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REVISTA

BRASILEIRA

DE

ANESTESIOLOGIA

PublicaçãoOficialdaSociedadeBrasileiradeAnestesiologia

www.sba.com.br

CLINICAL

INFORMATION

Severe

fat

embolism

in

perioperative

abdominal

liposuction

and

fat

grafting

Rodrigo

de

Lima

e

Souza

a,b,c,∗

,

Bruno

Tavares

Apgaua

a

,

João

Daniel

Milhomens

a

,

Francisco

Tadeu

Motta

Albuquerque

a

,

Luiz

Antônio

Carneiro

a

,

Márcio

Henrique

Mendes

a

,

Tiago

Carvalho

Garcia

a

,

Clerisson

Paiva

a

,

Felipe

Ladeia

a

,

Deiler

Célio

Jeunon

a

aCentrodeEnsinoeTreinamentodoHospitalMadreTeresa,BeloHorizonte,MG,Brazil

bUniversidadeFederaldeMinasGerais(UFMG),BeloHorizonte,MG,Brazil

cAssociac¸ãodeMedicinaIntensivaBrasileira(AMIB),SãoPaulo,SP,Brazil

Received3September2013;accepted26November2013 Availableonline12March2016

KEYWORDS

Fatembolism; Intraoperative; Liposuction

Abstract

Backgroundandobjectives: Fatembolismsyndromemayoccurinpatientssufferingfrom multi-pletrauma(longbonefractures)orplasticsurgery(liposuction),compromisingthecirculatory, respiratory and/or centralnervous systems. This report shows the evolution ofsevere fat embolismsyndromeafterliposuctionandfatgrafting.

Casereport: SSS,42yearsold,ASA1,noriskfactorsforthrombosis,candidateforabdominal liposuctionandbreastimplantprosthesis.Subjectedtobalancedgeneralanesthesiawithbasic monitoringandcontrolledventilation.After45minofprocedure,therewasasuddenand grad-ualdecreaseofcapnometry,severehypoxemiaandhypotension.Thepatientwasimmediately monitoredforMAPandcentralcatheter,treatedwithvasopressors,inotropes,andcrystalloid infusion,stabilizinghercondition.Arterial bloodsampleshowed pH=7.21; PCO2=51mmHg;

PO2=52mmHg;BE=−8;HCO3=18mEqL−1,andlactate=6.0mmolL−1.Transthoracic

echocar-diogramshowed PASP=55mmHg, hypocontractileVDandLVEF=60%.Diagnosisofpulmonary embolism.After24hofintensivetreatment,thepatientdevelopedanisocoriaandcoma (Glas-gowcoma scale=3).A brainCT was performedwhich showed severe cerebralhemispheric ischemiawithsignsoffatemboliinrightmiddlecerebralartery;transesophageal echocardiog-raphyshowedapatentforamenovale.Finally,after72hofevolution,thepatientprogressed tobraindeath.

Conclusion:Fat embolism syndrome usually occurs in young people. Treatment is based mainlyontheinfusionoffluidsandvasoactivedrugs,mechanicalventilation,andtriggering

CentrodeEnsinoeTreinamento(SBA)doHospitalMadreTeresa,BeloHorizonte,MG.

Correspondingauthor.

E-mails:[email protected],[email protected](R.deLimaeSouza).

http://dx.doi.org/10.1016/j.bjane.2013.11.006

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factorcorrection(earlyfixationoffracturesorsuspensionofliposuction).Themultiorgânico involvementindicatesaworseprognosis.

© 2014SociedadeBrasileirade Anestesiologia.Publishedby ElsevierEditoraLtda.Allrights reserved.

PALAVRAS-CHAVE

Emboliagordurosa; Peroperatório; Lipoaspirac¸ão

Emboliagordurosagravenoperoperatóriodelipoaspirac¸ãoabdominalelipoenxertia

Resumo

Justificativaeobjetivos: ASíndromedaEmboliaGordurosa(SEG)podeacontecerempacientes vítimasdepolitrauma(fraturadeossoslongos)ouoperac¸ões plásticas(lipoaspirac¸ão), com-prometendo circulac¸ão, respirac¸ãoe/ou sistema nervosocentral. Opresente relatomostra evoluc¸ãodeSEGgraveapóslipoaspirac¸ãoelipoenxertia.

Relatodocaso: SSS, 42 anos, ASA 1, sem fatores de risco para trombose, candidata a lipoaspirac¸ãoabdominal e implante deprótese mamária. Submetida à anestesia geral bal-anceadacommonitorizac¸ãobásicaeventilac¸ãocontrolada.Após45minutosdeprocedimento, houvequedasúbita eprogressivadacapnometria,hipoxemiaehipotensãograve. Imediata-mentefoimonitorizadacomPAMecatetercentral,tratadacomvasopressores,inotrópicose infusãodecristaloides,obtendoestabilizac¸ãodoquadro.Amostrasanguíneaarterialmostrou pH=7,21;PCO2=51mmHg; PO2=52mmHg;BE=−8; HCO3=18mEQ/l elactato=6,0mmol/l.

EcocardiogramatranstorácicomostrouPSAP=55mmHg,VDhipocontrátileFEVE=60%. Diagnós-ticodeemboliapulmonar.Após24hdetratamentointensivo,apacienteevoluiucomanisocoria ecomacomescaladeglasgow3.RealizadaTCdeencéfaloqueevidenciouisquemiacerebral grave,hemisférica,comsinaisdeêmbolosdegorduraemA.cerebralmédiaD;oecocardiograma transesofágicomostrou forameoval patente.Finalmente,após72hdeevoluc¸ão,apaciente evoluiuparamorteencefálica.

Conclusão:A SEGocorre geralmenteem jovens. Otratamentobaseia-se principalmente na infusãodelíquidosedrogasvasoativas,ventilac¸ãomecânicaecorrec¸ãodofatordesencadeante (fixac¸ãoprecocedefraturasoususpensãodalipoaspirac¸ão).Ocomprometimentomultiorgânico indicapiorprognóstico.

©2014SociedadeBrasileira deAnestesiologia.PublicadoporElsevierEditoraLtda.Todosos direitosreservados.

Introduction

The presenceof fat embolior freefatty acids inthe pul-monaryorsystemiccirculationcantriggerthefatembolism syndrome(FES), oftenoriginated from longbone fracture of the lower limbs and pelvis.On a smaller scale, it can resultfromcosmeticsurgerysuchasliposuctionand/orfat grafting,cardiopulmonarybypass,pancreatitis,jointrepair, severeburns,sicklecellanemia,diabetesmellitus,andlipid parenteralinfusion.1,2

FES is a relatively rare condition (0.3---5.0%), but

extremelysevere,withmortalityratesrangingfrom10%to

36%.1,2

Historically, the first description of FES happened in

themid-nineteenthcenturyonautopsyfindingsbyZenker.3

Later,stillinthesamecentury,VonBergmanmadethefirst

clinicaldiagnosisofFES,4describingtheclassictriad

charac-terizedbyacuterespiratoryfailurewithdiffusepulmonary

infiltrate,neurologicaldysfunctionandskinmanifestations

(petechiae).However,thistriadoccursinonly0.5---2.0%of

cases.5Thepassageofemboliintothesystemiccirculation

andthesevereneurologicalinvolvement(coma),aswellas

otherorgans,areindicativeofapoorprognosis,especially

thepossibilityofinteratrialcommunication(persistenceof

patentforamenovale).6

This report shows the fatal outcome of a massive fat

embolism case during the intraoperative period of an

abdominalliposuctionandfatgraftingduetothepresence

ofpatentforamenovale,culminatingwithsevere embolic

strokeandbraindeath.

Case

report

SSS, 42 years old, ASA 1, with no risk factors for deep

vein thrombosis, candidate for abdominal liposuction

and breast prosthesis implant. The patient was anxious

and fearful about the possibility of complication and

death. Therefore, general anesthesia was the option, a

less common practice for this type of procedure at the

Service (thoracic epiduralanesthesia withsedation is the

standard practice). The general anesthesia was balanced

withpropofol, remifentanil,atracurium, sevoflurane, and

controlled ventilation with 90% end-tidal oxygen. Basic

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Figure1 CTwithfatemboliinmiddlecerebralarteryandsignsofsevereischemia.

andNIBP).After45minofunchangedprocedure,therewas

a sudden and progressive fall in capnometry, hypoxemia,

andseverehypotension,coincidingwiththetimeofgluteal

fatgraftingintheproneposition.Immediately,thepatient

was placed in the supine position and monitored with

MAPandcentralcatheter.She wastreated with

vasopres-sors, inotropes, and infusion of crystalloid, obtaining the

stabilization of the clinical picture. Arterial blood

sam-ple showed pH=7.21; PCO2=52mmHg; PO2=51mmHg;

BE=−8; HCO3=18mEqL−1, lactate=6.0mmolL−1,

hemoglobin=11.8gdL−1, platelet count=120,000,

sodium=139mmolL−1, potassium=5.9mmolL−1, and

glucose=254mg%. Transthoracic echocardiography

per-formed in the operating room showed PASP=55mmHg,

hypocontractile RV, and LVEF=60%. The hypothesis of

pulmonary fat embolism was strengthened and it was

decided to refer the patient to the intensive care unit

(ICU) for supportive treatment. After 24h of intensive

care, the patient developed anisocoria and coma with

Glasgowscale 3. The brain CT performed showed severe

cerebralischemia,hemispherical,withsignsof fatemboli

in right middle cerebral artery (Fig. 1); transesophageal

echocardiographyshowed patent foramen ovale.

Unfortu-nately,after72hofevolution,thepatientdevelopedbrain

death.

Discussion

FESis clinicallyunderdiagnoseddue tothelow specificity

andsensitivityoflaboratorytestsandphysicalexamination.

Moreover, the diagnostic confusion with other syndromes

(e.g.,thromboembolism,myocardialinfarction,acute

respi-ratory distress syndrome, among others) often delay the

diagnosis.Theclassictriadinvolvingacuterespiratory

fail-ure,neurologicaldysfunction,andpetechiaeisinfrequent

and is manifested after 24---72h, usually after long bone

trauma.7 The increased serum concentration of lipase or

presenceoflipiduriamayassistindiagnosis,aswellas

imag-ingtests(MRI).

Schaikhetal.highlightedthe importanceof brainMRI,

especially in those patients who develop sensory

distur-bancesorneurologicaldeficits.8

Gurd and Wilson, in the 1970s, established major and

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Table1 Gurd’sdiagnosticcriteria.1

Majorcriteria:acuterespiratoryfailure,centralnervous systemdepression,skinandmucosaldisorders (petechiae)

Minorcriteria:tachycardia,fever,retinalchanges,low hematocrit(unexplainedanemia),increasederythrocyte sedimentationrate(ESR)andthrombocytopenia,fat globulesintheurineorinthesecretionof

bronchoalveolarlavage

andthreeminorcriteriaortwomajorandtwominorcriteria

toconfirmthesyndrome(Table1).1Theadoptionofthese

criteria is still useful for the diagnosis of FES in current

clinicalpractice.

Under generalanesthesia, respiratory symptoms,

espe-ciallyhypoxemia,maybemaskedbymechanicalventilation

withhigh fractionofinspiredoxygen.Inourcase, thefall

in capnography was the first change, indicating low

pul-monaryperfusion,followedbyoxygendesaturationaround

90%.Theearlydetectionofthecomplicationallowed

ther-apeuticmeasurestobetakeninatimelymanner,beforea

possiblecardiacarrest.Thelattercouldoccurifthe

anes-thetictechniquechosenwasepidural,becauseofthechance

ofpoorresponsetovasopressorsduetoinstalledvasoplegia

andrelativehypovolemia.

FES’s pathophysiology involves endothelial dysfunction

by the release of fatty acids from fat emboli,

lead-ing to vasculitis with activation of platelet aggregation

and consumption of clotting factors. This process may

beperpetuatedcausingmicrocirculationocclusion,

throm-bocytopenia, disseminated intravascular coagulation, and

bleeding, thelatterbeingrarer.8The centralnervous

sys-tem and other organs involvement indicates the passage

of fatty microemboliand/or free fattyacids into the

sys-temic circulation through anatomical pulmonary shunts

and/or communication between the right and left heart

chambers.6,8 The foramen ovale, which is an opening

(communication)betweenthetwoatriapresentinthefetal

circulation,isclosedrightafterbirth,butinabout10---25%of

theadultpopulationitmaybecomepatentbyanyincreased

pressureintherightchambersoftheheart.6,8

Inthepresentcase,thechoiceofgeneralanesthesiaand

theventilationmodewithpositiveexpiratorypressuremay

havecontributedtoopen thepatient’sinteratrial

commu-nication. The positive end-expiratory pressure used in

mechanicalventilationmayleadtohemodynamicchanges,

suchasincreasedcardiacwork,andpressurechangesinthe

right heart chambers,withconsequentright-left shunt,if

thereisanycommunicationbetweenthechambers.9

Clinically, it is not possible to screen patients for the

presence ofa patentforamen ovale inthe pre-anesthetic

evaluation,asthefunctionalcapacityandauscultationare

normalin mostcases.The gold standardfor thediagnosis

of patent foramen ovale is transesophageal

echocardiog-raphy, which should be performed in all patients eligible

for liposuction or fat grafting, a fact that would make

themajorityofthesesurgeriesunfeasible.3,6Muelleretal.

reported a case of paradoxical cerebral embolism due to

persistentforamenovale.Thepatientdeveloped

quadriple-giaandcognitiveimpairment.10Ontheotherhand,Folador

etal. reported a successfulcase afterliposuction, which

progressed to massive pulmonary fat embolism (without

cerebral embolization), and the patient survived without

sequelaeonlywithsupportivetreatment.11

FES treatment is supportive and includes the

manage-mentof respiratory dysfunction,hemodynamic, and early

fixationoflong-bonefractures.Corticosteroidsmaybe

use-fulforprevention,butithasnotbeenproventobeeffective

forovertsyndrome.Intheory,thesedrugslimitthe

endothe-lialdamagecausedbythefreefattyacids.12,13

Performing esthetic procedures in tertiary hospitals

referstothesecurityrequiredforanesthesiologiststo

exer-cisetheir function comfortably, which allowsofferingthe

patientthebesttechniqueindicationandthebest

diagnos-ticandtherapeuticresources.Plattetal.reporteddeaths

afterliposuctionoperationsduetopulmonaryfatembolism,

inadditiontootherdeathsbylidocainepoisoningandfluid

overload.14

Inthis report,theFESdiagnosis wasdone while inthe

operatingroom,throughclinicalsuspicionandthe

transtho-racicechocardiographyperformed.Theintensivecareunit

receivedthepatientwithinminutes,alreadywithinvasive

monitoringandvasoactiveaminesupport,afactthatmay

notoccurinanon-hospitalenvironment.

Conclusion

FEScanoccurbothincriticallyillpatients,victimsof

long-bone or multiple traumas, and in candidates for surgical

liposuction, a fact that should alert anesthesiologists for

earlydiagnosis andtreatment,aswellasfortheminimum

conditionsof workrequired toprovidesecurity.Fat

graft-ingispotentiallydangerousbecauseitincreasestheriskof

FESduetoaccidentalintravascularinjectionoffatemboli.

Neurologicalimpairmentanda highernumberof affected

organsindicateaworseprognosisofFES.15,16

Conflicts

of

interest

Theauthorsdeclarenoconflictsofinterest.

References

1.GurdA.Fatembolism:anaidtodiagnosis.JBoneJointSurg. 1970;52:732---7.

2.Filomeno LTB, Carelli CR, Silva NCLF, et al. Fat embolism: areviewfor currentorthopaedicspractice.Acta OrtopBras. 2005;13:196---208.

3.ZenkerFA.BeitragezurAnatomieundPhysiologiedeLung. Dres-den,Germany:JBraunsdorf.1861:31.

4.BergmannVE.Einfalltodlicherfettenbolic.BerlKlin Wochen-scher.1873;10:385---6.

5.OverellJR, Bone I,Lees KR. Interatrialseptalabnormalities andstroke:ameta-analysisofcase---controlstudies.Neurology. 2000;55:1172---9.

6.BuchholzS,ShakilA,FigtreeGA,etal.Diagnosisand manage-mentofpatentforamenovale.PostgradMedJ.2012;88:217---25. 7.ShaikhN.Emergencymanagementoffatembolismsyndrome.

JEmergTraumaShock.2009;2:29---33.

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9.TratadodeAnestesiologiaSAESP,vol.1,7thed.SãoPaulo: Edi-toraAtheneu;2011.p.1007---23.

10.Mueller F, Pfeifer C, Kinner B. Post-traumatic fulminant paradoxicalfatembolismsyndromeinconjunctionwith asymp-tomaticatrialseptaldefect:acasereportandreviewofthe literature.JMedCaseRep.2011;5:142---3.

11.FoladorJC,BierGE,CamargoRF,etal.SíndromedaEmbolia Gordurosa:relatodecasoassociadoàlipoaspirac¸ão.JPneumol. 1999;25:114---7.

12.Cavallazzi R, Cavallazzi AC. O efeito do corticosteroide na prevenc¸ãodasíndromedaemboliagordurosaapósfraturade osso longo dosmembros inferiores: revisão sistemática com meta-análise.JBrasPneumol.2008;34:34---41.

13.BedermanSS,BhandariM,McKeeMD,etal.Docorticosteroids reducetheriskoffatembolismsyndromeinpatientswithlong bonefractures?CanJSurg.2009;52:386---93.

14.PlattMS,KohlerLJ,RuizR,etal.Deathsassociatedwith lipo-suction:casereports andreviewoftheliterature.JForensic Sci.2002;47:205---7.

15.AkhtarS.Fatembolism.AnesthesiolClin.2009;27:533---50. 16.CostaAN,MendesDM,ToufenC,etal.13---Síndromeda

Imagem

Figure 1 CT with fat emboli in middle cerebral artery and signs of severe ischemia.

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