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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