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CentralMechanism
In1965,whenMelzackandWall20proposedthegatecontroltheoryofpaintransmissioninthe
spine, they also suggested a central biasing mechanism mediated through a system of
descendingfibers.Thesedescendingfibersarisefromthebrainstemreticularsystem,andthey
exertatonicinhibitiononthesomaticsensorysystematalllevels.Reducedsensoryinputafter
somaticnerveinjury(especiallywhenthenerveissevered)wouldresultinadecreaseinthe
descendingtonicinhibitionandthusallowanincreaseinthetransmissionoftheself-sustaining
neuronalactivitiesgeneratedeitherintheperipheryorwithinthespinalcord.Inthissituation,
theypostulatedthatprolongedpainmayleave“memorytraces”inthesomatosensorysystem,
making an individual more susceptible to recurrent pain. The practical application of this
theorybecomesrelevantinthetreatmentofpatientswithphantomlimbpain.
21,22
NeuronalPlasticityMechanism
This proposed theory, which has become more commonly accepted, suggests that the
perpetuationof abnormalfiring patternin the internuncial neuronpool inthe spinalcord is
responsible for abnormal painperception. Atthe spinal cord level, a class ofdorsal horn
neuronsthataremultireceptive,theso-calledwidedynamicrange(WDR)neurons,usuallydo
not contribute to painful sensations under normal conditions.23 Sustained stimulation of the
WDR by nociceptors, however, causes hyperexcitability and plasticity of the WDR by
nociceptors,resultinginexpansionoftheirreceptivefields.Thismayexplainwhyinnocuous
stimulations are now perceived as painful (hyperalgesia).22 Roberts and Foglesong
24
demonstrated that WDR neurons are the only spinal nociceptive neurons activated by
sympathetic efferent activity. Therefore, WDR neurons(i.e., thehigh-thresholdneurons) are
mostlikelytomediatethespinalcomponentofSMP.SympatheticactivationofWDRneurons
isabolishedbysubcutaneousinjectionoflocalanesthetic,coolingthereceptivefieldwithice,
andintravenousinjectionoftheα-adrenergicblockerphentolamine.
GlialCellActivation
It has recently been hypothesized that CRPS is associated with activation of glial cells
followingtissueinjuryorinflammation.Glialcell,suchasmicrogliaandastrocytes,secretes
substances that enhance pain transmission in the central nervous system once they are
activated.Thesesubstancesincludeproinflammatorycytokines,nitricoxide,andglutamate,to
name a few.Animalstudies haveshown thatactivation of glial cells augments nociception.
HumanautopsystudyofCRPSshowedthatlong-standingCRPSpatientshadsignificantglial
cellactivationaswellasneuronallossintheposteriorhorn,predominantlyatthelevelofthe
originalinjury.
25
PsychologicalPredisposition
Becausenoneofthepreviouslyproposedmechanismsofferanypredictabilityonwhoismore
susceptibletoCRPS,itisnotsurprisingthatsomesuggestedthatparticularpersonalitytraits
indicated predisposition toward developing CRPS. The patients’ seemingly exaggerated
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response to innocuous stimulations naturally led the physician to suspect psychological
disorders. There is literature on both adults and children that hypothesize the presence of
psychologicaldisorders,particularlyanxietyanddepression,whichpredisposeonetoCRPS.
Conversely,othersbelievethatanychronicpainandsuffering,inandofitself,willproducea
hostofpsychologicalcomplications.
DIAGNOSIS
A complete history and physical examination with high index of suspicion is crucial for
diagnosisofCRPSintheearlystageswhendisproportionatepainmaybethe onlyabnormal
feature.Differentiationfromotherconditionsmaybedifficult.Neuropathicpaincausedbyan
injured or entrapped peripheral nerve or a neuroma anywhere from its root to the terminal
branches may present similar symptoms, such as burning pain with hyperpathia. They are,
however, usually limited to the territory of the involved nerve and associated with little
sympatheticactivities.Inflammatoryprocessesnotinvolvingnerves,suchastenosynovitisand
bursitis, may produceburningpain,whichpersistsformonths.7 Theydonottypicallyshow
Tinelsign,whichisspecifictonerves.Vasculardiseasesthatcausedecreasedcirculationsuch
asRaynaudphenomenonordisseminatedlupuserythematosusmaymimicCRPS,althoughthey
usually affect more than one extremityat once.Therefore, the diagnosis is not infrequently
madebyexclusion,especiallyintheearlystagesofCRPS.Forsuchreasons,someclinicians
stilldonotacceptCRPSasadistinctivepathologicdisorder.
SeveralinvestigativetoolsmayhelptoconsolidatethediagnosisofCRPS:
Quantitativesweattestmayshowexcessivesweating.
Thermography can demonstrate a disorder in heat regulation. Heat loss from the skin
surface is mainlyregulated bysudomotor activity on thesweat glandsandthe dermal
microcirculation.26An affected hand or footmayat timesbehyperthermic, butrelative
coldness is the most common finding. These changes produce the observation of
vasomotor instability. They are related to sympathetic vasoconstriction and to
compensatoryorreboundvasodilatationofskincapillaries,whichare,inturn,influenced
byirritationofperipheralnervefibers.
27
Radiographicstudiesmayrevealcharacteristicthoughnotpathognomonicchanges.Patchy
osteoporosisisthe primaryroentgenographicmanifestationofearlydystrophicCRPS.
28
Other features such as patchyepiphyseal demineralizationofthe short boneswithsoft
tissueswelling;subperiostealresorption;striationandtunnelinginthecortex;aswellas
largeexcavationandtunnelingoftheendostealsurfacesmayalsobepresent.Onemustbe
aware, however, that similar pictures may also be seen in hyperparathyroidism,
thyrotoxicosis,andotherconditionswith increased boneturnover.29 In later dystrophic
stage,whendystrophy borders onatrophy, severe anddiffuseosteoporosisis the usual
finding.
Triple-phase bone scan using technetium-99 may demonstrate increased periarticular
uptake inthe involved extremity(Fig. 12-1).28 Apositive bone scanina patientwith
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clinical signs and symptoms of CRPS helps to confirm the diagnosis. Conversely, a
negative scanina patient with clinical CRPS does notrule out the conditionbecause
somepatientswillpresentwithinitialnegativescansthatbecomepositivelater.
30
Each finding, be it thermographic, radiographic, or scintigraphic, despite their sensitivity,
when present inisolation,tends to be nonspecific andimpossible to distinguishfrom other
metabolicorinflammatoryconditions.Takentogether,theygreatlystrengthenthediagnosis.
Thediagnostic“goldstandard”hasbeenpainrelieffromasympatheticnerveblock.When
evaluatingtheresultofasympatheticnerveblock,caremustbetakenthatsomaticnervesare
notanesthetizedduringthesympatheticblock,ortheoutcomecannotbeinterpreted.Evenwhen
doneproperly,thereisstilltheunavoidableconfoundingplaceboeffect.Tocircumventthis,it
has beenrecommended thatan α-adrenergic receptorblockersuch as phentolaminebeused
intravenouslyasapredictoragentbeforeinvasiveLSB.
31,32
Ofcourse,anegativeresponseto
sympatheticblocksdoesnotruleoutCRPS.
SincethenomenclatureconversionofRSDtoCRPS,therehavebeenmultipleconsensus
meetings convened to derive the diagnostic criteria for CRPS. In 1994, the International
AssociationfortheStudyofPain(IASP)cameupwiththefirstconsensus-drivendiagnostic
criteria.Insubsequentyears,theIASPcriteriawasfoundtobeadequatelysensitive,buthad
problemswith specificity, resulting inoverdiagnosis of CRPS.As a result,updatedcriteria
called the Budapest Criteria were recommended in 2003 when an international group of
researchersandclinicianexpertsinCRPSmetinBudapest,Hungary.TheBudapestconsensus
statementforCRPSisasfollows:
33
Generaldefinitionofthesyndrome:CRPSdescribesanarrayofpainfulconditionsthatare
characterized by a continuing (spontaneous and/or evoked) regional pain that is seemingly
disproportionateintimeordegreetotheusualcourseofanyknowntraumaorotherlesion.The
pain is regional (not in a specific nerve territory or dermatome) and usually has a distal
predominanceofabnormalsensory,motor,sudomotor,vasomotor,and/ortrophicfindings.The
syndromeshowsvariableprogressionovertime.
Tomaketheclinicaldiagnosis,thefollowingcriteriamustbemet:
Continuingpain,whichisdisproportionatetoanyincitingevent
Mustreportatleastonesymptominthreeofthefourfollowingcategories:
Sensory:Reportsofhyperesthesiaand/orallodynia
Vasomotor: Reports of temperature asymmetry and/or skin color changes and/or skin
colorasymmetry
Sudomotor/Edema: Evidence of edema and/or sweating changes and/or sweating
asymmetry
Motor/Trophic: Reports of decreased range of motion and/or motor dysfunction
(weakness,tremor,dystonia)and/ortrophicchanges(hair,nail,skin)
Must display at least one sign at time of evaluation in two or more of the following
categories:
Sensory:Evidenceofhyperalgesia(topinprick) and/orallodynia(tolighttouchand/or
temperaturesensationand/ordeepsomaticpressureand/orjointmovement)
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4.
Vasomotor:Evidenceoftemperatureasymmetry(1°C)and/orskin colorchangesand/or
asymmetry
Sudomotor/Edema: Evidence of edema and/or sweating changes and/or sweating
asymmetry
Motor/Trophic: Evidence of decreased range of motion and/or motor dysfunction
(weakness,tremor,dystonia)and/ortrophicchanges(hair,nail,skin)
Thereisnootherdiagnosisthatbetterexplainsthesignsandsymptoms
TREATMENT
Any treatment must be targeted toward relief of pain, avoidance of disuse atrophy, and
ultimatelya returnto normal function. Many patients, especially those with early stages of
CRPS,dorecovergraduallywithphysiotherapyandanalgesicdrugsalone.Inmoreadvanced
or chronic cases,moreaggressive treatmentsare neededto breaktheviciouscycle ofpain,
immobility, disuse atrophy, and more pain. For any patient, treatment should follow a
preplannedalgorithmtoeffectminimumtimelossbetweeneachchosenmethod.Psychological
evaluationwithongoingcounselingforthepatientsandtheirimmediatefamilymembersshould
be an integral part of the treatment regimen. The emphasis is toward a multidisciplinary
approach,whichensuresthatimportantaspectsofthepatient’scarearenotoverlooked.
NONINVASIVEMODALITIES
PhysicalTherapy
Physical therapy is themainstay ofovercoming disuse atrophy. Tominimize fear ofpainful
motion, patients should be given only active or actively assisted therapy within limits of
tolerance. Aggressive physical therapy without adequate pain management usually leads to
patient noncompliancewiththetreatmentprogramanddelayedrecovery.Therefore, passive
exercisemaybeundertakenonlywhenboththepatientandthetherapistthoroughlyunderstand
andaccepttheriskofmorepain,swelling,andstiffnessbyforcingmotionsbeyondthepointof
discomfort.
34
TranscutaneousElectricalNerveStimulation
Transcutaneouselectricalnervestimulationbecamepopularafterthegatetheory,proposedby
Melzackand Wall, became generallyaccepted. When delivered at levels that produce skin
tingling,ithasbeenpostulatedtoactivatebothlarge(Aβ,B)andsmall(Aδ,C)fibers.35The
large-fibersignals“closethegate”andblockthesmall-fibersignals.Alternatively,activation
of small fibers may facilitate the descending inhibitory system.
35,36
Using this modality,
Robainaandcolleaguesreportedexcellentresultsin 25% andgood resultsin45%ofRSD
patients.
37
NonsteroidalAnti-InflammatoryDrugs
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Althoughoftenusedasthefirst-lineanalgesicformostchronicconditions,nonsteroidalantiinflammatory drugs may be helpful during the acute stage when inflammatory changes and
tissueedemaarepresent.TheirefficacyinestablishedCRPShasnotbeenestablished.
TricyclicAntidepressants
Tricyclicantidepressantsblocknorepinephrineandserotoninreuptake.Theyalsoblocktheα1adrenergicreceptors,hencereducingsympatheticefferentactivity.Inanimalmodels,theyhave
beenshowntoblockthehyperalgesiainducedbyintrathecallyinjectedN-methyl-D-aspartate
(NMDA).
38,39
Theyhavebeenshowneffectiveinreducingsomeoftheneuropathicsymptoms
such as burningsensation. The popularity of this group of drugs has been limited by their
significantsideeffects.
Opioids
Opioidanalgesicshavebeenshowntoblockneuropathicpainlesseffectivelythannociceptive
pain.AlthoughopioidsarenotveryeffectiveintreatingCRPSpainsymptoms,theydoimprove
the qualityofpaincontrol. They areespeciallyhelpful topatientsgetting over severeacute
episodes.Becausetoleranceinevitablybuildsup,chronicusewillresultinescalatingdoses,
with increasing potential for side effects. These medications should, therefore, be given
judiciously.
Corticosteroids
Steroidshavebeenusedsince1953,whenfavorableresultswerereportedinthetreatmentof
shoulder-hand syndrome.40 The pharmacodynamics remains largely unknown. Kozin and
coworkers41 observed a chronic perivascular inflammatory infiltrate in synovial biopsy
specimens from involved extremities. Hence, thepotent anti-inflammatory properties ofthe
corticosteroids may partially account for their therapeutic effects. By stabilizing basement
membranes,theyreducecapillarypermeabilityanddecreaseplasmaextravasationcommonly
associatedwithearlystagesofCRPS.36Onepotentialadvantageofsystemic corticosteroids
overthe beneficialeffectsofsympathetic blockbecomesapparent whenmultiplebodyparts
are involved.A 1997reviewbyKingery39confirmedconsistentsupportinthe literaturefor
useofcorticosteroids,whichshowedlong-termeffectiveness.
Gabapentin
Gabapentin, an anticonvulsant, was initially used for partial seizures with or without
secondarygeneralization. Recently, it hasbeenused forneuropathicpainwithnotablygood
results,asreportedbyRosnerandassociates.42WhengiventopatientswithCRPS,dramatic
painreliefwasobservedand,insomecases, reversalofearlytrophic changes.Mellickand
Mellicy43 reported correctionsinskin temperature and color and lessening of andeventual
relieffromallodynia,hyperalgesia, andhyperpathia. Amajor advantage ofgabapentinisits
lowtoxicityandsideeffectprofile.Itisgenerallywelltoleratedbymostpatients.
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Carbocalcitonin
Whenbonescansshowincreasesinbloodflowanduptakeofthetracerintheinvolvedarea,
both porcine and salmon calcitonin have been reported to reduce local blood flow and
decreaselocal clinicalsignswithrelieffrompain.44Nuti andothers34demonstratedsimilar
improvements in thefeetofCRPS patients. Salmon calcitonin is now available as a nasal
spray,whichsignificantlyincreasespatientacceptanceovertheolderinjectableformulation.
ClonidineTransdermalApplication
Clonidinehasadualmodeofaction.Inthecentralnervoussystem,itactsasanα2agonist.In
the peripheral nervous system, it inhibits the release of norepinephrine from sympathetic
terminals.Thus,centrally,ithasanalgesiceffects,whereasperipherallyitreducestheongoing
activityofnociceptors,hencedecreasingthecentralsensitizationandrelievinghyperalgesia.
45
Itisavailableasatransdermalpatch,whichiseasytouse.Insomepatients,however,itmay
causeunacceptablehypotensionorsedation.
FIGURE12-5.Lumbarsympatheticblockunderfluoroscopyshowingthetipoftheneedleisatanteriorbodyofthe
L2vertebratoblockthelumbarsympatheticpainwithlocalanesthetic.
INVASIVEMODALITIES
Intermittent sympathetic nerve blocks doneinthe earlystages can be effective in achieving
remission.Eveninestablishedcases,theyarevaluableasanoptioninofferingtothepatients
periodic“breaks”fromtheviciouscycleofpainanddysfunction.Theprocedureisnotwithout
risk,andrepeatedblockstendtoloseefficacy.Whenjudiciouslydoneatthecrestofperiodsof
exacerbation, intermittent sympathetic nerve block can usually abort the need to resort to
opioid medication. Of course, this is applicable onlyto those who respond to sympathetic
blockade.Sympathetic nerve blockswith local anesthetics caneither be doneat thelumbar
sympatheticchainorasaregionalperfusioninthelimb.
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LumbarSympatheticBlock
The purpose of sympathetic blockade in patients with CRPS is to interrupt the abnormal
reflexes mediated by the autonomic nervous system. Sympathetic blockade can be both
diagnostic and therapeutic.36 In the early stage of CRPS, a prolonged remission may be
obtainedfromasinglesympatheticblock(Figs.12-5and12-6).Farmorecommonly,however,
repeatednerve blocksare required forprolonged paincontrol.14Typically,blocksaredone
closely,uptothreetimesperweekfor2weeksinearlycases,andthenaretaperedofftoonce
weeklyor lesswhensymptomssubsideorresponsesarestabilized.46Whentheconditionis
bilateral, LSB can be achieved bilaterally with an epidural infusion for inpatients.47 To
maximizebenefitfromthenerveblock,itshouldbefollowedbyacourseofphysicaltherapy
toimproverangeofmotion.
NeurolyticLSBwithInjectableChemicals
Chemical agents such as concentratedalcohol or phenol can produce longer duration nerve
blockslastingfromafewweekstoseveralmonths.HaynsworthandNoe48reportedthat89%
ofpatientsinthephenol groupshowed signs ofsympathetic blockadeafter 8 weeks.Some
controversysurroundstheuseoftheseagents,however,suchasahighincidence(5%to40%)
of postsympathectomy neuralgia resulting from inadvertent damage to somatic nerves (e.g.,
genitofemoralneuralgia).
49,50
FIGURE12-6.PatientwithCRPSofleftlowerextremity(A)withincreasedvascularflowandtemperatureafter
lumbarsympatheticblock(B).
SurgicalLumbarSympathectomy
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Becauseoftherelativeextensiveareainvolved,surgicallumbarsympathectomyisusuallynot
recommended,exceptwhendefinitelyindicated.Thesympatholyticeffectcanbetransientasa
resultofincompletedenervation.
IntravenousRegionalSympatholysis
DonewithguanethidineandreserpineasdescribedbyHannington-Kiff51in1977,intravenous
regionalsympatholysisisessentiallyamodificationoftheBierblockprocedureforregional
anesthesia. Pharmacologically, guanethidine acts as a false transmitter. It is taken up by
sympatheticnerveendingsanddisplacesnorepinephrinefromitsstoragesites.Thus,thereis
aninitialreleaseofnorepinephrinefollowedbydepletion.Excellentpainrelieflastsfrom12
to36 hours but may be as long as a few weeks.Wahren and colleagues demonstratedthat
patientswithSMP benefitedconsiderablyfor 2weeksormore, whereasnosignificantpain
relief was achieved in patients with SIP.52 Reserpine acts by reducing reuptake of
catecholamines,therebyslowlydepletingnorepinephrinestoresinsympatheticnerveendings.
Pain relief lasting from weeks up to a few months has been reported.53 Although reported
complications from these drugs have been few, prolonged orthostatic hypotension with
dizziness, somnolence, nausea, and vomiting can occur. Neither of these two agents was
approvedbytheU.S.FoodandDrugAdministrationforintravenousinfusion.Studiessuchas
thatbyBlanchardandassociates54havethrowndoubtontheefficacyofthesedrugswhenused
inthisfashion.Salineinfusionwasobservedtoproducecomparableresults.Thisledtosome
tocontendthattourniquetischemiawasactuallytheactiveingredient.
KetamineInfusion
CRPS patients that have refractory pain despite conventional treatment are likely to have
centralsensitizationofpainduetoreleaseofthemagnesiumblockadeoftheNMDAreceptor.
KetamineisanNMDAreceptorantagonistthatcanbeusedtotreatneuropathicpaininthese
patients. Double blind, randomized, placebo-controlled studies have shown that patients
treated with ketamine infusion have significant pain relief.
55,56
Furthermore, retrospective
studybyCorrelletal.57showedthatpatientshaveprolongedperiodofpainreliefwithrepeat
ketamineinfusioncomparedtosingleinfusion.Somepotentialsideeffectsofketamineinfusion
are diuresis, elevated liver enzyme, tachyarrhythmia, hallucination, flashbacks, and erratic
behavior. Thus, urine output, liver enzyme level, and EKGshould be monitored during the
infusion. Clonidine and benzodiazepine should be used to prevent tachyarrhythmia and
psychologicaleffectsofketamine.
Electroacupuncture
Electroacupunctureisclaimedtoreleaseendogenousopioids,endorphins,andenkephalinsin
the central nervous system, thereby achieving pain reduction. The electric current during
electroacupuncturemayalsoactlocallytorelaxthepostcapillarysphincters,thusreducingthe
localedemaandswelling.58Needlestimulationmayalsoincreaselarge-fibertransmissionand
“closethegate”tosmall-fiberpainsignalsaccordingtothegatecontroltheoryofMelzackand
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Wall.
20
NewInvasiveModalities
RadiofrequencyLumbarSympathectomy
Thistechniqueusesaheat-generatingradiofrequencydirectedthroughaninsulatedwireatthe
nerve or ganglion. It offers a limited, controlled thermal lesion, thus avoiding significant
neurologicdeficitsthatmayoccurwithinjectedchemicals.Also,lessscarisproduced,making
repeated procedures possible.59 Sri Kantha60 reported that the duration of relief from
radiofrequencysympathectomyappearstobelongerthanthatfromchemicalneurolyticagents
andmaybeaslongasthatfromopensurgery.Ontheotherhand,Roccoconcludedthatdespite
earlysuccessfulLSB,long-lastingpainreliefwasdifficulttoobtain.61Comparingincidenceof
postsympathectomy neuralgia, Haynsworth and Noe’s48 study showed 11% in the
radiofrequencygroupversus33%inthephenolgroup.
EpiduralClonidine
Clonidineis anα2-adrenoceptoragonist,whichbinds both pre-andpostsynapticneurons.It
decreases anesthetic requirement during surgery
62,63
and postoperative morphine
requirement.64Clonidine administered epidurallyproduces analgesia thatis not reversedby
opiate antagonist. Rauck and colleagues65 demonstrated extensive analgesia with epidural
clonidine. The proposed mechanisms include reduced norepinephrine release peripherally,
reductionofsympatheticoutflowcentrally,andthepostsynapticactionofhyperpolarizationof
dorsalhornWDRneurons.
65
Neuromodulation
Neuromodulation is based on the gate control theory proposed by Melzack and Wall,
20
whereby electrical stimulation of non-nociceptive Aβ nerve fibers inhibits dorsal horn
interneuronsandinterruptsthetransmissionofpainsignals.Theseinvestigatorswereableto
suppress pain with electrical stimulation of infraorbital nerves using peripheral nerve
stimulation(PNS).Peripheral stimulation may augmentblood flow, decrease excitability of
peripheral nerve fibers aswell as changingthe local concentrationofneurotransmitters that
produce chronic pain.
66,67
Case studies have shown that implantation of peripheral nerve
stimulatorproximaltothelesionwasabletoprovidelong-lastingreductionofpainscorein
patientswithCRPS.
68,69
Because ofthe initial complexityofPNSprocedureandunpredictabilityofitsoutcome,
electricalstimulationofthespinalcordforanalgesiawasproposedsoonafterpublicationof
the gate control therapy. Technically simplistic, it involves insertion of anelectrode-tipped
catheter into the epidural space attheappropriate spinal segment. This allows avariety of
currentstostimulatethespinalcorddirectly(Fig.12-2). Manydifferenttheories havebeen
proposed to explain how it works.70 Experience has shown that, inadditiontopainrelief,
spinalcordstimulationhasbeensuccessfultosomedegreeinreversingthe“inability”tomove
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injured extremities.71 It was also found helpful in patients who suffer recurrent pain after
surgicalsympathectomy.
72
PERIOPERATIVEMANAGEMENT
ThegeneralgoalsofperioperativemanagementofCRPSpatientsareaggressivepaincontrol
aswellaspreventingexacerbationofthiscondition.Surgery canprecipitatedevelopment of
CRPS.PreoperativefactorsthatprecipitateCRPSincludepreoperativeanxiety,preoperative
painintensity, andintraoperative factors.Intraoperativefactors includeprolonged tourniquet
time and motor nerve injury. Asaad and Glass73 have reviewed studies for different
perioperative approachesofthesepatients.Theyfound three components thatare critical to
management of these patients. Those include preventive measures, anesthetic and
intraoperativemanagement,andpostoperativepainmanagement.
Electivesurgeryshouldbeperformedwhensymptomsarewellcontrolled.Marxetal.
74
reported that administering calcitonin 2 to 4 days preoperatively and up to 4 weeks
postoperativelymaypreventrecurrenceofCRPS.Studiesalsofoundthatthreedailydosesof
vitaminCpreoperativelycandecreasetheincidenceofpostoperativeCRPS.
75–77
TheanestheticplanofCRPSisnotlimitedtothechoicebetweenregionalanesthesiaand
generalanesthesia.Inaprospective,controlledstudy,itfoundnodifferenceinthedevelopment
ofCRPSinpatients whoreceived general anesthesia, intravenous regional anesthesia with
lidocaine,orintravenousanesthesiawithlidocaineandclonidine,incomparisonwithpatients
who received a brachial plexus block. The same study also found a positive correlation
betweentourniquettimeandthedevelopmentofCRPS.
78
A multimodal approach is important in decreasing flare-up of CRPS symptoms
postoperatively.Patientsshould resumetheir oralmedicationasearlyaspossible.An early
mobilizationandrehabilitationshouldalsobetakingplace.74Inadditiontocontinuousregional
anesthesia,adjuvantmedicationsuchasclonidinemaybeaddedtotheinfusion.Subanesthetic
dose(10to20mgperhour)ofketamineintravenousinfusionintheimmediatepostoperative
periodcouldalsobehelpful.73Otheradjuvantpainmedicationssuchasgabapentincouldbe
partofthemultimodalpainmanagement.
79
PROGNOSIS
Twoimportantfactorsthatinfluencelong-termpatientoutcomeregardlessofetiologyare(1)
early recognition with appropriate treatments and (2) vigorous rehabilitation therapies. If
diagnosed early, the majority of patients with CRPS will respond to a course of prudent
physical therapy and adequate analgesia. Withdelayed treatment, the CRPS syndrome may
spread proximally from one extremity or even to the other extremities. It is potentially
devastating to patients in whom the disease progresses to the dystrophic–atrophic stages.
Evaluation of any particular treatment regimen must be tempered by the awareness that a
certain number of cases will show spontaneous resolution, whereas certain others will
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