Hepatic Pseudolesions

Transcription

1 5 Hepti Pseuolesions CONTENTS 5.1 Pthophysiologi Bkgroun Antomi Vrints of the Hepti Cirultion Vsulr Anormlities 5.2 Prenhyml Pseuolesions Fol Ftty Liver Fol Spre Ares in Ftty Liver Inflmmtory Pseuotumors Peliosis Heptis Confluent Hepti Firosis Segmentl Hypertrophy Prenhyml Compression 5.3 Vsulr Pseuolesions Trnsient Hepti Attenution Differenes Vsulr Mlformtions 5.1 Pthophysiologi Bkgroun The liver uniquely reeives ul loo supply; pproximtely ml/min of loo rrives vi the portl vein n pproximtely 400 ml/min rrives vi the hepti rtery. In non-irrhoti liver, loo perfusion ours t pressures of pproximtely 7 mmhg n 100 mmhg, vi the portl vein n hepti rtery, respetively. Arterioportl prenhyml perfusion emonstrtes the egree of reiproity of the rteril n portl venous ontriutions y virtue of vsulr flux through ynmi miroirultory rterioportl shunts (APS), lrgely t the level of the portl tri y trnsplexl, trnsvsl, or even trnstumorl routes [20, 24]. These shunts n trnsiently open uner the influene of ngiogeni moultors ut re frequently relte to pthology tht either ompromises portl flow or inreses rteril perfusion. APS n open to further extent in response to signifint portl loo flow reution or stoppge, whih in turn results in ompenstory inrese of the rteril flow through the orresponing liver segments. Connetions etween the intrhepti vsulr systems re not restrite to rterioportl ommunition ut my lso our etween the portl vein n the hepti or systemi veins, s seen in onitions suh s portl hypertension. Trnssinusoil shunts re governe y n rteriolr inlet sphinter uner the influene of ngiogeni ftors suh s vsulr enothelil growth ftor (VEGF) n ngioproteins. These shunts our in Bu-Chiri synrome, or my rise for no pprent reson or in response to fol infetion or noules of isese tht ompromise the portl perfusion of the sutene liver. The periiliry plexus or trnsplexl route is the most prominent venous system, n is ompose of vessels tht run roun the loulr uts. This system plys n importnt role when the portl vein is ompromise. Trnsvsl plexus often ours in onjuntion with periiliry shunting n vi the vs vsorum of the portl vein. It most ommonly ours in the setting of portl vein olusion or in ses of invsive heptoellulr rinom (HCC) [20]. Smll res of liver tissue my e supplie y nother venous system, the thir inflow whih omprises errnt veins tht enter the liver iretly, inepenently of the portl venous system. Suh veins ommunite with intrhepti portl rnhes to vrious egrees n le to folly erese portl perfusion. However, little overll hnge in the hepti rteril perfusion is seen. Beuse this hemoynmi stte is persistent, fol metoli hnges re osionlly oserve, typilly s spring in the ftty liver or s umultions of ft [20].

2 152 MRI of the Liver Antomi Vrints of the Hepti Cirultion Antomi vsulr vrints of the hepti irultion my involve the hepti rtery, the portl vein, n the hepti veins, n my our in the following mnner: A) The hepti rtery my hve mny ollterl vessels inluing the pnreti-uoenl rteries, the gstro-uoenl rtery, n the phreni inferior right rtery. Collterl routes y errnt hepti rteries my originte from the superior mesenteri rtery, the left gstri rtery or y extrhepti ollterl rteries, suh s the left gstroepiploi rtery, the gstrouoenl rtery, n the right gstri rtery. Outsie the eli trunk, ollterl flow my our vi the inferior phreni rtery [36]. B) The portl vein hs vrints n ollterl vessels. Frequently, portl vein vrints result in thir inflow in whih errnt veins tht re not onnete with the portl vein system enter the liver iretly. These errnt veins, whih re not erive from the gut venous ringe, re poor in nutritionl ftors. The thir inflow my involve the ysti vein, whih rins the glller e, n the priliry venous system, whih is within the heptouoenl ligment just nterior to the min trunk of the portl vein. The priliry venous system ollets venous loo from the he of the pnres, the istl prt of the stomh, n the iliry system ner the glller [13, 32]. These veins usully join the min trunk of the portl venous system s mjor rnhes, ut osionlly enter the liver iretly roun the port heptis, whih sometimes results in isolte perfusion. The epigstri-prumilil venous system is nother vrint of the portl vein n onsists of smll veins roun the fliform ligment tht rin the venous loo from the nterior prt of the ominl wll iretly into the liver. These veins re roughly ivie into three sugroups: the superior n inferior veins of Sppey tht rin the upper n lower portions of the fliform ligment, respetively, n the vein of Burow [47]. When ostrution of the ven v ours, eh of these veins my serve s ollterl hnnels for loo flow into the liver. C) There re numerous hepti vein vrints n essories. Most hepti vein vrints rin iretly into the inferior ven v. These usully enter the ven v on the right sie oth ully n orslly with respet to the level of the portl vein. The etetion of these vessels is importnt in Bu-Chiri synrome n lso for surgil plnning, sine they represent the min ringe route from the right liver loe [47] Vsulr Anormlities Due to the interreltionship etween ifferent vessels, when iniviul vessels eome ompromise, this immeitely hnges the loo flow in surrouning vessels (Fig. 1) Portl Vein Compromise A erese in portl loo flow my our in response to thromosis, stenosis, or to ompression of the min portl trunk or peripherl intrhepti rnhes. On ynmi omputer tomogrphy (CT) or mgneti resonne (MR) stuies of the liver, the erese portl loo flow les to res of prenhyml enhnement uring the rteril phse, referre to s trnsient hepti ttenution ifferene (THAD). This re of enhnement, representing inrese ompenstory rteril flow, is no longer visile uring the susequent portl venous phse ue to rpi equilirtion of ontrst ensity. Potentil linil prolems ssoite with THAD re tht fol liver lesions my e osure if they re lote within the res of hyperttenution, n tht the THAD res themselves my e mistken for hypervsulr lesions if they hve roun or ovl shpe. THAD re frequently seen roun liver - Fig. 1. Liver vessels. Shemti representtion of the inter-reltionship etween ifferent vessels in the liver, emonstrting hnges in the loo flow when n iniviul vessel is ompromise. (HA=Hepti Artery, PV=Portl Vein, HV=Hepti Veins)

3 5 Hepti Pseuolesions 153 sesses or ute holeystitis n these my evelop s result of inrese rteril perfusion eriving from lol hyperemi relte to the inflmmtory proess itself n/or euse of lolly reue portl flow ue to prenhyml ompression y the lesion. In irrhoti n non-irrhoti ptients, THAD re typilly fn- or wege-shpe n my e lor, segmentl, susegmentl, or supsulr in lotion. Another use of reue portl loo flow to the liver, espeilly t the periphery, is portl vernom [10] Hepti Artery Compromise The hepti rteries ommunite with eh other in the entrl portion of the liver n thus the lokge of these lrge rteries inues new routes of flow. However, ute ostrution of peripherl rteril flow oes not inue reognizle hnges in portl loo flow [43] Hepti Vein Compromise When the hepti vein is utely ostrute, the portl vein eomes rining rther thn supplying vein. The result is ompenstory inrese in hepti rteril flow s result of funtionl portl flow elimintion. Liver tumors my ostrut the hepti vein, in whih se prominent hepti enhnement is inue t site tht orrespons to the re of ostrute hepti venous ringe. A reution in the fferent loo flow vi the hepti vein is seen in Bu-Chiri synrome. In the ute phse, the post-sinusoil ostrution uses severe reution in the portl vein flow n ompenstory inrese in the rteril flow elivere through the hepti rtery. Sine loo flow is not le to perfuse the more peripherl liver res properly, n euse there is pressure grient etween the rteril vessels n liver veins, funtionl intrhepti APS evelop, tht my ultimtely le to omplete flow reversl within the portl vein. In the ltter phses of liver enhnement, the pperne of the prenhym is hrterize y stsis. This imging fining is lso seen in right sie ri filure, n is srile to the sme hemoynmi effets. In the hroni phse of Bu-Chiri synrome, n intrhepti network of venous ollterl vessels is prominent, whih evelops to ypss the ostrution. These norml vessels re more evient t the periphery, n re most prominent roun the ute loe, ue to its seprte utonomous venous ringe [31]. 5.2 Prenhyml Pseuolesions Hepti pseuolesions re non-neoplsti normlities whih my e su-ivie into prenhyml pseuolesions n vsulr pseuolesions. Prenhyml pseuolesions inlue fol ftty hnge, fol spring, inflmmtory pseuotumor, onfluent firosis, pseuotumor hypertrophy n hepti peliosis. Vsulr pseuolesions, on the other hn, re non-neoplsti hepti pseuolesions suh s APS, THAD, n vsulr normlities ssoite with Bu-Chiri synrome. Non-neoplsti normlities re lerly epite with moern imging tehniques n rise priniplly ue to loo flow normlities. These pseuolesions often our folly n n e foun in oth irrhoti n non-irrhoti livers. The min linil iffiulty is to etet n isriminte these non-neoplsti lesions from enign n mlignnt hepti neoplsms [32] Fol Ftty Liver Ftty liver infiltrtion is ommon, metoli omplition of vriety of toxi, ishemi n infetious insults to the liver, suh s oesity, ietes mellitus, loholi liver isese, mlnutrition, n hemotherpy. Other uses inlue hyperlimenttion, inherite metoli isturne, inflmmtory owel isese, severe heptitis, enogenous n exogenous steroi use, n pregnny [1]. Generlly, ft is eposite in response to ifferent metoli hnges, suh s inrese hepti synthesis of ftty is (ethnol), erese hepti oxition or utiliztion of ftty is (ron tetrhlorie, tetryline), impire relese of hepti lipoproteins (sterois), or exessive moiliztion of ftty is from ipose tissue (lohol, sterois). The prevlene of fol ftty infiltrtion of the liver inreses signifintly with vning ge; wheres it is unommon in infnts n young hilren, it is present in roughly 10% of the ult popultion [23]. There re oth iffuse n fol forms of ftty liver infiltrtion. Approximtely 30-40% of ses our folly, either s solitry res (10% of ses), or s multiple res with more wiespre istriution (20-30% of ses). Most ses of ftty liver infiltrtion re of the iffuse type with segmentl, lor, or irregulr istriution. A ommon site of ftty liver infiltrtion is the ventro-meil portion of the meil segment jent to the fliform ligment [6]. Portl flow erese leing to hepti nutritionl ishemi is ommon fining t this site n it is this erese in portl flow tht inues the eposition of ft. Frequently, sys-

4 154 MRI of the Liver temi veins, suh s the inferior vein of Sffey, supply this re in the sene of portl hypertension. Other ommon sites for the fol eposition of ft inlue supsulr regions n the orso-meil portion of the meil segment. When irregulr ftty liver or multiple fol ft eposits re seen, they re typilly istriute wiely with no ovious reltionship to vsulr flow. In mny ses ftty liver my e trnsient, ppering n isppering omprtively rpily. Moreover, it is often reversile with sustne stinene. On ultrsoun (US), key inition for ftty liver infiltrtion is entution of the rightness of prenhyml ehoes. While iffuse forms of ft infiltrtion typilly hve homogeneous pperne, in some ses n extremely heterogeneous or pseuonoulr pperne is note, simulting iffuse noulrity. In the se of fol ftty infiltrtion, res of ft eposition my e seen s solitry hyperehoi res, multiple onfluent hyperehoi res, hyperehoi skip noules, or irregulr hypern hypoehoi res (Fig. 2). Color Doppler exmintions typilly revel no mss effet or vsulr istortion (Fig. 3). Some stuies hve exmine the sensitivity n speifiity of US for reognizing ft, s ssesse on liver iopsy in ptients suspete of hving liver isese. Not surprisingly, the sensitivity of US imging for the etetion of ft inreses with inresing egrees of stetosis. The men sensitivity n speifiity vlues vry from 60% to 90%, n from 80% to 95%, respetively. Unfortuntely, US is not le to ifferentite simple stetosis from non-loholi stetoheptitis, oth of whih my o-exist [17, 22]. On CT, the ttenution of the norml liver is generlly Hounsfiel units (HU). Inrese hepti ft les to reution of the men hepti ttenution. Wheres in mil ses the CT ttenution of the liver might pproximte tht of the spleen, in vne ses the liver my pper prtiulrly hypoense, leit less ense thn the portl n hepti veins (Fig. 4). All forms of liver ft eposition (iffuse, lor, irregulr, n fol is- Fig. 2-. Fol ftty liver on US. On US exmintions, fol ftty res in the liver my pper with ifferent ptterns: () s hyperehoi noules (rrows), () s multiple, onfluent hyperehoi lesions (rrowhes), () s hyperehoi skip noules (rrowhes), n finlly () s irregulr hyper- (sterisk) n hypoehoi res (rrowhes)

5 5 Hepti Pseuolesions 155 Fig. 3. Fol ftty liver on olor Doppler US. On olor Doppler evlution, vsulr struture (rrowhes) ourses, without istortion, etween the hyperehoi noules tht represent fol ftty infiltrtion triution) re etetle on CT (Fig. 5). On unenhne CT iffuse istriution is seen s generl erese of ttenution throughout the orgn. Conversely, fol epositions of ft re ientifile s low-ensity, poorly emrte, spheril or non-spheril res tht show no mss effet n whih hve entrl ore of inonspiuous hepti tissue of norml ensity. However, multifol ftty liver isese tht simultes multiple lesions my lso e seen (Fig. 6) [25]. On unenhne T1- n T2-weighte MR imging, ft eposition is typilly hrterize y slight hyperintensity reltive to the norml liver prenhym. Wheres onventionl spin-eho sequenes re reltively insensitive to ft eposition, the use of short tu inversion reovery (STIR) or other ft-suppression tehniques my revel the presene of ft eposition s res of lower signl intensity. On the other hn, possily the est imging tehnique to etet n isriminte intrellulr ft is hemil-shift imging. On in-phse imges, the signls from ft n wter re itive, while on oppose-phse imges the ft signl is sutrte from the wter signl. Lesions or res ontining ft n wter therefore show loss of signl intensity on oppose-phse imges when ompre with in-phse imges (Fig. 7). On T1-weighte imges quire uring the rteril phse of ontrst enhnement fter the olus injetion of golinium ontrst gent, fol ft epositions generlly pper s isointense or slightly hypointense ompre to the surrouning liver prenhym, epening on the egree of stetosis (Fig. 8). Conversely, uring the liver-speifi heptoiliry phse fter G-BOPTA the typil pperne of fol ft epositions is slightly hypointense ompre to the norml liver. This ours euse of heptoyte llooning whih impees the ility of the otherwise norml heptoytes to tke up G-BOPTA. This is prtiulrly pprent on oppose-phse hemil shift imging (Fig. 9). With regrs to iffuse ftty liver, this is typilly seen uring the liver-speifi heptoiliry phse fter G-BOPTA ministrtion, s mrke homogeneous inrese in liver prenhym signl intensity. The pperne of fol ft res on T2-weighte imges fter the ministrtion of superprmgneti iron oxie (SPIO) ontrst gents is epenent on the Kupffer ell presene in the re of ftty hnge. Wheres some reports hve suggeste tht ftty res re not visile euse of the overll mrke erese in signl intensity fter SPIO umultion [28], other stuies hve shown Fig. 4,. Fol ftty liver on CT. Pre-ontrst CT sns show tht in moerte forms of fol ftty liver () the ROI vlues of the liver re lower thn those of the spleen. Conversely, in vne fol ftty liver () the liver is mrkely hypoense with ROI vlues ner 0 HU. Note tht in vne fol ftty liver, vessels re seen s hyperense ompre with norml liver tissue

6 156 MRI of the Liver e f g Fig. 5-g. Fol ftty liver on CT. Ftty liver with lor istriution (, ) is represente y lrge pseuolesion (sterisk) on the pre-ontrst CT sn () tht ppers slightly hypoense fter ontrst meium ministrtion (). In fol ftty liver with irregulr istriution (, ) numerous smll, ill-efine, hypoense noules (rrowhes) on the pre-ontrst sn () emonstrte heterogeneous enhnement in the portl venous phse fter ontrst meium ministrtion (). Ftty liver with fol istriution (e-g) is hrterize y well-efine hypoense noule (rrow) on the pre-ontrst exmintion (e) whih oes not show signifint enhnement fter ontrst meium ministrtion (f, g). Note the presene of n errnt vessel within the pseuolesion (rrowhe)

7 5 Hepti Pseuolesions 157 Fig. 6-. Multifol ftty liver. On the US exmintion () multiple ill-efine, slightly hyperehoi noules re etete (rrows). The orresponing pre-ontrst CT sn () revels numerous, ill-efine, slightly hypoense res (rrows), whih o not show signifint enhnement uring the rteril () n portl venous () phses fter ontrst meium injetion. Note some vsulr strutures within the fol ftty res (rrowhes in ) Fig. 7-. Diffuse ftty liver. On the pre-ontrst HASTE T2-weighte imge () n the GRE T1-weighte in-phse imge () the signl intensity of the liver is homogeneously inrese. Conversely, on the GRE T1-weighte out-of-phse imge () the signl intensity is mrkely n hrteristilly erese. GRE T1-weighte ft suppresse sequenes () re not suffiiently sensitive to smll quntities of ft, n so the liver ppers hyperintense s ompre with the spleen

8 158 MRI of the Liver e f Fig. 8-f. Fol ftty liver. On the pre-ontrst T2-weighte imge () the liver ppers homogeneously, slightly hyperintense, wheres on the pre-ontrst GRE T1-weighte in-phse imge () it ppers heteogeneous, n ill-efine slightly hyperintense res (rrows) n e seen. The orresponing pre-ontrst GRE T1-weighte out-of-phse imge () shows iffuse hypointense res (rrowhes) in oth liver loes initing fol ftty infiltrtion. During the T1-weighte ynmi stuy fter ontrst gent ministrtion, wek n heterogeneous intrlesionl enhnement n e etete in the rteril phse (). Note tht some vsulr strutures re lerly visile in the ffete res. In the portl venous phse (e), res of fol ftty infiltrtion (rrows) pper s slightly hypointense ompre to surrouning norml liver tissue. In the heptoiliry phse fter G-BOPTA ministrtion (f) the liver is reltively homogeneous in pperne, lthough some of the res of fol ftty infiltrtion show slightly erese signl intensity. The signl intensity of these res is reltively unhnge ompre with the unenhne imges; however, these res pper slightly hypointense euse of the inrese signl intensity of the surrouning norml liver tissue

9 5 Hepti Pseuolesions 159 Fig. 9-. Fol ftty liver. An ovl shpe, well-efine, slightly hyperintense re (rrowhes) in the posterior portion of segment IV n e etete on the pre-ontrst GRE T1-weighte in-phse imge (). The lesion is heterogeneously hypointense on the pre-ontrst GRE T1-weighte out-of-phse imge (). In the heptoiliry phse fter G-BOPTA ministrtion (, ) the re of fol ftty infiltrtion ppers isointense on the T1-weighte in-phse imge () n hypointense on the T1-weighte out-of-phse imge (). The erese uptke of G-BOPTA is ue to the ltere metoli funtion in the re of fol ftty infiltrtion erese uptke of SPIO in non-iffuse res of ft eposition [18]. While fol ft epositions my mimi the pperne of fol liver lesions, it is eqully the se tht fol ftty lesions suh s lipom n ngiomyolipom, ut more frequently HCC or hepti enom, my mimi fol ft. In orer to istinguish fol ft epositions from lesions with ftty metmorphosis, the signl intensity on T2- weighte imges, the prominent vsulrity, the presene of intrtumorl res of hemorrhge or nerosis, speifi imging signs suh s pseuopsule, n the enhnement ehvior fter ministrtion of liver-speifi ontrst gents shoul ll e tken into ount (Fig. 10).

10 160 MRI of the Liver e f Fig. 10-f. HCC with ftty metmorphosis. The pre-ontrst Turo SE T2-weighte imge () n the orresponing GRE T1-weighte in-phse imge () revel well-efine roun noule (rrow) whih is slightly hyperintense n heterogeneously isointense ompre to the norml liver prenhym, respetively. The signl intensity is reue on the GRE T1-weighte out-of-phse imge () ue to the ftty ontent of the lesion. On ynmi T1-weighte imging fter G-BOPTA ministrtion (, e) the lesion shows strong enhnement in the rteril phse () n thin, hypointense pseuopsule (rrowhe) in the portl venous phse (e). On the elye heptoiliry phse imge (f) the noule is slightly hypointense, suggesting tht the lesion is mlignnt in nture. In this se, however, the neoplsti ells in the well-ifferentite HCC still hve some pility to tke up G-BOPTA n to proue ile

11 5 Hepti Pseuolesions Fol Spre Ares in Ftty Liver Fol spring of ftty infiltrtion most frequently ours roun the glller n in the orsomeil portion of the meil segment where supply to the hepti prenhym my erive from systemi veins suh s the ysti vein of the glller or n errnt right gstri vein, rther thn from the portl vein. Fol spring n lso our jent to tumor ue to the presene of n rterioportl shunt or s rim roun n expnsively growing tumor. Unlike fol ft eposits, fol spre res hve hypoehoi pperne on US. However, neither fol ft eposits, nor fol spre res etermine mss effet with respet to vessels (Fig. 11). On multiphsi CT, fol spring hs hyperense pperne tht is vrile with the mount of ftty liver infiltrtion. As in the se of fol ft infiltrtion, roun res of fol spring my mimi hepti tumors (Fig. 12). On heptoiliry phse T1-weighte MR imges fter the ministrtion of G-BOPTA, fol spring in ftty liver hs n isointense or slightly hyperintense pperne (Fig. 13). A similr pperne is seen fter the ministrtion of other heptoiliry gents suh s G-EOB-DTPA or Mn- DPDP. Conversely, on T1- n T2-weighte imges fter SPIO ministrtion, fol spre res in ftty liver re seen s res of reltively low signl intensity refleting the reltively high uptke of SPIO in these res ompre with reue uptke in ftty res of the liver [18]. Wheres fol ftty infiltrtion n fol spre res with roun, regulr pperne my mimi hepti tumors (Figs. 12, 13), irregulr or iffuse res of infiltrtion or spring my osure fol liver lesions (Fig. 14) Inflmmtory Pseuotumors Hepti inflmmtory pseuotumor is n unusul n rre tumor-like onition tht is inresingly reognize s n importnt ifferentil ignosis in ptients presenting with liver msses. Synonyms use to efine this lesion inlue xnthogrnulom, firous xntom, plsmellulr grnulom, histioytom, pseuolymphom, n plsmoytom, ll of whih reflet the histologi omponents of the lesion. Most ommonly, the onition ours in hilren n in young men. Although the etiology is unknown, some uthors hve suggeste oliterns phleitis strting from the portl vein s possile use, with seonry iliry stsis n egenertion n nerosis of the iliry uts, leing to periutl sess or xnthogrnulom [27]. Mrosopilly, the inflmmtory pseuolesion is usully yellow-grey in olor n solitry, lthough multifol inflmmtory pseuotumor of the liver hs een esrie. The most frequent mirosopi omponents re plsmellulr ells, lthough vrile mounts of histioytes, mrophges, firomyolsts, n firous tissue re lso oserve. Three histologi sutypes hve een ientifie on the sis of the prevlene of single omponents, thus xnthogrnulomtous type lesions hve histioyti prevlene, plsmellulr type lesions ontin minly plsm ells, n sleroti type lesions hve preominntly firoti omponent [46]. Typilly, symptoms n lortory finings inite n ute inflmmtory proess, n reurrent pyogeni holngitis is the most frequent linil mnifesttion. Lrge lesions my use senstion of right upper ominl qurnt fullness or isomfort, with mlise, fever n weight loss. Liver funtion tests sometimes emonstrte the elevtion of lkline phosphtse n γ-glutmyltrnsferse. Fetures re non-speifi on US, with lesions presenting s heterogeneously hypoehoi or mosi ptterns, similr to those oserve in other fol liver neoplsms suh s HCC [19]. Similrly, the pperne of n inflmmtory pseuolesion is non-speifi on unenhne CT, with lesions invrily ppering hypoense. After ontrst meium ministrtion, n erly intense n peripherl enhnement is usully followe y homogeneous, omplete n persistent enhnement (Fig. 15). After few minutes, peripherl enhnement n hypoense ore n e oserve, the former omprising firolsti ells, n the ltter hroni inflmmtory ells [19]. On unenhne T1-weighte MR imges, inflmmtory pseuotumor is typilly hypointense, prtiulrly in the entrl portion. Conversely, on T2-weighte imges the lesion frequently emonstrtes isointensity or slight hyperintensity (Fig. 16). However, the pperne is vrile in reltion to the histologi omponents: for exmple, slight hypointensity my e oserve on T2-weighte imges in lesions with strong firoti preominne while stronger hyperintense pperne is initive of greter preominne of inflmmtory ells. Erly peripherl enhnement is typilly seen on T1-weighte ynmi imging fter olus injetion of ontrst gent, refleting the ellulr omponents n inflmmtory hnges within the lesion. Heptoiliry phse imging fter ministrtion of G-BOPTA or nother heptospeifi ontrst gent, frequently revels hypointense re representing the sene of heptoytes within the lesion (Fig. 17) [19, 37]. A rop in signl on T2-weighte imges fter SPIO ministrtion my revel resiul Kupffer ell funtion in liver prenhym in n sur-

12 162 MRI of the Liver Fig. 11,. Fol spring on US. B-moe US () revels hypoehoi re (rrowhe) with tringulr shpe ner the surfe of the liver. On olor Doppler US () n intrlesionl vessel is lerly visile. Note the sene of ny mss effet. This is typil of fol spring in ftty liver Fig Fol spring. Ptient with Burkitt lymphom fter hemotherpy. On the US exmintion () the liver is extremely right ue to hepti stetosis, n roun, hypoehoi noule (rrowhe) is visile in segment IV of the liver. On the CT stuy (-) the lesion (rrowhe) oes not show signifint enhnement. This is initive of fol spring in ftty liver

13 5 Hepti Pseuolesions 163 e f Fig. 13-f. Fol spring. Ptient with history of rest ner n hemotherpy. US evlution () revels n ovl shpe, hypoehoi re (rrowhe) within iffuse ftty liver. This is onsiere suspiious for metstsis. On the MR exmintion, this fol re (rrow) ppers slightly hypointense on the pre-ontrst TSE T2-weighte imge (), isointense on the GRE T1-weighte in-phse imge (), n hyperintense on the GRE T1-weighte out-of-phse imge (). On the ynmi imges fter G-BOPTA ministrtion (e, f) the lesion oes not revel inrese perfusion or wsh-out. This is more initive of n re of fol spring in ftty liver thn of metstsis

14 164 MRI of the Liver e f Fig. 14-f. Fol ftty liver. Ptient with history of renl ell rinom n hemotherpy. On the CT exmintion (-), n on the preontrst GRE T1-weighte in-phse n GRE T1-weighte out-of-phse imges (, e), the heterogeneous, iffuse ftty infiltrtion oes not permit the onfient efinition of ny lesion n in prtiulr smll n ill-efine re (rrowhe) in liver segment II. On the orresponing HASTE T2-weighte imge (f) two mrkely hyperintense lesions (rrows) n e seen, n the signl intensity is suggestive of hemngiom

15 5 Hepti Pseuolesions 165 e Fig. 15-e. Inflmmtory pseuotumor. Ptient with primry immunoefiieny. On the US exmintion () well-efine hypoehoi noule (rrow) is etete. On the orresponing pre-ontrst CT exmintion () well-efine, ovl, homogeneously hypoense lesion (rrow) is emonstrte in segment IV of the liver. After the olus ministrtion of ontrst meium, erly peripherl enhnement (rrowhe) is evient in the rteril phse (), while n isoense homogeneous pperne is seen in the portl venous () n equilirium (e) phses

16 166 MRI of the Liver e f g Fig. 16-g. Inflmmtory pseuotumor. On the pre-ontrst HASTE T2-weighte imge () slightly hyperintense lesion (rrows) in the re of the liver hilum is visile. On the orresponing pre-ontrst T1-weighte imge () the lesion is hypointense. The lesion shows heterogeneous enhnement in the rteril () n portl venous () phses of ynmi imging fter injetion of G-BOPTA. In the equilirium phse (e) entrl wsh-out of ontrst gent is evient, n the lesion now emonstrtes hyperintense rim (rrowhes). This most likely orrespons to n inflmmtory retion n eem of the surrouning liver tissue. In the heptoiliry phse (f) the lesion is hypointense in the enter, surroune y slightly righter rim. A HASTE T2-weighte imge (g) quire uring follow-up exmintion performe six months fter ntiioti therpy revels omplete restitution n no resiul tumor

17 5 Hepti Pseuolesions 167 e f Fig. 17-f. Inflmmtory pseuotumor. Sme se s emonstrte in Fig.15. On the pre-ontrst T2-weighte sequene () n on the GRE T1-weighte imge () the lesion (rrow) ppers hyperintense n heterogeneously hypointense respetively, ompre to the surrouning norml liver prenhym. Enhnement is seen in the periphery of the lesion uring the rteril phse () fter G-BOPTA ministrtion. During the portl venous phse (), the lesion ppers slightly hyperintense, prtiulrly in the entrl portion. During the heptoiliry phse (e) the noule ppers hypointense, ue to the sene of heptoytes. Follow-up MR imging fter six months (f) oes not revel ny fol lesions

18 168 MRI of the Liver rouning the inflmmtory pseuotumor. However, some uthors hve esrie lesions tht show no SPIO prtile uptke [37]. As it is iffiult to ignose inflmmtory pseuotumor of the liver on MR imging lone, supplementl lesion iopsy shoul lso e performe [26] Peliosis Heptis Peliosis heptis is rre entity hrterize y loo-fille ysti vities in the liver. Peliosis heptis frequently evelops in ssoition with mlignnies n hroni wsting iseses, suh s tuerulosis. However, it hs lso een esrie in ssoition with renl trnsplnttion, hemtologil isorers n infetion with humn immunoefiieny virus (HIV), s well s in ptients on long-term tretment with noli sterois, orl ontreptives, hormones, estrogen or Azthiprine. Regression is generlly oserve fter suh gents hve een stoppe or fter pproprite ntiioti therpy [44, 45]. Mrosopilly, peliosis is hrterize y ysti ilte sinusois fille with re loo ells n oun y ors of liver ells. Two vrieties hve een esrie: the phleetti type, in whih the loo-fille spes re line with enothelium n re se on neurysml ilttion of the entrl veins, n the prenhyml type, in whih the loo spes re not line with enothelium n re usully ssoite with hemorrhgi prenhyml nerosis. Peliosis n e ifferentite from hemngiom y the presene of portl trts within the firous strom of the loo-fille spes. Numerous theories hve een propose for the use of peliosis heptis, inluing outflow ostrution n heptoellulr nerosis leing to ysti loo-fille formtions. Peliosis heptis is usully foun inientlly t utopsy ut, rrely, it n use hepti filure or liver rupture with hemoperitoneum or shok. Ptients sometimes hve non-speifi signs suh s heptomegly n portl hypertension [44]. US finings re not speifi for the ignosis of peliosis heptis; the hepti ehopttern is usully non-homogeneous with oth hyperehoi n hypoehoi res [30]. On CT imges fter the olus ministrtion of iointe ontrst mteril, these lesions usully pper initilly hypoense, n eome isoense over time [42]. On unenhne T2-weighte MR imges, peliosis heptis frequently emonstrtes high signl intensity similr to tht seen in hemngiom. Conversely, low signl intensity is usully seen on unenhne T1-weighte imges. After golinium ministrtion, the lesions my show homogeneous or heterogeneous hypervsulriztion epening on flow, n my pper iso- or hyperintense on portl venous n equilirium phse imges fter G-BOPTA ministrtion. In the heptoiliry phse fter the ministrtion of G-BOPTA, Mn-DPDP or G-EOB-DTPA, the lesion gin ppers hypointense euse of the sene of heptoytes within the ysti ilte sinusois (Fig. 18). Fig. 18-j. Peliosis heptis. Ptient with non-hogkin lymphom uring hemotherpy. The pre-ontrst HASTE T2-weighte MR imge () revels multiple ill-efine res (rrowhes) with high signl intensity. On the orresponing unenhne GRE T1-weighte imge () these res hve low signl intensity. During the ynmi evlution fter ministrtion of G-BOPTA, the lesions show homogeneous hypervsulriztion in the rteril phse () n remin hyperintense uring the portl venous () n equilirium (e) phses. Beuse of the sene of heptoytes within the ilte sinusois, the lesions pper hypointense on T1-weighte (f) n T1-weighte ft-suppresse (g) imges quire uring the heptoiliry phse fter G-BOPTA ministrtion. A follow-up exmintion performe one yer fter hemotherpy (h-j) shows omplete resolution of the prenhyml hnges

19 5 Hepti Pseuolesions 169 e f g h i j

20 170 MRI of the Liver Confluent Hepti Firosis Confluent hepti firosis is mss-like firosis seen in pproximtely 15% of ptients with vne irrhosis who re nites for liver trnsplnttion. The imging finings of onfluent firosis result in it eing hrterize ue to its speifi lotion in the liver, whih is frequently the meil segment of the left n/or right loe. Clifitions or ilttion of the iliry uts re very rre. Imging tehniques suh s US re not speifi for the ignosis of onfluent hepti firosis; onfluent firosis typilly ppers s n ill-efine hyperehoi, heterogeneous re, often with pseuonoulr spet. On unenhne CT, onfluent firosis often ppers s wege-shpe fol re of low-ensity. After ontrst mteril ministrtion the lesion gin emonstrtes low level of vsulrity ut my pper slightly hyperense in the equilirium or lter phses ue to the pooling effet of firoti tissue. Typil fetures suh s retrtion of the overlying liver psule re evient on CT (Fig. 19). Morphologi informtion on onfluent firosis is ville lso fter MR imging, lthough the MR signl hrteristis re not unique n o not permit urte ifferentition of this lesion from hepti neoplsms. Wheres firoti tissue is typilly hypointense with either homogeneous or heterogeneous pperne on unenhne T1- n T2-weighte imges, onfluent hepti firosis ppers s region of lower signl intensity ompre to tht of the jent liver prenhym on T1-weighte imges, n s region of higher signl intensity on T2-weighte n STIR imges. The hyperintense pperne of onfluent hepti firosis on T2-weighte imges reflets eem within the firoti re [40, 41]. The pperne of onfluent firosis on ynmi phse imges fter the olus injetion of golinium ontrst gent is similr to tht oserve on CT, with hyperintensity typilly seen uring the equilirium phse. During the heptoiliry phse fter the ministrtion of heptospeifi ontrst gent, onfluent firosis typilly hs heterogeneously hypointense pperne ue to the reue numer of heptoytes (Fig. 20). Confluent firosis on SPIO-enhne T2- weighte imges hrteristilly presents s wege-shpe re of high signl intensity with internl res of low signl intensity. While the re of high signl intensity orrespons to the istriution of firosis, the low signl intensity regions reflet resiul funtioning liver prenhym tht is le to tke up SPIO prtiles [33]. The ifferentil ignosis of onfluent firosis in irrhoti ptients inlues non-neoplsti proesses suh s segmentl ftty liver or hepti infrtion n neoplsti proesses suh s infiltrtive slerosing HCC. Although irregulr ftty infiltrtion my pper with vrile shpe n is- Fig Confluent hepti firosis. The pre-ontrst CT sn () revels hypoense re (rrows) lote in segment VIII of the liver, ssoite with psulr retrtion. After ontrst meium ministrtion, this re shows minor enhnement in the rteril phse (), while the ensity inreses progressively in the portl venous () n equilirium () phses

21 5 Hepti Pseuolesions 171 e f Fig. 20-f. Confluent hepti firosis. Sme se shown in Fig.19. On the pre-ontrst T2-weighte imge () n on the GRE T1-weighte imge () n re (rrows) lote in segment VIII of the liver ppers homogeneously, slightly hyperintense n heterogeneously, slightly hypointense, respetively. The enhnement ehvior uring the ynmi series fter ministrtion of G-BOPTA is similr to tht seen on CT imging: the re oes not show signifint enhnement on rteril phse imges () ut shows progressive inrese in signl intensity uring the portl venous () n equilirium (e) phses (rrows). On the heptoiliry phse imge (f) fter injetion of G- BOPTA this re ppers slightly hypointense ompre with the norml liver

22 172 MRI of the Liver triution, the sene of psulr retrtion or segmentl shrinkge is often suffiient to istinguish this lesion from onfluent firosis. Similrly, hepti infrtion n pper s well-emrte wege-shpe re, ut these res typilly show little or no enhnement. Moreover, hepti infrtion is rre in irrhoti ptients, ourring more frequently in ptients with hemtologi isorers fter vsulr surgery or trnsplnttion. In the se of infiltrtive slerosing HCC, this lesion n e seen s nerly wege-shpe or peripherl n-like lesion, lthough it is usully hypervsulr uring the rteril phse of the ynmi stuy, showing wsh-out in the portl venous phse. Moreover, HCC is frequently ssoite with pseuopsule n often ontins res of nerosis, hemorrhge or ftty metmorphosis within the lesion [40, 41] Segmentl Hypertrophy In onitions suh s irrhosis, Bu-Chiri synrome or primry slerosing holngitis the liver my e ysmorphi in pperne. In the hroni phse of Bu-Chiri synrome, the norml vsulriztion tens to e lote more peripherlly n to e most prominent roun the ute loe ue to its seprte utonomous venous ringe. Consequently, this liver portion my inrese in volume. In slerosing holngitis, trophy n ompenstory hypertrophy of the liver prenhym re onsequenes of hroni ostrution of the segmentl ile ut. This les to trophy of the ffete segments n ompenstory hypertrophy in other segments in whih ile flow is mintine (Fig. 21). On CT n MR imging the resulting liver hypertrophy ppers more hyperense n hyperintense on T1-weighte imges respetively, ompre to tht of the surrouning prenhym Fig. 21. Segmentl hypertrophy. Ptient with primry slerosing holngitis. Color Doppler US revels prominent vsulr strutures lote roun segment I of the liver. This segment emonstrtes progressive inrese in size ue to trophy of other segments ffete y slerosing holngitis (Figs. 22, 23). In some ses the segmentl hypertrophy hs pseuotumorl spet Prenhyml Compression Diphrgmti ompression of liver prenhym ue to ontrtion of iphrgmti musle unles my rete hypoense pseuonoulr res espeilly in segments VII n VIII of the liver. This is typil ourrene t the time of the CT or MR exmintion when ptients inspire eeply using fol inrese in tissue pressure in the su-psulr region. The result is erese in portl perfusion while the hepti rteril perfusion remins reltively unhnge (Fig. 24). Pseuolesions ue to ri ompression re oserve in pproximtely 15% of ptients, n re most ommonly seen in the su-psulr region of liver segments V n VI [47]. Fig. 22,. Segmentl hypertrophy. Sme se s emonstrte in Fig. 21. On the CT exmintion the liver is ysmorphi in pperne, with pseuotumorl hypertrophy of segment I (sterisk). This segment ppers hyperense on the pre-ontrst imge () s ompre with the surrouning liver prenhym tht is ffete y the slerosing holngitis. Note the ilttion of-ile uts s typilly seen in primry slerosing holngitis (rrows). On the post-ontrst imge () the hypertrophy shows norml perfusion n is seen with omprle ensity to the surrouning liver tissue

23 5 Hepti Pseuolesions 173 e Fig. 23-e. Segmentl hypertrophy. On the GRE T1-weighte in-phse () n out-of-phse () imges the liver hypertrophy (rrows) ppers slightly hyperintense. The ynmi stuy fter ontrst gent ministrtion (-e) shows norml vsulriztion ompre to the surrouning liver Fig Prenhyml ompression. On the pre-ontrst T2-weighte () n GRE T1-weighte () imges, roun, slightly hypointense lesion (rrow) n e seen. In the rteril phse fter ontrst gent ministrtion () the re ppers hypointense ue to hnges in hepti rteril perfusion

24 174 MRI of the Liver 5.3 Vsulr Pseuolesions Trnsient Hepti Attenution Differenes (THAD) THAD is ssoite with numerous intrhepti vsulr onitions, prtiulrly intrhepti shunts. Intrhepti shunts n e ivie into rterioportl, rteriosystemi, n portosystemi, epening on the vsulr onnetion. APS re the most ommon form of intrhepti shunts, n re ommonly ssoite with HCC or with itrogeni uses, suh s liver iopsy (Fig. 25) or rio-frequeny (RF) ltion (Fig. 26). In APS iret ommunition etween the feeing rteril vessels of the neoplsm n the rining portl venules les to inrese rteril flow roun the tumor [29]. Erly enhnement of portl vein rnhes uring the rteril phses of CT n MR ynmi stuies is often initive of APS. APS n sometimes e seen in ssoition with smll hemngioms n seems to e relte to the hyperynmi vsulture of this tumor. APS re ommon in liver irrhosis, ue to the mge hepti flow (Figs. 27, 28), n n e soure of potentil onfusion with HCC, espeilly when they pper s smll, roun res uring the rteril phse (Figs. 29, 30). Non-tumorl roun APS show signl loss fter SPIO ministrtion, omprle to tht ourring in the norml liver prenhym. Homogeneous uptke of heptospeifi ontrst gents suh s G-BOPTA is generlly oserve, resulting in n isointense pperne reltive to the norml prenhym (Fig. 30 f, g) [48]. Well-ifferentite smll HCC my emonstrte the sme enhnement ehvior n the sme uptke fter SPIO n heptospeifi ontrst gents. As result, ifferentil ignosis my e iffiult n iopsy or strit follow-up shoul e performe. Diret ommunition etween the portl vein n systemi veins results in intrhepti portosystemi venous shunts. These re frequent in the setting of liver irrhosis with portl hypertension, n my e ompnie y extrhepti portosystemi ollterl irultion. THAD n e lssifie oring to morphology (setorl, segmentl, n lor), etiology (s result of enign or mlignnt tumors, rterioportl shunting, liver irrhosis, or venous thromosis), or pthogenesis (ue to low portl inflow, phlogosis, or sump effet). In the sene of iret reltionship to neoplsm, the most ommon use of THAD is thromosis of the portl vessels. The most frequent etiopthogenesis is therefore low portl inflow ue to ostrution or ompression of the portl vein [21]. Low portl inflow oul e result of APS. In this se, iversion of the portl flow y rteril flow uner higher pressure results in reltively low portl flow n inues ompenstory ollterl rteril flow whih intensifies n perpetutes the phenomenon. Thus, when THAD is relte to APS there is no portl lok, ut rther mixing of rteril n venous loo. This pthogenesis is frequently seen in hemngiom n HCC [9], s well s in rteril phenomen not ssoite with fol liver lesions. Setorl THAD re usully tringulr in shpe. If the lesion is present in the meil portion, low flow is inue y ompression n the THAD is fn-shpe. However, if the lesion is entrl the low flow is usully relte to thromosis or APS n the THAD is wege-shpe [21] (Fig. 31). On the other hn, it is well known tht APS rising in the ontext of irrhosis my proue THAD tht sometimes isply roun or pseuo-roun morphology (the xil setion of the onil shpe my pper roun or ovl). Thus, THAD is poorly istinguishle from smll HCC in irrhoti ptients, or from hypervsulr metstses in nonirrhoti ptients [11]. Osionlly, THAD my our s prelue to n otherwise oult fol lesion [12] n n sometimes msk the unerlying lesion Vsulr Mlformtions Aoring to the Mulliken n Glowki Clssifition, vsulr mlformtions n e suivie into: ) fst-flow forms, tht omprise rteriovenous mlformtions n rterioportl fistuls, ) slow-flow forms, tht omprise portosystemi shunts n venous s well s lymphti mlformtions, n ) omine forms [38]. The vst mjority of vsulr pseuolesions re ue to fst-flow form mlformtions Arteriovenous Mlformtions (AVMs) AVMs re ongenitl normlities in the formtion of loo vessels tht shunt loo through iret rteriovenous onnetions, without neoplsti tissue etween these nomlous vessels. Clinilly, these ongenitl normlities n e oserve in neontes with ongestive hert filure, heptomegly, portl hypertension, n nemi, or in lte hilhoo n in ults in the linil setting of hereitry hemorrhgi telengietsi ssoite with ongestive hert filure, hepti is-

25 5 Hepti Pseuolesions 175 Fig Arterioportl shunts. HCC fter liver iopsy. On the pre-ontrst CT sn () hypoense, roun, well-efine noule (rrowhe) n e seen. In the rteril phse fter ontrst meium ministrtion, mrkely hyperense, tringulr re (rrow) is visile ner the noule (). In the portl venous phse () the re gin ppers isoense ue to wsh-out of ontrst meium from this re n enhnement of the surrouning liver. Ctheter ngiogrphy () onfirms the presene of APS (rrow)

26 176 MRI of the Liver Fig Arterioportl shunts. HCC following tretment y RF ltion. On the pre-ontrst CT sn () well-efine, slightly hypoense noule (rrow) surroune y hypoense rim is emonstrte in segment VII of the right liver loe. During the rteril phse () fter ontrst meium ministrtion mrkely hyperense re (rrowhe) is seen ner the neroti lesion. This re eomes isoense in the portl venous phse () n represents n APS post RF ltion

27 5 Hepti Pseuolesions 177 Fig Arterioportl shunts. Ptient with liver irrhosis. On the pre-ontrst CT sn () no fol lesions re visile. During the rteril phse () fter ontrst meium ministrtion numerous, hyperense res (rrowhes) of vrile size re ppreile. In the portl venous phse () these res emonstrte rpi ontrst meium wsh-out resulting in isoensity. Unlike HCC, these lesions re not hypoense n there is no inition of pseuopsule on the portl venous phse sn

28 178 MRI of the Liver Fig Arterioportl shunts. Ptient with liver irrhosis. On the pre-ontrst CT sn () the liver is homogeneous in ensity. On the ynmi stuy, roun, mrkely hyperense lesion (rrowhe) n e etete in the rteril phse (). Rpi ontrst meium wsh-out ours in the portl venous phse () ut the lesion still ppers slightly hyperense ompre to the surrouning liver prenhym Fig Arterioportl shunts. On the pre-ontrst CT sn () no fol lesions re visile. On the rteril phse imge () fter ontrst meium ministrtion, severl hyperense lesions (rrowhes) with ifferent shpes re visile in the left loe of the liver. These res pper isoense in the portl venous () n equilirium () phses

29 5 Hepti Pseuolesions 179 e f g Fig. 30-g. Arterioportl shunts. Sme se s emonstrte in Fig. 29. On pre-ontrst T2-weighte () n GRE T1-weighte () imges, iffuse ill-efine res of signl heterogeneity (rrows) n e seen. On the rteril phse imge () fter injetion of G-BOPTA, the lesions (rrows) lote in the left loe pper mrkely hyperintense. Rpi wsh-out of ontrst gent ours from these lesions uring the portl venous () n equilirium (e) phses. The liver shows homogeneous signl intensity on T1-weighte (f) n T1-weighte ft-suppresse (g) imges quire uring the heptoiliry phse. This pperne mkes the ignosis of fol liver lesions unlikely n fvours the ignosis of APS

30 180 MRI of the Liver Fig THAD, fol spring n HCC. On the pre-ontrst GRE T1-weighte out-of-phse imge () tringulr re of fol spring (rrows) is lerly emrte in n otherwise iffuse stetosis of the liver. Within the fol spring roun hypointense lesion (rrowhe) representing n HCC n e etete. On the rteril phse imge () fter ontrst gent ministrtion THAD reproues the tringulr fol spre re. In the portl venous phse () the signl intensity in the fol spre re is similr to tht oserve in the preontrst phse, n the roun lesion is not lerly visile. On the orresponing SE T2-weighte imge () the fol spre re is not elinete, ut roun hyperintense lesion (rrow) orresponing to the HCC is reognizle Fig. 32,. Arteriovenous mlformtions. On the rteril phse CT imge (), multiple, irregulr n tortuous rteril vessels (rrowhes) re visile ner the ome of the liver. The left portl rnh (sterisk) is mlforme, inrese in size n shows erly opifition. The portl vein is etter elinete in the erly portl venous phse () n further mlforme venous vsulr strutures (rrowhes) re pprent surrouning the left portl rnh

31 5 Hepti Pseuolesions 181 hemi, n portl hypertension [4, 7]. Frequently, AVMs my our etween the hepti rtery n the hepti vein, s well s etween the hepti rtery n the portl venous system. On US, AVMs n pper s nest of tortuous, enlrge, nehoi vessels lote usully in one loe of the liver. Color Doppler US generlly emonstrtes signifint flow with high pek shifts oth in rteries n veins, low rteril resistive inex (RI), n inrese pulstility of veins. In lte stges of the isese, n rterilize spetrl pttern n e seen in the hepti veins [5]. On unenhne CT, AVMs generlly pper s hypottenuting res within the liver. In the rteril n erly portl venous phses fter ontrst mei ministrtion these lesions enhne intensely n homogeneously. Therefter, ontrst meium equilirtion results in similr ontrst ensity to tht oserve in the surrouning vsulr strutures (Fig. 32). Typil finings on ynmi MR imges of the liver for singulr AVMs post-iopsy or surgery inlue ilttion of the rining hepti vein n n erly enhnement of the hepti veins uring the rteril phse. Shunts etween the hepti rtery n the portl venous system typilly le to inrese portl venous pressure n thus to the usul finings of portl hypertension. MR imging is very useful tool for istinguishing AVMs from hemngioms. Speifilly, signl hypointensity on T2-weighte imges n the sene of progressive enhnement uring the ynmi series of quisitions fter ontrst gent ministrtion mke the ignosis of AVM most prole (Fig. 33) [5, 8]. On MR ngiogrphy, AVMs re foun with poor regionl emrtion of the lesion, rteriovenous shunting, vrile pooling of ontrst mteril in vsulr spes, n no prenhyml lush Arterioportl Fistuls Arterioportl fistuls my e quire or ongenitl, n my hve n intr- or extrhepti lotion. Common uses of quire rterioportl fistuls re irrhosis n hepti neoplsms, lunt or penetrting trum, perutneous liver iopsy, gstretomy, trnshepti holngiogrphy, n iliry surgery (Fig. 34). In the se of ongenitl rterioportl fistuls, these re typilly ssoite with hereitry hemorrhgi telengetsi, iliry tresi, n Ehlers-Dnlos Synrome. Often symptomti within the first yer of life, the first symptom of rterioportl fistul is usully portl hypertension ssoite with splenomegly, hypersplenism, vriel formtion, n sites [2]. US with olor Doppler is the most useful imging tehnique for mking the ignosis of rterioportl fistul. At Doppler US, ommon fetures inlue enlrgement of the hepti rtery n ilttion of the segment of the portl vein in whih the fistul is lote. In ongenitl rterioportl fistul, heptofugl flow in the portl vein n e etete long with olor spekling in the hepti prenhym jent to the fistul, whih is ue to virtion rtift [14]. Imging fetures of rterioportl fistuls on ynmi CT n MR inlue mrke enhnement of the min portl vein, segmentl rnhes, or mjor triutries, with ttenution or signl intensity pprohing tht of the ort uring the rteril phse. Perfusion nomlies of the surrouning liver prenhym suh s regionl inreses in rteril inflow s response to inverte portl flow, n inrese portl vein inflow ue to the shunt itself, my lso e oserve [16]. Angiogrphy is often inite for possile emoliztion Hereitry Hemorrhgi Telngietsi (HHT) HHT, lso lle Renu-Osler-Weer isese or Osler s isese, is vsulr, hereitry, utosomi ominnt isorer tht ours with frequeny of pproximtely ses/100,000 [15]. HHT is hrterize y the presene of muoutneous or viserl ngioysplsti lesions, the ltter most frequently seen in the liver, lung, rin, n gstrointestinl trt. Hepti involvement ounts for 10-40% of ses n is hrterize y the presene of intrhepti shunts (rterioportl, rteriosystemi, venous portosystemi), iffuse telngietses, n vsulr mss-forming lesions [3]. AVMs re usully istriute iffusely throughout the liver n my e ssoite with enlrgement of the hepti rtery n inrese tortuousity of vessels in the liver hilum n in the entrl portions of the liver loes. In Osler s isese, inrese rteril perfusion of the liver tissue frequently les to seonry noulr hypertrophy, whih my e misinterprete s mlignnt hepti tumor. These pseuotumors, s in fol noulr hyperplsi, represent lolize overgrowth of heptoellulr tissue n re not rel liver tumors. Ptients with hepti involvement n e symptomti, ut hert filure, portosystemi enephlopthy, holngitis, portl hypertension, n irrhosis hve een reporte [34]. Fol or iffuse hnges in hepti irultion re etetle on ll of the imging molities. US, prtiulrly in ssoition with olor Doppler, shows intrhepti shunts with rteril n venous vessels frequently inrese in size. However, this imging metho hs omprtively low sensitivity

32 182 MRI of the Liver e f Fig. 33-f. Arteriovenous mlformtions in helthy young ptient. An US sn () shows n norml ommunition (rrow) etween n rteril rnh n venous vessel. On pre-ontrst T1- n T2-weighte MR imges (, ) smll, hypointense re (rrowhes) is visile in the lower prts of segment VII of the liver. On the rteril phse imge () the lesion (rrowhe) shows intense n homogeneous enhnement. Erly enhnement of right portl vein rnh (rrow) is lso evient. The lesion shows the sme signl intensity s oserve in surrouning vsulr strutures in the portl venous (e) n equilirium (f) phses

33 5 Hepti Pseuolesions 183 e Fig. 34-e. Arterioportl fistul in irrhoti ptient. On the T2-weighte () n T1-weighte () MR imges, the fistul (rrows) ppers s hypointense, roun re, with signl voi lose to tht oserve in the ort n portl vein. In ll phses of the ynmi evlution fter ontrst gent ministrtion (-e) the enhnement of the vsulr re is similr to tht ourring in the ort n the left rnh of the portl vein tht inites n rterioportl fistul n sptil resolution for emonstrting smll rteriovenous shunts [39]. On multietetor CT, the possiility to perform seletive, multiphse stuy of hepti vsulr strutures permits oth rteril n venous vessels to e visulize. Hene, the visuliztion of rteriosystemi shunts is improve. Compre with onventionl spirl CT, multietetor CT improves imge qulity, n permits etter multiplnr n ngiogrphi reonstrution. Consequently, the pility to ientify n hrterize the vsulr lesions typil of HHT is improve [8]. Thus telngietses, whih re present in more thn 60% of ses of HHT, re seen s smll vsulr spots tht re reily reognizle on reonstrute multiplnr reformtte n mximum intensity projetion (MIP) imges. Likewise, lrge onfluent vsulr msses, whih re present in out 25% of HHT ses, re seen s lrge shunts or multiple telngietses tht olese. In reent stuy, multietetor CT (MDCT) ws le to etet hepti vsulr ltertions in out 80% of ptients with onfirme or suspete ignosis of HHT [35]. In this stuy rterioportl shunts n rteriosystemi shunts were etete s the only vsulr ltertions in roughly 50% n 20% of ptients, respetively, while oth shunt types were etete in pproximtely 30% of ptients. On MR imging, telngietses pper s smll hypo- to isointense lesions on unenhne T1- weighte imges n s iso- or hyperintense lesions on T2-weighte imges (Fig. 35). Wheres rteriovenous shunts re poorly etete on unenhne T1- n T2-weighte imges, iltte n tortuous vessels n usully e seen ner the rteriovenous shunts. Dynmi MR imging revels strong rteril phse enhnement n susequent isointensity with the surrouning liver tissue in the portl venous n equilirium phses. Norml enhnement of the ffete tissue in the heptoiliry phse n e note with the use of ontrst gents with heptoellulr properties suh s G-BOPTA (Fig. 36).

34 184 MRI of the Liver Fig. 35,. Hereitry hemorrhgi telengietsi. The pre-ontrst T2-weighte ft-suppresse TSE imge () revels lmost omplete exhnge of norml hepti struture y iffuse smll, roun mrkely hyperintense lesions. On the GRE T1-weighte imge () the lesions emonstrte similr hypointensity to tht oserve in the vessels Fig Hereitry hemorrhgi telengietsi. Diffusely istriute AV-mlformtions in ptient with Osler s isese. On the T2-weighte imge () res of flow voi (rrows) in the liver n e note initing inrese flow in rnhes of the hepti rtery. Aitionlly, some noulr-ppering liver lesions (rrowhes) in the right liver loe n e seen. These lesions (rrow) re lerly hypervsulr on the rteril phse imge fter injetion of G- BOPTA (). In the heptoiliry phse one hour fter injetion of G-BOPTA (), the lesions pper hyperintense ompre to the surrouning liver tissue ue to uptke of the ontrst gent into heptoytes. These liver lesions orrespon to lolize overgrowth of heptoellulr tissue similr to tht whih ours in FNH. The lesions pper hyperintense in the heptoiliry phse ue to the elye exretion of G-BOPTA into the newly forme n mlforme ile utules