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       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




                                                             2
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)




                                                                                 3
         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
                                                                                                   4
Modified from Blumberg, J. Auton. Nerv. Sys. 1983
                                                    5
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




                                                                         6
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




                                                                                7
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




                                                                               8
                             Thalamus



                   Sympathetics

                                  WDR Neurons



A Fiber Receptor

C Fiber Receptor


                                                9
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




                                                               10
CLINICAL HISTORY

 ANTECEDENT TRAUMA
    WHEN
    WHERE
    TYPE
    SEVERITY
    NERVE INVOLVEMENT




                         11
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




                                                           12
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?




                                             13
CLINICAL HISTORY(CONTINUED)

   TROPHIC CHANGES?
   PSYCHOLOGICAL COMPONENT?
   LITIGATION?
   PAST MEDICAL HISTORY
      SYMPATHOLYTC MEDICATIONS
      FACTORS LIMITING PHYSICAL ACTIVITY
      NICOTINE, CAFFEINE




                                            14
PHYSICAL EXAMINATION

 COMPLETE GENERAL EXAM
    CARDIOPULMONARY
    VASCULAR
    NEUROLOGIC
    MUSCULOSKELETAL
 GENERAL APPEARANCE
 AFFECT, MOOD
 APPREHENSION, PROTECTIVE AND PAIN BEHAVIORS




                                                15
PHYSICAL EXAMINATION

 AFFECTED LIMB
    SYMMETRICAL VISUAL INSPECTION
    PALPATION
    MOTOR/SENSORY EXAM




                                     16
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




                                       17
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




                                                        18
Physical Examination: Palpation

 Affected Limb
    allodynia
    hyperesthesia
    hyperalgesia
    warmth
    coolness
    sweaty
    coarse skin




                                  19
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




                                                                   20
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




                                                                      21
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



                                                         22
Diagnostic Tests

 Psychological
     Illness Behavior Questionnaire
         general hypochondria
         illness conviction
         psychological/somatic perception
         emotional inhibition
         dysphoria
         rejection
         irritability
     Depression and Anxiety Tests



                                             23
Treatment

 Overview
    Prevention
    Early Diagnosis
    Physical Therapeutics
    Pharmacological Therapeutics
    Psychological Therapy
    Prevention of Late Complications
    Outcome Measurement




                                        24
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




                                                25
Treatment: Early Diagnosis

 improved outcome
 high degree of suspicion
 early treatment




                             26
Treatment: Physical Therapeutics

 elevation
 compression
 heat/cold
 tens/ultrasound
 stretching/AROM/PROM
 stress loading
 exercise(active/passive)




                                   27
Treatment: Pharmacological Therapeutics

 Components of Pain
    inflammatory
    neuropathic
    sympathetic
    central nervous system




                                          28
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

                                                         29
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




                                                         30
Treatment: Pharmacological Therapeutics

 Calcitonin
    ? mechanism of action in CRPS I
    moderate efficacy in some studies




                                          31
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




                                                     32
Treatment: Prevention of Late Complications

 muscle atrophy/weakness
 osteoporosis
 contractures
 pain




                                              33
 A 29-year-old woman with reflex sympathetic dystrophy
  in the right foot demonstrates discoloration of the skin
  and marked allodynia.




                                                         34
 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.




                                                            35
 A 68-year-old woman with complex regional pain
  syndrome type II (causalgia).




                                                   36
 A 36-year-old woman with right arm reflex sympathetic
  dystrophy and dystonic posture (movement disorder).




                                                          37
 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.




                                                           38
 Laser Doppler study of the upper extremities in a patient
  with right hand reflex sympathetic dystrophy.




                                                          39
 Laser Doppler study of the lower extremities in a 25-
  year-old woman with reflex sympathetic dystrophy in the
  right foot.




                                                       40

				
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