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Algodystrophy

(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 Post traumatic painful osteoporosis.

o Regional migratory osteoporosis.

o Shoulder-hand syndrome.

o Transient osteoporosis.
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Historical
Clinical: Causalgia.
Painful soft tissue oedema

Radiological : Acute bone atrophy


1st: Sudecks bone atrophy 1900
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Main Aetiological Fractors In 250


Cases Of Algodystrophy
Literature
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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

with CNS distributions


• Hemiplegie.
• Meningeal and cerebral hage.
• Parkinsonian disease.
• Epilpsy.
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

Result: Localized Trabicular bone loss


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Neurocasular Theory
Vicious circle, pain stiffness, fear

over sympathetic tone, vasospasm,

ischemia, vasodilatation, oedema, pain

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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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.
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Diagnosis

• Clinical basis & staging


• Radiography
• Bone scintography
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 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).
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Clinical Picture and stages
Stage II:
* Trophic changes:
- Skin atrophy. - Atrophic hairs.
- Tappering fingers. - Atrophic nails
* Joints stiffness.
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Clinical Picture and stages
Stage III:
* Joints increase in stiffness to fibrous
ankylosis.

* Decrease in the pseudoinflammatory


signs.
Lab:-
not constant Hydroxyprolinuria
increased erosive reemodelling
(osteoclast) Osteocalcin level increase
increased osteoblastic activity ESR normal
Radiology
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• Diffuse rarifaction, spotty, patchy,


widened trabiculations
• Cortical erosions
• Total loss of bone structure, by moth
eaten appearance
• Normal joints
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Bone scan
Scintography
Hot area
[remodelling activity]
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Densitometry
Weak photon densitometry image

[ decrease bone mass]


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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

Sudecks´ bone atrophy


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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.
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Treatment
Medical treatment. Physical and rehabilitation.

Local injections. Accupuncture.

Sympathetic block. Psychotherapy.

Nerve block. Surgical treatment.


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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
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Calcitonin

*In Moderate Cases:

- 100 I.U. every day. For 3months.


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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.

• Local anaesthetic + hydrocortisone.


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• Sympathetic ganglion block.

• Nerve block.
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• Physical and rehabilitaon


therapy.

•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

PROF. HAZEM ABDEL-AZEEM


PROF. OF ORTH, SURGERY
CAIRO UNIVERSITY
Role of Miacalcic AD

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

• inhibition of the algystrophic process.

•Relief of symptoms.

•Restoration of normal density.


Miacalcic Relives pain and improves AD

the range of movement in


algodystrophy
Clinical presentation AD

Pain
Swelling

Algodystrophy Stiffness
Tendernes

Frozen shoulder
Vasomotor syndrome
disurbance
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Incidence after colle´s fracture
Long-term consequences AD

Pain & Malunio Bone loss


stiffness
 persists  Deformity.  > 10% loss in
for > 1  Shortening of cortical bone.
year &  > 25% loss in
may nead the radius.
trabecular
to loss of Radio-ulnar
bone.
function joint dislocation.
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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
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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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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.
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Treatment
comprehensive approach
Treatment of injury
Block of sympathetic flow
Active movements
Psyscological support
Calcition
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Focal Osteoporosis AD

© 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

© 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


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Algodystrophy 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
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Focal Osteoporosis
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Focal Osteoporosis 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

PROF. HAZEM ABDEL-AZEEM


PROF. OF ORTH, SURGERY
CAIRO UNIVERSITY
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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
AD

Algodystrophy
Event No. Pts Follow-
up
S&S Prev. %

Shoulder- hand Sy 27%


Stroke
136 24 W.
Tenderness 24 %
100 12 W. Vasomotor Sy.
Colles
Stiffness
Swelling
Tenderness 38%
Colles Vasomotor Sy. 40 %
60 9W. 40 %
Stiffness
Tenderness 36 %
Vasomotor Sy. 44 %
Colles 274 52 W. 37 %
Stiffness
45 %
Swelling
Incidence after AD

Colle´s fracture
Incidence after AD

Colle´s fracture
Pathophysiology AD

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.
Pathophysiology
The hypothesis of an abnormal sympathetic
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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.
Pathophysiology AD

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.


DIAGNOSIS
No gold standard for diagnosis.
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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
Disproportionate criteria
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 and
Increased 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 AD

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

Pain & Malunio Bone loss


stiffness
 persists  Deformity.  > 10% loss in
for > 1  Shortening of cortical bone.
year &  > 25% loss in
may nead the radius.
trabecular
to loss of Radio-ulnar
bone.
function joint dislocation.
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 AD

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
AD
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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