Complex Regional Pain Syndrome Power Point

COMPLEX REGIONAL PAIN SYNDROME

(the civil war disease)

By Gursangeet kaur

History“ long after the trace of wound has

gone….neuralgic symptoms are apt to linger, and too many carry with them throughout long years this final reminder of battle field..”

Silas Wier Mitchell

In 1867 SW Mitchell coined the term causalgia to describe pain syndrome affecting soldiers who had attained nerve injuries during American civil war.

(father of modern neurology)

In 1901,Sudeck described it as a syndrome characterized by bone changes after injury and named it as sudeck’s osteodystrophy

In 1946,Evans applied a generic term reflex sympathetic dystrophy (RSD)in describing a group of patients with chronic pain associated with skin changes

International association for study of pain(IASP)

• In 1993, a special consensus workshop held in Orlando, Florida, provided the umbrella term "complex regional pain syndrome," with causalgia and RSD as subtypes.

• Stanton-Hicks M, Janig W, Hassenbusch S, Haddox JD, Boas R, Wilson P (1995). "Reflex sympathetic dystrophy: changing concepts and taxonomy". Pain 63 (1): 127–33

CRPS I • Without nerve injury• RSD

CRPSII • causalgia• Nerve inury

IASP DEFINITION OF CRPS

Condition initiated by an injuryNot limited to distribution of single

peripheral nervePain disproportionate to inciting

event

Associated at some point with edema changes in skin,blood flow abnormal sweating allodynia hyperalgesiaSite usually distal extremity with distal to

proximal gradient

SYNONYMS FOR CRPS

• TYPE 1 TYPE IIRSD SUDECK’S ATROPHYALGODYSTROHYSHOULDER HAND SYNDROMEPOST TRAUMATIC PAIN SYNDROMEMINOR CAUSALGIA

CAUSALGIA MAJOR CAUSALGIAMITCHELL’S CAUSALGIA

CRPS

DemographyMean age of onset is 40 yearsMore female predominance (5:1)H/O any nociceptive injuryFracturesTraumatic and iatrogenic injuries of• median nerve• ulnar nerve• superficial radial nerveMedian nerve decompressionPalmar fasciectomy

Nociceptive injury

50%

Post fracture 20-40%

CVA 12-21%

Peripheral nerve injury 1-5%

Traumatic/iatrogenic injury

1-3%

Myocardial infarction 2-5%

Precipitating factors

• Physical stress • Emotional stress• Cold weather • Moving of affected limb• Cigarette smoking

Pathophysiology of CRPS

• Pathophysiology of CRPS is not fully understood• Despite of lack of knowledge of

CRPS,a number of hypothesis have been offered.

Classical view

• Hyperactivity of SNS.• Sympathetically mediated pain• Discredited in the past decade as SMP or

SNS abnormality does not provide an explanatory mechanism for certain aspects of individual presentations.

• (1990s ;cf.the authorative views of Bonica(1990) & Galer et al,2001)

LATER

• In 1993,Veldman et al focussed on an exaggerated regional inflammatory response.

• In 1996;Bennet & Robers; Coderre,katz & Melzack set in motion neuroplastic changes resulting in development of unusual symptoms.

Presently

“physiological wind-up” & CNS sensitization” are the key neurological processes that appear to be involved in induction and maintenance of CRPS.• Evidences that N-methyl-D-aspartate

(NMDA) receptor has significant involvement in CNS sensitization process.

• It is also hypothesized that elevated CNS glutamate levels promote “physiological wind-up” and CNS sensitization.

• (Correll GE, Maleki J, Gracely EJ, Muir JJ, Harbut RE (2004). "Subanesthetic ketamine infusion therapy: analysis of a novel therapeutic approach to complex regional pain syndrome". Pain Med 5 (3): 263–75.)

Clinical presentation of CRPS 1

autonomic

sensory

psychological

motor

inflammatory

pain

Sensory changes in CRPS

• Allodynia• Hyperalgesia• Allodynia• Hyperpathia• (Delayed pain response spreading beyond

normal dermatomal borders.)

Autonomic signs in CRPS

•Edema

•Colour change

•Temperature change(warmer orcooler)

•Sweating ↑ or ↓

Motor changes

• Weakness• tremors• Dystonia• myoclonus• Contractures• Decreased ROM

Trophic changes

• Altered nail growth

• Altered hair growth

• Skin changes

Psychological changes

• Depression• Anger • Fear• Anxiety• Suffering• Failure to cope

IASP diagnostic criteria• The presence of an initiating noxious

event/immobilization with (CRPS 1)or without nerve injury(CRPS II)

• PAIN + allodynia or hyperalgesia that is disproportionate in severity to any inciting event

• Evidence at some point in time of edema, changes in skin blood flow, temperature (abnormal pseudomotor activity in region of pain),trophic changes.

• Exclusion of conditions that would otherwise account for degree of pain and dysfunction

• diagnosis of exclusion:-• Vascular: DVT, vascular insufficiency• Inflammatory: cellulitis,trauma• Neuropathies: diabetic,entrapment• Erythromelalgia• Tumours

• Bruehl et al Pain,1999;81:147-154

Other diagnostic studies

• Thermometry/thermography• Bone X-ray• 3 phase bone scan• Sweat test• Response to sympathetic blockade

Clinical course of CRPS 1(RSD)

• Pain expands along the limb or migrates in other parts in almost 70% of the cases• Pain becomes bilateral in almost 50%

of the cases.

RSD/SHOULDER HAND SYNDROME

• Defined by Bonica;a disturbing and disabling secondary

complication following hemiplegia.ocurrs most commonly b/w 1st & 3rd

months following onset of stroke.if untreated can lead to permanent &

irreversible fixed deformity of hand & fingers which precludes functional use in future.

Acute stage

• Duration- 3months from the onset of symptoms• Hands swollen• Oedema • over dorsum of hand including MCP jt., • fingers & hand.• soft and puffy• ends just proximal to wrist joint• Loss of ROM

• Skin• loss of skin creases particularly over • knuckles,proximal and distal IP jt.• colour changes to pink or iliac hue.• warm and moist• Nails• undergo changes• appears whiter than those of other hand• Tendons of hand are no longer visible

Sub acute or dystrophic stage

• Swelling spreads more• Skin – cold,hydrotic,with or without cyanosis.• More intense pain• More marked oedema• Nails become cracked,brittle,grooved & spotty• Muscle atrophy remarkably seen.• Bones demineralisation increased• Increase in joint stiffness leading to more

marked decrease in ROM.

Chronic or atrophic stage

• Irreversible changes in skin and bones• Pain involves the entire skin• Marked muscle atrophy.• Severly limited range of motion• Flexor tendon contracture• Limb displaced from its normal position

and marked bone softening seen.

Treatment guidelines

Pain management

rehabilitation

Psychological treatment

Pharmacological treatment

• Anti inflammatory drugs(in acute cases)• COX inhibitors• piroxicam• Anti depressants- imipramine,doxepin• Anti convulsants-phenytoin,carbamazepine• Pain relief(chronic cases)• lidocaine• tocainide• Biphosphonates- calcitonin• Ca channel blokers-clonidine,reserpine

Invasive treatment

Sympathectomy• Spinal cord stimulation• Regional sympathetic nerve block• Ganglion block• Tender point injection

Blocks

• Intravenous regional sympathetic blocks• introduced in 1908 by Bier• Local anesthetic sympathetic blockade• done by placing a needle tip to the proximity

of sympathetic structures -Stellate ganglion -Lumbar sympathetic chain

nerve block Spinal cord stimulation

Rehabilitation

Early phase

Adequate analgesiaEncouragementEducation about disease process

Mid phaseIncreasing flexibilityStretchingStrengtheningPostural correctionOdema control

Later phaseNormalization of useAssessment of ergonomics & postureModifications at home&work