2 Definition of CRPS Type I a syndromeinitiating noxious eventnot limited to the distribution of a single peripheral nervedisproportionate to the inciting eventassociated with edema, vasomotor, sudomotor, allodynia, and hyperalgesia in the region of painAffects about 2% of the population and that’s about it.
3 CausesTraumasprain, strain, dislocation, fracture, laceration, contusion, crush injury, surgery, manipulation, tight cast, occupational repetitive traumaDiseaseintracerebral, intraspinal, nerve roots, ami, infection( joint, skin, periarticular), peripheral vascularIdiopathic ( about 1/3rd of all the cases)
4 Epidemiology Onset 9 – 85 years of age Median 42 years Women 3x > menVeldman PH, Reynen HM, Arntz IE: Signs and symptoms of reflex sympathetic dystrophy: prospective study of 829 patients. Lancet 1993 Oct 23; 342(8878):
5 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
6 Pathophysiology sympatholytic therapy abolishes pain and hyperalgesia Sympathetically maintained painsympatholytic therapy abolishes pain and hyperalgesiasympatholytic blockade followed by administration of adrenoceptor agonists, rekindles paindistal electrical stimulation of a freshly cut sympathetic nerve induced pain in a patient with sympathetically maintained painSympathetic 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.
7 Pathophysiology(continued) Ghostine et al - ephaptic transmissionerosion of nerve insulation -> abnormal internerve communicationshort circuiting between somatic afferents and sympathetic efferentsBennett (NIH) - sprouting of damaged nervessensitive to norepinephrinewill discharge upon exposure to norepinephrinesympathetic fibers as a source of norepinephrineproduce norepinephrine receptors at damaged endsnociceptors in intact nerves fire more in response to norepinephrine
8 Pathophysiology(continued) Schwartzman et al. - autoimmune etiologytissue injury -> nerve growth factor release -> activation of sympathetic neurons -> recruitment of neutrophils/monocytes -> complement activation -> interleukin 2Roberts - sensitization of intraspinal wide dynamic range (WDR) neuronsC fiber nociceptionA fiber mechanoreceptorsympathetic efferentsC fiber blockade fails alleviation of SMPmechanoreceptor response to sympathetic activityA fibers are the supertransmitters. C fibers are ?These are theories, none proven.
11 CLINICAL HISTORY ANTECEDENT TRAUMA WHEN WHERE TYPE SEVERITY NERVE INVOLVEMENT
12 CLINICAL HISTORY (CONTINUED) PAINBURNING, ACHING, THROBBING, STINGING, CONTINUOS WITH EXACERBATIONS, “EXCRUTIATING”, “UNBEARABLE”SYMPATHETIC PAIN: CONSTANT, SPONTANEOUS, WORSE AT NIGHT, WORSE WITH MOVEMENT, TACTILE AND THERMAL STIMULIIMMEDIATE OR DELAYED ONSET(WEEKS), GRADUAL INCREASE IN INTENSITYPROPENSITY TO DIFFUSE, IPSILATERAL/CONTRALATERAL LIMB INVOLVEMENTUsually starts on the same side then progresses to opposite side as condition continues.
13 CLINICAL HISTORY (CONTINUED) INITIAL DESCRIPTION OF PAINADEQUACY OF TREATMENTCHANGE IN CHARACTER/INTENSITYIMMOBILIZATIONHOW LONG, TO WHAT EXTENTHAS 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.
14 CLINICAL HISTORY(CONTINUED) TROPHIC CHANGES?PSYCHOLOGICAL COMPONENT?LITIGATION?PAST MEDICAL HISTORYSYMPATHOLYTC MEDICATIONSFACTORS LIMITING PHYSICAL ACTIVITYNICOTINE, CAFFEINEPsychological component – ideation, or depression due to long term pain. Nicotine and caffeine will trigger pain rsvp more.
15 PHYSICAL EXAMINATION COMPLETE GENERAL EXAM CARDIOPULMONARY VASCULAR NEUROLOGICMUSCULOSKELETALGENERAL APPEARANCEAFFECT, MOODAPPREHENSION, PROTECTIVE AND PAIN BEHAVIORSDo 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.
16 PHYSICAL EXAMINATION SYMMETRICAL VISUAL INSPECTION PALPATION AFFECTED LIMBSYMMETRICAL VISUAL INSPECTIONPALPATIONMOTOR/SENSORY EXAMAffected will be hotter or colder. Motor/sensory = heat, cool, touch, etc., including proprioception.
17 PHYSICAL EXAMINATION OF THE AFFECTED LIMB VISUAL INSPECTIONSWELLINGDISCOLORATION (ERYTHEMA, PALLOR, BLUISH MOTTLING, BRAWNY EDEMA)HYPERHIDROSISMUSCLE WASTINGPOSTURINGJOINT ABNORMALITYEVIDENCE OF TRAUMABrawny edema – may brown with long term edema. Posture refers to how they hold the body and whether you can see the pain there.
18 PHYSICAL EXAMINATION OF THE AFFECTED LIMB skin thickening, wrinkling, flakingskin thinning, smoothing, tightening, shininghair coarsening, lengthening, increase in distributionnail thickening, ridging, weakening with accelerated growth, growth asymmetryarthritic appearing jointsLong term joint disuse may appear arthritic.
20 Physical Examination: Motor & Sensory Exam Affected Limbweaknesstremorfine motor movementdecreased AROM/PROMallodyniahyperesthesiahyperalgesiaUnaffected Areasneck/shoulder stiffnesstrapezial spasm with shoulder elevation and loss of motionaltered gait with subsequent hip and back painFine motor movement can decrease. Stiffness and spasms even in unaffected areas, can’t shrug well. As you can tell, affects all body parts.
22 organic vs. nonorganic patient Diagnostic TestsPsychologicalExternal Motor Behavior (ADL, disability)Visual Analogue ScaleMcGill pain questionnaireMinnesota Multiphasic Personality Inventory (MMPI)chronic pain profileorganic vs. nonorganic patientSee the McGill Pain Questionnaire, also downloadable from the internet.
23 Diagnostic Tests Illness Behavior Questionnaire general hypochondria PsychologicalIllness Behavior Questionnairegeneral hypochondriaillness convictionpsychological/somatic perceptionemotional inhibitiondysphoriarejectionirritabilityDepression and Anxiety Tests
24 Treatment Prevention Early Diagnosis Physical Therapeutics OverviewPreventionEarly DiagnosisPhysical TherapeuticsPharmacological TherapeuticsPsychological TherapyPrevention of Late ComplicationsOutcome Measurement
25 Treatment: Prevention high risk patienttraumacvanerve injuryearly mobilizationAROM/PROMBrauspatents with stroke and hemiplegiaearly PT27% to 8% incidence of CRPS Type I
26 Treatment: Early Diagnosis improved outcomehigh degree of suspicionearly treatment
28 Treatment: Pharmacological Therapeutics Components of Paininflammatoryneuropathicsympatheticcentral nervous system
29 Treatment: Pharmacological Therapeutics Inflammatory ComponentNSAIDScentral effect of prostaglandinsIM/IV RB toradol - one study with good effectearly phase interventionPrednisone -efficacy comparable to sympatholytics1 mg/kg (up to 100 mg/day), 2 week tapermembrane stabilizing effectsbinding to lamina III and VII
30 Treatment: Pharmacological Therapeutics Neuropathic Componentanticonconvulsants - disappointingtricyclics - paucity of trialsgabapentin - at least one study: highly effectiveCNS ComponentopioidsTCAsanticonvulsantsNSAIDs, steroidsTricyclics are good antidepressants and also raise pain thresholds, but have nasty side fx. Amitryptaline is an example.Opioids, usually codeine, is extremely addicting.
31 Treatment: Pharmacological Therapeutics Calcitonin? mechanism of action in CRPS Imoderate efficacy in some studies
32 Treatment: Surgical Intervention Chemical Sympathectomyphenol, alcohollonger than sympathetic blockadepain recursRadiofrequency SympathectomyEndoscopic-guided SympathectomyOpen Surgical SympathectomyResults: 12-90% efficacy % recurrenceComplications: sympathalgia in 7-44% of patients
33 Treatment: Prevention of Late Complications muscle atrophy/weaknessosteoporosiscontracturespain
34 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.
35 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.
36 A 68-year-old woman with complex regional pain syndrome type II (causalgia). Nerve involvment on the left foot.
37 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.
38 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.
39 Laser Doppler study of the upper extremities in a patient with right hand reflex sympathetic dystrophy.
40 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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