Rev. Bras. Anestesiol. vol.66 número5

RevBrasAnestesiol.2016;66(5):529---532

REVISTA

BRASILEIRA

DE

ANESTESIOLOGIA

www.sba.com.br

MISCELLANEOUS

Correlation

of

computed

tomography,

magnetic

resonance

imaging

and

clinical

outcome

in

acute

carbon

monoxide

poisoning

Namik

Ozcan

,

Giray

Ozcam

,

Pinar

Kosar

,

Ayse

Ozcan

,

Hulya

Basar

_,

_Cetin

_Kaymak

a_{DepartmentofAnesthesiologyandReanimation,IntensiveCareUnit,AnkaraTrainingandResearchHospital,Ankara,Turkey} b_{DepartmentofRadiology,AnkaraTrainingandResearchHospital,Ankara,Turkey}

Received18February2014;accepted5May2014

Availableonline2June2014

KEYWORDS

Intensivecare; Carbonmonoxide; Imaging;

Poisoning

Abstract

Backgroundandobjectives: Carbonmonoxideisatoxicgasforhumansandisstillasilentkiller inbothdevelopedanddevelopingcountries.Theaimofthiscaseserieswastoevaluateearly radiologicalimagesasapredictorofsubsequentneuropsychologicalsequelae,followingcarbon monoxidepoisoning.

Case1: Aftercarbonmonoxideexposure,earlycomputedtomographyscansandmagnetic res-onanceimagingfindingsofa52-year-oldwomanshowedbilaterallesionsintheglobuspallidus. This patient was discharged and followed for 90 days. The patient recovered withoutany neurologicalsequela.

Case2: Ina58-year-oldwomanexposedtocarbonmonoxide,computedtomographyshowed lesionsinbilateralglobuspallidusandperiventricularwhitematter.Earlymagneticresonance imagingrevealedchangessimilartothatlikeinearlytomographyimages.Thepatientrecovered andwasdischargedfromhospital.Onthe27thdayofexposure,thepatientdeveloped disorien-tationandmemoryimpairment.Latemagneticresonanceimagingshoweddiffusehyperintensity inthecerebralwhitematter.

Conclusion: Whitematter lesions which progressto demyelinationand endup in neuropsy-chologicalsequelaecannotalwaysbediagnosedbyearlycomputedtomographyandmagnetic resonanceimagingincarbonmonoxidepoisoning.

©2014SociedadeBrasileiradeAnestesiologia.Publishedby ElsevierEditoraLtda.Thisisan openaccessarticleundertheCCBY-NC-NDlicense( http://creativecommons.org/licenses/by-nc-nd/4.0/).

∗_{Correspondingauthor.}

E-mails:namikozcan@gmail.com,namikozcan@yahoo.com(N.Ozcan). http://dx.doi.org/10.1016/j.bjane.2014.05.006

530 N.Ozcanetal.

PALAVRAS-CHAVE

Tratamentointensivo; Monóxidodecarbono; Imagem;

Intoxicac¸ão

Correlac¸ãodetomografiacomputadorizada,ressonânciamagnéticaeresultados

clínicosemintoxicac¸ãoagudapormonóxidodecarbono

Resumo

Justificativaeobjetivos: Monóxidodecarbonoéumgástóxicoparaossereshumanos,além deserumassassinosilenciosoempaísestanto desenvolvidosquantoemdesenvolvimento.O objetivodestasériedecasosfoiavaliarasimagensradiológicasiniciaiscomoumpreditivode sequelasneuropsicológicassubsequentesapósintoxicac¸ãopormonóxidodecarbono.

Caso1: Apósexposic¸ãoaomonóxidodecarbono,osachadosiniciaisemtomografias computa-dorizadaseressonânciasmagnéticasdeumamulherde52anosdeidademostraramlesõesem globopálidobilateralmente.Apacienterecebeualtaefoiacompanhadapor90dias.Apaciente serecuperousemsequelasneurológicas.

Caso2: Pacientedosexofeminino,58anosdeidade,expostaaomonóxidodecarbono.A tomo-grafiacomputadorizadamostroulesõesemglobopálido,bilateralmente,esubstânciabranca periventricular.A ressonância magnética inicial reveloualterac¸ões semelhantes àquelas em tomografias precoces. A paciente se recuperou erecebeu alta. No vigésimo sétimo dia de exposic¸ão,apacienteevoluiucomdesorientac¸ãoeperdadememória.Ressonânciamagnética posteriormostrouhiperintensidadedifusadasubstânciabrancacerebral.

Conclusão:Aslesõesdasubstânciabrancaqueprogridemparadesmielinizac¸ãoeresultamem sequelasneuropsicológicasnemsemprepodemserdiagnosticadasemtomografiase ressonân-ciasiniciaisemcasosdeintoxicac¸ãopormonóxidodecarbono.

©2014SociedadeBrasileiradeAnestesiologia.PublicadoporElsevierEditoraLtda.Este ´eum artigoOpen Accesssobumalicenc¸aCCBY-NC-ND( http://creativecommons.org/licenses/by-nc-nd/4.0/).

Introduction

Carbonmonoxide(CO)isawell-known,colorlessand odor-less gas that is toxic to all kinds of human tissues.1,2

FollowingexposuretoCO,morphologicchangesareseenin regionsofthebrainwithinhours.3---5_{Bilateraldemyelination}

ofthe cerebral whitematter, hyperintensities of centrum semiovale,andhemorrhagicnecrosisoftheglobuspallidus are some of the neuropathologic findings seen after CO poisoning.4,6

Theaimsofthisstudyweretoevaluatetheintegrityof brainwhitematterandbasalganglionswithmagnetic reso-nanceimaging(MRI)andcomputedtomography(CT)inthe acutephaseofCOexposure,andtoevaluateearly radiolog-icalimagesasapredictorofsubsequentneuropsychological sequelae,followingCOpoisoning.

Case

1

A52-year-oldwomanwasfound unconsciousat homeand referredtohospitalwithpossible COpoisoning.Her heart ratewas95beatsmin−1_{,respiratoryratewas25min}−1_and

bloodpressuremeasuredwas90/60mmHg.Resultsof arte-rialbloodgasanalysiswerepH:7.38,pO2:25mmHg,pCO2: 40mmHg,HCO3:20.9mEqL−1_{,COHb:46.4%,BE:}

−12.7,and

lactate:7mEqL−1 _{(<1.5).Laboratoryfindingsshowed}

Myo-globin:488ngmL−1_{(0---38.5),CK:147UL}−1_{(0---145),CK-MB:}

16.11ngmL−1 _{(0---5.6), andtroponin-I:0.048}

␮gL−1 (<0.1).

Inneurologicalexamination,thepatientwascomatosewith aGlasgowComaScale(GCS)scoreof9/15andpupilswere mydriatic.

AxialCTscansshowedbilateralhypodensityintheglobus palliduswithinfirst24h(Fig.1A).MRI findingsonthe7th dayofexposurewerebilateralhyperintensityintheglobus pallidusonaxial,coronalT2-weighted(T2)(Fig.1BandC), and axialFLAIR sequences.In addition, axialand sagittal unenhancedT1-weighted(T1)(Fig.1D)imagesinterestingly revealedperipheralhyperintensityoftheglobuspallidus.

The patient progressivelyrecovered within3 days and wasdischargedfromthehospitalonthe8thdayof admis-sion. The patient was followed for 90 days and did not developanyneurologicalsequela.

Case

2

A 58-year-oldwomanwas admittedtointensive care unit after several hours of CO exposure. The clinical exam-ination revealed heart rate 80beatsmin−1_{, respiratory}

rate15min−1_{, andblood pressure80/60mmHg.Results of}

blood gas analysiswere pH:7.18, pO2:11.6mmHg,pCO2: 50mmHg,HCO314.9mEqL−1_{,COHb:56.2%,BE:}

−12.7,and

lactate: 9mEqL−1 _{(<1.5). The laboratory findings showed}

myoglobin 4000ngmL−1 _{(0---38.5), CK: 247UL}−1 _(0---145),

CK-MB: 27.6ngmL−1 _{(0---5.6), and troponin-I 0.131␮gL}−1

(<0.1),andProBNP1040pmolL−1_{(<350).Physical}

examina-tionshowedmydriaticpupilsandpapilledema,theGCSscore of5/15,andthepatienthadgeneralizedconvulsions.

Radiologyandoutcomeincarbonmonoxidepoisoning 531

Figure1 (A)AxialCT,(B)axialT2MRI,(C)coronalT2MRI,and(D)axialT1MRIofCase1.

532 N.Ozcanetal.

capsuleinaxialT2,axialFLAIR(Fig.2C),coronalT2images. Cerebralwhitematterchangeswerenotobservedinanyof theimages.

Thepatientrecoveredwithin5days.Shewasdischarged fromthehospitalonthe8thdayofadmission.Thispatient haddeveloped disorientationand memory impairment on the27thdayof follow-up.Anotherdiffusion MRIwas per-formedonthe30thdayofexposure.Inadditiontoprevious findings,diffusehyperintensityinthecerebralwhitematter appeared,whichwasconsistentwithwhitematterdamage inaxialT2imagesanddiffusionT2images(Fig.2D).

Conclusion

Acute and intense CO exposure can lead to diffuse hypoxic---ischemic encephalopathy, including basal ganglia andcerebral whitematter involvement.3,7_{The globus}

pal-lidusisthemostcommonsiteofinvolvementofbasalganglia in CO poisoning.4,6,8 _{Several studies concluded that there}

may bea correlation between acute stage hypoperfusion areas and the neuropsychiatric symptoms which develop consequently.1,3,7,9,10 _{Ithasbeensuggestedthatwhite}

mat-terlesionsweremorecommonlyassociatedwithneurologic sequelaecomparedtolesionsintheglobuspallidus.10

After CO inhalation, globus pallidus damage usually occurs immediately, and cerebral white matter damage occurswithinhours.3---5 _{Ithasbeen reportedthatthemost}

commondemyelinationareasaretheperiventricularwhite matterandcentrumsemiovale.4,6,7_{Inseverecases,}

demyeli-nationcanextendtothesubcorticalwhitematter, corpus callosum,andexternalandinternalcapsules.Thesefindings correlatewellwiththeprognosis.4

In our cases,bilateral andsymmetrical hypodensity of globuspalliduswaspresentinearlyCTscansofbothcases. In early MRIs, globus pallidus was isointense in the first case and in the second, interestingly, the periphery of globuspalliduswashyperintenseinT1images.However,we observedthetypicalfindingofCOpoisoninginT2andFLAIR images,bilateral,symmetricalhyperintenseglobuspallidus forbothcases.Inaddition,theposteriorcrusofthe inter-nal capsule was hyperintense in T2 and FLAIR images for thesecond case.IncontrolMRIexaminationofthesecond case,which wasperformedone monthlater,we observed diffuselyhyperintensewhitematterinT2andFLAIRimages whichindicateswhitematterdamage.Restricteddiffusion inthe white matter, whichreflects cytotoxicedema, was observedinDWimagesandADCmap,atthesametime.

Inconclusion,ourcasesconfirmtheregionalspecificityof COpoisoninginthecerebralwhitematterandbasalganglia. Whitematterlesionsprogresstodemyelination,whichcan bepredictiveofoutcomeandneuropsychologicalsequelae. EarlyCTandMRIimagesdonotalwayscorrelatewellwith theclinicaloutcome.FurthercasesofCTandMRIwithlarger numbersofpatientsareneededtodemonstratetheclinical outcomeandprognosis.

Conflicts

of

interest

Theauthorsdeclarenoconflictsofinterest.

References

1.Kim HJ, Chang KH, Song IC, et al. Delayed encephalo-pathy of acute carbon monoxide intoxication: diffusivity of cerebral white matter lesions. Am J Neuroradiol. 2003;24: 1592---7.

2.OmayeST.Metabolicmodulationofcarbonmonoxidetoxicity. Toxicology.2002;180:139---50.

3.ThomSR, FisherD, ManevichY.Roles for platelet-activating factor and NO-derived oxidants causing neutrophil adher-ence after CO poisoning. Am J Physiol Heart Circ Physiol. 2001;281:H923---30.

4.Porter SS, Hopkins RO, Weaver LK, et al. Corpus callosum atrophy and neuropsychological outcome following car-bon monoxide poisoning. Arch Clin Neuropsychol. 2002;17: 195---204.

5.O’DonnellP,BuxtonPJ,PitkinA,etal.Themagneticresonance imagingappearancesof thebraininacute carbon monoxide poisoning.ClinRadiol.2000;55:273---80.

6.ChuK,JungKH,KimHJ,etal.Diffusion-weightedMRIand99m Tc-HMPAOSPECTin delayedrelapsing type ofcarbon monoxide poisoning:evidenceofdelayedcytotoxicedema. EurNeurol. 2004;51:98---103.

7.Chang KH, Han MH,Kim HS, et al. Delayed encephalopathy afteracutecarbonmonoxideintoxication:MRimagingfeatures and distributionofcerebral whitematterlesions. Radiology. 1992;184:117---22.

8.LoCP,ChenSY,LeeKW,etal.Braininjuryafteracutecarbon monoxidepoisoning:earlyand latecomplications. AJRAmJ Roentgenol.2007;189:W205---11.

9.Silver DA, Cross M, Fox B, et al. Computed tomography of the brain in acute carbon monoxide poisoning. Clin Radiol. 1996;51:480---3.