CRPS

Presented By/

Salah AlDekhayel
Wed 12th March 2008

5/3/12

Introduction
Definition:
An abnormally intense and inappropriately prolonged post

traumatic pain, that is not a reflection of actual or impending tissue damage, which might delay or prevent recovery

Synonyms:
RSD Algodystrophy Causalgia

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Classification
SMP (sympathetically maintained pain):
Type I classic Type II causalgia

SIP (sympathetically independent pain):

Type III >>> other pain dysfunction problems

SMP can become SIP overtime SIP has a poor prognosis

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Demographics
Between 30 55 yrs (mean 45) F:M >> 3:1 Smoking is statistically linked to RSD 80% Dx < 1 yr; will improve significantly 50% untreated > 1 yr; will have profound residual

impairment
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Traumatic:

Causes

v The most common >> distal radius & ulna fractures

(11-37%)
v Common intraoperative nerve injury causing CRPS:

Palmar cutaneous branch of median n. Superficial branch of radial n. Dorsal branch of ulnar n.

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Historical Review
Ambrose Pare (16th century) >>> burning pain after phlebotomy Percivall Pott (1771)>>> pain after nerve injury Silas Weir Mitchell (1864)>>> description of causalgia Sudek (1900) >>> bone demineralization inflammatory bone atrophy Leriche (1916)>>> post-traumatic burning pain Evan (1947) & Bonica (1973) >>> RSD
5/3/12 Robert (1980)>>> SMP vs. SIP

Pathophysiology
Cellular damage > 2ndry inflammation > activation of

mechanoreceptor & nociceptor afferent neurons > ectopic chemosensitivity to -adrenergic agonist > transduction through A, A, C fibers > dorsal horn spinal cord > sensitization of WDR neurons > excitatory transmitters;

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NMDA produce long lasting potentials refractory to

stimulation, & plays important role in SMP

modulation of nociceptive input via descending pathways >

determine pain intensity

Repetitive injury > alter protective response by sensitization

> early activation

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Symptoms
Pain Hyperalgesia >> 1ry vs. 2ndry Allodynia >> SMP Hyperpathia Trophic changes (30% of type I, within 10

days)
Autonomic dysfunction (in 80%)
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Signs
Trophic changes Autonomic >> ( in 80%) Classic dystrophic course:
acute (<3/12), dystrophic (3-6/12), chronic (>6/12)

Post-trauma with swelling, stiffness, pain, restlessness >> ???

Dystrophic response
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Physical Examination
Should include:
Cervical & thoracic spines Shoulder ROM Brachial plexus evaluation R/O thoracic outlet compression Hypersensitivity, vascularity, sensibility, ROM, edema, motor

function, pinch& grip, sweating, vasomotor tone, fibrosis

REMEMBER !!! >>> dystrophy can occur after any traumatic event

>>> a high index of suspicion aid in early Dx 5/3/12

Diagnostic Criteria
Veldman et al (1993) International Association for the Study of Pain (IASP) 1994 Bruehl criteria (1999):

(1) Continuing pain which is disproportionate to the inciting event (2) Must report at least 1 symptom in each of the 4 following categories: (a) Sensory (b) Vasomotor (d) Motor/trophic (c) Sudomotor/edema

(3) Must display at least 1 sign in 2 or more of the following categories: 5/3/12

Dx Testing
Pain threshold evaluation:
Success/failure of Rx can be assessed by repeated evaluations Rubber-tipped algometers, dolorimetry, monofilaments, computer-

controlled stimuli, thermal pain threshold hyperesthesia

Monofilaments>> the most practical method to monitor allodynia &

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Radiography:

Dx Testing

v Osteopenia in 80% of plain films v Classic Sudeks atrophy v Genant et al described FIVE patterns of

resorption:

Irregular resorption of trabecular bone in metaphysis >> patchy appearance

Subperiosteal Intracortical

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Dx Testing
Scintigraphy:
Three-phase technetium-99m bone scan Traditionally, +ve scan if asymmetrical flow in any phase Recent reports suggest >> diagnostic yield of stage III alone equals

that of three-phase bone scan

Highly specific(96-100%), but poorly sensitive (14-19%)
Clin J Pain Volume 23, Number 5, June 2007

+ve scan is not a prerequisite for Dx of CRPS/SMP. However, it

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provides objective support for Dx

Dx Testing
Evaluation of Autonomic Control:
Regulation of Microvascular Flow:
v

Nutritional deprivation is a common underlying finding in warm vs. cold hands

v v v

In warm-swollen hands >> it is caused by abnormal AV shunting In cold-stiff hands >> by decreased total flow Total digital flow can be assessed by:

Digital temperature measurment doppler fluxmetry

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Dx Testing
Evaluation of Autonomic Control:
Sudomotor function:
v v

assess sweat function Techniques:

Cumulative QSART

unstimulated resting sweat output

{quantitative sudomotor axon reflex test} skin response

Galvanic PASP

{peripheral autonomic surface potential}

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SSR {sympathetic skin response}

Dx Testing
Diagnostic Sympathetic Blockade:
SMP vs SIP phentolamine S/E >> headache, hypotension no therapeutic indications Regional Blockade:
v

Stellate ganglion, epidural, brachial plexus, or local. ganglion block:

v Stellate 5/3/12

Dx Testing
Thermography:
SN 45%, SP 50-89%
Clin J Pain Volume 23, Number 5, June 2007

Endurance Testing:
For functional capacity, gross and fine motor skills, strength, and

endurance

MRI:
Findings occur early, (SN 13-43%, SP 78-98%)
Clin J Pain Volume 23, Number 5, June 2007

Mild articular effusion, bone marrow edema, weak T1 signal

increased T2 signal

Few cases may show Swiss-cheese signal

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DDx
Connective Tissue disorders:
Scleroderma, RA

Psychiatric Disorders:
Malingering, factitious, conversion disorders (hysterical paralysis,

clenched-fist syndrome)

Myofascial Dysfunction:
Usually there is identified trigger point, which is relieved by

splinting or injection

Volkmanns ischemic contracture:

Classic Five Ps >> paresthesia, pallor, pulselessness, pain with

extension, paresis

5/3/12 Local nerve irritation:

Management
Principles:
Prevention High index of suspicion Psychological support least invasive Rx Identification of a nociceptive focus Before Rx >> clinical/lab testing should determine:
v v v

Extent of sympathetic tone Edema Total digital flow flow

5/3/12 v Nutritional

Management
Hand Therapy:
The entire limb Prevention of arthrofibrosis Concomitant pharmacologic, adaptive therapy, or surgery Mainstay >> AROM, PROM, stress-loading activities, TENS

(transcutaneous electrical nerve stimulation), desensitization, sensory re-education

Adaptive therapy
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Management
Pharmacologic Interventions:
q Oral/Topical agents:
v

Antidepressants:
Tricyclics

(TCA)

Tetracyclics

Atypical

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SSRIs

Management

Anticonvulsants:

Phenytoin, tegretol, depakene, gabapentin

Membrane-stabilizing
Rarely

agents:

used except in severe/refractory cases because of S/Es

Tocainide Mexiletine

>> less severe S/Es

Adrenergic

compounds:
diagnostic test >> poorly tolerated, but dramatic pain relief

Phentolamine

Phenoxybenzamine 5/3/12

Management

Steroids:

High starting dose rapidly tapered over 5-10 Long-term low doses have been advocated S/E

Neuromucular blockers:

Botulinum toxins A & B >> in acute / chronic pain

Free Radical Scavengers:

DMSO (dimethyl sulfoxide) >> favorable in warm CRPS I NAC (N-acetylcysteine) >> in cold CRPS More effective if patients treated early

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Management
Parentral Medications:
v Intravenous Regional Infusion:

Biers block For dystrophic pain was used first by Hannington-Kiff in 1970 reserpine, guanithidine, bretylium, steroids

v Percutaneous neural/ganglionic blockade continuous block:

E.g. stellate ganglion block, brachial plexus, epidural block

v Biofeedback-Acupuncture:

In selected patients

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Management
Surgical/Ablative Therapy:
v Sympathectomy:

Chemical:
o

Reversible axonotmesis in 3-6/12 For refractory CRPS

Surgical:
o

However, critical analysis of peer-reviewed literature concluded that this modality of Rx based on:
o

poor-quality evidence,

o o o

uncontrolled studies, personal experience, significant complications,

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Management Implantable Devices

CNS ablation:

Bilateral anterior cingulotomy

Mx of neural nociceptive foci:

50% most common >> neuroma, neuroma-in-continuity, secondary compression neuropathies

Surgery is indicated after failed non-operative Rx Options of surgery

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Management
Mx of Mechanical nociceptive foci:
v Internal derangement of wrist, injury to triangular fibrocartilage

complex, injury to distal radio-ulnar joint

Late-stage Rx (secondary joint deformities):
v CRPS >> arthrofibrosis >> fixed contractures v The best is prevention v Indications for surgery v Goal of surgery
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Prognosis
Natural history of CRPS is variable Residual pain and stiffness may occur not a progressive condition Patients should expect prolonged rehabilitation, long-term oral

medications (3-6 months), residual disability

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Conclusion
Dx is clinical + autonomic dysfunction, trophic changes, functional

impairment
Dx is supported by a variety of tests SMP is not a prerequisite for Dx Rx is based on physiologic staging and objective determination of

effectiveness
Surgery of underlying dystrophic foci is appropriate in selected patients Patients should understand the natural history of the disease
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THANKS
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