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CRPS Guide: Signs, Stages, Diagnosis & Treatment
- 1. Complex regional pain syndromeBy Petrus Iitula MBChB IHO
- 2. Table of content • Definition • Epidemiology • Etiology • Signs and symptoms • Pathophysiology • Types of CRPS (Stages) • Diagnosis • Investigations • Treatment Modalities
- 3. Definition The term complex regional pain syndrome (CRPS) describes a variety of painful conditions following injury. • minor trauma (fractures, sprain etc), elective surgeries, stroke. • exaggerated in both magnitude and duration of the expected clinical course • often result in significant impairment of motor function, and showing variable progression over time. • Complex : sensory sx, local autonomic instability, trophic changes, motor abnormalities.
- 4. Epidemiology • Females > males 2-4:1 • 5.5 – 26.2 cases per 100 000 persons/year. • Across all ages, peak at 40 years (range 50-70 yrs). • Arm > legs (in adults) • Preceding event: minor trauma, fracture, surgery. • No relation between severity of primary trauma and presentation. Risk Factors Immobilization of injured limb Use of ACE inhibitors Asthma Familial
- 5. Etiology • Most common triggers: - Fractures - Sprains - Soft tissue injuries – burns, cuts, bruises. - Limb immobilization (cast) - Surgery and medical conditions (stroke) or procedures (needle prick)
- 6. S&S • Key symptom is prolonged severe pain that may be constant. (burning, pins & needles, squeezing) • Radiate • Allodynia - ↑ sensitivity in affected area. • Skin: color, temperature, swelling of the limb, skin texture (shiny & thin), abnormal sweating patterns. • Changes in Nails and hair growth patterns. • Stiffness in the joints. • Muscle incoordination and Dystonia/ tremors
- 8. Pathophysiology Exact mechanism is still poorly understood - both peripheral & central factors involved. • Aberant inflammatory mechanisms. • Nociceptive sensitization. • Vasomotor dysfunction. • Maladaptive neuroplasticity.
- 9. Inflammatory mechanisms • Activation of cutaneous nociceptors following injury → Retrograde depolarization of primary afferents → Release of neuropeptides (substance P, CGRP) • Increase Interleukins and TNFα • ? Autoimmune mechanisms
- 10. Vasomotor dysfunction • A common problem in CRPS • Warm (4 months), intermediate (4-15 months) and cold type • Inhibition of cutaneous sympathetic vasoconstrictor activity • Increased sensitivity to circulating catecholamines (SMP) • Endothelial dysfunction
- 11. Central nervous system • Central sensitization • Structural changes to emotional centers - Distortion of mental image of affected area • Impaired motor control – dystonia • Cortical re-organisation
- 13. Types • CRPS type I (reflex sympathetic dystrophy) - minor injuries/ fractures • CRPS type II (causalgia) - develops after injury to a major peripheral nerve. These chronic pain syndromes comprise different clinical features, including spontaneous pain, allodynia, hyperalgesia, edema, autonomic abnormalities, and trophic signs.
- 16. CRPS Stage 1 (Acute) Immediately after injury (within weeks of injury) MOST LIKELY TO BE REVERSED AND CURED • SKIN: Red, warm, swollen, dry, inflamed. • DISTRIBUTION: Pain is not compatible with a single peripheral nerve, trunk, or root lesion. • SYMPATHETIC: - VASOMOTOR: Disturbances occur with variable intensity, producing altered color and temperature – SUDOMOTOR: Hyperhydrosis or diaphoresis • MOTOR: Decreased ROM, weakness • X-RAYS: Normal • BONE SCAN: Increased uptake
- 17. Stage 1 (Acute)
- 18. CRPS Stage 2 (Dystrophic) Within months of injury. • SKIN: Cool, moist, tight/shiny, swelling, coarse/sparse hair, brittle nails, discolored, edema • SYMPATHETIC: – VASOMOTOR: Mottled/cyanotic – SUDOMOTOR: Hyperhydrosis • MOTOR: Weakness, decreased ROM • BONE SCAN: No longer helpful.
- 20. CRPS Stage 3 (Atrophic) • Pain is somewhat decreased – less at rest, worse with passive motion • Changes are irreversible • SKIN: Atrophy, “waxy”, very thin, ulcerations, brittle nails • SYMPATHETIC: – VASOMOTOR: Cold, intermittently cyanotic/mottled • MOTOR: Decreased ROM, weakness, muscle & tendon atrophy, contractures, dystonia, tremor. Nonfunctional limb. • X-RAYS: Diffuse patchy osteoporosis (Sudeck’s Atrophy)
- 21. Sudeck’s Atrophy
- 23. Diagnosis • The diagnosis of CRPS is based solely on clinical signs and symptoms (BUDAPEST CRITERIA 2012). - Because poorly understood pathophysiological mechanisms of CRPS, mechanism based diagnosis is not yet feasible
- 25. Investigations • Objective testing (thermography, triple phase bone scan, quantitative sudomotor axon reflex test) is not necessary to make the diagnosis, but in some cases may be used to support a clinical diagnosis • There is no specific diagnostic test available for CRPS • Main purpose: to exclude other diagnoses – Lab: FBC,ESR,CRP to exclude infection/rheumatologic – Duplex / Ultrasound: exclude peripheral vascular disease – Nerve conduction velocity studies: exclude peripheral neuropathic disease, painful • Imaging: may demonstrate osteoporosis in affected limb (but no diagnostic value)
- 26. Differential Diagnosis 1. Diabetic (poly)neuropathy, 2. Vascular diseases ( Raynaud’s syndrome, DVT Vasculitis) 3.Cellulitis 4. Rheumatoid arthritis 5. Post Herpetic neuralgia
- 27. Management • Patient information and education • Pain relief and inflammatory control • Physical Rehabilitation • Psychological and Vocational rehabilitation
- 28. Treatment • Two types of treatment modalities: 1. Conservative treatment • Most important: early active mobilization physical therapy combined with pharmacotherapy, psychological therapy 2. Interventional management • Sympathetic block • Spinal cord stimulator
- 29. Conservative Treatment • Multidisciplinary approach • Pharmacotherapy - Steroids- acute phase - Oral prednisolone 30- 40 mg/day - Analgesia: Opioids - Antidepressants - Anticonvulsants - Lidocaine patch
- 30. Opiods
- 31. Antidepressants
- 32. Anti- convulsant
- 33. Others • Calcitonin • Biphosphonates • Vit.c • N-acetylcysteine
- 34. Interventional magement • Sympathetic block (stellate/lumbar block) – Break the vicious cycle of pain. – Permit more vigorous physical activity. • Neurolytic blocks - use alcohol – Give excellent results when performed early. – Diagnostic blocks using LA should be done prior to neurolytic block • Spinal cord stimulation -alters neuro-chemistry in dorsal horns, suppressing the hyperexcitability, increase GABA • Peripheral nerve stimulation • Intrathecal drug delivery system - Used for patients with dystonia , failed neuro-stimulation, long standing disease, multi limb involvement or need palliative care.
- 35. Complications • cause of significant morbidity and loss of quality of life. • It affects: - Anxiety, depression, stressed - cognition, - sleep (falling asleep and staying asleep), - bladder and bowel function, - -self-esteem, job, family • includes side effects of medications (such as dry mouth and constipation
- 36. Take Home Message • High index of suspicion for the clinician. • Treatment should be immediate after diagnosis - physiotherapy. • Multidisciplinary approach • Aim treatment: – toward restoration of full function of the affected area. • Intensity of therapy (in particular physiotherapy) should be adapted to the severity of the disease. – Gentle and below pain threshold and must not exacerbate the pain since every painful stimulus may worsen the syndrome
- 37. Thank you
- 38. References 1. Knobler, R., (2019). Hypervigilance in the Detection of Early Complex Regional Pain Syndrome, Type 1/Reflex Sympathetic Dystrophy— An Underutilized Tool in Treatment. Knobler Institute of Neurologic Disease, Fort Washington, PA, USA. 2. "Complex Regional Pain Syndrome Fact Sheet", NINDS, Publication date January 2017. NIH Publication No. 17-4173 https://www.ninds.nih.gov/Disorders/Patient-Caregiver-Education/Fact- Sheets/Complex-Regional-Pain-Syndrome-Fact- Sheet#:~:text=Complex%20regional%20pain%20syndrome%20(CRPS,peripheral% 20and%20central%20nervous%20systems. 3. Poree L, Krames E, Pope J, Deer TR, Levy R, Schultz L. Spinal cord stimulation as treatment for complex regional pain syndrome should be considered earlier than last resort therapy. Neuromodulation. 2013 Mar-Apr;16(2):125-41 https://www.neuromodulation.com/complex-regional-pain-syndrome-definition
Hinweis der Redaktion
- Primary trigger. the syndrome is complex because the patients affected may experience sensory symptoms i.e pain, paraesthesia (pins & needles), local autonomic instability such as oedema, temperature instabilty (hot and cold) skin color changes, trophic changes i.e changes in skin texture, nails and hair distribution with poor skin healing and motor abnormality.
- Relatively rare in the elderly. Very few children under 10. Almost no children under 5 years are affected.
- Unclear as to why some individuals develop CRPS and others with similar trauma do not. However in more than 90% of the cases, there is a clear history of trauma or injury.
- Radiate: may or may not radiate to the entire limb even if the injury might have only involved the finger or toe. Radiate to the contralateral limb in rare cases. Patients may also experience increased sensitivity in the affected area where by any normal contact or touch of the skin affected is experienced as very painful. This is termed as allodynia.
- CGRP - Calcitonin gene-related peptide There seem to be an aspect of an autoimmune mechanism as high levels of cytokines have been found in the tissues of people with CRPS. These also contributes to the redness, swelling and warth reported by pts. CRPS is common in pts with inflammatory and autoimune conditions such as asthma.
- Clinical experience has shown that CRPS1 is less likely to respond to treatment in its more advanced disease phases. For this reason, it is pertinent that clinicians are able to recognize the early, variable signs of CRPS1 which can provide the opportunity to initiate treatment early and facilitate resolution of this disorder, prior to the development of sequelae and spread. Despite the utility of the validated Budapest Criteria for diagnosing CRPS, the issues regarding early diagnosis and spread of CRPS, were not addressed in these criteria. Because the early features frequently are labile, the diagnosis may be delayed until they are more consistently displayed. This diagnostic uncertainty may contribute to a delay in the onset of treatment.
- Type 1 is further subdividd into phases. No definitive sequence of stages occurs in all patients.
- Diffuse patchy osteoporosis (Sudeck’s Atrophy
- For this reason, clinicians should be able to recognize the early, variable signs of CRPS1 which can provide the opportunity to initiate treatment early and facilitate resolution of this disorder, prior to the development of sequelae and spread. Despite the utility of the validated Budapest Criteria for diagnosing CRPS, the issues regarding early diagnosis and spread of CRPS, were not addressed in these criteria. Because the early features frequently are labile, the diagnosis may be delayed until they are more consistently displayed. This diagnostic uncertainty may contribute to a delay in the onset of treatment.
- There are four major categories in the Budapest Criteria utilized in order to diagnose CRPS. These criteria are widely accepted at this point. They have been under study for over 25 years and have been experimentally validated. In order to obtain information relevant to the clinical diagnosis of CRPS, the following nine diagnostic questions are proposed: 1. Is the pain out of proportion to the injury? 2. Is there a burning or aching quality to the pain? 3. Is there associated allodynia (pain from a non-painful stimulus), hyperpathia (exaggerated/prolonged pain to a painful stimulus), or hyperalgesia (increased sensitivity to a painful stimulus)? 4. Is there swelling (edema)? Is there sweating? 5. Are there associated color or skin temperature changes? 6. Is the skin smooth, shiny, or are there pronounced hair follicles? 7. Is there increased or decreased hair growth? 8. Are the nails cracked and grooved? 9. Are there abnormal movements, tone, posture (dystonia), reflexes or weakness? It deserves repeating that symptoms and signs will commonly vary with activity, posture, ambient temperature and/or humidity and with stress. These issues are not typically addressed in the conduct of a standard neurologic examination, but deserve consideration in the context of CRPS.
- Diagnoses readily confused with CRPS1/RSD could include those with fairly symmetrical symptoms, such as Raynaud’s syndrome and scleroderma, and possibly diabetic polyneuropathy. Alternatively, conditions with asymmetrical presentations could resemble CRPS, including diabetic neuropathy and post-herpetic neuralgia amongst others. However, these conditions tend to have distinct abnormalities on blood testing and do not have a specific traumatic origin preceding onset.
- Within the first week of symptoms, a short course of methylprednisolone, which affords 6 days of tapering therapy can be beneficial to jump-start treatment. This provides 24 mg, 20 mg, 16 mg, 12 mg, 8 mg, and 4 mg of methylprednisolone by mouth If untreated, or even incompletely treated, the severity of the pain from this disorder has driven people to suicidal ideation, and some to suicide. This problem is compounded by difficulties in obtaining adequate pain-relieving. Malingering.
- The natural history and pathophysiology of CRPS1/RSD is generally acknowledged as highly variable from individual to individual and from time to time within any given individual. This disorder can be the cause of significant morbidity and loss of quality of life. It affects mood, cognition,sleep (falling asleep and staying asleep), bladder and bowel function, self-esteem, job, family, home and includes side effects of medications (such as dry mouth and constipation). There do not appear to be psychological or psychiatric predisposing factors to the development of CRPS1/RSD, although there frequently are consequences of depression and anxiety following its onset.