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Cirrhosis: CT and MR imaging evaluation
Giuseppe Brancatelli a,b,c,∗ , Michael P. Federle c , Roberta Ambrosini d , Roberto Lagalla b , Alessandro Carriero d , Massimo Midiri b , Val´ erie Vilgrain e
Sezione di Radiologia, Ospedale Specializzato in Gastroenterologia, “Saverio de Bellis”—IRCCS, 70013 Castellana Grotte (Bari), Italy b Sezione di Scienze Radiologiche, Dipartimento di Biotecnologie Mediche e Medicina Legale, Universit` a di Palermo, Via del Vespro 127, 90127 Palermo, Italy c Department of Radiology, University of Pittsburgh Medical Center, 200 Lothrop Street, 15213 Pittsburgh, PA, USA d Department of Diagnostic and Interventional Radiology, “Maggiore della Carit` a” University Hospital, “A.Avogadro” Eastern Piemonte University, Corso Mazzini 18, Novara, Italy e Service de Radiologie, Hopital Beaujon, 100 Boulevard du General Leclerc, 92118 Clichy, France Received 7 July 2006; accepted 2 November 2006
Abstract In this article, we present the CT and MR imaging characteristics of the cirrhotic liver. We describe the altered liver morphology in different forms of viral, alcoholic and autoimmune end-stage liver disease. We present the spectrum of imaging ﬁndings in portal hypertension, such as splenomegaly, ascites and varices. We describe the patchy and lacelike patterns of ﬁbrosis, along with the focal conﬂuent form. The process of hepatocarcinogenesis is detailed, from regenerative to dysplastic nodules to overt hepatocellular carcinoma. Different types of non-neoplastic focal liver lesions occurring in the cirrhotic liver are discussed, including arterially enhancing nodules, hemangiomas and peribiliary cysts. We show different conditions causing liver morphology changes that can mimic cirrhosis, such as congenital hepatic ﬁbrosis, “pseudo-cirrhosis” due to breast metastases treated with chemotherapy, Budd-Chiari syndrome, sarcoidosis and cavernous transformation of the portal vein. © 2006 Elsevier Ireland Ltd. All rights reserved.
Keywords: Liver; Cirrhosis; Computed tomography; Magnetic resonance imaging
1. Introduction Cirrhosis is the ﬁnal result of chronic damage to the liver from various etiologies, characterized by parenchymal injury leading to extensive ﬁbrosis and nodular regeneration. The result is a diffuse disorganization of hepatic morphology with progressive loss of liver function. Although the mortality rate has been reduced by about 30% in the last few decades, within the European Union cirrhosis is still one of the leading causes of death and serious morbidity. Cirrhosis is most commonly the result of hepatitis B and C virus infection or chronic alcoholism; other causes are biliary, cryptogenic and metabolic. Usual clinical manifestations result from portal hypertension, portosystemic shunting and hepatic insufﬁciency. Common complications are ascites, gastrointestinal bleeding, encephalopathy and coagulopathy.
Corresponding author at: Via Villaermosa 29, 90139 Palermo, Italy. Tel.: +39 3291828155; fax: +39 0916552325. E-mail address: email@example.com (G. Brancatelli). 0720-048X/$ – see front matter © 2006 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ejrad.2006.11.003
In this review, we present the CT and MR imaging ﬁndings in the cirrhotic liver. 2. Liver morphology At an early stage of cirrhosis, the liver may appear normal on cross sectional imaging. With disease progression, heterogeneity of liver parenchyma and surface nodularity are observed. Caudate lobe hypertrophy is the most characteristic morphologic feature of liver cirrhosis (Fig. 1). A ratio of transverse caudate lobe width to right lobe width greater than or equal to 0.65 constitutes a positive indicator for the diagnosis of cirrhosis with high level of accuracy . A modiﬁed caudate lobe width to right lobe width ratio, using the right portal vein instead of the main portal vein to set the lateral boundary has recently been proposed . Other regional changes in hepatic morphology typically seen in advanced cirrhosis are segmental hypertrophy involving the lateral segments (II, III) of the left lobe (Fig. 2), and segmental atrophy affecting both the posterior
” regenerative nodules. Typical cirrhotic morphology at CT. Portal hypertension and mesenteric edema Fig. ﬁbrotic liver. and presence of right posterior hepatic notch (asterisk). abdominal wall (Fig. marked atrophy of the medial segment of the left hepatic lobe (arrowheads) and of the right posterior hepatic lobe (arrow). The increased pressure gradient is deﬁned as portal hypertension. Other shunts between the portal and the systemic circulation include splenorenal collaterals (Fig. 5B) . Typical cirrhotic morphology at MR imaging. 3C) . . moderate or severe form with pseudonodules surrounding mesenteric vessels and mimicking enlarged lymph nodes (Fig. pseudotumoral enlargement of the caudate lobe is In chronic liver disease. It can occur in mild. both draining into the portal vein. along with prominent “lacelike ﬁbrosis. observed in virtually all patients. The paraumbilical veins (Fig. Concomitant multiple irregular strictures of the intra.80. Late-stage primary biliary cirrhosis results in morphologic changes including a shrunken. Enlargement of hilar periportal space. segments (VI. Portal venous phase CT scan shows an enlarged left lateral lobe and caudate lobe (C). that is indistinguishable from other etiologies. 2). 2. Primary sclerosing cholangitis and primary biliary cirrhosis have some distinctive features in comparison to other types of cirrhosis. also reopen to form portosystemic shunts. the notch-sign  (Fig. and causes complications such as ascites and the development of engorged and tortuous collateral vessels that typically develop at the lower end of the esophagus (Figs.and extrahepatic bile ducts are also observed (Fig. 4) . 5C) and the left gastric vein.58 G. In primary sclerosing cholangitis induced end-stage cirrhosis. 3. / European Journal of Radiology 61 (2007) 57–69 Fig. 1. Brancatelli et al. an enlarged gallbladder fossa with the gallbladder (g) herniated toward the anterior abdominal wall. Gadolinium-enhanced T1-weighted fat-suppressed gradient-echo MR image (B) obtained during portal venous phase shows inhomogeneous liver enhancement and caudate to right lobe ratio of 1. 3A and B). 5D) and retroperitoneal collaterals. 3C and 5A) and at the gastric fundus (hypertensive gastropathy) (Fig. hemorrhoidal veins. along with atrophy of the peripheral hepatic segments resulting in a lobulated liver contour (Fig. 2). mildly lobulated liver margins (arrowheads) and regions of high attenuation (arrow) of hepatic parenchyma caused by patchy ﬁbrosis. 2)  and generalized widening of the interlobar ﬁssures are also considered typical ﬁndings of cirrhosis. 5B). VII) of the right lobe and medial segment (IV) of the left lobe  (Fig. Alteration of blood ﬂow is the likely explanation for these morphologic abnormalities. progressive hepatic ﬁbrosis leads to increased vascular resistance at the level of the hepatic sinusoids. 6). Increased venous pressure is also responsible for the prominent mesenteric edema and stranding occurring in 86% of patients with cirrhosis . Transverse T2-weighted fat-suppressed turbo spin-echo MR image (A) shows enlarged caudate lobe. Primary biliary cirrhosis typically produces early signs of portal hypertension while the liver is enlarged. and lymphadenopathy (Fig. an expanded gallbladder fossa (Fig.
(A) Transverse nonenhanced CT scan (narrow window setting) shows lacelike pattern of low-attenuating ﬁbrosis surrounding subcentimeter regenerative nodules that are hyperattenuating to normal liver or spleen. 4. The phenomenon of segmental hyperplasia associated with atrophy of other parts of the liver is known as the atrophy–hypertrophy complex. as a lacelike pattern. Primary sclerosing cholangitis at CT. Brancatelli et al.G. (C) Portal venous phase CT scan in a different patient with primary sclerosing cholangitis shows irregular dilatation of the intra-hepatic bile ducts (arrowheads). The lacelike type of ﬁbrosis is best described as thin or thick bands that surround regenerative nodules. This pattern is best visualized on nonenhanced CT (Fig. It is seen in about one-third of patients with primary biliary cirrhosis . (B) In the portal venous phase. Note esophageal varices (arrow) due to portal hypertension. Fibrosis Fibrosis is an inherent part of hepatic cirrhosis. and is typically detected as patchy ﬁbrosis (Fig. Fig. regenerative nodules are not easily recognized. 4. or as a conﬂuent mass. the attenuation difference between the caudate and the liver is lost. 1A). 3. (B) On portal venous phase CT scan obtained at the same level as A. The peripheral areas of the liver are hypodense due to atrophy. Splenomegaly and enlarged porta hepatis and portacaval lymph nodes (arrows) are also noted. 4B) . Primary biliary cirrhosis at CT. regardless of stage. / European Journal of Radiology 61 (2007) 57–69 59 Fig. 4A). (A) Nonenhanced CT shows severe lobulation (arrows) of the hepatic contour and compensatory hypertrophy of the caudate lobe (arrowheads). . and is usually not well visualized on portal venous phase images (Fig.
Brancatelli et al. persistent contrast enhancement. regenerative nodules are macronodular (≥9 mm). it may be mistaken for hepatocellular carcinoma. multiplanar reformatted in the coronal plane (B). as usually seen in chronic hepatitis B. / European Journal of Radiology 61 (2007) 57–69 Fig. or micronodular . however. Delayed.12] (Fig. Part (A) shows dilated and tortuous esophageal varices (arrow). 7). along with the characteristic capsular retraction and typical location and shape help to distinguish conﬂuent ﬁbrosis from hepatocellular carcinoma. part (B) shows varices in the gastric fundus (arrow) and a splenorenal shunt (double arrows). and is due to the retention of contrast by the ﬁbrotic tissue (Fig. V or VIII.60 G. with associated capsular retraction [11. 7D). part C shows recanalized parumbilical vein (arrow). Focal conﬂuent ﬁbrosis is observed in end-stage liver disease and is usually a wedge-shaped lesion located in the subcapsular portion of segment IV. and part D shows abdominal wall collaterals (arrowheads). This fea- ture. is typically observed. In those rare cases in which the lesion shows enhancement on arterial dominant phase. 5. 5. Axial (A). Regenerative nodules In the cirrhotic liver. axial maximum intensity projection (C) and sagittal maximum intensity projection (D) contrastenhanced CT images show different examples of collateral vessels developing in end-stage chronic liver disease due to severe portal hypertension.
6. Mesenteric edema in this case mimics the appearance of lymph-nodes. The accumulation of iron within regenerative nodules may cause hypointensity on T2-weighted images (Fig.G. T1-weighted gradient-echo fat-suppressed MR image (B) shows low intensity of focal conﬂuent ﬁbrosis lesion (arrow). 9B). usually best visualized using TEs greater than 10 ms. 6. Mesenteric edema in cirrhosis. Most regenerative nodules are difﬁcult to detect at CT or MR because they are too small or are too similar to surrounding liver parenchyma . Transverse T2-weighted fat-suppressed turbo spin-echo MR image (A) shows focal conﬂuent ﬁbrosis lesion (arrows) in segment four as an area of moderate to high intensity in comparison to background liver. as seen in other causes of cirrhosis. 7. hanced CT (Fig. Computed tomography detects regenerative nodules when they are surrounded by hypodense ﬁbrotic bands on nonen- Fig. MR imaging demonstrates regenerative nodules with greater sensitivity than any other imaging modality. . and therefore difﬁcult to detect. focal conﬂuent ﬁbrosis lesion shows delayed enhancement (arrow) due to presence of ﬁbrotic tissue. On equilibrium-phase (5 min) gadolinium-enhanced T1-weighted fat-suppressed gradient-echo MR image (D). They usually appear isointense (Fig. and marked hypointensity on T1-weighted gradient-Echo MR images (Fig. regenerative nodules usually enhance to the same degree than the background liver. 4A) or when they accumulate iron (siderotic nodules) . Note adjacent retraction (arrowhead) of liver capsule. 8B) to hyperintense relative to background liver parenchyma on T1-weighted sequences . 9A) because of magnetic ﬁeld inhomogeneities. / European Journal of Radiology 61 (2007) 57–69 61 Fig. Cirrhosis and focal conﬂuent ﬁbrosis at MR imaging. after contrast injection. Brancatelli et al. Due to their portal venous supply. Siderotic regenerative nodules are typically hyperattenuating to liver on nonenhanced CT and are isoattenuating to liver. Dysplastic nodules Dysplastic nodules are regenerative nodules containing atypical cells without deﬁnite histological signs of malignancy. Contrast-enhanced CT scan shows increased attenuation of the fat (arrows) around the mesenteric vessels due to congestion and edema caused by portal hypertension. and (3–9 mm). 8A) to hypointense on T2-weighted MR images relative to the surrounding inﬂammatory ﬁbrous septa and isointense (Fig. Gadolinium-enhanced T1-weighted fat-suppressed gradient-echo MR image obtained during arterial dominant phase (C) shows no apparent enhancement of focal conﬂuent ﬁbrosis lesion.
62 G. perihepatic ascites (a) and 1 cm hypointense mass (arrow). On transverse T1-weighted gradient-echo breath-hold MR image (B). nodules (arrows) are still isointense and surrounded by thick hyperintense septa of lacelike ﬁbrosis. Transverse T2-weighted fat-suppressed turbo spin-echo MR image (a) shows irregular liver margins. Arterial dominant phase (not shown) failed to show enhancement of nodules. Brancatelli et al. Cirrhosis and dysplastic nodule at MR imaging. surrounded by diffuse lacework of low-intensity ﬁbrosis. Arterial dominant phase (not shown) failed to show enhancement of nodule. nodules are hypointense. Transverse T2-weighted fat-suppressed turbo spin-echo MR image (A) shows multiple hypointense nodules (arrowheads). On transverse T1-weighted gradient-echo breath-hold MR image (b). the mass is hyperintense (arrow). Cirrhosis and multiple regenerative nodules at MR imaging. On transverse T2-weighted fat-suppressed turbo spin-echo MR image (B). 8. 9. . Cirrhosis and siderotic regenerative nodules at MR imaging. Transverse T1-weighted gradient-echo MR image (A) shows multiple subcentimeter isointense nodules (arrows). Fig. 10. / European Journal of Radiology 61 (2007) 57–69 Fig. Fig. consistent with diagnosis of regenerative nodules.
Cirrhosis and typical hepatocellular carcinoma at MR imaging. Brancatelli et al. lesion is hypointense in comparison to background liver. 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). On gadolinium-enhanced T1-weighted gradient-echo MR image obtained during portal venous phase (D). lesion becomes hypointense to surrounding parenchyma. . / European Journal of Radiology 61 (2007) 57–69 63 Fig.G. 11. Note hyperintense capsule (arrowhead) surrounding lesion. Gadolinium-enhanced T1-weighted gradient-echo MR image obtained during arterial dominant phase (C) shows marked enhancement of lesion (arrow) with central hypointense area due to necrosis.
ﬁbrosis. / European Journal of Radiology 61 (2007) 57–69 Fig. (B) On portal venous phase CT scan obtained at same level as A. Gadolinium-enhanced T1-weighted fat-suppressed gradient-echo MR image obtained during portal venous phase (C) shows washout of tumor portion that enhanced in arterial dominant phase. The ﬁbrotic capsule (arrows) surrounding lesion is well seen because of contrast retention. while remaining part is hypointense.64 G. . which contain small viable nodules with interspersed areas of necrosis. Mosaic appearance is caused by areas of different intensity level and results from peculiar growth pattern of hepatocellular carcinoma. Capsule and mosaic pattern are seen more frequently with increasing tumor diameter. Cirrhosis and benign arterially enhancing nodule at CT. Brancatelli et al. (A) Arterial dominant phase CT scan of the liver shows small enhancing lesion (arrows). Gadolinium-enhanced T1-weighted fat-suppressed gradient-echo MR image obtained during arterial dominant phase (B) shows that only peripheral portion of tumor enhances (arrow). 12. and cystic or fatty degeneration. 13. Fig. Transverse T2-weighted fat-suppressed turbo spin-echo MR image (A) shows large tumor (arrows) in right lobe of the liver that is slightly hyperintense to surrounding nontumorous parenchyma and heterogeneous due to presence of some hypointense areas. lesions are minimally hyperattenuating to isoattenuating compared to surrounding liver. Cirrhosis and large hepatocellular carcinoma with mosaic appearance at MR imaging.
10a). the so-called “nodule within a nodule” appearance on MR imaging . and Fig. (B) Transverse T2-weighted fat-suppressed turbo spin-echo MR image through the same level obtained 2 years later. Malignant transformation within a dysplastic nodule has been identiﬁed as early as 4 months after the ﬁrst detection of the dysplastic nodule .e. Dysplastic nodules are detected and characterized better by MR than by CT. 10b). Arterial phase enhancement should suggest development of a focus of hepatocellular carcinoma within a high-grade dysplastic nodule. Transverse T2-weighted fat-suppressed turbo spin-echo MR image (A) shows two hemangiomas (arrows) as strongly hyperintense in comparison to liver parenchyma. As with regenerative nodules. 14. and show hyperintensity on T1-weighted images (Fig. Dysplastic nodules are found in 15–25% of cirrhotic livers at the time of transplantation and are subclassiﬁed on the basis of the degree of cellular abnormalities: low-grade (containing hepatocytes with mild atypia) and high-grade (when the degree of atypia is moderate. (B) Delayed phase contrast-enhanced transverse CT scan demonstrates isoattenuation of right liver to the normal parenchyma. / European Journal of Radiology 61 (2007) 57–69 65 are considered an intermediate. (A) Arterial dominant phase CT scan shows hyperattenuation of the right lobe of the liver (arrowheads) in comparison to normal left liver due to thrombosis of the anterior branch of the right portal vein (arrow) and increased arterial ﬂow. dysplastic nodules and well-differentiated hepatocellular carcinoma. accurate diagnosis may be made in only about 15% of cases . but there is much overlap in imaging features between regenerative nodules. . Transient hepatic attenuation difference due to portal vein thrombosis in cirrhosis at CT. Therefore. marked arterial phase enhancement should suggest hepatocellular carcinoma rather than dysplastic nodule. The cavernous hemangioma in the right lobe is much smaller (arrow). Fig. but insufﬁcient for the diagnosis of malignancy) . whereas nontriadal arteries (i.G. Note splenomegaly. Characteristically. however. unaccompanied by portal venules and biliary ducts) develop to feed the nodules. Cirrhosis and multiple hemangiomas at MR imaging. hepatocellular carcinoma is hypoattenuating to liver on unenhanced CT. The presence of early arterial enhancement with rapid washout during the portal venous phase should be regarded as highly suspicious for the presence of hepatocellular carcinoma. Dysplastic nodules typically appear hypointense to the background liver parenchyma on T2-weighted images (Fig. premalignant step along the hepatocarcinogenesis process. quite in contrast to typical ﬁndings for hepatocellular carcinoma.. portal blood supply decreases. Hepatocellular carcinoma Hepatocellular carcinoma typically occurs within the cirrhotic liver. 15. dysplastic nodules receive predominantly portal venous ﬂow. while the cavernous hemangioma in the left lobe is no longer visible. and do not usually demonstrate bright enhancement on arterial phase CT or MRI. 7. Brancatelli et al. As the degree of (de-differentiation) malignancy increases.
24]. According to their guidelines. or hypervascularity in one imaging technique associated with wash out in the portal venous and/or delayed phase may be used to conﬁdently establish the diagnosis without biopsy . 12). mosaic appearance (Fig. with washout on portal venous and delayed phase [19. surgical resection and liver transplantation.g. 11D and 12C). imaging detection of a liver nodule 2. Transverse T2-weighted half-Fourier acquired single-shot turbo spin-echo MR image (A) shows organized cluster of high-intensity cysts (arrows) close to each other in left liver lobe. In patients with hepatocellular carcinoma. moderately enhancing lesion during the arterial phase.22]. Smaller lesions are more challenging. Both CT and MR are quite accurate in diagnosis of hepatocellular carcinoma nodule ≥2 cm in diameter [18. Note other single high intensity areas (arrowheads) in right liver lobe. dysplastic nodules. 16. multiplicity. whether by CT or Fig. the coincident ﬁndings of characteristic arterial vascularization that is seen on at least two imaging techniques (e.20]. should be subjected to an increase in the frequency of US surveillance. and hepatocellular carcinoma is usually hypointense to liver on T1-weighted imaging and hyperintense on T2-weighted imaging (Fig. .66 G. In evaluation of the cirrhotic liver. Other useful characteristics of hepatocellular carcinoma are heterogeneity. Distinction among regenerating nodules. separated by thin walls and lying along enhancing left portal vein. and hepatocellular carcinoma with varying degrees of differentiation requires an assessment of the hemodynamic nature of the mass.. an expert panel from the European Association for the Study of the Liver (EASL) distinguishes between lesions measuring less than 2 cm and those with larger diameters . Brancatelli et al. encapsulation (Figs. Gadolinium-enhanced T1-weighted fat-suppressed gradient-echo MR image (B) obtained during portal venous phase shows collection of discrete low intensity cysts (arrows) close to each other. Similar features are evident on MR imaging. likely representing biliary hamartomas. Accurate detection of small hepatocellular carcinomas is especially important because it offers the chance of curative therapy by percutaneous ablation. and portovenous or hepatovenous invasion. but these are the goal of surveillance programs in which patients with cirrhosis have imaging evaluation at intervals of 6–12 months or less [23.0 cm or smaller should always be conﬁrmed with needle biopsy. and in case of negative result. For a mass greater than 2. Cirrhosis and peribiliary cysts at MR imaging. / European Journal of Radiology 61 (2007) 57–69 manifests as a heterogeneous. Thick slab MR cholangiography (C) shows multiple peribiliary cysts at hepatic hilum and in left liver lobe.0 cm. 11) . multiphasic CT and MRI).
. Arterially enhancing nodules and perfusion anomalies With the increasing use of thin section CT and MR imaging and the rapid bolus injection of contrast. Hemangiomas In the cirrhotic liver. Perfusion anomalies can also result from occlusion of a portal venous branch with compensatory increased arterial ﬂow causing arterial phase hyperenhancement (Fig. Fig.. Conversely. Note splenomegaly. Fibrosis also causes progressive diminution in size. hemangiomas are more difﬁcult to recognize radiologically and pathologically. They represent cystic dilatation of the extramural glands in the periductal connective tissue. or even disappearance on subsequent imaging is the key to diagnosis of these vascular entities. 11. 13). / European Journal of Radiology 61 (2007) 57–69 67 MR. Fig.g. the characteristic feature of high signal intensity on heavily T2-weighted images remains. and isoattenuation with liver on all other phases. Diseases that mimic cirrhosis Several disease processes may result in distorted hepatic morphology that might be misinterpreted as cirrhosis on imaging. small enhancing nodules and perfusion anomalies are increasingly being observed in the cirrhotic liver [28. wedge shape. Usually. These perfusion pseudolesions can usually be distinguished from tumor by their peripheral location. ultimately resulting in obliteration of the hemangioma (Fig. 15) . we add an equilibrium or delayed phase acquisition as well . Congenital hepatic ﬁbrosis at CT. coursing adjacent to right or left portal vein. In congenital hepatic ﬁbrosis. CT scan obtained during the portal venous phase in a 16-year-old male with congenital hepatic ﬁbrosis shows an enlarged liver. 9. and portal venous phases of enhancement. Progressive ﬁbrosis alters the blood supply of the liver and causes loss of some identifying characteristics of hemangiomas. Unenhanced images are followed by dynamic acquisition of images during the arterial. it is essential to obtain multiple phases of imaging before and during the rapid (>4 ml/s) IV administration of contrast medium. and are not detectable on portal venous and delayed phase (Fig. 17. This network likely represent an hypertrophied peribiliary vascular plexus due to presinusoidal portal hypertension. i. Peribiliary cysts Peribiliary cysts are cystic lesions typically found on both sides of the intrahepatic portal venous branches.G.e. low attenuation at CT. Brancatelli et al. with no contrast enhancement  (Fig. 14) . 10. Both nodules and perfusion anomalies are likely due to intrahepatic shunts between a hepatic arterial branch and the portal venous system. 8. spherical shape or central location are features that may require close imaging follow-up (e. An abnormal network of small vessels representing a collateral circulation is seen running parallel to the intrahepatic portal veins (arrow). capsular retraction develops over those hemangiomas that regress in size. the liver generally shows variable segmental hypertrophy or atrophy. lack of mass effect. 16). however. or linear cluster (“string of beads”) of cysts. There is subtle capsular retraction adjacent to some of the lesions (arrow). 4–6 months) to exclude malignancy. Peribiliary cysts show the same imaging ﬁndings as simple cysts. with caudate lobe and left lateral segment enlargement and right lobe atrophy observed. Portal venous phase CT scan in a woman with metastatic breast carcinoma to the liver. with a prominent involvement of the left-sided intrahepatic ducts. Lack of growth. These pseudolesions may simulate a hypervascular hepatic lesion on the arterial dominant phase. and may increase in size and number as the cirrhosis progresses. The liver shows nodular contours (arrowhead) and a pseudocirrhotic appearance. With MR. These lesions may have variable size and morphology: linear and conﬂuent “tube-like” aspect.29]. low signal intensity on T1-weighted MR sequences and high signal on heavily T2-weighted MR sequences. 18. In some instances. simulating dilated bile ducts. Pseudocirrhosis at CT. helping to distinguish hemangioma from hepatocellular lesions. such as nodular peripheral enhancement and isoattenuation to blood vessels. .
as typically seen in cirrhosis.34]. Lack of washout on portal venous phase and the appearance of these nodules on T2. Note transjugular intrahepatic portosystemic shunt (arrowhead). 19.68 G. Sarcoidosis is a multisystem granulomatous disease that affects the liver in 24–79% of patients. Brancatelli et al. Multifocal nodular hypoenhancing lesions in the liver (and spleen) are typical ﬁndFig. splenomegaly and upper abdominal lymphadenopathy are features seen in cirrhosis and hepatic sarcoidosis. 20. / European Journal of Radiology 61 (2007) 57–69 However. lobular hepatic contour and enlargement of the caudate lobe. 18) . Fig. T1-weighted gradient-echo MR image obtained during arterial dominant phase (A) and portal venous phase (B) shows an enlarged caudate lobe and several nodules with marked enhancement (arrows). but widened ﬁssures. the left medial segment is of normal size or enlarged (Fig. large hypervascular regenerative nodules can be mistaken for hepatocellular carcinoma (Fig. a pattern that has been described as “pseudo-cirrhosis” (Fig. 19) [36–38]. ascites and splenomegaly. Budd-Chiari syndrome is characterized by hypertrophy of the caudate lobe and variable atrophy/hypertrophy of the remaining portions of the liver. In those patients with cavernous transformation of the portal vein. 12. Summary Both CT and MR provide valuable insights into the extent of hepatic injury from cirrhosis and complications including por- . and may result in hepatic injury that simulates or causes cirrhosis. ascites and splenomegaly. Patients with liver metastases from breast carcinoma treated with chemotherapy often develop retraction of the capsular surface with segmental volume loss. Sometimes. Sarcoidosis at CT. Portal venous phase CT scan in a patient with sarcoidosis shows enlarged left lobe and small right lobe. Splenomegaly and periaortic and hilar adenopathy also noted. along with heterogeneous liver enhancement. Liver morphology changes in a patient with cavernous transformation of the portal vein at CT. requiring liver biopsy for further evaluation (Fig. 21) . serial cross sectional studies have demonstrated hypertrophy of the central zones of the liver (segment 1 and 4) and hypotrophy of the left and right lobes due to the portal hypoperfusion of these peripheral areas (Fig. Portal venous phase CT scan performed 3 months after occurrence of portal vein thrombosis shows hypertrophy of the caudate lobe and relative atrophy of the peripheral portions of the liver. This morphologic ﬁnding has been considered useful in distinguishing patients with congenital hepatic ﬁbrosis from those with cirrhosis [33. Nodules showed low signal intensity on T2-weighted images (not shown) and high signal intensity on unenhanced T1-weighted images. 20) . Fig. ings. 17).and unenhanced T1-weighted images are opposite to what is expected for hepatocellular carcinoma. Chronic Budd-Chiari syndrome and large regenerative nodules at MR imaging. as opposed to cirrhosis. 21.
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