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Reflex Sympathetic Dystrophy
(CRPS I)
Presentation by : Somu Venkatesh
• In 1766, Hunter introduced the term algodystrophy in
describing pain of uncertain origin.
• In 1864 Mitchell introduced the term causalgia to
describe nerve pain following an amputation.
• More recently Evans forwarded the term reflex
sympathetic dystrophy (RSD) to identify a condition
that included pain, swelling, hyperhydrosis, skin color
changes, skin temperature changes, stiffness, and
underlying osteoporosis, with all symptoms potentially
reversible with stellate ganglion blockade.
Synonyms for CRPS:
• Algodystrophy
• Mimocausalgia
• Peripheral trophoneurosis
• Posttraumatic sympathetic dystrophy
• Reflex neurovascular dystrophy
• Shoulder-hand syndrome
• Sudeck’s atrophy
• Sympathetic neurovascular dystrophy
• The terms complex regional pain syndrome
(CRPS)types 1 and 2 are now used in place of
reflex sympathetic dystrophy (RSD) and
causalgia.
• CRPS type 1 is a regional pain syndrome that often
develops after tissue injury and most commonly affects
one limb.
• Examples of associted injury include minor shoulder or
limb trauma, fractures, myocardial infraction, or stroke.
• Allodynia (the perception of a nonpainful stimulus as
painful), hyperpathia (an exaggerated pain response to
a painful stimulus), and spontaneous pain occur.
• The symptoms are unrelated to the severity of the
initial trauma and are not confined to the distribution
of a single peripheral nerve.
• CRPS type 2 is a regional pain syndrome that
develops after injury to a specific peripheral
nerve, often a major nerve trunk.
• Spontaneous pain initally develops within the
territory of the affected nerve but eventually
may spread outside the nerve distribution.
• Pain(usually burning or electrical in quality) is the
primary clinical feature of CRPS.
• Vasomotor dysfunction, sudomotor abnormalities, or
focal edema may occur alone or in combination but
must be present for diagnosis.
• Limb pain syndromes that do not meet these criteria
are best classified as "limb pain - not otherwise
specified."
• In CRPS, localized sweating (increased resting sweat
output) and changes in blood flow may produce
temperature difference between affected and
unaffected limbs.
• CRPS type 1 (RSD) has been classically divided
into 3 clinical phases.
Phase 1
• Phase 1 consists of pain and swelling in the
distal extremity occuring within weeks to 3
months after the precipitation event.
• The pain is diffuse, spontaneous and either
burning, throbbing or aching in quality
• The involved extermity in warm and
edematous, and the joints are tender.
• Increased sweating and hair growth develop.
Phase 2
• In Phase 2 (3-6 months after onset), thin,
shiny, cool skin appears.
Phase 3
• After and additionall 3-6 months (Phase 3),
atrophy of the skin and subcutaneous tissue
plus flexion contractures complete the clinical
picture.
• The pathophysiology of CRPS is still unknown.
• To date the most reliable tool for the diagnosis
of CRPS is the physical examination.
• Other less reliable tests include the three-
phase bone scan, thermography, the
quantitative sudomotor axon reflex test
(QSART), and plain radiography.
• Increased uptake is anticipated in the later
phases of the bone scan while osteopenia is a
later finding in the CRPS patient.
• Autonomic testing or bone scans are
occasionally useful when the diagnosis is in
doubt.
• The natural history of typical CRPS may be
more variable than previously recognized.
• Most patients diagnosed within the first 6 to 8
weeks respond favorably to treatment.
Management
• Initially, hand therapy plays an important role in
the treatment of CRPS.
• Such techniques as massage, edema control,
gentle passive motion (to prevent contracture),
contrast baths, and use of the transelectrical
stimulator unit (TENS) have proven effective.
• The key concept to remember when embarking
on hand therapy is the patient must be exercised
within the limits of pain, otherwise a flare-up of
the condition may result.
• Initial drug therapies have included the use of ß-
blocker medication (propranolol), calcium
channel blockers medication (nifedipine),
guanethidine, neurontin (anticonvulsant
medication), nasal calcitonin, and 6-day medrol
dose packs—all with some limited success.
• The role of NSAIDs, although theoretically
attractive, has shown limited benefit.
• In patients with CRPS I or II, pain may be
sympathetically mediated or sympathetically
independent.
• In those with sympathetically mediated pain,
stellate ganglion blocks may be diagnostic as
well as curative for the condition.
• Multiple such injections may be necessary to
realize a benefit and are indicated when other
above-mentioned measures are not effective.
• Surgical stellate ganglion ablation is yet
another treatment alternative.
THANK YOU
Pharmacological interventions:
Physicians use a variety of drugs to treat RSD
• antidepressants
• anti-inflammatory such as corticosteroids
• COX-inhibitors such as piroxicam,
• vasodilators
• GABA analogs such gabapentin and pregabalin,
• alpha- or beta-adrenergic-blocking compounds,
and the entire pharmacy of opioids.
• Implantable drug pumps may also be used to
deliver pain medication directly to the
cerebrospinal fluid which allows
powerful opioids to be used in a much smaller
dose than when taken orally.
Drug pump
Sympathectomy
• Surgical, chemical, or radiofrequency
sympathectomy — interruption of the
affected portion of the sympathetic nervous
system — can be used as a last resort
Physiotherapy Management:
• Goal: ‘symptomatic treatment’
Pain
• TENS
• Thermal agents
• Cryotherapy
• Vibration
• Splinting-dynamic
• CPM
Edema
• Elevation
• Soft tissue manipulations
• Active exercises
• Compression- continuous
Allodynia
• Vibration
• Massage
• Progressive weight bearing
• Contrast bath
• Desensitization
– Peripheral to central
– Fine texture to coarse texture
Dystonia and joint stiffness
• Biofeedback and activities
• Active exercises
• Splinting
– Dynamic: pain and motion
– Static: prevention, assist weak muscles
– Static progressive: joint stiffness, tissue contracture
• CPM
• Modalities
– Superficial heat with gentle stretch
– Ultrasound with gentle stretch
Vasomotor instability
• Low-impact aerobic activities
• Thermal biofeedback
Vasoconstriction
Thermal agents
Massage
Ultrasound
TENS(burst)
Patient education-caffiene/nicotine
intake
Vasodilation
Cryotherapy
TENS
Neural mobilization
Patient education- alcohol

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CRPS

  • 1. Reflex Sympathetic Dystrophy (CRPS I) Presentation by : Somu Venkatesh
  • 2. • In 1766, Hunter introduced the term algodystrophy in describing pain of uncertain origin. • In 1864 Mitchell introduced the term causalgia to describe nerve pain following an amputation. • More recently Evans forwarded the term reflex sympathetic dystrophy (RSD) to identify a condition that included pain, swelling, hyperhydrosis, skin color changes, skin temperature changes, stiffness, and underlying osteoporosis, with all symptoms potentially reversible with stellate ganglion blockade.
  • 3. Synonyms for CRPS: • Algodystrophy • Mimocausalgia • Peripheral trophoneurosis • Posttraumatic sympathetic dystrophy • Reflex neurovascular dystrophy • Shoulder-hand syndrome • Sudeck’s atrophy • Sympathetic neurovascular dystrophy
  • 4. • The terms complex regional pain syndrome (CRPS)types 1 and 2 are now used in place of reflex sympathetic dystrophy (RSD) and causalgia.
  • 5. • CRPS type 1 is a regional pain syndrome that often develops after tissue injury and most commonly affects one limb. • Examples of associted injury include minor shoulder or limb trauma, fractures, myocardial infraction, or stroke. • Allodynia (the perception of a nonpainful stimulus as painful), hyperpathia (an exaggerated pain response to a painful stimulus), and spontaneous pain occur. • The symptoms are unrelated to the severity of the initial trauma and are not confined to the distribution of a single peripheral nerve.
  • 6. • CRPS type 2 is a regional pain syndrome that develops after injury to a specific peripheral nerve, often a major nerve trunk. • Spontaneous pain initally develops within the territory of the affected nerve but eventually may spread outside the nerve distribution.
  • 7. • Pain(usually burning or electrical in quality) is the primary clinical feature of CRPS. • Vasomotor dysfunction, sudomotor abnormalities, or focal edema may occur alone or in combination but must be present for diagnosis. • Limb pain syndromes that do not meet these criteria are best classified as "limb pain - not otherwise specified." • In CRPS, localized sweating (increased resting sweat output) and changes in blood flow may produce temperature difference between affected and unaffected limbs.
  • 8. • CRPS type 1 (RSD) has been classically divided into 3 clinical phases.
  • 9. Phase 1 • Phase 1 consists of pain and swelling in the distal extremity occuring within weeks to 3 months after the precipitation event. • The pain is diffuse, spontaneous and either burning, throbbing or aching in quality • The involved extermity in warm and edematous, and the joints are tender. • Increased sweating and hair growth develop.
  • 10. Phase 2 • In Phase 2 (3-6 months after onset), thin, shiny, cool skin appears.
  • 11. Phase 3 • After and additionall 3-6 months (Phase 3), atrophy of the skin and subcutaneous tissue plus flexion contractures complete the clinical picture.
  • 12. • The pathophysiology of CRPS is still unknown.
  • 13. • To date the most reliable tool for the diagnosis of CRPS is the physical examination. • Other less reliable tests include the three- phase bone scan, thermography, the quantitative sudomotor axon reflex test (QSART), and plain radiography. • Increased uptake is anticipated in the later phases of the bone scan while osteopenia is a later finding in the CRPS patient.
  • 14. • Autonomic testing or bone scans are occasionally useful when the diagnosis is in doubt. • The natural history of typical CRPS may be more variable than previously recognized.
  • 15. • Most patients diagnosed within the first 6 to 8 weeks respond favorably to treatment.
  • 16. Management • Initially, hand therapy plays an important role in the treatment of CRPS. • Such techniques as massage, edema control, gentle passive motion (to prevent contracture), contrast baths, and use of the transelectrical stimulator unit (TENS) have proven effective. • The key concept to remember when embarking on hand therapy is the patient must be exercised within the limits of pain, otherwise a flare-up of the condition may result.
  • 17. • Initial drug therapies have included the use of ß- blocker medication (propranolol), calcium channel blockers medication (nifedipine), guanethidine, neurontin (anticonvulsant medication), nasal calcitonin, and 6-day medrol dose packs—all with some limited success. • The role of NSAIDs, although theoretically attractive, has shown limited benefit. • In patients with CRPS I or II, pain may be sympathetically mediated or sympathetically independent.
  • 18. • In those with sympathetically mediated pain, stellate ganglion blocks may be diagnostic as well as curative for the condition. • Multiple such injections may be necessary to realize a benefit and are indicated when other above-mentioned measures are not effective.
  • 19. • Surgical stellate ganglion ablation is yet another treatment alternative.
  • 21. Pharmacological interventions: Physicians use a variety of drugs to treat RSD • antidepressants • anti-inflammatory such as corticosteroids • COX-inhibitors such as piroxicam, • vasodilators • GABA analogs such gabapentin and pregabalin, • alpha- or beta-adrenergic-blocking compounds, and the entire pharmacy of opioids.
  • 22. • Implantable drug pumps may also be used to deliver pain medication directly to the cerebrospinal fluid which allows powerful opioids to be used in a much smaller dose than when taken orally. Drug pump
  • 23.
  • 24. Sympathectomy • Surgical, chemical, or radiofrequency sympathectomy — interruption of the affected portion of the sympathetic nervous system — can be used as a last resort
  • 25. Physiotherapy Management: • Goal: ‘symptomatic treatment’
  • 26. Pain • TENS • Thermal agents • Cryotherapy • Vibration • Splinting-dynamic • CPM
  • 27. Edema • Elevation • Soft tissue manipulations • Active exercises • Compression- continuous
  • 28. Allodynia • Vibration • Massage • Progressive weight bearing • Contrast bath • Desensitization – Peripheral to central – Fine texture to coarse texture
  • 29. Dystonia and joint stiffness • Biofeedback and activities • Active exercises • Splinting – Dynamic: pain and motion – Static: prevention, assist weak muscles – Static progressive: joint stiffness, tissue contracture • CPM • Modalities – Superficial heat with gentle stretch – Ultrasound with gentle stretch
  • 30. Vasomotor instability • Low-impact aerobic activities • Thermal biofeedback Vasoconstriction Thermal agents Massage Ultrasound TENS(burst) Patient education-caffiene/nicotine intake Vasodilation Cryotherapy TENS Neural mobilization Patient education- alcohol