ORTHOPEDICS e d i t e d
Mikl6s
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Szendr6i
Semmelweis Publisher www.semmelweiskiado.hu
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ORTHOPEDICS e d i t e d
Mikl6s
�
@
b y
Szendr6i
Semmelweis Publisher www.semmelweiskiado.hu
B
u
d
a
p
e
st
, 2008
We would like to express our great thanks for the donations of our sponsors Dimenzi6 Egeszsegpenztar, Dimenzi6 Biztosit6 Egyesiilet, Berlin-ChemieIA.Menarini Kft. , ScanMedic Kft., Mr. Gyorgy Laszl6 whi ch enabled us to publish this book. Editor and authors Instru ctor in orthopaedi cs :
Pro! Tibor Vizkelety, M.D., Ph.D . , D . S c Orthopaedi c Department Semmelweis University, Budapest Pro! Kalman Szepesi, M.D., Ph.D., D.S c Orthopaedi c Depar tment University of Debre cen, Hungary
Language master:
Dr. David Durham
Translator:
Dr. Andras Vajda, M.D. Orthopaedi c Department Semmelweis University, Budapest George Szoke M.D., M . S c. (Oxon), Ph.D. Head of Pediatri c Orthopaedi c Department Department of Orthopaedi cs Semmelweis University, Budapest Tamas de Jonge M.D., Ph.D. Head of Orthopaedi c Department Markusovszky Hospital, Szombathely, Hungary
Photographer
Peter Kovacs Orthopaedi c Department Semmelweis University, Budapest
. © Mikl6s Szendroi, 2008
ISBN 978 963 9656 93 2 All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or trasnmitted in any from or by any means, electronic, mechanical, photocopyring, recording or otherwise, without either prior permission of the publishers. Semmelweis Publisher 1089 Budapest, Nagyvarad ter 4. www.semmelweiskiado.hu
Responsible editor: L asz 16 T an cos Editor-in- chief, layout: Judit Vin cze Illustrations : Csilla Koszeghy Cover design : L asz 16 T an cos SKD 1 75 Printed by Gyomai Kner Printing House Zrt., in Hungary Responsible exe cutive : Lajos Papp CEO
Editor: Pro! Mikl6s Szendroi, M.D., Ph.D., D.Se. Head of Orthopaedi c Department Semmelweis University, Budapest Authors: Pro! ArpQd Bellyei, M.D., Ph.D., D. Se. Orthopaedi c Department University of Pe cs, Hungary Pro! Tamas Bender, M.D., Ph.D. Poly clini c of the Hospitaller Brothers of St. John of God, Budapest Laszl6 Bucsi, M.D., Ph.D. Head of Orthopaedi c Department St. George Hospital, Szekesfeherv ar, Hungary Associate Pro! Zoltan Csernatony, M.D., Ph.D. Head of Orthopaedi c Department University of Debre cen, Hungary Pro! Laszl6 Hangody, M.D., Ph.D., D.Se. Head of Orthopaedi c Department Uzsoki Hospital, Budapest Pro! Tamas !llb, M.D. , Ph.D., D. Se. Head of Orthopaedi c Department University of Pe cs, Hungary Jeno Kiss, M.D. , Ph.D. Head of Orthopaedi c Department St. John Hospital, Budapest Katalin Kolto, M.D. Radiologist Orthopaedi c Department Semmelweis University, Budapest Pro! Janos Kranicz, M.D., Ph.D. Head of Orthopaedi c Department University of Pe cs, Hungary Prof. Lajos Kullmann, M .D ., Ph.D. Medi cal Rehabilitation Institute, Budapest Associate Pro! J6zsejLakatos, M.D., Ph.D. Orthopaedi c Department Semmelweis University, Budapest
Associate Pro! Ferenc Mady, MD., Ph.D. Orthopaedi c Department Semmelweis University, Budapest Associate Pro! Adam Mester, MD., Ph.D. Radiologist Radiologi c Department Semmelweis University, Budapest Pro! Tamas Meszaros, MD., Ph.D. Orthopaedi c Department University of Szeged, Hungary Pro! Gyula Poor, MD., Ph.D. Head of Rheumatology Department Semmelweis University, Budapest Pro! Miklos Szendroi, MD., Ph.D., D.Sc Head of Orthopaedi c Department Semmelweis University, Budapest Pro! Kalman Toth, MD., Ph.D. Head of Orthopaedi c Department University of Szeged, Hungary Peter Pal Varga, MD. Head of National Spine Centre, Budapest Pro! Tibor Vizkelety, MD., Ph.D., D.Sc Orthopaedi c Department Semmelweis University, Budapest
Contents
Preface . . . . . . . . . . . . . . . . . . . . . . . . . . .
. . . . . XVII
1.
History and subj e ct of orthopedi cs (Tibor Vizkelety) .
2.
Stru cture and development of bones (Zoltcm Csernatony) . 2 . 1 . Stru cture of bones . . . . . . . . . . . 2 . 1 . 1 . The composition of bone . 2 . 1 .2 . The bone tissue . . . . . . 2 . 1 .3 . Bones as organs . . . . . 2 . 1 .4. The development and growth of bones . 2.2. Biologi cal adaptation of bones . . . . . . . 2 . 3 . Hormones regulating the bone metabolism . . . . .
3.
Bone healing after various types of fra ctures (Mikl6s Szendroi) . . . . . . . 3 . 1 . Traumati c fra ctures . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 .2 . Fra cture healing. Types and stages. Factors influen cing fra cture healing 3 . 3 Pathologi cal fra cture healing. Pseudo-arthrosis . 3 .4. Pathologi cal fra ctures . 3 . 5 . Stress fractures . . . . . . . . . . . . . . . . .
11 11 11 13 14 16
4.
Examination methods in orthopedi cs (Katalin Kollo, Adam Mester, Tamas Meszaros) 4. 1 . Case history (anamnesis) . 4.2. Examination. . . . . . . 4.2. 1 . Inspe ction . . 4.2.2. Palpation . . . 4.2 . 3 . Alignment, axial deformities of the limbs. 4.2.4. Examination of the j oints . . . . . 4.2 . 5 . Range of motion of j oints (ROM) . 4.2.6. Assessment of mus cle power . 4.2.7. Assessment of mus cle tone . . . . 4.2 . 8 . Limb length assessment . . . . . . 4.2.9. Measurement of limb circumferen ce 4.3 . The standing position and the gait 4.3 . 1 . Standing position 4 . 3 . 2 . Gait . . . . . . 4 .4 . Limping . . . . . . . . . . . 4 . 5 . Neurologi cal examinations . 4.6. Laboratory tests . 4.7. Arthros copy . . 4 . 8 . Histology tests .
17 17 19 19 19 20 20 24 25 25 25 27 27 27 28 30 31 31 32 32
5 5 5 5 7 7 7 9
VIII
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4 .9. Imaging modalities . . . . . . . . . . . . . . . . . . 4 . 9 . l . X-ray tests, spe cial X-ray investigations 4.9.2. Mus culoskeletal ultrasonography : 4 . 9 . 3 . Isotope pro cedures 4.9.4. CT s canning . . . . . . . . . . . 4 . 9 . 5 . MRI . . . . . . . . . . . . . . . . 4.9.6. Invasive and interventional radiology .
32 32 35 36 37 38 38
5.
Surgi cal therapy i n orthopedi cs (Tamas Meszaros) . 5 . 1 . Mus cle - tendon operations . 5 .2 . Fas cia surgery . . . . 5 . 3 . Bone operations . . . 5 .4. Operations on j oints . 5 . 5 . Arthroplasty . . . . . 5 . 6 . Operation on nerves .
41 41 42 42 42 44 47
6.
Conservative treatment pro cedures (Zoltan Csernatony) . 6 . 1 . Immobilization . . . 6 . 2 . Mobilization . . . . 6 . 3 . Non-weight-bearing . 6.4. Irradiation . . . . . . 6 . 5 . Laser therapy . . . . 6 . 6 . Pharma ceuti cal treatment .
49 49 51 51 51 51 51
7.
Physiotherapy (Tamas Bender) 7 . l . Exercises . . . . . . . . . 7 . 2 . Immobilization, mobilization, exer cises 7 . 3 . Massage . . . . . . . . 7.4. Ele ctrotherapy . . . . . . . . . . . 7 . 5 . Ultrasound treatment . . . . . . . . 7 . 6 . Pulsating ele ctromagneti c treatment 7 . 7 . High-frequen cy treatment 7 . 8 . Cryotherapy . . . . . . . . 7 . 9 . Balneotherapy-health spas 7 . 1 0. Compresses and pa cks . .
57 57 58 59 59 60 60 60 61 61 62
8.
Manual therapy, acupun cture ( Tamas Bender)
63
9.
Amputation - artifi cial limbs (Lajos Kullmann) 9 . 1 . Lower limb amputation . . . . . . . . . . . 9 . l . l . Indi cations of lower limb amputations 9 . l .2 . Surgi cal te chnique of amputations 9 . l .3 . Criteria of proper stump . 9 . 2 . Lower limb prostheses . . . . . . . 9 . 2 . 1 . Temporary prostheses . 9.2.2. Final prosthesis . . . 9 . 3 . Upper limb amputation . . . . . . 9.4. Upper limb prosthesis appli cation 9.4. 1 . Cosmeti c prostheses .
65 65 65 66 66 68 68 69 70 70 71
Co n t e n s
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IX
9.4.2. Me chani cal prostheses . . . . . . . . 9.4. 3 . Prostheses powered by external force . Orthoses, applian ces for mobility (Lajas Kullmann) 1 0. 1 . Lower limb orthoses . . . . . . . . 1 0. 1 . 1 . Ankle - foot orthoses . . . . . 1 0. 1 .2. Knee orthoses . . . . . . . . 1 0. 1 .3 . Knee - ankle - foot orthoses . 1 0. 1 .4. Hip orthoses . . . . . . . . . 1 0. 1 .5 . Hip - knee - ankle - foot orthoses 1 0.2. Upper limb orthoses . . . . . . . . 1 0. 3 . Spinal orthoses . . . . . . . . . . . . . . . 1 0. 3 . 1 . Lumbosa cral orthoses . . . . . 1 0. 3 .2 . Thora co-Iumbo-sa cral orthoses 1 0. 3 . 3 . Cervi co - thora co - lumbo - sacral orthoses . 1 0.3 .4. Cervi cal orthoses . 1 0.4. Preventive sport applian ces . 1 0. 5 . Walking aids . . . . . . . . 1 0. 5 . 1 . Walking sti ck . 1 0. 5 . 2 . Crut ch . . . . . 1 0. 5 . 3 . Walking frame . 1 0. 5 .4. Wheel chair . . .
71 72 73 74 74 74 74 74 75 75 76 76 76 77 77 77 77 77 77 78 78
1 1.
Orthopedi c shoes and insoles (Kalmim T6th) . 1 1 . 1 . Shoes and orthopedi c shoe 1 1 .2. Shoes for children . . 1 1 . 3 . Shoe and sole insoles . . .
81 81 82 83
1 2.
Normal growth, growth disturbances (Kalman T6th) . 1 2 . 1 . Physiologi cal growth . . . . . . . . . . . . . 1 2 .2. Growth disturban ces . . . . . . . . . . . . . . . 1 2 .2. 1 . Treatment options for growth disturban ces 1 2 . 3 . Limb deformities . . . . . . . . . . . . . . . . . . . .
85 85 86 87 88
Bone dysplasias and developmental anomalies (Tibar Vizkelety) . 1 3 . 1 . Frequently o ccurring osteo chondrodysplasias . . . . . . . 1 3 . 1 . 1 . Skeletal dysplasias with predominant metaphyseal involvement . 1 3 . 1 .2 . Skeletal dysplasias with predominant epiphyseal involvement . 1 3 . 1 .3 . Skeletal dysplasias with maj or involvement of the spine . . . 1 3 . 1 .4. Dysostosis multiplex, complex carbohydrate storage diseases 1 3 . 1 .5 . Skeletal dysplasias with de creased bone density . . . . . . . 1 3 . 1 .6. Skeletal dysplasias with in creased bone density . . . . . . . . 1 3 . 1 .7 . Skeletal dysplasias due to the disorganized development of bone constituens . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
89 90 90 92 92 93 93 95
1 0.
.
13.
1 4.
Metaboli c diseases of the bone (Laszl6 Bucsi) . 1 4. 1 . Osteoporosis . . . . . . . . . . . . . . . 1 4.2. Osteomalacia (mollities ossium) . . . . 1 4.2. 1 . Ra chitis (ri ckets, avitaminosis D)
97 101 101 1 05 1 06
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Co n t e n s
1 4.2.2. Vitamin D resistant ra chitis (Fan coni syndrome, phosphate diabetes) . . . . . . . . . . . . . . . . . . . . . . . . . 1 4 . 3 . Hormonal metaboli c bone diseases . . . . . . . . . . . . . . . . . 1 4 . 3 . 1 . Hyperparathyroidism (Osteodystrophia fibrosa cysti ca generalisata, von Re cklinghausen ' s disease) . . . . . . 1 4 . 3 . 2 . Hypogonadism (Adiposogenital dystrophy, Frohli ch ' s disease) . 1 4. 3 . 3 . Cushing' s disease . . . . . . . . . . . . . . . . . . . . . . . . . 15.
Developmental anomalies o f the extremities (Tibor Vizkelety) . . . . . . . .
1 6.
Neuromus cular diseases (Tibor V izkelety) . . . . . . . . . . . . . . 1 6. 1 . Spinal dysraphisms, myelodysplasia . . . . . . . . . . . . . . . 1 6. 1 . 1 . Meningo cele, myelomeningo cele, myelodysplasia. 1 6.2. Cerebral palsy (infantile cerebral paresis, Little disease) . . . . 1 6. 3 . Poliomyelitis (poliomyelitis anterior a cuta, Heine-Medin disease) 1 6.4. Developmental anomalies and diseases of the mus cle system . 1 6.4. 1 . Congenital mus cle absen ces . . . . . . . . . . 1 6.4.2. Mus cular dystrophy . . . . . . . . . . . . . . . 1 6.4. 3 . Myopathies due to inflammation, polymyositis . 1 6.4.4. Myositis ossifi cans progressiva (fibrodysplasia ossifi cans progressiva) . . . . . . . . . . . . . . . . . . . . . . 1 6.4.5 Arthrogryposis (arthrogryposis multiplex congenita) . 1 6.4.6. Congenital laxity of the joints . . . . . . . . . . . .
.
.
.
1 08 1 08 1 08 1 09 1 09 . 111 1 15 1 15 1 15 1 18 1 22 1 23 1 23 1 23 1 25 1 25 1 25 1 26
1 7.
Tunnel syndromes (Zoltim Csernatony) . . . . . . . . . . . . . . . . . . . . . . . . 1 27
1 8.
Disorders of tendons, tendon sheaths, bursae, fas ciae and ligaments (Zoltan Csernatony) . . . . . . . . . . . . . . . . . . 1 8 . 1 . Disorders o f the tendons . . . . . . . . . . . . . 1 8 .2. Illnesses o f the paratenon and the tendon sheath 1 8 . 3 . Diseases o f the bursae . 1 8 .4. Illnesses of fas cia. . . . 1 8 . 5 . Disorders of ligaments .
1 9.
Diseases of joints (Zoltan Csernatony, JozsejLakatos, Tamas Meszaros, Gyula Poor, Miklos Szendroi) . . . . . . . 1 9. 1 . The stru cture of the joints . . . . . . 1 9.2. The biome chani cal aspe cts of j oints . 1 9. 3 . Arthritis . . . . . . . . . . . . . . . 1 9. 3 . 1 . Autoimmune lo comotor diseases . 1 9. 3 . 1 . 1 . Rheumatoid arthritis . . 1 9. 3 . 1 .2 . Polysystemi c auto immune diseases affe cting the lo comotor organs . . . . . . . . . . . . . 1 9. 3 . 2 . Seronegative spondarthritis . . . . . . . . . . . . . . . 1 9. 3 . 2 . 1 . Spondylitis ankylopoeti ca ( ankylosing spondylitis) 1 9. 3 .2 .2 . Other forms of seronegative spondarthritis (SNSA) . 1 9. 3 . 3 . Juvenile chroni c arthritis . 1 9. 3 .4. Crystal-indu ced arthritis 1 9. 3 .4. 1 . Gout . . . . . . .
135 135 136 1 36 1 37 137
1 39 1 39 1 40 1 40 1 40 141 1 44 1 44 1 44 1 47 1 48 1 49 1 49
Co n t e n s
�
XI
1 9. 3 .4.2. Other forms of crystal indu ced arthritis 1 9.4. Arthropathies . . . . . . . . . . . . . 1 9.4. 1 . Neurogeni c arthropathy . 1 9.4.2. Hemophili c arthropathy 1 9. 5 . Performing surgery in arthritis . . . . 1 9.6. Synovial chondromatosis . . . . . . 1 9. 7 . Pigmented villonodular synovitis (PVNS) . 1 9. 8 . Arthrosis (osteoarthritis) . . . . . . . . . . 1 9. 8 . 1 . Alterations in various parts of the joint . 1 9. 8 .2 . Alterations in the arti cular endings of bones . 1 9. 8 . 3 . Transformations in the non-loaded zone, osteophytes . 1 9. 8 .4. Changes in the arti cular capsule 1 9. 8 . 5 . Symptoms . . . . . . . 1 9. 8 . 6 . Treatment of arthrosis . . . . .
151 151 151 1 52 1 53 1 58 158 1 59 1 60 1 62 1 62 1 63 1 63 1 64
20.
Bacterial infe ctions of bones and joints (JozseJLakatos) 20. 1 . Osteomyelitis . . . . . . . . . . . . . . . . . . 20. 1 . 1 . A cute hematogeni c osteomyelitis . . 20. 1 .2 . Chroni c osteomyelitis . . . . . . . . 20. 1 .3 . Spe cial forms of primary chroni c osteomyelitis 20. 1 .4. Spe cial forms of inflammatory bone alterations . 20.2. Purulent arthritis . . . . . . . . . . . . . . . . . . . . . . 20.3 . Bone and joint tuberculosis . . . . . . . . . . . . . . . . . . 20.3 . 1 . Coxitis tuberculosa (tuber culosis of the hip) . . . 20. 3 . 2 Gonitis tuberculosa (tuberculosis of the knee-j oint)
1 65 1 65 1 65 171 1 72 1 74 1 77 1 79 1 82 1 83
21.
Tumors of the mus culoskeletal system (Miklos Szendroi) . 2 1 . 1 . General . . . . . . . . . . . . . . . . . . . . . . . . 2 1 .2. Primary bone tumors . . . . . . . . . . . . . . . . . 2 1 .2 . 1 . Histologi cal classifi cation of bone tumors . 2 1 .2.2. Bone forming (osteogeni c) tumors . . . . . 2 1 .2.2. 1 . Benign bone forming tumors . . . 2 1 .2.2.2. Malignant bone forming (osteogeni c) tumors 2 1 .2.3 . Cartilage-forming tumors . . . . . . . . . . . 2 1 . 2 . 3 . 1 . Benign cartilage-forming tumors . . 2 1 . 2 . 3 . 2 . Malignant cartilage-forming tumors 2 1 .2.4. Bone marrow tumors . . . . . . . . . . . 2 1 . 2 . 5 . Giant cell tumor of bone. (osteo clastoma, "brown tumor of bones") . 2 1 .2.6. Other rare bone tumors . 2 1 .3 . Bone metastases . . . . . . 2 1 .4. Tumor-like bone pro cesses . . . . . . 2 1 . 5 . Soft-tissue tumors . . . . . . . . . . 2 1 . 5 . 1 . Some soft-tissue tumors of orthopedi c signifi can ce
1 85 1 85 1 92 1 92 1 92 1 93 1 94 1 99 1 99 20 1 204 206 207 208 212 215 218
Reflex dystrophy (Sude ck ' s syndrome) (Zoltim Csernatony) . . . . . .
225
22.
XII
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Co n t e n s
23 .
Asepti c bone ne crosis (Arpad Bellyei) . . . . . . . . . . . . . . . . . . . . . . . . . 229 23 . 1 . Childhood bone ne crosis (j uvenile osteo chondrosis, juvenile osteo chondritis, 229 juvenile osteo chondrone crosis) 2 3 . 2 . Adult asepti c bone ne crosis . . . . . . . . . . . . . . . . . . . . . . . . . . . 23 1
24.
Diseases of the spine (Tamas Illes, J6zsejLakatos, Peter Pal Varga) . 24. 1 . Biome chani cs, fun ctional anatomy, fun ctional units of the spine . 24.2. Examination of the spine . . . . . . . . . . . . 24.2. 1 . Assessment of the cervi cal spine . 24.2.2. Assessment of the lumbar spine 24.2 . 3 . Radiologi cal assessment . . . . . 24. 3 . Classifi cation of deformities of the spine . . . 24. 3 . 1 . Chara cteristi cs of deformities in one plane . 24.3 . 1 . 1 . Fun ctional hyperkyphosis 24.3 . 1 .2 . Fun ctional hyperlordosis . . . . . 24.3 . 1 . 3 . Stru ctural kyphosis . . . . . . . . 24. 3 . 2. Spinal deformities 3 dimension: S coliosis . 24. 3 . 2 . 1 . Fun ctional (nonstru ctural) s coliosis 24. 3 .2 .2 . Stru ctural s coliosis . . . 24.4. Congenital abnormalities . . . . . . . . . . . . 24.4. 1 . Spondylolysis, spondylolisthesis . 24.4. 2 . Sacralization, lumbarization 24.4. 3 . O ccult spina bifida . . . . . . . . 24.5 . Other diseases . . . . . . . . . . . . . . . . . 24. 5 . 1 . Baastrup syndrome (interspinous arthrosis) 24. 5 . 2 . Sacrum a cutum . . . . 24. 5 . 3 . Co ccygodynia . . . . . . . . . 24. 6 . Degenerative disorders of the spine . . . . 24. 6 . 1 . Degenerative spinal disorders 24.6. 1 . 1 . Degenerative pro cess of the dis c . 24.6. 1 .2 . Dis c prolapse, hernia . . . . . . . 24.6. 1 .3 . Degenerative spine instability . . 24. 6 . 1 .4. Clini cal examination of degenerative spinal disorders . . . . . . . . . . . . . . . . . . . 24. 6 . 1 . 5 . Conservative treatment of a herniated dis c and degenerative spinal stenosis . . . . . . . . . . 24.6. 1 . 6. Surgi cal treatment of degenerative spinal disorders 24. 7 . Spinal changes in osteoporosis . 24. 8 . Tumors . . . . . . . . . . . . 24. 8 . l . Primary tumors . 24. 8 . 2 . Metastases . . . 24.9. Inflammations of the spine . . 24.9. 1 . Spondylitis tuberculosa (Pott ' s disease) 24. 9 . 2 . Pyogeni c spondylitis (spinal osteomyelitis) 24. 9 . 3 . Spondylodis citis . . . . . . . . . 24. 1 0. Chest deformities . . . . . . . . . . . . . . . 24. 1 0. 1 . Pe ctus ex cavatum (funnel chest) 24. 1 0.2. Pe ctus carinatum (pigeon chest) .
235 235 236 237 240 242 245 245 246 247 247 253 253 253 267 267 272 273 274 274 274 274 274 275 275 275 276 277 28 1 28 1 282 284 284 285 286 286 288 29 1 292 292 294
Co n t e n s
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XIII
25.
Disorders of the ne ck and the shoulder girdle (Jeno Kiss) . . . . . . 2 5 . 1 . Fun ctional anatomy and biome chani cs of the shoulder girdle . 25.2. Examination of the shoulder girdle . . . . . . . . . . . . . . 2 5 . 3 . The congenital and a cquired disorders of the of the shoulder girdle 25.4. Disorders of the shoulder . . . . . . . . . . . 2 5 . 5 . Other painful shoulder conditions briefly . . . 25.6. Glenohumeral instability, shoulder dislo cation
295 295 296 297 3 02 307 308
26.
Disorders of the elbow and forearm (Jeno Kiss) . . . 26. 1 . Fun ctional anatomy of the elbow and forearm 26.2. Assessment of the elbow . . . . . . . 26. 3 . Signifi cant developmental anomalies . . . . . 26.4. A cquired disorders of the elbow . . . . . . . . 26. 5 . Volkmann' s is chemi c contra cture of the forearm and the hand .
311 311 311 311 313 317
27.
Disorders of the hand and the wrist (Ferenc Mady) . 27. 1 . Fun ctional anatomy of the hand and the wrist . 27.2. Congenital anomalies of the hand . . . . . . . 27. 3 . A cquired hand disorders . . . . . . . . . . . . 27. 3 . 1 . Avas cular ne crosis of the carpal lunate bone (Kienb ock ' s disease) . . . . . . . . . . . . . 2 7 . 3 . 2 . Cyst and pseudoarthrosis of the s caphoid bone 27.3 . 3 . Osteoarthritis (OA) of the wrist and the hand 27.3 .4. Inflammatory pro cesses . . . . . . . . . . 27.3 . 5 . Ganglioni c cysts of the wrist and the hand . . 27.3.6. Dupuytren ' s contra cture . . . . . . . . . . . 27.3.7. Tumors and tumorous conditions in the hand
319 319 32 1 322
28.
Hip disorders (Arpad Bellyei, J6zsejLakatos, Mikl6s Szendroi) 28. 1 . Pediatri c hip disorders . . . . . . . . . . . . . . . . . . . 2 8 . 1 . 1 . Normal development of the hip joint . . . . . 2 8 . 1 .2. Congenital dislo cation and dysplasia of the hip 2 8 . 1 .3 . Osteo chondritis capitis femoris juvenilis (Perthes ' disease, Legg-Calve-Perthes ' disease) . . . . . . . . . . . . . . . . . 2 8 . 1 .4. Slipped capital femoral epiphysis (SCFE, epiphyseolysis capitis femoris juvenilis, coxa vara adoles cent) 2 8 . 1 .5 . Coxa vara infantum ( congenital) . . . . . . . 2 8 . 1 . 6 . Symptomati c coxa vara . . . . . . . . . . . . 2 8. 1 . 7 . Growth disturban ces of the proximal femur . 2 8 . 1 . 8 . Transitory arthritis coxae (transitory hip j oint inflammation) 2 8 . 1 .9. Juvenile a cetabular protrusion . . . . . 2 8 . 1 . 1 o . Snapping hip, external coxa saltans . . 2 8 . 1 . 1 1 . Inward o r outward rotation of the legs 2 8 . 1 . 1 2 . Limb shortening . . . . . . . . . . . . 2 8. 1 . 1 5 . Congenital hemiatrophy and hemihypertrophy . 28.2. Hip disorders i n adults . . . . . . . . . . . . . . . 2 8. 2 . 1 . Fun ctional anatomy . . . . . . . . . . 28.2.2. Deformities o f the hip - prearthrosis . 28.2.2. 1 . Valgus hip, coxa valga . . .
322 323 324 325 326 327 328 329 329 329 33 1 342 347 350 35 1 352 352 353 354 35 4 355 358 358 358 359 361
XIV
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Co n t e n s
2 8 . 2 . 2 . 2 . Varus hip, coxa vara . . . . . . . . . . . . . . . . . . 2 8 . 2 . 2 . 3 . Antetorsion and retrotorsion of the hip (coxa antetorta and coxa retrotorta) . . . . . . . . . . . . . . 2 8 .2.2.4. Other prearthroses . . . . . . . . . . . . . . . . . . 2 8 . 2 . 2 . 5 . Surgical treatment of prearthrotic conditions . . . . . 2 8 . 2 . 3 . Idiopathic femur head necrosis (aseptic, avascular femur head necrosis) . . . . . . . . . . . . . . . . . . . . . . . . . . . 2 8 .2.4. Coxarthrosis (hip osteoarthritis, arthrosis deformans coxae) . . 29.
30.
362 362 363 363 365 368
Disorders of the knee (Laszl6 Hangody, Mikl6s Szendroi) 29. 1 . Structure and functional anatomy of the knee . 29.2. Congenital developmental disorders . . . 29.2. 1 . Congenital knee dislocation . . . 29.2.2. Genu recurvaturn . . . . . . . . . 29.2 . 3 . Developmental disorders of the patella . 29.3 . Repeated patella dislocation and subluxation . . . . 29.3 . 1 . Habitual dislocation of the patella . . . 29.3 . 2. Recurrent dislocation and subluxation of the patella . 29.3 . 3 . Luxatio patellae congenita . . . . . 29.4. Developmental disorders of the menisci . . . . 29. 5 . Developmental disorders of the tibia and fibula . 2 9 . 5 . 1 . Tibia, fibula aplasia, hypoplasia 2 9 . 5 . 2 . Congenital tibia pseudarthrosis . 29.6. Axial deformities . . . . . . . . . . . . . . . 29.6. 1 . Genu varum - crus varum . . . 29.6.2. Tibia vara epiphysarea (Blount' s disease) . 29.6. 3 . Genu valgum - crus valgum . 29.6.4. Torsion o f the tibia . . . . . . . . 29.7. Aseptic osteochondroses around the knee . . . 29.7. 1 . Osteochondritis dissecans genus . 29.7.2. Osteochondritis of the tibial tubercle (Schlatter-Osgood' s disease) . . . . . 29. 7 . 3 . Adult aseptic femur condyle necrosis (Ahlb ack' s disease) . 29. 8 . Knee contractures . . . . . . . . . . . . . 29.9. Fluid accumulation (effusion) i n the knee . 29. 1 0. Cysts i n the knee region . . 29. 1 0. 1 . Ganglion . . . . . . . . . . . 29. 1 0.2 . Meniscus cyst . . . . . . . . 29. 1 0. 3 . Popliteal cyst (Baker' s cyst) . 29. 1 0.4. Bursitis praepatellaris . . . . 29. 1 1 . 1 . Collateral ligament injuries . 29. 1 1 .2 . Chronic collateral ligament insufficiency . 29. 1 1 . 3 . Cruciate ligament injuries . 29. 1 1 . 5 . Meniscal tear . . . . . . . . . . . . . . 29. 1 3 . Chondromalacia patellae . . . . . . . . . . . . . . . 29. 1 4 . Chondropathies, osteoarthritis (arthrosis) of the knee
375 375 377 377 377 377 378 378 378 379 379 379 379 379 3 80 380 381 381 3 82 3 82 3 82
Disorders of the foot (Janos Kranicz, Kalman T6th) . . . . 3 0. 1 . The functional anatomy and biomechanics of the foot
399 399
3 83 3 84 385 385 3 86 3 86 386 387 387 388 388 38 9 391 392 393
Co n t e n s
30.2. Foot deformities in childhood . . . . . . . . . . . . . . . . . . 30.2. 1 . Congenital foot deformities, developmental abnormalities 30.2.2. Pes equinovarus congenitus (congenital club foot) . 3 0 .2 . 3 . Pes adductus . . . . . . . . . . 3 0 .2.4. Pes excavatus . . . . . . . . . 3 0 . 2 . 5 . Pes calcaneovalgus congenitus 30.2.6. Accessory ossicles on the foot . 30 . 2 . 7 . Tarsal coalition . . . . . . . . . 3 0 . 2 . 8 . Osteochondrosis calcanei (apophysitis calcanei) 30.2.9. Osteochondrosis ossis navicularis pedis (K6hler' s I disease) 30.2. 1 0. Ostechondrosis capitis metatarsi 11. (K 6hler' s 11 disease) 3 0 . 3 . Foot deformities in adulthood . . . . . . . . . . . . . . . . . . 3 0 .3 . 1 . Pes planus (pes planovalgus, flat foot, fallen arch) . 3 0 . 3 . 2 . Hallux valgus, metatarsus I. varus 30 . 3 . 3 . Hallux rigidus . . . . . . . . . . 3 0 . 3 .4. Diseases o f the 5th ray . . . . . 30 . 3 . 5 . Diseases o f the sesamoid bone . 3 0 . 3 . 6. Metatarsalgia . . . . . . . . . 3 0 . 3 . 7 . Digitus malleus (hammertoe) . . 3 0 . 3 . 8 . Morton's neuroma . . . . . . . 3 0 . 3 . 9 . March fracture (stress fracture, fatigue fractures on the metatarsals) . . . . . . . . . . . . . . . . 30. 3 . 1 0. Achillodynia (paratenonitis of the Achilles tendon) 30 . 3 . 1 1 . Haglund heel . . . . . . . 30.3 . 1 2 . Calcaneus spur . . . . . . 30.3 . 1 3 . Arthrosis of the foot joints 3 0 . 3 . 1 4. Tarsal tunnel syndrome . 3 0 .3 . 1 5 . Diabetic foot . References . .
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400 400 40 1 405 406 407 408 408 409 409 410 41 1 41 1 414 417 417 418 418 419 419 420 420 420 420 42 1 42 1 422 423
Preface
One of the most dynamically developing fields of medicine is orthopedics. Products of high technology have become part of our ev eryday practice. One of the most successful operations is hip- and knee joint replacement using endoprostheses. More than 90 per cent of the devices last longer than 1 0 years in the patient. A separate branch of science tribology deals with their wear-out proce dures. The development of technology has en abled us to introduce arthroscopic techniques for joints like the knee, shoulder, hip, ankle and wrist. By this minimal invasive surgery we can remove menisci, replace the anterior crucial ligaments in the knee and refix the labrum in the shoulder joint. In tumor surgery limb saving procedures are more and more fa vored, which however requires the evolution of reconstruction surgery, i.e. development of
modular type tumor endoprostheses systems. The implementation of modem imaging tech niques, like CT, MR and PET examinations have made diagnostic procedures more pre cise and accurate, which is crucial for surgical planning. This book is intended to fill the need for up-to-date information on disorders and dis eases treated by orthopedic surgeons and re lated physicians. The numerous illustrations, photos taken of patients and removed surgical specimens, MRI and CT pictures as well as drawings have been carefully selected to max imize their benefits in pointing out orthopedic principles and concepts and serve the better understanding of diseases. M. Szendroi, MD, PhD, DrSc.
1.
T i b o r Vf z k e l e t y
History and subject of orthopedics
Orthopedic conditions are probably basi cally as old as mankind itself. Neolithic skele tal remains for instance show changes due to tuberculotic spondylitis. Tuberculotic gibbus or coxitis, clubfoot and degenerative disor ders are often to be seen on Egyptian mum mies. Throughout history achondroplastic dwarfs have frequently been the subject of il lustrations, and one picture suggests that epi demic poliomyelitis was not unknown. In an cient Baghdad, in Persia surgical and orthope dic patients were treated in separate wards in hospitals as long ago as 1 000 BC. In Hippocrates ' book on the joints we may read about congenital clubfoot, hip disloca tion and the treatment of spine curvatures, and his statements remain essentially today. Hip-
Fig. 1.1. Fabricius ab Aquapendente: Opera Chirurgica
pocrates was perfectly familiar with the con genital hip dislocation. Following Hippocrates, exercises were proposed by Celsus for the treatment of spinal deformities in the 1 st century AD . In the 2nd century Galenus created the nomenclature for the names of spinal curvatures : kyphosis, lordosis and scoliosis. In the Middle Ages, similarly to surgery the treatment of the musculoskeletal diseases was the task of healers and blacksmiths. This played a certain role in the predominance of mechanical treatment methods, enforced cor rections and fixations and by the 1 6th century the field of the mechanical orthopedics was established. The first and most noteworthy representatives of this trend were Ambroise Pare ( 1 5 1 0- 1 590) and Hieronymus Fabricius ab Aquapendente ( 1 5 3 7- 1 6 1 9), who de scribed the origin of congenital clubfoot, hip dislocation and torticollis and proposed vari ous treatment procedures. The book by Fabricius ab Aquapendente illustrates a con struction of metal frames to fix and correct all parts of the body and the j oints (Fig. 1 . 1 .) . The term ' orthopedics ' was first used by Nicolas Andry ( 1 65 8- 1 742) in his book titled "L 'Orthopedie ou I 'art de prevenir et de corriger dans les enfans des difJormites du corps" (Orthopedics, the art of preventing and correcting bodily deformities in children) published in 1 74 1 . The picture in this book il lustrating a growing curved tree fixed to a pole in an effort to make it erect has become the symbol of orthopedics (Fig. 1 .2.). The word ' orthopaedia' is of Greek origin created according to Andry is originated from the as sociation of words orthos (straight) and paidos (child). The book was also published not only in French, but also in English and in German.
2
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1 . H i st o ry a n d s u bject of o rt h o p e d ics
Fig. 1.3. Scu ltety 1666: appliance to correct spinal curvature
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Fig. 1.2. The symbol of orthopedics from And ry's book
With this name, the new specialty of or thopedics was born, and clear proof of its ex istence and development was the founding of the first specialist orthopedic institution of the world which was established in Orbe, Swit zerland in 1 779 by Jean Andre Venel ( 1 740- 1 79 1 ) . That institution, which may be considered most sophisticated even today provided the patients with medical treatment, aftercare, a supply of appliances and educa tion. During many decades orthopedic care tended primarily to concentrate on fixation, mobilization by means of various appliances, or manual correction (the mechanical trend) (Fig. 1 .3.). The dynamic trend, involving the utiliza tion of exercises also has a long history. The first book, titled "Medicina Gymnastica . " by Francis Fuller was published in 1 705 and was reprinted 9 times. The term "orthopedie" in Andry book likewise refers to the impor tance of exercises for the development of a straight posture. These exercises took the pa. .
tients to the open fields, adding the healing ef fects of the open air and the sunshine. In the early of 1 9th century, Ling in Sweden intro duced medical exercises, for the active and passive mobilization of certain parts of the body. Accepted into practice under the name of "Swedish gymnasty" and the essence of these procedures is made use of in modem times. Surgical procedures were resorted for the correction of contractures and deformities, es pecially in cases where mechanical solutions had failed. The sequence of evolution of sur gical treatment was first closed interventions, followed by subcutaneous tenotomies and fi nally open-exposure operations . The tech niques of asepsis and antisepsis introduced by Semmelweis and Lister played an important role in this development. The early surgical interventions were ob viously the work of the bone setters, who could successfully treat certain conditions, and who handed on their art through many generations. Revolutionary changes in the performance of mechanical and surgical treatment fol lowed the introduction of plaster of Paris casts, first used by Dutch physician Mathysen in 1 85 1 and applied extensively ever since. Thus the mechanical, functional and sur gi cal approaches for the treatment of orthopedic conditions developed in parallel. In recent de-
1. H i st o ry a n d s u bject of o rt h o p e d ics
cades, the changes have conside rably accele r ated and at p resent pe rhaps the most inten sively and dynamically developing b ranch of medicine. The p rog ress in science ove rall has naturally played a g reat role in this. The achievements in anesthesiology and intensive care now pe rmit successful extensive and timely surgical p rocedu res that we re ea rlie r impossible. The development is basically proceeding i n two directions: •
•
The prevention of diseases, and the early diagnosis and treatment, leading to the prevention of permanent deformities; Utilization of the available technical achievements in the therapy.
Medicine is most effective if disease is p revented when the rapy is unnecessa ry. The best example in o rthopedics is the int roduc tion of vaccination Salk and Sabin, which has eradicated poliomyelitis epidemics in those count ries whe re it is used systematically. Well-o rganized hip sc reening can p revent hip dislocation and dysplasia, fo r early t reat ment can solve it without any residual defo r mity. Besides the developments in su rge ry and anesthesiology p rog ress in othe r p rofessions has also played an impo rtant role in orthope dics. One good example is metallu rgy, with the p roduction of various new alloys, with special mechanical p rope rties, which have re sulted in the manufactu ring of app rop riately shaped endop rostheses and implants of excel lent quality which g reatly p romote successful surge ry. The re have simila rly been g reat develop ments in the field of tissue adaptive plastic mate rials, whe re the new techniques have rad ically changed the system of traditional limb- replacing p rostheses.
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3
Following the discove ry of x- rays and the int roduction of radiology, which was a revo lutiona ry step in o rthopedic diagnostics, the cu rrently applied imaging p rocedu res also re flect impo rtant imp rovements both in the di agnostics as well as in the surgical t reatment. The int roduction of a rth roscopic diagnos tics and su rge ry too has also resulted in revo lutiona ry changes in o rthopedics. O rthopedic activity sta rted in Hunga ry ve ry early. Some 50 yea rs afte r the establish ment of the fi rst o rthopedic institution in Switze rland by Venel, Agoston Schopj Merei founded a p rivate "Pesti Orthopedical P rivate Institute" in 1 836 . Modem su rgical o rthopedics was int ro duced by Gyula Dollinger. In a textbook pub lished in 1 942 J Kopits states that "the p res ent gene ration of physicians owe thei r thanks to Dollinger fo r thei r o rthopedic knowledge". A definite change was the inclusion of o r thopedics into the cu rriculum of the medical school, when the O rthopedic Clinic of Buda pest Unive rsity was established in 1 95 1 . The subj ect of o rthopedics being desc ribed b riefly as the specialty of medicine dealing with p re vention , t reatment and resea rch of diseases of the musculoskeletal system. In Hunga ry, simila rly as in Ge rman speaking a rea t raumatology and o rthopedics sepa rated from gene ral su rge ry, which was in cont rast with the situation elsewhe re in Eu rope. T raumatology deals with acute inj u ries, including polyt rauma, while o rthopedics t reats post-t raumatic conditions, axial defo r mities, congenital and inhe rited systemic bone diseases, limb developmental deficien cies, inflammato ry diseases of bones and joints, musculoskeletal tumo rs, etc . Natu rally howeve r, the re a re conside rable ove rlaps in the activities of these two p rofessions. Finan cial conside rations and effo rts to confo rm to the p ractice in Eu ropean Union will ce rtainly result in common t raining and ultimately the union of the two specialties.
Zo lta n Cse r n a t o n y
2.
Structure and development of bones
2.1. Structure of bones The bones have a numbe r of functions : they suppo rt the body, thei r rigidity playing role in maintaining the shape of the body. They fo rm the joints with thei r ca rtilaginous ends, the j oints a re fixed by ligaments. They se rve as leve r a rms around joints; the j ointed bones are moved and at the same time stabi lized by the muscles via the tendons . They p rotect vital o rgans and include a significant part of the hemopoetic system. Finally they are impo rtant as mine ral rese rves in the cal cium and phospho rus metabolisms of the o r ganism. Summa ry: the bones play p rotective, mechanical and metabolic roles in the body.
2.1.1. The composition of bone Chemically all bones have almost identi cal composition. Roughly 1 13 of the adult bone consists of wate r. D ry matte r content of 1
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fat free bone tissue contains 65% ino rganic mate rial (mainly hydroxyapatite), while 3 5 % i s o rganic (chiefly collagen). The bones ac counts fo r holds about 99% of the calcium content of the body.
2. 1.2. The bone tissue Histologically bone is st ructu red by cells and a mat rix. The cells which comp rise 1 -5% of the ove rall mass a re responsible fo r the bio logical p rope rties, the mat rix accounting fo r the mechanical p rope rties. The inte rcellula r mat rix, and specifically the osteons equips the adult bone with excellent mechanical quali ties. Mac roscopically the bone tissue can fo rm compact (substantia compacta) o r spongious (substantia spongiosa or cancellous) mate ri als. Since the compact fo rm mainly c reates the co rtex of the bones, it is often refe rred to as co rtical.
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Fig. 2.1. Histological structure of human bone
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4 vessels and nerves
5 6 7 8
osteocyte Volkmann-canal basic lamella cemen- line 9 Havers-canal 10 connecting lamella 11 bone trabecules
6
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2 . St r u ct u re a n d d eve l o p m e n t of b o n e s
The basic s truc tural elemen t of subs tan tia compac ta is the o s teon (Havers sys tem). This is a thick-walled tube tha t includes a narrow canal con taining, concen tric pipes 5 - 1 0 �m thick (Fig. 2 . 1 .) . Small plum- s tone-shaped holes loca ted sparsely in the walls of the os teons serve to accommoda te the real bone cells ( o s teocy te). These holes are connec ted via Volkmann canals, which are no t sur rounded by lamellar sys tems. The lamellae tha t form the wall of the os teons con tain colla gen fibers, which may be loca ted longi tudi nally, crosswise or in spirals. Calcium crys tals are connec ted to the collagen fibers, the orien ta tion of the collagen fundamen tally de ter mining the loca tion of the crys tals. The irreg-
1 2.......:: 3
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ular spaces be tween the "comple te" osteons are filled wi th the remnan ts of os teons . One of the mos t importan t phenomena ex hibi ted by bones is their permanen t res truc tur ing. In 1 year 5 - 1 0% of the os teons, and up to 20% of the cancellous bone in adul ts undergo res truc turing. Cancellous bone does no t display os teon s truc turing: i t con tains fine lamellae and tubes enclosing a complica ted cavi ty sys tem. The s truc ture of bone is perfec tly adap ted for i ts role in the body. The alignmen t and spi raling of the os teons ma tch the main load-bearing lines of the bone, they ru n ap proxima tely parallel to the longi tudinal axes of the bones.
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Fig. 2.2. Structu re of a long tubular bone (femur)
18
1 epiphysis
2 physis (growth plate)
3 4 5 6
apophysis metaphysis diaphysis metaphysis
7 physis 8 epiphysis 9 joint ca rtilage 10 spongiosa (cancellous bone) 1 1 periost 12 cortical bone 13 vessel 14 med ullar cavity 15 periost 16 nerve 17 vessel 18 joint cartilage
2 . St r u c t u r e a n d d eve l o p m e n t of b o n e s
2.1.3. Bones as organs The bones are built up of bone tissue con taining cancellous and compact bone in vari ous distributions and with complicated geom etry. Morphologically we may distinguish flat, cubic, cavital, short and long tubular bones. As regards their function we may refer to permanent load-bearing (the lower limbs and the spine), occasional load-bearing (the upper limbs) and non-load bearing (the facial skull) bones. The nomenclature of the tubular bones is based on the growth plate, the physis (phyestar to grow, Gr). The part between two physes is the diaphysis, the part in the vi cinity of physis is the metaphysis, and the ends form the epiphyses. The protruded bone - ends that have their own growing plate and serve for the origin and attachment of muscles are the apophyses (Fig. 2.2). =
2.1.4. The development and g rowth of bones Development of bones starts from the em bryonic connective tissue, the mesenchyma when the embryo is 2 months old. This pro cess requires a good supply of blood and oxy gen. There are three different developmental histological forms depending on the mechani cal environment: I. Desmal ossification
In locations subj ected to pulling forces a preliminary ossifying focus is created con taining connective fibers. The ossification starts from the so called ossification centers. 2. Chondral ossification
In locations subjected to compressive forces, a preliminary focus is created that con tains cartilage, which is a rough miniature replica ofthe final bone. The vessels enter this cartilaginous tissue and trigger the ossifica tion process via osteoblasts.
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7
3. Primary angiogenic ossification
This process occurs in areas lacking me chanical forces. It is characteristic for in stance, in the spaces between the skull bones. No precursor tissues are present, the bony de velopment starts with the invasion of vessels. In the growth plate in the vicinity of the end of the bone, the cartilaginous cells prolif erate, and on the opposite side the chondral ossification process continuously progresses. By the end of the growth the growth plates are ossified and closed. The whole procedure is regulated by hormones. The bones thicken by transversal growth. In the inner, cambium layer of periosteum covering the bone, bony apposition progresses via osteoblasts, while at the inner surface of the tubular bone the osteoclast activity leads to bone resorption. This is the reason why the proportions of tu bular bone are protected during the growing period (see Chapter 1 2. ) .
2.2. Biological adaptation of bones The composition, histological structure and shape of the bones are influenced not only genetically, but also by various mechanical factors . As living tissue, bone responds to chang ing external circumstances, and especially to compression and traction forces with perma nent restructuring, i.e. remodeling. For opti mal load distribution the bony trabeculae thicken so as to correspond to the compres sion - traction force alignments creating the traj ection lines. In this way, minimal material is required for the maximal bearing force. If the alignment of the load changes, e.g. in cases of different collodiaphyseal angles of the femoral bone, then the traj ection lines of the bony trabeculae also change (Fig. 2.3. a-b). As Julius Wolfformulated in his law: "The persistence or transformation of the shape of the skeleton is influenced by the forces acting on the bone." In other words : remodeling ad aptation of bone allows the musculoskeletal
8
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2 . St r u ct u re a n d d e ve l o p m e n t of b o n e s
system to adjust most appropriately to re peated utilization (Fig. 2.4. a-c. ) . The law of Jansen states that "The sensi tivity of the organism to external stimuli is proportional to the intensity of growth". As concerns the musculoskeletal system this means, that in response to a certain degree of
a
b
a
b
c
Fig. 2.4. Fig. 2.3. Traction and compression trajection lines in the fem oral neck. a. Normal trajection lines in the normal hip joint. b. Alteration of trajection lines in a subluxated, valgus femoral neck.
a. Lytic bone destruction in the calcaneus of an 8-year-old boy (arrows). b. Following cu rettage the cavity was filled with ho mologous bone chips. c. After 3 years, full restructuring and remodeling is apparent: a normal trajection bone structure match ing the loading conditions has been restored.
2 . St r u ct u re a n d d eve l o p m e nt of b o n e s
damage, the younger the organism, the more severe the deformity. At the same time the re generative capacity is larger. The law of Roux pronounces : "The ade quate stimulus for bone formation is the pres sure". This law is supplemented with impor tant elements by the law of Schultz-Arndt: "Small stimuli increase the living processes, large ones decrease them and huge ones ter minate them". This may be illustrated by the behavior of hyaline cartilage cells: their me tabolism increases during a normal cyclic load, but increase of the load above a certain limit results in the demise of the cells. According to the law of Pommer-Braus: "Bone is mechanically firm, but physiologi cally plastic". This is of significance in the pathophysiology of fractures (see Chapter
3 . l ).
These laws provide phenomenological de scription of the biomechanical responses of the skeletal system to certain stimuli (hor mones, injuries and loading). The background of the phenomena at a cell - tissue level in volves the mechanism of the internal or struc tural remodeling. The main point is that the
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Ag. 2.S. Regu lation of the ca lcium metabolism
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9
transformation of bones is effected by activa tion - resorption - formation.
2.3. Hormones reg u lating the bone metabolism A number of hormones and vitamins helps in regulate the bone and calcium metabolisms (Fig. 2.5.). Parathormone (in the parathyroid gland) increases the calcium resorption and phos phate excretion in the kidney. It enhances the osteoclast activity in the bones. It indirectly supports calcium absorption in the gastroin testinal tract. All these effects result in an in creased serum calcium level and a decreased serum phosphate level. Pathologically high parathormone levels cause transformation of the bone, creating cystic lesions (osteo dystrophia fibrosa cystic a generalisata von Recklinghausen 's disease, see Chapter 1 4.). Calcitonin (in the thyroid gland C cells) is an antagonist of parathormone. It inhibits the activity of osteoclasts, increases the number -
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ACTH
STH
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2. S t r u ct u re a n d d eve l o p m e n t of b o n e s
and function of osteoblasts, which results i n a decreased serum calcium level. The secretion of this hormone is regulated by the serum cal cium level. Its effects described above and its pain-killing action is utilized in the therapy of osteoporosis. Somatotropic hormone (STH, in the ante rior pituitary lobe) is responsible for the growth of the bones, until the epiphyses are closed. Its elevated secretion (pituitary adenoma) before the closure of the growth plates causes gigantism; after that period it causes extensive thickening of the bones and overgrowth of the acral areas (acromegaly). Sex hormones, such as testosterone play im portant roles in the increased growth during puberty; in this period changes in the propor tions of the somatotropic and sex hormones are manifested in a characteristic condition: slipped capital epiphysis, epiphyseolysis capitis femoris (see chapter 2 8 . 1 ). The de creased estrogen secretion in women in the postmenopausal period results in osteoporo sis.
An elevated adrenocorticotropic hormone (ACTH) secretion stimulates the function of the adrenal cortex, leading to a calcium defi cit. The increased secretion (or therapeutic ap plication) of corticosteroids also results in a decrease in bone mass, since it inhibits the ab sorption of calcium in the bowels, increases the secretion of calcium in the kidney and ends in secondary hyperparathyroidism. High dose steroid administration inhibits osteoblast activity. Active metabolites of vitamin D (e.g. 1 -25-dihydroxy-vitamin D) increase the ab sorption of calcium and phosphate both in the kidney and in the bowels. They mobilize the calcium ions in the bone and inhibit the secre tion of parathormone in the parathyroid gland. Overall vitamin D participates in bone forma tion, and it is therefore a basic drug in osteo porosis. Vitamin is of significance in collagen synthesis. A deficiency of vitamin C causes pathological disturbances in osteoid forma tion.
3.
Mi kl6s Szen d r6i
Bone healing after various types of fractures
3. 1. Traumatic fractu res In the event of a sufficient degree of trauma, when the stress on a bone exceeds its strength, the continuity of the bone sub stance is interrupted and a fracture occurs.
Etiopathology. There are many classifi � a tions for fractures. From the aspect of the sIte of action of the force, the fracture is said to be direct if it occurs at the site of stress; and indi rect if it occurs at some distance from the site of the stress. As concerns the pathomechanism, we dis tinguish bending, torsion, compression, sn:ain and stress fractures. Bone is weakest agamst torsional stresses, followed by distraction and compression forces. Special fracture types in children are epiphyseal plate fractures and plastic deformities. This involves bending of the long bones, mostly the fibula and the ulna, which often accompanies the greenstick frac tures of the tibia and the radius. Fractures can be classified according to the shape and the direction of the fracture li!le: transverse fractures, oblique fractures, spIral fractures, longitudinal, Y-shaped, fragmented and comminuted fractures. The patient' s history is usually typical permits conclusions concerning the direction of the stress, the shape of the fracture and the possible accompanying injuries. Clinical features. Definitive signs are the deformity of the limb with crepitus and patho logical mobility at the site of the frac �re. !he presence of pain, hematoma and an Impaired function (e.g. the patient is unable to put
weight on hislher leg) are features leading to the suspicion of a fracture. Radiological findings. Anteroposterior and lateral radiographs reveal the discontinu ity of the bone with or without displacement. The lesion is called a fissure if there is a frac ture gap in only one of the cortices. In some cases, if several bones are proj ected onto each other (pelvis, shoulder girdle, spinal facets, etc.), a eT-scan is required. If a ligament le sion is suspected, an MRI is required. Treatment. The earliest possible and pre cise reduction and fixation of the fracture is important for reestablishment of the circ� la tion of the soft tissues. The type of fixatlOn can be external (casting with plaster of Paris, or use of an external fixateur) or internal : ei ther on the surface or in the medullary canal of the bone. There are three categories of fixa tion stability: I . positional stability (pinning or plaster immobilization), 2. mobilization stability (the most types of plate fixation) and 3 . weigh-bearing stability (some intra medullary fixations) . In cases of rib fracture, chest bone fracture, clavicle and vertebral body fracture spontaneous healing may occur and stable fixation is not necessary.
3.2. Fract u re healing. Types and stages. Factors influencing fracture healing Fracture healing i s a complex process regu lated by neural and humoral factors.
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3 . B o n e hea l i n g aft e r v a r i o u s ty p e s o f fract u res
Direct bone healing (primary callus) develops if the fixation is stable (osteosynthesis with a plate or an intramed u l lary device), if the gap between the broken fragments is minimal and the fragments fit well with adequate compression, and if the blood supply is satis factory. Fracture healing is said to be indirect if the compression between the broken frag ments is low and it is the naturally developing callus which p rovides the stability (plaster im mobilization).
Stages of fracture healing (Fig. 3 . 1 .) :
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Stage 1 : Hematoma / inflammatory phase. Bleeding from the injured longitudinal endosteal and periosteal vessels leads to a hematoma. Stage 2 : Subperiostal-endosteal cell pro liferation. An intercellular matrix is formed, which is mostly composed of fibrous-like tis sue, but immature cartilage may also be pres ent. This matrix surrounds the broken frag ments . Stage 3 : Callus formation. Stem cells transform to osteoblasts, osteoclasts and chondroblasts which participate in the forma-
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Fig. 17.4. Compression of the n. cutaneus femoris lateralis in a case of meralgia paraesthetica.1: n. cutaneus femoris lateralis, 2: arcus iliopectineus (lig. iliopectinea)
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Compression of the peroneus nerve in a case of an terior tarsal tunnel syndrome. 1: n. peroneus profundus, 2: lateral branch of the n. peroneus profundus, 3: medial branch of the n. peroneus profu ndus, 4: retinaculum extenso rum
18.
Zo ltan Cse r n at o n y
Disorders of tendons, tendon sheaths, bursae, fasciae a nd lig a ments
The vanous elements of the musculo skeletal system are the contractile muscles and the non-contractile other constituents. The latter may be connected in series or in parallel. Those connected in series are the ten don ongms and attachments, fascia, aponeurosis, retinaculum, tendon sheaths, while those connected in parallel are the con nective tissue cover of the muscles and their framework, the epimysium, perimysium and endomysium, and the ligaments. Common or thopedic diseases of these elements are dis cussed below. All anatomic structures are designed for optimal function: the maximal efficacy is at tained with minimal mechanical effort. The muscle - tendon ensemble acts in complete harmony. If a structural disturbance or a par tial injury occurs, a reflex-like overall func tion failure may develop.
treatment of tendon injuries are discussed in connection with traumatology. �
Tendinopathies The tendinopathies may be divided into a number of groups :
1 . Mechanical edematous tendinopathy. The tendon is thickened, looses its white shine,
18. 1. Disorders of the tendons In view ofthe fact that the tendons are sub jected to a heavy mechanical load even in nor mal use, it is not surprising that they can be in volved in disturbances due to multiple micro trauma. This is obviously more common in heavy physical laborers and athletes, and some tendons are particularly involved, in the shoulder, knee and heel region (Fig. 18.1). In certain illnesses, or following long lasting immobilization, inflammation, or inju ries loose connective tissue may build up in the tendon making it weaker, fragile. The dis eases of the tendons may be divided into vari ous groups, affecting of the tendon itself, the osteo-periosteal attachment or the peri tendineal connective tissue. The onset and
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1 8 . D i s o r d e r s of t e n d o n s, t e n d o n s he a t h s , b u rsae, fa s c i a e a n d l i g a m e n ts
and becomes gray and matte. Histology re veals edema of the collagen fibers. 2 . Mechanical edematous tendinopathy. Af ter opening of the tendon sheath, the ten don is widened with fissures of various depth and length. Connective tissue scar ring and hypervascularization appear in the tendon sheath. 3 . Mechanical nodular tendinopathy. Hyper trophic nodules appear in the tendon, as an indication of an advanced stage of degen eration. Fibrosis may develop in the ten don-sheath (e.g. trigger finger, Chapter 27). 4. Mechanical necrotizing tendinopathy. This is the gravest stage, some fluid secre tion may start in the tendon sheath. Histologically various extent of necrosis may appear in the tendon and it may be se questrated. Usually, there are no inflam matory signs. �
Enthesopathies In the diseases classified here, the patho logical state is located in the bony anchorage of the tendons or ligaments. Five types are dif ferentiated:
1 . Inflammation (spondylarthritis ankylopoetica, spondy larthropathy) 2. Degenerative (Forestier' s illness). 3. Metabolic (gout, chondrocalcinosis). 4. Toxic and iatrogenic (synthetic vitamin A abuse, fluoride intoxication). 5 . Mechanical (overload).
18.2. I l lnesses of the paratenon and the tendon sheath The tendon sheath has multiple tasks : it protects the tendon, decreases friction, nour ishes, produces synovial fluid and ensures the blood and lymph supply. The structure and composition of the joint synovial membrane and the lining of the tendon-sheath is almost the same, and their pathologic processes therefore are very similar.
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Tenosynovitis, peritendinitis, peritendi nitis crepitans, tendovaginitis crepitans Tenosynovitis is inflammation of the in ner, synovial layer of the tendon sheath. The origin may be irritative, mechanical or bacte rial. Irritative tenosynovitis can be induced by an overload. The synovial layer of the tendon sheath shows evidence of mild inflammation and a small amount of exudate is excreted. In places, where tendon is covered only by the paratenon instead of by the tendon, such in flammation is called peritendinitis. �
Tenosynovitis purulenta, tenosynovitis tuberculosa Bacterial infection of the tendon sheath may take place in acute or chronic form. The chronic form is usually due to tuberculosis. �
Tendovaginitis In tendovaginitis, the outer fibrous wall of the tendon sheath is thickened. The etiology is unknown, but bacterial infection is not in volved. The inflammation is located at the ori fice of the tendon sheath (see trigger finger and de Quervain' s disease) .
18.3. Diseases of the bursae At positions, where the skin, muscles and tendons slide over each other or exhibit major angulations, the synovial bursae ensure the undisturbed motion and mechanical protec tion (e.g. between the heel bone and the Achil les tendon, or over the olecranon and the pa tella) . Accessory bursae can develop at any time, e.g. over the medial side of the 1 st meta tarsal head in hallux valgus, or over exostoses, around implants etc. �
Bursitis
1 . Traumatic bursitis. Swelling of the bursa may develop in consequence of a single mechanical effect or repeated microtrau ma (long-lasting kneeling or elbowing, e.g. a roofer, paver) . The bursa may con-
1 8 . D i s o r d e r s of t e n d o n s, t e n d o n s he a t h s , b u r s a e , f a s c i a e a n d l i g a m e n t s
tain blood (trauma, hemophilia) or syno vial fluid. It may be triggered by a foreign body. 2 . Microcrystal bursitis. Urate crystals may accumulate in gout (Fig. 1 8.2.), while apa tite may accumulated as a result of bleed ing or chronic bursitis, producing the ra diological picture of bursitis calcarea. 3. Infectious bursitis. This condition most of ten follows percutaneous infection and takes place either in the prepatellar or in the olecranon bursa. It is most frequently caused by classical pyogenic bacteria (bursitis purulenta), but it may also due to a fungal infection. 4. Rheumatoid and reactive bursitis. Bursitis may be initiated by rheumatoid arthritis, spondylarthritis ankylopoetica, or Reiter ' s disease.
18.4. Illnesses of fascia •
Muscle hernia Following injury or operations the fascia is not closed, and the underlying muscle pro-
137
trudes into the soft tissues. Apart from the es thetic discrepancy, in more severe cases this may be a source of functional disturbances and pain. •
Necrotizing fasciitis This severe condition occurs mainly in tropical areas and is caused by streptococcus. It may involve any fascia, causes extensive soft tissue necrosis and demands surgical in tervention. It can often cause a severe disfig urement.
18.5. Disorders of ligaments The j oint ligaments contain tendinous or compact collagen fiber connective tissue bun dles, which in some cases are purely the stron ger parts of the fibrotic joint capsule, but they also may be independent ligaments with a flat or cylindrical shape, located intra- or ex tra-articularly. Their role is to stabilize the ar ticulating bones. •
Fig. 18.2. Gout-induced olecranon bursitis
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Degeneration, rupture, insufficiency Various ligaments may degenerate either due to physiological aging, or as a result of certain rheumatologic disorders. Intact liga ments often undergo rupture following inju ries, and degenerated ligaments may be tom due to a minor trauma. The consequence may be instability and pathological j oint motion, inducing early osteoarthritis. The ligaments may become insufficient either because of tearing, or due to relative lengthening. An ex ample is the insufficient function of the spinal ligaments following disc degeneration: the vertebrae come close together, pathologic vertebral motions appear and the ligament be comes subj ected to strain.
19.
Zo lta n (se r nato ny, J6zsef La katos, Ta mas Mesza ros, Gyu l a Po6 r, M i kl6s Sze n d r6i
Diseases of joints
The bones constituting the skeleton are connected (juncturae ossium) to each other in two ways : either adj acent bones are connected continuously by connective tissue, cartilage or bone tissue (synarthrosis, syndesmosis, synchondrosis, synostosis); or there is a nar row gap Ooint space) between the bones. Bones are connected by a membrane consist ing of connective tissue, the joint capsule, the connections being called joints. (articulations, diarthroses) .
are made up of protein molecules and attached glucose-aminoglycan chains. Their role in volves consolidating water (70% of the carti laginous tissue is water). Cartilaginous tissue is completely avascular and does not contain nerve endings either. It receives its nourish ment partially through the veins surrounding
19. 1. The structure of the joints Bone endings connected to joints have to satisfy opposing criteria simultaneously: they must withstand pressure, but ensure mobility and stability. The shape of bone endings con nected to joints is fundamentally determined by the subchondral bone. The bone endings are enclosed in hyaline cartilage. The size of the articular surface is always proportional to the range of motion of the joint and is always larger on one of the bone endings connected to the joint. The hyaline cartilage is made up of chondrocytes and the intercellular matrix pro duced by these cells. Chondrocytes are capa ble of mitosis only while still in growth, and during this period minor cartilaginous injuries may heal . During adulthood, biomechanically much less valuable fibrous cartilage tissue is produced in the area of cartilage defects . Car tilaginous cells mainly produce type II colla gen and proteoglycan. Collagen accounts for 50% of the dry substance ofthe cartilage. Col lagen fibers are built up in a systematic fash ion: parallel to the surface and close to it, and in deeper segments perpendicular to the subchondral bone (Fig. 19.1). Proteoglycans
Structure of hyaline cartilage. 1. lamina splendens, 2. i ntercellular matrix, 3. chondrocytes, 4. borderline, S. calcified cartilage, 6. subchondral bone
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1 9 . D i se a s e s of j o i nts
the subchondral bone, but mainly via diffu sion from the synovial liquid. Cyclical pres sure increases the intake and metabolism of cartilage cells, but above a certain pressure level the cartilage cells die. The hyaline cartilage surrounding the bone-cortex of the j oint is made up of 4 layers : 1 . Tangential zone (small, round, flat cells parallel to the surface) 2. Transitional zone (irregular round cells) 3. Radial zone (perpendicular cell position ing) 4. Calcification zone (the layer in contact with the bone) The surfaces of the joints are comple mented by various structures composed of fi brous cartilages partially independent of the bone, increasing the pressure surface area of or even the stability. The joint capsule surrounds the j oint to gether with all of its structures. It is slim and loose in joints which have a higher range of motion, but in parts of the j oint that demon strate limited movement it is tighter and has segments that strengthened so as to become ligaments. Within the j oint capsule are the proprioception nerve endings, which are fun damental in proprioception. The cavity of the joint is padded by the synovial membrane. This is a very simple tis sue structure that includes an inner cell layer made up of synovial cells, with a fibrous layer rich in blood supply beneath it. It has two functions : assisting in the mobility between internal structures, as well as producing synovial fluid which has similar ingredients to those of the plasma: it is high in protein and is responsible for supplying the interior of the cartilaginous j oint and for lubricating the joint itself.
19.2. The biomechan ical aspects of joints The mobility of joints and to some extent their stability are determined chiefly by the
shape of the bone endings. Basically there are 6 different shapes, namely spherical (hip), el liptical (wrist joint), snail (elbow), cylinder (radius head), flat (smaller joints of the foot), and saddle (carpo-metacarpal joint of the thumb) (Fig. 1 9.2.). The possibilities of movement and their permanent range, how ever, are determined by the soft tissues mak ing up the joint and the muscles responsible for bringing the joint into motion. Apart from the movement possibilities of j oints, the positions of the participating bones relative to each other and the limb axis are of maj or significance. Both the upper and lower limbs define anato mic and constructional axes. The anatomic alignment is determined by the axis of the diaphysis, while the con structional axis is that around which the ex tended limb can be rotated.
19.3. Arthritis Arthritis is the collective term used for in flammatory diseases that affect the joints of the spine and the limbs. The reasons for these diseases vary: immune deficiencies, infective agents and pathogenic crystals may all be causes. Degenerative arthrosis, which is also often inflammatory, is not included here de spite the fact that in the Anglo-American medical literature it is (incorrectly) referred to as osteoarthritis. Nonbacterial arthritis can be divided into the following main groups: autoimmune loco motor diseases, seronegative spondarthritis, juvenile chronic arthritis (beginning in child hood), polymyalgia rheumatica, arthritis re lated to infections and arthritis induced by crystals.
19.3. 1. Autoimmune locomotor diseases Among the real auto immune rheumatoid diseases, rheumatoid arthritis primarily oc curs within joints, while the other diseases listed below often affect organs other than the j oints.
1 9 . D i s e a s e s of j o i nt s
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Fig. 19.2. Various joints.
19.3. 1 . 1 . Rheumatoid arthritis The causes of rheumatoid arthritis (RA) are unknown. It is a chronic progressive a rthritic disease, with an autoimmune pathomecha nism that affects multiple joints. Since the dis ease practically destroys the joints it affects, it is also responsible for causing serious disabil ity, often coupled with extra-articular changes. The serological characteristics in clude the positive rheumatoid factor (RF) and antifilaggrin levels.
Occurrence. The prevalence is between 0.2 and 1 . 5%. The number of RA patients in Hungary is between 50 - 1 00 thousand. Even though it may also occur in childhood and in the elderly, it primarily commences after the third or fourth decade and mainly affects fe males (female - male ratio : 2-3 : 1 ) . Etiopathogenesis. A maj or role i n the emergence of the disease is played by a ge netic predisposition. The human leukocyte antigen (HLA) DR4 and DRl loci, and to a
lesser extent the polymorphism of certain cytokines are related to the disease. Among the HLA DR4 subtypes, the DRB l * 040 1 , DRB 1 * 0404, DRB 1 * 0405 and DRB 1 * 04 1 0 alleles make one more prone to the disease. If subtypes pertaining to certain amino-acid se quences ("shared epitope " ) are present, the disease may be expected to be more severe. External factors that are considered to have an impact on the disease include viruses (e.g. hepatitis B and C virus, Epstein-Barr virus, parvovirus) and bacteria (e.g. enteral bacteria, mycoplasmas ) . The essence o f t h e disease is t h e T a n d B Iym phocytes, resulting of the autoimmune pro cess, as well as the macrophage activation, which leads to an i ncreased production of proinflammatory cytokines (chiefly TNFa and interleukin- l), the secretion of specific anti gens, pathologic cell adhesion, migration and angiogenesis, and finally joint pannus forma tion, cartilage and bone destruction (Fig. 19.3.).
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Clinical picture. In most cases the disease commences with symmetric polyarthritis, af fecting even the hands. The onset may be rapid, or the disease may develop slowly as oligo- or a monarthritis. Apart from the gen eral symptoms (fatigue, fever, loss of weight, nausea), morning stiffness in the smaller joints of the hand is also typical. During the evolution of the disease, remissions and exac erbations alternate, while the joints are slowly destroyed and various deformities appear, to gether with the consequent changes in the soft tissues. In the most frequently affected hand j oints, ulnar deviation and interosseous atro phy develop, while the fingers assume a swan-neck shape or buttonhole deformity and, due to the destruction of the ligaments in the wrist joints, the ulnar head becomes dor sally dislocated (Fig. 1 9.4.). The shoulders exhibit a painful restriction, while the elbow and knee joints often show signs of flexion contracture. A Baker cyst may develop in the popliteal fossa and its rupture may resemble the symptoms of deep vein thrombosis . Chronic inflammation of the metatarso phalangeal joints in the leg leads to sub luxation. Very rarely atlantoaxial subluxation develops, which may lead to grave and even fatal consequences. The disease may affect
changes in the wrist joint and hand in rheumatoid arthritis.
any j oint, even the temporomandibular or thy roid joints, but the back, the lumbar spine and the distal interphalangeal joints usually re main unaffected. The disease often produces extraarticular manifestations as well. Subcutaneous rheu matoid nodules appearing mainly in the extensor sides are indicative of a poor progno sis. Scleritis, episcleritis and secondary Sjogren syndrome may occur. Pleuritis, bronchiolitis and fibrosis may appear in the lungs, the latter possibly due to the frequently applied methotrexate therapy. In case of chronic and high inflammatory activity,
1 9 . D i s e a s e s of j o i n t s
amyloidosis may occur, which primarily af fects the kidneys. Necrotizing vasculitis of small and medium veins is a rare, but severe manifestation may lead to limb gangrene. Os teoporosis can take place, due to the basic dis ease and the frequent and lasting cortico steroid treatment. Cardiovascular complica tions significantly increase the mortality rate, as direct (e.g. coronary vasculitis) or indirect consequences of the basic disease. Due to immuno-suppressive treatment and long last ing steroid administration, various infections are common and relatively serious. The life expectancy for individuals with RA is 5 to 1 0 years less than for their healthy contemporar ies. The Felty syndrome is an unusual and rare form of RA and also includes the following: splenomegaly, hypersplenia and consequent leucopenia and thrombocytopenia. Diagnosis. Apart from the general inflam mation symptoms (increased We, CRP) labo ratory signs of RA include mild anemia and in 80% of the cases rheumatoid factor positivity. The seronegative form is rarer and has better prospects. The presence of antifilaggrin anti bodies (filaggrin, or cyclical citrullinated antipeptide) demonstrates high (above 95%) specificity in RA. The disease may be diag nosed if at least four of the following seven symptoms are present; the first four must per sist for at least six weeks (criteria set up by the American College of Rheumatology) : � � � �
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Morning stiffness for more than an hou r Inflammation o f three or more joint regions Inflammation of the hand joints in at least one region Symmetric arthritis Presence of rheu matoid nodes Radiological alterations Ouxtaarticular porosis, marginal erosion) Presence of rheu matoid factors in the serum
Therapy. If treated early, if the treatment starts 4-8 months after the symptoms first ap pear,- and adequately (aggressively), i.e. the
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method applied is a disease-altering basis therapeutic treatment, the destruction ofjoints can be significantly reduced or in some cases even halted. For such medication, metho trexate is the primary choice (in a dosage of 7,5-25 mg/week), which is well tolerable and has relatively few side-effects. However, due to its potentially dangerous hepatotoxicity and the damage it causes to the blood produc ing system, regular clinical and laboratory monitoring is required. Lejlunomid is a simi lar frontline medication. The following too are used in some cases as base-therapeutic medication, often in combination: hydroxy choloroquine, suJfasalazin, azathioprin and cyclosporine-A . If therapy refraction or seri ous disease progression should occur, biologi cal therapy (primarily TNFa-blockers) is an option which is very effective, though rather expensive. Additionally, local (intra-articu lar) or systemic corticosteroid administration is often required; non-steroid anti- inflamma tory drugs (NSAID) are often not enough to relieve the symptoms. In order to prevent bone loss due to the effects of the basic illness and lasting steroid treatment, the administra tion of calcium and vitamin D3 is necessary, while for therapeutic purposes, the adminis tration ofbisphosphonates is advised. Regular physiotherapy and related exercises, and the application of hand orthoses and various ap pliances can greatly reduce the progression of the disease and contribute to the preservation of the patient' s health. If conservative treat ment does not lead to an improvement and the progressive j oint alterations persist, surgery is advised. All patients with rheumatoid arthritis require treatment in which all the involved parties should act together as a team: the fam ily doctor, the rheumatologist, the physiother apist, the psychotherapist, the orthopedic sur geon, the patient and the family should all be involved in the long therapy, sometimes last ing a decade. In order to diagnose the disease at an early stage and to administer adequate treatment, an arthritis center was established in Hungary in 2004.
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19.3. 1.2. Polysystemic a utoimm u ne
diseases affecting the locomotor organs These include the Sjogren syndrome, dermatomyositis/polymyositis, progressive systemic sclerosis, mixed connective- tissue disease and systemic lupus erythematosus (SLE) which will be discussed in detail below. �
Systemic lupus erythematosus (SLE)
This is an autoimmune d isease that affect women of rep roductive age. It attacks several organs and its causes are unknown. It may a lso occur but much more rarely in childhood and old age and in males (female : male 10 : 1) The average p revalence is 0. 1-0.5%. =
The essence of the pathogenesis is the cel lular defect, the pathologic antibody and the immune complex secretion and deposition observed in genetically prone individuals fol lowing a T and B cell function disturbance, in ducing severe destruction of the organs and emergence of an extraordinarily colorful syn drome. Skin and mucosa symptoms (sensitivity to light, butterfly erythema, urticaria, vasculitis, discoid lesion, oral ulcers, alopecia, reticular livedo, and Raynaud 's syndrome) are com mon. The joints are also often affected, mostly in the form of symmetric non-erosive poly arthritis. Besides recurrent serositis (pleuritis, pericarditis), parenchymal alterations, pneu monitis and myocarditis may also occur. The neuropsychiatric symptoms can vary and may include psycho-organic syndrome, psychosis, epileptic seizure, central or peripheral neurop athy, lupus headache, mononeuritis multi plex. The kidney is generally affected in vari ous clinical forms and to different extents, the degree of this significantly influencing the prognosis of the disease. Of all the autoantibodies typical of SLE, the antinuclear antibodies, the antibodies tar geting the DNA double helix, the anti phospholipid antibodies and the anti-Srn anti bodies are worth noting because of their
diagnostical significance. Further laboratory discrepancies are leucopenia, anemia and thrombopenia, a low complement level and non- specific inflammatory parameters. The treatment of SLE is determined by the degree of inflammatory activity, the extent to which the organs are affected, and by other coexisting diseases. The therapy is individual and is based on the employment of immuno suppressive agents, corticosteroids and non steroid anti-inflammatory drugs.
19.3.2. Seronegative spondarthritis A common feature of seronegative spond arthritis (SNSA) also known as spondyl arthropathy is the arthritic transformation of the spinal and sacroiliac joints, which from a serological perspective means the lack of rheumatoid factor. Another common feature of the group is the solid or loose association with HLA (human leukocyte antigen) B27. Among these clinical entities spondylitis ankylopoetica is considered to be the most significant due to its frequency and severity. 19.3.2. 1. Spondylitis a n kylopoetica (an kylosing spondylitis) Spondylitis ankylopoetica (SPA), also known as ankylosing spondylitis (AS) is a chronic and progressive inflammation of the sacroiliac joints and the spine, which is usual ly associ ated with calcification of the ligaments, and fi nal ly the whole spine stiffens.
Occurrence. The prevalence is around 2% and there are around 20 thousand patients with this disease in Hungary; it is approxi mately seven times more frequent among males than among females. It usually appears in early adulthood but it has been known to occur in childhood. Etiopathogenesis. The clinical picture was independently described by Bechterew ( 1 892), Striimpel ( 1 897) and Marie ( 1 898). It has two types:
1 9 . D i s e a s e s of j o i n t s
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- Bechterew 's variant in which the alteration is concentrated in the spine; - Striimpel-Marie 's variant, in which apart from the spine, the peripheral joints also participate in the process.
There are also two groups depending on the direction in which it spreads : 1 . the ascending variety: This starts off from the sacroiliac j oint and the lumbar vertebra and progresses toward the cranial parts, sometimes incorporating the hips and the knees. 2. the descending variety: This starts off at the cervical spine toward the caudal seg ments, usually it does not affect the large joints. More than 90% of the patients are HLA B27-positive, however the role of this in the pathogenesis has not yet been established. Be sides the genetic association, it is assumed that infective agents (such as enteral bacteria) also play a part in the development of the dis ease. The role of TNFa in the development of SPA has been confirmed by successful bio logical therapy. The major feature of the pathomechanism is the synovitis coupled with proliferation and hyperplasia primarily in the fibrocartilaginous gaps, the intervertebral discs, the symphysis, the sternoclavicular joint and the sacroiliac j oint. As the disease progresses, the erosion of the cartilage of the joint and the destruction of the bone beneath it , lead to the development of fibrous and finally bony ankylosis. One of the pathological characteristics is enthesitis. The inflammation ofligaments, tendons origi nating from or attached to bones heals with bony apposition ( "hairy " sciatic bone or calcaneus ). Clinical picture and diagnostics. This disease usually occurs after the age of 20, but it has been known to affect youngsters and the elderly as well. Its development is rather in sidious. 1t begins with symptoms and ailments that are difficult to obj ectify for a long period.
Fig. 19.5. Lateral narrowing o f dorsolumbar spinal movements in ankylosing spondylitis.
Years can go by between the first symptom and the correct diagnosis. SPA usually starts with pain in the lumbosacral spine, in some cases in the hip or heel. The pain escalates during the night, but usually subsides in re sponse to movement. Thoracic tightness, with the sensation of wearing armor, may also oc cur. Among the general symptoms, sub febrility, loss of appetite and weight, and fa tigue are most common. Besides the charac teristic symptoms, an increase in the sedimen tation rate of the red blood cells helps to dis tinguish this condition from banal lumbar spi nal pains. The diagnosis is based upon the New York criteria: painful immobility in the dorsolumbar spine in all three directions (pri marily lateral) (Fig. 1 9.5.), a decrease in chest expansion while breathing in, and the radio logical signs of sacroileitis. The sacroileitis is usually bilateral and is coupled with special radiological alterations in the spine (syndesmophyte formation, cube vertebrae, spondylodiscitis, facet joint arthritis, etc). Signs of ligament calcification also appear, which are so typical. Calcification of the
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ligamentum longitudinale anterius and posterius appear in the X-ray image in the form of syndesmophytes. The complete de velopment of this is what leads to a "bam boo-like" spinal transformation (Fig. 1 9.6.). Additionally, enthesitis is often present and in one third of the cases the peripheral joints, also show signs of the disease. The extra-articular symptoms include iritis, aortitis, pericarditis, lung fibrosis, rarely neurological symptoms; in cases of prolonged inflammatory activity amyloidosis may also develop. Of the laboratory findings RF negativity, and HLA B27 positivity are typi cal, the latter is used in differential diagnostic problems . High inflammatory parameters are frequent, but these can be negative in the ac tive phase as well. In such cases the clinical signs and a specific questionnaire filled out by the patient (BASDAI index) help determine the severity of the activity. As the costovertebral joint may be affected at an early stage, the chest expansion during inspiration is significantly limited. By the fi nal stage only abdominal breathing may be observed. The breathing expansion may be limited to 1 -2 cm at the level of the nipples, which is an early sign and can lead to estab lishment of the correct diagnosis. With the gradual limitation of the spinal mobility and with spinal stiffening the extent of dorsal kyphosis also intensifies. Because of the curve of the spine, and the occasional hip j oint involvement, with flexion contracture, the patient is able to look forward only below the horizon. To look forward, the patient bends his/her knee j oints. It can occur, that the spine of the patient is deformed to such an extent that the patient looks back wards from between the legs (Fig. 1 9.7.). Patients with SPA can only lean to the side if the opposite limb is lifted from the ground and abducted. The patient' s condition is inten sified if the hip is affected, especially if ankylosis develops in the hip joints in flexion. Therapy. The most important part of the therapy is regular and proficient physiother apy. Teaching and the attainment of a correct
Fig. 19.6. a: Syndesmophyte development, " bamboo " shaped spine, and b: sacroiliac joint synostosis in advanced ankylosing spondylitis.
posture even in cases of complete spinal stiff ness are essential; of course, the patient must also cooperate fully to succeed. Non-steroid anti-inflammatory drugs are important, not only as symptomatic drugs, but also to exert a positive influence on the outcome. If the pe-
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briefly reviewed. A common feature i n con trast to SPA is that the sacroiliac joint is usu ally affected on one side and there is paravertebral ossification of the ligaments (development of parasyndesmophytes) on the spine. The clinical picture indicates a milder course than in SPA. �
Arthritis psoriatica 1 0-20% of the cases of psoriasis are usu ally combined with arthritis. This can lead to :
1 . most commonly to asymmetric oligo- or monarthritis and sausage fingers, 2 . distal interphalangeal j oint involvement, 3 . mutilation of fingers, 4. symmetric RA-like polyarthritis and 5 . spinal involvement resembling SPA.
Fig. 19.7. Stiffened Bechterew's spine in incorrect posture, leading to radical reduction of field of vision
ripheral joints are affected, basic therapy (methotrexate or sulfasalazin) may also be beneficial . Lately, TNFa blockers have been used in cases where SPA was not responding to drug treatment and have achieved excellent results. If arthrosis is affecting the larger joints, a hip arthroplasty is necessary (see later) . SPA seriously impairs the quality of life. Active and extra-articular forms are espe cially difficult to treat and the related mortal ity rates are close to those for RA.
19.3.2.2. Other forms of seronegative spondarthritis (SNSA)
In the following section the clinical pic tures for this group as well as SPA will be
Treatment involves basic therapeutic drugs (mainly methotrexate, leflunomid and more recently biological drugs) and non steroidal, or if needed, steroidal anti-in flammatories. Skin alterations are treated si multaneously. �
Reactive arthritis Urogenital or enteral infections followed by sterile arthritis are generally categorized as belonging to SNSA group. Arthrites follow ing urethritis are categorized as SARA (sexu ally acquired reactive arthritis). Reactive ar thritis caused by gonococcus, similarly to the gonorrhea infection process, is nowadays comparatively rare. No causative agents can be identified in the j oint. Forms relating to urogenital infections can occur at any age, but are most frequent in early adulthood. Mostly the lower limb are involved in oligoarthritis and sacroileitis, sometimes with lumbar spi nal pain. Reactive arthritis showing signs of the clinical triad urethritis, conjunctivitis and arthritis is termed Reiter disease. �
Enteropathic arthritis 1 5% of the patients suffering from Crohn disease or colitis ulcerosa develop arthro pathy, primarily in the lower limbs. Non-
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erosive asymmetric oligoarthritis with spinal and/or sacroiliac involvement often develops independently of the bowel symptoms.
19.3.3. Juvenile chronic arthritis Juvenile chronic arthritis (JCA) recently also termed juvenile idiopathic a rthritis (JIA), is a chronic a rthritic d isease beginning before the age of 16 (all other arthritic diseases must be excluded). It includes j uvenile SNSA's as well and is a heterogeneous disease group. An ac curate diagnosis can be established only dur ing later p hases of the disease.
Occurrence. The prevalence of lCA IS around 1 : 1 000 while the incidence is 1 : 1 0,000. Etiopathogenesis. Etiology of the dis ease, similarly to RA has not yet been firmly established, and due to its heterogeneous na ture it differs as a subcategory too. Immuno pathogenetic roles of genetic factors (e.g. HLA association) and inductive infective agents are understood to be responsible. Clinical picture and diagnosis. Accord ing to the initial symptoms, three diagnostic subcategories are distinguished: �
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systemic, polyarticular and oligoarticular form.
The symptoms within these subcategories differ considerably, often the only common factor is chronic arthritis, which interestingly does not cause significant pain as it does in adults (Fig. 1 9.8.). Therapy. The disease can only be influ enced appreciably if medication, physiother apy and, if needed, orthopedic surgery are ap plied concurrently. The multidisciplinary therapeutic team headed by the pediatri cian-rheumatologist must also include the teacher and the parents. The drug treatment
Fig. 19.8. Clinical picture of polyarticular juvenile chronic ar thritis in a boy treated with steroids.
policy varies according to the subcategory and the severity of the disease. The first step is usually non-steroidal anti-rheumatoid and, following j oint drainage, steroid medications. If this fails, systemic steroid treatment fol lows. In active or progressive cases, basis therapy (primarily methotrexate, azathioprin, sulfasalazin, chloroquine, etc.) is recom mended. , Excellent results have recently been achieved with etanercept, a biological sub stance inducing TNF blockade. Physiother apy and especially exercises are indispensable when it comes in the treatment in order to pre vent j oint deformities, contractures and im mobility. The activity of the disease can be stopped in children suffering with lCA
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through professional treatment; the progres sion may also be slowed down and, through the avoidance of severe consequences the child may become a useful member of the family and society.
19.3.4. Crystal-induced arthritis This category includes gout (arthritis urica) which is a well-defined and perfectly treatable disease, plus the less significant cal cium pyrophosphate dihydrate and hydroxy apatite arthropathies.
19.3.4. 1. Gout Gout is a joint disease caused by the accumu lation of monosodium-urate-monohydrate (M5U) crystals in the tissue. It is often coupled with extra-articular and visceral involvement. Hyperuricemia arises, when the uric acid level in the serum exceeds its solubility, this occurs in males over 20 IJmol/l, and in females over 360 IJmol/l.
Occurrence. Gout is the most common type of arthritis to affect overweight men above the age of 40. Its prevalence among men is 5 -2 81 1 000, while that among women is only one-fifth of this. The prevalence of gout is on the rise worldwide, primarily due to en vironmental factors (diuretics, alcohol, obe sity etc). Etiopathogenesis. Purine nucleotides are components of DNA and RNA molecules and the end-product of the human purine metabo lism is uric acid. The development of the dis ease is due to three significant factors: a high serum uric acid level, the formation of MSU crystals and the interaction between the crys tals and the inflammatory system. Gout is said to be primary, when the hyperuricemia, ini tially responsible for the precipitation of uric acid is a consequence of a hereditary meta bolic disease. Gout is considered secondary, if the hyperuricemia is a consequence of some
Fig. 19.9. Typical gout attack in the 1st metatarsophalangeal joint and the back of the foot.
other factor (e.g. increased cell disintegration in myeloproliferative diseases, or a decreased uric acid secretion due to an impaired renal function) . The pathomechanism of the hyper uricemia is related to the overproduction of uric acid (approximately 1 0%) or more fre quently (approximately 90%) to a deficiency in the transport of tubular urate which leads to a decreased excretion. The urate crystals ac cumulating in the tissue activate the inflam matory mediator systems and the effector molecules thereby released cause acute in flammation. Clinical picture. The clinical appearance of an acute attack of gout is typical. It usually occurs in the first metatarsophalangeal joint (podagra) (Fig. 1 9.9.). Intense pain in the j oint with a swelling often commences in the early morning hours, the skin is of purple-red and there is often fever. Acute gout is frequently induced by a purine-rich diet, alcohol, surgi cal intervention, trauma, medication and is of ten accompanied by general symptoms (fever, elevated sedimentation rate and white blood cell count). Following a period of acute at-
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b
u lcer. a: Clinical and b: radiological picture.
tacks chronic gout gradually develops accom panied by soft-tissue and bone tophus, serious joint destruction and changes in the visceral organs (Fig. 19.10. a, b). The most common internal complications are tubular nephro pathy gout and uric acid nephrolithiasis. Met abolic syndrome (obesity, hyperiipidemia, di abetes mellitus, hypertension, arteriosclero sis) often accompany gout. Diagnosis. The absolute criterion for a laboratory diagnosis is the presence of the negative bi-refractive needle-shaped MNU crystals in the synovial fluid. If this is not ob served, gout may be suspected in case a of a joint being affected, tophus, hyperuricemia, urate nephrolithiasis and remission within 48 hours after the intake of colchicine. In the X-ray image the bone edges are usurated, a urate deposit is formed, which is not absorbed. A circumscribed radiolucent area is visible, with a sharp edge and smooth contour, as though created by a punch. Dif fuse idiopathic skeletal hyperostosis may de velop in the spine and sometimes on the limbs, as part of the complex metabolic dis turbance.
Therapy. It is important to distinguish be tween the treatment of an acute gout attack and a steady decrease of the serum uric acid level. In cases of secondary gout causative therapy is possible. Colchicum salicylate is perfect for the treatment of joint seizures. An initial dose should be 1 mg followed by 0.5 mg every 2 hours till the seizure abates or di arrhea occurs. If colchicine is ineffective, non-steroidal anti-rheumatic drugs or if needed, steroid may also be administered. As part of the non-medical treatment a local cold pack and a tranquil environment are essential. If an intense attack persist, a daily dose of 0 . 5 - 1 .0 mg of colchicine salicylate may be ad ministered for a longer period. During sei zure-free periods, the serum uric acid level have to decrease below the safe level of 360 !lmol/l. A daily dose of300-600 mg of the uric acid synthesis inhibitor allopurinol is effec tive. Less commonly used uricosuria medica tion is applied if the tubular transport of uric acid is decreased. Non-drug therapy includes the elimination of environmental riskfactors such as obesity, a purine rich diet and alcohol consumption. Medication options for the treatment of chronic locomotor transforma-
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tions are supplemented by mechano-, electro and balneotherapeutic methods and, if needed, by orthopedic interventions. 19.3.4.2. Other forms of crysta l induced
arthritis
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(Fig. 1 9. 1 1 .). I n extreme cases, it causes de position similar to tophus or calcifying gout. The pathogenic crystals can be seen in the synovial liquid with an electron microscope. The treatment is symptomatic, X-ray irradia tion is often effective.
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Calcium pyrophosphate dihydrate (CPPD)-arthropathy This arthropathy is caused by crystal de posits of CPPD in the joint cartilage or in the periarticular area. The disease has numerous clinical appearances. The synovial fluid con tains non-inflammatory, small, rod-like, slightly positive, bi-refractive CPPD crystals. The X-ray picture of the affected joint reveals linear, pearl-like spottiness (chondro calcinosis) or irregular cartilage calcification (a few calcified nodes) During an acute attack of pseudo-gout colchicine, non-steroidal rheumatoid or steroid treatment may be ap plied. Rest, a cool compress and evacuation of the synovial liquid are necessary. The chronic forms are treated symptomatically with phys iotherapy and non-steroidal anti-inflam matory agents. It is important to treat the background disease. �
Hydroxyapatite arthropathy This involve the peri-articular and intra articular deposition of crystals of calcium hydroxyapatite. It appears most frequently in connection with inflammatory calcifying bur sitis (e.g. bursitis calcarea subacromialis)
Radiological picture of calcified subacromial bu rsitis.
19.4. Arthropathies 19.4. 1. Neurogenic arthropathy Neurogenic arthropathy (neuropathic arthro pathy, Charcot joint) is a disorder involving se rious articular destruction caused by damage to the central or peripheral nervous system leading to the loss of pain sensation deep and proprioceptive sensation.
Etiopathogenesis. As a result of the sen sory neurological disorder, due to loosening of the overloaded j oint, micro traumas, de struction of the cartilage and reactive hyper trophic bone transformations occur. Atrophic bone transformations are more characteristic in cases of peripheral nerve damage, while hypertrophic phenomena are primarily attrib uted to the central forms. Arthropathy is pri marily caused by insulin-dependent diabetes mellitus and alcoholism-induced polyneuro pathy, tabes dorsalis and syringomyelia, but the latter two nowadays are rather rare. Clinical picture and diagnosis. Neuro genic arthropathy induced by alcoholism and diabetes mellitus chiefly affects thefoot joints, while transformations caused by tabes dorsalis primarily involve the h ip and knee, and the syringomyelia form develops in the upper limbs. The process may in some cases be bilateral and symmetrical . Foot transfor mations caused by alcoholism and diabetes are accompanied by chronic edema, hyper emia, trophic skin and nail alterations, pain less ulcers on the soles of the feet, foot defor mities (see also chapter 30). Chiefly the tarso metatarsal and the metatarsophalangeal j oints are affected, and the joints of the ankle to a
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much lesser extent. The central leg and meta tarsal heads sink, causing hammer toes and serious deformations, leading to walking dif ficulties. Pain sensation is disturbed, numb ness and spasms develop, often coupled with motor disorders leading to muscle atrophy and weakening. Crepitation and subluxation may be detected, articular liquid collection develops which may occasionally be blood. There is great inconsistency between the seri ous clinical symptoms and the lack of pain sensation. Precise neurological examination is vital and must include tests of the sensation of position and vibration sense as well as re cording of electrophysiological parameters .
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bohydrate metabolism and elimination of the risk factors responsible for the damage of the vessels of the nerves (e.g. lipid metabolism disorder, hypertension, smoking) are all im portant. Medication of value for the symptom atic treatment includes various B vitamins, tricyclic antidepressants and anticonvulsive agents if needed. The limbs must be relieved from weight-bearing with the help of orthope dic insoles and shoes and protected from in jury. If the illness has progressed, orthopedic intervention will be the only effective treat ment.
Radiologically
19.4.2. Hemophilic arthropathy
Stage I.: osteoporosis, cortical defects and subluxations. Stage 11.: osteolysis, fractures, fragmentation and incipient periosteal reactions. Stage I ll.: severe hypertrophic arthrotic phenomena, serious bone defects, and in certain cases a n kylosis (Fig. 19. 12).
Hemophilic arthropathy is a degenerative ar ticular alteration due to repeated intra articu lar bleeding. It is mostly due to the lack of factor VI II. (hemophilia A) or factor IX. (he mophilia 8).
In the differential diagnostics, the distinc tion of septic arthritis, osteomyelitis and osteonecrosis is of primary importance . Therapy. Treatment of the basic illness, alcohol prohibition, correct control of the car-
Fig. 19.12. Neurogenic arthropathy caused by tabes dorsalis in both hip joints, with significant destruction and bi zarre bone formations.
The prognosis of the disease depends on the serum level of the factors : the condition is critical if the serum concentration level is be low 1 % of, intermediate, if it is between 1 -5%, and mild if it is between 5 - 1 5%. A mi nor trauma, or no trauma at all, may still ac company continuous articular hemorrhage (hemarthros). As a result the nourishment of the hyaline cartilage breaks down and chronic pigmented villonodular synovitis-like inflam mation develops on the synovial membrane which in turn extends to the cartilage (pannus development) and destroys it. Later cysts de velop in the subchondral bone leading to seri ous destructive arthrosis at a rather young age (Fig. 19.13 a-c). Hematological care and fac tor supplementation are important. If arthrosis or articular destruction has already occurred, arthroplasty has to be taken into consider ation. Serious contractures and axial deformi ties are contraindicated and it is important to note that the surgical complications are much more frequent than in normal cases of old-age arthroplasty.
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19.5. Performing surgery i n arthritis Rheumatoid symptoms chiefly indicate chronic multisytemic diseases affecting the cartilage, bone, tendon, muscle and internal organs. In rheumatoid arthritis, synovial inva-
a
b 5% 3%
1%
c
24%
11%
32% ----4
24% -----t
Fig. 19.13. a: Swollen knee joint of a hemophilic child b: X-ray image of the seriously destroyed knee joint in the same patient c: Surgical picture of articular destruction, pannus development.
Fig 19.14.
Distribution of ailments of 200 patients with some type of articular disease.
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sion destroys the articular surface, while the rheumatoid pannus damages adj acent tissues. Bone destruction, erosion, cyst formation and osteoporosis j eopardizes the skeletal integrity and, since ligaments and tendons are also af fected (destruction, rupture), the result is ar ticular instability. The aim of the treatment concerning patients with rheumatoid arthritis are to eliminate the pain and improve the j oint function and hence the quality of life for the patient. From a surgical point of view, rheumatoid patients pose numerous problems (Fig. 19.14): � �
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If many joints are affected it is difficult to choose the "target joint". In order to rehabilitate the patient, a series of surgical interventions are often necessary, cooperation of the patient in such cases is indispensable. As internal organs are affected, pre operative preparation and postoperative care are necessary. Rheumatoid patients frequently exhibit atlanto-axial articular synovitis, sub luxation and luxation, which requires anesthetic vigilance. Insertion of the intratracheal tube can pose a threat due to the possible neurological complications . Examination and if needed, stabilization
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of the neck segment of the spine for patients with RA are therefore essential. Steroid treatment and the basic illness itself can damage various structures. Accordingly, the most gentle surgical techniques are required. Because ofthe skin changes that occur in a rheumatoid patient, wound healing is often a problem. Because of the immunodepressed state, rheumatoid patients are more vulnerable as concern septic complications. For patients who have received steroid treatment, surgery is performed with an elevated amount of medication and the initial amount is gradually restored during the post operative phase. The preparation of the patient, defining the indication, forming the strategy, the post operative therapy and the long-term treatment is largely based on the close cooperation of the surgeon and the rheumatologist.
From a surgical aspect, the disease has an early, an intermediate and a late stage, corre sponding to the Steinbrocker stage classifica tion (Table 1 9. 1 .) . Surgical procedures can b e classified to operations performed on soft tissues, bones and joints .
Table 19.1. Surgical interventions according to the stages of rheumatoid diseases Surgical stages
Early
Intermediate
Late
I and (11) No radiological destruction, osteoporosis may occur locally
(11) and Ill. Various degree of osteoporosis, cartilage and bone destruction, deformities, subluxation, restricted mobility
IV. Rbrous or bony ankylosis, significant deformities, extra-articular soft tissue alterations
Nature of surgery
Preventive - curative
Plastic - reconstructive
Salvage
Type of surgery
Synovectomies tenosynovectomies
Ligament reconstruction, Resection, arthroplasty, arthrodesis tendon transpositions, tendon reconstructions i nterpositional arthroplasty, prosthesis implantation
Main symptoms (Steinbrocker stages)
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Surgery on soft tissues: synovectomies tenosynovectomies ligament transpositions ligament reconstructions Surgical procedu res on bones and joints: arthrodesis osteotomies resection arthroplasty interpositional arthroplasty alloarthroplasty (endoprosthesis im plantation) a
As regards to local preventative/curative interventions in rheumatoid arthritis, the main mean intervention is early synovectomy to eradicate the synovial invasion; this solves the ongoing complaints of the patient, and at the same time prevents or hinders the progression of the process in the specific joint.
b
Hand surgery. When synovitis that has been present for longer than 6 months and has not responded to conservative treatment af fects the metacarpophalangeal (MCP) joint, early stage synovectomy can help prevent the tri-articular system from reaching the col lapsed deformity stage (Fig. 1 9 . 1 5) . Correction ofthe typical ulnar deviation o f the fingers is achieved by centralization of the middle extensor tendon and its fixation at the level of the MCP j oint. If the "button hole" or "swan neck" deformities have already devel oped, surgery is possible only if it is suppleFig. 19. 16. a : Serious ulnar deviation of fingers o n a rheumatoid hand b: Arthroplasty of I I-V. MCP joints with silicon pros thesis implantation: the correction of the axis of the MCP joints can be clearly seen.
Fig. 19.15. Synovitis of the metacarpophalangeal joint and mild palmar subluxation of the fingers.
mented with ligament-plasty and tendon plasty. In order to restore the function of the hand arthroplasty has to be performed in the metacarpophalangeal articular line with the insertion of silicone prostheses (Fig. 1 9 . 1 6. a, b) This is also possible with the proximal interphalangeal (PIP) joints but arthrodesis in
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a functional position may also be performed. Stability of the distal interphalangeal (DIP) j oint in a pathologic position can be restored by performing arthrodesis. Wrist j oint surgery. Dorsal tenosynovitis requires synovectomy, whereas palmaris tenosynovitis causing median nerve compres sion requires tenosynovectomy and decom pression of the median nerve by incision of the transverse carpal ligament. The invasive synovial tissue destroys the tendons, if bone destruction occurs, the un even, protruding end of the ulnar bone (Lister tuberculum, or ulnar head syndrome) may in duce extensor tendon ruptures . It is extremely difficult to restore the continuity of the ten dons . When the tendons are fibrillated and de stroyed, uniting the ends is practically impos sible. Reconstruction can be performed only if the distal ends of the tendons are attached to the remaining mobile motor. This can be done with the tendon of the m. indicis proprius but also by suspending the distal parts of the de tached tendons IV. and V. to the remaining Ill. and 11. tendons in the shape of a roller-blind. If the rupture was caused by the ulnar head syndrome by the protruding ulnar end (piano key sign), ulnar head resection has to be performed. This involves retinaculum plasty and repositioning of the m. extensor carpi ulnaris. In case of ulnar head syndrome, ulnar head silicone prosthesis implantation surgery is also an option. Arthrodesis and wrist prosthesis implants are the key procedures when it comes to han dling wrist joint problems . If the wrist is af fected by pain, destruction or subluxation, re section of the destroyed surfaces, radiocarpal arthrodesis may be performed in a slight dor sal flexion and midposition. This is a favor able setting considering the function of the hand as the flexor, and the extensor muscles can therefore function optimally. If the patient does not engage in laborious physical work and does not have to exert large forces, and ifthere is a significant destruction, complete wrist joint silicone prosthesis im plantation may be performed, but it must be
borne in mind that this is a compromise be tween stability and mobility. Elbow j oint surgery. Synovectomy can be performed with radius head resection. In these cases, synovectomy is possible more ex tensively. However, some authors restrain from removing the radius head as it may cause instability. In the event of serious destruction, resec tion arthroplasty was earlier an accepted sur gical method which eliminated the pain, but it resulted in a limited functional outcome and in instability. If the degree of resection is minimal, interpositum can be used to cover resection surfaces. (e.g. fascia, dura mater). Some au thors report success, but the long-term func tional results are uncertain and instability and subluxation often occur. Arthrodesis used to be a standard surgical intervention, but today (especially if the prob lem is bilateral) it is avoided. Development in recent decades have had the aim of compen sating for the deficiencies of the firs generation wrist joint prostheses. Erosive destruction, a narrowed joint and significant pain are all indicatory. In summary, synovectomy and arthro plasty are currently the most accepted meth ods for the treatment elbow deformations in RA. Shoulder surgery. Surgery on rheuma toid shoulders also include various proce dures similar to those mentioned above. In rheumatoid arthritis extended inflammation of the subacromial bursa and the subdeltoid bursa, destruction and rupture of the rotator cuff and glenohumeral synovitis we are often observed. These conditions can be treated by arthroscopic synovectomy or open surgery. Reconstruction of the rotator cuff and acromioplasty can be performed similarly us ing both methods. In cases of major articular destruction, glenohumeral arthrodesis is a possibility, but from a functional point of view the most suit able procedure is shoulder joint endo prosthesis implantation.
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Hip surgery. Synovectomy has not be come very widespread in treating h ip joint transformations due to the special anatomic factors and the unique hip processes. The hip is the joint that is subjected most frequently to prosthetic procedures. Knee surgery. Arthroscopic or open sur gical synovectomy of the knee may delay the destruction of the cartilage for quite some time. If destruction should occur, arthrodesis is performed much less frequently nowadays. From a functional aspect, the best solution lies in the implantation of a total surface replacing endoprosthesis. Following a certain progression of the dis ease, the foot is also damaged in 80-90% of the cases. Foot surgery. The hindfoot is involved in 50-70% of advanced cases of the disease, and in 70-80% of the cases the forefoot. If the tar sus is involved, synovectomy and subtalar and Chopart arthrodesis may be necessary. Apart from the generally known proce dures mentioned above, complex rheumatoid forefoot deformities may be treated by resec tion of the metatarsus heads according to Clayton-Hibinette or by subcapital metarsal osteotomies according to Helal. Ankle and hallux j oint endoprostheses are not very popular. Arthrodesis may be per formed only if strict certain individual criteria are strictly satisfied, since, besides achieve-
ment o f stability, the ability to bear weight and painlessness, the articular mobility is lost. This leads to walking difficulties, which in turn means a limited environment, as well as overloading and acceleration of the degenera tive processes of the neighboring joints. Surgical treatment of spondylarthritis ankylopoetica (SPA). From a surgical as pect, the treatment of SPA poses a special problem. In about one-third of the cases arthrosis develops in the hip (usually bilater� ally) which ends up as a fibrous or bony ankylosis. If the hip is in a flexion position, this further worsens the limited ability to look forward, caused by the kyphosis. Conversion arthroplasty may be per formed by implanting a hip endoprosthesis. In such cases the flexion contracture of the hip joint resolves, extension becomes possible and the straightening of the torso increases the distance of forward vision. In certain cases, it may be necessary to consider bilateral hip arthroplasty in one ses sion. An applicable surgical procedure in cases of a maj or degree of kyphosis is spinal osteotomy. All procedures have the aim of wedge resection of the vertebral arches of the involved spinal segment CL 2-3 -4), exposure and preparation of the dura and the roots, then reclination and stabilization of the spine (Fig. 1 9 . 1 7 and 1 9.8).
b
Fig. 19.17. Picture of open wedge osteotomy.
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Fig. 19.18.
a
Picture of closed wedge osteotomy.
b
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19.6. S}'novial chondromatosis Synovial chondromatosis is a rare tumor-like transformation of the synovial membrane which usually occurs between the 2nd and 5th decade of l ife and is typically accom pa nied by cou ntless cartilaginous loose bodies p roduced by the synovial membrane.
Etiopathology. Initially microscopic metaplastic cartilage tissu begin to accumu late in the synovial membrane, later these islands grow to such an extent that clusters be come visible to the naked eye and are finally detached into the joint and behave as free bod ies. In the later phase of the disease, the ex panded articular cavity may contain many hundreds of cartilaginous free bodies, mea suring 0 . 5-2 cm. Clinical symptoms. The knee, hip, elbow and shoulder joints and the temporo mandibular j oint are most often affected. The j oint becomes swollen, the articular mobility is reduced and the patient complains of articu lar blocks and clicking. X-ray symptoms. Initially, the cartilagi nous bodies are not visible in the X-ray pic tures. They become visible only later when they become calcified (Fig. 1 9 . 1 9.). The MR
and eT images display typical intra-articular free bodies. Treatment. The surgical solution is expo sure of the joint, the removal of cartilaginous free bodies from the joint and subtotal synovectomy to prevent further development of the cartilaginous bodies. Very rarely, ma lignant transformations can occur in the carti laginous substance. In such cases, the process accelerates and becomes destructive.
19.7. Pigmented villonodu lar synovitis (PVNS) This disease i nvolves alterations in the synovial membrane in the joints, bursae and tendon sheaths and is categorized today as a benign tumor rather than an inflammatory disease. The proliferative tissue collection re sults in swelling of the joint, expansion of the capsule, but it may destroy the bone too.
Etiopathology. It is quite a rare condition. There are two forms : nodular and diffuse, also known as benign synovioma and primarily starts from the tendon sheaths of the fingers. From a histological aspect, both involve the proliferation of the cells lining the synovial membrane and the mesenchymal elements . Macroscopically, the synovial membrane padding the joint becomes thickened and the synovial villi, which are discolored brown ish-red from the haemosiderin also thicken to resemble the fingers of a glove. Clinical symptoms. It can occur at any age but is most frequent in young adults. It primarily affects the knee, the hip and the shoulder. The major symptoms include swell ing of the joints, pain, immobility, and in 75% of the cases intraarticular bleeding and hemarthros also develop.
Fig. 19.19. Widened elbow capsule surrounding numerous ar ticu lar free bodies with typical calcification
X-ray signs. Initially, there are no charac teristic X-ray alterations. In the later phase of the disease cystic defects may develop in the
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bones making the joint in question (Fig. 1 9.20. a-c) . An MRI demonstrates a charac teristic change in signal intensity due to the tissue proliferation and its increased haemo siderin content. Treatment. Exploration of the joint and removal of tissue proliferation by subtotal synovectomy are required; in some cases ra dio-orthesis is also an option, which in prac tice means that an isotope is inj ected in the cavity of the joint. Irradiation of the lesion is rarely used nowadays, due to the side-effects. Recurrence of the process is not rare. In case of serious bone destruction, synovectomy is combined with endoprosthesis implantation.
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19.8. Arthrosis (osteoarthritis) As concerns all of the tissues making up the skeleton, degenerative (regressive) trans formations, are most common and most pro nounced in the cartilaginous tissue. Damage to the metabolism of the cartilaginous cells and to the structure of the intercellular sub stance also causes the mechanical characteris tics of the cartilaginous cells to change. As a result ofthe degenerative processes relating to the tissue, the structure of the cartilaginous tissue may be completely disorganized and destroyed. The degenerative transfo rmations affecting the joint that are manifested i n typical clinical symptoms a re referred to as arthrosis
b c
a
Fig 19.20. a. Acetabulum destroyed by PVNS (area illustrated by arrows). b. The involvement of the femoral head and the acetabulum can be well observed in a a picture. c. The swollen synovial membrane removed from the joint.
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1 9 . D i se a s e s of j o i n t s a
b
Fig 19.21. Arthrosis of the hand, I. (PM joint in an X-ray and demonstrated in an overview histological picture.
deformans. The degeneration and g radual
devastation of the articular cartilage is accom panied by significant changes in the bone structure of the joint endings, d isordering of the synovial membrane (synovitis) and modifi cation of the structure of the tissues of the joint capsule. Besides degenerative processes, proliferative tissue development may also be observed at the joint endings (e.g. the devel opment of osteophytes). Alterations of this kind give rise to deterioration of a rticular function and pain (Fig. 19.21.).
The frequency of arthrosis increases rap idly after the age of 40. However, it also de pend on the joint. It is more common in the hand, hip, knee and spine, than in the ankles, wrist, elbow and shoulders. Arthrosis can de velop simultaneously in many joints, conse quently, 70% of people over the age of 65 have some kind of arthritic ailment. If some alteration in the metabolism or structure of the articular cartilage is related causatively only to a constitutional defect in the articular cartilage or to old age, it is re ferred to as a primary degenerative alteration (primary arthrosis). On the other hand, if the degeneration of the joint is initiated or pre-
ceded by a disease (arthritis, osteochondrosis, etc.) trauma or the incongruence of articular surfaces, it is called a secondary arthrosis. In the latter case, the articular transformation (disease) initiating the arthrosis is called a state of prearthrosis. The character of the structural change in articular cartilages and bone endings in joint areas, where the pressure is more intense (weight-bearing zones) differs from that in other areas where there is only limited or no pressure (non-weight-bearing zones).
19.8. 1. Alterations in various parts of the joint �
Weight-bearing zone, alterations of the hyaline cartilage The articular cartilage is the primary indi cator of the start of degeneration. In some places, the surface of the articular cartilage splinters and cracks, its chondroitin-sulfate content decreases, and the surface loses its smooth, shiny character. The structure of the deeper layers also changes, in some places this means swelling, in others the structure be comes crumbly. The number of cartilage cells
1 9 . D i s e a s e s of j o i n t s
a
b
•
Fig 19.22.
gradually decreases and irregular, island-like cell groupings develop at certain places. Cal cified salt deposits may also develop in cer tain layers of the articular cartilage. Conse quently, the integrity of the cartilaginous tis sue gradually ceases in these spots, and the forces affecting the surfaces of the j oint cause
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smaller parts o f the articular cartilage to drift off or become detached from the surface, and ulcers develop on the articular cartilage. In the degenerated areas ofthe j oint cartilage, newly formed blood vessels enter the basal layers of the cartilage from the medullary cavities of the cancellous bone through the subchondral bone, the hyaline tissue begins to degrade and new cartilage tissue of lower quality (fibrous cartilage tissue) commences to develop in the vicinity (Fig. 1 9.22. a, b). Impairment ofthe cartilaginous tissue usu ally starts in an overloaded segment of the ar ticular surface and later spreads to other areas. Various stages of the degenerative process may therefore be simultaneously observed in different segments of the articular surface. The situation is similar in the joint sur faces; if the degenerative process begins at one joint surface, the affected cartilage is ini tially in contact with the healthy cartilage of the other joint surface, but after a certain pro gression, degeneration appears here as well. As a result of the degeneration of the articular cartilage, the bone endings of the joints par tially or completely lose their cartilaginous coating, i.e. their surfaces consist of bare bone tissue. During arthroscopic examinations, the ar ticular cartilage can be examined. According to the above characteristics, such examina tions reveal four stages of articular cartilage alterations (chondropathies): •
a: Normal and b: degenerative articu lar cartilage.
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1st stage: the surface is rough, has lost its gleam and is soft 2nd stage: there a re cavities and fissures on the surface of the a rticular cartilage 3rd stage: the surface of the a rticular cartilage is cracked, discontinuous, some segments can be mechanically separated. 4th stage: there is an u lcer-like defect of cartilaginous tissue on articular surface, the subchondral bone appears (eburneation).
Extensive transformations, corresponding to 2nd-4th stage can be considered symptoms of arthrosis if they emerge during old age.
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1 9 . D i s e a s e s of j o i n t s a
b
Degenerative cysts in the femur head a: Overview histological picture, b: intra operative picture.
19.8.2. Alterations in the articular endings of bones The internal structure of the articular end ings of bones is also modified due to the change in the pressure conditions. In the vi cinity of the j oint surface the cancellous trabeculae thicken as a result of lamellar new bone formation in certain areas (sclerosis). In other regions bone cavities of various extent are formed due to the active resorption of the bone trabeculae (degenerative cysts, Fig. 1 9.23, a, b). Therefore, when the joint is placed under pressure, there is a morphologi cal possibility for the articular liquid to be squeezed toward the cysts and the cavities of the spongiosa which in turn will lead to an in crease of the intraosseal pressure and thus the development of pain.
tory area of the cartilage synovial membrane, multipotential cells begin to generate new bone tissue, and osteophytes develop (Fig. 1 9.24.). The gradual growth of osteophytes changes the shape of the endings of the joints and the j oint congruence as well as causes strain in the articular capsule.
19.8.3. Transformations in the non-loaded zone, osteophytes Even in the early phase of articular degeneration next to the articular edge in the transi-
Osteophytes in the edge zone of the femoral head.
1 9 . D i s e a s e s of j o i n t s
19.8.4. Changes in the articular capsule The cell layer covering the synovial mem brane becomes multilayered, thickens, and the villi become larger. The detached and de generated cartilage particles embed them selves in the synovial membrane, where they are finally absorbed. In the connective tissue layer of the synovial membrane, aspecific chronic inflammation develops (synovitis) . Similar processes take place i n the fibrous layer of the articular capsule: the articular capsule thickens and shrinks. Calcium salts may also be deposited develop in the articular capsule or in its vicinity (capsule calcifica tion).
19.8.5. Symptoms
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movement and load-bearing and ceases during rest. In most serious cases, a blunt or piercing pain becomes permanent and its intensity prevents all activities for the patient. The pain originating from the straining muscles in contracture also contributes to the increase in articular pain. Immobility (contracture). Due to the defensive contracture of the muscles and the shrinking of the articular capsule, the articular mobility range gradually decreases. Deformation of the joint endings leads to a decrease of articular movement and to changes in movement direction. Deformation. The shape of joints that are in a superficial position (elbow, fingers, knee) become more weighty and deform due to the osteophytes and the swelling of the joint. During examination the osteo-
Clinical symptoms. Arthrosis may de velop in any joint, but it occurs most fre quently in the vertebrae, in the smaller j oints of the hand and in the weight-bearing joints of the lower limbs (hip, knee, foot). Arthrosis rarely develops exclusively in a single joint, it usually affects numerous j oints. The clinical progression of the disease is indicated by the repeated appearance of symptoms and by an increase in their fre quency, so that they may even become perma nent. �
Pain is the primary indicator of arthrosis. In most cases the onset, intensity and type of the pain changes as the degenerative process progresses. The earliest, but not typical symptom is fatigue or blunt pain following strenuous work. The genuine early pain form is the initiating pain which occurs when the patient starts to move hislher j oints, e.g. when taking first the steps in the morning. During continuous movement the intensity of the pain subsides and it may even cease entirely: the joint has "warmed up". Simultan eously the articular stiffness also gradually abates. Later, the pain arises during
Fig 19.25. Degenerative cysts and sclerosis in the femoral head and the acetabulum, the joint space has narrowed in the pressure lone.
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1 9 . D i se a s e s of j o i n t s
phytes can be palpated and the patient is usually sensitive to pressure at these sites. Crepitation. A cracking can often be heard while the joint is in motion, which can be uncomfortable and painful for the patient.
X-ray signs. In the initial phase of the de generative process, no changes can be de tected on X-ray examination, however sec ondary arthrosis displays an abnormal articu lar picture (dysplasia, subluxation). Early signs of arthrosis include narrowing of the j oint space, subchondral sclerosis and osteophyte development. As the condition progresses, the articular gap steadily narrows and degenerative cysts of different sizes de velop in the subchondral zone. The j oint space in the pressure zone progressively contracts and the structural changes in the bone esca late. Finally, the joint endings are signifi cantly deformed, the j oint space disappears and the bone surfaces converge (Fig. 1 9.25).
The conservative and surgical procedures during treatment are closely harmonized. �
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19.8.6. Treatment of arthrosis The patient should be informed about the chronic and progressive character of the dis ease, as well as its expected outcome, and all possibilities which could lead to an improve ment, or with a reduction, or even complete termination of the complaints. The patient 's cooperation is vital to provide successful treatment. General advice. A reduction of the load (overload) on arthrotic joints is significant step. Overweight patients should therefore lose weight (by dieting) under medical super vision. A weight gain usually leads to an esca lation of the complaints. Exercises involving non-weight-bearing or swimming promote the metabolism of the cartilage cells and thus reduce pain. Permanent immobilization of an arthrotic joint should be avoided as it leads to a further deterioration in the metabolism of the joint and intensifies destruction. After pregnancy and child-bearing, a dete rioration of hip arthrosis and the escalation of related symptoms are to be expected.
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Conservative treatment Medication. No specific medication is currently available to cure for arthrosis, however chondroitin-sulfate medications does exert a positive effect on the progression of arthrosis. Pain killers, salicylates, non-steroidal anti-inflam matory drugs and muscle relaxants have beneficial effects. The use of steroids is very rarely necessary (in arthritis that does not respond to any other medical treatment and there is a large fluid collection in the j oint) . Physiotherapy. This too has a beneficial effect and can be of great help in the treatment of arthrotic patients. It is especially useful in reducing articular contractures and pain as are curative massages and underwater exercises. Extension treatment. This treatment can provide relative comfort and relief from pressure leading to a decrease in pain and possibly even termination of the contractures. It is primarily used in degenerative diseases involving the lower limbs and spine. Therapeutic X- ray irradiation. This may assist in relieving pain completely. However, depending on the patient' s radiation exposure this treatment can usually be repeated only after an interval of some years .
The various conservative treatment meth ods are usually employed simultaneously. Surgical treatment. The aims here are to reduce pain as well as, to improve the joint function and to correct the deformities that have developed. Accordingly, osteotomy, arthroplasty and arthrodesis may be per formed. Surgical procedures relating to spe cific joints are dealt with in the appropriate sections .
20.
J6zsef La katos
Bacterial infections of bones and joints
Inflammation of the musculoskeletal sys tem may be of various origins. �
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Reactive, sterile arthritis types: transitory after abdominal surgery caused by a metabolic disturbance (gout) accompanying arthrosis Viral, mycosis Specific (tu berculosis or syphilis) Accompanying rheumatic disease Bacterial Iatrogenic
The above classification is an arbitrary one. Transitory arthritis which appears in childhood and generally ceases spontane ously, will be discussed separately (see Chap ter 28. 1 ). Sterile inflammation can also be experi enced in degenerative diseases with articular erosion and as a result of the deposition of metabolic products in the j oints. In rheumatic diseases, one of the sites of the pathological process is the synovial membrane. The vari ous types of synovitis with quite different eti ologies mostly cause similar symptoms and have to be taken into consideration in the dif ferential diagnosis . Inflammations of the osteoarticular sys tem are from some respects different from those of the parenchymal organs. Some parts of the bone act as bradytrophic tissue and it is therefore difficult to attain a therapeutic con centration of antibiotics. There are a limited number of antibiotics that accumulate at an optimal concentration in the bone. Articular movement makes the elimination of the in flammation more difficult. An inflammatory process (mainly bacterial in origin), in some
circumstances can recrudesce in the bone or in the synovial membrane after years or decades. Hence, in many cases it is not possible to be certain whether the process has merely paused, or the healing is permanent. Acute and chronic inflammation of bones and j oints is often caused by bacterial infec tion . Before the discovery of antibiotics, these diseases were life- threatening. Since the in troduction of antibiotic treatment however, the results are more favorable, though the ability of the pathogens to resist antibiotics makes the selection of a potent antibiotic dif ficult.
20. 1. Osteomyel itis This is the inflammation of bone and bone marrow, caused by pyogenic pathogens. It can develop as a consequence of hematogenic or external (fractures or surgery) infection.
20. 1 . 1 . Acute hematogenic osteomyelitis This condition can occur in infancy, in the neonatal period, in childhood and in adult hood equally. The course depends on the age of the patient, the virulence of the pathogen, the immunological state of the organism, the localization of the infection, and the features of the bone blood supply. Staphylococcus aureus is most frequently responsible for the development of acute hematogenic osteomyelitis; it can be demon strated in about 90% of the cases. However this disease can also be caused by any kind of pyogenic, mycostic, parasitic or viral infec tion.
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In 75% of the cases, acute hematogenic osteomyelitis is encountered in children and adolescents, though in recent years the acute form of vertebral osteomyelitis has been seen more often among adults and the elderly too, as a complication of inappropriately treated pneumonia, cystopyelitis, abdominal and mi nor pelvis surgery and after discus hernia sur gery with a febrile postoperative period. Etiopathology. Rosenbach found evi dence that the hematogenic osteomyelitis is caused by infection ( 1 878), and the predomi nant role ofthe Staphylococcus strains was re vealed by Becker in 1 88 3 . The behavior o f Staphylococcus strains in the pathogenesis of hematogenic osteo myelitis was examined a century ago by the surgeon Laxer. It is typical of the Staphylo coccus strains that the pathogenic organisms adhere together in the shape of a bunch of grapes. These conglomerates (bacterial emboli) can collect in the capillary system of the bones and even in the nutrient arteries. The characteristics of the blood supply have been known since the researches of Treat ( 1 959). Because of the terminal arteries, the vascular system of the metaphysis provides the greatest potential for the bacterial emboli to adhere and thus the danger of the develop-
ment of osteomyelitis caused by pyogenics is most pronounced in the metaphysis. The extent and the course of the process and its localization in the bone depend on the anatomical features of the blood supply. �
Among neonates and infants (under the age of 1 year) the blood vessels penetrate the growth cartilage for the epiphysis. This makes it possible for the inflammatory focus in the metaphysis to break into the epiphysis, causing purulent arthritis in the joint (see Chapter 20.2). It is extremely important if the infection occurs at the proximal end of the femur, be cause of the intra-articular localization of the metaphysis (Fig. 20. 1 .). At this age severe destruction of the joint and the growth cartilage and longitudinal growth disorder are typical (Fig. 20.2.).
Fig. 20.2. Fig. 20.1. Epiphyseal osteomyelitis i n infancy, with destruction of the left hip metaphysis.
Late result of epiphyseal osteomyelitis that occurred in infancy: the right hip joint has been destroyed, the head and neck of the femur are damaged, the metaphysis is widened, and the limb is shortened.
2 0 . B a cte r i a l i nfect i o n s of b o n e s a n d j o i n t s
I n infancy, osteomyelitis I S called epiphyseal osteomyelitis. The process generally develops in the proximal and distal metaphysis of the femur,
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in the proximal metaphysis of the tibia and the humerus, and in the distal metaphysis of the radius (Fig. 20.3. a, b, c) .
a
b c
Fig. 20.3. a: Result of distal femora l metaphyseal osteomyelitis that began in a neonate: serious bone defect and deformity at the age of 2. b: At the age of 2 1/2, the medial femur condyle was re placed by a bone graft taken from the iliac crest. c: The redeveloped, sufficiently congruent femoral condyle at the age of 6 1/2.
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In childhood (after the age of I) the growth plate, except for a narrow peri pheral part, becomes impenetrable for the blood vessels, and accordingly the j oint is protected from the spreading of the in flammation that has developed in the metaphysis. After the course of the disease, growth im pairment is rarely experienced. Because ofthe excitement of the growth zone, hypertrophy of the bone can occur, similarly as in inflam mations caused by nonpyogenics e.g. in rheu matoid arthritis. �
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In adulthood, the growth cartilage ossifies, and because of the developed vascular system the purulent bone process can break into the joint. The periosteum adheres tightly to the bone, and therefore cannot be elevated easily from its base by the pus. The process mainly occurs inside the bone. In the absence of re storative ability, a chronic course and relapse are frequent. In general this condition can develop in the extremity bones, the short, flat bones, the pel vis, and the vertebrae. B acterial emboli that have entered the blood stream can become blocked in the capil lary system of the metaphysis, causing an acute inflammatory bone process and various extents of osteonecrosis. An abscess can de velop and can spread through the Haversian and Volkmann canals to the medullary space and the periosteum. The periosteum is lifted by the abscess, and in severe . cases it can break out into the soft parts . C linical symptoms. The onset of hemato genic osteomyelitis often remains unnoticed; the patient and the relatives merely recall the septic condition accompanied by fever. The patient frequently presumes a connection be tween the condition and some traumatic event. Thorough questioning generally re veals information concerning dermatological or dental illnesses, urinary infections, pneu monia or previous operations involving com plications.
The pain persists even when the patient is in a resting position, and at night it can inten sify and pulsate. The reason for this is the in creasing pressure in the medullary space, which is unable to expand. The limb can display pasty consistency, or a hard substance; if the abscess breaks through the bone into the soft parts, fluctua tion can be observed. An atypical, but not rare symptom in in flammations in deep-lying bones, is that above the infected area the temperature of the skin increases (calor heat); this may be de tected by comparative palpation of the two sides. The impaired function ofthe inflamed area (functio laesa), is caused by the pain and also by the muscular spasm induced by the pain. This is manifested in the resting of the limb, contracture, and restricted movement of the involved j oints. The disease usually begins rapidly and dramatically, with a high fever, shivering and prostration. Because of the frequent usage of antibiotics, these symptoms may be compara tively slight, assuming an atypical form, and this can impede an early, correct diagnosis. Laboratory examinations show numerous typical differences. In acute hematogenic osteomyelitis, the erythrocyte sedimentation rate ( l OO mmIh), and the protein level in the acute phase (C-reactive protein) can be ex tremely high. Besides a high leukocyte count, the differential blood count is noticeably shifted to the left. In a septic condition, the patient easily be comes anemic; a decreased red blood cell count, the hemoglobin level, the renal func tion, and the liver function are therefore im portant features. =
X-ray signs. In inflammatory bone pro cesses, the X-ray signs appear after 8- 1 0 days in children, and 2-3 weeks later in adults. The bidirectional X-ray image demonstrates typi cal alterations . The inflammatory process is surrounded by an atrophic bone structure. The purulent, confluent foci induce the resorption of the
2 0 . B a ct e r i a l i nfect i o n s of b o n e s a n d j o i n t s
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bone trabeculae, and i n these cases, an exten sive rarefied area can be seen inside the atro phic environment, with an indistinct periph ery and an elevated periosteum, which ap pears as a continuous, narrow strip (Fig. 20.4.
a, b). Later, the focus is surrounded by a scle rotic area with increased X-ray density; the thickness of the bone is increased by the periosteal reaction. Some parts of the bone can necrotize, and later the necrotic cortex is surrounded by a sequestrum: the necrotic bone part sequestrates (see: Chapter 20. 1 .2). If the inflammation breaks into a j oint, the articular surfaces can be rough, and the effu sion increases the distance between the sur faces. Later, if the process becomes chronic, since the chondronecrosis narrows the j oint space, the articular destruction increases. In destructive inflammatory processes of the tu bular bones, pathological fractures can occur. Bone scintigraphy is a useful, but nonspe cific examination technique which is per formed by the administration of 99mTechne tium phosphonate or 67Gallium citrate. Though the technetium procedure is non specific, it shows a technetium isotope con centration in inflammatory areas, even in the early stage of the inflammation, when the X-ray image still appears negative. This con centration is as a result of the increased circu lation and osteoblast activity. Fistulography is a radiological examina tion technique, adopted for the determination of advanced processes, the expansion of bone cavities or the presence of a sequestrum. For this examination, contrast material is inj ected into fistulous canals, after which X-ray exam ination is performed. Inflammatory bone destruction can be checked by means of CT, while the intra medullary extent of the process and the edema of soft parts can be demonstrated through MR!. These examinations have led to a great advance in the differential diagnosis of in flammatory bone processes, and especially in the distinction from other, generally tumorous processes.
Fig. 20.4. a: In the femur diaphysis, a lytic rarefaction can be observed, with a sclerotic edge at some sites, with a shadow that may indicate the presence of a sequestrum with a periosteal reaction. b: The MR image (horizontal reconstruction) reveals the edema of the neighboring muscles.
Diagnostic algorithm. The clinical pic ture, the X-ray signs, and the laboratory ex aminations provide a sufficient basis for the correct diagnosis. Identification of the patho gen is followed by the establishment of the an tibiotic sensitivity of the bacterium in order to
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formulate a treatment plan. Material including pus, tissue and detritus, taken by puncture or instrumental biopsy, is subj ected to general bacteriological examination, Koch culture, cytological examination and histological ex-
amination, so as to confirm the diagnostic sus picion. In a septic condition, with febrile periods, hemoculture examinations help to reveal the pathogen.
Table 20/1. Antibiotic treatment Generic name
Commercial name
Mode of administration
Most frequent side-effects
Clindamycin
Dalacin C
iv. or orally
Abdominal pain, nausea, vomiting, diarrhea, esophagitis
Ciprofloxacin
Ciprobay, Cifran
iv. or orally
Amoxicillin + clavulonic acid
Gastrointestinal side-effects, impaired renal function, psychic effects, chillorhexis, pseudomembranous colitis
Augmentin
iv. or orally
Diarrhea, nausea, pseudomembranous colitis, candidiasis, hepatitis, cholestatic icterus, erythema mu ltiforme
Cefu roxim
Zinacef, Zinnat, Xorim
iv. or orally
Allergic reactions, erythema multiforme, pseudomembranous colitis
Vancomycin
Vancocin CP
iv.
Urticaria, pru ritus, asphyxia, hypotension, shock, nephro- and ototoxicity, thrombocytopenia
Teicoplanin
Targocid
iv. or im.
Exanthema, pruritus, fever, colic, anaphylaxia, shivering, u rticaria
Carbapenem
Meronem, Tienam
iv.
Inflammation at the site of administration, thrombophlebitis, pain. Allergic reactions, abdominal pain, pseudomembranous colitis, convulsions, candidiasis, headache, paresthesias
Netilmycin
Netromycine
iv. or im.
Nephro- and ototoxicity, headache, weakness, visual disturbance, disorientation, fever, tremble
Gentamycin
Gentamycin
iv. or im.
Nephro- and ototoxicity, vertigo, tinnitus, nystagmus, deafness, peripheral neuropathy, articular pains, psilosis
Linezolid
Zyvoxid
iv. or orally
Abnormal liver fu nction values, dysgeusia, diarrhea, nausea, vomiting, vaginal moniliasis, other laboratory divergences
Rifampicin
Rifamed, Tubocin
orally (in combination)
Colors the body fluids orange, hepatitis, nausea, vomiting, diarrhea, pseudomembranous colitis, pru ritus, ataxia
Fusidic acid
Fucidin
orally or iv. (in combination)
Gastrointestinal complaints, jaundice, allergic reaction, granu locytopenia, thrombocytopenia
2 0 . B a ct e r i a l i nfect i o n s of b o n e s a n d j o i nt s
Differential diagnostics. The clinical pic ture must be distinguished from Ewing tumor which gives similar laboratory and radiologi cal results. In Ewing tumor, the periosteal re action reveals an "onion leaf' structure and the roughness of the cortex from the direction of the medullary space. These can be distinc tive features. Treatment. One of the most important methods for the treatment of acute bacterial inflammatory processes of bone articulations is rest. Depending on the age, the general condi tion and the region, this can be bed rest, exten sion treatment, the application of plaster (im mobilization splints), a plaster bed, corset, etc. The treatment should start with a broad spectrum antibiotic that accumulates in ap propriate concentration in the bone tissue. Af ter this in the knowledge of the results of the bacteriological culture, directed antibiotic treatment should be initiated (Table 20/1 .). Antibiotics, most freq uently used to treat bone-articular infections, osteomyelitis and puru lent arthritis, together with the mode of administration and the most frequent side-effects (the dosages are specified in the usage instructions).
If a few days after antibiotic therapy is be gun there is no spectacular clinical improve ment and regression of the laboratory data surgical treatment of acute hematogenic osteomyelitis may be recommended (verte bral processes can be exceptions; see Chapter 24). Important surgical interventions: - Exposure of an abscess, and drainage of the pus - Exposure of an enclosed bone abscess by trepanation - Focus cleaning - Sequestrotomy The healing process is indicated by the subsidence of the clinical symptoms and the
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regression of the radiological picture, with the laboratory findings progressively becoming negative.
20.1.2. Chronic osteomyelitis Despite appropriately performed surgical treatment and massive a ntibiotic therapy, it can occur that � � �
the treated acute form becomes chronic; acute osteomyelitis relapses years later and becomes chronic; the acute period is passed in a subclinical form, which is manifested as a chronic condition.
Chronic osteomyelitis does not endanger the life of the patient, because a balance sets in between the inflammatory bone process and the resistance capacity of the organism. In the cancellous bone, bacteria can survive in a larvate condition, encapsulated by the scarry environment, and can subsequently become virulent again, thereby reactivating a process thought to have been healed. In the area of old inflammation, the skin becomes tight and red, the limb swells up, and fluctuation may be ob served, accompanied by fever, a high sedi mentation rate, and typical blood test alter ations. A fistula can develop in the soft tis sues, leading to regression of the clinical symptoms. In the event of retention, a re peated febrile condition must be expected. The frequency of acute hematogenic osteomyelitis in childhood and also that of the ensuing chronic bone processes have de creased in the last few decades. Strong new bone formation is typical of chronic osteomyelitis in childhood. The affected limb can thicken, and can even be longer than the contralateral limb. The X-ray image may reveal that the bone structure is altered throughout the entire length of the diaphysis. In adulthood the X-ray symptoms exhibit a rather varied pic ture. However the bone thickening due to the sclerosis is always typical (Fig. 20.5. a, b). In the sclerotic areas, sequestra are frequently
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found. If the lytic and restorative processes are in equilibrium, the X-ray picture resem bles a honey comb. Depending on the viru lence of the pathogens, large bone abscesses can emerge, with a tendency to distal spread ing. As this process progresses, pathological
a
b
fractures can develop. Fistulography and a eT scan can reveal the location and size of the in flammatory focus and the position of the sequestrum. Treatment. The process can drag on for decades, and the treatment therefore demands patience on the part of both the patient and the physicien. A good result can be achieved only from radical surgical intervention . Opening of abscesses, excochleation, and excision of fistulas afford only a temporary solution. Af ter the removal of necrotized tissues and sequestra, suction and irrigation drainage may be the best surgical choice, but success is not guaranteed. For the local antibiotic treatment of a cleaned bone cavity, polymethyl metacrylate beads (PMMA Septopal chain) containing gentamycin or some other antibiotic may be implanted. This is required, because the struc ture of the walls of the bone cavities (inflam mation barrier) impedes the achievement of an effective local antibiotic concentration if general antimicrobial treatment is applied. After focus-cleaning surgery, the remain ing cavities can be filled with a muscle lobe, autologous bone, etc. However, it may be taken as a principle, that in cavities involving active inflammation and containing purulent fluid, the implanta tion of foreign material or bone is not expedi ent until the process has subsided.
20. 1.3. Special forms of primary chronic osteomyelitis
Fig. 20.S. a: Picture of chronic femur osteomyelitis, with thick ening of the femur, and with a variety of lytic and sclerotic bone structure changes. b: The a scan depicts the extended periosteal reac tion.
Some types of primary chronic osteo myelitis can diverge from the general in ap pearance and course. Etiologically, the possi bility of the presence of a pathogen of low vir ulence may arise, though in most cases the agent cannot be isolated. These types occur in adolescence or at a young age, which suggests that intense tissue-protective mechanisms may play a role in the process. The history of the patients does not reveal septic or febrile episodes.
2 0 . B a ct e r i a l i nfect i o n s of b o n e s a n d j o i n t s �
Brodie abscess
This is an inflammatory focus that develops in the metaphysis of the bones. The typical signs are pain, limited joint movement, and a marginated, round or oval region of lytic de struction with a sclerotic margin in the metaphysis demonstrated by X- ray. This a b scess is often observed as an accidental find ing.
Brodie distinguished this alteration from other types of osteomyelitis long ago as 1 863 . Because of the relatively strong resistance of the organism and the low virulence of the pathogen, the inflammation process inside the bones appears in a larvate form. The cavity contains necrotic cells, granulation tissue and a dense mucous liquid, from which bacteria can not be isolated. The cavity is enclosed in a connective tissue envelope. Clinical symptoms. Mild swelling (in the event of a superficial location), tenderness, and sometimes a dull, dragging pain can be observed. The neighboring j oint can respond to the close-lying inflammatory focus with ef fusion and limited movement. Fever is not typical, and the laboratory findings are rarely informatory. X-ray signs. In the metaphysis of the fe mur, tibia or humerus, a round or oval, scle rotic-edged lesion, 1 -2 cm in diameter can be seen. Rarely there is a mild periosteal reac tion. Depending on the size, it may be neces sary to consider osteoid osteoma, osteo blastoma, benign chondroblastoma and bone cyst in the differential diagnosis. The essence of the treatment is exposure, excochleation of the cavity and autologous bone implantation, all under in antibiotic pro tection. �
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in a spindle-like form on the metadiaphysis of long tubular bones.
Symptom: pain. Occurrence : in childhood and adoles cence. Clinical symptoms: there is a subdued onset that drags on, with uncertain pain and f�brility, but without particular laboratory sIgns. In the X-ray image the diaphysis of the tibia or the femur exhibits an expressed scle rosis, with a spindle-like thickening and con siderable narrowing or the possible disappear ance of the medullary cavity. Differential diagnosis : the possibility of osteoid osteoma must be considered (Fig. 20.6.).
Garre osteomyelitis
This disease, described by Garre in 1893, is also called sclerotizing osteomyelitis, because of the predominance of sclerotizing and proliferative elements in the inflammation of long tubular bones. The major feature of this disease is the sclerotic thickening, developing
Fig. 20.6. Garre's sclerotizing osteomyelitis in the mid part of the tibia
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Treatment. Longitudinal sawing of the thickened cortex and opening of the medullary cavity can relieve the complaints, and the process may subside. A culture of the removed bone tissue is generally negative. The process can recrudesce years later, and the complaints and the pain can recur.
20. 1.4. Special forms of inflammatory bone alterations � �
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Iatrogenic infections Posttraumatic osteomyelitis I nfections in the environment of stabilizing and mobile implants
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An iatrogenic infection is a result of a medical intervention. It can develop after surgery or intra articular inj ection treatment. Despite the in fection being a consequence of medical activ ity, it is difficult to determine in which phase of the intervention, or where and when the in fection occurred or even whether it was caused exogenously at all. These questions may be answered only if all of these issues are considered. �
As concerns post-traumatic infections, open fractures are regarded as potentially infected. In these cases any complications that oc cur after the surgical interventions are held to be iatrogenic. �
Infections, developing in the environ ment of stabilizing devices (metal plates) or mobile implants (endo prosthesis). Infections emerging early after the treat ment of closed fractures (after surgical stabili zation) should be considered iatrogenic. In the environment of implants, even if the operation is performed under ultra sterile cir cumstances, infection occurs in 0.3-0.5% of the cases, despite the sterile air flow, the spe cial surgical exhaust suit and the antibiotic
prophylaxis making the contamination virtu ally impossible. Under the customary conditions, the fre quency of septic complications after hip pros thesis operations can reach 2%. It is generally accepted in the literature that infections developing within 6 months af ter surgery are due to contamination, and can therefore be regarded as iatrogenic, while those that develop after 6 months (late infec tions) due to hematogenic dispersion. Never theless the cause of a late infection may also be contamination, but the virulence of the pathogen and the resistance of the organism are such as to allow only a late manifestation, so that can be classified as so called low-grade infection. The recognition ofpost-traumatic bone in fection does not pose any problem, because this is indicated by the open fracture or the fe brile condition after the osteosynthesis, and the laboratory alterations proving the inflam matory process The pain in the injured limb does not de crease, but becomes stronger. Inflammatory symptoms develop in the operated area. X-ray signs appear later. The first sign is bone atro phy, which is followed by a callus formation failure. The fractured bone-ends may undergo destruction and condensation, indicating that avascular necrotized bone parts have taken the place of live tissue. Broken-off bone pieces can sequestrate. Lytic, rarefied areas evolve around the screws, which therefore loosen and the fixa tion becomes insufficient. The inflammatory process is maintained and in many cases in tensified by the instability. Septic pseudarthrosis is a serious compli cation, treatment of which is a quite compli cated task. If it is accompanied by bone loss, it is defined as defect pseudoarthrosis (Fig. 20.7. a, d). The essential feature of the solu tion is the stabilization of the broken ends. As it is often necessary to remove all foreign ma terials from the area of the inflammatory fo cus, the method of choice is extrafocal osteo synthesis. The process can often be solved only by a series of surgical interventions. If
2 0 . B a cte r i a l i n fe ct i o n s of b o n e s a n d j o i n t s
a
b
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Fig. 20.7. a: Septic pseudarthrosis with a severe leg deformity, involving shortening and an u nstable limb. b: A bone defect can be observed in the X-ray image, with a fibula deformity. c: Postoperative picture: fibula implantation i nto the lateral condyle of the tibia, with screw fixation and spongiosa plasty, has been followed by bony consolidation. d: After surgery, the limb is stable, with a more favorable alignment.
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the fixing pins of the externalfixateur are po sitioned distant from the inflammation, in the healthy parts, the broken ends can be stabi lized which leads to subsidence of the inflam mation. Remodeling of the bone is often pos sible only by bone transplantation. Infections of mobile implants and articu lar endoprostheses belong in a different brand of orthopedic surgery. Infections can be either early or late com plications of surgery occurring within a year. The course can involve an acute, subacute or chronic inflammatory process, with the corre sponding clinical and laboratory symptoms. Clinical symptoms. A late haematoma, which is a subcutaneous or subfascial clot mass evolving as a result of a slowly oozing hemorrhage, and which can diffuse between the tissue layers, develops around postopera tive day 7. It may be accompanied by sub febrility or febrility. This gives rise to the sus picion of an early infection. Accordingly the prevention of hematoma formation is very important. If it does develop the earliest possible evacuation under sterile circumstances is mandatory. Acute infection can develop within 1 2 weeks after the operation. The patient suffers from permanent pain, and subfebrility or fever can be observed. In the operated area, induration and edema may be noted. Labora tory examinations indicate the infection. Be fore the healing of the wound, a purulent dis charge begins that can be long-lasting and abundant. In cases of subacute infection the erythro cyte sedimentation rate is slightly high. In ret rospect as concerns the early postoperative period, the former moderate fever, sub febrility, the edemic wound periphery nor malize spontaneously. The patient may feel well for months before the appearance of pain in the hip area. The occurrence of the com plaints is generally associated with the ap pearance of the radiological and isotopic signs of prosthesis loosening. Initially X-ray alterations can not be ob served, or they are merely very slight: peri-
prosthetic bone atrophy, a periosteal reaction, and a narrow discrete radiotransparent stripe at the boundary of the implant and the bone, or at the boundary of the cement and the bone. Laboratory examinations demonstrate a high sedimentation rate, CRP (C-reactive pro tein), and a differential blood count shifted to ward the left. Ultrasonography of the joint demonstrates an articular effusion, with in creasing density, which is a result of the tissue detritus in the fluid. An urgent puncture fur nishes information on the nature of the articu lar fluid (hematoma, infected hematoma or pus) . It is expedient to perform an immediate bacteriologic examination, and if the case is not acute, immediate exposure under antibi otic protection, cleaning and drainage are sug gested; if the case is subacute, after the culture and resistance results have been obtained, it is sensible to perform the exposure and lavage and to insert a suction drain as early as possi ble: experience indicates that an early expo sure (within some weeks) helps solve the pro cess meanwhile the prosthesis is retained. Slow infection generally appears months or even years after surgery that was thought to be successful. It is manifested as insidious, dull, monotonous pain, which cannot be eased by motion. When late septic complications develop, the leading clinical signs are a painful limita tion of movement, a sensation of instability, fever, and subfebrility. The operated area can be infiltrated and warm, but it can even be normal if the infection is of low grade. The laboratory tests may detect the classi cal signs of inflammation, depending on the virulence of the pathogen, but in a torpid case or if there is a fistulous process, they can be negative. Signs of septic implant loosening can be observed in the X-ray image: a periosteal re action, cirrus-cloud-like focal osteolysis in the bone structure, snowflake-like para-arti cular calcified shadows, and a transparent layer between the bone surface and the im plant (Fig. 20.8.). To clarify the diagnosis, articular puncture and bacteriologic examination are recom-
2 0 . B a cte r i a l i n fect i o n s of b o n e s a n d j o i nts
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Fig. 20.S. a: X-ray picture of the septic loosening of the hip endoprosthesis. Septic hip prosthesis: solution in two steps. b: Excisional arthroplasty - Girdlestone situation. c: After the healing of the process, reimplantation of hip endoprosthesis.
mended besides the above examinations . Un fortunately, after puncture, one-third of the traditional bacteriological cultures prove to be negative. There is a modem molecular biology method for isolation of the DNA of the bacte rial wall from the aspirate. If the typical symptoms are absent, per forming a gallium isotope scan can facilitate the differentiation of sterile and septic loosen ing. Treatment. Some decades ago, septic complications were solved by total reveal of the prosthesis, and Girdlestone surgery (pendular hip). After removal of the prosthesis and the head and neck of the femur, the remaining proximal part of the thigh bone was inclined against the pelvis, resembling the way in which a thinking individual bends the head into the palm. This led to a well-moving, pain less but unstable hip : the patients could walk
only with a walking aid. Nowadays, the solu tions chosen that are more appropriate for the patient. After the subsidence of the process and the eradication of the infection the aim is implantation of a new prosthesis. This can be performed as an immediate reimplantation, or in a two-step process. This latter also gives two options: 1 . Implantation of an antibiotic spacer, with reimplantation after the subsidence of the process. 2 . The removal of all foreign materials, with reimplantation 4-6 months after antibiotic treatment (Fig. 20.8. a, b, c).
20.2. Puru lent arthritis A condition of articular inflammation caused by pyogenic pathogens is called purulent a r thritis.
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The process in the joint depends consider ably on the virulence of the pathogen and on the resistance of the organism.
The inflam mation o f t h e joint can b e primary if the process begins initial ly in the a rticula tion, and secondary if the process com mences in a d ifferent part of the organism and spreads to the joint. Primary infections usually occur in childhood, at which age it is twice as frequent as osteomyelitis.
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Etiopathology. The pathogenic agent in 90% of the cases is Staphylococcus hemo lyticus, but all pathogens that may be in volved in osteomyelitis must be taken into consideration. Pathogens may enter an articulation in var ious ways: �
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In serous arthritis, the synovial membrane is purple and sanguine, while the exudate is transparent and serous. In serofibrinous arthritis, the joint is filled with a fibrin-containing turbid exudate, in which bacteria multiply. In purulent arthritis, which results from a severe infection, the j oint is filled with thin, yellow pus. The articular capsule and the synovial membrane are thickened: inflamed, sanguine and in some places necrotic. The articular cartilage is lifted from its base. The pus can easily break through and form a periarticular abscess or fistula.
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Via the blood stream, as a result of an infectious process in a different part of the organism. By direct spreading, as a result of sup puration occurring up in the metaphysis. As a result of an injury penetrating the joint. In an iatrogenic way, during an intra articular inj ection, and especially a steroid inj ection (sterility! ) .
Clinical symptoms. The general symp toms are manifested early: Prostration, fever, shivering and a loss of appetite. The labora tory findings reveal a high sedimentation rate and CRP and leukocytosis, with the blood count shifted to the left. The pain increases in a
b
Fig. 20.9. a: Septic arthritis induced by Staphylococcus in the left knee-joint. The articular surface has been destroyed, and deep destruction of the subchondral bone can be observed. b: Surgical exposure with serious destruction of the femur condyles and disorganization of the joint.
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response to the slightest movement of the ar ticulation. The joint is in a mid-position or a forced position; this is how the patient tries to ease the pain. The articulation is swollen, and its contours are blurred. The skin is warm to touch, and reddish. If the local symptoms worsen, the general condition can also deteri orate, and a serious septic, toxic state can de velop. X-ray signs. Initially, there are no signs, but the great amount of exudate enlarges the articular cavity. After 2-3 weeks, the bone structure becomes atrophic (local osteopenia) . The damage to the chondral surface leads to unevenness and tightening of the articular cavity. Subchondral cysts can appear (Fig. 20.9. a, b). Treatment. Before the discovery of anti biotics, a purulent inflammation of a large, weight- bearing j oint could threaten the life of a patient. Nowadays, thanks early diagnosis and the availability of modem antibiotic and surgical treatment, there is even an opportunity for the healing the process to end up with a moving articulation. By puncture of a diseased articulation, the tense, painful joint can be relieved, and mate rial can be collected for laboratory, bacterio logic examinations of the synovial fluid and exsudate. Until the results are obtained the pa tient should be treated with a broad spectrum antibiotic . Punctures can be repeated. The need for radical surgical exposure depends on the gen eral condition of the patient and on the local alterations. In some cases, rinsing and lavage performed under arthroscopic intervention, with the application of a suction-rinsing drain, may be sufficient. In a serious, purulent process, however ar ticular exposure, subtotal synovectomy and a suction or suction-rinsing drain should be chosen as a solution. When the clinical symptoms have sub sided, extremely careful moving of the articu lation is allowed.
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In advanced cases involving severe de struction a loss in function of the affectedjoint and sometimes the development of ankylosis should be expected.
20.3. Bone and joint tuberculosis This is a secondary tuberculotic process in the bone o r articulation. Symptoms are slowly de veloping pain, swelling and limitation of movement.
Occurrence. As for pulmonary and extra pulmonary (lymph node, urogenital, meningi tis) manifestations, articular tuberculosis was earlier a serious widespread disease in Hun gary, as elsewhere. Thanks to the organizations established in the 1 950s within the anti-tuberculosis net work, this grave illness was almost totally eradicated. In the past few years, however various negative changes, such as the increasing num ber of unemployed, the social problems of the homeless, alcoholism, and the spreading of immunodeficiency states (AIDS), have led to a resurgence of tuberculosis worldwide. Ac cordingly, the number of newly diagnosed extrapulmonary cases has moderately in creased. The data published in 2000, gave the inci dence of tuberculosis in Hungary as 36 per 100 000; the number of extrapulmonary cases was 246, of which 33 were newly diagnosed articular tuberculosis (Fig. 20.10.). Hence, al though relatively rare, the possibility of a rticu lar tuberculosis must be thought of, and suc cessful treatment demands a knowledge of the clinical pictu re.
Etiopathology. Articular tuberculosis is caused by Mycobacterium tuberculosis (Koch bacillus), discovered by Robert Koch in 1 882. In 90% of the cases, the primary focus is induced by bacteria invading the lungs and in fecting the regional lymph nodes (primary complex). As a result of hematogenic disper-
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pleuritis a n d others 42%
meningeal 2%
bone and joint 13%
Fig. 20.10.
Tubercu losis pie chart, showing the d istribution of extrapu lmonary forms.
sion, the bacteria can spread to other parts of the body (bones and urogenital organs), giv ing rise to post-primary tuberculotic lesions. Tuberculosis bacteria induce tuberculosis gemmation and caseous necrosis. The disease is caused by bacteria ofhuman or bovine type. The pathomorphologic alterations and the clinical pictures caused by the two types of bacteria do not differ. Bone and joint tuberculosis is a severely destructive disease. The mycobacterium ad heres in the terminal arteries of the epiphysis or in the vessels of the synovial membrane, which is where the focus develops (primary osteitis or primary synovitis) . The bone foci therefore appear first on bones and bone parts with a rich blood supply and with terminal arteries, that are rapidly growing and mechanically affected (meta physis of tubular bones, vertebrae and ossi cles) . In productive granulating processes, the tuberculous granulation tissue destroys the surrounding bone. In exsudative bone processes, a consider able proportion of the marrow undergoes caseation, and the blood supply and nutrition of the bone are therefore blocked. In the event of widespread necrosis, the necrotic detritus can dissolve, and a bone ab scess develops, often with sequestra. If the ab scess breaks through the bone, passing into the surrounding tissues, it can cause a cold ab-
scess (abscessusfrigidus) . This can move fur ther from the focus, sinking by gravitational force, so it is also called a migrating abscess (e.g. psoas abscess). If the abscess breaks through to the skin surface, a fistula develops. Clinical symptoms. The early diagnosis of articular tuberculosis is not easy. The de velopment of the symptoms is latent, with no typical signs. The pain of the affected joint differs in in tensity from other sharp pains, induced by acute bacterial inflammation. The pain in the articulations of the lower limb intensifies dur ing walking or weight-bearing, whereas in an inactive position it weakens or disappears . The patient easily becomes fatigued, suffers from night sweats, and is permanently subfeb rile. The erythrocyte sedimentation rate is slightly elevated, but only in very rare cases does this reach the level of acute inflamma tion. The differential blood count indicates relative lymphocytosis. If the bone destruction is severe and the treatment is delayed, the pus can break through the articular cavity, forming ab scesses in soft tissues at some distance from the focus. The fistula can be superinfected by banal pathogens. A microscopic smear, histological exami nation, culturing and animal inoculation facil itate an early diagnosis. These examinations
2 0 . B a ct e r i a l i n fect i o n s of b o n e s a n d j o i n t s
should be performed if possible before the start of medicinal treatment, though the toxic condition of the patient may necessitate im mediate antibiotic treatment. The presence of acid-fast rods in the smear, a positive animal inoculation test and the histo logical demonstration of Langhans cel ls help clarify the diagnosis. The tuberculin test is not as important as in the era before BCG vaccination. An organism that has recovered from an earlier infection can even react hyperergically in the tuberculin test. The skin reaction in the tuberculin test of an infected organism rather indicates the ac tivity of the process or the result of the treat ment.
X-ray signs. The X-ray signs are varied and change with the pathomorphologic alter ations. They are not always pathognostic, not even in advanced cases. The earliest X-ray sign is bone atrophy. This is a result of the toxin effect and inactivity. Prognostically, progressing bone atrophy is an unfavorable sign. As the process advances, the articular cavity can shrink, but if effusion is present it can expand too. The articular surface becomes rough, and in some places the subchondral bone may even crack, which suggests exten sive destruction of the articular cartilage. X-ray signs of articular deformities and se vere bone destruction may be observed. Cal cified abscess shadows can be seen at some sites distant from the bone. Reductions in the level of atrophy and of the local sclerotizing changes, and ossifica tion of the joint are radiological signs of heal ing. This is bony ankylosis of the articulation. If combined treatment with anti tuberculo sis inhibitors, and focus cleaning-surgery is carried out sufficiently early, the articular sur faces are not seriously damaged, and may re main intact, especially in processes limited to synovial primarily the knee-joints. Thus, the articulation can heal with a good function. However, even in these cases, the development of arthrosis few years later should be reckoned with.
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Treatment. In an early stage, the treat ment of the disease is primarily medicinal. The drugs most frequently used today are Rifampicin, INH, (isonicotinic acid hydra zide) PZA (pyrazin amide), Ethambutol, Streptomycin and PAS (para-amino salicyl acid) . Drug treatment is always carried out with a combination, of 2-3 medicines or in a serious case even four. Drug resistance may develop during chronic treatment, which necessitates drug sensitivity examinations on the discharges and the pathogens from time to time. Drug treatment alone is not always suffi cient to eliminate a bone focus, but it is an es sential addition to conservative or surgical treatment. If the general condition of the pa tient rules out surgical intervention, long-term drug treatment and conservative therapy are recommended. However the safe way to solve abscess and sequestral bone processes is to combine medicinal therapy with focus cleaning surgery. Sanatorium care in special institutes re mains important with the provision of heliotherapy dietetic treatment and climato therapy. Immobilization, rest, and freedom from stress must be continuous . Immobilization of the affected limb during the treatment of osteoarticular inflammatory processes has been regularly used since the observations of Jimos Balassa. The pain can be decreased and severe deformities can be avoided with plaster casts and traction. Appropriate weight- bear ing prevention can be achieved with walk ing -caliper treatment. In Hungary, the use of a sciatic-tuber supporting walking-caliper was introduced by Gyula Dollinger. If the pain in creases at any stage of the treatment, immobi lization must be ensured. The goal of the therapy is to achieve the maximum, possible painless movement, or perfect ankylosis in a proper position. Move ment limited to 1 5-20° indicates permanent pain and can induce the relapse of the process. The process can not be considered healed if an abscess or sequestrum is present, since these are frequent causes of relapse. The most im-
182
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portant goal is the permanent eradication of all possible sources of relapse by radical sur gery, focus cleaning, joint resection and verte bral focus cleaning. Abscesses and fistulae are accompanying signs of an osteoarticular
a b
Fig. 20.11. a: Caries trochanterica and coxitis tubercu losa on the left side. Because of the specific destruction of the g reater trochanter, a large, protruding cold abscess has developed in the area of the trochanter major and the gluteal region. b: The X-ray picture demonstrates that the a bscess and sequestral process of the trochanter has broken into the joint, destroying it.
tuberculotic process, and must be treated to gether with the bone focus. The connection between the fistula and the bone focus can be proved by fistulography. The role of surgical procedures in the treatment of osteoarticular tuberculosis is in creasmg. The widening of the indication of intra focal interventions is due to the availability of antituberculotics. However it is a general principle that active osteoarticular tuberculo sis demands a major surgical intervention only if the condition is life-threatening (sep sis, an abscess or a sequestral process, and the danger of development of paraplegia) as long as the process is not demarcated. In such a case, massive (a combination of 4 drugs) antituberculotic drug treatment should be car ried out to prevent the danger of tuberculosis dispersion (meningitis, pleuritis and wound suppuration).
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proportion of soft-tissue tumors and the ma j ority of bone tumors appears in the first two decades of life (Fig. 2 1 . 1 .), and the patients often relate their complaints to sports injuries and traumas. In cases involving unexpectedly long-lasting and increasing symptoms follow ing a trauma, tumor is to be considered and X-ray tests must be performed. The period of the complaints is dependent on the rate of growth of the tumor and may vary extremely wide. In cases of a rapidly ex panding Ewing 's sarcoma or a highly malig nant central osteosarcoma it is often a few weeks or months, but in cases with less malig nant chondrosarcomas it can be many years. The benign tumors and turnor-like lesions usually grow slowly. Malignant soft-tissue tumors may remain undetected for a long time, especially if they are localized deep down, covered by muscles. In these cases, dull pain is the only symptom, which does not disappear even at rest. Those tumors that penetrate the superficial fascia are detected earlier, they cause large swelling, the skin is warmer above them and the venous network is expressed. The most significant symptoms of bone tu mors are also swelling, a warmer skin and pain. The latter does not depend on the load, in the beginning it is intermittent and pricking, later radiating, constant pain is perceived. Both benign as well as malignant tumors in the vicinity of joints may induce a restriction Benign �
of j oint motion and reactive synovitis with j oint fluid collection. If a soft-tissue or bone tumor expanding from the bone involves ves sels, the significant symptom is radiating pain and edema of the limb. Pathologic fractures may occur as the first symptoms in cases of benign tumors (e.g. enchondroma) or turnor-like lesions (e.g. ju venile bone cyst), which may have been pres ent for a long time and extenuated the cortex. The fracture arises spontaneously or in re sponse to a minimal trauma. Malignant bone tumors, bone destructive soft-tissue tumors usually start with pain. X-ray and other imaging procedures. In the diagnosis of soft-tissue tumors X-ray tests are of modest help. Only the fat-tissue tumors (lipomas, liposarcomas) can be differentiated as they are more radiolucent than the sur rounding muscle and bone tissue. If a primary tumor is discovered, antero posterior (ap) and lateral chest X-ray is man datory to detect possible lung secondaries. As bone tumors grow, they change the shape and the structure of the bone, producing typical (but not absolutely specific) X-ray changes, so X-ray therefore plays a decisive role in the preoperative diagnosis and treat ment planning. Benign bone turnors usually grow slowly and there is time of the shape of the bone to change, and for a demarcation reaction to de-
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2 1 . Tu m o rs of t h e m u s c u l o s ke l eta l system
velop. The border o f the intact and affected bone tissue is usually well-defined, and the le sion is often surrounded by a sclerotic margin (non-ossifying bone fibroma, osteoid osteoma) (Fig. 2 1 .2.). Occasionally the bone appears "inflated" (e.g. enchondroma in pha langes of the fingers) (see Fig. 2 1 . 1 5.). With malignant tumors, the border be tween intact and affected bone tissue is vague il-defined, the sclerotic margin is missing. If the bone shows fusiform widening (e.g. chondrosarcoma), this is a sign of slow expan sion. Nevertheless the cortex and also the
Fig. 21.3. a: A- P film of the right pelvis, with a lmost invisible changes the iliac bone is slightly more radiodense b: The a image shows a tumor originating from the iliac bone, interspersed with calcifications invading both the gluteus muscles and the pelvic soft-tissues
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neighboring soft-tissues are soon infiltrated. There is often a periosteal reaction, such as spiculum formation in osteosarcomas (Fig. 2 1 . 1 2.),laminated "onion peel" reaction in Ewing 's sarcoma (Fig. 2 1 .2 1 .) . Indirect signs of extraosseal invasion o f the tumor are shown o n traditional X-ray films, as calcified foci deposited in a hyaline matrix (Fig. 2 1 .3. b), or spiculum fOrmation in osteosarcomas. It is important that the penetration of cer tain types of tumors (giant cell tumor of bone, metastasis, bone fibrosarcoma) into the cortex is never accompanied by a periosteal reaction. The availability of modem non-invasive imaging modalities, such as CT and MR, angiography and arteriography have lost much of their significance, but they are still useful diagnostic or therapeutic tools in cases of soft-tissue tumors and expansive, infiltrative bone tumors. Angiography can provide information on the extent, blood sup ply of a tumor, its relation to important ves sels, displacement or invasion of vessels (Fig. 2 1 .4. a). Arteriography may be supplemented by therapeutic interventions. Cytostatic drugs can be inj ected intra-arterially in high concen tration, directly into the tumor, or the supply ing vessels can be embolized. In this way, the tumor temporarily shrinks, its removal is eas ier and the bleeding can be reduced to a great degree. Computer tomography (CT) is useful di agnostic procedure mainly in cases of bone tu mors, and less for soft-tissue sarcomas. Tomographies are done in a horizontal plane, and even a very small bone destruction, intra and endosteal propagation can be demon strated. CT is mandatory in tumors of the shoulder girdle, pelvis and spine, where single bones, bone structures are proj ected in tradi tional X-rays to cover each other, and thus the localization of a tumor can not be accurate (Fig. 2 1 .3. a, b). The most significant method is the MR (magnetic resonance) imaging, which is based on a non ionizing radiation source, and is therefore harmless to the organ ism. It is excellent for visualization of the intramedullary and of bone tumors, and their
188
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2 1 . T u m o rs of t h e m u s c u l o s k e l eta l system
intraosseal extent, metastases (skip meta stases) (Fig. 2 1 .4. b). Since it is less sensitive than CT depicting possible cortex break through by the tumor, it is often applied in combination with CT. Common isotope test used for bone tumors is the 99 Tc-polyphosphate bone scan. Pathologically high osteoblast activity is indicated by a high uptake of the isotope (Fig.
2 1 .5.). The test is extraordinarily sensitive, but less specific : Apart from tumors, in creased activity can be induced by degenera tive, traumatic or inflammatory changes. Its main indication is the early detection of multi plex bone tumors or metastases and observa tion of the effectivity of chemotherapy. Fol lowing effective preoperative chemotherapy the isotope uptake of the turn or decreases. Iso tope tests are of little value in the diagnosis of soft-tissue tumors . In the recent years ultrasound investiga tions developed considerably and became more sensitive. They play no role in bone tu-
a b
Fig. 2 1.4. a. Angiography: hypovascularized periosteal osteosarcoma dorsally on the d istal metaphysis of the femur, d islocating the a rtery b. Sagittal MR image of the same periosteal osteosarcoma: the tumor has broken through the fe mur cortex in the area marked with arrows and has spread into the intramedullary cavity
Fig. 2 1.S. Bone scan: apart from the growth plates, there is high isotope uptake shown in the proximal meta diaphysis of the right femur (Ewing's-sarcoma).
2 1 . T u m o rs of t h e m u s c u l o s ke l eta l system
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189
crease may be indicative of recurrence. This level is also high in disseminated cancer metastases, when high quantities of calcium and phosphorus dissolve in the serum from the diluted bone tissue and the ion level may be elevated. The acid phosphatase level is in creased in metastases of prostate cancer, while in cases of neuroblastoma the excretion of vanillic-amygdalic acid and homovanillic acid are considered characteristic. Important diagnostic indicator in myeloma patients are the appearance of Bence-Jones protein in the urine, and increased levels of serum proteins. Paraproteins are generally detected by im mune-electrophoresis. Sternal puncture can be performed to detect affected plasmocytes, however a normal bone marrow does not ex clude this condition.
Fig. 21.6. Ultrasonografic image: the base of the picture is the femoral cortex, seen as a white line, above it, a re current chondrosarcoma is seen in the vastus mus cle, the calcifications in the tumor su bstance are visi ble as white spots
mor cases, since bone tissue "blocks" out intraosseal processes. With soft-tissue tu mors, it is an essential non-invasive and al ways repeatable examination method, the size of the tumor can be identified in three dimen sions, and the tumor can be differentiated from fluid-containing cysts (Fig. 2 1 .6.). A connected use is the ultrasound guided needle biopsy taking from soft-tissue tumors. Laboratory investigations. Bone tumors do not initially cause bone metabolism changes, which can be detected by laboratory tests. An early sign is the increased sedimen tation rate, but this is not specific. The serum alkalic phosphatase level is characteristically high in osteosarcomas (it is excreted by the tu mor cells), its decreased level proves the effi cacy of chemotherapy, whereas a repeated in-
Biopsy, histological test. Regarding to the diversity and the relative rarity of bone and soft-tissue tumors, which hampers a differen tial diagnosis, establishment of the exact diag nosis and surgical planning, almost always re quire biopsy and histological examinations. Amputation is contraindicated without a histological opinion ! In cases of soft-tissue tumors aspiration cytology is possible, the specimen is obtained by needle biopsy. In the overwhelming maj ority of bone tu mor cases open surgical biopsy is performed, with adherence to strict rules. The scar should be positioned so that the surgeon might re move it during the definitive surgery (there is a risk of recurrence in the scar) . Regarding the numerous differential diag nostic problems close cooperation and con sultation is essential between the pathologist, radiologist and surgeon. Treatment. The variety of surgical inter ventions depends on a number of factors for both soft-tissue and bone lesions, the age and general condition of the patient, the localiza tion of tumor, and particularly the surgical stage of the tumor. Latent, active and aggressive forms of be nign tumors are differentiated. A latent tumor
190
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usually does not cause clinical signs, it ap pears coincidentally, it does not grow, or only very slowly, and occasionally it may heal spontaneously. Examples include lipoma, osteoma, etc. An active benign tumor grows slowly, does not extend from its anatomic sheath, has its own capsule. Examples are enchondroma, chondromyxoid bone fibroma. Aggressive benign tumors can expand gradu ally, or rapidly, emerging from their anatomic casing (fascia border, periosteum), but usu ally do not metastasize (or very rarely). Ex amples are desmoids and giant cell bone tu mor. The surgical classification of malignant bone and soft-tissue tumors is based on three considerations (Table 2 1 . 1 .) : 1 . The level o f malignancy o f the tumor (low malignancy: G 1 , high malignancy: G2
Table 21.1. , Surgical classification of benign and malignant tumors (Enneking) Classification by histological g rade
Classification by localization
GO G1 G2 TO T1 T2
Classification by metastasis
benign low malignancy high malignancy
=
=
=
=
=
=
MO M1
intracapsular i ntracompartmental extracompartmental
=
=
no metastasis regional or distant
Benign tumors
1. latent
GO
TO
MO
2. active
GO
T1
MO
T1-T2
MO
3. aggressive GO
Malignant tumors
LA I. B
G1 G1
T1 T2
MO MO
11. A 11. B
G2 G2
T1 T2
MO MO
Ill. A Ill. B
G l-2 G l-2
T1 T2
M1 M1
2 . The relation of the tumors t o their ana tomic compartment, intracompartmental forms (T l ) and extracompartmental forms that broke through (T2). 3. Absent (MO) or apparent metastases (M I ) at the time o f discovery. The above 3 factors have the highest prog nostic value, so there are significant differ ences between the surgical stages regarding the 5 year survival rate. The radicality of the surgical intervention should be chosen in ac cordance with this. Group I contains tumors of low malignancy (e.g. chondrosarcoma, fibrosarcoma, differentiated liposarcoma); If A: tumors have not broken out from the compartment (e.g. intraosseal chondrosar coma), or lIB : have broken out from the com partment (e.g. soft-tissue infiltrative chondro sarcoma). Group 11 includes lesions with high malignancy (osteosarcoma, Ewing 's-sar coma, malignant fibrous histiocytoma, etc.), which (IlIA stage) are intracompartmental, or (IIIB stage) have already broken out from their compartment. Group III includes those tumors of low or high malignancy, where the prognosis is very poor, since distant meta stases are already present at the time of diag nOSIS. Beside modem therapy (chemo-, ra diotherapy) complete removal of the tumor is essential . Intralesional curettage or marginal resection is permitted only for benign lumps, since tumor cells may be left behind. In cases of malignant tumors, wide (the incision is di rected in a few centimeters deep in the healthy tissue) or radical resection must be performed or if the tumor has already invaded the ves sels, amputation or exarticulation is to be per formed (Fig. 2 1 .7.). Now that effective che motherapy is available, limb-saving opera tions are done in more than half of the bone tu mor cases, resection of tumor being followed by reconstruction of the bone defect. The bone defect, which is usually large and in cludes a j oint, can be replaced with the pa tient' s own bone ( autograft), or bone from a bone bank ( homograft), or by modular tumor endoprosthesis system.
2 1 . T u m o r s of t h e m u s c u l o s ke l et a l syst e m
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19
27
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1995
1998
2000
a m putation l i m b- saving o peration s
Fig. 2 1.S.
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Changes in the proportions of amputations and limb-saving pro cedures performed in the Dep. of Orthop. of the Semmelweis University
Fig. 21.7. Type of surgical procedures according their radicalities. 1: radical intervention: amputation, exarticu lation, 2: wide resection, 3:marginal excision, 4: intralesional (cu rettage of the defect)
Bone cavities are filled with homologous or autologous ground bone, or bone cement (Fig. 5.8. a, b). If the tumor has destroyed the j oint sur face, the joint must be replaced or the defect may be bridged over by a bone plate to stiffen it (resection arthrodesis). This has an advan tage that, after the bony union, the limb will be stable and can bear weight, the disadvantages are the stiff joint and the poor quality of life.
100 -li mb-saving o perations - - - - - - a m putation
90 80 70
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60
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ro >
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50 40 30 20 10 0 0
20
40
60
80
100
120
140
160
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Fig. 21.9. Survival rates after amputations and limb-saving proced ures in patients with osteosarcoma (Dep of Orthop. Semmelweis Univ.)
192
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The defect can be replaced b y a n osteo articular graft from bone a bank, but integra tion is slow (6 months- l year), and both early and late complications are common (ligament insufficiency, bone collapse, fatigue frac tures, etc.). More recently the use of tumor endoprostheses has become popular, they have the advantage that the moving joint pro vides good function, but the prosthesis may work loose after some years and the bone de fect will then be even larger. Chemotherapy. The overwhelming ma j ority of bone tumors were earlier considered as chemotherapy-resistant. In the most recent decades it became clear that besides Ewing 's sarcoma and central osteosarcoma, which lat ter were thought to be resistant are indeed sen sitive to adriamycin and to high doses of methotrexate. As a result of the introduction of pre- and postoperative chemotherapy the numbers of lung metastases and local recur rences have diminished and limb-saving oper ations have become possible even in cases of osteosarcomas, that have broken through the bone (Fig. 2 1 .8.). The survival rates are not significantly worse than in the amputation group (Fig. 2 1 .9.), and the 5 years survival rate has elevated from 20% to 60-70%. Chemotherapy is also being used in the treatment of soft-tissue tumors increasingly frequently, however the results are not so clearly beneficial as in osteosarcoma. The maj ority of soft-tissue sarcomas are moder ately sensitive to chemotherapy, and a tempo rary remission or an increased survival rate can be achieved through the use of very ag gressive protocols. Chemotherapy can be used as palliative treatment in cases of lung metastases. Radiotherapy. Bone tumors are generally radiotherapy resistant, except Ewing 's sar coma, where irradiation of the aimed bone may be effective to support chemotherapy and surgical therapy. At one time the maj ority of soft-tissue tu mors were considered to be radiotherapy-re sistant. Recently however, the available so-
phisticated radiation sources (linear accelera tors, high energy gamma-ray beams) permits the attainment of a greater deep dose that is better focused with a milder skin reaction. In soft-tissue tumors radiotherapy is used as an adjunct of surgical treatment preopera tively, to decrease the volume of the tumor and postoperatively, to expose the tumor bed, to inhibit local recurrence, specially following margin�l resections. In some forms oftumors, irradiation of the regional lymph glands may be needed.
2 1.2. Primary bone tumors 2 1.2.1. Histological classification of bone tumors This classification, based on histogenetic aspects, was prepared by a working party of the WHO (2002), it is generally approved and it has an advantage of an internationally stan dardized approach (Table 2 1 -2.).
2 1 .2.2. Bone forming (osteogenic) tumors Table 2 1.2. Histological classification of bone tumors
I.
Bone-forming tumors A) benign
1. osteoma 2. osteoid osteoma 3. osteoblastoma B) malignant
1.
conventional osteosarcoma (central, high-malignant) 2. central, low-malignant osteosarcoma 3. parosteal Ouxtacortical) osteosarcoma 4. periosteal osteosarcoma 5. su perficial, high-malignant osteosarcoma 6. teleangiectatic osteosarcoma 7. small cell osteosarcoma 8. secondary osteosarcoma
2 1 . T u m o rs of t h e m u sc u l o s ke l eta l syst e m 11.
Cartilage-forming tumors
A) benign lipoma B) malignant liposarcoma
1. 2.
8) malignant 1. 2. 3. 4. 5.
chondrosarcoma (primary and secondary) juxtacortical (peripheral) chond rosarcoma dedifferentiated chondrosarcoma mesenchymal chondrosarcoma clear cell chond rosarcoma
X. Neural tumors Neurilemmoma
XI. Notochordal tumor chordoma
XII. Other tumors 1. 2.
1. solitary bone cyst 2. aneurysmal bone cyst 3. juxtacortical bone cyst (intraosseal ganglion) 4. metaphyseal fibrous defect (non-ossifying bone fibroma) 5. eosinophilic granuloma 6. fibrous dysplasia 7. "myositis ossificans "
giant cell tumor (intermediate) malignant giant cell tumor
IV. Bone marrow (hematopoietic) tumors 1. 2.
plasma cell myeloma(solitary, multiple) malignant lymphoma (reticulum cell sarcoma)
IVIA Ewing's sarcoma I primitive neuroectodermal tumor
8.
Ewing's sarcoma family 9.
V. Vascular tumors A) benign hemangioma B) malignant angiosarcoma
VI. Fibrohistiocytic tumors A) benign benign fibrous histiocytoma B) malignant malignant fibrous histiocytoma
VII. Connective tissue (fibrogenic) tumors A) benign desmoplastic fibroma B) malignant fibrosarcoma
VIII. Smooth muscle tumors A) benign leiomyoma B) malignant leiomyosarcoma
adamantinoma metastatic tumors
Tumor-like bone lesions
Ill. Giant cell tumor of bone (osteoclastoma) 1. 2.
193
IX. Lipogenic tumors
A) benign
osteochondroma chondroma (enchondroma, periosteal chondroma) 3. chondroblastoma 4. chondromyxoid fibroma
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hyperparathyroidism-induced "brown tumor" intraosseal epidermoid cyst
2 1.2.2. 1 . Benign bone forming tu mors �
Osteoid osteoma
This is a benign, osteoblastic lesion, with a characteristic small size (ordinarily less than 1 cm), and reactive sclerosis surrounding the central radiolucent "nidus" (Fig. 2 1 . 10. a, b). The thickened hard cortex contains the nidus as a soft redd ish-gray a rea.
It is not uncommon, about 1 0 % of the be nign bone tumors. The tumorous origin of osteoid osteoma is not uniformly approved, some authors regard it as a reactive lesion. Symptoms. The disease starts usually at the age of 1 0-25 years. The special kind of pain is the leading symptom, it is severe, often occurs in the night and reacts well to salicy lates (salicylic test).
194
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About 1 0% are intracapsular, i n these cases a j oint-effusion, muscle spasm, cont racture are often present. Vertebral osteoid osteoma may result in an antalgic posture, and scoliosis. Femur and tibia are the most com mon sites of its occurrences. X-ray signs. The center of an osteoid osteoma is a radiolucent area 0,5-2 cm in di ameter ("nidus"), surrounded almost always by reactive sclerosis (Fig. 2 1 . 1 0. a, b). The nidus is often invisible due to the enhanced re- '
active sclerosis on regular films, in these cases a CT scan is advised. A bone scan shows a highly positive isotope uptake. Treatment. The aim is the total removal ofthe nidus. If this fails, the process may recur and the pain may persist. Surgical possibili ties: curettage or resection ofthe nidus. On the surface of the resected specimen the nidus is seen as a soft bluish spot. Very recently CT -guided drilling or radio-frequency thermo coagulation has been introduced. �
Osteoblastoma
This is a benign lesion, that is histologically equivalent to osteoid osteoma, but this is larger, exceeding 2 cm in the large tubular bones, and the sclerotic margin is usually missing or much less prominent.
Symptoms. This tumor occurs under the age of 20 years, it is much less common than osteoid osteoma. It is localized to the verte bral arches, long tubular bones, ribs, pelvis. The symptoms depend on the localization: the forms in the vertebral arches may cause neu rological complications, while osteoblasto mas in long tubular bones may be symptom less for a long time. X-ray signs. The X-ray image of osteo blastoma is not very distinctive. It generally causes extensive osteolytic destruction. The sclerotic margin is usually much less marked than in osteoid osteoma, occasionally it is mlssmg. Treatment. Osteoblastoma is one of the tumors that display active expansion. The choice of treatment should be curettage and filling with cancellous graft, or en-bloc exci sion in normal tissue. 2 1.2.2.2. Malignant bone forming
(osteogenic) tu mors Fig. 21.10.
a: A 16 year-old boy: osteoid osteoma in the metaphysis of the right femur b: a image: the intramedullary localization of the nidus and the surrounding sclerotic margin is clearly visible
�
Osteosarcoma
This is a malignant tumor, distinguished by the direct bone mass and osteoid production
2 1 . T u m o r s of t h e m u sc u l o s ke l eta l system
9%
-t---- 8 %
-f--rf.""'--- 5 %
-+--'-liHH/--- 5 %
f_�-+------ 32 % �¥�----- L5 %
-tt---- 3 %
Fig. 21.11. Incidence of central osteosarcoma
of the tumor cells. Osteosarcoma is the most common primary malignant bone tumor, comprising 25-30% of all bone sarcomas.
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195
It appears in many forms, its histological picture can be very variable. The conventional central osteosarcoma is most common, and is of greatest importance. In 60% of the cases, it appears in the first 2 de cades of life. It may involve any bone, but in about 50% of the cases it occurs around the knee, in the distal femoral or proximal tibial metaphysis (Fig. 2 1 . 1 1 .) . Symptoms. These are initially rather in significant: intermittent pain sets in, which later becomes persistent. The swelling ex pands rapidly, the skin is warmer, swollen subcutaneous veins appear. In an advanced stage pathologic fracture follows in app. 1 0% of cases. X-ray signs. Because of its fast progres sion, the osteosarcoma has usually broken through the cortex and infiltrated the soft-tissues even on the first X-ray film. Less frequently in forms producing a high volume of tumorous osteoid tissue, the involved bone is sclerotic, very radiodense (Fig. 2 1 . 1 2 . a, b). Fibroblastic, teleangiectatic or anaplastic osteosarcomas, that show hardly any bone production, induce osteolytic destruction. Most frequently mixed lytic -sclerotic forms occur. The border between the intact and in volved tissue is il-defined, with a "moth eaten" appearance. The growth plate, and the periosteum inhibit the expansion of the tumor somewhat. Similarly, the tumor destroys the joint cartilage and invades the joint only rarely. The pathological osteoblasts of the in, vasive tumor excrete osteoid in the soft tissues, this appearing as spiculum creation. eT and MR tests provide great help in as sessing the soft-tissue and intramedullary penetration (Fig. 2 1 . 1 2 . b, c). Pathology. The material of the tumor is determined by its osteoid content and by its calcification. Its texture may therefore vary from soft up to bone-hard. The cut surface often demonstrate visible bleedings, necrosis and cyst-like changes. At a distance of few cm from the tumor, inde pendent tumor islands, the so called "skip" metastases, are occasionally visible even macroscopically.
196
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2 1 . T u m o rs o f t h e m u s c u l o s ke l et a l syst e m
d e
a b
c
Fig. 2 1. 12. a: Sclerotic osteosarcoma invading the soft-tissue with spicula formation, located in the distal metaphysis of the femur b: a image showing the tumor invading to the joint in the level of patella c: MR image shows the soft-tissue extent of the osteosarcoma d: Histology of the osteoblastic osteosarcoma e: Limb-saving operation after resection of this osteosarcoma and implantation of a tumor prosthe sis (antero-posterior and lateral X-rays).
2 1 . T u m o rs of t h e m u s c u l o s ke l et a l system
The histological structure o f the tumor is variable, and often causes differential diag nostic difficulties. Osteoblastic (Fig. 2 1 . 1 2 . d), chondroblastic, fibroblastic, giant cell loaded, teleangiectatic, small cell and mixed forms are distinguished, depending on the dif ferentiation of the primitive connective tissue mesenchymal cells. Unfortunately, between osteosarcomas with a different tissue struc tures, the prognostic difference is negligible. Treatment. Central osteosarcoma is ra diotherapy-resistant, and accordingly chemo therapy and surgery are to be attempted. Cytostatic therapy is used both pre- and post operatively. Preoperative (neoadjuvant) che motherapy decreases the chances of the spread of tumor cell and metastasis formation during biopsy, the tumor shrinks, ("ripens"), and can be resected more easily.
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197
Thanks to the effective chemotherapy, the 5-year survival rate increased considerably, to 60-75 % (Fig. 2 1 .9.), and in more than half of the cases limb-saving procedures are success ful (Fig. 2 1 .8.). Some decades ago radical amputation pro cedures were almost always preferred, but nevertheless the 5 year survival rate did not exceed 20%. Today, surgical treatment, with wide removal of the tumor in the intact tissues is recommended, following preoperative che motherapy. Regarding metaphyseal location of the tumor the involved bone segment is re moved together with the j oint surface . Bone defects may be replaced by the patients own bone, or by bone from a bone bank, most often by tumor endoprostheses (Fig. 2 1 . 1 2. e).
Table 21.3. Other rare osteosarcomas
5 year survival rate
Diagnosis
Age Most frequent (years) Localization
X-ray appearance
Malignancy Therapy
Parosteal osteosarcoma
20-60
Femur, popliteal area, humerus, tibia
Intensely radiodense tumor on the bone surface
Grade 1
surgical
Periosteal osteosarcoma
15-30
Distal femur, tibia Blu rred, slightly (meta-diaphyseal) mineralized tumor on the bone surface
Grade 2
surgical 70% (chemotherapy ?)
Central osteosarcoma, low malignancy
15-45
Distal femur, proximal tibia
I ntramedullary lytic-sclerotic lesion, usually with a marked border
Grade 1
surgical
10-30 Superficial, highly malignant osteosarcoma
Distal femur, proximal tibia, humerus
Poorly mineralized superficial tumor, spicula formation
Grade 3
chemotherapy 55-65% surgical
Teleangiectatic osteosarcoma
10-25
Distal femur, proximal tibia metaphysis
Lytic destruction with blu rred border
Grade 3
Chemotherapy 65-75% surgical
Secondary osteosarcoma
30-60
Metaphysis of long tubu les bones
Lytic-sclerotic Grade 3 destruction with blurred border (+ basic disease Paget's disease, fibrous dysplasia, bone infarcts, postirradiation, etc.)
Chemotherapy 30-40% surgical
[-
-
90%
80-95%
198
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2 1 . T u m o rs of t h e m u sc u l o s ke l e t a l syste m
c
a: Parosteal osteosarcoma growing dorsally on the distal femoral metaphysis b: Operative specimen cut in half: it is clear, that the cortex is intact c: a images showing that the lump is situated on the outer surface of the bone, has not broken through the cortex.
�
Parosteal osteosarcoma (j uxtacortical osteosarcoma) This is an osteosarcoma localized on the surface ofthe bone, from the parosteal tissues, with relatively better prognosis (Fig. 2 1 . 1 3 . a, c).
�
Periosteal osteosarcoma This is located on the outer surface of the bone, in the periosteum, and usually in the diaphysis (Fig. 2 1 . 1 4.).
2 1 . T u m o rs of t h e m u s c u l o s ke l eta l syste m
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199
Fig. 21.14. Periosteal osteosarcoma on the surface of the tibia, the surgical specimen has been cut in half with a saw
Fig. 2 1. 15.
21.2.3. Cartilage-forming tumors 2 1 .2.3. 1. Benign cartilage-forming
tu mors �
Enchondroma
This is a benign tumor containing mature hyaline tissue. It is common, accounting for 20% of all benign bone tumors. It occurs in d h the 2n _4t decades, primarily involves the phalanges and the metacarpals of the hand.
Symptoms. It does not necessarily cause symptoms, and is often observed with un changed size for many years or expands only slowly. Stabbing pain may sometimes occur, or pathological fracture may be the first sign. The X-ray sign is specific, well delineated destruction is visible centrally in the meta diaphysis of the metacarpals, which inflates the bone without a periosteal reaction (Fig. 2 1 . 1 5.).
Lytic destruction in the base and mid-phalanx of the index finger inflating the bone -enchondroma
Pathology. Elevation of the cortical plate reveals a grey-white, debris-like material that fills up the medullary cavity. Micro scopically, this tumor is built up from hyaline cartilage, its structure is lobular. Occasionally it is difficult to differentiate the less malignant chondrosarcomas from the benign ones. One should not rely merely on the histology, but also consider the X-ray, the location and the clinical picture. It is essential to know that chondrosarcoma is very rare in the short tubu lar bones of the hand. It can present in a multi ple form as a systemic bone disease. In such cases, the risk of malignant transformation is higher, at 1 0%. Treatment. Excochleation and cavity fill ing the with autologous cancellous bone. In the active stage lesions may recur. About 0,5 - 1 % of solitary enchondromas produce secondary chondrosarcomas.
200 �
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2 1 . T u m o r s of t h e m u s c u l o s ke l eta l s y s t e m
osteochondroma may also be sources of com plaints . X-ray signs. Thin pedunculated or wide-based sessile forms are typical (Fig. 2 1 . 1 6, a, b). The peduncle bends in the direc tion of the diaphysis as a result ofthe dragging force of the neighboring muscles, resulting in the X-ray finding of a typical "hat-rack" shape. The size varies from a few cm up to 1 0 cm. Pathology. Macroscopically, the cortex of the bone continues in the shaft of the osteochondroma, and the end is widened as a butt, this area is covered by the hyaline cap. In the cartilage-bone border an ordinary enchondral ossification zone is visible. Treatment. The chiseling of osteo chondromas from their base ensures a perfect outcome. There may be a rare recurrence if parts of the cartilage or the covering connec tive tissue capsule are left behind. In less than I % of the cases, malignant transformation may occur in the substance of hyaline cartilage cap. The frequency is much
Osteochondroma (exostosis cartilaginea)
This is a bony lump covered with a hyaline cap, which p resents from the surface of the bone.
Osteochondroma is rather a hamartoma, than a real bone tumor, it is a cartilage bud that "migrates" out from the growth plate. It is quite common, giving 5 0-60% of all benign lumps. In 1 0% of the cases it is multiple and shows a familial accumulation, it is classified among the bone dysplasias (Chapter l 3 . 1 .7.). A solitary osteochondroma is usually di agnosed in the first decade, involving the metaphyses of long tubular bones. Distal fem oral, proximal tibial and proximal humeral metaphyses predominate. The osteochondr oma grows as long as the bones continue to grow. Rapid expansion with fast progression in adults is always a suspicious sign of malig nant transformation. Symptoms. At the beginning, there are al most no symptoms, the osteochondroma is discovered as an accidental finding. During its expansion it may compress the surrounding nerves and vessels, tendons snapping over the
a
b
Fig. 21.16. a: Ca uliflower-shaped osteochondroma in the proximal metaphysis of the fibula b: 3 dimension reconstruction a i mage of this osteochondroma
2 1 . Tu m o rs of t h e m u s c u l o s ke l eta l syst e m
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20 1
higher, (ca. 5 - 1 0%) in multiple osteo chondromas, in multiple cartilaginous exo stosis. These patients must be thoroughly fol lowed up, and control X-rays are to be done. A sudden enlargement following bone matura tion is usually a sign of a malignant transfor mation, these should be excised immediately. �
Chondroblastoma
This is a rare benign tumor located in the epiphysis, next to the joint.
Symptoms. It appears chiefly on the tibia, femur and humerus of boys before the end of growth. The early symptom is swelling of the limb with a restricted range of motion of the neighboring j oint. Later a joint collection may follow with reactive synovitis. X-ray signs. These are very specific : oval or rounded lytic bone destruction in the epiph ysis, usually centrally with a sharp, occasion ally sclerotic border (Fig. 2 1 . 1 7. a, b). Treatment. The most common procedure is intralesional excochleation and autologous cancellous bone grafting. �
Chondromyxoid bone fibroma This rare benign tumor elicits hardly any symptoms . It presents in the second decade in the metaphyses of the long tubular bones. The X-ray image shows an eccentric lytic lesion with an uneven sclerotic margin, which may occasionally lead to bone protrusion. Treatment. Excochleation, autologous or homologous cancellous bone grafting. 21.2.3.2. Malignant cartilage-forming
tumors �
Fig. 21.17. a: Lateral X-ray of the knee: round lytic destructions (arrows) in the epiphysis - chondroblastoma. b: MR image: the extent of the chondroblastoma can be well estimated.
Chondrosarcoma
This is a malignant bone tumor containing hyaline cartilage cells in various stages of mat uration and a matrix.
There are many groups of chondro sarcomas, which differ in histological appear-
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202
2 1 . T u m o rs of t h e m u sc u l o s ke l eta l system
s u rvival among
1,0 1 - -1- - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -� __q,�_5.. 0,9 0,8 0,7 0,6 0,5
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If the complaints or the deformity worsen, cardiopulmonary changes are observed, or the deformity causes psychological complica tions, surgery indication may be contem plated. About 40% of the patients are operated on between the ages of 4 and 1 0 years, and 50% under the age of 20.
24. 10.2. Pectus carinatum (pigeon chest) I n contrast with funnel chest, pigeon chest is a protrusion deformity. Less attention is paid to this deformity, but it may a lso occur in a d is figuring form that causes a major disturbance in the function of the thoracic organs. It may appear in combination form with funnel chest, with the predominance of either.
Etiopathology. The etiology is unclear. The deformity occurs in early childhood and becomes more sever at puberty (around the age of 1 0) . In the view of Lester, it may origi nate from rickets, but, similarly as for pectus excavatum, the congenital etiology prevails. Anomalies of the diaphragm may play a role, with the difference that the centrum ten-
dineum is widened and the tension of the lat eral fibers creates the deformity. The antero lateral part of the diaphragm is hypertrophied; this pulls in the rib arch, and paradox breath ing results. Clinical symptoms. These are similar to those described for funnel chest. The breath function test proves a reduction in the vital capacity, especially if the chest ex pansion is decreased by the expressed Harri son groove and the paradox breathing. The condition may be accompanied by a kyphotic back or kyphoscoliosis. The cosmetic and psychological problems are similar to those in cases of funnel chest. X-ray signs. In pectus carinatum ob liquum, the protrusion is obligue, whereas pectus carinatum arcuatum it is arched. It does not displace the heart. A chronic pulmonary circulation failure is detected as a late compli cation of severe deformities. Treatment. The surgical therapy and postoperative care of protrusion deformity cases are similar to those for pectus ex cavatum.
25.
Jeno Kiss
Disorders of the neck and the shoulder girdle
25. 1. Functional anatomy and biomechanics of the shoulder girdle The main function of the shoulder and the elbow, via the upper arm and the forearm is to adjust the main human working tool, the hand into the wanted position. Any operational dis turbance of these two large joints of our upper limb may impair the working capabilities and the regular daily activities. The degree of the function depends on whether the dominant or not dominant side is involved. A young la borer or a competing athlete has different ex pectations relative to the elderly, who mainly use their upper limbs for self-maintenance.
The movements of the shoulder girdle are combinations of the glenohumeral, acromio clavicular and sterno-clavicular movements . An additional function is the motion of the shoulder blade on the trunk, the three most important components of which are the eleva tion (lifting the arm in the plane of the shoul der blade), external rotation and the combina tion of extension and internal rotation which result in the ability to reach behind the back. This motion is ensured by the function of the thoraco-humeral, thoraco-scapular and scapulo-humeral muscles. The shoulder itself, the glenohumeral j oint has the largest range of motion of any joint of the human body, and at the same time it is the most unstable joint.
g ----��----
c
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d
Fig. 25. 1. Anterior aspect of the shoulder region: a: n. suprascapularis, b: n. axillaris, c: plexus brachia lis, d: hu merus, e: processus coracoideus, f: acromion, g: clavicula, h: lig. coraco-acromiale, i: m. subscapularis, j: m. supra spinatus, k: biceps tendon.
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Fig. 25.2. Posterior aspect of the shoulder region: a: n. supraspinatus, b: n. axiliaris, c: humerus, d: spina scapulae, e: m. supraspinatus, g: m. teres minor, h: m. teres major, i: m. deltoideus, k: m. infraspinatus.
Special significance is attributed from an orthopedic aspect to the rotator cuff (Fig. 25. 1 ., 25.2.). This comprises the tendons of four muscles that originate in the frontal and dorsal surfaces of the shoulder blade : the subscapular, supraspinate, infraspinate and teres minor muscles. Besides assisting the various rotational motion of the humerus, the most important task of the rotator cuff is to en sure the central position of the humeral head against the j oint cavity, in the glenoid fossa, in any position of the arm.
25.2. Examination of the shoulder girdle The most common complaints are pain, weakness, motion disturbance and instability. The onset of the complaints, and the circum stances of the possible injury must be ex plored. The details of the profession, possible sporting activity and the dominant side are also important. During the inspection atten tion should be paid to an abnormal posture, deformities, muscular atrophy, possible skin
redness, swelling. The assessment of the range of motion starts with the range of active motion, and in case of a deficit, it is compared with the range of passive motion, since impor tant conclusions can be drawn from the differ ences. The stability of the glenohumeral joint is evaluated via the various stability signs (sulcus sign, apprehension tests, drawer sign). The individual muscle and muscle group functions are checked. The muscles of the ro tator cuff are to be assessed extremely care fully. An indispensable part of the physical assessment of the shoulder girdle and the up per limb is the evaluation of the motion of the cervical spine and the neurological state of the upper limb. This may be supplemented if needed by connectivity testing of the upper limb nerves (ENG) and the muscles (EMG). The radiological evaluation requires bi directional films, one a-po and one lateral view. Depending on the actual disease a num ber of directed examinations are to be used. A cheap, swift and reliable procedure is ultrasonography test to evaluate the soft tis sues and especially the rotator cuff. The next step can be in assessment a native or con-
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trasted e T and MR assessment of the changes in the soft tissues, and bones, j oints. In certain cases, arthroscopic examination of the glenohumeral, subacromial or subscapular area may be required, these procedures are mainly used as the introductory phase of an endoscopic or open therapeutic method.
25.3. The congenital and acquired disorders of the of the shoulder girdle •
Torticollis, muscular congenital (wry neck)
The asymmetric posture of the head is caused by the shrinkage of the sternocleidomastoid muscle. The head is tilted lateral ly and rotated in different directions, the face is asymmetri cal, the sternocleidomastoid muscle is tensely prominent. From the age of 1-2 weeks a pain ful swelling is observed in the muscle. This oc curs in both genders, and is often associated with other developmental anomalies. The symptoms are usually observed as early as 1-2 weeks. This is the 3rd most common musculoskeletal disorder after hip dislocation and clubfoot.
Etiopathology. This is a congenital disor der. According to certain theories injury, or tearing occurs in the substance of the ster nocleidomastoid muscle during birth, leading to the scarring of the muscle. Others postulate the role of intrauterine in congruence, the neck is forced into an asym metrical position, this causes the shrinkage of the muscle. A further view consider the intra uterine ischemia as a causative factor. Besides the exogenous factors the role of endogenous, hereditary factors have also been supposed. In certain families, the wry-neck occurs with in creased frequency, often together with other hereditary disorders, such as hip dislocation, clubfoot. Clinical symptoms. In the substance of the sternocleidomastoid muscle a hazel nut-plum sized tender lump is palpable at
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one-two weeks of age. Later the lump disap pears from the muscle. It is palpable only ex ceptionally after the first or second year, but the shrunken muscle may still be detected. The shortened muscle is as tense as a tight string and protrudes under the skin. The head tilts to the involved side, while the face turns in the opposite direction. The shrinkage may involve one or both muscle parts. The shrink age of the sternal part causes the rotation, while the clavicular part tilts the head (Fig. 25.3.). If the torticollis persists for a long pe riod, the skull will become asymmetrical . The involved part of the face will be smaller, scoliosis may affect the cervical spine. Differential diagnosis •
•
•
•
• •
• • •
Congenital scoliosis of the cervical spine. The X- ray shows the possible vertebral anomalies. Ocular torticollis. I n cases of certain vision anomalies the child may hold the head asymmetrically to compensate. Torticollis caused by i nflammation. Various inflammatory processes may occur in the cervical spine. Painful motion restriction may occur in the neck related to about of common flu, which resolves within a few days. Traumatic torticollis. Pain commonly develops in children after sporting activity, during fighting, in adults following sudden jerks (e.g. looking backwards), causing an oblique posture of the neck. Rheumatoid torticollis. This occurs together with other rheumatoid symptoms. Spastic torticollis. This is a the possible consequence of neural illnesses, such as encephalitis, chorea. Scar related torticollis. This is caused by scars after burns, or various i nflammations. Torticollis may be caused by the individual's occupation. Torticollis may a lso be due to psychological reasons.
Treatment. If the disorder is detected in infanthood, conservative treatment may be commenced. The shortened muscle is to be stretched by means of passive exercises, the
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Fig. 25.3. Right sided torticollis. The right m. sternocleido mastoideus is tense, the head is tilted to the right and rotated to the left.
parents must be educated to do these. The in fant should be positioned in such a way as to have to make an active correction to see the environment: e.g. in the case of right sided torticollis the light and sound stimuli must be located on the right side and above, forcing the baby to look to the right and upward. The baby is to be fed in such a way that the head must move in the direction of correction. De pending on the severity of the disorder opera tion is advised at the age of 1 -2 years . The tense part of the muscle is incised-in some cases the entire muscle is detached from the sternum and the clavicle. Some experts pro pose the recession of the upper attachment of the muscle from the mastoid process. Surgery performed at an proper time usually results in complete correction. If the operation is de layed, the facial asymmetry may persist. Rehabilitation. Postoperatively soft col lar support in young individuals is used, or plaster of Paris fixation in older patients or in cases of severe deformity. The head is posi tioned into overcorrected state. After 2-4 weeks of rest, the neck exercises commence.
Fig. 25.4. Sprenge/'s deformity. The left shoulder blade is
higher.
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Klippel-Feil-syndrome syndrome)
(short
neck
The neck of the patient is very short, and the range of motion is restricted. The deformed vertebrae may resu lt in the mechanical irrita tion of the cervical nerve roots and occasion ally of the spinal cord, neural signs may there fore appear.
Etiopathology. This characteristic defor mity is caused by a multiple developmental anomaly. There is no unified etiology, so it is recommended to consider this anomaly as a syndrome. The basic disorder is a disturbance of segmentation, or the unification of the bi lateral half-segments of the vertebrae. Symptoms. In mild cases the X-ray done for some other reasons uncovers the disorder of the cervical spine, which is localized to a few vertebrae and symptomless. In severe forms of the condition, the short neck is spec tacular, which may be due to the extreme shortening of the neck, or it may also be vir tual due to the higher location of the scapulae.
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The neck motion is restricted, torticollis may develop. The X-ray shows the vertebral changes listed above. Treatment. Only the complaints and neu rological symptoms due to the degenerative changes in adults are to be treated. �
Elevated scapula (Sprengel's deformity, congenital high position of the shoulder blade)
This is a shoulder blade anomaly occu rs in both genders. The shoulder girdle with the shoulder blade is higher on one side or rarely on both sides, while the shoulder blade is de formed, hypoplastic and often rotated (Fig. 25.4.)
Etiopathology. During the development, the shoulder girdle does not descend in the usual way from the height of the cervical seg ments. The periscapular muscles are short ened due to the position of the bone, their path changes, in certain muscles fibrosis is ob served. From the upper apex of the shoulder blade a cartilaginous-bony bridge (omo vertebral bridge) is connected to the lower cervical spine in about one third or half of the cases. Symptoms. The shoulder blade and the shoulder are located higher, the upper angulus
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of the scapula protrudes in the line of the neck and shoulder, the tip of the shoulder is dis placed anteriorly. The elevation of the arm is hindered because of the restricted motion of the scapula. The X-ray shows the shoulder blade positioned higher than the opposite one, in some cases the bony bridge connected from the angulus superior to the lower cervical spine is also observed (Fig. 25.5. a-b). Treatment. This condition typically does not disturb the function of the limb, is not painful, therefore its correction is usually jus tified from a cosmetic point of view, primarily in unilateral cases. Quite a few procedures are recommended, one of the most simple and rel atively common interventions is incision of the omovertebral bridge. If the angulus supe rior protrudes considerably, a good cosmetic result may be achieved by excision of this part. �
Scapula alata (flying shoulder blade)
This scapula disorder may take place for vari ous reasons. In mild forms during elevation, in severe forms even at rest, the shoulder blade lifts off the trunk. Since the function of the upper limb and the u nlimited motion range of the shoulder girdle require stability and harmonic movement, the pathologic state of the shoulder blade may cause severe func tional loss.
a b
Fig. 25.5. a: X- ray: The right shoulder blade is higher. I n the cervicodorsal junction at many levels spina bifida is present. b: The shoulder blade limits the elevation of the arm.
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Etiopathology. The main motors and sta bilizers of the shoulder blade may weaken one by one (serratus anterior or trapezius muscle palsy) or simultaneously. The cause of serratus anterior muscle palsy is a lesion of the thoracic longus nerve, which may appear after a viral infection, lifting heavy obj ects, trac tion, direct contusion or iatrogenic injury. The accessory nerve may be injured in a similar way leading to palsy of the trapezius nerve. Symptoms. The shoulder blade lifts off the trunk on elevation of the arm. In severe forms, this sign is detected even at rest. Be cause of the disorder of the shoulder blade, the elevation of the arm is weaker or very limited (Fig. 25.6. a-b). In mild cases, only fatigue, shoulder girdle pain are detected. In case of facioscapulohumeral dystrophy (FSHD) com plex shoulder girdle weakness is observed. Treatment. In cases of isolated serratus anterior palsy, conservative treatment is ap plied first, including shoulder girdle exer cises, selective current stimuli and vitamin D . If conservative treatment is ineffective after 6 months, surgical exploration and neurolysis is to be considered. In cases of total palsy of the scapula stabi lizers the fixation of the shoulder blade to the trunk, the scapulo-thoracal fusion provides
a
the FSHD patients with dramatic improve ment in upper limb function and quality of life. �
Neuromuscular compression syndrome of the upper limb ( " thoracic outlet " syndrome)
This is a distinctive, complex syndrome caus ing complex sensitivity, innervation and circu lation disturbances in the upper limb. It is in creasingly referred to as the "thoracic outlet syndrome" (TOS). It is most common in mid d le-aged women.
The typical cause may be a cervical rib, when the brachial plexus and the subclavian vein and artery are all compressed at their exit from the chest, before they reach the upper limb (Fig. 25.7. 25.8.). Symptoms. These are due to sensory, mo tor and circulation changes. •
Sensory changes: Painfu l paresthesiae, often
marked pain, burning sensation appears in the ulnar part of the hand and fingers. Hypoesthetic zones may be present in areas supplied by the ulnar nerve.
b
Fig. 25.6. A young female with facioscapulohumeral dystrophy (FSHD): bilateral scapula alata (a), limiting the elevation of the arm (b).
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Fig. 25.7. Pathomechanism of the thoracic outlet" syndrome. " a: a. vertebral is, b: m. scalenus medius, c: m. scalenus anterior, d: a. su bclavia, e: v. subclavia, f: m. pectoralis minor.
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Motor changes: Paresis, muscle atrophy may take place mainly in the small muscles of the hand. The g rasping force may be diminished. Vasomotor changes: Cyanosis may appear in the limb, atrophic changes may appear on the fingers. The radial pulse may weaken or disappear if the limb is abducted and externally rotated.
Treatment. In mild cases conservative treatment is successful. It is important to per fonn exercises to strengthen the shoulder musculature and improve the posture. In stub born cases, an operation, removal of the 1 st rib or cervical rib may be needed to improve the compression signs.
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Fig. 25.S. Cervical rib (white arrow) and extended processus costotransversarius (black arrow).
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Cervicobrachial syndrome Detailed description of this clinical picture is to be found in the chapter of spinal disorders (Chapter 24). The symptoms are often similar those to of other upper limb illnesses, and therefore an assessment of the cervical spine is essential, occasionally with X-ray examina tion in cases of any upper limb symptoms, and a basic neurological assessment of the upper limbs. �
Obstetric paralysis (paralysis of the lower limbs after birth)
During birth, the brachial plexus or roots of the p lexus are injured leading to various ex tent of paralysis of the upper limb muscle.
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The involved upper limb o f the infant lies motionless, rotated internally beside the trunk. Later, the clinical picture depends on the extent of the paralysis. Three forms are distinguished, regarding the anatomy of the plexus : - Erb-Duchenne 's form involves the upper arm - Klumpke 's form involves the forearm - the third form involves the entire upper limb. Symptoms. The infant is lying with the floppy, motionless upper limb, internally ro tated beside the trunk. Later the extent of the paralysis and of the possible anesthetic, hypoesthetic areas are dependent on the type of the paralysis. These changes can usually be established only in older babies. In larger chil dren and adults a growth disturbance of the upper limb is observed, while the humerus or in more severe forms the entire limb is shorter. Treatment. In the first week after birth the limb is put to rest. The limb is usually posi tioned with the shoulder abducted to prevent contractures. The simplest way is to tie the shirt sleeve with a ribbon to the swad dling-clothes (Fig. 25.9.) . In the second week, passive exercises and electrical stimulation are commenced. After the 2nd year an im provement is not expected from further con servative treatment, the function of the limb may often be improved surgically.
25.4. Disorders of the shoulder In the common meaning shoulder joint is simply taken as the glenohumeral joint. How ever, in a wider sense, the shoulder joint refers to a joint performing all of the movements be tween the trunk and the humerus. �
Subacromial impingement
This syndrome is caused by the abnormal contact with and rubbing of the acromion by the g reater tubercle and the attached supra spinate tendon. Typical symptoms are the painful motion arc during lifting of the arm and the pain radiating to the upper arm, and increases at night. This syndrome is character istic of the individuals between 40-50 years.
Etiopathology. These symptoms may be caused by a number offactors. The most com-
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Fig. 25.9.
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The paralytic upper limb is fixed in an abducted po sition to the swaddling-clothes or to the bed.
Fig. 25.10. Painful arc, typical of the middle range of the eleva tion (a: painless, b: painfu l motion)
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mon are the anatomical changes o f the acromion as the age advances. Inflammation of the subacromial bursa for any reason, but usually after repeated trauma, tendinitis of the rotator cuff, may lead to impingement by nar rowing the subacromial space. Paralysis or only weakness of the rotator cuff, contracture due to shrinkage of the tendons or of the cap sule of the glenohumeral joint may cause im pingement by displacing the humeral head cranially. Symptoms. A typical complaint is the pain in the middle range of arm lifting, the so called painful arc (Fig. 25.1 0.). The night pain is also typical, the patient wakes many times and is unable to lie on the involved side. Apart from the painful arc examination reveals crep itation during elevation and rotation, and weakness of the muscles of the rotator cuff due to the pain. X-ray shows the possible changes in shape, osteophytes of the acromion, and scle rosis of the greater tubercle (Fig. 25. 1 1.). Ul trasound or MRI shows thickening of the sub acromial bursa, fluid collection, edematous thickening or degenerative thinning of the supraspinatus tendon. Treatment. Conservative treatment is first applied, depending on the causative fac tors . The possibly decreased range of motion
Fig. 25.11. Calcified attachment of the coraco-acromial liga ment leading to impingement.
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must be restored with active exercises of the rotator muscles. The pain and inflammation are alleviated with NSAID, physiotherapy and a few (at most 3) local steroid inj ections. The working environment, sport and occupa tional activity are to be adjusted. If the conser vative method fails, an operation may be con sidered. Subacromial decompression may be done with an open exposure or arthro scopically. The operation is followed by a number of month rehabilitation period, with the aim of restoring the motion rhythm, range and the muscle power. �
Tearing of the rotator cuff
Any tendon, but most often the supraspinate, may be torn partially or in total thickness, typ ically near to the attachment. The clinical pic ture is characterized by a painful arc during lifting of the arm, the pain, increasing at night and radiating to the upper a rm, and the func tion disturbance, depending on the muscle in volved.
This disorder, most common around the age of 40, is due to the degenerative changes of the tendons. Its frequency increases with the age. It may occur rarely at a younger age (throwing athletes, laborers) . Etiopathoiogy. A number of factors may play a role. The tendons of the rotator cuff, and specially the supraspinate have a hypovascular zone in the vicinity of the at tachment. The impaired circulation is accom panied by collagen degeneration due to aging, repeated microtrauma relating to the occupa tion or sporting, occasionally a significant trauma. The tear initially is rarely total, but usually a partial thickness tear (Fig. 25. 1 2 . a-b), and i t later becomes complete gradually or after a major injury. Tears are also de scribed regarding to their extent as well. When the tear is larger and persists longer, the possibly intact residue of the rotator cuff loses its centralizing effect on the humeral head. The humeral head is displaced cranially and gradual secondary degenerative changes take place.
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may be chosen. Active exercises are impor tant to strengthen the remaining components of the rotator cuff and other muscles of the shoulder girdle, and to improve the active mo tion. Pain and inflammation can be reduced with NSAID, physiotherapy or a few, (at most 3) local steroid injections. Operation is con sidered in older patients after failed conserva tive therapy, at an active age or even as pri mary treatment. In partial tears, open or ar throscopic acromioplasty and removal of the tom periphery are indicated. In cases of a total tear, rotator reconstruction, reinsertion of the tendon(s) to the bony base is recommended (Fig. 25. 13. a-b) .
a
b
Fig. 25.12. Partial tear of the supraspinate tendon in the prox imity of the joint (a) and the bu rsa (b)
Symptoms. This condition is also charac terized by the pain presenting in the middle range when the arm is elevated, the so called painful arc (Fig. 25.1 0.). Night pain is also common. The patient may experience pain and cracks, rubbing in certain movements. Active elevation of the arm is possible even in cases of massive tears, but examining the muscle functions one by one, the weakening is detected. In case the lesion has been present for a long time, the supraspinal or infraspinal fossa will be excavated, signaling the inactiv ity atrophy and degeneration of the muscles. X-ray shows the possible changes in shape, the sclerosis of the acromion, and the sclerosis of the greater tubercle. In more se vere cases, thinning of the subacromial space and secondary osteoarthritis of the gleno humeral j oint are observed. Ultrasound or MRI shows thickening of subacromial bursa, fluid collection, and degenerative thinning in cases of partial tear, and the loss of the supraspinate tendon in cases of total tear. Treatment. Depending on the age, occu pation, daily activities of the patient, and also on the extent of the tear, conservative therapy
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Adhesive capsulitis (frozen shoulder)
This is a typical syndrome caused by fibrotic tissue changes in the soft tissues surrounding the shoulder. The range of motion is limited, painful, but no significant X-ray changes are detected.
It is a common affliction mainly in middle aged adults, women are involved one and a half times more often. It is more common in association with diabetes mellitus and other metabolic diseases . The condition may be uni or bilateral with different severity and pro gression. Etiopathology : a number of factors may play role. Two basic forms are distinguished. - Primary adhesive capsulitis: the etiology is unknown. - Secondary adhesive capsulitis: the clinical symptoms are similar and the cause is known : injury of the shoulder, operation, intraor periarticular inj ection, infection, etc. Symptoms. Regardless of the etiology pain radiating to the upper arm is typical. The pain is present at rest, often it is worse at rest. The onset of pain is soon followed by a grad ual restriction of motion. As time goes by, the pain may decrease or disappear, but the re stricted motion persists for a long time.
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limitation of both active and passive shoulder motions the native X-ray does not prove any maj or changes. Treatment. Typically in a large propor tion of the cases this disorder heals without any particular therapy. This healing may last for 1 -3 years, and while the pain ceases and the motion improves, some restriction in the range persists. The aim of the conservative therapy is to relieve the pain. At the same time, gradual restoration of the range of mo tion should commence with exercises per formed a few times every day. In the over whelming maj ority of the cases conservative treatment results in a satisfactory improve ment, an additional procedure could be the manipulation of the joint under anesthesia. Some prefer operative treatment. a �
Glenohumeral arthrosis (osteoarthritis of the shoulder)
This condition causes a painful limitation of motion of the g lenohumeral joint it may be primary or secondary (following inflamma tion, degenerative, traumatic changes, infec tion, etc.). The primary form involves mainly elderly a bove the age of 60-65. The secondary forms may take place at any age, depending on the etiology.
Fig. 25.13. Reinsertion of torn supraspinate tendon with transosseal sutures (a: a-p view, b: upper view).
On examination typically severe restric tion of elevation and rotation is found. The ab solute diagnostic criterion is that besides the
Etiopathology. In primary arthrosis, the changes are similar to those for the other large joints (Fig. 25.14. a) . The rotator cuff is usu ally intact. In secondary osteoarthritis the outcome of the changes depends on the etiologic factor (Fig. 25.14. b, c, d) . Symptoms. Common symptoms of the primary and secondary osteoarthritis are the pain and the limited range of motion, which usually develops gradually. Because of the chronic instability or the rotator cuff tear, muscle atrophy takes place around the shoul der. In contrast with adhesive capsulitis radio logical changes are always detected in cases of arthrosis. Treatment. Since the load-bearing de mand on the upper limb is less than that on the
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c a
d
b
Fig. 25.14. Primary arthrosis of the shoulder (a), post-trau matic arthrosis (b), avascu lar humerus head -necrosis induced arthrosis (c), massive rotator cuff tear induced arthrosis (d).
lower limbs, conservative treatment can be applied for a long period. If an operation is necessary, it may be a j oint-preserving or a j oint-replacing procedure (arthroplasty). Joint-preserving methods include arthroscop ic lavage of the shoulder, endoscopic removal of cartilage debris, osteophytes, tom pieces of labrum and tendons, and in rheumatoid pa tients arthroscopic or open synovectomy. In severe cases, implantation of a shoulder pros thesis will improve the quality of life. De-
pending on the type and severity of the illness merely the head of the humerus (hemi arthroplasty) (Fig. 25.15. a), or both the head of the humerus and the glenoid surface can be replaced (Fig. 25.15. b). When both the glenohumeral joint and the deltoid muscle are destroyed, glenohumeral arthrodesis (Fig. 25.1 6.) could be the only solution to ensure pain relief and it provide an acceptable func tion by rotation of the scapula over the trunk.
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a b
Fig. 25.16. Glenohu meral arthrodesis, osteosynthesis with plates.
athletes and heavy laborers, is due to the phys ical overload and the special intra-articular path of the biceps caput longum tendon. If conservative treatment fails, arthroscopy is advised, this may show fragmentation or fi brillation, which may be smoothened arthro scopically. In cases of a severely degenerated tendon proximal detachment and tenodesis in the sulcus or more distally can be considered. Fig. 25.15. Shoulder hemiarthroplasty (a) and total arthroplasty, (b) X-ray picture.
25.5. Other painfu l shoulder conditions briefly �
Tendinitis of biceps brachii muscle Pain and local tenderness radiate from the area of the bicipital sulcus to the upper arm. This disease usually observed among young
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Calcifying tendinitis This is usually observed in women over 40, who experience very heavy shoulder pain without any antecedents. The diagnostic crite rion is a radiodense structure over the greater tubercle, which is less dense than the mature bone, but well circumscribed, corresponding to the calcium crystal deposits (hydroxy apatite) in the substance of the tendon, which proves an inflammatory process in the area. The treatment is basically symptomatic, since the condition heals spontaneously. Pain kill ers, NSAID are prescribed. A dramatic im-
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provement may b e achieved from a few ste roid inj ections into the subacromial space (not into the tendon ! ) . A further conservative tool is ultrasound shockwave therapy. When con servative therapy is unsuccessful, or extensive depositions lead to subacromial impingement, the focus is to be removed arthroscopically or by open surgery. �
Arthrosis of the acromio-c1avicular (AC) j oint A localized pain develops in the AC j oint mainly in middle aged or older patients, radi ating typically toward the neck. The local ten derness over the joint is also distinctive. Simi larly to other joints the AC changes may be caused by primary or post-traumatic arthrosis. The treatment is basically symptomatic, con servative. In stubborn cases resection of the lateral end of the clavicle and removal of the degenerated disc are justified. �
Disorders of the sterno-c1avicular (SC) j oint These are relatively uncommon. Instabil ity occurs as a part of general joint laxity, which rarely requires treatment, or as post-traumatic instability, when surgical sta bilization is considered. General j oint inflammations and degener ative processes may involve the SC j oint. There are some conditions of unknown origin, that cause deformity of this joint or the medial end of the clavicle (Tietze ' s syndrome, osteitis claviculae, etc.), which require con servative treatment in cases of complaints.
25.6. Glenohumeral i nstability, shoulder dislocation Symptomatic pathologic displacement of the humeral head relative to the g lenoid surface is cal led glenohumeral instability. Partial dis placement of the humeral head is subluxation. If the humeral head leaves the g lenoid fossa in its entirety, dislocation occurs.
The humeral head is usually luxated ante riorly and caudally, and can be reduced in the beginning only with medical assistance, after multiple repetitions, it can even reduce spon taneously. The younger the patient, the higher the probability recurrence of the shoulder dis location. About 96% of the dislocations are anterior or antero-inferior, the remaining 4% are posterior or multidirectional. Etiopathology. The stability of the shoul der is ensured by different static and dynamic factors. The static, passive stabilizers are the thickening of the joint capsule (glenohumeral ligaments), the glenoid labrum, the negative joint pressure and to a lesser extent the joint surfaces. The dynamic, or active stabilizers are primarily the muscles of the rotator cuff, secondarily the shoulder blade stabilizers and ultimately all the muscles in the shoulder gir dle. Shoulder instability may develop for many reasons, the type of the instability also varies. Because of the wide range of etiology the shoulder instability is classified in many dif ferent ways: �
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By the extent of the instability - subluxation - luxation By the direction of the instability - anterior - caudal - posterior - multidirectional By the time of the instability - acute - inveterate - recurrent By etiology - traumatic - habitual - voluntary
History. The majority of the patient men tion some kind of traumatic dislocation and recurrent luxations after that. The circum stances of the injury are essential. The most common anterior luxation typically develops
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) Fig. 25.17. Assessment of shoulder instability with su lcus sign.
following an extension-external rotation movement, while the posterior dislocation is induced by anteflexion and internal rotation. The first anterior luxation most often requires reduction performed by the doctor, later the patients are themselves able to reduce the shoulder. The first dislocation following a real injury may recur later even following the movements of the everyday life (dressing, washing, reaching backward, etc.). After many repetitions, the patient can even pro duce the luxation, this is not necessarily iden tical to the voluntary dislocation, which is usually related to psychiatric problems. Symptoms. Initially the dislocation causes a major sensation, with painful swell ing, elastic blockade of motion and often paresthesiae in the upper limb. If the shoulder is dislocated, the acromion protrudes, a de pression is seen under it and the humeral head is palpated caudally and frontally (anterior dislocation) or toward the back (posterior dis location). In cases of anterior dislocation, if the shoulder is externally rotated in 90 degrees of abduction, at the end point of the range the pa tient indicates that this motion causes discom fort with the feeling that the shoulder will dis locate during the assessment (anterior appre-
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hensive test). In cases of posterior dislocation, anteflexion and internal rotation provoke a similar sensation (posterior apprehensive test) . A further diagnostic sign is the subluxability of the humeral head caudally (sulcus sign, Fig. 25.1 7.), which is tested by axial pulling ofthe relaxed arm. A typical fea ture of multidirectional instability is the mo bility of the humeral head anteriorly or poste riorly (anterior and posterior drawer sign). X-ray signs. The direction of the disloca tion is detected by traditional X-ray test. After reduction, the native film gives information on the shape and direction of the glenoid cav ity, and on the possible bony B ankart' s lesion, (Hill- Sachs ' s lesion, Fig. 25.18. a). In case CT scan can also be done (Fig. 25. 1 8. b, c), CT arthrography is needed to clarifY the state of the bone anatomy and the labrum. MRI or ultrasonography may provide data on the con ditions of the labrum and the rotator cuff. Treatment. In case of acute luxation re duction and fixation of the shoulder in internal rotation for 3 -4 weeks results in lasting symptomless outcome only rarely. Following repeated dislocation the mode of treatment depends on the type of instability and the etiologic factors. If dislocation is intentional, the cause of the personal identity disturbance must be identified (psychiatric illnesses, family or school conflicts) and possibly cured. Disre garding the etiologic factors, ignoring the in stability complaint (the so called skillful ne glect) may be helpful, when the patient' s at tention is turned away from the significance of the instability. In cases of traumatic dislocation rehabili tation care for at least 6 months is essential, the most important elements of which are strengthening of the rotator cuff and scapula stabilizer muscles and improving the proprio ception in the shoulder area. Surgical treat ment is indicated only after failed conserva tive therapy, and the circular loose cap sule-ligament system is tightened (lower capsuloplasty) .
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b
c
Fig. 25.18. a: I n a case with rig ht habitual luxation the defect caused by the tear of the glenoid labrum is visible together with the a nterolateral head defect. b: Impression fracture at the posterior part of the humeral head (Hill-Sachs lesion): a image. c: Fracture of the anterior glenoid rim (bony Bankart's lesion) a image.
In case of real recurrent traumatic disloca tion operative procedure is the primary mode of therapy. The type of surgical method de pends on the type of injury and the direction of instability .
The postoperative rehabilitation is deter mined by the technique used. The patient may return to full physical activity (physical work, sport) usually after 6 months. The modem surgical procedures prevent recurrent luxation in 90-95% of the cases.
26.
Jeno Kiss
Disorders of the elbow and forearm
26. 1. Functional anatomy of the elbow and forearm While the movements ofthe glenohumeral joint can be compensated by the sliding of the scapula on the trunk, and similarly the motion restriction of the scapula can be compensated between certain limits by the glenohumeral joint movement, the flexion - extension of the elbow can not be replaced by any other func tion. Pronation - supination of the forearm can be compensated with the elbow extended ?� the movement of the shoulder. At all ages, It IS of utmost importance for every individual �o be �ble to reach both orifices of the gastro mtestmal tract. In case of a severe extension elbow contracture, the mouth is out of reach' in the event of a considerable flexion elbo� contracture, the patient is unable to reach the perineal area. Besides flexion - extension pronation - supination of the forearm is als � important, which is around 90° each. To per . form this complex movement, the integrity of the forearm bones, the attached interosseal membrane, and the proximal and distal ra dio-ulnar joints is essential . In consequence of the shape of the joint surfaces and the complexity of the ligament system, the elbow is a very stable joint. At the distal end of the humerus, the joint between the trochlea and olecranon ulnae ensures flexion - extension, while the joint between the capitulum humeri and the caput radii chiefly plays a role in the rotation and the sta bility of the elbow. Further important compo nents of the stability are the processus coronoides ulnae and the medial - lateral col lateral ligaments. The extension of the elbow is car:� ed ou� � y a single muscle, the triceps brachll, and It IS flexed only by the m. biceps
brachii and m. brachioradialis, but to some ex tent by practically all the muscles that origi nate over the elbow and are attached on the forearm or the wrist. The forearm is rotated by the pronator and supinator muscles with the assistance of the extensors and flexors . It should be pointed out th �t the biceps i � not only a flexor, but also a �Ulte strong supmator. When the palm is fac mg forward, the axis of the extended elbow positi ?ne � ? eside the trunk is 5-1 5 ° of valgus. It IS cntlcal from a surgical anatomical as pect that all three nerves and blood vessels are in the close vicinity of the elbow.
26.2. Assessment of the elbow The basic assessment criteria and methods are fully identical to those described in con nection with the assessment of the shoulder girdle (see details in Chapter 25 .2). In the course of the examination, the direction of movement and the anatomical features of the elbow j oint must naturally be taken into con sideration. A complex upper limb examina tion must always comprise such an assess ment.
26.3. Significant developmental anomalies �
Congenital dislocation of the radial head
This is a com plex developmental anomaly with axial deviations of the radius or the ulna, and the radial head is in a dislocated position. It is relatively rare, and may occur isolated or
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in association with other developmental anomalies.
Clinical symptoms. The deformity is rarely a source of complaint in childhood, and is mostly recognized accidentally. The pronation and supination of the forearm are restricted. In adults, the symptoms are arthrotic in character. Treatment. Reduction should be supple mented with correction osteotomy, and occa sionally with shortening of the radius or the ulna. When the symptoms present in adult hood, resection of the radial head is justified. �
Clinical symptoms. It is typical that the pronation - supination movements are miss ing. Treatment. Attempted restoration of pronation - supination movements through plastic surgery interventions usually fails, fol lowing removal of the bony bridge, even if a soft tissue interpositum is created, recurrence of the synostosis is common.
Congenital radioulnar synostosis
Because of a disturbance in the differentiation of the cartilaginous substance of the forearm bones, the separation of the two bones is in com plete. The synostosis between the radius and u l na is usually proximal to various extents (Fig. 26. 1.).
Fig. 26.2. Fig. 26.1. Bilateral radioulnar synostosis.
Bilateral Madelung deformity; clinical (a) and X- ray pictu re, demonstrating bending of the radius in the volar and ulnar directions (b), the dorsal protrusion of the ulna is clearly visible (c).
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Madelung's deformity
Mode/ung's deformity is a g rowth disturbance
of the distal epiphysis of the radius, resu lting in volar and ulnar bending of the distal radius. Its occurrence is often familial. It is more com mon in girls and often bilateral.
Clinical symptoms. The radius is short ened and the distal end of the ulna therefore protr�des over the wrist to the dorsal surface of the forearm (Fig. 26.2. a-c) . The deformity increases with growth. The symptoms are caused by the restriction of the extension and radialduction movements of the wrist, and by the restriction of the supination of the fore arm. When the deformity is severe, the grasp ing force of the hand may also diminish. Treatment. If the deformity is extensive, osteotomy on the distal metaphysis of the ra dius may correct the curvature of the bone. The ulna is shortened at the same time, or its distal end is resected.
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26.4. Acquired disorders of the elbow �
Arthrosis (osteoarthritis) of the elbow
Arthrosis is a painful restriction of the move ment of the elbow, with radiological changes, which can be primary or secondary (outcome of inflammation, degenerative, trauma, infec tion, etc.). Primary osteoarthritis involves mainly individuals over 40 who are engaged in heavy labor. Secondary changes may occur at any age, with varying incidence.
Etiopathology. In primary arthrosis the changes observed are similar to those in other large j oints . The changes primarily affect the j oint surface; the involvement of the radio humeral j oint precedes the ulnohumeral changes. In the late stages, osteophytes are typical at the tip of the olecranon and the coronoid process, obstructing the movements. In secondary arthrosis the type of the changes is dependent on the etiology factor (Fig. 26.3.). Clinical symptoms. Pain initially appears only after the exertion of physical effort, but it
Fig. 26.3. Elbow destruction caused by rheu matoid arthritis (lateral and anteroposterior X-ray)
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later becomes permanent. Early restriction o f the extension and supination is typical, but later movement is restricted in every dimen sion. Cracks van be heard and friction felt while moving the joint. The osteophytes sur rounding the ulnar nerve may cause the com pression of the nerve. In case of rheumatoid arthritis, swelling and occasional instability are also observed. Treatment. In any form of elbow osteo arthritis, conservative treatment is applicable for a relatively long period. Conservative treatment is employed to relieve pain, to maintain motion range and to protect the mus cles. In cases of systemic diseases (rheuma toid arthritis, hemophilia, gout, etc.) treatment of the basic disease is essential. If operative therapy is needed, joint- preserving and j oint-replacing procedures are available. Joint-preserving surgery involves arthroscop ic lavage of the joint, removal of inflamed synovial villi, and in rheumatoid arthritis ar throscopic or open synovectomy. Predomi nantly in post-trauma cases, the scarred j oint capsule and the hypertrophied callus that in hibits movements can be removed (arth rolysis). In severe cases, an elbow endoprosthesis is implanted to improve the quality of life (Fig. 26.4. a, b). This endoprosthesis ensures proper movement and stability, but the pa tients must refrain from excessive physical activity. �
during work (tennis players, typists, etc.). It is common among heavy laborers. Both variet ies are most frequent between the ages of 40 and 50. Lateral epicondylitis is 5 times more common than the medial form.
a b
Epicondylitis humeri lateralis et medialis (tennis elbow, golfers' elbow)
Lateral epicondylitis of the humerus is called tennis elbow, and medial epicondylitis is cal led golfers' elbow. The pain presenting at the lateral epicondyle is a consequence of overloading of the forearm extensors, while the pain occurring at the lateral epicondyle is the outcome of excessive use of the forearm flexors.
The symptoms are often detected in young adults who overload the extensor muscles of the wrist and fingers while playing sports or
Fig. 26.4. X-ray pictu res of an elbow following prosthesis im plantation in rheu matoid arthritis. Anetroposterior (a) and lateral view (b)
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Etiopathology. Repeated trauma and de generative changes in the area of the origin of the muscle result first in microscopic tears, then, in about 30% of the cases, macroscopic tears are observed. Clinical symptoms. In tennis elbow, the patients complain of gradually developing pain in the lateral part of the elbow. The pain initially occurs during active movements of the wrist and when grasping obj ects, but later it may be present even at rest. The pain in creases when the forearm extensors are ac tively stretched. The pain can be so intense that the patient is unable to grip, and drops grasped and lifted obj ects. The lateral epicondyle and the extensor muscles are ten der to palpation. Golfers ' elbow causes simi lar symptoms in the medial epicondyle area, and the medial epicondyle is tender. Differential diagnosis. In the case of ten nis elbow, radial nerve compression, cervical root compression and j oint ailments are to be considered. In golfers elbow, the compression syndrome of the ulnar nerve, collateral liga ment disorders and also cervical root com pression must be differentiated. Treatment. Conservative treatment, usu ally lasting for a number of months, proves successful in 90% of the cases of both disor ders. This includes the avoidance of overload ing movements, resting the wrist and hand if necessary, padding applied distally from the nonsteroidal ongm, anti muscle inflammatory drug creams or tablets, local lignocaine + steroid injections into the painful areas, and physiotherapy. If conservative treatment does not bring relief within a rela tively long period, various surgical interven tions are to be considered. �
Olecranon bu rsitis
Inflammation developing in the bursa over the olecranon is a relatively common condi tion. The inflammation is caused by chronic ir ritation of the tip of the elbow, metabolic dis ease, a blow in the elbow region, or hematogenous bacterial infection.
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Clinical symptoms. Depending in the eti ology, in acute cases moderate or severe swelling of the bursa, fluctuation and tender ness occur, in septic inflammation, hyperemia and warmth are detected. In case of chronic bursitis, the swelling varies, tenderness is moderate, and fluid accumulation, thickening of the wall of the bursa, and loose bodies in the bursa are palpable. Treatment. In case of sterile inflamma tion, the usual anti-inflammatory methods, and occasionally the drainage ofthe bursa and steroid inj ection are considered as conserva tive therapy. In stubborn cases, surgical re moval of the bursa is recommended. �
Instability of the elbow
Slack col lateral ligaments, usually acquired, but rarely of congenital origin, or deformed bones of the elbow result in instability of the joint.
Etiopathology. The elbow is a relatively stable j oint, nevertheless, elbow luxation due to high-energy injuries is the second most common dislocation after that of the shoulder. The instability may be acute or chronic. Chronic instability is relatively rare. With re gard to the direction, it may be medial, lateral, anterior or posterior, or usually some combi nation of these. Clinical symptoms. Acute elbow disloca tion is usually not difficult to diagnose, con sidering the obvious deformity and elastic block of movement. It is more difficult to prove chronic instability, which causes only subluxation. Even an experienced examiner can only establish proper diagnosis after sum marizing the circumstances of the onset of the complaints, the results of careful physical as sessment and an X-ray examination. Treatment. If no fracture is involved, an acute elbow dislocation, requires closed re duction and depending on the degree of insta bility following reduction, transitional immo bilization ( 1 -3 weeks), followed by early functional treatment. In cases of chronic insta bility, depending on the characteristics and
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extent and also on the physical activity and age of the patient, conservative treatment is advised: modification of the sporting and vo cational activities, strengthening of the mus cles bridging the elbow and occasionally ex ternal orthesis. Surgical procedures depend on the cause and type of the instability. �
Acquired axial deformities
In consequence of very frequent elbow frac tures in child hood, varus deformity is com mon due to the damage to the growth plate.
a b
A mild deformity is usually merely a cos metic problem. In more severe cases, how ever, the entire function of the upper limb is altered, especially when the varus deformity is complicated with a flexion contracture of the elbow. The diagnosis is unmistakable in view of the characteristic clinical and radiological signs. Milder cases do not need treatment. In more severe cases of varus with a flexion contracture, correction osteotomy in the hu merus distal metaphysis may be justified (Fig. 26.5. a, b) . �
Tunnel syndromes of the elbow
These clinical entities are characterized by pain and occasional paresthesia radiating from the elbow to various areas of the fore arm or of the hand. The ulnar nerve is most commonly involved. Compression of radial nerve is less frequent, and the median nerve compression is rare.
Fig. 26.5. 40° post-traumatic varus deformity of the rig ht el bow of a 10-year-old child (a), and following correc tion by humerus osteotomy (b)
Etiopathology. Nerve compression may take place where the nerve passes certain ana tomical locations and is compressed by a scar, an abnormal muscle belly, an osteophyte, a callus or a tumor. Stretching or tension of the nerve may be caused by severe post-traumatic or degenerative deformity of the elbow (see also in Chapter 1 7) . Treatment. Conservative therapy may be successful only in minor cases. Rest and use
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of a night splint in attempt to decrease the edema caused by the compression of the nerve. In more severe cases, surgical decom pression of the nerve may be necessary.
26.5. Volkmann's ischemic contracture of the forearm and the hand This clinical picture arises following injuries or the application of a tight plaster of Paris ban dages. The typical contractures are produced by the ischemic necrosis of the forearm mus culature. The syndrome was first described by Volkmann.
Etiopathology. This syndrome usually appears following a supracondylar humerus fracture in childhood, elbow luxation, or use of a tight plaster of Paris bandage applied for some other reason, but it can also be caused by a misplaced tourniquet cuff. Ischemic necro sis develops in the foreann musculature, re sulting in scarring of the muscles. In certain cases, damage to the ulnar, radial and median nerves is observed. Clinical symptoms. Early symptoms may be identified merely a few hours after the in jury. The hand is cool, swollen and purplish blue. A change in sensitivity and loss of mo tion to various extents may occur in the fin gers. The developed Volkmann contracture displays a typical picture: flexion contracture of the elbow, pronation ofthe foreann, flexion and a mild ulnar deviation contracture of the wrist, extension in the metacarpophalangeal joints, flexion in the interphalangeal joints, and an opposition contracture of the extended pollex. The fingers exhibit a claw hand defor mity (Fig. 26.6.) .
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Treatment. Prevention is essential. The risk of an ischemic contracture must be borne in mind in cases of elbow injuries, and reduc tion and positioning of the plaster of Paris must be carried out accordingly. A circular plaster must not be used in elbow injuries. The circulation must be checked regularly, and the attention of parents must be drawn to this. I f a minimal circulatory, sensory o r motor distur bance is detected in the hand, the bandage must be loosened immediately and close ob servation must follow. An important clinical symptom is the pain on passive flexion of the fingers, due to the increasing pressure in the muscle compartments. If this state does not improve quickly, fasciotomy of both flexor and extensor compartments on the elbow and the foreann must be perfonned immediately in order to decrease the pressure in the com partments and restore circulation. When a Volkmann contracture has already developed, the treatment is long-lasting. Contracture of the fingers may be improved by exercises, or in more severe cases by me chanical methods. In mild cases, these meth ods may even result in full recovery. In severe cases a surgical solution may be needed. De pending on the extent of the defonnity, the hand function may be improved by tenotomies, muscle transfers or wrist arthrodesis.
Fig. 26.6. Typical clinical picture of the Volkmann's contractures
Fe r e n c M a d y
27.
Disorders of the hand and the wrist
27. 1. Functional anatomy of the hand and the wrist Beside its motor function, the hand also acts as a sensory organ. The bones of the hand are the carpal bones, the metacarpal bones and the phalanges. Special attention should be paid to the first metacarpal bone due to the � a?dle joint and the metacarpophalangeal Jomt. The other metacarpals are characterized by the shape of their distal articular surface (ball joint). As concerns the joints, the loose ligaments ?� the saddle joint (the first carpometacarpal Jomt) and the eccentric location of the liga ments of the second to fifth metacarpo phalangeal joints should be taken into consid eration. The muscles of the hand are divided into three groups: the thenar, mesothenar and
Fig. 27.1.
a
hypothenar groups . These muscles provide the fine (but weaker) motions of the fingers . The peripheral nerves (the median and the ulnar nerve) reach the hand through pre formed anatomic tunnels (the carpal tunnel and Guyon ' s tunnel). Both nerves are of mixed type. There is a separate nerve on both sides of each finger. The blood supply of the hand is provided by the end-branches of the radial and the ulnar arteries. The anatomic structures of the hand are covered by the palmar fascia . Clinical examination of the hand. The easiest and quickest way to examine the hand is to apply the scheme described by Erik Moberg, which consists of four steps (Fig. 27.1 a-d) :
b
The Moberg's scheme: a method for rapid assessment of the hand-function.
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a) Examination of the integrity of the long flexors and extensors. The patient is re quested to extend the fingers fully, and then to flex them slowly while keeping the metacarpophalangeal joints extended. If this can be accomplished properly, the long flexor and extensor muscles and ten dons are intact. When the superficial flexor tendons are examined, the fingers are kept in extension, and the proximal interphalangeal j oints are then flexed one by one. If there is a lesion of the superficial flexor tendon, the finger cannot be flexed in the proximal interphalangeal joint in this way. b) The motor function of the ulnar nerve can be checked by adduction of the thumb and ab- and adduction of the long fingers. A weakened thumb adduction indicates a de teriorated function of the ulnar nerve. The patient is requested to hold a sheet of paper between the thumb and the edge of the palm. If the adduction function preserved, considerable force is required to remove the paper sheet. The abduction strength of the fingers is tested against resistance. The closing strength of the fingers is checked by attempting to open them. If the patient resists well, the innervations of the intrin sic muscles are intact. c) The median nerve is responsible for the opposition-reposition of the thumb. When testing the opposition, the patient is re quested to form a circle with the thumb and the little finger and to keep them tightly together. If the fingers can be sepa rated easily, the opponent muscle strength is weakened. d) The last step is to test the sensitivity of the hand according to the supply area of the three nerves . A small blunt obj ect is to be used for the examination. If the superficial sensation is preserved, the patient reports good sensation in the palm, in the lateral aspects of the fingers and in the palmar as pect of the fingertips . The limit between the sensory areas of the median and the ul nar nerves is the midline of the ring finger toward the wrist crease. The sensory areas
on the dorsal aspect of the hand differ from those in the palmar aspect. Distally from the proximal interphalangeal joints, the ar eas are the same, but the rest of the dorsal aspect is supplied by the radial and ulnar nerves. The border between them is the midline of the middle finger. More accurate methods for examining the sensitivity of the hand are the two-point dis crimination test; the touch test, the pain- and the pick-up tests. Recognition of objects is en sured by the simultaneous activity of the ther mal, pain and touch receptors. Ifthese are sev ered, the patient is not able to recognize smaller obj ects without eye control. If there is only a minor impairment, the two-point dis crimination increases from the normal 1 -2 mm up to 5-6 mm or even more. In case of more severe nerve damage, all the sensory functions are affected and the function of the hand deteriorates considerably. Both the regulation of the perspiration and the sensitivity of the hand are linked to the digital nerves. This can explain the phenome non that, if the digital nerve is severed, the skin is dry and the perspiration is impaired. On percussion of the damaged peripheral nerve, electric shock-like pain is evoked at the site of the nerve injury or nerve compression ( Tinel' s sign). The site of the nerve damage can therefore be accurately determined. The blood supply for the hand is provided by the radial and the ulnar arteries. The interosseal artery also provides some branches flowing from the wrist. These pres ent several anatomic variations and do not provide sufficient blood supply for the hand by themselves. The neutral 0 method is used to describe the range of movement of the hand. The joints are in the 0 position when the fingers are ex tended. The functional position of the hand: The optimal grip position is the best for the function of the hand (Fig. 27.2.). The functional position is borne in mind when the hand is immobilized: the articular ligaments adapt quickly (even within one or
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Surgery on the hand is performed under re gional or general anesthesia and with the use of tourniquet bloodless . The hand may be affected b y numerous or thopedic disorders . However their incidence can be different.
27.2. Congenital anomalies of the hand Fig. 27.2. Functional position of the hand. The metacarpo phalangeal joints are flexed at 60° in the second and 90° in the fifth finger. The wrist is in 30° dorsiflexion. The proximal interphalangeal and distal inter phalangeal joints are bent at 20-30°. The best grip is provided in this position of the hand.
two weeks) to the length they had during im mobilization. This explains the fixed deformi ties developing during immobilization. These deformities can be prevented by immobiliza tion in the functional position.
The upper and lower extremities develop simultaneously between the fourth and sev enth week of the embryonic life . The hand de velops through the growth and differentiation of the limb buds. If the embryo is exposed to genetic or direct toxic effects, various devel opmental failures may occur in the hand (and often in the foot) . �
Syndactyly In syndactyly, two or more fingers are par tially or completely j oined. Sometimes only
Fig. 27.3. Types of syndactyly a: Sketch of an X-ray image indicating that in cutaneous syndactyly the bones are not affected and separated as in a normal hand. b: In osseous syndactyly the bones are missing or joined. c: In spoon-hand, all the fingers have a common skin glove; certain bones are missing or deformed.
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Fig. 27.4. Cutaneous syndactyly. The middle and ring fingers are joined in their entire length. Due to the growth of the fingers, the otherwise longer middle finger bends ulnarward. After separation, the fingers continue growing proportionately.
the skin is common (cutaneous syndactyly), but in more severe cases, the bones are also common (bony syndactyly) . In the most se vere case, all five fingers are involved (spoon hand) (Fig. 27.3. a-c). In cutaneous syndactyly, the otherwise separate fingers are covered by a common skin (Fig. 27.4.). The nail may be deformed at its base. Possible variations of the blood ves sels should be clarified before surgery is de cided on. Angiography is to be performed to exclude any vascular abnormalities. Separation of the fingers needs an experi enced surgeon. A preferred age for such inter ventions is at the age of 2-3 years . Accurate reconstruction of the web between the fingers is essential in order to avoid scars and conse quent fixed deformities. �
Ectrodactyly This is the congenital absence of a fin ger(s). �
Cleft hand This congenital absence of one or more of the central (second to fourth) fingers is also called lobster-claw hand. The cosmetic ap pearance is usually worse than the functional impairment. �
Polydactyly This denotes the presence of an extra digit, which may be complete or the rudimentary part of a finger or thumb.
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Congenital trigger thumb This involves congenital stenosis of the flexo tendon sheath ofthe thumb. Surgical in cision of the tendon sheath is indicated at an early age. Congenital anomalies of the hand exhibit great variety and many combinations are ob served. The optimal timing for surgery is around the age of 2-3 years . If several interventions are necessary, these should be completed be fore the first school year.
27.3. Acquired hand disorders 27.3.1. Avascular necrosis of the carpal lunate bone (Kienbock's disease) This d isease comprises necrosis, fragmenta tion and collapse of the l unate bone in adults; it is of unknown etiology. It was first de scribed by KienbOck who presumed a blood supply distu rbance leading to bone necrosis.
The pathomechanism and the outcome dif fer from those in juvenile osteochondritis. In Kienbock' s disease the necrosis of the lunate bone is definitive, while in juvenile osteo chondritis the necrosis is followed by regener ation of the bone.
2 7 . D i s o r d e r s of t h e h a n d a n d t h e w r i st
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The disease occurs most frequently in males who perform heavy manual work, (re peated micro traumas, use of a pneumatic hammer, or activities in a smithy) around the age of 3 0 . Clinical features. Pain o n palpation and a painful swelling of the dorsal aspect of the wrist. The patients usually connect the onset of the symptoms to some trauma in the past. Pain increases upon exertion. Movements of the wrist are painful and limited in all three planes . In a later stage, the range of extension decreases markedly, and a fixed flexion deformity and atrophy of the forearm muscles can be observed.
Fig. 27.S. Avascu lar necrosis of the lu nate bone. The X-ray im age clearly shows the smaller, sclerotic, deformed lunate bone with cystic lesions.
Radiological signs. In the early stages, there are no characteristic radiological alter ations. Later, the bony structure of the lunate changes, and it exhibits an increased density with cystic lesions . In the lateral view, there is a dip in the lunate (Fig. 27.5.). Treatment. Physiotherapy and immobili zation of the wrist (splint or brace) in the early stage. The administration of nonsteroidal anti-inflammatory drugs can relieve the pain considerably. If conservative treatment fails, surgery is indicated.
27.3.2. Cyst and pseudoarthrosis of the scaphoid bone Fracture of the carpal scaphoid bone, the most common fracture of the carpus, can re sult in nonunion in a considerable number of cases.
Fig. 27.6. Pseudo-articulation of the scaphoid bone. The ar row indicates the fracture. In the radiograph, the en largement of the false joint line is clearly visible. The bone has not yet deformed.
This fracture is often not diagnosed at the first examination. The precarious blood sup ply of the scaphoid is at risk and pseudo arthrosis may develop in the fracture line, fol lowed by necrosis of the proximal broken fragment (Fig. 27.6.). Cystic changes may oc cur in the fracture line or even without a frac ture.
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Clinical features. There is usually an old injury in the medical history which is often re vealed only when the patients are requested to recall a possible injury that they suffered in the past. The fovea radialis (fossa tabatiere) is swollen. Dorsiflexion and radial abduction of the wrist provoke pain. There is tenderness over the scaphoid bone. Radiological signs. If a scaphoid fracture is suspected, radiographs of the wrist are taken in four planes (scaphoid views) . Treatment. If nonunion has developed, surgical treatment is usually performed. Sev eral techniques are available, but their princi ples are the same : removal of the dead bone fragments; filling with cancellous bone grafts; and internal fixation (pin, screw, Ender 's plate etc.).
27.3.3. Osteoarthritis (OA) of the wrist and the hand Osteoarthritic changes a re more common in the hand than in the hip or knee joint. They are of great importance because they can compromise the function of the hand.
Etiology. A previous injury, an articular fracture or chronic exertion (activities of a typist or a decorator) may be found in medical history. It may also develop spontaneously in the elderly. Clinical features. There is gradually in creasing pain in the j oints of the hand, usually in the midline of the dorsal aspect of the wrist. The affected j oint becomes swollen and pain ful, and the strength and ability to grip obj ects diminish. The most commonly affected joints are the radiocarpal joint, the saddle j oint and the first metacarpophalangeal joint. Radiological findings. The usual osteo arthritic changes can be detected. In wrist osteoarthritis, the styloid of the radius be-
Fig. 27.7. Osteoarthritis of the saddle-joint. The joint su rfaces of the os trapezium and the first metacarpal that are facing each other are deformed, the bones are sclerotic. The first metacarpal subluxates towards the radial.
comes elongated. The radiocarpal joint space becomes thin first on the radial side. The proximal carpal bones flatten and deform, and degenerative bone cysts may appear. In osteoarthritis of the saddle joint, the base o fthe first metacarpal subluxates or may even dislocate. The radius of the thumb short ens (Fig. 27.7.). Osteoarthritis of the radiocarpal joint (wrist) is treated first conservatively, with im mobilization, pain control and physiotherapy. (Fig. 27.8.). In contrast with the earlier practice, ad ministration of topical steroids is to be avoided. The use of cortisone preparations can result in disintegration of the substance of the joint capsule, ligaments and tendons, lead ing to an impaired mechanical quality.
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(tendon sheath and bursa). Edema and soft tissue distension can lead to a deterioration of the circulation causing necrosis and/or loss of a part of the hand. �
Tendovaginitis crepitans
This is a non-pyogenic inflammation of the tendon sheath. Its mildest form occurs in the dorsum of the wrist due to overexertion of the hand (typist or pianist activities). Synovial effusion develops inside the tendon sheath and fibrin precipitation occurs there.
Clinical features. Pain and swelling in the dorsal aspect of the wrist. Crepitation (a snow- crunching-like sensation) may be expe rienced along the extensor tendons while the wrist is moving. There is tenderness on palpa tion over the swollen j oint. The grip strength of the hand diminishes considerably. Treatment. Immobilization of the wrist and the fingers for 2-3 weeks and administra tion of nonsteroidal anti-inflammatory drugs. Fig. 27.8. Osteoarthritis of the radiocarpal joint. The joint sur faces are thin, and the styloid process is pointed. The scaphoid bone displays pseudo-articu lation (secondary wrist osteoarthritis)
Immobilization can be achieved by the ap plication of plaster of Paris splints or wrist braces. Other types of braces can involve the saddle joint kept in opposition.
27.3.4. Inflammatory processes During work, the hand is exposed to a wide variety of physical effects. Besides overexertion, injuries varying in severity can occur. Injuries in the skin enable pathogenic mi crobes to penetrate the hand, causing various pyogenic infections. Septic conditions of the hand are dangerous because the infection can spread rapidly along the anatomic structures
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Stenosing tenosynovitis
This condition is characterized by stricture of the tendon sheath. Depending on which ten dons are affected, De Quervain's disease and trigger finger (or trigger thumb) are distin guished.
De Quervain ' s disease. Chronic inflam mation and stenosis occur in the common ten don sheath of the abductor pollicis longus and extensor pollicis brevis tendons at the level of the styloid process o fthe radius. The mobility of the thumb is reduced and the grip strength is greatly diminished due to pain (Fig. 27.9.). Clinical features. Besides the pain there is swelling and tenderness on palpation in the radial aspect of the wrist. The pain is severe on palpation in the styloid process. Finkelstein ' s test is usually positive : pas sively abducting the hand ulnarward provokes pain at the site of the tenderness. The inj ection of hydrocortisone results in only short-term pain relief, therefore this type of drug should
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be avoided. Surgical incision of the tendon sheath results in a definitive recovery. Trigger finger and thumb (digitus saltans -
pollex saltans). A nodule is observed on the tendon with relative stenosis of the tendon sheath. As the tendon glides through the sheath, a snapping movement can be seen and palpated usually accompanied by pain. I n more severe cases, there is not enough space for the nodule to glide through the constric tion. The patient is u nable to flex or extend the affected finger. The stenosis is located at the level of the metacarpophalangeal joint.
At the entry of the tendon sheath, there is a strong fibrous annulus, stabilizing the tendon on its base thus providing smooth gliding. Either the tendon sheath becomes thicker due to inflammation or the tendon develops a swelling (intratendinous ganglionic cyst or tu mor) . This can lead to relative stenosis there. The tendon moves through the stenosis only upon forced flexion or extension, accompa nied by a snapping (Fig. 27.1 0.). In adults,
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Fig. 27.9. The abductor pollicis longus tendon (1) and the extensor pollicis brevis tendon (3)in the first dorsal compartment. Close attention should be paid to the radial nerve and its sensory branches. The sur gery comprises the incision of the first dorsal tendon compartment (2).
trigger finger usually occurs on the long fin gers. Trigger thumb may be observed congen itally in children. If the constriction is severe, the thumb remains fixed in flex ion (congeni tal pollex flexus ). Treatment. Conservative treatment usu ally fails or provides only temporary results. Surgical treatments results in an immedi ate and definitive recovery, and thus attempt ing conservative methods for a longer period is meaningless. Surgery comprises longitudi nal incision of the constricted part of the ten don sheath.
27.3.5. Ganglion of the wrist and the hand Gangli onic cysts usually arise from struc tures lined with synovial membrane Uoints, bursae and tendon sheaths). They contain yel lowish synovial fluid. They have an outer fi brous capsule and an inner synovial mem brane. Fig. 27.10.
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Mechanism of digitus saltans: the thickening on the entry of the tendon sheath or on the tendon itself blocks the movement of the ten don. Passed this stenosis the tendon moves freely. 1. metacarpus, 2. flexor tendon, 3. thickening of tendon, 4 and tendon sheath
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Fig. 27.12.
Ganglion of the hand. The cystic lesions arise most frequently from the dorsal capsule of the scapholunate joint.
Dupuytren's contracture. A strong nodular thicken ing affects the palmar fascia above the IV. ray, which decreases significantly the range of movement in the MP and PIP joints.
Pathology. The cause of ganglionic cysts is unclear. They commonly develop on the dorsal (Fig. 27.1 1 .), or occasionally on the palmar surface of the wrist. Ganglionic cysts in the wrist area are usually attached to the capsule of the radiocarpal joint. While the cysts are growing, tissue around the cysts is lifted, i. e. tissue wraps around the cyst. In case they develop on the palmar surface, they may encompass the radial artery.
carpophalangeal j oint is fixed in a 90° flexion (Grade Ill), and then a proximal inter phalangeal flexion contracture occurs (Grade IV, Fig. 27.1 2.) and the patient is unable to move the finger. The other fingers are much more rarely involved. The sensory ability of the fingers is not af fected. Repeated trauma may be a cause but more than half of the patients have never been heavy physical workers .
27.3.6. Dupuytren ' s contracture
Pathology. The nodules initially consist of curly connective tissue bundles rich in cells and poor in fibers . These bundles may extend to the distal phalanges and start to shrink. At this stage mature connective tissue with an in creasing amount of collagen fibers can be de tected. The subcutaneous tissue between the cord and the skin gradually disappears and the thick palmar fascia is covered by only a very thin layer of skin.
This is a benign but aggressive superficial proliferative fibroplasia involving shrinking of the palmar or plantar fascia and resulting in contracture of the finger joints.
Clinical features. The lesion usually be gins with a small nodule (rarely several nod ules) situated in line with the ring or the little finger (Grade I). After a few months or even a year, these nodules develop into a cord (Grade II). In parallel with its thickening, extension of the affected finger becomes limited and a flexion contracture develops. Later the meta-
Treatment. In the early stages, the pa tients usually have no complaints and only ob servation is necessary. When the bundles start to form, surgery can be performed.
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27.3.7. Tumors and tumorous conditions i n the hand Any tumor that may arise in the locomo tion system and the dermal tissue may also oc cur in the hand, but each has its own charac teristic incidence. Malignant tumors are rare. Among the tumorous conditions, seba ceous cysts are often found beneath the skin of the palm or the fingers. These cysts grow slowly, lying just underneath the skin. They are bordered by a white and strong fibrotic capsule filled with a white mass consisting of liquefied dermal elements, sebum and corneous debris. Among benign tumors, benign synovioma, the giant cell tumor of the tendon sheets, is frequent. This tumor is usually
found in the fingers and grows slowly. The X-ray films reveal a lytic lesion with a sharp margin (like an impression) on the bones next to the tumor. When surgically exposed, a grayish- white lobular structure with yellow ish spots in some places can be seen. The tu mor can be easily dissected from the sur rounding tissue, but often involves as much as three-quarters of the circumference of the digit. After excision, recurrence often occurs. The most common benign tumor is the enchondroma, which is a tumor of cartilagi nous origin (See chapter 2 1 , Fig. 2 1 . 1 5 .). Malignant tumors in the hand are ex tremely rare. Among these, synovial sar coma and chondrosarcoma are relatively of ten observed.
28.
Arpad B e l lyei, J6zsef La katos, M i kl6s Sze n d r6i
Hip disorders
28. 1. Pediatric hip disorders 28. 1.1. Normal development of the hip joint �
Development of the acetabulum and pelvis The three bones that together form the acetabulum and the pelvis develop from three ossifying centers . The bony center of the iliac bone, which forms the upper part of the acetabulum appears in the third embryonic month, followed in the fourth month by the ossifying center of the sciatic bone, which forms the posterior part of the acetabulum, and in the sixth month by the ossifying center the of pubic bone, which forms the anterior part of the acetabulum. The ossifying centers rapidly develop, and at the time of birth these three bones are divided by the Y-shaped growth plate located in the depth of the acetabulum, ossification occurring at the end of development, between the ages of 1 4 and 1 6 years . The growth of the edge of the acetabulum is controlled by an extra ossifying center (os acetabuli) . The fully developed acetabulum is a 1 70- 1 75° segment of a sphere that contains loose fat and connective tissue in its base (pulvinar acetabuli). There is a hyaline cover only on that half-moon-shaped part, which is in contact with the femoral head. The fibrous - cartilagi nous rim on the edge of the acetabulum, the acetabular labrum, makes the cup deeper, so that it contains almost three-quarters of the femoral head. The femoral head is held in a central position in the acetabulum by the cap sule, the enforcing ligaments and the muscles bridging over the joint. The posterior bony part of the acetabulum (the sciatic bone) is
better developed and covers the femoral head better than the anterior part (the pubic bone; Fig. 28.1.). The anterior segment of the femo ral head is only partially covered; the further shell is provided by the active anterior acetabulum wall, the tense substance of iliopsoas muscle, which is of maj or clinical significance. Ossification of the proximal and middle parts of the femoral bone is organized by three centers : in the second embryonic month, a bony center appears in the middle of the diaphysis and progresses in both directions of the diaphysis. The epiphyseal bony center of
Fig. 28.1. Right hip frontal view: the bone cover is less anteri orly than posteriorly.
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the femoral head emerges i n the fourth-sixth month of extrauterine life, the ossifying center of the greater trochanter at the age of three years, and that of the lesser trochanter at the age of 8. The epiphysis later forms the j oint; it is covered by hyaline cartilage, while the apophysis serves as the origin and attachment for muscles. �
Progress of collodiaphyseal angle In adults, the angle between the femoral neck and stem is 1 25 - 1 3 5 ° . This angle varies from early embryonic life to puberty. In em bryonic, life the angle first decreases, then gradually increases, and its average value at birth is 1 40°. During the first year it increases to 1 48°, and it then gradually decreases to the adult level. If this angle exceeds the normal value for the given age, the condition is called a valgus deformity, if it is less, it is a varus de formity. Accordingly, mild physiological coxa valga is observed in early infancy rela tive to the adult situation. When the roof of the j oint is steep and dysplastic, and its covering
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pressure effect on the loaded femoral head is therefore insufficient, valgus hip develops. �
Development of antetorsion Under normal circumstances, the projec tion of the femoral head and neck and transcondylar axis in the horizontal plane has an anteriorly open angle; this is the angle of antetorsion (Fig. 28.2.). The origin of this an gle is the forward torsion of the proximal fem oral bone (the head looks forward and the greater trochanter slightly rearward). The av erage value of antetorsion in adults is 1 0- 1 4°. �
Blood supply of the proximal femoral bone The blood supply in extrauterine life must be considered in three phases : - Between the ages of 1 and 3 years, the blood supply of the proximal two-thirds of the femoral head, the epiphysis, is provided via the artery of the liga mentum teres capitis femoris from the arteria obturatoria (Fig. 28.3.). The growth plate is located distal to the epiphysis; it is an avascular area pre senting a vascular blockage between the epiphysis and the metaphysis.
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Fig. 28.2.
Right hip frontal view: the collodiaphyseal (a) and antetorsion (�) ang les; the line d rawn through the distal femur condyles represents the frontal plane.
Fig. 28.3. The ligamentum teres capitis femoris with the sup ply artery.
28. Hip disorders
- Between the ages of 3 and 1 4 years the proximal epiphysis of the femur is subject to relative ischemia, since the capacity of the arteria obturatoria is then greatly decreased. From this period, the blood is supplied to the proximal epi physis by the lateral epiphyseal artery related to the vessel plexus around the metaphysis (a. circumflexa femoris lateralis et medialis). This vessel runs around the growth plate laterally and posteriorly and then enters the j oint space, reaching the ossifying center of the epiphysis and providing the blood supply directly (Fig. 28.4.). This means that a short segment of the supply artery runs unprotected, in an extraosseal and intracapsular position and is exposed to injuries. In this period, any process under the tense hip joint capsule (syno vitis or edema) may occlude the supplying artery, causing necrosis (see Perthes ' disease). - Around the age of 14 years, the growth plate gradually ossifies, and the intra osseal arteries of the metaphysis
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gradually invade the distal part o f the epiphysis and take part in its blood supply. �
Nerve supply of the hip j oint About two-thirds of the hip j oint is sup plied with sensory fibers by the obturator nerve, which originates from segments L2-4 and runs in the medial edge of the psoas maj or muscle, reaching the medial aspect of the thigh through the lateral - upper aspect of the canalis obturatoria. It provides sensory branches to the hip joint, and then runs dis tally between the adductor muscles providing motor branches most of the adductor muscles and a sensory branch for the small skin area at the distal - medial aspect of the thigh and the knee. The essence of these features is, that in adults, but particularly in children, the pain re lated to hip disorders appears not so much in the hip area, but also in the distal thigh or in the knee.
28. 1.2. Congenital dislocation and dysplasia of the hip Synonyms of this condition are hip dysplasia, acetabulum hypoplasia, congenital dislocation of the hip, developmental disloca tion ofthe hip, and dislocation of the hip in in fants. Definition. This is congenital dysplasia of the acetabulum, which may lead to either intra- or extrauterine consecutive hip dislocation.
Fig. 28.4. The lateral epiphyseal artery runs round the growth plate and supplies the epiphysis.
Pathologic forms - The mildest form is hip dysplasia (acetabulum hypoplasia), when the femoral head is located centrally in the acetabulum, but the acetabulum is underdeveloped, and the acetabulum angle is steep (Fig 28.5.) . - Subluxation: In cases of maj or acetabulum hypoplasia, the femoral head may be displaced cranially. The cartilaginous elements of the aceta-
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Pathologic forms of hip d islocation: dysplasia, subluxation and luxation.
bulum and the femoral head are still partially coupled. - Luxation: The femoral head is displaced proximally and dorsally from the acetabulum. Incidence. Hip dysplasia is classified as a frequent developmental disorder; its inci dence in Hungary is estimated to be around 0 . 5 % . This includes both dysplastic and dislo cation cases which require treatment. Its incidence is dependent on the geo graphical regions and on the ethnicity. In Cen tral Europe the incidence is high, but in Negro sub race and in China the incidence is very low. In Japan however the incidence is very high. Hip dislocation is 6 times more frequent in girls than in boys . This entity was already described by Hip pocrates, however, the current nomenclature and approach are associated with the activity of Lorenz ( 1 895). He stated, that children are not born with hip dislocation, but only with a predisposition; the dislocation occurs only as a result of walking - loading, due to the under developed hip j oint. As early as 1 879, Roser explained that hip dislocation, or a predisposi tion to it, can be recognized in newborns, and added, that these children may heal, provided they wear special nappies right after birth, which ensure an abducted position. Hilgenreiner introduced the term hip dys-
plasia, denoting the maldevelopment of the entire hip joint. As proposed by the European Pediatric Orthopedic Society, the present terminology is: developmental dislocation of the hip (DDH) . Etiopathology. DDH is a multifactorial developmental abnormality. The term multi factorial means that both the inheritance fac tors (mainly a predisposition) and the envi ronmental factors acting collectively are re sponsible for the occurrence of luxation. The genetic, hereditary factors (predispo sitions) appear as acetabulum hypoplasia, which is the primary cause of this polygene inheritance. Hereditary factors may also be manifested as the dominantly inherited gen eral joint laxity. Both intra- and extrauterine environmen tal factors may contribute. Intrauterine causes include any compartmental disproportion (such as breech presentation, other position ing disorders, or tight intrauterine situations), and transitional joint laxity is particularly im portant. The essence of this is that in the sec ond and third trimesters of pregnancy, the lev els of estrogen and progesterone increase in both the mother' s and the embryo ' s blood, since their circulation is common. It is well accepted that both estrogen and progesterone cause j oint laxity. The transitional joint laxity endorses the expansion of the vaginal mus cles, and increases the flexibility of the joints of the embryo. The newborn ' s hormone level gradually decreases, and normalizes by the 3 -4th week. Hence, the newborn is in a bor derline state for 3 weeks regarding joint sta bility, when the femoral head may separate from the joint (unstable hip). The two most important extrauterine factors are the inappro priate use of nappies fitting tightly on the lower limbs, and the erect position, i.e. the at tainment of walking itself. From the moment of birth, the newborn assumes the so called re laxed - sleeping or sprawled posture, which is characterized by almost 90° offlexion and ab duction of the hip joint (Fig. 28.6.). In a sprawled position, the femoral head is sunk
28. H i p d isorders
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Fig. 28.6. Relaxed - sleeping posture of the newborn: almost 90° flex ion, abduction and external rotation.
deeply in the acetabulum, enhancing the nor mal development of the acetabular roof, even in dysplastic-hypoplastic cases. The treatment follows the same path. Many clinical findings relate to environmental factors, e.g. 1 6% of babies with hip dislocation exhibit breech pre sentation. Etiologic forms of hip dislocation. 1 . Hip dysplasia or consequential dislocation on the basis of acetabular hypoplasia (polygenic form) can be well managed with conservative treatment; the disloca tion can be easily reduced. 2 Dislocation is already present at the mo ment of birth as a feature of general, inher ited connective tissue laxity (dominant form). Besides the luxation, other signs of general, inherited connective tissue laxity are also detected (knee hyperextension and lax wrist). It reacts well to conserva tive treatment; the dislocation is easily re duced.
Symptomatic hip dislocation is a symptom of identified monogenic (dominant or re cessive) hereditary abnormality (e.g. Ehler-Danlos syndrome, Marfan 's syn drome, Morquio 's syndrome, congenital multiplex arthrogryposis, etc.). It reacts less to conservative treatment, though this may be attempted. It usually requires sur gical intervention. 4 Secondary hip luxation is due to primary neurological or muscular disorders. The dislocation is not present at birth, it ap pears only during childhood (e.g. infantile cerebral palsy, poliomyelitis, etc.). It barely reacts to conservative treatment, and usually requires surgical intervention. 5 Teratological hip luxation is induced by a teratogenic factor in the first third of intrauterine life, it is not inherited. It is of ten seen as a part of the multiple develop mental abnormality of the limb. The series of developmental abnormalities is local ized only to the involved limb, in contrast with symptomatic hip dislocation, where it is part of a general developmental abnor mality involving the entire body. It does not react to conservative treatment, and the outcome of surgical intervention is also generally poor. �
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Pathology of dislocated hip j oint Bony elements - Acetabulum hypoplasia - primary path ologic factor. - Increased antetorsion of the proximal femur (this is a consequence of loosening of the active anterior acetabular wall (iliopsoas muscle). - Coxa valga (this is a consequence of the missing pressure of the body weight transferred to the head and neck by the acetabulum) .
Soft-tissue components The soft tissue at the bottom of the acetabulum proliferates, the limb is inverted, the iliopsoas and adductor muscles are tense, and the gluteus medius and minimus muscles are insufficient.
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Clinical symptoms. The clinical symp toms are classified as follows : � �
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Signs arousing suspicion Signs indicating probability Hip instability Definite signs Late signs X- ray and u ltrasonographic signs (imaging signs)
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Signs arousing suspicion Signs arousing suspicion feature among the history data obtained from the parents : the occurrence of hip dislocation or dysplasia, a pathological pregnancy, an abnormal delivery or the intrauterine posture (breech presenta tion) and other data relating to the behavior of the newborn: an asymmetric movement of a lower limb, or any other factors worth men tioning. �
maius. When the baby is prone, the gluteal folds are also asymmetric and positioned proximally on the involved side (Fig. 28.7.). - Adduction contracture. The hip ab duction of newborns is between 70° and 90° and symmetrical. An abduction of less than 70° bilaterally or asymmetrical abduction is considered a sign indicating probability. - An increased greater trochanter mass. In cases of hip luxation or subluxation, the greater trochanter is displaced proximally and laterally, and on palpation it is felt to be an enlarged mass (Fig. 28.8.). - External rotation of the limb. In hip dysplasia and even more in luxation, the limb is externally rotated. This has no specific diagnostic value, but it may be Impressive.
Signs indicating probability - Fold asymmetry. This is considered only if it is consequently present together with other signs indicating probability. The fold asymmetry is presumed to be consequent when the thigh folds are deeper and proximal, and perhaps more numerous . In girls, the most proximal fold may partially conceal the labium
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Fig. 28.7. In cases of hip dysplasia and luxation the thigh and gluteal folds are asymmetric. I n the involved side, there are more and deeper folds.
Fig. 28.8. The baby is assessed with bent hips and knees. The thigh is shorter on the luxated side, while the greater trochanter is displaced proximally and later ally, and on palpation it gives the feeling of an in creased mass, in the middle of the buttock, there is a fold.
28. Hip d isorders
- Limb shortening (Bettmann 's sign). Limb shortening is associated with hip dislocation, since the femoral head is displaced from the acetabulum proximally, resulting in limb shortening (Fig. 28.8.). - Axial deviation. In Lorenz 's abduction, the femoral axis points above the acetabulum instead of its center. - Atrophy, and flattening of the gluteal muscles. With the hip flexed to 90° the buttocks are asymmetrical and on one side, a dent is visible in the middle of the buttock (Fig. 28.8.). •
Hip instability (Barlow' s sign) The essence of this sign is that the hip is not displaced, but it is dislocatable, luxatable from the acetabulum. The sign is caused by two factors : acetabulum hypoplasia and tran sitional hormonal laxity. Consequently, it is a false-positive sign in 90% of the cases in the first 3 weeks. The mode of assessment is the following: The hips of the supine baby are flexed to 90° with knees fully flexed. The hips are t4en mildly adducted and mild pressure is exerted backward with the examiner' s thumb. In positive cases, a click is palpable in the hip, when the femoral head leaves the acetabulum
Fig. 28.9. Hip instability (Barlow's sign). The pressure of the examiner's thumb dislocates the hip.
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(positive Barlow 's sign, Fig. 28.9.) . A s soon as the force is released, the head slips back into the acetabulum. •
Definite signs (Ortolani 's sign). This is the only definite sign of hip dislo cation; it can also be evaluated as a reduction sign. The assessment is performed as follows : The hips of the supine baby are flexed to 90° and abducted. During abduction a click is ex perienced, signaling that the femoral head is reduced (Fig. 28.1 0.). In cases involving hips that undergo reduction with difficulty, this maneuver is to be supplemented with axial traction of the femur to facilitate reduction (Lorenz 's reposition). •
Late signs Late signs are detected after the child has started to walk. Fortunately these are seen very rarely nowadays. - The Trendelenburg sign. This is de tected in all other disorders besides hip dislocation, where a gluteus medius and mlll1mus muscle insufficiency 1S present. The standing patient is requested to stand on only one leg, and to lift the other leg up while bending the hip and the knee. In normal individuals,
Fig. 28.10. Reposition sign (Ortolani's sign): during a bd uction, a click is felt and the femoral head is reduced
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28. Hip d isorders
walking, and also during assessment in a prone position. - Increased lumbar lordosis. Mainly in high bilateral dislocations, the lack of proper hip support results in an increase in the pelvic slope, and this is com pensated by increased lumbar lordosis.
the gluteal muscles o n the supporting side (hip abductors) hold the un supported side of the pelvis in a horizontal plane. In case of an in sufficiency of the gluteal muscles, the pelvis on the unsupported side sinks below the horizontal plane and the patient tilts with the trunk toward the supported side, because this is the only way he/she is able to maintain balance (Fig. 28. 1 1 .). In unilateral cases, the trunk tilts toward the supported side with every step during walking, in bilateral cases, the trunk tilts in both directions (duck gait). - Telescope sign. In cases of total dis location, the protruding trochanter (and the femoral head) moves proximally and distally in the axis of the femur during
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Fig. 28.12. Fig. 28. 11. Left side positive Trendelenburg sign; the unsup ported, right side of the pelvis sinks u nder the hori zontal plane
Ultrasonographic assessment of the hip. The draw ing: the angle alpha is not less than 60° and beta is not larger than 55° for in normal hips. The image shows a phase I Il.a dysplastic hip: a: bony acetabular roof; b: cartilage acetabular roof, c: baseline.
28. Hip disorders •
U1trasonographic and X-ray signs (imaging signs) Ultrasonographic signs. Under the age of 4 months X-ray examinations are not per formed on the hips, because the ossifying cen ter is undetectable. Instead of the harmful X-ray radiation, a modem and harmless ultra sonographic assessment is carried out. This reveals dysplasia at an early stage and the de velopment of the hip joint is easily followed up (Fig. 28.1 2.). The examination may be re peated at any time. Ultrasonography is recom mended in case of any existing clinical sign, or when risk factors are recorded (familial oc currence, or breech presentation) . This noninvasive scan helps in the evaluation of the bony and cartilaginous elements of the acetabulum as primary factors. X-ray signs. Hip X-rays may be per formed above the age of 4 months with the following indications : - when ultrasonography and physical assessment lead to a questionable conclusion, - in suspected dysplasia or luxation, - in cases of familial occurrence.
The presence of the ossifying center of the femoral head contributes a great deal to the evaluation of the X-ray film. Before its mani festation, various ancillary lines facilitate ori entation.
Fig. 28.13. 4-month-old baby. Hip X-ray: the acetabular roof is steep on the left side (dysplasia).
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- Acetabular roof angle (Hilgenreiner 's angle) : this is normally symmetrical and less than 3 0°, in cases of dysplasia the value increases (Fig. 28.13.). Assess ment of the acetabular roof angle : a horizontal line is drawn through the identical points of the Y -shaped car tilage, representing the horizontal plane, and the angle is measured between this and the line following the acetabular roof. - Kopits 's rectangle. This is outlined by the lines drawn between the two end-points of the acetabular roof and the two end-points of the femoral neck metaphysis. In normal cases, this is a regular square, and, if the ossifying cen ter is already apparent, it is positioned in the central area (Fig. 28.14.). In cases of dysplasia or luxation, the square is irregular, and the ossifying center is excentric and lateralized. - Menard-Shanton 's line. The cranial arch of the foramen obturatorium is normally the continuation of the lower arch of the femoral neck. In cases of subluxation or dislocation, this arch is interrupted, and the lower arch of the femoral neck is moved proximally (Fig. 28.14) . - Ombredanne 's line. This is a per pendicular line drawn from the lateral edge of the acetabulum distally to the horizontal line connecting the Y -line,
Fig. 28. 14. Kopits's quadrangle (K), Menard-Shanton's line (MS)
and Ombredanne's line (0).
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described above. These two lines divide the hip joint into 4 segments. If the hip is normal, the ossitying center is located in the inner-lower quadrant; in cases of subluxation or dislocation it is located laterally (Fig. 28. 1 4.). - Hilgenreiner 's H-distance. This is the distance between the medial spine of the femoral neck and the sciatic bone, which is normally parallel with the Y-line and it is at most 5 mm. Before the age of 6 months, a larger distance may mean lateralization of the femoral head (Fig. 28.1 5.). Prevention of hip dislocation . The es sence of prevention is to ensure the relaxed resting position for the newborn following birth (Fig. 28.6.). It is not coincidental that hip dislocation is rare in Far-Eastern countries and in Africa, where children are carried on their mother' s back with their legs spread. In contrast, in countries, where babies are wrapped in nappies or swaddled with tightly adducted lower limbs (Eskimos, Canadian In dian tribes, in some places in Ecuador and in Central and Eastern Europe), dislocation is very widespread.
Prevention and recognition are closely re lated. Accordingly, three compulsory infant screenings are performed in Hungary: The first is carried out 3 -4 days after birth, usually in neonatal wards, and is easy to organize. The next is due at the age of 3 -4 weeks, and the third at the age of 3 -4 months. The hips must be checked on all occasions when the child is due to participate at other regular pediatric check-ups or inoculation. Conservative treatment. The methods of conservative treatment depend on the time and severity of the diagnosis. When dysplasia is noticed at the first or second screening, merely exercises and
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Fig. 28.16.
Fig. 28.15. Various ancillary lines and ang les for evaluating hip dysplasia or dislocation on the X- ray film. (Y: Y- line; vsz: acetabular roof angle; d l,d2: socket metaphysis d istance; h: Y-line - metaphysis dis tance). On the left, the situation is normal; on the right, dislocation is seen. Vsz and d values are larger, and distance h is lower
a: Right side: normal; left hip: acetabulum hypoplasia is seen in an extended position. The femoral head is pressed against the acetabular roof; no improve ment is expected. b: I n the abducted - flexed position, the femoral head is pressed centrally into the socket, ind ucing normalization of the acetabulum. c: Recovered state.
2 8 . H i p d i s o r d e rs
spreading nappies are recommended (Fig. 28. 1 6. a, c). The method advocated for spreading nappies is the use of "Rugi pants" (Fig. 28.1 7.), which ensures continuous ab duction with the elastic spongious lining. In cases of dysplasia recognized at the third screening and confirmed by ultrasonography or X-ray examination, the application of Pavlik ' s harness is advised (Fig. 28.1 8.). Pavlik 's harness is a functional treatment mo dality popular worldwide. The essence of this functional treatment is that it limits only the extension of the hip; all the other movements can be freely performed. Flexion and abduc tion centralize the femoral head and enhance the development of the acetabular roof. The use of Pavlik 's harness is possible only until the infant sits up (at the age of 6-8 months), since the main effect is eliminated in a sitting position. Instability. As described in the above, at the time of the first screening, instability is a
Fig. 28.17. Sprawling abduction nappies.
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Fig. 28.18. Pavlik's harness. 90° of flexion is secu red in the hip
joint
pseudo-positive symptom induced by transi tional hormonal laxity. At the next screening, it may be decided whether real dysplasia is present: if the instability has ceased, the hip is classified as normal. If the instability persists, severe acetabulum hypoplasia is in the back ground and Pavlik 's harness should be con sidered. The severity of the acetabulum hypo plasia may be defined by an ultrasonographic scan. In cases of instability persisting up to the age of 4 months, Pavlik' s harness is also indi cated. Ortolani 's positive hip (luxation) . If this is detected at the first screening, abduction exer cises and spreading treatment are advised for a short period, knowing that Pavlik 's harness is needed (Fig. 28.1 8.). Pavlik 's harness is not to be applied before the I O- 1 4th day after birth, since it may harm the newborn and the skin adaptation is still underway. Pavlik' s har ness can be used on an outpatient basis. In the maj ority of cases (95%), it results in total re covery. Below the age of 6 months, other modes of conservative treatment may be attempted if Pavlik 's harness fails (5%). One ofthese is the "overhead extension" (Fig. 28.1 9.). In cases
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a ------
Fig. 28.20. Abd uction splint.
Conservative treatment is recommended until the age of 6 months. Above this age, sur gical intervention is advised.
Fig. 28.19. Overhead extension, first vertically (a), and later in the a bd ucted position (b).
of irreducible or barely reducible hip disloca tions, distal traction is applied via cords at tached to the legs by adhesive tapes, which may loosen the hip joints. With gradually in creased abduction, spontaneous reduction may occur. In cases of instability, when the femoral head leaves the acetabulum at 1 0-20° of adduction, a more rigid fixation device, the abduction splint (von Rosen ' s splint) is tem porarily applied (Fig. 28.20.).
Surgical management. In surgical reduc tion, following exposure of the hip joint cap sule, the soft tissue that fills the joint is re moved, together with the inverted limbus. The iliopsoas muscle is separated from the lesser trochanter, and fixed to the capsule at the an terior part of the femoral neck. After removal of the obsolete parts of the capsule, reduction of the femoral head is easily achieved and, by narrowing the capsule, the reduced femoral head can be stabilized. Postoperatively, the hip must be functionally immobilized in the abduction - flexion position with a splint or in Pavlik 's harness. After the age of 2 years, besides the cor rection of soft-tissue components by the open reduction procedure described above, the bony components must also be corrected. In cases of mild acetabular hypoplasia, the cor rection of the proximal femur can be satisfac-
28. Hip disorders
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Fig. 28.21. A 2-year-old girl with a developmental dislocation of the left hip. Open reduction, varus and derotation osteotomy. The steep acetabular roof is normalized, and the head is central. Normal hip at the ages of 6, 8 and 31 years.
tory: varus and derotation osteotomy ensures the development of the acetabular roof after the centralization of the femoral head (Fig. 28.2 1 . a, b) .
Correction of the acetabulum can be sub divided into complete and incomplete pelvic osteotomies (pericapsular pelvic osteotomy and acetabuloplasty).
Fig. 28.22. Pelvic osteotomies for correction of the steep acetabulum: 1: Salter's pelvic osteotomy, 2: Pemberton's in complete pericapsular pelvic osteotomy, 3: Chiari's pelvic osteotomy, 4: triple osteotomy.
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The most widespread and popular tech niques are as follows : - Chiari 's pelvic osteotomy is a complete pelvic osteotomy over the acetabulum, the distal part being displaced medially (Fig. 28.22.). The center of rotation of this motion is the symphysis. The disadvantage is that the femoral head is covered by fibrous cartilage instead of hyaline. It is nowadays used only in exceptional cases, when no 'other procedures are reasonable. - Salter 's pelvic osteotomy is also a complete pelvic osteotomy over the acetabulum, but the distal part is displaced laterally, providing a hyaline cartilage cover for the femoral head (Fig. 28.22.). The center of rotation of this motion is again the symphysis. The correction effect is limited, depending on the mobility of the symphysis, and it can therefore be used under the age of 6. - Pemberton 's incomplete pelvic oste otomy, acetabuloplasty, is a rounded and arched pelvic osteotomy starting above the upper edge of the acetabulum and extending to the Y -shaped cartilage in the depth of the acetabulum (Fig. 28.22.). The steep acetabulum is folded
down over the femoral head, and the correction achieved is ensured by a bone wedge inserted into the gap. The center of rotation of this motion is the Y -shaped cartilage. It may be ideal until the closure of Y -shaped cartilage. The surgical intervention on the hip joint which corrects the bony and soft tissue ele ments in a single session is called one-stage osteotomy (Fig. 28.23.). The outcome is ex cellent if it is done in time and with good tech nical conditions. Later, the child may take part in sports activities and gymnastic exercises.
28. 1.3. Osteochondritis capitis femoris juvenilis (Perthes' disease, Legg-Calve-Perthes' disease) This is necrosis of the proximal femur epiphy sis in childhood, leading to a deformity of the femoral head.
Incidence. It occurs between the ages. of 3 and 1 3 years; it is the second most common hip illness with an incidence of between 0, 1 - 1 %. It is 3 times more common in boys
Fig. 28.23. A 5-year-old girl with subluxation; one-stage osteotomy which corrects the bony and soft tissue elements in a single session.
28. Hip disorders
than in girls. It is usually unilateral, but in 1 5%, it is a bilateral condition. Etiology. The definite cause of the disease is unknown, there is however both direct and indirect evidence pointing to a disturbance of the blood supply of the femur proximal epiph ysis. The condition is unquestionably related to occlusion of the lateral epiphyseal artery, which supplies the epiphysis and it is apt to occlude in response to a pressure increase in the hip joint, on the short and vulnerable seg ment of the artery, where it runs on its intra-articular and extra-osseal path. It has been proven, that in 5% of the cases, this con dition is preceded by transitory hip arthritis. It occurs in the temperate zone, in both the northern and southern hemisphere. It is not observed in cold and hot zones where the cli mate is usually more balanced. The influenza common in spring and autumn may be the etiologic factor. It is also characteristic, that the incidence of this condition in childhood corresponds to that of transitoric coxitis. Pathology. In consequence of primary or reactive intra-articular irritation, the synovial membrane swells and becomes hyperemic. In the early stages, the histology of the epiphysis ossifying center reveals an enchondral ossifi cation disturbance besides necrosis. The osteocytes expire and the necrotic foci are gradually surrounded by scar tissue, while os teoclasts form from monocytic elements . The necrotic bone substance is gradually degraded and the osteoblasts produce new bone (keep ing substitution). In the regenerative stage, the bone production is increased. In the stage in which the necrotic areas undergo degradation, the bone is not sufficiently solid enough, and the granulation tissue gradually occupying the necrotic bone does not have appropriate me chanical rigidity, and is therefore not suitable for weight-bearing. Accordingly, the femoral head becomes flattened and mush room-shaped, and may protrude laterally. History. A typical feature is an intermit tent, strange gait or limp lasting for weeks or
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months. I n a number of cases however, the child has no complaints. In early stages, the strange gait or limp temporarily ceases after resting. The child locates the pain in the thigh or in the knee instead of the hip (due to the obturator nerve). As a general rule therefore, in case of knee pain in childhood, the hip must be thoroughly assessed. Occasionally, the child presents acute hip pain, and is unable to bear weight on the involved limb. In these cases, primary or secondary synovitis pre dominates. Clinical symptoms. The first obj ective sign is a decrease in the internal rotation of the involved hip compared to the contralateral side. In advanced cases, the limitation of the internal rotation becomes more severe, and an external rotation contracture may develop to gether with the limited extension. This is a se lective limitation of movement, since the pro cess always involves only one plane of the three axial planes of movement of the hip j oint. The child limps protectively; atrophy of the thigh muscles is also observed. In ne glected cases, the flattening of the femoral head and the shortening of the metaphysis cause moderate limb shortening. Imaging diagnostics. When Perthes ' dis ease is suspected, bilateral anteroposterior and Lauenstein X-ray films are to be taken. Lauenstein ' s position is the flexed, abducted and externally rotated hip. On the basis of X-ray picture, 4 stages are defined: Early stage. The early X-ray image does not show bony changes; medially, the j oint space is wider than on the other side. The cause is the synovitis and edema of the pulvinar acetabuli. 2 Sclerotic stage. The structure of the bony center of the proximal epiphysis is cloudy, and the density is increased; it becomes sclerotic, which is the radiological sign of necrosis (Fig. 28.24.). The bone center is moderately flattened. 3 Fragmentation stage. The previously ho mogenous bone center is even more flat-
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Fig. 28.26. Perthes' disease: epiphysis flattened and widened.
Fig. 28.24. Perthes' disease: sclerotic stage.
Fig. 28.27. Perthes' disease: end stage.
Fig. 28.25. Perthes' disease: fragmentation stage.
tened and fragmented (Fig. 28.25.). Radiolucent areas appear in the bone cen ter as the granulation tissue disintegrates the necrotic bone. The entire epiphysis may flatten, it widens and protrudes later ally, and the widening of metaphysis in creases (Fig. 28.26.). 4 Final stage. The femoral head is flattened to some extent, and its height is less than the contralateral height. The structure of the newly built bone center is normalized. In untreated or severe cases an enlarged,
Fig. 28.28. Bone scan: no perfusion of the involved epiphysis
flat, protruding femoral head is formed (coxa magna, Fig. 28.27.). In cases of clinical suspicion, when the X-ray finding is negative, a bone scan may confirm the diagnosis, showing no or only limited perfusion of the involved epiphysis (Fig. 28.28.).
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Laboratory tests are negative. Treatment. The course of Perthes ' dis ease lasts 3-5 years; the treatment is influ enced to a large extent by the known risk fac tors listed below.
I . Catterall 's stages (Fig. 28.29.) . � �
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Stage I: 25% of the epiphysis is involved. Stage 11: 50% of the epiphysis is involved. Stage I l l : 75% of the epiphysis is involved. IV. stage: The entire epiphysis is necrotized.
The more extensive the necrosis, the worse the prognosis. 2. Lateral pillar sign. Even if the necrosis is extensive, in cases when the small lateral segment of the epiphysis remains un harmed and its structure is intact, the prog nosis is expected to be good (Fig. 28.30.).
Fig. 28.30. The small lateral pillar of the epiphysis remains un harmed and its structure is intact.
1
3
Fig. 28.29. CatteraWs stages of Perthes's disease according to the extent of the affliction.
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3 . The age. This is the most important factor regarding therapy. Comparative clinical studies of treated and untreated cases have proved that below the age of 6 years, a good outcome is to be expected, almost re gardless of the method applied. This is probably due to the good regenerative ca pability of the young organism. After the age of9- l 0, the outcome is poor in the ma j ority of cases, regardless of the therapy. 4 . Metaphyseal involvement. If the process involves the metaphysis, the prognosis is poor (Fig. 28.3 1 .). The current treatment strategy relates to two major points: B elow the age of 6 years, the outcome is expected to be favorable even without treatment. Hence active therapy should only be considered in cases of Catterall 's stage IV of complete necrosis. After the age of 1 0 years, the result is poor with or without treatment. Above this age, therefore, only those interventions are indicated that ensure centralization of the femoral head proven by functional X-ray examination; otherwise only observation and palliative treatment should be provided. The centralizing ( containment) treatment has become predominant in both conservative and surgical methodology. Methods of centralizing treatment Conservative techniques. The basis of the treatment is that abduction and internal ro tation of the hip ensure the central location of the femoral head in the acetabulum. This posi tion decreases the load by distributing it evenly on the surface of the biologically softer femoral head and enhances its new modelation to the shape of the acetabulum (re ciprocal remodelation) . To achieve this obj ective (in either uni-, or bilateral cases), various calipers have been de vised to ensure abduction and internal rotation (Fig. 28.32.). Walking in these calipers and their utilization for 3 - 5 years involves a sub stantial restriction of activity for the child. An alternative approach is the use of crutches or bed rest, but in view of the 3-5
Fig. 28.31. Metaphysea l necrosis.
Fig. 28.32. Calipers used in Perthes' disease to ensure abduc tion and interna l rotation.
28. Hip d isorders
years progress, this appears impracticable and maybe even impossible to implement. Operative therapy. Varus derotation osteotomy of the proximal femur. This method is popular in Hungary and in all of Eu rope, since 8 weeks after the surgically achieved centralization and following the healing of the osteotomy full, weight-bearing and activity may commence. The osteotomy close to the pathology increases the decompo sition and rebuilding of the necrotized femo ral head and virtually halves the usual 3-5 -year period of progression (Fig. 28.33.). �
Pelvic osteotomies A full cover of the femoral head and a de crease of the load on the surface can also be achieved by pelvic osteotomy, which is an other mode of centralization. Mainly Salter ' s osteotomy has become widespread. I t has a biomechanical disadvantage since it increases the pressure on the femoral head. Further more, the author recommends that it is to be
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performed before the age of6. After the age o f 1 0, Chiari ' s complete pelvic osteotomy may be performed mainly as a palliative interven tion (especially when a large lateral femoral head protrusion is detected, Fig. 28.22.). Perthes ' disease is one of the causes of hip osteoarthritis in adults . Therefore, after the healing of Perthes ' disease, school gymnastic exercises and sports are advised as follows : 1 . Cases that have healed without deformity: all activities are allowed. 2. A slightly flattened, but round, central femoral head (physiologic incongruence) : all activities (including sports) are al lowed. 3. A considerably flattened, laterally pro truding deformed femoral head (coxa magna) : moderate gymnastic exercises, swimming and cycling are allowed.
28. 1.4. Slipped capital femoral epiphysis (SCFE, epiphyseolysis capitis femoris juvenilis, coxa vara adolescent) The origin of this entity is the slipping of the capital femoral epiphysis backward and medi ally on the femoral neck. The process is often bilateral.
Fig. 28.33. Perthes's disease on the right side, following varus derotation osteotomy: full recovery. The head is round.
The types: - Epiphyseolysis lenta: This is a gradual slipping, with intermittent knee, thigh and hip pain; the limb is in a position similar to that when the neck of the femur is fractured: mild shortening and external rotation are seen with a restricted range of internal rotation. - Acute epiphyseolysis: The slip happens suddenly, following a fall or a faulty movement. It is accompanied by acute hip and knee pain. The limb is in a position similar to that when the neck of the femur is fractured. The limb is shortened and externally rotated, with a severely restricted range of motion.
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I ncidence. This is the third most common hip condition after hip dysplasia and Perthes ' disease. I t occurs i n the age interval 1 0- 1 5 years. It i s twice as common in boys, as in girls. It is often bilateral, and therefore close observation of the other hip is crucial. The lenta form of epiphyseolysis predominates (95%) . Etiopathology. It is currently believed that the background of this condition involves the development of a latent hormonal dys function between the growth hormones (that control the ossification) and the sex hormones in puberty. In response to the effects of the growth hormones, the proliferation of carti laginous elements in the growth plates in creases, and the growth plates widen. At the
Fig. 28.34. Shearing forces acting on the growth plate (ny), since the load (R) is not perpendicular to the growth plate.
end of growth, the secretion of the growth hormone gradually diminishes. The sex hor mones lessen the proliferation of the cartilagi nous elements, and the growth plates become thinner and ultimately disappear. The diverse secretion activity undergoes a crossover in puberty. If the secretion of sex hormones starts later, the growth plates persist and can not resist the biomechanical load pro duced by the considerable body weight and height gain in puberty, and may be displaced. This is common in the hip joint, because this is the only epiphysis in the body that is not perpendicular to the axis of the body weight, but is inclined obliquely and medially. It is therefore subj ected not only to pressing forces, but also to substantial shearing forces (Fig. 28.34.).
Fig. 28.35. Dystrophia adiposogenital constitution of a 14-year-old boy with right-sided epiphyseolysis.
28. H i p d i s o r d e rs
The condition is common in two constitu tions. One exhibits all the features of hypo gonadism: fat, a lack of secondary sexual signs, an a eunuchoid constitution (relative hypogonadism; Fig. 28.35.). The other type is a tall, thin constitution with long powerful arms (relative growth hormone overproduc tion). History. In cases of epiphyseolysis lenta, the child presents chronic complaints. Usually knee and thigh pain, but occasionally hip pain and fatigue are mentioned and the child avoids physical activity. The gait is peculiar, and an occasional limp is observed. In acute cases a stabbing hip, thigh or knee pain occurs following a fall or faulty move ment and the child is unable or hardly able to stand. Clinical symptoms. Walking with a slight limp is usually detected with an externally ro tated lower limb. One of the constitutions de scribed above is observed (eunuchoid relative hypogonadism, or a tall, thin constitution) . When the hip is assessed in a supine posi tion, the internal rotation is observed to be re stricted, and in most of the cases an external rotation contracture is present. The abduction and extension may also lessen, especially in major slips. Drehmann ' s sign is distinctive: on passive flexing of the hip, constrained ab duction and external rotation occur. This sign is a consequence of the dorsal and medial dis placement of the femoral head. Another com mon feature is the crossing sign: the child is asked to kneel, and the legs will cross each other. In acute cases, besides the intense pain the symptoms are similar to those detected when the neck of the femur is fractured: the limb is shortened and externalIy rotated, and any at tempted movement elicits severe pain. X-ray signs. Similarly as in other hip con ditions, bilateral anteroposterior and Lauenstein films are to be taken. On the Lauenstein views, slippage of the epiphysis is noticeable earlier, since the backward slip is
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then detected on this view and this is always larger than the medial displacement. In the anteroposterior views, the very early signs (preceding the significant slipping) is the wid ening and unevenness of the growth plate (Fig. 28.36.) . A moderate slip is indicated if the decrease in height of the bony center of the epiphysis is mild, compared to the other side. Another valuable sign is that when the lateral contour of the femoral neck is extended, nor mally, this line cuts few mm-s off the edge of the epiphysis (Fig. 28-36.). If the line is pe ripheral to the epiphysis, this may be a radio logical evidence of a mild slip. If a line drawn along the lower contour of the femoral neck on a Lauenstein film is prox imalIy elongated, and this line marks off a small segment from the posterior edge of the epiphysis, this is evidence of a mild slip (Fig. 28.37.). The extent of the slip can be defined by an exact angle on the Lauenstein films : the angle between the axis of the femoral neck, and the line drawn through the edges of the epiphysis. Normally, its value is 90° (Fig. 28.37., and 28.38.). Treatment. Both forms of epiphyseolysis require surgical treatment. Until the operation is performed, immediate bed rest is ordered so as to prevent progression, but a further slip may still occur.
Fig. 28.36. A 12-year-old boy with left sided chronic epiphyseolysis: anteroposterior. X-ray.
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Fig. 28.37. Same boy: Lauenstein X-ray.
Fig. 28.39. Epiphyseolysis with moderate slip: " in situ " epiphyseodesis with 2 spongiosa screws.
a b
In cases involving a slip of less than 30° in epiphyseolysis lenta, surgical fixation in situ is indicated, ifthis is technically possible. One or more K-wires, cancellous screws or cannulated screws (Fig. 28.39.) are intro duced through the neck into the epiphysis. Because of the stabilization of the epiphy sis, the pain and the contractures rapidly sub side postoperatively. The child may get out of bed on crutches the day after the operation, or in the event of pain, a few days later, and al lowed to bear weight and go to school after 3 weeks. When the slip is more than 3 0°, wedge osteotomy of the neck after Dunn can be car ried out, and the reduction is supplemented with corrective shortening of the femoral neck. In cases of acute si ip, gentle open or closed reduction and fixation is indicated in the first week. The attempt at reduction however, may result in a blood supply deficit and necrosis of the head.
28. 1.S. Coxa vara infantum (congenital) Fig. 28.38. A 14-year-old girl with acute epiphyseolysis. antero posterior (a) and Lauenstein radiographs: total slip (b).
This is a congenital ossifying malfunction of the femoral neck: the collodiaphyseal angl
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e gradually decreases and causes limb short ening. The condition is al ready present at birth, but is usually recognized at the age of 3-4 years. It involves both genders and is usu ally bilateral. It is a rare congenital condition.
Etiopathology. The etiopathology is un known. It is not inherited. The pathological process is progressive; the collodiaphyseal angle gradually decreases during childhood, often to under 90°. The growth plate becomes almost vertical, and may even create a state corresponding to acute epiphyseolysis be cause ofbiomechanical factors, since the ver tical growth plate is subj ected almost exclu sively to shearing forces. The limb is gradu ally shortened, and the maj or trochanter moves cranially. The origin and attachment of the gluteus medius and minimus muscles come closer to each other, and they become insufficient, Trendelenburg ' s gait develops. Clinical symptoms. The condition may already be discovered in infants by a skilled orthopedist, or at least the suspicion arises. Fold asymmetry and limited abduction are typical. The child is usually referred to a spe cialist at about 3 -4 years of age, with a pain less peculiar gait and limp. A higher and thicker trochanter mass, limb shortening and Trendelenburg ' s gait are observed. The hip abduction is slightly restricted. X-ray signs. Before the appearance of the ossifying center of the femoral head epiphy sis, early films merely indicate the irregularity of the proximal metaphysis. Later, the de creased collodiaphyseal angle is unequivo cally determined, and it is less than the aver age for the age group . The direction of the growth plate changes, it becomes close to ver tical. A characteristic X-ray sign is the pres ence of a triangle-shaped component between the distal-medial part of the epiphysis and the medial part of the neck (Fig. 28.40.). The growth plate may close earlier, around the age of 1 0- 1 2 years, because of the ossifying error,
Fig. 28.40. Bilateral coxa vara infa ntum.
or permanent pseudo-arthrosis may often de velop in the femoral neck. Treatment. This deformity can only be treated surgically. In progressive cases, val gus osteotomy is to be carried out in the early years. It must be realized however, that a gradual recurrence may follow because of the progression of the condition. In these cases, valgus osteotomy must be repeated at a later age.
28. 1.6. Sym ptomatic coxa vara A number of illnesses and general conditions, such as epiphyseolysis capitis femoris, fibrous dysplasia, Paget's disease, etc., may ind uce secondary varus hip.
Clinical symptoms. The clinical symp toms are similar to those described on coxa vara infantum (congenital) : limited hip ab duction, limb shortening and Trendelenburg' s gait. Treatment. If the deformity is part of a systemic disease, the latter should be treated, which may or may not cure the ossifying dis turbance.
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28. 1.7. Growth disturbances of the proximal fem u r Various extents o f hypoplasia or aplasia o f the proximal femur may occur for u n known rea sons. A primary teratogenic noxa is presum ably in the background during embryo genesis. It is not inherited.
The main point of this disorder is that ossi fication of the proximal femur is delayed. Os sification of the epiphysis is late and hypo plastic, and occasionally involves more than one ossifying center; moreover, the proximal ossification of the diaphysis is retarded (Fig. 28.4 1 .) . The hypoplastic or aplastic proximal femur is often dislocated. Treatment. In infants, no treatment is needed but observation is recommended. Af-
Fig. 28.41. Right congenital femur hypoplasia.
ter the start of walking, conservative treat ment is advised, depending on the extent of limb shortening. If the shortening amounts to 3 -5 cm, length equalization using surgical shoes is necessary. If the shortening is more extensive, equalizing calipers are prescribed.
28. 1.8. Transitory arthritis coxae (transitory hip joint inflammation) This is an acute, painful hip arthritis, which re solves by itself within a few days. It occurs most frequently between the ages of 2 and 14 years, affecting both genders equally.
Etiopathology. In the majority of the cases, the arthritis is preceded within 1 -3 weeks by influenza. It may occur after any other inflammation or trauma. As an immune response to an inflammation, reactive syno vitis may occur in any joint (not purulent). This is usually a condition in the temperate zone (similarly to Perthes ' s disease), and the incidence of the two disorders is also very similar. Clinical symptoms. It usually appears as an acute condition, the child is unable to bear weight on the upper limb in the morning or daytime, indicating hip, thigh or knee pain. The child protects the hip, and this indicates the hip involvement, despite the fact that the pain seems to be distal . The condition often occurs in a less acute form: the parents com plain that the child limps and avoids loading the involved limb, but the pain is not domi nant. Examination reveals a selective restric tion of movement is similar to that in Perthes' disease. The most outstanding sign is de creased internal rotation, and occasionally an external rotation contracture; the abduction (or adduction) and extension may also be lim ited. The laboratory tests are usually negative; a mildly increased sedimentation rate and a left shifted differential blood test may possi bly be observed in consequence of the earlier influenza.
28. H i p d isorders
Imaging diagnostics. On ultrasono graphy, the accumulation of fluid in the joint is detected unmistakably. It is more important to evaluate whether the hip synovitis and fluid accumulation have caused any impairment to the circulation of the femoral head. The bone scan may demonstrate perfusion loss in the proximal femur area, but this is rarely neces sary. In all cases of transitory arthritis, bilat eral anteroposterior and Lauenstein X-ray im ages are advised, and the diagnosis should be confirmed in case of negative X-ray findings. Treatment. The patient must rest and the basic condition (influenza) is to be dealt with. If not contraindicated, nonsteroidal anti inflammatory drugs are advised. The com plaints cease within a few days. Walking and weight-bearing are allowed after the motion of the hip has become unrestricted.
28. 1.9. Juvenile acetabular protrusion Protrusion is the invasion and distension of the medial wall of the acetabulum toward the pelvis. Juvenile acetabular p rotrusion, which is usually unilateral, causes intermittent intense hip joint pain.
Fig. 28.42. Protrusio acetabuli in an elderly person with sec ondary arthrosis. The Wieberg CE angle is greater than the normal 20-40°.
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Three types of acetabular protrusion are differentiated: 1 . Juvenile protrusion : This is a rare condi tion, with intermittent hip complaints. Exonerative rheumatoid arthritis or non-differentiated collagenosis is possible in the background. The condition involves only the hip joint. 2. Acetabular protrusion in the elderly: Sec ondary osteoarthritis of the hip gradually develops on the basis of bilateral acetabular protrusion, usually in subj ects over the age of 5 0. 3 . Secondary acetabular protrusion : The pro trusion is due to some other identified ill ness (osteoporosis, osteomalacia, sys temic bone disorders, etc.). History. There is a gradual onset of inter mittent hip pain, the hip pain sometimes being severe. The pain is localized to the hip and groin and possibly the thigh and knee too. It occurs 4 times more frequently in girls and young females, than in males. Clinical symptoms. The restriction of hip motion and pain in response to passive move ments are typical. The restriction of hip mo tion is not selective, but homogenous. Both the external and internal rotation and also the ab- and adduction are limited to some extent. The flexion - extension usually remains intact. As the condition progresses, the hip gradually becomes uniaxial : flexion - extension is possi ble, but other movements may completely dis appear. The end-stage of the process is osteo arthritis in early adulthood with joint space narrowing and destruction. X-ray signs. The medial wall of the acetabulum is thinner, and in advanced cases it protrudes toward the pelvis. K6hler ' s drop figure disappears or is crossed over. The fem oral head is seated deep in the acetabulum, and the Wieberg ' s CE angle is larger than 40° (Fig 28.42.).
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Treatment. I n case protrusion is diag nosed, consultation with a rheumatologist or clinical immunologist is needed to verify any possible background disease. Most cases are seronegative, and the rheumatologist gives a negative opinion. In these cases, treatment with nonsteroidal anti-inflammatory drugs is advised according to the complaints, supple mented by a few days of rest. If the hip com plaints persist, intra-articular depot cortisone may be administered. The result is usually spectacular: the complaints cease almost im mediately. If the complaints and arthrosis per sist, hip replacement is indicated, even in early adulthood.
28. 1. 10. Snapping hip, external coxa saltans Coxa saltans i s present when t h e tractus iliotibialis, the thick, strong bundle of the fas cia lata, jumps over the tip of the g reater trochanter with a click. It takes place in late childhood or early adulthood and involves both genders. It is relatively rare.
Etiopathology. The occurrence is usually unilateral if it is due to an accident or scar. If its etiology is related to congenital develop ment, or to a connective tissue deficiency, then it is observed bilaterally. Coxa saltans has no relation to the hip joint, though the pa tients dramatically report that their hip "jumps out". The bursa, normally located between the greater trochanter and the iliotibial tract, de creases friction of the fascia lata. In cases of coxa saltans the smooth friction turns into stretched click, resulting in bursitis. History. The patients recount, that their hip "jumps out" upon certain movements first on one side, an then possibly bilaterally with varying intensity. Clinical symptoms. The patients can re produce the click while walking or squatting, and the sign is well palpable when the exam-
iner ' s hand is placed on the trochanter. It is of ten palpated better with the patient in a supine position, while the hip is flexed and extended, with simultaneous adduction and internal ro tation. The greater trochanter may be tender, indicating bursitis. Treatment. When the pain and bursitis is predominate, conservative therapy is advised with some days of rest and nonsteroidal anti-inflammatory drugs. When the click is the main complaint, the tense bundle of the tractus iliotibialis may be incised.
28. 1 . 1 1 . Inward or outward rotation of the legs Child ren may walk rotating their legs inward or less often outward. This is common and is not pathological, but rather a normal variant. Its incidence is 15-20% between the ages of 2 and 6. It affects both genders.
Etiopathology. It may be regarded as a physiological episode, since the gait is stabi lized this way. The intoeing gait terminates or improves in 95% of the cases in consequence of the changes in muscle power. The anatomi cal and clinical factors may be as follows :
- The decrease in the retrotorsion of the acetabulum and in the antetorsion of the femoral neck is delayed. These levels are more pronounced in childhood, gradually decreasing to adulthood. - Overactivity or weakening of the ilio psoas muscle, the active component of the anterior acetabular wall. The former may result in intoeing, and the latter in an externally rotated gait. - An imbalance between the external and internal rotating hip muscles. - A valgus knee deformity (more frequent in girls). The compensatory gait in the valgus knee could be a mild intoeing gait. - A rotation, ossification deformity of the leg, when the leg is internally rotated
28. H i p d i s o r d e r s
while the kneecaps look anteriorly. It is often accompanied by varus leg, proving the mild ossification disturbance of the leg. - Flatfoot, when the chi Id compensates the valgus heel with internally turned feet. - A structural or dynamic form of pes adductus. (In the dynamic form, the deformity is seen only during walking due to the overactivity of the abductor hallucis muscle, it discontinues at rest). Clinical symptoms and treatment. The child is taken to the doctor because of the strange gait, with inward turned legs. The walking pattern frequently shows a familial accumulation (an inherited alternative gait). Other features of underdeveloped muscles are often seen (e.g. flatfoot, valgus knee, sagging belly or a negligent posture). If no obvious etiology is found, spontane ous correction is expected by puberty. In cases of flatfoot or valgus knee, application of a supinating heel wedge to the footwear is ad vised. Sporting activity, swimming and ball games should be encouraged. Exemption from physical exercises at school is inappro priate. In cases of extreme rotation of the legs, with a valgus knee of more than 1 50, a marked metatarsus varus operative correction may be required.
28. 1. 12. Limb shortening Limb shortening is considered t o exist, if the difference in length between the lower limbs exceeds 1 cm.
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Types Functional shortening: This is caused by an adduction and flexion contracture of the hip. It is resolved if the primary source is eliminated (apparent shortening). An abduction contracture of the hip results in a relative elongation, which is also solved when the primary source is eliminated.
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Absolute shortening: The distance between the anterior superior iliac spine and the lateral (or medial) ankle is shorter than on the other side. It may be caused by: - Hip dislocation - Coxa vara - Perthes ' disease - A congenital local ossification malfunction in the growth plates - Inflammation of the growth plates - Trauma of the growth plates - Radiotherapy or the action of an iatrogenic noxa on the growth plates - Congenital limb hypoplasia
Shortening may involve the upper or the lower limbs. A major functional problem is caused in the lower limbs. Due to the asym metric load, lumbar spine changes may occur. Treatment. The treatment is determined by the age of the patient, the cause and the ex tent of the shortening. It is also influenced by the height of the patient relative to the average height of his age group. Limb shortening categorization : - 1 -3 cm: conservative treatment, foot wear correction - 3 - 1 5 cm: surgical intervention is con sidered - over 1 5 cm: amputation at the middle leg is considered, and application of a mo dem light prosthesis. Surgical solutions: Epiphyseodesis, obstruction of growth on the longer limb. Staples bridging the distal femur and prox imal tibia growth plates may achieve tempo rary epiphyseodesis. This procedure may be repeated. �
Limb lengthening or shortening procedures in one session This involves metaphyseal or diaphyseal shortening of the longer limb. Metaphyseal shortening may be carried out at the proximal and distal metaphysis of the femur and at the
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a
c
Fig. 28.43. Met ho ds of metaphyseal shortening on femur (a, b) and tibia (c) a: Proximal femural metaphysis, b: distal femural metaphysis, c: proximal tibial metaphysis.
b
Fig. 28.44. Methods of diaphyseal shortening of the longer limb in one ses sion. a: femur, b: tibia.
proximal metaphysis of the tibia (Fig. 28.43.). Diaphyseal shortening is performed at the midshaft on both the femur and the tibia (Fig. 28.44.). This is advocated in case of tall chil dren when the length discrepancy is less than 4 cm. Elongation osteotomy at the midshaft of the femur or the tibia in one sessIOn: - This comprises transverse osteo tomy in the middle part of the femur diaphysis. With use of a distractor, an elongation of 2-3 cm can be achieved. - Corrective osteotomy of the femur distal metaphysis with moderate elongation is performed. This is particularly indicated when mild shortening is associated with substantial valgus knee. These procedures are carried out rela tively rarely, since merely 2-3 cm elongation is achieved.
28. Hip d isorders �
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Continuous limb lengthening in multiple sessions: - This procedure is applied most frequently nowadays; the original limb length can be restored. It is indicated for shortenings between 3 and 1 5 cm. The larger the shortening, the longer the procedure. It may be performed either in childhood or in young adults. The collaboration of the child may be expected after 8 years of age, the procedure demands continuous cooperation between child, parents and physician. Devices for continuous limb lengthen ing (Fig. 28.45. a, b) : - Wagner type telescopic external fixateur: Transverse osteotomy is performed in the middle of the femur or tibia diaphysis. The fragments are fixed with strong screws (Schanz screws) driven into the distal and proximal metaphysis, and the screws are held by the external fixateur. This procedure is able to exert either distraction or
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compression. The modem systems have elastic telescopic solutions built in. - When Ilizarov type rings are used, the fragments are stabilized with stretched K-wires. The rings are fixed by 3 axial telescopes parallel to the limb axis. Both distraction as well as compression can be achieved. This device is more useful in fixing metaphyseal osteotomies, where the ossification is better. Both procedures have advantages and dis advantages. Ilizarov rings have recently be come more popular. �
The steps in continuous elongation : 1 Psychological training: This is neces sary to convince the child, together with detailed, repeated discussions of the working process between physi cian, parents and physiotherapist. This is the only way compliance of the child can be assured. 2 Special exercises are implemented be fore the operation in order to elongate the neighboring muscles and tendons .
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b
Fig. 28.45. Devices for continuous limb lengthening. a: Wagner's diaphyseal lengthening, b. llizarov's metaphyseal lengthening.
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This may decrease the necessity of sup plementary operations. 3 The procedure of continuous elonga tion: After the insertion and stabiliza tion of the external fixateur, the trans-
verse osteotomy of the diaphysis or metaphysis is carried out via a small in cision. On the operating table, an im mediate lengthening of 1 cm is accom plished. After a few days rest, further I mm lengthening may be achieved once or twice daily. This is continued until the required length has been attained, or contracture takes place in the neigh boring joints (Fig. 28.46. a, b). In cases of severe shortenings, the continuous elongation can be repeated once or more after an interval of one year. The rate of complications continuous elongation is relatively high (3 0%). Osteo myelitis, or transient or permanent paresis may occur, as may damage and restriction of motion in the neighboring joints .
28. 1. 15. Congenital hemiatrophy and hemihypertrophy This is a condition with unknown etiology and is not uncommon; one side of the body is deficiently grown and hemiatrophic. The limb length discrepancy may already be apparent in the first year and usually progresses slowly. Very minor length and circumferential differ ences are sometimes detected in both the up per and lower limbs; on other occasions, the dissimilarity progresses. Congenital hemi hypertrophy is diagnosed when ill-defined growth is observed on one side. It is often dif ficult to decide whether the length difference is due to hemihypertrophy or hemiatrophy.
28.2. Hip disorders in adu lts 28.2 . 1 . Functional anatomy Fig. 28.46. a: Following a d istal femur metaphysis fractu re: the growth plate is closed on the left, resulting in a 1O-cm limb shortening. b: After the limb lengthening, ossification is seen between the frag ments.
The hip joint is a spherical or limitless joint. The socket is the acetabulum, and the head is the femoral head. The elements of the acetabulum (the hyaline-covered C-shaped facies lunata, the ligamentum transversum acetabuli, bridging the incisura acetabuli, the
28. Hip d isorders
pulvinar, the fat tissue filling the fossa acetabuli, and the circular labrum) surround the femoral head over its equator, and the j oint is therefore classified as an enarthrosis. The capsule is very strong, reinforced by three ligaments, the iliofemoral, pubofemoral and ischiofemoral ligaments. These are at tached to the femoral neck in the same direc tion, turning from the caudal and posterior di rection. This is important from a mechanical point of view. The ligamentum capitis femoris plays a role mainly in the blood supply of the femoral head. Flexion and extension of the hip are ac complished around the transverse axis con necting the centers of the femoral heads. Dur ing flexion, the spiral twisted external liga ments loosen, during extension they tighten. In the hip, 5- 1 5 ° of extension is possible. Ab duction and adduction are achieved around the sagittal axis. The internal and external ro tation are performed around the construction axis. Combination of the above-mentioned motions effects the conical circumduction. The movement of the hip j oint is powered by a number of inner and outer muscles. Since these muscles have a mixed function, it is use ful to discuss them according to their main function. - M. iliopsoas : the only real flexor of the hip, which also has adduction and internal rotation effects. - M . tensor fasciae latae: a flexor of the hip, a knee extensor and a hip internal rotator. - M . gluteus maximus : a hip extensor. - M. gluteus medius and minimus: hip abductors. - M. piriformis : an external rotator and abductor. - M. obturator internus, gemellus superi or, inferior, obturator externus and quadratus femoris : external rotators. - Adductor muscle group : m. adductor longus, adductor brevis, gracilis and adductor magnus : adductors, internal rotators.
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28.2.2. Deformities of the hip prearthrosis Prearthrosis is a condition in which the joint cartilage cover is present, and the complaints a re minimal (fatigue and intermittent pain), but early osteoarthritis is expected, consider ing the deformity, changed biomechanics, or joint incongruence as a resu lt of earlier ill nesses or trauma. Cartilage damage is a consequence of essen tially the fol lowing major mechanisms: � �
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A pressure increase on any given loading surface A decrease of the loading surface Incongruence between the joint su rfaces Direct damage to the cartilage su rface
Etiologic factors. - Pediatric hip diseases that healed with deformity (congenital dislocation of the hip, epiphyseolysis capitis femoris, Perthes ' disease, etc. - Changes in collodiaphyseal angle (coxa vara, valga, or increased anteversion) - Acetabular protrusion - Post-traumatic conditions - Inflammation (bacterial, rheumatic, etc.) - Metabolic diseases with direct cartilage damage (gout or ochronosis) - Tumors destroying the joint surfaces
The most common factor, the effect of the increased collodiaphyseal angle, due to the valgus deformity is analyzed in Pauwels ' biomechanical system a s follows. In certain phases of the gait, the ipsilateral limb is loaded, while the contralateral limb is advanced. At these moments, the j oint is sub j ected to forces, which maintain balance and prevent pelvic tilt on the other side, the pelvis therefore remaining horizontal. This is ac complished by the hip abductor, namely the gluteus medius muscle. Pauwels' demonstrated that at these mo ments the following forces are acting (Fig. 28.47. a-c) .
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b
a
A
B
c
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b
a
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kIVcm 2
./
25,2
kIVcm 2
Fig. 28.41. Loading conditions A: A normal col lodiaphyseal angle (ratio of force / lever arm (b:a) 3:1). B: Coxa valga (b:a 6:1). C: I ncongruence (a) congruence (b) (following cor rection osteotomy). =
=
The system works by the lever principle. In the balanced position: force
x
lever arm
=
load
x
load arm.
The lever arm is the horizontal proj ection of the distance between the hip center and the force vector of the balancing abductors (Fig. 28.47. A). The load arm is the projection of the distance between the weight line and the hip center. Under normal circumstances, the ratio of these two arms is 1 : 3 . The hip abduc tors balance a 50 kg load with a 1 50 kg force. The rotation point of the lever (the hip joint) is loaded by 1 50+50 kg. If the power arm is
shorter, the force in hip abductors increases. In cases of a steep (valgus) femoral neck, the ratio may even increase to 1 : 6 (Fig. 28.47. B) . Thus the load acting on the hip in this case may reach even 3 5 0 kg ! The extent of cartilage wear is dependent on the pressure, friction and congruence of the joint surface. If a small area is subjected to high pressure, or certain areas do not touch the other joint surface, degeneration takes place (Fig 28.47. C). Deviations of the collodia physeal angle (coxa valga, coxa vara, incon gruence or subluxation) may lead to hyaline degeneration, and this condition may there fore be considered as prearthrosis.
28. Hip disorders
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If the coliodiaphyseal angle in adults is g reater than 130- 135°, the condition known as valgus hip is determined (Fig. 28.48. c).
ral head i s only partial because o f acetabular dysplasia, coxa valga subluxans is present (Fig. 28.49.). Depending on the extent of subluxation, a number of groups are differentiated (after Hartofilakidis) :
The collodiaphyseal angle depends on the age: the nonnal range at the age of 9 years is 1 3 5 - 1 38°, at 15 years, it is 1 3 3 ° , decreasing to 1 20° in elderly ages. The values for valgus de fonnities are therefore dependent on the age. Coxa valga is rarely an independent entity, it is often a component of other diseases, such as congenital dislocation and dysplasia, if these persist after treatment, or i f subcapital coxa valga develops. Infantile cerebral paresis and any noxa affecting the lateral part of the proximal femur growth plate also cause valgus defonnity. If the coverage of the femo-
Stage 1 : Dysplastic hip. The head is attached to the original acetabular hyaline (inde pendently of the extent of subluxation) . The X-ray picture shows an upper seg mental defect: the acetabulum is shallow because of the osteophytes padding up the fossa acetabuli. Stage 2: Low dislocation. The head is in a sec ondary socket, partially connected to the primary acetabulum. The X-ray picture shows an anterior/posterior segmental de fect: the acetabulum is shallow, with in creased socket and femur anteversion.
28.2.2. 1. Valgus hip, coxa valga
Fig. 28.48. Collodiaphyseal angle ranges in adults. a: Varus deformity (95°), b: Normal (126°), c: Va lgus deformity (150°)
Fig. 28.49. Right-side subluxed femoral head; 3D a image.
a b
Fig. 28.50. The left hip is in high dislocation, with severe hip osteoarthritis on the right side. a: Anteroposterior X-ray of pelvis. b: 3 dimension a reconstruction.
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Fig. 28.51.
(_10 ° )
b ( 12 ° )
c
(45 ° )
Different types of torsions of the proximal femur. a: Retrotorsion. b: Normal. c: Antetorsion.
Stage 3: High luxation. The X-ray picture shows a cranial and dorsal secondary socket, which is totally independent of the primary acetabulum. A segmental defect is seen in the entire acetabular edge.
The highly luxated hip (Hartofilakidis Stage 3) is a special form of prearthrosis. The femoral head is located 5- 8 cm proximally, in the substance of the gluteus medius muscle, attached in a pseudoarthrosis to the iliac crest (Fig. 28.50. a, b). The patient overloads the intact, longer limb (especially if the length discrepancy is not equalized), and early osteoarthritis of the uninvolved hip therefore occurs (Fig. 28.50. a) . Constitutional varus or valgus hips are of ten detected in adults with well-developed sockets and congruence. These are not consid ered to be prearthrotic conditions. 28.2.2.2. Va rus hip, coxa vara
- congenital developmental deformities of the femur - fibrous dysplasia, Paget' s disease, osteomalacia or rickets - malunited fractured neck of the femur 28.2.2.3. Antetorsion and retrotorsion
of the hip (coxa antetorta and coxa retrotorta) Rotation of the proximal femur around the longitudinal axis of the bone is torsion. This may take p lace in two directions. In ante torsion, the ventral angle of the line connect ing the centers of the head and the greater trochanter exceeds the normal 15°. In retro version, this angle is less than 15° (Fig. 28.51. a, c).
Antetorsion is much more common. It rarely occurs on its own, usually being de tected in association with infantile cerebral
Coxa vara deformity is present, when the collodiaphyseal angle in adults is less than 120° (Fig. 28.48. a). Coxa vara is a conse quence of pediatric hip afflictions, which leave residual symptoms despite treatment:
- osteochondritis after the treatment of congenital hip dislocation - femoral head deformities after Perthes ' disease - coxa vara deformity after epiphyseolysis capitis femoris - congenital developmental deformities of the femur (coxa vara infantum, or a proximal femoral deficiency)
Fig. 28.52. Infantile cerebral palsy: bilateral coxa valga antetorta deformity.
2 8 . H i p d i s o r d e rs
palsy (Fig. 28.52.), or hip dysplasia with a valgus deformity. In cases of maj or ante torsion, the patient walks with typical inter nally rotated lower limbs, in order to achieve that their hip j oints act in normal position. 28.2.2.4. Other p rearthroses
Inflammatory illnesses in childhood may also be considered as prearthrotic conditions. The systemic inflammatory illnesses are in cluded here : rheumatoid arthritis, epiphyseal osteomyelitis, or purulent arthritis, which even after healing may end up with osteo arthritis in adulthood. The primary acetabular protrusion occurs in puberty (see Chapter 2 8 . 1 ) . Medialization of the femoral head leads to a bio mechanically disadvantageous state, which may result in severe arthrosis in adulthood with monoaxial (hinge) hip motion. The secondary acetabular protrusion may develop in consequence of an inflammatory hip disease (e.g. rheumatoid arthritis); it de stroys the bottom of the socket, causing medialization of the head. This is the "thin wall" protrusion. It bears significance in rela tion to bone grafting. 28.2.2.5. Surgical treatment of
prearthrotic conditions The objective is to restore the normal ana tomical and biomechanical situation and axis. This way the arthrosis is prevented, or the pro cess may be slowed down. Preventive operations in the hip area: �
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Femur osteotomies a) Intertrochanteric varus osteotomy b) McMurray's medialization osteotomy c) Valgus intertrochanteric osteotomy d) Subtrochanteric osteotomy Pelvic osteotomies
Femur osteotomies Femur osteotomies may be carried out in the intertrochanteric or subtrochanteric seg-
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ment. They normalize the axial deformities and power arms. Each one involves a different way to achieve the same goal, namely to change the morphology or static of the limb, thereby improving the function (sub trochanteric osteotomies). a) Intertrochanteric varus osteotomy This intervention is performed in prearthrosis or early arthrosis, to correct the axis of the steep femoral neck, to improve the loading aspects and j oint congruence (Fig. 28.53. a, c). A medially based triangular wedge is sawn out from the intertrochanteric area of the femur. After removal of the wedge, the bone ends are united and firmly fixed (sta ble osteosynthesis). During the operation, si multaneous derotation is possible to decrease the enlarged antetorsion of the femur so as to further improve the congruence ofthe femoral head to the socket. Precondition ofthis operation is the appro priate abduction of the j oint, since the varus mechanism decreases part of the abduction range of the joint. Another precondition is, that the femoral head must be more centralized on the abduc tion film, with better joint congruence. b) McMurray's medialization osteotomy The femur is cut through in the intertrochanteric area in a plane inclined slightly upwards, and the distal bone end is displaced medially by half the width of the bone and fixed in this position. No wedge is removed. Through the displacement of the lower bone end, the muscles relax, causing an ad vantageous effect. This operation is currently rarely performed because of the availability of arthroplasties. The bone displacement causes a deformity in the medullary canal, which may make it impossible to insert of the stem of the artificial hip. c) Valgus intertrochanteric femur osteotomy The aim of this procedure is to correct a varus femoral neck to enhance the congru-
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Fig. 28.53. a: Outline and effect of varus and medializing intertrochanteric osteotomy (1: hip abductor m., 2: m. iliopsoas, 3: hip adductor m.). b: Femur valgus deformity - preoperative X-ray. c: After varus osteotomy. (Because of the shallow socket, Chiari's pelvic osteotomy was performed later.)
a b
c
ence, to decrease the tension of selected mus cles (adductors and iliopsoas) and to increase the tone of the hip abductors (Fig. 28.54. a, b). In the operation, a laterally based wedge is sawn out from the intertrochanteric area of the femur. After removal of the wedge, the bone ends are reduced and firmly fixed with stable osteosynthesis. Due to the valgus, the femoral head is turned laterally in the socket, the con gruence improves and the distance between the origin and attachment of the muscles changes beneficially. A precondition of this operation is the adduction reserve of the joint, since the varus mechanism decreases part of the adduction range of the j oint. Simultaneous derotation is also possible. The intertrochanteric femur osteotomy is preceded by a careful examination of the pa-
tient and geometrical planning based on the X-ray films. The size of the wedge removed is determined by the measured collodiaphyseal angle. The effects of intertrochanteric femur osteotomy may be summarized as follows: - By centralization of the femoral head, the joint congruence improves, the loaded surface increases, and the pressure is better dispersed, and therefore decreases. - The power of the abductors, adductors and iliopsoas is altered advantageously by the changed distance between the origin and the attachment of the muscles. - The alteration of the collodiaphyseal angle changes the length of the power arm (varus osteotomy) in accordance
2 8 . H i p d i s o r d e rs
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3 a b
Fig. 28.54. a: Outline and effect of valgus intertrochanteric osteotomy. b: X-ray of valgus intertrochanteric osteotomy.
with Pauwels' theory, and consequently the pressure generated by the abductors on the joint decreases. - The consolidation of the osteotomy rearranges the circulation of the pro ximal femur, and decreases venous stagnation, giving rise to an advan tageous, not negligible biological effect. �
Pelvic osteotomies Pelvic osteotomies are discussed in the chapter on congenital hip dislocation. Chiari ' s osteotomy i s performed i n cases o f pre arthrosis in early adulthood (Fig. 28.55. a, b). On the same principle, acetabular roof con struction is also considered (see Chapter 28. 1 ) .
Fig. 28.55. Chiari's pelvic osteotomy in hip dysplasia: a: X-ray picture of dysplastic hip. b: After medial displacement of the proximal part of the iliac bone, the coverage of the femoral head and the loading conditions are better.
28.2.3. Idiopathic fem u r head necrosis (aseptic, avascular fem u r head necrosis) This is ischemic necrosis involving the frontal and u pper lateral weight- bearing area of the femoral head, leading to severe joint defor mity.
Symptoms. Pain in the hip, restriction of the range of motion and a limp. The X-ray pic ture shows a wedge-shaped sclerotic area in the upper perimeter of the femoral head,
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28. H i p d isorders
which may collapse. I n a large proportion o f the cases (30%) the process is bilateral. Incidence. Zizic and Hungerford report that every thousandth individual is exposed to the possibility of developing avascular femur head necrosis. It is common between the ages on 0-60 years. The male - female ratio is 4: 1 . The pathophysiological basis of the condi tion was discovered in 1 948 by Chandler, who compared the circulation disturbance of the femur head with the occlusion of coronary ar teries in the heart and called the avascular fe mur head necrosis "the coronary disease of the hip". Etiopathology. This has not been clarified precisely. Data in the literature point to vari ous factors which predispose avascular femur head necrosis: �
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chronic steroid therapy alcohol a buse cytostatic treatment and X-ray irradiation a n occupation involving a risk of caisson disease sickle cell anemia or other he mo globinopathy (thrombus production) metabolic diseases (lipid metabolic d isorder, hyperg lycemia, hyperuricemia) storage illnesses (Gaucher's disease)
a
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autoimmune diseases (rheumatoid arthritis, systemic lupus erythematodes, etc.) injuries
Chronic steroid therapy and alcohol abuse are among the causes in 65-75% of idiopathic femur head necrosis. The blood supply of the femoral head is ensured by the circumflex ar tery of the femur. The arteria capitis femoris only rarely functions in adults. The anastomo ses ensure the blood supply of the femoral head, but the circumflex branches are re garded as terminal arteries, in the event of oc clusion, the supplied area necrotizes. Clinical symptoms. The onset of the ill ness is uncertain: pain is felt in the hip, the thigh, or possibly in the knee, and becomes stronger on loading. As the affliction pro gresses, the pain intensity fluctuates. Fluid ac cumulation is associated with joint inflamma tion, increasing both the pressure as well as the pain. Resolution of the inflammation may ease the soreness. Thigh muscle atrophy is also seen. The hip internal rotation, abduction and adduction become limited. Flexion - exten sion is maintained for a relatively long time. The limp is caused primarily by the pain, but later by the limited motion.
b
Fig. 28.56. Bilateral femur head necrosis: Stage 3 on the right-side, Stage 1 on the left. a: X-ray. b: MR image (horizontal plane).
28. Hip disorders
X-ray signs. The radiological phases of this condition were determined by Arlet and Ficat. These phases affect the therapeutic ac tivity. Since the changes in the early phase of the condition are difficult to identify on an X-ray picture, not only an anteroposterior film, but also Lauenstein views are taken. Both hips must be observed because of frequent bilat eral involvement. Ficat 's phases: Phase 0: This is the preclinical and pre radiological phase ("silent hip", no clini cal or radiological signs). The intra medullary pressure is increased. In 60% of the cases, the condition later progresses to Phase 1. Phase I. There are early clinical symptoms, but no radiological signs. A bone scan is advised. MRI is invaluable. The leading symptom is a sudden groin pain that radi ates to the thigh, which intensifies during the night. Movements are restricted (Fig. 28.56. a, b).
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Phase /1. Typical X-ray changes are observed: a wedge-shaped area with a sclerotic mar gin; the joint surface is intact (precollaptic state) . The clinical symptoms stagnate or progress. Transient phase If-Ill: S ickle sign: a sickle-shaped line appears under the j oint surface due to a subchondral fracture. Seg mental collapse is seen. Phase Ill: The joint surface has collapsed, and a sequestrum has separated. The j oint space is intact or wider. There is evidence of inflammation and fluid accumulation. The pain is severe and motion is limited (Fig. 28.56. a, b, 28.57). Phase IV: This is the terminal phase, evidence of secondary arthrosis is seen. The j oint space progressively narrows; osteophyto sis; the head is deformed. Limited j oint motion. Differential diagnosis. Having identified the clinical and radiological signs the diagno sis is not problematical, especially if the his tory has been precisely identified. This condi tion is to be differentiated from hip algo dystrophy, inflammation and tumors . Besides the X-ray image, the bone scan helps to verify the bone necrosis. CT defines the contours of the head. MRI and 3D CT tests provide particularly valuable assistance in confirming the diagnosis and in deciding on the treatment. Treatment. In the early phases non weight-bearing, swimming, gymnastic exer cises, nonsteroidal anti-inflammatory drugs, pain killers, physiotherapy and medical spa treatment may be recommended. However, the condition progresses and the conservative treatment does not lead to substantial results. The surgical treatment varies in the differ ent phases.
Fig. 28.57. Left side: Stage 3 femur head necrosis: with im ploded wedge-shaped sequestrum.
- In Ficat phases 1. and 11. , when, despite the bone necrosis, the j oint surface is still intact, drilling of the necrotized area, cancellous grafting and a vas-
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28. Hip d isorders
cularized implant may produce reasonable results . - In Ficat phase Ill. , unloading and transposition of the collapsed area may be attempted. This is done by inter trochanteric flexion osteotomy. A pre condition of this intervention is that the extent of the necrosis must be less than 50%. If it is more (in the maj ority of cases), total prosthesis implantation is the method of choice. - In Ficat phase Ill . , the condition presents as secondary osteoarthritis, and total prosthesis implantation is in dicated.
28.2.4. Coxarthrosis (hip osteoarthritis, arthrosis deformans coxae) This entity is characterized by deformity, pain and limited movement in the hip due to carti laginous and bone degeneration.
Symptoms. Pain, with progressing restric tion of movement, contractures and a limp. The j oint space becomes thinner, the joint contours are uneven, the j oint surfaces are de formed, and osteophytes, and degenerative cysts may develop. Incidence. In the population aged 65-74 years, X-ray signs (Kellgren) of hip osteo arthritis are present in 1 6-25%. Symptoms re quiring treatment are considerably less fre quent: 6- 1 0%. Male - female ratio is 1 : 2 . 5 . The ratio of primary and secondary hip osteoarthritis in the operated population is 65 and 3 5 % respectively. Etiopathology. Hip osteoarthritis has two different forms :
I . Primary hip osteoarthritis: Its cause is un known, however literature data suggest that the condition is determined. In paral-
lel with aging, the function of the cartilage cells changes, their proteoglycan produc tion decreases, which leads to a decrease in the water content of the intercellular matrix, and to damage of the integrity of the collagen network. Behind the genetic predisposition, gene mutations producing faulty collagen, or ill-defined antigen as sociations may be part of the cause. 2 . Secondary hip osteoarthritis : This devel ops on the bases of other hip disorders. These may originate from childhood or adulthood. The roles of congenital dislo cation, Perthes ' disease, epiphyseolysis capitis femoris, primary acetabular protru sion and inflammatory diseases were dis cussed in the chapter on prearthrosis. In adults, inflammatory diseases (septic arthritis, rheumatoid arthritis and spondyl arthrosis ankylopoetica), idiopathic aseptic necrosis of the femoral head, fractures involv ing the joints, post-traumatic conditions near joints, metabolic diseases, bone dysplasia, and arthropathy may all result in secondary hip osteoarthritis. The pathology of osteoarthritis was dis cussed earlier in connection with diseases of the j oints (Chapter 1 9). Macroscopically, the cartilage is no longer gleaming, its mother-of-pearl white color has turned to yellowish brown. The hyaline is fiberized and softened in places. The areas subj ected to the greatest surface load have no cartilage cover, and ebumated (condensed) bone is visible. The subchondral cavities and degenerative cysts often communicate with the j oint cavity. The femoral head gradually loses its ball shape, and widens due to the marginal osteo phytes. The appositions that grow around the facies lunata in the center of the acetabulum may block the fossa, and a double acetabular bottom may be formed. These central osteoarthritic products (socket bottom osteo phytes) literally displace the femoral head and secondary subluxation is observed. B esides the changes in the cartilaginous bony structures, thickening, inflammation or
2 8 . H i p d i s o r d e rs
shrinking of the capsule may also play a role in the complaints and symptoms. In consequence of the changes listed above, the condition known as hip osteoarth ritis or arthrosis deformans coxae develops. Clinical symptoms. The main complaints are pain, limited movement and a limp. Ini tially, the pain presents only after getting out of bed in the morning, or upon standing up from a chair. It may subside during moving. Later on, the pain increases and becomes con tinuous, both in the daytime and at night. The pain may be located deep in the hip, in the groin, around the greater trochanter or the sacrum, or in the front of the thigh, radiating to the knee. The patient' s quality of life depends on the extent of the pain. As the condition pro gresses, the patient' s working and walking ability diminishes, and he / she may ulti mately become unable to take care of him selflherself. The limiting of their movements is recog nized while they attempt to carry out everyday tasks. In the beginning it may be difficult to put on a pair of socks, or to get on a bus . The limits of movements of the joint gradually narrow. First the extension becomes limited, i.e. a flexion contracture arises. Later the in ternal rotation decreases, which is followed by abduction and adduction. Monoaxial movements may succeed when the hip joint has only flexion and extension, but ultimately the flexion also becomes limited, and the hip is in such a state that only very limited move ment remains . Flexion, adduction and an ex ternal rotation contracture usually prevail. The limp is due to the clinical symptoms listed above, the pain resulting in a protective limp. Because of the flexion contracture, the hyperextension phase of the step is missing. Adduction flexion contractures cause an ap parent limb length difference, which increases the limp. X-ray signs. In the evaluation ofthe radio logical picture of the primary and secondary forms of hip osteoarthritis are differentiated.
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Primary forms (Fig. 28.58) : The j oint space is narrow. - The j oint contours are uneven. - Subchondral sclerosis is observed (on loaded areas) . - Degenerative cysts develop. - Osteophytes are seen at the socket margin and on the head - neck border (collar osteophytes). - A double socket bottom may be present. -
The primary form may be associated with protrusion. The head may be lateralized, when the thickened double socket bottom sublux ates the head from the central position.
Fig. 28.58. X-ray image of bilateral primary hip osteoarthritis.
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Secondary forms (Fig. 28.59) : - When the head is not central and the incongruence is severe, the hip osteoarthritis is usually secondary. - The same X-ray signs are present as in the primary form. - The X-ray signs depicting former disorders, which have not fully recovered anatomically may be identified (e.g. congenital dislocation (Fig. 28.60.), epiphyseolysis capitis femoris, Perthes disease or other types of head necrosis, j oint infection, etc. ) . '
Differential diagnosis. This condition is identified without any difficulty thanks to the
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28. Hip disorders
(arthritis and inclplent spondylarthritis ankylopoetica), or knee diseases (meniscal tear, arthrosis, etc.). On the other hand, pain radiating from the hip to the knee may suggest the presence of a knee disorder.
Fig. 28.60. Secondary hip osteoarthritis on basis of bilateral de velopmental dislocation of the hips with typical short neck and high trochanter.
clinical and radiological characteristics. Symptoms of diseases of the neighboring re gions may occasionally hinder establishment of the clinical diagnosis. These can include degenerative involvement of the lumbar spine accompanied by root irritation (e.g. lumbar disc hernia), diseases of the sacroiliac joint
Treatment. Before an account of the treatment methods, mention should be made of the means of prevention. In the prevention of both types of hip osteoarthritis, a healthy lifestyle, based on healthy nourishment and regular exercise, is essential . Body weight must be kept at the optimal level or weight loss should be considered if necessary. Even in the presence of a prearthrotic state, regular swimming, gymnastics and sports are those factors, which are able to protect the compen sated state of the hip musculature for a long period and to slow down the progress of the disease, which eventually requires either con servative or surgical attention. Apart from changes in lifestyle, it may also be necessary to change schools or working conditions. To prevent secondary hip osteoarthritis, the best possible treatment of the primary dis ease is indispensable. The incidence of con genital dislocation of the hip has decreased significantly in recent decades due to the early screening and successful treatment. The ef fective management of epiphyseolysis capitis femoris and Perthes ' disease has also led to a decrease in the incidence of hip osteoarthritis. Septic arthritis and hip tubercolosis, which earlier resulted in ankylosis (full stiffness of the joint) have now become conditions that rather induce hip osteoarthritis. Early diagnosis and early and appropriate treatment may delay severe hip osteoarthritis. The results are modest in cases when the hip osteoarthritis develops after femoral head ne crosis and fractures involving the joint. Conservative treatment: is applied in hip osteoarthritis to decrease the pain, to ease the contractures and the limp, and to increase the range of motion, and muscle power. Medica tion, physiotherapy and spa treatment may be employed. The following medications or their combi nations may be effective :
28. Hip disorders �
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Pain killers Nonsteroidal anti-inflammatory d rugs Steroid d rugs Muscle relaxants.
The most important goal is to relieve the pain. Instead of general pain killers, non steroidal anti-inflammatory drugs are pre ferred, since the osteoarthritis-induced in flammation is a significant source of the j oint pain. Muscle spasm and contracture may be alleviated by a combination of these drugs and muscle relaxants. Steroid therapy is a very effective element of the anti inflammation treatment. It does have harmful local and general side effects, however, caused by the chronic steroid ther apy: gastrointestinal ulcer, osteoporosis, ste roid necrosis, steroid diabetes and Cushing 's syndrome. Local steroid use (intra- or para-articular) may be indicated for a certain time period and in a limited dose. A traction device is often applied to unload the hip joint, and to decrease the spasm and contractures and the pain. It can be used even at home, combined with other methods. A walking stick is also useful. Surgical treatment. In prearthrosis or moderate hip osteoarthritis, femoral and pel vis osteotomies are performed to improve congruence and containment (see Chapters 2 8 . 1 . and 2 8 .2 . 2 . 5. ). I n advanced cases, the obj ective of surgi cal treatment is to decrease pain and restore movement and stability. Primarily a hip endo prosthesis is implanted; occasionally, stiffen ing of the hip or (after prosthesis removal) pseudoarthrosis formation is carried out. - Hip arthroplasty - Hip arthrodesis - Resection, or excision arthroplasty
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The system of hip endoprostheses i s the fol lowing: �
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surface replacement endoprostheses cervicocapital endoprostheses total hip endoprostheses cemented uncemented hybrid
Surface replacement endoprostheses. The key procedure of this method is double cup arthroplasty. After the removal of the dam aged joint surfaces, a plastic socket is ce mented into the acetabulum, and a matching metal cup is cemented onto the femoral head. Earlier, the results of this operation were modest, but it has nowadays been resurrected in a form involving a metal cup - metal head. Cervicocapital endoprostheses. Follow ing removal of the head and the neck, a cervicocapital endoprosthesis can be inserted into the medullary cavity of the femur. The metal head, moving in the cartilage-covered bony acetabulum, ensures the joint function. This procedure is mainly employed in opera tions involving the elderly, following frac tures of the femoral neck. This endoprosthesis is also manufactured in a bipolar form: a large metal ball is positioned in the cartilage cov ered bony acetabulum, inside this ball is a plastic bushing containing a small metal ball. The bipolar design increases the range of mo tion and the lifetime of the implant.
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Hip arthroplasty The total hip endoprosthesis embodies the most noteworthy achievement in orthopedics. A patient with a painful restriction of move ment can by this means be freed from all the complaints, and the mobility and quality of life restored to normal.
total hip endoprosthesis. Augmentation (:;,���
of the acetabular roof with bone block a nd screws.
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28. Hip d isorders
Total hip endoprosthesis / cemented (Fig. 28.61). After exposure of the hip j oint, the head and neck are resected. The acetabular cartilage is removed, the socket is deepened and the artificial cup is cemented home. After the preparation of the femur medullary cavity, a corresponding prosthesis stem is fixed. A metal head is assembled onto the cone of the metal neck, which is reduced to the polyethyl ene artificial socket. Bone cement (consisting of polymethyl metacrylate) is made from two components (fluid + powder). After mixing of the compo nents, they polymerize, and the cement sets through an exothermic reaction (ca. 80 QC) the cement is setting. This substance fixes the prosthesis firmly in the bone cavity surface. Total h ip endoprosthesis / cementless (Fig. 28.62.). The cementless implants are different in shape and surface from the ce mented ones. No bonding material is utilized in these cases. The cup consists of two com ponents : an external metal ring and a plastic lining. The surface of the external metal ring is threaded, and can be screwed into the bony acetabulum, but may also be designed to be pressed firmly into the bony bed (press fit). The plastic lining covers the head of the pros thesis. The stem of the femoral components matches the anatomical configuration of the medullary cavity (anatomical prostheses). The medullary cavity is prepared with ream-
ers matching the shape of the prosthesis, which will therefore wedge into the cavity (press fit). After the operation, the wedge ef fect and the press fit will ensure primary sta bility; later, especially in cases of a porous surface, bony ingrowth takes place, and sec ondary, biological fixation evolves. The po rous surface ensures attachment to the bony bed over a large surface. Total hip endoprosthesis / Hybridfixation. One component is fixed with, while the other without cement. The expected survival of both cemented and cementless endoprostheses is similar: 90% at 1 0 years . After the setting of the cement, the ce mented prosthesis is totally stable and ready for weight bearing. This prosthesis has the negative feature, that if the implant becomes loose, removal of cement may cause bone loss. The biological fixation of cementless im plants may take some time, but in the event of its loosening, the exchange does not create bone deficiency. The indications of a cementless implant are young age and a good bone structure ensuring the proper primary stability. In cases of poor bone quality (osteo porosis or necrosis), defective anatomical sit uation (previous operations, a dysplastic acetabulum, etc.) the cemented procedure is recommended. Minimally invasive endoprosthesis tech nique. This is the newest enterprise of pros thetic surgery. In a selected patient cohort (young, active patients with no obesity, etc.), the surgical incision is short (under 10 cm), and the joint capsule is preserved as much as possible, possible using minimal trauma tization. The postoperative pain and blood loss are expected to decrease, mobilization is swift, with a better cosmetic outcome. There are also some risks to be considered, e.g. mis placed components due to the limited view, unexpected tissue damage and bleeding. �
Fig. 28.62. Cementless total hip endoprosthesis.
Fusion of the hip j oint, arthrodesis This has almost totally been abandoned. The procedure, which ensures pain-free sta bility, was used in young patients who ac-
28. Hip disorders
quired a severe unilateral hip condition, while performing standing or physically demanding jobs. A good function of the lumbar spine and the knee are preconditions of this arthrodesis, since these structures will take over the lost motion of the hip and their load will increase. The increased load will sooner or later result in the degenerative changes in the mentioned joints, and the ipsilateral knee and contra lateral hip osteoarthritis will also develop. These are the drawbacks of the arthrodesis. �
Resection (excision) arthroplasty Resection (excision) arthroplasty is the fi nal solution in septic/aseptic failures of hip endoprosthesis procedures. The stem,
Fig. 28.63. Girdlestone situation following removal of total hip endoprosthesis.
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acetabulum (and possibly the cement) are all removed ( Girdlestone operation; Fig. 28.63 . ) . This state was earlier considered t o be final. Today however, the patients demand a good quality of life, therefore if the eradication of the infection is safe and the anatomical cir cumstances allow, prosthesis replantation may be attempted. �
Sterile loosening of a hip endoprosthesis and revision arthroplasty According to wide-range statistics, 90% of cemented and cementless endoprostheses re main stable at 1 0 years . This proportion is lower for young adults and in certain cases of secondary hip osteoarthritis (75-80%). The cause of the sterile loosening is that the bone, the cement and the material of the implants all have different moduli of elastic ity. The wear on the substances of the im plants is also a contributing factor. Granules of polyethylene, metal and cement can accu mulate in the joint, together with hystiocytes and foreign body giant cells, which may gen erate tissue reaction. This persevering granu lation tissue invades between the implant and the bone and induces osteolysis, leading to loosening of the implant. In these cases revi sion arthroplasty is advocated, which ac counts for 20-25% out of all endoprosthesis interventions. The success of the revision is dependent on the anatomical circumstances perceived during operation. If no bone loss is revealed, revision is not problematical. Some years ago, in the event of maj or bone loss, only the Girdlestone state was reasonable : the patient walked on the pseudo-arthrosis with a sup porting walking aid, with a pronounced limp but without much pain. Today there are de vices to replace bony defects of both the acetabulum as well as of the femur. The new bone bed receives the new implant with a sta bility matching that ofa primary intervention. The 1 0-year survival rate of revision arthroplasties is similar (about 80%) to that of the primary interventions .
29.
Laszl6 Hangody, M i kl6s Szen d r6i
Disorders of the knee
29. 1. Structure and functional anatomy of the knee The knee is the largest joint of the body, with one of the most complicated structures; it is classified by its motions as a trocho ginglymus. The longitudinal axes of the femur and the tibia in the frontal plane (anatomical axis) enclose a lateral angle (the physiological valgus angle of the knee, which is approxi mately 1 73°). The knee is slightly eccentric: the lateral condyle is somewhat flatter, while the medial one is larger. The loading axis, however, runs along the line drawn from the femoral head through the center of the knee to the ankle joint, and the loads on the medial
1 --��------��.� ______*H�_ 2 � 3
15
14 13
12 --+'���
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1. 2. 3. 4. 5. 6. 7.
7
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8 9 11 ----t--_+_
Fig. 29.1. Anatomy of the knee joint
and lateral half of the knee are therefore equal under normal circumstances. The knee joint may be divided into 3 com partments : patellofemoral, medial and lateral tibiofemoral j oints. The practicality of this di vision is that certain disorders (e.g. osteo arthritis) have different affinities for different compartments. During motion and walking, the joint sur face is loaded by extremely large forces. The stability of the joint in each phase is provided not by the bony structure and shape, but by strong ligaments with complicated paths (pas sive stabilizers) and muscles (active stabiliz ers) (Fig. 29. 1 .) . The medial stabilizers that prevent valgus displacement are the following structures : the dorsomedial capsule, the su-
10
9. 10. 11. 12. 13. 14. 15.
anterior cruciate ligament, posterior cruciate ligament, medial collateral ligament, semimembranosus muscle, medial superficial collateral ligament, menisci, patellar tendon, gracilis muscle, semitendinosus muscle, sartorius muscle, membrana interossea, tractus iliotibialis, tendon biceps femoris, lateral collateral ligament, popliteus tendon
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2 9 . D i s o r d e rs of t h e k n e e
perficial layer of the medial collateral liga ment, the medial capsule ligament, the poste rior oblique ligament, the muscles of the pes anserinus and the semimembranous muscle. The latter muscles are also internal rotators; they produce 20 an internal rotation of 20° at the knee bent to 90°. The lateral stabilizers are : the dorsolateral capsule, the lateral collat eral ligament, the m. popliteus, the iliotibial tract and the m. biceps femoris. (The popliteus muscle has an important function in addition to stabilization: it rotates the tibia inward at the start of flexion.) The other muscles ensure the approximately 40° of external rotation of the leg with the knee bent. The active rotation around the longitudinal axis of the leg is pos sible only with the knee bent and relaxed col lateral ligaments. To achieve this, the flexors attached to both sides of the tibia like reins ro tate the knee in and out. The internal rotation is limited to 20° by the tense cruciate liga ments, and the external rotation to 40° by the collateral ligaments. The central stabilizing system of the knee involves the menisci and the cruciate liga ments. The anterior cruciate ligament origi nates from the mediodorsal part of the lateral femoral condyle and is attached widely in the intercondylar eminence, between the anterior horns of the two menisci. It contains 3 bun dles, which are partially twisted around them selves. In each stage of flexion, a different bundle comes under tension. The posterior cruciate ligament originates from the ventro lateral part of the medial femoral condyle and runs backward and down to the tibial inter condylar fossa; it contains 2 bundles. Functions: � �
Both cruciate ligaments participate in protecting the lateral stability. The anterior cruciate ligament prevents a nterior subluxation of the tibia, while the posterior cruciate ligament prevents the posterior subluxation of the tibia and the a nterior skidding of the femur over the fi xed tibia d u ring walking.
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I n every phase of the knee flexion, when the collateral ligaments are somewhat loosened, they ensure the stability of femur on the tibia, and the axis of the control led rolling-slide movement d u ring knee flexion.
The foremost motion of the knee is exten sion - flexion, which is effected around the transverse axis connecting the epicondyles. The extent varies individually; it is generally around 1 3 0°, depending on the tension of the extensor apparatus, and the soft tissue-mass in the popliteal fossa. In extension, the collateral ligaments are stretched, for the radius of the sagittal curvature of the femoral condyles is greater frontally. The end-point of extension is secured by a number of factors, at the same time inhibiting hyperextension. These com ponents are the collateral ligaments, the ex tremely strong posterior capsule, and the tense cruciate ligaments. In the normal knee, about 1 0° of end-rotation occurs externally at the end of extension. In this situation, the passive stabilizers are tense, and the active ones (mus cles) may relax; thus standing with extended knees does not require much muscle activity to stabilize the joint. In this position, the joint is stable. Apart from flexion, all other move ments are pathological and relate mostly to damage to the passive stabilizers . Physical examination of the knee: the follow ing factors are to be assessed: � �
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The axis (anteroposterior. and sagittal plane) Fluid accumu lation Stability (anteroposterior and lateral, rotational) Range of movement Muscle power Contractures (soft tissue, skin, muscle, capsular or bony) The patel la reflex Meniscal tear Chondropathy and arthrosis signs
The technique of assessment is discussed in the section on each disorder.
29. D i s o r d e r s of the k n e e
29.2. Congenital developmental disorders 29.2. 1. Congenital knee dislocation This rare disorder, which is frequently associ ated with other developmental anomalies, may occur bilateral ly. The tibia is subluxed o r fu lly dislocated anteriorly in t he sagittal plane. The tibia plateau is attached to the ventral surface of the femu r condyle.
Clinical symptoms. This disorder is usu ally detected at birth or in babyhood; the se verity varies. In cases of subluxation, the proximal tibia is positioned anteriorly on the femoral condyles to different extents, the fe mur and the tibia of the patient enclose a fron tally open angle. In mild cases, the knee flexion is generally full, but in more severe forms it may be badly limited. When luxation is total knee flexion is possible, the flexor muscles are displaced in front of the joint and they act as extensors enhancing the hyper extension. In severe bilateral cases, the patient is unable to walk, or occasionally stands and walks on the posterior surface of the leg and popliteal fossa. X-ray signs. The lateral views clearly re veal the ventral subluxation of the tibial condyles. The confronting joint surfaces may be flattened. Therapy. The hips and the entire lower limbs must also be assessed, since the knee disorder may be associated with multiple de velopmental disorders . In minor cases, early conservative treatment may be successful. Gentle reduction may be attempted even in the first week after birth, followed by a circu lar plaster cast up to the groin. With a frequent change of plaster and pas sive exercises, the knee flexion can gradually be increased. In cases of subluxation or full dislocation, surgery is indicated. Elongation of the quadriceps tendon, and incision of the shrunk ventral capsule are followed by appli-
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cation of a plaster cast for 4-6 weeks. After that, intensive rehabilitation is essential.
29.2.2. Genu recurvatum The range extension o f the knee surpasses the normal 5- 0°.
Causes : - Congenital: the tibial plateau is inclined forward - Idiopathic: abnormal load, standing with a loose posterior capsule - Post-traumatic: the ventral part of the tibia growth plate is blocked - Compensatory: in neuromuscular disorders (quadriceps palsy caused by poliomyelitis, and forced knee hyper extension in cases of equinus foot) . Therapy. Depending on the etiology osteotomy or orthosis may be selected.
29.2.3. Developmental disorders of the patel la Complete absence of the patella (aplasia patellae) or hypoplasia is a rare congenital de velopmental disorder. The knee extension strength may be weakened, but usually does not cause a major functional deficit; the pas sive range of movement is full. It is more common that the patella devel ops from two or more ossifying centers, and they do not unite at the end of growth (bipar tite or tripartite patella). The hyaline surfaces of the patella are even, and the disorder is not a source of complaints, or only in the event of overload. A common finding is the high or deep po sition of the patella (patella alta or patella baj a) . Together with the factors discussed above, a high patella increases the chances of habitual dislocation; in the baj a position, the patella is compressed to the femur on flexion, leading to chondropathy and chondromalacia.
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2 9 . D i s o r d e r s of t h e k n e e
29.3. Repeated patella dislocation and subluxation 29.3.1. Habitual dislocation of the patella The patella dislocates laterally on every occa sion, when the knee is flexed. It is clearly seen and palpated. This occurs between the ages of 5 and 9 years, i n older i nd ividuals it is ob served only occasional ly.
Etiopathology. The explanation is the contracture of the quadriceps femoris muscle. The contracture may be congenital or the ef fect of palsy, but the most common reason is an inj ection (mainly antibiotics) into the quadriceps femoris muscle in infancy or early childhood. The inj ections lead to fibrosis, which is the cause of the extension knee contracture in the maj ority of cases; patella dislocation also occurs in around 20% of the patients. C linical symptoms. At every flex ion of the knee, the patella slides down from the lat eral femoral condyle to the lateral side. Ifknee flexion is attempted while the examiner man ually holds the patella in place to prevent the lateral luxation, only 3 0-40° of flexion can be achieved and the muscle is very tense. Treatment. The patella slides over the prominent edge of the lateral condyle at every luxation, and its hyaline surface may therefore be damaged after a time. Surgery is recom mended to elongate the quadriceps tendon, to incise the lateral capsule and to tighten the medial capsule.
29.3.2. Recurrent dislocation and subluxation of the patella The patella occasionally undergoes dislocation or subluxation lateral. Fol lowing the acute epi sode, swelling and pain are observed. This
disorder occurs in pU berty. It is 3 times more common among girls than among boys.
Etiopathology. Similarly to habitual dis location, this is lateral and presents first as a traumatic luxation. The history may indicate and injury, but this is usually not a direct ef fect on the patella. The dislocation is induced by a critical knee movement with distortion during some activity, jumping or sport. In re current cases, the patient knows exactly what movement causes luxation and tries to avoid it. The dislocation recurs again with various incidence, but usually increasingly more com mon. It may initially present once or twice a year, but without a surgical solution it may be come a daily event. An important factor in this disorder is the loosening of the medial capsule and reti naculum. Contributions may also be made by the following factors : a high patella, a hypo plastic lateral femoral condyle or lateral part of the patella, valgus knee or a lateral position of the tibial tubercle due to torsion of the leg. Clinical symptoms. It is not easy to estab lish from the history whether the patient origi nally suffered a patella dislocation or a meniscal tear. If the situation recurs the diag nosis is easier. Following an acute incident, the knee is swollen, and an accumulation of fluid or blood may be present. After a time, patella chondromalacia may develop. The medial edge of the patella is tender, and pressing the patella in a lateral direction elicits sudden and severe pam. X-ray signs. Serial films taken with dif ferent flexions of the knee of the prone patient demonstrate hypoplasia and a tendency to dis location. Treatment. The patient usually arrives following reduction of the dislocated patella (or it may have reduced spontaneously). If blood has accumulated it is evacuated and a plaster cast is applied. Active quadriceps ex-
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ercises are recommended later. Even after multiple luxation, a conservative method can be attempted, especially active quadriceps training. A special orthosis can be prescribed, enabling the patient to play sports . If the com plaints persist, surgical methods follow. Many procedures have been published, the es sence being incision of the lateral retina culum, tightening the medial and correcting the path of the ligamentum patellae by trans posing the tibial tubercle medially.
29.3.3. Luxatio patellae congenita This disorder is well differentiated from the above form, since it is present at birth. The patella lies on the lateral part of the femoral condyle (Fig. 29.2.), and is not reduced during motion; in fact, it is often irreducible even manually. The patella is hypoplastic, and the ligament is shortened. The knee is in valgus and externally ro tated. Swift operation is warranted, but it is not easy to reduce and fix the patella even surgi cally.
Fig. 29.2. Congenital patella luxation with characteristic lateralized patella, and shallow patellar groove on the femoral surface.
29.4. Developmental disorders of the menisci �
Discoid meniscus
The embryonic meniscus has a discoid shape. If this persists after birth, the condition is called discoid meniscus: instead of the normal
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sickle shape, the meniscus resembles a disc. In 95% of the cases, the lateral is involved.
Clinical symptoms. Discoid meniscus is detected among toddlers. At the beginning of knee flexion and at the end of extension, a typ ical clicking sound is heard, with a few de grees of valgus - varus or external - internal rotation movement. This condition is more vulnerable than with the normal meniscus, and it is symptomatic if a central tear appears after minor trauma or distortion. Treatment. The weak, thin, tom central part is excised via arthroscopy, leaving the pe ripheral part intact.
29.5. Developmental disorders of the tibia and fibula 29.5. 1. Tibia, fibula aplasia, hypoplasia Tibia hypoplasia results in a shorter leg. Partial or total aplasia often presents together with other developmental disorders (see Chapter 1 5) . The leg is usually bent to varus, while the foot is in equinovarus because of the missing medial ankle.
29.5.2. Congenital tibia pseudarthrosis At birth, the leg may be bent in an anteriorly convex shape. Fradure o r pseudoarthrosis de velops later, usual ly in childhood. The typical findings are the angulation between the mid d le and distal third of the leg and occasional pathological movements.
Clinical symptoms. Curvature with fron tal and lateral angulation is seen between the middle and distal third of the leg. If fracture has occurred, acute angulation and irregular movements are detected. The X-ray picture shows the described bend of the tibia with sclerosis or cystic zones,
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o r interruption of the bone integrity. The fib ula may be intact, curved or also pseudo arthrotic. The etiology is unclear. It often accompa nies neurofibromatosis (see Chapter 1 3) . Cafe au lait spots are then found on the skin, and neurofibromatosis nodules. It may also be as sociated with fibrous dysplasia. Spontaneous fracture often occurs at the location of the curve detected after birth. The tendency of pseudoarthrosis to heal is ex tremely poor. Surgery (possibly repeated) succeeds. Otherwise, a caliper splint is pre scribed.
29.6. Axial deformities 29.6. 1. Genu varum - crus varum This deformity i s characterized b y the medially convex angle enclosed in the frontal plane between the axes of the femur and the leg (Fig. 29.3.).
Symptoms. The distance between the me dial surfaces of the knees, which is normally a few centimeters, may be greatly increased. The condition may be present unilaterally, but more often it is bilateral, giving rise to bowleg. Incidence. This situation is normal in in fants and toddlers, and gradually turns to a mild valgus position (knock knee) by the age of 8- 1 0 years. Varus deformities that persist after this age and progress are considered to need correction. The disorder appears in both genders, but is more common among boys. Etiopathology. Varus deformities may be idiopathic or of known origin. A number of conditions may lead to varus knee : - Metabolic bone disease (the weakened, occasionally soft bone bends under a load), e.g. rickets, fibrous dysplasia, Paget ' s disease or osteomalacia. - Congenital connective tissue weakness, or loose ligaments - Tibia vara epiphysarea
Fig. 29.3. Genu varum; the loading axis of the lower limb is displaced from the medial part of the knee in the direction of the medial line of the body; the medial knee compartment is overloaded.
- Medial damage to the tibial proximal or femoral distal growth plate - Malunited femur or tibia fractures with axial deformity - Compensation (as a consequence of an abduction hip contracture) - Medial osteoarthritis Clinical symptoms. The deformity is usu ally bilateral. It is symptomless in childhood, and the parents take the child to the doctor merely because of the deformity. Later the leading symptoms are quickly developing tiredness, pain after loading, and an uneven gait. Common further signs are internal rota tion of the leg and flatfoot. In untreated cases, overloading of the me dial part of the knee joint (Fig. 29.3.) results in early arthrosis and instability. In severe cases, the lateral ligaments may become distended, and the knee will wobble. X-ray signs. The extent and the punctum maximum of the axial deformity are best visu alized on a film of the entire lower limb. In
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later stages the X-ray signs of osteoarthritis are seen in the medial joint surfaces (narrow ing of the joint space, marginal osteophytes, sclerosis, etc.) (Fig. 29.3.). Treatment. The etiology should be identi fied and the deformity should be prevented (e.g. recognition and treatment of rickets, osteomalacia and osteoporosis). A mild defor-
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mity detected in a toddler does not require treatment. At a later age, the marked varus is presumed to be a prearthrotic factor, warrant ing a surgical solution. Corrective osteotomy is performed at the metaphysis near the punctum maximum of the deformity, most of ten on the tibia.
29.6.2. Tibia vara epiphysarea (Blount's disease) This is a relatively uncommon disease, which involves dysostosis of the proximal epiphysis metaphysis of the tibia, resulting in a varus knee deformity. The rapidly progress ing varus deformity usually starts in child hood, occasionally around the age of 1 0 years (Fig. 29.4. a, b). The treatment in tall children is temporary closure of the distal growth plate with staples (epiphyseodesis), or usually valgus tibia osteotomy. Because of the pro gression of the condition the operation must sometimes be repeated.
29.6.3. Genu valgum - crus valgum
a b
Fig. 29.4. Bilateral severe Blount disease with varus deformity. a: Clinical picture. b: X- ray image
I n cases o f valgus knee, the axis o f the thigh and the axis of the leg enclose a lateral con vex angle i n the frontal plane (Fig. 29.S.). The distance between the medial ankles with the knees closed together is considerably in creased. In childhood, this deformity is often physiological, and at the age of 8- 10 sponta neous correction is expected.
Etiopathoiogy. The condition may be of idiopathic or known origin. The causes can be similar to those of varus knee, but resulting in the opposite deformity: - Metabolic bone disease e.g. rickets (but this usually causes a varus deformity). - Dyschondroplasia, and multiple exo stosis. - Connective tissue weakness, and loose ligaments. - Damage to the lateral part of the distal femoral growth plate (osteomyelitis, tu mor, trauma or injuries).
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- Malunited femur o r tibia fractures with an axial deformity. - Muscle paralysis. - Loosening following medial collateral ligament injuries. - Compensation (as a consequence of an adduction hip contracture) . Clinical symptoms. When the knees are closed together, the medial ankles can not come into contact, and the patella is turned upward. This is recorded in centimeters. The valgus is the most common deformity of the knee joint; it is often associated with recurvatum. In toddlers, this situation is not considered abnormal if the distance between the medial ankles is not more than 5 cm; it corrects spon taneously by the age of 8- 1 0 years. Valgus knee is usually associated with mild valgus heel, and the parents take the child to the doc tor not because of any complaints, but be cause of the ugly gait. In these cases, only a supination heel elevation and foot exercises are needed. In adults, a pronounced valgus deformity is a prearthrotic factor (Fig. 29.5.). Early
chondropathy and osteoarthritis can develop, with knee instability, leading to serious com plaints. X-ray signs. The extent of the deformity is well visible on weight-bearing films. In a later stage, evidence of osteoarthritis is seen in the lateral compartment. Treatment. It is important to determine the cause and to treat this condition early, be fore the deformity develops. In more serious cases, surgery is advised: If the growth plate persists, temporary epiphyseodesis with sta ples in the medial side (Blount ' s procedure) is possible. Corrective varus osteotomy can be carried out on either the femur or the tibia, as described in the Chapter 29.6. 1 .
29.6.4. Torsion of the tibia Varus and inward torsion of the tibia is a common condition under the age of 1 year, and later it can improve spontaneously (see Chapter 1 2) .
29.7. Aseptic osteochondroses around the knee 29.7. 1. Osteochondritis dissecans genus
-' UIII�....lI..Q9&
Fig. 29.5. I n valgus deformity, the loading axis is lateralized, and the lateral compartment of the joint is there fore overloaded.
This entity i nvolves aseptic bone necrosis which occurs in the joints. In the majority of cases it affects the lateral part of the medial tibial condyle. The necrotized cartilage - bone piece may be detached, forming a loose body and leaving a crater-like hollow 1-2 cm in di ameter in its place. It is observed in young adults, i n half of the cases bilateral ly.
Etiopathology. The cause is not clear: roles may be played by constitutional factors, repeated micro injuries (athletes), circulation anomalies, and the closure of end-arteries. Clinical symptoms. Initially mild pain and swelling are experienced, the flex ion may
29. D i s o r d e r s of the k n e e
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be restricted, and the limit may be painful. If the necrotized osteochondral piece is partially detached, the condition may mimic a meniscal tear; if it is fully detached, forming a loose body, it may cause a joint block or become palpable. X-ray signs. The anteroposterior views of the knee, or rather the special views, show a bean-shaped bony body measuring about 3 cm on the lateral side of the femoral condyle. Treatment. If the disorder is in an early stage, the extent is limited and the joint con gruence is intact (MRl scan), the cessation of overloading (sport) may result in spontaneous healing, especially in adolescents. If partial detachment occurs, the surface of the crater is refreshed, the necrotized parts are removed and the fragment is fixed with absorbable "pins" in an arthroscopic procedure. If the crater is too large and predominantly involves the weight-bearing surface, autologous or ho mologous grafting may be indicated.
29.7.2. Osteochondritis of the tibial tubercle (Schlatter-Osgood's disease) Schlatter-Osgood's disease is juvenile osteochondrosis of the tibial tubercle. It is most common in the age range 1 1- 16 years and affects both boys and girls.
Etiopathology. This is aseptic bone ne crosis of the tibial tubercle. Clinical symptoms. The complaints often start following heavy loading or after direct pressure on the tibial tubercle. Forced knee extension against resistance may elicit pain. A swelling is seen over the tibial tubercle, but other signs of inflammation are missing. X-ray signs. The lateral view of the knee the apophysis of the tibia is fragmented, scle rotic and protruding (Fig. 29.6. a, b).
Schlatter-Osgood disease.
a. The lateral X-ray picture shows the tibial tubercle as an independent bony fragment. b. Characteristic prominent tu bercle when the knee is bent.
Treatment. The ossification disorder usu ally heals in 2 years. It responds well to con servative treatment, several weeks or months of rest, avoidance of physical exercises, occa sionally cold compress, creams, and non steroidal anti-inflammatory drug administra tion. In stubborn cases, a plaster cast up to the groin may be applied for 4 weeks. The com plaint may recur up to the end of growth at around 1 8-2 1 years, when the tibial tubercle
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unites with the tibia. If the tibial tubercle pro trudes to a maj or extent· and disturbs the pa tient during kneeling, the persisting bone frag ment is excised.
29.7.3. Adu lt aseptic femur condyle necrosis (Ahlbiick's disease) Spontaneous aseptic osteonecrosis usually starts after the age of 60 years on the load bearing area of the medial condyle of the fe mur, less frequently of the tibia . .
a b
Fig. 29.7. A 71-year-old female with necrosis of the right medial femoral condyle (M. Ahlbiick disease). a: Anteroposterior X-ray picture; the joint su rface of the medial femoral condyle is flattened and cracked (arrow). b: MR shows the intraosseal extent of the necrosis. c: I ntraoperative picture: the almost separated femoral su rface is visible; the cartilage of the knee is intact else where. d: Unicondylar prosthesis inserted (immediate postopera tive film).
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Etiopathogenesis. The reason is unclear. It is usually unilateral, and the extent is al ways larger than in juvenile osteochondritis. It often results in varus knee. Symptoms. The knee becomes progres sively more painful, and the range of move ment is extremely restricted. The diagnosis is established by X-ray examination. The surface of the condyle is uneven, later becoming flat. The MRI scan illustrates the extent of the defect (Fig. 29.7. a-d) . Treatment. Condyle necrosis in the el derly warrants sledge prosthesis insertion.
29.8. Knee contractures Flexion may be restricted (extension contracture), or extension may be restricted (flexion contractu re), or both may be limited, for many reasons. The contracture may be due to a muscu lar disorder, an innervation anomaly or shrinkage of the capsule, the liga ments or the skin. A special form is postoper ative arthrofibrosis (fibrous a nkylosis).
Etiopathology: - Inflammation and swelling - Trauma and distortion - Neuromuscular diseases (Heine-Medin disease, or infantile cerebral paresis) - Congenital anomalies (knee dislocation) - Bums or scars after operations or InJunes - Arthrosis - Tumors adj acent to j oints - Iatrogenic or repeated knee operations
Flexion contractures and spasms of the knee muscles are most common in cases of in fantile cerebral palsy Extension contractures of the knee are dis cussed separately. Etiopathology. The cause of its congeni tal form is unknown; it often appears with other developmental abnormalities. The
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flexion is limited t o 1 0-20°. The quadriceps femoris muscle is fully or partially shortened. The most common cause of the acquired form is the scarring that follows antibiotic inj ec tions into the thigh, or the m. vastus lateralis or intermedius in infancy. Clinical symptoms. The child walks with a stiff knee, and the hip is therefore abducted and externally rotated. The child is unable to squat, and keeps the knee extended while sit ting. The thigh circumference is less than on the other side, and the quadriceps muscle is atrophic, and scarred. One special form of this extension contracture is isolated shortening of the m. rectus femoris, which can be congenital or a consequence of inj ections. The symptoms are similar to those mentioned above. This mus cle bridges over two joints, and the physical findings are therefore different when the hip flexed or extended. If the child is supine, the knee flexion seems to be complete with the hip flexed. In the prone position with the hip extended the knee flexion may be only 5 - 1 0°, and further flexion is possible only with flexion of the hip. Treatment is surgical, the tendinous part of the hip flexor/knee extensor muscles being lengthened above the knee.
29.9. Fluid accumulation (effusion) i n the knee This condition causes swelling of the suprapatellar pouch, patella ballottement and restriction of the range of movement. The fluid may be serous (hydrops), bloody (hemarthros) or inflammatory (serous, sero fibrinous or purulent) . Genicular synovitis may be due to: - bacterial infection (via direct or hematogenous spread) - viral infection - specific conditions (e.g. tuberculosis)
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Genicular abacterial synovitis may b e due to:
- postbacterial allergic processes (tran sitory arthritis) (rheumatoid diseases - rheumatic arthritis, etc. ) - metabolic diseases (gout, ochronosis, pseudo-gout, etc.) - osteoarthritis - post-traumatic joint deformities - neural diseases (syringomyelia, neurosyphilis, etc. ) - tumors adj acent t o j oints Hemarthros may be due to: - hemophilia (spontaneous bleeding or microtrauma) - hemorrhagic diathesis - trauma (fractures involving the j oint or cruciate ligament and meniscus rup tures) - a tumor or tumor-like condition in vading the j oint (e.g. villonodular synovitis ) . Clinical symptoms. In acute synovitis, the knee is swollen and hot, and the skin is red. The suprapatellar pouch is swollen, and patella ballottement is detected. Diffuse ten derness and strong pain are present. The range of movement is severely restricted; the joint may be blocked in mid-position. In chronic synovitis, the severe pulsating pain and the hot skin may be missing. The joint may be "dry", when patella ballottement is absent, but the knee is swollen due to the thickened synovial membrane, and the parapatellar fossa is smoothed. In the form where considerable amounts of synovial fluid are secreted, the patella ballottement is pres ent, the amount of fluid may reach 1 50-200 ml. The range of movement is moderately re stricted. The X-ray signs are not characteristic; the j oint space may be widened, but there is no di rect evidence relating to the basic disease. MRI and ultrasonography may give more in formation (loose body, tumor, etc .) .
Treatment. The exact diagnosis and the underlying condition must be established. In cases of post-traumatic hemarthros (if this is proven by joint puncture), acute knee arthroscopy may be performed. Diagnostic joint puncture is usually considered neces sary. The aspirated fluid is sent for laboratory tests (to detect crystals, proteins, leucocytes, fungi, LE cytes, bacteria, etc.). The local treatment depends on the source illness, e.g. conservative treatment is preferred in primary osteoarthritis, whereas in rheumatoid arthri tis, if conservative treatment fails, syno vectomy is advocated. If pus is evacuated via the puncture, the subsequent therapy is in ac cordance with the treatment of acute or chronic bacterial synovitis outlined in Chap ter 1 9. 3 . 5 . 1 .
29.10. Cl'.sts in the knee region Cysts are common in the knee region. They may communicate with the joint, have a synovial lining and contain thickened synovial fluid.
29. 10. 1. Ganglion This type of cyst is common in the knee re gion, and also in the wrist, ankle and foot. It originates from the tendinous parts of the extensor muscles attached to the fibula head, with a size between 4 and 7 cm, and is easy to palpate. Exposure reveals a membranous cyst with a yellow, gelatinous content. Surgical re moval is advised, but recurrence is common.
29.10.2. Meniscus cyst This is a degenerative cyst, ongmating from the meniscus; it is 7 times more common laterally. Clinical symptoms. In young adults a thick nodule may be palpated at the lateral j oint line, possible be accompanied by im pingement, a click, and a blocking sign, char-
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acterized by a meniscal tear. It may be ob served at the edge of the meniscus or within the meniscus, when it is not palpable, then ne cessitating arthroscopy or an MRI scan. Treatment. Surgical removal of the me niscus cyst is recommended, in some cases with the entire meniscus. The residual menis cus may result in recurrence.
29.10.3. Popliteal cyst (Baker's cyst) This cyst, containing thickened synovial fluid, appears in the popliteal fossa on t he basis of processes causing chronic synovitis in the knee joints of adu lts. It is usually connected with the joint. Both genders are affected. It is also frequent in chi ldren. The cause is un known.
Etiopathology. This is not clear. Weak ness of the posterior capsule is assumed, for the synovial membrane may protrude by this route. On the other hand, chronic synovitis is considered to play a role, and based on an intra-articular cause (osteoarthritis, loose body, tom meniscus, etc.). It is often seen in rheumatoid arthritis. Clinical symptoms. At the outset the complaints are vague. Squatting is difficult, a
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and some radiating pain may appear. The cyst "expands" in osteoarthritis, following an overload, longer weight-bearing, and be comes palpable in the popliteal fossa (Fig. 29-8. a, b); during rest it decreases in size. The cyst is connected with the knee joint and an increase in knee j oint pressure pumps synovial fluid into the cyst. Later, the connec tion may become unidirectional and work as a vent, when no fluid may return from the cyst to the joint space. The size of the cyst may be constant or increasing. It must be differenti ated from aneurysms and tumors by ultra sonography, which is easy to perform and has 95% surety. In the event of doubt, an MR scan is performed. Treatment. The cause of chronic syno vitis of the knee must be eliminated first. If there are complaints, surgical removal is ad vised. In adults, recurrence is common, espe cially if the chronic synovitis of the knee per sists.
29. 10.4. Bursitis praepatellaris This is chronic inflammation of the prepatellar bursa, usually due to excessive mechanical loading (kneeling occupations, mason, or parquet layers). The inflammation may be acute, chronic, serous or rarely puru-
b
a: b: Intraoperative picture of the cyst, with a membranous wall and a transparent content.
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lent. The skin over the kneecap is hot, red, ten der and hyperkeratotic; the size of the swell ing varies between 7 and 1 0 cm. Treatment. In acute cases, the limb is put at rest, and a cold compress is applied, which together with aspiration, may heal the pro cess. In purulent bursitis, incision, drainage and surgical excision may be the solution.
29. 1 1. 1 . Col lateral ligament injuries Etiopathology. These injuries may be classified in terms of the extent of the force and the damage: overstretching of the liga ment which does not result in instability (sprain or distortion); or partial or total rup ture. The latter may involve the ligament itself or the bony attachment can be broken out. In ruptures, the damage usually disrupts differ ent layers of the ligament at different heights . A purely lateral force may result in a contralateral collateral ligament rupture to gether with tearing of the adj acent capsule, causing simple or uniplanar moderate knee in stability. More common is the complex rota tional knee instability that arises when the force acts in several planes . Flexion - valgus external rotation injuries lead to anteromedial instability, usually with simultaneous tearing of the medial collateral ligament, anterior cruciate and medial meniscus ("unhappy triad ''), sometimes associated with tearing of the capsule and the posterior oblique liga ment. Less frequent are the flexion - varus internal rotation injuries, when the lateral cap sule, lateral collateral and anterior cruciate ligament are damaged, with consequent anterolateral knee instability. Hyperextensive forces or injuries forcing the head of the tibia dorsally cause posterior instabilities, which may likewise be combined with medial, lateral and rotation components, as above. In extremely high-energy injuries (e.g. a traumatic knee dislocation), the complexity is even greater: the anterior and posterior com ponents are combined with lateral elements,
possibly aggravated by bone, vascular, neural and tendon injuries. Clinical symptoms. In fresh injuries pain, swelling, hemorrhage and direct tenderness to palpation are detected along the path and over the attachment of the collateral ligament. Iso lated collateral ligament rupture can not be identified with the knee fully extended, since the strong posterior capsule partially takes over the function of the collateral ligament. Accordingly, the test for the integrity of the collateral ligaments is performed at 1 0-200 of flexion, with valgus stress for the medial, and the varus test for the lateral collateral liga ment. In the event of damage, mild ' opening' is detected in response to the above stresses, denoted by , +, ++ or +++, depending on the extent of the ill-defined movement. In cases of isolated collateral ligament tears the intact cruciate limits the mild ' opening' to + or ++ ; in cases of +++ ' opening ' , therefore, cruciate and oblique posterior ligament ruptures are also present. To substantiate these findings, X-ray examinations can be performed, the joint being hold in a stressed position (the pain-induced muscle spasm may hide the in stability) . In cases of doubt, ultrasonography and MRI can be added to confirm the diagno sis. -
Treatment. Isolated tears of the collateral ligament can be treated conservatively be cause of the excellent blood supply due to the location of this ligament. Bone disruptions are treated surgically.
29. 1 1.2. Chronic collateral ligament insufficiency Etiopathology. This is exceptional as iso lated damage; it usually occurs following the partial healing of a complex ligament rupture. In the majority of cases, it is an element of an anteromedial or posterolateral instability. The following additional factors may lead to a chronic knee collateral ligament insuffi ciency:
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- a marked varus or valgus deformity - a marked hip abduction or adduction contracture as a compensatory symptom - rheumatologic diseases - arthrosis Clinical symptoms. An isolated collateral ligament insufficiency elicits a moderate varus or valgus instability feeling, which pres ents during a physical load, sports activity or walking on uneven ground as an occasional knee distortion. The main complaint is the feeling of a lack of stability. Stress X-ray ex amination, ultrasonography or MRI may con firm the diagnosis. Treatment. The treatment depends on the degree of instability and naturally the associ ated injuries. Ifthe lateral instability is signifi cant, surgical treatment of the associated inj u ries (anterior or posterior cruciate ligament re placement, and replacement of the collateral ligament with autologous tendon fixed via bone holes) can be considered. The latter is a very delicate task, how with regard to how to position the graft isometrically. The best re sults are achieved laterally by cutting the bi ceps tendon in half, and medially by using one of the hamstrings.
Outline of the anterior cruciate ligament rupture.
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29. 1 1.3. Cruciate ligament inju ries These lesions are o bserved following a trauma; they lead mainly to various extents of sagittal i nstability of the knee.
Etiopathology. Cruciate injuries occur from the action of complex forces exerted in the sagittal plane; they may be isolated or as sociated with injuries of other components (Fig. 29.9.) . Injury to the anterior cruciate lig ament (ACL) is 1 0 times more common than one to the posterior cruciate ligament (PCL). The ACL usually undergoes tearing in the middle third of the ligament, and the ends are fringed, resembling a broom. Bony abruption is distal and more frequent in children. Clinical symptoms. These include pain, swelling, blood accumulation and instability, which may cause an inability to bear weight. In fresh cases, locking of the joint or an exten sion deficit may also occur, caused by the im pinged ligament parts. In chronic ACL or PCL inj uries, the patient often describe an in stability feeling, even on horizontal ground (the knee occasionally gives way), but it is more pronounced on uneven ground when the direction is changed.
\
Fig. 29.9.
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Fig. 29. 10. Drawer sign.
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In chronic cases, there are only slight signs of instability. The sagittal stability of the knee is characterized by the drawer sign, which is limited in fresh cases in muscular patients be cause of the pain due to the fixing ability of the active stabilizers. In cases of an ACL tear, the head of the tibia can be moved anteriorly on the femoral condyles to various extents with the knee flexed at 90°. This is the anterior drawer sign, and its extent is denoted simi larly to the lateral instability, on a +, ++ and +++ scale (Fig. 29.1 0.). In PCL injuries in the same flexed position the head of the tibia may be displaced posteriorly because of the rup ture. From this position, it may be reduced to normal and redisplaced posteriorly (posterior drawer sign). This may be pseudo-positive due to the general joint laxity: a comparative assessment with the other knee is advised. Ultrasonography may suggest cruciate lig ament injuries; the MRI almost certainly proves them. Treatment. Acute reconstruction of the ligament is not advised, even in fresh cases, because of the frequent failures. The only ex ception is distal bony abruption of the liga ments, which is currently treated with anchor ing of the abrupted bone and the attached liga ment. In the other cases, the first procedure is arthroscopy (treatment of other intra-articular injuries, meniscal tears and hyaline surface damage, and careful limited resection of the tom, impinging fibers of the cruciate) ; then conservative therapy is advised. Satisfactory stability may be achieved by training of the thigh muscles. When long-term conservative treatment does not terminate the patient ' s complaints of instability and a limited ability to bear weight, if the patient is younger than 50, ACL or PCL replacement may be per formed. The improving results of arthroscopic lig ament reconstruction have led to these proce dures becoming increasingly popular all over the world. This is supported by the observa tion that injured patients who have no instabil ity feeling may exhibit a certain "micro instability", and ACL or PCL-injured knees
therefore degenerate faster and severe carti lage wear may take place within a few years. The main role is definitely played by autologous grafts. Occasionally (especially in revisions), allografts may be used, but the ear lier popular plastic ligaments are no longer recommended. Ten years ago, the bone patellar tendon - bone graft was applied al most exclusively, whereas the positive experi ence has resulted in the replacement being carried out nowadays with four times folded semitendinous tendon, twice folded se mintendinous + gracilis tendon, or rarely quadriceps tendon grafts (Fig. 29. 1 1 .). During this procedure, which is usually performed
us grafts: the semitendinosus tendon is seen above, and the bone - patella tendon - bone
, - -..,- - � - ---,
Arthroscopic picture 1 year after insertion of a four times folded semitendinosus tendon graft.
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arthroscopically, the most important goal is the isometric position and stable fixation of the graft. To achieve this, interference screws are utilized in bone - patellar tendon - bone grafts, and (semintendinous + gracilis tendon) plates, staples, anchors and other special fix ing elements are used in cases involving ten don use (Fig. 29.1 2.).
29. 1 1.5. Meniscal tear These are very common i nj u ries of the knee. The meniscus becomes trapped between the femoral and tibial condyles and sustains rup tures varying in extent and loca lization.
Etiopathology. The mechanism of the in jury is usually a rotational force : while the leg
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is fixed, the femur is rotated inward or out ward. The femoral condyles push the menisci in front of them, and the meniscal edges may become trapped between the contacting joint surfaces. Predisposing factors are earlier or concomitant ligament injuries (most often the ACL), and axial deformities of the knee (genu varum, valgum or recurvatum), and the exten sively loose joints. In cases of osteoarthritis or rheumatologic conditions and in the elderly, degenerative changes of the menisci may result in frequent tears as a result of the repeated microtraurnas . I n the majority of cases (90%) the medial me niscus is involved, which is the less mobile, as it is anchored to the medial capsule and collat eral ligament. The tear takes place most often at the posterior horn and in the middle part of the meniscus (Fig. 29. 13. and 29.1 4.). Regardless of whether if the tear is lobular or bucket-handle-shaped, its interposition be tween the loading surfaces causes gradual hyaline cartilage damage. Clinical symptoms. In a typical case, the patient has a history of sports injury or trauma. Impingement during physiological motion relates to previous degeneration. The injury causes strong pain and is accompanied by the accumulation of serous j oint fluid. Blood accumulates when the meniscus is tom
Normal menisci (a). Longitudinal fissu re (b) and bucket-handle tear in the medial meniscus (c).
Arthr(),rnnir picture of a bucket-handle tear and
impingement of the medial meniscus.
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29. D i s o rders of the knee
a t the base. One of the most important symp toms, which is often missing, is the joint lock due to the impingement of the tom part of the meniscus. In chronic cases, very little or no fluid may be accumulated, and the patient ex periences repeated locking and painful clicks in response to certain movements . The joint space is tender to direct pressure. In cases of suspected meniscal injury, the ligaments of the knee must also be assessed. X-ray signs. The ultrasonographic and MRI images reveal the location of the meniscal tear with relatively high accuracy. Treatment. Resection and particularly full excision of the menisci predisposes to osteoarthritis . The basic principle of the surgi cal treatment is to remove only the irreparably tom parts. Unfortunately, partial resection of the meniscus is a necessary intervention in most cases. At present the meniscus operation is almost exclusively performed arthro scopically. In young individuals, fresh and not too long tears may be reconstructed if they are lo calized near the base (this meniscus substance has a blood supply); this involves arthroscop ic resuturing of the meniscus. Reinsertion of the meniscus is possible only in a small pro portion of the cases and resection is usually considered necessary. The practice in these cases is removal of the tom, impinging parts of the meniscus and smoothing of their base with a shaver. If there are extensive ruptures near to the base in youngsters, and the j oint is otherwise intact, the expected osteoarthritis may be prevented by implantation of a fresh meniscus allograft. �
Cartilage damage The sliding surfaces of the knee j oint are covered with hyaline cartilage, which has ex cellent mechanical and weight distribution qualities, but a very poor disposition to regen erate (Chapter 1 9.8). There are zones of this surface which are heavily loaded, and others which bear less weight. The maximal load affects the central
areas of the femoral and tibial condyles; the peripheral areas which are covered by the menisci and the parts next to the intercondylar eminences are loaded with somewhat less weight. The 4-5 -mm-thick hyaline cartilage is un changed structure and is an excellent buffer: it ensures movement with almost no friction for many decades. On the other hand, if this struc ture is damaged, it has a very poor disposition to heal spontaneously.
29.13. Chondromalacia patellae This d isorder (involving early degenerative changes) has long been known, its name char acteristica l ly meaning softening of the carti lage su rface of the kneeca p.
Etiopathology. This clinical picture is only the introductory stage to a progressive degenerative process: the same clinical diag nosis applies to the more advanced stage of patella cartilage damage. For grading of the cartilage damage, the Outerbridge classifica tion is the most popular. In stage I, the cartilage softens, but its surface remains smooth; its color may differ from that of the adjacent. In stage 11, the surface becomes "hairy", i.e. covered with small villi, and the involved area loses its shine. Small superficial fis sures may be present. In stage 111 the degeneration progresses, and the fissures become numerous and spread through the entire thickness to the bone. Stage IV is characterized by large defects ex tending deep to the bone, resulting from the action of shearing forces on the dam aged, cracked cartilage surface.
The latter two stages are regarded as the initial stages of osteoarthritis (see Chapter 1 9 . 8 .). Biomechanical factors often play a role in the development of patella chondromalacia. In a large proportion of the cases, formal de-
2 9 . D i s o rd e r s of t h e k n e e
Fig. 29.15. Patellofemoral arthrosis with lateral hyperpression syndrome.
fects are present: incongruence of the patellotrochleal junction, anomalies of the traction route of the quadriceps (increased Q angle), and a high or low position of the knee cap (patella alta or patella baj a), with repeated luxation or subluxation as a consequence of the former factors, or patellofemoral hyper pressure (Fig. 29.1 5.). Exposure of the knee cap to a direct or indirect trauma leads to hyaline contusion, contusion and hematoma of the subchondral bone or an occasional pa tella fracture. In a large number of cases, none of these factors can be identified; these cases are classified as idiopathic. This is often the situation with young schoolgirls who do not play any sports, when severe hypotrophy of the vastus medialis muscle is observed. Clinical symptoms. Walking up or down stairs, or standing up from a squatposition may produce severe retropatellar pain, and later prolonged flexion without loading may also cause complaints. A long period of sitting with the knees flexed can produce complaints that are known as ' drive-in movie sign ' . Fluid accumulation is not common. Direct pressure on the kneecap, tapping or attempted sub luxation, either laterally or medially, pro vokes pain (the Frond and Zohlen signs). It is important to assess the angle between the di rection of traction of the quadriceps apparatus and the axis of the patellar ligament (Q-angle). The mobility and possible ten dency of the kneecap to undergo dislocation must also be assessed. X-ray signs. X-ray tests play a decisive role in the identification of etiology. In the lat-
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era I view, the high o r low position of the knee cap, or the relative length of the j oint surface (the Blackburne or Insall-Salvati indices) may preconditioning factors. Patella lateralization too may be visualized in accurate antero posterior X-ray images, and the patello femoral views taken at 3 0-60 and 90° of flexion may demonstrate the pathologic match in the different phases of motion. The congruency disturbances relating to the shape anomalies of the patella or the trochlea are of great importance. Treatment. Apart from those cases where there is a severe biomechanical background, the therapeutic approach is basically conser vative. Rest, nonsteroidal anti-inflammatory drugs, various physiotherapeutic processes (iontophoresis, ultrasonographic treatment, selective current stimulation of the vastus medialis, etc.) and well-selected exercises play a deciding role. The most important fea tures are the strengthening of the vastus medialis and of the entire quadriceps muscle, and proprioceptive exercises. Underwater ex ercises and bicycling are useful supplements. If the conservative attempts fail, or if a well-defined biomechanical cause is proven, operative treatment may be considered. The most common procedure is minimally inva sive arthroscopy, when the surface changes exceeding stage 1 1 are smoothed with a shaver, and the patellofemoral pressure condi tions in cases of hyperpression are advanta geously affected by incision of the lateral retinaculum. In stubborn or severe cases, the tibial tubercle may be ventralized to correct the direction of patellofemoral traction.
29. 14. Chondropathies, osteoarthritis (arthrosis) of the knee A lengthy series (many yea rs) of pathologic events usua l ly occur from the mild cartilage damage (chondro pathy) to the end-stage (osteoarthritis o r a rthrosis of the knee).
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I n itially, macroscopic changes take place i n t h e carti lage, followed b y deformation a n d destruction o f t h e joint, involving t h e majority of the adjacent structu res, resulting in a re stricted range of movement and pain.
Etiopathology. Primary osteoarthritis of the knee is the most common process destroy ing the large j oints, followed by hip and shoulder degeneration. In the age group over 65 years, the radiological prevalence is 20-34%, but only 7- 1 1 % require treatment of their complaints . The diagnosis is secondary osteoarthritis of the knee, when the destruction is due to a previous illness, trauma or biomechanical anomalies . The most common factors are: - instability (rupture of the collateral or cruciate ligaments, meniscectomy, capsule tear, or a change in muscular balance in neuromuscular disorders) - overweight - axial anomalies - meniscal injuries, or loss - rheumatologic diseases - inflammatory or metabolic diseases - overloading - a post-traumatic state
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- osteochondritis dissecans, or loose joint bodies One of the most common causes is knee j oint instability, when abnormal, pathologic joint movements occur leading in a vicious circle to destruction of the cartilage (Fig. 29.1 6.). The destruction of the cartilage alters the biomechanical conditions and causes inflam matory and reactive changes; the hyaline sub stance may disappear, and subchondral scle rosis and cysts may develop accompanied by osteophyte formation in the non-loaded areas and contractures of the joint capsule. Clinical symptoms. When the changes in volve only the cartilage and a limited area, the symptoms are said to be moderate. The most characteristic symptoms are a decrease in load-bearing, intermittent fluid accumulation, pain, tenderness of the involved compart ment, click and crepitation. Later, the swell ing and fluid accumulation become more common, pain is present even in the resting period, the range of movement decreases and the joint gradually becomes deformed. In the maj ority of cases, the axial anomalies of the knee joint give rise to a severe varus defor mity with flexion contracture.
i n sta bi lity of the knee
path ologi ca l movements
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2 9 . D i s o r d e rs of t h e knee
X-ray signs. Anteroposterior X-ray films in the loaded position provide indirect data on the thickness of the cartilage of the weight-bearing surfaces in extension. The Rosenberg views at 30° of flexion furnish in formation on the quality of the posterior parts of the joint surface. As the condition pro gresses, the joint space diminishes or disap pears, the subchondral bone undergoes sclero sis and peripheral osteophytes are formed. Treatment. The process of primary osteoarthritis of the knee usually lasts for many years from the first complaints to the end-stage of the joint destruction. During this period, the symptoms are present with various intensity, the painful stages of inflammation alternating with long symptomless periods. Initially, conservative treatment is advised. The aim is to decrease the symptoms and signs and the contractures. Nonsteroidal anti-inflammatory drugs, muscle relaxants and painkillers are prescribed, together with oral chondroprotective medication (glucose amine sulfate and chondroitin sui fate ) and a
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Fig. 29.17. Closing-type valgus high tibial osteotomy. a: Preoperative loaded anteroposterior view: mild varus deformity. b: Six months following the closing-type valgus high tibial osteotomy (lateral based wedge removal and staple fixation).
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intra-articular hyaluronic acid. Adjuvant ther apy may include cooling, electrotherapy, vari ous iontophoreses, the use of ultrasound and medical spa treatment. The most significant therapy is movement of the j oint without a load, swimming and underwater exercises, the aim of which is to improve the knee func tion and resolve the contractures. The surgical treatment in prearthrotic chondropathies can be divided into two cate gories. One category involves treatment of the biomechanical factors presumed as prea rthrotic factors, while the other deals with the existing cartilage damage. In the former group, the correction of mainly varus and rarely valgus axial deformities is of great im portance. The varus deformity occurs chiefly on the tibia. The correction is most often a clos ing-type high valgus tibia osteotomy with re moval of the laterally based wedge proximal to the tibial tubercle (Fig. 29.17. a, b); more rarely, a varus osteotomy is carried out in the same area with the opening of a medial wedge (Fig. 29. 1 8. a, b). Apart from these techa
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���:;:;:" valgus high tibial osteotomy. a. preoperative loaded a nteroposterior view: mild varus deformity. b. Six months following the high tibial osteotomy, the axis is good and the osteotomy has healed.
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29. Diso rders of the k n e e
a b
Fig. 29.19. "Microfracture" technique: arthroscopic picture.
niques, dome-shaped or sphere osteotomies are also performed, allowing minimal rota tional correction. For the treatment of carti lage damage, arthroscopic debridement and lavage may be of value, but only for short pe riods. The sliding surface reconstruction of limited, local cartilage defects (hyaline and osteochondral defects) is attempted by one of the surface reconstruction techniques, such as Pridie ' s procedure, abrasive arthroplasty or mosaic plasty. Via small holes made with a sharp surgical awl, radial fissures are created in the bone, forming an ideal attachment sur face for the regeneratum. The most important elements of the postsurgical aftercare are 4-8 weeks of movements without weight-bearing and a further 2-4 weeks of partial weight bearing. The popular procedure of ' micro fracture' is performed arthroscopically, even in cases of multiple degenerative cartilage de fects (Fig. 29.1 9.). In optimal cases, a satis factory gliding surface can be created, rich in collagen fibers of types I, IX and X. The other direction of cartilage surface creation is the treatment of the circumscribed small and medium-sized full-thickness hyaline defects. In these cases, the aim is to produce a hyaline-type and quality sliding surface instead of the above-mentioned fi-
Fig. 29.20. Open mosaic plasty on the lateral femoral condyle. 2 a: 4 cm bony defect caused by osteochondritis b: the defect is filled with grafts 4.5 mm in diameter.
Fig. 29.21. Arthroscopic view of mosaic plasty performed 5 years earlier on the medial femoral condyle.
2 9 . D i s o r d e r s of t h e k n e e
a b
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hyaline cartilage and the intermediate fibrous cartilage takes place (Fig. 29.2 1 .) . This is clearly shown by MRI (Fig. 29.22. a, b). The most common indications of mosaic plasty are osteochondritis dissecans, and traumatic or degenerative defects. Because of the limits of transplantation (limited donor sites and technical difficulties), the future solution may be cartilage formation via cell proliferation (autologous chondrocyte transplantation). So far, however, the struc tural organization of the resulting surface is significantly different form that of the joint hyaline cartilage, and a number of technical and financial problems limit the application of this method. The trend of the present technical development is the integrated use of holding matrices (scaffolds) and biologically active hyaline-inducing materials. The best outcome is expected at present from the transplantation of fresh osteochondral grafts. �
Fig. 29.22. MR view of the mosaic plasty. (29-27 a b) a: Preoperative sagittal MR view of osteochondritis dissecans on the lateral femoral condyle. b: 20 weeks following mosaic plasty.
brous cartilage surface. The ' mosaic plasty' procedure (introduced by L. Hangody) has been performed in a large number of cases since 1 992. Small cylindrical osteochondral grafts ( 1 -4 cm2 ) replace the damaged surface of the loading area (usually arthroscopically) to ensure congruent surface reconstruction and to decrease the damage to the donor site (Fig. 29.20. a, b). During the postoperative period, fibrous cartilage produced between the transplanted cylinders in the transplanted area, generating a composite gliding surface, where the integration of the transplanted
Surgical solutions in osteoarthritis If the degenerative processes are severe and extensive, it is too late for the procedures listed above and a good result cannot be ex pected. Arthrodesis, the stiffening of the de stroyed j oint, is not well tolerated nowadays, even if this procedure eliminates the pain. Re moval of the cartilage and lasting fixation of the joint can fix the bony elements and stop the pain, but the joint function is lost. The stiff
Fig. 29.23. I ntraoperative picture of a total bicondylaer knee endoprosthesis.
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Fig. 29.24. Secondary arthrosis due to rheumatoid arthritis. Pre- and postoperative x-ray pictures of total knee prosthesis.
j oint changes the basic dynamics of the gait and exerts an extreme overload on the neigh boring j oints, the contralateral hip and knee j oints, and the lumbar spine, which may lead to early secondary osteoarthritis. Implantation of an artificial joint (endoprosthesis) can lead to a much better quality of life. Depending on the extent of the damage, a part or the entire j oint is replaced. When only the surface of one of the femorotibial compartments is damaged (usually the medial one), a unicondylar (sledge) prosthesis may be indicated (Fig. 29.7.). A precondition of this procedure is the intact state of the ligaments and the other compartments and normal axial circum stances . In cases of severe cartilage damage in volving a number of compartments, the proper solution is implantation of a total j oint replacement (Figs. 29.23. and 29.24.). An im portant precondition of this procedure is the intact function of both collateral ligaments. During surgery, the anterior cruciate ligament
is sacrificed and stability is ensured by the changed geometry of the replaced surfaces. The above-mentioned severe destruction is treated by means of constrained (hinged) prostheses, which permit flexion and limited rotation. These can give rise to complications, as they loosen more often than ordinary pros theses. In a consideration of the indication of an endoprosthesis, it must be borne in mind that the implantation will presumably not be the fi nal solution, and there may well be complica tions. The forces acting at the prosthesis bone junction may eventually loosen the im plant long run (according to present statistics, in 1 0- 1 6 years). This will require revision sur gery, with even higher risks. The chances of sterile loosening are higher for younger pa tients, who generally demand increased phys ical activity. The prostheses mentioned above are designed both with and without bone ce ment fixation. When all the factors are taken into account, prostheses are implanted as late as possible, usually after the age of 60 years.
30.
J a n o s K r a n i cz, Ka l m a n T6t h
Disorders of the foot
30. 1. The functional anatomy and biomechanics of the foot The function of the foot is to transfer body . weIght onto the ground, and at the same time to ensure the mobility necessary for walking : In orde� to meet this twofold requirement, a system IS needed that can withstand large im pacts of pressure, and guarantee good mobil ity and elasticity in response to different dy namic effects . Regarding its anatomic construction ' the foot resembles an arrangement of pillars con nected by a system of arches (Fig. 30. 1 .) . Five longitudinal arches are distinguished from the calcaneus to the metatarsus . The transverse arch is positioned in a medial lateral direction. The arches are maintained by two stabilizing systems : the passive stabiliz ing system, comprising the following ele-
Fig. 30.1. The bony structure of the foot is constructed of arches.
� ents : the joint capsules to connect the joints m the foot, and the collection of minuscule liga�ents to s �pport these j oints; and the dy . . namic stablhzmg system, which is composed of the short muscles in the foot and the set of long muscles originating on the tibia and at tached to the foot. By themselves, neither the passive nor the active stabilizers are sufficient to support the normal arch system, they operate flawlessly only when complementing each other. As mo tion becomes more and more dynamic, the arch system gains increasing significance in each phase of walking. In the heel-strike phase, for example, the arch system acts as a sho � k-absorbe� in order to neutralize a pro portIOn of the mertial forces originating from the contact with the ground. In the push-off phase, the elasticity of the arch increases the strength of the push-off. Computerized pres sure-distribution analyses have unequivocally proven that higher levels of pressure are ex erted under the second, third and fourth metatarsus heads than under the first and fifth metatarsals (Fig. 30.2a), even in the standing phase. The explanation for this is that the t� ick adipose tissue under the sole plays a sig . pressure distribution. This is lllficant role m also indicated by the clinical experience that the atrophy of the adipose tissue of the foot in rheumatoid arthritis patients leads to severe metatarsalgia. During the gait cycle, the pressure factors b�tween �he g�ound and the foot undergo cy clIc modificatIOn (Fig. 30.2b). The force in creases on every area of the sole, but the load inc �eases fr0 t? the rear to the front. The expla . that the middle metatarsals natIOn for thIS IS are longer than the first and fifth. With the lift ing of the heel, the short metatarsals lift off the
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30.2. Foot deformities in childhood
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Identified congenital foot deformities demonstrate an extremely wide range of pre sentations. Depending on the direction of the defor mity, joint contractures occurring in the fron tal or sagittal plane are identified. These may occur in an isolated manner, limited to one j oint, but combined contracture groups are more common. These are well known as uni form diagnoses (e.g. clubfoot or navicular foot).
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30.2. 1. Congenital foot deformities, developmental abnormalities
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Deformities of the foot occurring in the sagittal plane �
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Pes equinus (talipes eq u i nus): the foot is in a plantar flexion position at the a nkle joint. Pes calcaneus: the foot is constantly i n an u pwa rd, dorsal flexed position. Pes cavus (excavated foot): the anterior part of the foot is in a cu rved position compared to the tarsus and the longitudinal a rch is higher than average.
Deformities of the foot occurring in the fron tal plane
ground earlier, and thus the transfer of energy takes place via the metatarsals maintaining contact. The more dynamic the movement, the higher the load on the anterior part of the foot. Walking is a harmoniously structured string of movements resulting from actively coordinated operations of both the upper and lower extremities and the axial muscles. An understanding of each phase of walking is necessary in order for the physician to recog nize deviations, detailed descriptions of which are to be found in the chapter on patient examination (Chapter 4).
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Pes varus: the heels i nvert i nward from the median at the subtalar joint. Pes valgus: the heels turn o utward from the median at the subtalar joint. Pes adductus, metatarsus varus (intoe): the forepart of the foot is bent toward the medial at Chopart's joint. Pes supinatus (inverted foot): the forepart of the foot supinates at Chopart's joint. Pes abductus: the forepart of the foot is bent latera l ly at Chopart's joint.
Congenital foot deformities that occur less frequently: - Cleft foot (the transverse arch is missing). - Developmental abnormalities of the toes : polydactyly, oligodactyly, syndac-
30. D i s o r d e r s o f the f o o t
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tyly, digitus varus, valgus, subductus and superductus. - Different amnion stricture disorders.
30.2.2. Pes equinovarus congenitus (congenital clubfoot) Terminology. This is a case of congenital contractu res affecting all joints of the foot, which can best be described by the Lati n term: p e s equ inovarus add uctus et plantiflexus congenitus (Fig. 30.3). �
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Equinus: A flexion contracture is present in the ankle, the talus in the mal leolar fork is set in a flexed position, and the m. triceps surae has shrunk. Varus: The calcaneus in the subtalar joint is tilted toward the medial and the forepart of the foot, and it is a lso twisted, supinating toward the medial. Supination of the forefoot: As regards the d irection of deform ity, this corresponds to the varus position of the heel, but due to the different position, heel varus and supination of the forepart of the foot a re d isti nguished in clinica l practice. The forefoot may take up a pronated position relative to the heel. Adductus: The forepa rt of the foot bends toward the medial at the Chopart's and Lisfranc joints. Plantiflexus: The a nterior part of the foot is in a further cu rved position as compared to the tarsus at Chopart's joint and the sole is excavated.
Occurrence. Congenital club foot, which is present at birth, is more frequent among males population, the male-female ratio being approximately 2: 1 . Most cases are bilateral, but it occurs with Similar frequency on the left or right side. The incidence in Europe is between 0, 1 -0,2 %, in Hungary, it is 0, 1 25 %. Its incidence demonstrates racial charac teristics. Occurrence among the Polynesian Maoris is 0,6- 0,7 %.
Fig. 30.3. Congenital, severe bilateral clu bfoot, the a nterior part of the foot displays 90° adduction and supination.
Etiology. There are only hypothetical the ories relating to the etiology of congenital structural club foot: �
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mecha nical reasons, endogenous reasons, mu ltifactorial reasons (genetic + environmental effects)
The multifactorial origin is most widely ac cepted, i.e. congenital clubfoot tends to de velop as a result of the joint presence of a ge netic predisposition and environmental effects.
Familial aggregation. Congenital club foot demonstrates a familial aggregation, the risk of multiple occurrence depending on the familial incidence. The higher the number of cases of congenital clubfoot in the index fam ily, the higher the familial incidence, and con sequently, the higher the expectancy ofthe re peated occurrence of congenital clubfoot. Thus, if two siblings are affected, the ex pected incidence among subsequent siblings is 3-5%. If one parent has congenital club foot, the risk is 2%, and if one parent and one sibling
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3 0 . D i s o rd e r s of t h e f o o t
are both affected, the risk of further occur rence is approximately 25%. Pathology. Disease-induced lesions affect all structures of the foot. Diagnosed alter ations of the bones are mostly secondary and are consequences of adaptation to a chronic malfunction. - Changes in shape such as a shortened calcaneus, an elongated talus neck or a wedge-shaped deformity of the navicular bone are most typical. - Regarding the altered articulation of the bones, the twisting of the calcaneus under the talus is significant, it is situated high above the horizontal plane, the talus is in a flexed position, or the navicular bone and the os cuboideum have slipped towards the medial at Chopart ' s joint. - The malleolar fork is rotated toward the medial. - The soft tissue shrinks on the posterior, medial surface and the sole. - The attachment of the tendons widens, and is often atypical. - The tibial muscle mass decreases and becomes atrophic.
Fig. 30.4. Untreated severe bilateral clubfoot. The bursa de veloping on the instep impairs walking.
ward. A toddler, who is able to stand or walk, will position the weight on the outer soles, or even stand on the dorsum of the foot (Fig. 30.4.). In the course of a joint mobility examina tion, the degree of contracture and the passive correction are determined. Feet that are short, with an elevated heel position and a transverse fold of skin behind the heel are indicative of a poor prognosis. The contractures are rigid, the first toe is shorter, and there is pronounced muscle atro phy along the tibia.
Clinical symptoms. Congenital club foot is easily diagnosable at birth due to character istic contractures, it can be said that the foot is "bean-shaped" and turned entirely toward the medial, while the inner sole is concave, the outer sole is convex, the heel is upright, and high located, and often only fat tissue is palpa ble behind the ankle. In severe cases, the sole faces backward, with the instep facing for-
Radiological symptoms. Taking an X-ray picture in order to determine the diagnosis is not necessary, but during treatment proce dures, an antero-posterior (a-p) and a lateral X -ray image should be taken in order to evalu ate the results of conservative treatment and establish a surgical plan.
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Fig. 30.5. The ang les of the tarsal bones diverge char acteristically in case of foot deformities. A de creased angle causes clubfoot and an in creased angle resu lts in navicular feet. (30-9) a: Clubfoot, angle: 0° . b: Excavation, angle: 20°. e: Normal, angle: 35°. d: Flat feet, angle: 50°. 80°. e: Navicu lar foot, angle:
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The X-ray image depicts the position of the tarsal bones in relation to each other and also the shapes and structure of the bones. In order to describe the position of the tar sal bones, the anteroposterior and the lateral talocalcaneal angles are used, which are smaller than normal in patients with clubfoot (Fig. 30.5.). The relation of the posterior and the ante rior parts of the foot can best be described through the talometatarsal and the naviculo metatarsal angles (Fig. 30.6.). Treatment principles �
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Conservative treatment Treatment is primarily conservative: the methods applied a re early passive and active p hysica l exercise, g rad ual correction with plaster casts, o rthoses and specia l footwear. Surgical treatment Ea rly soft-tissue surgery, which is nowadays usually a conseq uence of unsuccessful conservative treatment. Reoperation i n recu rrent cases. Broader surgical i ntervention on soft tissue and bones at a later age. Nursing Organized care should be offered at specialized treatment centers. Regular physiotherapy is carried out until the p hase of foot g rowth ends, after which orthopedic technical support and continuous o rthopedic specia list fol low- u p is needed.
Detailed description of conservative treatment implementation. Passive physical exercises of the foot (unless contraindicated) and correction of the j oints in the direction op posite to the contraction should be com menced immediately after birth. This may be performed by infant ward nurses, physiother apists and parents alike. Stimulation of the skin of the sole (e.g. with a soft toothbrush) will induce active foot movements. The opti mal instance for commencing gradual correc tion with plaster casts is on day 5-7.
Fig. 30.6. I ncreased talometatarsal angle in clubfoot. a: Normal. b: C1u bfoot.
Gradual correction with plaster casts may be implemented according to the Lorenz prin ciples in the following order: inflexion, adduction, supination of the forefoot, varus of the heel and finally correction ofthe equinus. Correction methods aimed at reducing or eliminating all possible contractures (as long as the foot can endure them) are also acknowl edged. In both cases, the achieved result is to be stabilized in a circular plaster cast with the knee in a 90° position and the cast running from mid- or upper thigh to the end of the toes, with the top of the toes left uncovered. Felt sheets should be attached corresponding to the bones running directly under the skin, and the skin itself should be protected with a thin layer of cotton wool. It is advisable to inspect the plastered foot after 20-30 minutes in order to ensure that no blood circulation disorders have arisen. If any such problems are perceived, loosening or re placement of the cast is necessary. The plaster should initially be changed weekly and, after manual exercising, a new circular plaster cast should be applied.
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A t later ages, alternating plaster correction should be applied every 2-3 weeks. Special care should be paid not to place the foot in a "rocking chair" position, which would mean over-correction of Chopart 's j oint and initiat ing subluxation in the dorsal direction. It is advisable to verify the situation by means of an antero-posterior and a lateral X-ray picture. When untreated clubfoot is encountered in infants or early childhood, the conservative treatment applied is identical to that for the newborn. In these cases, gradual correction with plaster casts is merely capable of reduc ing the contractures and the establishment of better conditions for surgical treatment. In recurrent cases of clubfoot or after re peated surgery, the application of a long-term plaster cast may be necessary, sometimes with use of the Kite method (following surgical correction and stabilization of the foot in plas ter, a wedge is removed from the cast after which the cast can be further corrected). A plastic orthosis may be applied at any point after removal of the plaster cast. Following the conclusion of conservative or surgical treatment, the foot and the muscles should be exercised and strengthened, primar ily by means of physiotherapy. Standard shoes are generally adequate for walking, but it may be necessary to acquire antivarus shoes with a straight sole-axis and an elongated inner counter reaching to the front of the shoe. In recurrent cases, an orthopedic shoe spe cially constructed for the patient' s foot may be necessary, with a straight sole-axis, a fron tally extended pronated heel, and a stronger inner counter. �
Surgical treatment Surgical indication . It is a general princi ple, that all structures sustaining contractures should, as far as possible, be eliminated in the course of surgery. Surgery is advised in the fol lowi ng cases: �
After 6 months of age, fol lowing conservative therapy, i n o rder to correct
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residual disorders, dorsal, or dorsa l-inner soft-tissue release. In u ntreated, late cases in older children, or as repeated su rgery for recu rrence between the ages of 1 and 3, extensive soft-tissue surgery or peritalar a rthrolysis may be indicated. Between the ages of 3 and 12, the treatment may be as mentioned above, access being ensured laterally for repositioning of the os navicu lare: calca neocuboidal wedge resection according to Evans, resection of the cuboidal su rface of the ca lcaneal joint according to Lichtblau or calcaneus osteotomy. Above the age of 3 years, muscle transplantation is possible in order to ensure recovery of the muscle ba lance. As soon as the g rowth of the foot has ended after pu berty, wedge resection, subtalar or Chopart's joint a rthrodesis may be carried out. Supramal leolar rotational tibial osteo tomy of the i nverted foot has the aim of palliative correction.
Surgical methods. Dorsal release. This involves "Z" shaped Achilles tendon length ening, dorsal capsulotomy of the ankle and hindfoot joints, and posterior incision of the talofibular ligament. Dorsal and medial release. Posterior tenotomy of the m. tibialis is performed, to gether with the previous interventions, medial and plantar capsulotomy of the talonavicular joint, ad capsulotomy of the frontal and dor sal-medial segments of the subtalar joint, capsulotomy of the naviculocuneiform and the metatarsocuneiform joints. Aspects of physical exercise. These in clude alleviation of contractures, passive cor rective exercise, active exercise, and strength ening of the femur and the foot muscles. Electric stimulation of weakened muscle groups may be performed and the patient may be provided with walking instruction, walking
3 0 . D i s o r d e r s of t h e f o o t
correction, implementation of passive sup porting and stabilizing orthoses, and lifestyle and vocational guidance. Orthopedic shoes should be worn. Suggested sports that ensure regular mus cle strengthening for the feet are short- and long-distance running, cycling and ball games.
30.2.3. Pes adductus The forefoot bends medially at Chopart's joint. The situation is similar to clubfoot, a l though it is well distinguishable, since the heel is not in varus or equ i n us. Although to various extents, the heel is i n a valgus position, and it is therefore often referred to as pes adductus planovalgus.
Occurrence. It is easily diagnosed imme diately after birth. Some consider it to be a genuine developmental abnormality, while others assume it to be an abnormality due to the constraint of maintaining the foot in a varus position while in the womb . The condition is in most cases bilateral; it occurs more frequently in the male popula tion, the male-female proportion being 3 : 1 .
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position of the heel, the diagnosis may b e es tablished on the basis of the medial (metatarsus varus) inflexion of the first toe (Fig. 30.7. and 30.8.). The increase of the dis tance between the first and the second toes is clinically also clearly visible. Radiological symptoms. The angles of the talus and the calcaneus are larger than nor mal, the navicular bone at the head of the talus is displaced laterally, directed in a subluxed position, and the metatarsals deviate toward the medial side. Treatment. In mild cases, there is a ten dency to spontaneous correction. Release of the adduction contracture of Chopart ' s joint is necessary, by conservative methods if possible. Manual correction. Axial traction of the forefoot by fixed calcaneus, and exercising the forefoot in abduction and pronation is ad vised with the application ofBebax redressing sandals.
Diagnosis. Besides the adduction contracture of Chopart ' s j oint and the valgus
a
Fig. 30.7. Pes adductus, the forefoot curves medially at Chopart's joint.
b
Fig. 30.S. Graphic illustration of a normal foot (a) and a pes adductus (b).
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Active physical exercise is also recom mended with the concurrent application of skin stimulation. Surgical treatment. Incision of the m. ab ductor hallucis and the medial joint capsules may be carried out after 2 years of age. Metatarsus base osteotomy in order to correct the deformity is possible at a later age.
30.2.4. Pes excavatus The term hol low foot (pes varus o r pes cavovarus) describes such foot defo rmities when t he longitudinal arch is higher than av erage, rega rd less of the cause i n itiating the condition.
Clinical symptoms. This unmistakable foot deformity takes shape by about the age of 1 0- 1 2 ; the foot is relatively short, the longitu dinal arch is higher, the anterior part of the foot is in adduction, the heel in varus position, and the 1 st metatarsus head is situated low down, which appears more explicitly due to the strongly constrained dorsal-flexed posi tion of the big toe and the other toes in the condition known as hammertoe (Fig. 30.9. a, b). The aponeurosis plantaris is stretched like a taut string, which intensifies during the dorsiflexion of the forefoot and raises the skin of the sole. Soreness and callosities may emerge on the plantar side of the forefoot over the meta tarsal heads.
a: Excavated foot, the longitudinal arch is elevated (X-ray). b: In cases of excavated foot, the patient is unable to rest the heel on the ground because of the exten sive inflexus.
Initiating causes. This deformity gener ally develops as a consequence of a mus cle-balance disorder. The lumbrical and interosseus muscles weaken, and therefore the effects of the long flexors and extensors take over. The reason for the muscle-balance disor der is generally myelodysplasia or spina bifida occulta, though other neuromuscular disorders may also occasionally be diag nosed.
Treatment Conservative treatment. The treatment of mild cases of pes excavatus is in conservative. Physical exercise is advised to stretch the shortened muscles, and the wearing of ortho pedic shoes if necessary. Surgical treatment. In childhood, Steindler 's operation is carried out: the aponeurosis plantaris and the short plantar muscles are detached from the heel . This may
Fig. 30.9.
3 0 . D i s o r d e r s of t h e f o o t
be supplemented with incision of the capsules on the plantar surface of Chopart 's joint. Tendon and muscle transplantation may be needed to correct the arched position of the toes, especially the big toe. In the event of a pronounced deformity af ter 1 0- 1 2 years of age, osteotomy of the cunei form bones with removal of a dorsal-based wedge will ensure an improvement in appear ance, due to the shortening of the longitudinal arch. After the foot has finished growing, arthrodesis of Chopart 's joint and the tarsal joint may come into consideration.
30.2.5. Pes calcaneovalgus congenitus This is a congenital developmental va lgus de formity of the foot, with varying extents of severity.
In line with the appearance of the defor mity, the condition is often referred to as rock ing chair foot, navicular foot or congenital flatfoot. With regard to the main pathogenetic fac tor behind these deformities, the disease is of ten referred to as vertical talus . Clinical symptoms. In all cases, the sole is convex, the instep is slightly concave, the forefoot is abducted, pronated and extended at
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Chopart 's joint, furthermore, the tarsus is in equinus and the heel is in a distinct valgus (Fig. 30. 1 0.). Etiology. Foot deformities described as vertical talus do not form a closed etiological entity; similarly to clubfoot, several varieties are defined. - Structural navicular foot: This is a distinct developmental deformity of the foot; its isolated occurrence is very rare. - Symptomatic navicular foot: This deformity is present already at birth, as one symptom of many relating to a complex syndrome (e.g. Freeman Scheldon 's syndrome) . It is often regarded as a result of arthrogryposis multiplex congenita. It is generally bilateral, the contractures are rigid, and respond very poorly to corrective treatment. - Myelodysplasia-related navicular foot. This too is often already present at birth. A muscle-balance disorder plays the main role in its development. It has been reported by Sharrard, that if the lesion is present in or above the 3 rd lumbar vertebra, the contractures are extremely rigid. In case of lesion between L5 and S I , looser contractures are perceived. - Spastic navicular foot. This develops in most cases after the patient has learned
Fig. 30.11. Fig. 30.10. Oinical depiction of bilateral congenital navicular foot.
Talus positioned vertically, demonstrating the pathological relation of the talocalcaneal joint and Chopart's joint.
408
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to walk and is a consequence of a muscle-balance disorder, with the heel in an equinus position. Radiological symptoms. The steep posi tion of the talus, the pathological correlation of the tibiotalaris and the talocalcaneal is, and the dislocated or dorsolaterally subluxed posi tion of the os naviculare on the talus-neck (Fig. 30. 1 1 .) are characteristic of all above listed foot deformities . Treatment. The obj ective is repositioning of the talus and the os naviculare, normaliza tion of the position of the tarsus and the ante rior part of the foot and preservation of the corrected position. Conservative treatment. If any type of navicular foot is noticed at birth, passive physical exercising should be commenced immediately, followed by gradual correction with plaster casts. In case of navicular foot developing as a result of spastic or flaccid paralysis, gradual correction with plaster casts is rarely imple mented, treatment is primarily surgical. Surgical treatment. From the age of 6 months to 3 years, posterolateral or, if neces sary, medial release is performed.
30.2.6. Accessory ossicles on the foot Generally, no complaints are caused by this condition, although its occurrence is fre quent, most often involving the os tibiale externum ( 1 0%), the os trigonum (8%), and the os peroneum (5%). �
Os tibiale externum This is found on the inner side of the foot, beside the os naviculare. It is associated via either fibrous tissue or cartilage with the navicular bone, together forming a horn shape, which is why it is also referred to as os naviculare cornutum. Its clinical significance is that it protrudes in the medial part of the foot, on the inner side, and consequently, the wearing of shoes will
Fig. 30.12. Accessory bones on the medial side of both navicular bones: os tibiale externum.
eventually cause painful inflammation and hyperkeratosis. On an X-ray, it is easily detectable, espe cially in an antero-posterior position beside the os naviculare as a separate bone center (Fig. 30.1 2.). Treatment. The use of insoles may reduce discomfort, but only surgical removal will re sult in complete elimination of the irritation. Special attention should be paid to maintain ing the posterior attachment of the m. tibialis.
30.2.7. Tarsal coalition This is a pathologic connection(s) between different tarsal bones.
When stiff flat feet are detected in adoles cence, possible pathologic bindings between different tarsal bones should be taken into consideration. Depending on which bones are connected, the following forms are identified: calcaneo navicular coalition, talonavicular coalition and calcaneocuboid coalition. In most cases, calcaneonavicular coalition is diagnosed. The binding tissue may be fi brous, cartilaginous or bony. The possibility of this disorder is often suspected on a lateral
3 0 . D i s o r d e r s of t h e foot
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X-ray picture, but a cartilaginous or bony co alition is weII perceivable on an oblique im age (Fig. 30.13.). Treatment. The disorder is not curable by conservative treatment. In childhood, resection of the bony bar, and in adulthood, subtalar and Chopart ' s j oint arthrodesis is performed in order to terminate the complaints. Fig. 30.13.
30.2.8. Osteochondrosis calcanei (apophysitis calcanei)
The bony fusion between the os naviculare and the calca neus can be observed in an oblique image.
This mostly develops between the ages of 7 and 13 in male patients, often bilatera l ly. It is believed that besides ossification d isorders, an i ncreased functional load and d isorders of the blood supply of the apophysis a lso p lay a part in its development.
Clinical symptoms. Children complain of rapid exhaustion, and of tarsal pain and sensi tivity around the adherence of the Achilles tendon, which escalates when subjected to ex tensive strain. The pain is more intense in re sponse to the dorsiflexion of the foot, it de creases upon plantiflexion. Walking up and down stairs is especiaIIy difficult. The heel is slightly thickened. Radiological symptoms. The apophysis of the calcaneus is indistinct, with an unclear contour and an irregular shape. The ossifying center is fragmented (Fig. 30.1 4.). Treatment. Treatment of the disorder is conservative. Complaints should cease upon relaxation and lifting of shoe-heels.
30.2.9. Osteochondrosis ossis navicu laris pedis (Kohler's I disease) The essence of this d isorder is aseptic necrosis occu rring in the os navicu lare pedis. The d iag nosis was described by Kohler i n 1908. It ge-
Fig. 30.14. The apophysis of the calcaneus is shattered and sclerotic.
nera l ly occurs between the ages of 3 and 10. The d isorder is more freq uent in males and approximately 30% of the cases a re bilateral.
Etiology. The etiology has not yet been clarified; the most probable cause is an ossifi cation disorder. Some associate the iIIness with trauma. Clinical symptoms. The condition often develops without causing any particular com plaints and only an X-ray image taken for some other reason will shed light on its exis tence. The complaints are manifested in rapid exhaustion, limping, and local pain and swell ing in the area of the navicular bone in the in step. The limping intensifies after extensive walking. Passive movement of Chopart ' s j oint is limited, and may even be painful.
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Radiological symptoms. The structure of the navicular bone is irregular, it is porotic. During the progression of the process, the bone decreases in size, gradually forms a disk shape, becomes sclerotic and diminishes. At rophy may be observed on other bones of the foot. In the process of healing, the os naviculare regains its original form and shape (Fig. 30. 1 5). Treatment. Shoe inserts are recom mended, through which the navicular bone can be partially relieved of body weight. There is no need for surgical treatment.
Fig. 30.15. Kohler's I disease: the ossifying center of the os
naviculare is cracked and the bone is flattened.
30.2. 10. Ostechondrosis capitis metatarsi 11. (Kohler's 11 disease) This disease denotes aseptic necrosis occur ring in the 2nd, (rarely the 3rd or 4th) meta tarsa l head. It genera l ly develops between the age of 10 and 18 and is three times as fre q uent i n female popu lation as in males, rarely, it is bi latera l.
Etiology. It generally occurs in cases of pes transversoplanus. Its development is ex plained by the fact that since the arch of the foot is descended, the 2nd metatarsal head is set deeper and is exposed to increased weight pressure. An inadequate blood supply of the epiphysis may also play a role in its develop ment. Clinical symptoms. The symptoms vary in accordance with the 3 stages of the disor der.
a) In the early stage, the dorsal surface of the metatarsal head is sensitive to pressure. Rapid exhaustion occurs, which intensi fies upon exertion, and the patient there fore tends to walk on the edge ofthe sole. b) In the middle or compression stage, swell ing and painful disability arise in the fore foot. The patient tries to evade the regular rolling phase of the feet, since the pain in-
Fig. 30.16.
Kohler's 11 disease: deformation of the metatarsal
head.
tensifies during the roll and when standing on tiptoe (plantarflexion of the foot). c) In the final stage, arthrotic symptoms pre dominate. Exostosis is palpable on the metatarsal head, and the toes sub luxate. Callosity develops in the corresponding spot on the sole. Radiological symptoms. No changes are perceivable in the initial period. In the com pression stage, the first sign is the sub-
3 0 . D i s o r d e r s of t h e f o o t
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chondral, transverse radiolucency in the meta tarsal head; later, the joint surface becomes flattened and deformed, but it remains well defined. Arthrosis and deformed joint sur faces are characteristic in the final stage; the metatarsal head is cylindrically deformed (Fig. 30.1 6.). Treatment. Treatment of this deformity, if possible, is conservative, the chief objective being to relieve the load on the forefoot and the metatarsal head. Suitable insoles and spe cially designed rocking bottom shoes will eliminate the discomfort. During the develop ment of normal bone structure, the deformity will heal in 1 -2 years . Resection of the head will result in total re cuperation. Excochleation of the necrotic seg ment and spongiosa plasty may also be at tempted.
a
30.3. Foot deformities in adu lthood 30.3. 1. Pes planus (pes planovalgus, flat foot, fallen arch) This is the most frequent foot d isorder of static orig in. The background of the condition is the collapse of the a rched system of the foot, since the active and passive stabilizing systems supporting the arch a re insufficient. The d isorder is cal led pes pla novalgus if the predomi nant factor is collapse of the longitu dinal arch together with the va lgus heel. If the transverse arch has fa llen with the calcaneus i n the normal position, the condition is ca l led pes transversoplanus.
It is worthwhile to reflect on the different types concurrently, since they are often asso ciated and the triggering causes are mostly the same. Etiopathology. When the active and pas sive stabilizing systems of the foot are not ca pable of equalizing the pressure of body weight placed on the feet, the valgus position of the calcaneus will develop and the longitu-
c d
Fig. 30.17. Normal longitudinal arch (al and pes planus b: The descent of the lon.gitudinal arch. c: This image of the patient clearly reveals how the medial side of the foot almost touches the g round; calluses are also well observable. d: X-ray picture of a flattened longitudinal arch in a standing patient.
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dinal arch will descend (Fig. 30. 1 7. a-c). This is generally followed by the collapse of the transverse arch as well. The reasons for the disruption of the bal ance: - overloading of the foot (body weight or pregnancy) - the decreased weight-carrying capacity of the foot - insufficient functioning of the passive stabilizers (congenital weakness of connective tissue, Ehlers-Dahnlos syndrome, hormonal effects or preg nancy) - insufficient functioning of the active muscles (paralysis, stabilizers Heine-Medin disease or myelodys plasia) - improper loading of the foot: com pensatory (infantile cerebral paresis) - following trauma or inflammation, or in case a tumor can damage the bony structure, tendons or ligaments of the foot arch
more, medially from the tip of the medial an kle, distally and slightly anterioriy, the con tour of the talus head protrudes. Under normal conditions, body weight is transferred onto the trochlea of the talus, and from here is dis tributed toward the calcaneus and the metatarsus. With weakening of the m. tibialis posterior, the m. extensor hallucis longus, the m. extensor digitorum longus and the pero neus muscle group, the talus head will tilt
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Clinical symptoms. The height of the nor mal longitudinal arch decreases, or in extreme cases it may disappear totally. Posterior ob servation of the patient reveals the position of the calcaneus valgus (Fig. 30.1 8.). Furthera b
Fig. 30. 19.
Fig. 30.18. Pes calcaneovalgus. The axes of the leg and the calca neus are at a n angle of approximately 20°.
a: Graphic image of a normal (1) and a collapsed transverse arch (2) and an expanded forefoot (3). b: Calluses developed on the sole below the 2nd-4th metatarsal heads (as a sign of increased pressure on the sole) in the case of a fallen trans verse arch.
3 0 . D i s o r d e r s of t h e foot
downward, toward the medial. The medial contour of the foot will therefore become con vex and the forefoot will assume a pronated position in relation to the heel. Collapse of the transverse arch is also a static deformity, its triggering causes corre spond to those of pes planovalgus, with which it is often associated, generally in the mid dle-aged. Because of the increased weight af fecting the metatarsal heads, the transverse arch drops (Fig. 30.19. a), and the foot spreads out. Calluses may develop under the 2nd, 3rd and 4th metatarsal heads on the sur face of the sole (Fig. 30.19. b). In cases of rheumatic diseases, the decay of the ligaments and the inflammated bursa on the sole of the foot intensify the deformity and the pain. In case of neonates, the arch system of the foot is not yet developed, and similarly, their physiological curves are not yet perceptible on the spine. These features develop later, in response to the appropriate stimuli . Parents often worry that the transverse and longitudi nal arches have not yet developed on the foot of their infant, who is about to start walking. The development of the arch system is time-consuming, and furthermore, the muscu lar system of the foot has to grow used to the muscle exertion necessary for walking. The final development of the arch system is con sidered normal up to the age of two years . Throughout growth (bearing in mind that growth is not a linear process) there are peri ods when the foot is exposed to increased ex ertion. One of these periods is the commenc ing of school, when the wearing of a backpack and walking to school may trigger an over loading of the feet. Adolescence is similarly a critical stage, owing to the significant increase in body weight and the changing circum stances (intensive sporting activity and per haps the commencing of employment) on the other. In cases of fixed, muscularly affixed flat foot, both the ligamental system and the dy namic stabilizing system are insufficient, but the disorder can still be corrected: in this con dition, the arch may be restored under anes thesia. When ligamental fixation has devel-
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oped, the arches can not be restored, not even under narcosis. This condition is referred to as bony rigidity. Naturally, there are certain circumstances or occupations that may bring about an insuf ficiency of the arch system by straining it ex cessively. Such occupations include those of waiters, hairdressers and surgeons. Physio logical changes too may cause the develop ment of flat feet, as in pregnancy, when the enhanced loosening of tissue results in a de crease in the passive stabilizing effect of the ligamental system. With a normal ligament and muscular system, obesity will lead to the collapse of the arches because of the excess weight load. Treatment. One of the most important ob j ectives is prevention. In childhood, the child should not be forced to walk and should be carried when tired. Strengthening of the foot muscles is also very important. One technique is to encourage walking on uneven surfaces. It is very impor tant, that walking barefoot on artificially flat surfaces such as wooden floors or boarding is explicitly harmful, since in these cases there is no need for the active operation of the foot muscles, and thus the muscles will wither. In contrast, on pebbly, bumpy, grassy or sandy surfaces, the foot is forced to adapt to the given surface owing to its uneven nature, which results in the strengthening of the dy namic stabilizing system. At the same time, it is possible to actively fortify the foot muscles by means of playful activities, e.g. picking up pens and pencils from the floor with the toes. It is possible to encourage the strengthening of the muscles of the sole through such exer clses. Insoles are not prescribed automatically for children aged 6-7 with flatfoot. In a pes calcaneovalgus condition, the valgus position of the heel is compensated by the lifting of the medial part of the shoe heels. A 5 -mm wedge is positioned medially under the heel, sloping toward the lateral. Thus, the elevation corrects the axis of the valgus positioned calcaneus. Physical exercising of the foot is especially
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important for these children. Insoles are not recommended, since relieving of the foot muscles and passive support of the arch will lead to further weakening of the muscles. When fixed flatfoot develops in older chil dren, loosening of the rigidity may be achieved conservatively through application of a cold compress, and after loosening, the corrected position should in certain cases be maintained with a plaster cast. If no results can be attained through appli cation of a cold compress, manipulation should be performed under narcosis and a plaster cast should possibly be applied. In adolescence and adulthood, patients with flatfoot are recommended insoles. In soles correct the valgus position of the calcaneus, thereby establishing the longitudi nal arch and they may also support the trans verse arch. In case conservative treatment does not bring the desired results, surgical so lutions may also come into question. Instead of the former practice of positioning a bony wedge into the sinus tarsi in order to achieve an extra-articular arthrodesis, corrections are nowadays executed through the utilization of screws. Another possibility is calcaneus osteotomy, in the course of which the patho logic axis is corrected through wedge resec tion and/or shifting. When marked arthrosis is associated with axis deviation, fusion of the talocalcaneal and Chopart 's j oints may be considered.
part of the 1 st metatarsal in the medial direc tion (Fig. 30.20. a, b). One of the conse quences of this displacement is that the m. ab ductor hallucis slides onto the surface of the sole and pronates the hallux. The flexors and extensors with the sesamoid bones lateralize relative to head of the I st metatarsal, pulling the hallux into adduction (valgus) (Fig. 30.2 1 . a ) . Hyperactivity of the m. adductor hallucis and the position of the flexors results in a vi cious circle that constantly amplifies the de formity.
a b
30.3.2. Hallux valgus, metatarsus I. varus This is a valgus deformity (subluxation in the metatarsop halangeal joint) of the ha llux of static origin with a variable extent of varus position of the 1st metatarsal.
Etiopathology. Congenital, constitutional (loose ligaments or falling of the transversal arch) and external factors (tight, fashionable or pointed shoes) can all play a role in the de velopment of a bunion. The most common cause of this disorder is a shift of the distal
Fig. 30.20. a: Severe hallux valgus. b: X- ray image of the above patient.
3 0 . D i s o r d e r s of t h e f o o t
i i
i
a
b
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Fig. 30.2 1. Hallux valgus. a: The pathological pulling direction of the tendons intensifying the valgus (1: m. extensor hallucis longus, 2: m. flexor hallucis brevis, 3: m. add uctor hallucis, 4: m. flexor hallucis longus, 5: m. abductor hallucis). b: Graphic illustration of an orthotic device to cor rect hallux valg us.
Treatment. Pain killers, insoles, the wear ing of wide or orthopedic shoes and perhaps a hallux valgus-correcting appliance (Fig. 30-2 1 . b) at night may come into consider ation as forms of conservative therapy. A sat isfactorily improved condition may be ex pected only after surgical treatment. Radiological parameters, which play a role in the surgical indication are demon strated in Fig. 30.22. There are more than 1 50 possible surgical interventions for the correction of hallux valgus. These may be divided into three basic groups: operations involving only soft tissue, operations of only bony tissue, and a combi nation of the two. One factor that significantly influences the surgical indication is whether arthrosis is present in the 1 st metatarso phalangeal joint. If it is, correctional osteo tomy can not come into question. Soft-tissue operations are generally carried out before the closure of the growth plates. In adulthood, the indication of combined surgery depends on the following factors :
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Fig. 30.22. Radiological parameters playing a part in the indica tion: 1: interphalangeal angle, 2: hallux valgus angle, 3: the angle formed by the metatarsus axis and the joint su rface, 4: the angle formed by the axes of the 1st and 2nd metatarsi.
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a b
c d
Fig. 30.23. Osteotomy of the 1st metatarsus base and Akin osteotomy of the proximal phalanx. a: Clinica l image before su rgery. b: Antero-posterior X-ray image of the foot before surgery. c: Antero-posterior X-ray image of the foot after surgery. d: Clinical image after su rgery.
Phase 1 : The hallux valgus angle is smaller than 2 5° , the intermetatarsal angle is smaller than 1 2° , the mobility of the 1 st metatarsophalangeal j oint is complete, and the dislocation of the sesamoid bone is smaller than 25%. In this case, Schede ' s operation and/or distal metatarsal and/or distal phalanx osteotomy may come into question concurrently with a soft-tissue correction (which generally involves shortening on the medial side and release on the lateral side), supplemented with tenotomy of the adductor hallucis. Schede 's operation: chiseling away the exostosis that has developed on the medial side of the 1 st metatarsal, together with re-
moval of the irritative bursa formed be tween the exostosis and the skin. Phase 2: The hallux valgus angle is 25-3 5° (possibly even 40°), the intermetatarsal angle is 1 2 - 1 8°, there may be subluxation in the 1 st metatarsophalangeal joint, and the dislocation of the sesamoid bones is 25-50%. The interventions applied in this phase: besides removal of the exostoses and soft-tissue interventions, distal (possi bly diaphyseal) or proximal 1 st metatarsal osteotomy and if necessary, proximal pha lanx osteotomy. Phase 3: The hallux valgus angle is larger than 40°, the intermetatarsal angle is larger than 1 8°, the 1 st metatarsophalangeal joint
3 0 . D i s o r d e r s of t h e f o o t
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is subluxed and/or the 1 sI ray is hyper mobi le. Surgical interventions imple mented in this phase (at a young age, if no arthrosis is present in the metatarso phalangeal joint) are proximal 1 st metatar sal osteotomy (Fig. 30.23. a-d) or meta tarsocuneiform arthrodesis and if neces sary, proximal phalanx osteotomy.
30.3.3. Hallux rigidus Hallux rigid us is the term used to describe pain-ind ucing, isolated limitation of move ment of the 1st metata rsophalangeal joint, it is genera l ly caused by arthrosis. I n these cases, valgus deformity is minimal or not p resent at all. The ROM may be minimal i n the functional aspect, but enough is left to sustai n the pain (Fig. 30.24.).
The clinical symptoms of osteoarthritis of the 1 st metatarsophalangeal j oint: pain, crepi tation and a significantly decreased ROM. The condition may develop as a result of trauma or inflammation, or a preceding bun ion operation. The patient ' s gait is disturbed by the pain induced and the lift-off phase of the patient' s gait i s perturbed because of the absence o f the 1 st metatarsophalangeal j oint extension. Rocking bottom orthopedic shoes are recom mended as conservative treatment. Besides
Fig. 30.25. Schematic illustration of cheilectomy. 113 oblique dorsal resection of the distal joint surface of the 1st metatarsus, and 113 dorsal resection of the proximal joint su rface of the proximal phalanx.
the radiological and clinical condition, the in dication of surgical treatment is strongly de pendent on the patient' s age and the level of his/her requirements . The surgical treatment of hallux rigidus may be categorized as follows : a) An operation retaining the 1 sI metatarso phalangeal joint, which consists in remov ing with a chisel the bony osteophytes that have developed on the metatarso phalangeal joint area of the metatarsus and the proximal phalanx dorsally, in this way re-enabling dorsiflexion of the j oint (cheilectomy) (Fig. 30.25.). b) Operations sacrificing the 1 st metatarso phalangeal j oint, consisting in either re section of the base of the proximal phalanx of the hallux or arthrodesis of the meta tarsophalangeal joint.
30.3.4. Diseases of the 5th ray Bony irregularities and axia l deformities may develop on the 5th ray on the latera l side of the metata rsus (Fig. 30.26. a, b).
Fig 30.24. X- ray image of hallux rigid us. The joint space of the metatarsophalangeal joint is significantly narrowed, and osteophytes may be observed on the edge of the bones.
These disorders are essentially equivalent to lateral deviation or increase of the 4th-5th intermetatarsal angle. They may cause dis comfort and/or problems even when normal shoes are worn.
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1
2
b
3
4
Fig. 30.26. a: Categorization of deformities of the 5th metatarsus: Type 1: Exostosis on the lateral side of the 5th metatarsus head; no lateral deviation on the metatarsus, the 4th-5th intermetatarsal angle is normal. Type 2: I ntense lateral deviation of the 5th metatarsus. No real hypertrophy can be observed on the lateral side of the metatarsus head; the intermetata rsal angle is within the normal range. Type 3: I ncreased i ntermetatarsal ang le; no hypertrophy and the extent of deviation is normal. Type 4: Combined variation: hypertrophy and/or increased deviation is present with an increased intermetatarsal ang le. b: Schematic drawing of a correctional osteotomy performed on$ a type 4 deformity as described above.
Treatment. In cases of exostosis, if no other disorder is observed (an increased 4th-5th intermetatarsal angle or enlarged curve of the 5th metatarsus), removal of the exostosis is recommended. When deformities of the 5th metatarsus are observed, osteotomy may be considered. If the 5th toe is super posed over the 4th toe (digitus V varus super ductus, which may be present congenitally), the above solutions may be supplemented with plastic surgical interventions carried out on the joint capsule, the tendon or the skin, through the formation of artificial syndactyly.
30.3.5. Diseases of the sesamoid bone The most frequent pathological disorders are fractures, avascular necrosis and arthrosis.
30.3.6. Metatarsalgia Metatarsalgia is the term used to describe the pain ind uced by load ing of the metata rsals. Hyperkeratosis is a lso generally present under the metatarsal heads concerned. The d isorder usua l ly develops as a resu lt of pes transversoplanus.
Conservative treatment may prove to be successful with well-adapted insoles, other wise, surgical treatment is recommended. Metatarsalgia of static origin generally affects the central (2nd, 3rd and 4th) metatarsi; in these cases, it is advisable to carry out surgery on the 2nd-4th rays concurrently (e.g. sub capital osteotomy according to Helal), since osteotomy involving only one ray may lead to metatarsalgia of the other rays.
3 0 . D i s o r d e r s of t h e f o o t
30.3.7. Digitus malleus (hammertoe) The flexor-extensor balance on the forefoot is disrupted as a resu lt of the dropping of the transverse arch, and a characteristic condition develops. The metatarsophalangeal joint takes up a hyperextended position, the proximal interphalangeal (PIP) joint fixes in a flexed po sition and the distal interphalangeal (DIP) joint assumes a n extended position.
A clavus forms on the dorsal side of the toe, corresponding to the proximal inter phalangeal joint as a result of the pressure in duced by wearing shoes. A sensitive, irritable bursa develops between the clavus and the skin (Fig. 30.27. a, b). Treatment. In the early stage, the process may be reversible by the wearing of insoles and regular toe exercises; later, after the de formity becomes rigid, only surgical interven tion may yield a good result. Of the several
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possible surgical solutions, the most common is surgical resection of the proximal phalanx head. In neglected cases, when subluxation or luxation has developed in the metatarso phalangeal joint, arthrodesis of the proximal interphalangeal joint, or possibly capsul ectomy in the metatarsophalangeal joint, re section of the base of the proximal phalanx or temporary wire fixation may be necessary.
30.3.8. Morton's neuroma The essence o f t h i s d isorder is a typica l spin d le-shaped neuroma on t he digita l nerve be tween the 3rd and 4th, less freq uently be tween the 2nd and 3rd metatarsi, located d i rectly p roximally from the partition of the nerve.
Clinically, a sharp, flashing pain occurs in the supply area of the nerve, after which a per sistent pain of lower intensity remains. It is important to distinguish the disorder from metatarsalgia, which may be achieved through a simple physical examination. In metatarsalgia, the metatarsals are sensitive to direct pressure from underneath, while the pain is not induced upon transverse pressure of the anterior part of the foot. In contrast, in Morton' s neuralgia, the foot is not sensitive to pressing of the metatarsals from below, but the pain may be provoked by transverse com pression of the metatarsus heads . Treatment. Lidocaine infiltration admin istered in the area of the neuroma eliminates the pain immediately, this may partially be utilized for diagnostic purposes. A local ste roid inj ection may be attempted once, or pos sibly twice. If no improvement is experi enced, removal of the thickened nerve seg ment may be considered.
Fig. 30.27. a: Schematic illustration of a hammertoe deformity. b: Hammertoe.
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30.3.9. March fracture (stress fracture, fatigue fractures on the metatarsals) The term "ma rch fracture" also implies the es sence of the i l l ness. It was first described among soldiers, as a syndrome occu rring after persistent strain, marching.
The fundamentals of the disorder are stress fractures which develop most commonly on the 2nd and 3rd metatarsi, as a result of per sisting, repeated strain; these fractures can not be spotted immediately in the X-ray picture. A few days later, upon osteolysis of the edges of the fracture, it can be well distinguished, and after a few weeks, a large mass of callus may be observed (See Chapter 3 and Fig. 3 . 5). The significance of this diagnosis is chiefly the differential-diagnostic aspect: if it is not taken into consideration, a turnor may be suspected. Later, metatarsalgic complaints may arise subsequent to march fractures. Treatment. The condition heals spontane ously if the legs are rested.
30.3. 10. Achillodynia (paratenonitis of the Achilles tendon) This d isorder is cha racterized by pain in the Achilles tendon and the surrounding paratenon, possibly accompanied by its thick ening.
The condition is characteristic at a young age, or in male patients who earlier exercised regularly and resume physical exercise after a long intermission. The increased strain on the Achilles tendon causes pain, pressure sensi tivity and a palpable, reel-shaped swelling 1 -2 cm above the point where the tendon is at tached to the calcaneus. In certain cases, crep itation is also observed above the tendon upon movement of the feet. When further physical exercise is forced, the total rupture of the damaged Achilles tendon often occurs.
Differential diagnosis. This disorder must be distinguished from partial or total rupture of the Achilles tendon. If a rupture has occurred, an indent is palpable in the affected area, and the patient can not support him/her self on tiptoe on one foot. The Thomson test may be of assistance in establishing the cor rect diagnosis: with the patient lying in prone position, in normal cases, compression of the flexing muscles of the leg results in plantarflexion of the foot; with a ruptured Achilles tendon, the foot does not move. Treatment. This comprises resting, eleva tion of the leg and the administration of nonsteroidal anti-rheumatic drugs. After the temporary discontinuance of physical exer cise, it is very important to recommence and build up the exercising program gradually, corresponding to the load-bearing capacity of the tendon. Locally administered steroid products may reduce the discomfort, but they are not recommended, for they increase the danger of rupture of the Achilles tendon.
30.3. 1 1. Haglund heel This disorder involves a bony enlargement developing in adolescence, after the end of the growth phase, on the upper part of the dorsal surface of the calcaneus, in the area where the Achilles tendon adheres to the bone. The upper rim of the shoe presses on the bony enlargement, causing severe discomfort. This is not genuine exostosis, the disorder is rather a variation of form, or excessive bone mass. Treatment: by means of periodic change of the shoes and conservative treatment (cold compresses and nonsteroidal anti-inflamma tory cream) the complaints usually cease. Rarely, in stubborn cases, resection of the bone excess may be carried out.
30.3. 12. Calcaneus spur The essence of this disorder is that a small, spur-like protrusion develops at the origin of
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30.3.13. Arthrosis of the foot joints
Fig. 30.28.
This d isorder develops most frequently in the subtalar joint and Chopart's joint. Primary a rthrosis occurs in elderly patients. The sig nifi cance of secondary a rthrosis is higher. These cases a re genera l ly recognised as end stages of progressive prearthrotic conditions (pes excavatus, clu bfoot, etc.) o r as a conseq uence of some other d isease (inflammation, aseptic bone necrosis, or trauma).
X-ray picture of a calcaneal spur.
the plantar fascia, originating from the tuber of the calcaneus, which is sensitive to strain or direct pressure. Patients generally complain of a stinging pain in the heel area, which they compare to stepping on a sharp pebble. The sensitive area is well palpable, and the pain (usually originating at the medial perim eter of the calcaneus tuber) can be provoked by applying pressure. In a lateral X-ray pic ture, a spike-shaped protuberance can be ob served at the origin of the aponeurosis plantaris in the maj ority of cases (Fig. 30.28). Considering that in many cases, a calcaneus spur is not always seen in spite of the intense pain, and as a spur may develop without caus ing the patient any discomfort, it may be pre sumed, that the pain is not induced by the exostosis, but by the overstraining of the plan tar structures and periostitis. Treatment is generally conservative: in most cases, relaxation, the wearing of insoles to relieve the foot and the administration of anti-inflammatory agents will improve the pa tient's condition. Also, local steroid inj ections often have a good effect. If conservative treat ment does not produce acceptable results in 3-6 months, incision of the aponeurosis plantaris adjacent to the calcaneal origin may be considered. Recently, by means of an ar throscopic intervention, the aponeurosis can be detached through a minimally invasive procedure as an outpatient operation.
Clinical symptoms. Pain localized in the arthrotic area causes discomfort on movement of the affected joint. The area is sensitive to pressure, and osteophyte formation is often palpable upon external examination. Radiologically, narrowing of the joint space is characteristic in osteoarthritis, with subchondral sclerosis, subchondral cysts and osteophytes. Treatment. In mild cases, non steroidal anti-rheumatic agents, symptomatic treatment and therapeutic X-ray irradiation may be highly effective. Orthopedic shoes may be recommended later. In case conservative treatment does not prove successful, surgical treatment may be considered, with arthrodesis of the arthrotic joint. When the entire tarsus is affected, combined arthrodesis (triple arthrodesis) of the talocalcaneal j oint and Chopart ' s j oint is performed. It is important to distinguish arthrosis from diabetes-related arthropathy, which in its early stage may dis play a picture similar to that of conventional osteoarthritis, but demonstrates only a few of the clinical symptoms of the disorder.
30.3. 14. Tarsal tunnel syndrome This involves compression of the tibial nerve on the inside of the medial ankle at the entrance of the tarsal tunnel . The mechanism of its development corresponds to that of the carpal tunnel syndrome. The causes of the dis order may be any of the following : inflamma tion, trauma, a venous circulation disorder, or
422
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3 0 . D i s o rders of the foot
functional reasons. Patients describe nightly paresthesia on the sole of the foot, around their toes. The symptoms can be provoked by applying direct pressure to the tarsal tunnel. An EMG examination may help establish the diagnosis. Treatment. Conservative treatment, shoe inserts to support the medial side of the sole, and the administration of non steroidal anti-inflammatory drugs lead to an improve ment. Rarely, surgical decompression may be indicated.
30.3. 15. Diabetic foot Diabetic foot is a collective term for foot p roblems relating to diabetes: macro and microangiopathy and foot deformities devel oping as a conseq uence of neuro pathy, ac companied by u lcers o r necrosis in severe cases.
The nutrition and oxygenization of the tis sues is diminished because of the impaired blood circulation, and wounds therefore heal with greater difficulty, than under normal conditions. Because of the sensation disorders developing as an accessory symptom of the neuropathy, minor injuries of the foot do not
Fig. 30.29. Characteristic symptoms of a diabetic foot: the skin is d ry and cracked, the toenails are dry and are mycosis-infected, and a circulation disorder in an early stage may be perceived u nder the 1st metatarsus head.
attract attention, until more severe complaints occur, resulting from the disorder not having been treated (Fig. 30.29.). Clinical experience shows that certain diabetic ulcers develop not on the sole (under pressure), but on the dor sum ofthe foot, this proving that ulcers are not caused merely by pressure. It is most impor tant to diagnose the neuropathy and also to prevent it. The risk factors of ulcers develop ing on the diabetic foot are as follows : - retinopathy, - old age, - previous foot ulcers, - alcohol consumption, - smoking, - known cardiac disease, - foot deformity (hallux valgus, hammertoe, etc.), - limited joint mobility. The following measures may be recom mended as forms of prevention. The diabetic patient should wash hislher feet regularly with warm water. The temperature of the water should be checked before stepping into it. The patient should examine hislher soles every day with the help of a mirror. Drying-out of the skin should be avoided by the application of skin cream. Before putting on shoes, the pa tient should ascertain that there are no wrin kles in the socks and no other pressure-induc ing obj ects are present. The patient should not walk barefoot or wear new shoes for long pe riods. If the patient perceives any problems, he/she should turn to a physician immedi ately, and should not treat the complaint at home. The development of ulcers and rapid progression of the infection is a serious risk in case of diabetic feet and in certain cases may lead to amputation of the foot. It is most im portant, therefore, to control the patient's blood sugar level. From an orthopedic aspect, total contact shoe inserts and the provision of diabetic orthopedic shoes are of great signifi cance as concerns the avoidance of the devel opment of ulcers and other complications .
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