Reflex Sympathetic Dystrophy (RSD), now known as Complex Regional Pain Syndrome (CRPS), is a chronic pain condition that usually affects an extremity like an arm or leg following an injury. It causes ongoing pain that is out of proportion to the original injury and involves changes in skin, bone, and blood vessels in the affected area. CRPS is classified into two types depending on whether there is confirmed nerve damage present. Treatment involves a multidisciplinary approach including medications, physical therapy, sympathetic nerve blocks, and in severe cases, surgical sympathectomy to relieve pain.

1. Reflex Sympathetic
Dystrophy

2. HISTORY
Ambroise Pare 17th
century: “burning pain after nerve
injury”
Weir Mitchell 1872: “Causalgia”
a. burning pain
b. Allodynia
c. Autonomic Changes
Sudeck 1900: Regional demineralisation with post
traumatic pain
Evans 1946: “RSD”
International Association For Study of Pain:
“CRPS 1” = RSD
“ CRPS 2” = Causalgia

3. CRPS
 RSD
 Algodystrophy
 Sudeck’s Atrophy
 Shoulder Hand Syndrome
 Causalgia

4. 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

5. 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

6. 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

7. 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

8. INJURY
REACTIVE VASOMOTOR SPASM
LOSS OF VASCULAR TONE
VASODILATION
BONE RESORBTION
DECREASED MOBILITY
DECREASED CIRCULATON
FIBROSIS/SHORTENING OF INVOLVED LIGAMENTS

9. SIGNS & SYMPTOMS
 Pain
 Vasomotor changes
 Trophic changes
Within
3 weeks – 6 months
of original injury

10.  AUTONOMIC
1. B/L temp. difference (Dynamic)
2. Skin Discoloration
3. Subcutaneous Thickening
4. Peripheral Oedema
 RADIOLOGIC: Osteopenia

11.  SENSORY
1. Sensitivity
2. Muscle belly
tenderness
3. Hyperalgesia over
bony prominences,
hyperpathia
 MOTOR
1. Muscle atrophy/
weakness
2. Joint stiffness
3. Muscle contractures
4. Mechanical allodynia

12.  3 Patterns of spreading Symptoms
1. Continuous type
2. Mirror Image type
3. Independent type

13. STAGES
Based 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

14. STAGE II :
Increased chronicity
Increased symptom severity
Limb increasingly cold
Oedema +
Skin mottled
Lasts 3-12 months
Immobilization – Joint stiffness

15. STAGE III: ATROPHIC
Most severe
Symptoms near intolerance
Occurs > 1 year on
Dystrophic changes in skin, muscle and bone
UNRESPONSIVE TO Rx - PERMANENT

16. 3 PREREQOISITES FOR
DIAGNOSIS
 Persistent lesion or injury
 Predisposing constitution
 Abnormal sympathetic arc

17. 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

18.  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

19.  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

20. BEST DIAGNOSTIC &
PROGNOSTIC TEST
LA block of appropriate sympathetic ganglia
Novocain (5% Procaine hydrochloride) used as a
pharmacologic neural blocker
STELLATE GANGLION – UL
LUMBAR PARAVERTEBRAL GANGLIA – LL
Guanethadine: Initially symptoms increase then
decrease
Phentolamine test: Alpha adrenoceptors blocked

21. TREATMENT
 Educate regarding therapeutic goals
 Minimize pain
 Physiotherapy
 Determine contribution of SNS to the pain

22.  Physiotherapy
Elevation, massage, contrast baths, stockings
AIM: improve jt. ROM & muscle strength
 Acupuncture
 TENS- 1. Non invasive 2. No side effects

23.  Psychiatric treatment
 Alternative treatments
a. Qi emission b. Qi instruction
Thermal biofeedback, Relaxation training,
supportive psychotherapy

24. PHARMACOLOGY
1. 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 week
4. Dimethyl sulfoxide cream 50% on the skin
5. N-acetyl cysteine 600mg tid

25.  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

26. SYMPATHETIC BLOCKS
 3-6 tries
 Diagnostic, therapeutic, prognostic
 Continuous sympathetic block preferred
over serial blocks

27.  Stellate ganglion block
 Axillary Sympathectomy
 Lower limb Sympathectomy

28. Effective Sympathetic Denervation
 Horner’s syndrome
 Skin temp 34 deg.
 50% increase in skin blood flow
 Abolition of skin resistance response

29.  Post sympathectomy pain
1. Proximal to original pain
2. Resolves on its own
OR
After sympathetic blocks

30. THANK YOU