral head 8. Where is most bone removed from the typical osteoarthritic femoral head during preparation for the femoral head component? A. B. C. D. E.
Superior part of the head Inferior part of the head Superior and anterior parts of the head Posterior and inferior parts of the head Equal removal, simply shaving off a circumferential surface layer
9. How should osteophytes be dealt with during preparation of the femoral head? A. Remove all osteophytes as they distort the anatomy
323 B. Preserve all osteophytes to reduce the risk of neck fracture C. Remove all mature, corticated osteophytes D. Remove all soft osteophytes and those mature ones that might cause impingement or oversizing E. Remove all osteophytes except those situated at the area that will be situated at the margin of the prosthesis once the head component is in place 10. Which of the following factors is not considered in calculating the Surface Arthroplast Risk Index? A. B. C. D. E.
Femoral cysts Activity level Femoral head shape Patient weight Previous surgery to hip
11. What is the mean length of follow up in currently available observational studies on resurfacing hip arthroplasty? A. B. C. D. E.
o1 year 1–2 years 2–4 years 4–6 years 6–10 years
12. What observation has been made on histological studies that raises the possibility of a novel mode of failure for metal on metal resurfacing implants? A. Metal particles are found in lymphoreticular tissue B. Elevated levels of metal ions are found in periprosthetic tissues C. There is a significant risk of metal sensitivity D. A lymphocyte rich membrane develops around the cement mantle E. There is a marked perivascular infiltrate of lymphocytes and plasma cells around some metal on metal articulations
ARTICLE IN PRESS 324
CME SECTION
Please fill in your answers to the CME questionnaire above in the response section provided below. A return address and fax number is given at the bottom of the page. ...........................................................................................
Responses Please shade in the square for the correct answer. 1 2 3 4 5 6 7 8 9 10 11 12
A A A A A A A A A A A A
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B B B B B B B B B B B B
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C C C C C C C C C C C C
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D D D D D D D D D D D D
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Your details (Print clearly) NAME. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ADDRESS. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . FAX NO. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . EMAIL. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . RETURN THE COMPLETED RESPONSE FORM by fax to +44-113-206-6791, or by post to CME, Current Orthopaedics, Orthopaedic Surgery, Clinical Sciences Building, St. James’s University Hospital, Beckett Street, Leeds LS9 7TF, UK.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 325
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CME SECTION
Answers to CME questions in Vol. 19, issue 2 Please find below the answers to the Current Orthopaedics CME questions from Vol. 19, issue 2 which were based on the article—‘Acetabular Fractures’ by J. McMaster and J. Powell from the same issue. 1 A&
B&
C&
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2 A&
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4 A&
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doi:10.1016/j.cuor.2005.04.005
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 326
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Book review
The Essentials of Musculoskeletal Imaging is the second book in the Essentials series published by the American Academy of Orthopaedic Surgeons. Those familiar with the first book, Essentials of Musculoskeletal Care, will recognise the format, which is carried over into the present text. There are four general sections (imaging modalities, general orthopaedics, tumours and paediatric orthopaedics) and seven anatomic sections. The chapters within each section describe a specific clinical problem, which can be as complex as spinal osteomyelitis or as humble as the heel bump. There then follows a brief description of the condition and the imaging studies required for diagnosis and those required for a comprehensive evaluation. There is a very brief description of the imaging findings, which often includes only one or two radiographs or a few representative sections from an MRI scan. There is an accompanying CD-ROM, which contains over 700 images. The text therefore does not set out to provide an in-depth coverage of the conditions and imaging findings but aims to provide an easy to use reference, to guide the clinician in requesting the appropriate imaging modality. It is certainly easy to use with a clearly set out six pages of contents, which usually direct the reader straight to the clinical condition of interest. A comprehensive list of synonyms for each condition is listed at the beginning of each chapter, all fully indexed, so there is usually no problem tracking down a particular condition. Whilst the text does not set out to be comprehensive I suspect that many Orthopaedic trainees at the beginning of their training will find the easy reference style and very
doi:10.1016/j.cuor.2005.04.001
concise text a quick way of assimilating a lot of knowledge. It is certainly easy enough to flick through the pages between patients in the outpatient clinic, though the size of the book lends itself more to a desktop reference rather than handbook. More established Orthopaedic surgeons would find it of use when they stray out of their area of expertise. My only major area of concern with the book is the lack of emphasis on musculoskeletal ultrasound, which is acknowledged in the text and reflects local practice in America. Radiologists on this side of the Atlantic who use all imaging modalities available to them, recognise that ultrasound provides images of far greater resolution than MRI, is quick and easy to use and provides dynamic information that MRI can never provide. The comment that ultrasound for the diagnosis of biceps pathology is difficult’’ is complete nonsense; anything is difficult if you have not been trained to do it. The recommendation of five radiographic views followed by MRI for the diagnosis of long head of biceps rupture is totally inappropriate for what is usually a clinical diagnosis, which can be confirmed within minutes by ultrasound if necessary. This book therefore fails in its aim of guiding the clinician in selecting the appropriate imaging modality; at least in those centres that use ultrasound. There is, however, still much in this book to recommend it, as long as the reader remembers that it is only a guide and the appropriate imaging modality will often depend on the local expertise of the radiologist. ’’
T.R. Johnson, L.S. Steinbach, Essentials of Musculoskeletal Imaging, American Academy of Orthopaedic Surgeons, ISBN: 089203324X, 2004 (900pp; £94.95)
James J Rankine St James’s University Hospital Leeds, Department of Radiology, Beckett Street, Leeds, West Yorkshire LS9 7TF, UK E-mail address:
[email protected]
Aims and Scope Current Orthopaedics presents a unique collection of international review articles summarizing the current state of knowledge and research in orthopaedics. Each issue focuses on a specific topic, discussed in depth in a mini-symposium; other articles cover the areas of basic science, medicine, children/adults, trauma, imaging and historical review. There is also an annotation, self-assessment questions and an exam section. In this way, the entire postgraduate syllabus will be covered in a 4-year cycle. The Journal is cited in: Cochrane Center, EMBASE/ Excerpta Medica, Infomed, Reference Update and UMI Microfilms.
Editor Professor R. A. Dickson MA, ChM, FRCS, DSc St James’s University Hospital Trust, Leeds, UK
Editorial Committee President of BOTA, M. A. Farquharson-Roberts (Gosport, UK), I. Leslie (Bristol, UK), D. Limb (Leeds, UK), M. Macnicol (Edinburgh, UK), J. Rankine (Leeds, UK)
Editorial Advisory Board E. G. Pasion (Philippines) L. de Almeida (Portugal) G. P. Songcharoen (Thailand) R. W. Bucholz (USA) J. W. Frymoyer (USA) R. W. Gaines (USA) S. L. Weinstein (USA) M. Bumbasirevic (former Yugoslavia)
J. C. Y. Leong (Hong Kong) A. K. Mukherjee (India) A. Kusakabe (Japan) A. Uchida (Japan) M.-S. Moon (Korea) R. Castelein (The Netherlands) R. K. Marti (The Netherlands) G. Hooper (New Zealand) A. Thurston (New Zealand)
D. C. Davidson (Australia) J. Harris (Australia) S. Nade (Australia) G. R. Velloso (Brazil) J. H. Wedge (Canada) S. Santavirta (Finland) P. N. Smyrnis (Greece) P. N. Soucacos (Greece) M. Torrens (Greece)
Available online at www.sciencedirect.com
Amsterdam
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Boston
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Jena
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London
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New York
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Oxford
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Paris
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Philadelphia
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San Diego
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St Louis
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 327–333
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MINI-SYMPOSIUM: PELVIC FRACTURES
(i) Injuries to the pelvic ring: Incidence, classification, associated injuries and mortality rates B.A. Petrisora,, M. Bhandarib a
Orthopaedic Trauma Service, 6N Hamilton Health Sciences: General Division, 237 Barton St. E., Hamilton, Ontario, Canada L8L 2X2 b Division of Orthopaedics, Department of Surgery, McMaster University, 7N Hamilton Health Sciences: General Division, 237 Barton St. E., Hamilton, Ontario, Canada L8L 2X2
KEYWORDS Pelvic fractures; Trauma; Associated injuries; Epidemiology; Mortality; Incidence
Summary High energy injuries to the pelvic ring often result from motor vehicle collisions. The incidence of severe pelvic ring injuries may be increasing in some areas. They are often associated with significant injuries to other major bodily organ systems resulting in high degrees of both morbidity and mortality. & 2005 Elsevier Ltd. All rights reserved.
Introduction Pelvic ring injuries commonly result from high energy trauma, with motor vehicle accidents accounting for up to 73% of injuries.1–3 The National Trauma Registry of major injury in Canada which collects data on all those with ISS412, has reported that for the years 2001–2002 motor vehicle collisions accounted for 47% of all cases.4 Mortality rates following pelvic trauma have ranged from 9 to 27%.2,5,6 Morbidity following pelvic injuries is high—often the result of the high energy trauma and a number of associated injuries. In this article we will address the incidence and classificaCorresponding author. Tel.: +1 905 527 4322 44648.
tion of high energy injuries to the pelvic ring as well as associated injuries.
Incidence Pelvic injuries include approximately 3% of all skeletal injuries and can occur in 4–18% of those sustaining high energy injuries (ISS412).7–10 Males are twice as likely to sustain a pelvic injury compared to females (66% vs. 34%, respectively).2,7 The Canadian National Trauma Registry have recorded that out of 109 738 major injuries occurring in 1999, 4531 had a pelvis fracture (4%).11 At the Hamilton Health Sciences, General Division, a Level 1 Tertiary trauma centre, pelvic
0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2005.06.006
ARTICLE IN PRESS 328 injuries made up 13.3% of orthopaedic injuries seen in the trauma population with ISS412 over a 10 year period.12 This correlates with reports from other North American centres. Clancy et al. found an incidence of pelvic fractures in trauma patients admitted to a US level 1 trauma centre to be 11.9%.9 This was relatively consistent with the level 2 trauma centres in the area with an incidence of 12.1%.9 Figures derived from UK data have shown an incidence of 8–14% depending on the ISS included in the respective databases.10,13 An increase in the number of severe pelvic injuries, those with a pelvic abbreviated injury severity score (pelvic AIS) of X4 in those vehicle occupants involved in a motor vehicle collision (MVC) has occurred in Canada.7 The incidence increased from 3.9% to 7.5% from 1994 to 1999, respectively.7 Suggested reasons for this are an increase in motor vehicle speed as well as an increase in subcompact and sports utility vehicles (SUV). Also, lateral impact crashes, which are known to be associated with an increased incidence of pelvic injuries, increased during the study period.7,14 Similarly, other North American and German data echo this trend and report that 59.7–73.4% of those sustaining a high energy pelvic ring injury were involved in an MVC.1–3 In an evaluation of the risk factors associated with severe pelvic injuries (AISX4), Demetriades et al. suggest that motorcycle injuries result in the highest incidence of pelvic fractures (15.5%) followed by pedestrian injuries (13.8%), falls from height 415 ft (12.9%) and car occupants (10.2%).15 Muir et al. agreed that pedestrians had the highest incidence of pelvic injuries (44%), however this was followed by occupant MVC’s (35%),10 falls from height and motorcycle accidents. Within the group of occupants involved in an MVC, the highest incidence of pelvic fracture was seen in the driver, followed by the front seat passenger and then the rear seat passenger.10 Although geographic differences may exist, most reports support motor vehicle collisions, either occupant, pedestrian or motorcycle as the major source of pelvic injuries worldwide.
Open pelvic injuries Open pelvic fractures occur in approximately 2–4% of pelvic injuries and, as with high energy pelvic ring injuries in general, occur more frequently in males.8,16–18 Several reports reveal that automobile or motorcycle accidents cause the highest proportion of open pelvic injuries.16–18 Brenneman
B.A. Petrisor, M. Bhandari et al. report this to be as high as 49% with automobile–pedestrian accidents following a close second (31%).16 Other reports have either an MVC, motorcycle or pedestrian accident as the primary cause of open pelvic fractures in over 50% of cases.18 Clearly, a high proportion of open pelvic fractures are the result of an MVC or related cause. A high incidence of Gustilo and Anderson Type 3 injuries has been reported—up to 60% in some reports.8,16,19 Strict categorical classification is difficult with pelvic injuries due in part to the complex anatomical relationship of soft tissues around the bone and also its proximity to potential levels of high bacterial contamination. In order to help with classification, some reports place those open pelvic fractures with wounds extending into the perineum or rectum as automatically Gustilo and Anderson type 3 injuries.8
Classification Pelvic injuries are most commonly classified either mechanistically (that of Young and Burgess5) or based on stability and mechanism (that of Tile and Pennal, adopted, modified and recommended by the Orthopaedic Trauma Association20,21). The OTA classification groups pelvic injuries into three main divisions: A-type injuries have a stable pelvic ring, B-type have a partial posterior disruption and C-type have a complete posterior disruption.21 Gansslen et al. using the OTA classification, reported a series of 2551 pelvic ring injuries.2 They found that 54.8% were type A fractures, 24.7% were type B fractures and 15.7% were type C fractures.2 However, Rommens and Hessman reviewed 222 patients with either B or C type injuries and found a higher proportion of C type injuries (55%).3 Within this classification, the severity of injury increases from type A to type C.2,3,20 Reports have shown that C type injuries have a higher injury severity score (ISS); as well, documented injuries in those motor vehicle collisions that were rapidly fatal have shown a predominance of C type patterns in those who had pelvic fractures.20,22 Using the classification of Young and Burgess, initial reports found an incidence of 41.4% for lateral compression injuries, 25.7% for anteroposterior compression, 4.7% for vertical shear, and 9.9% had a combined mechanism.5 This is consistent with other case series reviews of high energy pelvic injuries which have shown lateral compression injuries to have the highest incidence and vertical shear injuries to have the lowest.23
ARTICLE IN PRESS Injuries to the pelvic ring: Incidence, classification, associated injuries and mortality rates In open pelvic fractures, studies have reported differing incidences of A, B or C injuries. A type injuries range from 11% to 31%, B type (with the majority being B1 or open book injuries) range from 26% to 43% and C type injuries range from 43% to 45%.16,19 These figures again correlate with an increased preponderance of severe pelvic ring injuries in the open fracture subgroup. Classification systems for open pelvic fractures have also been described.19,24 Jones et al., have classified open pelvic injuries into three major categories: class 1 injuries are open pelvic fractures with a stable pelvic ring, class 2 are injuries in which the pelvic ring is either rotationally or vertically unstable and there is no rectal or perineal wound with the potential for fecal contamination and class 3 are open pelvic fractures that are either rotationally or vertically unstable but have a rectal or perineal wound present with the potential of fecal contamination.19 In their series, class 1 injuries accounted for 30% of open pelvic fractures, class 2 injuries accounted for 46% and class 3 injuries accounted for 23%.19 They found this classification to be predictive of both sepsis and mortality. Bircher and Hargrove classify open pelvic fractures into one of three categories, each with three subsets.24 A type injuries are predominantly ‘outside–in’ injuries, B type injuries are predominantly ‘inside–out’ injuries and C type injuries are those associated with severe soft tissue injury or loss and fecal contamination.24 Further studies are needed both to determine the specific incidence of each type and subtype and for further validation. A further subgroup of open fractures, which have a very high energy variant of the C type pelvic fracture pattern, is the traumatic hemipelvectomy. This lesion can be characterized by significant softtissue disruption, avulsion or occlusion of the iliac or femoral vessels and wide separation of the hemipelvis.25 The incidence has been reported to be 0.55%. However, the true incidence may be unknown as a significant number of cases may be fatal at the scene.25,26 In a review of the survivors of this injury, most were injured on motorcycles, were pedestrians or were occupants involved in MVC’s (driver most commonly).25 Once again this reveals the significant association of motor vehicle trauma and high energy injury patterns.
Associated injuries Injuries to other organ systems are commonly seen with high energy pelvic ring injuries (Table 1). The incidence of associated injuries varies with reports
329
Table 1 Associated injuries and their respective reported incidences. Associated Injuries
Reported incidences (%)
Head Chest Abdomen Genitourinary Anorectal Neurologic Requiring angiography Other MSK injuries
33.3–692,5,8,26 27–56.42,5,8,26 17–585,13,18,26 6.3–44.65,26,27 0.95–2.314,16 3–463,26,38,52 4.7–9.15,13,45 27–833,5,8
ranging from 30% to 93%.1,3,27 Some authors have shown an increased constellation of associated injuries as the severity of the pelvic fracture increases.5,27 In this review we will focus on significant injuries to other major bodily systems.
Thoracic and abdominal injuries Thoracic injuries occur in 27–65% of those with high energy pelvic injuries.3,7,10,27 Some have found this the most common extrapelvic lesion while others suggest it is more commonly associated with certain fracture types.5,27 Initial reports found the incidence of thoracic injury to range from 19% to 39% depending on the fracture pattern, with the Young and Burgess anteroposterior compression (APC) type 2 injury (39%) and the lateral compression (LC) type 2 injury (36%) having the highest association.5 Documentation on the severity of thoracic injury suggests that severe thoracic trauma is more commonly seen with an incidence up to 30%.3,7 Intra-abdominal injuries can take the form of solid organ damage or damage to the bowel. Initial reports documented splenic injuries as the most common with an incidence ranging from 9% to 24% depending on the fracture pattern, the highest being associated with the vertical shear injury.5 More recent reports suggest that liver injuries are the most common intra-abdominal organ injury with an incidence of approximately 6%. This is followed by splenic injuries with an approximate incidence of 5% and injuries to the bowel with an incidence of 4%.15 This pattern is consistent throughout the range of pelvic AIS.15 Using stepwise logistic regression Demetriades et al., found that involvement in an MVC and a pelvic injury of at least AIS ¼ 4 were predictors of liver injury.15 Thus those with severe pelvic injuries (AISX4) had a
ARTICLE IN PRESS 330 relative risk of liver injury of 1.9 and this combined with MVC as the mechanism of injury increased the relative risk to 3.15
Urogenital and rectal injuries Reports of bladder and urethral injuries range from 6% to 21% depending on the fracture morphology.3,5 Some series have found the APC injury pattern to be significantly associated with these injuries.3 Recent reports have focused on determining predictors of associated bladder and urethral injuries.15 Male gender and a pelvic AISX4 have been documented to be independent risk factors associated with bladder or urethral injuries. Males and those patients with AISX4 are 1.9 and three-fold more likely to have a urethral injury following pelvic trauma compared to controls. Both risk factors together resulted in a incidence of 4.8% for bladder or urethral injury.15 Aihara et al., reported that of bladder and urethral injuries, bladder injuries were the most commonly associated injury, with an incidence of 4.6%.28 Urethral injuries occurred in 1.1% of pelvic ring injuries and combined injuries occurred in 0.8%.28 Widening of the SI joint, widening of the symphysis pubis and fractures of the sacrum were associated with a bladder injury with widening of the symphysis pubis the strongest predictor of bladder injury.28 In regard to urethral injury, fractures of the inferior rami, widened symphysis pubis and SI joint widening were associated, however only symphysis pubis widening and fracture of the inferior pubic ramus were independently predictive of urethral injury.28 Within the subcategory of open pelvic fractures the incidence of urogenital injuries has been reported to be as high as 61.4%.16 Jones et al., in a multicentre retrospective review reported the incidence of vaginal lacerations to be 33%, bladder injuries to be 23% and urethral injuries to be 10%.19 Urethral injuries may be associated with decreases in sexual function, as well, sexual function may be decreased in the absence of obvious urethral injuries.29,30 In a review of 90 patients, King et al., found the incidence of sexual dysfunction to be 5% in those without urologic injury and 42% in those with urologic injury.30 Rates can be higher as seen in those with documented posterior urethral injuries referred for late reconstruction.31 Seventy-two per cent had sexual dysfunction as demonstrated by nocturnal tumescence studies.31 When looking at all high energy pelvic fractures, an incidence of erectile dysfunction of 12% and dyspareunia in 2% of women has been reported.32 When looking specifically at male sexual function
B.A. Petrisor, M. Bhandari using validated outcome measures for this, the complaints of erectile dysfunction range from mild to severe. This was shown to correlate with a significant decrease in overall sexual satisfaction. Interestingly, 20% of those with complaints of erectile dysfunction had no previously associated urethral disruption. The only factor identified by Malavaud et al. to be associated with this decrease in erectile function was pubic diastasis.29 Copeland et al. reviewed two groups of female multitrauma patients: those with pelvic fractures and those with only fractures to the extremities.33 They found increased urinary complaints in those with pelvic fractures than in those without (21% compared to 7%, respectively). Dyspareunia was seen in those with pelvic fractures and was more common when the residual displacement of the fracture was X5 mm (43% compared to a 25% incidence in those with displacement o5 mm).33 Between groups there was no difference in the rates of miscarriage or infertility.33
Anorectal injury Anorectal injuries occur with an incidence of 0.95–2.3%.16,18,28 Although infrequent they are a significant source of both morbidity and mortality.34 Reviews of open fractures have found rectal and perineal injuries to occur in 23–64% of patients with open pelvic injuries.18,19,35,36 The presence of perineal injuries incurs a high rate of sepsis—up to 77% in some reports.19 Aihara et al., have shown that the primary and independent predictor of rectal injuries was a widened symphysis with a relative risk of 3.3.28
Head and neurologic injuries Head injury occurs in 37–69% of high energy pelvic fractures.3,7,10 The higher percentages are often seen in those patients with pelvic AISX4. Early reports suggested an association with the anteroposterior compression injury pattern.5 Most head injuries are closed injuries, with subdural hematoma and cerebral contusion making up approximately 6% and 9%, respectively.7 Peripheral neurologic injuries have been reported to occur with an incidence ranging from 3% to 46% depending in part on the severity of the injury, fracture morphology and the presence of an associated sacral fracture.2,37–39 A higher incidence of neurologic injury has been reported with a completely unstable injury pattern (OTA C type injury).3 With the partially unstable pattern (OTA B type), a higher incidence of neurologic injuries are
ARTICLE IN PRESS Injuries to the pelvic ring: Incidence, classification, associated injuries and mortality rates seen in the B1 (APC equivalent) as compared to the B2 (LC equivalent) pattern.3 When looking at the type of nerve injury, the majority (60%) are a mixed motor and sensory loss, while the rest have a sensory deficit alone.39 Approximately half of these injuries may go on to recover.39 Sacral fractures, in association with fractures of the pelvic ring have been shown to increase the likelihood of neurologic injury.40–42 Denis et al. classified these injuries as being either in zone 1 (involving the sacral ala, lateral to the foramina), zone 2 (transforaminal) or zone 3 (extending into the sacral canal).41 The incidence of neurologic injury increased accordingly from zone 1 (5.9%), to zone 2 (28%) to zone 3 (56%). The type of neurologic injury also correlates with placement, as injury to the L5 nerve root is most frequent in zone 1, unilateral sacral root lesions occur in zone 2 and injuries to the cauda equina are most frequent in zone 3.40,42 An uncommon variant of sacral fracture that has been reported is the midline sagittal fracture associated with anterior–posterior compression type injuries.43 These fractures occur with an incidence of 0.6% of pelvic fractures and 1.4% of sacral fractures as seen in a review of 10 cases.40 Interestingly, there were no objective neurologic deficits at 31 months of follow-up with this type of injury. This type of fracture pattern may protect the nerve roots from injury by hinging open through the posterior aspect of the canal.40
Hemodynamic complications The incidence of those requiring transfusion of blood products in patients with high energy pelvic ring injuries ranges from 38% to 75%.15 Transfusion rates can increase significantly as severity of pelvic injury increases and as the number of other associated major organ injury increases.6,7,15,44 Indeed it has been suggested that the requirement for major blood transfusions and threat of hemorrhage is significantly due to associated non-pelvic injuries.44 Recent reports have determined factors found to be predictive of the risk of undergoing a transfusion. Using information available at presentation as factors in a logistic regression model predictors of transfusion include increasing age (460), shock on arrival (systolic blood pressure o90 mmHg), revised trauma score and base deficit.23 In a similar report, age 455, ISS425, pelvic AISX4 and angiographic embolization have also been identified as significant independent risk factors associated with major blood transfusions (42 L).15
331
Open fractures have been also been shown to have higher initial 24 h transfusion requirements as compared to closed injuries.16 Indeed, in some reports of open pelvic fractures, exsanguination was as high as 7% with documented transfusion rates as high as 33.6 units.16,45 Pelvic angiography is reported to be necessary in 4.7–9.1% of pelvic injuries.7,15,46 Of these up to 18.8% may require a repeat angiography and embolization.47 Shapiro et al., found that predictors of repeat angiography were continued or recurrent hypotension (SBPo90), absence of intra-abdominal injury, and persistent base deficit of 10 for greater than 6 h.47 Early reports revealed that APC type injuries were significantly associated with hemodynamic instability and transfusion requirements and this continues to be the case.5,48 In comparing an APC group to an LC group in a series of pelvic fractures treated with angiography, the APC group was found to be more commonly hemodynamically unstable on arrival.48 The APC group contained the highest number of posterior division arterial injuries (52%) while the LC group contained a higher proportion of anterior division arterial injuries (59%). When converting to the OTA classification, all type A injuries had internal iliac posterior division injuries, type B had a high proportion of anterior division injuries (56%) and Type C had a high proportion of posterior division injuries (40%). Previous reports have shown a high degree of internal iliac posterior division arterial injury, most commonly the superior gluteal artery, with unstable posterior injury patterns. Similarly anterior division injury patterns result in anterior division arterial injury, most commonly the pudendal.46
Other soft tissue injuries Closed soft tissue injuries can also occur with pelvic trauma. The closed internal degloving injury associated with acetabular fractures and occurring over the greater trochanter as described by MorelLavallee can also be seen in pelvic injuries.49–50 Degloving may also occur over the trunk, buttock or thighs.49 Hak et al., reviewed 24 patients with this lesion. In their series, six patients (25%) had lateral compression fractures with sacral and ramus fractures and six patients (25%) had sacroiliac disruptions. The rest were associated with acetabular fractures.49 These injuries may initially be missed and indeed Hudson et al. found that onethird were missed with the majority resulting from a motor vehicle accident.51
ARTICLE IN PRESS 332
B.A. Petrisor, M. Bhandari
Mortality
References
Rates of mortality associated with high energy pelvic fractures range between 9% and 28% and are composed of an early mortality, usually due to hemorrhage and a later mortality commonly associated either with sepsis or multiple organ failure.2,15,23,52 In a certain number of patients the pelvic injury is determined to be the primary cause of death and this has been reported to be from 0.8% to 1.4%.1,2,15 Mortality increases as the severity of the injury increases.2,15,23 Indeed, type A injuries are associated with the lowest mortality rate of 9%.2 This increases to 14–28% in those with type B or C injuries and those with a pelvic AISX4.2,15,27 Predictors of mortality have been determined using logistic regression analysis and they include presentation to the trauma suite with a revised trauma score less than 11, age 460 or in shock.23 Those who have one or more of these factors are at significant risk of dying regardless of fracture pattern.23 Starr et al., found that mortality was highest within the first 24 h. Open pelvic fractures have an increased mortality when compared to closed pelvic injuries.16,19,36 Jones et al., report an overall incidence of mortality of 25% in their open fracture series, and Brenneman et al., report an incidence of mortality of 25% of those with open pelvic fractures compared to 16% in those with closed pelvic injuries. The incidence of death increased from 0% in Jones et al., class 1 open pelvic fractures to 33% in class 2 and 44% in class 3 injuries. Half of the patients died early as a result of hemorrhage and 10% died later due to multiple organ failure.19 Factors seen to influence this rate are ISS, age in years and associated significant soft tissue damage.2,36 With these factors mortality rates reach over 30%.2,36 In those patients requiring angiography, the overall mortality rate is also seen to be higher and is reported to be as high as 57%.23,46 Those presenting with shock on arrival (systolic blood pressure o90 mmHg) were seen to have the highest mortality.46
1. Poole GV, Ward EF. Causes of mortality in patients with pelvic fractures. Orthopedics 1994;17:691–6. 2. Gansslen A, Pohlemann T, Paul C, Lobenhoffer P, Tscherne H. Epidemiology of pelvic ring injuries. Injury 1996;27 (Suppl 1):S20. 3. Rommens PM, Hessmann MH. Staged reconstruction of pelvic ring disruption: differences in morbidity, mortality, radiologic results, and functional outcomes between B1, B2/B3, and C-type lesions. J Orthop Trauma 2002;16:92–8. 4. Canadian Institute for Health Information. National Trauma Registry 2003 Report. 7. 2003 (GENERIC). 5. Dalai SA, Burgess AR, Siegel JH, et al. Pelvic fracture in multiple trauma: classification by mechanism is key to pattern of organ injury, resuscitative requirements, and outcome. J Trauma 1989;29:981–1000. 6. Burgess AR, Eastridge BJ, Young JW, et al. Pelvic ring disruptions: effective classification system and treatment protocols. J Trauma 1990;30:848–56. 7. Inaba K, Sharkey PW, Stephen DJ, Redelmeier DA, Brenneman FD. The increasing incidence of severe pelvic injury in motor vehicle collisions. Injury 2004;35:759–65. 8. Grotz MR, Allami MK, Harwood P, Pape HC, Krettek C, Giannoudis PV. Open pelvic fractures: epidemiology, current concepts of management and outcome. Injury 2005;36: 1–13. 9. Clancy TV, Gary MJ, Covington DL, Brinker CC, Blackman D. A statewide analysis of level I and II trauma centers for patients with major injuries. J Trauma 2001;51:346–51. 10. Muir L, Boot D, Gorman DF, Teanby DN. The epidemiology of pelvic fractures in the Mersey Region. Injury 1996;27: 199–204. 11. Canadian Institute for Health Information. National Trauma Registry. 1999 (GENERIC). 12. Canadian Institute for Health Information. National Trauma Registry: Hamilton Health Sciences: General Division. 2005 (GENERIC). 13. Bircher M, Giannoudis PV. Pelvic trauma management within the UK: a reflection of a failing trauma service. Injury 2004;35:2–6. 14. Rowe SA, Sochor MS, Staples KS, Wahl WL, Wang SC. Pelvic ring fractures: implications of vehicle design, crash type, and occupant characteristics. Surgery 2004;136:842–7. 15. Demetriades D, Karaiskakis M, Toutouzas K, Alo K, Velmahos G, Chan L. Pelvic fractures: epidemiology and predictors of associated abdominal injuries and outcomes. J Am Coll Surg 2002;195:1–10. 16. Brenneman FD, Katyal D, Boulanger BR, Tile M, Redelmeier DA. Long-term outcomes in open pelvic fractures. J Trauma 1997;42:773–7. 17. Perry Jr JF. Pelvic open fractures. Clin Orthop Relat Res 1980:41–5. 18. Ferrera PC, Hill DA. Good outcomes of open pelvic fractures. Injury 1999;30:187–90. 19. Jones AL, Powell JN, Kellam JF, McCormack RG, Dust W, Wimmer P. Open pelvic fractures. A multicenter retrospective analysis. Orthop Clin North Am 1997;28:345–50. 20. Tile M. Describing the injury: classification of pelvic ring injuries. In: Tile MHDKJ, editor. Fractures of the pelvis and acetabulum. Philadelphia: Lippincot Williams and Wilkins; 2003. p. 130. 21. Orthopaedic Trauma Association Committee for Coding and Classification. Fracture and Dislocation Compendium, J Orthop Trauma 1996;10:V–IX.
Conclusion Significant injuries to the pelvic ring, most commonly the result of high energy trauma, carry with them high rates of both morbidity and mortality. This is in part due to their frequent association with other injuries.
ARTICLE IN PRESS Injuries to the pelvic ring: Incidence, classification, associated injuries and mortality rates 22. Adams JE, Davis GG, Alexander CB, Alonso JE. Pelvic trauma in rapidly fatal motor vehicle accidents. J Orthop Trauma 2003;17:406–10. 23. Starr AJ, Griffin DR, Reinert CM, et al. Pelvic ring disruptions: prediction of associated injuries, transfusion requirement, pelvic arteriography, complications, and mortality. J Orthop Trauma 2002;16:553–61. 24. Bircher MHR. Is it possible to classify open fractures of the pelvis. European J Trauma 2004;30:74–9. 25. Rieger HDK-H. Traumatic hemipelvectomy: an update. J Trauma 1998;45:422–6. 26. Pohlemann T, Paul C, Gansslen A, Regel G, Tscherne H. Traumatic hemipelvectomy. Experiences with 11 cases. Unfallchirurg 1996;99:304–12. 27. Siegmeth A, Mullner T, Kukla C, Vecsei V. Associated injuries in severe pelvic trauma. Unfallchirurg 2000;103:572–81. 28. Aihara R, Blansfield JS, Millham FH, LaMorte WW, Hirsch EF. Fracture locations influence the likelihood of rectal and lower urinary tract injuries in patients sustaining pelvic fractures. J Trauma 2002;52:205–8. 29. Malavaud B, Mouzin M, Tricoire JL, et al. Evaluation of male sexual function after pelvic trauma by the International Index of Erectile Function. Urology 2000;55:842–6. 30. King J. Impotence after fractures of the pelvis. J Bone Joint Surg Am 1975;57:1107–9. 31. Shenfeld OZ, Kiselgorf D, Gofrit ON, et al. The incidence and causes of erectile dysfunction after pelvic fractures associated with posterior urethral disruption. J Urol 2003; 169:2173–6. 32. Pohlemann T, Tscherne H, Baumgartel F, et al. Pelvic fractures: epidemiology, therapy and long-term outcome. Overview of the multicenter study of the Pelvis Study Group. Unfallchirurg 1996;99:160–7. 33. Copeland CE, Bosse MJ, McCarthy ML, et al. Effect of trauma and pelvic fracture on female genitourinary, sexual, and reproductive function. J Orthop Trauma 1997;11:73–81. 34. Woods RK, O’Keefe G, Rhee P, Routt Jr ML, Maier RV. Open pelvic fracture and fecal diversion. Arch Surg 1998; 133:281–6. 35. Sinnott R, Rhodes M, Brader A. Open pelvic fracture: an injury for trauma centers. Am J Surg 1992;163:283–7. 36. Hanson PB, Milne JC, Chapman MW. Open fractures of the pelvis. Review of 43 cases. J Bone Joint Surg Br 1991;73: 325–9.
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37. Failinger MS, McGanity PL. Unstable fractures of the pelvic ring. J Bone Joint Surg Am 1992;74:781–91. 38. Majeed SA. Neurologic deficits in major pelvic injuries. Clin Orthop Relat Res 1992:222–8. 39. Reilly MC, Zinar DM, Matta JM. Neurologic injuries in pelvic ring fractures. Clin Orthop Relat Res 1996:28–36. 40. Bellabarba C, Stewart JD, Ricci WM, DiPasquale TG, Bolhofner BR. Midline sagittal sacral fractures in anterior–posterior compression pelvic ring injuries. J Orthop Trauma 2003;17:32–7. 41. Denis F, Davis S, Comfort T. Sacral fractures: an important problem. Retrospective analysis of 236 cases. Clin Orthop Relat Res 1988;227:67–81. 42. Gibbons KJ, Soloniuk DS, Razack N. Neurological injury and patterns of sacral fractures. J Neurosurg 1990;72:889–93. 43. Carter TR, Lambert K. Pubic diastasis with longitudinal fracture of the sacral body: case report. J Trauma 1990; 30:627–9. 44. Poole GV, Ward EF, Muakkassa FF, Hsu HS, Griswold JA, Rhodes RS. Pelvic fracture from major blunt trauma. Outcome is determined by associated injuries. Ann Surg 1991;213:532–8. 45. Raffa J, Christensen NM. Compound fractures of the pelvis. Am J Surg 1976;132:282–6. 46. O’Neill PA, Riina J, Sclafani S, Tornetta III P. Angiographic findings in pelvic fractures. Clin Orthop Relat Res 1996:60–7. 47. Shapiro M, McDonald AA, Knight D, Johannigman JA, Cuschieri J. The role of repeat angiography in the management of pelvic fractures. J Trauma 2005;58:227–31. 48. Metz CM, Hak DJ, Goulet JA, Williams D. Pelvic fracture patterns and their corresponding angiographic sources of hemorrhage. Orthop Clin North Am 2004;35:431–7 v. 49. Hak DJ, Olson SA, Matta JM. Diagnosis and management of closed internal degloving injuries associated with pelvic and acetabular fractures: the Morel-Lavallee lesion. J Trauma 1997;42:1046–51. 50. Collinge C, Tornetta III P. Soft tissue injuries associated with pelvic fractures. Orthop Clin North Am 2004;35:451–6 v. 51. Hudson DA, Knottenbelt JD, Krige JE. Closed degloving injuries: results following conservative surgery. Plast Reconstr Surg 1992;89:853–5. 52. Wubben RC. Mortality rate of pelvic fracture patients. Wis Med J 1996;95:702–4.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 334–344
www.elsevier.com/locate/cuor
MINI-SYMPOSIUM: PELVIC FRACTURES
(ii) Acute management of pelvic ring fractures Marius Keela,, Otmar Trentzb a
Division of Trauma Surgery, University Hospital Zurich, Zurich, Switzerland Division of Trauma Surgery, University Hospital Zurich, Raemistrasse 100, CH-8091 Zurich, Switzerland
b
KEYWORDS Pelvic ring fracture; Life-saving surgery; Damage control; Pelvic C-clamp; Pelvic packing; Angiographic embolisation; Second look; Vacuum-assisted closure; Early total care; Delayed definitive surgery
Summary During the primary survey, patients with pelvic ring fractures undergo decision making for day 1 surgery including life-saving surgery, damage control surgery and early total care or delayed definitive surgery dependent on haemodynamic status, physiologic criteria (hypothermia, coagulopathy, acidosis), scoring of injury severity and personal or operative resources. The staged sequential procedures of ‘pelvic damage control’ include damage control surgery with control of haemorrhage and contamination, decompression of abdominal and pelvic compartment syndromes, de´bridement of soft tissue injuries as well as temporary or definitive osteosynthesis, followed by resuscitation in the intensive care unit, ‘second-look’ operations, scheduled definitive surgery and secondary reconstructive surgery. External fixation of the posterior pelvic ring by pelvic C-clamp and pelvic packing represent the work horses for haemorrhage control of severe pelvic ring injuries in haemodynamically unstable patients, whereas angiographic embolisation is an option for haemodynamically stable patients or persistent bleeding after or during damage control surgery. & 2005 Elsevier Ltd. All rights reserved.
Introduction Severe pelvic ring fractures are often associated with severe bleeding and major intraabdominal injuries.1,2 Therefore, the acute management of pelvic ring injuries is complex and demands an algorithm for deciding which patient should be operated immediately and which operative strategies should be chosen.2,3 Day 1 surgery of patients with severe pelvic ring fractures includes lifeCorresponding author. Tel.: +41 44 255 3657; fax: +41 44 255 4406. E-mail addresses:
[email protected] (M. Keel),
[email protected] (O. Trentz).
saving surgery, damage control surgery and early total care. The decision for one of these strategies or for delayed definitive surgery is made dependent on haemodynamic status, physiologic criteria (hypothermia, coagulopathy, acidosis), scoring of injury severity and personal or operative resources.4 The term ‘damage control’ was popularised by Rotondo in 1993 for the successful treatment of penetrating abdominal injuries5. This strategy has become the gold standard of care for abdominal trauma of severely injured patients and was defined as rapid abbreviated laparotomy to stop haemorrhage and peritoneal soiling and staged sequential repair after ongoing resuscitation and recovery from the lethal triad of hypothermia,
0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2005.09.009
ARTICLE IN PRESS Acute management of pelvic ring fractures
335
acidosis and coagulopathy.4–8 Based on the damage control concept for abdominal injuries, the application of the same principles to the management of multiply injured patients with associated fractures of the long bones and pelvic ring fractures was named ‘damage control orthopaedics’ (DCO).9 The philosophy of ‘pelvic damage control’ is to abbreviate surgical interventions by deferring repair of anatomical lesions before the development of irreversible physiologic endpoints according to the classical staged laparotomy.2,4–8 This operative concept reduces the mortality rate and the incidence of posttraumatic complications in patients with severe pelvic ring fractures.2,3,10 The aim of this review article is to summarise the principles and steps of the acute management of severely injured patients with pelvic ring fractures.
Initial management and decision making for day 1 surgery According to the Advanced Trauma Life Support (ATLS&) principles, severely injured patients with pelvic ring fractures undergo the primary survey of airway (A), breathing (B), circulation (C), neurologic status (D; disability) and core temperature (E;
environment) (Fig. 1).4,11 Pelvic stability is tested by manual compression in anterior–posterior and lateral–medial directions. Patients with severe trauma who are unconscious (Glasgow Coma Scale (GCS) o9 points) or in shock benefit from immediate endotracheal intubation and oxygenation. Simultaneous with airway management, a quick assessment of the patient will determine the degree of shock present. A patient with a systolic blood pressure o90 mmHg, a thready pulse and flat neck veins is assumed to have hypovolaemic shock. If the patient’s primary problem in shock is blood loss, the intention is to stop the bleeding and replace the volume deficit. Obvious blood loss such as external bleedings and occult blood loss e.g. into the abdomen or retroperitoneum should be immediately detected clinically or by basic imaging which includes chest, pelvis and lateral cervical spine radiographs (Fig. 1). In addition, focused assessment for sonographic examination of the trauma patient (FAST) has become a standard procedure in the primary survey. Free abdominal fluid is a strong indicator for intraperitoneal lesions in addition to profuse retroperitoneal bleedings in patients with severe pelvic injuries.12 As soon as possible blood work is obtained that includes arterial blood gas analysis, haematocrit,
Primary survey - ATLS ©
Resuscitation Preservation of perfusion and oxygenation
• Clinical examination - ABCDE • Basic imaging (chest, pelvis, lateral cervical spine), FAST
“in extremis
„
_
“transient „ responder Life saving surgery • Crash thoracotomy: aortic clamping, open cardiac resuscitation if cardiac arrest
• Crash laparotomy: aortic cross clamping, abdominal and pelvic packing
• Pelvic C-clamp
“responder
Vital functions? Response?
„
+ Secondary survey - ATLS© • Head to toe examination • Extended imaging: extremity x-rays, CT-scan
?
Damage control • Control of hemorrhage • Control of contamination • Decompression of compartment syndromes • Débridement of soft tissue injuries • Temporary or definitive pelvic ring osteosynthesis
“borderline„ Physiologic
Staged sequential procedures • Resuscitation„ in ICU • “Second look and scheduled definitive surgery • Secondary reconstructive surgery
_
balance? Scoring? Resources?
+ Early total care or Delayed definitive surgery
Figure 1 Algorithm of the acute management and treatment of patients with pelvic ring fractures. See text for details and explanations.
ARTICLE IN PRESS 336 haemoglobin, lactate level, base deficit, pH, blood type and cross-match, and a screening battery of other laboratory tests including coagulation parameters. The fluid used to resuscitate and the further workup will depend on the patient’s response to initial fluid load (2 l prewarmed crystalloids), the laboratory and further clinical analyses.11 The ‘responder’ may require no more than crystalloids to replace the volume deficit and progress to the secondary survey, which focuses on a complete physical head to toe examination that directs further diagnostic studies (extended imaging) such as CT scan trauma protocol and extremity radiographs (Fig. 1).4 The ‘transient responder’ may need typed and cross-matched blood. The application of platelets, fresh frozen plasma (FFP) or fibrinogen is well established in patients with unstable pelvic fractures, whereas the treatment of coagulopathy with recombinant activated factor VII (rFVIIa) is undergoing trials. Patients with a ‘transient response’ to resuscitation with a hypotension (o90 mmHg) in excess of 70 min or a transfusion rate of 10–15 units of packed red blood cells should be transferred to the operating room without delay and undergone damage control procedures.4 Furthermore, attempts have been made for ‘responders’ to define physiologic criteria for the initiation of damage control based on hypothermia (o34 1C), coagulopathy (prothrombin time 419 s or partial thromboplastin time 460 s; platelet count o90,000) and acidosis (pH o7.2 or lactate serum level 45 mmol/l), called the lethal triad.7,9 Then the failure to normalise an abnormal serum lactate level by 48 h after trauma has been correlated with mortalities ranging from 86% to 100%.4 Further citied indications especially for DCO concern type and severity of injury: injury severity score (ISS)435 points; severe head injury, the abbreviated injury scale (AIS)42 points; multiple injuries with an ISS420 points and additional thoracic trauma AIS42 points; multiple injuries with abdominal/pelvic trauma and haemorrhagic shock; severe soft tissue injuries, radiographic evidence of bilateral pulmonary contusion as well as type of surgery (presumed operation time 460 min and expecting major blood loss).9 These first-hit (trauma load) and second-hit (interventional load) phenomena predispose these patients ‘at risk’ or ‘borderline’ for the development of severe systemic inflammation (host defense response) after surgery with a high incidence of local infections, sepsis, multiple-organ dysfunctions and high mortality rate.4,6 They justify the decision for damage control of pelvic ring injuries instead of early total care or delayed definitive surgery (Fig. 1).
M. Keel, O. Trentz Fluid replacement in patients with severe haemorrhagic shock and no response to the initial fluid replacement ‘in extremis’ is controversially discussed.4 It is suggested that immediate massive volume replacement before surgical control of bleeding might disrupt a blood clot that had obliterated a bleeding vessel. Therefore patients with unstable pelvic ring fractures and persistent severe haemorrhagic shock should undergo lifesaving procedures. In addition, the patient ‘in extremis’ may need type 0 blood and clotting factors.
Life-saving surgery The left anterolateral ‘crash’ thoracotomy (emergency room thoracotomy (ERT)) or sternotomy with thoracic aortic cross-clamping and open cardiopulmonary resuscitation as a life-saving intervention represents a controversial indication for patients with unstable pelvic ring injuries and severe haemorrhagic shock who arrive in trauma centres after a short scene/transport time with witnessed and/or objectively measured vital parameters (patients ‘in extremis’) (Fig. 1).2,4 In addition, this access allows cannulation of the right atrium with a catheter for massive resuscitation. However, ERT or sternotomy should be performed selectively due to its very low survival rate in patients sustaining cardiopulmonary arrest secondary to blunt trauma (1.5%). Furthermore, for patients with pelvic ring injuries and exsanguinating abdominal or retroperitoneal haemorrhage without response to fluids ‘crash’ laparotomy can be life saving. To control haemorrhage, blood and clot are removed digitally and by suction. Thereafter, lateral retraction of the abdominal wall is performed to enable four-quadrant packing. The abdominal aorta is controlled digitally at the aortic hiatus or by placement of an aortic infradiaphragmatic cross-clamp. After successful resuscitation, life-saving procedures for patients ‘in extremis’ with unstable pelvic ring injuries should be completed with closed reduction and stabilisation of the posterior pelvic ring by the pelvic C-clamp.3
Damage control surgery If patients ‘in extremis’ survive life-saving procedures or after decision making for damage control as ‘preemptive intervention’ on the basis of clinical and laboratory findings, patients with severe pelvic fractures should undergo damage control surgery
ARTICLE IN PRESS Acute management of pelvic ring fractures immediately. The concept of ‘pelvic damage control’ includes stepwise control of haemorrhage and contamination, decompression of abdominal or
337 pelvic compartment syndromes, de´bridement of soft tissue injuries and finally the temporary or definitive pelvic ring osteosynthesis.
Figure 2 (a) Plain film of the pelvis of a haemodynamically unstable young lady after a rollover injury showing a vertical shear injury with a transforaminal sacral fracture on the left side and bilateral rami fractures combined with an open anterior hip dislocation on the right side. (b) Preoperative state of anteriorly dislocated femoral head. (c) Intraoperative status after closed reduction of posterior pelvic ring and placement of pelvic C-clamp, laparotomy with pelvic packing, reduction and de´bridement of open hip dislocation, placement of supraacetabular pins for anterior external fixator and installation of catheters for the measurement of bladder pressure to monitor the intraabdominal pressure. (d) Postoperative plain film of the pelvis with the placed pelvic C-clamp, supraacetabular external fixator and pelvic packing. (e) Plain film of the pelvis after posterior local plating of sacral fracture and lumbo-iliac distraction osteosynthesis at the end of the first week after injury. (f) Plain film of the pelvic 1 year after injury with formation of ectopic ossification.
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Control of haemorrhage Pelvic C-clamp and external fixator The immediate recognition of haemorrhagic shock and effective control of the bleeding play a pivotal role for the survival and posttraumatic course of patients with severe pelvic ring injuries. However, the treatment of exsanguinating haemorrhage after pelvic ring fractures is controversial.2–4,10,13,14 Though acute closed reduction and external stabilisation of the disrupted pelvis is well accepted, which technique and device used still give rise to debate. According to prehospital experience, the use of a pelvic binder or belt is established in different trauma centres as temporary external stabilisers.1,13 The pelvic C-clamp as a posterior device for vertical shear injuries (C-type fractures) is mechanically superior to these non-invasive external fixation systems or anterior external fixator (Fig. 2).2,3,15 However, the application of the C-clamp can be complicated by vascular injuries, nerve injuries through overcompression in sacral fractures, perforation of pelvic organs, displacement of the unstable hemipelvis into the true pelvis, loss of reducion, loosening of the pins, and pin tract infections. To avoid the displacement of the hemipelvis, an additional anterior supraacetabular external fixator should be applied in very unstable fractures (Fig. 2). In addition, the pelvic C-clamp is not applicable in fractures of the iliac bone and most trans-iliac fracture dislocations.15
Pelvic packing The reduction and stabilisation of the posterior pelvic ring mostly does not result in complete spontaneous haemostasis ‘self-tamponade’ of retroperitoneal bleeding by decreasing pelvic volume and fracture haemorrhage.3,10 Then severe pelvic ring injuries lead to damage of the constraining ligaments of the pelvic ring, the pelvic floor and the iliopectineal fascia. Moreover, the retroperitoneal space is not separated cranially by constraining compartments. Thus, the retroperitoneal haema-
M. Keel, O. Trentz toma can drain into the abdomen or into the chest along the psoas muscle (called chimney effect) with a circulatory decompensation and a fatal outcome. Therefore, in patients with persistent haemorrhagic shock after external stabilisation of the pelvic ring, laparotomy and pelvic packing are recommended to control retroperitoneal presacral and the paravesical venous bleeding.2,3,10 The rare arterial haemorrhage (10–20%) in an unstable pelvic fracture can also be successfully treated by pelvic packing. Furthermore, the high incidence of associated intraperitoneal lesions (31%) in patients with severe pelvic fractures emphasises the rationale for laparotomy and pelvic packing (Fig. 3).1 Direct surgical haemostasis Severe pelvic fractures have often associated intraabdominal solid organ injuries such as liver (10%) or spleen (6%) and rarely bleeding from largebore vessels.1 After initial four-quadrant packing and pelvic packing for severe pelvic injuries, temporary infradiaphragmatic aortic occlusion or balloon catheter tamponade may be necessary for completion of haemorrhage control. Intraabdominal or pelvic vascular injuries can be managed by simple lateral repair whereas end-to-end anastomosis or graft interposition is time consuming. As a damage control procedure the internal iliac artery can be ligated. However, ligation of the aorta, vena cava, common or external iliac artery or veins often precipitates significant ischaemia with a high mortality and should be reserved only for desperate situations. An alternative to ligation may be the rapid placement of temporary arterial or venous shunts to preserve the leg.16 Blood loss through vascular injuries in open fractures or traumatic haemipelvectomy should be stopped by manual compression followed by tamponade, clamping and ligation (Fig. 4). Techniques to control liver bleeding during damage control include perihepatic packing after Pringle manoeuvre, direct ligation of bleeding vessels, hepatorrhaphy, cauterisation, topical haemostatic agents, partial resection or hepatic artery
Figure 3 (a) Plain film of the pelvis of a haemodynamically unstable boy after a rollover injury with a sacroiliac dislocation on the right side, a sacroiliac fracture dislocation on the left side, symphysis dislocation and rami fractures of the left side and associated injuries of the external iliac artery, rectum, bladder and ureter as well as a Morel–Lavalle lesion. (b) Postoperative plain film of the pelvis after anterior iliosacral and symphysis cerclages and pelvic packing. (c) Intraoperative status of the open abdomen with a zipper after laparotomy with packing, colostomy, and repair of left ureter, iliac vascular repair and fasciotomy of the leg. (d) Open abdomen with abdominal V.A.C.& and colostomy after second look. (e) Second look with de´bridement of the Morel-Lavalle´ lesion and status after decompressive fasciotomy of the leg. (f) Plain film of the pelvis after disarticulation of the left hip because of ischemia-reperfusion damage with muscle and skin necrosis of the left leg. (g) Plain film of the pelvis after surgical hemipelvectomy 8 weeks after injury. (h) Situs 9 months after injury with healed abdominal wall and colostomy.
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Figure 4 (a) Plain film of the pelvis of a haemodynamically unstable patient after a motorcycle accident with a traumatic haemipelvectomy on the left side. (b) Radiograph of amputated leg and hemipelvis. (c) Intraoperative status after packing and clamping of iliac arteries and veins.
ligation.4,7,8 Splenic injuries require mostly an immediate splenectomy, whereas splenorrhaphy or partial resection should be reserved for haemodynamically stable patients.4,7,8 In the presence of diffuse retroperitoneal bleeding renal injury should be excluded by exploration. Severe renal injury in the exsanguinating patient is best dealt with by nephrectomy if a contralateral kidney is palpable, alternatively retroperitoneal packing is carried out primarly.
Transcatheter arterial embolisation Transcatheter arterial embolisation to control haemorrhage in patients with severe pelvic ring fractures is recommended in some trauma centres.13,14 However, several dangerous complications and a mortality up to 50% are reported.10,17 In addition, the technique is time consuming and simultaneous treatment of associated injuries is inhibited.10 Data from different studies describing patients undergoing pelvic packing, respectively,
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Figure 5 (a) Plain film of the pelvis of a haemodynamically unstable patient after a fall from a great height with an open iliac wing fracture. (b) Intraoperative status after packing and de´bridement of the open fracture. (c) Intraoperative angiography and transcatheter embolisation of the active bleeding of superior gluteal artery. (d) Plain film of the pelvis 8 months after injury and several second-look operations with aggressive de´bridement showing extended ectopic ossification.
and embolisation are not comparable. Studies with patients who underwent crash or emergency laparotomy and pelvic packing always represent patients ‘in extremis’ or ‘transient responders’, whereas patients with embolisation are haemodynamically more stable.2,3,10,13,14,17 However, angiographic arterial embolisation can be helpful in patients with ongoing haemorrhage after damage control laparotomy and pelvic packing or repacking at the first ‘second-look’ operation or in those patients who can be haemodynamically stabilised with volume replacement. This technique is not only practicable in angiographic interventional facilities but also intraoperatively e.g. to embolise selectively the superior gluteal artery in patients with severe pelvic ring fractures (Fig. 5).
Control of contamination Severe pelvic fractures are also accompanied by hollow viscus injuries, small bowel in 9% and colon or rectum in 4%.1 These injuries must be controlled with clamps, staples, suturing, or resection without anastomosis.4,7,8 Very seldom injuries of the pancreas in patients with pelvic fractures (0.4%) should be primarily managed by drains and packing.1,4,7,8 Urethra and bladder injuries of patients with severe pelvic fractures are common (15%) and are managed temporarily with suprapubic catheter drainage and/or repair.1,4,7,8 After control of haemorrhage, contamination and definitive packing a decision for rapid skin closure (Fig. 2) or primary installation of a zipper (Fig. 3) must be made according to the physiologic parameters
ARTICLE IN PRESS 342 (hypothermia, coagulopathy, acidosis), visceral oedema and cardiopulmonary parameters.7,18,19
Decompression of compartment syndromes The disruption of the retroperitoneal muscle compartments after severe pelvic ring injuries can lead to uncontrolled haemorrhage especially from on-going coagulopathy with the risk of abdominal compartment syndrome (ACS) or pelvic compartment syndrome.2,18 In addition, following crystalloid resuscitation and prolonged laparotomy progressive and sustained oedema and distension of the bowel in combination with the insertion of abdominal packs increases the volume and may lead to an increase in the intraabdominal pressure (IAP) following the closure of the abdominal fascia. The indication for abdominal decompression in situations without primary laparotomy or after closure of the damage control laparotomy depends on the renal, respiratory and cardiac dysfunctions to raised IAP, measured by the bladder pressure (Fig. 2).18 The development of oliguria/anuria, high airway pressures, inadequate oxygenation or a bladder pressure of 425 mmHg are indications for decompression of the abdomen. As prevention of ACS the abdomen should be not closed after life saving or damage control laparotomies.18 The abdomen can be closed temporarily with a zipper (Fig. 3). Following stabilisation of coagulation the vacuum-assisted closure (V.A.C.) technique (Fig. 3) is recommended because it facilitates the subsequent definitive abdominal wall closure (Fig. 3).19 The risk for pelvic compartment syndromes such as iliopsoas, gluteus maximus or gluteus medius are very low after pelvic ring injuries because of the trauma-induced decompression of the fascia through the dislocated iliac wing fractures. However, severe contusions, haematoma or distended skin on the lateral side or the buttock area after closed pelvic ring fractures are suspicious for the development of a pelvic compartment syndrome. If in doubt, surgical decompression of these muscle compartments is mandatory to prevent muscle necrosis with crush syndrome, skin necrosis and secondary infections (Fig. 3). In addition, preventative decompression of the muscle compartments of the leg should be done in patients with pelvic ring fractures and associated iliac or femoral vascular injuries (Fig. 3). The incision should be chosen according to the approaches for the acute or definitive osteosynthesis. The soft tissue defects can be closed temporarily by textile tamponades or synthetic skin substitue (Epigard&) and in patients with a compensated coagulation system by V.A.C.& dressings.20 Secondary wound closure or skin graft-
M. Keel, O. Trentz ing should be done after second-look operations and the certainty that the extremity will survive. However, extended muscle necrosis especially after vascular injuries is complicated by crush syndrome and septic posttraumatic courses with multipleorgan failure. Disarticulation in the hip or surgical hemipelvectomy can represent the final life-saving solution (limb for life!) (Fig. 3). The decision for these mutilating procedures should be made during the second-look operations to avoid exacerbating the posttraumatic course.
De ´bridement of soft tissue injuries Extended soft tissue injuries of the pelvis were described by Morel–Lavalle´. These pelvic de´collements result from crush and shearing mechanisms and are characterised by a degloving of the subcutaneous fat from the pelvic fascia (Fig. 3). An aggressive de ´bridement with resection of avital soft tissue reduces local septic complications. In the same manner open pelvic fractures should be managed with an complete resection of necrotic tissues and extended irrigation to minimise the risk of infections (Fig. 5). In situations with diffuse persistent bleeding after de´bridement, textile tamponades can be placed temporarily (Fig. 5), otherwise V.A.C.& can be applied.20
Temporary or definitive pelvic ring osteosynthesis The damage control concept for pelvic ring injuries does not exclusively include pelvic C-clamp or external fixators for the stabilisation of the pelvic ring. For iliac fractures or transiliac fracture dislocations as well as symphysis disruptions, primary open reduction, mostly through the transabdominal approach, and internal fixation of the iliac wing, iliosacral joint or the symphysis with plates or screws and cerclages (Fig. 3) represent a perfect method as abutment for pelvic packing to control the haemorrhage. In addition, internal fixation has shown a superior stability in comparison with external fixation in several biomechanical studies. However, open reduction and internal fixation is time-consuming and imprecise reduction of the iliosacral joint or the symphysis can render the definitive reduction and osteosynthesis of associated posterior pelvic ring injuries, especially sacral fractures and acetabular fractures, more difficult.
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Figure 6 (a) Plain film of the pelvis of a haemodynamically stable young lady with a transforaminal sacral fracture and anterior iliosacral dislocation, both colum acetabular fracture and rami fractures on the left side of the pelvis. (b) Postoperative film of the pelvis after anterior iliosacral plating, placement of transiliosacral screw and plating of the acetabulum through an ilioinguinal approach, operated 1 week after accident because of associated head and thoracic injuries.
Staged sequential procedures The concept of damage control can be described as staged sequential procedures.4 Following the abbreviated damage control surgery the patient is moved to the intensive care unit (ICU), where ongoing core rewarming, correction of coagulopathy, fluid resusciation and optimisation of haemodynamic status with correction of the acidosis and reexamination of the patient ‘tertiary survey’ to diagnose missed injuries are carried out. Endpoints include a core temperature 435 1C, normalisation of the prothrombin time, and a systemic lactate level o2.5 mmol/L within 12 h. Additionally, an array of supportive therapies or diagnostic tools (measurement of bladder pressure) are established to avoid secondary hits such as septic complications, ischaemia-reperfusion injuries, ACS and organ damage.4,6 When normal physiology has been restored, ‘second-look’ operations with removal of pelvic or abdominal packing, reconstruction of the digestive tract, colostomy formation can be undertaken usually within 24–72 h after trauma (Fig. 1). Recurrent or persistent bleeding (more than 10 units of packed red blood cells in the early postoperative period) will necessitate immediate repacking or angiographic embolisation. Concerning definitive pelvic or other fracture fixations there is a ‘window of opportunity’ between days 4 and 10 after trauma (scheduled definitive surgery).4,6 Secondary reconstructive surgery after severe pelvic injuries includes abdominal wall reconstruction, anastomosis after
colostomy or secondary hip prosthesis and is recommended after recovering from the status of immunosuppression, respectively, from the catabolic metabolism (X4 weeks) (Fig. 1).4,6
Early total care or delayed definitive surgery During early total care of pelvic ring fractures such as plating of the symphysis in cases with isolated symphysis dislocation, intraoperative problems can arise or unexpected associated injuries are found. In addition, inability to achieve haemostasis due to coagulopathy, inaccessible major venous injury, time-consuming procedures in a patient with suboptimal response to resuscitation, reassessment of intraabdominal contents and inability to reapproximate abdominal fascia due to visceral oedema are reasons for turning to the damage control concept as a ‘bail-out’ procedure.4 Furthermore, ancillary issues indicating benefits of damage control or of delayed definitive surgery in haemodynamically stable patients (Fig. 6) with pelvic ring fractures are limited resources, limited experience of the surgical team in complex injuries, or a fatigued and overwhelmed surgical team (Fig. 1). However, selecting damage control too carelessly may mean an unnecessarily premature termination of surgery in patients who would otherwise have recovered from a single definitive procedure.
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References 1. Demetriades D, Karaiskakis M, Toutouzas K, Alo K, Velmahos G, Chan L. Pelvic fractures: epidemiology and predictors of associated abdominal injuries and outcomes. J Am Coll Surg 2002;195:1–10. 2. Ertel W, Eid K, Keel M, Trentz O. Therapeutical strategies and outcome of polytraumatized patients with pelvic injuries—a six-year experience. Eur J Trauma 2000;6:14–7. 3. Ertel W, Keel M, Eid K, Platz A, Trentz O. Control of severe hemorrhage using C-clamp and pelvic packing in multiply injured patients with pelvic ring disruption. J Orthop Trauma 2001;15:468–74. 4. Keel M, Labler L, Trentz O. ‘‘Damage control’’ in severely injured patients. Why, when, and how? Eur J Trauma 2005; 31:212–21. 5. Rotondo MF, Schwab W, McGonigal MD, Phillips 3rd GR, Furchteman TM, Kauder DR, et al. ‘‘Damage control’’: an approach for improved survival in exsanguinating penetrating abdominal injury. J Trauma 1993;35:375–82. 6. Keel M, Trentz O. Pathophysiology of polytrauma: a review. Injury 2005;36:691–709. 7. Moore EE. Staged laparotomy for the hypothermia, acidosis, and coagulopathy syndrome. Am J Surg 1996;172:405–10. 8. Shapiro MB, Jenkins DH, Schwab CW, Rotondo MF. Damage control: collective review. J Trauma 2000;49:969–78. 9. Pape H-C, Giannoudis PV, Krettek C, Trentz O. Timing of fixation of major fractures in blunt polytrauma: role of conventional indicators in clinical decision making. J Orthop Trauma 2005;19:551–62. 10. Ga ¨nsslen A, Giannoudis P, Pape H-C. Hemorrhage in pelvic fracture: who needs angiography? Curr Opin Crit Care 2003; 9:515–23. 11. Advanced Trauma Life Support for DoctorsATLS. Instructor course manual. Chicago: American College of Surgeons; 1997.
M. Keel, O. Trentz 12. Ruchholtz S, Waydhas C, Pehle B, Taeger G, Ku ¨hne C, NastKolb D. Free abdominal fluid on ultrasound in unstable pelvic ring fracture: Is laparotomy always necessary? J Trauma 2004;57:278–86. 13. Velmahos GC, Toutouzas KG, Vassiliu P, Sarkisyan G, Chan LS, Hanks SH, et al. A prospective study on the safety and efficacy of angiographic embolization for pelvic and visceral injuries. J Trauma 2002;52:303–8. 14. Hagiwara A, Murata A, Matsuda T, Matsuda H, Shimazaki S. The usefulness of transcatheter arterial embolization for patients with blunt polytrauma showing transient response to fluid resuscitation. J Trauma 2003;57:271–7. 15. Ganz R, Krushell R, Jakob R, Kuffer J. The antishock pelvic clamp. Clin Orthop Relat Res 1991;267:71–8. 16. Reber PU, Patel AG, Sapio NL, Ris HB, Beck M, Kniemeyer HW. Selecitve use of temporary intravascular shunts in coincident vascular and orthopedic upper and lower limb trauma. J Trauma 1999;47:72–6. 17. Cook RE, Keating JF, Gillespie I. The role of angiography in the management of haemorrhage from major fractures of the pelvis. J Bone Joint Surg [Br] 2002; 84-B:178–82. 18. Ertel W, Oberholzer A, Platz A, Stocker R, Trentz O. Incidence and clinical pattern of the abdominal compartment syndrome after ‘‘damage control’’-laparotomy in 311 patients with severe abdominal and/or pelvic trauma. Crit Care Med 2000;28:1747–53. 19. Miller PR, Meredith JW, Johnson JC, Chang MC. Prospecitve evaluation of vacuum-assisted fascial closure after open abdomen. Planned ventral hernia rate is substantially reduced. Ann Surg 2004;239:608–16. 20. Labler L, Keel M, Trentz O. Vacuum-assisted closure (V.A.C.s) for temporary soft tissue coverage in type III open fracture of lower extremities. Eur J Trauma 2004;5: 305–12.
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www.elsevier.com/locate/cuor
MINI-SYMPOSIUM: PELVIC FRACTURES
(iii) Management of open pelvic fractures$ Efstathios Katsoulis, Emmanuel Drakoulakis, Peter V. Giannoudis Department of Trauma & Orthopaedics, St James’s University Hospital, Beckett Street, Leeds LS9 7TF, UK
KEYWORDS Open pelvic fractures; Pelvic ring injury; Management; Outcome; Mortality
Summary Open pelvic fractures are potentially devastating injuries. Although rare, they are frequently associated with other system injuries. Their early, aggressive and multidisciplinary management has contributed over the years to reduced mortality rates. This review article is focused in the current concepts of the management of these fractures and their outcome. & 2005 Elsevier Ltd. All rights reserved.
Introduction Pelvic fractures account for approximately 3% of all skeletal fractures and their associated mortality ranges from 10% to 16%.1–5 They range from lowenergy stable fractures to high-energy unstable ones and they can be classified as closed and open (2–4% of all pelvic fractures in adults).1,6–10 In children, the bone, cartilage and joints of the pelvis are more pliant and they can provide a significant buffer for energy absorption. The fractures are more frequently sustained at the chondro-osseous interface than on the bony parts of the pelvis (50% of the osseous pelvic ring fractures in children are ramus fractures with most of them being unilateral and primarily involving the superior ramus).11 $
No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. No funds were received in support of this study. Corresponding author. Tel.: +44 113 20 66460; fax: +44 113 20 65156. E-mail address:
[email protected] (P.V. Giannoudis).
By definition, an open pelvic fracture is a fracture that communicates with the rectum, vagina or the environment through a break in the skin. They usually result from a high-energy trauma from either direct or transmitted forces.12 The adult patients are usually males involved in road traffic accidents.1,8 Falls, crush injuries and penetrating trauma are less frequent causes.8,13 Classifications describing the variety of pelvic fractures patterns include the original Pennal classification modified by Tile in 198814 and the Young–Burgess classification.15 Recently, one comprehensive classification by Bircher and Hargrove (awaiting validation) was proposed for the classification of open pelvic injury patterns.16 The mortality rate following open pelvic fractures was as high as 50% in the 1970s and 1980s, being then significantly higher than the 10–15% mortality of closed pelvic fractures.9,10,17,18 In the early 1990s, there was an improvement in the management of these injuries and the mortality dropped to 25–30%, although some authors described mortality rates as low as 5%.6,19
0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2005.06.008
ARTICLE IN PRESS 346 Several factors have been shown to influence mortality including age, injury severity score (ISS), pelvic instability, size and status of the wound, presence of rectal injury, number of blood units transfused and other associated injuries.1,7–10,20–22 The overall ISS in open pelvic fractures ranges from 25 to 48.1,6–8,20,23–25 Only one direct comparison of the ISS in open and closed pelvic fractures is available in the literature and no significant difference was found.1 The overall improvement of the mortality in open pelvic fractures could be attributed to the advances made in modern critical care medicine, the implementation of early multidisciplinary protocols, the aggressive fracture stabilization and selective faecal diversion.
Emergency management The initial assessment and management of these patients should be carried out according to the ATLS protocol26 with special attention to be given to the haemodynamic parameters (Fig. 1). The resuscitation should be aggressive, with intravenous fluids, blood products and clotting factors.27 Brenneman et al. reported that in open pelvic fractures (because of the loss of tamponade effect) patients need four times more blood during the first 24 h than in the closed ones.1,7 If possible, a swab and a photograph of the wounds should be taken initially and a sterile pressure dressing with antiseptic solution should be applied in order to reduce the blood loss, primarily, and the risk of infection.1 Before radiological assessment, two steps will guide further management28:
The haemodynamic status of the patient. A single bimanual compression-distraction of the pelvis should assess the mechanical instability.
An anteroposterior plain radiograph will help identify the fracture pattern and the stability of it.26,29 In case of a haemodynamically unstable patient, an abdominal ultrasound scan or a diagnostic peritoneal lavage could contribute to the diagnosis of the source of bleeding. Because of the higher energy related to open pelvic fractures, intraabdominal injuries have a higher incidence than in closed ones.8,25,30,31 If the patient remains in an unstable haemodynamic condition and the abdominal or chest cavity have been excluded as the source of bleeding, urgent temporary stabilization of the pelvis is indicated. The venous tamponade effect can be
E. Katsoulis et al. obtained by different means, including: application of a circumferential sheet, pelvic binder, internal rotation of both legs, traction of the lower limbs, and application of an external fixator or the C-clamp.9,32–35
Assessment of osseous and ligamentous structures In most cases, the anteroposterior plain radiograph can identify the ligamento-osseous injuries and can provide information about pelvic stability. If the patient is haemodynamically stable, inlet (beam directed caudad at 601), outlet (beam directed cephalad at 451)36 and Judet (Iliac and obturator oblique) pelvic radiographs will help more with the fracture identification. As open pelvic fractures are high-energy fractures and other organs and soft tissues are involved, a computed tomography scan (CT scan) is used for the assessment of pelvis in the haemodynamically stable patients; osseous and soft tissue windows are used as well as 3D reconstruction of the pelvis.37 Extraluminal gas, haemorrhage or bowel wall thickening will help in the assessment of the intestinal injuries. Vaginal lacerations or previous diagnostic peritoneal lavage can provide false positive results and should be taken into account.38–42 Also, independently of the patient’s consciousness, it must not be neglected the assessment of all four limbs, thorax and spine is essential in order to identify any fractures that will need immobilization and could influence the decision making process. Depending on the available publications, the distribution of the type of open pelvic fractures is type B8,43 or type B and C with an equal distribution amongst them.1 The incidence of associated acetabular fractures in unstable open pelvic fractures ranges between 40% and 60%.1,24 The presence of a pelvic fracture in a child, particularly if displaced, assumes even more clinical significance. During the initial assessment of paediatric pelvic fractures, one must be more aware of the intraabdominal and intrapelvic injuries rather than the osseous injuries that are of a secondary importance.
Assessment of the soft tissue injury Two systems can be used for this assessment:
The Gustilo—Anderson classification for the extent of the soft tissue injury.44,45
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Figure 1 (a) Management of open pelvic fractures. (b) Forty-five year old female sustained an APII open pelvic fracture following a motor cycle accident. (c) Following debridement and diverting colostomy the fracture was stabilized with an external fixator.
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The site of the soft tissue injury classified as Zone 1 (perineum, anterior pubis, medial buttock, posterior sacrum), Zone 2 (medial thigh, groin crease) and Zone 3 (posterolateral buttock, iliac crest).1,46
Because of the forces applied during the accident, most of the open pelvic fractures are Gustilo type III8 and most of the wounds are situated in the perineal region, Zone 1.1,12,25 A high level of suspicion is necessary because missed injuries are not uncommon. Inspection of the soft tissues both anteriorly and posteriorly is essential.38,39,47–52 Rectal injuries Their incidence varies from 17% to 64%.6–8,23–25 They can be assessed first by inspection and secondly by digital examination (anal sphincter tone, contents of the rectal ampulla, blood on the examination glove, rectal wall weakness). Cases of assessment by sigmoidoscopy and rectoscopy had already been described and rigid sigmoidoscopy has already been suggested as a mandatory investigation.41 Urogenital tract injuries They have an incidence from 23% to 57%.6–8,23–25 Urethral and vaginal injuries are the commonest.33 Vaginal lacerations result from either penetration of a bony fragment or from indirect forces from diastasis of symphysis pubis.53 Delayed diagnosis is associated with mortality and infections.50,53 Injuries to cervix, uterus and ovaries are rare.23,54 Inspection of the external genitalia is the first action to take and then a more meticulous digital examination can reveal lacerations, blood at the external urethral meatus, a high riding prostate, perineal haematoma, haematuria and vaginal bleeding. Any of these findings or the inability to urinate in association with an anterior pelvic ring fracture should be an indication for a retrograde urethrogram52,55–57 and a cystogram should follow through an eventual suprapubic catheter if a urethral injury has been diagnosed. In this way we can assess both the urethral and bladder integrity.
Sepsis control The same principles of open fracture management of the extremities apply in the pelvis as well. A swab for microbiological examination and a photograph of the wound (for later decision-making, without re-exposure of the wound) can be taken initially, independently of the haemodynamic sta-
E. Katsoulis et al. tus of the patient. Once the patient is stable, a meticulous irrigation can be instituted and the wounds should be packed open in order to prevent the development of gas gangrene. Broad-spectrum intravenous antibiotics against aerobic and anaerobic organisms can be administrated. At a later stage, after the microbiological sensitivity testing, the antibiotics can be adjusted accordingly.9,12,58 Also, the antitetanus vaccinal status of the patient should not be neglected. The perineal wounds must be judged (because of their location) for the potential to contaminate the fracture site and/or a retroperitoneal haematoma. The presence of a rectal laceration is an absolute indication for urgent diverting colostomy (end or loop colostomy) with rectal washout. Most centres now accept that a distal loop washout is appropriate as soon as practical. Urethral injuries generally are managed conservatively, by primary realignment or suprapubic catheter insertion. In case of intraperitoneal bladder rupture, direct repair is undertaken whereas extraperitoneal bladder ruptures are often managed by urethral catheter drainage alone.Suprapubic catheters should be discouraged if surgery for anterior pelvic ring injury or acetabular fracture repair will be undertaken.
Surgical management A multidisciplinary team approach is needed as the surgical management includes wound irrigation and debridement, fracture stabilization (temporary or definitive), laparotomy for repair of any intrapelvic and or intraabdominal injury, repair of urogenital injuries and plastic surgical techniques for covering of the soft tissue defects. In cases where ongoing haemodynamic instability is encountered, pelvic packing can complement the external fixation. It is effected through a lower abdominal laparotomy, adjusted to the pelvic wound. Packs have to be inserted in the prevesical and presacral spaces and have to be removed or changed within 48 h.2,23,59 In cases of large vessel bleeding, operative control of haemorrhage should be considered. For such patients, being in extremis clinical condition, clamping of iliac vessels or distal aorta can be performed.59 The aortic clamp should be placed below the L3 level as the Radicularis Magna Artery, communicating with the Spinalis Anterior Artery, emerges from the aorta between T12 and L3 level. Another adjunct to haemorrhage control (when fracture stabilization is insufficient) is the angio-
ARTICLE IN PRESS Management of open pelvic fractures graphic embolization in cases where arterial bleeding is suspected. However, this technique is time consuming and can be performed in only approximately 10% of cases.34,59–62 The initial fracture management of the patient assuming that end points of resuscitation have been achieved will depend on the location of the soft tissue injury and the degree of contamination. The plan for the definitive stabilization should be effectuated according to the principles of ‘‘damage control orthopaedics’’.63–66 Temporary stabilization can be achieved as previously stated with either an anterior external fixator or a C-clamp.67–73 Application of an external fixator involves two to three pins inserted in each iliac crest, a simple frame is constructed and is generally turned down in order to permit the general surgeons to perform a laparotomy if needed.35,74,75 In unstable patterns, skeletal traction could supplement the external fixator in order to prevent shortening or malrotation of the hemipelvis. Definitive stabilization in closed pelvic fractures with internal fixation is recommended between the third and seventh day post-injury. In open fractures, the timing is not adequately covered and fixation techniques are controversial. Traditionally, only external fixation has been used76,77 but there are authors publishing good results after internal fixation24 or suggesting internal fixation when there is no gross contamination of the fracture site.28 In comminuted iliac wing fractures, early open internal fixation is preferred since external fixation cannot be applied.78 Combinations of internal and external fixation have been also described by Leenen et al.24 and percutaneous internal fixation has been used for open fractures with less complications.2,27,32,79–84 The surgical treatment of pelvic fracture wounds includes extensive irrigation, debridements (up to healthy tissue with capillary bleeding) and removal of foreign bodies and bony fragments. For the washout, either free flow or pulsed lavage techniques can be used. The wounds can either be left open or vacuum-sealed dressings can be used in order to drain them. A second look, with or without closure, should be done after 48–72 h.28,43,78,85–90 The possibility of a compartment syndrome associated with the above-mentioned injuries should not be neglected. The major pelvic compartments are the iliopsoas, the gluteus maximus and the gluteus medius/minimus. Measurement of their pressure is mandatory.91 Plastic surgical techniques can be undertaken in order to treat these wounds and eliminate dead spaces.12,92–94 Split or full thickness skin grafts are used as well as
349 suction drains, vacuum-sealed drainage or free flaps. Diverting colostomy (end or loop)1,43,95,96 or ileostomy with washout of residual rectal faeces7,95,96 is a widely accepted treatment for all open pelvic fractures, with rectal, vaginal and perineal wounds.10,18,19,25,31,46 Perineal wounds also require early sphincter repair.29,83 When placing the stoma, we should bear in mind the eventual location of any orthopaedic incision, suprapubic catheter and external fixator pins.46,97 With this technique, both pelvic sepsis and the related mortality are reduced1,43 although in Woods et al. study, the incidence of local infection was not necessarily reduced by the selective colostomy and he suggested that only patients with extensive soft tissue injury might benefit from it.98 The colostomy is traditionally taken down and the continuity restored 6 weeks to 3 months after the injury.99,100,101 Recently, the trend is to rely on the patient’s condition and reverse the colostomy early.95,96 But, until now there are no clinical studies available evaluating the ideal timing. The restoration of continuity has an important rate of complications and therefore awareness of the patient with regards to this issue is of paramount importance.101–104 In case of vaginal lacerations, surgical repair with absorbable sutures, in order to prevent abscess formations, is indicated.53,105 Care must be taken not to injure the uterine arteries laying along the lateral borders of the vaginal vault. Early assessment of urethral or bladder injuries is essential,106–108 as previously stated using a retrograde cysto-urethrogram. If a partial or complete tear is present, a suprapubic catheter needs to be inserted in order to ensure and measure the urinary output and prevent sepsis from infected urine.55,97,109 If possible, early realignment is considered today as the choice of treatment.110 Delayed end-to-end repair is undertaken 3 months post-trauma and generally a transperineal approach is used.73,111–114 The intraperitoneal rupture of the bladder is an emergency and has to be treated surgically.109
Complications Complications following open pelvic fractures can be classified as early and late ones. The early complications include perineal intraoperative injury (from prolonged traction against a pudental post),60,115,116 paralytic ileus, deep vein thrombosis and pulmonary embolism (2–10%),58
ARTICLE IN PRESS 350 acute respiratory distress syndrome and multiple organ failure,2,63 infection (deep sepsis has an incidence of around 2%)60 and neurological injuries as a result of the initial injury or following the surgical procedure. The overall prevalence of neurologic injury in pelvic trauma, including temporary neurological injuries, is between 10% and 15%.11 Iatrogenic neurological injuries have an overall range from 3% to 10%.60 Sacral fractures and sacroiliac joint (SIJ) disruptions have a high prevalence of neurological injuries, including avulsion of the lumbar nerve roots, avulsion of the superior gluteal nerve, femoral nerve lesion, involvement of the obturator and sciatic nerves as well as cauda equina syndrome. The incidence of neurological injuries in sacral fractures is approximately, 6% for the Zone 1, 28% for the Zone 2 and 57% for the Zone 3.11 The diagnosis and evaluation of such injuries can be helped by nerve conduction studies and electromyography. The long-term prognosis depends on the level and degree of the nerve root involved.11 Late complications include abdominal herniation, non-union/mal-union of the fractures (the incidence is around 3%, causing severe disability, complaints of constant pain, problems with sitting, leg-length discrepancy). Complex major operations are required and they are often associated with high co-morbidity. Chronic pain is present in approximately 30% of patients having had an unstable pelvic fracture. The pain is usually situated at the posterior SIJ and the lower lumbar spine. Calcification of the sacrotuberous (ST) ligament after pelvic trauma can be another source of pain.60 Non-union and residual SIJ dislocation has to be excluded before attributing the pain to a calcified ST ligament. Other complications that could present following open pelvic fractures include infections (perineal wound infection, pelvic abscess, sepsis, osteomyelitis), rectal incontinence1 and septic arthritis of the hip following rectal tear associated with pelvic fracture (rare).40
Outcome There is a lack of information in the literature regarding the long-term outcome of patients after open pelvic fracture. Assessment of patients with the SF-36 evaluation tool suggested some differences between closed and open pelvic fractures and long-term survivors require longer periods in rehabilitation.11 Brenneman et al.1 reported the outcome of 44 patients with open pelvic fractures after a 4-year follow-up. More than the half of
E. Katsoulis et al. them had chronic sequelae (urinary and faecal incontinence, impotence and dyspareunia) and slightly more than half of the employed ones returned to work. They scored worse on body pain, physical functioning and physical role scales compared to a closed pelvic fracture female group.117 Ferrera et al.7 described a good outcome in 8/15 patients and a fair outcome in 7/15 patients requiring assistance with their daily activities. Fallat et al.118 described 2/6 women with genital injuries having minor dyspareunia. In general terms, further studies are required to evaluate accurately the long-term outcome following open pelvic fractures.
Conclusion Open pelvic fractures are frequently associated with other system injuries. They require an early aggressive multidisciplinary approach in order to reduce the mortality rate and improve the outcome. Their management consists of an ‘‘early treatment phase’’ (external pelvic stabilization, pelvic packing, faecal diversion, wound/soft tissue management, urogenital injury treatment) and a ‘‘definitive treatment phase’’ (fracture stabilization according to the ‘‘damage control orthopaedic principles’’, definitive soft tissue management). Long-term complications could prevail including chronic pain, residual disability in physical functioning, incontinence, impotence, and dyspareunia.
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ARTICLE IN PRESS Current Orthopaedics (2005) 19, 354–361
www.elsevier.com/locate/cuor
MINI-SYMPOSIUM: PELVIC FRACTURES
(iv) Pelvic fractures and genitourinary injuries Jonathan Yerasimides, Craig S. Roberts Department of Orthopaedic Surgery, University of Louisville School of Medicine, 210 East Gray Street, Suite 1003, Louisville, Kentucky 40202, USA
KEYWORDS Pelvis; Fracture; Genitourinary; Urethral tears; Dyspareunia
Summary The association between pelvic fractures and genitourinary injuries, particularly bladder ruptures and posterior urethral tears, is well known. Sexual dysfunction (erectile dysfunction and dyspareunia) is also becoming a wellrecognised frequent sequela of pelvic fractures. The management of combined genitourinary injuries and pelvic fractures is controversial, as there is evidence that the acute management of urethral tears may have a profound effect on future sexual function and continence. Currently, a trend exists toward more aggressive treatment of the bony injuries, genitourinary injuries, and sexual dysfunction with the hope of improving overall long-term functional outcomes. & 2005 Elsevier Ltd. All rights reserved.
Introduction Although the association between pelvic fractures and genitourinary injuries is well known,1–6 there is increased recognition in the medical community of the morbidity of concomitant urogenital injury and its deleterious effects on sexual function. Harwood et al.7 reported that 42% of patients with a urethral injury had sexual dysfunction. Less common consequences of pelvic fractures include vaginal lacerations in women and erectile dysfunction from damage to the autonomic cavernosal supply in men.8,9 The management of concomitant pelvic fractures and genitourinary injuries is controversial. We present an overview of the anatomy,
Corresponding author. Tel.: +1 502 852 6964; fax: +1 502 852 7227. E-mail addresses:
[email protected] (J. Yerasimides),
[email protected] (C.S. Roberts).
diagnosis, and treatment of genitourinary injuries associated with pelvic fractures.
Anatomy The close proximity of the bladder, prostate, and urethra within the pelvic ring make these structures highly susceptible to injury when fractures occur to the bony pelvis. The bladder is an extraperitoneal sac that lies anterior and inferior to the peritoneal cavity and posterior to the pubic symphysis. In children, the bladder is an abdominal organ that lies above the pubic symphysis and does not fall into its adult position below the symphysis until about the sixth year of life.2 The empty bladder is rarely superior to the symphysis pubis in the adult, but as it fills with urine, it ascends into the abdominal cavity along the anterior abdominal wall. The urethral orifice in the most inferior portion of the bladder marks the neck. In men,
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ARTICLE IN PRESS Pelvic fractures and genitourinary injuries the neck is contiguous with the prostate which makes the urethra more vulnerable because the dense puboprostatic ligaments firmly fix the prostate (and therefore urethra) to the posterior surface of the symphysis pubis. Diastasis of the pubic symphysis has been reported to be associated with impaired sexual potency.7 In women, the bladder is directly attached to the pubic symphysis by the pubovesical ligaments.2 Because the female urethra is short and mobile compared to the long, well-fixed male urethra, it is injured less frequently that the male urethra. Support to the urethra is provided by the pelvic floor inferiorly and the rectum posteriorly. With the exception of the fixed bladder neck, the bladder is free to move. The superior portion, or dome, is the weakest and least supported portion of the bladder.2,10 The prostate divides the male urethra into anterior and posterior portions. The posterior portion is comprised of the prostatic and membranous segments and is the most commonly injured region. The prostatic segment is approximately 3 cm in length and lies between the bladder neck and verumontanum. The membranous segment is the portion of the urethra that traverses the urogenital diaphragm. It is firmly fixed and averages 2.0–2.5 cm in length.2 The urogenital diaphragm has traditionally been considered a separate anatomic structure consisting of two fascial layers with a thick layer of skeletal muscle in between these layers. However, anatomic and radiographic studies in cadavers by Colapinto and McCallum11 refuted this concept by demonstrating that the prostate and urogenital diaphragm are a single unit. In their investigation, the muscle in the urogenital diaphragm was shown to be contiguous with the substance of the prostate gland. These enveloping fibres formed the voluntary sphincter of the urethra. These authors found that the prostate, membranous urethra, and urogenital diaphragm worked as a fixed single unit during traumatic urethral avulsion. The weakest point was the inferior surface of the urogenital diaphragm or the bulbomembranous urethral junction, and not the prostatomembranous junction as was previously believed.11 This finding was supported by radiographic evidence of contrast extravasation into the perineum in patients with complete urethral disruption. Contrast would be expected to be contained in the pelvis if the urogenital diaphragm was intact.11,12
Mechanism of genitourinary injury The most common injuries to the lower urinary tract associated with pelvic fractures are bladder
355 rupture and urethral disruption as a result of motor vehicle collisions, an automobile striking a pedestrian, a fall from a significant height, and motorcycle collisions.6 Malgaigne’s fracture has been shown in multiple studies to be the predominant type of pelvic fracture associated with urethral injury.5,13,14 Bladder injury can occur in either the extraperitoneal or intraperitoneal regions; both regions are rarely injured simultaneously. Classically, intraperitoneal injury consists of a large, horizontal tear in the bladder dome which occurs as a result of a force applied to the abdomen or symphyseal region associated with a full bladder. The intravesical and intra-abdominal pressure becomes acutely elevated and the bladder ruptures at its weakest point in the dome. This can occur without associated pelvic ring disruption as a result of a seatbelt injury in a motor vehicle accident.12 The incidence of extraperitoneal rupture is approximately 85% and most commonly involves the anterolateral wall near the neck.2,10 Extraperitoneal bladder rupture classically occurs from direct penetration by a sharp, bony spicule.15 In contrast, intraperitoneal ruptures occur 15% of the time. Nonetheless, there have been previously published reports disputing this classic concept. Carroll and McAninch16 noted only 35% of bladder injuries occurred on the same side as the pelvic fracture. This was corroborated by Cass and Luxenberg who proposed that severe lower abdominal trauma caused a rupture of the empty bladder similar to the known mechanism of intraperitoneal rupture.17 The incidence of injury to the male urethra associated with pelvic fractures ranges from 1.4% to 11%.2 Urethral injury in females is uncommon because of the relative mobility of the untethered urethra. The most common fracture pattern is an anterior ring disruption, especially with posterior involvement, such as Malgaigne’s fracture.5 The main mechanism is a shearing force against the points of fixation of the urethra. When a fracture of the pelvis occurs, either the symphysis is mobilsed or the pelvic contents are compressed. In the former, the prostate is displaced with the symphysis, stretching the urethra. In some cases the displacement is not significant enough to cause complete disruption and a partial tear occurs. When the pelvic contents are significantly compressed, such as in a lateral compression fracture, the prostate is forced upwards, tearing the puboprostatic ligaments and subsequently the urethra.5 The disruption occurs at the inferior portion of the membranous urethra, or the bulbomembranous junction. Radiographically,
ARTICLE IN PRESS 356 displacement of the pubic ramus relative to the ischium produces the classic urethral disruption.3 Giannoudis et al.7 noted that damage to the delicate vascular structures and nerves to the genitalia can occur after fracture of the pelvis even in the absence of urological injury. Neurological injury usually involves the lumbosacral plexus. There is a lack of consensus about the precise vascular injury that can cause sexual dysfunction. Sharlip18 reported impotence in three patients in whom obliteration of both of the internal pudendal arteries occurred at the level of the urogenital diaphragm. Levine et al.19 investigated impotent patients and reported that all who had sustained a fracture had also suffered injury to the posterior urethra. These authors identified vascular lesions in both hypogastric-cavernous beds in all patients, and lesions of the pudendal or common penile arteries in 90% of patients with a fracture. Munarriz et al.20 reported that 80% of patients who had sustained trauma to the pelvis had an abnormality of venous outflow, and 70% had an abnormality of venous occlusion. Angiography most frequently detected abnormalities in the common penile and cavernous arteries. These investigators found pure arterial damage in 30% of patients. Others have stated that erectile dysfunction is unlikely to be caused by venous abnormalities, but probably represents inadequate smooth muscle function as a result of arterial or neural damage.7,21
Diagnosis There should be a heightened suspicion of urologic injury in any patient presenting with a pelvic ring injury. The classic clinical signs of urologic injury are blood at the urethral meatus, inability to void despite the sensation of a full bladder, and a high riding or ‘absent’ prostate on rectal examination.2–4 Blood and/or urine extravasate into the perineum producing the classic perineal butterfly hematoma is diagnostic of urethral injury. If a urologic injury is suspected by initial clinical assessment, the Foley catheter should be placed by a urologist because of the significant risk of completing a partial tear or contaminating a retroperitoneal haematoma.2–4 A retrograde urethrogram should be performed first to assess the integrity of the urethra. This is usually performed with 30–40 ml of a water-soluble contrast medium which is gently instilled into the urethra. A film is obtained as the last 10 ml is instilled.2 Spirnak described a simple technique in which the tip of a 14-Fr or 16-Fr Foley catheter was inserted in the
J. Yerasimides, C.S. Roberts urethral meatus and advanced enough to inflate the balloon with several milliliters of saline.2 A syringe was used to administer the contrast medium through the catheter. If the urethra was normal, the balloon was deflated and the catheter advanced into the bladder where a cystogram could be performed. When the posterior urethra is disrupted, the contrast medium can be seen extravasating into the perineum or above the urogenital diaphragm. Historically, a urethrogram in the presence of a urethral injury demonstrated spread of contrast material above the urogenital diaphragm. A review of 100 cases by Sandler et al. supported Colapinto and McCallum’s earlier studies that showed that the disrupted urethra occurred at the inferior border of the urogenital diaphragm.11,22 Sandler and associates demonstrated predominant extravasation into the perineum, indicative of a tear located below the level of the urogenital diaphragm. Following retrograde urethrogram, the integrity of the bladder should be assessed. If the urethra is intact, the cystogram is performed retrograde through the urinary catheter. To avoid a falsenegative result, the bladder must be overdistended to assure sufficient filling. Weyrauch and Peterfy experimentally demonstrated in dogs that bladder incisions as large as 2 cm could be missed if the bladder was not sufficiently distended.23 In the adult, 300–500 ml of contrast medium is administered with gravity and films are taken. A complete bladder study includes anteroposterior, oblique, lateral, and post-drainage films.2 Post-drainage films are important because some bladder wall defects can be obscured by a fully contrast filled bladder. When the contrast is emptied from the bladder, residual extravasated medium can be seen. Cystographic findings of an extraperitoneal bladder rupture are a teardrop-shaped bladder and extravasation of contrast confined to the pelvis. It is easily contrasted to the intraperitoneal rupture where the contrast medium fills the peritoneal cavity with no distinct pattern.2
Treatment of urologic injuries The treatment of patients with combined urologic and pelvic fractures requires coordination between orthopaedic, urologic, and general surgeons. Abdominal organ injury occurs in 50% of patients with pelvic and urologic injury.3 These patients may require exploratory laparotomy at which time orthopaedic and urologic pathology can be
ARTICLE IN PRESS Pelvic fractures and genitourinary injuries addressed if the patient is stable. Many orthopaedic surgeons fear contamination from combined orthopaedic and urologic procedures. Routt et al.1 reported the results of a protocol in which 23 patients with unstable pelvic fractures with associated urologic injuries were treated with open reduction and internal fixation of the anterior pelvic ring injury using the same anesthetic and surgical exposure as the urethral realignment or bladder repair. Only one of 23 cases (4%) was complicated by late, deep infection. Zingg et al.24 also reported that infection occurred in only one of 10 patients treated with simultaneous urologic repair and open reduction and internal fixation of pelvic ring injuries. Intraperitoneal bladder perforation requires surgical exploration, repair, and placement of a suprapubic catheter.2,3,25 Symphyseal plating can be done under the same anaesthetic and appears to have an acceptable risk of infection when performed within 48 h of placement of the suprapubic catheter.1 Beyond this point, alternative methods such as external fixation should be considered. Prior to the 1970s, extraperitoneal bladder rupture was considered an injury that required surgical treatment. Currently, if patients with extraperitoneal bladder rupture are undergoing exploratory laparotomy for abdominal injuries, the bladder should be addressed at the same sitting. All other patients should be managed nonoperatively unless a bony spicule perforating the bladder is suspected.2 Non-operative management requires urinary catheter placement and close observation. Broad spectrum antibiotics are given and a cystogram performed 7–10 days prior to catheter removal. Most ruptures heal by 10 days, and virtually all heal by 3 weeks with non-operative management.2,3 Urethral tears are classified as complete or partial (35%). The incidence rate of these injuries is approximately 65%. The treatment of partial urethral injuries is relatively straightforward, as most are managed with a urinary catheter placed by a urologist. If the catheter cannot be advanced across the partial tear easily, a suprapubic cystostomy tube is placed to divert urine. The catheter is maintained for 2–3 weeks before radiographic evidence of healing is confirmed. A retrograde urethrogram is performed in patients managed with a urinary catheters. A voiding cystourethrogram is performed in patients who have a cystostomy tube. The catheter is removed when the urethra is healed.2 Management of complete urethral disruption is controversial. There are three main treatment options: immediate surgical exploration and realignment over a urinary catheter, primary urethro-
357 plasty, and suprapubic cystostomy drainage with delayed urethroplasty.1–4 One of the most frequently cited studies is that of Webster and associates who reviewed more than 300 patients from 15 reported series in order to determine the incidence of complications associated with each treatment option.2,26 Of the patients who underwent primary realignment, 69% developed strictures, 44% had impotence, and 20% were incontinent. Those with suprapubic cystotomy and delayed reconstruction showed a decreased incidence of impotence (11.6%) and incontinence (1.7%), but had a urethral stricture rate of 100%. Routt et al.1 reported that urologic complications occurred in 30% of their patients treated with primary urologic repair at the same sitting as the orthopaedic fixation. These authors also reported that urethral stricture was present in 44% and impotence in 16.7%. The complications of impotence, stricture, and incontinence are not necessarily complications, but consequences of these severe injuries. Harwood et al.7 noted that primary suturing of urethral injuries was associated with high rates of incontinence and impotence at followup. Urethral realignment fell out of favour in the early 1970s. Currently, urologic reconstruction in the face of pelvic fracture remains an area of interest and development. Acute management of urethral injury uses early suprapubic catherisation. It has been noted that early urethral realignment is an alternative to suprapubic catheterisation if the patient is stable and institutional expertise is available.7 The ultimate goal of early and more aggressive treatment of urethral injury is the improved outcomes and genitourinary function at follow-up. Treatment involves urinary diversion either through a suprapubic catheter if there is a leak on the urethrogram, or a urethral catheter if no leak is found. Repair of the urethra when necessary is most commonly not performed acutely, but rather is done on a delayed basis.7 Routt et al.1 presented an alternative approach with combined early repair of the urethral injury and symphyseal disruption in a series of 28 patients; however, strictures and impotence were relatively frequent complications. With new techniques involving fluoroscopic and endoscopic guidance, primary realignment techniques can be performed with delayed reconstruction. Simultaneous antegrade and retrograde urethroscopy can be used to pass urethral catheters with a reduced risk of iatrogenic injury to the periurethral tissues.7 Catheters remain in place for 6–8 weeks, at which time a repeat urethrogram is performed to assess stricture formation and the need for delayed reconstruction.
ARTICLE IN PRESS 358
J. Yerasimides, C.S. Roberts
In summary, we propose a simple algorithm for the workup and management of suspected urologic injury in association with a pelvic fracture (Fig. 1). The main decision point after a retrograde urethrogram/cystogram is the diagnosis of either a urethral injury or a bladder injury. If it is determined that the urethra is injured, the next decision point is between a partial tear and a complete tear. If it is determined that the bladder is injured, the main decision point is between an extraperitoneal injury and an intraperitoneal injury.
Sexual dysfunction in males after pelvic fracture Patients are often reluctant to discuss sexual dysfunction after pelvic injuries, and will only do
so when the clinician questions them directly during a follow-up evaluation. The clinician needs to gather information about the temporal relationship between the pelvic ring injury and the sexual dysfunction, role of medications, diabetes, neurologic disease, vascular disease, and basic psychological profile. If the patient relates nocturnal or early morning erections, serious underlying organic pathology is thought to be unlikely, and the case is more likely to be psychogenic.27 King28 reported sexual impotence in 16 (20%) of 90 male patients which was more likely to be associated with a urethral injury. Ellison et al.29 reported on a series of 42 men with pelvic fractures and noted that at 20-month follow-up, persistent impotence was associated with vasculogeneic trauma. Mark et al.30 reported that 57 of 92 (62%) patients who had undergone delayed perineal repair following a pelvic fracture and urethral
Displaced pelvic fracture with suspected urologic injury
Retrograde urethrogram/cystogram
Urethral injury
Partial tear
Urinary catheter
Bladder injury
Complete tear
Suprapubic catheter
Extraperitoneal
Intraperitoneal
Urinary catheter
Surgical repair
Primary realignment with combined retrograde/antegrade urethroscopy
6 to 8 weeks Urethrogram Stricture
Delayed reconstruction
No Stricture
Monitoring for stricture
Figure 1 A proposed algorithm for the diagnosis and management of suspected urologic injury in association with a displaced pelvic fracture.
ARTICLE IN PRESS Pelvic fractures and genitourinary injuries injury remained impotent in the long term with a median follow-up of 4 years. The pattern of the pelvic ring injury appears to affect the prognosis. Bellabarba et al.31 reported on the outcome of an uncommon variant of the anterior-posterior compression injury in which the posterior ring injury was a midline sagittal sacral fracture extending into the spinal canal. In their series of 10 patients followed an average of 31 months, there were no objective neurologic findings that could be attributed to sacral nerve root injury. Three patients had sexual dysfunction at final follow-up, but none had evidence of sacral root/plexus injury secondary to the fracture. One additional patient who sustained a urethral tear required a chronic suprapubic catheter because of a stricture. Six patients, including one who required a repair of a retroperitoneal bladder tear, had no urogenital sequelae. The authors concluded this Denis Zone III variant had a lower incidence of associated neurologic deficits (450%), particularly compared to those reported in patients with transverse zone III sacral fractures. The midline sagittal fracture variant and simultaneous lateral displacement of both bony and neural elements through the midline may have protected the sacral nerve roots and plexi from injury. Harwood et al.7 suggested an algorithm for management of post-traumatic erectile dysfunction. If appropriate basic screening tests show no underlying primary pathology, initial management should consist of pharmacologic agents. Phosphodiesterase inhibitors, such as Sildenafil Citrate or Viagra (Pfizer, New York, NY), have been successful in treating erectile dysfunction. The drug acts by inhibiting phosphodiesterase type 5 to facilitate normal erection in men with normal neurovascular status. Therefore, only men with intact nerve and vascular status will respond to this treatment. Patients who fail oral agents can be tried on intracavernosal injections. The most commonly used agent is prostaglandin E1, which is injected directly into the corpora cavernosa to induce erection. It acts as a smooth muscle relaxant and has generally good results although some patients report penile pain or prolonged erection. Again, this treatment will be ineffective in those with neurologic damage. Failure of oral and injectible agents should be followed with further investigations such as Doppler scanning and arteriography. Treatment options beyond this point usually revolve around mechanical prostheses or vacuum devices. Micro-surgical revascularisation has been used with varying success but has limited indications.
359 There are many treatment options; however, no recommendation for preferred treatment are currently available.7 Mark et al.30 reported on 92 patients who underwent delayed perineal repair following a pelvic fracture and urethral injury. They found that 57 patients (62%) remained impotent in the long term with a median follow-up of 4 years. Self-injection with vasoactive agents was successful in 24 of 27 (89%), suggesting a neurogenic etiology. They concluded that disruption of the cavernosal nerves lateral to the prostatomembrananosus urethra behind the symphysis pubis was the most likely cause of impotence injury. Bilateral pubic rami fractures had a high incidence of associated impotence.
Sexual dysfunction in females alter pelvic fracture Female sexual dysfunction involves pain during sexual intercourse (dyspareunia) and future difficulty with vaginal childbirth with resultant need for Caesarean section. Kiely and Williams32 reported the results of a questionnaire sent to women who had sustained major pelvic fractures and sacro-iliac disruption. Seven of the 11 patients who were sexually active reported dyspareunia. Four of the 11 patients had given birth, and only one required a Caesarian section. Copeland et al.33 reported the results of a study of the effect of trauma and pelvic fracture on genitourinary, sexual, and reproductive function. Urinary complaints occurred significantly more often in the study group (with pelvic fractures) than in controls (21% and 7%, respectively), in patients with residual pelvic fracture displacement45 mm than in those without displacement (33% and 14%, respectively), and in patients with residual lateral (60%) or vertical (67%) displaced fractures than in those with medially displaced fractures (21.4%). Caesarian section rates were significantly more frequent in subjects with fractures initially displaced 45 mm than in those with fractures initially displaced o5 mm (80% and15%, respectively). There was no difference in the incidence of infertility or miscarriage between groups. Dyspareunia was more common in subjects with fractures displaced 45 mm than in those with non-displaced fractures (43% and 25%, respectively). The authors concluded that pelvic trauma negatively affected the genitourinary and reproductive function of female patients.
ARTICLE IN PRESS 360 Fallat et al.34 studied 31 women treated at a Level I trauma centre who had sustained reproductive tract injuries. The injuries were divided into coital (all of whom had vaginal lacerations) and non-coital injury groups. At follow-up, seven women in the combined group had subsequent pregnancies, and only two patients who had sustained pelvic fractures had dyspareunia. The authors concluded that even severe injuries do not preclude normal pregnancy and sexual function. Treatment of female sexual dysfunction focuses mainly on the treatment of dyspareunia and maintenance of ability to bear children through the birth canal. Gynaecologic referral should be made in most cases of dyspareunia after a pelvic fracture. Dyspareunia may be relieved by excision of a bony exostosis in select cases.35 In addition, female patients who sustain a pelvic fracture should be counselled about the increased risk of a Caesarian section for childbirth.
Conclusion Traditional understanding and treatment of urologic injuries associated with pelvic fractures has been coupled with an increased awareness of risk of future sexual dysfunction. Contemporary management continues to evolve, with an increased trend towards more aggressive treatment of the pelvic fractures and dislocations, urologic injuries, and sexual dysfunction with the hope of improved overall long-term functional outcome.
References 1. Routt ML, Simonian PT, Defalco AJ, Miller J, Clarke T. Internal fixation in pelvic fractures and primary repairs of associated genitourinary disruptions: a team approach. J Trauma 1996;40:784–90. 2. Spirnak JP. Pelvic fracture and injury to the lower urinary tract. Urol Surg 1988;68:1057–69. 3. Taffet R. Management of pelvic fractures with concomitant urologic injuries. Orthop Clin N Am 1997;28:389–96. 4. Colapinto V. Trauma to the pelvis: urethral injury. Clin Orthop Relat Res 1980;151:46–55. 5. Koraitim MM, Marzouk ME, Atta MA, Orabi SS. Risk factors and mechanism of urethral injury in pelvic fractures. Br J Urol 1996;77:876–80. 6. Aihara R, Blansfield JS, Millhan FH, LaMorte WW, Hirsch EF. Fracture locations influence the likehood of rectal and lower urinary tract injuries in patients sustaining pelvic fractures. J Trauma 2002;52:205–9. 7. Harwood PJ, Grotz M, Eardley I, Giannoudis PV. Erectile dysfunction after fracture of the pelvis. J Bone J Surg 2005;87-B(3):231–90. 8. Niemi TA, Norton LW. Vaginal injuries in patients with pelvic fractures. J Trauma 1985;25:547–51.
J. Yerasimides, C.S. Roberts 9. Machtens S, Ga ¨nsslen T, Stief CG. Erectile dysfunction in relation to traumatic pelvic injuries or pelvic fractures. Br J Urol Int 2001;87:441–8. 10. Jones AL, Burgess AR. Fractures of the pelvic ring. In: Bucholz RW, Heckman JD, editors. Rockwood and Green’s fractures in adults. Philadelphia: Lippincott Williams and Wilkins; 2002. p. 1495–6. 11. Colapinto V, McCallum RW. Injury to the male posterior urethra in fractured pelvis: a new classification. J Urol 1977;118:575. 12. Wolk DJ, Sandler CM, Corriere Jr JN. Extraperitoneal bladder rupture without pelvic fracture. J Urol 1985;134:1199–201. 13. Lowe MA, Mason JT, Luna GK, Maier RV, Copass MK, Berger RE. Risk factors for urethral injuries in men with traumatic pelvic fractures. J Urol 1988;140:506–7. 14. Pokorny M, Pontes JE, Pierce Jr JM. Urological injuries associated with pelvic trauma. J Urol 1979;121:455–7. 15. Sandler CM, Harris Jr JH, Corriere Jr JN, Toombs BD. Posterior urethral injuries after pelvic fracture. Am J Roentgenol 1981;137(6):1233–7. 16. Carroll PR, McAninch JW. Major bladder trauma: mechanism of injury and a unified method of diagnois and repair. J Urol 1984;132:254–7. 17. Cass AS, Luxenberg M. Features of 164 bladder ruptures. J Urol 1987;138:743–5. 18. Sharlip ID. Penile arteriography in impotence after pelvic trauma. J Urol 1981;126(4):477–81. 19. Levine FJ, Greenfield AJ, Goldstein I. Arteriographically determined occlusive disease within the hypogastric-cavernous bed in impotent patients following blunt perineal and pelvic trauma. J Urol 1990;144(5):1147–53. 20. Munarriz RM, Yan QR, Nehra A, Udelson D, Goldstein I. Blunt trauma: the pathophysiology of hemodynamic injury leading to erectile dysfunction. J Urol 1995;153(6):1831–40. 21. Siroky MB, Azadzoi KM. Vasculogenic erectile dysfunction: newer therapeutic strategies. J Urology 2003;170s:S24–30. 22. Sandler CM, Phillips JM, Harris JD, Toombs BD. Radiology of the bladder and urethra in blunt pelvic trauma. Rad Clin N Am 1981;19(1):195–211. 23. Weyrauch Jr HM, Peterfy RA. Tests for leakage in the early diagnosis of the ruptured bladder. J Urol 1940;44: 264–73. 24. Zingg EJ, Casavona GA, Isler B, Sohn M. Pelvic fractures and traumatic lesions of the posterior urethra. Eur Urol 1990;18(1):27–32. 25. Oliver JA, Taguchi Y. Rupture of the full bladder. Br J Urol 1964;36:524–5. 26. Webster GD, Mathes GL, Selli C. Prostatomembranous urethral injuries: a review of the literature and a rational approach to their management. J Urol 1983;130: 898–902. 27. Giannoudis PV, Veysi VT, Pape H- C, Krettek C, Smith MR. When should we operate on major fractures in patients with severe head injuries? Am J Surg 2002;183:261–7. 28. King J. Impotence after fractures of the pelvis. J Bone J Surg 1975;57-A(8):1107–9. 29. Ellison M, Timberlake GA, Kerstein MD. Impotence following pelvic fracture. J Trauma 1988;28(5):695–6. 30. Mark SD, Keane TE, Vandemark RM, Webster GD. Impotence following pelvic fracture urethral injury: incidence etiology and management. Br J Urol 1995;75(1):62–4. 31. Bellabarba C, Stewart JD, Ricci WM, DePasquale TG, Bolhofner BR. Midline sagittal sacral fractures in anteriorposterior compression pelvic ring injuries. J Orthop Trauma 2003;17(1):32–7.
ARTICLE IN PRESS Pelvic fractures and genitourinary injuries 32. Kiely N, Williams N. Sexual dysfunction in women following pelvic fractures with sacroiliac disruption. Injury 1996; 27(1):45–6. 33. Copeland CE, Bosse MJ, McCarthy ML, et al. Effect of trauma and pelvic fracture on female genitourinary, sexual, and reproductive function. J Orthop Trauma 1997;11(2):73–81.
361 34. Fallat ME, Weaver JM, Hertweck SP, Miller FB. Late follow-up and functional outcome after traumatic reproductive tract injuries in women. Am J Surg 1998;64(9):858–61. 35. Wilkes RA, Seymour N. Dyspareunia due to exostosis formation after pelvic fracture. Br J Obstet Gynaecol 1993; 100(11):1050–1.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 362–372
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MINI-SYMPOSIUM: PELVIC FRACTURES
(v) Delayed reconstruction of pelvic fractures John Keating Department of Orthopaedic Trauma, Royal Infirmary, Lauriston Place, Edinburgh EH3 9YW, Scotland, UK
KEYWORDS Pelvic fracture; Pelvic ring; Internal fixation; External fixation
Summary Unstable pelvic fractures are usually the result of high energy trauma and 70% of patients have other significant injuries. The initial priorities are to identify all injuries and stabilise the patient. Delayed reconstruction should be considered in patients with unstable fracture patterns (lateral compression, anteroposterior compression or vertical shear) that are displaced. Open reduction and internal fixation with plating techniques remains the most commonly used surgical technique. However, combinations of internal fixation, percutaneous fixation and external fixation are also possible and have a role to play. The ilioinguinal and Pfannestiel approaches are the most frequently employed. Posterior approaches are generally reserved for displaced sacral fractures. Percutaneous fixation can be used for fractures where closed reduction has been achieved. Sacroiliac screws and the medullary ramus screw are the two common techniques. Anatomical results are superior with internal fixation compared to non-operative treatment or external fixation. Late morbidity rates remain high due to persistent pelvic pain and associated visceral injury. & 2005 Elsevier Ltd. All rights reserved.
Introduction Pelvic ring disruptions are rare injuries but present a significant challenge for the treating orthopaedic surgeon. The majority of pelvic ring disruptions occur as a result of high energy trauma and 70% of patients have other serious injuries. The management of associated injuries may have a significant influence on the emergency and definitive management of the pelvic fracture. Patients who are haemodynamically unstable with other life-threatening injuries at the time of admission may be too Tel.: +44 131 536 3720; fax: +44 131 536 3810.
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unfit to undergo definitive internal fixation of the pelvic ring disruption. Application of pelvic external fixation has been the most commonly employed urgent orthopaedic intervention in the acute setting. However, there are drawbacks to use of external fixation as definitive mode of treatment. They are cumbersome, poorly tolerated by patients and are associated with a high rate of malunion, particularly with more unstable fracture patterns. Once the patient is stabilised there is therefore a need to consider delayed reconstruction. This article reviews the current indications for pelvic reconstruction, the techniques available and aspects of outcome, including complications and function.
0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2005.09.006
ARTICLE IN PRESS Delayed reconstruction of pelvic fractures
Clinical assessment Initial clinical assessment should be in accordance with ATLS guidelines. This facilitates a thorough evaluation of the patient and identification of those with other injuries. As part of the secondary survey a careful examination of the perineum, rectum and vagina is required to identify wounds that communicate with the fracture. Open pelvic fractures are found in 5–10% of cases. Although rare they are associated with a significantly higher morbidity and mortality and early identification of open wounds is essential to institute early appropriate treatment, which may include a defunctioning colostomy. Once the patient is stabilised some other clinical aspects need to be taken into account when considering definitive fixation. A careful assessment of the skin condition of the pelvis is necessary to determine if a surgical approach can be safely undertaken. Skin in the lateral and posterior aspect of the pelvis may be extensively contused and degloved and surgical incisions in these circumstances have an increased risk of infection and wound breakdown. Contamination of external fixation pin-tracks or supra-pubic catheter sites may necessitate altered planning of incisions or consideration of alternative approaches. A careful neurological assessment should be undertaken before definitive fixation if possible. This will allow the surgeon to document any preexisting neurological deficit which might otherwise be attributed to the surgical procedure. The status of the bladder and urethra should have been established as part of the initial assessment but if there is any doubt a retrograde urethrogram and cystogram should be performed. The presence and extent of any apparent leg-length discrepancy should be documented, as this may influence the decision to operate or not. Rectal, vaginal and perineal examinations should have been carried out in the acute phase of treatment but may need to be repeated if there is any clinical doubt regarding the findings. Ideally definitive fixation should be undertaken in a haemodynamically stable patient, with urethral catheter drainage of the bladder and with no other adjacent contaminated wounds. This is not always possible in practice and therefore surgical decisions may have to be modified depending on the clinical situation.
Radiographic assessment Plain AP radiographs will identify most pelvic fractures and allow classification of the injury.
363 Additional imaging helps more accurate classification and detection of the pathology in more detail. The inlet and outlet views allow identification of subtle degrees of superior and posterior migration that may not be evident on the AP view (Fig. 1). The outlet view also shows the sacral foramena more clearly and may help identify sacral fractures in the transforamenal region which may be difficult to detect on the AP view. Patients with associated acetabular fractures should have additional iliac oblique and obturator oblique views if possible. In patients who are haemodynamically unstable at the time of presentation, these additional views may have to be deferred until the patient is stabilised. The CT scan is the most useful additional investigation in these patients. The majority of patients will require imaging from the head down to the level of the pubic symphysis. This is the most accurate way of identifying associated head, thoracic and intra-abdominal trauma. The scan will also define accurately the extent of the posterior pelvic ring disruption. It is particularly useful in
Figure 1 (a) Inlet view of pelvic fracture showing posterior displacement of right hemipelvis with disruption of pubic symphysis; (b) outlet view showing sacral foramena. Note the superior displacement of the right hemipelvis with incongruity of the symphysis and a fracture through the iliac wing.
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J. Keating stable. Type C3 injuries are bilateral vertically unstable injuries. The mechanistic classification is less comprehensive but relates the mechanism of injury to the fracture pattern and the likely associated soft tissue injuries. The main categories are lateral compression (LC), anteroposterior compression (APC, ‘‘open book’’ pattern) and vertical shear (VS). Fractures with mixed patterns of injuries are classified as combined mechanical injuries (CMI). LC injuries are associated with visceral injuries. APC patterns increase pelvic volume and hypotension is common due to pelvic haemorrhage. Vertical shear injuries are the most unstable pattern and are associated with visceral trauma, hypotension and pelvic neurological injury.
Figure 2 CT scan of transforamenal sacral fracture. These fractures are difficult to visualise on plain radiographs.
showing the morphology of sacral fractures, which may be difficult to discern on plain radiographs (Fig. 2). More sophisticated imaging, including twodimensional and three-dimensional reconstructions, is most useful for imaging acetabular fractures but is not mandatory for most pelvic fractures. Some additional views of the pelvis are useful during surgical reconstruction and can be obtained with image intensification. For percutaneous fixation of sacroiliac dislocation or sacral fractures, a true lateral view of the sacrum is required during surgery to ensure correct screw placement in a safe zone. For insertion of the medullary ramus screw combination views of the iliac oblique and inlet view and the obturator oblique and the outlet view are required.
Classification The most commonly used classification systems are the AO system1 and the mechanistic classfication of Young and Burgess.2–4 The AO classification patterns comprise stable patterns (type A), rotationally unstable (type B) or vertically unstable patterns (type C). Rotationally unstable patterns are divided into unilateral open book patterns (B1), unilateral lateral compression (B2) or combinations involving both sides of the pelvic ring (B3). Type C vertically unstable injuries may involve one side of the pelvis (type C1), or both sides (C2 and C3). The C2 pattern is a vertical unstable hemipelvis on one side with the contralateral side rotationally un-
Options for reconstruction Non-operative management Many pelvic ring fractures do not require surgical reconstruction. Lateral compression fractures are the most common variety of pelvic ring disruption. In many of these fractures there is minimal distortion of the pelvic ring. In addition, this pattern of injury does not disrupt the internal pelvic ligaments (sacrospinous and sacrotuberous) or the posterior ligaments so late displacement is rare. APC (open book) injuries with less than 2.5 cm symphyseal diastasis are also inherently stable since this degree of distraction is not associated with any significant posterior or internal pelvic ligament injury. These injuries can be treated nonoperatively. If other injuries allow, patients can be mobilised weight-bearing as tolerated, often with crutches. Patients with stable unilateral pelvic fractures can be allowed mobilise with crutches fully weight-bearing on the intact side. If nonoperative treatment is chosen repeat radiographs on two occasions within a month of injury are advisable to detect any loss of position that might warrant consideration of operative intervention. Progression to full-weight bearing can usually begin at 6–8 weeks assuming there is on radiographic evidence of callus formation.
Operative management There are several options available for definitive surgical management of an unstable pelvis. These include external fixation alone, combined external fixation and internal fixation, sequential external fixation followed by internal fixation or definitive
ARTICLE IN PRESS Delayed reconstruction of pelvic fractures internal fixation, sometimes by percutaneous techniques. The indications for operative treatment are summarised in Table 1. Fixation needs to be considered for any pelvic ring disruption with significant displacement. The degree of displacement considered acceptable depends to a large extent on the pattern of injury. As already indicated most lateral compresssion patterns can be treated non-operatively. However, some variations of this injury do occur that merit surgical intervention. Lateral compression fractures may be associated with considerable rotation of one hemipelvis in relation to the other and this may result in the development of an apparent leglength discrepancy. Although the anterior lesion in most lateral compression disruptions is an isolated or multiple pubic ramus fractures, disruption of the pubic symphysis with overlapping of the symphysis (a ‘‘locked symphysis’’) can occur (Fig. 3). Displacement of the ramus fractures in lateral compression injuries is normally not severe enough to merit fixation but a tilt fracture of the pubic ramus is occasionally seen. These fractures involve a fracture of the superior and inferior pubic ramus laterally with disruption of the symphysis medially (Fig. 4). The symphyseal-ramus fragment then protrudes into the perineum. This is a particular problem in female patients where it will lead to late pain and dyspareunia later. Finally the iliac wing component of a lateral compression fracture may displace considerably with a risk of non-union (Fig. 5). In any of these situations internal fixation of the fracture is preferable to non-operative treatment. For APC (open book) injuries, most pelvic surgeons consider internal or external fixation Table 1
365 when the degree of diastasis exceeds 2.5 cm. With this degree of displacement, there is usually a significant disruption of the anterior sacroiliac ligaments and the internal ligaments, allowing for rotational instability. Vertical shear injuries are often associated with marked anterior and posterior displacement. In general displacement in any plane exceeding 1 cm is considered an indication for fixation. These injuries are very variable in morphology. Occasionally there may be anterior ramus fractures and a posterior transforamenal sacral fracture with limited displacement. Nonoperative treatment can be considered in this situation. Vertical shear patterns with symphyseal disruption and/or sacroiliac dislocation are highly unstable patterns and are not suitable for nonoperative management.
Figure 3 Lateral compression injury with iliac wing fracture and locked symphysis.
Indications for pelvic fracture treatment.
Non-operative treatment APC injuries with o2.5 cm anterior disruption Lateral compression injuries with minimal displacement Indications for operative treatment APC injures 42.5 cm disruption Lateral compression injuries with apparent LLD Lateral compression injuries with tilt fracture/locked symphysis Vertical shear injuries with displacement in any plane 41 cm Poor results of vertical shear injury with external fixation Indications for external fixation as definitive management Unstable fracture in patient too ill to tolerate major surgery Unstable open pelvic fracture with perinal/rectal communication Indications for fixation of pubic ramus fractures Lateral compression injury with tilt fracture Lateral compression injury with rotation of hemipelvis and apparent leg length discrepancy Vertically unstable patterns with displacement
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Figure 4 Vertical shear injury with sacroiliac disruption and pubic symphysis disruption. There was an additional fracture of the superior and inferior pubic ramus on the right side with displacement of the right symphyseal segment into the perineum—a tilt fracture.
Figure 5 Lateral compression injury shown in Fig. 3. This fracture was associated with a displaced crescent fracture of the iliac wing and a disruption of the pubic symphysis. Nonoperative treatment would have been associated with a poor outcome and a significant risk of non-union. Position after internal fixation with plate fixation of iliac wing and symphysis.
Acute management Approximately 50% of patients with unstable pelvic ring disruptions are haemodynamically unstable at the time of presentation. Internal fixation at this stage is often impractical. The most common mode of pelvic stabilisation is application of external fixation.5 The rationale for use of external fixation is a reduction in the volume of the pelvic cavity to tamponade haemorrhage and to achieve reduction
J. Keating of the pelvic ring conferring some skeletal stability. The use of external fixation has been reported to improve survival rates but its use remains controversial and there are some drawbacks associated with application of a frame on the pelvis. Technical errors in frame application are common, particularly in surgeons with limited experience of pelvic ring disruptions. The commonest error is imperfect pin placement in the iliac wing, which may result in early loosening and loss of reduction. More seriously application of a frame to the anterior pelvis may actually increase the extent of posterior displacement in vertical shear patterns. In general acute external fixation is best avoided if the patient is haemodynamically stable, irrespective of the fracture pattern. Pin track infection may compromise surgical exposures required for delayed reconstruction. There are other drawbacks to the use of external fixation for definitive management. External fixation is biomechanically inferior to rigid internal fixation. The devices are cumbersome and mobilisation of the patient with a pelvic external fixator in situ is difficult. External fixation alone for vertical shear fractures is associated with malunion rates of up to 95%6 and if possible should not be used as the definitive treatment. However, in a proportion of patients the circumstances favouring successful internal fixation may never occur. In patients with open fractures contaminating the perineum with the presence of a colostomy the risk of undertaking fixation may be too high. Some patients remain too ill to withstand major open surgery and in elderly patients osteoporosis is associated with an increased risk of fixation failure.
Timing of surgery The timing of definitive pelvic fixation depends on achieving haemodynamic stability, treatment of other life-threatening injury and correction of any associated coagulopathy. This frequently occupies the first 24–48 h following admission. At that stage definitive reconstruction can be considered, assuming the haematological indices are normal and coagulopathy is reversed. Ideally definitive stabilisation of the pelvic ring should be achieved within 5–7 days7,8. Delay beyond this time frame increases the technical difficulty of the surgery. Closed reduction and percutaneous fixation becomes less feasible as the delay to surgery increases. While awaiting an appropriate window of opportunity to perform definitive fixation, traction or external fixation (or both) can be used to maintain reduction. However, as already indicated, external
ARTICLE IN PRESS Delayed reconstruction of pelvic fractures fixation may compromise subsequent surgical access by pin track infection and should be avoided unless there is persistent haemodynamic instability during the acute phase of treatment.
Surgical approaches Prior to surgery a urinary catheter should be inserted in all patients to minimise the risk of bladder injury and to monitor urinary output. Anterior and posterior lesions may be present and the approach chosen depends on the pattern of injury and fixation techniques selected. Pubic symphyseal disruptions are approached using the Pfannenstiel incision. A horizontal incision is made 2 cm above the level of the pubic symphysis. After division of subcutaneous tissue the rectus sheath is identified. In most symphyseal disruptions, the rectus abdominis on one side is avulsed with extensive stripping of the symphysis, which simplifies the surgical exposure. Fractures of the pubic ramus are not accessible for plate fixation using the Pfannenstiel incision and an ilioinguinal approach is required. Although this is a more extensive surgical procedure it allows simultaneous access to the iliac wing and sacroiliac joint which is an advantage if anterior and posterior elements of pelvic disruption need to be addressed. The approach will allow fixation of pubic ramus fractures, iliac wing fractures and sacroliac dislocations. Sacral fractures are too medial to be fixed via this exposure. The pelvis is approached via an incision along the iliac wing extending medially to the pubic symphysis. The inner table of the iliac wing is exposed by subperiosteal elevation of the iliopsoas muscle. The external oblique aponeurosis is divided in line with the incision and the inguinal ligament is split along its length. Access to the pelvis is gained via three sugical ‘‘windows’’. In the lateral window the iliac wing is accessible. A second interval is developed between the iliopsoas and femoral vessels giving access to the iliopectineal eminence, the pelvic brim and quadrilateral plate. The femoral nerve remains on the surface of the iliopsoas. Between the iliopsoas and femoral vessels is the iliopectineal fascia which runs down onto the brim of the pelvis and must be divided to make full use of this interval. The third and most medial window is developed between the femoral vessels and spermatic cord. This allows access to the superior pubic ramus and symphysis. Additional exposures may be required for posterior ring disruptions, particularly for sacral fractures. These can be approached via posterior
367 longitudinal incisions situated adjacent to the posterior superior iliac spine. The incision can be made medial to the spine if the lesion is a sacral fracture but lateral if the lesion involves the iliac wing. A subperiosteal exposure can be made of the iliac wing or the posterior aspect of sacrum. Bilateral incisions can be used for bilateral posterior disruptions. This approach has a number of advantages—sacroiliac dislocations and sacral fractures can be accessed via this exposure. For patients with sacral nerve root injury, decompression is possible although the benefit of this latter procedure remains uncertain. The main drawback is the requirement for prone or lateral positioning of the patient. Simultaneous access to the anterior lesion is therefore not possible with prone positioning and obviously external fixation has to be removed. The other problems with these incisions are soft tissue complications. Degloving and extensive bruising of the posterior pelvic skin is a common accompaniment of these major injuries and increases the risk of open surgery, with attendant risks of wound breakdown and infection. Percutaneous fixation has become popular for fixation of some types of pelvic ring disruption. These techniques have some particular advantages for these patients. It avoids the need for extensive exposures, which is an advantage in patients who may have other major injuries. Blood loss is minimal and the risk of wound infection is negligible. Percutaneous iliosacral screws7 and the medullary ramus screw8 are the most common techniues used. Percutaneous iliosacral screws can be used for sacral fractures and sacroiliac dislocations. They can be used for patients with bilateral posterior disruptions, which greatly limits the degree of soft tissue dissection. The supine postion is preferred if possible, since simultaneous anterior access to the pelvis is possible. The patient is placed on a radiolucent table in order to obtain inlet, outlet and lateral sacral views. The procedure is facilitated by a small midline support behind the sacrum pelvis to elevate the pelvis slightly which makes the entry point easier to obtain. The starting point is chosen with the lateral sacral view to identify the body of S1. A curved sclerotic line denotes the slope of the ala and care must be taken to remain below this to avoid penetration above the ala and the risk of L5 root injury. A guide wire is introduced and advanced with the use of the inlet and outlet views to ensure correct placement into the body of S1, avoiding the S1 formen and anterior or posterior malposition of the screw. The medullary ramus screw may be inserted from the antegrade approach via the iliac wing or the
ARTICLE IN PRESS 368 retrograde approach with an entry point adjacent to the pubic ramus. Two views are necessary to guide placement of this screw. One is a combination of the outlet and obturator oblique view and the other is a combination of the inlet and iliac oblique view. These two views allow visualisation of the superior pubic ramus in two different planes to ensure the screw remains within the medullary canal. The main practical limitations of this type of surgery are the difficulty in achieving a satisfactory closed reduction and the need for high quality imaging to minimise the risk of neurovascular injury. Computer CT guided pelvic surgery is currently being developed. Current systems are evolving but at the moment remain expensive and time consuming to use. There is no widely available system at present. In the future improved methods of closed reduction using percutaneous clamps and traction with more user-friendly imaging technology may increase the applicability of this approach.
Reduction and fixation techniques
J. Keating symphysis which can usually be achieved by use of a pointed reduction clamp applied on either side of the pelvis in the obturator ring (Fig. 6). In vertical shear injuries achieving reduction can be much more difficult—one hemipelvis is shifted in a superior and posterior direction, with associated rotation in many of these cases, and the reduction requires correction of this muliplanar deformity. Techniques of reduction include use of traction on the leg and pointed reduction clamps applied to the obturator foramen on either side. Application of the plates may be needed to achieve the final reduction. There is no consensus about the configuration of plating. Most surgeons use at least one 4.5 mm (or equivalent) plate applied to the superior aspect of the symphysis with two screws on either side of the symphysis. The use of a second anterior plate increases the stability of the construct and is worth considering, particularly in vertical shear injuries (Fig. 7). Alternatives such as the two hole plate or tension band wiring systems are now less popular as they are less rigid and the risk of loss of reduction with fixation failure is higher.
Most procedures are performed with the patient in the supine position. Intraoperative screening is essential in all cases to verify fracture reduction and guide implant placement. The patient therefore needs to be placed on a table that allows visualisation of the pelvic using intraoperative radiography. Some tables have the advantage of allowing application of skeletal traction, which may facilitate reduction. For rotationally unstable patterns it may be sufficient to stabilise the anterior disruption alone but in vertical shear injuries with displacement anterior and posterior stabilisation is necessary. Posterior approaches to the sacrum or sacroiliac joint require the patient to be positioned prone.
Pubic symphysis disruption Surgical treatment of pubic symphysis diastasis can be achieved by internal or external fixation. Internal fixation has a number of advantages. Biomechanically it is stronger than external fixation. The use of an external frame is associated with a less precise reduction and the frame has to be maintained for at least 6–8 weeks. Pin track infection is almost invariable and patients find the frame cumbersome. Mobilisation is difficult and risks loss of reduction. Plating of pubic symphyseal disruption is usually straightforward in rotationally unstable injuries. Reduction requires closure of the
Figure 6 (a) APC (open book) injury with pubic symphyseal disruption (b) after plating of pubic symphysis.
ARTICLE IN PRESS Delayed reconstruction of pelvic fractures
369
Figure 8 Pelvic instrumentation trays with a selection of specialised reduction clamps and plates.
Figure 7 (a) Vertical shear injury with pubic symphysis disruption and sacroiliac dislocation (b) insertion of percutaneous iliosacral screws on outlet view. Note screw position above S1 foramen (c) completion of fixation with augmentation of posterior screw fixation with sacroiliac plate.
Pubic ramus fracture Pubic ramus fractures are most commonly found in association with lateral compression vertical shear patterns. If the fracture configuration is a lateral compression injury then the pelvic ligaments are usually intact and fixation is often not required.
With more significant degrees of displacement fixation may need to be considered. The ilioinguinal exposure is the usual surgical approach. In order to make full use of this exposure, a range of specialised pelvic clamps and the ball spike pusher are necessary (Fig. 8). The fracture is reduced either indirectly with traction or directly using pelvic clamps. The fracture is usually fixed with application of a 3.5 mm pelvic reconstruction plate extending from the iliac wing across the superior pubic ramus fracture to the pubic symphysis. An alternative to plating is the use of retrograde or antegrade pubic ramus screws.8 Reduction must be achieved by closed or open methods, after which a medullary ramus screw is inserted retrograde from the symphysis or antegrade from the iliac wing. The retrograde screw is difficult to insert in obese patients or if there is a lot of perineal or scrotal swelling. The antegrade screw may be a better choice in these patients but obesity or marked gluteal swelling will increase the technical difficulty. Closed reduction must be achieved to allow safe insertion of these screws.
Posterior fixation Fixation of the posterior component of the injury is not always required. In APC injuries, there is usually opening of the SI joint on one or both sides but reduction of the anterior disruption will reduce the posterior component of the injury. Fixation of the posterior lesion is indicated principally for vertical shear patterns with sacroiliac dislocations or sacral fractures. Lateral compression injuries with displacement of crescent iliac wing fractures
ARTICLE IN PRESS 370 may also require posterior fixation. In vertical shear injuries fixation of both anterior and posterior lesions is required to achieve and maintain an acceptable reduction. Fixation of the anterior lesion alone is not adequate. The surgical approach is determined by the anatomy of the posterior disruption and other considerations including the state of the posterior skin and soft tissues. Crescent iliac wing fractures and sacroiliac dislocations can be accessed using the ilioinguinal approach. This has the advantage of allowing simultaneous anterior and posterior access which greatly facilitates fracture reduction. In patients with sacroiliac dislocation the precision of reduction is more easily judged from the anterior approach. However, the L5 nerve root lies on the ala of the sacrum and is vulnerable to injury. It also limits medial access for plating. In obese patients or those with marked abdominal swelling access may be very difficult. Reduction of sacroiliac dislocation is usually achieved with a combination of direct and indirect manipulation. Application of longitudinal traction on the leg is usually needed. Pelvic clamps can then be applied to the iliac wing to internally rotate the bone and close the SI joint. Anterior fixation by one or two plates is then carried out. Specially designed plates have been used for this purpose but 3.5 mm plates are the usual implants employed. The limited space on the medial side limits fixation in each plate to one screw in the sacral ala (Fig. 7). Sacral fractures are commonly classified by location.9 Type I are lateral to the sacral foramena, type II are transforamenal and type III are medial to the sacral foramena. The risk of neurological injury increases with more medial patterns. Sacral fractures are too medial to be accessed using the ilioinguinal exposure. There are three options for fixation: transiliac bars, plate fixation or percutaneous fixation. Fixation may be percutaneous or by a direct open posterior approach. The posterior exposure allows plate fixation of sacral fractures and sacral nerve root decompression. However, there is no possibility of simultaneous anterior access and clearly any external fixator frame cannot be left in situ during the procedure. Skin in this area is also quite frequently extensively contused and there may be degloving. If these features are present the risk of wound breakdown and infection increases considerably.10 In posterior approaches plate fixation is usually employed although iliosacral screws can be inserted via this approach. Reduction is generally achieved by use of pelvic clamps. The sciatic notch can be accessed and palpation of the anterior
J. Keating sacroiliac joint is possible to verify reduction in sacroiliac dislocations. In sacral fractures direct visualisation of the two sides of the fracture is possible after subperiosteal dissection. If bony impingement caused by loose fragments has been indentified on preoperative CT scans then a posterior nerve root decompression is possible via this exposure. A laminar spreader can be used to distract the fracture to allow this to be carried out. Once this is achieved the fracture is reduced with clamps. Plate fixation may be achieved with large plates applied across the sacrum to each iliac wing11 or with small fragment plates applied across the fracture line between sacral foramena.12 Percutaneous fixation of posterior pelvic disruptions is an alternative surgical option. It can be utilised for sacral fractures and sacroiliac dislocation. However, it is only an option in situations where adequate closed reduction can be achieved. This sometimes requires traction or application of an external frame. Excellent quality image intensification is mandatory to safely insert percutaneous screws with inlet, outlet and lateral sacral views being required. The main risk of procedure is nerve injury to the L5 or sacral roots from misplaced screws. If the reduction cannot be obtained and verified with good quality imaging, then an alternative method of fixation must be chosen. The one exception to this rule is a sacroiliac dislocation where the level of the iliac wing is restored but residual widening of the joint is present. A percutaneous screw in this situation may be used to close the joint and complete the reduction. In sacral fractures, percutaneous screw fixation can be used but care must be taken in transforamenal injuries not to overcompress the fracture, which may inflict a neurological injury.
Sequence of reconstruction The sequence of reconstruction will vary with the pattern of injury. Rotationally unstable APC injuries with symphysis disruption only require anterior plating. Lateral compression and vertical shear injuries may have anterior and posterior disruption to deal with. In this situation the ilioinguinal exposure allows access to both. Temporary reduction of the anterior lesion is first achieved with clamps and traction. The posterior lesion can then be reduced. Fine tuning the quality of reduction is then carried out if required. Fixation of the anterior lesion and then the posterior lesion is carried out.
ARTICLE IN PRESS Delayed reconstruction of pelvic fractures
Complications Early Major pelvic disruptions are severe injuries and there is considerable risk of complications associated with the injury and the subsequent treatment. Associated visceral trauma is not uncommon. The incidence of these injuries varies with the type of disruption. Urological injuries to the bladder or urethra are present in 15–25% of unstable pelvic fractures. Open book patterns in particular are associated with a high risk of urethral and bladder injury. Lateral compression patterns of injury are associated with blunt force delivered to the abdomen and chest. These patients often have lung contusions and liver or spleen injury. Vertical shear injuries are the most violent pattern of disruption and any combination of visceral injury may be associated. Neurological injury is the highest in this group and is present in 30–50% of cases. Infection rates following surgery are generally low (o5%) with anterior plating procedures. Access via posterior skin incisions has been associated with higher rates of sepsis due to the associated soft tissue damage in that area. Neurological injury as a consequence of surgery should be kept to a minimum with modern imaging and reduction techniques. The lateral cutaneous nerve is frequently subjected to traction forces during the ilioinguinal exposure and some disturbance of nerve function is common. Sacral roots and the L5 nerve root are vulnerable to injury during reduction and implant placement. Percutaneous fixation carries particular hazards. Adequate imaging, a satisfactory reduction and awareness of the relevant surgical anatomy will minimise this risk. Iatrogenic visceral injury is much less common but can occur. Bladder damage is the main risk but can be minimised by use of a urinary catheter and avoiding over penetration of drills during anterior plating procedures. Deep venous thrombosis and pulmonary embolus are particular problems in this group of patients. Prevention is controversial. Many patients are coagulopathic due to blood loss in the early stages of treatment and preventative measures may be inappropriate. I generally commence DVT prophylaxis with enoxoparin (or another suitable pharmacological prophylactic agent) when haematological parameters are normal and any coagulopathy has been reversed.
Late Malunion was common when external fixation alone was used as definitive treatment. More widespread
371 use of internal fixation has been associated with superior anatomical results. However, loss of fixation leading to malunion still occurs and is more common in vertical shear patterns of fracture. Rigid anterior and posterior plating minimises this risk. Patients with bladder and urethral injury often have long-term problems including urinary incontinence, urethral stricture and impotence in men. Malunion in female patients may be associated with dyspareunia and problems in labour following pregnancy.
Functional outcome There are a number of advantages associated with internal fixation of unstable pelvic fractures. Patients can mobilise more easily, pain control is better and the anatomical result is superior to nonoperative treatment or external fixation alone. Published studies of outcome suggest that results after internal fixation are superior to other methods.13–18 Improvements in imaging and instrumentation have been associated with better anatomical results, but poor functional results with chronic disability are still common. Patients with with APC and LC patterns of injury do better since the anatomical results of fixation are better and the incidence of severe soft tissue injury is lower. Although anatomical reductions are easier to achieve in APC (open book) patterns, these fractures tend to have a poorer functional outcome than the LC patients probably because they have a higher incidence of urethral and bladder trauma with late sexual dysfunction.19 In general more severe degrees of disuption with associated visceral or neurological injury are associated with poorer outcomes, as might be expected. Most published studies identify vertical shear patterns with a poorer prognosis since these injuries have a higher incidence of associated injury. Chronic posterior pelvic pain is common and has been reported in 30–70% of cases. Sacroiliac dislocations and sacral fractures are both associated with this problem. Although up to 70% of patients will have pelvic pain, about two-thirds return to some type of occupational and recreational activity. However 30% never return to work or recreation and remain chronically disabled due to the combined effects of pain, visceral and neurological injury.18 Malunion and non-unions of the pelvis after fracture can be corrected surgically. However, the surgery is technically demanding, although satisfactory outcomes have been reported in the hands of experienced surgeons.20 Union rates after
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surgical correction are 490%, but anatomical reductions are possible in only 50% of cases. However, Mears20 reported 71% of patients had very little or no pain and 64% were very satisfied with the outcome. United malunions appear to have a better prognosis than unstable ununited malalignments which had a higher risk of a poor outcome and neurological complications.
The future Modern methods of pelvic reconstruction have contributed to a significant improvement in the quality of anatomical results of pelvic reconstruction compared to older methods of non-operative treatment or reliance of external fixation as definitive treatment. The late morbidity of these injuries remains high. As motor vehicle safety improves and traffic speeds gradually reduce there may be a reduction in the proportion of more severe patterns of pelvic disruption. Computer assisted surgery systems are becoming more sophisticated and may eventually have an integral role in fixation of these injuries. This may assist in achieving better quality reductions and will minimise risk of iatogenic injury. However, the violence required to disrupt the pelvis means that these patients will continue to represent the more severe end of the spectrum of orthopaedic trauma. A residual degree of significant morbidity can therefore be expected even with the best reconstructive treatment.
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Practice points—delayed reconstruction
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Consider fractures with significant displacement for fixation (41 cm any plane) Definitive fixation easier within first 7 days Ilioinguinal and Pfannenstiel approaches most common Fixation of both anterior and posterior lesions required in vertical shear patterns Percutaneous fixation an option only if closed reduction can be achieved Anatomical results better with anterior and posterior internal fixation Late morbidity significant due to pelvic pain and visceral/nerve injury
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19.
References 20. 1. Tile M. Classification of fractures of the pelvis and acetabulum. In: Tile M, editor. Fractures of the pelvis and
acetabulum. 2nd ed. London: Williams & Wilkins; 1995. p. 66–101. Young J, Burgess AR, Brumback RJ, et al. Pelvic fractures; value of plain radiography in early assessment and management. Musculoskeletal Radiol 1986;160:445–51. Burgess AR, Eastridge BJ, Young JWR, et al. Pelvic ring disruptions: effective classification system and treatment protocols. J Trauma 1990;30:848–56. Dalal SA, Burgess AR, Siegel JH, et al. Pelvic fracture in multiple trauma: classification by mechanism is key to pattern of organ injury, resuscitative requirements, and outcome. J Trauma 1989;29:981–1000. Riemer BL, Butterfield SL, Diamond DL, et al. Acute mortality associated with injuries to the pelvic ring: the role of early patient mobilization and external fixation. J Trauma 1993;35:671–7. Lindahl J, Hirvensalo E, Bo ¨stman, Santavirta S. Failure of reduction with an external fixator in the management of injuries of the pelvic ring. J Bone Joint Surg 1999;81B: 955–62. Routt ML, Kregor PJ, Simonian PT, Mayo KA. Early results of percutaneous iliosacral screws with the patient in the supine position. J Orthop Trauma 1995;9:207–14. Routt ML, Simonian PT, Grujic L. The retrograde medullary ramus screw for the treatment of anterior pelvic ring disruptions: a new technique. J Orthop Trauma 1995;9: 35–44. Denis F, Davis S, Comfort T. Sacral fractures: an important problem. Retrospective analysis of 236 cases. Clin Orthop 1988;227:67–81. Kellam JF, McMurtry RY, Tile M. The unstable pelvic fracture. Orthop Clin N Am 1987;18:25–41. Mears DC, Capito CP, Deleeuw H. Posterior pelvic disruptions managed by the use of the double cobra plate. Instr Course Lect 1988;87:143–50. Pohlemann T, Bosch U, Gansslen A, Tscherne H. The Hannover experience in the management of pelvic fractures. Clin Orthop 1994;305:69–80. Goldstein A, Phillips T, Sclafani S, et al. Early open reduction and internal fixation of the disrupted pelvic ring. J Trauma 1986;26:325–33. Henderson R. The long-term results of non-operatively treated major pelvic disruptions. J Orthop Trauma 1989;3: 41–7. Latenser BA, Gentilello LM, Tarver AA, Thalgott JS, Batdorf JW. Improved outcome with early fixation of skeletally unstable pelvic fractures. J Trauma 1991;31:28–31. Gruen GS, Leit ME, Gruen RJ, et al. Functional outcome of patients with unstable pelvic ring fractures stabilized with open reduction and internal fixation. J Trauma 1995;39: 838–45. Tornetta P, Matta JM. Outcome of operatively treated unstable posterior pelvic ring disruptions. Clin Orthop Relat Res 1996;329:186–93. Keating JF, Werier J, Blachut P, et al. Early fixation of the vertically unstable pelvis: the role of iliosacral screw fixation of the posterior lesion. J Orthop Trauma 1999;13: 107–13. Rommens PM, Hessmann MH. Staged reconstruction of pelvic ring disruption: differences in morbidity, mortality, radiologic results, and functional outcome. J Orthop Trauma 2002;16:92–8. Mears DC, Velyvis J. Surgical reconstruction of late pelvic post-traumatic nonunion and malalignment. J Bone Joint Surg 2003;85B:21–30.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 373–378
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CHILDREN
Missed posttraumatic radial head dislocation Sanjeev Agarwala, B.W. Scottb, a
St. James’s University Hospital, Beckett Street, Leeds, LS9 7TF, UK Leeds General Infirmary, Gt. George Street, Leeds, LS1 3EX, UK
b
KEYWORDS Monteggia fracture; Forearm injury; Elbow dislocation; Radial head dislocation; Elbow injury
Summary Radial head dislocations, either alone, or in association with fracture of forearm bones, are best managed acutely. If the injury is missed on initial radiographs, then treatment of the chronic injury involves open reduction of the radial head and reconstruction of the annular ligament. Alternatively, an ulnar elongation and corrective osteotomy may be done. In this article we describe the different methods that have been used to treat this injury and present illustrative cases with treatment guidelines. & 2005 Elsevier Ltd. All rights reserved.
Introduction
In 1814, Giovanni Battista Monteggia described fracture of the proximal ulna with dislocation of the radial head. In the most widely used classification system of these injuries published by Bado, four types are described. Type I is an anteriorly angulated fracture of the proximal ulna with an anterior dislocation of the radial head. Type II is a posteriorly angulated fracture of the proximal ulna and posterior dislocation of the radial head. Type III is a laterally angulated fracture of the proximal ulna and lateral dislocation of the radial head. Type IV is a fracture of proximal radius and ulna with an anterior dislocation of the radial head. Three variants have also been described:
isolated dislocation of the radial head;
Corresponding author. Tel.: +0113 392 6697;
fax: +0113 392 3770. E-mail address:
[email protected] (B.W. Scott).
fracture of proximal ulna with fracture of the radial neck; and fracture of proximal ulna and radius with the radial fracture being more proximal than the ulnar fracture.
In an acute Monteggia injury, reduction of the radial head is generally possible by manipulation and correction of ulnar angulation. In some instances the annular ligament or capsule may be interposed and prevents reduction of the radial head. This necessitates an open reduction and repair of the annular ligament. If the injury is less than 3 weeks old, closed reduction is generally possible; if between 3 weeks and 3 months, open reduction is more commonly required with repair of the annular ligament. Injuries that are diagnosed with a delay of more than 3 months may be classified as chronic injuries1 and these are best managed by reconstruction to maintain alignment of the radiocapitellar joint.
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ARTICLE IN PRESS 374 Stabilisation of the ulna by internal fixation may be needed in older children, or if the ulnar fracture is oblique or comminuted.2 There is a relatively high incidence of myositis and synostosis in this region and periosteal stripping should be minimal.
Missed injuries Missed Monteggia injuries are fortunately rare, but by no means non-existent. Most reports of missed injuries in the literature are from referral centres and document series of 5–15 cases over periods of many years. The injury can be missed if adequate radiographs are not obtained in a child with an injury to forearm or elbow. All such injuries should have two orthogonal views centred on the elbow in addition to the appropriate imaging for the forearm injury. Failure to recognise the loss of alignment of the radial head and the capitellum on initial radiographs is another cause of missed injuries. A line drawn through the centre of the shaft and head of the radius should intersect the capitellum in all X-ray views and in any position of the elbow. If the radial head is not anatomically reduced after correction of ulnar alignment, this generally signifies an interposed annular ligament or biceps tendon. In these situations, open reduction of the radial head and internal fixation of the ulna should be undertaken. On follow-up after reduction of the radial head, a close watch should be kept for any recurrence of subluxation or dislocation which should be managed accordingly.
Natural history of persistent dislocation One of the earliest reports on the natural history of an unreduced Monteggia injury was by Blount. His recommendation was against any treatment as late reduction was thought to result in a poorer functional outcome when compared to leaving an unreduced radial head. Many other contemporary reports supported this view.3,4 Wiley reported poor results with reconstruction in late cases of traumatic dislocation of the radial head; all patients undergoing reconstruction in his series ended up with an excision of the radial head. In general, excision of the radial head in young children is avoided because of concerns about valgus deformity, ulnar neuropathy and wrist pain. However, the literature on this issue is equivocal. Watson Jones5 believed that excision of the radial head in the growing child led to proximal migration of the radius and secondary subluxation of the
S. Agarwal, B.W. Scott distal radio–ulnar joint. Additionally, lack of the proximal radius may lead to valgus deformity and instability of the elbow6. In a series7 of 25 patients with a mean age of 14.2 years and average followup of 7.8 years, excision of the radial head was not associated with any of the aforementioned problems and resulted in good to excellent results in 19 out of 27 elbows. The salient feature was reoperation for removal of appositional bone growth in seven patients. Another article8 showed improved arc of motion and reduced pain following radial head excision for congenital dislocation of the radial head at an average age of 13 years in eight elbows. Over the years, there has been steadily mounting evidence that unreduced radial head dislocation is fraught with problems and poor function and hence reconstruction is now the preferred treatment. One of the earliest papers on reconstruction of the annular ligament was by Bell Tawse9 and in his series of six patients, there was a block to flexion and a progressive valgus deformity as a result of unreduced dislocation. Similarly, Best10 and Hirayama et al.11 recommended reconstruction in cases of late presentation because of deformity, reduced movements and pain.
Treatment options Reduction of the radial head at a later stage may require open reduction and stabilisation of the radial head along with corrective osteotomy of the ulna. The two broad categories of procedures to achieve stability of the radial head include either open reduction of the radial head with reconstruction of the annular ligament, or corrective wedge osteotomy of the ulna to stabilise the radial head or a combination thereof.
Annular ligament reconstruction The landmark paper regarding annular ligament reconstruction was written by Bell Tawse9 from Pontefract, England. He described reconstruction of the ligament using a strip of the central part of the triceps fascia, which is left attached to the ulna and is passed around the radial neck to stabilise the radiocapitellar joint. Ulnar osteotomy was not done in any patient. The patients included eight patients with posttraumatic radial head dislocation and one with congenital dislocation of the radial head. All patients regained a full or good range of movement except the one with congenital dislocation of the radial head who was left with a 401 fixed flexion deformity.
ARTICLE IN PRESS Missed posttraumatic radial head dislocation A modification to this technique was proposed by Lloyd Roberts and Bucknill6 in which the lateral portion of the triceps fascia was used, as it has a rolled edge and is thicker, instead of the central slip. In addition, a transcapitellar Kirschner wire passed into the proximal radius was used to supplement stability in the early postoperative period. The strip of triceps fascia is passed around the radial neck and then through a drill hole in the ulna and sutured to itself. Eight patients were operated with a time lag of 4 months to 3 years between injury and surgical reconstruction. Only one patient out of eight required an ulnar osteotomy to correct bowing of the ulna. All patients regained a full or functional range of flexion and extension and pronation—supination except one patient with a 3 year old injury who had 451 of pronation and supination. Another series of five late presentation Monteggia injuries was reported by Fowles et al.2 The five patients were managed by open reduction of the radial head. Three had reconstruction of the annular ligament; in one the ligament was sutured and the last did not have a repair. Two had an ulnar osteotomy for correction of angulation. A Kirschner wire was used to stabilise the radial head in all patients. The average flexion arc improved by 50% as compared to the preoperative range of motion. There was lateral subluxation of the radial head in the patient who did not have reconstruction or repair of the annular ligament. A more recent article1 from the Mayo clinic describes seven female patients treated by reconstruction over a 28 year period. The average age was 5 years and 10 months whilst the time since injury ranged from 3 months to 7 years. The prerequisite for surgery was a concave proximal radial articular surface evident on plain radiographs. One patient had significant posterior bowing of the proximal ulna and had an ulnar osteotomy and intramedullary stabilisation at the time of annular ligament reconstruction. At final follow-up, all patients were pain-free and had no elbow instability. The preoperative pronation and supination was a full or almost full range in all patients. Postoperatively, all had a functional or full range of supination but one had pronation of only 51 and two others had pronation of 401 and 451. One patient had a restricted flexion—extension range from 401 to 951 which was previously full range. The authors recommended annular ligament reconstruction for a child of any age and after any duration of dislocation. The prerequisites for surgery were a concave proximal radial articular surface and normal contour and shape of the radius and ulna. Any significant deformity of either bone
375 should be corrected by osteotomy at time of reconstruction.
Ulnar osteotomy The ulnar osteotomy has been proposed to stabilise the radial head either on its own (through overcorrection) or along with open reduction of the radial head and reconstruction of the annular ligament. The ulnar osteotomy was first described by Judet et al.12 in 1962. Hirayama et al.11 reported a series of nine patients managed by over correction and elongation of the ulna. The patients were 2–12 years old and the injury occurred 2 months to 3 years before surgical reconstruction. The scar tissue obstructing reduction was excised and an ulnar osteotomy performed 5 cm distal to the olecranon. The ulna was distracted by 1 cm and angulated by 151 at the osteotomy site. To correct an anteriorly dislocated radial head, the ulnar osteotomy is angulated posteriorly, producing a convexity towards the posterior aspect and thus stabilising the proximal radius. Similarly, for a lateral dislocation (Type III), the osteotomy was angulated medially. No attempt was made to repair the annular ligament. A cast was applied keeping the elbow in 901 flexion and the forearm supinated. Three patients had residual loss of pronation, and one patient who was operated 3 years following the injury had a poor result with restricted extension and pronation. The remaining patients did well. Tension in the interosseous membrane is said to stabilise the radial head following ulnar elongation osteotomy. The position of postoperative immobilisation was changed to midpronation in the later cases due to problems of residual restriction of pronation in patients immobilised in supination. Biceps tendon lengthening was required in some cases to enable full extension. Open reduction of the radial head with ulnar osteotomy is relatively simpler than formal annular ligament reconstruction and, based on reports in the literature, seems to provide comparable results.
Authors’ preferred treatment option The experience of the senior author (BWS) is based on reconstruction of the annular ligament in accordance with the recommendation and operative technique reported by Seel and Peterson.1 A lateral Kocher’s approach is used and the fibrous tissue and remnants of the annular ligament obstructing reduction are excised. Stability of
ARTICLE IN PRESS 376 reduction is assessed. If there is a significant ulnar bowing deformity, a corrective ulnar osteotomy is done and stabilised with a four-hole plate. The lateral margin of triceps fascia is used as a graft and the strip is harvested through an extension of the approach proximally, aiming to keep the graft as long as possible. A drill hole is made in the ulna from the posterior border to the antero-lateral edge, which corresponds to the antero-medial attachment of the annular ligament. The fascial strip is passed in the drill hole in the ulna from the back to exit anteriorly, then around the radial neck and then onto the lateral surface of the ulna to be sutured to itself at the starting point (Fig. 1A). An alternative is to make two drill holes crossing each other and after
S. Agarwal, B.W. Scott looping round the radial neck, the strip is passed back into the second drill hole and exits posteriorly to be sutured back to the starting point (Fig. 1B). The second drill hole provides a more anatomic posteromedial line of pull on the radial head. A transcapitellar Kirschner wire may be used for additional stability in the early postoperative period if there is any concern regarding the integrity of reconstruction and the wire is removed at the time of cast removal at 6 weeks. We have not had any instances of wire breakage as long as the arm is immobilised in a cast for the same duration. Active movement is started after 6 weeks. In patients who are operated within 3 months of injury, it may be possible to define the annular ligament and repair it.
Illustrative cases Case 1
Figure 1 Direction of drill holes through the proximal ulna to pass the triceps fascia strip. Single (A) or double (B) drill holes may be used and the resultant stabilising force maintains alignment of the radial head.
A 7 year old girl sustained a low energy injury to her elbow when she fell whilst playing. On X-rays, there was no obvious fracture in the forearm. The radial head dislocation was not detected and the injury was treated as an undisplaced supracondylar fracture of the humerus and a cast was applied for 3 weeks. On removal of the cast, repeat radiographs showed the dislocated radial head (Fig. 2). A referral was made to our centre and at that point, she was 5 weeks following the injury. A closed reduction was unsuccessful at that stage and an open reduction and reconstruction of the annular ligament was performed (Fig. 3). No
Figure 2 (A) and (B) Preoperative radiographs showing the dislocated head of radius without forearm deformity.
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Figure 3 (A) and (B) Postoperative radiograph showing relocation of the radial head and a congruent joint.
Figure 4 (A) and (B) Preoperative radiograph showing the ulnar deformity and anterior dislocation of the radial head.
osteotomy was necessary, as the shape of the radius and the ulna was normal. A transcapitellar wire was used for stability and removed after 6 weeks. At last follow-up, she had a stable elbow with a nearly full range of motion.
Case 2 A 10 year old boy sustained an injury to his forearm. The radial head dislocation was missed and the injury treated as a fracture of the ulna. Ten months
following injury, he presented back to the clinic with a bony swelling on the anterior aspect of the elbow, which on radiographs (Fig. 4) was confirmed to be the dislocated radial head. At this point he was referred to our centre. There was an anterior dislocation of the radial head with an anteriorly angulated fracture of the ulna. This was managed by open reduction of the radial head, corrective osteotomy of the ulna and reconstruction of the annular ligament using the triceps fascia strip (Fig. 5). The transcapitellar wire was removed at 6 weeks when active movements were started. At
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Figure 5 (A) and (B) Postoperative radiograph showing the reconstruction. Ulnar osteotomy has been stabilised with a plate and the radial head is reduced.
last follow-up, he had a flexion—extension range of 25–1151 and had regained almost full supination but little pronation.
Summary Dislocation of the radial head can be managed by closed reduction if recognised and treated within 3 weeks of injury. Beyond 3 weeks, open reduction is often required. If there is a delay in treatment of over 3 months, the reconstructive options to restore anatomy are either to reconstruct the annular ligament with a triceps fascia strip, or to correct the ulnar angulation by ulnar osteotomy. The two procedures can be combined for old unreduced dislocations with a significant ulnar deformity. The reported results with both these procedures are good in most patients with the main problem being restricted range of elbow movements. Practice points
High index of suspicion for the Monteggia injury in children with elbow or forearm trauma Adequate radiographic evaluation is essential Annular ligament reconstruction using the triceps fascia passed through drill holes in the proximal ulna is a reliable procedure
References 1. Seel MJ, Peterson HA. Management of chronic posttraumatic radial head dislocation in children. J Pediatr Orthop 1999; 19:306–12. 2. Fowles JV, Sliman N, Kassab MT. The Monteggia lesion in children. Fracture of the ulna and dislocation of the radial head. J Bone Joint Surg Am 1983;65(9):1276–83. 3. Hurst LC, Dubrow EN. Surgical treatment of the symptomatic chronic radial head dislocation: a neglected Monteggia fracture. J Pediatr Orthop 1983;3:227–30. 4. Freedman L, Luk K, Leong JCY. The radial head reduction after a missed Monteggia fracture: brief report. J Bone Joint Surg Br 1988;70:846–7. 5. Watson-Jones, Sir R. Fracture and joint injuries, vol. 2. 4th ed. Edinburgh and London: E. and S. Livingstone; 1955. p. 579. 6. Lloyd-Roberts GC, Bucknill TM. Anterior dislocation of the radial head in children. Aetiology, natural history and management. J Bone Joint Surg Br 1977;59(4):402–7. 7. Hresko MT, Rosenberg BN, Pappas AM. Excision of the radial head in patients younger than 18 years. J Pediatr Orthop 1999;19(1):106–13. 8. Campbell CC, Waters PM, Emans JB. Excision of the radial head for congenital dislocation. J Bone Joint Surg Am 1992; 74(5):726–33. 9. Bell Tawse AJS. The treatment of malunited anterior Monteggia fractures in children. J Bone Joint Surg Br 1965; 47(4):718–23. 10. Best TN. Management of old unreduced Monteggia fracture dislocations of the elbow in children. J Pediatr Orthop 1994;14:193–9. 11. Hirayama T, Takemitsu Y, Yagihara K, Mikita A. Operation for chronic dislocation of the radial head in children. J Bone Joint Surg Br 1987;69(4):639–42. 12. Judet R, Lord G, Roy-Camille R. Osteotomy of the cubital diaphysis in old dislocations of the radial head in the child. Presse Med 1962;70:1307–8.
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FOOT
The surgical treatment of Morton’s neuroma$ Samrendu K. Singh, James P. Ioli, Christopher P. Chiodo Brigham Foot and Ankle Service, Department of Orthopaedic Surgery, 1153 Centre Street, Suite 56, Jamaica Plain, Boston, MA 02130, USA
KEYWORDS Morton’s neuroma; Surgery; Release; Metatarsalgia
Summary Morton’s neuroma is a painful forefoot disorder caused by thickening and fibrosis of an interdigital nerve. The aetiology is unknown. On physical examination, care should be taken to differentiate it from metatarsalgia or joint synovitis/instability. The lateral squeeze test is often positive. The sensitivity and specificity of MRI and ultrasound for confirming the diagnosis has been questioned. Surgery is considered if symptoms persist after 3 months of non-operative treatment. In this article we describe our recommended surgical technique for neuroma resection. & 2005 Elsevier Ltd. All rights reserved.
Introduction Lewis Durlacher,1 the surgeon chiropodist to Queen Victoria, was actually the first to describe a ‘‘form of neuralgic affection’’ involving the ‘‘plantar nerves between the third and fourth metatarsal bones’’ in 1845. In 1876, Thomas G. Morton,2 a Philadelphia based surgeon, further localised the problem to the region of the fourth metatarsophalangeal joint. While Morton’s neuroma is a relatively common painful disorder of the forefoot characterized by thickening and fibrosis of an interdigital nerve, its aetiology and pathogenesis is not entirely under$
Work undertaken at the Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA. Corresponding author. Tel.: +1 617 983 7361; fax: +1 617 983 7201. E-mail address:
[email protected] (C.P. Chiodo).
stood. Morton speculated that a neuroma or hypertrophy of the digital branches of the lateral plantar nerve was the cause of the pain. Betts3 subsequently attributed the condition to a ‘‘neuritis of the interdigital nerve.’’ Nissen4 suggested that pressure on the digital artery from local structures causes intermittent neural ischaemia. Betts proposed that a communicating branch to the fourth web space tethers the interdigital nerve of the third web space, rendering the nerve vulnerable to repetitive shear on the edge of the intermetatarsal ligament. Other proposed aetiologies for interdigital neuroma formation include entrapment of the interdigital nerve at the anterior edge of the transverse intermetatarsal ligament5 and compression of the interdigital nerve by a swollen intermetatarsal bursa.6 The current authors speculate that it may be a combination of peripheral entrapment, tethering, ischaemia and repetitive trauma that is ultimately
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ARTICLE IN PRESS 380 responsible for the development of the interdigital neuroma.
Clinical presentation The diagnosis of Morton’s neuroma is based primarily on history and physical examination. It should be considered in all patients with forefoot pain, but establishing an accurate diagnosis can be challenging as several other forefoot conditions have similar clinical presentations. The typical patient with a Morton’s neuroma complains of a sharp, burning pain localized to either the second or third web space or metatarsal interspace. Approximately 80% of neuromas occur in the third web space with the remainder occurring in the second web space. The condition occurs so rarely in the first and fourth web spaces that in these cases an alternative diagnosis should be sought. The pain is usually plantar at the level of the metatarsal heads, and often radiates into the toes and may be associated with distal numbness. Interestingly, one differentiating feature is that a patient with a Morton’s neuroma often feels the need to remove the shoe and massage the area.7 On examination, maximal tenderness is localized to the involved interspace at the level of the metatarsal heads. Care should be taken to differentiate this tenderness from that felt under the metatarsal heads in metatarsalgia or from that felt over the metatarso-phalangeal joint with synovitis or instability. Thus, the metatarso-phalangeal joint drawer test for instability should routinely be performed. With a Morton’s neuroma, cutaneous sensation may be decreased in the distal distribution of the affected digital nerve. Additionally, the ‘‘lateral squeeze test’’ is often positive. This test is performed by applying plantar and dorsal pressure with the examiner’s thumb and index finger to the involved interspace at the level of the metatarsophalangeal joints while gently squeezing the forefoot with the other hand. It is positive if a palpable or painful click is produced. The pain disappears very suddenly when the compression is relieved. The click is commonly referred to as a ‘‘Mulder’s click’’, and is thought to result from the neuroma subluxing between the adjacent metatarsal heads.8 The differential diagnosis for Morton’s neuroma is extensive and includes metatarsalgia, metatarsophalangeal synovitis/instability, stress fracture, Frieberg’s infraction, infection and tumours. For this reason we recommend routine radiographs of the foot when evaluating a patient with a possible neuroma.
S.K. Singh et al. Beyond radiographs, further imaging is usually unnecessary. Recently, the sensitivity and specificity of MRI and ultrasound for confirming the clinical diagnosis of a Morton’s neuroma has been questioned.9–11 Sharp et al.12 reported 29 histologically confirmed cases that had a physical examination, ultrasound and MRI. In this series, physical examination was the most sensitive and specific modality. The accuracy of ultrasound and MRI was similar and dependent on the size of the lesion. We feel that this is important, as in our experience, the size of the lesion correlates neither with preoperative nor postoperative pain.
Treatment Non-operative therapy should be attempted for 3 months before proceeding with surgery. Initially, non-steroidal anti-inflammatory medications and shoe wear modification are recommended. The shoe should have a soft upper and a wide toe-box. Second-line treatment options include metatarsal padding, orthotics, and steroid injections. We inject the web space through the dorsum of the foot. It is essential that the needle be passed deep to the transverse intermetatarsal ligament. This can be confirmed by looking for tenting of the plantar skin. Surgical excision of a symptomatic neuroma is an effective and reliable treatment option for those patients who have not responded to non-operative measures for a persistently painful neuroma. Contraindications to surgery include ongoing infection and compromised perfusion. In the foot with poor pulses, Doppler evaluation is a valuable tool to assess perfusion and wound healing capacity. If the ankle/brachial pressure index (ABPI) is less than 0.5, surgery should be delayed, and the patient referred for a vascular opinion. All surgical candidates should be counseled preoperatively with regard to the general risks of foot surgery and the possibility of developing a symptomatic ‘‘stump’’ or ‘‘bulb’’ neuroma, and warned that there will be permanent numbness in the affected webspace.
Surgical treatment Several procedures have been described13,14 including isolated inter-digital nerve excision, isolated transverse metatarsal ligament division, and inter-digital nerve excision combined with transverse ligament division.
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Our preference is nerve resection with intermetatarsal ligament division, as there is little evidence supporting simple ligament division. We do not favour resection without ligament division, as the painful stump cannot be buried sufficiently proximally. The concern that division of this ligament may lead to a splayed foot has been disproved.15
Dorsal approach For primary surgery, a dorsal approach is to be preferred. The patient is positioned supine and local or regional anesthesia used. An ankle or thigh tourniquet may be used. A three to four centimeter longitudinal incision is made in the midline of the involved interspace. The incision starts proximal to the metatarsal heads and extends distally into the web space.16 Because the skin in the web space is thin, the distal incision must be adequate to prevent uncontrolled tearing with retraction. The subcutaneous tissues are bluntly dissected with a finger or the back of a forceps. Just deep to the skin there is a small vein that crosses the field and should be cauterized. Additionally, care should be taken to avoid damaging the dorsal digital nerves. The deep fascia of the foot is a distinct layer and is divided sharply in line with the skin incision. This layer should not be confused with the deeper, transverse intermetatarsal ligament. A small self-retaining retractor, or ideally a lamina spreader, is then placed between the metatarsals to put the transverse metatarsal ligament under tension. With this, the proximal and distal borders are readily identified and a blunt elevator or haemostat can be passed deep into it to protect the underlying nerve (Fig. 1). The ligament is then released sharply (Fig. 2). Next, the two distal branches of the common digital nerve are identified and isolated. After supplemental infiltration of the region with plain lignocaine, the distal branches are transected. The cut distal ends of the nerve are grasped with a hemostat. The nerve is then gently elevated and dissected proximally. The small plantar branches of the nerve should be identified and divided (Fig. 3). While traction is applied to the nerve, the area is again infiltrated with lignocaine and the nerve is transected as proximal to the metatarsal heads as possible (Fig. 4). The deep tissues are closed with buried interrupted 4-0 absorbable sutures. The skin is closed with 4-0 nylon sutures using a ‘no-touch’ technique.
Figure 1 A lamina spreader is placed between the metatarsals to put the transverse metatarsal ligament under tension. A haemostat protects the underlying nerve.
Figure 2 The transverse metatarsal ligament has been divided revealing the neuroma.
Plantar approach A symptomatic stump neuroma may develop in patients who have undergone a primary interdigital neurectomy.17,18 This is characterized by plantar burning or a stabbing pain that is exacerbated by weight bearing and reproduced by applying plantar pressure just proximal to the metatarsal heads. For resection of a recurrent stump neuroma, a plantar approach is recommended, as this will allow better exposure of the proximal nerve trunk.19,20
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A plantar incision is made just proximal to the web space and extends at least 4 cm proximally, equidistant between the metatarsal heads and shafts.
Minimal deep dissection is needed, as the neuroma is usually located subcutaneously (Fig. 5). The neuroma is dissected and freed from adjacent tissues. Dissection is then continued proximally to a normal segment of the nerve trunk. At this level, the nerve is transected sharply and the proximal stump buried into the intrinsic musculature of the foot. The deep tissues are closed with buried interrupted 4-0 absorbable sutures. The skin is closed with 4-0 nylon sutures.
Post-operative care and return to activity
Figure 3 The cut distal ends on the nerve are grasped with a haemostat. The nerve is gently elevated and dissected proximally. The small plantar nerves should be identified and divided.
In all cases, a compression dressing is applied and the foot protected with a post-operative shoe. After primary neurectomy through a dorsal approach, immediate weight bearing is allowed and the skin sutures are removed at 10–14 days postoperatively. After revision neurectomy through a plantar approach, weight bearing and suture removal are delayed for 2–3 weeks. Cross training for high-level athletes should be delayed until the skin has healed. Thereafter, appropriate exercises include pool training and the use of an exercise bike. The patient may progress to a regular shoe in 3–4 weeks. High-level sports participation is generally restricted for 4–6 weeks.
Figure 4 Traction is applied and the nerve transected as proximal to the metatarsal heads as possible.
ARTICLE IN PRESS The surgical treatment of Morton’s neuroma
383 segment deep within the intrinsic musculature of the foot. The absorbable suture is then cut under tension at the level of the dorsal skin and allowed to retract subcutaneously.
Conclusion Reports in the literature on patient satisfaction following this procedure range from 80% to 93%.14,17,18,21 Patients should be counseled about the specific residual effects including interdigital numbness (68%17,72%18) and plantar numbness (50%17, 65%18). Practice points
Figure 5 The plantar approach for revision surgery. The nerve is subcutaneous.
Pearls and pitfalls Careful handling of the soft-tissues and meticulous haemostasis will minimize post-operative swelling and pain. Good knowledge and understanding of the local anatomy and good surgical exposure is essential to avoid damaging and/or mistakenly excising the lumbrical tendon or the digital artery. Exposure is facilitated by an adequate incision, the use of a tourniquet, and loupe magnification. Placing a self-retaining retractor or lamina spreader between the metatarsal heads puts the intermetatarsal ligament under tension, greatly facilitating identification and division of this structure. Transection of the nerve trunk as proximal to the metatarsal heads as possible decreases the chances of developing a painful ‘‘stump’’ neuroma. To this end, dividing the small plantar branches of the nerve proximal to the level of transection allows the proximal segment to retract more readily. With burial of a recurrent stump neuroma into the intrinsic musculature of the foot, it is helpful to place a 4-0 absorbable stitch through the epineural layer of the distal aspect of the proximal nerve segment. The suture is attached to a straight free needle, which is then delivered through the dorsum of the foot. This pulls and buries the proximal nerve
Morton’s neuroma is a common cause of forefoot pain. The diagnosis is based primarily on history and physical examination. Surgery should be considered only after 3 months of non-operative therapies have failed. We recommend a dorsal approach with division of the transverse intermetatarsal ligament and neuroma resection.
References 1. Durlacher L. A treatise on corns, bunions, the diseases of nails, and the general management of feet. Simpkin: Marshall and Co; 1945. 2. Morton TG. A peculiar and painful affection of the fourth metatarso-phalangeal articulation. Am J Med Sci 1876; 71:37–45. 3. Betts LO. Morton’s metatarsalgia. Med J Aust 1940;1:514–5. 4. Nissen KI. Plantar digital neuritis: Morton’s metatarsalgia. J Bone Joint Surg (Br) 1948;30:84–94. 5. Gauthier G. Thomas Morton’s disease: a nerve entrapment syndrome. A new surgical technique. Clin Orthop Relat Res 1979;142:90–2. 6. Bossley CJ, Cairney PC. The intermetatarsal bursa: its significance in Morton’s metatarsalgia. J Bone Joint Surg (Br) 1980;80-B:184–7. 7. Lutter LD. Atlas of adult foot and ankle surgery. St Louis, Missouri: Mosby; 1997. p. 115–20. 8. Mulder JD. The causative mechanism in Morton’s metatarsalgia. J Bone Joint Surg (Br) 1951;33-B:94–5. 9. Terk MR, Kwong PK, Suthar M, Horvath BC, Colletti PM. Morton neuroma: evaluation with MR imaging performed with contrast enhancement and fat suppression. Radiology 1993;189:239–41. 10. Resch S, Stenstrom A, Jonsson A, Jonsson K. The diagnostic efficacy of magnetic resonance imaging and ultrasonography
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11.
12.
13. 14.
15.
in Morton’s neuroma: a radiological–surgical correlation. Foot Ankle Int 1994;15:88–92. Zanetti M, Strehle JK, Zollinger H, Hodler J. Morton neuroma and fluid in the intermetatarsal bursae on MR images of 70 asymptomatic volunteers. Radiology 1997;203:516–20. Sharp RJ, Wade CM, Hennessy MS, Saxby TS. The role of MRI and ultrasound imaging in Morton’s neuroma and the effect of size of lesion on symptoms. J Bone Joint Surg (Br) 2003; 85-B:999–1005. McGlamry ED, Banks AS, Downey MS. Comprehensive textbook of foot surgery. Baltimore: Williams & Wilkins; 1992. p. 304–20. Thomson CE, Gibson JN, Martin D. Interventions in the treatment of Morton’s neuroma. Cochrane Database Syst Rev 2004;(3):CD003118. Hamilton WG. Morton’s neuroma surgery. The Foot: Surgical Update. Seattle, Washington: AAOS Summer Institute; 1992.
S.K. Singh et al. 16. McKeever DC. Surgical approach for neuroma of plantar digital nerve (Morton’s Metatarsalgia). J Bone Joint Surg 1952;34A:490. 17. Mann RA, Reynolds JC. Interdigital neuroma—a critical clinical analysis. Foot Ankle 1983;3:238–43. 18. Coughlin MJ, Pinsonneault T. Operative treatment of interdigital neuroma: a long-term follow-up study. J Bone Joint Surg 2001;83A:1321–8. 19. Johnson JE, Johnson KA, Unni KK. Persistent pain after excision of an interdigital neuroma. Results of reoperation. J Bone Joint Surg Am 1988;70:651–7. 20. Beskin JL, Baxter DE. Recurrent pain following interdigital neurectomy—a plantar approach. Foot Ankle 1988;9:34–9. 21. Keh R, Ballew K, Higgins K, Odom R, Harkless L. Long term follow-up of Morton’s neuroma. J Foot Surg 1992;31(1): 93–5.
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HIP
Girdlestone resection arthroplasty of the hip: Current perspectives H. Sharma, C.R. Dreghorn, E.R. Gardner Victoria Infirmary, Glasgow G42 9TY, UK
KEYWORDS Girdlestone operation; Resection arthroplasty; Excision arthroplasty; Hip
Summary Modern technological advancements in revision hip arthroplasty have revolutionised the treatment of failed primary total hip replacements. The decision to perform a Girdlestone operation is taken as a last resort, particularly for medically sub-optimal and functionally compromised patients, who have a high anaesthetic and operative risk at one-stage and two-stage reimplantations. Girdlestone resection arthroplasty should be considered as a salvage procedure, primarily aimed at pain relief and infection control. Such patients must be warned to expect 2–3 in of limb shortening and reliance upon a walking aid postoperatively. & 2005 Elsevier Ltd. All rights reserved.
Introduction With an increase in life expectancy, the number of patients with primarily replaced and revised hips is increasing dramatically. Although, revision total hip arthroplasty has revolutionised the treatment of failed primary total hip replacements, medically sub-optimal and functionally compromised patients, who have a high anaesthetic and operative risk, may not be suitable for any further major interventions, especially one-stage and two-stage reimplantations. In such cases, Girdlestone resection arthroplasty (i.e. removal of prosthesis and/or cement) is considered to be an acceptable salvage option. Corresponding author. Tel.:+44 141 639 3697;
fax: +44 141 201 5082. E-mail addresses:
[email protected] (H. Sharma),
[email protected] (C.R. Dreghorn),
[email protected] (E.R. Gardner).
There are several retrospective studies published on long-term outcome of this salvage procedure, mainly infected total hip arthroplasty with variably reported results.1–10 The indication for the Girdlestone operation has now become a salvage procedure. This article is an overview of Girdlestone resection arthroplasty of the hip with special regard to indications, patient selection, surgical technique, mortality and morbidity characteristics, outcome analysis and prognostic factors influencing outcome.
Historical perspectives The first report of resection arthroplasty (removal of the head and the neck of femur) as a treatment for septic arthritis of the hip was published by White in 1849.11 In 1928, Gathorne Robert Girdlestone
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(1881–1950), an orthopaedic surgeon from Oxford, described a similar procedure for the tuberculous hip joint.11 In 1943, Girdlestone popularised it for the treatment of late septic arthritis. Girdlestone himself did not report any long-term functional results. In 1945, Batchelor recommended dividing the femoral neck distally, flush with the lesser trochanter, to achieve smooth surfaces. He observed that irregular osseous spurs or prominences might cause considerable pain with motion. He also advocated performing an abduction osteotomy in conjunction with the resection of the femoral head and neck to improve stability.11 The modern Girdlestone procedure predominantly consists of removal of the prosthesis and/or cement following septic and aseptic loosening of total hip arthoplasty or hemiprosthesis.11
Types of girdlestone resection arthroplasty The Girdlestone procedure can be described into two main categories:
Primary Performed for primary hip disorders like septic hip, tuberculous hip, and rarely for osteoarthritis and rheumatoid arthritis.
Secondary or modified Used for failed hip replacements or failed construction after hip trauma (Figs. 1 and 2). For all practical purposes, any Girdlestone procedure performed nowadays can be considered as a secondary or modified Girdlestone procedure.
Why resection, why not revision? The modern Girdlestone operation involves the removal of the prosthesis and/or cement following septic or aseptic loosening of a total hip prosthesis, hemi-prosthesis or a failed osteosynthesis. It has proved to be an effective salvage procedure, for controlling pain and infection. With the advancements in revision hip technique and technology, Girdlestone resection arthroplasty is rarely indicated as a primary procedure. It is a salvage procedure, and it should not be considered as an alternative to one- or two-stage reimplantations. Indications include infective and aseptic loosening of total or hemi-arthroplasties, recurrent dislocations and un-united operated femoral neck fractures. Girdlestone pseudarthrosis may also be considered as the first stage of a two-stage revision. The decision to perform a resection arthroplasty without reimplantation of a second prosthesis is based upon multiple factors. Important considerations include infection with multiple organisms or bacteria resistant to antibiotic therapy, poor quality
Figure 1 Early Girdlestone for septic total hip arthroplasty.
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Surgical technique of girdlestone procedure A standing anteroposterior radiograph of the pelvis should be taken to plan the resection. The role of preoperative traction is debatable. A direct lateral or posterior approach through the previous scar should include the excision of any sinus or scar. Iliopsoas tenotomy and/or adductor tenotomy may be required. Femoral preparation comprises removal of the prosthesis (with or without trochanteric osteotomy), removal of cement and smoothing of the transected femoral surface. Utmost care should be observed to prevent femoral shaft fractures intraoperatively. Tissue specimens should be sent for both bacteriology and histology. Acetabular preparation consists of the removal of the prosthesis and cement. Primary wound closure is preferred even in infected cases.14 Intra- and immediate postoperative blood loss may vary from 1 to 5 l.
Radiographic classification Grauer et al.11 described four possible levels of proximal femoral resection: Figure 2 Late Girdlestone with proximal migration of greater trochanter nearly abutting against lower ilium. Table 1
Indications for resection.
Infection with multiple organisms or bacteria resistant to antibiotic therapy Poor quality local soft tissues Unacceptable complexity of any possible reconstruction Refusal by the patient to have another operation after removal of the implant Patients with systemic disease or poor overall health Inadequate bone stock Or combinations of these factors
local soft tissues, unacceptable complexity of the reconstruction, refusal by the patient to have another operation after removal of the implant, and patients with systemic disease, poor overall health, inadequate bone stock or combinations of these factors.12,13 The problem of repeated operations, prolonged morbidity, intercurrent illnesses and repeated invasive investigations after an infected prosthesis leads to depression and dissatisfaction. Table 1 therefore summarises the circumstances when resection may be the appropriate option.
Type I—a substantial portion (41.5 cm) of the femoral neck remains, usually performed for failed resurfacings, Type II—a small portion of the femoral neck remains (1.5 cm or less), Type III—intertrochanteric resection, Type IV—sub-trochanteric resection. The obvious clinical implication of this classification is that the more proximal the resection, the better is the overall function, walking and activity of the patient. Contrary to this observation, no correlation could be found between the radiological appearances and the quality of the result in some studies.15,16
Overall outcome Girdlestone arthroplasty patients cannot be assessed with the usual parameters routinely applied for hip evaluation.3 The functional outcome in previous studies on Girdlestone arthroplasty is illustrated in Table 2. The reported results of Girdlestone arthroplasty are not uniform. Satisfactory results have been reported by Campbell et al.,19 Mallory,21 Ahlgren et al.,17 Grauer et al.,11 Bohler and Salzer18 and Castellanos
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77.77% 59.3 79 —
83
18 88.88% 100% 94.4% — 27 — 81.5 100 5.2 78 83 86 100 4.1 33 91 97 85 4 30 90 80 100 4–7.5
Esenwein et al.2 Castellanos et al.20 Bourne et al.12 Clegg1
Old patient (Marchetti et al.,3 Bittar and Petty22 found poor results in younger patients) Male Unilateral16 Healed wound5 Non-diabetic (Rittmeister et al.27 found poor results in diabetics) Smooth inter-trochanteric line5 No cement left in the femoral canal1,27. Contrary paper by Ballard et al.15 Less limb shortening/conservative proximal femoral resection11 Reduced level of expectation Unfavourable preoperative condition with strong pain or persistent infection
et al.,20 while poor outcomes were recorded Clegg,1 Petty and Goldsmith,5 Bittar and Petty,22 McElwaine and Colville4 and Esenwein et al.2 In Table 3, the favourable outcome determinants with Girdlestone resection arthroplasty have been listed.
Mallory21
10 90 100 100 3.8
90
27 89 100 100 4–5
100
Intra- or postoperative mortality is reported to be between 7% and 62% following Girdlestone operation for infected total hip replacements.20 A higher postoperative mortality follows the Girdlestone procedure for failed hip fractures than after revision for failed arthroplasty.23
45 Good 73 100 —
88 15
Morbidity analysis
21 0 76 100 5.4
Petty and Goldsmith5
Campbell et al.19
Ahlgren et al.17
Mortality analysis
No. of patients Relief of pain Control of infection Need for walking aid Leg length discrepancy (in cm) Patient satisfaction
Table 2
Summary of the functional outcome with Girdlestone resection arthroplasty of the hip in the previously published studies.
Sharma et al.23
Table 3 Favourable outcome determinants with Girdlestone resection arthroplasty.
Complications include infection with persistent discharging sinuses and fistulae, haemorrhage and hypovolaemia, proximal femoral fracture, tractionrelated problems (pin-site infection, common peroneal nerve compression, joint stiffness, contractures), the effects of immobilisation (decubitus ulcers, urinary infection, chest infection, disuse osteoporosis, muscle wasting), persistent pain, thrombo-embolism, psychological disturbances (depression, psychosis, suicidal tendency), a Trendelenburg gait and generalised fatigue.
Age, sex, side and body mass index Younger patients have higher functional demands and expectation so they are likely to be dissatisfied
ARTICLE IN PRESS Girdlestone resection arthroplasty of the hip: Current perspectives with the operation. The results are reported to be significantly poorer in women, particularly older ones as reported by Grauer et al.11 The patients were satisfied with the operation in unilateral cases as a secondary operation, but it was generally unsatisfactory as a primary procedure or when performed bilaterally.16 Grauer et al.11 also observed that body weight, height and body habitus pose no statistically significant influence on pain, walking or function.
Pain relief The primary goal of the Girdlestone procedure is pain relief. Adequate pain relief was observed in 60% (Scalvi et al.), 77% (Ballard et al.), 80% (Parr et al.), 83% (Castellanos), 91% (Bourne et al.) and 89% (Sharma et al.).6,12,15,20,23,24
Infection control Control of infection has been reported in 73–100% cases postoperatively following the Girdlestone operation.1,5,11,18 Sharma et al.23 achieved 100% infection control in the surviving patients, similar to Mallory21 and Ahlgren et al.17. Infection control was achieved in the majority of the studies
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(83%—Parr et al.; 86%—Castellanos; 97%—Bourne et al.).12,20,24 Castellanos et al.20 found no correlation between the type of organisms and the persistence of infection, although, Kantor et al. identified worse functional results in patients with chronic drainage.10 Clegg1 advocated a complete removal of all the cement in order to achieve an eradication of infection. Practically, it can be quite difficult to get rid of all cement remnants (Figs. 3–5). We agree with the views of Petty and Goldsmith,5 Ahlgren et al.,17 Bourne et al.12 that small amounts of retained cement do not seem to influence wound healing after resection arthroplasty.
Leg length discrepancy and need for walking aids Most of the studies reported limb shortening of approximately 4–6 cm.2,12,20,25 The degree of shortening is often dependent on the amount of bone lost from the proximal femur and the quality of the scar tissues at the time of surgery.11 Associated gluteus medius insufficiency magnifies the need for walking aids. McElwaine and Colville4 noted that calipers were found to be unacceptable in the majority of patients. Grauer et al.11 reported a positive correlation between shortening and level of resection, patients with less shortening walking
Figure 3 Septic failure of revision total hip arthroplasty with recurrent dislocation is a common indication for Girdlestone procedure.
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Figure 4 Pre-Girdlestone radiograph showing aseptic recurrent dislocation of total hip arthroplasty.
better, although the difference was not statistically significant. Electromyocinesigraphic26 examination performed in Girdlestone patients in order to study the automatic function of the muscles with patients standing and walking confirmed that there was no innervation of the hip abductors but high activity in the rectus femoris during standing. The contralateral abductor group and the trunk muscles were hyperactive during standing and walking.
Overall satisfaction Subjective satisfaction varies between 14% and 100%.5,12,18,23 in the reported series. It is hard to attach much credibility to this overall measurement in view of this major discrepancy in reported results.
Failed total hip replacements versus failed hip fractures The mortality was higher in the failed fracture group (68%) in comparison to those with failed arthroplasty23 (48%) (Figs. 6 and 7).
H. Sharma et al.
Figure 5 Post-Girdlestone radiograph of the same patient. Note that stable components, cement and circlage wires could be left alone in these relatively high anaesthetic risk patients.
Delayed reimplantation following girdlestone arthroplasty Rittmeister et al.27 reported greater patient satisfaction and better function if Girdlestone hips were converted to a hip arthroplasty rather than being left with the excisional procedure. The incidence of postoperative complications and revisions were similar for both groups. Charlton et al.28 in retrospective study showed a high rate of dislocation (11.4%) and persistent limp (39%) following delayed conversion. A high dislocation rate following conversion of the Girdlestone procedure to secondary total hip arthroplasty relates to soft tissue contracture, limb length discrepancy, deficient bone stock and malpositioning of the components. A constrained acetabular component should be considered to reduce the dislocation rate. Schroder et al.29 followed two groups of patients: 32 patients had a long-standing pseudarthrosis; in the other group of 16 patients, a total hip replacement was reimplanted at an average of 3 years after a pseudarthrosis. The improvement in
ARTICLE IN PRESS Girdlestone resection arthroplasty of the hip: Current perspectives
Figure 6 Aseptic loosening of Thompson’s uncemented hemi-arthroplasty subsequently underwent Girdlestone procedure.
hip function after the reimplantation was marginal and the results were comparable to a wellfunctioning pseudarthrosis. Personal satisfaction and the activities of daily living were marginally better in the reimplantation group, (Harris hip score 64 compared to 58 in those with a pseudarthrosis). Brandt et al.30 stated that prosthesis removal and delayed reimplantation arthroplasty is an effective treatment to limit the recurrence of Staphylococcus aureus prosthetic joint infection, provided there is no evidence of infection at the time of reimplantation arthroplasty.
Conclusions Various studies have confirmed that the Girdlestone procedure is very effective in achieving its primary goals of infection control and pain relief for irreversibly failed total hip joints and to salvage failed operated hip trauma. A high mortality and a poor functional outcome could be attributed to a higher age group, poor general health and highly selected group of patients, who were unfit for reimplantation surgery. Patients who have had
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Figure 7 While performing Girdlestone operation in the same patient, an intraoperative femoral shaft fracture occurred. It was successfully treated non-operatively.
resection arthroplasty following failed operated hip trauma do considerably worse than after failed total hip arthroplasty. There is no significant difference between the long-term outcomes of Girdlestone procedures performed at a District General Hospital compared to a University Teaching Hospital. The decision to perform a Girdlestone operation is mostly taken as a last resort, as all the suitable candidates are filtered off for revision surgery, before reaching the stage of this salvage operation. The decision between revision and resection should not be taken lightly and it should not be considered as an alternative to one-stage or two-stage reimplantations. Such patients must be warned to expect 2–3 in of limb shortening and reliance upon a walking aid postoperatively. This operation can be made acceptable by proper explanation to the patient with realistic expectations.
Practice points
The primary goals of the Girdlestone operation are pain relief with infection control. It
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H. Sharma et al. is a salvage procedure, and should not be considered as an alternative to one-stage or two-stage reimplantations A high mortality is observed in the literature with such groups of patients which can be attributed to higher age group, poor general health and highly selected group of patients, who are unfit for reimplantation surgery Patients must be warned to expect 2–3 in of limb shortening and invariable assisted mobility postoperatively
10.
11.
12.
13.
Research directions
14.
15.
Future studies with larger number of patients utilising results from multiple centres may reveal more meaningful results with primary pathology diagnosis stratification Need for a separate questionnaire for assessing Girdlestone patients To compare the long-term outcome of patients with septic retained implants with those treated by excisional arthroplasty To assess the role of Girdlestone resection arthroplasty for MRSA (Methicillin Resistant Staphylococcus Aureus) infected hips
16. 17.
18. 19.
20.
21.
References 1. Clegg J. The results of the pseudarthrosis after removal of an infected total hip prosthesis. J Bone Joint Surg Br 1977;59:298–301. 2. Esenwein SA, Robert K, Kollig E, Ambacher T, Kutscha-Lissberg F, Muhr G. Long-term results after resection arthroplasty according to Girdlestone for treatment of persisting infections of the hip joint. Chirurg 2001;72:1336–43. 3. Marchetti PG, Toni A, Baldini N, Binazzi R, D’Elia L, Sudanese A, et al. Clinical evaluation of 104 hip resection arthroplasties after removal of a total hip prosthesis. J Arthroplasty 1987;2:34–41. 4. McElwaine JP, Colville J. Excision arthroplasty for infected total hip replacements. J Bone Joint Surg Br 1984;66:168–71. 5. Petty W, Goldsmith S. Resection arthroplasty following infected total hip arthroplasty. J Bone Joint Surg Am 1980; 62:889–96. 6. Scalvi A, Campacci A, Marcer M, Cassini M, Guerra C, Ferraresi M, et al. Girdlestone arthroplasty for loosening of the total hip prosthesis: evaluation and results. Chir Organi Mov 1995;80:279–85. 7. Vatopoulos PK, Diacomopoulos GJ, Demiris CS, Gorgolis J, Papathanassiou BT. Girdlestone’s operation: a follow-up study. Acta Orthop Scand 1976;47:324–8. 8. Renvall S, Einola S. Girdlestone operation. An acceptable alternative in the case of unreconstructable hip arthroplasty. Ann Chir Gynaecol 1990;79:165–7. 9. De Laat EA, van der List JJ, van Horn JR, Slooff TJ. Girdlestone’s pseudarthrosis after removal of a total hip
22. 23.
24.
25.
26.
27.
28.
29.
30.
prosthesis; a retrospective study of 40 patients. Acta Orthop Belg 1991;57:109–13. Kantor GS, Osterkamp JA, Dorr LD, Fischer D, Perry J, Conaty JP. Resection arthroplasty following infected total hip replacement arthroplasty. J Arthroplasty 1986;1:83–9. Grauer JD, Amstutz HC, O’Carroll PF, Dorey FJ. Resection arthroplasty of the hip. J Bone Joint Surg Am 1989;71: 669–78. Bourne RB, Hunter GA, Rorabeck CH, Macnab JJ. A six-year follow-up of infected total hip replacements managed by Girdlestone’s arthroplasty. J Bone Joint Surg Br 1984;66: 340–3. Muller RT, Schlegel KF, Konermann H. Long-term results of the Girdlestone hip. Arch Orthop Trauma Surg 1989;108: 359–62. Horan FT. Robert Jones, Gathorne Girdlestone and excision arthroplasty of the hip. J Bone Joint Surg Br 2005;87:104–6. Ballard WT, Lowry DA, Brand RA. Resection arthroplasty of the hip. J Arthroplasty 1995;10:772–9. Haw CS, Gray DH. Excision arthroplasty of the hip. J Bone Joint Surg Br 1976;58:44–7. Ahlgren SA, Gudmundsson G, Bartholdsson E. Function after removal of a septic total hip prosthesis. A survey of 27 Girdlestone hips. Acta Orthop Scand 1980;51:541–5. Bohler M, Salzer M. Girdlestone’s modified resection arthroplasty. Orthopedics 1991;14:661–6. Campbell A, Fitzgerald B, Fisher WD, Hamblen DL. Girdlestone pseudarthrosis for failed total hip replacement. J Bone Joint Surg Br 1978;60:441–2. Castellanos J, Flores X, Llusa M, Chiriboga C, Navarro A. The Girdlestone pseudarthrosis in the treatment of infected hip replacements. Int Orthop 1998;22:178–81. Mallory TH. Excision arthroplasty with delayed wound closure for the infected total hip replacement. Clin Orthop 1978;137:106–11. Bittar ES, Petty W. Girdlestone arthroplasty for infected total hip arthroplasty. Clin Orthop 1982;170:83–7. Sharma H, De Leeuw J, Rowley DI. Girdlestone resection arthroplasty following failed surgical procedures. Int Orthop 2005;29:92–5. Parr PL, Croft C, Enneking WF. Resection of the head and neck of the femur with and without angulation osteotomy. A follow-up study of thirty-eight patients. J Bone Joint Surg Am 1971;53:935–44. Herzog T, Link W, Engel S, Beck H. Resection arthroplasty: middle- and long-term results. Arch Orthop Trauma Surg 1989;108:279–81. Chamay A, Taillard W, Kritsikis N, Burckhardt A. Girdlestone’s hip resection. Clinical and electromyocinesigraphic study. Orthopade 1987;16:287–94. Rittmeister M, Manthei L, Muller M, Hailer NP. Reimplantation of the artificial hip joint in girdlestone hips is superior to girdlestone arthroplasty by itself. Z Orthop Ihre Grenzgeb 2004;142:559–63. Charlton WP, Hozack WJ, Teloken MA, Rao R, Bissett GA. Complications associated with reimplantation after girdlestone arthroplasty. Clin Orthop 2003;407:119–26. Schroder J, Saris D, Besselaar PP, Marti RK. Comparison of the results of the Girdlestone pseudarthrosis with reimplantation of a total hip replacement. Int Orthop 1998;22: 215–8. Brandt CM, Duffy MC, Berbari EF, Hanssen AD, Steckelberg JM, Osmon DR. Staphylococcus aureus prosthetic joint infection treated with prosthesis removal and delayed reimplantation arthroplasty. Mayo Clin Proc 1999;74:553–8.
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TUMOURS
The use of massive bone allografts in bone tumour surgery of the limb Davide Donati, Claudia Di Bella, Marco Col angeli, Giuseppe Bianchi, Mario Mercuri Orthopaedic Surgery, Bone Regeneration Laboratory, Musculoskeletal Oncology Department, Rizzoli Institute, University of Bologna, Via Pupilli 1, 40136 Bologna, Italy
KEYWORDS Bone tumour; Reconstruction; Massive allograft
Summary Massive bone allograft reconstruction is commonly used for limb salvage after malignant bone tumour resection. Since the early 1980s, we have performed 540 operations in the limb with more than 2 years follow-up. The major complication was infection with a high risk of implant failure and significant risk of amputation. Structural failure of the graft is a common reason for further surgery, as is non- or delayed union. Additional autograft gives better results and half of our allografts survived 216 months. & 2005 Elsevier Ltd. All rights reserved.
Introduction Limb salvage surgery for bone tumours started at the Rizzoli Institute in the early 1980s, used in more than 95% of our cases. We have a used a wide variety of reconstructive techniques including cemented and non-cemented metallic implants, biological techniques, fixation with plates and nails, use of associated vascularised transplants, as well as intramedullary cementation and revision prostheses. While most of the cases were treated with modular mega-prostheses, in more than 30% of the procedures, we used massive bone allografts.
Corresponding author. Tel.: +39 51 63 66 885;
fax: +33 951 3317 10. E-mail address:
[email protected] (D. Donati).
Use of bone allografts is dependent on reliable bone banks. In Italy we were reliant on massive bone allografts imported from other European countries until we were able to set up a modern musculoskeletal tissue bank in the late 1990s. The requirement for a large bone selection and good bone bank practices is emphasised. Concerns remain about the reliability of massive bone reconstruction.1 Prior to using massive bone allografts, the ‘biological’ alternative was intercalary autograft and arthrodesis.2–5 The limitations and disadvantages of this type of reconstruction are well known, and in a many cases a temporary cement spacer was used.6 Since allografts have become a real alternative, the indications have widened, e.g. intercalary, arthrodeses and more recently, osteochondral reconstructions. Allograft is a more
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ARTICLE IN PRESS 394 flexible and reliable technique than mega-prostheses. Early clinical studies demonstrated more frequent early complications with massive allograft compared to prosthetic replacement. This reflected the more demanding surgical technique and the need for carefully planned physical therapy. Nonetheless allografts were felt to provide a more reliable reconstruction in the longer followup,7–10 because while metallic implants were easier to implant and allowed simpler rehabilitation they would inevitably fail with time. Since the early 1980s we have performed more than 600 massive allograft replacements in various sites. This paper considers only those to limbs. Over 20 years the indications, fixation methods and the use of adjuvants have all changed. However, it seems appropriate to take an overall view of this large series. The aim of this review is to give data on the long-term follow-up of allografts, irrespective of variables, such as resection length, reconstruction type, and cause of failure.
Material and methods From 1980 to 2002, we performed 540 massive allograft replacements, 95 in the upper limb (73 humerus, 18 radius, 1 ulna and 3 metacarpals) and 445 in the lower limb (242 femur, 202 tibia and 1 metatarsal). Three hundred and five patients were male and 235 female. Age ranged from 1 to 77 years, with an average of 22.5. Postoperative chemotherapy was given in 338 procedures. The earliest technique used was intercalary reconstruction in 194 cases. Starting from 1988 in 83 selected cases we supplemented the allograft with vascularised fibula.11,12 Fourteen intercalary reconstructions were performed in the humerus, 1 in the radius, 111 in femur and 68 in the tibia. Massive allografts were also used for arthrodeses: 65 of the knee, 12 ankle and 3 wrist. The last knee arthrodesis was performed in 1996. After 1989 we started carrying out osteochondral reconstruction and have now performed 135; 75 in the upper limb (46 proximal humerus, 2 total humerus, 9 distal humerus, 1 proximal ulna, 13 distal radius, 1 proximal radius and 3 metacarpal) and 60 lower limb: 2 proximal femur, 25 distal femur, 31 proximal tibia, 1 distal tibia and 1 metatarsal bone. Around the knee, there were 6 femoral and 2 tibial condylar replacements. Because of high numbers of fractures we started to use allograft prosthetic composite (APC)13 in 131 cases; 3 in the humerus, 59 proximal
D. Donati et al. femur and 69 around the knee (4 distal femur, 65 proximal tibia). Survival analysis was performed using life tables. Comparison of survival experience was analysed by the Wilcoxon test and multivariate analysis using Cox regression with Wald method.
Results Infection Infection was one of the most challenging complications. There were 47 cases of infection (8.7%) and it was the cause of failure of the implant in 70% of these cases and 15% amputation. However, if we exclude the first 28 patients treated in the series (6 infected cases), performed with poor quality bone supply, the percentage decreases to (8%). Twentyone patients had early infection (within 6 months of surgery), while among 26 late infections, 13 occurred after repeat surgery for allograft fracture, and 8 occurred in tibia APCs. In the upper limb the percentage was lower (2.1%) than it was in the lower limb. The tibia is still the most common site involved (15.3%), particularly in APC reconstructions (20%), while in the femur the rate is 5.7%. These figures are similar or less than in modular replacement prosthesis.
Fracture Fracture occurred in 129 cases (23.8%), in almost half of the cases (62) within 24 months of surgery. In 22 cases they were subchondral, 19 metaphyseal, 67 diaphyseal. Eighteen were due to avulsion of an apophysis and three were stress fractures. Osteochondral reconstructions (29.6%) were the most affected while the smallest number was in APCs (15%). In the APC group, 18 fractures were located in the proximal femur due to trochanteric gluteus medius pullout. These fractures caused no functional deficit on gait and did not require surgical treatment. The rate of fractures in arthrodesis was average, but occurred later than in the other groups (from 12 to 137, 60 months mean). In the upper limb fracture occurred in 19% (all humeral), while in the lower limb 26%. Allograft fracture caused implant failure in 47% of the cases. In another 18% a new osteosynthesis successfully treated the fracture, while the remaining 35% healed without operation. In intercalary reconstruction, since we started (in 1993) using cement in the medullary canal, this complication has markedly decreased.
ARTICLE IN PRESS The use of massive bone allografts in bone tumour surgery of the limb
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Delayed or non-union Delayed or non-union was the most frequent complication, occurring in 148 patients (27.4%). The rate was higher in chemotherapy-treated patients: 31.3% vs. 21% in non-chemotherapy patients. It was commoner in arthrodesis (43.7%) and least in APC (14.5%). Approximately half of the patients with delayed union did not require surgery (42.5%), while only 6% of the cases had allograft failure.
Failure 120 cases failed (22%). A new allograft was performed in 26 cases (four combined with a vascularised fibula), 27 with a modular prosthesis, four with an APC and one was treated by an Ilizarov technique. Seven patients could not be treated successfully and 29 underwent amputation. The remaining 27 patients did not undergo a complete change of the reconstruction. Ten intercalary reconstructions were successfully treated with vascularised fibula augmentation, 14 osteochondral fractures were salvaged with a standard prosthesis, and three infected proximal tibia APCs were treated by removing the allograft and applying antibiotic-impregnated cement around the prosthetic stem. In these latter cases the functional evaluation did not differ before or after the complication was treated. If they are excluded, the number of failures decreases to 93 (17%). With regard to the type of reconstruction, osteochondral reconstruction around the knee had the highest failure rate, 38.5%, followed by knee arthrodesis, 23%, and proximal tibia APCs with 21.5%. In terms of site, the proximal tibia was the site most affected by complications, with a failure rate of 28%.
Figure 1 Contingency types of failure (120 survival at 216 months in a linear pattern and
table of the series including all cases). The expected allograft is 56.6%. The curve is decreasing becomes stable at 156 months.
Figure 2 Contingency table of the series excluding salvaged allograft (93 cases). The expected allograft survival at 216 months is 71.8%. The curve becomes stable at 132 months.
Functional results Including all patients followed-up for more than 24 months (346), according to the MSTS functional evaluation, 87% of results were excellent or good. This excludes all the failed cases.
Statistics The overall expected allograft survival at 216 months is 56.6%. Excluding the salvaged allograft, the expected allograft survival at 216 months increases to 71.8% (Figs. 1 and 2). Univariate analysis was performed to analyse the effect of several variables, such as age, type of
diagnosis, site (upper vs. lower limb) and use of postoperative antiblastic chemotherapy in relation to the rate of failure. None were statistically significant. Among the causes of failure, infection and fracture were highly significant (Figs. 3 and 4), while delayed or non-union was not. The probability of maintaining the allograft was 57.4% in cases of delayed union, and 62.6% in non-delayed union. Finally, univariate analysis showed that the type of reconstruction was only close to significance (po0:052). Multivariate analysis performed (Cox regression) included all the variables reported above. Only fracture was highly significant (po0:0002), while
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Figure 3 The probability of survival of the allograft in non-infected cases is 61.6% at 156 months, while in infected cases is 15.3% at 120 months. (po0:0001).
D. Donati et al.
Figure 5 The best chance to retain the allograft over time is in intercalary reconstruction with allograft and vascularised fibula, followed by APCs, arthrodesis, intercalary and osteochondral reconstruction. The significance is related to the better outcome of the intercalary with vascularised fibula. There were no significant differences among any of the other groups. Legend: 5 ¼ Intercalary with vascularised fibula, 4 ¼ Intercalary, 3 ¼ APCs, 2 ¼ Arthrodesis, 1 ¼ Osteochondral.
Figure 4 The probability to maintain the allograft in nonfracture cases is 86% at 108 months, while in the fractured cases is 33% at 156 months. (po0:0001).
infection was not. However, another significant parameter was the type of reconstruction (po0:0487; Fig. 5). Excluding the fractured cases, the different type of reconstruction was particularly significant: details are reported in the diagram (Fig. 6).
Discussion For nearly 30 years we have used massive bone allografts for limb salvage experience in a wide variety of sites and methods. Over that period, our
Figure 6 Excluding the fractured cases, APCs score significantly worse than intercalary reconstruction with vascularised fibula (po0:03) and osteochondral (po0:001) reconstruction. Legend: 5 ¼ Intercalary with vascularised fibula, 4 ¼ Intercalary, 3 ¼ APCs, 2 ¼ Arthrodesis, 1 ¼ Osteochondral.
techniques have improved with experience, both operative and in decision making as well as improvements in surgical devices. Major allograft in tumour surgery has limitations. The number of failures was significantly high, and
ARTICLE IN PRESS The use of massive bone allografts in bone tumour surgery of the limb an unexpected finding was the time of occurrence. In the actuarial tables the curves become stable at 156 and 132 months. We first found soft tissue integration as the biggest advantage of allograft surgery, specifically tendon and ligament reattachment is the key factor that leads to a good functional performance, as confirmed by 87% excellent or good results in ‘nonfailure’ cases. Additionally the soft tissue adherent sleeve formation around an allograft is very important in preventing late allograft infection, which is more common in metal implants. Only 13 cases in the series were affected by late infection without a recognised risk factor, and eight of them were proximal tibia APCs. While the overall results of 8.7% of infection is considered acceptable for this type of surgery,14,15 we are now limiting the use of APCs in the proximal tibia by excluding cases treated with postoperative chemotherapy and when the gastrocnemius rotation is feasible.16 There is more concern with regard to allograft bone integration and regeneration. The 27.4% delayed or non-union indicates a slow and limited ability of allograft host integration. We know from allograft retrieval studies17–19 that the cutting cone formation at the junction is frequently insufficient to achieve a sound fusion in a reasonable course of time. Over time the fixation devices have improved (e.g. titanium DCP plates) as well as the frequent use of step cut junctions.20 The failure rate for this complication is low at 6%, however we are still very conservative in allowing weight bearing to our patients, particularly when postoperative chemotherapy is used.21–24 Lack of bone regeneration is shown by the rate of mechanical failure of the allograft. Fracture occurred in one-fourth of the patients with a high probability of failure. The probability of maintaining the allograft in non-fracture cases is 86% at 108 months, while in the fracture cases it is 33% at 156 months. Fracture can occur very late, even after 10 years’ follow-up, indicating that allograft bone regeneration is hardly ever complete.25,26
Table 1
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It is clear that some questions still need to be answered. How long does the remodelling process last in a massive allograft? Is the allograft remodelling a positive process or just a weakening of the implanted structure? Is it better to go towards the use of artificial adjuvants, such as APCs, intramedullary cementation,27 or more invasive fixation devices, or, on the other hand, towards the use of more biological solutions, such as associated bone transplant, better muscle coverage, use of mesenchymal autologous cells, growth factors, etc.? A variety of factors affect the answer, such as age of the patient, the length and type of reconstruction, the type of fixation, the use of adjuvants, the quality of surrounding soft tissue, etc. Our series provides part of the answer. The combination of vascularised fibula with the allograft was the best performing reconstruction, whereas APCs were the less reliable, mostly related to the proximal tibia cases. Arthrodesis is less and less acceptable to patients. In the knee, the failure rate was 23% with the tendency to increase even after 10 years.28,29 While osteochondral allografts performed very well at the start, over time, mostly due to allograft fracture, this reconstruction had the highest failure rate. Hence we no longer use this type of reconstruction in the lower limb. While APCs are still the technique of choice in the proximal femur,30 we now limit its use in the proximal tibia. We consider that the proximal tibia remains the most complicated site for any type of reconstruction.31,32 In our hands, massive bone allograft replacement in tumor surgery still has indications. In the upper limb intercalary massive bone allograft, as well as osteochondral allograft reconstructions, remain the first choice in many sites. We have more than satisfactory results in the proximal humerus33 and distal radius, but the elbow remains a difficult area to be replaced34 (Table 1). In the lower limb, APC in the proximal femur is still the gold standard because of the good range of
Current indications for massive allograft replacement in the upper limb.
Type of resection
Type of reconstruction
Proximal humerus (sparing rotator cuff and axillary bundle)
Osteochondral allograft with intramedullary cementation and plate fixation with opposite cortical bar Osteochondral allograft, plate fixation and step cut junction Bone allograft with plate fixation Free autologous tibia with plate fixation
Distal radius Humerus intercalary Radius intercalary
ARTICLE IN PRESS 398 Table 2
D. Donati et al. Current indications for massive allograft replacement in the lower limb.
Type of resection
Type of reconstruction
Proximal femur
APC cemented in the allograft, press fit in the femoral host bone, revision hip prosthesis Bone allograft, intramedullary cementation and plate fixation with opposite cortical bar Bone allograft associated to central vascularised fibula, plate fixation Bone allograft, intramedullary cementation and plate fixation Bone allograft associated to central vascularised fibula (from opposite side), plate fixation Osteochondral allograft with screw fixation APC cemented in the allograft, press fit in the femoral host bone, revision hip prosthesis with medial gastrocnemius rotation Osteochondral allograft with plate fixation Osteochondral allograft with screw fixation Ankle arthrodesis with locked nail
Femur intercalary (standard resection) Femur intercalary (extended resection) Tibia intercalary (standard resection) Tibia intercalary (extended resection) Femur condyle Proximal tibia (patients without chemotherapy)
Tibia condyle Distal tibia (standard) Distal tibia (extended)
motion achievable. Complications are limited and failures are only related to local recurrence and infection.30 Reconstruction with massive allograft around the knee is much less reliable than using a metal implant. Arthrodesis has been abandoned due to the patient’s discomfort, while osteochondral reconstruction and APCs have a high complication rate, particularly fracture and infection. We still use allografts in condyle resection and APCs in proximal tibia, but only when a benign or low-grade tumor is resected to avoid the use of postoperative chemotherapy. In the distal tibia in the majority of cases an arthrodesis with allograft and nail is performed (Table 2). Current thinking is to avoid sacrificing as much of the joint as possible during resection, achieving intercalary reconstructions. This requires a sound bone allograft integration in difficult situations with the help of biological augmentation. The use of the vascularised fibula combined with a structural allograft makes for ready fusion of the critical osteotomy lines even in chemotherapy-treated patients.20,35,36 For some years we have been performing in vitro and in vivo experiments on the use of mesenchymal stem cells in allograft bone integration.37–39 The goal is to improve the formation of early cutting cones at the osteotomy line as the periphery of the allograft. This process may reduce the time of junction healing first, and bone regeneration after, to avoid early clinical complications, such as nonunion and fracture in massive allografts replacements.
Conclusions There are still indications for massive bone allograft replacement in skeletal tumor surgery. However, in our series, the overall expected allograft survival at 216 months was 56.6%, while the last event was registered at 156 months. This shows the need for more reliable implants. The relative weakness of the allografted bone is the lack of quick and complete bone integration and regeneration. The use of biological solutions combined with the allograft may give better results, reducing late failures.
References 1. Hernigou P, Delepine G, Goutallier D, Jiulieron A. Massive allografts sterilised by irradiation. Clinical results. J Bone Jt Surg Br 1993;75:904–13. 2. Donati D, Capanna R, Campanacci M, et al. Innesti ossei omoplastici massivi utilizzati per ricostruzioni intercalari ed artrodesi dopo resezione per tumore. Studio policentrico europeo. Chir Organi Mov 1993;88:81–94. 3. Donati D, Capanna R, Casadei R, et al. L’artrodesi di ginocchio dopo resezione per tumore: innesti autoplastici ed omoplastici a confronto. Chir Organi Mov 1995;80:29–37. 4. Scarborough MT, Helmstedter CS. Arthrodesis after resection of bone tumors. Semin Surg Oncol 1997;13:25–33. 5. Wolf RE, Scarborough MT, Enneking WF. Long-term followup of patients with autogenous resection arthrodesis of the knee. Clin Orthop 1999;358:36–40. 6. Donati D, Giacomini S, Gozzi E, et al. Knee arthrodesis with temporary spacer performed in malignant tumor around the knee. Arch Orthop Trauma Surg 2002;122:123–8.
ARTICLE IN PRESS The use of massive bone allografts in bone tumour surgery of the limb 7. Aho AJ, Ekford T, Dean PB, et al. Incorpotation and clinical result of large allografts of the extremities and pelvis. Clin Orthop 1994;307:200–13. 8. Mankin HJ, Gebhardt MC, Jennings LC, Springfield DS, Tomford WW. Long term results of allograft replacement in the management of bone tumors. Clin Orthop 1996;324: 86–97. 9. Mnaymneh W, Malinin T. Massive allografts in surgery of bone tumors. Orthop Clin N Am 1989;20:455–67. 10. Muscolo DL, Petracchi LJ, Ayerza MA, Calabrese M. Massive femoral allografts followed for 22 to 36 years. Report of six cases. J Bone Jt Surg Br 1992;74:887–92. 11. Capanna R, Bufalini C, Campanacci M. A new technique for reconstructions of large metadiaphyseal bone defects. Orthop Traumatol 1993;2:159–77. 12. Manfrini M. The role of vascularized fibula in skeletal reconstruction. Chir Organi Mov 2003;88:137–42. 13. Gitelis S, Piasecky P. Allograft prosthetic composite arthroplasty for osteosarcoma and other aggressive bone tumors. Clin Orthop 1991;270:197–201. 14. Eckardt JJ, Lesavoy MA, Dubrow TJ, Wackym PA. Exposed endoprosthesis. Management protocol using muscle and myocutaneous flap coverage. Clin Orthop 1990;251:220–3. 15. Scarborough MT. Allograft-allograft healing? Salvage of massive allografts after fracture. Clin Orthop 2001;382: 28–33. 16. Capanna R, Donati D, Masetti C. Effect of electromagnetic fields on patients undergoing massive bone graft following bone tumor resection. A double blind study. Clin Orthop 1994;306:213–21. 17. Caldora P, Donati D, Capanna R, et al. Studio istomorfologico degli espianti di innesti omoplastici massivi: risultati preliminari. Chir Organi Mov 1995;80:191–205. 18. Enneking WF, Mindell ER. Observations on massive retrieved human allografts. J Bone Jt Surg Am 1991;73:1123–42. 19. Mankin HJ. The changes in major limb reconstruction as a result of the development of allografts. Chir Organi Mov 2003;88:101–13. 20. Sorger JI, Hornicek FJ, Zavatta M, et al. Allograft fractures revisited. Clin Orthop 2001;382:66–74. 21. Beccheroni A, Lucarelli E, Donati D, et al. Recovery of stromal stem cells in bone sarcomas patients after chemotherapy: implication for cell-based therapy in bone defect reduction. Oncol Rep 2003;10:891–6. 22. Donati D, DiLiddo M, Zavatta M, et al. Massive bone allograft reconstruction in high-grade osteosarcoma. Clin Orthop 2000;377:186–94. 23. Hazan EJ, Hornicek FJ, Tomford W, Gebhardt MC, Mankin HJ. The effect of adjuvant chemotherapy on osteoarticular allografts. Clin Orthop 2001;385:176–81.
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24. Van Boerum DH, Randall RL, Mohr RA, Conrad EU, Bachus KN. Rotational stability of a modified step-cut for use in intercalary allografts. J Bone Jt Surg Am 2003;85:1073–8. 25. Dick HM, Strauch RJ. Infection in massive bone allografts. Clin Orthop 1994;306:46–53. 26. Hornicek FJ, Gebhardt MC, Tomford WW, et al. Factors affecting nonunion of the allograft–host junction. Clin Orthop 2001;382:87–98. 27. Gerrand CH, Griffin AM, Davis AM, Gross AE, Bell RS, et al. Large segment allograft survival is improved with intramedullary cement. J Surg Oncol 2003;84:198–208. 28. Casadei R, Donati D, Ferraro A, et al. Artrodesi di ginocchio con innesto omoplastico dopo resezione per tumore osseo: studio a lungo termine. Chir Organi Mov 2003;88:123–35. 29. Donati D, Giacomini S, Gozzi E, et al. Allograft arthrodesis in the treatment of bone tumors: a two center study. Clin Orthop 2002;400:217–24. 30. Donati D, Gozzi E, Giacomini S, Mercuri M. Proximal femur reconstrucion by an allograft prosthesis composite (APC). Clin Orthop 2002;394:192–200. 31. Brien EW, Terek RM, Healey JH, Lane JM. Allograft reconstruction after proximal tibial resection for bone tumors. An analysis of function and outcome comparing allograft and prosthetic reconstructions. Clin Orthop 1994;303:116–27. 32. Enneking WF, Campanacci DA. Retrieved human allografts: a clinicopathological study. J Bone Jt Surg Am 2001;83: 971–86. 33. DeGroot H, Donati D, Di Liddo M, Gozzi E, Mercuri M. The use of cement in osteoarticular allografts for proximal humeral bone tumors. Clin Orthop 2004;427:190–7. 34. Delloye C, De Nayer P, Vincent A. Osteochondral allografts in arm and forearm surgery. Acta Orthop Belg 1991;57: 75–83. 35. Manfrini M, Gasbarrini A, Malaguti C, et al. Intraepiphyseal resection of the proximal tibia and its impact on lower limb growth. Clin Orthop 1999;358:111–9. 36. Manfrini M, Vanel D, De Paolis M, et al. Imaging of vascularized fibula autograft placed inside a massive allograft in reconstruction of lower limb bone tumors. Am J Roentgenol 2004;182:963–70. 37. Jeon DG, Kawai A, Boland P, Healey JH. Algorithm for the surgical treatment of malignant lesions of the proximal tibia. Clin Orthop 1999;358:15–26. 38. Lucarelli E, Donati D, Cenacchi A, Fornasari PM. Bone reconstruction of large defects using bone marrow derived autologous stem cells. Transfus Apher Sci 2004;30:169–74. 39. Lucarelli E, Fini M, Beccheroni A, et al. Stromal stem cells and platelet rich plasma improve bone allograft integration. Clin Orthop 2005;435:62–8.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 400–402
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Three external CME points available The following series of questions are based on the CME designated article for this issue—‘Management of open pelvic fractures’ by E. Katsoulis, E. Drakoulakis and P.V. Giannoudis. Please read the article carefully and then complete the self-assessment questionnaire by filling in the square corresponding to your response to each multiple-choice question. For true or false questions, please fill in one square only. After completing the questionnaire, either post or fax the answer page back to the Current Orthopaedics Editorial Office at the address at the bottom of the RESPONSE sheet. Please photocopy this page if you wish to keep your copy of Current Orthopaedics intact. Replies received before the next issue of Current Orthopaedics is published will be marked and those reaching an adequate standard will qualify for three external CME points. You will be notified of your marks and a CME certificate will be despatched for your records.
Questions 1. Which of the following has not been shown to be associated with mortality rates in open pelvic fractures? A. B. C. D. E.
Age Injury Severity Score Presence of vaginal injury Pelvic instability Number of units of blood transfused
2. What are the blood requirements in open pelvic fractures in the first 24 hours after injury when compared to similar closed fractures? A. B. C. D.
Slightly less Approximately the same Blood requirements approximately twice as high Blood requirements approximately four times as high E. Blood requirements approximately six times as high
3. How are the X-ray beams aligned to obtain pelvic inlet and outlet views? A. Inlet 45 degrees caudad, outlet 45 degrees cephalad B. Inlet 45 degrees caudad, outlet 60 degrees cephalad 0268-0890/$ - see front matter doi:10.1016/j.cuor.2005.10.001
C. Inlet 60 degrees caudad, outlet 60 degrees cephalad D. Inlet 60 degrees caudad, outlet 45 degrees cephalad 4. What is the approximate incidence of acetabular fractures in patients with open fractures of the pelvic ring? A. B. C. D. E.
75% 50% 25% 10% 5%
5. Which of the following is an incorrect assignment of a region of soft tissue injury to its zone in the description of open pelvic fractures? A. B. C. D. E.
Perineum—zone 2 Medial buttock—zone 1 Posterolateral buttock—zone 3 Anterior pubis—zone 1 Medial thigh—zone 2
6. What is the approximate incidence of rectal injury in open pelvic fractures? A. less than 1% B. 2% C. 5%
ARTICLE IN PRESS CME SECTION D. 10% E. 40% 7. What is the approximate incidence of urogenital tract injury in open pelvic fractures? A. B. C. D. E.
1% 5% 10% 40% 70%
8. What is the most appropriate management of a rectal laceration associated with a pelvic fracture? A. Two layer repair of the laceration and rectal washout B. Excision of a segment of rectum with end to end repair and pelvic drainage C. Rectal repair and temporary ileostomy D. End colostomy with rectal washout E. Loop colostomy alone
401 10. Which of the following statements about embolisation in the management of pelvic bleeding is true? A. It is the first choice procedure in most cases B. It is useful in only about 10% of cases C. It is useful in the management of venous bleeding D. It is a rapid means of obtaining haemodynamic control E. If unsuccessful, a pelvic external fixator should be applied 11. What is the approximate incidence of sepsis after modern treatment of open pelvic fractures? A. B. C. D. E.
Less than 1% 2% 5% 10% 30%
9. What is the appropriate management for most extraperitoneal bladder ruptures associated with open pelvic fractures?
12. What is the approximate incidence of chronic pain after unstable pelvic fractures?
A. B. C. D. E.
A. B. C. D. E.
Urethral catheter Suprapubic catheter Direct repair Diversion procedure No intervention
2% 5% 10% 30% 50%
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Answers to CME questions in Vol. 19, issue 3 Please find below the answers to Current Orthopaedics CME questions from Vol. 19, issue 3 which were based on the articles—‘Examination of the wrist: Parts I and II’ by R. Srinivas Reddy and J. Compson. 1
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doi:10.1016/j.cuor.2005.06.002
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 404–406
Book reviews Diagnostic Imaging: Orthopaedics. Stoller, Tirman, Bredella, Beltran, Branstetter and Blease, 2004. The ‘‘Stoller’’ textbook has for many years been the definitive text for the application of MRI in orthopaedics and sports medicine. This all-new textbook takes a radical departure from the dense prose text of old and presents an image and graphic-packed visual feast, born of the computer generation. Each condition is presented in a standardised format with concise, bulleted text, key-facts boxes and thumbnail images. Once familiar with the format the reader knows where to look for specific information, since all the text, key-fact boxes and illustrations are presented in the same place for each condition. The illustrations, by Salvador Beltran, warrant particular mention. These are full colour computer-generated illustrations that have a real three-dimensional quality. Presented alongside the MRI images, they help bridge the divide of visualising the threedimensional structure of a pathological process from a single, two-dimensional, MRI cross-section. The concise, fact-filled text, lends itself to a quick reference guide, rather than leisurely reading around a subject. The detailed description of the MRI findings for each MRI sequence is not likely to interest the orthopaedic surgeon, but the standardised layout allows the reader to jump straight to the ‘‘key-facts box’’ or the ‘‘image gallery’’. While each condition has a section on the clinical features, the conditions are set out in the contents
with their specific imaging diagnosis, rather than with presenting clinical scenarios. This is, after all, a radiological textbook rather than a clinical one. Orthopaedic surgeons in training, and those straying from their area of expertise, are most likely to find this book of use as a reference guide when provided with an MRI diagnosis on one of their patients. Even the most experienced of shoulder surgeons is likely to find the detailed description of the nine grades of SLAP lesion illuminating. This is a textbook which is primarily all about the use of MRI in orthopaedics, and as such makes no reference to the use of ultrasound. This very much reflects local practice in America where, for various reasons, ultrasound in the musculoskeletal system has been slow to take off. In centres where the radiologist provides a musculoskeletal ultrasound service, the description of the MRI features for a significant proportion of the conditions in this textbook will be merely of academic interest. This textbook does not cover the spine, but there is a separate textbook devoted to spinal imaging in the same series, which follows the same format. The real strength of this textbook is the visual layout. This is likely to be copied and herald a whole new breed of textbook for the 21st century.
James J. Rankine St. James’s University Hospital, Leeds LS9 7TF, UK E-mail address:
[email protected]
doi: 10.1016/j.cuor.2005.05.005
Dennis J. Winner, Paediatric Orthopaedics for Primary Care Physicians, Cambridge University Press, Cambridge, ISBN 0521825644 (166pp., £55). This is a hardback book of 158 pages that is well illustrated with X-rays, figures and drawings. The format of each of the seven chapters is very simple
and clear to follow. It is written as a narrative and not in point form, which makes it easy to read. All common and a few uncommon children’s orthopaedic conditions are covered in the chapters, which include growing bones and joints, lower extremity developmental attitudes, common orthopaedic conditions from birth to walking then from toddler to adolescence plus adolescence and
ARTICLE IN PRESS Book reviews puberty, miscellaneous disorders and genetic disorders. This book is intended for primary care physicians and general practitioners. It does not include any surgical detail. Some of the chapters include orthopaedic vocabulary, e.g. ‘‘Cobb angles’’, ‘‘varus’’ and ‘‘valgus’’, etc. and I believe an extra chapter on terminology, or else a glossary, would be helpful.
405 This is a beautiful book aimed at primary care physicians. It is very enjoyable to read but does not add any information to that which orthopaedic trainees can obtain from their standard textbooks.
P.A. Templeton
doi: 10.1016/j.cuor.2005.04.003
J.P. Fulkerson (Ed.), Common patellofemoral problems, American Academy of Orthopaedic Surgeons, USA. ISBN 0892033495, 2005 (99pp., US$50). This publication is a softback book of 99 pages in the monograph series of the AAOS. It is edited by John Fulkerson who is one of the major names in patellofemoral orthopaedic surgery. For any general orthopaedic surgeon or specialist knee surgeon, patellofemoral disorders are one of the most difficult to understand and to manage. It is divided into 9 chapters with a logical progression of headings from patellofemoral pain to malalignment and instability and appropriate management, through to patellofemoral osteoarthritis. The editor of this multi-authored volume was a senior author of another well-known book on the subject, but this particular edition is exceptionally practical and user-friendly. There are an
adequate number of clear black and white diagrams and photographs to illustrate and explain the underlying pathology. This is the first book, albeit a small volume, which I have felt that I will be able to use actively to make clinical decisions on specific patients. Even for the busy surgeon or trainee, it is not too long to read from cover to cover. Each chapter is well referenced and this is particularly useful in assessing the success rate of the various surgical procedures which are quoted in the text. On balance, I would thoroughly recommend this particular edition. It will be a friend to the subspecialist knee surgeon but equally, provide a clear background and sensible approach to these problems for the trainee.
Stuart Calder
doi: 10.1016/j.cuor.2005.08.003
Jeffrey Fischgrund (Ed.), Neck Pain, American Academy of Orthopaedic Surgeons, ISBN 0892033347, 2004 (70pp., £ 31). Neck pain is a 94 page overview of a common condition which practitioners in orthopaedic medicine will see in everyday practice. Written by American orthopaedic surgeons on behalf of the American Academy of Orthopaedic Surgeons, it takes the reader through epidemiology, imaging, pharmacological treatment, injections and manual therapies. It has a whole section on whiplash injury that would be useful for those practicing medicodoi: 10.1016/j.cuor.2005.08.004
legal work. However, for the orthopaedic trainee, it is difficult to read for the FRCS(Orth) and much of it would be irrelevant. There is a paucity of diagrams and no summary points. The surgical section is brief and certainly not comprehensive. This book is more suited for those who practice manipulative therapies such as physiotherapists and chiropractors and I would not recommend this book for the orthopaedic trainee whose time may be better spent on the core syllabus.
Jake Timothy
ARTICLE IN PRESS 406 Vincent D. Pellegrini Jr. (Ed.), Instructional Course Lectures, vol. 54, American Academy of Orthopaedic Surgeons, ISBN 0892033452, 2005 (650pp., plus accompanying DVD ROM, $170 ðd112:00Þ). The preface of the 54th in this series of publications, which reproduces a collection of presentations from the 71st AAOS Annual Meeting in San Francisco (2004), promises to provide the reader with ‘a smorgasbord of subspecialty topics for the general orthopaedic practitioner’. This hardback volume is well indexed with a clear table of contents. The text is nicely laid out in logical sequence with appropriate subheadings. As one might expect from an AAOS publication the tables are well presented with good quality black and white reproductions of clinical photographs, diagrams and radiographs. The articles are extensively referenced allowing the reader to delve deeper into particular topics of interest. The author list of the instructional course lectures reads like a ‘who’s who’ of American and Canadian orthopaedic surgery. This North American dominance is broken only by European contributions from Leeds, Hanover and Lund. Broad areas of orthopaedics covered by the work include orthodoi: 10.1016/j.cuor.2005.06.010
Book reviews paedic medicine, adult reconstruction, adult spine, trauma, sports medicine (the knee), paediatric orthopaedics with small sections discussing oncology and basic science. The book is accompanied by a generally well filmed and narrated DVD containing practical and theoretical demonstrations to supplement seven of the lectures. The DVD has an easy to navigate menu, though I found it disappointing that comparatively few of the lectures were supported by multimedia. Of particular interest to the trainee preparing for specialist examinations was the video accompanying the chapter ulnar-sided wrist pain: diagnosis and management, which threw some much needed light on this often neglected topic. As acknowledged by the editor in the preface it is increasingly difficult to produce a publication such as this that aims to cover the breadth of the speciality but inevitably ends up giving a few ‘in depth’ snapshots of certain areas. It is not a volume that orthopaedic surgeons working in specialist areas would turn to and is perhaps most appropriate for the orthopaedic surgeon who still believes that variety is the spice of life.
Angus Robertson
Aims and Scope Current Orthopaedics presents a unique collection of international review articles summarizing the current state of knowledge and research in orthopaedics. Each issue focuses on a specific topic, discussed in depth in a mini-symposium; other articles cover the areas of basic science, medicine, children/adults, trauma, imaging and historical review. There is also an annotation, self-assessment questions and an exam section. In this way, the entire postgraduate syllabus will be covered in a 4-year cycle. The Journal is cited in: Cochrane Center, EMBASE/ Excerpta Medica, Infomed, Reference Update and UMI Microfilms.
Editor Professor R. A. Dickson MA, ChM, FRCS, DSc St James’s University Hospital Trust, Leeds, UK
Editorial Committee President of BOTA, M. A. Farquharson-Roberts (Gosport, UK), I. Leslie (Bristol, UK), D. Limb (Leeds, UK), M. Macnicol (Edinburgh, UK), J. Rankine (Leeds, UK)
Editorial Advisory Board L. de Almeida (Portugal) G. P. Songcharoen (Thailand) R. W. Bucholz (USA) J. W. Frymoyer (USA) R. W. Gaines (USA) S. L. Weinstein (USA) M. Bumbasirevic (former Yugoslavia)
A. K. Mukherjee (India) A. Kusakabe (Japan) A. Uchida (Japan) M.-S. Moon (Korea) R. Castelein (The Netherlands) R. K. Marti (The Netherlands) G. Hooper (New Zealand) A. Thurston (New Zealand) E. G. Pasion (Philippines)
D. C. Davidson (Australia) J. Harris (Australia) S. Nade (Australia) G. R. Velloso (Brazil) J. H. Wedge (Canada) S. Santavirta (Finland) P. N. Soucacos (Greece) M. Torrens (Greece) J. C. Y. Leong (Hong Kong)
Available online at www.sciencedirect.com
Amsterdam
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ARTICLE IN PRESS Current Orthopaedics (2005) 19, 407–414
www.elsevier.com/locate/cuor
MINI-SYMPOSIUM: SURGERY FOR KNEE ARTHRITIS
(i) Novel treatments for early osteoarthritis of the knee S.P. Krishnana, J.A. Skinnerb, a
Joint Reconstruction Unit, Royal National Orthopaedic Hospital, Stanmore, UK Royal National Orthopaedic Hospital, Stanmore, UK
b
KEYWORDS Primary osteoarthritis; Knee; Conservative treatment
Summary While partial/total knee replacement remains the cornerstone of treatment of end stage osteoarthritis (OA), there is a large population of patients with painful knees and early arthritis for whom arthroplasty is inappropriate. Weight loss, anti-inflammatory analgesics, physiotherapy, use of sticks, and activity modification remain the basis of treatment in this group. In this article we review the evidence for a number of popular treatment options and review possible future therapeutic strategies. Once considered a safer alternative, COX-2 inhibitors have become the subject of intense scrutiny with recent evidence suggesting cardiac and CNS side effects. Current evidence supports the use of intra-articular viscosupplementation and corticosteroids but the role of oral glucosamine and chondroitin sulphate remains debatable. Arthroscopic debridement and microfracture techniques are shown to be effective in selected patients. & 2005 Published by Elsevier Ltd.
Introduction The treatment of osteoarthritis (OA) continues to evolve. Primary OA of the knee affects one-tenth of the population aged over 55 years and the number and proportion of patients involved may increase as both longevity and body mass index rise. OA appears to arise if there is an imbalance between degeneration and repair of the articular cartilage. Aetiological factors associated with OA include age, gender, race, obesity, metabolic factors, occupation, genetic influences and mechanical factors. Corresponding author. Tel.: +44 208 909 5529; fax: +44 208 954 3036. E-mail addresses:
[email protected] (S.P. Krishnan),
[email protected] (J.A. Skinner).
0268-0890/$ - see front matter & 2005 Published by Elsevier Ltd. doi:10.1016/j.cuor.2005.10.004
OA cannot be cured. The primary goals for OA therapy are to relieve pain, delay progression, maintain or improve function, and prevent or correct deformity. In this article, we discuss the evidence for various novel treatment modalities in an attempt to clarify their current role in the management of early OA of the knee.
Non-pharmacological modalities Transcutaneous electrical nerve stimulation Transcutaneous electrical nerve stimulation (TENS) is the most commonly used form of electroanalgesia in the treatment of arthritis pain in the
ARTICLE IN PRESS 408 knee. Clinically TENS is applied at varying frequencies, intensities, and pulse durations of stimulation. When high-frequency TENS is applied at low intensity it is referred to as conventional TENS. The analgesic effect with this setup is immediate. Pain relief lasts while the stimulus is turned on, but it usually abates when the stimulation stops. In contrast, when low-frequency TENS is applied at high intensity so that a motor contraction is produced, it is referred to as acupuncture-like TENS (AL-TENS). Although this method may be more effective than conventional TENS, it is uncomfortable, and many patients do not tolerate it. The mechanism of the analgesia produced by TENS is best explained by the gate control theory of pain. Complications arising from the use of TENS are rare. Skin irritation is reported and often is due to the drying out of the electrodes or to reaction to adhesive tape. TENS is ineffective in patients with morphine tolerance and is contraindicated in those with demand-type pacemakers and in pregnancy. A Cochrane review (2000) of seven studies (148 patients received TENS and 146 patients received placebo treatment) concluded that active TENS and AL-TENS treatment for at least 4 weeks effectively reduce pain and knee stiffness.1 However, this review was limited because of heterogeneity in study designs and outcome measurements. Betterdefined studies are required to determine the optimum duration, mode of application and clinical effectiveness of TENS.
S.P. Krishnan, J.A. Skinner oscillation of the particles of that material thus generating heat. In addition to thermal changes, the vibration of the tissues may have a separate mode of action. Pulsed ultrasound has been recommended for acute pain and inflammation, and continuous ultrasound for the treatment of stiffness. Few trials are available in the literature and they suggest no benefit over placebo or short wave diathermy for people with knee OA. These conclusions are limited by overall poor methodological quality of available comparative trials.
Low level laser therapy Low level laser therapy (LLLT) is a light source that generates extremely pure light, of a single wavelength. The effect is not thermal, but rather related to photochemical reactions in the cells. A recent meta-analysis (2004) revealed that the pooled results show no effect of 1 month of LLLT on pain or overall patient-rated assessment of disease activity. However, three trials showed positive effects on pain relief and three trials found no effect. Lower dosage of LLLT was found as effective as higher dosage for reducing pain and improving knee range of motion.3 There is lack of data on how LLLT effectiveness is affected by four important factors: wavelength, treatment duration, dosage and site of application over nerves instead of joints.
Electromagnetic fields Electromagnetic fields (EMF) have been postulated as a treatment for OA since their use has stimulated cartilage growth in vitro. EMF causes physical stress on bone leading to the generation of piezoelectric potentials. These then act as transduction signals to promote bone formation and stimulates chondrocytes to increase proteoglycan synthesis. A Cochrane review (2002)2 investigating the clinical use of EMF showed statistically significant improvements in function and pain in OA, but it remained unclear as to whether this improvement was noticeable clinically. Further well-defined studies are needed to establish its clinical relevance. There are no reported side effects of this therapy.
Therapeutic ultrasound Ultrasound uses mechanical vibrations at frequencies between 1.0 and 3.0 MHz. As the energy within the sound wave is passed to a material, it causes
Pharmacological therapy Analgesic and anti-inflammatory medicines This includes the use of both systemic and topical application of non-opioids, opioids and compound analgesic preparations. There remain a very important group of drugs with undoubted efficacy but side effects are common. COX-2 inhibitors Once considered a safer alternative, COX-2 inhibitors have become the subject of intense scrutiny with recent evidence suggesting potential cardiac and CNS side effects. Rofecoxib (Vioxx) was voluntarily withdrawn from global markets in October 2004 after it was shown that long-term use (greater than 18 months) could increase the risk of myocardial infarction and stroke. There remain a number of questions over both the benefits and risks associated with COX-2 selective agents4 and work is ongoing.
ARTICLE IN PRESS Novel treatments for early osteoarthritis of the knee
Glucosamine and chondroitin sulphate Public interest in the use of glucosamine for OA, gained momentum after the 1997 publication of ‘The Arthritis Care’ which described its ability to provide symptomatic relief with few side effects. Glucosamine is the hexosamine constituent of keratan sulphate, the glycosaminoglycan found in hyaline cartilage along with chondroitin sulphate. Glycosaminoglycans are the major constituents of proteoglycan molecules of hyaline cartilage. The proteoglycan moiety gives hyaline cartilage its visco-elastic property and allows it to act as a cushion. Glucosamine and chondroitin sulphate are thought to influence cartilage metabolism as suggested by in-vitro models and animal studies. These effects have not been established in-vivo, nor it has been shown that the observed metabolic responses occur in senescent or arthritic cartilage. Proponents have promoted glucosamine and chondroitin sulphate as chondro-protective dietary supplements with matrix modifying properties. Both agents have more than one mechanism of action. They may stimulate production of cartilaginous matrix and downregulate the production of proteolytic enzymes. They may also improve synovial fluid characteristics and may have anti-inflammatory properties. It remains unclear as to whether these effects are physiologically significant. A Cochrane review (2005) of eight well-controlled studies failed to show benefit of glucosamine for pain and Western Ontario and McMaster Universities (WOMAC) function.5 Collective analysis of 20 randomised control trials (RCTs) (including those without adequate allocation concealment) with 2570 patients found that glucosamine showed significant improvement in pain and Lequesne function, over placebo. However, results have not been uniformly positive, and the reasons for this remain unexplained. WOMAC pain, function and stiffness outcomes did not reach statistical significance. Reviews done at 6 weeks showed a decrease in pain and improved function, but studies reporting at 3 months show little difference. Two RCTs showed that a glucosamine preparation was able to slow radiological progression of OA of the knee over a 3-year period. However, the reliability of radiographic assessment of the progression of OA remains controversial.6 The reported minor side effects of glucosamine include gastro-intestinal complaints, headache, leg pain, oedema, and itching. However, it is generally well tolerated. Evidence based on animal studies suggests that glucosamine may affect the metabolism of glucose and insulin and hence its use in
409 diabetics may be restricted until human studies are available.
Visco-supplementation Originally described by Balazs and Denlinger in the 1960s, it was first used (intravenously) to treat racehorses with traumatic arthritis. Hyaluronic acid is a component of normal synovial fluid and an important contributor to joint homeostasis. In OA, both the concentration and the molecular weight of hyaluronic acid are decreased, which reduces the visco-elasticity of synovial fluid. The exact mechanism of action of visco-supplementation is unclear. Although restoration of the visco-elastic properties of synovial fluid seems to be the explanation, other mechanisms may exist. The actual period that the injected hyaluronic acid stays within the joint space is in the order of hours to days, but the time of clinical efficacy is several months. Other postulated mechanisms to explain the long-lasting effect of visco-supplementation include possible anti-inflammatory and analgesic properties or stimulation of in-vivo hyaluronic acid synthesis by the exogenously injected hyaluronic acid. Visco-supplementation involves the use of hyaluron and hylan derivatives (Adant, Arthrum H, Artz, BioHy, Durolane, Fermathron, Go-On, Hyalgen, Hyalan G-F 20 (Synvisc Hylan G-F 20), NRD101, Orthovisc, Ostenil, Replasyn, SLM-10, Suplasyn, Synject and Zeel compositum). Hylans are cross-linked hyaluronic acids, which gives them a higher molecular weight and increased visco-elastic properties. The higher molecular weight of hylan is thought to make it effective and to make it reside longer in the joint space (i.e., slower resorption). The recommended injection schedule is one injection per week for 3–5 weeks for various commercial preparations although higher molecular weight preparations can be given as a single injection. Repeat courses of visco-supplementation can be performed after 6 months and are shown to be effective in patients who had a previous favourable clinical response. If effusion is present, aspiration of the joint is recommended before the injection to prevent dilution of the injected hyaluronic acid. A meta-analysis (2004)7 on the therapeutic effects of hyaluronic acid on OA knee, found significant improvements in pain and functional outcome. However, there was significant betweenstudy heterogeneity in the estimates of the efficacy of hyaluronic acid. Patients older than 65 years of age and those with the most advanced radiographic stage of OA (complete loss of joint space) were
ARTICLE IN PRESS 410 found to be less likely to benefit from viscosupplementation therapy. The only significant side effect reported is a painful acute local reaction (incidence ¼ 2–8%). Good quality studies are required to resolve the continued uncertainty about the therapeutic effects of different types of hyaluronic acid products. A more recent Cochrane review (2005)8 also concluded that visco-supplementation is an effective treatment for OA of the knee with beneficial effects on pain, function and patient global assessment. The maximal improvement in symptoms occurred between 5 and 13 weeks following the injection. The benefits were comparable to the use of NSAIDS but without any reported systemic side effects, and longer-term benefits were noted when compared to the use of intra-articular (IA) corticosteroids.
Intra-articular corticosteroids Corticosteroids inhibit the inflammatory and immune cascade at several levels: they suppress immune cell migration, inhibit macrophage presentation to lymphocytes, suppress immune/ inflammatory effector cell activation and differentiation, increase apoptosis of immature and activated T-lymphocytes, and suppress pro-inflammatory cytokine production. Contraindications include sepsis, joint prostheses and overlying infection in the soft tissue. Although widely used, there are concerns regarding possible adverse effects, including long-term joint damage and the risk of infection. A RCT on the long-term efficacy and safety of IA corticosteroids concluded that there was no evidence that steroids accelerated joint space narrowing.9 Moreover, long-term treatment of knee OA with repeated steroid injections resulted in significant reduction in the clinical symptoms of the disease. A Cochrane review (2005) of 26 trials (1721 patients) showed definite superiority of IA corticosteroids over IA placebo for pain reduction and patient global assessment between 1 and 3 weeks post-injection.10 However, there was no significant improvement in function during this period. These initial improvements in pain and patient global assessment were not seen in studies at 4–24 weeks post-injection, and there was no significant improvement in function during this period. When corticosteroids are compared with HA products, no statistically significant differences were detected at 1–4 weeks post-injection. The onset of effect was similar with IA HA products, but was less durable. HA products showed more effectiveness in
S.P. Krishnan, J.A. Skinner terms of pain and function between 5 and 13 weeks post-injection. Comparisons of IA corticosteroids showed that triamcinolone hexacetonide was superior to betamethasone for the number of patients reporting pain reduction up to 4 weeks post-injection. Comparisons between IA corticosteroid and joint lavage showed no differences in any of the efficacy or safety outcome measures.
Conservative surgical options Arthroscopic debridement The techniques used include lavage and debridement, marrow stimulation techniques and laser or thermal chondroplasty. The mechanism of action is multifactorial and may include stimulation of fibrocartilage formation and tissue repair secondary to enzymatic digestion of the extra-cellular matrix. Clinical results are unpredictable. Concerns include the durability of the fibro-cartilage repair tissue in subchondral penetration procedures and thermal damage to subchondral bone and adjacent normal articular cartilage in laser/thermal chondroplasty. With proper selection, patients with early degenerative arthritis and mechanical symptoms of locking or catching can benefit from debridement. Despite its widespread use, few prospective studies of effect exist. A recent prospective, randomised, double-blinded study11 has shown that outcomes after arthroscopic lavage/debridement were no better than placebo (sham surgery) for knee OA. A prospective analysis12 of 126 patients who underwent arthroscopic debridement procedures including resection of unstable chondral flaps and meniscal tears showed that 56 patients (44%) had a clinically important reduction in pain, as determined with the WOMAC pain scale, at 2 years after the procedure. Clinical variables such as the presence of medial joint-line tenderness, a positive Steinman test and the presence of an unstable meniscal tear at arthroscopy predicted a successful result after the arthroscopic debridement. Another prospective study,13 involving 254 patients with moderate knee pain due to early OA treated by arthroscopic debridement, found that 75% had minimal discomfort and improved function at a mean follow-up of 44 months; and 85% were satisfied with the treatment. The mean age of patients was 49 years. Only 14% required further surgery after an average period of 4 years. Those
ARTICLE IN PRESS Novel treatments for early osteoarthritis of the knee with less radiographic arthritis, less severe cartilage damage at operation and younger age had most improvement. A retrospective study on 204 knee debridements,14 found that 63% (129 knees) were better, 21% (43 knees) were unchanged and 16% (13 knees) were worse after the surgery. They also concluded that patients with less deformity do better than those with significant varus or valgus angulations. Satisfaction decreased with increasing number of previous operations. Increasing age predicted poorer outcome but this was secondary in importance to angular deformity. Other positive prognostic factors include a preoperative flexion contracture of less than 101 and hospital for special surgery (HSS) scores greater than 22.15 Arthroscopic debridement clearly has a role in patient management, whether it is temporising or palliative. This is especially true in patients who fail to respond to medical management and when arthroplasty must be deferred because of young age.
411
Figure. 1 Arthroscopic picture demonstrating microfracture technique for an isolated degenerative lesion of the cartilage.
Micro-fracture This procedure was introduced by Steadman 20 years ago and is a technique in which accurate debridement of all unstable and damaged articular cartilage is performed, down to the subchondral bone plate while maintaining a stable perpendicular edge of healthy cartilage. An arthroscopic awl is used to make multiple holes in the defect, while ensuring the subchondral plate is kept intact. After micro-fracture, the defect fills with haematoma, thus producing an environment for pluripotential marrow cells to differentiate into fibrocartilage (Fig. 1). Micro-fracture is a modification of the Pridie drilling technique. Advantages of micro-fracture over drilling may include reduced thermal damage to subchondral bone and the creation of a rougher surface to which repair tissue might adhere more easily. It is also easier to penetrate a defect perpendicularly with a curved awl during an arthroscopic procedure as compared with a drill. There are currently no published studies which compare micro-fracture with drilling. An evaluation of patient satisfaction and outcome after micro-fracture16 for isolated degenerative lesions on 81 patients at a mean follow-up of 26 years showed significant improvement in mean Lysholm score for function. However, 18 patients (22.2%) required a revision procedure within the next 5 years (13 adhesiolysis and 5 repeat microfracture). There is insufficient data to determine the role of micro-fracture in overt OA.
Figure. 2 Arthroscopic appearance of the repaired osteochondral defect at 1 year following ACI.
Autologous chondrocyte implantation (ACI) Published data is limited to its use in the treatment of isolated symptomatic osteo-chondral defects of the knee. Autologous chondrocyte implantation (ACI) is shown to be superior to mosaicplasty in the treatment of symptomatic osteochondral defects.17 However, a short-term comparison of ACI with micro-fracture found no difference in clinical outcome.18 ACI produces durable outcome for as long as 11 years19 (Fig. 2). ACI may play a role in the prevention/postponement of the onset of OA. The technique shows
ARTICLE IN PRESS 412 inferior results with increasing age20 and hence degenerative osteochondral lesions are considered as a relative contraindication for ACI. However, ACI has been shown to be useful21 for salvage in patients with knee OA in whom arthroplasty was deferred for various reasons. Pain relief and comfort with activities of daily living were the desired preoperative goals in this group of 71 salvage patients. They noted significant improvement in SF-36 quality of life scores and 490% patient satisfaction at 24 months and concluded that ACI could be an option for salvage in patients with knee OA when they have realistic expectations of its outcome.
S.P. Krishnan, J.A. Skinner kine-induced degradation. Genetic modification involves transfer of genes using in vivo or in vitro strategies. The in vitro techniques are complex and involve several steps including the removal of synovium from the joint, transfection of the cells by a viral or non-viral gene transfer method and reintroduction of the transfected cells into the joint. However, such reintroduced cells have only a transient effect and may perish before any transgene expression occurs. In vivo strategies aimed at genetically enhancing chondrocytes or their progenitors may improve transgene expression and could serve as a continual source for cytokine receptor antagonists.
Bisphosphonates
Potential therapies for the future Cytokines The cytokines IL-1b and TNFa play a major role in the inflammatory process associated with cartilage damage in OA. IL-1b is formed as a precursor protein and must be cleaved in order to be active. The enzyme responsible for the cleavage is IL-1 bconverting enzyme (ICE). An in-vitro study of ICE showed that its inhibition effectively reduces the production of the active form of IL-1 b in OA cartilage and synovium.22 Pralnacasan (an oral inhibitor of ICE) has been shown to be effective in reducing OA damage in two mouse models.23 Also, IA injection of IL-1 receptor antagonist (IL-1 Ra) has been shown to produce pain relief and improved function in people.24
Growth factors In response to injury, chondrocytes synthesise macromolecules to repair damaged tissue. Growth factors such as insulin-like growth factor-1 (IGF-1) contribute to this repair process. A pilot study of the use of recombinant IGF-1 in patients with severe OA found no differences in pain or mobility when compared to a control group. As a result of high cost and suboptimal delivery systems, these growth factors have not undergone extensive clinical testing. However, interest remains, fuelled by promising in-vitro results.25
Gene therapy This includes genetic modification of chondrocytes and/or synovial cells to facilitate the production of cytokine receptor antagonists (e.g. IL-1 Ra), thus rendering the cartilage/synovium resilient to cyto-
Bisphosphonates inhibit osteoclasts directly, either by increasing cellular apoptosis or by affecting the cell’s metabolic activity. In OA, they appear to act on subchondral bone, where affected joints have decreased bone mineral density and quality and there is increased bone turnover similar to that observed in patients with osteoporosis. Early studies using the bisphosphonate risedronic acid have shown its possible use in reducing joint space narrowing measurements.
Hormone replacement therapy Epidemiological studies suggest that post-menopausal women are at increased risk for developing OA. Oestrogen may thus play a role in OA aetiology. No randomised, prospective, controlled trials are presently available to assess the direct impact of HRT on the structural progression of OA. Furthermore, HRT is not without risk. HRT cannot be recommended as a treatment for OA at the present time.
Matrix metalloproteinase inhibitors MMPs are a group of zinc-dependent proteolytic enzymes that degrade cartilage matrix macromolecules. After secretion, MMPs are activated by proteolytic removal of their propeptides. Once activated, regulation in the extracellular matrix is the function of tissue inhibitors of matrix metalloproteinase inhibitors (TIMPs). Faulty regulation of MMPs may have a role in the pathogenesis of OA. Clinical trials using MMP inhibitors to treat OA have frequently encountered problems with toxicity and the development of such adverse effects as arthralgia, myalgia and tendonitis. This often required patient withdrawal from trials. Antibiotics
ARTICLE IN PRESS Novel treatments for early osteoarthritis of the knee of the tetracycline class (including doxycycline and minocycline) have been found to inhibit MMP activity and have likewise reduced the severity of OA in animal models. Their clinical use in reducing the progression of OA is currently being investigated.
413
Research directions
Nitric oxide Excess production of nitric oxide (NO) and its byproducts (reactive oxygen species [ROS]), in response to inflammation, are thought to be involved in the pathogenesis of OA. One of the enzymes responsible for its synthesis is inducible NO synthase (iNOS). Reducing excess production of NO may alleviate OA symptoms and halt disease progression. Animal studies on therapeutic doses of the iNOS inhibitor N-iminoethyl-L-lysine have been shown to reduce the size of cartilage lesions and the incidence of osteophytes in a dose-dependent manner.26 Also, iNOS knock-out mice have been shown to be resilient to experimental OA.27
Artificial meniscus Early animal studies and mechanical tests using a polyvinyl alcohol-hydrogel (PVA-H) artificial meniscus showed encouraging results.28 Mechanical tests using a higher water content PVA-H showed viscoelastic behaviour similar to that of human meniscus and its frictional coefficient against natural articular cartilage was also effective. Also, early results of animal studies suggest it may delay the onset of OA following menisectomy.
Conclusion Current evidence supports the use of IA viscosupplementation and corticosteroids in selected patients with early OA of the knee, but further long-term studies are required to establish the role of oral glucosamine and chondroitin sulphate. Arthroscopic debridement is useful for younger patients with less radiographic OA and deformity, with meniscal lesions or chondral flaps amenable to treatment. The treatment of OA knee has evolved from symptomatic treatment to possible prophylactic and disease-modifying solutions. Established treatments are still being researched and perfected, and disease modification therapy is still in its infancy. The need for both may be critical, in an ageing population where OA becomes an increasing burden and cause of morbidity.
Risk of cardio-vascular and CNS complications on long-term use of NSAIDs In-vivo studies on the effectiveness of glucosamine and chondroitin sulphate on cartilage metabolism Disease modifying drugs for OA knee Biological replacement of senescent cartilage using tissue engineering techniques Therapy to prevent cartilage senescence
References 1. Osiri M, Brosseau L, Mc Gowan J, et al. Transcutaneous electrical nerve stimulation for knee osteoarthritis. Cochrane Database Syst Rev 2000;23(4):CD 002823. 2. Hulme JM, Judd MD, Robinson VA, Tugwell P, Wells G, de Bie RA. Electromagnetic fields for the treatment of osteoarthritis. Cochrane Database Syst Rev 2002;21(1):CD 003523. 3. Brosseau L, Gam A, Harman K, et al. Low level laser therapy (Classes I, II and III) for treating osteoarthritis. Cochrane Database Syst Rev 2004;19(3):CD 002046. 4. Howes LG, Krum H. Selective cyclo-oxygenase-2 inhibitors and myocardial infarction: how strong is the link? Drug Saf 2002;25(12):829–35. 5. Towheed TE, Maxwell L, Anastassiades TP, et al. Glucosamine therapy for treating osteoarthritis. Cochrane Database Syst Rev 2005;20(2):CD002946. 6. Mazzuca SA, Brandt KD, Buckwalter KA, Lequesne M. Pitfalls in the accurate measurement of joint space narrowing in semiflexed, anteroposterior radiographic imaging of the knee. Arthritis Rheum 2004;50(8):2508–15. 7. Wang CT, Lin J, Chang CJ, Lin YT, Hou SM. Therapeutic effects of hyaluronic acid on osteoarthritis of the knee. A meta-analysis of randomized controlled trials. J Bone Jt Surg Am 2004;86-A(3):538–45. 8. 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 2005;18(2): CD005321. 9. Raynauld JP, Buckland-Wright C, Ward R, et al. Safety and efficacy of long-term intraarticular steroid injections in osteoarthritis of the knee: a randomized, double-blind, placebo-controlled trial. Arthritis Rheum 2003;48(2):370–7. 10. Bellamy N, Campbell J, Robinson V, Gee T, Bourne R, Wells G. Intra-articular corticosteroid for treatment of osteoarthritis of the knee. Cochrane Database Syst Rev 2005;18(2):CD 005328. 11. Moseley JB, O’Malley K, Petersen NJ, et al. A controlled trial of arthroscopic surgery for osteoarthritis of the knee. N Engl J Med 2002;347(2):81–8. 12. Dervin GF, Stiell IG, Rody K, Grabowski J. Effect of arthroscopic debridement for osteoarthritis of the knee on health-related quality of life. J Bone Jt Surg Am 2003; 85-A(1):156–7. 13. Aichroth PM, Patel DV, Moyes ST. A prospective review of arthroscopic debridement for degenerative joint disease of the knee. Int Orthop 1991;15(4):351–5.
ARTICLE IN PRESS 414 14. Harwin SF. Arthroscopic debridement for osteoarthritis of the knee: predictors of patient satisfaction. Arthroscopy 1999;15(2):142–6. 15. Fond J, Rodin D, Ahmad S, Nirschl RP. Arthroscopic debridement for the treatment of osteoarthritis of the knee: 2- and 5-year results. Arthroscopy 2002;18(8):829–34. 16. Miller BS, Steadman JR, Briggs KK, Rodrigo JJ, Rodkey WG. Patient satisfaction and outcome after microfracture of the degenerative knee. J Knee Surg 2004;17(1):13–7. 17. 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 Jt Surg Br 2003;85(2):223–30. 18. Knutsen G, Engebretsen L, Ludvigsen TC, et al. Autologous chondrocyte implantation compared with microfracture in the knee. A randomized trial. J Bone Jt Surg Am 2004; 86-A(3):455–64. 19. Peterson L, Brittberg M, Kiviranta I, Akerlund EL, Lindahl A. Autologous chondrocyte transplantation. Biomechanics and long-term durability. Am J Sports Med 2002;30(1): 2–12. 20. 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 Jt Surg Br 2005;87(5):640–5. 21. Minas T. Autologous chondrocyte implantation in the arthritic knee. Orthopedics 2003;26(9):945–7.
S.P. Krishnan, J.A. Skinner 22. Saha N, Moldovan F, Tardif G, et al. Interleukin-1 betaconverting enzyme/caspace-1 in human osteosrthritic tissues: localisation and role in the maturation of interleukin1beta and interleukin-18. Arthritis Rheum 1999;42(8): 1577–87. 23. Rudolphi K, Gerwin N, et al. Pralnacasan, an inhibitor of interleukin-1 beta conerting enzyme, reduces joint damage in two murine models of osteoarthritis. Osteoarthritis Cartilage 2003;11(10):738–46. 24. Goupille P, Giraubeau B, et al. Safety and efficacy of intraarticular injection of IL-1ra in patients with painful osteoarthritis of the knee: a multicenter, double-blind study [abstract 1822]. Arthritis Rheum 2003;48(Suppl):S696. 25. Haupt JL, Frisbie DD, McIlwraith CW, et al. Dual transduction of insulin-like growth factor-I and interleukin-1 receptor antagonist protein controls cartilage degradation in an osteoarthritic culture model. J Orthop Res 2005;23(1): 118–26. 26. Pelletier JP, Jovanovic DV, Fernandes JC, et al. Reduced progression of experimental osteoarthritis in vivo by selective inhibition of inducible nitric oxide synthase. Arthritis Rheum 1998;41(7):1275–86. 27. van den Berg WB, van de Loo F, Joosten LA, et al. Animal models of arthritis in NOS2-deficient mice. Osteoarthritis Cartilage 1999;7(4):413–5. 28. Kobayashi M, Chang YS, Oka M. A two year in vivo study of polyvinyl alcohol-hydrogel (PVA-H) artificial meniscus. Biomaterials 2005;26(16):3243–8.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 415–427
www.elsevier.com/locate/cuor
MINI-SYMPOSIUM: SURGERY FOR KNEE ARTHRITIS
(ii) Osteotomy for osteoarthritis of the knee Vittorio Franco, Guglielmo Cerullo, Massimo Cipolla, Enrico Gianni, Giancarlo Puddu Clinica Valle Giulia, Via G. De Notaris 2B, 00197 Roma, Italy
KEYWORDS Osteotomy; Osteoarthritis; Opening wedge; Mechanical axis
Summary Osteotomy is a classic operation in the treatment of uni-compartimental osteoarthrosis of the knee. In the modern context it is used to correct initial varus, or valgus, deformity before slight chondral damages advance to become progressive irreversible articular disease. It has been presented as an alternative to prosthetic joint replacement, but the indications depend on the stage and articular spread of degenerative changes and on the patient’s general state. Indications for surgery are very different, in most of the cases, from the indications for uni or total knee replacement. Since the early nineties we have practiced a modern and relatively new technique in performing knee osteotomies based on a special dedicated system of instruments and plates. This opening wedge technique, when compared to Coventry’s antivarus closing wedge osteotomy, inverts the method of correction, adding the wedge medially instead of removing it laterally; in case of valgus deformity osteotomy is carried out on the femoral side with a lateral opening wedge. Operative techniques of high tibial osteotomy and osteotomy of the distal femur will be illustrated with particular attention to all details of the two operations in ‘step by step’ descriptions. & 2005 Published by Elsevier Ltd.
Introduction Deformity of the knee associated with osteoarthrosis (OA) is a common presenting complaint to the orthopaedic surgeon. In a normal knee, approximately 60% of the weight-bearing forces are transmitted through the medial compartment and 40% through the lateral compartment. The varus Corresponding author. Tel.: +39 06 324791;
fax: +39 06 3230707. E-mail address:
[email protected] (V. Franco). 0268-0890/$ - see front matter & 2005 Published by Elsevier Ltd. doi:10.1016/j.cuor.2005.10.008
knee with uni-compartimental OA of the medial compartment has an altered alignment and consequently more load is distributed to the affected compartment. Then the medial half of the tibial plateau supports most of the body weight and the malalignment accentuates the stress on damaged articular cartilage, causing further degenerative changes and more angular deformity. In valgus deformity, the lateral plateau is the overloaded half of the joint with progressive chondral damage due to malalignment, which also makes the deformity worse as time goes by.
ARTICLE IN PRESS 416 Osteotomy is the classic operation, in the standard orthopaedic armamentarium, to treat early degenerative arthritis of the knee and correct deformity. This procedure has a long history in orthopaedics. The first reports on osteotomies can be found in the German literature as early as the nineteenth century. Much later in modern English literature, Jackson,1 in 1958, and Wardle,2 in 1962, described the earliest techniques of proximal tibial valgus osteotomies with a lateral closing wedge. Only in 1965 was the method popularised by Coventry.3 He modified the previously performed procedures by executing the osteotomy proximal to the tibial tubercle. This had several advantages. The osteotomy was performed closer to the area of the deformity, the bone involved was cancellous and tended to heal rapidly, and the patient could bear weight on the leg immediately, since the pull of quadriceps stabilised the osteotomy. The medial opening wedge technique came about 10 years later. Hernigou et al.4 in 1987 presented a 10–13 years follow-up of 93 patients operated with the opening technique and considered that this was a suitable procedure for medial compartment narthrosis, but cautioned that ‘precise correction of malalignment is essential’ for a good long-term outcome. Fowler et al.5 in 2000 described a modification of the Puddu and co-workers6,7 opening wedge technique and pointed out how ‘small corrections of 51 or less are technically easier to achieve than with a closing wedge osteotomy’. Proximal tibial osteotomy is not so effective in cases of valgus knee, especially when the deformity is more than 101. A major valgus deformity is often associated with a joint line that slopes superolaterally in the anterior–posterior plane, and this abnormal plane cannot be corrected unless the osteotomy is done proximal to the joint. Coventry8 in 1973 stated that if a knee is more than 121 valgus, or if the plane of the joint deviated from the horizontal by more than 101, distal femoral varus osteotomy, rather than a proximal tibial varus osteotomy, should be done. The Manual of Internal Fixation, 1979 edition,9 contains a brief description of the use of the 901 offset blade-plate for the femoral osteotomy. More recently, some authors10,11 discussed in detail their methods to perform the distal femoral osteotomy. In the following paragraphs, we present our techniques to perform opening wedge osteotomies in the proximal tibia/distal femur using Puddu plates.
Indications/contraindications OA of the knee has many causative factors. Degenerative changes of the articular cartilage
V. Franco et al. can occur through tension, compression or shear. Genetic factors are known to play a part. Specific trauma and trauma from overload caused by obesity or occupational factors are aetiologically important. In essence, the biophysical cause for OA is an overload, or a concentration of forces, beyond the ability of the cartilage and subchondral bone to cope. Malalignment into a varus position will overload the medial condyles of the femur and tibia, while valgus deformity overstresses the lateral compartment of the joint. It follows that alignment of the lower extremity plays an important role in uni-compartimental OA of the knee. The rationale behind the osteotomy is to correct the angular deformity at the knee and, thereby, decrease the excessive weight-bearing load across the affected compartment, which is the most involved by the degenerative process. Since alternative treatments for severe degenerative and inflammatory diseases of the knee in the 1960s were limited, tibial osteotomy was initially used for OA, rheumatoid arthritis and secondary arthrosis regardless of the aetiopathogenesis and the magnitude of the angular deformity. Nowadays we think that the patients selected for an osteotomy should have uni-compartimental OA with axial malalignment. However, fracture and other trauma, congenital and acquired deformities, and idiopatic osteonecrosis could be, in particular cases, indications for this procedure. There is no definite chronologic age below which one should do an osteotomy and above which one should do an arthroplasty. The age of 60 is the most often cited, but activity level, lifestyle and general health must be considered. As long-term studies of arthroplasty demonstrate, age considerations may change. But it still remains that the age group of osteotomy patients is generally younger than that for knee arthroplasty. Furthermore, the actual trend seems to be orientated towards early treatment of uni-compartimental OA in relative young patients since better results have to be expected when the articular changes are in the initial stages of the degenerative process. Osteotomy would be best done for primarily unicompartimental OA in knees with generally wellmaintained range of motion (ROM) (at least 901 of flexion, less than 151 of flexion contracture). Osteotomy should probably not be done in patients with rheumatoid arthritis, patient with very unstable knees, nor in knees with greater than 201 of varus deformity or 151 of valgus deformity, because, according to Insall et al.,12 these knees are complicated by an associated severe ligamentous laxity and subluxation. The last one is
ARTICLE IN PRESS Osteotomy for osteoarthritis of the knee a relative contraindication; in fact, even if the correction of the mechanical axis in such a great deformity can result in a relaxed collateral ligamentous complex, often the knee finds itself a new functional stability so that many authors, including ourselves, do not routinely perform retightening of the ligamentous structures. A medial or lateral meniscectomy that leads to a symptomatic deformity is a frequent indication for an osteotomy. Too often the menisci are sacrificed in the young sporting patient who undergoes an operative procedure after a sprain of the knee. In such a patient, the timing of reparative surgery is very important because the osteotomy is much more effective if it is performed in the earliest stage of the disease to prevent the later unavoidable degenerative changes. In the same way, a young patient with a congenital deformity who has developed pain can be considered a candidate for an early preventive osteotomy before articular damages start to involve the overloaded compartment. A patient who has varus deformity and anterior cruciate ligament (ACL) insufficiency may be treated with proximal tibial osteotomy, eventually, in addition to the ACL reconstruction. A technically demanding procedure, osteotomy with ligament reconstruction, addresses the underlying disorder and simultaneously corrects the problems. Because this is not routine procedure, it will not be discussed here. Symptoms of pain and instability must be separated as clearly as possible. When pain prevails, especially in sedentary patients, correction of alignment, with consequent relief of medial compartment pain can be a satisfactory treatment. Obesity is a controversial topic and has a negative effect on the outcome of surgery in many orthopaedic operations. Most would agree that excess of body weight could make a patient better candidate for osteotomy than for arthroplasty, but it is also true that obesity will represent a negative factor in view of the possible general postoperative complications. When a patient is overweight, then the weight should be brought to near normal before surgery since worse long-term results for osteotomy related to obesity have been demonstrated. A contraindication to osteotomy is severe bone loss (more than a few millimetres) of the medial or lateral tibia or femur. When medial or lateral compartment bony support is insufficient, congruent weight bearing on both tibial plateaus following the osteotomy is not possible. In this situation, tibiofemoral contact will teeter on the relatively prominent intercondylar tibial spines.
417 The presence of severe varus or valgus deformity may be associated with lateral or medial subluxation of the tibia, respectively. Subluxation greater than 1 cm is an absolute contraindication to osteotomy and some authors suggest that osteotomy should not be performed if any translation or subluxation is present. Studies on the biomechanics of dynamic gait accurately addressed the issue of varus or lateral thrust of the knee during ambulation. The term ‘adductor moment’ was used to describe the amount of lateral or varus thrust of the knee observed during gait. Patients with a high adductor moment have worse results following osteotomy than patients with a low adductor moment. Furthermore, patients with a high adductor moment are more likely to have a recurrent varus deformity following valgus osteotomy. When osteotomy is chosen for those patients in spite of a high adductor moment, overcorrection of the deformity may be helpful. Osteotomy of the proximal tibia or distal femur is designed to relieve pain caused by medial or lateral tibiofemoral OA. Slight degenerative changes of the patellofemoral joint are not a contraindication to osteotomy. But following proximal tibial osteotomy with a medial opening wedge, the anterior tibial tubercle is lowered at about one-half of the angular correction. Therefore, the condition of ‘patella baja’ is a contraindication to this kind of operation.
Preoperative planning The goal of knee osteotomy is to realign the mechanical axis of the limb thereby shifting the weight bearing line (WBL) from the diseased compartment to the more normal compartment. Full-length radiographs of the lower extremity best measure the alignment of the limb. The measurement of the WBL is a line drawn from the centre of the femoral head through the centre of the knee to the centre of the ankle mortise. The anatomic axis is a line drawn through the centre of the shaft of the femur and through the centre of the shaft of the tibia. In the normal knee, the two lines cross each other in the centre of the joint making an angle of 51 (physiologic valgus), and the mechanical axis, which in this case almost coincides with the WBL, passes also through the centre of the joint, or slightly varus (about 11 medially). According to these parameters as the reference points of ‘normality’, the deformity is measured. In the case of a varus knee, we wish to move the WBL through the neutral alignment (approximately the
ARTICLE IN PRESS 418 centre of the knee) to a more lateral point at about two-thirds (63%) of the tibia plateau to get 51 of mechanical valgus alignment and, therefore, overcorrect the anatomic valgus from the ‘normal’ 51 to 9–101. Extensive experience has shown that overcorrection is absolutely essential if one wants to optimise the long term results of valgus osteotomy. It is insufficient to correct to normal valgus and bring the extremity back to the position from which it originally deformed and does not properly unload the medial compartment. In the normal knee, approximately 60% of weight-bearing forces are transmitted through the medial compartment and approximately 40% through the lateral compartment; even in severe valgus deformity (up to 301 valgus) the medial plateau load never falls below 30%. A young patient with a symptomatic congenital varus could be a candidate for early valgus osteotomy but, only in this situation, the correction must not be an ‘overcorrection’. In such a patient it is quite sufficient to restore the physiological alignment of the knee. We prefer to make our plans on a double leg standing radiograph, instead of a single weightbearing X-ray, to reduce the risk of overcorrection. The resulting deformity of the knee, measured on a single leg stance examination, is the amount of the osseous geometric malalignment plus the malalignment due to the ligamentous laxity. The osteotomy is able to realign the limb by means of a bony correction. The remaining part of the deformity, depending on the ligaments, can spontaneously recover simply because the new balance between the femur and tibia inverts the convexity and concavity side of the joint each other canceling the effects of the pre-existing laxity on varus/valgus alignment. In case of a valgus knee, we wish to reposition the mechanical axis to the neutral alignment at approximately 01 in the centre of the joint that means 51 of anatomic and physiologic valgus. The biomechanics of varus and valgus deformities of the knee differ. In fact, the intrinsic valgus angle between femur and tibia determines an asymmetric overload of the medial compartment, at about 60% of the whole, already in the normal knee. Thus, the overbalance of the knee towards a varus alignment will result in a functional disaster because of the additional overload of the medial compartment and the consequent dramatic acceleration of the degenerative changes of the more normal side too. The osteotomy we propose here is based on the opening wedge technique. Special plates with a spacer ‘tooth’ were designed for this aim. We need
V. Franco et al. to know the size of the base of the wedge, calculated in millimetres, to choose the plate and fix the osteotomy at the desired correction, we have planned in angular degrees. Different widths of the tibia, at the level of the osteotomy cut, correspond to different wedge sizes, for the same value of angular correction. The WBL method13 is a simple and reproducible technique for determining the desired correction angle. Divide the tibial plateau from 0% to 100% from the medial to the lateral margin. Draw two lines, the first one from the centre of the femoral head and the second one from the centre of the tibiotalar joint to the same point at the 63% point of the tibia plateau. The angle formed by these two lines equals the angle of correction. Once the desired angle of correction has been determined the opening wedge height can be calculated by drawing a schematic triangle in which the apex angle is the one measured with the just described method (Fig. 1). Now, on the drawing itself is possible to read how many millimetres wide has the base of the osteotomy to be to get the planned correction. To complete the evaluation of the knee, we look at the different radiographic views including the standard lateral and the axial of the patellofemoral joint. The Rosenberg et al.14 view, comparative posteroanterior weight-bearing radiograph at 451 of knee flexion, facilitates the diagnosis when the standard AP view is not sensitive enough. The Rosenberg exam has a strong predictive value when the deformity is associated with a cruciate insufficiency and, therefore, the chondral wear prevails in the posterior part of the tibial plateaus. Most authors do not recommend computed tomography (CT) scans or magnetic resonance imaging (MRI) in studying a candidate for knee osteotomy, but we think that the stress reaction of the subchondral bone, detectable by MRI, could be the only positive sign of a degenerative process, at its earlier stage, but, already, with all the stigmata of the condemned knee.
Dedicated surgical instrumentation The object of valgus osteotomy is to obtain after the operation, a new mechanical axis overcorrected up to 51 of valgus, while our purpose with varus osteotomy is to reposition the lower limb to align the physiologic 01 of the neutral mechanical axis.
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Figure 1 Normal alignment (A), with the weight-bearing line passing through centre of the knee. With varus angular deformity related to loss of the osteocartilaginous complex, angle CBD results in 61 of deformity (B). With abnormally slack lateral soft tissues, the lateral articular surfaces separate, resulting in an additional a1 of varus angular deformity (C) (angles exaggerated for illustration). A properly executed high tibial osteotomy results in a weight-bearing line that passes through the lateral compartment (D).
We present here our technique to perform the opening wedge osteotomy and, to accomplish reproducible results with less technical difficulty. The senior author developed a complete, but simple and easy, system of dedicated instruments and plates. We obtain valgus correction of the knee by means of proximal tibial osteotomy and varus correction by distal femoral osteotomy. In varus deformity, the tibiofemoral joint line is usually parallel to the floor and proximal tibial osteotomy has been demonstrated to effectively transfer load from the medial to the lateral compartment. In valgus deformity, the joint line has a valgus tilt with a corresponding obliquity from superolateral to inferomedial direction. While tibial varus osteotomy may realign a valgus limb, it is not able to correct the joint line tilt because the procedure is performed distally to the joint. The mechanical consequence of it, in patients with severe valgus deformities (over 10–121 according to various authors), is to transfer the load transmission medially not more than the lateral portion of the tibial spine, and the resultant increased valgus tilt of the joint line leads to
greater shear forces and lateral subluxation during gait. On the contrary distal femoral varus osteotomy may realign a valgus limb and correct valgus tilt of the joint line when used to treat lateral tibiofemoral OA with valgus deformity. The plates specially designed for this osteotomy are butterfly shaped with four holes for the tibia and ‘T’-shaped with seven holes for the femur (Fig. 2). Their peculiarity is a spacer, a tooth as it were, available in many different sizes from 5 to 17.5 mm in thickness (up to 20 mm for the femur). The size of the spacer tooth increases about 1 mm from the thinnest to the thickest. Tibial plates with trapezoidal spacers are also available to permit correction of the coronal and, eventually, the sagittal deformity, the so-called tibial posterior slope, in one surgical procedure. The tooth enters the osteotomy line, holding the position and preventing later collapse of the bone with recurrence of the deformity. The thickness of the spacer must coincide with the desired angle of correction, calculated in advance by preoperative planning. The two upper holes of the tibial plate and the three of the horizontal lower arm of the
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Figure 4 ‘Osteotomy jack’ is a simple innovative tool that consists of two osteotomes, which permits, intraoperatively, by means of the screw, to gently distract and easily open the osteotomy. Figure 2 Femoral plate.
Figure 3 New tibial plate forged in a special titanium alloy.
femoral ‘T’ plate allow the introduction of AO 6.5 mm cancellous screws, while the lower holes of the tibial plate and the holes in the vertical arm of the femoral plate are cut for the AO 4.5 mm cortical screws. Innovative new plates, forged in a special titanium alloy, are now available (Fig. 3). The most important improvement, compared to former plates consist of the new special holes. Through them screws can be freely orientated in every preferred direction and then locked in the plate, like in a sort of internal mini-fixator, thanks to a special device of the hole itself, originally realised
by the manufacturer (Arthrex, Naples, FL). Dedicated cortical and cancellous screws for the new plates, also of titanium alloy, are now available. The crucial point of the operation is the opening of the metaphysis, where the osteotomy has cut the bone, at the desired angle of correction to allow introduction of the plate tooth. Recently, we introduced a new innovative tool the ‘osteotomy jack’ (Fig. 4) which greatly facilitates this step. Introduced into the osteotomy line, the jack gently retracts the bone to create the space for the plate and the grafts. It consists of two osteotomes coupling with a screw long enough to separate the blades and open the osteotomy. Then a very simple ‘wedge opener’ enters the already prepared osteotomy site. It looks like a fork with two wedge-shaped tines, graduated to hold the opening correctly, and a removable handle to allow positioning of the plate. The other two dedicated tools are the special Homan retractor for vastus lateralis, to be used in the femoral osteotomy, and a long rod guide with an ankle support to check intraoperatively the mechanical femorotibial alignment.
Surgical technique of tibial osteotomy Step 1: patient position We prefer a normal operating table with the patient in a supine position and the C-arm of an image intensifier set up opposite to the surgeon. The patient is draped as usual in knee surgery; we also prepare the iliac wing and cover the foot using a very fine stockinette and a transparent adhesive drape to minimise the bulging at the ankle so that it will be possible to better realise the femorotibial
ARTICLE IN PRESS Osteotomy for osteoarthritis of the knee alignment after the correction. The tourniquet may be inflated.
Step 2: arthroscopy Arthroscopy of the knee is carried out before the osteotomy to assess the relative integrity of the controlateral tibiofemoral compartment and of the patellofemoral joint and to treat any intraarticular pathology: appropriate joint surface debridement, partial meniscectomy or loose body removal is performed if needed.
Step 3: incision and exposure We expose the anteromedial aspect of the tibia through a vertical skin incision centred between the medial border of the anterior tibial tubercle and the anterior edge of the medial collateral ligament and extending 6–8 cm distally to the joint line. Sharp dissection is carried to the sartorius fascia and the pes anserinus tendons are identified and detached from the bone. The pes anserinous is now retracted (Fig. 5) and the anterior half of the underlying superficial collateral ligament is horizontally cut. There is no risk of instability because the deepest, and much more stabilising, tibiomeniscal bundle of the ligament remains intact.
Figure 5 Pes anserinus tendons are retracted to expose the superficial collateral ligament.
421 A blunt retractor is placed dorsally, deep to the collateral ligament, to protect the posterior vessels exposing the posteromedial corner of the tibia. Anteriorly a second retractor is placed under the patellar tendon. The procedure is facilitated by flexion of the knee.
Step 4: osteotomy The authors’ preferred method is a ‘free’ technique. With the knee in extension and under fluoroscopic control, a guide pin (Steinmann) is drilled, by the ‘free hand’, through the proximal tibia from medial to lateral. This is obliquely oriented starting approximately 4 cm distal to the joint line and directed across the superior edge of the tibial tubercle to a point 1 cm below the joint line (Fig. 6). The original instruments system also provides an osteotomy cutting guide to help the surgeon in the placement of the second guide pin and to facilitate the use of the oscillating saw with the proper orientation. The guide may be adjusted to accommodate variations in size and anatomy and different choices in tilting the osteotomy cut in both coronal and sagittal planes are also possible. The osteotomy is then performed keeping the oscillating saw blade below and parallel to the
Figure 6 Guide Steinmann pin is drilled through the proximal tibia from medial to lateral, obliquely oriented and directed across the superior edge of the tibial tubercle to point 1 cm below the joint line.
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guide pin, to prevent an intraarticular fracture. The saw is used to cut the medial cortex only. Then a sharp osteotome is used to finish the osteotomy, making certain that the all the cancellous metaphysis and, especially, the anterior and the posterior cortices are completely divided, but preserving a lateral hinge of about 0.5 cm of intact bone. Fibular osteotomy is not necessary.
Step 5: wedge opening The osteotomy line is easily opened by the help of the jack (Fig. 7) that gently moves the tibial axis and realigns the knee. Then the wedge opener is introduced and slowly advanced into the metaphysis. The surgeon measures the dimensions of bone gap directly on the graduated tines of the wedge opener and chooses the plate.
Step 6: plate fixation By removing the handle and, if necessary, one of the wedges, with the other one still in the osteotomy, the plate can easily be positioned on the medial cortex of the tibia with the spacer tooth introduced into the osteotomy line. Before fixing the plate, we check under fluoroscopy the mechanical axis by means of the special guide rod, long enough to extend from the centre of the femoral
Figure 8 Before fixing the plate we check under fluoroscopy the mechanical axis by means of the special guide rod, long enough to extend from the centre of the femoral head through the knee to the centre of the ankle.
head through the knee to the centre of the ankle (Fig. 8). When the rod crosses the knee at a lateral point about two-thirds (63%) of the tibia plateau, we know the angular correction corresponds to the 101 of anatomic valgus we had planned in advance. But if the correction is under or oversized, we can still exchange the plate with one having a thicker or thinner tooth as needed. Now the plate is fixed proximally with two 6.5 mm cancellous screws and distally with two 4.5 mm cortical screws. In the valgus knee, the medial side is the convex side so that the plate can act as a tension band device obeying an important biomechanical principle for the effectiveness of the internal fixation.
Step 7: bone grafting
Figure 7 Osteotomy is easily opened with the help of the jack.
With a skin incision extending from the anterosuperior iliac spine 8–10 cm above the iliac crest, we take two or three corticocancellous bone grafts with the same wedge shape of the osteotomy, the larger one measures the full correction, while the others are proportionately smaller. The grafts are press-fit introduced to fill the defect. It is also
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Surgical technique of femoral osteotomy Steps 1 and 2: patient position. Arthroscopy There are no differences at all in positioning and preparing the patient for femoral osteotomy compared with the tibial procedure. The arthroscopy has here the same justification and it is performed with the same intentions as in the tibial procedure.
Step 3: incision and exposure We expose the lateral aspect of the femur with a standard straight incision through the skin and the fascia starting two fingers breadth distal to the epicondyle and extending the incision about 12 cm proximally. The dissection is carried down to the vastus lateralis, which is retracted from the posterolateral intermuscular septum by the special dedicated Homan retractor placed ventrally. Perforating vessels are to be expected and should be controlled with ligature or electrocautery. We leave the joint capsule intact. The lateral cortex is now exposed. The procedure is facilitated by flexion of the knee.
Step 4: osteotomy
Figure 9 (A, B) A case of arthritic varus knee, pre- and post-operative radiographs.
possible to use different grafts, such as bone from the bank or synthetic Hatrics (Arthrex Inc., Naples, FL) or bovine freeze-dried bone or, according to some other authors, no grafts at all. The correct position of the plate and grafts is confirmed with AP (Fig. 9) and lateral radiographs. One (two) drain(s) (the second intraarticular if needed) is (are) prepared and the wound is closed in a routine fashion.
Again the authors’ preferred method consists of drilling the guide pin into the femur by the ‘free hand’, but, still once, the osteotomy cutting guide may be helpful in the proper positioning of the second guide pin and, then, to perform the osteotomy with the proper orientation. After perfect positioning of the Steinmann guide pin in a slightly oblique direction (about 201), from a proximal point on the lateral cortex, three fingers breadth above the epicondyle, safely off from the troclear-groove, to a distal point on the medial cortex, a second Homan is placed dorsally to avoid soft tissue damage and the osteotomy is started with the powered saw just to cut the cortical bone. It is very important to carry on the osteotomy with the blade, the saw and then the osteotome, parallel and proximal to the guide pin to help prevent intraarticular fracture. The osteotomy must be perpendicular to the long axis of the femur to have later on the ‘T’ plate well oriented with the femoral shaft. After the first few centimetres with the saw a sharp flexible thin osteotome is introduced and driven in all directions into the femur to separate the cancellous bone and the anterior and posterior cortices ending the
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osteotomy 0.5 cm before the medial cortex, to preserve a hinge of intact bone.
Step 5: wedge opening After the distraction by the jack (Fig. 10), the opener is introduced and slowly advanced until the osteotomy has been opened to obtain the planned realignment of the knee and the handle is removed. The surgeon measures the dimension of bone gap directly on the graduated wedges of the opener and chooses the plate.
Step 6: plate fixation By removing the handle of the opener, the plate can easily be positioned on the lateral cortex of the femur with the spacer tooth introduced into the osteotomy line. If the plate does not fit the femoral cortex properly, we must pre-contour it by modelling with the bending pliers. Before fixing the plate, we make control the mechanical axis by means of the special guide rod, long enough to extend from the centre of the femoral head to the centre of the ankle, which we check under fluoroscopy at the knee joint, approximately the centre of the tibial spine for neutral mechanical axis. When the correction is under or oversized, we choose a different plate with a thicker or thinner tooth as needed. We then fix the plate with four cortical screws proximal to the osteotomy and two cancellous screws distally (Fig. 11). A lateral plate instead of a medial one is recommended for an important biomechanical reason. When a normal knee with a valgus femorotibial angle is loaded in single leg stance, the lateral femur is the tension side
Figure 11 Plate is secured to the femoral cortex with two (rarely three) distal cancellous screws and the all four cortical screws.
secondary to the extrinsic varus component of body weight. In severe genu valgum, the mechanical axis moves laterally and, therefore, the convex medial side is subjected to tensile forces. After osteotomy, the mechanical axis is again moved medially, which returns the tension side of the knee to the lateral side. To act as a tension band, the plate must be applied to the lateral femur. Application of the plate to the medial femur after the osteotomy, as in the closing wedge osteotomy with the AO 901 angled blade-plate, violates this principle and would be expected to lead to a high incidence of failure.
Step 7: bone grafting We always fill the osteotomy defect normally with grafts of autologous bone, or in rarer circumstances with synthetic bone substitute. According with other authors bone grafting is recommended in all opening wedge osteotomies greater than 7.5 mm to prevent delayed or non-union and/or fixation failure. In osteotomies 7.5 or smaller, the decision to bone graft should be individualised. The correct position of the plate and grafts is confirmed with AP (Fig. 12) and lateral radiographs. One or two drains (one intraarticular) are prepared and the wound is closed in a routine fashion.
Technical pitfalls and complications Figure 10 Osteotomy is easily opened with the help of the jack.
The risk of intraarticular fracture is always present. This is more often due to a mistake in positioning
ARTICLE IN PRESS Osteotomy for osteoarthritis of the knee
Figure 12 (A, B) A case of arthritic valgus knee, pre- and post-operative radiographs.
the guide pin too close to the joint, leaving a very poor metaphyseal bone stock between the osteotomy and the articular surface. It may also be due to
425 imperfect completion of the osteotomy, without complete interruption of the anterior or, more often, posterior cortex that produces an articular fracture at the moment the knee is stressed, to open the osteotomy. The osteotomy jack greatly reduces, but cannot cancel, this risk. Usually, it is possible, if not easy, to fix the fracture with the proximal screws in the tibial, or the distal ones in the femur, introduced, as usual, through the plate. When the surgeon does not respect the hinge of intact bone the osteotomy can displace. Checking under fluoroscopy the fixation and the alignment of the bone, the osteotomy angle looks subluxed with the tibia (or the femur) diaphysis slipped laterally (or medially) respectively. The trick to prevent this technical problem starts with the proper choice of the site of the osteotomy cut that should be proximal enough in the tibia, or distal in the femur, to avoid the maximum step-off of the bone profile and address a more stable fixation but, mainly, an intact bone hinge is essential for stability. This, when correctly preserved, prevents the osteotomy from any possible dislocation. But if undesired subluxation has nevertheless occurred, then a possible solution for this problem is a staple fixation by a contralateral incision. Failure of the hardware, especially the plates, should be a very rare event. However, it can happen that a screw breaks, when too early weight bearing is allowed during the post-operative period contravening the rehabilitation protocol. But sometimes, there is a technical pitfall if a screw breaks. An imperfect congruence of the tooth plate into the osteotomy space overloads the screws with a lever arm that they cannot resist. An intact hinge maintains a sort of intrinsic elasticity and, as a spring, closes the osteotomy on the tooth making the system plate–bone congruent and tight; conversely, a fissured hinge fails to exert this elastic compression on the opposite side of the bone. The plate could be loose on the bone and the spacer tooth not in contact with both cortices. The screws have to support part of the effort to prevent osteotomy collapse until the bone heals, but they break because of a fatigue fracture of the metal before complete recovery. The lateral positioning of the ‘T’ plate is critical. The osteotomy has to be perfectly oriented in the sagittal plane, perpendicular to the longitudinal axis of the femur to have the long arm of the plate completely lying on the bone, just in the centre of the diaphysis. In fact, the spacer tooth forms a right angle with the plate that prevents the correct positioning of the long arm on the bone when the osteotomy is oblique with the femur. If the vertical arm is not parallel to the diaphysis the last upper
ARTICLE IN PRESS 426 holes of the plate project from the bone, anteriorly or posteriorly to the cortex, and make it very difficult to fix the all screws properly. Injuries to the vessels are not frequent. In the literature, accidental tears to the anterior tibial artery are reported, but only when an extensive lateral approach to the tibia is performed. The posterior vessels should be safely protected by correct use of a posterior Homan retractor and by keeping the knee flexed during surgery. Thrombophlebitis and infections are generic complications in common with all other surgical procedures on the lower limb. Delayed union may occur, but most osteotomies will go on to union with time and partially assisted early weight bearing. Non-union is also a possibility. In our series (43 tibial and 21 femoral osteotomies), we had no non-unions and this follows the systematic use of the bone grafts to fill the osteotomy. Peroneal palsy was always a potential complication of tibial valgus closing wedge osteotomy; we have never seen this complication in the opening wedge technique. However, in severe valgus deformities, when distal varus osteotomy is performed, a transitory peroneal neuropraxia can occur because of the overstretching of the nerve due to the correction. It may be incorrect to include loss of the desired correction as a true complication. In opening wedge osteotomy, collapse of the grafts might cause a decrease of the angular correction, but the new plates have been demonstrated to be effective in preventing it. Of course continuing degenerative changes and high adduction moments contribute to a gradual loss of correction as time goes by.
Post-operative management and rehabilitation After the operation the knee is immobilised with a ROM brace in full extension or at slight flexion of about 101 that allows a full ROM when unlocked. Passive flexion and extension in a continuous passive motion device are started the day after surgery. The drains are removed 48 h later. The patients are allowed to walk with no weight bearing on the operated limb, from the second postoperative day and they are dismissed from the hospital after 4–5 days. When post-operative knee pain and effusion have been minimised, restoring normal lower limb ROM and musculotendinous extensibility is fundamental to implementing an exercise programme that integrates the trunk, hip and ankle muscles into dynamic knee stabilisation
V. Franco et al. while addressing isolated quadriceps femoris deficiencies. Physical therapy intervention with the knee osteotomy patient requires continual attention to the balance of protection and function. Although progressive weight-bearing and ROM exercises are vital to recovery, early excessive joint loading and terminal knee flexion–extension with external loads can compromise the integrity of the surgical realignment. Usually, within the first 4 weeks, patients are able to completely flex the knee. After 4 weeks (six in femoral osteotomy) functional weight bearing is allowed. Full weight bearing is normally possible after 6–7 weeks (eight or nine in femoral osteotomy) when the radiographs show satisfactory healing. Then greater emphasis needs to be placed on restoring proprioceptivekinesthetic normality at the involved lower limb. While the rehabilitation programme progresses to address both anaerobic and aerobic physiological energy systems, increasing fatigue resistance as evidenced by prolonged maintenance of appropriate body control during functional exercises without apparent discomfort or movement-avoidance patterns assures the therapist that neuromuscular control for dynamic knee stabilisation is improving. Rehab may need to be delayed for older patients, particularly if they have not recently participated in a physical exercise programme and rehabilitation should be changed towards an emphasis on active ROM to facilitate articular cartilage nourishment and preservation.
Conclusions The treatment of uni-compartimental OA of the knee remains a challenge to the orthopaedic surgeon. The causes are varied and the therapeutic options are numerous. When non-operative and arthroscopic procedures fail and the patient is considered too young for uni or total knee replacement, osteotomy is the standard operation in the orthopaedic armamentarium to treat axial deformities of the knee and subsequent uni-compartimental OA. The opening wedge technique we have presented here is a modern interpretation of a classic operation. Also new and up-to-date are the dedicated instruments and plates. Some variations in the shape and dimension of the plate tooth are planned for the next months. Tibial plates with trapezoidal spacers will be available to permit the correction of the coronal and, eventually, the sagittal deformity, the so-called tibial posterior slope, at one surgical
ARTICLE IN PRESS Osteotomy for osteoarthritis of the knee sitting. The new femoral and tibial plates will have the tooth increasing one size for each millimetre, from the thinnest to the thickest, and, in their titanium version, work as a mini-internal fixator securing more stability to the osteotomy. The ideal candidate for an osteotomy is a patient who has only early uni-compartimental OA with limb malalignment, no flexion contracture, ROM of the knee at least 1001, intact ligaments, or anterior instability, and no severe osseous defects. Good results depend on the precision of the angular correction; in the case of varus knee a limited overcorrection up to 101 of valgus prevents the early recurrence of the deformity and provides time without compromising a later total joint replacement.
References 1. Jackson JP. Osteotomy for osteroarthritis of the knee. In: Proceedings of the Sheffield Regional Orthopaedic Club. J Bone Jt Surg (Br) 1958;826. 2. Wardle EN. Osteotomy of the tibia and fibula. Surg Gynecol Obstet 1962;115:61–4. 3. Coventry MB. Osteotomy of the upper portion of the tibia for degenerative arthritis of the knee. J Bone Jt Surg (Am) 1965;47:984–90. 4. Hernigou P, Medevill D, Debeyre J, et al. Proximal tibial osteotomy with varus deformity: a ten to thirteen year follow-up study. J Bone Jt Surg (Am) 1987;69:332.
427 5. Fowler PJ, Tan JL, Brown GA. Medial opening wedge high tibial osteotomy: how I do it. Oper Tech Sports Med 2000;1:32–8. 6. Puddu G, Franco V. Femoral antivalgus opening wedge osteotomy. Drez Jr D, DeLee JC, editors. Operative techniques in sports medicine ‘‘osteotomies about the athletic knee’’, vol. 8, no. 1. Orlando, FL: W.B. Saunders; 2000. 7. Puddu G, Franco V, Cipolla M, et al. Opening-wedge osteotomy—proximal tibia and distal femur. In: Jackson DW, editor. Reconstructive knee surgery. Master techniques in orthopaedic surgery. Philadelphia: Lippincott Williams & Wilkins; 2003. p. 375–90. 8. Coventry MB. Osteotomy about the knee for degenerative and rheumatoid arthritis. J Bone Jt Surg (Am) 1973; 55:23–48. 9. Muller ME, Allgower M, Schneider R, Willenegger H. Manual of internal fixation. Techniques recommended by the AO-group, 2 ed, supplement. New York: Springer; 1979 [p. 376]. 10. Healy WL, Anglen JO, Wasilewski SA, Krackow KA. Distal femoral varus osteotomy. J Bone Jt Surg 1988;70A:102–9. 11. McDermott A, Finklestein J, Farine I, et al. Distal femoral varus osteotomy forvalgus deformity of the knee. J Bone Jt Surg 1988;70A:110–6. 12. Insall JN, Joseph DM, Msika C. High tibial osteotomy for varus gonarthrosis. J Bone Jt Surg (Am) 1984;66: 1040–8. 13. Dugdale TW, Noyes FR, Styer D. Preoperative planning for high tibial osteotomy. The effect of lateral tibiofemoral separation and tibiofemoral length. Clin Orthop 1992;274:248–64. 14. Rosenberg TD, Paulos LE, Parker RD, et al. The forty-fivedegree posteroanterior weight-bearing radiograph of the knee. J Bone Jt Surg (Am) 1988;70:1479–83.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 428–445
www.elsevier.com/locate/cuor
MINI-SYMPOSIUM: SURGERY FOR KNEE ARTHRITIS
(iii) Modern unicompartmental knee replacement Gregory C.R. Keene, Mark C. Forster SPORTSMED.SA, 32 Payneham Road, Stepney, Adelaide, SA 5069, Australia
KEYWORDS Unicompartmental knee replacement; Unicompartmental knee arthroplasty; Minimally invasive knee arthroplasty
Summary Unicompartmental knee replacement (UKR) or arthroplasty (UKA) has undergone a resurgence of interest and usage in recent years. This is partly due to the development of minimally invasive surgery (MIS) techniques for UKR. Many experienced arthroplasty surgeons correctly consider that UKR is more technically demanding than total knee replacement (TKR). However, in appropriately selected patients and with carefully performed surgery, the known benefits of UKR can be safely offered. Many previously learned lessons have had to be rediscovered to enable this technically demanding procedure. MIS has been demanded by patients and offered by surgeons but the limited surgical access makes the technical intricacy of UKR surgery even more demanding. Computer aided surgery (CAS) has emerged as a probable solution to this problem. This article examines the current place of UKR in arthroplasty surgery with particular reference to the new techniques of MIS and CAS. UKR has an important place in the selection of surgical options for the treatment of unicompartmental knee arthritis because of the rapid recovery, lower complication rate and high success rate compared to other available procedures. & 2005 Elsevier Ltd. All rights reserved.
Introduction Unicompartmental knee replacement (UKR) has been shown in published papers to enjoy results superior to both total knee replacement (TKR) and high tibial osteotomy (HTO) in terms of speed of recovery, functional results and complication rates in properly selected patients.1,2 National arthroplasty registry data3,4 reveals that UKR surgery has only a marginally higher 10 year revision rate than TKR and that higher volume UKR surgeons have significantly lower revision rates for Corresponding author. Tel.: +61 8 83627788;
fax: +61 8 83620071. E-mail address:
[email protected] (G.C.R. Keene).
mobile bearing but not fixed bearing UKR.5 There have been reports of very long term success of UKR.6 In most instances where a revision of a UKR to a TKR is required this can be achieved almost as easily as a primary TKR and certainly much more easily than conversion of an HTO to a TKR or revision of a TKR. UKR is cheaper than TKR in cost to the patient and to the health care systems, both public and private. UKR performed with MIS has further advantages in terms of patient recovery and lowered risk, especially with regard to blood loss and transfusion requirements.7 UKR has some unique differences when compared to TKR, particularly with alignment and ligament balance. In addition lateral UKR poses a different
0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2005.10.003
ARTICLE IN PRESS Modern unicompartmental knee replacement set of surgical difficulties to medial UKR. We have been performing UKR surgery since 1981 and currently perform about 150 UKR cases and 150 TKR cases per year. In 2000 we changed to MIS for UKR. From 2000 the senior author was involved in an eight member international team of experienced unicompartmental knee arthroplasty (UKA) surgeons designing a new minimally invasive unicompartmental arthroplasty system (PreservationDePuy). In 2002 we began using computer aided surgery (CAS) for both UKR and TKR. We estimate that in our practice up to 30% of knee arthritis patients needing an arthroplasty may be suitable for UKR. Many arthroplasty patients require bilateral surgery and 25% of our patients have bilateral simultaneous UKR. We find this procedure to be physiologically less stressful on the patient than a bilateral TKR. Our enthusiasm for UKR in appropriate patients also extends to the patello-femoral joint and we perform approximately 20 isolated patello-femoral replacements (PF UKR) per year. We have used most of the available prostheses in our 20 year experience with this procedure and currently use the LCS PF UKR. We agree with the opinions and results of the Avon group led by Chris Ackroyd. We have not included any details of this procedure in this paper due to the space needed, but we recommend the reader to published works.
History Introduced in the 1950s, the first UKRs were hemiarthroplasty spacers, only resurfacing the tibial plateau. The MacIntosh (1958) was initially made of acrylic but later was manufactured from cobalt-chrome (1964). The McKeever (1960) was made from Vitalium and had the advantage of a keel for improved fixation into the tibia. The first designs to feature a femoral and tibial component were the Marmor Modular Knee and the St Georg Sled (both 1972). These designs featured a resurfacing metallic femoral component and a fixed all-polyethylene tibial component. Both components were cemented. Beuchel introduced the LCS mobile bearing UKR in 1977. The tibial component featured a polyethylene meniscal bearing that could move anteroposterior (AP) in a track in the metal tibial tray. Although originally cemented, the components were later modified with a porous coating of sintered beads to also allow uncemented fixation. The Robert-Brigham prosthesis (1980) was the first to feature a fixed bearing metal backed tibial
429 component. The Oxford mobile bearing design followed in 1982 which used an unconstrained mobile bearing. Since then a number of these designs have been modified and developed further into the range of currently available prostheses.
Indications and contraindications The indications for UKR vary according to different authors. In our experience and in talking to other experienced UKR surgeons we have found that indications gradually become broader with increasing and successful experience with UKR. Patients with mild to moderate patello-femoral degeneration, younger heavier patients and those with nonsymptomatic ACL laxity can be included as the surgeons experience and confidence grows. Also, as technical expertise with the chosen UKR grows, the length of the incision can also be safely reduced. We also strongly recommend that the use of a mobile bearing UKR be delayed until the surgeon has become an experienced and frequent UKR fixed bearing user. We recommend that new UKR surgeons choose limited or ‘tight’ indications. Thus the perfect patient is a well motivated, slim, low activity, older patient requiring a medial UKR. A fixed bearing UKR should be chosen and the surgeon should use a longer incision. Table 1 summarizes our current indications but we acknowledge the differences suggested by other authors in brackets. Contraindications are perhaps easier to summarise. There are again differences as indicated in brackets in Table 2.
Patient selection The majority of patients suitable for UKR fall into the above categories without difficulty. Weight bearing X-rays are important to show joint space narrowing but are usually taken in full extension. We also use the 451 flexed posterior–anterior (PA) weight bearing X-ray described by Rosenberg8 to show more clearly the wear on the femur. Often an arthroscopy has been performed recently enough for the surgeon to use that data to help in decision making. We sometimes perform a bone scan in patients where very minor patellofemoral X-ray changes are noted.9 If the bone scan shows a significant increase in patello-femoral activity we are hesitant to perform a UKR and recommend a TKR. Figure 1 shows a weight bearing X-ray of a patient with isolated medial pain in the left knee and similar but less severe pain in the
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Table 1
Indications for UKR.
Symptoms localised to joint line X-ray joint space narrowed on symptomatic side (Cartier-total loss) Age 440 (Cartier 460) Sedentary lifestyle-no impact sports or heavy manual work Near normal weight Both cruciate ligaments intact but non symptomatic ACL laxity may be acceptable Malalignment correctable without major soft tissue release Flexion, varus or valgus deformity o151 Moderate patello-femoral degeneration acceptable
Table 2
Contraindications to UKR.
Morbid obesity (490–100 kg Cartier). (Goodfellow disagrees) Uncorrectable deformity—varus, valgus or flexion 4151 Bi or tri compartment arthritis—PFJ is ‘‘forgiving’’ (Cartier avoids advanced PFOA) Very active lifestyle. (Goodfellow disagrees) Soft bone—severe porosis Inflammatory arthritis—rheumatoid or chondro-calcinosis
Figure 1 X-rays of a patient with bilateral medial osteoarthritis.
right knee with some associated patella pain on stairs. Figure 2 are the patient’s patella skyline Xrays showing mild patello-femoral arthritis in both. The single photon emission computer tomography (SPECT) bone scan in Fig. 3 shows the expected activity in the medial compartment. Figure 4 however shows a dramatic hot spot in the right femoral trochlea but not in the left. We are happy to perform a UKR in the left knee but prefer a TKR in the right. We do not routinely use an MRI to evaluate these patients as we feel that a bone scan shows arthritic activity in the other compartments more clearly, but we acknowledge this test as useful.
We often perform a preliminary arthroscopy at the time of the UKR to check the other compartments, as this is more accurate than inspecting the lateral compartment through a medial incision or vice versa for a lateral UKR. As a result, about one in 50 planned UKR change to a TKR intraoperatively due to bi or tri-compartmental involvement. Patients should be warned of this possibility. Younger patients should also be warned that they have an increased risk of revision to a TKR compared with older patients.3 We are particularly insistent that younger patients stop running activities and explain to them the loosening, wear and prosthesis fracture risks involved.
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Figure 2 Mild bilateral patello-femoral osteoarthritis.
We have used AP stress X-rays to try and assist us in determining the alignment to be achieved at surgery and whether correction is achievable. Unfortunately the technique of varus–valgus stress X-rays is difficult and provides variable results. In addition correction of alignment is significantly improved after osteophytes removal at surgery. We no longer use these X-rays and prefer to use ligament balance at surgery as our principal guide to alignment correction.
Figure 3 SPECT scan showing increased activity in the medial compartments bilaterally.
Figure 4 SPECT scan showing increased activity in the right patello-femoral joint.
X-ray templating and stress X-rays Templating the preoperative X-rays provides an indicative estimate of prosthesis sizes, minimal tibial resection and posterior slope. All of these should however be checked at surgery after opening the joint, resecting the osteophytes and performing ligament balancing and alignment decisions.
Anterior cruciate ligament (ACL) status Deschamps10 from the French Cartier group who are very experienced with UKR and both O’Connor11 and Goodfellow12 from the Oxford group, all strongly recommend that UKR not be performed in ACL deficient patients. However, there is some evidence that UKR can be successfully performed when there is ACL laxity without instability, particularly in the elderly.13 In our experience ACL laxity without instability is not a contraindication to UKR. We have on a few occasions performed a preliminary ACL reconstruction followed by a later UKR in patients with arthritic pain and symptomatic ACL laxity that was otherwise ideal for a UKR. Some surgeons have performed both procedures at the same operation with good results.
Bearing selection There are basically three different types of tibial bearings (Table 3). Some surgeons have a preference for particular bearing types for a whole variety of reasons. However we think that the three different bearing types do have different pros and cons and therefore different indications. The all poly fixed bearing gives the greatest thickness of poly for the least amount of tibial bone
ARTICLE IN PRESS 432 Table 3
G.C.R. Keene, M.C. Forster Types of bearing.
All poly fixed bearing Modular metal backed fixed bearing Mobile bearing
resection. There is evidence that a minimal thickness of poly required for a UKR is 6 mm.14 We prefer designs with a keel, which strengthens AP flexibility and enhances component fixation. The all poly is also surgically the easiest to insert. We use the all poly fixed bearing in older inactive patients, currently 40% of our UKR patients. Some of these prostheses have a thin nonmodular metal backing (moulded) to decrease component AP flexibility. They usually do not have a keel. The modular metal backed fixed bearing has a snap in exchangeable poly tibial component sitting in a metal tray. They require slightly more tibial resection for less thickness of poly and a revision may have to be done earlier in the event of poly wear. However a poly exchange is a very small, easy operation in these patients. We have performed approximately 450 MillerGalante UKR’s in the late 80’s and many of these have now had this simple poly exchange. We use the modular metal backed fixed bearing in older patients (460 years) who are moderately active or overweight where we think there is some risk of early poly wear. This is 20% of our UKR patients. The mobile bearing has the advantage of very superior poly wear compared with fixed bearings, perhaps up to 10:1 according to the work of Fisher.15 Hence it is likely to last longer in younger, more kinematically active patients. However, it is more technically demanding surgically due to component complexity and the need for very accurate component to component alignment and positioning. For these reasons malposition of mobile bearing UKR is frequent and the consequence is a much higher revision rate in low volume surgeons,5 who presumably do not do the operation frequently enough to retain the skills necessary to avoid revision causing errors. There are essentially only two mobile bearing UKR types. Firstly there is the Oxford and several close imitations. They have full congruency on the femoral to bearing surface but are unconstrained on the backside tibial bearing surface permitting multi-directional movement at this surface. Secondly, there is the Preservation, which borrows its mobile bearing design from the previously very successful LCS design and has full congruency
on the femoral to bearing surface in the weight bearing 0–401 range but less congruency after 401. This is the so-called J curve reproducing normal condylar shape. On the tibial to bearing surface the bearing is unconstrained AP but constrained mediolateral in a track, permitting unidirectional AP movement. This design is to reproduce normal meniscal mobility. Both of these designs have their strengths and weaknesses but high revision rates for both have been reported. We acknowledge that the reported incidence of revisions does not favour mobile bearings except in specialised centers. The arguments in favour of superior poly wear are lost in the complexity of the surgical procedure to the point where infrequent UKR surgeons may more safely consider fixed bearing in the majority of their UKR knees. For these reasons we think that the mobile bearing should only be used by experienced high volume UKR surgeons in their younger patients (o60 years of age) or in very active patients of any age. This is 40% of our patients. In the Preservation system the femoral component is the same for all three tibial bearing types. There are varying reports and theories concerning the merits of metal backing or non-metal backed, all-poly tibial components in terms of anterior–posterior (AP) deformation and cold flow of the poly with subsequent aseptic loosening. This issue clearly links with the structural design of the tibial prosthesis and the presence of fins or pegs for enhanced fixation. All poly proponents say that the all poly tibia and the cement layer have a modulus of elasticity closer to bone and loosening is less likely than in the stiffer metal backed components. The metal backed proponents say the opposite, which is that the non-flexible tibia is less like to flex and loosen and is therefore preferable! We believe that an AP keel enhances fixation on the all poly and at the same time makes the component stiffer. Testing for AP stiffness of the Preservation all poly tibia versus the modular metal backed showed virtually no difference. A tibial keel slot is easier to prepare in MIS UKR access than two peg holes, particularly the posterior peg for which access in poor. Figure 5 shows the three different tibial bearing options and the single matching femoral component in the UKR that we use. Figure 6 shows the keel design that is the same for all three tibial components. This has the advantage that the tibial and femoral preparation and component insertion has a common surgical technique for all three bearing types.
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Figure 5 The femoral component and tibial bearing options of the Preservation knee.
use a medial (or lateral for lateral UKR) parapatellar incision about 8–10 cm in length in both the skin and capsule. In obese patients the incision must be larger. Removal of osteophytes from the medial (or lateral in a lateral UKR) edge of the tibia and femur is required before alignment and ligament balance can be achieved. Soft tissue releases should not be performed, as alignment is determined largely by ligament balance and there is an assumption that in a UKR patient arthritic ligament shortening has not yet occurred. A ligament release will risk overcorrection of the joint alignment and early opposite compartment degeneration.
Alignment and ligament balance Figure 6 A metal backed tibial component showing the fixation keel.
Surgical principles Exposure We recommend the use of a tightly applied Esmarch bandage (or similar) and tourniquet to create a completely bloodless field to help with vision in the restricted space. It is, in our opinion, an unnecessary struggle to perform this demanding procedure in a restricted, blood filled space, which also compromises cement penetration and fixation. Surgeons new to UKR should use a sufficiently long incision to permit the important surgical principles to be easily followed. More experienced surgeons are able to steadily reduce the surgical exposure as their familiarity with the procedure increases. We
Alignment correction is possibly the most important issue in the longevity of a UKR.16 It is also possibly the most difficult element, especially compared with TKR where 01 mechanical axis is the generally accepted, and relatively easily achieved, standard. After resection of osteophytes the knee can be placed in the desired alignment. In a medial UKR we bring the knee into near full extension and correct the varus position until the medial collateral ligament is slightly looser than firm. In other words we correct alignment to normal collateral ligament tension. This will usually mean that a varus knee is slightly under corrected with respect to mechanical axis alignment. Similarly for a lateral UKR we perform the same procedure except that we try to leave the lateral ligament slightly looser than the medial reflecting the normal tension differences in the collateral ligaments (lateral looser). This again leaves a lateral UKR slightly under corrected.
ARTICLE IN PRESS 434 It is important to understand the reason for not trying to achieve a neutral mechanical axis alignment. In varus arthritis the knee has probably been in varus for the entire patient’s life and correcting to 0 degrees will overload the lateral compartment. The same applies to the lateral UKR. Studies have shown that over correcting the knee by 51 will increase the load in the opposite normal compartment by 50–100% and result in arthritic degeneration.17 Having said this, it is also important to realise that if the deformity is significantly under corrected then the prosthesis will be subjected to abnormally high peak adduction moment loads with excess poly wear18 and possible failure.19 This delicate balance between under and overcorrection, and the resulting failure if the narrow window of optimum alignment position is not achieved, is the exquisite challenge for the UKR surgeon. It is also one of the fundamental differences between UKR and TKR and highlights why UKR is a procedure for delicate surgeons who like to be challenged! In the Preservation system, the flexion space is always balanced after the extension space, as the extension space determines limb alignment and we spend far more time weight bearing in extension than flexion. Sometimes a slight trim off the posterior aspect of the femur in flexion is required make the flexion space balanced to the extension space. Leaving the flexion space tight will restrict flexion post-operatively. It is important to select a UKR prosthesis that is instrumented to allow this degree of refinement in alignment selection and ligament balancing, as the kinematic behaviour of the replaced compartment must coexist with the non-replaced compartment. Conflict between the 2 compartments will obviously result in grief.
Intramedullary versus extramedullary instrumentation Extramedullary instrumentation lowers the risk of fat embolism20 and usually assists minimally invasive approaches. On the other hand, intramedullary instrumentation is perhaps more accurate for those surgeons who prefer mechanical axis alignment. In our opinion UKR should always achieve optimal limb and prosthesis alignment and we recommend surgeons avoid UKR systems that are not well instrumented.
Component alignment and posterior slope In UKR knees limb alignment is determined by the bony resection and subsequent thickness of the UKR
G.C.R. Keene, M.C. Forster components. In TKR limb alignment is determined by the varus/valgus alignment of the components. Therefore in a UKR slightly greater freedom is allowed in selecting component varus/valgus position without disastrous alignment problems. Some surgeons prefer a tibial component to be at a right angle to the long tibial axis whereas some prefer to have a slightly physiological varus position. We believe that either is permitted and not critical to the longevity of the procedure. In tibia vara this can be important. CAS permits refinement of this component positioning. However posterior slope is very important and must be matched to the patients natural slope, which we have seen (and has been reported) to vary from 01 to 201.21 If this is not done then mismatch occurs between the UKR side and the normal side of the knee and will create kinematic problems, especially tight flexion and possible early failure of the prosthesis. This is quite different from TKR where a standard posterior slope is often selected then ligament releases and bone resection levels are used to balance the flexion and extension spaces. Figures 7 and 8 show extremes of posterior slope.
Medial and lateral differences It is more difficult to perform a lateral UKR because it is generally more difficult to sublux the patella medially than it is laterally for a medial UKR. Also a high Q angle tends to increase this difficulty and decrease lateral access. To overcome this problem we extend both the skin and capsule incision (proximally into the quads tendon a little if necessary). Another difficulty with the lateral side involves ligament balance. The lateral collateral ligament is normally significantly more lax than the medial collateral and this laxity must be recreated or the knee will be overcorrected, with early progression to medial compartment degeneration. This issue of lateral compartment ligament tension is the reason why the fully unconstrained Oxford mobile bearing UKR is not advised for the lateral side.22 The semi-constrained Preservation mobile bearing UKR and most fixed bearing UKR’s are suitable for lateral use. About 18% of our UKR cases are lateral and our short and long term results are similar to medial UKR, although the Swedish Knee Arthroplasty Register does report a 2% higher 10 year revision rate in lateral UKR compared with medial UKR.
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Figure 7 A knee with a 01 posterior slope.
Tibial preparation It is important to resect the minimum amount of tibial bone, as the metaphyseal bone is stronger and wider closer to the joint line. A deep tibial resection places the prosthesis on weaker, narrower (medio-lateral) bone with a higher risk of prosthesis sinkage or tibial collapse.23 For similar reasons the number of pins drilled into the tibia should be kept to a minimum and away from the cortical bone. All tibial preparation should be gentle, including insertion the tibial prosthesis, to avoid tibial fracture and these complications.
Patella impingement Some UKR designs are better than others in this area and those with a femoral shape that closely matches the polycentric or J curve shape of the normal femoral condyle may perform better than single radius designs.
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Figure 8 A knee with a 201 posterior slope.
The Preservation has a small ‘‘kick back’’ anterior chamfer that was specifically designed for this feature. While it does involve another small surgical step, it is important to recess the anterior edge of the femoral component to avoid patella impingement in early flexion.
Component insertion If the surgeon is new to UKR surgery we recommend that the tibial and femoral components be inserted with separate mixes of quick curing cement. This particularly applies to mobile bearing UKR’s. With experience both components can be cemented together with longer curing cement (we use SmartSetTM (CMW) for this). We also recommend that early in a surgeons UKR experience a trial insertion be performed with the components or trials in order that the insertion sequence and soft tissue retraction can be rehearsed. This is particularly important if a minimally invasive incision is being used. The femoral
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component is inserted with the knee at 901 of flexion (or more) and a good assistant and patella retraction are required. Designs with the femoral peg(s) parallel to the posterior femoral cut are much easier to insert via an MIS incision than designs with diverging femoral pegs.
Cementing technique It is very important to clean and dry the bone thoroughly before cementing the components to increase microinterlock, which produces higher values of ultimate shear strength of the cement– bone interface.24 Small 1–2 mm depth drill holes can be very carefully made in sclerotic bone to increase cement penetration and fixation. Figure 9 shows a fully prepared tibia (with drill holes) and femur after cleaning and drying the bone in a bloodless field. Cement must be digitally pressurised into the cut bone surfaces prior to insertion of the components to enhance fixation. Most components provide for the tibia to be inserted first. Excess cement must then be removed from the back of the tibia. We have reported a cement probe designed for this purpose.25 Finally, the femoral component is inserted after pressurising cement into the accessible cut surfaces of the femur. Figures 10a and b shows the dramatic increase in cement penetration achieved with simple digital pressurising of the cement.
Cementless fixation We have not had any experience with MIS UKR cementless fixation but have previously used the LCS porous coated UKR successfully. This is a cementless femoral and tibial prosthesis but is not
Figure 9 A prepared medial compartment.
Figure 10 (a) and (b) Improved cement penetration following digital pressure.
suitable for MIS due to the very long peg on the tibial component. Bernasek26 reported that porous coating in cementless UKR did not have uniform bony ingrowths. Hydroxyapatite (HA) coated uncemented TKR has been reported more favourably.27 We are currently working on an HA porous coated modification to the femoral component of the Preservation UKR and will be trialing the first components soon. Cementless fixation of the tibial component is of more concern because of the higher stresses on the cement–bone interface and the more compromised fixation options due to MIS. However the tibial component is usually inserted first and
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cement retrieval from the posterior aspect and between the prosthesis and collateral ligament is fairly easy. After insertion of the snap in poly component in the fixed modular metal backed or the mobile bearing, the space becomes very restricted. When the femoral component is then inserted there is literally no room to retrieve cement from the posterior femoral recesses. Therefore we believe that an HA porous coated femoral component would overcome this problem.
X-rays Figures 11–13 show post-operative X-rays of the three different bearing that we use. Consideration should be given to regular check X-rays in fixed bearing knees to monitor early poly wear especially in young, active or overweight patients.
Aftercare and rehabilitation After skin closure and the insertion of a gravity drain we apply a very firm compressive bandage to the knee. Our hospital phase physiotherapy program begins on day 1. The goal is that by discharge 2 days after surgery patients should be independent with respect to gait (+/ aids), their exercises, and most activities of daily living, and should have obtained 901 knee flexion. We use ice therapy, continuous passive motion (CPM) 3 h per day from 01 to 901, soft tissue treatment and massage and gait training. Exercises involve passive flexion and extension and active quads and hamstring exercises. Most of our patients are discharged home on day two. Patients are given a very detailed exercise booklet on discharge and most are not seen again by the physiotherapist until the same time as their outpatient appointment with the surgeon at two weeks. Some patients that are having trouble with their exercises in hospital are seen by the physiotherapist earlier than two weeks. At 2 weeks the physiotherapist institutes the stage 2 programme. The goals of this are to reinforce expectations and outcomes, progress range of motion, strength exercises and continue gait training. Supervised hydrotherapy classes are encouraged and some higher demand, more active patients, begin a gym and bike program. Usually at 2 weeks patients have over 1001 of flexion.
Figure 11 (a) and (b) All-polyethylene tibial component.
Patients are discharged from the physiotherapist 2–3 months after surgery. Full or close to full range of motion is achieved in most patients.
Permitted activities The generally accepted limitations of TKR apply equally to UKR. High impact activity has been shown in the laboratory to increase poly wear and helps explain the higher revision rates in younger patients. We permit and encourage walking, swimming, cycling and golf. We permit with less enthusiasm
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Figure 13 (a) and (b) Mobile bearing tibial component.
Complications Aseptic loosening
Figure 12 (a) and (b) Metal-backed modular tibial component.
snow skiing (blue slopes only) and social doubles tennis although we encourage patients to learn to say and use ‘‘yours’’ and ‘‘good shot’’!
Loosening can be caused by poor surgical or cementing technique, under correction of the deformity, component or joint line malposition. Loosening is far more common on the tibial component than the femoral. Apart from complaints of increasing pain localised to the component area, the most helpful investigation is plain X-ray, fluoroscopically guided, to show the prosthesis–cement–bone interface clearly and any associated radiolucent lines. If in doubt that the prosthesis is loose and the radiolucent lines are not indicative of loosening we think it is appropriate to adopt a wait and see
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Figure 15 Retained posterior cement.
Figure 14 A loose tibial component.
policy after frank discussion with the patient. We also ask the patient to see our physiotherapist to rule out any extra-articular causes of the pain. We see the patient 3 months later with a further X-ray and judge if the pain and radiolucent lines have worsened. Figure 14 shows such an X-ray. If still in doubt at this point we usually recommend an arthroscopy to evaluate possible other causes of the pain. There is published evidence that this is useful.28
Retained cement Symptomatic retained cement is most common on the tibial side and can be posterior as in Fig. 15 where it can limit flexion or extension or under the collateral ligament as in Fig. 16 where it causes pain. Cement must be thoroughly cleaned from the prosthesis–bone rim after component insertion as described. Small cement particles are a common cause of ‘third body’’ poly wear as shown in Fig. 17.
Component wear and fracture The main causes are under correction of alignment deformity or component malposition causing poly
Figure 16 Cement under medial ligament.
overload and wear on the tibial component as shown in Fig. 18 or component fracture as shown in Fig. 19 if severe overload occurs.
Tibial collapse and fracture Over resection of tibial metaphyseal bone, under sizing (AP or ML or both) of the tibial component, soft tibial bone, excess pins holes in the tibia, rough handling of the tibial preparation or component insertion are all causes
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Figure 19 A fractured mobile bearing. Figure 17 Cement particle 3rd body wear on tibial prosthesis.
Figure 20 Internal fixation following tibial plateau fracture.
Figure 18 An eccentrically loading tibial component showing polyethylene wear.
of this mini disaster which will usually require internal fixation as in Fig. 20 or conversion to a TKR.
Radiolucent lines Radiolucent lines are common and probably represent less than ideal fibro-osseous fixation. If seen soon after surgery the patient is usually pain free or still improving. A stable fibrous union lucency is usually less than 1–2 mm and has a sclerotic margin, such as seen on the X-ray in Fig. 21 taken 3 years
ARTICLE IN PRESS Modern unicompartmental knee replacement post-UKR in a happy pain free patient. Lucencies representing loosening are wider, have a fuzzy margin and are associated with progressive pain.
Opposite compartment degeneration Provided the opposite compartment was normal at the time of UKR, this complication nearly always means the knee was overcorrected. Figure 22 shows
441 the X-ray of a patient who had successful bilateral LCS UKR 11 years previously but had recent right lateral knee pain. The right lateral joint space is narrowed and this patient’s bone scan in Fig. 23 shows the extent of lateral arthritis activity. A TKR revision is necessary in such cases, although there have been reports of the insertion of another UKR in the now degenerate compartment, making a bicompartment double UKR.
Component malposition The most serious issue here is usually early poly wear from edge loading such as is seen in Fig. 24. Different prostheses have different tolerances for this error, which is probably common in minor degrees. The Preservation was designed with a transitional radius on the edges of the femoral
Figure 21 A radiolucency from a stable fibrous union.
Figure 23 SPECT scan showing increasing activity in the lateral compartment.
Figure 22 Lateral progression of osteoarthritis.
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Figure 24 Femoral component edge loading.
Figure 26 An Oxford UKR with a dislocated bearing.
tension determines bearing stability. The bearing can pop out anteriorly or posteriorly when the correct ligament balance and tension has not been achieved. Figure 26 shows an anteriorly dislocated Oxford UKR. For this reason the Oxford prosthesis cannot be used on the lateral side and should also not be used in the occasional patient with physiological medial laxity.
Joint line malposition Figure 25 Tibial component overhanging medially.
component to provide edge loading tolerance up to 101 of component malposition. A fully ML congruent design such as the Oxford is also tolerant of this error in varus–valgus component malalignment. Sometimes malposition can cause soft tissue impingement especially with components that overlap the edge of the tibia as in Fig. 25. Tibial components that are non-anatomical in shape have a higher risk of this problem.
This can occur in three different planes—horizontal (superior/inferior); coronal (varus/valgus) and sagittal (posterior slope). Each malposition disturbs normal joint kinematics and results in restricted range of motion, pain and early failure due to secondary shear stresses in the prosthesis. Figure 27 shows a joint malposition that is significantly low. In a natural tibia vara this problem can easily occur unless the normal vara is reproduced. CAS will assist in this delicate issue of three-dimensional joint line positions.
Bearing dislocation
Arthrofibrosis
This is a special problem for the fully unconstrained prostheses of the Oxford type where ligament
This is much less common in UKR than in TKR and can be caused by post-operative bleeding, rough
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443 an intra-articular injection of steroid before the arthroscopy.
Patello-femoral pain and degeneration Sometimes the patello-femoral joint will slowly deteriorate after a UKR. An arthroscopic debridement may help or conversion to a full TKR may become necessary. Most UKR patients will complain that their knee is a bit stiff to get going after a prolonged sit or in the morning but that it is fine after a few steps. This is normal for all knee arthroplasties and needs only reassurance.
Results
Figure 27 A UKR with a lowered joint line.
tissue handling and poor rehabilitation. A careful arthroscopic debridement of scar tissue and a gentle MUA should be performed if physiotherapy fails to relieve the problem.
Slowly resolving pain Many experienced UKR surgeons say that some UKR patients have medial metaphyseal pain or up to six months after surgery. This may be due to remodelling of the bony stresses in the knee and patients need to be warned about his and surgeons resist the call to do something surgical in this time! Reassuring the patient is a good alternative!
Synovial impingement In our experience patients who complain of joint line pain and tenderness and in whom the symptoms are settled by a local anesthetic injection, may benefit from an arthroscopy to check for synovial impingement.28 We are happy also to try
Published series of UKR patients report up to 98% 10 year survival in both fixed bearing and mobile bearing UKR. The Swedish knee arthroplasty register; however, reports that across the Swedish hospitals the 10 year revision rate for medial UKR is 9% and for lateral UKR is 11% in contrast to TKR at 7%. We have now performed nearly 500 Preservation UKR cases with a 16% incidence of bilateral simultaneous cases and a 15% incidence of lateral UKR. We have completed a review of the first 144 Preservation UKR patients with 188 knees at 2 year follow-up. We were able to follow-up 100% of the cases. Table 4 shows the preoperative, 1 and 2 year Oxford and American Knee Society scores highlighting a dramatic improvement in both results at 1 year and maintaining of these results at 2 years.
Table 4 Preoperative, 1 and 2 year Oxford and American Knee Society scores.
ARTICLE IN PRESS 444 There was one revision in an all poly tibia for loosening early in the series due to poor cementing technique. The tibial prosthesis was recemented successfully. Our results show that excellent results can be achieved in a high proportion of patients with modern UKR techniques but the procedure is technically demanding and patient selection is important.
G.C.R. Keene, M.C. Forster their results and extend their indications cautiously. Practice points
Good patient selection is vital A technically demanding procedure CAS improves alignment and may improve results UKR is a good option for unicompartmental arthritis
Computer assisted surgery (CAS) CAS has been shown to increase accuracy of limb and prosthesis alignment in both UKR29 and TKR.30 There is a direct and strong relationship between alignment and prosthesis longevity.18 We have been using the Ci prosthesis specific system for the Preservation UKR in well over 100 cases. There are many different types of CAS systems. Some of the earlier systems permit limb alignment accuracy only. While we acknowledge that this is a very important factor in prosthesis longevity we feel that it is worth having implant specific software to control limb and prosthesis alignment, joint line level and slope and finally kinematics and ligament balancing. We have reported our own results in a randomised trial of bilateral simultaneous MIS UKR where one side was performed with CAS and the other side with standard extramedullary instruments. There was an average improvement of 21 in alignment on standardised full leg alignment films. This improvement was highly significant and pushed 26% of our patients from outside a desired alignment window into a safer range.31 CAS requires a short learning curve and a willingness to trust the computer and spend the time it takes to use the system, usually about 15 min extra. We think that the improved alignment achieved makes this worthwhile.
Summary UKR results continue to delight those surgeons who have gained the skills and understanding to enable good results to be reliably achieved. Unfortunately there remain some surgeons who do not have that confidence in UKR for a variety of reasons. We hope that his article will help those surgeons to discover the joys of good UKR patient results and for established UKR surgeons to perhaps improve
Research directions
Mobile versus fixed bearing results Alignment and ligament balance relationship Cementless fixation Replacement bearings
References 1. Newman JH, Ackroyd CE, Shah NA. Unicompartmental or total knee replacement? Five year results of a prospective, randomized trial of 102 osteoarthritic knees with unicompartmental arthritis. J Bone Jt Surg 1998;80B: 862–5. 2. Newman JH, Weale AE. Unicompartmental arthroplasty and high tibial osteotomy for osteoarthrosis of the knee. A comparative study with a 12 to 17 year follow up period. Clin Orthop 1994;302:134–7. 3. Swedish Knee Arthroplasty Register 2004 Report. http:// www.ort.lu.se/knee/pdf/skar2004engl.pdf 4. Australian National Joint Registry 2004 Report. http://www. dmac.adelaide.edu.au/aoanjrr/documents/aoanjrrreport_ 2004.pdf 5. Robertsson O, Knutson K, Lewold S, Lidgren L. The routine of surgical management reduces failure after unicompartmental knee arthroplasty. J Bone Jt Surg 2001;83B:45–9. 6. Callaghan JJ, Gardner J, Goetz D, et al. Unicompartmental knee replacement: a minimum 21 year follow up end result study. #AR5. Presented at the 118th Annual Meeting of the American Orthopaedic Association. June 22–25, 2005. Huntington Beach, California. 7. Jeer PJS, Cossey AJ, Keene GCR. Haemoglobin levels following unicompartmental knee arthroplasty: influence of transfusion practice and surgical approach. Knee 2005; 12:358–61. 8. Rosenberg TD, Paulos LE, Parker RD, Coward DB, Scott SM. The forty five degree posteroanterior flexion weight bearing radiograph of the knee. J Bone Jt Surg 1988; 70A:1479–983. 9. Jeer PJS, Mahr CC, Keene GCR, Oakeshott RD. Single photon emission computed tomography in planning unicompartmental knee arthroplasty. A prospective study examining the association between scan findings and intraoperative assessment of osteoarthritis. Knee 2005; in press.
ARTICLE IN PRESS Modern unicompartmental knee replacement 10. Deschamps G, Lapeyre B. La rupture du ligament croise ante ´rieur: une cause d’e´chec souvent me´connue des prostheses unicompartimentales du genou. A propos d’une se´rie de 79 prosthe `ses Lotus revues au-dela ` de 5 ans. Rev Chir Orthop 1987;73:544–51. 11. Goodfellow J, O’Connor JJ. A risk factor in unconstrained meniscal prostheses. Clin Orthop 1992;276:245–52. 12. Goodfellow J, Kershaw CJ, Benson MKD’A, O’Connor JJ. The Oxford knee for unicompartmental osteoarthritis. J Bone Jt Surg 1988;70B:692–701. 13. Engh GA, Ammeen D. Is an intact anterior cruciate ligament needed in order to have a well-functioning unicondylar knee replacement? Clin Orthop 2004;428:170–3. 14. Lewold S, Robertsson O, Knutson K, Ligren L. Revision of unicompartmental knee arthroplasty. Outcome in 1135 cases from the Swedish knee arthroplasty study. Acta Orthop Scand 1998;69:469–74. 15. McEwen HMJ, Fisher J, Goldsmith AAJ, Auger DD, Hardaker C, Stone MH. Wear of fixed bearing and rotating platform mobile bearing knees subjected to high levels of internal and external tibial rotation. J Mater Sci: Mater Med 2001; 12:1049–52. 16. Whiteside LA, McCarthy DS. Laboratory evaluation of alignment and kinematics in a unicompartmental knee arthroplasty inserted with intramedullary instrumentation. Clin Orthop 1992;79:238. 17. Bensadoun JL, Vidal J, Maury P. Unicompartmental arthroplasty. Orthop Trans 1989;13:708. 18. Hernigou P, Deschamps G. Alignment influences wear in the knee after medial unicompartmental arthroplasty. Clin Orthop 2004;423:161–5. 19. Chassis EP, Mikosz RP, Andriacchi TP, Rosenberg AG. Functional analysis of cemented medial unicompartmental arthroplasty. J Arthroplasty 1996;5:553–9. 20. Morawa LG, Manley MT, Edidin AA, Reilly DT. Transesophageal echocardiographic monitored events during total knee arthroplasty. Clin Orthop 1996;331:192–8.
445 21. Matsuda S, Miura H, Nagamine R, Urabe K, Ikenoue T, Okazaki K, et al. Posterior tibial slope in the normal and varus knee. Am J Knee Surg 1999;12:165–8. 22. Gunther TV, Murray DW, Miller R, Wallace DA, Carr AJ, O’Connor JJ, et al. Lateral unicompartmental arthroplasty with the Oxford meniscal knee. Knee 1996;3:33–9. 23. Hvid I. Trabecular bone strength at the knee. Clin Orthop 1988;227:210–21. 24. Reading AD, McCaskie AW, Barnes MR, Gregg PJ. A comparison of 2 modern femoral cementing techniques: analysis by cement–bone interface pressure measurements, computerized image analysis, and static mechanical testing. J Arthroplasty 2000;15:479–87. 25. Keene GCR, Jeer PMS. Cement retrieval in minimally invasive knee surgery. The 901 ball probe. J Arthroplasty 2005;20:798–9. 26. Bernasek TL, Rand JA, Bryan R. Unicompartmental porous coated anatomic total knee arthroplasty. Clin Orthop 1988;236:52–9. 27. Cross MJ, Parish EN. A hydroxyapatite-coated total knee replacement: prospective analysis of 1000 patients. J Bone Jt Surg 2005;87B:1073–6. 28. Klinger HM, Baums MH, Spahn G, Ernstberger T. A study of effectiveness of knee arthroscopy after knee arthroplasty. J Arthroplasty 2005;21:731–8. 29. Jenny J-Y, Boeri C. Unicompartmental knee prosthesis implantation with a non-image-based navigation system: rationale, technique, case-control comparative study with a conventional instrumented implantation. Knee Surg Sports Traumatol Arthrosc 2003;11:40–5. 30. Chauhan SK, Scott RG, Reidahl W, Beaver RJ. Computer assisted knee arthroplasty versus a conventional jig based technique. A randomized, prospective trial. J Bone Jt Surg 2004;86B:372–7. 31. Keene G, Simson D, Kalairajah Y. Limb alignment in computer assisted minimally invasive unicompartmental knee replacement. J Bone Jt Surg, in press.
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www.elsevier.com/locate/cuor
MINI SYMPOSIUM: SURGERY FOR KNEE ARTHRITIS
(iv) Total knee replacement J. Bellemans, H. Vandenneucker, J. Vanlauwe Department of Orthopaedic Surgery, University Hospital Pellenberg, Katholieke Universiteit Leuven, Weligerveld 1, 3012 Pellenberg, Belgium
KEYWORDS Total knee replacement; Arthroplasty; Overview
Summary Total knee arthroplasty is today a successful procedure in relieving pain and functional restoration of patients with advanced knee disease. Our knowledge on indications, surgical technique and prosthetic design have evolved over the past years to such an extent that a consistent and durable outcome can be obtained in the majority of cases. Some controversies that were debated in the past have today been resolved; others are still open for discussion. In this paper, a general overview on the current ‘state of the art’ in primary knee arthroplasty is given. & 2005 Elsevier Ltd. All rights reserved.
Introduction Total knee arthroplasty (TKA) is today one of the most successful reconstructive procedures in orthopaedic surgery. Relief of pain and restoration of function can be obtained in the majority of cases to a level which is satisfactory to both the patient and the surgeon. Numerous successful implant designs are currently in use, including implants that retain or substitute the posterior cruciate ligament (PCL), implants that can be inserted with or without the use of cement, with a mobile or fixed bearing Corresponding author. Tel.: +32 16 338800; fax: +32 16 564536. E-mail addresses:
[email protected] (J. Bellemans),
[email protected] (H. Vandenneucker),
[email protected] (J. Vanlauwe).
insert, as well as many other variables. History has, however, taught us in the meantime that some of these variables have been tried and abandoned because so-believed improvements turned out to be associated with inferior results. Others turned out to make little difference in outcome, whereas some innovations became commonly accepted as clear improvements. Together with this evolution in design and technology, our knowledge with respect to diagnosis, patient selection, outcome assessment, and other aspects has also evolved dramatically.
Indications and patient selection Just as for any operative procedure, proper patient selection is crucial when performing TKA. Total knee replacement is a resurfacing procedure where
0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2005.09.007
ARTICLE IN PRESS Total knee replacement damaged cartilage and the underlying bone are replaced by artificial implants, and therefore only patients with sufficient cartilage damage should be considered. It is generally accepted that full thickness cartilage damage in at least one of the three compartments (medial, lateral, and patellofemoral) should be present, causing severe subjective discomfort to the patient. Subjective complaints should match the objective cartilage damage observed on weight-bearing radiographs or other imaging techniques (arthroscopy, MRI). Evidence exists that patient satisfaction is inversely related to the preoperative status, where patients with important cartilage destruction are usually much more satisfied after the procedure than patients with only mild or moderate preoperative cartilage wear. As a guideline, a comfortable walking distance of 500 m is frequently considered as a valuable subjective threshold below which knee arthroplasty should be considered when conservative measures have failed. Conservative treatment should always be prescribed first, since this may delay or even defer indefinitely the need for knee arthroplasty surgery. Medical treatment, physiotherapy and weight reduction are sometimes more effective in pain reduction than expected, depending on the severity of the arthritis. Controversy exists on the usefulness of steroid and hyaluronic acid injections, arthroscopic lavage and debridement, shoe insoles, or bracing. In a number of cases non-arthroplasty surgical alternatives should be considered. Tibial or femoral osteotomy, bone marrow stimulation techniques, or chondrocyte transplantation procedures can be indicated in younger patients with localised cartilage damage with or without malalignment, but play no role for the knee with diffuse erosive and degenerative cartilage damage. Unicompartmental resurfacing is an alternative to total knee replacement in cases where only one compartment of the knee is damaged. The reported success rates after unicompartmental knee replacement, as well as patellofemoral arthroplasty, are comparable to those obtained after TKA with respect to pain reduction. Function is generally better preserved after partial knee replacement due to preservation of the non-damaged compartments and the cruciate ligaments.1 With respect to long-term survival of partial knee arthroplasty, it is clear these are not as durable as total knee replacements. The survival rates of most unicompartmental knee series do not surpass 90% at 10 years, and this should be taken into account when the decision for knee arthroplasty is made.2,3
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Surgical principles and operative technique Successful surgical replacement of the articulating surfaces by prosthetic components can only be achieved when proper knee and limb alignment as well as soft tissue equilibrium are restored. Restoration of the correct mechanical axes of the lower limb should be obtained, which means that at the end of the procedure the mechanical axis of the femur should be in line with the mechanical axis of the tibia, and the line connecting the centre of the hip with the centre of the ankle joint should pass through the centre of the knee joint (Fig. 1A and B). Pre-existing deformities should therefore be corrected during the procedure by appropriate bone resection, while maintaining correct mediolateral soft tissue balancing. Residual medio-lateral soft tissue imbalance may lead to instability or ligament tightness with pain and loss of motion. This implies that during surgery osseous reconstruction should be performed in such a way that mechanical joint alignment is restored while maintaining or restoring a correct soft tissue envelope
Figure 1 Restoration of preoperative varus deformity (left) to correct alignment after TKA (right).
ARTICLE IN PRESS 448 around the knee joint. Soft tissue envelope deformities are present in many patients with deformed knee osteoarthritis, due to either soft tissue stretching or contracture, and should be corrected during surgery to obtain a stable and symmetrically balanced knee joint. Two types of surgical techniques are today commonly employed to achieve this. In the so-called ‘‘bone referencing technique’’, bony landmarks are used for restoration of osseous alignment, with subsequent soft tissue balancing after the bone cuts are made. In the ‘‘ligament referencing technique’’ (also sometimes called ‘‘tibia cut first technique’’ or ‘‘LCS technique’’), the tibial cut is made first, with subsequent ligament balancing, which is only followed by the other bone cuts when adequate soft tissue equilibrium has been obtained. Although both schools have strong believers and disbelievers, no outcome data exist today to support one over the other and both options can be considered as appropriate. Most of the controversy between these techniques is associated with the rotational positioning of the femoral component, which is critical with respect to patellar tracking and rectangularity of the flexion space. Although some agreement exists on the acceptable margins within which a well-performed TKA procedure should fall, no hard evidence is available with respect to most of these variables. Mechanical alignment of the femoral and tibial components in the frontal plane should generally lie between neutral 731, but in some cases outliers can be accepted or even preferred. The same is true for sagittal alignment, where down-slope of the tibial component between 01 and 101 is usually acceptable, whereas upslope should be avoided. On the femoral component, hyperextension should be avoided. Femoral rotational position should be parallel to the epicondyles and perpendicular to the anteroposterior line of Whiteside.4 Some deviation from this cannot always be avoided during surgery with the current instrumentation available, but should not lead to excessive internal component rotation because this will lead to trochlear medialisation and patellar maltracking. Some external malrotation is better tolerated by the patient. Because of the fact that current instruments are associated with some degree of imprecision, computer-assisted surgery was recently introduced and has gained some popularity in the meantime. Early reports have demonstrated increased precision with respect to coronal plane positioning of the components, while there is growing evidence that this is also true for sagittal and rotational position-
J. Bellemans et al. ing.5 Despite this, however, today there does not yet seem to exist a sufficient scientific basis to support the widespread use of these systems, mainly because of the extra associated costs, the extra operative time, and the lack of clinical data demonstrating superior outcome.
Prosthetic design Contrary to what might have been expected, total knee designs have changed relatively little during the past two decades. It is only very recently that important innovations have been introduced compared to the implants that have been in use for almost 20 years now, and which were based upon the success of the Insall–Burstein, Miller–Galante and LCS knee systems. These systems have generally been considered as satisfactory in terms of pain relief and functional restoration. Long-term performance and survival have gradually improved over the years due to better knowledge of the process of polyethylene wear, its influencing factors and the biological consequences. For this reason most design innovations over the past two decades have been related to the implant materials and to factors which are known to influence the wear process. Today it is commonly accepted that cobalt–chrome alloys for femoral components and titanium or cobalt–chrome alloys for tibial base plates are adequate for long-term mechanical performance. The same is true for ultrahigh molecular weight polyethylene, which has functioned well in the past as bearing material in most joint replacements. In most knee implant designs, however, relatively large contact stresses are applied across relatively non-comforming articulating surfaces, potentially exceeding the polyethylene material’s strength. The potential of wear damage with generation of polyethylene wear debris has therefore been one of the main concerns in knee arthroplasty component design, since it leads to subsequent osteolysis, implant loosening and implant failure (Fig. 2A and B). Today it is well known that not only the material properties but also the components’ shape can influence this process. Chemical, physical, and mechanical properties of polyethylene can be affected by a number of factors, including the resin from which the material is fabricated, the production process, the method of sterilisation and shelf storage. Today there is still no clear consensus with respect to many of these factors, although some commonly used techniques in the past (such as gamma irradiation in air
ARTICLE IN PRESS Total knee replacement
449
Current options in TKA Cemented or cementless fixation
Figure 2 Severe polyethylene wear with significant osteolysis and component loosening.
sterilisation) have been abandoned because of detrimental results. Highly cross-linked polyethylene has recently been introduced in an effort to reduce wear even further, but its application in knees may be limited since cross-linking reduces the mechanical properties of the polyethylene, such as fatigue crack propagation resistance, tensile strength, and yield strength, despite the fact that cross-linked polyethylene has been shown to reduce abrasive and adhesive wear in hips. Component shape parameters that have an important effect on polyethylene wear are the polyethylene thickness and the contours of the polyethylene and metallic articulating surfaces. It is today generally accepted that the polyethylene thickness should never be under 7 mm, and that maximal articulating contact areas should be obtained to reduce contact stress. This results in a difficult compromise, since large contact areas can only be achieved through the use of conforming components, whereas it is well known that the restoration of kinematics and function compatible with the soft tissues around the knee requires the use of relatively non-conforming implants. In an attempt to solve this paradox, mobile bearing implants have been introduced, generating the opportunity to achieve high conformity and large contact areas, while reducing the constraint of the system through the use of a mobile bearing polyethylene insert. The choice between mobile or fixed bearings is, however, only one of the several options that need to be decided upon by the surgeon.
Poly-methylmetacrylate (PMMA) has been used for a long time as an excellent anchoring system for arthroplasty components. In the knee it has been shown that cement fixation can lead to implant survival in as high as 91% of the cases at 21 years.6 Despite these satisfactory results, a number of potential downsides associated with the use of cement exist. Cement is prone to fatigue failure and is a poor transmitter of tensile and shear stresses, it is a potential source of third body wear, it is associated with increased thromboembolic activation, and it may increase the susceptibility to local infection. The cementing technique itself is not free of technical problems either, and inevitably increases operative time. Opponents of cemented TKA have argued that the above-mentioned disadvantages associated with the use of cement can be avoided by using cementless fixation. This option has become increasingly popular since published series of uncemented TKA have become available, showing that at least equal results can be obtained compared to cemented TKA at up to 10–15 years follow-up.7 Cementless TKA however is generally considered as technically more challenging than cemented TKA, since a tight interface gap smaller than 0.5 mm is necessary for successful component integration, together with immediate initial component stability (Fig. 3). Cemented TKA is more forgiving with respect to both of these aspects, and therefore remains for many surgeons the standard.
PCL retaining or posterior stabilised Theoretically the PCL can be saved during TKA, since its insertion on the tibia is located distal to the usual resection plane. We know that the PCL plays an important role in the kinematic and functional behaviour of the knee, and it is therefore of interest to consider its retention during the procedure. The fact that TKA designs with substitution of the PCL by a system of cam–post interaction (‘‘posterior stabilised’’) have been as successful as, or even more successful than, PCL-retaining TKAs, has lead to a continuous debate between PCL-retainers and substitutors. It is today clear that PCL-retaining TKAs do not demonstrate normal kinematics. Instead an aberrant pattern characterised by paradoxical motion is seen in the majority of PCL-retaining knees, with
ARTICLE IN PRESS 450
Figure 3 Cementless TKA requires more aggressive initial fixation stability for successful component integration.
forward translation of the femur onto the tibia during flexion.8,9 The absence of the anterior cruciate ligament (ACL) together with the inability to reproduce normal and consistent PCL tension with our modern implants and instrumentation, are believed to be the main causative factors. Contrary to this, better kinematics have been reported for cam–post-type substituting PS knees, at least in the sagittal plane. Although PS knees demonstrate reproducible roll-back during flexion, it is however predominantly symmetric on the medial and lateral side, whereas in the normal knee asymmetric roll-back occurs, predominantly on the lateral side. In other words, PCL-retaining knees do not perform better with regard to kinematics when compared to cam–post PS knees, although the latter are associated with more normal femoral roll-back. Likewise, other theoretical advantages that may have been in favour of PCL-retention, have not withstood the test of time. Long-term clinical studies have indeed failed to show an advantage of PCL retention versus substitution, and the longest success rates have indeed been reported on posterior stabilised knees.
Mobile bearing or fixed bearing insert Mobile bearing inserts have been in use for more than 20 years, and although other designs have had
J. Bellemans et al. some success, it is mainly the rotating LCS knee that is today considered as the prototype mobile bearing knee. The theoretical advantage of mobile bearing knees is mainly the fact that increased conformity of the articulating surfaces is possible without increasing the constraint of the system, with less polyethylene wear as the end result. Laboratory data using knees simulators as well as retrieval specimens obtained from mobile bearing unicompartmental knees have confirmed this, but concern exists on the potential increase of volumetric wear (versus linear wear) and the size of the wear particles, which may be smaller and therefore more aggressive in mobile bearing knees.10 Other theoretical advantages of mobile bearing knees are the potential reduction of the bone– implant interface stresses, and the self-aligning nature of the implant which makes it more forgiving towards rotational mistakes in implant positioning during the operation. Downsides of mobile bearings are however the potential risk for bearing dislocation, functional instability, and backside wear or damage on the underside of the bearing. Clinical studies have in general shown comparable results between fixed bearing knees and knees with mobile bearing inserts that allow rotation, and therefore the debate continues. Mobile bearing designs allowing both rotation and translation of the insert have however been associated with less favourable reports, and their use is therefore today somewhat more controversial.
Patellar resurfacing Although the first generation of knee arthroplasty designs did not provide replacement of the patella, most surgeons advocate today replacement of the patellar surface during TKA. Initial follow-up studies have noted a 10–20% incidence of residual anterior knee pain when TKA was performed without patellar resurfacing. The introduction of modern TKA designs with more patellar friendly trochlear shapes, providing a smooth support for the patella during the whole range of motion, has lead to a renewed interest in leaving the patella unresurfaced (Fig. 4A and B). Despite the fact that studies have shown that even with such patellar friendly designs, residual peripatellar pain and discomfort is often seen in some 10% of cases, proponents of this strategy have argued that this percentage equals the complication rate of patellar resurfacing and therefore continue to defend nonresurfacing the patella. A recent meta-analysis of the existing literature showed however that knees
ARTICLE IN PRESS Total knee replacement
Figure 4 Unresurfaced (left) versus resurfaced (right) patella.
with replacement of the patella generally performed better than knees without patellar replacement on most of the outcome variables.11
Medio-lateral stabilisation Unlike to the very first (hinged) knee prostheses that were used, contemporary TKA designs do not provide medio-lateral stabilisation. Medio-lateral stabilisation requires the use of an intrinsic rigid link between the femoral and tibial components, and experiences from the past have shown that such a link is susceptible to mechanical failure, and also leads to high interface stresses between the implants and the underlying bone. It is therefore no surprise that these early hinge designs were associated with high failure rates at short-term follow-up. Modern TKA designs have, therefore, deliberately been developed without medio-lateral constraint, since in most primary cases adequate medio-lateral ligament stability can be obtained without supplementary stabilisation by the implant. In exceptional cases, such as the severe valgus knee with deficiency of the medial collateral ligament, a design with additional medio-lateral constraint may be indicated to obtain a stable joint. In those cases the surgeon can use a so-called ‘‘CCKtype’’ of implant or a rotating hinge design. CCKdesigns provide medio-lateral stability through a central cam–post system, whereas rotating hinges do so by a rigid central link which excludes varusvalgus play, but allows axial rotation. Consensus exists that both implant options are, however, associated with inferior long-term results, and therefore their use should be retained for exceptional cases only. The CCK option is then considered more as the back-up solution for moderate medio-lateral instability, whereas the rotating hinge designs should be reserved for severe medio-lateral instability.
451 270,000 procedures performed in the USA in 1999. There is a consensus that an average of 90% or more of the patients who have knee replacement can expect 10–20 years of satisfactory function, with relief of pain, and increased social mobility and interaction. Furthermore, TKA has been shown to be a cost-effective medical intervention that is associated with significant improvements in quality of life. Resumption of physical activity after TKA leads to an overall improvement of cardiovascular fitness and general health.12,13 These results are relatively uniform for most TKA systems available today, without major differences with respect to prosthetic design or implant manufacturer. Nonetheless, some patients achieve a poor result early after surgery or the implants fail prematurely and a revision operation is required. Early postoperative dissatisfaction is often related to unfulfilled patient expectations, which may have been unrealistic. Activities of daily life are usually possible without problems, but as much as two-thirds of the patients report difficulties in squatting and kneeling, and half of the patients are limited in turning and cutting manoeuvres. Only 15% of the patients are able to kneel with little or no difficulty.12 Maximal flexion after TKA is often limited, usually somewhere between 1001 and 1201, and is influenced by many factors such as preoperative flexion, patient motivation, technical operative factors, and implant related features9 (Fig. 5). Although the incidence of failure after TKA is low, yet it has been reported that 22,000 knee replacements are revised every year. The reasons for failure in order of prevalence are polyethylene wear, aseptic loosening, instability, infection, arthrofibrosis, malalignment or malpositioning, extensor mechanism deficiency, avascular necrosis of the patella, and periprosthetic fracture. Approximately half of the revision operations are performed less
Outcome after TKA The number of TKA procedures has increased tremendously over the past decade, with over
Figure 5 Patient with limited maximal flexion (1051).
ARTICLE IN PRESS 452 than 2 years after the primary operation, mostly for reasons of instability, malalignment, prosthetic malpositioning, and prosthetic loosening.14 The current overall incidence of infection is 1–2%, but is higher in patients with rheumatoid arthritis, diabetes, obesity, or concurrent infection at other sites. Durability of the implant is a greater concern in younger patients because of the higher activity level, with a cumulative revision rate of 13% at 8.5 years for patients younger than 60 years, versus 6% for patients older than 60.15 Both long-term survival as well as immediate functional performance that is obtained today after TKA, has therefore a significant margin for further improvement, and is the basis for continued research and development of knee arthroplasty designs and surgical technique.
References 1. Chassin E, Mikosz R, Andriacchi T, Rosenberg A. Functional analysis of cemented medial unicompartmental knee arthroplasty. J Arthroplasty 1996;11:553–9. 2. Cartier P, Sanouiller J, Grelsamer R. Unicompartmental knee arthroplasty surgery: 10 year minimum follow-up period. J Arthroplasty 1996;11:782–8. 3. Tabor O, Tabor OJ. Unicompartmental arthroplasty: a longterm follow-up study. J Arthroplasty 1998;13:373–9. 4. Whiteside L, Arima J. The anteroposterior axis for femoral rotational alignment in valgus total knee arthroplasty. Clin Orthop 1995;321:168–72.
J. Bellemans et al. 5. Chauhan S, Clark G, Lloyd S, Breidhall W, Sikorski J. Computer assisted total knee replacement. A controlled cadaver study using a multi-parameter quantitative CT assessment of alignment (the Perth CT protocol). J Bone Jt Surg 2004;86B:818–23. 6. Gill G, Joshi A, Mills D. Total condylar knee arthroplasty: 16 to 21 year results. Clin Orthop Rel Res 1999;367:210–5. 7. Whiteside L. Cementless total knee replacement. 9 to 11-year results and 10-year survorship analysis. Clin Orthop Rel Res 1994;309:185–92. 8. Banks S, Harman M, Bellemans J, Hodge A. Making sense of knee arthroplasty kinematics: news you can use. J Bone Jt Surg 2003;85A:64–72. 9. Bellemans J, Banks S, Victor J, Vandenneucker H, Moermans A. Fluoroscopic analysis of the kinematics of deep flexion in total knee arthroplasty. The influence of posterior condylar offset. J Bone Jt Surg 2002;84-B:50–3. 10. Huang C, Ma H, Liau J, Ho F, Cheng C. Osteolysis in failed TKA: a comparison of mobile bearing and fixed bearing knees. J Bone Jt Surg 2002;84A:2224–9. 11. Nizard R, Biau D, Porcher R, Ravaud P, Bizot P, Hannouche D, et al. A meta-analysis of patellar replacement in total knee arthroplasty. Clin Orthop Rel Res 2005;432: 196–203. 12. Aglietti P, Cuomo P, Baldini A. Sports and activity levels after TKA. In: Bellemans J, Ries M, Victor J, editors. Total knee arthroplasty: a guide to get better performance. Heidelberg: Springer; 2005. p. 393–7. 13. Ries M, Philbin E, Groff G, Sheesly K, Richman J, Lynch F. Improvement in cardiovascular fitness after TKA. J Bone Jt Surg 1996;78A:1696–701. 14. Sharkey P, Hozack W, Rothman R, Shastri S, Jacoby S. Why are total knee arthroplasties failing today? Clin Orthop Rel Res 2002;404:7–13. 15. Harrysson O, Robertsson O, Nayfeh J. Higher cumulative revision rate of knee arthroplasties in younger patients with osteoarthritis. Clin Orthop Rel Res 2004;421:162–8.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 453–460
www.elsevier.com/locate/cuor
TISSUE ENGINEERING
Current concepts and applications in the musculoskeletal and peripheral nervous systems Panayotis N. Soucacosa,, Elizabeth O. Johnsonb a
Department of Orthopaedic Surgery, University of Athens, School of Medicine, KAT Accident Hospital, 2 Nikis str, Kifissia 14561, Athens, Greece b Department of Anatomy, Histology and Embryology, University of Ioannina, School of Medicine, Ioannina, Greece
KEYWORDS Biotechnology; Tissue engineering; Tissue regeneration; Tissue replacement
Summary Biotechnology and tissue engineering have broad applications over several medical disciplines. The advances in the fields of biotechnology and tissue engineering offer new possibilities in the repair or regeneration of tissue lost to disease or injury. Consequently, a major portion of the research effort has focused on applications in orthopaedics with emphasis on the development of techniques for developing bone, articular cartilage, ligaments, tendons and nerve. Tissue engineering represents a multidisciplinary approach to solving some of the most demanding medical problems, particularly the creation of new tissues similar to those in the living organism. These new technical approaches include strategies in using new synthetic polymer formulations and various alternatives in tissue regeneration. This paper will examine the possible impact of biomolecular medicine in areas critical to the future of hand surgery, including tissue replacement, tissue regeneration, wound healing, and bone, tendon, cartilage, ligament and nerve repair. & 2005 Elsevier Ltd. All rights reserved.
Introduction Tissue replacement and tissue regeneration Tissue loss related to disease or trauma has been traditionally managed with autografts or allografts. Autograft is the best method for replacing defects, but the problem of donor site defects (structural or
functional) of the host donor site has never been overcome. Although the development of immune suppressing agents has expanded the allograft era, the number of donors with perfectly matching recipient HLA is still limited. As a result of these inherent difficulties, the possibility of replacing tissue defects with biologically functioning materials has been the focus of recent investigations. The ultimate goal is to regenerate normal tissue. The
Corresponding author. Tel.: +30 210 628 0209; fax: +30 210 628 0765.
E-mail address:
[email protected] (P.N. Soucacos). 0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2005.06.009
ARTICLE IN PRESS 454 advances in the fields of biotechnology and tissue engineering offer new possibilities in the repair or regeneration of tissue loss in disease or injury. Although tissue engineering has broad applications over several medical disciplines, a major portion of the research effort has focused on applications in orthopaedics with emphasis on the development of bone, articular cartilage, ligaments, tendons and nerves. With the recent progress of new technologies in cell modulation, extracellular matrix fabrication and the synthesis of synthetic polymers that mimic bodily structures, the self-regeneration of bodily defects by host tissue can now be considered a possibility. Conventionally, tissue replacement focused on the use of non-biologic and non-viable materials, such as metals, ceramics and synthetic polymers. Restoration of defects was usually limited to re-establishing support for mechanical functions in skeletal and circulatory systems or to the replacement of morphological defects with bioinert materials. Recently, research focusing on constructing artificial tissues by combining modulated cells with extracellular matrixhybridized synthetic polymers has produced exciting results with biologically functioning artificial tissues.1 With the extension of knowledge from cell biology and embryology, the focus on tissue restoration has slowly shifted to tissue regeneration or generation of site-specific normal tissue as it occurs in embryonic development. Embryonic and mesenchymal stem cells have become attractive resources because of the potential for differentiation into various tissue types in response to signal transduction mediated by cytokines.1 Embryonic pluripotential stem cells and adult human stem cells have the potential to differentiate into various cells types.2,3 Embryonic tissue is characterized by high concentrations of pluripotent and progenitor cells and relatively little matrix.
Components for tissue engineering All tissues consist of cells, extracellular matrix and ionic body fluid. The extracellular matrix plays a fundamental role in providing a suitable living environment for cells and in maintaining the tissue’s structure. By hybridizing the extracellular matrix with polymers, cultured cells can be then introduced, resulting in a biomimicking material with biological properties appropriate for tissue replacement. Thus, three essential components are required for tissue engineering; these are a scaffold or matrix, cells and cellular signals in the form of growth factors or transfected genes.
P.N. Soucacos, E.O. Johnson
The scaffold or matrix A scaffold or matrix to provide a construct for the cells to grow is a crucial component for tissue engineering. A scaffold is an artificial construct using polymers. Human tissues are comprised of biologically and structurally complex acellular fabrics that provide a supportive scaffold for cellular growth and have biologically important chemical properties that profoundly affect cell growth and differentiation. Initially, scaffolds or matrices that were developed focused on biodegradable polymers which supported the initial growth and differentiation of cells. However, they had inherent properties allowing them to degrade over time, thus allowing the cells themselves to produce matrix components specific to that particular tissue. Of the new polymers developed, polylactic acid, polyglycolic acid and polypropyl fumarate have exhibited novel biomechanical properties and in particular, the ability to promote growth of tissue. As our awareness of the extracellular matrix constituents increases, more tissue-specific scaffolds can be developed or scaffolds that incorporate cellular signals that enhance cell growth and differentiation can be devised.
The cells Most investigators have used fully differentiated cells, such as osteoblasts, chondrocytes or others in tissue engineering. However, tissues are complex structures comprising various cell types. For example, skin is composed of multiple differentiated cell populations including keratinocytes, melanocytes, neural cells, fibroblasts, adipocytes, smooth muscle cells, endothelial cells, etc. Thus engineering anatomically precise tissues would entail the use of numerous differentiated cell types such as those described for skin. In light of the knowledge that new cells in any tissue emanate from a quiescent population of stem cells and which are responsible for maintaining the long-term integrity of the tissue, research has recently focused on the application of cells that are undifferentiated4 (Table 1, Fig. 1). The advantage of using stem cells is that they can differentiate into individual specific cell types and also recreate themselves so as to maintain the population of stem cells. Recently, investigators have proposed methods to obtain autologous stem cells, embryonic stem cells or cloning.5,6
The cellular signals The regulation of cellular processes that occur during tissue repair is complex, and includes
ARTICLE IN PRESS Current concepts and applications in the musculoskeletal and peripheral nervous systems central roles for growth factors and cytokines. With the advances in molecular biology we now have a clearer picture of how growth factors influence repair through receptor activation, signal transduction and changes in target gene expression, which in turn alter cell proliferation and migration, as well as other cellular metabolic activities. It is very likely that during the 21st century new treatment paradigms will entail adding or subtracting growth factors to induce changes in cell function. Various growth factors have a prominent role in the regulation of wound healing,7 and they are predominately released by various activated cells at the wound site (Table 2). Recently, healing rates in normal wounds were found to be accelerated by adding exogenous TGF-beta, PDGF, IGF-1, or FDF2.8 In addition, these growth factors also augment repair in organisms with impaired wound healing conditions, such as chronic steroid use or diabetes.9
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Table 1 Some sources of mesenchymal stem cells with multilineage differentiation potential. Tissue source
Differentiation potential
Muscle
Adipocyte Osteocyte Chondrocyte
Adipose
Chondrocyte Muscle Osteoblast Stromal Cell
Bone Marrow
Adipocyte Chondrocyte Muscle Osteoblast Stromal Cell
Trabecular Bone
Adipocyte Chondrocyte Osteoblast
Tissue engineering
Periosteum
Chondrocyte Osteoblast
Biomaterials
Blood
Adipocyte Fibroblast Osteoblast Osteoclast
In the development of biomaterials for orthopaedic applications, several important requirements must be adhered to including biocompatibility, mechanical properties, promotion of tissue formation, sterilizability, and ease of handling. Any biomaterial used in hand surgery must be biocompatible, that is, it must not elicit extreme immunogenicity or cytotoxicity. Because these materials degrade in vivo, their degradation products must also be biocompatible.10 The initial mechanical properties of the biomaterial that is implanted must be as similar as possible to those of the tissue that is to be regenerated. This ensures proper support in early healing stages, and graded load transfer later in the process for creation of replacement tissue that is identical to the original.11 Several mechanical properties need to be considered for materials to be used in orthopaedics, including compression, tension and torsion. Compressive properties are an important consideration for cancellous bone, while tensile properties are important for cortical bone. Properties such as the amount of void space and degradation time are selected to encourage tissue growth and vascularization within the material.10 Biomaterial should be easily sterilizable to help prevent infection12 and easy to handle.13
Bone Bone tissue engineering has focused primarily on repairing bony defects with polymeric materials
and ceramics. Ceramics, such as calcium phosphate hydraulic cement are biocompatible and harden in situ.14 These have often been chosen to aid in fracture fixation and filling of bony defects as they promote bony ingrowth. Despite considerable focus on cements that are quickly resorbed, many existing calcium phosphate materials degrade relatively slowly, which can lead to decreased bone regeneration at the site of the implant.15 While these cements show good biocompatibility and perform well in compression, tensile strengths are still below that of natural bone.15,16 In an effort to address these concerns, researchers have chosen to investigate polymeric materials. Polymers are also injectable and harden in situ. Although polymers may be less biocompatible and more difficult to sterilize than ceramic cements, mechanical properties and degradation times are more easily tailored giving them distinct advantages. A promising candidate for clinical application is polypropylene fumarate (PPF) which shows versatility and excellent mechanical properties.13 The mechanical properties of PPF can vary greatly according to the synthetic method and the cross-linking agents used. Its degradation time is dependent on polymer structure and other components that comprise the composite material.
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P.N. Soucacos, E.O. Johnson
Figure 1 Differentiation potential of human mesenchymal cells. Mesenchymal cells demonstrate a multilineage differentiation potential, with the ability to differentiate into muscle, tendon, adipose tissue, bone and cartilage. Some of the factors that promote the tissue-specific differentiation processes are indicated. BFGF, basic fibroblast growth factor; BMP, bone morphogenetic protein; FGF, fibroblast growth factor; GDF, growth/differentiation factor; PDGF, platelet-derived growth factor; TGF-b, transforming growth factor beta.
Table 2 Various growth factors have a prominent role in wound healing. Growth factor or cytokine
Effect on wound
Transforming growth factor b
Reduced scar formation Neovascularization Increased granulation tissue & collagen Acute wound healing
Granulocyte macrophage-colony Fibroblast growth factor Platelet derived growth factor
Interleukin 1-b
Neovascularization Re-epithelialization Increased granulation tissue & collagen Neovascularization Re-epithelialization Infected wound healing
proliferation and differentiation of osteoblastic functions of rat marrow stromal cells.18 Moreover, recent studies indicate that the initial mechanical properties can be improved by directing cell migration and differentiation within the material with the use of growth factors (TGF-b1).19 As periosteum has osteogenic potency through the release of periosteum-derived osteoblasts, it can be used to generate bone. Periosteum grafts have been successfully applied to induce new bone formation, with vascularized periosteum showing a constant or even increasing level of osteogenic capacity over time.20,21 Endochondral ossification bone formation can be induced when periosteum is placed directly onto a polyglycolic acid polymer, resulting in the migration of the periosteal cells from the tissue and their attachment and spreading on the polymer.21
Many are released by activated cells at the wound site.
Cartilage Although initially a mild inflammatory response was observed and a fibrous capsule formed around the implant, PPF does not exhibit a deleterious longterm inflammatory response when implanted subcutaneously in rats.17 Recent in vitro studies indicated that the PPF/b-TCP construct has significant osteoconductive properties and demonstrated that the composite encourages attachment,
Cartilage tissue engineering differs significantly from bone tissue engineering. Cartilage biomaterials are required to withstand compressive loads, like bone. However, as cartilage must provide a frictionless movement at the joints, an important consideration for appropriate cartilage biomaterials include the ability to withstand shear forces at the joint surface. Both naturally derived and
ARTICLE IN PRESS Current concepts and applications in the musculoskeletal and peripheral nervous systems synthetic polymers have been used in cartilage repair with significant differences in biocompatiblity and promotion of tissue formation. Transplantation of chondrocytes on polyglycolic acid polymer mesh has been shown to regenerate cartilage.22 Of the naturally derived polymers, fibrin glues and alginate gels have been the most widely studied for injectable cartilage applications. Several investigators have explored the application of a degradable fibrin mesh produced by injecting fibrinogen and thrombin as a scaffold for chondrocytes.23 The advantage of this method is that the patient’s own fibrinogen and thrombin can be used, thus eliminating concerns of biocompatibility, sterilizability and temperature changes during setting. Recent experimental data found that when the cell–fibrinogen–thrombin mixture was injected into defects, hyaline-like cartage was formed with more glycosaminoglycan and type II collagen present than untreated defects.24 Alginate is a liquid derivative of seaweed that can be cross-linked with calcium and injected into the cartilaginous defect. Histologic evaluation showed the architecture of the newly formed tissue to be similar to that of the native cartilage, there was little sign of alginate degradation and there is some evidence that it may be immunogenic.25
Tendons Tendon defects are a major concern in hand surgery because of the limited availability of a proper tissue source for tendon grafting. In many cases, unfavorable results are attributed to the lack of ideal grafts, rather than the surgical technique. Although autografts are considered ideal for repairing tendon defects, there are limited donor sites and harvesting an autologous tendon often leads to minor functional disabilities. On the other hand, tendon allografts are generally difficult because of immune rejections. Most prosthetic replacements (e.g. carbon fibers, silastic sheets dacron grafts, etc) fail to achieve a satisfactory long-term result as they are unable to properly heal with tendon tissue and they cannot sustain the mechanical forces required for movement.26 Compared to other tissue types such as bone and cartilage, tendon engineering has not been extensively studied. To date several studies have tested the feasibility of engineering tendon tissues with autologous tenocytes to bridge tendon defects.27–30 One of the pioneer experiments in tendon engineering was performed in nude mice. The results demonstrated for the first time that tendon tissue could be engineered using polyglycolic acid fibers
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seeded with tenocytes.27 However, because an immunodeficient animal model was used, no imformation was gathered regarding the biocompatibility of polyglycolic acid with host tissues and seed cells. In addition, this study did not address the effects of mechanical loading on the engineered tendons. The same research team presented one study recently using a hen model and demonstrated that tendon tissue could be engineered in vivo to bridge the tendon defect.28 Moreover, the engineered tendon resembled natural tendons not only in gross appearance (structure, color and texture), but also their histologic structure was similar to that of natural tendons regarding collagen bundle alignment and cell-tocollagen ratio. An important finding was that the strength of the engineered tendons was about 83% of the normal tendon breaking strength and the engineered tendon gained tensile strength gradually over the entire period of tissue construction, indicating similar biomechanical properties.28 The teams of Awad and Young mixed bone marrow stromal cells with collagen gel to repair tendon defects in a rabbit model. Although the biomechanical properties were improved when compared to the control tissue, the enginnered tissues did not display a histologic structure similar to that of normal tendons.29,30 Critical evaluation of the results of these four studies underscores two of the fundamental elements in tissue engineering, the biomaterial applied and the seed cell. The biomaterial applied as the scaffold material used is of primary importance. In the hen model, the scaffold material used was unwoven polyglycolic acid fibers which otherwise are unable to sustain any tension. To provide additional mechanical strength, the investigators wrapped the fibers with a biomembrane of intestinal submucosa, and allowed the severed ends to retract to a set degree to avoid overloading.28 The seed cell is the second key element. In the study by Cao28 the tenocytes were selected as seed cells to engineer tendon tissue. The disadvantage of using tenocytes for tendon construction is the need to harvest autologous tendon tissue, which may not be practical clinically. However, tenocytes from other mammalian sources (e.g. pigs) are difficult to culture and grow. Thus, a remaining important step for the future success of tendon engineering is the ability to identify an alternative source of seed cells, such as dermal fibroblasts. A common clinical problem is adhesion of the repaired tendon to surrounding tissues. Generally, it is believed that preservation of paratenon tissue helps reduce adhesion. The tendons engineered in these studies were not surrounded by paratenon,
ARTICLE IN PRESS 458 and therefore adhered strongly to the surrounding tissues. Thus, a remaining challenge in the area, will be how to engineer a composite tendon tissue that includes a paratenon. In last few years, several groups have been interested in applying methods in cell culture and molecular biology to flexor tendon research. Banes and colleagues31 developed a method to separate and propagate chicken fibroblast/tenocyte populations from the other synovium (epitenon) and the internal tendon. Others were able to grow a third cell line composed of fibroblasts derived from the surrounding tendon sheath. Growth factors such as TGF-b1 have been implicated in the process of tendon wound healing.
Vessels Polyvinylchloride (PVC) was first used to restore resected vessels in 1952. Since then, synthetic polymers have been regarded as one of the most important biomaterials, mostly because of its malleable chemical and physical characteristics. To protect against the formation of thrombosis from blood plasma proteins adhering to the polymer surface of these artificial blood vessels, the use of chemical modifications of the lumen with hydrophilic–hydrophobic phase segregation or grafting protein repellant on the polymer surface have been attempted with encouraging results.32,33
Nerves Current issues in peripheral nerve surgery include improvement of regeneration and creation of alternative sources of donor nerves. Several advances have been made in the surgical technique, including introduction of the end-to-side neurorrhaphy and baby-sitter nerve anastomoses. Biotechnological advances include allotransplantation of nerves, growth factors and artificial nerve conduits. Nerve allografts or xenografts are considered a good alternative for nerve conduits if imunosuppression is found safe and efficacious. Nerve allotransplantation has already been performed in patients with adequate sensory reinnervation34 (Table 3). Neurotrophic factors play an important role in nerve regeneration and as a result, there is great clinical interest in addressing whether they can supplement damaged nerve and nerve repairs in order to enhance sensory or motor recovery, or alternatively to avoid excessive tissue inflammation and scarring.
P.N. Soucacos, E.O. Johnson Tissue engineering of peripheral nerves has focused on means to create either natural or synthetic tubular nerve guidance channels as alternatives to nerve autografts. The various options for guidance channels include synthetic substances, such as lactate polymer, polyglactin mesh, polyethylene, silicone and silicone-polymer tubes, as well as to biologic conduits, including autologous collagen, arterial grafts, veins and acellular muscle grafts.35 These are selected for their ability to help direct axons sprouting from the regenerating nerve end, provide a conduit for diffusion of neurotrophic factors secreted by the damaged nerve stumps and minimize infiltration of fibrous tissue.36 Good axonal regeneration has been observed with the use of autologous vein grafts, and vein conduits have been used clinically to bridge short digital nerve gaps.37 Acellular muscle has been used for the repair of digital nerves, but because of the lack of viable Schwann cells their was failure of regeneration.38 As Schwann cells play a crucial role in regeneration of peripheral nerves due to their neurotrophic and neurotropic influence,39 recent studies have been aimed at evaluating the possibility of creating tissue engineered nerve grafts from biologic matrices combined with viable Schwann cells.35 Schwann cells produce and accumulate trophic factors for regenerating axons and thus are essential for axonal regneration, particularly for long gaps.40 Schwann cells produce basal lamina components, such as collagen IV, which provide the extracellular matrix for attachment of the regenerating axons. More importantly, the Schwann cells form a column of cells, the band of Bungner, within the basal lamina tube after Wallerian degeneration has taken place. This cell column serves as the pathway for the regenerating axons to reach their target.41 Recent studies have found several advantages with the application of acellular muscle in combination with cultured Schwann cells for nerve regeneration. This combination provides the advantage of large basal lamina tubes which can serve as pathways for the regenerating axons and the necessary effects of viable Schwann cells (production and accumulation of neurotrophic and neurotropic factors) to support early axonal regeneration.35
Conclusions All tissues consist of cells, extracellular matrix and ionic body fluid. The extracellular matrix plays a
ARTICLE IN PRESS Current concepts and applications in the musculoskeletal and peripheral nervous systems Table 3 Types of conduits used for peripheral nerve regeneration. Natural conduits
Synthetic conduits
Biological tissue Basal membrane Natural polymers Laminin Fibronectin Non-biodegradable
Vein Collagen
Silicone
Biodegradable PLA PGA PLGA
fundamental role in providing a suitable living environment for cells and in maintaining the tissue’s structure. By hybridizing the extracellular matrix with polymers, cultured cells can then be introduced, resulting in a biomimicking material with biological properties appropriate for tissue replacement. Thus, three essential components are required for tissue engineering; these are a scaffold or matrix, cells and cellular signals in the form of growth factors or transfected genes. Biotechnology and tissue engineering represent a multidisciplinary approach to solving some of the most demanding medical problems, particularly the creation of new tissues similar to those in the living organism. These new technical approaches include strategies in using new synthetic polymer formulations, biologic constructs as well as various alternatives in tissue regeneration. Although cell transplantation on artificial matrices is rapidly being successfully applied to form several specific tissue types (bone, cartilage, tendon, nerve, etc), the construction of anatomical units, such as an entire joint, present special challenges in tissue engineering. These anatomical units are composed of multiple cell-tissue types, each with its tissuespecific extracellular matrices. The next challenge in biotechnology and tissue engineering is to be able to combine the formation of several musculoskeletal tissue components into a functional anatomical unit. Very recent studies have presented the application of three different cell types (periosteum, cartilage and tendons) to form an entire phalangeal joint with a predetermined shape and composition.
References 1. Suh H. Recent advances in biomaterials. Yonsei Med J 1998;39(2):87–96.
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2. Pittenger MF, Mackay AM, Beck SC, et al. Multilineage potential of adult human mesenchymal stem cells. Science 1999;284:143–6. 3. Thomason JA, Itskovitz-Eldor J, Shapiro SS, et al. Embryonic stem cell lines derived from human blastocysts. Science 1998;282:1145–7. 4. Solter D, Gearhart J. Enhanced: putting stem cells to work. Science 1999;283:1468. 5. Ferber D. From the lab to the clinic. Science 1999;284:423. 6. Pennisi E. Cloning: the lamb that roared. Science 1997;278: 2038. 7. Brueing K, Andrec C, Helo G, et al. Growth factors in the repair of partial thickness porcine skin wounds. Plast Reconstr Surg 1997;100:657. 8. Cromack DT, Porras-Reyes B, Mustoe TA. Current concepts in wound healing: growth factor and macrophage interaction. J Trauma 1990;30S:129. 9. Cromack DT, Pierce GF, Mustoc TA. TGF-beta and PDGF mediated tissue repair: Identifying mechanisms of action using impaired and normal models of wound healing. Prog Clin Biol Res 1991;365:359. 10. Thomson RC, Wake MC, Yaszemski MJ, Mikos AG. Biodegradable polymer scaffolds to regenerate organs. Adv Polym Sci 1995;122:245–74. 11. Yaszemski MJ, Payne RG, Hayes WC, Langer R, Mikos AG. In vitro degradation of a poly(propylene fumarate) based composite material. Biomaterials 1996;17:2127–30. 12. Yaszemski MJ, Payne RG, Hayes WC, Langer R, Migos AG. Evolution of bone transplantation: molecular, cellular and tissue strategies to engineer human bone. Biomaterials 1996;17:175–85. 13. Temenoff JS, Mikos AG. Injectable biodegradable materials for orthopedic tissue engineering. Biomaterials 2000; 21(23):2405–12. 14. Ikenaga M, Hardouin P, Lemaire J, Andrianjatovo H, Flautre B. Biomechanical characterization of a biodegradable calcium phosphate hydraulic cement: a comparison with porous biphasic calcium phosphate ceramics. J Biomed Mater Res 1998;40:139–44. 15. Frankenburg EP, Goldstein SA, Bauer TW, Harris SA, Poser RD. Biomechanical and histological evaluation of calcium phosphate cement. J Bone Jt Surg 1998;80A: 1112–24. 16. Constanaz BR, Ison IC, Fulmer MT, et al. Skeletal repair by in situ formation of the mineral phase of bone. Science 1995;267:1796–9. 17. Peter SJ, Miller ST, Zhu G, Yasko AW, Mikos AG. In vivo degradation of poly(propylene fumarate)/b-tricalcium phosphate injectable composite scaffold. J Biomed Mater Res 1998;41:1–7. 18. Peter SJ, Lu I, Kim DJ, Mikos AG. Marrow stromal osteoblast function on a poly(propylene fumarate)/b-tricalcium phosphate biodegradable orthpedic composite. Biomaterials 2000;21:1207–13. 19. Lu I, Stamatas GN, Mikos AG. Controlled release of transforming growth factor-b1 from biodegradable poylmers. J Biomed Mater Res 2000;50:440–56. 20. Ishida H, Tamai S, Yajima H, Inoue K, Ohgushi H, Dohi Y. Histologic and biochemical analysis of osteogenic capaciaty of vascularized periosteium. Plastic Reconstr Surg 1996;97:512–8. 21. Isogali N, Landis W, Kim H, et al. Formation of phalanges and small joints by tissue-engineering. J Bone Jt Surg 1999;81A:306–16. 22. Vacanti CA, Langer R, Schloo B, Vacanti JP. Synthetic polymers seeded with chondrocytes provide a template for
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new cartilage formation. Plast. Reconstr Surg 1991;88: 753–9. Sims CD, Butler PEM, Cao YL, et al. Tissue engineered neocartilage using plasma derived polymer substrates and chondroytes. Plast Reconstr Surg 1998;101:1580–5. Hendrickson DA, Nixon AJ, Grande DA, Todhunter RJ, Minor RM, Erb H, Lust G. Chondrocyte-fibrin matrix transplants for resurfacing extensive articular cartilage defects. J Orthop Res 1994;12:485–97. Paige KT, Cima LG, Yaremchuk MJ, Schloo BI, Vacanti JP, Vacanti CAQ. De novo cartilage generation using calium alginate-chondrocyte constructs. Plast Reconstr Surg 1996; 97:168–80. Milthorpe BK. Xenografts for tendon and ligament repair. Biomaterials 1994;15:745. Cao Y, Vacanti JP, Ma X, et al. Generation of neo-tendon using synthetic polymers seeded with tenocytes. Transplant Proc 1994;26:3390. Cao Y, Yongtao l, Liu W, Shan Q, Buonocore SD, Cui L. Bridging tendon defects using autologous tenocyte engineered tendon in a hen model. Plast Reconstruc Surg 2002;110:1280–9. Awad HA, Butler DI, Boivin GP, et al. Autologous mesenchymal stem cell-mediated repair of tendon. Tissue Eng 1999;5:267. Young Rg, Butler DL, Weber W, Caplan AI, Gordon SL, Find DJ. Use of mesenchymal stem cells in a collagen matrix for Achilles tendon repair. J Orthop Res 1998;16:406. Banes AJ, Donlon K, Link GW, et al. Cell populations of tendon: a simplified method for isolation of synovial cells and internal fibroblasts: confirmation of origin and biologic properties. J Orthop Res 1988;6:83.
P.N. Soucacos, E.O. Johnson 32. Wesolowski SA, Fries CC, Domingo RT, Liebig WJ, Sawyer PH. The compound prosthetic vascular graft: a pathologic survey. Surgery 1963;53:19–44. 33. Lee J, Lee D, Suh H, Park DK, Kim YH, Park J. Complement functional activity of PEG modified polyurethane films with different end groups. Biomater Res 1999;3: 103–6. 34. Mackinnon SE, Hudson AR. Clinical application of peripheral nerve transplantation. Plast Reconstr Surg 1992;90: 695. 35. Fansa H, Keilhoff G, Wolf G, Schneider W. Tissue engineering of peripheral nerves: a comparison of venous and acellular muscle grafts with cultured Schwann cells. Plast Reconstr Surg 2001;107:485–94. 36. Hudson TW, Evans GR, Schmidt CE. Engineering strategies for peripheral nerve repair. Orthop Clin North Am 2000;31:485–98. 37. Strauch B, Ferder M, Lovell-Allen S, More K, Kim DJ, Llena J. Determining the maximum length of a vein conduit used as an interposition graft for nerve regeneration. J Reconstr Microsurg 1997;8:605. 38. Fawcett JW, Keynew RJ. Muscle basal lamina: a new graft material for peripheral nerve repair. J Neurosurg 1986;65: 354. 39. Bunge RP. Expanding roles for the Schwann cell: ensheathment, myelination, tropism and regeneration. Curr Opin Neurobiol 1993;3:805. 40. Ide C. Peripheral nerve regeneration. Neurosci Res 1996;25:101. 41. Gulati Ak, Rai DR, Ali AM. Influence of cultured Schwann cells on regeneration through acellular basal lamina grafts. Brain Res 1993;705:118.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 461–466
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Hallux flexus: Review of current opinion on aetiology and management Nicholas E. Ohly, Malcolm F. Macnicol Royal Hospital for Sick Children, Sciennes Road, Edinburgh EH9 1LF, UK
KEYWORDS Hallux flexus; Dorsal bunion; Clubfoot; Cerebral palsy
Summary Hallux flexus is a deformity of the foot characterised by elevation of the first metatarsal head and fixed flexion at the first metatarsophalangeal joint. The deformity is predominantly seen in children following clubfoot surgery or with cerebral palsy. In this article, current opinion on the aetiology and treatment of hallux flexus is reviewed. We argue that a conservative approach to management is appropriate initially, with subsequent soft tissue or skeletal surgery if appropriate. & 2005 Elsevier Ltd. All rights reserved.
Aetiology Hallux flexus (also termed the ‘dorsal bunion’) is a deformity of the foot characterised by elevation or dorsiflexion of the first metatarsal and fixed flexion at the first metatarsophalangeal joint. There is often associated hallux valgus or varus, and the deformity is evident at rest, but is usually more pronounced during the push-off phase of gait (Figs. 1 and 2). There are 3 main groups of patients in which hallux flexus is seen: 1. children who have had clubfoot surgery 2. children with cerebral palsy 3. children with poliomyelitis paralysis. Hallux flexus has also been described in other abnormalities of muscle function such as CharcotCorresponding author.
Marie-Tooth syndrome.1 The deformity will either be diagnosed on routine post-operative follow up, or the patient will present with a fixed deformity when abnormal pressure over the dorsum of the first metatarsal head starts to cause symptoms. The patient may also present late with problems such as excessive medial arch weight bearing secondary to pronation or calf weakness (calcaneus). Hallux flexus has been classified in a number of ways. Lapidus2 originally described the deformity and divided the condition into 4 groups: 1. 2. 3. 4.
associated with hallux rigidus in paralytic deformities of the foot after surgical correction of clubfoot secondary to severe planovalgus.
Park and Goldenberg3 preferred to describe hallux flexus as either related or unrelated to an underlying muscle imbalance. We suggest that the
0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2005.09.001
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Figures 1 and 2 Views of established hallux flexus in a 12-year old boy who underwent posteromedial release for clubfoot aged 4 months.
deformity should be considered as either primary or iatrogenic. Historically, theories about the underlying cause of the deformity are confusing and varied. In order to consider the different theories, an appreciation of the anatomy of the first ray is required. The first metatarsal base is elevated by tibialis anterior, and depressed at its base by peroneus longus. The proximal phalanx is plantarflexed at the metatarsophalangeal joint by both flexor hallucis longus and brevis, and is dorsiflexed by extensor hallucis longus. Therefore, it follows that an imbalance between these muscles is required to produce the deformity. In primary hallux flexus the muscle imbalance is secondary to the natural progression of the underlying disease. In iatrogenic hallux flexus, the muscle imbalance results from the surgery which has been carried out (Figs. 3 and 4). Lapidus2 felt that extensor hallucis longus dysfunction was the cause of hallux flexus, either due to paralysis or following transfer to the first metatarsal. Hammond4 postulated that an unop-
N.E. Ohly, M.F. Macnicol
Figures 3 and 4 Prosection of tendons/muscles acting on the (white arrow), flexor hallucis hallucis longus (yellow pin), arrow).
normal foot showing the first ray. Tibialis anterior brevis (blue pin), flexor peroneus longus (black
posed or overactive tibialis anterior with secondary plantarflexion of the hallux caused the deformity, or that strong plantarflexion of the hallux and a resultant upward displacement of the first metatarsal head was responsible. Goldner5 amalgated these theories in his report on a series of 26 toes with combined hallux flexus and hallux valgus secondary to cerebral palsy. He argued that it was a weak extensor hallucis longus, overpull of tibialis anterior on the first metatarsal and spasticity or contracture of the flexor hallucis longus or brevis that caused the deformity. Furthermore he asserted that a weak peroneus longus muscle was not implicated in the deformity. Bleck6 stated that hallux flexus was a late complication of triple arthrodesis for long-standing and severe equinovalgus, and that it was predominantly tibialis anterior spasticity combined with fixed dorsiflexion of the first metatarsal that resulted in a dorsal bunion. McKay1 assessed muscle function in 24 feet with hallux flexus, half (12) of which had undergone
ARTICLE IN PRESS Hallux flexus: Review of current opinion on aetiology and management posteromedial release for clubfoot. The remaining feet had undergone peroneus longus transfer and Achilles tendon lengthening for poliomyelitis (9 feet), triple arthrodesis (3 feet) or represented the muscle imbalance in cerebral palsy (2 feet). He found that the bunions were caused either by a weak or absent peroneus longus (18 feet) or by weakness of the triceps surae (16 feet), or both. The flexor hallucis brevis was strong in all 24 feet. His feeling was that hallux flexus develops as the first metatarsal is elevated against the strong flexor pull of the flexor hallucis brevis. However, McKay also noted that some of the patients in his series had weakness in other muscles, notably the flexor hallucis longus (12 patients) and tibialis anterior (7 patients). This imbalance was not considered to be directly causative of hallux flexus, and neither muscle was involved in his technique for operative correction of the deformity. In his opinion, the deformity probably occurred due to overpull of the long, and especially short, toe flexors, with weak plantarflexion and a calcaneus gait. He emphasized that flexor hallucis brevis and abductor hallucis were responsible for the deformity. Thus in the post-operative clubfoot with a weak calf, the flexor hallucis longus and brevis overact during the pushoff phase of gait as part of an effort to compensate for the weak plantarflexion. Since the peroneus longus is usually weak the flexion deformity of the first metatarsophalangeal joint worsens if the tibialis anterior is functioning unopposed. Kuo9 also agreed with this theory. We suggest that the underlying cause of the deformity in both primary and iatrogenic hallux flexus is the same. There is loss of the depressant force of peroneus longus upon the first metatarsal head and unopposed elevation by tibialis anterior, with unopposed flexion at the first metatarsophalangeal joint by flexor hallucis longus and brevis. In primary hallux flexus this may be due to functional inadequacy of the peroneus longus because of lack of excursion in a rigid abducted foot, for example, in calcaneovalgus, or peroneus longus may be intrinsically weak in cerebral palsy (Fig. 5). Iatrogenic hallux flexus is most commonly seen following surgery for clubfoot or cerebral palsy. A standard posteromedial release for clubfoot involves extensive ankle and subtalar capsulotomies, Achilles tendon lengthening, abductor hallucis and tibialis posterior lengthening, and flexor hallucis longus and flexor digitorum longus tenotomy or lengthening. In clubfoot, muscles innervated by the L4 nerve root are strong whilst those innervated by the L5 and S1 roots are weak. Therefore, following posteromedial release, tibialis anterior (L4) elevates the first metatarsal head unopposed by
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Figure 5 Radiograph of the foot in Figs. 1 and 2 showing elevation of the first metatarsal and flexion at the first metatarsophalangeal joint.
Table 1 Suggested progression of treatment for hallux flexus. I
Supportive shoes
II III IV V VI
Orthoses Tendon7soft tissue release Tendon transfers Osteotomies Arthrodesis
peroneus longus (L5/S1), and the first metatarsophalangeal joint is flexed by flexor hallucis longus (S2) and brevis (S3) unopposed by extensor hallucis longus (L5/S1). When surgery is indicated to correct the deformities caused by poliomyelitis and cerebral palsy, peroneus longus transfer and sometimes Achilles tendon lengthening is performed. If a rigid deformity is present, triple arthrodesis may be advisable.
Management A review of the current orthopaedic literature favours operative management of hallux flexus, with most authors incorporating either osteotomy or arthrodesis as part of their overall correction. We would advocate a more conservative initial approach, with an emphasis on early recognition of the deformity in children at risk of hallux flexus, and a preference for only soft tissue correction if surgery is indicated. Table 1 gives a summary of the suggested progression of treatment.
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Non-operative If the deformity is mild, flexible and asymptomatic then an entirely non-operative approach should prove sufficient. Orthoses are helpful if extra support for the foot is required provided the deformity is functionally acceptable. In our unit we recognised 13 cases of hallux flexus following clubfoot surgery, and 10 of these were treated nonoperatively.7 To date none have required any further treatment for hallux flexus.
Operative Depending upon the theory concerning the causation of the deformity, various corrective procedures have been described. Lapidus2 originally described a first metatarsal–cuneiform joint arthrodesis, with a possible cuneiform–navicular joint arthrodesis, as well as a first metatarsophalangeal capsulorrhaphy, flexor hallucis longus transfer dorsally to the distal end of the first metatarsal, and transfer of tibialis anterior posteriorly to the tibialis posterior tendon. Hammond4 treated 42 toes in 38 patients with a similar arthodesis to Lapidus, but using cortical bone graft, and with tibialis anterior transferred to the middle of the first metatarsal and no flexor hallucis longus transfer. Tachdjian8 advocated osteotomy of the base of the first metatarsal, capsulorrhaphy of the first metatarsophalangeal joint and transfer of the insertion of flexor hallucis longus to the head of the first metatarsal. Goldner5 reported on a series over 25 years of 26 toes with combined hallux flexus and hallux valgus in 16 patients with cerebral palsy. He advocated tibialis anterior transfer to the second metatarsal base, adductor hallucis transfer to the first metatarsal neck, plication of abductor hallucis, plantarlateral osteotomy of the first metatarsal base, dorso-medial osteotomy of the proximal phalangeal base, lateral first metatarsophalangeal joint capsulotomy, flexor hallucis longus transfer to the dorsum of the first metatarsophalangeal joint and realignment of the phalanges. Mean follow up was not stated, however, he reported that 22 of the 26 toes (84.6%) maintained their correction, with the other 4 ultimately requiring either metatarsophalangeal joint arthrodesis or arthroplasty. McKay1 wrote about his experience with hallux flexus in 24 feet (22 patients) over a 17-year period. He also advocated both first metatarsal– cuneiform arthrodesis and metatarsal osteotomy. However, he pointed out that neither of these addresses the primary muscle imbalance. Furthermore, he stated that the correction of the under-
N.E. Ohly, M.F. Macnicol lying muscle imbalance must be accompanied by a first metatarsophalangeal joint capsulorrhaphy. Tibialis transfer to either tibialis posterior or the middle of the first metatarsal failed to correct the metatarsal elevation, and flexor hallucis longus transfer to the first metatarsal led to very weak plantarflexion of the first metatarsal. He felt that much stronger plantarflexion could be achieved by transfer of flexor hallucis brevis to the first metatarsal neck, and that this would also remove the primary deforming force. McKay thus developed a technique for correcting a dorsal bunion while the foot is still supple. He transferred abductor hallucis, both heads of flexor hallucis brevis and adductor hallucis (oblique and transverse heads) to the dorsal aspect of the neck of the first metatarsal, along with excision of the sesamoids, and a first metatarsophalangeal joint capsulotomy. Bony correction was achieved with either arthrodesis of the interphalangeal joint or flexor hallucis longus tenodesis to the base of the proximal phalanx (in order to prevent a postoperative fixed flexion deformity). A slight modification was made in the presence of either hallux valgus or varus, with omission of either abductor hallucis or adductor hallucis transfer, respectively. Bleck6 reported the correction of dorsal bunions in children with cerebral palsy. He described a procedure in 2 patients, involving tibialis anterior lengthening, plantar wedge osteotomy of the first metatarsal, arthrodesis of the first metatarsal–cuneiform joint and arthrodesis of the cuneiform–navicular joint. Soft tissue release was achieved by flexor hallucis longus lengthening and myotomy of the insertion of flexor hallucis brevis. If the articular cartilage of the first metatarsophalangeal joint was eroded then the proximal half of the proximal phalanx was excised. Kuo9 was more conservative in his approach and described a technique for correcting dorsal bunion following clubfoot surgery. He reported satisfactory outcomes in 10 out of 11 toes by using what he termed a ‘Reverse Jones’ procedure. Flexor hallucis longus was transferred to the head of the first metatarsal, a capsulorrhaphy was performed if there was a rigid metatarsophalangeal or interphalangeal deformity, and only occasionally would bony correction be required. This would involve either a plantarflexion osteotomy of the first metatarsal or triple arthrodesis. He also described split tibial tendon transfer. Most recently, Mestdagh10 described 9 cases of hallux flexus which were corrected by plantar wedge resection of the base of the first metatarsal or cuneiform, transfer of the flexor hallucis longus to the distal dorsal segment of the first
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metatarsophalangeal joint capsule, release of the tibialis anterior tendon and insertion to tibialis posterior. The first ray was pinned for a month to position its axis.
Clinical experience in Edinburgh The incidence of dorsal bunion following clubfoot surgery is not well reported in the literature. McKay described the lesion as ‘a significant number’ among the post-operative deformities he managed.11,12 In Edinburgh, from a total of 234 cases of clubfoot (grades II and III) in 151 children reported in 2000,7 13 feet developed hallux flexus of varying severity post-operatively. In 3 cases the deformity was sufficiently severe to produce a dorsal bunion. In 10 feet the hallux flexus was flexible and functionally acceptable so orthotic support was effective. Peak pressure distribution studies13 are useful in this assessment, showing that reduced loading through the first metatarsal head is relatively common after clubfoot release. It may also be evident to a lesser degree in the opposite ‘normal’ foot in unilateral cases. In the 3 severe cases a lengthening of the flexor hallucis longus tendon by a step-cut technique was combined with a plantar first metatarsophalangeal joint capsulotomy. The sesamoids were preserved, no tendon transfers were effected and osteotomy or arthrodesis were avoided. In the case illustrated (Figs. 1 and 2) the flexor hallucis longus tendon had not been released at the time of the posteromedial release when the patient was 4 months of age. Mild calcaneus deformity may coexist with hallux flexus, as noted in this case and the orthopaedic literature. The operative approach that we suggest is relatively simple in comparison to any of the techniques that have been described in the past. However, it has been sufficient to achieve and maintain a satisfactory correction in the 3 cases that have required operative correction (Figs. 6 and 7).
Conclusions Hallux flexus in an uncommon deformity of the first ray that is seen in a selected sub-group of patients. With the advent of widespread polio immunisation, it is now children with cerebral palsy, or patients who have had corrective foot surgery for cerebral palsy or clubfoot that are seen with this deformity. Since the development of hallux flexus can be anticipated in these patients, it follows that hallux flexus should be looked for in this group during
Figures 6 and 7 Post-operative photographs of the foot seen in Figs. 1 and 2 taken 8 weeks after surgery (2 weeks after the cast had been removed).
routine follow up. When diagnosed, it is important to treat early and conservatively if at all possible. During initial posteromedial release for clubfoot, it is important to avoid overcorrection of the hindfoot. Hallux flexus usually develops in an overcorrected valgus foot with poor triceps surae function, especially if a horizontal breach deformity is present, and an ‘overactive’, unlengthened flexor hallucis longus tendon is contributory. Unopposed great toe flexion is a major component in the development of hallux flexus. Moreover, it is possible that tibialis posterior (and tibialis anterior) tenotomy effectively shortens the flexor hallucis longus muscle to such an extent that it is unable to accommodate the increased medial dimension of the foot following clubfoot correction. We would therefore propose incorporating flexor hallucis longus release in the posteromedial release to avoid this complication. As discussed earlier, in clubfoot the L4 myotome is strong and L5/S1 weak, therefore it is unclear whether flexor hallucis longus and brevis (S2/3) are
ARTICLE IN PRESS 466 indeed strong in hallux flexus, or if it is merely weak hallux extension that leads to unopposed flexion at the metatarsophalangeal joint. Alternatively, the apparent strength of the flexor hallucis longus and brevis could be a phenomenon secondary to weak foot plantarflexion by triceps surae leading to mild calcaneus gait and compensatory overactivity of flexor hallucis longus and brevis during push-off. Finally, it is worth considering whether conservative treatment of clubfoot with the Ponseti approach would decrease the incidence of iatrogenic hallux flexus. Although only the Achilles tendon is lengthened in the Ponseti approach, with the inherent L4 strength and L5/S1 weakness it is still conceivable that hallux flexus could develop. To our knowledge, this complication of the Ponseti technique has not been reported. From the preceding discussion it is clear that a large variety of opinion exists for both the causation and best treatment for hallux flexus. This lack of consensus suggests that the precise cause of the deformity is often unknown, or is multifactorial. The dearth of any long-term results for the various treatment options described in the literature makes accurate prescriptive treatment difficult.
References 1. McKay DW. Dorsal bunions in children. J Bone Jt Surg Am 1983;65:975.
N.E. Ohly, M.F. Macnicol 2. Lapidus PW. ‘‘Dorsal bunion’’: its mechanics and operative correction. J Bone Jt Surg 1940;22:627–37. 3. Park DB, Goldenberg EM. Dorsal bunions: a review. J Foot Surg 1989;28:217–9. 4. Hammond G. Elevation of the first metatarsal bone with hallux equines. Surgery 1943;13:240–56. 5. Goldner JL. Hallux valgus and hallux flexus associated with cerebral palsy: analysis and treatment. Clin Orthop Relat Res 1981;157:98–104. 6. Bleck EE. Forefoot problems in cerebral palsy—diagnosis and management. Foot Ankle 1984;4(4):188–94. 7. Macnicol MF, Nadeem RD, Forness M. Functional results of surgical treatment in congenital talipes equinovarus (clubfoot): a comparison of outcome measurements. J Pediatr Orthop (Part B) 2000;9:285–92. 8. Tachdjian MO. Treatment of dorsal bunion by open-up osteotomy of base of first metatarsal: pediatric orthopaedics, vol. 2. Philadelphia: WB Saunders; 1972. p. 994–5. 9. Kuo KN. ‘‘Reverse Jones’’ procedure for dorsal bunion following clubfoot surgery. In: Simons GW, editor. Clubfoot. New York: Springer; 1994. p. 412–26. 10. Mestdagh H, Cassagnaud X, Barouk P, Audebert S, Maynou C. Correction of acquired metatarsus elevatus and hallux flexus: technique used in nine cases. Rev Chir Orthop Reparatrice App Moteur 2004;90(2):147–51. 11. McKay D. New concept and approach to clubfoot treatment. Section III. Evaluation and results. J Pediatr Orthop 1983;3: 141–8. 12. McKay DW. Correction of the overcorrected clubfoot. In: Simons GW, editor. Clubfoot. New York: Springer; 1994. p. 374–6. 13. Herd F, Macnicol MF, Abboud RJ. The need for biomechanical evaluation in the assessment of clubfoot. Foot 2004;14: 72–6.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 467–470
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SYNDROMES
Achondroplasia Rouin Amirfeyza, Martin Garganb, a
Trauma and Orthopaedics, Yeovil District Hospital, Yeovil, UK Bristol Royal Hospital for Sick Children, Bristol, UK
b
Introduction Achondroplasia is a disorder of chondrocytes. Mucinoid degeneration occurs and endochondral ossification is affected. It is the commonest of the small stature skeletal dysplasias.
Epidemiology and genetics The prevalence of achondroplasia is about 1 in 30 000 live births.1 Eighty per cent of the cases are due to new mutations, probably from paternal origin, as they are associated with increasing paternal age. Achondroplasia is transmitted as a fully penetrant autosomal dominant trait. The achondroplasia gene is located on chromosome 4p16.3, which encodes fibroblast growth factor receptor 3 (FGFR3). This receptor is expressed in articular chondrocytes.2
Clinical presentation
summarises the differences between these two entities.3 Head circumference is around the 97th centile and clinically there is macrocephaly. The characteristic snub nose and prominent forehead is secondary to relative hypoplasia of the mid-third of the face. The elbows and hips show flexion contractures. The hands have digits of equal length (trident or starfish). The thoracic cage is relatively small and there may be mild hypotonia.
Infants Developmental milestones are delayed. Independent walking starts at an average of 16 months. Upper airway obstruction is secondary to mid-third facial hypoplasia. Individuals presenting with symptoms of sleep apnoea need further investigations. Foramen magnum stenosis can cause cervicomedullary junction stenosis, which increases the risk of death in the first year of life. Thoraco-lumbar kyphosis is usually present, becoming more marked in a sitting child. This normally corrects without treatment once the child starts walking.4 However, in 10% of children with achondroplasia kyphosis may progress. This is an indication for surgical referral.
Neonates The main differential diagnosis at birth is spondyloepiphyseal dysplasia congenita (SEDC). Table 1 Corresponding author. Tel.: +44 117 923 2121; fax: +44 117 928 2659. E-mail address:
[email protected] (M. Gargan).
Childhood The fibulae are relatively long, which can cause bow leg deformity. An increase in lumbar lordosis is normal and is associated with hip flexion contracture. Despite general joint laxity, the elbows tend to retain a mild flexion contracture.
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R. Amirfeyz, M. Gargan
Table 1 The differences between achondroplasia and SEDC. Radiograph
Achondroplasia
SEDC
Head Disproportion
Large Short limbs
Vertebrae (lateral X-ray) Cleft palate Epiphyseal delay Soft tissues Pubis ossification
Square
Normal Short limbs and spine Ovoid
No Mild Redundant Present
Some Marked Normal Delayed
Adolescents Back pain is a common complaint from adolescence onwards and up to 17% will develop complications associated with spinal stenosis. The nature of short stature is disproportionate, with a mean adult height of 132 cm in males and 124 cm in females. Limb shortening is rhizomelic, affecting the proximal long bones, and the hands cannot reach the top of the head. Increasing consciousness of stature difference leads patients to seek advice regarding leg lengthening. Life expectancy is normal after the first year of life and the risk of degenerative joint disea se is low as the epiphyses are not affected.
Fig. 1 Lateral skull radiograph of a patient with achondroplasia. Note the enlarged vault, narrow foramen magnum and hypoplasia of the mid-third of the face.
Radiological features Radiological features of achondroplasia5 Skull:
Enlarged vault (Fig. 1). Small posterior fossa. Narrow foramen magnum. Face:
Hypoplasia of the mid-third of the face (Fig. 1). Spine:
Short and flat vertebral bodies. Posterior scalloping. Anterior wedging (Fig. 2).
Fig. 2 Lateral and anteroposterior views of spine. The vertebral bodies are short and flat, have anterior wedging and posterior scalloping. The interpedicular distance is normal on the anteroposterior radiograph.
Iliac wings: Hands:
Trident (starfish) appearance.
Elephant ear (square). Short and narrow sciatic notches.
ARTICLE IN PRESS Achondroplasia
469 Hips:
Flat acetabular roofs. ‘‘Ball in socket’’ epiphysial–metaphysial junctions. Hemispherical femoral heads. Flared metaphyses. Short femoral neck (Fig. 3).
Treatment
Fig. 3 Anteroposterior view of an achondroplastic pelvis. The acetabular roof is horizontal. The femoral necks are short.
Non-surgical. J Upper airway obstruction and sleep apnoea need investigation and treatment. J Sitting modifications and bracing for kyphosis. J Footwear prescription for foot disproportion. Surgical (to relieve symptoms and improve function). J Spinal column. – Treatment of kyphosis may start with bracing but if proved to be progressive, may need spinal fusion.6 – Spinal stenosis may need decompression if severe enough (especially cervicomedullary junction stenosis). Long laminectomies may be required to prevent recurrent stenotic symptoms from a higher level. Widening of
Fig. 4 Radiograph of humerus and both knees in achondroplasia.
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R. Amirfeyz, M. Gargan inter-apophyseolaminar diameter has also been tried with good results.7 – Leg lengthening is now an established technique. The principle is distraction of the callus following a corticotomy by means of a circular frame. However, as the treatment is onerous, prolonged and with high complications, preoperative counselling is mandatory.8 Both femora and tibiae need to be lengthened. It is usually deferred till young adult life when the patient can make a decision and choose to undergo the surgery. – Bowlegs: the Ilizarov technique is the most satisfactory method for correction of proximal bowlegs in early childhood. Distal tibial osteotomy and fibular shortening is recommended for correction of distal bow legs in older children (Fig. 4).9 – Future treatments: PTH and C-type natriuretic peptide (CNP) are currently being investigated in the treatment of achondroplastic animals.10,11
2.
3.
4.
5. 6. 7.
8. 9. 10. 11.
References 1. Wynne-Davies R, Gormley J. The prevalence of skeletal dysplasias. An estimate of their minimum frequency and the
number of patients requiring orthopaedic care. J Bone Joint Surg Br 1985;67(1):133–7. Bonaventure J, Rousseau F, Legeai-Mallet L, Le Merrer M, Munnich A, Maroteaux P. Common mutations in the gene encoding fibroblast growth factor receptor 3 account for achondroplasia, hypochondroplasia and thanatophoric dysplasia. Acta Paediatr Suppl 1996;417:33–8. Amirfeyz R, Taylor A, Smithson S, Gargan M. Orthopaedic manifestations and managements of spondyloepimetaphyseal dysplasia Strudwick Type. JPOB, in press. Witherow PJ, Gargan MF. Management of rare and complex disability: achondroplasia and hypochondroplasia. Curr Paed 1996;6:178–82. Wynne-Davies R, Hall CM, Apley AG. Atlas of skeletal dysplasias. Edinburgh: Churchill Livingstone; 1985. p. 181–212. Ain MC, Shirley ED. Spinal fusion for kyphosis in achondroplasia. J Pediatr Orthop 2004;24(5):541–5. Thomeer RT, van Dijk JM. Surgical treatment of lumbar stenosis in achondroplasia. J Neurosurg 2002;96(3 Suppl): 292–7. Aldegheri R, Dall’Oca C. Limb lengthening in short stature patients. J Pediatr Orthop B 2001;10(3):238–47. Beals RK, Stanley G. Surgical correction of bowlegs in achondroplasia. J Pediatr Orthop B 2005;14(4):244–8. Tanaka H. PTH in the treatment of achondroplasia. Clin Calcium 2003;13(12):1582–5. Komatsu Y, Yasoda A, Chusho H, Nakao K. The possible novel treatment of achondroplasia, C-type natriuretic peptide (CNP). Clin Calcium 2003;13(12):1578–81.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 471–473
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CASE STUDY
Hip Adnan A. Faraj Department of Orthopaedics and Trauma, Airedale General Hospital, Skipton Road, Steeton, Keighley BD2 06T, UK
A 30-year-old bus driver presented to the Accident and Emergency department having been assaulted. On arrival, he had difficulty weight bearing but managed to limp into the department. He recalled being repeatedly kicked in the head and the right buttock and had been pushed down 12 stairs. He was complaining of right hip pain with tenderness and swelling over the greater trochanteric area. There was pain on all movements of the right hip. There were no chest or abdominal injuries.
Questions 1. What does the plain right hip AP X-ray show? (Fig. 1) 2. What further investigations do you suggest? 3. How would you manage this case?
Answers 1. Plain X-ray showed a fracture of the acetabular lip on the right side (Fig. 1). 2. Computerised tomography scan of the hip (Fig. 2). This confirmed a fracture involving the superior and anterior margin of the right acetabulum with two long thin main fragments 3.0 cm 0.6 cm and a small joint effusion. There was a degree of subluxation. Corresponding author.
E-mail address:
[email protected].
Figure 1
3. A case could be made for fixation of the acetabular fracture and reduction of the subluxation by an expert. However, it is obvious from both the plain X-ray and the CT scan that it is an unusual fracture and reconstruction might not be possible. This patient was managed with bed rest for 6 weeks followed by non-weightbearing mobilisation for a further 6 weeks and gradual weight bearing 12 weeks after injury.
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A.A. Faraj
Figure 2 Figure 3
However, his progress was hampered by symptoms of hip instability and groin pain. On pressing the accelerator of his bus, he felt the hip moving abnormally and causing pain.
Questions 1. How would you investigate this patient for his continuing problems with his right hip? 2. What do you think is the main source of pain? 3. What are the options? 4. What do you know about post-traumatic hip subluxation?
Answers 1. Plain films and an MRI scan. AP X-ray of the right hip 10 months after accident shows avascular necrosis and lateral acetabular impingement with early osteoarthritis (Fig. 3). Subsequently, MRI scan of the hip revealed avascular necrosis of the head adjacent to the weight-bearing part of the acetabular fracture (Fig. 4). Additionally there may be post-traumatic chondrolysis. 2. Thus, his symptoms are the result of early hip arthritis, osteonecrosis, and hip instability with impingement. 3. Reconstruction of the joint 10 months following the initial injury was thought unlikely to be beneficial and joint replacement was thought a better option. 4. Traumatic hip subluxation is a potentially devastating injury often misdiagnosed as a simple hip sprain or strain.1–3 Management is not easy.
Figure 4
Subluxation rather than complete dislocation most likely reflects lower energy injury. In the case of traumatic hip dislocation, prompt reduction is of paramount importance to decrease the risk of subsequent osteonecrosis,4 as reduction may relieve tension across the femoral and circumflex vessels. Despite the lowerenergy trauma seen in patients with traumatic hip subluxation, osteonecrosis can develop.5 Although the cause of osteonecrosis following hip subluxation is not completely understood, several studies have evaluated the effect of posterior dislocation on blood flow to the femoral head.5,6 In this case osteonecrosis developed, with extensive joint space narrowing over a 6-month period without subchondral collapse, indicating chondrolysis in addition to
ARTICLE IN PRESS Hip
473
osteonecrosis. Post-traumatic chondrolysis could be explained by ischaemia brought about by increased capsular pressure immediately following injury rather than later collapse of the head of femur.7 Thus, several authors have suggested acute aspiration of the hip to reduce the incidence of osteonecrosis. However, this is still controversial,8 e.g. how can intra-articular pressure be elevated when the fractured acetabular rim creates an opening of the hip joint? Indeed, it is debatable whether early management will alter the progress of the joint damage.
Question 1. What type of arthroplasty would you choose in a patient who is only 30?
Answer The outstanding problem in the young active patient who undergoes total hip replacement (especially in males) is a high rate of loosening. Cemented total hip replacements have relatively good outcomes, particularly in the short term. In one study 90% of hips implanted were still functioning at 15 years of follow-up. However, at 20–25 years of follow-up, successful results drop to 70–75%. Uncemented prostheses, once the bone/prosthesis has bonded, are unlikely to loosen. As to bearing surfaces, alumina-on-alumina seems to be one of the best choices in young and active patients, provided that sound socket fixation is maintained in the long term. Total hip resurfacing has become popular, as it is associated with a lower incidence of hip dislocation and preserves bone stock, but follow-up is still short. We felt in our patient this was the best option available. There were concerns about failure because of the avascular necrosis of the head, the level of activity and the age of the patient. To date, 3 years later, the patient is still fine and still works full time as a bus driver (Fig. 5).
Figure 5 AP X-ray of the hip 6 months after surface replacement.
References 1. Brink O, Vesterby A, Jensen J. Pattern of injuries due to interpersonal violence. Injury 1998;29(9):705–9. 2. Cooper DE, Warren RF, Barnes R. Traumatic subluxation of the hip resulting in aseptic necrosis and chondrolysis in a professional football player. Am J Sports Med 1991;19:322–4. 3. Moorman III CT, Warren RF, Hershman EB, Crowe JF, Potter HG, Barnes R, et al. Traumatic posterior hip subluxation in American football. J Bone Jt Surg Am 2003;85-A(7):1190–6. 4. Dreinhofer KE, Schwarzkopf SR, Haas NP, Tscherne H. Isolated traumatic dislocation of the hip. Long-term results in 50 patients. J Bone Jt Surg Br 1994;76:6–12. 5. Poggi JJ, Callaghan JJ, Spritzer CE, Roark T, Goldner RD. Changes on magnetic resonance images after traumatic hip dislocation. Clin Orthop 1995;319:249–59. 6. Soto-Hall R, Johnson LH, Johnson RA. Variations in the intraarticular pressure of the hip joint in injury and disease: a probable factor in avascular necrosis. J Bone Jt Surg Am 1964;46:509–16. 7. Harper WM, Barnes MR, Gregg PJ. Femoral head blood flow in femoral neck fractures. An analysis using intra-osseous pressure measurement. J Bone Jt Surg Br 1991;73:6. 8. Yue JJ, Wilber JH, Lipuma JP, Murthi A, Carter JR, Marcus RE, et al. Posterior hip dislocations: a cadaveric angiographic study. J Orthop Trauma 1996;10:447–54.
ARTICLE IN PRESS Current Orthopaedics (2005) 19, 474–477
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Radiology quiz Case 1. History 24-year-old man with knee pain (Fig. 1a and b).
History 68-year-old man with 4-month history of neck pain. No history of trauma (Fig. 2).
Question 1 (1) What are the images? (2) What is the diagnosis?
Figure 1 0268-0890/$ - see front matter doi:10.1016/j.cuor.2005.07.001
Question 2 (1) What is the investigation? (2) What is the abnormality?
Figure 2
ARTICLE IN PRESS Radiology quiz
475
History
History
30-year-old man with a non-traumatic painful hip (Fig. 3a and b).
56-year-old man with knee pain and history of alcohol abuse (Fig. 4).
Figure 4
Question 4 Figure 3
Question 3 (1) What is the investigation? (2) What is the abnormality?
(1) What is the diagnosis on the lateral radiograph of the knee?
ARTICLE IN PRESS 476
Radiology quiz
History
History
15-year-old female with lower limb muscle atrophy and club foot (Fig. 5a and b).
72-year-old man with a 3 month history of back pain (Fig. 6).
Figure 5
Question 5 (1) What is the investigation? (2) What is the diagnosis?
Figure 6
Question 6 (1) What is the abnormality on the lateral radiograph of the lumbar spine?
ARTICLE IN PRESS Radiology quiz
477
Answer 1
Answer 4
(1) The images are coronal and sagittal proton density magnetic resonance images of the knee. (2) An oblique tear of the posterior 13 of the medial meniscus with an associated para-meniscal cyst.
There is a well defined densely sclerotic lesion with serpiginous borders in the medullary cavity within the proximal tibia. The findings are consistent with a bone infarct. The differential diagnosis includes a cartilage tumour. Any pathology that leads to vessel occlusion can result in bone infarcts. This includes sickle cell anaemia, vasculitis, corticosteroid use and ethanol abuse.
Para-meniscal cysts most commonly occur in the anterior horn of the lateral meniscus or the posterior horn of the medial meniscus. They vary in size and can exceed 1 cm. They can be loculated. They occur due to joint fluid being forced though a meniscal tear. There is a ball valve effect allowing accumulation of fluid within the cyst.
Answer 2 (1) Lateral radiograph of the cervical spine. (2) There is almost complete bony destruction of C7 with prominent pre-vertebral soft tissues. This patient was known to have myeloma. Classically spinal myeloma spares the posterior elements of the vertebrae due to lack of red marrow. Extra-dural extension with prominent paraspinal soft tissues can be a feature. As the process is one of destruction with little osteoblastic activity, bone scans are relatively insensitive with approximately only 10% of lesions visible compared to 30% with plain radiographs.
Answer 3 (1) Antero-posterior radiograph of the pelvis and a T1 weighted coronal image of the pelvis. (2) There are erosions seen on both sides of the left hip joint. The T1 weighted MR image shows that these are due to synovial masses that are of low and intermediate signal. The low signal is due to haemosiderin. The diagnosis is pigmented villonodular synovitis (PVNS). PVNS usually affects a single large joint, most commonly the knee. Bony pressure erosions are present in approximately 50% of cases. PVNS is a highly vascular synovial proliferation. There is repeated haemorrhage with the formation of haemosiderin which is of low signal on all MRI sequences.
Answer 5 (1) Sagittal and axial T2 weighted MR image of the lumbar spine (2) Diastematomyelia. There are 2 hemicords separated by a bony spur at L2. This is a congenital abnormality of the notochord. The 2 hemicords are either covered with a single meningeal sheath, or each has its own arachnoid/dural sheath. In the latter either a bony spur is present (in 75%) or there is a fibrous band (25%). Other associated abnormalities are myelomeningocele, congenital scoliosis due to vertebral anomalies (block, butterfly and hemivertebrae), tethered cord and multi-level spina bifida.
Answer 6 There is a ureteric stent in situ. L3 and L4 are diffusely sclerotic. The findings are suggestive of metastatic prostatic carcinoma. Densely sclerotic vertebrae are described as ivory vertebrae. The differential includes, metastases (breast, prostate or an initially lytic metastasis that has been treated), lymphoma, Paget’s disease and haemangioma. The ureteric stent favours the diagnosis of prostatic metastatic disease with associated treated ureteric obstruction. M Shaw, C Wakeley Department of Radiology Bristol Royal Infirmary Marlborough Street Bristol, BS1 3NU UK E-mail address:
[email protected] (M Shaw)
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CME SECTION
Three external CME points available The following series of questions are based on the CME designated article for this issue—‘Novel treatments for early osteoarthritis of the knee’ by S.P. Krishnan and J.A. Skinner. Please read the article carefully and then complete the self- assessment questionnaire by filling in the square corresponding to your response to each multiple-choice question. For true or false questions, please fill in one square only. After completing the questionnaire, either post or fax the answer page back to the Current Orthopaedics Editorial Office at the address at the bottom of the RESPONSE sheet. Please photocopy this page if you wish to keep your copy of Current Orthopaedics intact. Replies received before the next issue of Current Orthopaedics is published will be marked and those reaching an adequate standard will qualify for three external CME points. You will be notified of your marks and a CME certificate will be despatched for your records.
Questions 1. Which of the following treatments has been shown in vitro to stimulate cartilage growth? A. High-frequency, low-intensity transcutaneous nerve stimulation (TENS) B. Low-frequency, high-intensity TENS C. Electromagnetic fields D. 1.0 MHz ultrasound E. Low-level laser therapy 2. Which of the following modalities relies principally on the generation of heat in treated tissue for its effect? A. High-frequency, low-intensity transcutaneous nerve stimulation (TENS) B. Low-frequency, high-intensity TENS C. Electromagnetic fields D. 1.0 MHz ultrasound E. Low-level laser therapy 3. What is the main current concern about the long-term use of COX2 inhibitors, in particular
doi:10.1016/j.cuor.2005.10.006
Rofecoxib, which has been withdrawn from the market? A. Tolerance B. Addiction C. Interactions with intra-articular preparations of steroid D. Increased risk of myocardial infarction and stroke E. CNS side effects 4. Which of the following best describes Glucosamine? A. B. C. D. E.
It is a hexosamine Keratan sulphate is a typical glucosamine It is a protreoglycan It is a glycoprotein It is a glycosaminoglycan
5. Which of the following is NOT a likely mechanism of action of glucosamine? A. Stimulation of cartilage matrix production B. Downregulation of the production of proteolytic enzymes
ARTICLE IN PRESS CME SECTION C. Inhibition of lysosomal enzyme release D. Improve the characteristics of synovial fluid E. Antiinflammatory properties 6. In which category of patients should the use of glucosamine be restricted until proper studies have been conducted to detect possible adverse effectsstudies? A. B. C. D. E.
Migraine sufferers Those with lymphoedema Those with inflammatory bowel disease Diabetics Epileptics
7. How long does an intra-articular injection of hyaluronic acid stay in the joint? A. B. C. D. E.
30 min 2h 2–3 days 2–3 weeks 2–3 months
8. If a patient with osteoarthritis is being treated by viscosupplementation and has a moderate effusion in the joint that has not altered in size for several weeks and is not associated with systemic symptoms or upset, what is the correct course of action? A. Aspirate the effusion and inject the hyaluronic acid derivative B. Inject the hyaluronic acid derivative into the effusion C. Aspirate the effusion, culture it and if cultures are negative at 48 h inject the hyaluronic acid derivative D. Inject the hyaluronic acid derivative with antibiotic cover E. Hyaluronic acid derivative viscosupplementation is contra indicated
479 9. Which of the following is a pharmacological effect of corticosteroids? A. Enhanced immune cell migration B. Increase apoptosis of immature and activated T lymphocytes C. Enhanced activation of immune cells D. Upregulation of pro-inflammatory cytokine production E. Facilitation of macrophage presentation to lymphocytes 10. Which of the following is not a good predictor of a successful result from arthroscopic debridement for early osteoarthritis of the knee? A. The presence of unstable chondral flaps on arthroscopy B. Medial joint line tenderness pre-op C. Positive Steinman test D. Presence of an unstable meniscal tear E. Osteophytes at the lateral edge of the patellofemoral groove 11. Up to how long has autologous chondrocyte implantation been shown to improve clinical outcome for patients with early knee arthritis? A. B. C. D. E.
3–6 months 1 year 5 years 10 years 20 years plus
12. Upon which trace element do the matrix metalloproteinases depend for their activity? A. B. C. D. E.
Iron Zinc Magnesium Manganese Selenium
ARTICLE IN PRESS 480
CME SECTION
Please fill in your answers to the CME questionnaire above in the response section provided below. A return address and fax number is given at the bottom of the page. ....................................................................................
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CME SECTION
Answers to CME questions in Vol. 19, issue 4 Please find below the answers to the Current Orthopaedics CME questions from Vol. 19, issue 4 which were based on the article—‘Resurfacing arthroplasty of the hip’ by P. Roberts, P. Grigoris, H. Bosch and N. Talwaker. 1 A&
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doi:10.1016/j.cuor.2005.07.002
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ERRATUM
Erratum to ‘‘Resurfacing arthroplasty of the hip’’ [Current Orthopaedics (2005) 263–279] Paul Robertsa,, Peter Grigorisb,c, Hendrik Boschd, Nilesh Talwakerd a
Royal Gwent Hospital, Cardiff Road, Newport, NP9 2UB, UK Department of Medical Engineering, School of Engineering, Design and Technology, University of Bradford, Richmond Road, Brardford, West Yorkshire, BD7 1DP, UK c 2nd Orthopaedic Department, University of Athens, Ag. Olga Hospital, 142 33 N. Ionia, Athens, Greece d Department of Orthopaedics and Trauma, Royal Gwent Hospital, Cardiff Road, Newport, NP9 2UB, UK b
The publisher regrets that an error occurred in Table 4. Two points are given for a weight of o82 kg and not 482 kg. We apologise for any inconvenience caused.
DOI of original article: 10.1016/j.cuor.2005.05.004
Corresponding author. Tel.: +44 1633 238917; fax: +44 1633 656293.
E-mail address:
[email protected] (P. Roberts). 0268-0890/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.cuor.2005.10.009
Author Index A ADERINTO J, 59 AGARWAL S, 373 ALAM A, 27, 34 AMIRFEYZ R, 309, 467 ANJUM SN, 40 ANWAR R, 40 ATKINS R,155
FRANCO V, 415 FUNK L,135, 209 G
B BACCI G,119 BARBOSA K,135 BARRON D, 20 BELLEMANS J, 446 BHANDARI M, 327 BIANCHI G, 393 BOSCH H, 263, 482 BRADLEY K, 34 BRENKEL IJ, 59 BRICCOLI A, 305 BRIGGS PJ, 85 BRITTENDEN J,13 BUMBASIREVICØ M, 49, 314 BUMBASIREVIC V, 314
GARDNER ER, 385 GARGAN M, 309, 467 GARNAVOS C, 294 GEORGE S,1 GIANNI E, 415 GIANNOUDIS PV, 345 GOOSEN JHM, 288 GRAYA,1 GRIGORIS P, 263, 482 H HARRISON JWK,190 I INGHAM E, 280 IOLI JP, 379 J
C JANE MJ, 68, 215 JIN ZM, 280 JOHNSON EO, 453
CALLEJA M, 34 CASTELEIN RM, 288 CERULLO G, 415 CHAN PKH, 59 CHIODO CP, 379 CIPOLLA M, 415 CLARKC, 309 COL ANGELI M, 393 COLQUHOUN K, 27 COMPSON J,171,180
K KARAMARKOVIC A, 314 KATSOULIS E, 345 KEATING J, 362 KEEL M, 334 KEENE GCR, 428 KRISHNAN SP, 407 D L
DEWEY P,1 DI BELLA C, 393 DONATI D, 393 DRAKOULAKIS E, 345 DREGHORN CR, 385
LAING P, 94,101 LEARMONTH ID, 255 LESICØ A, 49, 314 LONGHI A,119 F
FAHMY NRM,190 FARAJ AA, 471 FISHER J, 280 FORSTER MC, 428
M MACEWEN GD, 223 MACNICOL MF, 461 MAKWANA NK,108, 231 MCBRIDE A,155
II
CURRENT ORTHOPAEDICS
MCBRIDE DJ, 94,101 MCCARTHY JJ, 223 MCKIE S,13 MCMASTER J,140 MERCURI M, 393 MOHANDAS P, 247 MUIRHEAD-ALLWOOD S, 247
SCOTT BW, 373 SETOLA E,119 SHARMA H, 68, 215, 385 SHAW M, 474 SIDDIQUI NA, 247 SINGH SK, 379 SKINNER JA, 407 SOUCACOS PN, 453 N
NICHOLL JE, 40 NUTHALLT, 247
T
O OHLY NE, 461
TALWAKER N, 263, 482 TIPPER JL, 280 TORRENS MJ,127 TRENTZ O, 334
P V PETRISOR BA, 327 POWELL J,140 PUDDU G, 415 R RAMAMURTHY C, 94,101 RANKINE JJ, 326, 404 REDDY RS,171,180 REID R, 215 ROBERTS CS, 354 ROBERTS P, 263, 482 ROBERTSON, A, 406 ROBINSON P,196 ROCCA M, 305
VAN LIEFLAND MR, 231 VANDENNEUCKER H, 446 VANLAUWE J, 446 VERHEYEN CCPM, 288 VERSARI M,119
W WAKELEY C, 474 WILSON D, 27, 34
S Y SALONE M, 305 SCOLES PV, 223
YERASIMIDES J, 354
Subject Index A Acetabular fractures,140 Anatomy, 40 Angiographic embolisation, 334 Arthroplasty, 446 Arti¢cial discs,127 Assessment,140 Associated injuries, 327
Excision arthroplasty, 385 Extensor mechanism injuries, 49 External ¢xation, 362 F
B Biotechnology, 453 Bone, 68 Bone tumour, 393
Femoral component, 255 Foot, 40, 85 Forearm injury, 373 Fracture, 85, 231, 354 FractureFdislocation,108 G Genitourinary, 354 Giant cell tumour of the tendon sheath, 215 Girdlestone operation, 385
C Calcaneal fractures, 94,101 Calcaneocuboid, 85 Cancer,1 Carpal bones,171,180 Causalgia,155 Cerebral palsy, 461 Cervical arthroplasty,127 Cervical spondylosis,127 Classi¢cation,140,190 Clearance, 280 Clinical features,190, 309 Clinical ¢ndings, 40 Clubfoot, 461 Complex regional pain syndrome,155 Complications, 94,101,140 Computed tomography, 20 Conservative arthroplasty, 255 Conservative treatment, 407 Cuboid, 85 Cuneiform, 85
H Hallux £exus, 461 Head diameter, 280 Hindfoot dislocations, 94,101 Hindfoot fractures, 94,101 Hip, 223, 247, 385 Hip arthritis, 255 Hip arthroplasty, 59, 263 Hip resurfacing, 263 Humeral nails, 294 I Incidence, 327 Infection, 59 Injuries, 49 Instability, 223 Internal ¢xation, 362 Intramedullary nailing, 294 Ionising radiation,1
D Damage control, 334 Delayed de¢nitive surgery, 334 Developmental, 223 Diabetes, 59 Diaphyseal humeral fracture, 294 Disc prostheses,127 Dislocation, 85, 223 Distal radio-ulnar joint,180 Dorsal bunion, 461 Dyspareunia, 354 Dysplasia, 223
K Kinematics, 280 Knee, 407 Knee arthroplasty, 59 L Life-saving surgery, 334 Ligaments,196 Lisfranc,108 Lubrication, 280 M
E Early total care, 334 Elbow dislocation, 373 Elbow injury, 373 Epidemiology, 327
Magnetic resonance imaging,13 Management, 94,101, 345 Massive allograft, 393 Mechanical axis, 415 Metal-on-metal, 263, 280
IV
CURRENT ORTHOPAEDICS
Metastatic osteosarcoma, 305 Metastatic soft tissue sarcoma, 305 Metatarsal, 85 Metatarsalgia, 379 Metatarsophalangeal, 85 Midcarpal joint,180 Midfoot fracture, 231 Minimally invasive knee arthroplasty, 428 Minimally invasive surgery, 247 Monitoring, 288 Monteggia fracture, 373 Mortality, 327, 345 Morton’s neuroma, 379 MR Arthrography,196 MR Imaging,196 MRI physics,13 MRI safety,13 MRI sequences,13 Multiple organ failure, 314 Musculoskeletal, 20, 27, 34 N Navicular, 85 Non-operative treatment,140 Nuclear medicine, 34 O Open pelvic fractures, 345 Opening wedge, 415 Operative treatment,140 Orthopaedic,13 Os calcis, 85 Os Calcis fractures, 94,101 Osteoarthritis, 415 Osteosarcoma, 68 Osteotomy, 415 Outcome, 59,140, 345 Overview, 446
Radio-carpal joint,180 Radiotherapy, 215 Reconstruction, 393 Recurrence, 215 Re£ex sympathetic dystrophy,155 Release, 379 Resection arthroplasty, 385 Review,140 S Sarcomatous degeneration, 68 Second look, 334 SED, 309 SEDC, 309 SEDT, 309 Sepsis, 314 Sesamoids, 40 Spondyloepiphyseal dysplasia, 309 Stress fracture, 231 Subtalar, 85 Surface anatomy,171 Surgeon,1 Surgery, 255, 379 Surgical approaches,140 Surgical technique,140 Survival, 68 Synovectomy, 215 Systemic in£ammatory response, 314 T
P Paget’s disease, 68 Patella fractures, 49 Patellar tendon, 49 Pavlik harness, 223 Pelvic C-clamp, 334 Pelvic fractures, 327, 362 Pelvic packing, 334 Pelvic ring, 362 Pelvic ring fracture, 334 Pelvic ring injury, 345 Pelvis, 354 Periacetabular osteolysis, 288 Peri-traperial arthritis,190 Physics, 20, 27, 34 Pigmented villonodular synovitis, 215 Plantar aponeurosis, 85 Polyethylene wear, 288 Primary osteoarthritis, 407 Pulmonary metastases, 305 Q Quadriceps tendon, 49
Talonavicular, 85 Talus, 85 Talus fractures, 94,101 Tarsal fracture, 231 Tarsometatarsal, 85 Tarsometatarsal injury,108 Therapy, 314 Tissue engineering, 453 Tissue regeneration, 453 Tissue replacement, 453 Total disc replacement,127 Total hip arthroplasty, 288 Total hip replacement, 247 Total knee replacement, 446 Trauma, 314, 327 Treatment, 40,190, 288, 309 Triangular ¢brocartilage complex,180 Tribology, 263 U Ultrasound, 27,196 Unicompartmental knee arthroplasty, 428 Unicompartmental knee replacement, 428 Urethral tears, 354 V Vacuum-assisted closure, 334 W Wear particles, 280 Wrist,196 Wrist examination,171,180
R Radial head dislocation, 373 Radiation protection,1
X X-ray,1 X-ray ¢ndings, 40
