CRPS Flashcards
CRPS - Definition
presence of regional pain combined with autonomic dysfunction, atrophy and functional impairment affecting muskuloskeletal, neural and vascular structures
Type 1: not associated with a real nerve injury
Type 2: associated with a real nerve injury
Type 3: nontraumatic causes producing extremity pain such as myofascial syndrome (controversial discussion about!!!)
Neuropathic pain:
pain initiated or caused by a primary lesion or lesions or dysfunction of the peripheral nervous system or central nervous system (allodynia, hyperalgesia, hyperesthesia, sympathetic pain, hypoesthesia, hyperpathia, dysesthesia, paresthesia)
Diagnosis is based on the patient’s history and physical examinations, CRPS maybe include SMP (sympathetically maintained pain) or SIP (sympathetically independent pain) - can be tested with sympatholytic medications or sympathetic blocks - SMP can change to a SIP
physiology of pain
pain is only present if there is a damage of cellular tissue damage, leads to secondary inflammation with activating and sensitizing polymodal low-threshold mechanoreceptors und nociceptor afferent neurons
transduction over small myelinated (Alpha-Gamma), large myelinated (Alphpa-beta) and small unmyelinated C afferent fibers to the dorsal horn of the spinal cord
Transmitters include N-glutamate, aspartate, alpha-amino-3-hydroxy-5-methyl-4-isoxazoproprionic ace (AMPA), N-methyl-d-aspartate (NMDA) and Substance P are the principal neurotramsmitters
NMDA the most important with long-lasting potentials and refractory to stimulation to develop an CRPS Type 1 and Type 2
Nociception is modulated by via descending pathways - peripheral and central factors are required for the perception of pain
Pain intensity is determined by the magnitude and extent of the initiating or ongoing event, afferent input, efferent modulation and CNS interpretation
Concious appreciation of nociceptive experiences is dependent on a complex interplay of afferent and efferent infromation
Vasomotor disturbance may result from variety of mechanism, including antidromic vasodilation, vasoparalytic dilatation, normal somatosensory reflexes and denervation supersensitivity. Presence of nociceptive-induced inappropiate transmitter-receptor activity can affect peripheral microcirculation - leads to impaired nutritive blood flow and may sensitize CNS pathways.
gate theory of pain
finite amount of information can be received at the spinal cord or cortical level - this “gate” is the dorsal horn.
Thus painful information displaced or modified by less noxious input cannot be processed through the gate.
acute versus chronic pain
acute:
warning from direct trauma or damage with physiologic reaction, which protect the host
chronic pain that occurs in absence of ongoing tissue destruction or that provides an inappropiate reflection of the intensity, magnitude or duration of the tissue damage/compromise is PATHOLOGIC!!!!
CRPS may be considered an abnormally severe or prolonged manifestation of a normal postinjury response
damage or compromise the arteriovenous shuntmechanism, produce arthrofibrosis, cause excessive osteopenia, alter neuroceptor function or result in central pain imprinting or any combination of these sequelae.
demographics of CRPS
incidence USA Minnesota 5,46 per 100.000 person/years, four times more than male, dutch study 26,2 per 100.000 person/years with femal effected three times more often
mean age at onset USA 46 - Dutch study 53
upper extremity more involved than the lower extremity - fracture the most precipitating event
incidence of cigarette smoking is higher in RSD, statistically linked to RSD
genetic or familial predisposition to RSD have been presented
predisposition for CRPS type 1 has been suggested with hemiplegic patients on the involved side
80% with RSD in the first year will improve significantly - 50% of patients with untreated symptoms lasting longer than 1 year will have profound residual impairment
distal radius and ulnar fracture - associated with CRPS - complicates postinjury in 28% of patients - finger stiffness or poor functions
CRPS more likely occur with patient of distal radius fracture with:
tight cast, compression of the median nerve, overdistraction, instability of DRUG or with ulnar fracture
common nerve injuries occuring during operative procedures that may precipitate CRPS include:
- injury to the palmar cutaneous branch of the median nerve
- damage of the superficial branch of the radial nerve
- trauma to the dorsal branch to the ulnar nerve
- devastating consequences of Dupuytren-Surgery with decompression of the median nerve at the wrist
psychological effects
CRPS is not psychogenic condition,
58% of 283 consecutive patients to pain center fulfilling the criteria for personality disorders
dependent, passive-aggressive and histrionic personalities are most common
DD
conversion disorders
clenched fist syndromes
SHAFT (sad, hostile, anxious, frustrated, tenacious) difficult to discern (multiple operations, absence of consistent clinical findings, multiple treating physicians, myriad of medications, psychiatric treatment, absence from work, disproportionate self-characterization and verbalization of symptoms, crying from pain, family history of disability)
CRPS: MCP and PIP are extended, moderate swelling
(flexion is uncommon for CRPS, lack of objective findings - trophic changes, edema, osteopenia, radiographic or fixed contractures suggest another disease, massive swelling not typical for CRPS)
Symptoms and signs
pain:
burning, throbbing, cutting, searing, shooting, aching
localization of the nociceptive focus
Allodynia: typical for sympathetically maintained CRPS
Hyperpathia - pain produced by painful stimuli that appears with delay
difficulties to sleep because of burning pain is common and may be an early portent of progressive symptoms and signs
Instruments:
VAS - visual analog scala
SF-36 - 36-item health status questionnaire
McGill Short Form Pain questionnaire
self-administered questionnaires used for carpal tunnel syndrome
DASH
McCabe Cold Sensitivity Severity Scale
Trophic changes:
stiffness, edema, osteopenia, atrophy of the hair, nails, skin, hypertrophy of the skin or hyperkeratosis
changes in skin, hair, nails are seen 10 days after onset, later bone demineralization (dual-photon absorptiometry or quantative scintigraphy
later stiffness, atrophy of muscles and tendons, movement disorders and dystonic posturing
testing autonomic function
98% of patients during the painful stages of CRPS
digital perfusion:
digital temperatures measurements
laser Doppler fluxmetry
plethysmography
vital capillaroscopy
stage 1 only increased blood flow and unchanged vasoconstriction
stage 2 decreased bloodflow and stronger vasoconstriction
sweating:
sudomotor axon reflex test (QSART)
galvanic skin response
asymmetry of somatosensory evoked potentials in the affected and contralateral extremity
Handfunction:
Moberg pickup test
stages:
acute - less than 3 month
dystrophic: 3 - 6 month
chronic: more than 6 month
Pain threshold evaluation
specific standardized evaluations and tests
rubber-tipped algometers
dolorimetry
monofilaments (best way to assess and monitoring treatment for allodynia and hyperesthesia)
computer-controlled stimuli
Radiography
osteopenia in 80% of cases extremities affected with CRPS
5 radiograph patterns:
- irregular resorption of trabecular bone in the metaphysis
- subperiosteal bone resorption
- intracortical bone resorption
- endosteal bone resorption
- surface erosions
MRI
functional magnetic resonance imaging may be valuable in evaluating the pathophysiology associated with CRPS and in monitoring patients response to interventions
abnormalities in the size of the cortical representations of the affected hand on the primary and secondary somatosensory cortices have been reported
Bone Scan (Scintigraphy)
3-phase technetium 99m bone scanning is performed commonly
- phase: 2 to 3 minutes - assessment of digital perfusion
- phase: 3-to 5 minutes - blood pool image or tissue phase assessment of total perfusion
- phase: standard bone scan evaluates the uptake of the tracer in bony structures
Mackinnon and Holder strictly interpreted Phase III with diffuse increased uptake in the delayed image is diagnostic for RSD
high specifity but poor sensitivity, adds useful diagnostic information
cave: positive phase III bone scan is not a prerequisite for the diagnosis of CRPS or SMP
bone scan
…do not correlate with traditional staging criteria for RSD
…not part of the diagnosis of SMP or CRPS
…do not predict recovery
…will not predict the potential for response to treatment
…BUT …positive phase III scan can provide objective support for the clinical diagnosis of CRPS
Evaluation of autonomic control
sweating and microvascular perfusion
evaluate the sympathetic dysfunction associated with characteristic pain from CRPS in a clinical suspicion of CRPS
evaluation of:
- regulation of the microvascular flow (inappropriate AV-shunting)
- sudomotor function
microvascular flow
others
diagnostical regional and sympathtic blockade
thermography
treatment
multimodal aspect in special units
pharmacologic:
antidepressants (tryclic or tetracyclic (Ludiomil), Trazadone (Desytel), selective serotonin reuptake inhibitors
anticonvulsants
membrane-stabilizing agents (Mexitil and Tonocard)
Adrenergic compounds (phentolamine, Phenoxybenzamine, prazosin, terazosin, clonidin)
calcum channel blockers
others:
corticosteroids, neuromuscular blocking agents, bisphosphonates, calcitonin, ketamine, free radical scavengers
percutaneous neural or ganglioncic blockade
outcome:
less pain, decreased swelling, diminished hypersensitivity to touch
