whatever happened to rsd? andrew muir. history 1872 mitchell described a syndrome of causalgia:...
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History
1872 Mitchell described a syndrome of causalgia: Limbs of American Civil War soldiers who
sustained nerve injuries Burning pain, hyperaesthesia, trophic
changes with glossy skin The nomenclature relates to the Greek ‘kausis’
burning and ‘algos’ pain after a nerve injury 1901 Sudeck (bone changes after injury) 1940 Reflex Sympathetic Dystrophy (RSD)
CRPS: Nomenclature
The nomenclature of CRPS Types I, II was adopted after a Consensus Conference in 1993 Standardised terminology Avoid unsustainable pathophysiological implications Take up has been patchy but increasing: 11% of
articles between 1995 and 1999 used it but 3.5% 1995 & 27.5% in 1999
Type II refers to major nerve injury, Type I to the rest.
CRPS: Diagnostic Criteria
A. Presence of an initiating noxious event or cause of immobilisation.
B. Continuing pain, allodynia or hyperalgesia with which the pain is disproportionate to any inciting event.
C. Evidence at some time of oedema, changes in skin blood flow, or abnormal sudomotor activity in the region of pain.
D. This diagnosis is precluded by the existence of conditions that would otherwise account for the degree of pain or dysfunction.
CRPS: Diagnostic Criteria
One group found that the criteria did not discriminate between CRPS I and Diabetic Peripheral neuropathy and positive predictive value between 40 and 60%.
Criteria used in a check list can improve PPV to 0.91, sensitivity to 0.71 and specificity to 0.95
Baron suggests current presence of 3 symptoms and 2 signs.
Pathophysiology:
It can be shown that cooling the body with affected limb isothermic causes pain associated with sympathetic tone.
Controversial pharmacological challenge of Raja etc
Some studies have demonstrated an overall decrease in sympathetic nervous system activity explaining the Acute ‘hot’, hypercirculation phase Chronic ‘denervation supersensitivity’ phase with the cold
blue limb.
Pathophysiology:
Most of the following have been demonstrated in animal models of nerve damage.
Peripheral changes Expression of adrenoceptors on a subset of C-fibres,
OR Noradrenaline mediated release of prostanoids
Central changes ‘wind up’ Autonomic/somatic crosstalk & sprouting after nerve
injury.
Pathophysiology:
Sympathetic nervous system elaboration of noradrenalin can activate mast cells, inviting a immuno-inflammatory aspect to this.
Na+
Ca++
AMPA-R
PKCactivation
L-argNos
NO
Ca++
Geneexpression
Mg++
IP3
G
mGluRNMDA-R
Glu SPGluGlu
Mao et al, Pain, 1995
Practical Clinical Features:
Pain Allodynia Temperature change Colour change Sweating Dystrophy Motor change
Non dermatomal Should be marked Should be marked
Uncommon Non-specific
Practical Clinical Features:
A continuum from:Icy cold, immobile, dripping with sweat, profound allodynia
TO
Hey! The X-ray looks OK … so how come it still hurts?
Practical Clinical Features:
There exist a number of potential differential diagnoses, the most common and important one is DISUSE secondary to persistent pain, (where the clinical signs are likely to be less marked).
Unrecognized local pathology(sprain, #, sepsis, cellulitis, allergy) Vascular insufficiency (Raynaud’s disease, thromboangiitis
obliterans, thrombosis)
Practical Clinical Features:
In all cases, the aims of treatment must be considered through the same process as any other patient with chronic pain.
RESTORATION OF FUNCTION !
Treatment algorithms
Guideline published in 1998 Functional restoration Physical and psychological methods To move through to another modality if no
response in defined period Consensus report Complex Regional Pain
Syndrome: Guidelines for therapy Stanton Hicks et al Clin J of
Pain 14: 155-66 1998 (now more recent)
Response to Algorithm
100 experienced pain specialists Referral
32% orthopaedic specialist 12% neurologist, 12% GPs 9% self referred, 9% anaesthetist 8%neurosurgeon, 8%physiotherapist 6% lawyer/ case manager 4% podiatrist
Frequency of Treatments
85% Pharmacotherapy
67% Nerve Blocks
66% Physiotherapy
51% Psychological Tx
35% Invasive therapies
19% Sympathectomy
Pharmacotherapy
79% Anticonvulsants 73% Antidepressants 50% Opioids 39% Non Steroidals 32% Topical agents 10% Corticosteroids 2% Bisphosphonates
Evidence based guidelines
Don’t really exist Cochrane data base of RCTs Critical analysis of 22 RCTs
Poor methodology Only looking at one modality Difficult to compare Calcitonin deceases pain of CRPS
Perez et al Journ of Pain and Sympt Mgt 21, No6, June 2001
What do we know?
Oral corticosteroids are effective (2 papers, 1 RCT) Bisphosphanates:
Alendronate improved bone density with a trend to decrease in pain and swelling
Clodronate improved pain substantially Spinal cord stimulation – moderate improvement Some support for:
DMSO cream Epidural clonidine Intravenous bretyllium, ketanserin
What do we know?
IVRB guanethidine is ineffective, bretyllium works (single trial) Ketanserin effective Ketorolac effective (1 paper)
A Reasonable Approach:
Physiotherapy – (rest or mobilisation) Adequate analgesia Early pulse of corticosteroids Early referral to Pain Clinic for:
Repeated temporary sympathectomiesEpidural clonidineBisphosphanates
Long term management of chronic pain
Case study 1: History
Mrs C Italian woman 70 years old
History: 3mths ago gardening Stick pierced palm R hand Hot, swollen, dry, painful Treated antibiotics, sling deteriorated
Case 1: History
Referred to orthopaedic hand surgeon ? Hysterical, ?CRPS type 1 unable to move arm, fingers unable to hold knife and fork unable to do washing, cooking
Case 1: History
Investigations x-ray, bone scan, ultrasound inflammatory markers
Referred to pain clinic
Case 1: Examination
Pain on light touch, Increased reaction to pain in most of arm viz
palm, classic tender points Motor neglect. All upper limb movements impaired tissue swelling temperature cooler than other limb colour change
Case 1: Management
Management: Initial TCA, oxycontin, physiotherapy cease sling, start hanging washing on clothes line
Series of 3 stellate ganglion blocks Good response for some days with lasting
improvement(SMP) Combined with physiotherapy: EMLA cream to palm, trigger point injections extensor
origin
Case 1: Management
Outcome good. Swelling gone, Movements substantially improved Function: returned to most activities Residual thickening of palmar flexion tendon
middle finger Swelling substantially reduced Pain Medications ceased
Case 2: History
Mr U Turkish man aged 48 Injured at work end 1999 conveyor belt fault results in open injury to R
hand laceration palmar branch of digital nerve repair of digital nerve
Case 2: History
Pain increased burning, painful on light touch extending up arm
No progress with hand therapy Referred to pain clinic for SGBs
Case 2 : Examination
Wearing glove Holding arm up close to chest
difficulty swinging arm/initiating movement decrease grip strength Hand cold blue sweaty, swollen
Case 2 : Management
Diagnosis of CRPS type 2 Trial of oral medications
neuorpathic agents, SR opioids, TCAs Trial of stellate ganglion blocks/ activation
temporary improvement (SMP) poor compliance
Multi-disciplinary pain assessment
Case 2 : Management
Not suitable for pain management seeking cure unresolved anger/ litigation Referred for in-patient rehabilitation
program (Plan: Cx epidural/ phys ther) Unsuccessful
Case 2 : Management
further interventional Mx by pain specialist number 3 guanethidine blocks Spinal cord stimulation
Unsuccessful
Case 2 : Management
Further deterioration now back and leg pain, using stick not working/ low function at home depressed arm wasted, sweaty hand, no movement heavily involved with litigation, still focussed on cure and blame seeking multiple medical opinions
Case 3 : History
Mr M.R. Aged 24, Australian born Had a venipuncture from R cubital fossa
(lateral aspect) November 2000 Felt pain shoot up to shoulder/ felt faint 36hrs later woke up with clawed R hand Has not been able to open hand since Has not worked since
Case 3 : History
Referred by GP for pain management 2 overdoses Had been working at previous job for 3 days
prior to Venipunture No real indication for VP did not attend a doctor prior to VP Litigation in progress against pathology firm
Case 3 : History
Now living with grandparents who are “looking after him”
Has initiated referral to multiple specialists No reports available Difficulty contacting referring GP Using self prescribed splints at night
Case 3 : Examination
Presentation agitated conflicting history with Mother Pain not a major complaint Both hands cool sweaty Holding R hand in tight claw Resistance to opening
Case 3 : Management
No wasting in arm in general Increased forearm muscle bulk Possibly some wasting dorsum of hand
No difference in temperature, swelling, sweating No allodynia No motor akinesia of arm in general Normal movements of shoulder and upper arm.
Cannot move fingers
Case 3 : Management
Diagnosis? ??????????Nerve injury ?????????CRPS ??Conversion disorder
Management Full assessment (multi-disc) Counselling/ Reassurance No medications, general gym program
Case 3 : Management
Participating in competitive manner in Gym program
Enjoys being videoed Has taken up a correspondence course
(sports psychology) Will have an EUA Unable to get any reports
Case 4 : History
MRS B 58 year old woman (Australian born) Working as nurse in aged care
MCA 1997: injured shoulder and ankle(soft tissue)
Recovered, RTW Persistent swollen R leg Intermittent shoulder stiffness
Case 4 : History
1998 R leg gave way, fell fractured ankle POP/ int fixn pain and spasm swelling persistent problem
when in POP prolonged rehabilitation 2X 3 mths IP persisting pain, swelling, spasm 2 further operations No progress, Referred to pain clinic
Case 4 : Examination
Pleasant co-operative woman Wearing rigid ankle brace/ using wheelchair leg swollen, cool compared to L side intense allodynia, skin dry, discoloured multiple tender points over entire leg, back
shoulder out of brace grossly abnormal gait and devel
of spasm on light touch/ movet
Case 4 : Management
Management initial Oxycontin/ gabapentin: Good analgesia No improvement in function/spasm Lumbar sympathetic block Excellent block with no change in symptoms
(SIP)
Case 4 : Management
Case conference Rehab/ Physio in-patient admission: epidural opiate/ clonidine/ Local
Anaesthetic Allodynia/ spasm disappeared gait re-training, gym program ceased all analgesics returned to normal activities no splint/ no wheelchair skin/ temp/ swelling abated
Case 4 : Management
12 months later noted recurrence of spasm and pain skin changes/ allodynia trial hydrotherapy/ gym finding this difficult, further deterioration requested epidural treatment underwent multi-disc assessment
Case 4 : Management
Cure focussed, not interested in CBT Program Admitted for epidural
Similar response to previous Pt anxious that found walking difficult.
Had persistent muscle cramp Referral to IP rehab (Not accepted by TAC) OP physio attempted: poor progress
Case 4 : Management
became increasingly frustrated by TAC Frustrated that not cured Told that time to accept as chronic
problem Reacted to this Now overall improvement, walking/
holidaying in USA
Role of Primary Care Physician
(1) DIAGNOSIS early (2) Early Use of adequate analgesia to
promote normal activity/ posture active physio/ not passive/ gentle reactivation. if physio cannot progress 1st step is increase
in time based analgesia (3) Early referral to Multi disciplin PU
urgent, not to go on long waiting list
Be Aware
Some pain specialists unimodal approach diagnostician eg phentolamine infusion/
guanethidine block/ no response/ discharge interventionist: blocks/ more blocks/ spinal
cord stimulation/ no rehab/ psych rehab/ no intervention/ pain relief psych/ no intervention/ rehab
Be Aware
Adequate education/ counselling patients ill informed/ self help groups/
Internet: progressive disease explanation of the importance of return to
normal function avoid surgery if possible/ only if appropriate
and covered by analgesia Role of cognitions/ depression/ litigation as
mediating factors
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