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CRPS Images Complex Regional Pain Syndromes (CRPS)
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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 Affects about 2% of the population and that’s about it.
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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):
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Modified from Blumberg, J. Auton. Nerv. Sys. 1983
All of the vaso-sudo motor responses are reactions. Causes wrong signals sent to and from the brain, causing abnormal motor responses which then feeds back distorted information sent to the brain via the spinal cord, etc. All are under sympathetic control – if blood flow is disrputed then there can be swelling and chronic atrophy, trophic changes. Result is an atrophic limb. Modified from Blumberg, J. Auton. Nerv. Sys. 1983
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Pathophysiology sympatholytic therapy abolishes pain and hyperalgesia
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 Sympathetic system was once blocked by surgery – cut the affected ganglion nerve and thus no sx…and also no pain, sweating, feeling, etc. Pretty drastic stuff.
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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 A fibers are the supertransmitters. C fibers are ? These are theories, none proven.
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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 Usually starts on the same side then progresses to opposite side as condition continues.
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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? Vascular = swelling/sweating. Will rsvp to sympathetic manipulation like needling. Sudomotor = pain upon movement. Produces atrophy of the muscles.
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CLINICAL HISTORY(CONTINUED)
TROPHIC CHANGES? PSYCHOLOGICAL COMPONENT? LITIGATION? PAST MEDICAL HISTORY SYMPATHOLYTC MEDICATIONS FACTORS LIMITING PHYSICAL ACTIVITY NICOTINE, CAFFEINE Psychological component – ideation, or depression due to long term pain. Nicotine and caffeine will trigger pain rsvp more.
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PHYSICAL EXAMINATION COMPLETE GENERAL EXAM CARDIOPULMONARY VASCULAR
NEUROLOGIC MUSCULOSKELETAL GENERAL APPEARANCE AFFECT, MOOD APPREHENSION, PROTECTIVE AND PAIN BEHAVIORS Do all vitals, reflexes, gait, cranial nerves, cerebellar signs, then flexion/extension/tonicity. General appearance is how do they look overall. Protective refers to protecting the affected area.
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PHYSICAL EXAMINATION SYMMETRICAL VISUAL INSPECTION PALPATION
AFFECTED LIMB SYMMETRICAL VISUAL INSPECTION PALPATION MOTOR/SENSORY EXAM Affected will be hotter or colder. Motor/sensory = heat, cool, touch, etc., including proprioception.
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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 Brawny edema – may brown with long term edema. Posture refers to how they hold the body and whether you can see the pain there.
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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 Long term joint disuse may appear arthritic.
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Physical Examination: Palpation
Affected Limb allodynia hyperesthesia hyperalgesia warmth coolness sweaty coarse skin Hyperesthesia = hypersensitive. Hyperalgesia = excess pain response.
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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 Fine motor movement can decrease. Stiffness and spasms even in unaffected areas, can’t shrug well. As you can tell, affects all body parts.
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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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organic vs. nonorganic patient
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 See the McGill Pain Questionnaire, also downloadable from the internet.
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Diagnostic Tests Illness Behavior Questionnaire general hypochondria
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 Prevention Early Diagnosis Physical Therapeutics
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 - 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 Tricyclics are good antidepressants and also raise pain thresholds, but have nasty side fx. Amitryptaline is an example. Opioids, usually codeine, is extremely addicting.
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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 % 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. Right foot is more swollen, color differentiations. Vascular blockage.
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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).
Nerve involvment on the left foot.
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A 36-year-old woman with right arm reflex sympathetic dystrophy and dystonic posture (movement disorder). Note right hand – can’t straighten fingers. Dystonic posture too.
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Normal laser Doppler study of the upper extremities
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 25-year-old woman with reflex sympathetic dystrophy in the right foot. Better supply to the left foot – the darker blue indicates less inervation and less flow.
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