Reflex sympathetic dystrophy (1)

Reflex Sympathetic Dystrophy

HISTORYAmbroise Pare 17th century: “burning pain after nerve

injury”Weir Mitchell 1872: “Causalgia” a. burning pain b. Allodynia c. Autonomic ChangesSudeck 1900: Regional demineralisation with post

traumatic painEvans 1946: “RSD”International Association For Study of Pain: “CRPS 1” = RSD “ CRPS 2” = Causalgia

CRPS RSD

Algodystrophy

Sudeck’s Atrophy

Shoulder Hand Syndrome

Causalgia

CRPS 1

1. Without nerve lesion

2. Burns, blunt trauma, sprain, stroke, shingles

3. A/w: Anxiety disorder Dependency, insecurity Personality disorders, Sense of Dissatisfaction

CRPS 2

1. With nerve lesion

2. Crush injury, laceration

IASP CRITERA “Initiating Noxious Event:-External/Internal Hyperalgesia, continuing pain, allodynia out

of proportion to the inciting event e/o oedema, changes in skin blood flow or

abnormal sudomotor activity in region of pain Absence of any alternative explanation for

the symptoms +FOR CRPS II: Known nerve injury

PATHOLOGY Poorly understood Theories: CRPS 1:-

1. Ongoing nociceptor input that maintains a central state of hyper excitability for prolonged periods

2. Inflammatory cause: resembles it and relieved by steroids

Sympathetically

maintained pain

Nociceptor input

maintained by ineracn

btw Primary afferents

and sympathetic

efferents through

alpha adrenergic

mechanism

Sympathetically

independent pain

Maintaining nociceptor

input comes from other

causes such as

peripheral nerve

stimulation

Eg: Neuroma

INJURY

REACTIVE VASOMOTOR SPASM

LOSS OF VASCULAR TONE

VASODILATION

BONE RESORBTION

DECREASED MOBILITY

DECREASED CIRCULATON

FIBROSIS/SHORTENING OF INVOLVED LIGAMENTS

SIGNS & SYMPTOMS Pain

Vasomotor changes

Trophic changes

Within 3 weeks – 6 months of original injury

AUTONOMIC1. B/L temp. difference (Dynamic)2. Skin Discoloration3. Subcutaneous Thickening4. Peripheral Oedema

RADIOLOGIC: Osteopenia

SENSORY1. Sensitivity

2. Muscle belly tenderness

3. Hyperalgesia over bony prominences, hyperpathia

MOTOR1. Muscle atrophy/

weakness

2. Joint stiffness

3. Muscle contractures

4. Mechanical allodynia

3 Patterns of spreading Symptoms

1. Continuous type

2. Mirror Image type

3. Independent type

STAGESBased on severity and chronology

STAGE I. MILD

Days/wks after injury

Pain/swelling/dysfunction - localized

Exaggerated symptoms

Limb relatively immobile and sensitive

May last up to 3 months

STAGE II :Increased chronicity

Increased symptom severity

Limb increasingly cold

Oedema +

Skin mottled

Lasts 3-12 months

Immobilization – Joint stiffness

STAGE III: ATROPHIC

Most severe

Symptoms near intolerance

Occurs > 1 year on

Dystrophic changes in skin, muscle and bone

UNRESPONSIVE TO Rx - PERMANENT

3 PREREQOISITES FOR DIAGNOSIS

Persistent lesion or injury

Predisposing constitution

Abnormal sympathetic arc

DIAGNOSTIC CRITERIA BY KOZEN

Persistent and Diffuse pain

in the hand

Loss of function of the hand

Autonomic Dysfunction

Relief by interruption of Sympathetic reflex

RADIOGRAPHY

1/3rd pts. Normal X ray picture

Osteopenia in affected limb

(after 2-4 weeks of symptoms)

Increased Power Doppler Flow in RSD of Lower Extrimity

BONE SCAN / SCINTIGRAPHY

Preferred Diagnostic test

INCREASED UPTAKE—CRPS INDUCED OSTEOPENIA

MacKinnon & Holder- strictest criteria for diagnosis of RSD in hand

REQUIRED DIFFUSE INCREASE IN DELAYED PERIARTICULAR UPTAKE IN ALL JOINTS OF

AFFECTED HAND

BEST DIAGNOSTIC & PROGNOSTIC TEST

LA block of appropriate sympathetic ganglia

Novocain (5% Procaine hydrochloride) used as a pharmacologic neural blocker

STELLATE GANGLION – ULLUMBAR PARAVERTEBRAL GANGLIA – LL

Guanethadine: Initially symptoms increase then decrease

Phentolamine test: Alpha adrenoceptors blocked

TREATMENT Educate regarding therapeutic goals

Minimize pain

Physiotherapy

Determine contribution of SNS to the pain

Physiotherapy

Elevation, massage, contrast baths, stockings

AIM: improve jt. ROM & muscle strength

Acupuncture

TENS- 1. Non invasive 2. No side effects

Psychiatric treatment Alternative treatments

a. Qi emission b. Qi instruction

Thermal biofeedback, Relaxation training, supportive psychotherapy

PHARMACOLOGY1. Corticosteroids :- Prednisolone 30mg /day x 12 weeks DECREASES: pain, edema, inflamn, ectopic

electrical activity after nerve injury

2. Bisphosphonates :-7.5 mg/250 ml of saline daily x 3 days INCREASES ROM

3. Mannitol 10%, 1000ml/24 hrs x 1 week4. Dimethyl sulfoxide cream 50% on the skin5. N-acetyl cysteine 600mg tid

CONSTANT PAIN+ INFLAMMATION N.S.A.I.D.S CONSTANT PAIN – INFLAMMATION Tramadol CONSTANT PAIN – SLEEP DISTURBED Anti-depressants, Oral lidocaine, Mexiletine SPONTANEOUS PAROXYSMAL JABS Anticonvulsants SYMPATHETICALLY MEDIATED PAIN Clonidine patch MUSCLE CRAMPS/ DYSTONIA Baclofen

SYMPATHETIC BLOCKS 3-6 tries Diagnostic, therapeutic, prognostic Continuous sympathetic block preferred

over serial blocks

Stellate ganglion block

Axillary Sympathectomy

Lower limb Sympathectomy

Effective Sympathetic Denervation Horner’s syndrome

Skin temp 34 deg.

50% increase in skin blood flow

Abolition of skin resistance response

Post sympathectomy pain

1. Proximal to original pain

2. Resolves on its own

OR

After sympathetic blocks

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