Download Whatever happened to RSD?

Whatever happened to RSD?
Andrew Muir
History
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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
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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
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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
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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
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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:
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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
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Acute ‘hot’, hypercirculation phase
Chronic ‘denervation supersensitivity’ phase with the
cold blue limb.
Pathophysiology:
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Most of the following have been demonstrated in
animal models of nerve damage.
Peripheral changes
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Expression of adrenoceptors on a subset of C-fibres,
OR
Noradrenaline mediated release of prostanoids
Central changes
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‘wind up’
Autonomic/somatic crosstalk & sprouting after nerve
injury.
Pathophysiology:
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Sympathetic nervous system elaboration
of noradrenalin can activate mast cells,
inviting a immuno-inflammatory aspect to
this.
Mao et al, Pain, 1995
Glu
Glu
Glu
SP
NMDA-R
AMPA-R
Mg++
mGluR
G
Na+
IP3
Ca++
PKC
activation
L-arg
Nos
NO
Ca++
Gene
expression
Practical Clinical Features:
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Pain
Allodynia
Temperature change
Colour change
Sweating
Dystrophy
Motor change
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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:
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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).
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Unrecognized local pathology(sprain, #, sepsis, cellulitis, allergy)
Vascular insufficiency (Raynaud’s disease, thromboangiitis
obliterans, thrombosis)
Practical Clinical Features:
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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
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Guideline published in 1998
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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)
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Response to Algorithm
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100 experienced pain specialists
Referral
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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%
73%
50%
39%
32%
10%
2%
Anticonvulsants
Antidepressants
Opioids
Non Steroidals
Topical agents
Corticosteroids
Bisphosphonates
Timing of treatment
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97% believed better outcome if referred
within 3 months of onset
Evidence based guidelines
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Don’t really exist
Cochrane data base of RCTs
Critical analysis of 22 RCTs
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Poor methodology
Only looking at one modality
Difficult to compare
Calcitonin deceases pain of CRPS
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Perez et al Journ of Pain and Sympt Mgt 21, No6, June 2001
What do we know?
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Oral corticosteroids are effective (2 papers, 1
RCT)
Bisphosphanates:
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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:
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DMSO cream
Epidural clonidine
Intravenous bretyllium, ketanserin
What do we know?
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IVRB
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guanethidine is ineffective,
bretyllium works (single trial)
Ketanserin effective
Ketorolac effective (1 paper)
A Reasonable Approach:
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Physiotherapy – (rest or mobilisation)
Adequate analgesia
Early pulse of corticosteroids
Early referral to Pain Clinic for:
Repeated temporary sympathectomies
Epidural clonidine
Bisphosphanates
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Long term management of chronic pain
Case study 1: History
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Mrs C
Italian woman 70 years old
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History: 3mths ago gardening
Stick pierced palm R hand
Hot, swollen, dry, painful
Treated antibiotics, sling
deteriorated
Case 1: History
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Referred to orthopaedic hand surgeon
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? Hysterical, ?CRPS type 1
unable to move arm, fingers
unable to hold knife and fork
unable to do washing, cooking
Case 1: History
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Investigations
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x-ray, bone scan, ultrasound
inflammatory markers
Referred to pain clinic
Case 1: Examination
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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
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Management: Initial
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TCA, oxycontin, physiotherapy
cease sling,
start hanging washing on clothes line
Series of 3 stellate ganglion blocks
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Good response for some days with lasting
improvement(SMP)
Combined with physiotherapy:
EMLA cream to palm, trigger point injections extensor
origin
Case 1: Management
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Outcome good.
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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
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Mr U
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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
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Pain increased
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burning, painful on light touch
extending up arm
No progress with hand therapy
Referred to pain clinic for SGBs
Case 2 : Examination
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Wearing glove
Holding arm up close to chest
difficulty swinging arm/initiating movement
decrease grip strength
Hand cold blue sweaty, swollen
Case 2 : Management
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Diagnosis of CRPS type 2
Trial of oral medications
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Trial of stellate ganglion blocks/ activation
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neuorpathic agents, SR opioids, TCAs
temporary improvement (SMP)
poor compliance
Multi-disciplinary pain assessment
Case 2 : Management
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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
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further interventional Mx by pain specialist
number 3
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guanethidine blocks
Spinal cord stimulation
Unsuccessful
Case 2 : Management
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Further deterioration
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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 2 : Management
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ASSESSED AS “NOT READY” for CBT
based Pain Management Program
Case 3 : History
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Mr M.R.
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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
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Referred by GP for pain management
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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
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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
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Presentation
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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
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No wasting in arm in general
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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
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Diagnosis?
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??????????Nerve injury
?????????CRPS
??Conversion disorder
Management
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Full assessment (multi-disc)
Counselling/ Reassurance
No medications, general gym program
Case 3 : Management
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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
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MRS B
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58 year old woman (Australian born)
Working as nurse in aged care
MCA 1997: injured shoulder and ankle(soft
tissue)
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Recovered, RTW
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Persistent swollen R leg
Intermittent shoulder stiffness
Case 4 : History
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1998 R leg gave way, fell
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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
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Pleasant co-operative woman
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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
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Management initial
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Oxycontin/ gabapentin: Good analgesia
No improvement in function/spasm
Lumbar sympathetic block
Excellent block with no change in symptoms
(SIP)
Case 4 : Management
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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
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12 months later
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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
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Cure focussed, not interested in CBT Program
Admitted for epidural
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Pt anxious that found walking difficult.
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Similar response to previous
Had persistent muscle cramp
Referral to IP rehab (Not accepted by TAC)
OP physio attempted: poor progress
Case 4 : Management
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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
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(1) DIAGNOSIS early
(2) Early Use of adequate analgesia to
promote normal activity/ posture
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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
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urgent, not to go on long waiting list
Be Aware
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Some pain specialists unimodal approach
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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
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Adequate education/ counselling
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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