1-17 Algodystrophy---

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

AD

AD

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

AD

AD

AD

AD

AD

AD

AD

AD

AD

AD

AD

AD

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

AD

AD

AD

AD

AD

AD

AD

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

AD

AD

AD

AD

AD

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

AD

AD

AD

AD

AD

AD

AD

Treatment

comprehensive approach

Treatment of injury

Block of sympathetic flow

Active movements

Psyscological support

Calcition

AD

AD

AD

AD

AD

AD

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

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

AD

AD

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

AD

AD

AD

AD

AD

AD

AD

AD