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.
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.
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.
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