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Algodystrophy (AD)
Prof. Hazem Abdel Azeem (MD)
Cairo University
Transient osteoporosis of hip
Algodystrophy 1987
H. Azeem H. Mohammadi
New Egyptian Journal of Medicine
PublicationPublicationAD
AD
Alogodystrophy a Neurodystrophic
Disorders
Alogodystrophy a Neurodystrophic
Disorders
AD
Characters:
Pain.
Swelling.
Trophic changes.
Functional incapacity.
ADAlgodystrophy
Definition
“The term Algodystrophy covers a group of
painful conditions with association of pain,
vasomotor and trophic changes, functional
impairment localized in the distal parts of the
body”
ADTerminology* Algodystrophy (AD)
o Sudecks bone atrophy 1900.
o Reflex sympathetic dystrophy (RSD).
o Decalcifying alogdystrophy.
AD
o Post traumatic painful osteoporosis.
o Regional migratory osteoporosis.
o Shoulder-hand syndrome.
o Transient osteoporosis.
AD
Historical
Clinical: Causalgia.
Painful soft tissue oedema
Radiological : Acute bone atrophy
1st: Sudecks bone atrophy 1900
AD
Main Aetiological Fractors In 250
Cases Of Algodystrophy
AD
Sudecks
Vincent
Lequesne
Mohamadi & Azeem
Réne
1900
1962
1967
1987
1994
Literature
AD
Algodystrophy Following trauma
Neglected Minor Trauma
* Sprains. * Fractures.
* Conyusions. * Dislocations.
AD
Algodystrophy with locomotor disorders
* Arthritis.
* Tendonitis.
* Gout…etc.
AD
Algodystrophy with metabolic disorders
* Diabetes mellitus.
* Gout.
Drug induced:
-Barbiturates. - Antithyroid.
- AntiTB. - Alocohol.
AD
Algodystrophy with peripheral nerves disorders
* Radiculagia..
* Neuroma.
* Nerve entrapment.
* Neuropathy.
AD
Algodystrophy
with vascular disease
• Ischaemia.
• Peripheral arterial disease.
ADAlgodystrophy
with CNS distributions
• Hemiplegie.
• Meningeal and cerebral hage.
• Parkinsonian disease.
• Epilpsy.
ADAlgodystrophy
Following surgery
Minor Soft Tissues inte
• Meningeal and cerebral hage.
• Parkinsonian disease.
• Epilpsy.
AD
AD
Pathophysiology
Theories:
• Neurovascular dystrophy
• Bone remodeling
• Hormonal regulation
• Biomechanical
AD
Biochemical Theory
AD
Hemoral Theory
? Parathyroid
? Calcitonin
? 1-25 diydroxicalciferol
Relation to ostoclastic activity
AD
Disturbance of Bone Remodelling Unbalanced
Cellular Coupling Osteoblaste X osteoclast
Result: Localized Trabicular bone loss
AD
Neurocasular Theory
Vicious circle, pain stiffness, fear
over sympathetic tone, vasospasm,
ischemia, vasodilatation, oedema, pain
mediators, etc
Neurovascular
Vasospasm
ischaemia
Vasodilation
Oedema Pain Stiffness
Over sympathetic tone
AD
Pathology
Synoial membrane normal
Articular cartilage normal
Periarticular tissue normal
No inflammatory signs
ADPathology
Osteoblastic poor activity
Subchondral cortical and
cancellous resprotion
Wide marrow spaces
Micro fractures
AD
The sites most commonly affected are the
wrist and hand (28%;, shoulder (27%),
ankle and foot (24%), knee (10%), elbow
(6%) and hip (5%). The condition occurs
mainly in people aged between 40 and 65
years.
AD
AD
• Clinical basis & staging
• Radiography
• Bone scintography
Diagnosis
AD
MRI
Densitometry
Lab. work up
Histopathology
Biopsy [core]
Clinical Picture and stages
Stage I: 2 to 3 months. * Pain : - Dull - Causalgic * Vasomotor:
- Redness to bluishness.
-Swelling. - Wormth - Oedema.
* Refrain from movement (Painful)
(Pseudoinflammatory signs).
AD
Stage II:
* Trophic changes:
- Skin atrophy. - Atrophic hairs.
- Tappering fingers. - Atrophic nails
* Joints stiffness.
Clinical Picture and stages
AD
Stage III:
* Joints increase in stiffness to fibrous
ankylosis.
* Decrease in the pseudoinflammatory
signs.
Clinical Picture and stages
Lab:-
not constant Hydroxyprolinuria
increased erosive reemodelling
(osteoclast) Osteocalcin level increase
increased osteoblastic activity ESR
normal
ADRadiology• Diffuse rarifaction, spotty, patchy,
widened trabiculations
• Cortical erosions
• Total loss of bone structure, by moth
eaten appearance
• Normal joints
AD
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AD
Bone scanScintography
Hot area
[remodelling activity]
AD
AD
Densitometry
Weak photon densitometry image
[ decrease bone mass]
AD
AD
Pathology
Core biopsy:•Periosteocytic lysis of cortical and
cancellous bone
• Foci of remodelling activity
• Osteoclastic bone resorption
AD
AD
Personal Experience
Post traumatic
Sudecks´ bone atrophy
AD
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Treatment The short-term aims of the treatment of
algodystrophy are the following: To relieve the pain. To correct or prevent vasomotor disorders. To prevent bone demoralization. To prevent trophic change and ankylosis. To reduce the duration of functional incapacity.
AD
Treatment
Medical treatment.
Local injections.
Sympathetic block.
Nerve block.
Physical and rehabilitation.
Accupuncture.
Psychotherapy.
Surgical treatment.
AD
Medical Treatment
NSAIDA.
Vasodilators.
Corticosteroids.
Betabolckers.
Calcitonin.
Calcitonin ( synthetic salmon Calcitonin)
Significantly shortens the duration of
functional incapacity, which can otherwise last for
a year or more, by preventing further bone
demineralization and promoting rapid
remineralization.
Is safe and well tolerated; there are known I
contraindications.
Calcitonin ( synthetic salmon Calcitonin)
Particularly when given in early-stage disease
Rapidly relieves pain, often completely.
Alleviates the other symptoms.
Increases joint mobility.
Next
AD
Calcitonin
*In Moderate Cases:
- 100 I.U. every day. For 3months.
AD
Calcitonin *In Severe Cases:
- 100 I.U. every day. For 2 to 4
weeks followed by 100 IU every other
day for 2 months.
AD
Calcitonin *Dose is versatile.
- course can be repeated spaced 3
monthly.
AD
Local Injection
•Periarticular (not intraarticular) and in
trigger points.
• Local anaesthetic + hydrocortisone.
AD
• Sympathetic ganglion block.
• Nerve block.
AD
• Physical and rehabilitaon
therapy.
•Accupuncture.
• Psychotherapy.
AD
Surgical Treatment * In persistent Acute Manifestation
- Sympathectomy
Cervical or Lumber.
* In Chronic Cases
- For release
AD
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Alogodystrophy?
AD
* Prognosis:
√ Recovery is common
Or √ Stiff atrophic hand
AD
Unsatisfactory situation
AD
*Problem: Diagnosis
Clinical diagnosis
Aetiological diagnosis
Pathological diagnosis
Unsatisfactory situation
Thank You
AD
AD
AD
Algodystrophy
Reflex sympathetic dystrophy PROF. HAZEM ABDEL-AZEEM
PROF. OF ORTH, SURGERY
CAIRO UNIVERSITY
Role of Miacalcic
Miacalcic
Relieves oedema
Inhibits the Alogodystrophy
process Relives pain
Increases the rang of
movement Helps in restoration
of normal bone density
Reduces redness
& hypothemia
AD
•A localized syndrome involving pain, oedema and vasomotor disturbances around a joint of joints
•Occurs due to: (1) Trauma eg. Sprains, contusions & dislocations.
(2) Locomotor disorders eg. Arthritis * tenditis
(3) Other disorders eg. Neuropathy, ischaemia & hemiplegia.
Alogodystrophy AD
• Antiosteoclastic
• Anti-inflammatory
• Analgesic
• Vascular effect
Mode of action of Miacalcic AD
• inhibition of the algystrophic process.
•Relief of symptoms.
•Restoration of normal density.
The patient need AD
Miacalcic Relives pain and improves the range of movement in
algodystrophy
AD
Clinical presentation
Algodystrophy
Swelling Pain
Tendernes
Vasomotor
disurbance
Frozen shoulder syndrome
Stiffness
AD
Incidence after colle´s fracture AD
Long-term consequences
persists for > 1 year & may nead to loss of function
Bone loss Malunio Pain & stiffness
Deformity. Shortening of the radius.Radio-ulnar joint dislocation.
> 10% loss in cortical bone. > 25% loss in trabecular bone.
AD
Miacalcic in Alogodystrophy
• Caldtonin has proved to be the most e/fei agent in
the treatment of Sudeck's disease. It proves
microcirculatory disturbances.
• Reduces bone pain.
• Inhibits the pathologically increased
resorption“
Ada Bossany, Endocr, Jugoslav., 1997
AD
Problem: Treatment
AD
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Difficult task:-
Low incidence
Refusing interference
Neurotic
Expensive lab & Rad. Work up
? Expensive drugs
AD
AD
Calcitonin *In Severe Cases:
- 100 I.U. /day.
- Sc. Or IM. For 2 to 4 weeks.
*In Moderate.
AD
AD
Miacalcic reduces vasomotor and inflammatory symptoms (e.g. oedema and changes in the appearance of the skin) and restores the mobility of the affected joint.
AD
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Treatment
comprehensive approach
Treatment of injury
Block of sympathetic flow
Active movements
Psyscological support
Calcition
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© Algodystrophy: * Local treatment:
- physiotherapy
- Sympathectomy: medical or surgical
* Systemic Treatment: - Steroids
- Calcitonin: is the most widely used drug with many reports confirming its efficacy
Focal Osteoporosis
AD
AD
© Clinical Trial (Sawiki A. et al.1992) :
* Synthetic Salmon Calcitonin is not only potent inhibitor of the algodystroph
process but may also contribute in some was to the activation of the skeletal restoration normal bone density.
Clinical Rheumatology,1992
Algodystrophy
AD
AD
© Clinical Trial (Sawiki A. et al.1992) (Cont.):
* * A marked clinical improvement
occurred; pain diminished, motion range increased oedema, redness and hypothermia substantially decreased.
Clinical Rheumatology,1992
Algodystrophy
ADFocal Osteoporosis
AD
AD
© Algodystrophy: * Clinical syndrome characterized by:
- Pain- Tenderness- Dystrophic skin changes- Swelling - Stiffness - Vascular instability
Focal Osteoporosis
AD
© Algodystrophy: * Radiological changes include:
- Loss of bone density
- Patchy radio translucencies
- Subchondral radiio-translucencies
- Loss of trabecular definition
Focal Osteoporosis
AD
Transient Osteoporosis
of the Hip in Pregnancy
Focal Osteoporosis
AD
© Transient Osteoporosis of the Hip : * Occurs in women during third trimester.
* Clinical manifestations include hip pain and limitation of movements.
* ESR may be raised.
* X-ray shows osteoporsis particularly the femoral head.
Focal Osteoporosis
ADFocal Osteoporosis
AD
Calcitonin New interesting Publication
Calcitonin New interesting Publication
AD
AD
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Algodystrophy
Reflex sympathetic dystrophy PROF. HAZEM ABDEL-AZEEM
PROF. OF ORTH, SURGERY
CAIRO UNIVERSITY
AD
Definition "Algodyitrophy is a clinical syndrome characterized by prominent locoregional pain, vasomotor and trophic changes and delayed recovery, occurring after even minor trauma or surgery
Nomenclature of Algodystrophy
* Out of > 45 names the commonest are :- Algodystrophy
- Complex regional pain syndrome type 1 (CRPS1- port trauma or surgery)
- Complex regional pain syndrome type 2 (CRPS2- alter nerve Injury)
- Reflex sympathetic dystrophy
- Sudeks atrophy
Nomenclature of Algodystrophy* In retrospective studies the incidence
was:- 1-2% after various fractures and- 2-5% alter peripheral nerve Injury.
* In prospective studies, the incidence was much higher:- 7-3SV. of Colles' fracture ,- 27% after stroke with shoulder trauma and- 8%after stroke when shoulder trauma was avoided.
Associated events related to
Algodystrophy* Trauma:- without fracture
» minor trauma » major trauma
- withfracture» limbs » vertebra
* Neurological lesions* Spontaneous
* Other precipitating/ associated factors eg : - Surgery- Stroke - Coronary artery disease.
AD
Incidence of Algodystrophy Event No. Pts Follow-
up S&S Prev. %
Stroke 136 24 W.
Shoulder- hand Sy 27%
Colles 100 12 W.
TendernessVasomotor Sy.StiffnessSwelling
24 %
Colles 60 9W.
Tenderness Vasomotor Sy.Stiffness
38%40 %40 %
Colles 274 52 W.
TendernessVasomotor Sy.StiffnessSwelling
36 %44 %37 %45 %
ADIncidence after Colle´s fracture
ADIncidence after Colle´s fracture
ADPathophysiology The clinical signs suggest the involvement of
the neurological system, and
The scintigraphic and radiological changes
indicate increased vascularity and accelerated
bone loss.
Which of the changes is cause or secondary
remains, however, to be proven.
ADPathophysiology The hypothesis of an abnormal sympathetic
nervous reflex Is, challenged by: The variable effect of local blockade of the sympathetic system
or of gympathectomy.
Furthermore, In a large group of patients with algodystrophy,
early symptoms of an exaggerated regional Inflammatory
response were found In most patients, but clinical symptoms of
a disturbance of the sympathetic nervous system, such as
hyperhydrosts, were only rarely present.
The lower level of noradrenallne In the affected site does not
support Increased sympathetic overactlvlty.
ADPathophysiology Tissue injury in the inciting event, and biochemical processes have
been involved.
Recently α-adrenerglc receptors have been emphasized, in controlling
thermoregulatory modulation.
Psychological symptomps were found in up to 50% of the patients,
BUT many of them were described in patients with severe illness as
well.
The changes in bone density on X-ray, with patchy osteoporosis, are
considered to be secondary to an inflammation-like component of the
syndrome and to disuse.
ADDIAGNOSIS No gold standard for diagnosis.
Diagnosis is based on the combination of clinical signs and in some,
cased by X-ray and radionuclide scintigraphic pictures.
In clinical research setting additional methods have been applied such as;
Thermography,
Volume measurement of the affected limb.
measurement of resting sweat.
Quantitative pseudomotor axon reflex tests.
Asymmetry, ultrasound, Doppler and bone densitometry.
RISK FACTORS FOR DEVELOPING ALGODYSTROPHY
Some studies, (thawed that Collet' fracture as evaluated by severity (usingthe Frytanan's dassHlcatton) will associated with the severity of algodystrophy.
Risk factor* alter itroke Included subluxation and paresis of the shoulder
girdle, moderate •pasticlty and vliual disturbances.
Transient osteoporosls of the hip Is a typical presentation hi pregnancy or
early postpartum.
The hypothesis of a special personality structure for developingaigodystrophy has not been found in a large overview of the literature.
Patients with severe complications were younger,
Females, had more often lower limb Involvement or multiple localizations and had Initially a 'cold* presentation on clinical examination.
Modified clinical diagnostic criteria Disproportionate pain to inciting event with:
- At least one symptom In each of the following categories:
• Sensory; hyperesthesla
• vasomotor : Temp. Asymmetry and /or skin colour changes and /or skin color asymm.
• Sweating /Oedema : Oedema and /or sweating changes and/or sweating asymm.
• Motor/ Trophic: Dei ease range of motion and /or motor dysfunction (weaqkness, tremor, dystonla) and / or trophic changes (hair ,nall, skin) B - Plus at least one sign In 2 or more of the same categories
Radionuclide scintigraphy Typically, the scintigraphic analysis includes a
radionuclide angiogram, a blood pool or tissue phase image and a delayed image.Three stages have been described
increased perfusion with increased and delayed activity of bone images, followed by.
Normal perfusion with persistent changes in bone images and lastly,
Normal or decreased vascularity with normalization of the bone images.
Typical positive image can be supportive but it’s the absence does not rule out typical clinical presentation.
Radionuclide changes Patchy or diffuse osteopenia are found in 50%
of cases.
The radiographic appearance is however non-specific.
Osteopenia may be seen 2 to 3 weeks after the onset of symptoms.
In a later stage: Affected bones may have a ground glass appearance.
cortical crosions around the joints andIncreased joint effusion.
Radionuclide changes (Cont.)
Localized osteoprosis :
After 7 weeks, bone loss was significantly highrt in
patients with alogodystrophy at cortical (14% versus-6%, P<
0.05) and trabecular sites ( -23% versus- 10% p< 0.001) in
the forearm compared to patients without algodystrophy.
in patient without algodystrophy, bone loss recovered
after 19-32 weeks, in patients with algodystrophy, bone loss
persisted after 6 to 12 months.
Clinical presentation
Algodystrophy
Swelling Pain
Tendernes
Vasomotor
disurbance
Frozen shoulder syndrome
Stiffness
AD
SPECTRUM OF CLINICAL SIGNS AND
SYMPTOMS Algodystrophy typical occurs in an extermity after a sometimes trivial event, such as trauma or surgry:
The clinical picture includes the combinations of
o intense pain that is disropportionate to the incting event.
o Vasomotor changes with oedema and changes in skin colour and
temperature.
o Delayed functional recovery, and
o Various associated tropic changes
The key feature is disroprotionate pain, and this may be the initial
manifestation of algodystrophy.
SPECTRUM OF CLINICAL SIGNS AND SYMPTOMS - The clinical picture of Algodystrophy is
different in children as compared to adults. It is
mostly characterised by hypothermia, and mild
and incomplete forms have been described
SPECTRUM OF CLINICAL SIGNS AND SYMPTOMS Stages of Algodystrophy :
Stage I (weeks to months):
o Non-focal pain of often progressively increasing intensity that is
disproprtionate to the incliting evevt, associated with joint stiffness,
decreased rang of motion, increased skin temperature and dyshydrosis.
Stage II (several months):
o Persisting pain with tendency to decrease in most but not all cases, oedema
with thicking of the skin and fascia, and muscular atrophy. Development of
localized patchy osteoporosis.
Stage III :
o Persisting, atrophy of skin and muscles, stiffness of the joint, cooling of the
involved extermity.
Long-term consequences
persists for > 1 year & may nead to loss of function
Bone loss Malunio Pain & stiffness
Deformity. Shortening of the radius.Radio-ulnar joint dislocation.
> 10% loss in cortical bone. > 25% loss in trabecular bone.
AD
The patient need
inhibition of the algodystrophic process.
Relief of symptoms.
Restoration of normal density
MANAGEMENT • Management of algodystrophy has been complicated by all the
above mentioned uncertainties
• Furthermore, management of chronic evolution can become
complicated by associated psychosodal problems of the
patient
• Physical therapy Is suggested as the mainstay of therapy, but
no controlled trial Is available,
• Caldtonln Induced a rapid decline In pain In 64% of patients
compared to 23% on placebo after 2 weeks (P < 0,001),
• Intranasal calcltonln was superior to placebo In ameliorating
pain and mobility, and resulted In Increased work ability after
60 days,
Role of Miacalcic
Miacalcic
Relieves oedema
Inhibits the Alogodystrophy
process Relives pain
Increases the rang of
movement Helps in restoration
of normal bone density
Reduces redness
& hypothemia
AD
Miacalcic in Algodystrophy• Clinical Trial (Sawiki A. et al.1992):
* Synthetic Salmon Calcitonin is not only a po inhibitor
of the algodystrophic process but may also contribute
in some way to the activation of the skeletal
restoration of normal bone density.
* A marked clinical improvement occurred; pain
diminished, motion range increased oedema, redness
and hypothermia substantially decreased.
Miacalcic Relives pain and improves
the rang of movement in
algodystrophy.
AD
“ Calcitonin has proved to be the most effective agent in the treatment of Sudeck's disease. It proves microcirculatory disturbances.
• Reduces bone pain.
•Inhibits the pathologically increased bone resorption"
Miacalcic Relives pain and improves
the rang of movement in
algodystrophy.
Thank You
AD
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