Transcript Acute Pain: An Introduction

When is it Reasonable to
Speak about CRPS?
Rasha S. Jabri , MD
Dubai Anesthesia March 2012
Tawam Hospital-JHMI
Al Ain Abu Dhabi, UAE
History
• American Civil War: GSW near neves
• 1864 : term “causalgia” long years final
reminder of the battle-field
• Dr. Sudeck: trivial injuries result in
osteoporotic changes near the site of injury
(Sudeck’s atrophy)
History
• Rene Leriche : sympathetic nervous system
as a mediating factor in the condition
• “Reflex sympathetic dystrophy” (RSD)
• Since the early descriptions of this painful
condition many names have been applied to
the syndrome
Terms for CRPS
•
•
•
•
•
•
•
•
•
•Algodystrophy
•Algoneurodystrophy
•Causalgia
•Post-traumatic pain syndrome
•Post-traumatic dystrophy
•Post-traumatic osteoporosis
•Reflex sympathetic dystrophy
•Shoulder-hand syndrome
•Sudeck’s atrophy
Classification
• 1986 (IASP) formal description and
classification of RSD but NO clear
diagnostic criteria, NO specific underlying
mechanisms.
• Many neuropathic pain conditions were
included in the diagnosis of RSD,
specifically those resistant to traditional
treatments
Classification
• 1994 IASP new taxonomy of complex
regional pain syndrome (CRPS), which
would more accurately describe RSD and
causalgia.
• New diagnostic criteria for CRPS which
focused on clinical diagnosis from patient
history, symptom description, physical
signs and pain.
Classification
• CRPS : inciting events:
– type I =RSD, follows a soft tissue injury
– CRPS II= (causalgia) follows a well-defined
nerve injury
CPRS
• syndrome including,
– complexity of the varied presentations
– regionally, symptoms, which are typically nondermatomal
– pain, usually out of proportion to the inciting
trauma
– syndrome, denoting the constellation of signs
and symptoms
• varied contribution of the sympathetic
nervous system
Epidemiology
• Overall incidence of CRPS to be 26.2 per
100,000 person
• CRPS I to be 5.46 per 100,000 person years
at risk and a prevalence of 20.57 per
100,000.
• The incidence of CRPS II has been
reported at 0.82 per 100,000 person years at
risk and prevalence of 4.2 per 100,000
person years.
Risk Factors
•
•
•
•
•
•
Extremities trauma/MVA↑
Surgeries/Orthopedic↑( Knee, Ankle, CTS)
Stroke, or unknown cause very rare
Most cases between 50 and 70 years of age
CRPS female predominance: 2.0-3.5:1.13
Mainly Caucasian
Pathophysiology
• Theories peripheral mechanisms as well as
central mechanisms for CRPS.
• In CRPS II biochemical, morphological
(structural) and physiological changes of the
injured and adjacent intact primary afferent
neurons may occur
CPRS II
• The loss of DRG cells degeneration of
the centrally projecting afferent axons and
to denervation of dorsal horn neurons
• Secondary changes in the central
representations  changes in central
representations (in the spinal cord, brain
stem, thalamus and forebrain)
CPRS I
• CRPS I central representations of the
sensory, autonomic, and somatomotor
systems account for the clinical presentation
in CRPS
• CRPS, particularly type I, is a systemic
disease of neuronal systems:
somatosensory, sympathetic, somatomotor,
and peripheral (vascular, inflammatory)
systems
Pathophysiology
• Marked increase in alpha 1 adrenoreceptors
which appears in the injured extremity: skin
muscle and nerve tissue
• Augment depolarization in nerve and
muscle tissue resulting in an amplification
effect of any stimuli
• Increase in pain w increase in either
endogenous or exogenous catecholamines.
Tissue damage initiates a number of alterations of the
peripheral and the central pain pathways
Dahl, J. B. et al. Br Med Bull 2004
71:13-27; doi:10.1093/bmb/ldh030
.
Bruehl S. An Update on the Pathophysiology of CRPS
Anesthesiology .September 2010;113(3):713-725
Bruehl S. An Update on the Pathophysiology
of CRPS Anesthesiology .September
2010;113(3):713-725
Speculative Model
of Interacting
Pathophysiologic
Mechanisms in
CRPS
Clinical Stages
• Classically: three distinct sequential
progressive stages
• Disputes the traditional staging of CRPS
• Subtypes/subgroups exist in CRPS
Clinical Stages (Bonica)
I warm acute CRPS pain, sensory abnormalities,
hyperalgesia, allodynia, vasomotor dysfunction,
edema and sudomotor disturbance.
II (dystrophic stage) 3 to 6 mons more pain/sensory
dysfunction and vasomotor dysfunction, with
significant motor/trophic changes.
III (atrophic stage) cold extremity with decreased
pain/sensory disturbance, continued vasomotor
disturbance, increased motor/trophic changes.
General definition
• An array of painful conditions regional pain
disproportionate in time or degree to the
usual course of any known dz
• Regional: not in a specific nerve territory or
dermatome usually has a distal
predominance of abnormal sensory, motor,
sudomotor, vasomotor, and/or trophic
findings.
IASP CRPS subgroups NOT
Sequential stages
(1) Relatively limited syndrome with vasomotor
signs predominating
(2) Relatively limited syndrome with neuropathic
pain/sensory abnormalities predominating
(3) Florid CRPS syndrome similar to ‘‘classic RSD’’
descriptions
Pattern and Spread
32. IE, et al. Signs and
symptoms of reflex
sympathetic dystrophy:
prospective study of 829
patients. Lancet
1993;342:1012-1016.
Veldman PH.Signs and symptoms of RSD: prospective study of 829 patients.
Lancet 1993;342:1012-1016.
Clinical Features
• CPRS is a painful and debilitating disorder
primarily affecting one or more extremities.
key features
• Spontaneous pain, allodynia, hyperalgesia,
edema, temperature change, abnormal
vasomotor and sudomotor activity, trophic
changes, and motor dysfunction
IASP
Diagnostic criteria to establish the diagnosis
of CRPS (type I):
(3) Edema, changes in skin
(1) initiating noxious event
blood flow, or abnormal
or immobilization
sudomotor activity
(2) continuing pain,
• (4) the exclusion other
allodynia, or hyperalgesia
medical conditions
with pain disproportionate
CPRS II IASP
(1) continuing pain, allodynia, or
hyperalgesia after an nerve injury
(2) Edema, changes in skin blood flow,
or abnormal sudomotor activity
• (3) the exclusion other medical
conditions
Sudomotor Changes & Edema
Trophic Changes
Trophic Changes
Conclusions and Clinical
Implications
• IASP standardized, common methodology
for making DX of CRPS or not
• Treatment for two distinct conditions
• CRPS and non-CRPS neuropathic
pain groups
IASP_
• Controversy about the value of consensus-based
dx criteria
• Absence of evidence-based information
• Necessity of validating in light of systematic
validation research
Harden RN. Proposed new diagnostic criteria for CRPS. Pain Med.
May-Jun2007;8(4):326-331
CRPS DX ?????
• “looser” vs “tighter” criteria?!!
• Validity dx of the criteria ?
• Sensitivity vs Specificity?
Harden RN. Proposed new diagnostic criteria for CRPS. Pain Med.
May-Jun2007;8(4):326-331
IASP/CRPS dx Criteria
Adequately Sensitive
(rarely miss a case of actual CRPS)
Problems of overdiagnosis due to
Poor Specificity
Harden RN. CRPS : Are the IASP diagnostic criteria valid and sufficiently
comprehensive? Pain 1999;83:211–9
Harden RN. Proposed new diagnostic criteria for CRPS. Pain Med. MayJun2007;8(4):326-331
Objective
signs on PE
Subjective
symptom
• The modified criteria requires the
presence of both for CRPS diagnosis
Clinical Diagnostic
Criteria by the Budapest group
• 2/4 sign categories and ¾ symptom
categories for diagnosis
• Sensitivity of 0.85
• Specificity of 0.69
• Clinical vs research purposes2/4+4/4
more sensitivity and specificity around 80,
90%
Diagnostic Examination
• No single objective test for diagnosis
• Diagnostic tests may assist in determining
the likelihood of the syndrome
Diagnostic Examination
• Sympathetic Blockade
– sympathetically maintained pain or sympathetic
independent pain
• Skin Temperature Measurement
– Infrared thermography
– Difference of more than 2.2°C has a sensitivity
of 76% and a specificity of 93% for diagnosis
of CRPS
Quantitative Autonomic Function
Testing
– The quantitative sudomotor axon reflex test
(QSART)
– difference in sweat production between an
affected extremity and an unaffected extremity
– QSART test may help predict response to
sympathetic block
– Research needs to be conducted to further
assess the utility of the test
Vasomotor Testing
– Acute CRPS increase in vascular flow to the
affected extremity secondary to neurogenic
inflammation
– Decrease in sympathetic activity at the
extremity
– Measured by doppler flowmetry
– Additional studies to assess the utility in the
diagnosis of CRPS
Trophic Change Measurement
• Chronic CRPS present with changes in skin,
nails or bone
• Evaluation of trophic changes to the bone
by triple-phase bone scintigraphy has been
used to substantiate the diagnosis of CRPS,
although distinguishing between CRPS and
acute trauma may difficult
Therapy
Pharmacological Therapy
– Antidepressants (tricyclic & dual inhibitors) are
effective agents for treating a variety of
neuropathic pain condition
– SSRI + DPNP, PHN? CRPS
• Anticonvulsants (Antiepileptics)
– The gabapentinoid group of drugs, gabapentin
(GBP) and pregabalin (PGB), are the most
commonly used antiepileptics drugs (AEDs) for
CRPS
• Opioids
– There are no long-term studies
– Considered in CRPS if pain limits the patient’s
participation in physical restorative therapies
– Fent Patch VAS↓, fx (Agarwal, Pain Med 2007)
• Calcium Regulating Medications
(Bisphosphonates)
• Effective agents for the treatment of CRPS
– Mechanism of action is unknown
– (alendronate, pamidronate, clodronate)
– May inhibit bone resorption and their
effectiveness have been confirmed in
randomized controlled studies
– Manicourt (Arthritis Rheum 2004)
• Calcitonin
– Thyroid gland, inhibit osteoclastic bone
resorption
– Gobelet ( Pain 1992)
– Intranasal calcitonin in 63 pts with CRPS in a
double-blind randomized study
– Significant reduction in pain at rest and with
motion and increased mobility
– Meta-analysis_Perez concluded that calcitonin
could provide effective pain relief in CRPS
patients (J Pain Symptom Manage 2001)
Free Radical Scavenger
• Dimethylsulfoxide (DSMO)
• N-acetylcysteine (NAC)
• Effective in treating CRPS
• Perez (Pain 2003)
Interventional Procedures
• Sympathetic Nerve Blockade
– Diagnosis and treatment for CRPS
• Epidural Infusion
– local anesthetic and opioid
– fluoroscopic guidance catheter tip on the
affected side at the appropriate spinal segmental
level
– Tunneled 5 days to 12 wks physiotherapy
Neuromodulation
• Only one in five CRPS patients is capable
of returning to a normal level of functioning
• Spinal cord stimulation (SCS) is an
intervention modality that may be used in
patients with refractory pain
• Symptoms of CRPS have been ranked the
second most frequent indicator for SCS
therapy in the USA after post-laminectomy
pain syndrome
SCS
•
•
•
•
•
Pain relief as high as 70%
when conservative therapies fail
Kemler (J Neurosurg 2008)
-------------------long term effect
Harke (Eur J Pain 2005)
Intrathecal Drug Delivery
• Data citing the benefits is limited
• Case reports/series
• Viable consideration for patients that do not
respond to SCS or w multiple sites of pain
• Alternatively ziconitide a nonopioid
analgesic, has shown some promise in the
treatment of severe chronic nonmalignant
pain, including CRPS
Summary
• CRPS is a painful and debilitating disorder
primarily affecting one or more extremities
• No specific etiology identified
• ? underlying pathophysiology
• Difficulties in diagnosis and treatment
• No single diagnostic test or a single or
combination of therapies that are
universally effective for CRPS
Conclusions
• Treatment of CRPS focuses on an early
aggressive multimodal approach targets
pain reduction and functional restoration
• Medications CRPS are approved for the
treatment of other pain conditions
• Continued research may reveal additional
mechanisms of the disease leading to
preventive measures and additional targets
for drug activity