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Rasha S. Jabri , MD Dubai Anesthesia March 2012 Tawam Hospital-JHMI Al Ain Abu Dhabi, UAE

When is it Reasonable to Speak about CRPS?. Rasha S. Jabri , MD Dubai Anesthesia March 2012 Tawam Hospital-JHMI Al Ain Abu Dhabi, UAE. History. American Civil War: GSW near neves 1864 : term “causalgia” long years final reminder of the battle-field

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Rasha S. Jabri , MD Dubai Anesthesia March 2012 Tawam Hospital-JHMI Al Ain Abu Dhabi, UAE

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  1. When is it Reasonable to Speak about CRPS? Rasha S. Jabri , MD Dubai Anesthesia March 2012 Tawam Hospital-JHMI Al Ain Abu Dhabi, UAE

  2. History • American Civil War: GSW near neves • 1864 : term “causalgia” long years final reminder of the battle-field • Dr. Sudeck: trivial injuries result in osteoporotic changes near the site of injury (Sudeck’s atrophy)

  3. History • Rene Leriche : sympathetic nervous system as a mediating factor in the condition • “Reflex sympathetic dystrophy” (RSD) • Since the early descriptions of this painful condition many names have been applied to the syndrome

  4. Terms for CRPS • •Algodystrophy • •Algoneurodystrophy • •Causalgia • •Post-traumatic pain syndrome • •Post-traumatic dystrophy • •Post-traumatic osteoporosis • •Reflex sympathetic dystrophy • •Shoulder-hand syndrome • •Sudeck’s atrophy

  5. Classification • 1986 (IASP) formal description and classification of RSD but NO clear diagnostic criteria, NO specific underlying mechanisms. • Many neuropathic pain conditions were included in the diagnosis of RSD, specifically those resistant to traditional treatments

  6. Classification • 1994 IASP new taxonomy of complex regional pain syndrome (CRPS), which would more accurately describe RSD and causalgia. • New diagnostic criteria for CRPS which focused on clinical diagnosis from patient history, symptom description, physical signs and pain.

  7. Classification • CRPS : inciting events: • type I =RSD, follows a soft tissue injury • CRPS II= (causalgia) follows a well-defined nerve injury

  8. CPRS • syndrome including, • complexity of the varied presentations • regionally, symptoms, which are typically non-dermatomal • pain, usually out of proportion to the inciting trauma • syndrome, denoting the constellation of signs and symptoms • varied contribution of the sympathetic nervous system

  9. Epidemiology • Overall incidence of CRPS to be 26.2 per 100,000 person • CRPS I to be 5.46 per 100,000 person years at risk and a prevalence of 20.57 per 100,000. • The incidence of CRPS II has been reported at 0.82 per 100,000 person years at risk and prevalence of 4.2 per 100,000 person years.

  10. Risk Factors • Extremities trauma/MVA↑ • Surgeries/Orthopedic↑( Knee, Ankle, CTS) • Stroke, or unknown cause very rare • Most cases between 50 and 70 years of age • CRPS female predominance: 2.0-3.5:1.13 • Mainly Caucasian

  11. Pathophysiology • Theories peripheral mechanisms as well as central mechanisms for CRPS. • In CRPS II biochemical, morphological (structural) and physiological changes of the injured and adjacent intact primary afferent neurons may occur

  12. CPRS II • The loss of DRG cells degeneration of the centrally projecting afferent axons and to denervation of dorsal horn neurons • Secondary changes in the central representations changes in central representations (in the spinal cord, brain stem, thalamus and forebrain)

  13. CPRS I • CRPS I central representations of the sensory, autonomic, and somatomotor systems account for the clinical presentation in CRPS • CRPS, particularly type I, is a systemic disease of neuronal systems: somatosensory, sympathetic, somatomotor, and peripheral (vascular, inflammatory) systems

  14. Pathophysiology • Marked increase in alpha 1 adrenoreceptors which appears in the injured extremity: skin muscle and nerve tissue • Augment depolarization in nerve and muscle tissue resulting in an amplification effect of any stimuli • Increase in pain w increase in either endogenous or exogenous catecholamines.

  15. Tissue damage initiates a number of alterations of the peripheral and the central pain pathways Dahl, J. B. et al. Br Med Bull 2004 71:13-27; doi:10.1093/bmb/ldh030 .

  16. Bruehl S. An Update on the Pathophysiology of CRPS Anesthesiology .September 2010;113(3):713-725

  17. Bruehl S. An Update on the Pathophysiology of CRPS Anesthesiology .September 2010;113(3):713-725 Speculative Model of Interacting Pathophysiologic Mechanisms in CRPS

  18. Clinical Stages • Classically: three distinct sequential progressive stages • Disputes the traditional staging of CRPS • Subtypes/subgroups exist in CRPS

  19. Clinical Stages (Bonica) I warm acute CRPS pain, sensory abnormalities, hyperalgesia, allodynia, vasomotor dysfunction, edema and sudomotor disturbance. II (dystrophic stage) 3 to 6 mons more pain/sensory dysfunction and vasomotor dysfunction, with significant motor/trophic changes. III (atrophic stage) cold extremity with decreased pain/sensory disturbance, continued vasomotor disturbance, increased motor/trophic changes.

  20. General definition • An array of painful conditions regional pain disproportionate in time or degree to the usual course of any known dz • Regional: not in a specific nerve territory or dermatome usually has a distal predominance of abnormal sensory, motor, sudomotor, vasomotor, and/or trophic findings.

  21. IASP CRPS subgroups NOT Sequential stages (1) Relatively limited syndrome with vasomotor signs predominating (2) Relatively limited syndrome with neuropathic pain/sensory abnormalities predominating (3) Florid CRPS syndrome similar to ‘‘classic RSD’’ descriptions

  22. Pattern and Spread 32. IE, et al. Signs and symptoms of reflex sympathetic dystrophy: prospective study of 829 patients. Lancet 1993;342:1012-1016. Veldman PH.Signs and symptoms of RSD: prospective study of 829 patients. Lancet 1993;342:1012-1016.

  23. Clinical Features • CPRS is a painful and debilitating disorder primarily affecting one or more extremities.

  24. key features • Spontaneous pain, allodynia, hyperalgesia, edema, temperature change, abnormal vasomotor and sudomotor activity, trophic changes, and motor dysfunction

  25. IASP Diagnostic criteria to establish the diagnosis of CRPS (type I): (3) Edema, changes in skin blood flow, or abnormal sudomotor activity (1) initiating noxious event or immobilization (2) continuing pain, allodynia, or hyperalgesia with pain disproportionate • (4) the exclusion other medical conditions

  26. CPRS II IASP (1) continuing pain, allodynia, or hyperalgesia after an nerve injury (2) Edema, changes in skin blood flow, or abnormal sudomotor activity • (3) the exclusion other medical conditions

  27. Sudomotor Changes & Edema

  28. Trophic Changes

  29. Trophic Changes

  30. Conclusions and Clinical Implications • IASP standardized, common methodology for making DX of CRPS or not • Treatment for two distinct conditions • CRPS and non-CRPS neuropathic pain groups

  31. IASP_ • Controversy about the value of consensus-based dx criteria • Absence of evidence-based information • Necessity of validating in light of systematic validation research Harden RN. Proposed new diagnostic criteria for CRPS. Pain Med. May-Jun2007;8(4):326-331

  32. CRPS DX ????? • “looser” vs “tighter” criteria?!! • Validity dx of the criteria ? • Sensitivity vs Specificity?

  33. Harden RN. Proposed new diagnostic criteria for CRPS. Pain Med. May-Jun2007;8(4):326-331

  34. IASP/CRPS dx Criteria Adequately Sensitive (rarely miss a case of actual CRPS) Problems of overdiagnosis due to Poor Specificity Harden RN. CRPS : Are the IASP diagnostic criteria valid and sufficiently comprehensive? Pain 1999;83:211–9

  35. Harden RN. Proposed new diagnostic criteria for CRPS. Pain Med. May-Jun2007;8(4):326-331

  36. Subjective symptom Objective signs on PE • The modified criteria requires the presence of both for CRPS diagnosis

  37. Clinical DiagnosticCriteria by the Budapest group • 2/4 sign categories and ¾ symptom categories for diagnosis • Sensitivity of 0.85 • Specificity of 0.69 • Clinical vs research purposes2/4+4/4 more sensitivity and specificity around 80, 90%

  38. Diagnostic Examination • No single objective test for diagnosis • Diagnostic tests may assist in determining the likelihood of the syndrome

  39. Diagnostic Examination • Sympathetic Blockade • sympathetically maintained pain or sympathetic independent pain • Skin Temperature Measurement • Infrared thermography • Difference of more than 2.2°C has a sensitivity of 76% and a specificity of 93% for diagnosis of CRPS

  40. Quantitative Autonomic Function Testing • The quantitative sudomotor axon reflex test (QSART) • difference in sweat production between an affected extremity and an unaffected extremity • QSART test may help predict response to sympathetic block • Research needs to be conducted to further assess the utility of the test

  41. Vasomotor Testing • Acute CRPS increase in vascular flow to the affected extremity secondary to neurogenic inflammation • Decrease in sympathetic activity at the extremity • Measured by doppler flowmetry • Additional studies to assess the utility in the diagnosis of CRPS

  42. Trophic Change Measurement • Chronic CRPS present with changes in skin, nails or bone • Evaluation of trophic changes to the bone by triple-phase bone scintigraphy has been used to substantiate the diagnosis of CRPS, although distinguishing between CRPS and acute trauma may difficult

  43. Therapy

  44. Pharmacological Therapy • Antidepressants (tricyclic & dual inhibitors) are effective agents for treating a variety of neuropathic pain condition • SSRI + DPNP, PHN? CRPS

  45. Anticonvulsants (Antiepileptics) • The gabapentinoid group of drugs, gabapentin (GBP) and pregabalin (PGB), are the most commonly used antiepileptics drugs (AEDs) for CRPS • Opioids • There are no long-term studies • Considered in CRPS if pain limits the patient’s participation in physical restorative therapies • Fent Patch VAS↓, fx (Agarwal, Pain Med 2007)

  46. Calcium Regulating Medications (Bisphosphonates) • Effective agents for the treatment of CRPS • Mechanism of action is unknown • (alendronate, pamidronate, clodronate) • May inhibit bone resorption and their effectiveness have been confirmed in randomized controlled studies • Manicourt (Arthritis Rheum 2004)

  47. Calcitonin • Thyroid gland, inhibit osteoclastic bone resorption • Gobelet ( Pain 1992) • Intranasal calcitonin in 63 pts with CRPS in a double-blind randomized study • Significant reduction in pain at rest and with motion and increased mobility • Meta-analysis_Perez concluded that calcitonin could provide effective pain relief in CRPS patients (J Pain Symptom Manage 2001)

  48. Free Radical Scavenger • Dimethylsulfoxide (DSMO) • N-acetylcysteine (NAC) • Effective in treating CRPS • Perez (Pain 2003)

  49. Interventional Procedures • Sympathetic Nerve Blockade • Diagnosis and treatment for CRPS • Epidural Infusion • local anesthetic and opioid • fluoroscopic guidance catheter tip on the affected side at the appropriate spinal segmental level • Tunneled 5 days to 12 wks physiotherapy

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