脾臟影像學資料課件

脾臟

影像診斷學放射學院劉林祥1脾臟影像檢查技術(shù)X線：價值有限，血管造影USCT：為更清楚顯示小病變，可應用5mm的層厚和層距平掃發(fā)現(xiàn)可疑應增強2MRImagingTechniqueCoronalT2WIhalf-Fourierrapidacquisitionwithrelaxationenhancement(RARE)AxialFSET2WIorlongechotimeinversion-recoveryimagingperformedduringabreathholdAxialGRET1WIchemicalshiftin-phaseandout-of-phaseimagingperformedduringabreathholdAxial3DGREbreath-holdsequencesuchasvolumetricinterpolatedbreath-holdexamination(VIBE)withpre-contrastanddynamicenhanced3AnatomyThelargestductlessglandandthelargestsinglelymphaticorganinthebodymesodermalinorigintothecirculatorysystemasthelymphnodesfunctionsincludeimmunologicsurveillance,redbloodcellbreakdown,andspleniccontractionforbloodvolumeaugmentationduringhemorrhageAwiderangeofpathologycanaffectthespleen5AnatomyAnintraperitonealorganwithasmoothserosalsurfaceandattachedtotheretroperitoneumbyfattyligamentssurfaces:diaphragmatic(phrenic)andvisceral

VisceralsurfaceisdividedintoananteriororgastricridgeandaposteriororrenalportionSplenicarteryandveinemergefromthesplenichilumintheformofsixormorebranches;thesplenicarteryisremarkableforitslargesizeandtortuosity.slightlysuperiortothevein6MicroscopicAnatomydividedintotwocompartments,theredandwhitepulps,separatedbythemarginalzoneThewhitepulpismadeupofTandBlymphocytesandlocatedcentrallyTheredpulpiscomposedofrichplexusesoftortuousvenoussinuses7脾的大小新月形或內(nèi)緣凹陷的半月形，密度均勻略低于肝前后徑7～10㎝寬徑4～6㎝上下徑11～15㎝8ArciformnormalenhancementpatternAxial3DGREVIBEImmediatelyafteradministrationofcontrastmaterialArciformnormalenhancementpattern10MRI影像分析橫斷面大小、形態(tài)與CT相似冠狀面顯示脾的大小、形態(tài)及其與鄰近器官的關(guān)系優(yōu)于橫斷面T1WI信號低于肝T2WI信號高于肝血管流空無信號副脾、多脾及異位脾，信號強度始終與脾相同脾腫瘤呈稍長T1長T2信號如腫瘤伴出血壞死，則為混雜信號囊性病變呈圓形長T1低信號和長T2高信號脾內(nèi)出血的信號與出血時間有關(guān)脾內(nèi)鈣化呈黑色低信號12PolyspleniaAssociationwithabdominalsitusandcardiovascularanomalies.morecommoninfemalesNumeroussmallsplenicmassesinhypochondriumAxialin-phaseGREimageshowssitusinversuswithmultiplemassesintherightupperquadrant14PolyspleniaCoronalGREcineandaxialin-phaseGREimagesAcardiacanomalyintheformofpulmonarystenosisandsmallmassesintheleftupperquadrant15脾外傷易發(fā)生外傷，脾包膜下、脾實質(zhì)內(nèi)和脾周圍出血據(jù)脾破裂時間，早發(fā)性脾破裂和遲發(fā)性脾破裂可因感染、腫瘤、血液病等引起自發(fā)性脾破裂急性脾破裂可出現(xiàn)劇烈左上腹疼痛并向背部放射遲發(fā)性脾破裂，癥狀可隱匿數(shù)天至出現(xiàn)大出血16脾外傷平片和透視左上腹脾區(qū)致密塊影；結(jié)腸脾曲因血腫壓迫而下移；左膈抬高，活動受限?？砂橛衅渌鈧?，如氣胸、氣腹、肋骨骨折脾動脈造影重度：脾破裂，大血管分支破裂中度：脾內(nèi)、外有較多的對比劑外溢輕度：脾內(nèi)血腫，呈小范圍無血管區(qū)改變或少量對比劑外溢17脾外傷CT脾挫裂傷表現(xiàn)為脾內(nèi)不規(guī)則形的低密度區(qū)，還可伴有小點、片狀高密度影脾血腫表現(xiàn)為團塊狀高密度影包膜下血腫呈半月形高密度影，隨出血時間延長，血腫逐漸變?yōu)榈让芏饶酥恋兔芏仍钇て屏岩娖⒅芑虿⑸细骨环e液（積血）增強掃描有助于顯示較輕的病變18脾外傷急性脾破裂CT平掃在稍高密度的膈下液體中見脾輪廓斷裂快速注射對比劑，脾的活組織與周圍的血液分界清楚20脾外傷、破裂根據(jù)脾的形態(tài)，提示脾實質(zhì)裂傷脾周液體的CT值超過50HU，表明腹腔內(nèi)存在出血212324TraumaCoronalT2WIhalf-FourierRAREC-3DVIBEAnacuteorsubacutesubcapsularhematoma26脾腫瘤原發(fā)脾腫瘤少見，惡性以淋巴瘤多，良性以血管瘤多脾惡性淋巴瘤CT可見脾增大，脾內(nèi)單發(fā)或多發(fā)稍低密度灶，邊界不清。增強掃描病灶輕度不規(guī)則強化，與正常脾實質(zhì)分界清楚脾海綿狀血管瘤CT平掃為邊界清楚的低密度區(qū)，增強早期顯示病灶周邊結(jié)節(jié)狀強化，延遲掃描對比劑逐漸向中心充填，最后病灶呈等密度脾血管瘤在T2WI呈明顯高信號，Gd-DTPA增強多明顯強化。淋巴瘤表現(xiàn)為單個或多個大小不等的圓形腫塊，邊界不清，在T1WI及T2WI表現(xiàn)為不均勻性混雜信號27InflammationAbscessesbefoundin0.14-0.7%autopsycasesPrevalenceincreasedduetoincreasednumberofimmunosuppressedpatientssuchasAIDSSolitary,

multiple,ormultilocularLowsignalintensityonT1WIandhighsignalintensityonT2WIMinimalperipheralenhancementwhenthecapsuledevelops28CandidiasisThemostcommoninfectioninvolvingtheliverandspleeninimmunocompromisedMRIbesuperiortoCTindetectionofmicroabscessessecondarytocandidiasismultiplehypointense,ring-enhancinglesionslessthan1cmonenhancedimages30CandidiasisE+3DVIBEimmunocompromisedMultiplesmall,hypointenselesions31HistoplasmosisAlthoughseeninpatientswithcompetentimmunesystems,theprevalenceofhistoplasmosisisgreaterinimmunocompromisedpatientsMRIdemonstratestheacuteandsubacutephasesofdiseaseasscatteredhypointenselesionsonbothT1WIandT2WIOldgranulomascanbecalcified,causingcharacteristicsignalintensitychangeswithbloomingartifactsonMRIThisappearanceisbestappreciatedonGRET1WI,especiallythoseobtainedwithalongechotime32HistoplasmacapsulatumAxialE+3DVIBET2WIIRScatteredlowsignalintensitylesionsrepresentinfectionofspleen33AxialT1WIandT2WIoldcalcifiedsplenichistoplasmomaAlowsignalntensitylesionwithcharacteristic"blooming"34SarcoidosisAgranulomatoussystemicdiseaseofunknownetiologythatcaninvolvenumeroussites,infrequentlyinvolvingthespleenNodularsarcoidosisdemonstratelowsignalintensitywithallMRIsequencesLesionsaremostconspicuousonT2WIFSorearlyphaseenhancedimagesSarcoidosislesionsenhanceinaminimalanddelayedpattern35Sarcoidosismultiplesmall,hypointense,focalspleniclesions,representsarcoidosisnotenhanceonearlyphasebutenhanceondelayedphase

36脾腫瘤非何杰金淋巴瘤平掃見脾大注射對比劑后可見多發(fā)低密度區(qū)37非何杰金淋巴瘤境界清楚的低密度病灶，注射對比劑后周邊強化38非何杰金淋巴瘤多發(fā)微小低密度病灶，對比增強后清楚化學治療后消失39404142脾囊腫分為先天性和后天性，真性和假性真性囊腫見于單純性囊腫和多囊脾，假性囊腫見于外傷出血和炎癥之后。脾包蟲囊腫多見于流行區(qū)CT和MRI表現(xiàn)類似于肝腎囊腫寄生蟲性囊腫?？梢娔夷[壁弧形鈣化，外傷性囊腫內(nèi)由于出血和機化，囊內(nèi)密度高于水43脾囊腫囊腫壁鈣化，考慮為寄生蟲性44BenignNeoplasmsorCystsTruespleniccystsareepithelialcelllined,asopposedtopseudocystsIncludeepidermoidandparasiticcystsMRIcharacteristicsfollowthoseofcystsinotherorgansofthebody,withlackoftissuearchitectureandhighwatercontentlongerT1andT2relativetonormalsplenictissuenoenhancementfollowingadministrationofGDDTPAMRIisusefulwhenUSandCTresultsareequivocal45SpleniccystAxialE+T1WI3DVIBET2WIhalf-FourierRARETypicalfeatures46脾梗死常見原因是左心系統(tǒng)血栓脫落，脾周圍器官的腫瘤和炎癥引起脾動脈血栓并脫落，某些血液病和淤血性脾增大多無癥狀，少數(shù)可有上腹疼痛脾動脈造影見受累動脈中斷，并見三角形無血管區(qū)，尖端指向脾門MRI梗塞區(qū)的信號強度根據(jù)梗塞時間長短不同急性和亞急性梗塞區(qū)在T1WI和T2WI分別為低信號和高信號區(qū)慢性期梗塞區(qū)瘢痕和鈣化形成，T1WI和T2WI均為低信號47脾梗死CT脾內(nèi)三角形低密度影，尖端指向脾門，邊界清楚。增強后無強化快速注射對比劑，腫大的脾內(nèi)可見局限性低密度區(qū)，脾被膜輕度凹陷48脾梗死脾臟完全梗死，周圍脾實質(zhì)接受被膜血管的血供49SplenicInfarctionSeeninthesettingofarterialembolisuchasinsicklecellanemia,Gaucherdisease,hematologicmalignancies,cardiacemboli,torsion,collagenvasculardisease,andportalhypertensionPeripheralwedge-shapeddefectsthatexhibitdecreasedsignalintensityonbothT1WIandT2WIanddonotenhanceafterintravenouscontrastmaterialadministration50SplenicInfarctionAxialE+3DVIBEnonenhancingwedge-shapedareaofinfarction51SplenicarteryaneurysmsSecondarytomultiplecausessuchasmedialdegenerationwithsuperimposedatherosclerosis,congenitalcauses,mycoticcauses,portalhypertension,fibromusculardysplasia,andpseudoaneurysmsfromtraumaandpancreatitisMRIallowseffectivediagnosisandcharacterizationoftheselesions3DGREsequencessuchasVIBEordedicated3DMRangiographicsequencesarethebestforevaluatingtheselesions52SplenicarteryaneurysmsE+3DGREVIBEAneurysmaldilatationofdistalendofsplenicartery53SplenicveinthrombosisMostcommonlysecondarytopancreatitisAtleast20%withchronicpancreatitisCompressionandfibrosiscausedbypancreatitisErosionofapseudocystintothesplenicveinMayresultingastricvaricesandattimeseitheresophagealorcolonicvaricesanintraluminalfillingdefectafteriv.contrastE+MRAhasthepotentialtoreplaceia.DSAasthestandardmethodofassessingtheportalvenousanatomy54SplenicveinthrombosisAxialvenousphaseE+3DGREVIBEThrombusfillingthesplenicveinAppearsasanareaofsignalvoid55ArteriovenousmalformationsCanoccuranywhereinthehumanbodybutrarelyoccurinthespleenAmachinery-typebruitintheupperleftabdominalquadrantrepresentsanimportantandsimplediagnosticsymptomfoundatclinicalexaminationduringauscultationMRimagingcandemonstratearteriovenousmalformationsasmultiplesignalvoidswithallnonenhancedpulsesequencesArteriovenousmalformationsdemonstrateserpentineenhancementafterintravenousinjectionofgadoliniumcontrastmaterial56ArteriovenousmalformationsAxialT2-weightedinversion-recoveryandcontrast-enhanced3DVIBEimagesAspleniclesionthatappearsasanareaofsignalvoidThelesiondemonstratesserpentineenhancementontheenhancedimageandrepresentsanarteriovenousmalformation57HematologicDisorders

SickleCellDiseaseCommonintheblackpopulationwithaprevalenceof0.2%(homozygousform)and8%–10%(heterozygousform)ThespleenistheorganmostcommonlyinvolvedbysicklecelldiseaseAppearsasanearlysignalvoidareaduetoirondepositionfrombloodtransfusionAutosplenectomyisoftenfoundinpatientswithhomozygoussicklecelldisease58SickleCellDiseaseT2WIhalf-FourierRAREDecreasedsignalintensityisduetorepeatedbloodtransfusion59SickleCellDiseaseAxialE+T1WIGREAverysmallspleenisindicativeofautosplenectomy60ExtramedullaryhematopoiesisAcompensatoryresponsetodeficientbonemarrowcellspredominantlyaffectsthespleenandliverAlthoughusuallyshowsdiffuseinfiltrationmicroscopically,maybefocalmasslikeinvolvementofliverandspleenSignalintensitydependsonevolutionofhematopoiesisActivelesionsshowintermediatesignalintensityonT1WI,highsignalintensityonT2WI,andsomeenhancementOlderlesionsshowlowsignalintensityonT1WIandT2WIandmaynotshowanyenhancementusuallyexhibitreducedsignalintensityonin-phaseT1WIGREcomparedwiththatonopposed-phaseimagesowingtothepresenceofiron61ExtramedullaryhematopoiesisThelesionhasreducedsignalintensityonthein-phaseimagecomparedwiththatontheout-of-phaseimageThisdifferenceissecondarytoirondeposition62HemangiomaThemostcommonprimarybenignneoplasmofthespleenComposedofendothelium-linedvascularchannelsfilledwithbloodMostarehypointensetothespleenonT1WIandhyperintenseonT2WIEarlynodularcentripetalenhancementanduniformenhancementatdelayedimaging63SplenichemangiomaAxialT2WIFSEandE+3DVIBETypicalMRIfeatures64DiffusehemangiomatosisArarebenignvascularconditionoccurringasamanifestationofsystemicangiomatosisAssociationswithKlippel-Trénaunay-Weber,Turner,Kasabach-Merritt–like,andBeckwith-Wiedemannsyndromeslesscommonly,confinedtothespleenSometimesaccompaniedbyseveredisturbanceofbloodcoagulation65AxialE+3DVIBEandT2WIofaKlippel-Trénaunay-WebersyndromeDiffuseangiomatosisofthespleenandchestwall66HamartomasBenignasymptomaticlesions,usuallysingle,composedofamixtureofnormalsplenicstructuressuchaswhiteandredpulpCommonlyassociatedwithtuberoussclerosisHeterogeneouslyhyperintenserelativetothespleenonT2WIanddemonstratediffuseenhancementonearlypostcontrastimagesandmoreuniformenhancementondelayedimages67HamartomasLesionwithhighsignalintensityonT2WI,lowsignalintensityonT1WI,andmoreuniformenhancementonthedelayedimage68SplenicSarcomaPrimarysplenicangiosarcomasareextremelyraretumorswithaverypoorprognosis.highlyaggressiveandmanifestwithwide-spreadmetastaticdiseaseorsplenicruptureLowsignalintensityonT1WIandheterogeneoushighsignalintensityonT2WIHeterogeneousenhancementwithmultiplehyperintensenodularfociandhypointenseregionsMRIseemstobemorepreciseintheoverallassessmentandstagingofthistypeoftumorandisofparticularvaluefortimelydiagnosisofthisrapidlyfataldisease69AngiosarcomaE+3DVIBET2WIhalf-FourierRARELowonT1WIHighonT2WIHeterogeneousenhancement70LymphomaThecommonestmalignanttumorofthespleenItisimportanttodetectsplenicinvolvementbecauseitcanalterthemanagementLymphomatousdepositshaveT1andT2similartothoseofnormalsplenicparenchymaEnhancedsequencesaremoresensitivefortheevaluationofspleniclymphomaDiffuseinvolvementmaybeseenaslargeirregularlyenhancingregionsMultifocaldiseaseisalsocommonandcanbeseenasmultiplefocallesionsthatarehypointenserelativetotheuniformlyorarciformenhancingspleen71LymphomaE+3DGREVIBEMultifocalinvolvementofthespleenbymultiplehypointenselymphomatouslesions72MetastasesRelativelyuncommonUsuallyinwidespreaddisseminatedmalignanciesIsolatedsplenicmetastasesalsorecognizedTypicallyashyperintensemassesonT2WIandhypo-toisointensemassesonT1WIThedegreeandcharacteristicsofenhancementdependonthenatureandtypeoftheunderlyingprimaryneoplasm73MetastasesT2-WIhalf-FourierRAREApatientwhounderwentleftnephrectomyforrenalcellcarcinomashowshyperintensesplenicmetastases74SplenicenlargementCausedbyvariousdiseasesLymphomaMalariaLeukemiaportalhypertensionmetabolicdiseases(eg,Gaucherdisease)75PortalhypertensionThemostcommoncauseofsplenomegalyMRIoftenrevealsassociatedsignsofhepaticcirrhosiswithorwithoutchangein