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8/7/2019 CRPS-A Most Challenging Pain Syndrome
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CRPSCRPS-- A Most ChallengingA Most Challenging
Pain SyndromePain Syndrome
Chhaya V VermaChhaya V VermaProfessorProfessor-- School of physiotherapySchool of physiotherapy
KEM Hospital & Seth G.S. MedicalKEM Hospital & Seth G.S. Medical
College, Parel, MumbaiCollege, Parel, Mumbai
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Reflex Sympathetic Dystrophy(RSD)Reflex Sympathetic Dystrophy(RSD)
Sudeck in 1900- as Syndrome of
osteoporosis of bones of hand & foot
following trauma
Is a generic term- describes post traumatic
pain accompanied by abnormal autonomic
activity and impaired extremity function
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IASP 1993 proposed term CRPS-
Complex Regional Pain Syndrome
Based on clinical features, location of pain
and type, location of injury without
implying mechanism, cause or abnormal
behaviour of sympathetic tone
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CRPS Type I (traditional RSD) without
identifiable PNI
CRPS Type II (Causalgia- Clinical RSD)
with peripheral nerve injury
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Physiology of CRPSPhysiology of CRPS
Normal responses to initial noxious insult
are prolonged abnormally
Persistence of responses in absence of
ongoing insult or impending cellular
damage
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Neuromuscular DisturbancesNeuromuscular Disturbances
Pain- out of proportion, constant,
aggravated by movement
Hyperaesthesia- tenderness, burning Swelling- initially soft, later brawny
Discoloration - initially angry red,
later pale- blue cyanotic Stiffness finger joints
Temperature- initially increased,
later decreased
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Dystrophic ChangesDystrophic Changes
Trophic changes of skin and subcutaneous
fascia
Osteoporosis of bones Palmar fascitis
Sudomotor changes
Pilomotor activity
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Lee LankfordsLee Lankfords
Classification of RSDClassification of RSD(In ascending order of severity) Minor Causalgia- following minor injuries to
sensory nerve in distal part of limb
Minor Traumatic Dystrophy- following minortrauma, other than nerve lesion
Shoulder-Hand Syndrome-following proximaltrauma to shoulder or neck, painful visceral lesion eg
Heart attack, stomach ulcer, hemiplegia, pulmonary
lesion, etc
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Classification of RSDClassification of RSD
Major Traumatic Dystrophy- most commoninvolving whole wrist of hand eg crush injury, colles
fracture, etc
Major Causalgia- following partial injury to mixedmajor nerve proximally
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RSDRSD-- IncidenceIncidence
Secondary to Trauma- 45-50%
due to # around wrist joint
Cardiac Conditions- 3%
Neurological- 20%
Age- mostly after 35-45 yrs
Sex- Female > Male
Personality- People with anxiety, emotionallysensitive, insecured, grumbling type,
Diasthesis very sensitive to cold, who sweat alot, have low pain threshold
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Abnormal Sympathetic ReflexAbnormal Sympathetic Reflex
Trauma
Normal response- sympatheticvasoconstriction to prevent bleeding
followed by Vasodilation to speed uphealing
Abnormal Response- initialvasoconstriction fails to shut down painfullocalised ischemia PAIN
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DrDrLorenteLorente DeNosDeNos
Theory ofTheory of internuncialinternuncial PainPain
Pain Impulses
Spinal Cord(post and lateral horn)
Increased sympathetic
Activity(tissue ischemia)
Constant pain
Syndrome of RSD
(pain, parasthesia, oedema, stiffness)
internuncial
neurons
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Vicious Cycle of RSDVicious Cycle of RSD
PAIN
hyperesthesia
IMMOBILIY(Reflex
splinting)
Circulatorystasis
EDEMA
Poornutrition
TISSUEREACTION
fibrosis
VASOSPASM(Abnormal
autonomic reflex)
tissue ischemia
Stiff NonFunctional
Dystrophic
Stiff NonFunctional
dystrophic
extremity
Traumaticpainful
lesion
DependentDiathesis
Patient gain
Emotional
Stress
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RSDRSD
3 stages
No specific demarcation of duration
Usually overlap each other
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Stage I (Acute)Stage I (Acute)
Stage of sudden abnormal release ofsympathetic tone
Starts immediately / within few weeks post
injury Lasts for 2-3 months
Constant pain, burning/ aching, increases onmovement, disproportionate to injury
Marked oedema, redness and warmth Dryness of skin
Increased nail and hair growth
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StageStage --II (Dystrophic)II (Dystrophic)
pevious stage of hyper vascularity
replaced
Sympathetic over activity
Marked vasoconstriction
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Stage II(dystrophic)Stage II(dystrophic)
Hard, brawny swelling
Restricted ROM
Cool, pale, cyanotic skin
Nails crack
Hair sparse and coarse
Increased stiffness leads to decreased ROM
Fibrous ankylosis of periarticular structures ofdigital joints of fingers
Spotty osteoporosis
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Stage III(Atrophic)Stage III(Atrophic)Stage of Residual dystrophic ChangesStage of Residual dystrophic Changes
Constant dull pain, spreads proximally
Irreversible tissue changes
Atrophied skin & fingertips
Fixed joint structures
X-rays- bony demineralisation
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Managemant of RSDManagemant of RSD
KEY- Early detection of Symptoms
- minimises distressing pain and further
complications
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Aims of TreatmentAims of Treatment
To prevent painful stimuli which would add to
existing pain
To treat existing Pain
To treat Hypersensitivity / Allodynia
To maintain maximum function of the hand
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Prevention of Painful StimuliPrevention of Painful Stimuli
Splinting at Rest
2 types of hand attitudes-
Wrist in Flexion
Wrist in Extension
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Aim- to maintain maximum functional positionof hand
Wrist 20 degrees Extension
MP 60-70 deg flexion
Thumb Opposition
IP jts Kept free for active mobilisation
To be worn at night & intermittently during day
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Active Mobilisation- within patients limits
Active Exercises
Decreases patients discomfort
Activation of large diameter afferent fibrestimulation& opioid stimulation
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Oedema ControlOedema Control
Elevation
Compression
Active Exercises
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Treatment of existing PainTreatment of existing Pain
Recognising Patients vasomotor state
Vasodilation Vasoconstriction
Cryotherapy(immersion Thermal agents-hot
In cold water) water bath, PWB,
fluidotherapy
TENS-brief intense type TENS- burst type(high intensity train
of pulses)
Vasoconstrictor effect Vasodilator effect
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Mechanism of action of TENSMechanism of action of TENS
Constant stimulation ofLarge Diameter
Myelinated Afferent nerve fibres
closes gate for
Small Non-Myelinated Slow conducting
C-fibres of pain
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TENSTENS--CRPSCRPS
Conventional Brief Intense Burst
Freq 50-100hz 100-250hz 70-100hz
Perception Parasthesia Tetanic/Non Rhythmic Strong rhythmicTingling contraction contraction
Effect Pain Vasoconstriction Vasodilation
modulation pain modulation pain modulation
Duration Continuous 10-15min/session 30-45min/session
until pain relief
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Sequential Electrode Placement(TENS)Sequential Electrode Placement(TENS)
Anatomical site
Proximal to Pain / Hyperaesthesia
Dermatomal Distribution
Peripheral/cutaneous nerve
Trigger point / acupuncture points
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Treatment of Hypersensitivity & AllodyniaTreatment of Hypersensitivity & Allodynia
Desensitization Programme- Barber et al 1984
Determine patients baseline hypersensitivity
Determine patients Tolerance for tactile
stimulation without exacerbation of pain(sensory
and pain threshold)
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Treatment of Hypersensitivity & AllodyniaTreatment of Hypersensitivity & Allodynia
Program includes use of Textures, Pressure,Percussion(tapping), Vibration, use of everydayobjects
Progress from area outside of hypersensitivity toarea of greatest sensitivity
Allow use of padded gloves, garments toprotect hypersensitive area from enviromentalstimuli
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Treatment of Hypersensitivity & AllodyniaTreatment of Hypersensitivity & Allodynia
Include Active ROM
Include functional activity programme wrt ADL
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Stress Loading ProgrammeStress Loading Programme
Watson & carlson 1987Watson & carlson 1987
3 Component Programme
Compressive loading of upper extremity(scrubbing with brush) 3 -10min 3 times a day
Distraction- carrying weight in hand whilestanding, walking
Use of other modalities
splinting
active mobilisation with functional activities
close kinetic chain exercises- form of stress
loading exercises
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Neural Tissue Mobilisation TechniquesNeural Tissue Mobilisation Techniques
Shaclok & Butler, 1991Shaclok & Butler, 1991
Dynamic mobilisation of hypomobile Brachial
Plexuseg. ULNTT 1 for Median Nerve
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Improvement of EnduranceImprovement of Endurance
Patients Sedentary Lifestyle
Deconditioning
Less Tolerance for ADL,occupational
& vocational activites
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Improvement of EnduranceImprovement of Endurance
Importance of 6 min walk test
Low impact aerobic activities(walking)
increases total body circulation & Cardiac output
increases circulation to affected extremity
may assist by providing stability to symp. tone
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Multidisciplinary ApproachMultidisciplinary Approach
Complex and devasting problem
Needs Team Approach
Medical intervention- medications, regional &local blocks, surgical techniques
Professional Psychologic Support
Physiotherapy
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Immediate Post Block AnesthesiaImmediate Post Block Anesthesia
During pain free state, gentle, passive mobility
exercise as long as symptoms are not
exacerbated
Followed by active exercise programme
Myofascial trigger points managed by
physiotherapy or medically-post injection,
stretching techniques are taught (MFR, US
therapy)
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CRPS is the most challenging painsyndrome. It is a dynamic problem with
multiple therapies of etiology andmaintenance.
Early recognition is the key in alleviatingmost CRPS problems
The exercise programme should beplanned according to individual patientssymptoms and evaluation
Successful exercise of CRPS is directlyrelated to active participation andmotivation of patient.
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A- rapid onset of pain
B- plateau on a high level B (6month- 2 years)
C- without exercise pain graduallyfades down
D- pain comes down at low level,persists for long duration
E- early treatment, if earlydetection, pain comes downearly
F- pain comes down but not muchif treatment is less effective orlate stage
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Assessment of Treatment outcomeAssessment of Treatment outcome
MeasuresMeasures
ROM-universal Goniometer
Pinch Strength- Pinch Gauge
Grip Strength- Grip Dynamometer
Pain- Mcgill pain questionaire scale
Sensory & Pain Threshold
Hand Functions- DASH score
Physical aerobic capacity- 6 MWT
QOL- SF 36
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THANK YOU