Although this syndrome occurs in both the upper and lower extremities, it is of interest that the success of pharmacologic and other treatment modalities differs between the upper and lo
Trang 1The normal physiologic response of
an extremity to a painful injury
in-volves humoral and neural signals
that give rise to increased blood
flow, edema, limited joint excursion,
and hypersensitivity to pain These
signs and symptoms are usually
proportional to the severity of the
injury and resolve with healing of
the damaged tissues When this
injury response is prolonged, a
chronic pain syndrome results
With time, painful symptoms may
expand from the site of injury to
involve the entire extremity, leading
to a persistently swollen, painful,
and ultimately functionless limb
This progressive pain pattern
has been recognized for over 100
years and has been described
vari-ously as causalgia, minor causalgia,
major causalgia, mimocausalgia,
pseudocausalgia, reflex sympathetic
dystrophy, algodystrophy,
algo-neurodystrophy, posttraumatic dystrophy, Sudeck’s atrophy, and sympathetically maintained pain syndrome To minimize the confu-sion in terminology, the Interna-tional Association for the Study of Pain coined the term complex re-gional pain syndrome (CRPS) to describe this constellation of symp-toms Within this diagnosis are two subtypes, which differ only by the presence of a definable peripheral nerve injury in type II
CRPS involving the lower ex-tremity presents a diagnostic and therapeutic challenge to the ortho-paedic surgeon Often discomfort is severe and patients are unable to gain relief Although this syndrome occurs in both the upper and lower extremities, it is of interest that the success of pharmacologic and other treatment modalities differs between the upper and lower extremities.1-5
Frequently, the symptoms in the lower extremity are more refractory
to intervention than those in the upper extremity.6 This differential response has led some to suggest that CRPS of the legs and feet is a discrete clinical entity.1,7-10 Narcotic pain medications are of little restorative value and, if used, fre-quently result in drug dependence without improving limb function Complicating management are social issues, such as liability or worker’s compensation or disability, that may provide a financial disincentive for patients to report improvement Often there is overlying psychologi-cal dysfunction, as well Because of the many physiologic and psycho-logical factors involved in pain, a multidisciplinary approach should
be developed for each patient, in-tegrating the efforts of the ortho-paedic surgeon, anesthesiologist, physiatrist, physical therapist, occu-pational therapist, and psychiatrist
Dr Hogan is Orthopaedic Surgeon, United States Navy, Norfolk, VA Dr Hurwitz is S Ward Casscells Professor, Department of Orthopaedic Surgery, University of Virginia Health Sciences Center, Charlottesville, VA Reprint requests: Dr Hurwitz, University of Virginia Health Sciences Center, Department
of Orthopaedics, PO Box 800159, Charlottes-ville, VA 22908.
Copyright 2002 by the American Academy of Orthopaedic Surgeons.
Abstract
Complex regional pain syndrome, formerly known as reflex sympathetic
dystro-phy or causalgia, is a difficult therapeutic problem for the orthopaedic surgeon
treating an affected lower extremity Despite many divergent and often
con-flicting theories, the cause of the severe pain, alterations in regional blood flow,
and edema is unknown Interventions that have proved successful for treating
similar conditions in the arm and hand frequently do not relieve pain similarly
in the lower extremity Common treatment regimens target individual
compo-nents of this symptom complex, namely, sympathetic or afferent nerve
hyperac-tivity, vasomotor instability, or regional osteoporosis Despite widespread use
of some of these treatments, few controlled clinical trials quantify their
effective-ness This challenging syndrome is best managed by a multidisciplinary team,
including chronic pain management specialists, physical therapists, and
orthopaedic surgeons.
J Am Acad Orthop Surg 2002;10:281-289
of the Lower Extremity
Christopher J Hogan, MD, and Shepard R Hurwitz, MD
Trang 2The pathophysiology of CRPS
re-mains unknown, and little clinical
evidence explains why certain
treat-ment protocols appear to be
suc-cessful Divergent theories abound,
likely because the spectrum of
pre-sentations of this syndrome is so
diverse This suggests that responses
to treatment vary because
heteroge-neous conditions are being treated
The older term reflex sympathetic
dystrophy describes a pathologic
reflex of the sympathetic nerves that
causes blood flow irregularities,
resulting in constant pain, muscle
atrophy, and fibrosis The
propo-nents of this etiology cited the pain
relief from sympathetic block as
supportive evidence They also
ad-vocated the use of calcium channel
blockers to counteract the
vasocon-striction of increased
sympathetic-adrenergic activity Sympathetic
block, however, did not prove to be
a reliable predictor of treatment
re-sponse and for this reason, the term
reflex sympathetic dystrophy was
discarded.11,12
Several other theories were
offered based on response of
periph-eral or systemic antagonism to α- or
β-adrenergic agonists.1,5,13-16 The theories of injury-induced hypersen-sitivity to circulating catecholamines are based on many reports of posi-tive clinical response to pharmaco-logic block using phentolamine, phenoxybenzamine, or propranolol
A subset of the catecholamine hypersensitivity theories suggested that the site of the pathologic recep-tors is in the skin rather than in the small vessels
Local inflammatory factors were the rationale for the use of high-dose corticosteroids.17,18 This seemed a logical explanation for the swelling and pain in an area that was physi-cally traumatized The advocates of this theory suggested that the pain-ful inflammation, in turn, disrupted local autoregulation of blood flow, and thus explained the classic phases
of reflex sympathetic dystrophy
A group of regional pain syn-dromes is associated with known nerve injury, previously referred to
as causalgia The concept of a pain-ful local nerve injury establishing constant pain through a central mechanism in the spinal cord or spinothalamic network was an
explanation that did not involve cate-cholamines or the sympathetic nerves A variation on the centrally mediated pain mechanism was the proposal that peripheral nerve in-juries created aberrant neuronal connections between peripheral sensory and sympathetic nerves To support their theory, advocates of neural injuries cited success with membrane-stabilizing medications, such as bretylium, gabapentin, and calcium channel blockers.3,10,19-22
Diagnosis and Clinical Course
The diagnosis of CRPS is based on physical examination findings be-cause no laboratory or radiologic tests can reliably confirm or exclude the diagnosis Traditionally, the clinical course of CRPS has been divided into three stages that de-scribe the physical characteristics of the syndrome (Table 1) In the hand, these stages are relevant to the effectiveness of intervention, with earlier intervention more likely
to result in successful outcomes Whether early intervention
im-Table 1
Stages of Complex Regional Pain Syndrome
Usual Time Stage Course (mo) Clinical Features Radiographic Findings
Acute 0 to 3 Warm, red, edematous extremity; Normal plain radiographs; may
aching, burning pain; intolerance have abnormal uptake of imaging
to cold; altered sweat pattern; agent on bone scan joint stiffness without any significant
effusion; hyperesthetic skin; no fixed joint contractures
Dystrophic 3 to 6 Cool, cyanotic, edematous extremity; Subchondral osteopenia; patellar and
shiny, hyperesthetic skin; fixed medial femoral condyle osteopenia contractures; fibrotic changes occur on sunrise view; may have abnormal
in the synovium uptake of imaging agent on bone scan Atrophic 6 to 12 Loss of hair, nails, skin folds; Bone demineralization
fixed contractures; muscle wasting
Trang 3proves the prognosis in CRPS of the
lower extremity, however, is
disput-ed.1,7-10
In the acute stage (within 3
months after the injury), patients
report a burning or aching pain that
generally does not respond to
nar-cotics and is considerably more
in-tense than expected for the degree
of injury Symptoms typically begin
soon after the injury—within hours
or days—but may develop more
in-sidiously over several weeks One
of the first clinical signs is an extreme
intolerance to cold, and patients
often state that motion, dependency
of the limb, and touch aggravate
their symptoms The skin is usually
warm and hyperemic and frequently
demonstrates an altered pattern of
perspiration that ranges from dry to
increased sweating Early in its
course, the pain may follow the
dis-tribution of a cutaneous nerve, but
with time this may progress to
involve the entire extremity Mild
edema around the joints is common,
but true joint effusions are rare (Fig
1) Although patients report a
sensa-tion of joint stiffness, examinasensa-tion
under anesthesia usually reveals a full range of motion
Plain radiographs help determine whether other definable lesions, such
as stress fractures, are responsible for the symptoms, but for CRPS in the acute phase, there are neither radio-graphic changes nor evidence of osteoporosis Technetium 99m bone scans are commonly used to attempt
to confirm the diagnosis of CRPS, but they have a specificity of 75% to 98% and a sensitivity of only 50% for this condition.11 The most common finding is increased periarticular uptake of the imaging agent in each phase, although decreased flow has been reported in the acute setting.2,23
As a result, bone scan findings are generally reported as “abnormal”
compared with those for the unaf-fected contralateral extremity
In the dystrophic stage, which begins approximately 3 months after the initial injury, pain is con-stant and aggravated by any stimu-lus If the ankle is involved, a fixed equinovarus deformity of the hind-foot may develop, with firm indura-tion around the tibiotalar joint.11
The skin is frequently cool to the touch, cyanotic, and shiny, and hair may be scant Radiographs of the involved extremity may reveal patchy subchondral osteopenia from both the disuse and the hyper-emia of the acute stage (Fig 2), although this finding may be absent
in up to 20% of patients who meet the diagnostic criteria for CRPS.11 If the knee is involved, osteopenia of the patella and medial femoral condyle on the sunrise view charac-teristically is present.7,24-26 Bone scan imaging at this time frequently demonstrates altered uptake of the imaging agent in the affected limb, particularly in the periarticular region.27 Synovial biopsies demon-strate increased fibrosis and synovial proliferation without any evidence
of inflammatory changes.25 This degree of fibrosis increases with the duration of symptoms
The atrophic stage begins about 6 months to 1 year after the onset of symptoms, when the skin and per-fusion changes become fixed, lead-ing to the clinical appearance of cyanotic, shiny, pale skin, with loss
Figure 1 Left foot of a woman with CRPS
after sustaining what she described as a
“slight sprain” of the ankle.
Figure 2 Anteroposterior (A) and lateral (B)
radio-graphs of the right foot of a middle-aged woman 3 months after open reduction and fixation for a talar neck fracture She had pain in the entire foot and stiffness of the ankle and all joints She could not tol-erate bearing weight or wearing shoes The amount
of osteopenia is beyond that expected from disuse, a finding typical of the dystrophic stage.
A
B
Trang 4of the usual skin folds The joint
motion is severely restricted, and
fixed contractures are common
Sig-nificant muscle wasting is apparent
on inspection, and there is
radio-graphic evidence of profound bone
demineralization
Treatment
No current consensus exists
regard-ing the most effective treatment
regi-men for CRPS of the lower extremity
Several studies report treatment
re-sults with the modalities used in
upper extremity cases However,
these studies had either small
num-bers of patients or limited clinical
follow-up.11-13,28 In addition, the
heterogeneity of the patient
popula-tions precludes a single algorithm to
guide treatment Clinical trials for
CRPS of the lower extremity are
list-ed in Table 2
The use of intravenous regional
sympathetic blocks was first
popu-larized by Hannington-Kiff in 1974, who suggested that guanethidine might relieve pain for patients with CRPS The goal of this therapy is to reduce the sympathetic input to the limb, based on the theory that chronic pain results from either a central hyperactivity of the sympa-thetic nervous system33or a periph-eral hypersensitivity to circulating catecholamines.34,35 To achieve a block, the affected extremity is exsanguinated and placed under tourniquet control, and a sympa-tholytic agent is infused into a vein
The medication suffuses the tissues via the venous pathways while the tourniquet prevents the circulation
of the medication into the systemic vasculature The drugs that have been used in intravenous regional blocks are guanethidine, reserpine, and bretylium, all of which inhibit release of norepinephrine by dis-placing it from neuronal storage vesicles In the United States, intra-venous preparations of
guanethi-dine and reserpine are no longer available, leaving bretylium as the only option
The efficacy of intravenous re-gional sympathetic blocks in the treatment of CRPS is unclear because separate studies dealing with very similar patient populations report contradictory levels of response to treatment Some studies showed no difference between guanethidine, reserpine, and saline control,5,36,37 whereas some demonstrated pain relief in about half of the lower ex-tremity patients,33,38and others, improvement in approximately 75%
of patients.29 None of these studies mentioned the duration of benefit Similarly, the efficacy of bretylium for intravenous regional sympathetic blocks is uncertain Although bre-tylium has been reported to be an effective treatment for CRPS, the largest published series does not discriminate between upper and lower extremity involvement.39 Of two studies that used bretylium,
Table 2
Clinical Trials for Treatment of Complex Regional Pain Syndrome of the Lower Extremity
No of Patients With Lower Duration of Study Drug Extremity Symptoms Results Relief
Intravenous
regional block
Eulry et al29 Guanethidine 87 Improvement, 64 Not given
Lumbar
sympathetic block
O’Brien et al8 Bupivacaine 60 Good, 34; fair, 21 Not given
Wang et al1 Bupivacaine 43 Initial improvement, 30 Not given
Cooper et al30 Epidural bupivacaine 14 Complete resolution, 11 7 to 48 mo
and narcotic
Oral agents
Cortet et al31 Pamidronate 17 Improvement/resolution in all >90 days
Devogelaer et al32 Pamidronate 15 Improvement/resolution in all Not given
Ghostine et al14 Phenoxybenzamine 17 Improvement/resolution in all No recurrences in 6 mo
to 6 yr follow-up
Intravenous agents
Poplawski et al6 Lidocaine and 8 Excellent results, 4 Not given
methylprednisolone Poor results, 4
Trang 5comprising a total of five cases, one
claimed total resolution of
symp-toms3 and the other, no benefit.19
Such conflicting reports of treatment
response are difficult to reconcile,
especially with the small number of
patients included
Several authors have used
lum-bar sympathetic blocks with either
lidocaine or bupivacaine to manage
CRPS of the knee.1,8,10,40 This
tech-nique involves introducing a needle
into the region of the paravertebral
lumbar sympathetic ganglia under
either fluoroscopic or computed
to-mographic guidance and infiltrating
the area with the local anesthetic
As an essential criterion for the
diagnosis of CRPS, three of these
protocols required that patients
demonstrate pain relief following
the administration of phentolamine,
a criterion that may favorably bias
the patient population toward this
therapy Although 93 of 112 total
patients had some degree of pain
relief, most had residual symptoms
In one series, only 12% of patients
were pain free at 3 years’
follow-up,1 whereas in another, only 57%
of patients had a good response,
al-though there was no mention of the
duration of pain relief.8 With
lum-bar sympathetic block, in contrast to
most other types of treatments,
there appears to be no correlation
between the duration of symptoms
and the response to treatment.1,8,10,40
Use of either continuous epidural
anesthesia or an intrathecal narcotic
pump allows either low-dose
nar-cotics or local anesthetics to be
ad-ministered locally, resulting in fewer
systemic side effects than are seen
with intravenous administration
When delivered locally, narcotics can
help break the pain cycle, whereas
the anesthetic agents provide a
rela-tively selective sympathetic
block-ade The narrow diameter of the
unmyelinated sympathetic fibers
allows for a block of these nerves
with minimal inhibition of the motor
or sensory fibers
Two published series report suc-cessful treatment with this interven-tion, either through placement of an indwelling morphine pump41or ad-ministration of continuous epidural anesthesia in conjunction with con-tinuous passive motion.30 Despite this success, the risks and costs of these treatments are considerable
Continuous epidural anesthesia requires hospitalization for the duration of treatment and carries the risks of urinary retention, skin breakdown, and hypotension Intra-thecal morphine pumps are rela-tively expensive and require periodic refilling of the narcotic reservoir
The use of α-adrenergic blocking agents is based on addressing the altered blood flow demonstrated in patients with CRPS, which is theo-rized to result from increased local secretion of norepinephrine and vas-cular endothelial hypersensitivity to this neurotransmitter Normally, peripheral blood flow is determined largely by sympathetic activity at the α1-adrenergic receptors, with increased stimulation leading to vasoconstriction Inhibition of the receptors leads to dilation of the arterioles and increased blood flow
Phentolamine is an α1-adrenergic sympathetic blocking agent with a very short duration of action Pain relief following intravenous admin-istration has been proposed as a diagnostic test for CRPS as well as a prognostic guide for favorable re-sponse to sympathetic block.15,42 The 15-minute plasma half-life of this medication, however, precludes its use as a therapeutic intervention
Phenoxybenzamine and prazosin have been used successfully in patients with lower extremity CRPS, although none of these reports states whether patients required long-term treatment.14,43,44 In contrast, another
α-adrenergic antagonist, droperidol, had no clinical benefit.45
Intravenous or oral clonidine or the combination is commonly used
as an intervention, likely on a
theo-retical basis because no published series documents its efficacy One small series demonstrated temporary relief with topical use.42
There is some clinical evidence that an oral beta blocker may im-prove symptoms Although the most dramatic property of propran-olol is its peripheral beta blockade, this drug also demonstrates central nervous system activity via antago-nism of serotonin A total of five patients with acute CRPS treated with oral propranolol has been re-ported Three of the patients were free of symptoms at their last
follow-up,16,46 and two demonstrated no change in their symptoms.47 Pain relief occurred several weeks after beginning treatment in those who had relief We found no reports of the use of intravenous beta blocker therapy or the use of any other beta blocker
Oral calcium channel blockers oppose the vasoconstriction medi-ated by the sympathetic nervous system by causing smooth-muscle relaxation in arteriole walls, leading
to increased peripheral blood flow These drugs have been used success-fully in vasospastic conditions, such
as Reynaud’s disease The largest reported clinical series of CRPS pa-tients treated with oral calcium chan-nel blockers did not distinguish between the results of treating upper and lower extremity symptoms, although a high degree of pain relief was reported.43 Prough et al20 re-ported success in three patients with lower extremity CRPS with this intervention, but two required main-tenance doses of nifedipine to pre-vent a recurrence of symptoms Reports of the efficacy of the se-lective serotonin blocker ketanserin
in treating CRPS mostly have not differentiated between upper or lower extremity involvement This use is based on the fact that sero-tonin demonstrates significant vaso-constrictive properties, and low concentrations of this
Trang 6neurotrans-mitter applied topically have been
shown to cause pain Bounameaux
et al48 stated that, although oral
ketanserin effectively increased
blood flow to the involved leg in the
majority of patients, none of the
eight patients with lower extremity
involvement reported any lasting
pain relief From this finding, the
authors concluded that decreased
peripheral blood flow might not be
the crucial factor in some patients
with CRPS
Treatment with bisphosphonates
is based on the concept that pain
results from the osteopenia created
by blood flow derangements and
chronic disuse Adami et al49reported
that alendronate was effective in
treating patients with long-standing
CRPS, but their results did not
dis-tinguish between upper and lower
extremity involvement Rehman et
al50showed that these patients have
lower than normal bone density and
that this relative osteoporosis
im-proves with the use of pamidronate
The time to improvement in bone
density in this study parallelled the
time to improvement of symptoms
seen by Cortet et al31and Devogelaer
et al.32 These studies, comprising a
total of 32 patients symptomatic for
at least 6 months, reported
improve-ment in symptoms in all cases but
did not mention the duration of pain
relief or whether patients required
chronic therapy
The rationale for the clinical use
of anticonvulsants in patients with
CRPS is that injured neurons have
abnormal sensitivity and may send
impulses spontaneously that lead to
the perception of pain Although
review articles have reported
treat-ment of lower extremity CRPS with
carbamazepine, clonazepam,
val-proic acid, and phenytoin,11,12we
have uncovered no clinical studies
substantiating the effectiveness of
these drugs
The only anticonvulsant studied
clinically and reported in the
litera-ture to date is gabapentin, which
acts both peripherally and centrally
to depress the excitatory pathways and stimulate the inhibitory path-ways This drug increases central nervous system levels of serotonin, which is an inhibitory neurotrans-mitter Mellick and Mellick21 reported that gabapentin relieved pain in a series of six patients with CRPS, two of whom had symptoms
in the lower extremity for 3 years
They did not mention the duration
of pain relief or whether these patients required chronic treatment with the medication
Antiarrhythmic medications also have been used to suppress the spon-taneous discharge of injured neu-rons and depress C fiber–mediated reflexes at the level of the spinal cord The efficacy of bretylium, a class III antiarrhythmic, has been discussed Mexiletine is an oral agent similar in action to lidocaine, which was used by Chabal et al22to treat three patients with chronic type
II CRPS of the lower extremity
They found improvement in two of three patients but did not mention the duration of benefit or whether the patients required long-term treatment
Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit the enzyme cyclooxygenase This inhibition leads to a decreased production of prostaglandins and thromboxanes, substances that increase the sensitiv-ity of nociceptors to painful stimuli and promote vascular constriction
Despite the widespread use of this class of medications, no published trials report the use of oral NSAIDs
to treat CRPS The benefits of intra-venous ketorolac were reported in a single small series.17 All three pa-tients with lower extremity symp-toms demonstrated temporary pain relief, which increased in duration with serial doses The average dura-tion of benefit was 15 days, allowing most patients to begin edema con-trol measures and attempt to regain joint motion
The potent anti-inflammatory effects of corticosteroids make these drugs an attractive option for treatment of CRPS because, theoretically, decreased tissue edema will lessen pain and im-prove joint motion Use of pred-nisone, prednisolone, or methyl-prednisolone is commonly cited in the treatment of lower extremity CRPS,11,13,28 but most studies sup-porting their use combine the re-sults of patients with upper and lower extremity involvement or in-clude only those with upper ex-tremity symptoms.18
Poplawski et al,6 however, re-ported on a series of 27 patients with CRPS, 8 of whom had lower extremity involvement Using intra-venous regional lidocaine and meth-ylprednisolone, they found that 60% of patients with upper extrem-ity involvement had a good or ex-cellent result compared with 50%
of those with lower extremity symptoms No definitive studies support the benefit of oral cortico-steroids in the treatment of lower extremity CRPS
Gentle physical therapy both to control edema and prevent joint contracture is beneficial in all stages
of CRPS Activity is thought to improve function, but it has little proven effect on pain There is no compelling evidence that any exer-cise or activity is curative Overly ag-gressive therapy should be avoided because this can exacerbate the patient’s sense of loss of control in the treatment process Although the use of transcutaneous electrical nerve stimulation (TENS) units is widespread, their usefulness has been demonstrated only in a small series in the pediatric literature,51 and there is no published report of the efficacy of this intervention in adults In a small study, other modalities, such as daily ultrasound treatments, have been shown to be beneficial in treatment of CRPS of the foot.40
Trang 7Treatment Overview
Several conclusions can be drawn
about CRPS of the lower extremity
There are no defined risk factors for
developing CRPS, and this
syn-drome has been described after both
major and incidental trauma to the
lower extremity The pain and
edema generally do not resolve
without treatment, and patients
fre-quently have residual symptoms,
despite prompt intervention.1 The
treating orthopaedic surgeon who
suspects CRPS should keep in mind
that these patients may have other
mechanical derangements
contribut-ing to their pain, such as a stress
fracture or degenerative arthritis A
careful, detailed history and
physi-cal examination should be done in
every case to eliminate the
possibili-ty of concomitant pathology
Intra-articular pathology requiring
surgi-cal intervention should be addressed
after the symptoms of CRPS have
subsided; even in this setting, CRPS
recurs after surgery in up to 47% of
patients.7,8,30 Because of this high
reported risk of recurrence,
explor-atory surgery should be avoided
Radiographs and nuclear bone scans
are helpful in confirming the
diag-nosis but may be falsely negative
early in the course of the syndrome
Magnetic resonance imaging has no
proven diagnostic value
When the patient has no
appar-ent mechanical derangemappar-ent,
ancil-lary services should be recruited
within 4 weeks to 3 months to break
the pain-impairment cycle of CRPS
A multidisciplinary approach, using
physical therapy and pain control
measures, is preferred to a single
physician dispensing treatment
Physical therapy is useful in all
stages, but forced motion should be
avoided because patients’ sense of
losing control can be exacerbated by
overly aggressive manipulation
Edema control can most effectively
be accomplished with compression,
gentle motion, and distal-to-proximal
massage Ice or ultrasound may be helpful, but often patients do not tolerate extremes of heat and cold well, limiting the usefulness of these modalities Progressive tactile desensitization may provide a use-ful adjunct, although this is less important than in patients with upper extremity CRPS because ambulation commonly provides adequate stimulation
Many different medications have been used in the treatment of CRPS
of the lower extremity, with varying degrees of success Narcotic pain medications should come from one physician to minimize the risk of drug dependence and drug interac-tions Orthopaedic surgeons do not commonly prescribe these medica-tions and therefore should consult early with a specialized pain clinic
Patients should be referred to pain clinic services within 3 months of the diagnosis of CRPS Gabapentin, prazosin, propranolol, nifedipine, and mexiletine all have been used in successful treatment protocols, but studies with these drugs involved fewer than five patients with lower extremity symptoms, making it dif-ficult to draw conclusions regarding the efficacy of each intervention
The greatest clinical experience is with the use of intravenous regional administration of sympatholytic agents, NSAIDs, or corticosteroids
Considered as one large group, pa-tients treated with guanethidine, reserpine, or bretylium responded similarly to those treated with ketorolac, prednisolone, or methyl-prednisolone, with approximately half reporting relief This suggests that other mechanisms may con-tribute to the clinical response
Some of the controversy surround-ing intravenous regional techniques comes from studies suggesting that the pain relief results, not from the infusion of a sympatholytic agent, but from the tourniquet-induced ische-mia Rocco et al5and Blanchard et
al36demonstrated no difference in
results between guanethidine, reser-pine, and normal saline infusion administered to patients with lower extremity CRPS, a finding supported
by Jadad et al,37who demonstrated
no difference between guanethidine and saline infusions These authors suggest that tourniquet-induced ischemia may provide enough pain relief to allow for increased physical therapy, but no studies have tested this hypothesis
More encouraging results were seen after paravertebral sympathetic blocks and after treatment with con-tinuous epidural anesthesia All of the studies of these two interven-tions used response to phentolamine
as a diagnostic criterion for CRPS, a factor that may select for a better response to treatment with anti–α -adrenergic agents
Pamidronate, a bisphosphonate, has demonstrated encouraging re-sults in the treatment of CRPS of the lower extremity Although it is difficult to ascribe all of the clinical features of CRPS to osteopenia, this medication reportedly led to im-provement or resolution of symp-toms in all patients in the study populations
Summary
CRPS of the lower extremity poses a management challenge The etiology
is unclear, and theories to explain the condition, as well as proposed therapies, abound Therapies that may be effective for upper extremity CRPS are often not as effective for lower extremity CRPS, leading some to conclude that it is a differ-ent differ-entity
No laboratory or radiologic tests can reliably confirm the diagnosis
In the acute stage, burning or aching pain that cannot be controlled by narcotics is the major feature In the dystrophic stage, beginning approx-imately 3 months after injury, bone scans often demonstrate altered
Trang 8up-take of the imaging agent in the
affected limb In the atrophic stage,
6 months to 1 year after injury, fixed
contractures, significant muscle
wasting, and profound bone
de-mineralization are common
The greatest clinical experience in
managing CRPS is with intravenous
regional administration of
sympa-tholytic agents, NSAIDs, and
corti-costeroids Numerous systemic
medications have been studied for
relief of pain in CRPS, but no clear evidence advocates the use of any of these drug therapies for lower extremity CRPS Published evi-dence seems best to support the use
of the anticonvulsant gabapentin, the α-adrenergic blocking agent pra-zosin, the oral beta blocker propran-olol, the calcium channel blocker nifedipine, and the antiarrhythmic mexiletine Results with bisphos-phonates have been encouraging
Gentle physical therapy is bene-ficial in all stages of CRPS both to control edema and prevent joint contracture, but it has little proven effect on pain Overly aggressive therapy can increase pain A multi-disciplinary team approach to management is recommended, including chronic pain manage-ment specialists and physical thera-pists as well as orthopaedic sur-geons
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