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Reflex Sympathetic Dystrophy is a chronic pain disorder
involving the sympathetic nervous system. It usually is
the result of an injury or trauma, but can also be a complication
of surgery, infection, casting or splinting and myocardial
infarction (heart attack).
The
trauma sets off the body's mechanism for pain recognition,
but then the "normal system of pain perception"
begins to misfire and an abnormal cycle of intractable
pain begins. As RSD progresses, the abnormal pain of the
sympathetic nervous system has an effect on other areas
of the body and can result in total disability as muscles,
bones, skin and the autonomic immune system become involved.
The
first indication of RSD is prolonged, intractable pain
usually more severe than the injury. The symptoms are:
- chronic
burning pain in a localized area,
-
intense sensitivity to temperature and light touch,
and
- a
color change to the skin.
Most
physicians agree that there are three stages to RSD, which
progress at a different pace in each person.
Stage
1 (Acute,
1 - 3 months): Burning pain, edema, increased
nail and hair growth, hyperthermia or hypothermia, muscle
spasm, and vasospasm.
Stage
2
(Dystrophic, 3 - 6 months): Pain
becomes more intense and proximal, sometimes crossing
the midline, cold insensitivity, brawny edema, swollen
digits, hyperhidrosis, early atrophy and loss of ROM,
mottled skin, changes in the nails, with osteopenia late.
Stage
3
(Atrophy, > 6 months): Pain involving
the entire limb becomes more diffuse and subsides to a
degree. Skin is pale and cyanotic with a smooth shiny
appearance. Further bone loss and contractures are associated
with worsening atrophy and irreversible changes. There
may be a wasting of affected muscles, contraction of tendons,
and a definite withering of the affected limb.
In
all of the stages, severe chronic pain continues to be
a major complaint. Depression can accompany the life changes
of RSD and psychological therapy may help.
Although
RSD can be a progressive disorder, it should not be assumed
that all cases will advance and present all clinical symptoms
and dysfunction. Early and effective treatment may lesson
the effect of RSD in some individuals.
RSD may result from --
- minor
trauma,
- inflammation
following surgery,
-
infection,
-
lacerations,
- degenerative
joint disease,
- burns
and
- any
compression (such as casting or swelling due to injury)
that may cause prolonged pressure on peripheral nerves.
"Peripheral
neuropathies, nerve-entrapment, neuromas, thoracic outlet
syndrome and carpal or tarsal tunnel can coexist with
RSD.
It
is hard for some physicians to accept a dual disease process
and not just focus on only one of the diseases. Many other
chronic pain disorders may be mistakenly diagnosed as
sympathetically maintained pain or RSD because of similarities
in clinical presentations.
Diagnosing
RSD is very important so proper therapy can be
applied. A wrong diagnosis is like having carburetor problems
with the engine of your car and using a tire pump to try
to fix it."
DIAGNOSIS:
It is important to make an RSD diagnosis
as early as possible !
A.Early
diagnosis includes a thorough history and examination.
1.
Look for: allodynia, burning pain, edema,
color or hair growth changes, diaphoresis,
temperature changes in the skin, muscle weakness.
2. Rule out musculoskeletal, rheumatologic,
infectious, vascular, or psychiatric disorder.
B.Diagnostic
studies:
1.
Plain film x-rays - patchy periarticular
osteoporosis (in mid to later stages)
2.
Triple-phase bone scan- high specificity
and sensitivity in early to mid stages. Static
phase is most sensitive and shows increased uptake in
periarticular bone.
3.
CT scan- swiss cheese appearance of involved
bone
4.
Thermography/Doppler- blood flow and
temperature
5.
Sympathetic block- decreases sympathetic
effector response on cutaneous nerves
TREATMENT
(Excerpt from Neurological
Pain Associates Pain Management Center,
by Dr.
H. Hoosahmand
February 2002
A.
Treat the Underlying Process !
B.
Conservative/Modalities:
1.
A&PROM exercises - as tolerated to
desensitize and prevent contractures
2. Desensitization - increase the patient's
tolerance for normal sensory input
3. Contrast baths- decreases vasomotor
activity/sensitivity
4. Edema control
5. TENS- modulates inhibitory control
of afferent input (large fibers) - early
6. Ultrasound - provides inhibiting effect
on the sympathetic ganglia.
C. Pharmacological:
1.
Adrenergic agents- propranolol, guanethidine,
clonidine
2. Tricyclics - elavil, imipramine
3. Anti-convulsant's - gabapentin, carbamazepine
4. Topical - Capsaicin (substance P/may
take weeks) and EMLA cream (fast acting)
5. Steroids - Prednisone 60mg day then
taper over 2 weeks
6. Calcium channel blockers
D. Interventional:
1.
Sympathetic blockade - injection of local anesthetic
and cortico-steroid to the sympathetic ganglia to inhibit
sympathetic tone to involved extremity.
2. Local peripheral nerve blocks
3. Surgical sympathectomy - refractory
pain (may recur in 6-12 months)
4. Amputation
D.
Other
1.
Psychologic counseling
2. Pain management counseling or program
PROGNOSIS
1.
Spontaneous remission is rare
2. Mild cases may resolve in weeks to months with early
management
3. Upper extremity involvement usually involves a longer
course than lower extremity
4. Disease course may last up to 2 years or longer
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