CRPS Images - CatsTCMNotes
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CRPS Images
Complex Regional Pain Syndromes (CRPS)
Definition of CRPS Type I
a syndrome
initiating noxious event
not limited to the distribution of a single peripheral nerve
disproportionate to the inciting event
associated with edema, vasomotor, sudomotor,
allodynia, and hyperalgesia in the region of pain
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Causes
Trauma
sprain, strain, dislocation, fracture, laceration, contusion, crush injury,
surgery, manipulation, tight cast, occupational repetitive trauma
Disease
intracerebral, intraspinal, nerve roots, ami, infection( joint, skin,
periarticular), peripheral vascular
Idiopathic ( about 1/3rd of all the cases)
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Epidemiology
Onset 9 – 85 years of age
Median 42 years
Women 3x > men
Veldman PH, Reynen HM, Arntz IE: Signs and symptoms of reflex sympathetic dystrophy: prospective
study of 829 patients. Lancet 1993 Oct 23; 342(8878): 1012-6
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Modified from Blumberg, J. Auton. Nerv. Sys. 1983
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Pathophysiology
Sympathetically maintained pain
sympatholytic therapy abolishes pain and hyperalgesia
sympatholytic blockade followed by administration of
adrenoceptor agonists, rekindles pain
distal electrical stimulation of a freshly cut sympathetic nerve
induced pain in a patient with sympathetically maintained pain
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Pathophysiology(continued)
Ghostine et al - ephaptic transmission
erosion of nerve insulation -> abnormal internerve communication
short circuiting between somatic afferents and sympathetic efferents
Bennett (NIH) - sprouting of damaged nerves
sensitive to norepinephrine
will discharge upon exposure to norepinephrine
sympathetic fibers as a source of norepinephrine
produce norepinephrine receptors at damaged ends
nociceptors in intact nerves fire more in response to norepinephrine
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Pathophysiology(continued)
Schwartzman et al. - autoimmune etiology
tissue injury -> nerve growth factor release -> activation of sympathetic
neurons -> recruitment of neutrophils/monocytes -> complement
activation -> interleukin 2
Roberts - sensitization of intraspinal wide dynamic range (WDR) neurons
C fiber nociception
A fiber mechanoreceptor
sympathetic efferents
C fiber blockade fails alleviation of SMP
mechanoreceptor response to sympathetic activity
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Thalamus
Sympathetics
WDR Neurons
A Fiber Receptor
C Fiber Receptor
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Pathophysiology(continued)
Sympathetic postganglionic neuron/afferent neuron coupling
direct noradrenergic coupling
within traumatized nerve
within dorsal root ganglion
via microvascular bed
indirect noradrenergic coupling
ephaptic coupling
? Abnormal inflammatory response
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CLINICAL HISTORY
ANTECEDENT TRAUMA
WHEN
WHERE
TYPE
SEVERITY
NERVE INVOLVEMENT
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CLINICAL HISTORY (CONTINUED)
PAIN
BURNING, ACHING, THROBBING, STINGING, CONTINUOS WITH
EXACERBATIONS, “EXCRUTIATING”, “UNBEARABLE”
SYMPATHETIC PAIN: CONSTANT, SPONTANEOUS, WORSE AT NIGHT,
WORSE WITH MOVEMENT, TACTILE AND THERMAL STIMULI
IMMEDIATE OR DELAYED ONSET(WEEKS), GRADUAL INCREASE IN
INTENSITY
PROPENSITY TO DIFFUSE, IPSILATERAL/CONTRALATERAL LIMB
INVOLVEMENT
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CLINICAL HISTORY (CONTINUED)
INITIAL DESCRIPTION OF PAIN
ADEQUACY OF TREATMENT
CHANGE IN CHARACTER/INTENSITY
IMMOBILIZATION
HOW LONG, TO WHAT EXTENT
HAS THE PRECIPITATING FACTOR RESOLVED?
VASOMOTOR CHANGES?
SUDOMOTOR CHANGES?
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CLINICAL HISTORY(CONTINUED)
TROPHIC CHANGES?
PSYCHOLOGICAL COMPONENT?
LITIGATION?
PAST MEDICAL HISTORY
SYMPATHOLYTC MEDICATIONS
FACTORS LIMITING PHYSICAL ACTIVITY
NICOTINE, CAFFEINE
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PHYSICAL EXAMINATION
COMPLETE GENERAL EXAM
CARDIOPULMONARY
VASCULAR
NEUROLOGIC
MUSCULOSKELETAL
GENERAL APPEARANCE
AFFECT, MOOD
APPREHENSION, PROTECTIVE AND PAIN BEHAVIORS
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PHYSICAL EXAMINATION
AFFECTED LIMB
SYMMETRICAL VISUAL INSPECTION
PALPATION
MOTOR/SENSORY EXAM
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PHYSICAL EXAMINATION OF THE AFFECTED
LIMB
VISUAL INSPECTION
SWELLING
DISCOLORATION
(ERYTHEMA, PALLOR,
BLUISH MOTTLING,
BRAWNY EDEMA)
HYPERHIDROSIS
MUSCLE WASTING
POSTURING
JOINT ABNORMALITY
EVIDENCE OF TRAUMA
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PHYSICAL EXAMINATION OF THE AFFECTED
LIMB
skin thickening, wrinkling, flaking
skin thinning, smoothing, tightening, shining
hair coarsening, lengthening, increase in distribution
nail thickening, ridging, weakening with accelerated
growth, growth asymmetry
arthritic appearing joints
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Physical Examination: Palpation
Affected Limb
allodynia
hyperesthesia
hyperalgesia
warmth
coolness
sweaty
coarse skin
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Physical Examination: Motor & Sensory Exam
Affected Limb
weakness
tremor
fine motor movement
decreased AROM/PROM
allodynia
hyperesthesia
hyperalgesia
Unaffected Areas
neck/shoulder stiffness
trapezial spasm with shoulder elevation and loss of motion
altered gait with subsequent hip and back pain
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Diagnostic Tests
Sensory
Von Frey hairs, brush hairs, feather
Sudomotor
ninhydrine sweat test, skin conductance response, cobalt blue
test
Swelling
tape measure
water displacement
Joint mobility
goniometer
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Diagnostic Tests
Psychological
External Motor Behavior (ADL, disability)
Visual Analogue Scale
McGill pain questionnaire
Minnesota Multiphasic Personality Inventory (MMPI)
chronic pain profile
organic vs. nonorganic patient
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Diagnostic Tests
Psychological
Illness Behavior Questionnaire
general hypochondria
illness conviction
psychological/somatic perception
emotional inhibition
dysphoria
rejection
irritability
Depression and Anxiety Tests
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Treatment
Overview
Prevention
Early Diagnosis
Physical Therapeutics
Pharmacological Therapeutics
Psychological Therapy
Prevention of Late Complications
Outcome Measurement
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Treatment: Prevention
high risk patient
trauma
cva
nerve injury
early mobilization
AROM/PROM
Braus
patents with stroke and hemiplegia
early PT
27% to 8% incidence of CRPS Type I
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Treatment: Early Diagnosis
improved outcome
high degree of suspicion
early treatment
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Treatment: Physical Therapeutics
elevation
compression
heat/cold
tens/ultrasound
stretching/AROM/PROM
stress loading
exercise(active/passive)
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Treatment: Pharmacological Therapeutics
Components of Pain
inflammatory
neuropathic
sympathetic
central nervous system
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Treatment: Pharmacological Therapeutics
Inflammatory Component
NSAIDS
central effect of prostaglandins
IM/IV RB toradol - one study with good effect
early phase intervention
Prednisone -
early phase intervention
efficacy comparable to sympatholytics
1 mg/kg (up to 100 mg/day), 2 week taper
membrane stabilizing effects
binding to lamina III and VII
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Treatment: Pharmacological Therapeutics
Neuropathic Component
anticonconvulsants - disappointing
tricyclics - paucity of trials
gabapentin - at least one study: highly effective
CNS Component
opioids
TCAs
anticonvulsants
NSAIDs, steroids
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Treatment: Pharmacological Therapeutics
Calcitonin
? mechanism of action in CRPS I
moderate efficacy in some studies
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Treatment: Surgical Intervention
Chemical Sympathectomy
phenol, alcohol
longer than sympathetic blockade
pain recurs
Radiofrequency Sympathectomy
Endoscopic-guided Sympathectomy
Open Surgical Sympathectomy
Results: 12-90% efficacy
30% recurrence
Complications: sympathalgia in 7-44% of patients
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Treatment: Prevention of Late Complications
muscle atrophy/weakness
osteoporosis
contractures
pain
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A 29-year-old woman with reflex sympathetic dystrophy
in the right foot demonstrates discoloration of the skin
and marked allodynia.
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This photo shows the same patient as in the above
image, following a right lumbar sympathetic block.
Marked increase in the temperature of the right foot is
noted, with more than 50% pain relief.
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A 68-year-old woman with complex regional pain
syndrome type II (causalgia).
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A 36-year-old woman with right arm reflex sympathetic
dystrophy and dystonic posture (movement disorder).
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Normal laser Doppler study of the upper extremities.
When the patient performs inspiratory gasp repeatedly
during laser Doppler image acquisition, the transient
capillary flow decreases are displayed easily and
dramatically (as dark bands) in the pseudocolor image.
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Laser Doppler study of the upper extremities in a patient
with right hand reflex sympathetic dystrophy.
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Laser Doppler study of the lower extremities in a 25year-old woman with reflex sympathetic dystrophy in the
right foot.
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