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P. Doury Y Dirheimer S. Pattin
Algo dys trophy Diagnosis and Therapy of a Frequent Disease of the Locomotor Apparatus
With a Foreword by IVilliaumey
Translated by M.-Th.Wackenheim
With 46 Figures
Springer-Verlag Berlin Heidelberg New York 1981
Professeur PAUL DOURY Service de Rhumatologie des Armees, H6pital Begin F-94160 Saint-Mande
Dr. YVES DIRHElMER Service de Neuroradiologie, Centre Hospitalier Universitaire F-67091 Strasbourg Cedex
Dr. SERGE PATTIN Service de Rhumatologie des Armees, H6pital Begin F-94160 Saint-Mande
Translator
MARIE-THERESE W ACKENHEIM Institut de Radiologie, Universite de Strasbourg, II, rue Humann F-67085 Strasbourg Cedex
The cover design shows a classical algodystrophy of the wrist and of the hand
ISBN-13: 978-3-642-67991-9 DOl: 10.1007/978-3-642-67989-6
e-ISBN-13: 978-3-642-67989-6
This work is subject to copyright. All rights are reserved, whether the whole or part of the material is concerned, specifically those of translation, reprinting, re-use of illustrations, broadcasting, reproduction by photocopying machine or similar means, and storage in data banks. Under § 54 of the German Copyright Law where copies are made for other than private use a fee is payable to "Verwertungsgesellschaft Wort", Munich.
© by Springer-Verlag Berlin Heidelberg 1981
Softcover reprint of the hardcover 1st edition 1981
The use of registered names, trademarks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use.
Reproduction of the figures: Gustav Dreher GmbH, Stuttgart
2127/3130-543210
Foreword
It is with great pleasure and ,much interest that I accepted to write the foreword to this book by Paul Doury, Yves Dirheimer, and Serge Pattin on the subject of "algodystrophy." First, because I know the extent of their personal experience, from which they have selected the best for this book. Second, because it seemed to me that their detailed analysis of the numerous works on the subject, works which have been published all over the world and which provide diverse physiopathologic interpretations, would provide a comprehensive study meeting a real need.
Algodystrophy, to adopt the term used by the authors, merits rheumatologists' careful attention. It is indeed a frequent condition and, as is now well known, occurs in the most varied etiologic circumstances; it is not solely posttraumatic, a notion on which diagnosis had long been based. This variable etiology suggests the complexity of algodystrophy's pathogenic mechanism.
The condition usually shows a pseudoarthritic inflammatory pattern and/or localized and painful demineralization of the bones, which naturally leads the patient to consult a specialist. Recently much has been learned about algodystrophy, on the one hand as a result of modern investigation techniques such as bone scintigraphy, which make possible a more accurate diagnosis of the early stages or of the localized forms of the disease, and, on the other hand, with regard to the possibilities of a better adapted therapy, liable to modify markedly the evolution of the disease. The opening chapter of this book demonstrates the recent escalation of progress in this field.
This brief preface can unfortunately not provide an exhaustive account of the authors' personal contribution. I would, nevertheless, like to place special emphasis upon their essential conceptions. I feel that their governing thought has been to show the basic unity of the various types of algodystrophy, the clinical features and the mode of occurrence of which are so variable that one cannot wonder that so many authors have attempted to dismember this pathologic group and to individualize several related but nevertheless distinct entities. Doury, Dirheimer, and Pattin's approach is quite different and leads them to investigate uniting characteristics found in the fields of physiopathology and pathology and in the clinical picture of algodystrophy.
First of all, what is the genesis of this painful condition and of the trophic changes that characterize it? Many factors, from almost all fields of medicine and of surgery, seem to provoke or to favor algodystrophy. It seems, however that this condition never has one particular cause, but that it is nearly always the result of several pathogenic mechanisms occurring on receptive ground. This explains the absence of a strict or exclusive parallelism between the provoking or favoring factor and the resulting symptomatic and evolutive patterns. This is particularly so in cases following trauma, since the latter can be of vastly differing nature and severity, and it is far from true that the most severe always cause the most severe and most extended algodystrophic
VI Foreword
syndrome. The posttraumatic forms are considered to be the consequence of a pathologic reflex leading to direct lesion of the cutaneous, subcutaneous, muscular, tendinous, capsular, or bony tissues, or to the development of a large locoregional vascular disturbance with a complex evolution responsible for multiple alterations. - But it seems that such a reflex mechanism can also be the consequence of very diverse and non traumatic affections of the locomotor apparatus or of visceral, coronary, mediastinal, and pleuropulmonary irritative stimuli. This mechanism can be determined or governed by central nervous system lesions or by neurosympathetic disturbances. Also involved are biochemic agents, such as serotonin, liable to be mobilized by metabolic disturbances or drug intoxications. Many unknowns still persist on the nature and evolution of the pathogenic process of algodystrophy, but it is very likely that there is a common response pattern to these very diverse stimuli.
A critical analysis allows the authors to describe a general symptomatology which is common to the different varieties of algodystrophy. They also underline the importance they attach to this unity by devoting a chapter to the general data on which the diagnosis of algodystrophy is based: - A clinical syndrome comprising painful, mechanical, and inflammatory
or mixed manifestations which affect more or less intensely the articular regions and are sometimes accompanied by synovial effusion of the mechanical type;
- Absence of any biologic changes of an inflammatory type; - Radiologic changes not involving the interspaces and consisting predomi-
nantly of locoregional demineralization in differing degrees and times of occurrence;
- Almost constant and usually early occurring increased uptake of isotopes. This is, of course, not a specific but nevertheless a significant sign, especially when there is no radiologic evidence of the changes, in contrast to the clinical findings; A very peculiar cyclic development leading to spontaneous regression of the pseudoinflammatory clinical syndrome and of the scintigraphic and radiologic anomalies, occurring slowly with sometimes very marked tendinoaponeurotic sequels. Quite naturally~ this comprehensive study has led the authors to elaborate
diagnostic criteria, the value and usefulness of which they have pertinently established. All this is the result of a detailed study of all clinical types of algodystrophy aimed at throwing light on the less well-known pecularities of the most classic forms as well as describing the hitherto undescribed features of the disease. The authors' personal experience makes this chapter a very original contribution. The description of the radiologic and scintigraphic anomalies is very carefully given, and abundant and accurate illustrations of remarkable quality are provided, for which the Editor must be congratulated.
In spite of their concern to demonstrate the unity of the disease, the authors also emphasize its polymorphism and describe in detail its many clinical forms, particularly their topography, evolution, symptomatology, and etiology. They thus draw attention to the localized variants of the algodystrophic syndrome, involving only the coxofemoral area and the knee. The latter forms, the diagnosis of which is difficult, have been made known thanks to the authors' personal studies. Equally fascinating is the description of the atypical evolutive forms, such as those which are immediately plurifocal, in a patent or latent manner, or secondarily plurifocal, in an extensive or recurrent way.
Foreword VII
Finally, the authors rightly emphasize the incomplete or atypical forms, hyperinflammatory or pseudophlegmonous forms, and fibrous or pseudosclerodermal forms, demonstrating the extreme variability of the clinical features of the disease without casting doubt upon its fundamental unity. This polymorphism justifies the comprehensiveness of the chapter on differential diagnosis, which makes reference not only to the effusional type of rheumatic disease but also to the many conditions which may mimic, clinically or radiologically, some of the features of algodystrophy in their classic forms or in their unusual aspects.
Trauma remains by far the most frequent cause of algodystrophy, but several diseases as well as certain drugs can also be held responsible, as has already been shown. This has very important theoretical and practical implications. The authors have made a detailed review of such facts, providing an exhaustive summing up of all the available data.
The reader will also be interested by the other chapters of this book, for instance the pathologic study which includes an original description of a synovial involvement. The latter is all the more interesting as such documentations are very rare.
Finally, the treatment of algodystrophy has been dealt with in detail; the authors describe the drug and physical treatments which are applied simultaneously and the results which can be expected. Neither prevention nor medicolegal considerations are neglected, proof that Doury, Dirheimer, and Pattin wish to provide their readers with a complete handbook, combining theoretical data and the most useful practical indications. We can but congratulate them on their eclecticism and wish their book the success it deserves.
J. VILLIAUMEY
Acknowledgements
We are grateful to Prof. J. Villiaumey, president of the French Society of Rheumatology for having accepted to write the foreword for this book.
We wish to thank Prof. A. Wackenheim, Head and Chairman of Radiology, University of Strasbourg for his advices and constant support.
We thank also Mrs. M.-Th. Wackenheim for her English translation of our text and for her kindness and disponibility.
Many people in a variety of ways have made this volume possible and it gives us pleasure to identify them here: Prof. J. Arlet, rheumatology, Toulouse; Prof. R.P. Delahaye, radiology, Paris; Dr. R. Granier, nuclear medicine, Paris; Dr. L. Heraut, neurophysiology, Paris; Prof. R. Lagier, pathology, Geneva; Prof. P.J. Metges, radiology, Paris; Prof. P. Meunier, rheumatology, Lyon; Dr. B. Moyses nuclear medicine, Strasbourg; Dr. A. Norton, general practitioner, London; Dr. A. Ramsheyi, general practitioner, Teheran.
We thank also our technical assistants Mrs. C. Butterlin, L. Fischer, M. Reinheimer, R. Walter.
P. DOURY
Y. DIRHEIMER
S. PATTIN
Contents
Introduction
Chapter 1 Historical Review .... Chapter 2 Why Study this Condition?
Part 1 Symptomatology
Chapter 1 General Data in Algodystrophy
A. Clinical Syndrome . . B. Biochemical Syndrome C. Radiological Syndrome D. Scintigraphic Syndrome E. Clinical Course
Chapter 2 Clinical Description Chapter 3 Topographic Forms
A. Algodystrophy of the Upper Limb
I. Onset ......... . II. First Stage . . . . . . . .
1. Involvement of Hand and Wrist 2. Involvement of the Shoulder
III. Second Stage . . . 1. Hand and Wrist 2. Shoulder 3. Elbow .....
IV. Evolution V. Topographic Forms
1. Isolated Involvement of the Hand 2. Isolated Involvement of the Shoulder 3. Associated Involvement of the Elbow 4. Associated Involvement of the Sternoclavicular
Articulation .............. . 5. Algodystrophy Localized to Two or Three Fingers
of One Hand ....... . 6. Bilateral and Extensive Forms
B. Algodystrophy of the Lower Limbs I. Algodystrophy of the Foot
II. Algodystrophy of the Knee 1. The Classical Form . . 2. Partial Algodystrophy . 3. Highly Localized Algodystrophy
2 7
10
10 10 10 11 11
11 12
12
13 13 13 13
13 13 14 14
14 14 14 14 15
15
15 15
15 15 17 17 18 18
XII Contents
III. Algodystrophy of the Hip 1. General Data 2. Clinical Signs 3. Clinical Course
C. Algodystrophy of the Spine D. Other Localizations
Part 2 Complementary Investigations
Chapter 1 Biochemistry
A. Nonspecific Indicators of Inflammation . . . . . . B. Calcium and Phosphorus Levels in Blood and Urine C. Calcitonin Test ..... . D. Hydroxyproline in the Urine E. Parathormone F. HL-A Antigen . . G. Synovial Fluid . . H. Muscular Enzymes
Predisposition to Algodystrophy in Certain Preexisting Metabolic Disturbances . . . . . .
1. Diabetes Mellitus 2. Hyperlipidemia
Chapter 2 Radiology . . . .
A. Techniques ..... .
I. Magnification Radiology II. Tomography ....
III. Xeroradiography IV. Electron Radiography V. Logetronography
B. Involvement of Soft Tissues C. Involvement of Bone . . .
I. Elementary Radiographic Signs 1. Osteopenia . . . . . . . . 2. Subchondral Lysis .... 3. Resorption of Cortical Bone 4. Juxta-articular Erosions
II. Association of Primary Lesions Producing Different Types of Image . . . . .
III. Evolution Features .......... . 1. Early Demineralization ...... . 2. Evaluation of the Radiologic Intensity of
Algodystrophy . . . . . . . . . . . 3. Classification into Stages ..... . 4. Forms Without Bone Demineralization
D. Topographic Forms ........... .
I. Partial Algodystrophy . . . . . . . . . II. Highly Localized or Parcellar Algodystrophy
III. Algodystrophy of the Upper Limb IV. Algodystrophy of the Foot V. Algodystrophy of the Knee . . . .
18 19 19 20 21 23
26
26 26 26 27 28 28 29 29
29 29 29
29
30
30 31 31 31 31
31 32 32 32 32 32 33
33 34 34
34 34 35
35
35 36 36 37 37
Contents
VI. Algodystrophy of the Hip VII. Algodystrophy of the Spine
E. Articular Involvement F. Arthrography . . . . G. Arteriography . . . . H. Pertrochanteral and Intra-femoral-head Phlebography
Chapter 3 Scintigraphy
A. Bone Scanning .
I. Technique II. Results
1. Increased Uptake 2. Iso and Hypofixation 3. Usefulness of Bone Scanning for Diagnosis
of Algodystrophy . . . . . . . 4. Limits of Bone Scanning . . . . . 5. Significance of Scintigraphic Data .
B. Isotopic Exploration of the Vascular Sector C. Isotopic Exploration of the Interstitial Area D. Joint Scanning . . .
Chapter 4 Densitometry Chapter 5 Thermography Chapter 6 Vascular Investigations
A. Oscillometry . B. Capillaroscopy . . . . . C. Doppler Effect . . . . .
Chapter 7 Electromyography Chapter 8 Pathology
A. Synovia. B. Cartilage C. Bone ..
I. Macroscopy II. Microscopy
III. Electron Microscopy IV. Microradiography . . V. Static and Dynamic Histomorphometry
VI. Attempt at a Histodynamic Interpretation of the Algodystrophic Mechanism
D. Periarticular Tissues .....
I. Capsule . . . . . II. Aponeuroses, Bursae and Tendons
III. Muscles . . . . . IV. Cutaneous Tissues V. Vessels
VI. Nerves
Part 3 Clinical Forms
Chapter 1 Topographic Forms Chapter 2 Evolutive Forms .
XIII
38 38
38 44 52 53
53
53
55 55 55 56
59 60 60
61 61 61
61 63 64
64 65 65
66 67
68 68 71
71 71 73 74 74
76
80
80 80 81 81 82 82
86 86
XIV
A. Initial Plurifocal Forms
1. Patent Forms . . 1. In the Upper Limb 2. In the Lower Limb 3. Simultaneous Involvement of the Four Limbs
II. Latent Forms
B. Secondarily Extensive Forms C. True Recurrent Forms D. Partial Forms
1. Radial Forms II. Zonal Forms
E. Parcellar Forms
Chapter 3 Incomplete Forms
A. Clinical . . . B. Radiological . . . . . C. Scintigraphic ....
Chapter 4 Atypical Forms
A. Hyperinflammatory Forms B. Pseudophlegmonous Forms C. Fibrotic Forms (Pseudo-Dupuytren) D. Pseudosclerodermic Forms ....
Part 4 Differential Diagnosis
Chapter 1 Inflammatory Process
A. Synovitis B. Phlebitis
Chapter 2 Infection
A. Osteitis . . . . B. Abscesses . . . C. Septic Arthritis
Chapter 3 Tumors .
A. Benign Tumors B. Malignant Tumors
Chapter 4 Bone Necrosis Chapter 5 Arthrosis Chapter 6 Miscellaneous
A. Fatigue Fractures B. Chondromatosis - Osteochondromatosis C. Dupuytren's Contracture D. Dupuytren's Disease of the Foot E. Scleroderma . . . . . . . F. Osteolysis . . . . . . . . . .
1. Idiopathic Osteolysis II. Idiopathic Aero-osteolysis
III. Secondary Osteolysis
Contents
86 86 86 86 87
87
88 89 89 89 89
90
90 90 90
91
91 91 91 91
94
94 95
95
95 96 96
96
96 97
97 98 98
98 98 99 99 99 99
99 99 99
Contents
G. Osteoporosis Following Immobilization H. Posttraumatic Paget's Disease . . . . 1. Sprains . . . . . . . . . . . . . .
K. Somatic Conversion Syndromes: Hysteria
Part 5 Positive Criteria
xv
100 100 100 100
Clinical Criteria 102 Radiological Criteria 102 Biochemical Criteria 102 Scintigraphic Criteria 102 Criteria Related to the Clinical Course and to the Treatment 103
Part 6 Etiology
A. General Etiologic Circumstances 106
1. Age . . . . . . 106 II. Sex . . . . . . 106
B. Favoring Circumstances 106
1. Traumatism 106 1. The Severity of the Causal Traumatism 107 2. The Nature of the Traumatism . . . . 107 3. The Site of the Traumatism ..... 107 4. Algodystrophy of the Limbs and Immobilization 108
II. Nontraumatic Affections of the Locomotor Apparatus 108 III. Diseases of the Nervous System . . . . . 108
1. Involvement of the Peripheral Nerves 108 2. Diseases of the Central Nervous System 109
IV. Cardiovascular Diseases 109 V. Pleuropulmonary Diseases 109
VI. Hyperthyroidism 110 VII. Diabetes Mellitus . . . . 110
VIII. Hyperlipidemia . . . . . 110 IX. Iatrogenic Algodystrophies 110
1. Phenobarbitals 110 2. Tuberculostats III 3. Pregnancy . . 112
X. Other Etiologic Factors 112 XI. Apparently Primary Algodystrophies 112
XII. Etiologic Factors in Our 250 Cases of Algodystrophy 113
Part 7 Physiopathology
Part 8 Treatment
Chapter 1 Chemotherapy
A. Analgesics .......... . B. Nonsteroid Anti-Inflammatory Drugs C. Systemic Corticosteroids D. Local Corticosteroids . . . . . E. Therapy Aimed at Vasodilatation
I. Systemic Treatment 1. Alpha-blockers . . . .
120
120 120 120 120 120
120 120
XVI
2. Ganglioplegics . . . . 3. Postganglionic Blockers
II. Local Treatment
F. Griseofulvin . G. Beta-blockers H. Calcitonin . .
Chapter 2 Physical Treatment
A. Massage ...... . B. Hydrotherapy, Crenotherapy, Thalassotherapy C. Kinesitherapy and Rehabilitation D. Electrotherapy . E. Roentgentherapy F. Acupuncture
Chapter 3 Surgery . Chapter 4 Management of A1godystrophies Chapter 5 Prevention ..... .
Part 9 Clinical Course and Prognosis
Chapter 1 Clinical Course
A. Clinical Course of Untreated Algodystrophy B. Clinical Course of Treated Algodystrophy
Chapter 2 Prognosis
Part 10 Medicolegal Considerations
Causality ........ . Past Status . . . . . . . . . Duration of Total Transient Disability Date of Consolidation . . . . . . . Fixation of Permanent and Partial Disability The Pretium Doloris
References . .
Subject Index.
Contents
121 121
121
121 121 122
124
124 124 125 126 126 127
127 128 129
132
132 132
133
136 136 136 136 136 137
138
163