complex regional pain syndrome workshop
DESCRIPTION
Complex Regional Pain Syndrome Workshop. Dr Jason Brooks Consultant Anaesthesia and Pain Medicine Belfast Trust November 2013. CRPS. What is it? Diagnosis Treatment – general principles Pain Clinic treatment. Key Messages. Clinical Diagnosis of exclusion Uncertain cause - PowerPoint PPT PresentationTRANSCRIPT
Complex Regional Pain Syndrome
WorkshopDr Jason Brooks
Consultant Anaesthesia and Pain Medicine
Belfast Trust
November 2013
CRPS
• What is it?• Diagnosis• Treatment – general
principles• Pain Clinic treatment
Key Messages
• Clinical Diagnosis of exclusion• Uncertain cause• No specific treatment• Rehabilitation key treatment• Other treatments aimed to facilitate
above
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 dystrophyCausalgiaMinor causalagiaSudek atrophyShoulder-hand syndromeReflex 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
• 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)
• 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
• 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)
How common is CRPS?
deMos et al 2007
? 1-2% following #7-35% following colles2-5% following nerve injuryVeldman et al 1993
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
Signs% Symptoms%
Burning pain 80
Hyperethesia 65
Temperature diff 55 78
Colour changes 66 85
Sweating 24 52
Oedma 56 21
Nail Changes 9 24
Hair changes 8 18
Weakness 20 75
Tremor 9 23
Dystonia 14 20
Reduced ROM 70 80
Hyperalgesia 63
Allodynia 74
Features - Harden 2001
Dr Brooks www.paindocni.co.uk
Early CRPS of the right hand; clearly visible signs include swelling, red colour and a shiny skin.
Goebel A Rheumatology 2011
Dr Brooks www.paindocni.co.uk
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
Sign>2
Symptom>3
1) SensoryAllodynia(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
FeaturesPAIN
Spontaneous
Disproportionate to initiating event
Allodynia / Hyperalgesia (variability in reported prevalence)
WHAT IS 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
The Eradicator – Consumed by Chronic Pain
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
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
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
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 injuryPain, disability and work incapacity not same thingDifferent people respond very differentlySocial issues profound influence
Biopsychosocial Model Pain
CultureSocial interactions
Sick role
Illness behaviourBeliefs, coping strategies
Emotionsdistress
NeurophysiologyPhysiologic dysfunction
(Tissue damage?)
SOCIAL
PSYCHO
BIO-
BIOLOGICAL
Psyc
Social
Pain Experience
Biopsychosocial Model Pain
Social
Psychological
Pain ExperienceBio
Biopsychosocial Model Pain
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
Proposed coupling between sympathetic NS and afferent neurones
Peripheral couplingIndirect via vascular bedVia adrenal medulla
Vasomotor changes
Colour – red, cyanotic or pale
Typically temp in acute stages < 6mths
ß in chronic state
? Reliability of HISTORYOften difficult to examine /
variable
Thermography
Difference 0.6 Sens & Spec 67% (Bruehl 1996)
Difference 2 Sens 32 % spec 100% (Wasner 2002)
Diagnostic value increases if multiple sitesVery dynamic measures
Not a reliable clinical test
Sudomotor & Oedma
Increased or decreased sweat production
? Reliability of history? Clinical assessment
Sweat testing – research settingResting sweat output
• Trophic– Advanced – atrophy skin/
nails– Demineralisation bone– 7% develop severe
changes / refractory
• Motor– Weakness, poor
coordination, tremor and myoclonus
– ? Related to disuse / neglect
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??
• Radiography– Demineralisation– ? Related to disuse– Considered non-specific & late– Not part of screening procedure
Three-phase bone scintigraphy
Unilateral Uptake tracerHigh sensitivityLow Specificity
Not useful in the work –up of patients
Neither makes or excludes the diagnosis
Integrative conceptual model of CRPSCentral SensitisationDriver CRPSDynamic changes in spinal cord increasing transmission of pain signal
Inflammatory Process↑ inflammatory agentsNeurogenic inflammationSkin reddening / oedma
Cortical ReorganisationReduced sensory representation in homouculus altered.Improves with RxMirror Therapy / GMI
Autoimmune ConditionNovel conceptEvidence antineuronal Ab’sIVIG effective in reducing pain short term
Ischaemia reperfusion injurySome evidence for low oxygen tension in peripheral tissues
Goebel A Rheumatology 2011
Sympathetic Dysfunction
Management
The Four Pillars of Treatment in CRPS.
Goebel A Rheumatology 2011;rheumatology.ker202
DCRPSPain Mx oral/topical meds
Psychological Rx with focus on Education
InterventionalPain Mx
SNBIVRASomatic
Epidural/PlexusNeurostimIntrathecal
Surgical /
Rehab
ReactivationDesensitisation
IsometricFlexibilityOedma control
ROM, Stress LoadIsotonic Aerobic conditioning
Other
Psychological
Assess for axis 1Pain copingBiofeed/RelaxCBT
Freq or psycotherapy
Fai
lure
to P
rogr
ess Failure to P
rogress
Medication
Very little good data for CRPS
Initial - Codeine / Paracetamol / NSAIDS
Next Step – Antiepileptics / Antidepressants used in Neuropathic pain conditions
Anticonvulsants Pregabalin/ Gabapentin
Antidepressants Amitriptyline
Opiates – Care with prescribing especially ↑ doses Not increase above equivalent 60 mg morphine per 24 hrs No short acting
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
Other Medications
• Iv palmidronate• Early CRPS
• Vit C• Steroids
Self Management Strategies
• Activities to help the patient plan and pace activities
• Sleep hygiene• Vocational support, eg for return to work
(where appropriate)• Self-management
Psychological interventionsAll pain conditions complex biopsychosocial
disorder
Pain Disuse/Emotional arousal
Several case reports / series reporting benefits
RCTs contain psychological therapy as part physical/medical therapy
• 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
Multidisciplinary Rehabilitation– Functional restoration via interdiciplinary approch
essential– Evidence small– Physical/OT improved pain and restored mobility Oerlemans
1999
• Physical therapy
– Rx pain / oedma– ROM– muscle strength– Improve limb function
Active motionStress loading
Posture changesDesensitisation
MassageTENS
Oedma – garments/gentle movements
OT early protective splints reduce pain oedma
Dynamic splints
Stress loading - level 3 evidence
A controlled pilot study of the utility of mirror visual feedback in the treatment of complex regional pain syndrome (type 1)
McCabe et al 2003
? CRPS consequence of disrupted cortical processing.? Congruent visual feedback restore
8 CRPS Pts
3 Pts < 8 weeks - Good improvement
2 Pts 5mts - 1 yr - 2/3 improved
3 Pts >1 year no response
Interventional therapies
• Stellate ganglion block• Lumbar sympathetic chain
• Intravenous Regional anaesthesia– Guanethidine– Bretyllium
Sympathetic Block
Stellate Ganglion Block
• Upper Limb Chronic Regional Pain Syndrome Type I (CRPS I)
• Sympathetic supply to the ipsilateral arm / hemi-face
Lumbar Sympathetic Block
• sympathetic chains–overlying anterior portion of vertebral bodies
• posterior to aorta/IVC• anteromedial to kidneys/ureter
LSB Needle Insertion
Dr Brooks www.paindocni.co.uk
Intravenous Regional Sympathetic Block
• Depletion of norepinephrine in sympathetic nerve terminals
• guanethidine• bretylium
• IVRA–Guanethidine – essentially little evidence efficacy
BUT ALL THE STUDIES– entry criteria / all included
Dr Brooks www.paindocni.co.uk
Sympathetic nerve blocks
• Very little evidence benefit or evidence to base judgement
• Still used routinely
• ? role
Titrate to responseAllow Physio therapy3 studies demonstrated improvements
Epidural Infusions
Epidural Infusions
Study No. Pts Infusion Results Complications
Cooper 89 14 Bupiv-opioid4 days
Improved pain/ROM 13/14
none
Konnig 95 29 Bupiv7 days
83% improved pain
Infection catheter site
Rauck 93 19 Clonidine3 days
Improved pain
InfectionsNauseaDizziness
Brachial Plexus Catheter
Several Case reports (level 4 evidence)
1-3 weeksAllow physiotherapy
Even less evidence
Spinal Cord StimulationMeta-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 efficacyUse if other Rx failed
NICE approved
Take Home Message
• Clinical Diagnosis• Uncertain cause• No specific treatment• Rehabilitation key treatment• Moderate/Severe CRPS needs
multidisciplinary team management!
The Four Pillars of Treatment in CRPS.
Goebel A Rheumatology 2011;rheumatology.ker202
NHS Website CRPS
