Cirrhosis CT and MR Imaging Evaluation

European Journal of Radiology 61 (2007) 5769

Cirrhosis: CT and MR imagierl

sima de Be

nolog90127200 Lggioro MaGeneovem

Abstract

In this art tic livforms of vir specsplenomegaly, ascites and varices. We describe the patchy and lacelike patterns of fibrosis, along with the focal confluent form. The process ofhepatocarcinogenesis is detailed, from regenerative to dysplastic nodules to overt hepatocellular carcinoma. Different types of non-neoplastic focalliver lesions occurring in the cirrhotic liver are discussed, including arterially enhancing nodules, hemangiomas and peribiliary cysts. We showdifferent conditions causing liver morphology changes that can mimic cirrhosis, such as congenital hepatic fibrosis, pseudo-cirrhosis due tobreast metastases treated with chemotherapy, Budd-Chiari syndrome, sarcoidosis and cavernous transformation of the portal vein. 2006 Else

Keywords: L

1. Introdu

Cirrhosivarious etiing to extena diffuse dsive loss ofreduced bypean Unionserious moatitis B andare biliary,tations resuand hepaticgastrointes

CorresponTel.: +39 329

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0720-048X/$doi:10.1016/jvier Ireland Ltd. All rights reserved.

iver; Cirrhosis; Computed tomography; Magnetic resonance imaging

ction

s is the final result of chronic damage to the liver fromologies, characterized by parenchymal injury lead-sive fibrosis and nodular regeneration. The result is

isorganization of hepatic morphology with progres-liver function. Although the mortality rate has beenabout 30% in the last few decades, within the Euro-cirrhosis is still one of the leading causes of death and

rbidity. Cirrhosis is most commonly the result of hep-C virus infection or chronic alcoholism; other causescryptogenic and metabolic. Usual clinical manifes-lt from portal hypertension, portosystemic shuntinginsufficiency. Common complications are ascites,

tinal bleeding, encephalopathy and coagulopathy.

ding author at: Via Villaermosa 29, 90139 Palermo, Italy.1828155; fax: +39 0916552325.dress: [email protected] (G. Brancatelli).

In this review, we present the CT and MR imaging findingsin the cirrhotic liver.

2. Liver morphology

At an early stage of cirrhosis, the liver may appear normal oncross sectional imaging. With disease progression, heterogene-ity of liver parenchyma and surface nodularity are observed.Caudate lobe hypertrophy is the most characteristic morpho-logic feature of liver cirrhosis (Fig. 1). A ratio of transversecaudate lobe width to right lobe width greater than or equalto 0.65 constitutes a positive indicator for the diagnosis ofcirrhosis with high level of accuracy [1]. A modified caudatelobe width to right lobe width ratio, using the right portal veininstead of the main portal vein to set the lateral boundary hasrecently been proposed [2]. Other regional changes in hepaticmorphology typically seen in advanced cirrhosis are segmentalhypertrophy involving the lateral segments (II, III) of the leftlobe (Fig. 2), and segmental atrophy affecting both the posterior

see front matter 2006 Elsevier Ireland Ltd. All rights reserved..ejrad.2006.11.003Giuseppe Brancatelli a,b,c,, Michael P. FedRoberto Lagalla b, Alessandro Carriero d, Mas

Sezione di Radiologia, Ospedale Specializzato in Gastroenterologia, Saveriob Sezione di Scienze Radiologiche, Dipartimento di Biotec

Universita` di Palermo, Via del Vespro 127,c Department of Radiology, University of Pittsburgh Medical Center,

d Department of Diagnostic and Interventional Radiology, MaA.Avogadro Eastern Piemonte University, Cors

e Service de Radiologie, Hopital Beaujon, 100 Boulevard duReceived 7 July 2006; accepted 2 N

icle, we present the CT and MR imaging characteristics of the cirrhoal, alcoholic and autoimmune end-stage liver disease. We present theng evaluatione c, Roberta Ambrosini d,o Midiri b, Valerie Vilgrain ellisIRCCS, 70013 Castellana Grotte (Bari), Italyie Mediche e Medicina Legale,Palermo, Italy

othrop Street, 15213 Pittsburgh, PA, USAe della Carita` University Hospital,zzini 18, Novara, Italyral Leclerc, 92118 Clichy, Franceber 2006

er. We describe the altered liver morphology in differenttrum of imaging findings in portal hypertension, such as

58 G. Brancatelli et al. / European Journal of Radiology 61 (2007) 5769

Fig. 1. Typicafat-suppressedmildly lobula(arrow) of hepT1-weighted fvenous phaseratio of 1.80.

segments (the left lobexplanationof hilar pergallbladderthe interlobcirrhosis.

Primaryhave somecirrhosis. Icirrhosis, pl cirrhotic morphology at MR imaging. Transverse T2-weightedturbo spin-echo MR image (A) shows enlarged caudate lobe,

ted liver margins (arrowheads) and regions of high attenuationatic parenchyma caused by patchy fibrosis. Gadolinium-enhancedat-suppressed gradient-echo MR image (B) obtained during portalshows inhomogeneous liver enhancement and caudate to right lobe

VI, VII) of the right lobe and medial segment (IV) ofe [3] (Fig. 2). Alteration of blood flow is the likelyfor these morphologic abnormalities. Enlargement

iportal space, the notch-sign [4] (Fig. 2), an expandedfossa (Fig. 2) [5] and generalized widening of

ar fissures are also considered typical findings of

sclerosing cholangitis and primary biliary cirrhosisdistinctive features in comparison to other types ofn primary sclerosing cholangitis induced end-stageseudotumoral enlargement of the caudate lobe is

Fig. 2. Typicaan enlarged lewith the gallbatrophy of theright posterior(asterisk).

observed iperipheral h(Fig. 3A anintra- and ePrimary bilhypertensiolacelike fi(Fig. 4) [7]phologic cindistingui

3. Portal h

In chronto increasesinusoids.tal hypertethe develothat typical3C and 5Athy) (Fig. 5left gastricto form potal and the(Fig. 5B),retroperiton

Increasenent mesepatients wisevere formand mimicl cirrhotic morphology at CT. Portal venous phase CT scan showsft lateral lobe and caudate lobe (C), an enlarged gallbladder fossaladder (g) herniated toward the anterior abdominal wall, markedmedial segment of the left hepatic lobe (arrowheads) and of thehepatic lobe (arrow), and presence of right posterior hepatic notch

n virtually all patients, along with atrophy of theepatic segments resulting in a lobulated liver contourd B). Concomitant multiple irregular strictures of thextrahepatic bile ducts are also observed (Fig. 3C) [6].iary cirrhosis typically produces early signs of portaln while the liver is enlarged, along with prominent

brosis, regenerative nodules, and lymphadenopathy

. Late-stage primary biliary cirrhosis results in mor-hanges including a shrunken, fibrotic liver, that isshable from other etiologies.

ypertension and mesenteric edema

ic liver disease, progressive hepatic fibrosis leadsd vascular resistance at the level of the hepaticThe increased pressure gradient is defined as por-nsion, and causes complications such as ascites andpment of engorged and tortuous collateral vesselsly develop at the lower end of the esophagus (Figs.) and at the gastric fundus (hypertensive gastropa-B) [8]. The paraumbilical veins (Fig. 5C) and thevein, both draining into the portal vein, also reopenrtosystemic shunts. Other shunts between the por-systemic circulation include splenorenal collateralshemorrhoidal veins, abdominal wall (Fig. 5D) andeal collaterals.d venous pressure is also responsible for the promi-nteric edema and stranding occurring in 86% ofth cirrhosis [9]. It can occur in mild, moderate orwith pseudonodules surrounding mesenteric vessels

king enlarged lymph nodes (Fig. 6).

G. Brancatelli et al. / European Journal of Radiology 61 (2007) 5769 59

Fig. 3. Primacaudate lobeother parts oflost. (C) PortaNote esophag

Fig. 4. Primasubcentimeterregenerative n

4. Fibrosi

Fibrosiscally detecor as a cory sclerosing cholangitis at CT. (A) Nonenhanced CT shows severe lobulation (arro(arrowheads). The peripheral areas of the liver are hypodense due to atrophy. The pthe liver is known as the atrophyhypertrophy complex. (B) In the portal venous phal venous phase CT scan in a different patient with primary sclerosing cholangitis showeal varices (arrow) due to portal hypertension.

ry biliary cirrhosis at CT. (A) Transverse nonenhanced CT scan (narrow window settiregenerative nodules that are hyperattenuating to normal liver or spleen. (B) On

odules are not easily recognized. Splenomegaly and enlarged porta hepatis and porta

s

is an inherent part of hepatic cirrhosis, and is typi-ted as patchy fibrosis (Fig. 1A), as a lacelike pattern,nfluent mass. The lacelike type of fibrosis is best

describednodules. T(Fig. 4A),phase imagpatients wiws) of the hepatic contour and compensatory hypertrophy of thehenomenon of segmental hyperplasia associated with atrophy ofse, the attenuation difference between the caudate and the liver iss irregular dilatation of the intra-hepatic bile ducts (arrowheads).

ng) shows lacelike pattern of low-attenuating fibrosis surroundingportal venous phase CT scan obtained at the same level as A,caval lymph nodes (arrows) are also noted.

as thin or thick bands that surround regenerativehis pattern is best visualized on nonenhanced CTand is usually not well visualized on portal venouses (Fig. 4B) [10]. It is seen in about one-third ofth primary biliary cirrhosis [7], regardless of stage.


Fig. 5. Axialenhanced CTdilated and toparumbilical

Focal confland is usualar portionretraction [shows enhataken for heenhancemeretention o(A), multiplanar reformatted in the coronal plane (B), axial maximum intensity projeimages show different examples of collateral vessels developing in end-stage chron

rtuous esophageal varices (arrow); part (B) shows varices in the gastric fundus (arrow)vein (arrow), and part D shows abdominal wall collaterals (arrowheads).

uent fibrosis is observed in end-stage liver diseaselly a wedge-shaped lesion located in the subcapsu-of segment IV, V or VIII, with associated capsular11,12] (Fig. 7). In those rare cases in which the lesionncement on arterial dominant phase, it may be mis-patocellular carcinoma. Delayed, persistent contrastnt, however, is typically observed, and is due to thef contrast by the fibrotic tissue (Fig. 7D). This fea-

ture, alonglocation anhepatocellu

5. Regene

In the ci(9 mm), action (C) and sagittal maximum intensity projection (D) contrast-ic liver disease due to severe portal hypertension. Part (A) showsand a splenorenal shunt (double arrows); part C shows recanalized

with the characteristic capsular retraction and typicald shape help to distinguish confluent fibrosis fromlar carcinoma.

rative nodules

rrhotic liver, regenerative nodules are macronodulars usually seen in chronic hepatitis B, or micronodular


Fig. 6. Mesenteric edema in cirrhosis. Contrast-enhanced CT scan showsincreased attenuation of the fat (arrows) around the mesenteric vessels due tocongestion and edema caused by portal hypertension. Mesenteric edema in thiscase mimics the appearance of lymph-nodes.

(39 mm), as seen in other causes of cirrhosis. Most regenera-tive nodules are difficult to detect at CT or MR because theyare too small or are too similar to surrounding liver parenchyma[13]. Computed tomography detects regenerative nodules whenthey are surrounded by hypodense fibrotic bands on nonen-

hanced CT (Fig. 4A) or when they accumulate iron (sideroticnodules) [14]. Siderotic regenerative nodules are typicallyhyperattenuating to liver on nonenhanced CT and are isoatten-uating to liver, and therefore difficult to detect, after contrastinjection.

MR imaging demonstrates regenerative nodules with greatersensitivity than any other imaging modality. They usually appearisointense (Fig. 8A) to hypointense on T2-weighted MR imagesrelative to the surrounding inflammatory fibrous septa and isoin-tense (Fig. 8B) to hyperintense relative to background liverparenchyma on T1-weighted sequences [13]. The accumulationof iron within regenerative nodules may cause hypointensityon T2-weighted images (Fig. 9A) because of magnetic fieldinhomogeneities, and marked hypointensity on T1-weightedgradient-Echo MR images (Fig. 9B), usually best visualizedusing TEs greater than 10 ms. Due to their portal venous supply,regenerative nodules usually enhance to the same degree thanthe background liver.

6. Dysplastic nodules

Dysplastic nodules are regenerative nodules containing atyp-ical cells without definite histological signs of malignancy, and

Fig. 7. Cirrholesion (arrowsshows low intgradient-echogadolinium-eof fibrotic tisssis and focal confluent fibrosis at MR imaging. Transverse T2-weighted fat-suppress) in segment four as an area of moderate to high intensity in comparison to backgroun

ensity of focal confluent fibrosis lesion (arrow). Note adjacent retraction (arrowhead) oMR image obtained during arterial dominant phase (C) shows no apparent enhanceme

nhanced T1-weighted fat-suppressed gradient-echo MR image (D), focal confluent fibue.ed turbo spin-echo MR image (A) shows focal confluent fibrosisd liver. T1-weighted gradient-echo fat-suppressed MR image (B)

f liver capsule. Gadolinium-enhanced T1-weighted fat-suppressednt of focal confluent fibrosis lesion. On equilibrium-phase (5 min)rosis lesion shows delayed enhancement (arrow) due to presence


Fig. 8. Cirrhosis and multiple regenerative nodules at MR imaging. Transverse T1-weighted gradient-echo MR image (A) shows multiple subcentimeter isointensenodules (arrows), surrounded by diffuse lacework of low-intensity fibrosis. On transverse T2-weighted fat-suppressed turbo spin-echo MR image (B), nodules(arrows) are still isointense and surrounded by thick hyperintense septa of lacelike fibrosis. Arterial dominant phase (not shown) failed to show enhancement ofnodules, consistent with diagnosis of regenerative nodules.

Fig. 9. Cirrhosis and siderotic regenerative nodules at MR imaging. Transverse T2-weighted fat-suppressed turbo spin-echo MR image (A) shows multiple hypointensenodules (arrowheads). On transverse T1-weighted gradient-echo breath-hold MR image (B), nodules are hypointense.

Fig. 10. Cirrhosis and dysplastic nodule at MR imaging. Transverse T2-weighted fat-suppressed turbo spin-echo MR image (a) shows irregular liver margins,perihepatic ascites (a) and 1 cm hypointense mass (arrow). On transverse T1-weighted gradient-echo breath-hold MR image (b), the mass is hyperintense (arrow).Arterial dominant phase (not shown) failed to show enhancement of nodule.


Fig. 11. Cirrhosis and typical hepatocellular carcinoma at MR imaging. Transverse T2-weighted half-Fourier acquired single-shot turbo spin-echo MR image (A)shows 2 cm mildly hyperintense lesion (arrow) in right hepatic lobe. On T1-weighted gradient-echo MR image (B), lesion is hypointense in comparison to backgroundliver. Gadolinium-enhanced T1-weighted gradient-echo MR image obtained during arterial dominant phase (C) shows marked enhancement of lesion (arrow) withcentral hypointense area due to necrosis. On gadolinium-enhanced T1-weighted gradient-echo MR image obtained during portal venous phase (D), lesion becomeshypointense to surrounding parenchyma. Note hyperintense capsule (arrowhead) surrounding lesion.


Fig. 12. Cirrh(A) shows larsome hypointperipheral poobtained duriis well seen bcarcinoma, wmore frequen

Fig. 13. Cirrhportal venousosis and large hepatocellular carcinoma with mosaic appearance at MR imaging. Trge tumor (arrows) in right lobe of the liver that is slightly hyperintense to surroundingense areas. Gadolinium-enhanced T1-weighted fat-suppressed gradient-echo MR imrtion of tumor enhances (arrow), while remaining part is hypointense. Gadoliniumng portal venous phase (C) shows washout of tumor portion that enhanced in arterialecause of contrast retention. Mosaic appearance is caused by areas of different intensihich contain small viable nodules with interspersed areas of necrosis, fibrosis, and ctly with increasing tumor diameter.

osis and benign arterially enhancing nodule at CT. (A) Arterial dominant phase CTphase CT scan obtained at same level as A, lesions are minimally hyperattenuating tansverse T2-weighted fat-suppressed turbo spin-echo MR imagenontumorous parenchyma and heterogeneous due to presence of

age obtained during arterial dominant phase (B) shows that only-enhanced T1-weighted fat-suppressed gradient-echo MR imagedominant phase. The fibrotic capsule (arrows) surrounding lesionty level and results from peculiar growth pattern of hepatocellularystic or fatty degeneration. Capsule and mosaic pattern are seen

scan of the liver shows small enhancing lesion (arrows). (B) Ono isoattenuating compared to surrounding liver.


are considered an intermediate, premalignant step along thehepatocarcinogenesis process. Malignant transformation withina dysplastic nodule has been identified as early as 4 monthsafter the first detection of the dysplastic nodule [15]. Dysplasticnodules are found in 1525% of cirrhotic livers at the time oftransplantation and are subclassified on the basis of the degreeof cellular abnormalities: low-grade (containing hepatocyteswith mild atypia) and high-grade (when the degree of atypiais moderate, but insufficient for the diagnosis of malignancy)[16].

As with regenerative nodules, dysplastic nodules receive pre-dominantly portal venous flow, and do not usually demonstratebright enhancement on arterial phase CT or MRI. Therefore,marked arterial phase enhancement should suggest hepato-cellular carcinoma rather than dysplastic nodule, but there ismuch overlap in imaging features between regenerative nod-ules, dysplastic nodules and well-differentiated hepatocellularcarcinoma. Dysplastic nodules typically appear hypointenseto the background liver parenchyma on T2-weighted images(Fig. 10a), and show hyperintensity on T1-weighted images(Fig. 10b), quite in contrast to typical findings for hepatocel-lular carcinoma. Arterial phase enhancement should suggestdevelopment of a focus of hepatocellular carcinoma within a

Fig. 14. Tranin cirrhosis aation of the rliver due to thand increasedscan demonstsplenomegaly

high-grade dysplastic nodule, the so-called nodule within anodule appearance on MR imaging [17].

Dysplastic nodules are detected and characterized better byMR than by CT; however, accurate diagnosis may be made inonly about 15% of cases [18].

7. Hepatocellular carcinoma

Hepatocellular carcinoma typically occurs within the cir-rhotic liver. As the degree of (de-differentiation) malignancyincreases, portal blood supply decreases, whereas nontriadalarteries (i.e., unaccompanied by portal venules and biliary ducts)develop to feed the nodules. The presence of early arterialenhancement with rapid washout during the portal venous phaseshould be regarded as highly suspicious for the presence ofhepatocellular carcinoma. Characteristically, hepatocellular car-cinoma is hypoattenuating to liver on unenhanced CT, and

. Cirrhted(arrowsvers

e leveuchger vsient hepatic attenuation difference due to portal vein thrombosist CT. (A) Arterial dominant phase CT scan shows hyperattenu-ight lobe of the liver (arrowheads) in comparison to normal leftrombosis of the anterior branch of the right portal vein (arrow)arterial flow. (B) Delayed phase contrast-enhanced transverse CT

rates isoattenuation of right liver to the normal parenchyma. Note.

Fig. 15T2-weiggiomas(B) Tranthe samlobe is mis no lonhosis and multiple hemangiomas at MR imaging. Transversefat-suppressed turbo spin-echo MR image (A) shows two heman-s) as strongly hyperintense in comparison to liver parenchyma.

e T2-weighted fat-suppressed turbo spin-echo MR image throughl obtained 2 years later. The cavernous hemangioma in the rightsmaller (arrow), while the cavernous hemangioma in the left lobeisible.


manifests as a heterogeneous, moderately enhancing lesion dur-ing the arterial phase, with washout on portal venous and delayedphase [19,20]. Similar features are evident on MR imaging,and hepatocellular carcinoma is usually hypointense to liver onT1-weighted imaging and hyperintense on T2-weighted imag-ing (Fig. 11) [21]. Other useful characteristics of hepatocellularcarcinoma are heterogeneity, mosaic appearance (Fig. 12), mul-tiplicity, encapsulation (Figs. 11D and 12C), and portovenousor hepatovenous invasion.

Both CT and MR are quite accurate in diagnosis of hepato-cellular carcinoma nodule 2 cm in diameter [18,22]. Smallerlesions are more challenging, but these are the goal of surveil-lance programs in which patients with cirrhosis have imagingevaluation at intervals of 612 months or less [23,24]. Accu-rate detection of small hepatocellular carcinomas is especiallyimportant because it offers the chance of curative therapy by per-cutaneous ablation, surgical resection and liver transplantation.

In patients with hepatocellular carcinoma, an expert panelfrom the European Association for the Study of the Liver (EASL)distinguishes between lesions measuring less than 2 cm andthose with larger diameters [25]. According to their guidelines,imaging detection of a liver nodule 2.0 cm or smaller shouldalways be confirmed with needle biopsy, and in case of negativeresult, should be subjected to an increase in the frequency of USsurveillance. For a mass greater than 2.0 cm, the coincident find-ings of characteristic arterial vascularization that is seen on atleast two imaging techniques (e.g., multiphasic CT and MRI),or hypervascularity in one imaging technique associated withwash out in the portal venous and/or delayed phase may be usedto confidently establish the diagnosis without biopsy [26].

Distinction among regenerating nodules, dysplastic nodules,and hepatocellular carcinoma with varying degrees of differen-tiation requires an assessment of the hemodynamic nature ofthe mass. In evaluation of the cirrhotic liver, whether by CT or

Fig. 16. Cirrh r acqucluster of high ced Tduring portal ach ovein. Thick sl nd inin right liver losis and peribiliary cysts at MR imaging. Transverse T2-weighted half-Fourie-intensity cysts (arrows) close to each other in left liver lobe. Gadolinium-enhan

venous phase shows collection of discrete low intensity cysts (arrows) close to eab MR cholangiography (C) shows multiple peribiliary cysts at hepatic hilum aobe, likely representing biliary hamartomas.ired single-shot turbo spin-echo MR image (A) shows organized1-weighted fat-suppressed gradient-echo MR image (B) obtainedther, separated by thin walls and lying along enhancing left portalleft liver lobe. Note other single high intensity areas (arrowheads)


MR, it is essential to obtain multiple phases of imaging beforeand during the rapid (>4 ml/s) IV administration of contrastmedium. Usition of imof enhancephase acqu

8. Arteriaanomalies

With theand the rapules and pethe cirrhotiare likely dbranch andsimulate aphase, and(Fig. 13). Limaging ission anomabranch witrial phasepseudolesioperipheraltenuation wshape or cimaging fo

9. Heman

In the ciognize radalters the bidentifyingperipheralUsually, hintensity odistinguishalso causesing in oblitinstances, cthat regress

10. Peribi

Peribiliasides of themay havetube-likesimulatingof cysts, whepatic ducglands in thsize and nushow the sauation at CT

and high signal on heavily T2-weighted MR sequences, with nocontrast enhancement [32] (Fig. 16).

iseases that mimic cirrhosis

eral disease processes may result in distorted hepatic mor-y that might be misinterpreted as cirrhosis on imaging.ongenital hepatic fibrosis, the liver generally shows vari-gmental hypertrophy or atrophy, with caudate lobe and

eral segment enlargement and right lobe atrophy observed.

Congenital hepatic fibrosis at CT. CT scan obtained during the portalphase in a 16-year-old male with congenital hepatic fibrosis shows an

liver. An abnormal network of small vessels representing a collateralon is seen running parallel to the intrahepatic portal veins (arrow). Thislikely represent an hypertrophied peribiliary vascular plexus due to

oidal portal hypertension. Note splenomegaly.

Pseuic brend ato sonenhanced images are followed by dynamic acqui-ages during the arterial, and portal venous phases

ment. With MR, we add an equilibrium or delayedisition as well [27].

lly enhancing nodules and perfusion

increasing use of thin section CT and MR imagingid bolus injection of contrast, small enhancing nod-rfusion anomalies are increasingly being observed inc liver [28,29]. Both nodules and perfusion anomaliesue to intrahepatic shunts between a hepatic arterialthe portal venous system. These pseudolesions may

hypervascular hepatic lesion on the arterial dominantare not detectable on portal venous and delayed phaseack of growth, or even disappearance on subsequentthe key to diagnosis of these vascular entities. Perfu-lies can also result from occlusion of a portal venous

h compensatory increased arterial flow causing arte-hyperenhancement (Fig. 14) [30]. These perfusionns can usually be distinguished from tumor by their

location, wedge shape, lack of mass effect, and isoat-ith liver on all other phases. Conversely, spherical

entral location are features that may require closellow-up (e.g., 46 months) to exclude malignancy.

giomas

rrhotic liver, hemangiomas are more difficult to rec-iologically and pathologically. Progressive fibrosislood supply of the liver and causes loss of somecharacteristics of hemangiomas, such as nodular

enhancement and isoattenuation to blood vessels.owever, the characteristic feature of high signaln heavily T2-weighted images remains, helping tohemangioma from hepatocellular lesions. Fibrosisprogressive diminution in size, ultimately result-

eration of the hemangioma (Fig. 15) [31]. In someapsular retraction develops over those hemangiomasin size.

liary cysts

ry cysts are cystic lesions typically found on bothintrahepatic portal venous branches. These lesions

variable size and morphology: linear and confluentaspect, coursing adjacent to right or left portal vein,

dilated bile ducts, or linear cluster (string of beads)ith a prominent involvement of the left-sided intra-ts. They represent cystic dilatation of the extramurale periductal connective tissue, and may increase inmber as the cirrhosis progresses. Peribiliary cystsme imaging findings as simple cysts, i.e., low atten-, low signal intensity on T1-weighted MR sequences

11. D

Sevpholog

In cable seleft lat

Fig. 17.venous

enlargedcirculatinetworkpresinus

Fig. 18.metastathead) aadjacentdocirrhosis at CT. Portal venous phase CT scan in a woman withast carcinoma to the liver. The liver shows nodular contours (arrow-pseudocirrhotic appearance. There is subtle capsular retractionme of the lesions (arrow).


However, as opposed to cirrhosis, the left medial segment is ofnormal size or enlarged (Fig. 17). This morphologic finding hasbeen considered useful in distinguishing patients with congenitalhepatic fibrosis from those with cirrhosis [33,34].

Patients with liver metastases from breast carcinoma treatedwith chemotherapy often develop retraction of the capsular sur-face with segmental volume loss, lobular hepatic contour andenlargement of the caudate lobe, a pattern that has been describedas pseudo-cirrhosis (Fig. 18) [35].

Budd-Chiari syndrome is characterized by hypertrophy of thecaudate lobe and variable atrophy/hypertrophy of the remainingportions of the liver, along with heterogeneous liver enhance-ment, ascites and splenomegaly. Sometimes, large hypervascularregenerative nodules can be mistaken for hepatocellular carci-noma (Fig. 19) [3638].

Sarcoidosis is a multisystem granulomatous disease thataffects the liver in 2479% of patients, and may result in hep-atic injury that simulates or causes cirrhosis. Multifocal nodularhypoenhancing lesions in the liver (and spleen) are typical find-

Fig. 19. Chroimaging. T1-winant phase (Aand several nsignal intensitunenhanced Tthe appearancare opposite tointrahepatic p

Fig. 20. Sarcoidosis at CT. Portal venous phase CT scan in a patient with sar-coidosis shows enlarged left lobe and small right lobe, as typically seen incirrhosis. Splenomegaly and periaortic and hilar adenopathy also noted.

Fig. 21. Liver morphology changes in a patient with cavernous transformationrtal vein at CT. Portal venous phase CT scan performed 3 months afterce of portal vein thrombosis shows hypertrophy of the caudate lobe and

atrophy of the peripheral portions of the liver.

ut widened fissures, splenomegaly and upper abdominaladenopathy are features seen in cirrhosis and hepatic sar-is, requiring liver biopsy for further evaluation (Fig. 20)

hose patients with cavernous transformation of the portalerial cross sectional studies have demonstrated hyper-of the central zones of the liver (segment 1 and 4) and

ophy of the left and right lobes due to the portal hypop-n of these peripheral areas (Fig. 21) [40].

mmary

h CT and MR provide valuable insights into the extent ofc injury from cirrhosis and complications including por-nic Budd-Chiari syndrome and large regenerative nodules at MReighted gradient-echo MR image obtained during arterial dom-) and portal venous phase (B) shows an enlarged caudate lobe

odules with marked enhancement (arrows). Nodules showed lowy on T2-weighted images (not shown) and high signal intensity on1-weighted images. Lack of washout on portal venous phase ande of these nodules on T2- and unenhanced T1-weighted imageswhat is expected for hepatocellular carcinoma. Note transjugular

ortosystemic shunt (arrowhead), ascites and splenomegaly.

of the pooccurren

relative

ings, blymphcoidos[39].

In tvein, strophyhypotrerfusio

12. Su

Bothepati


tal hypertension. Distinction among small hepatic focal lesionsremains challenging, while both CT and MR are quite accu-rate in detection and characterization of larger (>2 cm) lesions,including hepatocellular carcinoma. Attention to scan techniqueis key, including the use of multiphasic imaging with a rapid IVbolus of contrast medium.

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Cirrhosis: CT and MR imaging evaluationIntroductionLiver morphologyPortal hypertension and mesenteric edemaFibrosisRegenerative nodulesDysplastic nodulesHepatocellular carcinomaArterially enhancing nodules and perfusion anomaliesHemangiomasPeribiliary cystsDiseases that mimic cirrhosisSummaryReferences

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Cirrhosis CT and MR Imaging Evaluation

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