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Complex Regional Pain Syndrome

Complex Regional Pain Syndrome. Dr Jason Brooks Consultant Anaesthesia and Pain Medicine Belfast Trust Orthopaedic Update June 2013. CRPS. What is it? Diagnosis Treatment – general principles Pain Clinic treatment. Key Messages. Clinical Diagnosis of exclusion Uncertain cause

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Complex Regional Pain Syndrome

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  1. Complex Regional Pain Syndrome Dr Jason Brooks Consultant Anaesthesia and Pain Medicine Belfast Trust Orthopaedic Update June 2013

  2. CRPS • What is it? • Diagnosis • Treatment – general principles • Pain Clinic treatment Dr Brooks www.paindocni.co.uk

  3. Key Messages • Clinical Diagnosis of exclusion • Uncertain cause • No specific treatment • Rehabilitation key treatment • Other treatments aimed to facilitate above Dr Brooks www.paindocni.co.uk

  4. Health-care services involved in the care of patients with CRPS. Goebel A Rheumatology 2011

  5. In 1993, the IASP introduced the term Complex regional pain syndrometo describe all pain states that previously would have been diagnosed as RSD or causalgia-like syndromes Posttraumatic dystrophy Causalgia Minor causalagia Sudek atrophy Shoulder-hand syndrome Reflex sympathetic dystrophy

  6. CRPS • Complex: Varied and dynamic clinical presentation • Regional: Non-dermatomal distribution of symptoms • Pain: Out of proportion to the inciting events • Syndrome: Constellation of symptoms and signs Dr Brooks www.paindocni.co.uk

  7. The term “sympathetic” was avoided in the revised definition because its contribution is not constant across patients • CRPS pain may be “sympathetically maintained pain” (SMP) • or “sympathetically independent pain” (SIP) Dr Brooks www.paindocni.co.uk

  8. CRPS can be separated into two types based on the presence or absence of a nerve injury • CRPS type I: A syndrome that develops after an initiating noxious event that may or may not be associated with a period of immobilization • CRPS type II: Differs from CRPS type I by the presence of a known injury to a nerve or nerves

  9. How common is CRPS? • Incidence: 26/100,000 life years Hip OA = 88 per 100,000 person years • Female:Male ratio: 3-4:1 • 80-85% have experienced preceding trauma (fractures, surgery) ? 1-2% following # 7-35% following colles 2-5% following nerve injury Veldman et al 1993 deMos et al 2007

  10. Natural History • Natural history uncertain • 30% consider resolved by 6yrs • 50% disease stable • 15% no improvement • Later improvement less common with time deMos etal 2009 Dr Brooks www.paindocni.co.uk

  11. Features - Harden 2001 Dr Brooks www.paindocni.co.uk

  12. Early CRPS of the right hand; clearly visible signs include swelling, red colour and a shiny skin. Goebel A Rheumatology 2011

  13. Dr Brooks www.paindocni.co.uk

  14. Budapest Diagnostic criteria A) Continuing pain disproportionate to initiating event B) At least 1 sign in 2 or more categories C) The patient symptoms in 3 or more categories D) No other diagnosis can better explain the signs and symptoms

  15. Features PAIN Spontaneous Disproportionate to initiating event Allodynia / Hyperalgesia (variability in reported prevalence) Dr Brooks www.paindocni.co.uk

  16. WHAT IS PAIN ?

  17. The Eradicator – Consumed by Chronic Pain This artwork represents my daily struggle with constant pain. The only part of my body that does not hurt yet is still reaching out for help because I am not giving up. The artwork also glows in the dark representing the relentless nature of my pain 24/7

  18. A Definition “an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage” International Association for the Study of Pain

  19. A Definition “an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage” International Association for the Study of Pain

  20. A Definition “an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage” International Association for the Study of Pain

  21. A Definition “an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage” International Association for the Study of Pain

  22. Pain is whatever the experiencing person says it is, existing whenever the experiencing person says it does McCaffery

  23. Disease Model Pain Pain = tissue injury Tissue damage = impairment = disability = incapacity work Cure pain – disability will recover Problem Pain  tissue injury Pain, disability and work incapacity not same thing Different people respond very differently Social issues profound influence

  24. Culture Social interactions Sick role Illness behaviour Beliefs, coping strategies Emotions distress Neurophysiology Physiologic dysfunction (Tissue damage?) Biopsychosocial Model Pain SOCIAL PSYCHO BIO-

  25. Biopsychosocial Model Pain Social BIOLOGICAL Pain Experience Psyc

  26. Biopsychosocial Model Pain Social Pain Experience Bio Psychological

  27. Sympathetically Maintained Pain Proportion of CRPS symptoms improved with sympathetic blockade If  symp outflow to limb  stimulus evoked pain in those who responded to block Peripheral coupling Indirect via vascular bed Via adrenal medulla Proposed coupling between sympathetic NS and afferent neurones

  28. Vasomotor changes • Thermography • Difference 0.6 Sens & Spec 67% (Bruehl 1996) • Difference 2 Sens 32 % spec 100% (Wasner 2002) • Diagnostic value increases if multiple sites • Very dynamic measures • Not a reliable clinical test Colour – red, cyanotic or pale Typically  temp in acute stages < 6mths • in chronic state ? Reliability of HISTORY Often difficult to examine / variable

  29. Sudomotor & Oedma Increased or decreased sweat production ? Reliability of history ? Clinical assessment Sweat testing – research setting Resting sweat output Dr Brooks www.paindocni.co.uk

  30. Trophic • Advanced – atrophy skin/ nails • Demineralisation bone • 7% develop severe changes / refractory • Motor • Weakness, poor coordination, tremor and myoclonus • ? Related to disuse / neglect Dr Brooks www.paindocni.co.uk

  31. Other Investigations • QST • Not specific • No additional diagnostic information • Neurophysiological procedures • CRPS  - borderline delay NCV / distal motor latency • > 20% suggest underlying peripheral nerve lesion • Useful to distinguish between CRPS  &  • Is that important??

  32. Radiography • Demineralisation • ? Related to disuse • Considered non-specific & late • Not part of screening procedure

  33. Three-phase bone scintigraphy Unilateral Uptake tracer High sensitivity Low Specificity Not useful in the work –up of patients Neither makes or excludes the diagnosis Dr Brooks www.paindocni.co.uk

  34. Central Sensitisation Driver CRPS Dynamic changes in spinal cord increasing transmission of pain signal Cortical Reorganisation Reduced sensory representation in homouculus altered. Improves with Rx Mirror Therapy / GMI Integrative conceptual model of CRPS Ischaemia reperfusion injury Some evidence for low oxygen tension in peripheral tissues Sympathetic Dysfunction Inflammatory Process ↑ inflammatory agents Neurogenic inflammation Skin reddening / oedma Autoimmune Condition Novel concept Evidence antineuronalAb’s IVIG effective in reducing pain short term Goebel A Rheumatology 2011

  35. Management

  36. The Four Pillars of Treatment in CRPS. Goebel A Rheumatology 2011;rheumatology.ker202

  37. CRPS Pain Mx oral/topical meds Psychological Rx with focus on Education Interventional Pain Mx Rehab SNB IVRA Somatic Reactivation Desensitisation Psychological Assess for axis 1 Pain coping Biofeed/Relax CBT Isometric Flexibility Oedma control Failure to Progress Failure to Progress Epidural/Plexus Neurostim Intrathecal ROM, Stress Load Isotonic Aerobic conditioning  Freq or psycotherapy Other Surgical /

  38. Medication Very little good data for CRPS Initial - Codeine / Paracetamol / NSAIDS Next Step – Antiepileptics / Antidepressants used in Neuropathic pain conditions AnticonvulsantsPregabalin/ Gabapentin AntidepressantsAmitriptyline

  39. Opiates – Care with prescribing especially ↑ doses Not increase above equivalent 60 mg morphine per 24 hrs No short acting Dr Brooks www.paindocni.co.uk

  40. Medication Second / Third Line Therapies Lidocaine patches NMDA antagonist Ketamine iv infusion 5 days Topical capsaicin No evidence in trials but still used CannabinoidsNabilone

  41. Other Medications • Iv palmidronate • Early CRPS • Vit C • Steroids Dr Brooks www.paindocni.co.uk

  42. Pain Disuse/Emotional arousal Psychological interventions All pain conditions complex biopsychosocial disorder • Several case reports / series reporting benefits • RCTs contain psychological therapy as part physical/medical therapy Dr Brooks www.paindocni.co.uk

  43. In general: • Relaxation therapy • Coping skills • Behavioural intervention to address disuse • CBT • Active participant in therapy • Potentially as part of more formal Pain Management Programme Dr Brooks www.paindocni.co.uk

  44. Physiotherapy / Rehabilitation See Louis Talk!

  45. Interventional therapies Sympathetic Block • Stellate ganglion block • Lumbar sympathetic chain • Intravenous Regional anaesthesia • Guanethidine • Bretyllium Dr Brooks www.paindocni.co.uk

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