Complex Regional Pain Syndrome

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

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

Key Messages Clinical Diagnosis of exclusion Uncertain cause No specific treatment Rehabilitation key treatment Other treatments aimed to facilitate above Dr Brooks

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

In 1993, the IASP introduced the term Complex regional pain syndrome to 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

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 Dr Brooks:

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 Dr Brooks:

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 Dr Brooks:

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) A retrospective cohort study was conducted during 1996–2005 in the Integrated Primary Care Information (IPCI) project, a general practice research database with electronic patient record data from 600,000 patients throughout the Netherlands. Potential CRPS cases were identified by a sensitive search algorithm including synonyms and abbreviations for CRPS. Subsequently, cases were validated by electronic record review, supplemented with original specialist letters and information from an enquiry of general practitioners. ? 1-2% following # 7-35% following colles 2-5% following nerve injury Veldman et al 1993 deMos et al 2007 Dr Brooks:

Natural History Natural history uncertain 30% consider resolved by 6yrs 50% disease stable 15% no improvement Later improvement less common with time OBJECTIVES: The outcome of complex regional pain syndrome (CRPS) is relatively unknown. High disease resolution rates have been reported, but also long-lasting impairments in many patients. This study aims to assess CRPS outcome in a population-based cohort of CRPS patients. METHODS: CRPS patients were retrospectively identified (1996 to 2005) in a Dutch general practitioners database, the integrated primary care information project, and included if at onset (ie, in the past) they had complied with the International Association for the Study of Pain (IASP) diagnostic criteria. The disease status at minimum of 2 years since onset was assessed during visits using questionnaires, interviews, and physical examination. Symptoms and signs were compared with reference patients with an identical past injury but without CRPS. Actual fulfillment of the IASP criteria, treatment status, self-reported recovery, and working status were recorded. Moreover, to identify the potential prognostic factors, baseline patient characteristics were compared across subgroups according to the CRPS outcome. These subgroups were derived by cluster analysis on actual symptoms and signs. RESULTS: One hundred and two CRPS patients were assessed at on average 5.8 years (range: 2.1 to 10.8) since onset. CRPS patients displayed higher symptom and sign prevalences in all categories (sensory, vasomotor, sudomotor, and motor/trophic) than controls. Sixteen percent (95% CI: 9-22) reported the CRPS as still progressive, whereas 31% (95% CI: 19-43) were incapable of working. Patients in the poorest outcome cluster more often had their upper extremity affected, event other than a fracture, and cold CRPS. DISCUSSION: Severe CRPS outcome is rare, but a majority of patients has persistent impairments at 2 or more years since onset. deMos etal 2009 Dr Brooks Dr Brooks:

Features - Harden 2001 Signs% Symptoms% Burning pain 80 Hyperethesia 65 Temperature diff 55 78 Colour changes 66 85 Sweating 24 52 Oedma 56 21 Nail Changes 9 Hair changes 8 18 Weakness 20 75 Tremor 23 Dystonia 14 Reduced ROM 70 Hyperalgesia 63 Allodynia 74 These patients often report a burning spontaneous pain felt in the distal part of the affected extremity. Characteristically, the pain is disproportionate in intensity to the inciting event. The pain usually increases when the extremity is in a dependent position. Stimulus-evoked pains are a striking clinical feature; they include mechanical and thermal allodynia and/or hyperalgesia. These sensory abnormalities often appear early, are most pronounced distally, and have no consistent spatial relationship to individual nerve territories or to the site of the inciting lesion. Typically pain can be elicited by movement of and pressure on the joints (deep somatic hyperalgesia), even if these are not directly affected by the inciting lesion. Autonomic abnormalities include swelling and changes of sweating and skin blood flow. In the acute stages of CRPS I the affected limb is often warmer than the contralateral limb. Sweating abnormalities-either hypohidrosis or, more frequently, hyperhidrosis-are present in nearly all CRPS I patients. The acute distal swelling of the affected limb depends very critically on aggravating stimuli. Since it may diminish after sympathetic blocks it is likely that it is maintained by sympathetic activity. Trophic changes such as abnormal nail growth, increased or decreased hair growth, fibrosis, thin glossy skin and osteoporosis may be present, particularly in chronic stages. Restrictions of passive movement are often present in longstanding cases and may be related to both functional motor disturbances and trophic changes of joints and tendons. Weakness of all muscles of the affected distal extremity is often present. Small accurate movements are characteristically impaired. Nerve conduction and electromyography studies are normal, except in patients in very chronic and advanced stages. About half of the patients have a postural or action tremor representing an increased physiological tremor. In about 10% of cases dystonia of the affected hand or foot develops (Harden et al 2001).d Dr Brooks Dr Brooks:

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

Sensory abnormalities and pain
Based on numerous animal experimental findings spontaneous pain and various forms of hyperalgesia at the distal extremity are thought to be generated by processes of peripheral and central sensitization. In addition to positive sensory phenomena, up to 50% of patients with chronic CRPS I develop hypoaesthesia and hypoalgesia on the entire half of the body or in the upper quadrant ipsilateral to the affected extremity. Systematic quantitative sensory testing has shown that patients with these generalized hypoaesthesias have increased thresholds to mechanical, cold, warmth and heat stimuli compared with the responses generated from the corresponding contralateral healthy body side. Patients with these extended sensory deficits have a longer disease duration, greater pain intensity, a higher frequency of mechanical allodynia and a higher tendency to develop changes in the somatomotor system than do patients with spatially restricted sensory deficits. These changed somatosensory perceptions are likely due to changes in the central representation of somatosensory sensations in the thalamus and cortex. Accordingly, positron emission tomography (PET) studies demonstrated adaptive changes in the thalamus during the course of the disease (Fukumoto et al 1999). Furthermore, recent magnetoencephalographic (MEG) and functional magnetic resonance imaging (fMRI) studies demonstrated a shortened distance between little finger and thumb representations in the first somatosensory (SI) cortex on the painful side (Maihofner et al 2003, 2005, Pleger et al 2004b, 2005). The MEG SI responses were increased on the affected side, indicating processes of central sensitization (Juottonen et al 2002) (cf. Fig. 64.2). These central changes depend on continuous nociceptive input from the affected extremity and may disappear after successful treatment of the pain (Maihofner et al 2004, Pleger et al 2005).g Dr Brooks:

Dr Brooks: www.paindocni.co.uk

Sympathetic denervation and denervation hypersensitivity cannot completely account for vasomotor and sudomotor abnormalities in CRPS. First, in CRPS I there is no overt nerve lesion and second, in CRPS II the autonomic symptoms spread beyond the territory of the lesioned nerve. In fact, there is direct evidence for a reorganization of central autonomic control in these syndromes (Janig & Baron 2002, 2003). Hyperhidrosis, for example, is found in many CRPS patients. Resting sweat output, as well as thermoregulatory and axon reflex sweating are increased in CRPS I patients (Birklein et al 1997). Increased sweat production cannot be explained by a peripheral mechanism since, unlike blood vessels, sweat glands do not develop denervation supersensitivity. Dr Brooks Dr Brooks:

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 Dr Brooks:

1) Sensory 2) Vasomotor 3) Sudomotor/ Vasomotor 4) Motor/Trophic Sign
>2 Symptom >3 1) Sensory Allodynia (to light tough or temperature deep somatic pressure or hyperalgesia to pinprick 2) Vasomotor Temperature asymmetry and or skin colour changes and or skin colour asymmetry Must be > 1C 3) Sudomotor/ Vasomotor Oedema and or sweating and or sweating asymmetry 4) Motor/Trophic Decreased range of motion and or motor dysfunction

Features PAIN Spontaneous Disproportionate to initiating event Allodynia / Hyperalgesia (variability in reported prevalence) In order to study cutaneous sympathetic vasoconstrictor innervation in CRPS I patients, we have analysed central sympathetic reflexes induced by thermoregulatory (whole-body warming, cooling) and respiratory stimuli (Baron & Maier 1996, Wasner et al 1999, 2001). Sympathetic effector organ function, i.e. skin temperature and skin blood flow, was measured bilaterally at the extremities by infrared thermometry and laser Doppler flowmetry. Under normal conditions these reflexes do not show interside differences. In CRPS patients three distinct vascular regulation patterns were identified related to the duration of the disorder:･In the warm regulation type (acute stage, < 6 months) the affected limb was warmer and skin perfusion values were higher than contralaterally during the entire spectrum of sympathetic activity. Even massive body cooling failed to activate sympathetic vasoconstrictor neurons (Wasner et al 1999). Consistently, direct measurements of norepinephrine levels from the venous effluent above the area of pain show a reduction in the affected extremity (Harden et al 1994, Wasner et al 1999).･In the intermediate type temperature and perfusion were either elevated or reduced depending on the degree of sympathetic activity.･In the cold type (chronic stage) temperature and perfusion were lower on the affected side during the entire spectrum of sympathetic activity. Norepinephrine levels, however, were still lower on the affected side (Wasner et al 2001). Dr Brooks Dr Brooks:

WHAT IS PAIN ?

Perhaps the best known artwork involving pain and the spine was done by Frida Kahlo.ﾊ At the age of 15 Kahlo was in a severe bus accident in which a long metal rod penetrated her chest, injured her spine, and exited through her pelvis.ﾊ Her life was permanently affected by this accident, and she lived and painted in pain for the rest of her life.

This self portrait depicts Kahloﾍs despair with her neuropathic pain problem, showing a fractured spine, nails penetrating her skin, emotionless tearing, and an overall outlook of hopelessness.ﾊ The backdrop is barren and desolate, purportedly reflecting social isolation.

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

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

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

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

Biopsychosocial Model Pain
Culture Social interactions Sick role SOCIAL PSYCHO BIO- Illness behaviour Beliefs, coping strategies Emotions distress Beliefs – Fear avoidance Personal responsibility Beliefs and expectations Coping Passive / active / health care Distress Axiety/fear/depressive/anger Illness behaviour Social interactions Culture/family Neurophysiology Physiologic dysfunction (Tissue damage?)

BIOLOGICAL Pain Experience Psyc

Experience Bio Psychological

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 Common in early CRPs – unusual in late schattshneider j 2006 Short term relief in pateints On the basis of experience and recent clinical studies the term 'sympathetically maintained pain' was redefined. Neuropathic pain patients presenting with similar clinical signs and symptoms can clearly be divided into two groups by the negative or positive effect of selective sympathetic blockade or antagonism of alpha adrenoceptor mechanisms. The pain component that is relieved by specific sympatholytic procedures is considered to be sympathetically maintained pain (SMP). Thus, SMP is now defined as a symptom or the underlying mechanism in a subset of patients with neuropathic disorders and not a clinical entity. The positive effect of a sympathetic blockade is not essential for the diagnosis. On the other hand, the only way to differentiate between sympathetically maintained pain (SMP) and sympathetically independent pain (SIP) is the efficacy of a correctly applied sympatholytic intervention (Stanton-Hicks et al 1995). Peripheral coupling Indirect via vascular bed Via adrenal medulla Proposed coupling between sympathetic NS and afferent neurones Dr Brooks:

Vasomotor changes Thermography Colour – red, cyanotic or pale
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 Red warm – reduced symp outflow Cold blue – adrenoreceptor upregulation increased sensitivity Reduce over time Dr Brooks:

Sudomotor & Oedma Increased or decreased sweat production ? Reliability of history ? Clinical assessment Sweat testing – research setting Resting sweat output Dr Brooks Dr Brooks:

Trophic Advanced – atrophy skin/ nails Demineralisation bone 7% develop severe changes / refractory Motor Weakness, poor coordination, tremor and myoclonus ? Related to disuse / neglect Motor abnormalities page 1016 page 1017 About 50% of the patients with CRPS show a decrease of active range of motion, an increased amplitude of physiological tremor and reduced active motor force of the affected extremity. In about 10% of cases dystonia of the affected hand or foot develops, especially in chronic cases. It is unlikely that these motor changes are related to a peripheral process (e.g. influence of the sympathetic nervous system on neuromuscular transmission and/or contractility of skeletal muscle). These somatomotor changes are more likely generated by changes of activity in the motor neurons, i.e. they have a central origin. Furthermore, we used kinematic analysis of target reaching as well as grip force analysis to quantitatively assess motor deficits in CRPS patients (Schattschneider et al 2001). These results pointed to abnormalities in cerebral motor processing. A pathological sensorimotor integration located in the parietal cortex was found that may induce abnormal central programming and processing of motor tasks. Interestingly, the motor performance is also slightly impaired on the contralateral unaffected side (Ribbers et al 2002). According to this view, a neglect-like syndrome was clinically described as being responsible for the disuse of the extremity (Galer et al 1995). A recent controlled study also supports an incongruence between central motor output and sensory input as an underlying mechanism in CRPS. Using the method of mirror visual feedback the visual input from a moving unaffected limb to the brain was able to re-establish the pain-free relationship between sensory feedback and motor execution. After 6 weeks of therapy pain and function were improved as compared with the control group (McCabe et al 2003, Moseley 2004). Furthermore, a sustained inhibition of the motor cortex was found in CRPS patients on the contralateral as well as the ipsilateral hemisphere (Juottonen et al 2002, Schwenkreis et al 2003).e Dr Brooks Dr Brooks:

Other Investigations QST Neurophysiological procedures 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?? Dr Brooks:

Radiography Demineralisation ? Related to disuse
Considered non-specific & late Not part of screening procedure Plain radiographs and X-ray bone densitometry: Endosteal and intracortical excavation, subperiosteal and trabecular bone resorption, spotty and localized bone demineralization or osteoporosis have been thought to be specific signs of CRPS, but these are only positive in chronic stages. A comparison of radiography and three-phase scintigraphy in early post-fracture CRPS showed a lower sensitivity and specificity of the radiography. MRI scans are suggested as being more reliable than radiographic examination and scintigraphy but have to prove their value in further studies Dr Brooks:

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 Bone scintigraphy: Osseous changes are common in CRPS. Thus three-phase bone scintigraphy can provide valuable information. A homogenous unilateral hyperperfusion in the perfusion (30 s post-injection [p.i.]) and blood-pool phases (2 min p.i.) is characteristic and will help to exclude differential diagnoses (e.g. osteoporosis due to inactivity). At 3 h p.i. the mineralization phase will show an increased unilateral periarticular tracer uptake (Fig. 64.6). A pathological uptake in the metacarpophalangeal or metacarpal bones is thought to be highly sensitive and specific for CRPS. However, a gold standard to compare with is as yet unknown but it is useful to rule out pain syndromes of other origin. It should be noted that bone scintigraphy only shows significant changes during the subacute period (up to 1 year). Dr Brooks Dr Brooks:

Integrative conceptual model of CRPS
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 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 antineuronal Ab’s IVIG effective in reducing pain short term Goebel A Rheumatology 2011 Dr Brooks:

Management Dr Brooks:

The Four Pillars of Treatment in CRPS.
The four pillars of treatment in CRSP. Information/education, physical rehabilitation, psychological intervention and drug/procedural interventions have equal importance for the treatment of CRPS. Emphasis is on an individualized, integrated interdisciplinary approach. Goebel A Rheumatology 2011;rheumatology.ker202 Dr Brooks:

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

Medication Initial - Codeine / Paracetamol / NSAIDS
Very little good data for CRPS Initial - Codeine / Paracetamol / NSAIDS Next Step – Antiepileptics / Antidepressants used in Neuropathic pain conditions Anticonvulsants Pregabalin/ Gabapentin Antidepressants Amitriptyline Antidepressants: Tricyclic antidepressants (TCAs) have been intensely studied in different neuropathic pain conditions, but not in CRPS. There is solid evidence that reuptake blockers of serotonin and noradrenaline (e.g. amitriptyline) and selective noradrenaline blockers (e.g. desipramine) produce pain relief in diabetic or postherpetic neuropathy. The effectiveness of selective serotonin reuptake inhibitors in neuropathic pain states is still discussed. Only one of four studies performed so far showed a significant pain reduction in painful diabetic neuropathy. None has been performed on CRPS patients. Gabapentin and pregabalin: Promising preliminary evidence was revealed by studies on patients with CRPS that showed an analgesic effect of gabapentin (Mellick & Mellick 1995, Serpell 2002, van de Vusse et al 2004). Gabapentin and pregabalin are is effective in painful diabetic neuropathy and postherpetic neuralgia. Dr Brooks:

Opiates – Care with prescribing especially ↑ doses Not increase above equivalent 60 mg morphine per 24 hrs No short acting Dr Brooks

Medication Second / Third Line Therapies Lidocaine patches
NMDA antagonist Ketamine iv infusion 5 days Topical capsaicin No evidence in trials but still used Cannabinoids Nabilone N-methyl-D-aspartate (NMDA) receptor blockers: Clinically available compounds that are demonstrated to have NMDA receptor blocking properties include ketamine, dextromethorphan and memantine. Dextromethorphan, for example, is effective in the treatment of painful diabetic neuropathy and not effective in postherpetic neuralgia and central pain. NMDA receptor blockers may therefore offer new options in the treatment of CRPS pain but studies that would help clinicians to fully utilize these agents are not yet available. Calcium-regulating drugs: Calcitonin administered three times daily intranasally demonstrated a significant pain reduction in CRPS patients (Gobelet et al 1992). Clodronate 300 mg daily i.v. and alendronate 7.5 mg daily i.v. showed a significant improvement in pain, swelling and movement range in acute CRPS (Adami et al 1997, Varenna et al 2000). The mode of action of these compounds in CRPS is unknown. Sodium channel blocking agents: Lidocaine (lignocaine) administered intravenously is effective in CRPS I and II regarding spontaneous and evoked pain (Wallace et al 2000). Carbamazepine has not been tested in CRPS. Dr Brooks:

Other Medications Iv palmidronate Early CRPS Vit C Steroids Dr Brooks

Psychological interventions
All pain conditions complex biopsychosocial disorder Pain Disuse/Emotional arousal Several case reports / series reporting benefits RCTs contain psychological therapy as part physical/medical therapy Dr Brooks Dr Brooks:

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 Dr Brooks:

Physiotherapy / Rehabilitation
See Louis Talk! Active motion Stress loading Posture changes Desensitiseation Massage TENS Oedma – garments/gentle movements OT early protective splints reduce pain oedma Dynamic splints Stress loading - level 3 evidence Dr Brooks:

Interventional therapies
Sympathetic Block Stellate ganglion block Lumbar sympathetic chain Intravenous Regional anaesthesia Guanethidine Bretyllium Dr Brooks Dr Brooks:

Stellate Ganglion Block
Upper Limb Chronic Regional Pain Syndrome Type I (CRPS I) Sympathetic supply to the ipsilateral arm / hemi-face Sympathetic ganglion blocks: One controlled study in patients with CRPS I has shown that sympathetic ganglion blocks with local anaesthetic have the same immediate effect on pain as a control injection with saline (Price et al 1998). However, after 24 h patients in the local anaesthetic group were much better, indicating that non-specific effects are important initially and that evaluating the efficacy of sympatholytic interventions is best done after 24 h. With these data in mind, the uncontrolled studies mentioned above must be interpreted cautiously. Only 10 out of the 24 studies we reviewed assessed long-term effects. Dr Brooks:

Lumbar Sympathetic Block
sympathetic chains overlying anterior portion of vertebral bodies posterior to aorta/IVC anteromedial to kidneys/ureter Dr Brooks:

LSB Needle Insertion Dr Brooks Dr Brooks:

Intravenous Regional Sympathetic Block
Depletion of norepinephrine in sympathetic nerve terminals guanethidine bretylium Dr Brooks:

IVRA Guanethidine – essentially little evidence efficacy BUT ALL THE STUDIES– entry criteria / all included Fig. 3. Individual and summary effect sizes for subgroup 3.[13, 26, 30, 31, 33, 35, 36, 39 and 40] Displayed are the effect sizes with 95% CI. Tuq3: subgroup 3, IRSB versus control plus quality weighting; Tu3: subgroup 3, IRSB versus control without quality weighting; Tuq3plac: subgroup 3, IRSB versus placebo with quality weighting Intravenous regional sympatholysis (IVRS) - open studies: No improvement compared with baseline was found for reserpine (IVRS) and guanethidine (IVRS) (Jadad et al 1995). No differences were obtained between guanethidine (IVRS) or lidocaine (lignocaine) (IVRS) (Ramamurthy & Hoffman 1995). Guanethidine and pilocarpine versus placebo showed no differences after application of four blocks (Livingstone & Atkins 2002). However, stellate blocks with bupivacaine as well as regional blocks with guanethidine (IVRS) demonstrated a significant improvement of pain compared with baseline but no differences between these two therapies (Bonelli et al 1983). One study demonstrated that IVRS bretylium and lidocaine (lignocaine) produce significantly longer pain relief than lidocaine(lignocaine) alone (Hord et al 1992). No effect was obtained by droperidol(IVRS) (Kettler & Abram 1988). Hanna and Peat (1989) demonstrated a significant improvement of pain due to a single (IVRS) bolus of ketanserin. Bounameaux et al (1984) failed to show any significant effect with the same procedure. There is a desperate need for controlled studies that assess the acute as well as the long-term effect of sympathetic blockade and IVRS on pain and other CRPS symptoms, in particular motor function. Well performed sympathetic ganglion blocks should be performed rather than IVRS (Hord & Oaklander 2003) Oa Dr Brooks Dr Brooks:

Sympathetic nerve blocks
Very little evidence benefit or evidence to base judgement Still used routinely ? role One study demonstrated efficacy bretylium One study Guanethidine comparable to stellate Dr Brooks Dr Brooks:

Epidural Infusions Titrate to response Allow Physio therapy
3 studies demonstrated improvements Dr Brooks:

Epidural Infusions Study No. Pts Infusion Results Complications Cooper 89 14 Bupiv-opioid 4 days Improved pain/ROM 13/14 none Konnig 95 29 Bupiv 7 days 83% improved pain Infection catheter site Rauck 93 19 Clonidine 3 days Improved pain Infections Nausea Dizziness Dr Brooks Dr Brooks:

Brachial Plexus Catheter
Several Case reports (level 4 evidence) 1-3 weeks Allow physiotherapy Even less evidence Dr Brooks Dr Brooks:

Spinal Cord Stimulation
Meta-analysis Grabow 2003 15 studies 1 RCT / 14 observational case series Only 1 RCT – 50% response ( 50% relief) Kemler MA 2000 Suggest benefit still questions re efficacy Use if other Rx failed NICE approved Dr Brooks:

Take Home Message Clinical Diagnosis Uncertain cause No specific treatment Rehabilitation key treatment Moderate/Severe CRPS needs multidisciplinary team management! Dr Brooks

Autonomic abnormalities
Denervation supersensitivity A partial nerve lesion is the important preceding event in CRPS II. Therefore, it has generally been assumed that abnormalities in skin blood flow within the territory of the lesioned nerve are due to peripheral impairment of sympathetic function and sympathetic denervation. During the first weeks after transection of vasoconstrictor fibres, vasodilatation is present within the denervated area. Later the vasculature may develop increased sensitivity to circulating catecholamines, probably due to upregulation of adrenoceptors.f Dr Brooks:

NHS Website CRPS Dr Brooks Dr Brooks:

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