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Complex Regional Pain
Syndrome
A.Sridhar, MPT
1864 - Colonel Weir Mitchell, MD
“severely painful dystrophic syndrome following ballistic
injuries” in Civil War soldiers: Causalgia
History
Paul Sudeck
Suggested that the signs and symptoms of RSD may be caused by an exaggerated inflammatory response to injury or operation of an extremity.
Sudeck’s Atrophy: Bone
loss associated with RSD
Rene Leriche
Sympathetic
nervous system
dysfunction as a
cause of pain.
Therapeutic surgical
sympathectomy
John Bonica
The syndrome much as we
know it today
Promoted the term RSD
Described 3 stages
CRPS History
CRPS (complex regional pain syndrome) initially considered in early 1800s by Claude Bernard et al.
During the Civil War it was seen that soldiers who suffered from low-velocity, high-mass missile injuries developed a neuropathic pain that was termed "causalgia" by Silas Weir-Mitchell.
In 1940s the term of reflex sympathetic dystrophy came into use relating the belief of an abnormal efferent reflex from the sympathetic nervous system to bodily injury.
Since that time much study and frustration has come from this relatively rare condition of which the pathophysiology is still not fully understood.
Basics
Often seen after injury to a limb or related to
some inciting event.
The patient complains of and can manifest
skin color/ temperature/ appearance changes
in the affected limb.
Pain often excruciating – burning, tingling,
electric-like, etc. are often symptoms that
patients feel. The pain is often out of
proportion to stimulus or the event.
Physical Appearance
Diagnostic Criteria
IASP (International Assoc for the Study of Pain) diagnostic criteria include 4 subjective and/ or objective findings:
1. The presence of an initiating event or a cause of immobilization – peripheral injury or central (stroke, etc)*. (Injury)
2. Continuing pain, allodynia, or hyperalgesia in which the pain is disproportiate to inciting event. (Sensory)
3. Evidence of edema, changes in skin blood flow, or abnormal sudomotor activity in region of pain. (Vasomotor)
4. Diagnosis is excluded by the existence of other conditions that would otherwise account for the degree of pain/ dysfunction.
One symptom from each category (except #1 as 5% of pts lack known event) and at least one sign from 2 categories must be evident to diagnose CRPS, at least by research criteria.
*Not always present or identifiable.
CRPS More Widely Diagnosed
Quickly becoming more recognized, and
possibly overly diagnosed for several
reasons:
The standardization of diagnosis.
The "discovery" by personal injury lawyers
who use it as a tool for settlements.
New treatments and research for chronic
pain.
Patient self-research and the internet.
Diagnostic Si/Sx
The most common pain finding is a "burning" and "stinging” sensations that occur spontaneously. This is seen in as many as 87% of cases.
69% of patients report hyperesthesia with light touch (such as clothing laying on the skin or even draughts of blowing wind).
Vasomotor dysfunction is manifested by asymmetrical edema in affected limb, skin color and temperature changes, abnormal sweating (either hyperhidrosis or anhidrosis), and skin/ nail changes.
Patients may also complain of muscle jerking, myoclonus, or rigidity in affected limb including contractures of hands and feet.
RSD RENAMED
Reflex Sympathetic Dystrophy renamed as
Complex Regional Pain Syndrome in 1995
CRPS type 1 is RSD
CRPS type 2 is Causalgia (nerve lesion)
Current evidence suggests CRPS 1 is minute
nerve injury in C fibers (Oaklander AL MD
PhD et al Pain 2006)
CRPS II
The majority of patients seen are diagnosed with
CRPS type I – or reflex sympathetic dystrophy
(RSD). This is the less painful, debilitating of the two.
CRPS II (causalgia) is related to a known injury to a
specific major nerve with neuropathic pain frequently
following along the distribution of that nerve alone,
though not always.
While the diagnostic criteria of the IASP may apply,
these patients may also demonstrate hypoesthesia in
the nerve distribution associated with electrical shocks
and extreme allodynia. This is rarer than CRPS I and
the patients are often more debilitated.
IASP Nomenclature
CRPS I = Reflex Sympathetic Dystrophy
CRPS II = Causalgia
The only difference between the two is the inciting event: minor trauma (I) versus major peripheral nerve injury (II).
���Algodystrophy, Sudeck’s atrophy, sympathetically maintained pain, shoulder/hand syndrome, transient osteoporosis, and acute atrophy of bone.
Clinical Presentation
Precipitating event:
CRPS I
Minor trauma, contusion, sprain or strain
Fracture (especially colles fx)
Post surgical
Immobilization
Less frequently: CVA, spinal cord injury
CRPS II
Documented peripheral nerve injury and concordant
focal deficits (but the signs and symptoms of CRPS are
not limited to the same distribution as the affected nerve.)
Clinical Presentation
Time Course
Three stages:
Stage 1 (acute)
Stage 2 (dystrophic)
Stage 3 (atrophic)
CRPS Stage 1 (Acute) Immediately after injury--3 months MOST LIKELY TO BE REVERSED AND CURED
SKIN: Red, warm, swollen, dry, inflamed. Later color may
change to mottled and colder with marked hyperhydrosis. Changes back and forth especially with painful use.
DISTRIBUTION: Pain is not compatible with a single peripheral nerve, trunk, or root lesion.
SYMPATHETIC:
VASOMOTOR: Disturbances occur with variable intensity, producing altered color and temperature. Hyperemic Mottled
SUDOMOTOR: Dry Hyperhydrosis
MOTOR: Decreased ROM, weakness
X-RAYS: Normal
BONE SCAN: Increased uptake
Stage 1 (Acute)
Stage 1 (Acute)
QuickTime™ and a decompressor
are needed to see this picture.
CRPS Stage 2 (Dystrophic)
Pain remains SEVERE. Same characteristics
as Stage 1.
CRPS Stage 2 (Dystrophic)
6 weeks--1 year SKIN: Cool, moist, tight/shiny, swelling,
coarse/sparse hair, brittle nails, discolored, edema
SYMPATHETIC: VASOMOTOR: Mottled/cyanotic
SUDOMOTOR: Hyperhydrosis
MOTOR: Weakness, decreased ROM
BONE SCAN: No longer helpful.
Stage 2 (Dystrophic)
Stage 2 (Dystrophic)
QuickTime™ and a decompressor
are needed to see this picture.
Stage 2 (Dystrophic)
CRPS Stage 3 (atrophic)
6 months--Forever? Pain is somewhat decreased (but still debilitating)
less at rest, worse with passive motion
Changes are irreversible, poor outcomes, permanent disability
SKIN: Atrophy, “waxy”, very thin, ulcerations, brittle nails
SYMPATHETIC: VASOMOTOR: Cold, intermittently cyanotic/mottled
MOTOR: Decreased ROM, weakness, muscle & tendon atrophy, contractures, dystonia, tremor. Nonfunctional limb.
X-RAYS: Diffuse patchy osteoporosis (Sudeck’s Atrophy)
Atrophic Stage 3
Severe Mottling
Atrophic Stage 3
Contractures
Skin Ulceration
Migratory/progressive
CRPS I Diagnostic Criteria - IASP
1. The presence of an initiating noxious event or a cause of immobilization.
2. Continuing pain, allodynia or hyperalgesia with which the pain is disproportionate to the inciting event.
3. Evidence at some time of edema, changes in skin blood flow or abnormal sudomotor activity in the painful region.
4. The diagnosis is excluded by the existence of conditions that would otherwise account for the degree of pain and dysfunction. note: Criteria 2,3 and 4 are necessary for a
diagnosis of complex regional pain syndrome. International Association for the Study of Pain: Diagnostic Criteria for Complex Regional Pain
Syndrome with 1997 ICD Codes
Merskey H, Bodguk N, eds. Classification of chronic pain, descriptions of chronic pain syndromes and definitions of pain terms. Id ed. Seattle: IASP Press, 1994:40-3.
CRPS II (Causalgia) - IASP
1. The presence of continuing pain, allodynia or hyperalgesia after a nerve injury, not necessarily limited to the distribution of the injured nerve.
2. Evidence at some time of edema, changes in skin blood flow or abnormal sudomotor activity in the region of the pain.
3. The diagnosis is excluded by the existence of conditions that would otherwise account for the degree of pain and dysfunction.
note: All three criteria must be satisfied. International Association for the Study of Pain: Diagnostic Criteria for Complex Regional
Pain Syndrome with 1997 ICD Codes
Merskey H, Bodguk N, eds. Classification of chronic pain, descriptions of chronic pain syndromes and definitions of pain terms. Id ed. Seattle: IASP Press, 1994:40-3.
Mirror Therapy The brain wants congruence between motor intention,
peripheral sensory input and visual input. Mirror
therapy “restores” this relationship.
Treatment
Treatment usually consists of several objectives:
Functional restoration of affected limb - often should be considered first before other treatments
Sympathetic and/or motor blocks
Cognitive behavioral techniques
Psychotherapy
Pharmacotherapy
Occupational and physical therapy
Tx – Functional Restoration
Functional restoration involves steady progression from gentle movements to gentle, weight bearing movement. Results in more active load bearing with expected gradual desensitization and increased functionality of limb.
Examples include moving from silk stimulation to other cloths and textures, the scrub and carry technique, and contrast baths that widen the temperature range that the patient can tolerate.
If limitations occur then addition of blocks, pharmacotherapy, etc. can help increase the patient's tolerance and improvement.
Tx - Psychotherapy
Psychotherapy is critical to improvement in patients with CRPS. There is a high incidence of depression and anxiety noted in many CRPS patients. Unknown at this time if antecedent psychological factors prior to injury are common.
CRPS patients also develop a type of PTSD termed "kinesophobia" or fear of movement related to prior pain or initial injury. The patient develops "negative reinforcements" through fear of initial movements that caused the injury of prior movements that resulted in extreme pain in the past. Fear of movement often results in contractures and reduced functionality.
Cognitive behavioral therapy is the most beneficial psychotherapy to help patients with these concerns, though other interventions including family therapy are also beneficial.
Tx - Pharmacotherapy
Pharmacotherapy is often on a trial and error basis and
is very patient specific. Drugs are considered based
on neuropathic pain treatments and then used for
CRPS and have yet to be shown effective in RCTs.
- initial drug(s) to consider include gabapentin and
pregabalin (both used for neuropathic pain) and are
approved for these conditions
- TCAs often used for patients with sleep
disturbances, but are hindered by their numerous
side effects and drug interactions; not currently
approved for pain treatment
Tx - Pharmacotherapy
- SSRIs and SNRIs like fluoxetine and duloxetine,
resp, are often used with the latter being approved for
neuropathic pain conditions.
- Opioids should be avoided as much as possible as
their effectiveness is not well proved and
dependence/ addiction are serious concerns in CRPS
patients.
- Intrathecal baclofen, IV steroids, IVIG, and
anticonvulsant medications are all treatments that
have been considered and used with variable
success, though studies are still lacking.
Tx – Interventional Approaches
Considering the nature of the sympathetic involvement in the patient, blocking the sympathetic nervous system seems inherent towards improvement.
Cervical and lumbar sympathetic blocks are frequently performed as outpatient procedures with patients receiving a few weeks or months of relief. Often done to help with movement therapies.
Beir blocks with local anesthetics, guanethidine, or other neurolytic agents have been performed with varying success.
SCS, pump implantation, and thermocoagulation have also been used to treat patients with CRPS with variable success rates.
Despite the belief that blocking the sympathetic
nervous system will result in reduced pain,
many patients do not gain substantial benefit
from these procedures for any substantial
length of time and the procedures themselves
may actually exacerbate the patient's pain.
CRPS Prognosis
Overall the prognosis for patients with CRPS is
relatively low. Effective treatments are very patient
specific and patient satisfaction, mental state,
willingness to be involved in their treatment all
contribute to their pain reduction.
Many patients report extreme lack of satisfaction with
their pain control and are usually disabled.
More research is required into chronic pain and
developing better methods to treat chronic autonomic
dysfunctional pain.
References
Harden RN, Complex Regional Pain Syndrome, British Journal of Anesthesia, 2001, 87, pp. 99-106.
Schott GD, Complex? Regional? Pain? Syndrome? Practical Neurology. 2007, 7, pp. 145-157.
Forouzanfar T, et al. Treatment of Complex Regional Pain Syndrome Type I. European Journal of Pain. Vol 6, issue 2. Apr 2002. pp. 105-122.
Thank U