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I.

AbdominalAorticReconstriction
a. Patientselection
b. AorticCrossClamping
i. Hemodynamicalterations
ii. Metabolicalterations
iii. EffectsonregionalCirculation
iv. AorticCrossclampRelease
1. Theaortaisoccluded,metabolitesthatareliberatedasaresultofaneaerobicmetabolism,suchasserumlactate,
accumulatebelowtheaorticcrossclampandinducevasodilationandvasomotorparalysis.
2. Asthecrossclampisreleased,SVTdecreases,andbloodissequesteredintopreviousdilatedveins,whichdecreases
venousreturn.
3. Reactivehyperemiacausestransientvasodilationsecondarytothepresenceoftissuehypoxia,releaseofadenine
nucleotides,andliberationofanunnamedvasodepressorsubstance,whichmayactasamyocardialvasodepressor
substance,whichmayactasamyocardialdepressantandperipheralvasodilator.
4. Declampingshocksyndromecanoccurthatcauseshemodynamicinstabilitythatmayensueafterthereleaseofan
aorticcrossclamp.
5. Venousendothelinmaybepartiallyresponsibleforthehemodynamicalterationsthataccompanydeclapmingshock
syndrome.VenousET1hasapositiveinotropiceffectontheheartandavasoconstrictingandvasodilatingactionon
bloodvessels.
6. AlthoughSVRandMAPdecrease,intravascularvolumemayinfluencethedirectionofmagnitudeofchangeinCO.
7. Resrotarionofcirculatingbloodvolumeisparamountinprovidingcirculatorystabilitybeforerelaseofaorticclamp.
8. Thesiteanddurationofcrossclampapplication,aswellasthegradualrelaseoftheclamp,influencethemagnitudeof
circulatoryinstability.
9. Interventions:254
a. Increasefluids
b. Decreasedepth
c. Decreasevasodilators
d. Increasevasoconstrictordrugs
e. Reapplycrossclampforseverehypotention
f. Consideradministrationofmannitorandsodiumbicarb
c. SurgicalApproach
i. Thestandardapproachforelectiveabdominalaorticreconstructyionisthetransperitonealincision.
ii. Advantagesofthisrouteincludeexposureofinfrarenalandiliacvessels,abilitytoinspectintraabdominalorgansandrapid
closure.
iii. Unfavorableconsequencesassociatedwiththisapproachincludeincreasedfluidlosses,prolongedileus,postoperativeincisional
pain,andpulmonarycomplications.
iv. Theretroperitonealapparoachisanalternative.Advantagesincludeexcellentexposure(especiallyforjuxtarenalandsuprarenal
aneurysmsandinobsesspatients),decreasedfluidlosses,lessincisionalpain,andfewerpostoperativepulmonaryandintestinal
complications.
d. Managementoffluidandbloodloss.
i. Extremelossofextracellularfluidandbloodshouldbeeexpectedwithabdominalaorticaneursymectomies.
ii. Thedegreeofsurgicalandevaporativelossesandthirdspacingwilldeterminethemagnitudeofthepatientsfluidvolumedeficit.
iii. Mostbloodlossoccursbecauseofbackbleedingfromthelumbarandinferiormesentericarteriesafterthevesselshavebeen
clampedandtheaneurysmisopened.
iv. Thesuseofheparinalsocontributetobloodloss.
v. Excessivebleeding,however,canoccuratanypointduringsurgeryandbloodreplacementiscommonlyadministeredduringAA
resections.
vi. 3optionsareavailablefordadministeredingautologoustransfusions
1. preoperativedeposit,
2. intraoperativephlebotomyandhemodilution
3. intraoperativebloodsalvage.
vii. Preoperativedepositisbecomingmorefeasiblebecauseasymptomaticaneurysmsarebeingdeterctedwithgreaterfrequency.
Ideallypatientsdoneattheirwwnbloodtominimizetheintraoperativeuseofhomologousbloodproductsandthesubsequentrisk
oftransfusionrelatedviruses.
viii. Withanemiaanddecreasedhemoglobin,oxygentransportisdecreased,thusmakingthepatientwithsystemicvasculardiseaseat
increasedriskforMIandstroke.
ix. Autotransfusionsystemsmaybeusedforreplacingintraoperativebloodloss.
e. Presenceofconcurrentdisease(preoperativemanagement)
i. ThepresenceofunderlyingCASADinpatientswithvasculardiseasehasbeenwelldocumented.
ii. ReportsuggestthatCADexistsinmorethan50%ofpatientwhorequireabdominalaorticreconstructionandisthesinglemost
significantriskfactorinfluencinglongtermsurvivability.
iii. MIareresponsiblefor4070%ofallfatailitiesthatoccurafteraneurysmreconstruction.
f. Intraoperativemanagement
i. Anestheticselection:
1. Anestheticselectionshouldbebasedonthefollowingobjectives:providingoptimumanalgesiaandamnesia,
facilitatingrelaxaiotn,maintaininghemodynamicstability,preservingrenalbloodflow,andminimizingmorbidityand
mortality.

ii.

GA
1.
2.
3.
4.

iii.

RA

CirculatorystabilityisdesirableforpatientsundergoingAAAreconstrictuion,especiallyforthosewithCAD.
Highconcentrationsofinhalationagentsinpatientswithmoderatetoseveredecreasedejectionfractionshouldnotbe
usedbecausetheydepressthemyocardiumandcausehemodynamicinstability.
Becausethedegreeofmyocardialdepressionisdosedependendt,itisacceptabletoadministerinhalationagentsat
lowerinhaledconcentrations.
Cardiovascularstabilitycanbeprovidedbyoptiodsandisgoodforpatientswthischemicheartdiseaseandventricular
dysfunction.

1.
2.

g.

h.

Epiduralanesthesiaforabdominalaneursymectomiesiscommonlyconsidered.
Thebenefitsofepiduraluseincludedecreasedpreloadandafterload,preservedmyocardialoxygenationreducedstress
response,excellentmusclerelaxation,decreasedincidenceofpostoperativethromboembolism,increasedgraftflowto
thelwerextremieies,decreasedpulmonarycomplicationsandimprovedpostoperativeanalgesia.
3. Potentialdisadvantagesincludeanticoagulationandthepossibilityofepiduralhematoma,andiflocalanesthesiais
employedintraoperatively,severehypotensionduringbloodlossordeclamping.
4. Maintainingintravascularcolumemaybeanextremechallengeduringabdominalaorticresections.
5. Controversyexistsregardingwhethertheadministrationofcrystalloidsorcolloidsaffectstheoverallincidenceof
morbidityandmortality.
6. Crystalloidsmaybeusedforreplacingbasaland3rdspacelossesatanapproximaterateof10mL/kg/hr.
7. Bloodlossesinitiallycanbereplacedwithcrystallloidsataratioof3:1.
8. Combinationofcrystalloidandcolloidadministrationisacceptable.
9. Fluidreplacementshouldbesufficienttomaintainnormalcardiacfillingpressures,cardiacoutputandurineoutputof
atleast1mL/kg/hr.
iv. Combinationtechniques
v. Hemodynamicalterations
1. Expectfluctuationsinheartrateandbpsduringinductionqandintubation.
2. Preoperativereplacementoffluiddeficitspreventsexaggeratedresponsestovasodilatinginductionagent.
3. Forpatientswithadequateleftventricularfunction,hemodynamicstabilitycanbepreservedwithaslowinduction
usingopiodsandbetaadrenergicblockingagents.
4. Etomidatehasminimalmyocardialdepressantreffectsandmaybemostsuitableforpatientswithlimitedcardiac
reserve.
vi. Renalpreservation
1. Topreserverenalfunctionduringaorticcrossclampingincludemaintaintingadequatehydration,avoidsevereand
prolongedhypotension,andusingrenalprotectionagentssuhasmannitol,dopamine,furosemideandNacetylcysteine.
2. Withsuprarenalclampplacement,theuseofrenalcoldperfusionat5*Cofhypoosmolarcystalloidsolutioninstilled
intothekidneymaybeaneffectiverenalprotectionstrategy.
3. Thetheorizedmechanismisadecreasedinrenalmetabolicrateresultingina7%reductioninoxygenconsumptionfor
eachdegreeCelsiusdropintemperature.
4. Hoewever,thebestpredictorofpostoperativerenaldysfunctionisbasedonthepatientspreoperativerenalfunction.
Postoperativeconsiderations
i. Cardiac,respiratory,andrenalfailurearethemostcommoncomplicationsobservedposoperativelyinpatientsrecoveringfrom
abdominalaorticreconstruction.
ii. CardiovascularmonitoringmustbecloselymonitoredintheICUforatleast24hoursaftersurgery.
iii. MaintainingadequateBP,intravascularfluidvolume,andmyocardialoxygenationisparamountduringthisperiod.
iv. Mostpatientsrequireventilatorassistanceduringthepostoperativeperiod.
v. Vigilantmonitoringofrespiratoryfunctionismandatory,especiallywhenepiduralcathetersareusedforposoperateiveanalgesia.
Juxtarenalandsuprarenalaorticaneurysms
i.

Belowthekidneys(infrarenal)

ii.

Atthesamelevelasthekidneys(juxtarenal)

iii.

Abovethekidneys(suprarenal)

iv.
v.
vi.

i.

AlthoughmostAAAsoccurbelowtheleveloftherenalaretiers,2%extendproximallyandinvolvetherenalorvisceralarteries
Renalfailureoccursmoreoftenbecauseofsuprarenalaorticocclusion.
Maintainingadequateintravascularvolumeandadministeringosmoticandloopdiureticsmayminimizerenalischemiaand
dysfunction.
vii. Paraplegiaispossiblewhenthebloodsupplytothespinalcordisinterruptedbyaorticcrossclampingatorabovethelevelof
thediaphragm.
viii. IncreasingtheMAPordecreasingtheCSFpressurebyplacingacatheterinthesubarachnoidspacetodrainSCFmaybeusedas
ameanstoincreasespinalcordperfusionpressure.
ix. Totalbodyhypothermiaandmultimodalneurologicalmonitoringincludingsomatorsensoryandmotorevokedpotentialscanbe
usedtodecreasetheincidenceofparaplegia.
x. Neurologicdeficitscanbecomeevidentweeksaftersurgery.
RupturedabdominalAorticaneurysm

i.

II.

Ahighmortalityrateof8090%isassociatedwitharupturedAAA,whereaspostoperativemortalityisestimatedtorangefrom
4050%.
ii. EndovascularaorticrepairisbeingusedtotreatrupturedAAAsandmaydecreasetheoverallmortality.
iii. ThemostcommonsymptomsofrupturedAAsincludeatriadofsevereabdominaldiscomfortorbackpain,hypotension,anda
pulsatilemass.
iv. Othersymptomsinclude;
1. Syncope,groinorflankpain,hematuria,andgroinhernia.
v. RiskfactorsassociatedwithanincreaseinmortalityinpatientswitharupturedAAA
vi. Poorprognosis=hypotensionandahistoryofcardiacdisease.
vii. Cardgiovascularstabilityistheprimaryfocusuntilbloodlossfromtheproximalaortaiscontrolledbysurgicalintervention.
viii. Fluidresusciatationcanbeginwithcrystalloids;colloidsandbloodproductscanbeadministeredastheybecomeavailable.
ix. Coagulationstudiesandotherlabsincludeinghemoglobin,bct,andioniczedcalciumvaluesshouldbeobtained.
x. Largeamountsofcitrateusedasapreservativeinbankedbloodbindcalciumionsandresultinrelativehypocalcemia.
xi. Hypocalcemiacancausedecreasedmyocardialcontractilityasevidencedbyhypotension,increasedleftventricularenddiastolic
pressure,andincreasedCVP.
xii. Calciumchloridecanbeadministeredifhypocalcemiaoccurs.
xiii. Dilutionalthrombocytopeniaisthemostcommonreasonforcoagulopathytodevelopaftermassiveintravenousfluidandblood
administration.
xiv. TheuseofFFPhasbeenshowntodecreasethetotaltransfusionrequiremen5sandtheincidenceofcoagulopathies.
xv. Afterfluidresuscitationhasbeenperformedandhemodynamicstabilityhasbeenensured,directarterialBPmonitoringmustbe
instituted.
xvi. AcentralvenousorPACmaybeinserted.
Thoracicaorticaneurysms
a. Classification
i. Aneursmsofthethoracicaortamaybeclassifiedwithrespecttotype,shape,andlocation.
ii. Typically,aneurysmsinvolvingall3layersofthearterialwalltunicaadventitia,tunicamedia,andtunicaintimaareconsidered
tobetrueaneurysms.
iii. Falseaneurysmsinvolvethetunicaadventitiaonly.
iv. Theshapeofthelesionalsocanserveasameansofcharacterizinganeurysms.
1. Fusiformaneurysmshaveaspindleshapeandresultindilationoftheaorta.
2. Sacullaraneurysmsarespehericaldilationsandaregenerallylimitedtoonlyonesegmentofthevesselwall
3. Aorticdissectionistheresultofaspontaneoustearwithintheintimathatpermitstheflowofbloodthroughafalse
passagealongthelongitudinalaxisoftheaorta.
4. Thereare2majorclassifcationsshcemesofaorticdissectionbasedonthelocation.Theyarethedebakeyandstanfor
classiciations.
a. Debakey
i. TypeI:originatesintheascendingaortaandextendsatleasttotheaorticarchandoftentothe
descendingaortaandbeyond
ii. TypeII:originatesintheascendingaorta;confinedtothissegment
iii. TypeIII:originatesinthedescendingaorta,usuallyjustdistaltotheleftsubclavianartery,and
extendsdistally
b. Standford
i. TypeA:dissectionsthatinvolvetheascendingaorta(withorwithoutextensionintothedescending
aorta)
ii. TypeB:dissectionsthatdonotinvolvetheascendingaorta.

v.

b.

III.

IV.

Thoracoabdominalaorticaneurysmsareclassifiedusingthecrafordclassificationasshowninfigure254.
1. TypeIdistaltotheeleftsubclavianarterytoabovetherenalarteries.
2. TypeIIdistaltotheleftsubclavainarterytobelowtherenalarteres.
3. TypeIIIfromthe6thintercoastalspacetotherenalarteries
4. Type4fromthe13thintercoastalspacetotheiliacbifurcation
5. Types5belowthe6thintervostalspacetojustabovetherenalarteries.

Etiology
i. Atheroscelrosisisthemostcommoncauseofaneurysmalpathology.
ii. Atheroscleroticlesionsoccurmostofteninthedescendinganddistalthoracicaortanadaremostoftenclassifiedasfusiform.
iii. Lesscommoncausesincludeaorticdissectionandvariousmechanical,inflammatory,andinfectionsprocesses.Thevarious
causesofaorticaneurysmsareclassifiedinbox2q58.
c. Diagnosis
i. Symptomsrelatedtoaorticinsufficiencymaybeobservedinaneurysmsoftheascendingaorta.
ii. AnuppermediastinalmassmaybeanincidentalfindingonconventionalCXRinanasymptomaticpatient.
d. Treatment
i. Resectionoftheascendingaortaandgraftreplacementnecessiateatetheuseofcardiopulmonarybypass.Theaorticvalvealso
mayrequirereplacement.
ii. Surgicalresectionoflesionsinthetransversearchcompromisescerebralperfusion,althoughvariousbypasstechniques
combinedwithprofoundhypothermiaandcirculatoryarresthavebeenused.
Aorticdissection
a. Ischaracterizedbyaspontaneoustearofthevesselwallintima,permittingthepassageofbloodalongafalselumen.
b. Althoughthecauseofthedissectionisunclea,lesionsthatwerethoughttoberelatedtocysticnecroticprocessesmayactuallybecausedby
varioationsinwallintegreity.
c. HTNisthemostcommonfactorthatcontributestotheprogressionofthelesion.
d. Manipulationoftheascendingaortaduringcardiacsurgerymaybeassociatedwithaorticdissection.
e. TypeAdissctionshavethehighestincidenceofruputesandrequireimmediatesurgicalintervention
f. TuypeBmayinitiallybemanagedmedically,withtheadministrationofarterialdilatingandBadrenergicblockingagents.
Descendingthoracicandthoracoabdominalaneurysms
a. Preoperativeassessment
i. Mostpatientsdevelopingdescendingthoracicaortifcaneurysmareasymptomatic
ii. Operativesurgicaldecisionsarebasedonthesize,extent,andrateofexpansionoftheaneurysm.
iii. Forpatientswithdegenerativeaorticdisease,surgicalrepairisadvisedfornaeurysms6cmorlarger.
iv. Specialattentionshouldbedirectedtowardcardiac,renal,andneurologicfunction.
v. Althoughmostfatalitiesrelatedtothoracicaorticsurgeryarecardiacinorigin,renalandneurologicdysfunctioncontributeto
poorsurgicaloutcomes.
vi. Preoperativerenaldysfunctionisdirectlyrelatedtopostoperativerenalfailureandisthoughttobeoneofthestrongest
contributorstorenaldeteriorationaftersurgery.
vii. Neurolicfunctionshouldbecarefullyassessedinthepreoperativephase.Becauseparaplegiaisoneofthemostdevastating
consequesnecesofthoracicaorticsurgery,anyalterationinlowerextremityfunctionshouldbenoted.
viii. HoarsenessrelatedtocompressionoftheRLNshouldbeassessedanddocumented.
ix. LRLNismostsusceptibletodamagebecauseofitscloseproximitytotheaorticarch.
x. BilateralrecurrenltLNcompressionordamagecanresultinrespiratorycompromise.
b. Intraoperativemanagement
i. Monitoring

1.
2.

V.

Sameasabdominalanurysmectomies.
Iftheaneurysmsinvolvesthethoracicregionorthedistalaorticarch,rightradialarteriallinemonitoringispreferred
becauseleftsubclavianarterialbloodflowmaybecompromisedduringsurgery.
3. UseofTEEissuggestedforcardiacmonitoringinpatientswithmyocardialdysfunction.
4. Indwellingurinarycatheterisusedforassessingrenalfunction.
5. Tofacilitateexposingthedescendingthoracicaorta,adoublelumenentodtrachealtubeisinsertedtoallowforone
lungventilation.
6. Asaresult,carefulmonitoringofoxygenatonismandatory.
7. Routineuseofpulseoximetrymaybelimitediftheleftsubclavianarteryismanipulated.Thereforetherighthandthe
ear,orthenasalpassagesshouldbeusedformonitoringoxygensaturation.
8. LumbarintrathecalcatheterisinsertedtoaccessCSF.
9. SomatosenseoryevokedpotensialsorMEPSareoftenusedtomonitoranddeterctneurolicdysfunction.
ii. Spinalcordischmia
1. Theprimarypreoperativeriskfatorsfoedelayedparaplegiaincludetype2neurysms,emergencyprocedures,numberof
sacrifiecedsegmentalsegments,andrealfailure.
2. Themainposoperatiefactoresinflucedhemodynamicinstabilitycausedbyatrialfibrillation,bleeding,multiorgan
failure,andsepsis
3. Neurolicdeficitsaretheresultofhypoperfusiontothepsnalcordduringthoracicaorticreconstruction.
4. Thearteryofadamkieqiczalsoknownasthegreaterradicularartery,originatesfromanintercoastalbranchbetweenT8
toL2andprovidesthemajorityofbloodflowtotheanteriorspinalartery.
5. Theanteriorspinalofthearteryperfusesthevenrralaspectofthespinalcord,whichisresponsiblefofrmotorcontrol.
6. Althoughattemptsaremadetoremimplanttheintercostalbranchesthatcontributebloodflowtothespinalcord,these
effortsdonotalwaysdecreasetheincidenceofparaplegia.
7. Severaltechniqueshavebeensuccessfulinanefforttodecreasetheincidenceofneurlicdysfunctionafterthoracic
aorticsurgery.
8. TheseincludeSSEPandMEPmonitoring,CSFdrainage,hypothermia,reattachmentofintercostalarteries,anddistal
aorticperfusion.
9. Systemichypothermianadselectivecoolingofthespinalcordmaylengthenischemictimeintervals;hoever,the
clinicalbenefitsofthesehypothermiamethoedsareunclear.
10. SpinalcordperfusionpressurecanbeestimatedbycalculatingthearterialbloodpressureminustheCSFpressure.
11. Duringaorticclamping,CSFpressureincreaseswhilearterialpressuredecreasesdistaltotheclamp.
12. ThespinalcordperfusionppressurecanthereforebemanipulatedbyalteringarterialBPandrainingCSFthorughthe
interathecalcatheter.
13. IfwemodifyarterialpressureanddecreaseCSFpressurewecanmanipulatespinalcordperfusionpressure.
iii. Renaldysfuynction
1. Theincidenceofrenaldysfunctionafterthoracoabdominalaorticresectionisestimatedtobebetween1020%.The
majorcausesofrenalinsufficiencyistypeandsizeofaneurysmaldisease,ischemictime,andthedegreeof
preoperativerenaldysfunction.
iv. Anestheticmanagement
1. Sameasabdominal
v. Postoperativeconsiderations
1. IfadoublelumenETTwasused,itshouldbereplaedwithastandardendotrachealtubetoprovideasecureairway
sincepostoperativeventilatorassistanceisusuallyrequired.
2. Airwayanatomymaybeedematousduringsurgery,causingdifficultywithventilationandreintubation.Undertehse
circumstances,,doublelumenETTmaybeleftinplace.Replafementcanproceedinthepostoperativeperiodafter
airwayedemaisdissipated.
3. Epidruarlanalgesiausinglocalanestehtics,narcotics,orbothcanbeadministeredforpainrelief.
Endovascularaorticaneurysmrepair
a. Firstendovascularstentwasperformedtorepairaninfrarenalaorticaneurysmin1991.
b. Endovascularaorticaneurysmrepairwasinitiallydevelopedtohelppatientswithseverecoexistingdiseasewhowerenotconsideredtobe
surgicalcandidates.
i. Procedure
1. Endovascularaorticaneurysmrepairinvolvesthedeploymentofanendovascularstentgraftwithintheaorticlumen.
Thegraftrestrictsbloodflowtotheportionoftheaortawheretheaneurysmexcists.
2. ThispressurecanbeperformedforpatientshwohavedescendingthoracicaorticaneurysmsorAAAs.Cannulationof
bothefemoralarteriesisperformed
3. Afuidgwireisthreaededthroughtheiliacarterytotheleveloftheaneurysm.Asheathisinsertedovertheguidewire
andpositionedattheaneurysmlocationthorughtheuseoffluoroscopy.
4. Theproximalendofthesheathmustextendbeyondtheaneurysm.
5. Oncethesheathisdeployed,radialforceorfixationmechanismssuchashooksorbarbsonthestentbecomeembedded
intotheaorticwalltopreventstenmigration.
6. Theprocedurefrequentlytakesplaceinaninterventionalradiologysuite.
7. Comparedwiththeconventionalsurgicalmethod,advantagesoftheendovascularapproachincludenoaorticcross
clamping,improvedhemodynamicstability,decreasedincidenceofembolicevents,decreasedbloodloss,reduced
stressresponse,decreasedincideneofrenaldysfunctionanddecreasedpostoperativediscomfort.
8. Systemicanticoagulationwithheparin,50100units/kgisadministeredpriortocathetermanipulation.
9. Antibioticcoverageisrecommendedatthebeginningofsurgery.

10. Theanesthetictechniquesthatcanbeusedforevarincludegeneralanesthesia,neuraxialblockade,orlocalanesthesia
withsedation.
11. ComplicationsfromEVARapproachincludeendograftthrombosis,migrationorrupture,graftinfection,iliacartery
rupture,andlowerextremityischemia.
12. Endovasculargraftdesignanddurabilitycontinuetoimprove.
13. Graftdevicesareeitherunibody(comesinonepiece)ormodular(comesinmulstiplepieces).
14. Theendograftfabriciseitherwovenpolyester(Dacron)orpolytetrafluoroethylene.
15. Endoleakisaseriouscomplicationwithendovasculargraft.Endoleadisapersistentbloodflowandpressurebetween
theendovasculargraftandaorticaneurism
16. Differenttypesofendoleaksx
a. TypeI:attachmentsiteleak
b. TypeIIbranchleak(lumbarartery,renalartery,internaliliacartery,
c. TypeIIIgraftdect(fabrictear)
d. TypeIV:graftwallfabricporosity
e. ENdotension:systemicpressureinaneuryssacdespitenoevidenceofendoleakds.

VI.
1.
2.
3.
4.

VII.

MostaretypeIIand70%spontaneouslyclosewithinthe1stmonthafterimplantation.
TypeIIendoleaksarecausebycollateralretrogradeperfusion.
TypeIandIIendoleaksarecausedbydevicerelatedproblems.
Mostcommonfrequentinterventionsusedtocorrectthesecomplicationsincludeimplantationofasecondendograftor
openrepair.
5. ContrastCTarerecommendedat1,6,12,18monthspostoperativeandthenannually.
6. Lilfelongradiographicevaluationandsurveillanceisnecessarytomonitoraneurysmsize,graftmigration,andendoleak
7. Intensivefollowupcare,theneedforreinterventionsnadthecostoftheendograftmakeEVARmoreexpensivethan
openrepair
Cerebrovascularinsufficiencyandcarotidendarteractomy
a. CarotidendarterectomyisthesecondmostcommonvascularoperationperformedintheUS(firstbeingcoronaryrevascularization).
b. CVA,orstrokes,arethe3rdleadingcauseofdeathintheUS.Moststokesarecausedbycerebralischemiaascomparedwithintracranial
hemorrhage.
c. Incarotidatheroscleroticdisease,subintimalfattyplaquescanincreaseinsizeovertimeandincrementallyoccludethevascularlumen,
whichresultsindecreasedcerebralbloodflow.
d. Theplaquemayruptureandreleasefibrin,calcium,cholesterol,andinflammatorycells.Thisphenomenoncanleadtoabruptocclusionof
thelumenfromthrombosisduetoplateletactivation,oranembolusmayformanddecreasecerebralbloodflowdistaltothecarotidartery.
e. Ineachscenario,anabruptdecreaseincerebralbloodflowleadstoTIAorstrokes.
f. Cartoridendarterectomy,thesurgicalprocedureinwhichtheinternalcarotidarteryisincisedandtheplaquewithinthecarotidarterial
lumenremovedtoimprovecerebralbloodflow.
i. Indications
1. TheinitialindicationforCEAwassymptomaticstenosisbutnotcompleteocclusivecarotiddisease.
2. Thispresentationoccursinmostpatientswhoundergocarotidsurgery.
ii. Morbidityandmortality
iii. Patientselection
1. ThosepatientswhohavethegreatestbenefitfromCEAarethosewithstenosisofgreaterthan70%anditisoflesser
benefitinsymptomaticpatientswith5069%stenosis.
2. Surgicalinterventionwasmostbeneficialinmenwhoareolderthan75yearsofageandwithin2weeksoftheirlast
ischemicevent.
iv. Diagnosis
1. Amaurosisfagux,ormonocularblindess,occursin25%ofpatientswithhighgradecarotidarterystenosis.This
syndromeisbelievedtobecausedbymicrothombithattravelintotheinternalcarotidarteryanddecreasetheblood
supplyoftheopticnerveviatheophthalmicartery.
2. Duplexultrasonographydigitalsubtractionangiographycomputedtomographicangiographyandmagnetic
resonsenanceangiography(MRA).
v. Preoperativeassessment
1. TheprecenseofconcurrentCADandcartoridstenosisiswelldocumented.
2. AthothoughstrokeisadevastatingconsequenceofCEA
vi. Intraoperativeconsiderations

1.

vii.

viii.

ix.

Cerebralphysiology
a. Cerebralbloodflowcanremainrelativelyconstantatdifferentcerebralperfusionpressuresasaresultof
cerebrovascularautoregulation.
b. CerebralperfusionpressurecanbeexpressedasthedifferencebetweenMAPandICP.
c. DuringCEA,intracranialpressureisusuallynotelevated;therefore,MAPplaysthepredominantrolein
determiningCPP.
d. WhenMapismaintainedbetween60160mmHg,CBFremainsconstant.
e. However,theadverseeffectsofchronicsystemicHTNshiftthepatientscerebralautoregulatorycurcveotthe
right,andthereforeahigherthannormalMAPmayberequiredrtoensureadequatecerebralperfusion.
f. NormalCBFisapproximately50mL/100g/min.
g. Neuronalfunctionisgenerallymaintainedatlevelsgreaterthan25mL/100g/min.
h. Levelslessthathiscriticalvaluejeopardizecellularfunction.Decreasedperfusionandischemiacanbe
reflextedinchangesinconsciousness.Cellulardeathoccursatlevelslessthan6mL/100g/min,asevidenced
byflatteningseenonanEEG
i. DuringCEAtheanesthetifcgoalsmustfocusonimprovementandpreotectionofCBFanddiligent
monitoringofbrainfunction.
2. Cerebralmonitoring
a. Carbondioxidehasapotenteffectoncerebrovasculartone.
i. Hypocapniadecreases
ii. HypercapniaincreasesCBF
iii. Normocapniaisparamount.
b. Duringrepairthecarotidarterycrossclampisapplied.
c. CerebralmonitoringmodalitiesduringGAforCEA
i. EEG:assessescorticalelectricalfunction
ii. SSEP:assessessensoryevokedpotentials
iii. Carotidstumppressure:assessesperfusionpressureintheoperativecarotidartery
iv. TranscranialDoppler:assessesbloodflowvelocityinthemiddlecerebralartery
v. Cerebraloximtery:assessescerebralregionaloxygensaturation.
d. Themostsensitiveandspecificmeasureofadequatecerebralbloodflowisresponsivenessinanawake
patient.
e. EEGmonitoringconstitutesthegoldstandardinidentifyingneurologicdeficitsrelatetocarotidarterycross
clamping.
f. EEGhasdemonstratedreliabilityinmonitoringcorticalelectricalfunction
g. LossofBetawaveactivity,lossofamplitude,andemergenceofslowwaveactivityallareindicativeof
neuroligcdysfunction
h. Carotidstumptpressurehasbeenusedasameansofassessingcollateralflow.Afterthecarotidcrossclamp
isplaced,distalpressureintheoperativeinternalcarotidarteryismeasure.Acarotidsttmppressureofless
tha4050mmhgreflectsneurologivchypoperfusionandisacriterionforshuntplacement.
i. Complicationswithshuntplacementisemobilizationandinjurytotheartery.
3. Cerebralprotection
a. GoaltomaintainCBFanddecreasecerebralischemia
b. CanpreventCIbyincreasingcollateralfloworbydereasingcerebralmetabolicrequirements.
c. Avoidhyperflycemia,hemodilutionkmaintenanceofnormocarbia,andtightcontrolofarterialbloodpressure
toprotectcerebrum.
4. Cerebralmetabolism
a. Propofoldecreasescerebralmetabolismby40%.
b. Dexmedetomidinealsodecreasescerebraloxygenconsumptionandcerebralbloodflow.
c. AvoidNitrousoxide.
BPcontrol
1. Allpatientsshouldcontinuetotaketheirpreoperativeantihypertensivemedicationsuntiltimeofsurgery.
2. PtswithBP>180mmHgmaybeatincreasedriskofstrokeanddeath.
3. Theuseofpharmacologicadjuncts,suchasshortactingBadrenergicblockers,maystabilizebloodpressureduring
inductionandemergence.
4. ContinuousintravenoususeofnitroglycerinorsodiumnitroprussideshouldbeavailabletotreatHTN.
5. PatientswithchronicHTNarepredisposedtodramaticdecreasesinBPaftertheinductionofgeneralanesthesia.This
conditionmustbetreatedpromptlyandcanbesucressfullymanagedbyprovidingIVfluidsoradministering
appropriatevasopressors.
6. Hypotensionandbradycardia,mayresultfromcarotidsinusbaroreceptormanipulation,maybeinhibitedbystopping
surgicalstimulationandinfiltratingwithalocalanesthetic.
Anestheticmanagement:GoalsspecifictoCEAincludemaintainingcerebralandmyocardialperfusionandoxygenation,
minimizingthestressresponse,andfacilitatingasmoothandrapidemergence.Goalistooptimizeperfusiontothebrain,
minimizemyocardialworkload,ensurecardiovascularstability,andallowforrapidemergence.
1. Anestheticselection
2. Regionalanesthesia
3. Generalanesthesia
Postoperativeconsiderations
1. InpostoperativeperiodmostcommonproblemisHTN

2.
3.

VIII.

SBPgreaterthan180mmHgisassociatedwithanincreasedriskofTIA,stroke,orMI
PostoperativehypotensionislesscommonbutcanbeamoredifficultproblemtotreatbecauseraisingtheBPtoomuch
mayundulystresstheheart.
4. Reestablishingnormalpressurescanbeaccomplishedbycarefultitrationoffluidsandvasopressors.
5. Hemorrhagecanoccurtothecarotidarteryrequiresquickintervention
6. Respiratoryinsufficiencycanbeproblematic.
7. Tensionpneumocanoccurbecausetheapicesofthelungsextendabovetheclaviclestowardthesurgicalsite.
8. Cerebralhyperrperfusionsyndromemayresultfromincreasedbloodflowtothebraincasaresultoflossofcerebral
vascularautorregulation.Themechanismofactioncausingthisphenomenonisunclea;however,itishypothesizedthat
CHSmayoccurasaresltofchroniccerebralischemiaoralteredcerebrovascularautoregulation.Signsandsymptoms
ofCHSincludesevereheadache,visualdistrubancesALCC,seizzures.
Carotidarteryangioplastystenting
a. PriortoCASprocedure,patientsreceiveanaorticarch,carotid,andcerebralangiogramorahighresolutionMRI.
b. Thisallowsevaluationoftheindividualanatomyandangiopathologyoftheaorticarch.Determinationofthetypeofsheaths,stents,and
cerebralembolicprotectiondevicecanthenbeplanned.
c. Femoralarteryaccessisobtained,thenasheathisthreadedthroughthearoticarchandintotheoperativecarotidartery.
d. Theguidwire/embolicprotectiondeviceisadvancedthroughthesheathandpositionedacrossthestenoticregion.
e. Anembolicprotectiondevicesequestiersemboliduringangioplastyandstentingtoavoiddistalocclusionincerebralarteries.
f. Adistalembolicprotectionlowerstheriskfofintraoperativeandpostoperativeadverseevents.
g. Thisfilerlikedeviceisinserteddistaltotheareaofstenosispriortotheangioplastyandstentdeploymenttocatchmicrothrombiandpieces
ofplaquethatcouldlodgewithinthebrain.
h. Angioplastywitha5mmballoondilatesthecarotidartery,thenthestentisdeployed.Theguidwire/devicewireisremovedafter
angioghraphicconficmationthatcarotidarterydissectionorocclusionhasnotoccurred.
i. Anestheticconsiderations
1. TheanesthetictechniqueusedmostoftenforpatientshavingCASislocalanesthesiaatthefemoralinsertionsiteand
minimalsedation,antithrombotictherapy,andobservationforhypotentionandbradycardia.
2. Anticoagulationisinitiatedwithaheparinbolus,50100units/kgtomaintainactivatedclottingtime(ACT)atgreater
than250seconds.
3. Ballooninflationintheinternalcarotidarterycanstimulatethebaroreceptorresonse,resultinginprolongedbradicardia
andhypotension.
4. Glycopyrrolateoratropinecanbegivenpriortoinflationtooffsetthisvagalresponse.
5. Fluoroscopywillbeusedthroughoutthesurgery,soitisimportantthatalloperatingroompersonalareprotectedwith
leadshielding.
6. ComplicationsassociatedwithCoronaryarterystenting(CAS):
a. Stroke,
b. MI
c. Bradycardia
d. Hypotension
e. Deformationofexpandablestent
f. Stentthrombosis
g. Hornersyndrome
h. Cerebralhyperperfusionsyndrome
i. Carotidarterydissectioncarotidcarterydissection
j. Carotidarteryrupture
k. Hemorrhageresultingfromanticoagulation.
7. OnlytreatementapprovedforacuteischemicstorokeisIVrecombinanttissueplasminogenactivator.
8. Acarotidduplexscanisperformedpriortodischarge,andthenroutinelyobtainedat6wks,6mtns,1yearandthen
yeartly.

9.

PtswillremainonASAandanticoagulationforlife.

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