Beruflich Dokumente
Kultur Dokumente
(AD)
Prof. Hazem Abdel Azeem (MD)
Cairo University
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Publication
Transient osteoporosis of hip
Algodystrophy 1987
H. Azeem H. Mohammadi
New Egyptian Journal of Medicine
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Alogodystrophy a
Neurodystrophic
Disorders
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Characters:
Pain.
Swelling.
Trophic changes.
Functional incapacity.
Algodystrophy AD
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”
Terminology
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* Algodystrophy (AD)
o Sudecks bone atrophy 1900.
o Reflex sympathetic dystrophy (RSD).
o Decalcifying alogdystrophy.
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o Shoulder-hand syndrome.
o Transient osteoporosis.
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Historical
Clinical: Causalgia.
Painful soft tissue oedema
Sudecks 1900
Vincent 1962
Lequesne 1967
Mohamadi & Azeem 1987
Réne 1994
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Algodystrophy Following
trauma
Neglected Minor Trauma
* Sprains. * Fractures.
* Conyusions. * Dislocations.
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Algodystrophy with
locomotor disorders
* Arthritis.
* Tendonitis.
* Gout…etc.
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Algodystrophy with
metabolic disorders
* Diabetes mellitus.
* Gout.
Drug induced:
-Barbiturates. - Antithyroid.
- AntiTB. - Alocohol.
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Algodystrophy with
peripheral nerves disorders
* Radiculagia..
* Neuroma.
* Nerve entrapment.
* Neuropathy.
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Algodystrophy
with vascular disease
• Ischaemia.
• Peripheral arterial disease.
Algodystrophy AD
Following surgery
Minor Soft Tissues inte
• Meningeal and cerebral hage.
• Parkinsonian disease.
• Epilpsy.
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Pathophysiology
Theories:
• Neurovascular dystrophy
• Bone remodeling
• Hormonal regulation
• Biomechanical
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Biochemical Theory
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Hemoral Theory
? Parathyroid
? Calcitonin
? 1-25 diydroxicalciferol
Relation to ostoclastic activity
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Disturbance of Bone
Remodelling Unbalanced
Cellular Coupling
Osteoblaste X osteoclast
Neurocasular Theory
Vicious circle, pain stiffness, fear
mediators, etc
Oedema Pain Stiffness
Vasodilation
Neurovascular
ischaemia
Over sympathetic
Vasospasm tone
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Pathology
Synoial membrane normal
Articular cartilage normal
Periarticular tissue normal
No inflammatory signs
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Pathology
Osteoblastic poor activity
Subchondral cortical and
cancellous resprotion
Wide marrow spaces
Micro fractures
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years.
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Diagnosis
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.
Bone scan
Scintography
Hot area
[remodelling activity]
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Densitometry
Weak photon densitometry image
Pathology
Core biopsy:
•Periosteocytic lysis of cortical and
cancellous bone
• Foci of remodelling activity
• Osteoclastic bone resorption
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Personal Experience
Post traumatic
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.
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Treatment
Medical treatment. Physical and rehabilitation.
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)
Next
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Calcitonin
Calcitonin
*In Severe Cases:
- 100 I.U. every day. For 2 to 4
weeks followed by 100 IU every other
day for 2 months.
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Calcitonin
*Dose is versatile.
- course can be repeated spaced 3
monthly.
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Local Injection
•Periarticular (not intraarticular) and in
trigger points.
• Nerve block.
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•Accupuncture.
• Psychotherapy.
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Surgical Treatment
* In persistent Acute Manifestation
- Sympathectomy
Cervical or Lumber.
* In Chronic Cases
- For release
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Alogodystrophy?
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* Prognosis:
√ Recovery is common
Or √ Stiff atrophic hand
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Unsatisfactory
situation
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Unsatisfactory situation
*Problem: Diagnosis
Clinical diagnosis
Aetiological
diagnosis
Pathological
Thank
You
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Algodystrophy
Reflex sympathetic dystrophy
Inhibits the
Alogodystrophy
Relives pain Relieves oedema
process
Miacalcic
Increases the
rang of
movement Reduces redness
Helps in restoration & hypothemia
of normal bone
density
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Alogodystrophy
• 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.
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Mode of action of Miacalcic
• Antiosteoclastic
• Anti-inflammatory
• Analgesic
• Vascular effect
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The patient need
•Relief of symptoms.
Pain
Swelling
Algodystrophy Stiffness
Tendernes
Frozen shoulder
Vasomotor syndrome
disurbance
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Incidence after colle´s fracture
Long-term consequences AD
Problem:
Treatment
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Difficult task:-
Low incidence
Refusing interference
Neurotic
Expensive lab & Rad. Work up
? Expensive drugs
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Calcitonin
*In Severe Cases:
- 100 I.U. /day.
- Sc. Or IM. For 2 to 4 weeks.
*In Moderate.
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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
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Algodystrophy 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 AD
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Calcitonin
New interesting Publication
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Algodystrophy
Reflex sympathetic dystrophy
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
* Trauma:
Algodystrophy
- without fracture
» minor trauma
» major trauma
- withfracture
» limbs
» vertebra
* Neurological lesions
* Spontaneous
* Other precipitating/ associated factors eg :
- Surgery
- Stroke
- Coronary artery disease.
Incidence of
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Algodystrophy
Event No. Pts Follow-
up
S&S Prev. %
Colle´s fracture
Incidence after AD
Colle´s fracture
Pathophysiology AD
been involved.
thermoregulatory modulation.
well.
In clinical research setting additional methods have been applied such as;
Thermography,
Pain
Swelling
Algodystrophy Stiffness
Tendernes
Frozen shoulder
Vasomotor syndrome
disurbance
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 AD
Relief of symptoms.
Inhibits the
Alogodystrophy
Relives pain Relieves oedema
process
Miacalcic
Increases the
rang of
movement Reduces redness
Helps in restoration & hypothemia
of normal bone
density
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.
improves the rang of
movement in
algodystrophy.
Miacalcic Relives pain
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and improves the rang
of movement in
algodystrophy.
“ 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"
Thank
You
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