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Thrombosed great saphenous vein aneurysm accompanied by venous thrombosis

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www.elsevier.es/rmuanl

SCIENTIFIC

LETTER

Thrombosed

great

saphenous

vein

aneurysm

accompanied

by

venous

thrombosis

F.G.

Rendón-Elías

a,∗

,

R.

Albores-Figueroa

a

,

L.S.

Arrazolo-Ortega

a

,

F.

Torres-Alcalá

a

,

M.

Hernández-Sánchez

b

,

L.H.

Gómez-Danés

a

aServiceofThoracicandCardiovascularSurgeryofthe‘‘Dr.JoséEleuterioGonzález’’,UniversityHospitaloftheUANL,Mexico bServiceofPediatrics,UMAE

·21,IMSSMonterrey,NuevoLeón,Mexico

Received14May2014;accepted22July2014 Availableonline23June2015

KEYWORDS

Greatsaphenousvein; Venousaneurysms; Vascular

malformations; Venousthrombosis

Abstract Superficialvenousaneurysmsofthelowerextremitiesareconsideredrareandtheir clinicalsignificanceispoorlydefined.Thepurposeofthisarticleistoreportacaseofa 72-year-old womanwithathrombosed greatsaphenousveinaneurysmalongwithdeepvenous thrombosisandreviewitsclinicalpresentation,diagnosisandtreatment.

©2014UniversidadAutónomadeNuevoLeón.PublishedbyMassonDoymaMéxicoS.A.Allrights reserved.

Introduction

Venousaneurysms(VA)areararevascularpathology. First describedbySirWilliamOslerin1913,1VAscanbelocated

anywherethroughoutthevenoussystemanddonothavea preferenceregardingsexorage.2

VAs are usually located in the lower extremities, and can be deep or superficial, depending on whether the affected vein is over or under the muscle fascia. Deep VAs are the most frequent, because the popliteal vein is the most commonly affected (between 60% and 70% of

Correspondingauthorat:ServiciodeCirugíaTorácicay

Cardio-vasculardelHospitalUniversitario‘‘Dr.JoséEleuterioGonzález’’, delaUniversidadAutónomadeNuevoLeón,Av.MaderoyGonzalitos S/N,CP.64460,Monterrey,NuevoLeón,Mexico.

E-mailaddress:[email protected](F.G.Rendón-Elías).

the cases), and the most studied because of their high thromboembolismrisk.3

SuperficialVAsarerare,withunder60reportedcasesin medicalliterature4 andaretakenless seriouslythan deep

VAs,due tothefactthatsuperficial VAsareconsidered to havealowriskoflife-threateningcomplications.

Thepurposeofthisarticleistopresentacaseofapatient affectedby athrombosed greatsaphenous vein aneurysm alongwithdeepvenousthrombosis.Additionally,the liter-atureisreviewedwithadiscussiononclinicalimplications andthediagnosticandtherapeuticapproachof thislesser knownvascularpathology.

Clinical

case

The patient is a 72-year-old female, with no positive background of chronic degenerative diseases or of any othertype,andanegativehistoryofsmoking.Thepatient

http://dx.doi.org/10.1016/j.rmu.2015.02.002

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Figure1 Reconstructedultrasoundimagewhichshowsaninternalsaphenousveinvenousaneurismof9×5cm,whichcompression

didnotremove.

presentedanincreaseinvolumeoftherightpelviclimb10 daysafterundergoing surgerytocorrect adirect inguinal herniausingtheBassini---Shouldice technique.The subject pointed out that for over 40 years she presented a soft tumorofapproximately10cm,locatedinthemiddlethird ofthemedialpartoftherightthigh22cmfromtheinguinal fold. The tumor was soft, palpable and painless with a variationinvolumedependingonthepositionanddidnot causeanydiscomfort. Subsequenttothe hernioplastythe patientbegannoticingthatthetumorhardenedandcaused pain,alongwithrednessandanincreaseinlocal tempera-ture,consequently thephysiciandiagnosedacellulitisand prescribedantibiotictherapy.Thesymptomatologydidnot improvewiththeprescribedtreatmentandnowpresented anincreaseinvolumeoftheentirepelvicmember.Shewas thereforereferredtoourservice.Duringtheexaminationa differenceof5cminvolumebetweenbothpelvicmembers wasobserved,noticingahard,non-mobile,painfullumpof 9×6cm.The restof the examination wasnormal. A

vas-cular ultrasoundwas performed, showing a non-palpable, anechoic growth,connectedto thegreat saphenousvein, of9×5cm(Fig.1)without the presenceof venous reflex

neitherinthe greatsaphenousnorin thesaphenofemoral junction.Moreover,a posterior tibialveinthrombosis was detected.Withagreatsaphenousveinaneurysmdiagnosis, thepatient wastransferredtosurgery where an aneurys-mectomyandSFJligationwereperformed(Figs.2and3).

Therewerenocomplicationsduringtheprocedure,the evolutionwasgoodandthepatientwasdischargedonthe secondpostoperativedaywithacompressiveand anticoag-ulantDVTtreatmentforaperiodof3months.

Discussion

The terminology used to describe venous dilatations can cause confusion. The terms phlebectasia, varicose vein and/or venous aneurysm are considered synonyms in the medicalcommunity;however,theymeandifferentthings. Phlebectasiais defined asa fusiform and diffusely dilated vein.Theassociationofdilatedandtortuousveinsisknown as varicose veins.5 There is no precise criteria regarding

sizeandwhenavenousdilationisconsideredananeurysm; however,Mateo6 andMcDevitt7established thatwhenever

Figure 2 Surgical excision of the internal saphenous vein venousaneurisms.

thevein’sdiameteristwiceaslargeasthenormal diame-ter,thenitisconsideredtobeananeurysm(thesaphenous vein’snormalsizeat thesaphenofemoraljointis3---5mm, 2---4mmatthethighand1---3mmattheankle).8

.

Neverthe-less,inordertoconsideritaprimaryvenousaneurysmsize is notthe onlyfactor considered. Itmust alsobe a local-izeddilation,conformedbythreehistologicallayerswhich constitutethenormalvenouswall.Thiscouldbesaccularor

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fusiform (animportant distinctionbecauseofits hemody-namicimplicationsthatinfluencethecourseoftreatment) andshouldonlycommunicatetothecorrespondingveinina proximalanddistalmannerandneitherbesecondarytoan arteriovenousfistula,9norberelatedtoavaricosevein.10

Hilschercoined the term primaryvenous aneurysm, mak-ingacomparisontoarterialaneurysms.Abbottwastheone whointegratedthecriteriatodefineVAs.11Ourpatientmet

therequired criteriatoclassifyhervenous pathologyasa primaryvenousaneurysm.

PrimaryVAsoccurintheheadandneck,thoracicand vis-ceralveinsaswellasveinsofthe extremities.Aneurysms of the deep venous system are characteristic on the extremities,whereagreaterincidenceofthromboembolic complicationsisreported.

Theincidenceofsuperficialvenousaneurysmsis approx-imately0.1%,12withaprevalenceof1.5%,13equallyinboth

sexesanditmayoccuratanyage.

Thepathogenesisofvenousaneurysmsisunknown; sev-eralmechanismshavebeenimplicatedinitsformation,such ashemodynamicchanges,arteriovenousfistulae, inflamma-toryprocesses,infections,trauma,congenitalweaknessof the venous wall and degenerative changes.5,14 The most

accepted theory states that it is a result of the loss of connective tissue components of the venous wall, which can be caused by a congenital defect or secondary to a degenerative process due toaging.15,16 In a recent study,

tissue from the wall of venous aneurysms was examined anditwasreportedthatstructuralchangesofthe aneurys-matic wall can be related tothe increased expression of metalloproteinase,17whichcanbetranslatedtoareduction

ofthemusclelayer,fragmentedelastictissue,anincrease inthefibroustissueandinfiltration ofinflammatorycells. SchatzandFine,18believedthatedophlebohypertophywas

a majorfactor in the formation of VA, which begins with anincreaseinvenousflowleadingtoahypertrophyofthe venouswall, thendilation andsclerosis.Pascarellaetal.4

informedthatsuperficialVAsonlowerlimbsweregenerally locateddistaltoanincompetentvenousvalve,whichcauses venousreflex,hittingthevenouswallandproducinga tur-bulentflow,causing structuralchanges onthe wallof the spleen,whilethoseindeepveinsaresecondarytointrinsic changesofthevenouswall.

The difference among findings in the reports suggests thattheetiologyofVAsisdiverseanddependsontheir loca-tionandnaturalhistory.16,19---22Inourcase,theetiologymay

come asaresultof acongenitaldefect in theconnective tissuestructure,whichgeneratedaweakvenouswall sus-ceptibletodilation,hencecontributingtotheonsetofthe inguinalhernia.

Accordingtotheetiopathogeny,VAscanbedividedinto primary (congenital) or acquired. Based on the Hamburg classificationfor congenital vascular malformations,23 VAs

correspondtoavenousmalformationofthetronculartype, which can be presented as aplasia, hyperplasia, stenosis (i.e.the leftiliac veinin May-Turnersyndrome),dilations oraneurysms(themostcommonbeingthepoplitealvein).24

CongenitalVAsarelesscommonbutcanoccurinanyvein ofthebody.Inastudy,Guillespieetal.,2reportedthat77%

of VAs were located in the lower extremities(57% in the deepvenoussystem),10%intheupperextremitiesand13% intheneck.

The clinical presentation of superficial VAs in lower extremitiesis that of a palpablesoft lump. It can change itssizeandlocationwiththebody’spositionortheValsalva maneuver;theycanbecompletelyasymptomaticorpainful withedema,andhavesignsandsymptomssimilartothose describedinourcase.

The diagnosis can be made by the clinical history and physical examination in most cases,but it is usually con-firmed by image studies. Within image studies, vascular ultrasoundis themethodofchoice forthestudy ofVAs.25

Intheultrasound,VAsarepresented asananechoic cystic structure,withwell-definedwalls,whichcanbesecularor fusiformandwithalowflowvolume;also,theyprovideus withinformationonvascularconnections,theexistenceof thrombosis,or if thereis an associated arteriovenous fis-tulaorany other pathologies,26 in additiontoguiding the

therapeuticapproach.TheCATscan,theMRIandthe phle-bography are studies which can be performed in case of diagnosticdoubtorwhenmoreexactinformationisrequired (size,extension, associatedlesionsand vascular origin).27

Clinicalhistoryandexaminationarethebasisfor reaching any diagnosis, but in the case of venous problems, vas-cular ultrasound evaluation is fundamental to reaching a correctdiagnosis,andthuschoosingthepropertreatment. Itis only in case of doubt,where further imagingstudies arerequired.Inthedifferentialdiagnosis,wemustconsider varicoseveins,softtissuetumors,hygromas,hemangiomas and, depending on location, inguinal hernias. Vascular aneurysmcomplicationsare:thrombophlebitis,deepvenous thrombosis, pulmonary embolism and bleeding caused by rupture.

CoagulationdisordersassociatedwithVAsare character-izedby blood stasisin thedilated vesselsandwitha low bloodflow,whichactivatesthecoagulationcascadewiththe subsequentproduction of thrombin andthe conversion of fibrinogenintofibrin.28,29Thenthefibrinolysisprocessbegins

which is reflected in the rise in fibrinogen derived prod-ucts,including D-dimer. This is the simplified description oflocated intravascularcoagulopathy whichcharacterizes coagulopathy associated with venous malformations.30,31

Newlyformed microthrombusattachtocalciumand phle-boliths are formed.32,33 These can be detected during

physicalexamination andverifiedby imagingstudies. The presenceofphlebolithsinVAscanindicatetreatmentwith anticoagulants, especially in large and extensive VAs.34

Localized intravascular coagulopathy is of utmost impor-tancebecause it is linked to the presence of local pain, thrombophlebitis,deep venous thrombosisand pulmonary embolism.

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tothepresenceofsuperficialanddeepvenous thrombosis describedinourreport.

RegardingtheriskofVArupture,itrepresentssomething theoreticalsincetherearenoreportedcasesofthis compli-cation.

SuperficialVA treatment canbeconservative, endovas-cular or surgical. If the VA is not toolarge and does not causesymptomsit maybetreated conservativelythrough compressive therapy and prophylaxis in order to avoid thrombophlebitis or deep venous thrombosis. The indica-tions for surgical treatment in superficial VAs are: the presence of symptoms, the risk of thrombosis, compres-sion of nearby structures and, more commonly, esthetic problems.35 Surgical treatment36 consists of ligation and

total excision of the aneurysm. However, in some cases, endovascular methods can be used, like foam, laser or radiofrequencysclerotherapy.37 Inthecaseofpatientswho

present superficial venous thrombosisabove the knee (as inourcase)or deepvenousthrombosisatanylocation,it is important to treat with anticoagulants for 3---6 months in patients with normal thrombophilic profiles, otherwise theanticoagulantisprescribedindefinitely.Inthepresented case,thereisnodoubtthatthechosensurgicaltreatmentis adequateandthetreatmentwithanticoagulantsduetothe presenceofdeepthrombosisforaperiodofthreemonthsis acceptable.

Theresultsofthetreatment ofthesetypes of patholo-giesareexcellent aslongastheyarenotassociated with othervascular malformationsor pathologies;thereareno reportsofmortalityinsuperficialVAsurgicalinterventionin thelowerextremitiesandthemorbidityisthesameasany venoussurgicalprocedure.36

In our case, the primary care physician diagnosed the increaseinvolumeasasofttissuetumor(firstdifferential diagnosis whichshould bemade) andsince itwas asymp-tomatic,theydidnotgiveitmuchimportancedespitethe fact that the patient reported that the tumor was grow-ing progressively. As a result of the inguinal hernioplasty thepatientwasonbedrestfortwoweeks.Surgicaltrauma andprolongedbedrestareriskfactorsforthrombosis.The patientdidnotreceiveprophylaxisforthrombosis.

At first, and because the tumor looked red and was causing severe pain, it was treated as if it was cellulitis (thrombophlebitis, which is commonly confused withsoft tissueinfections).Itwasnotuntilthesizeofthepatient’s legbegantoincreasethattherewasasuspicionofvenous thrombosisandthecasewasreferredtoourservice.

Thus we conclude that it is important to: (1) perform theclinicalhistoryandathoroughphysicalexaminationin allof ourpatients, (2)we must keepin mindall possible differentialdiagnosesbeforegivingadefiniteone,(3)one mustneverforgetprophylaxis fordeepveinthrombosisin surgicalpatients,(4)notallskinrednessequalsinfection, (5)venous thrombosis must beruled out in every patient whopresentsasuddenincreaseinlegvolume,(6)vascular ultrasoundisanessentialtoolfor diagnosisand(7)venous aneurysmsdoexistandtheyarenotjustvaricoseveins.

Conflict

of

interest

Theauthorshavenoconflictsofinteresttodeclare.

Funding

Nofinancialsupportwasprovided.

References

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Figure

Figure 1 Reconstructed ultrasound image which shows an internal saphenous vein venous aneurism of 9 × 5 cm, which compression did not remove.

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