crps-a most challenging pain syndrome

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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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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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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crps-a most challenging pain syndrome

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