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FIGURE20.1 A,Gasgangrenevisiblewithradiolucencybyfirstmetatarsophalangealjoint.B,Statuspostpartial
firstrayresectionwithexcisionaldebridementofallnonviablesofttissueandbone.C,Postoperativeday2.
Peripheralneuropathyisthemostcommoncauseoffootulcerations,withdiabetesmellitusbeingthemost
commoncauseofneuropathy.1Othercausesalso exist,includingmetabolic,toxins,viralandbacterial
infections,genetics, ischemia,andinflammatory conditions.Patientswithdiabeteshavea15% lifelong
incidenceofdevelopingfootulcers, resultinginover 50%ofnontraumaticlowerlimb amputations.
2-6
Reducedvascularperfusionanddecreasedoxygentothelowerlimbdiminishesthebody’sabilitytoheal
suffocatedwoundsites,leadingtoprolongedexposureofopentissuetobacteriaandincreasedlikelihood
of bone and soft tissue infection. Additionally, abnormal perfusion of blood to the foot can lead to
weakeningof bones.Combiningweakened bones and neuropathycanlead to Charcotneuroarthropathy
andmajordeformitiesatriskforwoundsandinfections,increasingthethreatformajorlowerextremity
amputation.
7,8
II.InfectionControl
A.RiskFactors
Infection, particularly of an ulcer site, is a significant risk factor for lower extremity amputation.
4,5
Infectionscancauseadelayinwoundhealingwithdeteriorationofthesurroundingtissue.9Causesfor
lower extremity infections include vascular impairment, neuropathy, and decreased resistance to
infection.
9-12
B.Antibiotics
Control of infection is typically via culture-guided antibiotics. Severe infections require intravenous
antibioticswithprophylacticpolymicrobialcoveragepriortocultureresultsincludinggram-positiveand
gram-negativeanaerobesandaerobes.13Asdeepwoundculturesbecomeavailable,antibioticcoverage
canbenarroweddependingongrowth.Mildsofttissueinfectionsgenerallyrequire2weeksoftherapy.
14
Deepersofttissueinfectionsmayrequireupto2monthsoftreatment.14Osteomyelitisrequires6weeks
orlongerofanantibioticregimeninadditiontosurgicalbonedebridement.15Prolongedulcerationsover
osseousprominencesshouldbeevaluatedforosteomyelitis.Improperfootwearisthemostcommoncause
ofneuropathiculcerations,particularlywhenbonyprominencesorfootdeformitiesexist.
16
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C.Examinations
A biomechanical examination and wound offloading removes abnormally high-pressure areas in a
neuropathic patient. Techniques for offloading include accommodative inserts, total contact casting,
braces,andtheuseoffelt.Computerizedgaitanalysiseffectivelyassesseshighpedalpressurelocations,
leadingtoincreasedorthoticcustomization.Studiesfoundthattotalcontactcastinghealsulcerationsfaster
thanhalf shoesandremovablecasts.17Patientsgivenaremovablecastwerefoundtowear itforonly
28% oftheir steps.18Patients undergoing total contactcasting have increased healing asdemonstrated
histologicallywithevidenceofangiogenesisandformationofgranulartissueascomparedwithpatients
treated with debridement alone.19 Contraindications to nonremovable casts include infection and/or
ischemic wounds. Offloading via surgical procedures, such as exostectomies, tendon lengthenings or
transfers, fusions,osteotomies,applicationofexternalfixation,and/oramputationsmaybe requiredfor
adequate offloading of sites and ultimate wound reduction and prevention. Advanced wound healing
productscanalsobeattempted.
D.Osteomyelitis
1.Osteomyelitis,whichonthefoottypicallyoccursatulcerativesiteswithboneprominencesoratdeep
infectionsites,isahighlydestructivecomplicationoftennecessitatinglong-termintravenousantibiotics,
surgical debridement, or amputation. The average 5-year patient survival rate after amputation in the
diabetic population is 39%.20 Surgically, eliminating thesource of infectionis the primarygoal. The
secondary goal involves salvaging the extremity for functional, efficient, and low energy ambulation.
During resection, specimens should be obtained of both the infected site and clean margins for
pathological and microbiological evaluation. Next, “dead space” must be managed to avoid further
complications,includinghematomasandcreationofareasallowingfurtherinfectiousreactions.
2.Sharpdebridementofulcerationsoff-loadssitesbyremovinghyperkeratosis,necrotictissue,foreign
material,andinfectiousorganisms.
15,21
Sharpdebridementshould includethe removal ofallnonviable
softtissueandboneuntilhealthygranularwoundbedsareobtained.Onceinfectionhasbeeneradicated,
woundscanbeclosedorcoveredwithprimarywoundclosure,splitthicknessskingrafts,localflaps,or
freeflaps.Ifvascularperfusiontotissuesarenotadequate,clostridialcollagenaseisusedforenzymatic
debridement of the wound site.22 Hydrocolloid and hydrogel dressings lead to autolysis of necrotic
tissues.
3.Avarietyofdressingoptionsforulcerationsareavailableandaredependentuponwoundetiologyand
patientcharacteristics.Treatmentofperipheraledemaisalsobeneficial.
4.Negativepressurewoundtherapy(NPWT)canbeusedtostimulateangiogenesisandtheformationof
granulartissue,decreasingoverallhealingtimeofwounds.
23,24
5. Ifvascular flow is the chiefissue delayingwound healing, revascularization should be attempted.
VascularassessmentincludesDopplerultrasound, duplexultrasound,anklebrachial index, toebrachial
index,andangiography.
25,26
Prakashetalfoundthatthepresenceofneuropathyincreasesfootulcerations
and the ischemia worsens the overall presentation.
27,28
Peripheral vascular disease in patients with
diabetes typically involves occlusive arterial lesions involving the femoral-popliteal segment and the
tibial arteriesbelowtheknee.28In thediabeticpopulation, chronichyperglycemia leads toendothelial
celldysfunction,resultingin anincreaseinthromboxaneA2andadecrease in vasodilators,leadingto
hypercoagulationandvasoconstriction.29Inpatientswithperipheralarterialdisease,graftsandbypasses
maybeindicated.Ifvascularinterventionsareindicated,theproceduresshouldbeperformedassoonas
possible to avoid further tissue degeneration distally. In situations that vascular interventions are not
feasible,amputationofthelimbmaybewarranted.
1
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III.AdvancedWoundHealing
A.Phases
Wound healing consists of three phases: acute inflammatory, proliferative, and maturation. The acute
inflammatoryphaseconsistsofvasoconstrictionofarteriolesandcapillaries,plateletaggregation,andthe
inflammatory cell cascade. The proliferative phase includes fibroblastic activity, extracellular matrix
reorganization, and angiogenesis.
30-32
The maturation phase involves the formation of scar tissues in
additiontothesynthesisandbreakdownofcollagen.Numerousadvancedwoundhealingtherapiesexist,
ranging from complex biologic dressings, stem cells, laser treatments, hyperbaric oxygen therapies,
negativepressurewoundtherapies(NPWT),splintthicknessskingraftsandflaps.
30,31
B.ExtracellularMatrix
Collagen-based modalities provide collagen, themajor protein inthe extracellular matrix. Sustainable
extracellularscaffoldsarecompromisedinulcerations,andtreatmentwithcollagenprovidesastructural
scaffold matrix to support extracellular components, increase fibroblast proliferation, mediate cell
migrationandorganization,andinhibitexcessiveMMPs.
15,33,34
C.NoninvasiveVascularStudies
1.Whenthereisconcernforlimbischemiaorvascularinsufficiencyinthefaceofachronicnonhealing
wound, noninvasive vascular studies can be obtained. Noninvasive vascular studies with preferred
parametersincludeanklebrachialindex(ABI)of<0.7,toebrachialindex(TBI)<0.4,ortranscutaneous
oxygen tension (TcPO2) levels <30 mm Hg. Abnormal values increase wound complications.
35-37
Arteriographycanbeperformedforevaluationofthearterialtree.Sixangiosomesexistinthefootand
ankle38:threefrom the posterior tibialartery,twofromtheperonealartery,andonefromthedorsalis
pedisartery.38Arteriographycandetermine ifanangiosomeisnotperfusedatan areaofulceration.It
alsoassistswithlocationofflapformationorincisionplacement.Ifrevascularizationcanbeperformed,
directrevascularizationofanulceration’sangiosomeyieldsahigherhealingrateofwoundhealing.39If
revascularizationcannotbeachieved,hyperbaricoxygentherapycanbeattemptedwithischemicwounds.
It exposes patients to 100% oxygen at 2-3 times the normal atmospheric pressure, increasing the
saturationofoxygeninthebloodtodecreasehypoxiaandedemaandpromotewoundhealing.
40
2. After revascularization, when a healthy and granular wound bed is achieved, split thickness skin
grafting (STSG) can be performed. The procedure includes harvesting skin from a donor site and
transplantingittoarecipientsite.Duringthisprocess,theharvestedskinisseparatedfromitslocalblood
supplyandiscompletelydependentontherecipientsite’sbloodsupplyforsurvival(Fig.20.2).41Ifthe
typeofwounddoesnotindicateSTSGforclosureanddirectclosurecannotbeattained,flapclosurecan
beattempted.
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FIGURE20.2 Dorsalrightfootwoundtreatedwithexcisionaldebridement,STSGapplication,andnegative
pressuretherapy.A,Dorsalfootwound,(B)postsurgicaldebridement,(C)applicationofSTSG,(D)negative
pressuretherapy,(E,F)completionofwoundclosure.
3.Flapsaretissuesutilizedfortransplantationvascularizedbyastemorpedicle.
42
Flaps may include
epidermis,dermis,subcutaneoustissue,underlingfascia,ormuscle.Differentflaptechniquesutilizedin
plasticandreconstructiveinterventionsforwoundsincludeadvancement,rotational,andtranspositional
flaps(Fig.20.3).Fourmainfeaturesforconsiderationindeterminingincisionsforflapformationinclude
adequate exposure, adequate blood supply, sparingof sensory and motor nerves, and attention toskin
tensionlines.43Skinincisionsplacedperpendiculartoskintensionlinescanincreasescarcontractures.
These types offlaps are perfused by a perforator artery from the dermis tothe subdermal plexus and
differ from an axial flap, which has a direct cutaneous vascular supply. Angiosomes evaluation is
essentialasrandomflapsrelyonperforatorsforsurvival.
44
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FIGURE20.3 Rhomboidtranspositionalflap.A,Drawingflapoutpriortoincisiontoensureappropriateskintension
forclosureandmeasurementsforcoverage,(B)raisingtheflapfullthicknesstolevelofbone,(C)flapinsetwith
closure,(D)finalclosureappearance.
4.Chokevesselslinkadjacentangiosomesandcanbeusedtoenhanceperfusiontoanangiosome.
44
The
delayphenomenonresultsinthedilationofexistingchokevesselswithintheflapratherthananingrowth
ofnewvessels,increasingoverallperfusiontothesite.45Raisingtheflapcausesalocalsympathectomy
inthedelayphenomenon,leadingtovasodilation.44Distantaxialflaps,tissueexpansion,andfreeflaps
can be performed when split thickness skin grafting and local random flaps are not suitable. These
techniquesaremorecomplexwithincreasedriskformorbidity.
IV.Summary
Ischemia,trauma,gasgangrene,septicjoints,necrotizingfasciitis,anddeformitiesandulcerationsleading
toinfectionsandosteomyelitiscanhavedetrimental effectsofthelower extremity.Salvagingthelower
extremityforfunctional,efficient,andlowenergyambulationistheultimategoalaftertreatingtheprimary
source for an at risk foot. When ischemia is leading to the pedal complications, the limb requires
evaluation to determine whether efficient blood flow exists for tissue oxygenation. If inefficient flow
exists, revascularization should be attempted. If revascularization is unable to be attempted or is
ineffective, modalities, including hyperbaric oxygen, can be used. When open wounds exist without
infectionandare delayedinclosure,negativepressurewoundtherapy, collagen-basedmodalities, skin
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grafts,andskinflapscanbeutilizedtoattemptclosurepriortonewinfectionagainputtingthefootatrisk
foramputation.Limb salvageis nottypicallya one-stagesurgical procedureandmay require multiple
interventionsbeforedesiredresultsareattained.Ultimately,inadditiontoaskilledmultispecialtyhealth
careteam,extensiveamountsoftimeandcompliantpatientswithpostoperativeprotocolsarenecessaryto
achievelimbsalvage.
References
1.SumpioBE.Footulcers.NEnglJMed.2000;343:787-793.
2.BoultonAJ,ArmstrongDG,AlbertSF,etal.Comprehensivefootexaminationandriskassessment:areportofthetaskforceofthefoot
careinterestgroupoftheAmericandiabetesassociation,withendorsementbytheAmericanassociationofclinicalendocrinologists.
DiabetesCare.2008;31(8):1679-1685.
3.ReiberGE,LipskyBA,GibbonsGW.Theburdenofdiabeticfootulcers.AmJSurgery.1998;176(suppl2A):5S-10S.
4.ReiberGE,VileikyteL,BoykoEJ,etal.Causalpathwaysforincidentlower-extremityulcersinpatientswithdiabetesfromtwosettings.
DiabetesCare.1999;22:157-162.
5.PecoraroRE,ReiberG,BurgessEM.Pathwaystodiabeticlimbamputation:basisforprevention.DiabetesCare.1990;13:513-521.
6.EnerothM,ApelqvistJ,StenstromA.Clinicalcharacteristicsandoutcomein223diabeticpatientswithdeepfootinfections.FootAnkle
Int.1997;18:716-722.
7.LeeL,BlumePA,SumpioB.Charcotjointdiseaseindiabetesmellitus.AnnVascSurg.2003;17(5):571-580.
8.KnoxRC,DutchW,BlumeP,SumpioBE.Diabeticfootdisease.IntJAngiol.2000;9(1):1-6.
9.LipskyBA,BerendtAR.Principlesandpracticeofantibiotictherapyofdiabeticfootinfections.DiabetesMetabResRev.2000;16:(suppl
1):S42-S46.
10.LaingP.Thedevelopmentandcomplicationsofdiabeticfootulcers.AmJSurg.1998;176(2Asuppl):11S-9S.
11.CaputoGM,CavanaghPR,UlbrechtJS,GibbonsGW,KarchmerAW.Assessmentandmanagementoffootdiseaseinpatientswith
diabetes.NEnglJMed.1994;331:854-860.
[a]
12.ShahBR,HuxJE.Quantifyingtheriskofinfectiousdiseasesforpeoplewithdiabetes.DiabetesCare.2003;26:510-513.[b]LipskyBA,
BerendtAR,DeeryG,etal.Diagnosisandtreatmentofdiabeticfootinfections.IDSAGuidelinesforDiabeticFootInfectionsCID.
2004;39:885-910.
13.JoshiN,CaputoGM,WeitekampMR,KarchmerAW.Infectionsinpatientswithdiabetesmellitus.NEngJMed.1999;273:721-723.
14.SumpioBE.Contemporaryevaluationandmanagementofthediabeticfoot.Scientifica.2012:435487.
15.LipskyBA,BerendtAR,CorniaPB,etal.2012InfectiousdiseasesocietyofAmericaclinicalpracticeguidelinesforthediagnosisand
treatmentofdiabeticfootinfections.ClinInfectDis.2012;54(12):e132-e173.
16.MacfarlaneRM,JeffcoateWJ.Factorscontributingtothepresentationofdiabeticfootulcers.DiabetMed.1997;14:867-870.
17.ArmstrongDG,NguyenHC,LaveryLA,vanSchieCH,BoultonAJM,HarlessLB.Off-loadingthediabeticfootwound:arandomized
clinicaltrial.DiabetesCare.2001;24:1019-1022.
18.ArmstrongDG,LaveryLA,KimbrielHR,NixonBP,BoultonAJM.Activitypatternsofpatientswithdiabeticfootulceration:patients
withactiveulcerationmaynotadheretoastandardpressureoff-loadingregimen.DiabetesCare.2003;26:2595-2897.
19.PiaggesiA,ViacavaP,RizzoL,etal.Semi-quantitativeanalysisofthehistopathologicalfeaturesoftheneuropathicfootulcer:effectsof
pressurerelief.DiabeticCare.2003;26:3123-3128.
20.TentolourisN,Al-SabbaghS,WalkerMG,BoultonAJ,JudeEB.Mortalityindiabeticandnondiabeticpatientsafteramputations
performedfrom1990to1995:a5-yearfollow-upstudy.DiabetesCare.2004;27(7):1598-1604.
21.SteedDL,DonohoeD,WebsterMW,LindsleyL.Effectofextensivedebridementandtreatmentonthehealingofdiabeticfootulcers.
JAmCollSurg.1996;183:61-64.
22.TallisA,MotleyTA,WunderlichRP,etal.Clinicalandeconomicassessmentofdiabeticfootulcerdebridementwithcollagenase:results
ofarandomizedcontrolledstudy.ClinTher.2013;35(11):1805-1820.
23.WagnerFW.Thediabeticfoot.Orthopedics.1987;10(1):163-174.
24.BusSA.Offloadingthediabeticfoot;evidenceandclinicaldecisionmaking.EWMAJ.2012;12(3);13-15.
25.SumpioB,ThakorP,MahlerD,BlumeP.Negativepressurewoundtherapyaspostoperativedressinginbelowkneeamputationstump
closureofpatientswithchronicvenousinsufficiency.Wounds.2011;23(10):301-308.
26.ParkSC,ChoiCY,HaYI,YangHE.Utilityoftoe-brachialindexfordiagnosisofperipheralarterialdisease.ArchPlastSurg.
2012;39(3):227-231.
27.PrakashSS,Krishnakumar,PrabhaC.Theinfluenceofperipheralneuropathyandperipheralvasculardiseaseintheoutcomeofdiabetic
footmanagement–aprospectivestudy.IntJMedResHealthSci.2014;4(2):258-264.
https://t.me/med1917

28.LoGerfoFW.Peripheralarterialocclusivediseaseandthediabetic:currentclinicalmanagement.HeartDisStroke.1992;1(6):395-397.
29.ParaskevasKJ,BakerDM,PompellaA,MikhailidisDP.Doesdiabetesmellitusplayaroleinrestenosisandpatencyratesfollowing
lowerextremityperipheralarterialrevascularization?Acriticaloverview.AnnVascSurg.2008;22(3):481-491.
30.SnyderRJ,KirsnerRS,WarrinerRA,LaveryLA,HanftJR,SheehanP.Consensusrecommendationsonadvancingthestandardof
carefortreatingneuropathicfootulcersinpatientswithdiabetes.OstomyWoundManage.2010;56(4suppl):S1-S24.
31.GarwoodC,SteinbergJ,KimP.Bioengineeredalternativetissuesindiabeticwoundhealing.ClinPodiatrMedSurg.2015;32(1):121-
133.
32.EnnisWJ,LeeC,GelladaK,CorbiereTF,KohTJ.Advancedtechnologiestoimprovewoundhealing.PlastReconstrSurg.
2016;138:94-104.
33.AmberM,GazesM,BlumeP.Assessingcollagen-basedmodalitiesfordiabeticfootulcerations.PodiatryToday.2016;29(5).
34.BakkerK,ApelqvistJ,LipskyB,VanNettenJ.The2015IWGDFguidancedocumentsonpreventionandmanagementoffoot
problemsindiabetes:developmentofanevidence-basedglobalconsensus.DiabetesMetabResRev.2016;32(suppl1):2-6.
35.AttingerCE.Useofsofttissuetechniquesforsalvageofthediabeticfoot.In:KominskyS,ed.MedicalandSurgicalManagementof
theDiabeticFoot.St.Louis:Mosby;1994:323-366.
36.AttingerC,BulanEJ,BlumePA.Pharmacologicalandmechanicalmanagementofwounds.In:MathesSJ,ed.Plasticsurgery.Vol.1.
St.Louis:Elsevier;2006:863-899.
37.BenitezE,SumpioB,ChinJ,SumpioB.Contemporaryassessmentoffootperfusioninpatientswithcriticallimbischemia.SeminVasc
Surg.2014;27:3-15.
38.AttingerC,EvansK,BulanE,BlumeP,CooperP.Angiosomesofthefootandankleandclinicalimplicationsforlimbsalvage:
reconstruction,incisions,andrevascularization.PlastReconstrSurg.2006;117(7S):261S-293S.
39.NevilleR,AttingerC,BulanE,DucicI,ThomassenM,SidawyA.Revascularizationofaspecificangiosomeforlimbsalvage:does
thetargetarterymatter?AnnVascSurg.2009;23:367-373.
40.LipskyB,BerendtR.Hyperbaricoxygentherapyfordiabeticfootwounds.DiabetesCare.2010;33(5):1143-1145.
41.BarrattGE,KoopmannCF.Skingrafts:physiologyandclinicalconsiderations.OtolaryngolClinNorthAm.1984;17:335-351.
42.AlnaebME,BoutinA,CrabtreeVP,etal.Assessmentoflowerextremityperipheralarterialdiseaseusinganovelautomatedoptical
device.VascEndovascularSurg.2007;41(6):522-527.
43.BrobynTJ,CramerLM,HulnickSJ.Facialresurfacingwiththelimbergflap.ClinPlastSurg.1976;3(3):481-490.
44.BlumeP,DoneganR,SchmidtB.Theroleofplasticsurgeryforsofttissuecoverageofthediabeticfootandankle.ClinPodiatrMed
Surg.2014;31:127-150.
45.DharS,TaylorI.Thedelayphenomenon:thestoryunfolds.PlastReconstrSurg.1999;104:2079.
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C H A P T E R 2 1
PulmonaryVascularDiseasesandInterventions
EileenM.HarderMD
WassimH.FaresMD,MSc
I.PulmonaryVascularDisease
II.AcutePulmonaryEmboli
A.Epidemiology
B.RiskFactors
C.Pathophysiology
D.Classification
E.Presentation
F.Diagnosis
G.Treatment
III.PulmonaryHypertension
A.Definition
B.Epidemiology
C.PulmonaryArterialHypertension(WHOPHGroup1)
D.AtrialSeptalDefects
E.OtherFormsofPAH-CHD
F.PortopulmonaryHypertension
G.ChronicThromboembolicPulmonaryHypertension
IV.Conclusions
KeyPoints
■Depending onpatient comorbidities and theseverity ofthe insult,PEsmaycauseawide
varietyofsymptoms,rangingfromnonetodyspneatosuddendeath.
■PEscanbeclassifiedbymortalityrisk:high(massive),intermediate(submassive),andlow
(nonsubmassive).Thesegroupsaredefinedclinicallybycertainprognosticfactors.
■PEtreatmentdependsontheriskgroup.
■PHhasmanydifferentetiologies,andtheWorldHealthOrganization(WHO)separatesthis
diseaseintofivedifferentclasses.
■ThebestscreeningtestforanysuspectedPHistransthoracicechocardiography(TTE).
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■WHOgroup1PHispulmonaryarterialhypertension(PAH).Itcanbeidiopathic,heritable,
drugortoxinrelated,orassociatedwithcertainconditionsincludingcongenitalheartdisease
orportalhypertension.
■IfTTEsuggestsPAH,definitivediagnosisismadebyrightheartcatheterization(RHC).
■PAHtreatmentdependsonthecauseofPHanddiseaseseverity.Itofteninvolvesadvanced
medicaltherapy;certainformsofPAHmayrequiresurgery.
■WHOgroup4PHiscausedbychronicpulmonaryemboli(CTEPH).
ClinicalPearls
■High-riskPEsaredefinedbyhemodynamicinstability(sustainedhypotensionorshock).
■IntermediatePEsarehemodynamicallystablebuthaveevidenceofRVdysfunctionand/or
myocardialinjury.Allofthesefeaturesareabsentinlow-riskPEs.
■Inhemodynamicallyunstablepatients,PEcanbediagnosedbyTTE.Stablepatientsshould
undergoCTpulmonaryangiogram(CTPA).
■Patients with high-risk PEs should receive urgent treatment with systemic thrombolysis,
surgicalembolectomy,orcatheter-basedmethods,asappropriate.
■Intermediateandlow-riskPEsshouldreceiveanticoagulation.
■PAHonRHCisdefinedasameanPAP≥25mmHgwithpulmonaryarterywedgepressure
(PAWP)≤15mmHgandpulmonaryvascularresistance(PVR)>3Woodunits.
■Treatment of PAH may entail calcium channel blockers (for the small number of
vasoreactivepatients)oradvancedtherapy.
■Uncorrected atrial septal defects (ASDs) may also cause PAH. Patients with ASD-PAH
shouldundergoearlyclosure,providedthattheydonothaveEisenmengersyndrome.
■PortopulmonaryhypertensionisaformofPAHassociatedwithportalhypertension.Liver
transplantisindicatedinpatientswithmPAP<35mmHgandPVR<5Woodunits.
■CTEPHshouldbeconsideredinacutePEpatientswhosedyspneaandothersymptomsdo
notresolveafter3-6months.
■In suspected CTEPH, a positive TTE is followed by a ventilation/perfusion scan. RHC
and/orpulmonaryangiographyarerequiredtoconfirmthediagnosis.
■The only definitive treatment for CTEPH is pulmonary endarterectomy (PEA). Balloon
pulmonaryangioplastyoradvancedtherapymaybeconsideredinnon-PEAcandidates.
I.PulmonaryVascularDisease
Pulmonaryvasculardisease(PVD)referstoanydiseasethataffectsthepulmonaryvessels.Thetwomost
commonconditions are pulmonaryemboli and pulmonaryhypertension, and this chapter will focus on
thesediseasesandtheirmanagement.
II.AcutePulmonaryEmboli
A.Epidemiology
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Anacutepulmonaryembolus(PE)occurswhenapulmonaryartery(PA)oroneofitsbranchesbecomes
obstructed,mostcommonlybythrombus.TheincidenceofPEsisunknown,andthismaybeduepartlyto
underdiagnosis—silentPEsmayoccurinupto30%-50%ofdeepvenousthrombosis(DVT)cases,and
theyareoftenonlynotedincidentallyonautopsy.
1-3
Recentestimatessuggestthatthereareapproximately
600,000 PEs inthe UnitedStates per year, and it may contribute to death in up toone-third of these
patients.
4-7
B.RiskFactors
TherearemanyinheritedandacquiredPEriskfactors.Inheritedfactorsincludehypercoagulablestates,
such as factor V Leiden or prothrombin mutations, protein C or S deficiencies, and antithrombin
deficiency. Important acquired risk factors include older age,major or orthopedic surgery, leg or hip
fractures,cancer,immobility,spinalcordinjury,priorPE/DVT,obesity,pregnancy,oralcontraceptiveor
hormone replacement therapy, andantiphospholipid antibody syndrome, among others.
2,8
For patients
withDVTs,PEriskisparticularlyhighwithproximalthighclots.
C.Pathophysiology
PEsandDVTsaretypesofvenousthromboembolism,inwhichclotformationisbasedonVirchowtriad
ofvenousstasis,hypercoagulability,andendothelialinjury.Innormallungs,perfusionmatchesventilation
—hypoxic vasoconstriction occurs in poorly ventilated areas, and well-oxygenated regions remain
perfused.PEscreateaventilation-perfusionmismatch.Inthemostseverecases,perfusioniscompletely
absentandsystemicshuntingofdeoxygenatedbloodoccurs.
5,9
Thisresultsinhypoxemia,whichisfurther
worsenedbycytokinesthatpromoteinflammationandvasocontriction.9Compensatoryhyperventilation
occurs and as a result, respiratory alkalosis with low P
CO2
is usually present.9 Hypercapnia should
increasesuspicionforamassiveembolism.
9
PEs also cause circulatory dysfunction. Generally, hemodynamic abnormalities occur only when
≥30%-50% of the pulmonary arterial system is occluded, although even a small clot can cause
dysfunction in patients with heart and lung disease.
8,10,11
Obstructed vessels and the accompanying
vasoconstrictionofnormalvasculaturecauseasuddenriseinpulmonaryvascularresistance(PVR)and
acute pulmonary hypertension (PH).The increased afterloaddilatesthe rightventricle (RV), decreases
myocardial contractility, and diminishescoronaryvessel perfusion.12 A normal, nonweakened RV can
generatea systolicpressureupto 40 mmHg,but abovethisin theacute setting,RV failureoccurs.
11
Right-sided strokevolume (SV) and cardiac output(CO) are reduced. Asthe RV furtherstretches,the
septummovesintotheleftventricle(LV).Theendresultisdecreasedleft-sidedfilling,preload,andCO.
13
ThebodytriggersacomplexcompensatorycascadeincludingsympatheticactivationtoincreasePAflow
andpreservesystemiccirculation.8Dependingontheseverityoftheinsult,aPEcanmanifestasawide
spectrumoffindingsrangingfromnohemodynamicabnormalitiestoRVfailure,hypotension,andshock.
In the most severe cases, compensation is inadequate and sudden death occurs, often by pulseless
electricalactivityorasystole.
8,11
D.Classification
AlthoughPEscanbeclassifiedinmultipledifferentways,themostclinically relevantsystem stratifies
disease severity based on mortality risk—high, intermediate, or low.
2,11
These terms correspond to
massive,submassive,andnonsubmassivePEs,respectively.
High-risk(massive)diseaseisdefinedbythepresenceofsustainedhypotensionorshockinthesettingof
https://t.me/med1917
Соседние файлы в папке Библиотека им академика М.И. Перельмана
