CT in hepatic cirrhosis and chronic hepatitis

CT in Hepatic Cirrhosis and Chronic Hepatitis Carlos Vails, Eduard Andia, Yolanda Roca, Mbnica Cos, and Juan Figueras Cirrhosis is a diffuse liver disease with premalignant potential in which hepatocellular carcinoma (HCC) frequently develops. The hemodynamics of contrast material are the key to diagnosis of focal liver lesions with computed tomography (CT). Lesions with arterial-dominant vascularity, such as HCC, show brisk enhancement during the arterial phase, whereas lesions with portal blood supply can appear as hyperenhancing lesions in the portal phase. The advent of helical CT has significantly improved the CT examination of the liver because the arterial phase can be displayed independently of the portal phase. The addition of arterial phase imaging to conventional portal phase imaging seems to improve tumor detection and characterization. Although HCC is the single most frequent tumor seen in chronic liver disease, other lesions such as peripheral cholangiocarcinoma and hemangioma should be considered in the differential diagnosis. Optimization of helical CT techniques may allow better detection and characterization of these lesions. In addition to tumor detection, CT plays an important role in preoperative staging of HCC as well as in preoperative assessment of patient candidates to hepatic transplantation. The use of CT angiography with maximum intensity projection techniques may allow for better preoperative work-up and vascular mapping in HCC patients. This article shows the spectrum of helical CT findings in chronic liver disease and specifically in the imaging of HCC and other focal lesions. Copyright 2002, Elsevier Science (USA). All rights reserved.

HE LIVER IS A COMPLEX, metabolically active organ with important homeostatic and digestive functions. The vascular supply of the liver is complex and relatively unique because the liver depends on 2 vascular inflows: the hepatic artery accounts for 25% of the blood supply and the portal vein provides about 75%. a'2

rial variant and is found in 18% to 20% of individuals (Fig 2). Accessory vessels have a different origin than the standard anatomy but they do not replace the standard vessel. A left hepatic artery arising from the left gastric artery is the most frequent accessory vessel found.

ANATOMY AND PHYSIOLOGY OF HEPATIC BLOOD FLOW

The portal vein arises from the confluence of the splenic vein and the superior mesenteric vein, at the level of the pancreatic neck. The portal vein courses anteriorly and superiorly to the porta hepatis, where it bifurcates into fight and left portal veins. Portal vein variations (Fig 3) are found in 20% of individuals 4 and include immediate trifurcation of the main portal vein with absence of the right portal vein, a right anterior portal branch arising from the left portal vein, and a right posterior portal branch arising from the main portal trunk.

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Hepatic Artery The hepatic arterial supply has a standard distribution in 55% to 60% of individuals. 3 In these typical cases, the celiac trunk arises from the anterior aspect of the abdominal aorta immediately caudal to the esophageal hiatus. The celiac trunk rapidly trifurcates and gives rise to the common hepatic artery, the left gastric artery, and the splenic artery. The common hepatic artery courses anteriorly and to the right, through the lesser omenturn, giving off several branches: the gastroduodenal, the supraduodenal, and the right gastric arteries. Distal to the gastroduodenal artery origin, the common hepatic artery is called the proper hepatic artery. The latter vessel enters the porta hepatis and bifurcates into right and left hepatic arteries (Fig 1). In 40% to 45% of patients, different anatomic variants can be found. There are 2 basic types of arterial variants: replaced and accessory vessels. Replaced vessels have a different origin than the standard anatomy and replace the normal vessel. A replaced right hepatic artery arising from the superior mesenteric artery is the most common arte-

Portal Vein

Arterioportal Communications In addition to its complex, dual blood supply, the liver has multiple physiologic intercommu-

From the Institut de DiagnOstic per la Imatge (IDI), Hospital Duran i Reynals; the Department of Surgery, Hospital Princeps d'Espanya; Ciutat Sanithria i Universitgtria de Bellvitge; Autovia de Castelldefels km 2,7; and L'Hospitalet de Llobregat; Barcelona, Spain. Address reprint requests to Carlos Valls, MD, PhD, Institut de DiagnOstic per la Imatge (IDI), Hospital Duran i Reynals, Ciutat Sanit~ria i Universitdwia de Bellvitge, Barcelona, Spain; e-mail: [email protected] Copyright 2002, Elsevier Science (USA). All rights reserved. 0887-2171/02/2301-0003535.00/0 doLl O.lO53/sult.2002.30123

Seminars in Ultrasound, CT, and MR/, Vol 23, No 1 (February), 2002: pp 37-61

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Fig 1. Standard arterial anatomy of the liver. Maximum intensity projection (MIP) image in the coronal plane shows normal arterial distribution. Early trifurcation of the celiac trunk is well seen, with the celiac giving off the common hepatic artery (CHA), the left gastric artery (LGA), and the splenic artery (SA). Note that the proper hepatic artery (PHA) begins distal to the gastroduodenal artery (GDA) and continues to the hepatic bifurcation, into the right (RHA), and left hepatic arteries (LHA).

liver parenchyma and hepatic tumors. These differences are usually small and barely discernible on noncontrast computed tomography (CT). To maximize the differences in density between normal liver parenchyma and focal liver lesions it is necessary to inject contrast material. Rapid intravenous injection of iodinated contrast material increases the attenuation differences between normal parenchyma and focal liver lesions, and allows optimal visualization of vascular structures. Iodinated contrast material, like any other extracellular space contrast material injected intravenously, rapidly distributes from the vascular to the extravas-

nication systems between the high-pressure arterial system and the low-pressure portal venous system. A sound knowledge of these physiologic communications is necessary to understand the pathophysiology and hemodynamics of hepatic vascular abnormalities. Previous angiographic studies have shown different arterioportal communications: transinusoidal, transplexal, and transvasal. In transinusoidal communications, the blood flow arrives at different levels of the sinusoids. Depending on the resistance to anterograde flow, retrograde back-flow to the portal system can occur. Transplexal communications occur through the peribiliary plexus. This venous plexus drains into the portal veins and the sinusoids. On arterialdominant phase CT studies, transplexal communication presents as transient, homogeneous, hepatic hyperattenuation in the segment of the liver drained by a thrombosed portal vein. Transvasal communications occur via portal vasa vasornm that enter the wall of the portal vein. This communication can be found in neoplastic portal thrombosis, in which case tumor neovessels give rise to the classic "thread and streaks" sign. MULTIPHASIC HELICAL COMPUTED TOMOGRAPHY TECHNIQUE

Detection of focal liver lesions on CT is based on the differences in attenuation between normal

Fig 2. Replaced right hepatic artery arising from the superior mesentaric artery. (A) MIP image in the axial plane shows a replaced RHA arising from the SMA. (B) MIP image in the oblique coronal plane shows the replaced RHA coursing inferior to the LHA, which arises from the celiac trunk (arrowhead).

CT IN HEPATIC CIRRHOSIS AND CHRONIC HEPATITIS

Fig 3. Portal vein variations. (A) MIP image in the axial plane shows a right anterior portal branch (arrow) arising from the left portal vein. (B) MIP image in the axial plane in another patient shows trifurcation of the main portal vein, with absence of the right portal vein. MPV, main portal vein; RAPV, right anterior portal vein branch; RPPV, right posterior portal vein branch; LPV, left portal vein.

cular or interstitial space. 5 In the liver, the degree of parenchymal enhancement depends on the dose of iodine administered. With older, nonhelical CT units, contrast material could only be delivered during the portal-dominmlt phase. In this phase, hypovascular lesions are well seen, but hypervascular lesions are usually missed because they can be isodense relative to the liver parenchyma. The advent of helical CT has significantly improved the examination of the liver because of a marked reduction in acquisition time. It is possible now to complete the examination of the entire liver

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during the arterial-dominant and portal-dominant phases of contrast enhancement. In addition, the advent of multirow detector CT scanners has further improved multiphasic study of the liver, allowing a triple-pass CT technique during the early arterial, late arterial, and portal venous phases. 6 The vascular hemodynamics of contrast material is the key to detection and characterization of hypervascular lesions such as hepatocellular carcinoma (HCC). Arterial-dominant phase imaging results in scanning the liver 20 to 40 seconds after the start of contrast injection. During this phase, the normal liver parenchyma receives opacified blood from the arterial system, but also receives 4 times more nonopacified blood from the portal system. HCCs receive most of its blood supply from the hepatic artery, whereas normal liver parenchyma is supplied mainly through the portal vein system. Therefore, lesions with arterial-dominant vascularity show brisk enhancement during the arterial phase and are easily detected in the background of normal liver parenchyma, which remains relatively hypovascular during this phase. Previous studies have shown that a significant number of additional HCC lesions can be found during the arterial phase compared with the portal or delayed phases. 7,s Portal-phase dominant imaging requires scanning the liver 60 to 90 seconds after the start of contrast injection. During this phase, the liver still receives opacified blood from the arterial system but also receives 4 times more opacified blood from the portal system. Therefore, during this phase, hypervascular lesions such as HCC can be isodense relative to the normal liver because both HCC and normal parenchyma enhance similarly. In our institution, helical CT is obtained with 5-mm collimation and a 1:1.5 pitch and subsequent reconstruction of the images at a 5-ram interval. Contrast material (170 mL) is injected at 5 mL/s (biphasic helical CT). The helical acquisition starts at 20 seconds for the arterial phase and at 60 to 70 seconds for the portal phase. We inject contrast material with an automated power injector (Medrad, Pittsburgh, PA) through large-bore venous catheters (18-G for 5-mL/s rate). In addition, we routinely perform equilibrium-phase images 10 to 15 minutes after the administration of contrast material because most HCCs are clearly hypovascular relative to the liver parenchyma during this phase.

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SIGNS OF CHRONIC LIVER DISEASE ON CT

Parenchymal Changes Cirrhosis is a diffuse liver disease produced as a common final response of the liver to a wide variety of chronic injuries. In western countries, chronic hepatitis C virus infection and alcohol ingestion are the most common causes of cirrhosis. Histologically, cirrhosis is defined as an impaired regeneration of lobular hepatic parenchyma, accompanied by extensive necrosis, and the development of regenerative nodules, which consist of normal hepatocytes surrounded by fibrosis. In cirrhosis, irreversible fibrous bridging develops between the portal spaces, with remodeling and destruction of the underlying parenchymal architecture. 9 From the standpoint of imaging, morphologic changes in cirrhosis greatly depend on the severity of the disease. In early cirrhosis, morphologic changes may be subtle and easily missed with all imaging modalities, whereas in advanced disease, morphologic changes are usually obvious. Therefore, early parenchymal changes may not be visible on CT. Recently, enlargement of the hilar periportal space, with increased fatty tissue in the porta hepatis, has been described as a helpful indirect sign of cirrhosis on magnetic resonance (MR). m These morphologic changes may also be detected with CT. In the later stages of cirrhosis, morphologic changes are easily seen, and include

VALLS ET AL

nodularity of liver surface caused by regenerating nodules, fibrous scarfing, and nonuniform segmental atrophy or hypertrophy (Fig 4). In addition, extrahepatic changes related to portal hypertension, such as splenomegaly and venous collaterals, are usually found. Nodularity of the liver contour on CT directly correlates with the gross appearance of the cirrhotic liver. Histologically, this nodularity is related to regenerative nodules that grossly distort the hepatic architecture. Regenerative nodules are usually not seen on CT (other than as surface nodularity), though they can occasionally be seen as hyperdense parenchymal nodules on noncontrast examinations, or as tiny hypodense nodules on postcontrast, delayed-phase, images. In some patients with advanced cirrhosis, confluent fibrotic masses are present, which generally are associated with atrophic changes in the anterior part of the liver. This so-called confluent hepatic fibrosis has been reported in a large series of cirrhotic patients studied with conventional nonhelical CT. 11 In this series, confluent hepatic fibrosis was found in 14% (59 of 420) of the patients who underwent liver transplantation. These fibrotic lesions are generally wedge shaped, and radiate from the porta hepatis. They are associated with retraction of the liver capsule and segmental parenchyreal shrinkage (Fig 5). Confluent hepatic fibrosis

Fig 4, Parenchymal changes in cirrhosis. (A) Contrast-enhanced helical CT in the portal phase shows nodularity of the contour of the left hepatic lobe (small arrows), Note a dilated left gastric vein in the lesser peritoneal space (large arrow), (B) Contrastenhanced CT in another patient with multicentric HCC shows advanced cirrhotic changes with marked hypertrophy of the left lobe (large arrow) and enlargement of the caudate lobe (small arrow),

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Fig 5. Confluent hepatic fibrosis with parenchymal shrinkage. (A) Noncontrast CT shows marked parenchymal loss and subcapsular shrinkage of segment IV, Note the hypodense wedge-shaped area radiating from the porta hepatis (arrows). (B) Portal-phase imaging at the same level shows that the fibrotic area is virtually isodense relative to liver parenchyma. Note slight enhancement of an area of normal parenchyma (arrow}. (C) Equilibrium-phase CT scan shows slight hyperenhancement of the fibrotic lesion (arrows},

may also present as a peripherally located band of tissue that does not extend to the porta hepatis, as shown in Figure 6. Contrast enhancement of confluent hepatic fibrosis is variable, and the fibrotic area can be isoattenuating, hypoattenuating, or hy-

perattenuating in comparison with the remainder of the liver parenchyma. In the series of Ohtomo et al, 11 most areas of confluent fibrosis were iso(50%) or hypoattenuating (28%), and only 22% were hyperattenuating after contrast administra-

Fig 6. Confluent hepatic fibrosis. (A) Nonenhanced CT shows a low-attenuation wedge-shaped lesion in a subcapsular location extending to the hepatic hilus (arrow). (B) Corresponding contrast-enhanced axial image during the portal phase shows marked contrast enhancement of the fibrotic area (arrow),

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tion. However the investigators did not perform biphasic CT studies, and therefore the relative enhancement on arterial and portal phase was not described. In some cases, poorly marginated confluent hepatic fibrosis may be difficult to differentiate from infiltrative neoplasms. 12

Portosystemic Collaterals Cirrhosis-related fibrotic changes in the liver parenchyma may cause compression and distortion of vascular structures, leading to increased portal venous flow resistance at the postsinusoidal level. As hepatic venous outflow is restricted, hydrostatic pressure in the portal system rises (portal hypertension), and the portal vessels become distended. In severe portal hypertension, the outflow hepatic vein resistance becomes so great that portal venous flow eventually decreases. Ultimately, hepatofugal flow develops as blood flow is diverted away from the liver. The alternative pathways for portal blood flow are found at sites where venous drainage is shared by both the hepatic and systemic venous systems] 3 These sites are called portocavaI or portosystemic anastomosis. The portosystemic collateral pathways can be shown by cross-sectional imaging, and it is important to identify these collaterals before planning the appropriate treatment for cirrhosis. Left gastric vein collateral pathways. The most relevant portosystemic collaterals are those around the gastroesophageal junction because they are the main cause of gastrointestinal bleeding and hepatic encephalopathy. These collaterals are tributaries of a dilated left gastric vein (LGV). The LGV normally is a branch of the portal vein that drains the anterior and posterior surface of the stomach. The LGV ascends through the lesser curvature up to the esophageal junction, where it receives the esophageal veins. The LGV is considered to be dilated when it exceeds 5 to 6 mm in maximum diameter (Fig 4A). Therefore, in generalized portal hypertension, dilated veins develop around the stomach (gastric varices), and within and outside the wall of the esophagus (esophageal and paraesophageal varices) (Fig 7). The latter usually drain into the azygos/hemiazygos system, but they may also connect with the subclavian system through the left pericardiophrenic vein or the inferior phrenic vein. 13 The short gastric veins, which are small veins that drain the gastric fundus and greater curvature, are located between the

Fig 7. Gastric and paraesophageal varices. (A) Contrastenhanced helical CT in the portal phase shows dilated vascular structures (arrow) in the posterior wall of the gastric cardia, consistent with gastric varices. {B) Axial helical CT shows tortuous vessels in the posterior wall of the esophagus (arrows) corresponding to paraesophageal varices.

splenic hilum and the gastric wall. Occasionally, these veins can also be dilated in portal hypertension. SpIenorenal shunts. Another group of portosystemic collateral vessels develops between the splenoportal system and the left renal vein (Fig 8A), forming spontaneous splenorenal shunts. These collaterals, in turn, communicate with the LGV, and the posterior and short gastric veins. The connection between the LGV and the left renal vein can also be formed through the left inferior phrenic and left adrenal veins. 13

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Fig 8. Splenorenal shunt and dilated paraumbilical vein. {A) MIP image in the axial plane shows a tortuous vessel (arrows) connecting the splenic vein and the left renal vein (arrowheads). (B) MIP image in the axial plane shows a dilated paraumbilical vein (arrowheads) arising from the left portal vein and running through the ligamentum teres to the umbilical region. Note the presence of a dilated left gastric vein (arrow).

Paraumbilical vein. The last relevant alternative collateral pathway is the paraumbilical vein system. Hypertrophy of this collateral venous pathway is clinically detectable as the classic caput medusae around the umbilicus (Cruveilhier-von Baumgarten syndrome). Normal paraumbilical veins originate around the umbilicus and extend upward along the round ligament, ending in the left branch of the portal vein. They drain into the superior vena cava or the external iliac veins through the inferior epigastric veins, or through the superior epigastric and/or internal thoracic veins. A dilated paraumbilical vein is seen on contrastenhanced CT as a serpentine tubular vessel running in the fissure of the round ligament, anterior to segments II and IIl of the liver (Fig 8B). DIAGNOSTIC FEATURES OF HCC

Epidemiologic Data HCC is the most common primary liver malignancy, with a reported incidence ranging between 250,000 and 1,000,000 new cases per year. la Most patients with HCC have underlying liver cirrhosis and chronic hepatitis B or C virus infection. HCC is a very common hepatic cancer in some eastern and African countries where chronic hepatitis B virus (HBV) infection is endemic. Although the incidence of HCC in the United States and northern Europe is low, the incidence in southern Europe and Mediterranean countries is moderate, as'16 Recent epidemiologic data show an increase in the incidence of HCC in the United States over the

past 2 decades, rising from 1.4 per 100,000 in 1980 to 2.4 per 100,000 in 1995. a7 Recent studies have shown a high prevalence of hepatitis C virus (HCV) antibodies in patients with cirrhosis and HCC in countries where HBV infection is not endemic (75% in Barcelona and 70% in northern Italy). On the other hand, in countries with endemic HBV infection, such as Taiwan or South Africa, the prevalence of HCV antibodies is less than 30%. 18 These epidemiologic data suggest, therefore, an etiologic relationship between chronic HCV infection and HCC in cirrhosis. 19 In the United States, approximately 2.7 million people are chronically infected with HCV, which is a leading cause of chronic liver disease. 2° In most cases, transmission of HCV occurs among young adults, as a result of injection drug use and highrisk sexual practices) ° In approximately 85% of adults infected with HCV, the infection becomes chronic, and at least 20% of patients with chronic HCV infection develop cirrhosis.17 Once cirrhosis is established, HCC develops during the next 20 years. Overall, the incidence of HCC is 1.9% to 6.7% in all patients with chronic HCV infection. 17 HCV infection, therefore, appears to be a formidable health problem in developed countries. The problem is particularly acute because most HCVinfected patients are younger than 50 years of age. Consequently, infection-related complications such as cirrhosis and HCC will certainly increase during the next few years as these patients reach the age at which such complications typically oc-

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<

Fig 9, Hyperenhancement pattern of HCC in the arterial phase. (A) Helical CT shows a heterogeneously hyperenhancing lesion (arrow) in segment II of the left lobe. (B) Arterialphase CT scan in another patient shows a tiny hypervascular lesion (black arrow) in segment IV and a larger lesion (white arrow) in the caudate lobe. Histologically, both lesions corresponded to HCC.

cur. 2° In Spain, the majority of HCC cases have underlying cirrhosis (92.8%). Only a minority of Spanish patients (8.2%) are HBV-antibody positive,21 and the majority (75%) are HCV-antibody positive.22 Contrast Enhancement Features

The histologic features are the key to understanding the pattern of contrast enhancement of HCC. Well-differentiated HCCs are hypervascular lesions with a predominant arterial blood supply.23'24 Generally, HCCs show brisk transient hyperenhancement during the arterial phase, and are readily detected with biphasic helical CT against the background of minimally enhancing, normal liver parenchyma (Fig 9). HCCs rapidly become iso- or hypoattenuating during the portal phase (Fig 10). In a small number of cases, however, HCC lesions may be hypoenhancing and nearly isodense in the arterial phase and persist as hypoattenuating lesions during the portal phase. These lesions may be better shown in the portal

Fig 10. HCC nodules isodense in the portal phase. (A} Arterial-phase helical CT shows multiple, tiny, hypervascular lesions (arrowheads) consistent with HCC in segments II, IV, and VII. (B) Portal-phase imaging at the same level shows that most lesions are now isodense with the liver. Only the lesion in segment VII (arrow) is barely discernible as a slightly hyperdense nodule.

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seven of these lesions were hypervascular in the arterial phase, and all of these turned out to be HCC at histopathologic study. The positive predictive value (PPV) of tumor hypervascularity for diagnosis of HCC was 100%. The PPV of hypovascularity for the diagnosis of HCC was 81% for all hypovascular lesions (some of these lesions were coexisting with hypervascular lesions), and only 66% in patients with only hypovascular lesions. These results show, therefore, that in patients with hepatic cirrhosis, an enhancement pattern consisting of hyperattenuation in the arterial phase and hypoisodensity in the portal phase is virtually diagnostic of HCC. 25

Morphologic CT Features

Fig 11. HCC best seen in the portal phase. (A) Helical CT in the arterial phase shows a slightly hypodense lesion (arrow) in segment Ill, without significant contrast enhancement. (B) Corresponding axial CT scan in the portal phase shows much greater conspicuity of the hypodense lesion (arrow) against the background of normally enhancing liver parenchyma.

phase than in the arterial phase (Fig 11). In general, HCCs become clearly hypoattenuating, relative to the surrounding liver parenchyma, on equilibriumphase CT The significance of the HCC enhancement pattern in a clinical setting of cirrhosis has been recently addressed by Lee et al, 25 who evaluated the diagnostic significance of hypervascular lesions in 26 cirrhotic patients who underwent biphasic helical CT before hepatic transplantation. A total of 58 lesions were detected by CT. Thirty-

Additional features suggesting the diagnosis of HCC include a peritumoral capsule, a mosaic enhancement pattern (defined later), portal vein thrombosis, fatty infiltration within the mass, and arteriovenous shunting. 23'24 Tumor capsule. Histologically, the tumor capsule that surrounds HCC is a fibrous band with 2 layers. The outer layer is composed of compressed normal hepatic parenchyma and peritumoral vessels. 23 The inner layer forms from the condensation and colagenization of reticuline fibers as normal hepatocytes collapse and disappear with the expansive growth of HCC. is On CT, the tumor capsule is defined as a thin, sharply marginated rim of tissue that surrounds an expanding tumor. Enhancement features of the capsule are highly variable, 24 but, generally, the capsule is hypovascular on arterial-phase images and hypervascular on portal and delayed images (Fig 12). In a nonhelical CT series, Freeny et al23 reported a tumor capsule in 13% of the patients. In 93% of the cases, the capsule was hyperattenuating relative to the liver parenchyma, but the investigators do not mention specifically the phase of contrast enhancement in which hyperattenuation occurred. In the series by Stevens et al, 24 a tumor capsule was found in 31% of HCC cases, 24 and in another series by Honda et al, 26 a tumor capsule was present in 57% of lesions. Mosaic pattern. On CT, a mosaic pattern is defined as an internal tumoral structure, with nodules and septa of different attenuation and different degrees of contrast enhancement (Figs 13 and 14). 23,24 These imaging features correlate with the gross morphologic appearance of the tumor. Histologically, a mosaic enhancement pattern corm-

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Fig 12. Peritumoral capsule in HCC. (A) Helical CT in the arterial phase discloses a hyperenhancing lesion in segment VIII, consistent with HCC. Note the hypodense peritumoral capsule (arrow). (B) Corresponding portal-phase axial image shows near isoattenuation of the tumor, as compared with normal liver parenchyma. The peritumoral capsule (arrow) now is hyperenhancing. (C) On this axial CT scan in the equilibrium phase, the HCC nodule is now clearly hypoattenuating. Note hyperenbancement of the peritumoral capsule (arrow).

lates with macroscopic heterogeneity of the tumor. 1s'26 The mosaic pattern has been found in 63% of the patients in a Japanese series, z7 and in 46% of the patients in an American series. 24 Vascular invasion. The association of a focal liver lesion and vascular invasion (mainly of the portal vein) strongly suggests the diagnosis of HCC. Vascular invasion is defined as intraluminal tumor in the portal or hepatic veins, generally associated with an expanded diameter of the vessel. In contradistinction to bland (nontumor) thrombus, which is hypovascular relative to cir-

rhotic liver parenchyma, tumor thrombus shows contrast enhancement in the arterial phase, and tumor neovessels can occasionally be detected (Fig 15). In both Asian 27 and American 24 series, the incidence of vascular invasion in HCC is relatively high (48% and 33%, respectively). In some cases of vascular invasion, arterioportal shunting can also be seen, as indicated by early opacification of portal vessels in the arterial phase (Fig 16). On CT scans, an arterioportal shunt is defined as enhancement of a segment of the portal vein and adjacent liver parenchyma during the arterial phase.

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Fig 13. Mosaic pattern in HCC, (A) Contrast-enhanced helical CT in a 66-year-old man shows a mosaic pattern of multiple coalescent hypervascular nodules within the mass (arrow). (B) Corresponding axial image in the portal phase shows persistent hyperenhancement of the lesion (arrow).

Fig 14. Multiphasic CT in mosaic pattern. (A) CT scan in the arterial phase shows a heterogeneous liver tumor with areas that differ in attenuation. Note the hyperenhancing area in the posterior aspect of the lesion (arrow). (B) Corresponding portal-phase image shows slight hyperenhancement of the lesion and a hypodense intratumoral nodule (arrow). (C) In the equilibrium phase, the lesion is globally hypodense, but hypoattenuation persists in the anterior nodule (arrow).

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Fig 15, Tumor thrombus in HCC, (A) Axial CT scan in the arterial phase at the level of the porta hepatis shows multinodular HCC in the right hepatic lobe (arrowheads). Note hyperenhancing thrombus in the main portal vein, with enlarged neovessels (arrow) consistent with tumor thrombus. (B) CT scan at the same level in the portal phase shows hypodense thrombus in the main portal vein, (C) An image slightly caudal from B in the portal phase shows extension of tumor thrombus into the splenic vein (arrow).

Fatty metamorphosis. Histologically, HCC shows variable degrees of fatty metamorphosis2S; however, detection of gross lipomatous areas with CT is very infrequent (Fig 17). In an Asian series, only 1.6% of the patients (10 of 600) showed areas of low attenuation consistent with fatty infiltration, whereas in a Western series, this feature was even less fiequent. 23a4 DIFFERENTIAL DIAGNOSIS OF FOCAL LIVER LESIONS IN CHRONIC LIVER DISEASE

As more cirrhotic patients are screened with biphasic helical CT, an increasing number of lesions are being detected. Although a majority of nodules in the setting of chronic liver disease will turn out to be HCC, other lesions can also be

found. In the series of Krinsky et al, 29 concerning 71 consecutive patients who underwent liver transplantation, histopathologic study disclosed hepatic neoplasms in 15%, dysplastic nodules in 25%, and benign lesions (cysts, hemangiomas, and hamartomas) in 16% of the patients. Radiologists should be aware of differential diagnosis of hepatic masses, as well as the imaging features that, in some cases, may permit a specific diagnosis to be made.

Hypervascular Lesions Hyperenhancing lesions in the arterial-dominant phase include HCC, small hemangiomas, atypical dysplastic nodules, transient hepatic attenuation differences (THAD), focal nodular hyperplasia, liver cell adenoma, and hypervascular metasta-

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or equilibrium phase includes hypovascular HCC, peripheral cholangiocarcinoma, dysplastic nodule, and regenerative nodule. Other lesions such as hyalinized or sclerosed hemangiomas, necrotic nodules, or liver metastases from other primary tumors are exceedingly rare.

Hemangioma

Fig 16. Arterioportal shunting in HCC. Arterial phase helical CT shows arterioportal shunting with early enhancement of the left portal vein (arrow). Note infiltrating HCC (arrowheads) invading the left portal vein.

ses. 3° In the setting of chronic liver disease, however, the differential diagnosis of HCC can be limited to hemangiomas, THAD, and the extremely rare hypervascular dysplasfic nodule.

Hypovascular Lesions In patients with chronic liver disease, the differential diagnosis of hypodense lesions in the portal

Hemangioma is the most common benign liver lesion, with an overall incidence as high as 7%. These masses are always benign and in the great majority of cases are either asymptomatic or produce minimal symptoms. Microscopically, cavernous hemangiomas consist of normal sinusoids with blood-filled spaces lined by endothelial cells. On contrast-enhanced CT, hemangiomas initially present globular peripheral enhancement, as shown in Figure 18. According to Freeny and Marks, 31 hepatic hemangiomas can be confidently diagnosed when a focal lesion is hypodense, compared with normal liver, on precontrast scans, which shows early peripheral contrast enhancement, and fills in, becoming iso- or hyperdense on delayed scans. More recently, Leslie et a132 and van Leuveen et a133 have shown that globular, noncontinuous enhancement that is isodense with the aorta in the portal phase is highly characteristic of cavernous hemangiomas on CT, with a positive predictive value of 100% and a sensitivity ranging between 67% and 86%. Roughly, 30% of hemangiomas

Fig 17. Fatty metamorphosis in HCC. (A) Noncontrast CT shows a large, heterogeneous lesion in the right lobe of the liver, Note the intratumoral low-attenuation areas (arrows) consistent with fatty metamorphosis. (B) No enhancement occurs in these areas during arterial phase-contrast enhanced CT.

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Fig 18. Typical enhancement features of hemangiomas. (A) Contrast-enhanced CT in the arterial phase in a 54-year-old patient shows a focal lesion in segment II. Note globular, peripheral, and discontinuous contrast enhancement (arrows). (B) Corresponding axial image in the portal phase shows progressive peripheral tiff-in of the lesion. (C} In the equilibrium phase, 10 minutes later, the lesion shows homogeneous enhancement (arrow). Note that the lesion is isodense to normal vascular structures such as the middle hepatic vein (arrowhead).

may appear as homogeneously hyperenhancing lesions in the arterial phase, 34 and may mimic HCC, particularly in the setting of virus- or alcoholrelated liver disease. However, most small hemangiomas tend to be progressively hyperdense in the portal and equilibrium phases, allowing distinction from HCCs, which are usually hypovascular in the portal or equilibrium phases (Fig 19). In addition, hemangiomas are exceedingly rare in patients with cirrhosis. In the series by Miller et al, 12 114 malignant lesions were found in 40 of 200 cirrhotic patients who underwent transplantation (103 HCCs and 11 cholangiocarcinomas), whereas only 6 hemangiomas were found. In another series, Dodd et al35 found only 9 hemangiomas in a series of 508 consecutive patients who underwent transplantation. In a recent study by Brancatelli et al, 36 reported 21 hemangiomas in cirrhotic patients undergoing transplantation during a 6-year period. Five lesions were not detected with imaging, even in retrospect. In the remaining patients, 14 lesions had characteristic nodular peripheral enhancement, and only 2 (11%) showed uniform hyperenhancemerit in the arterial phase that mimicked HCC. In the setting of chronic liver disease, hemangiomas

may decrease in size and show capsular retraction (Fig 20). Small hemangiomas with fibrotic changes (hyalinized hemangiomas) rem~tin a difficult diagnosis with CT, and generally require histologic proof. 37 THAD

Structural alterations in cirrhosis may lead to microvascular changes in the form of spontaneous arterioportal communications. Occlusion of the peripheral hepatic veins, with subsequent retrograde filling of portal flow through arterioportal anastomoses, has been proposed as the cause of spontaneous arterioportal communications in cirrhosis. 38 Experimental microscopic studies have shown that the peribiliary plexus is hypertrophied in the cirrhotic liver39 and that transplexal arterioportal communications occur through the plexus. On arterial-phase CT, transplexal communication may present as THAD. On a day-to-day basis, showing a hypervascular lesion in a cirrhotic patient is virtually diagnostic of HCC. However, nonneoplastic hyperattenuating lesions may be found, especially in patients with chronic liver disease,4° and occasionally these le-

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Fig 19. Small hemangioma in a 57-year-old woman with HCV cirrhosis. (A) Arterial-phase CT scan shows a small hyperenhancing nodule in segment II (arrow). In that setting, the lesion is indistinguishable from HCC. (B) Corresponding portal-phase image shows that the lesion (arrow) clearly remains hyperenhancing. (C) Delayed-phase axial CT shows that the lesion remains hyperattenuated relative to the liver parenchyma (arrow). Note that the lesion is isodense with adjacent venous structures (arrowhead) and, therefore, a confident diagnosis of hemangioma can be made. (Figures A and C reprinted with permission from the American Journal of Roentgeneology.3°)

Fig 20. Hemangioma with decreasing size in a cirrhotic patient. (A) Axial, contrast-enhanced CT in the portal phase shows a subcapsular hemangioma (arrows} with typical globular peripheral and discontinuous contrast enhancement. (B) Portal-phase CT at the same level 7 years later shows a decrease in the size of the lesion (arrow) and absence of the typical enhancement pattern. Histopathologic examination after transplantation: only a fibrotic scar was found at the site of the hemangioma. (Reprinted with permission from Radiology.3s)

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sions may mimic HCC. Kim et al4° reported the CT findings of nonneoplastic arterioportal shunts in a series of 803 patients with suspected HCC who were referred for arterial embolization. All lesions were hyperattenuating in the arterial phase and remained slightly hyperattenuating or isoattenuating in the portal phase. Interestingly, none of these lesions was hypoattenuating in the portal phase, as is typical of HCC. On biphasic helical CT, nonneoplastic THAD are usually subcapsular, wedge-shaped lesions with a straight border (Fig 21). Subcapsular location is more frequent because hypertrophy of the peribiliary plexus is more prominent in the subcapsular area of the liver. The wedge-shaped appearance, subcapsular location, and absence of hypoattenuation in the portal and equilibrium phases are the key to differentiate THAD from small HCCs (Fig 21). Occasionally, early opacification of a small portal branch can be seen within the THAI).4° This feature, also called the Dot sign, is virtually diagnostic of a nonneoplastic arteriopo~al shunt (Fig 21). Although very infrequent, some THADs may have a pseudonodular shape. 29'41 In these selected cases, differential diagnosis with HCC may be difficult. In our experience, nodular THAD are usually subcapsular and often are located near the round ligament or paraumbilical vein (Fig 22). Occasionally, confirmatory findings including follow-up studies or fine-needle aspiratiofi biopsy are required for definitive diagnosis.

Dysplastic Nodules Dysplastic nodules are premalignant neoplastic nodules that are found in the setting of cirrhosis. 42 It has been estimated that dysplastic nodules develop in 15% to 25% of cirrhotic livers. A multistep process of carcinogenesis has been shown in the cirrhotic liver, from dysplastic nodule (formerly called adenomatous hyperplasia) to H C C . 43 The blood supply of dysplastic nodules comes mainly from the portal vein, but an arterial blood supply has been shown occasionally. A recent series reported a relatively high incidence (24%) of dysplastic nodules in patients with advanced cirrhosis undergoing hepatic transplantation.44 In this series, the sensitivity of helical CT was 39% (9 of 23) for detecting these nodules, and all lesions were hypoattenuating. In a recent study, Krinsky et a129 reported the results of multiphasic MR imaging (MRI) in the diagnosis of HCC and

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dysplastic nodules in transplanted patients. Only 15% (9 of 59) of dysplastic nodules were detected with MRI, and most of these lesions were hypovascular. Interestingly, 4 high-grade dysplastic nodules were hyperenhancing in the arterial phase and were misinterpreted as HCC. Therefore, hyperenhancing dysplastic nodules may be indistinguishable from small HCCs (Fig 23).

Regenerative Nodules Histologically, regenerative nodules in the cirrhotic liver are formed by regenerative hepatocytes surrounded by fibrotic septa. The architecture and blood supply of regenerative nodules is very similar to normal hepatic parenchyma; therefore, CT visualization of regenerative nodules is difficult. Regenerative nodules can be seen occasionally as slightly hyperdense lesions on noncontrast studies. More frequently, regenerative nodules appear in the equilibrium phase as tiny hypodense regions (Fig 24). Although they occur very infrequently, large regenerative nodules may present as low-density lesions in the arterial, portal, and equilibrium phases, mimicking hypovascular HCCs (Fig 25). Another infrequently seen lesion that may be found in the clinical setting of chronic liver disease is the necrotic nodule of the cirrhotic liver (Fig 26). We have found one such case that was considered to be HCC preoperatively. Although the lesion was hypodense, it clearly showed peripheral linear enhancement. At histologic diagnosis, only necrosis could be found.

Intrahepatic Peripheral Cholangiocarcinoma Intrahepatic peripheral cholangiocarcinoma (IPCC) is a primary adenocarcinoma arising from the intrahepatic bile duct epithelium. Although this tumor accounts for less than 10% of all primary hepatic malignancies, it is the second most common primary malignant hepatic neoplasm after N e e . 45 On contrast-enhanced CT, IPCC has been described as a predominantly hypodense mass, with irregular margins and mild peripheral enhancement, which becomes hyperdense on delayedphase images.46-48 Recently, the CT features of ICC have been described with 2-phase spiral CT. 49'5° In most cases, IPCC presents as a hypodense lesion with rim-like peripheral enhancement in both the arterial and portal phases (Fig 27A and 27B). The hyperenhancing pattern of ICC on de-

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Fig 21. THAD. (A) Transverse, arterial-phase, helical CT in a patient with peripheral cholangiocarcinoma in segments II and I|1 (white arrow) and neoplastic portal vein thrombosis (arrowhead). Note the subcapsular wedge-shaped hyperattenuating area in segment IV with a straight border (black arrow) consistent with THAD. (B) Axial CT scan in the portal phase in another patient shows a small subcapsular wedge-shaped hyperenhancing lesion with straight borders (arrow), consistent with a small THAD. (C) Corresponding portal-phase image shows that the lesion is isoattenuating with normal liver parenchyma. (D) Transverse arterial-phase CT section in another patient shows a subcapsular wedge-shaped hyperenhancing lesion in segment VI, consistent with THAD. Note early opacification of a small portal vessel within the lesion (arrow). (Part A reprinted with permission from Abdominal Imaging.) 49

Fig 22. Nodular THAD mimicking HCC. (A) Transverse late-arterial phase CT scan in a 58-year-old woman with cirrhosis shows a hyperenhancing nodular lesion in segment IV (arrow) adjacent to the umbilical portion of the left portal vein. Note that the lesion is slightly less enhancing than a dilated paraumbilical vein (arrowheads). (B) Corresponding portal-phase image shows that the lesion is now isodense with normal parenchyma, The paraumbilical vein (arrowheads) remains hyperattenuating in this phase. At transplantation and histopathologic examination, no lesion was found in this location.

Fig 23. Hyperenhancing dysplastic nodule mimicking HCC.

(A) Arterial-phase axial CT scan shows a hyperenhancing lesion (arrow) in segment VIII. (B) Corresponding image in the equilibrium phase shows that the lesion (arrow) is hypodense relative to the liver parenchyma. (C) Corresponding specimen, after liver resection, shows a nodular solid lesion macroscopically indistinguishable from HCC. On microscopic examination, the lesion was found to be a low-grade dysplastic nodule.

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Fig 24. Small regenerative nodules. (A) Axial portal-phase CT shows tiny hypodense nodules (arrows) scattered throughout the liver. (B) During the equilibrium phase, these regenerative nodules (arrows) remain hypodense and are slightly more conspicuous.

layed-phase imaging seems to be related to the large amount of interstitial space in the fibrous stroma of the tumor. Slow diffusion of contrast medium from the vascular to the interstitial space may account for the delayed and prolonged enhancement of the tumor on images obtained 10 to 15 minutes after contrast injection (Fig 27C and 27D). 47 Variable degrees of delayed enhancement in ICC during the equilibrium phase have been reported previously. 48'5° In the appropriate clinical setting, however, the combination of a focal hypodense mass with peripheral enhancement in the arterial and portal phases, accompanied by capsular retraction and/or hyperenhancement on the equilibrium phase, may be valuable in suggesting the diagnosis of ICC. 49 This diagnostic approach is especially important in patients with chronic fiver disease, which is associated with ICC (25%). In the series reported by Valls et a149 6 of 25 (25%) patients with ICC had chronic liver disease. In patients with chronic liver disease, HCC is generally the most frequent diagnosis suggested; however, for any hypovascular lesion, the diagnosis of ICC should be seriously considered because it is the second most frequent hepatic malignancy. If imaging findings on arterial or portal phase CT show a hypovascular lesion with peripheral-rim enhancement, a delayed series should be obtained at l0 to 15 minutes

to took for hyperenhancement of the lesion. In the setting of chronic fiver disease, this constellation of findings is highly suggestive of intrahepatic peripheral cholangiocarcinoma. PREOPERATIVE IMAGING

Preoperative Staging of HCC Surgery is stiU the only chance for cure of HCC, though for the majority of patients with HCC, the prognosis is poor. Accurate tumor staging, therefore, is critical in patients with HCC for whom surgical treatment, either resection or transplantation, may be attempted. Unfortunately, only a minority of patients proves to be candidates for curative resection because of intrahepatic tumor extension and the frequent association with chronic fiver disease. Nevertheless, recent reports indicate that potentially curative surgery can be performed in a select group of patients. Because modem imaging techniques allow us to define more accurately the intrahepatic extension of HCC, we may be able to select the patients who are best suited for surgical treatment. In the past years, technologic improvements in CT, sonography, and MRI have allowed radiologists to improve noninvasive imaging of HCC. The advent of helical CT has dramatically enhanced our ability to detect and stage H C C . 6'7'25

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Fig 25. Large regenerative nodule mimicking HCC. (A) Transverse arterial-phase helical CT image shows a hypervascular nodule (white arrow) in segment VII, consistent with HCC. More anteriorly, in segment VIII, there is another hypodense lesion (black arrow) without contrast enhancement. (B) Portal-phase imaging at the same level shows that the HCC nodule (white arrow) is now nearly isodense. The lesion in segment VIII (black arrow) is still hypodense. (C} On delayed phase imaging, both lesions (arrows) are hypodense. (D) Histopathoiogic examination after liver transplantation showed that the hypervascular lesion in segment VU was an HCC and that the hypovascular lesion in segment VUl (black arrow) was a large regenerative nodule. Note the grayish portion of the HCC (white arrowheads) is viable tumor, and other areas (black arrow) are necrotic. Specimen obtained after chemoembolization.

The addition of arterial-phase imaging to conventional portal-phase imaging seems to improve tumor detection, especially in patients with HCC and coexistent cirrhosis. However, these techniques are relatively new, and studies with substantial pathologic correlation are not yet available. Baron 7 reported the results of biphasic helical CT in 66

patients. Arterial-phase imaging showed 95% of HCCs, whereas portal-phase imaging detected 82%. In 7 cases (11%), lesions were only visible in the arterial phase. This study, however, has the inherent flaw of the lack of pathologic correlation. It is difficult to determine the exact sensitivity and specificity of helical CT in the detection of

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Fig 26. Necrotic liver nodule, (A) Arterial-phase helical CT section shows a hypodense lesion that does not enhance in segment VII (arrow). (B) Corresponding portal-phase imaging shows that the lesion is hypodense (arrow). (C) On equilibrium-phase imaging, the lesion remains hypodense and shows a definite peripheral rim enhancement (arrowheads). The imaging findings were suggestive of hypovascular HCC, but on histopathologic examination, only a necrotic nodule was found.

HCC because pathologic examination of the whole liver after hepatic transplantation is needed. In a large series with nonhelical CT, Miller et a112 reported a sensitivity of 68% for the detection of HCC. In another series using helical CT, Baron and Oliver 51 studied 195 patients with chronic liver disease and without known HCC who underwent hepatic transplantation. These investigators report a sensitivity of 59.3% (19 of 32). In a more recent series of 41 patients with transplantation correlation, Lira et a144 report a sensitivity of 71% (15 of 21) for helical CT in the detection of HCC. The results of imaging techniques largely depend on the size of the lesions. In the Lim et al44 series, the detection rate for HCCs less than 2 cm was 60% and the detection rate for HCCs larger than 2 cm was 82%. In our experience, based on

a recent series of 37 consecutive patients studied before liver transplantation, helical CT had a sensitivity of 79.5% (39 of 49) and a PPV of 86.6% in the detection of HCC. We had 6 false-positive findings that were related to macronodular regenerative nodules, dysplastic nodules, nodular THAD, and necrotic cirrhotic nodules (Figs 25 and 26). In a recent pretransplantation series, Krinsky et a129 used MRI to study 71 patients with chronic liver disease but without a known HCC. These investigators report a sensitivity of 50% (5 of 10) for the detection of HCC. These results may appear modest but, in this study, patients with known HCC were excluded to avoid positive bias, and this series, therefore, represents the worst possible scenario, which is not usually found in clinical practice. A large number of

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Fig 27, Peripheral intrahepatic cholangiocarcinoma in a 74-year-old man with hepatic cirrhosis. (A) Transverse arterial-phase helical CT shows a focal lesion in segments V and VI (arrow) with peripheral rim-like enhancement. (B) On portal phase images, the lesion is hypodense, and peripheral enhancement is also well seen. Note the marked capsular retraction (arrowheads). (C) Delayed-phase axial CT atthe same level shows marked hyperattenuation of the lesion (arrow). (D) Microscopic study (hematoxylin and eosin, 100×) after percutaneous liver biopsy shows proliferation of epithelial cells consistent with adenocarcinoma and abundant fibrous stroma (arrowheads). (Figures A and C reprinted with permission from Abdominal Imaging. 4s)

false-positive findings also occurred in this series (15 lesions in 10 patients). The false-positive findings were related to hypervascular dysplastic nodules, as well as nodular forms of

THAD related to arterioportal shunts. In our experience, false-positive findings have been related to large macroregenerative nodules and hypervascular dysplastic nodules.

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Pretransplantation Imaging Conventional hepatic transplant.

Preoperative assessment of candidates for hepatic transplantation is a multidisciplinary issue that includes clinical, surgical, and imaging evaluation. The main objective is to detect any factor that may contraindicate transplantation or change the surgical technique. Preoperative imaging is useful to assess the hepatic parenchyma, portal and mesenteric vessel patency, signs of portal hypertension, and to rule out underlying neoplastic conditions in the abdomen. Excluding patients in whom the indication for transplantation is HCC, the standard pretransplantation evaluation can be accomplished with sonography and CT. It is important to assess patency of the portal vein and especially to exclude the presence of superior mesenteric vein thrombosis because this finding may be a contraindication to transplantation. The preoperative assessment of arterial anatomic variants with CT angiography by using MIP techniques may be useful in selected cases, but in most cases, hepatic vascular assessment can be performed at the time of the surgical procedure. Domino hepatic transplantation. Familial amyloid polyneuropathy (FAP) is the most common type of hereditary amyloidosis. It is related to transthyretine (TTR) protein mutation and characterized by systemic deposition of variant TTR. 52 Clinically, FAP presents with severe peripheral and autonomic neuropathy and amyloid deposits in the spleen, kidneys, heart, adrenal gland, and eyes. More than 95% of the TTR is synthesized in the liver; therefore, hepatic transplantation is the only curative treatment for TTR patients. However, liver function itself is not affected in FAP, in contradistinction to other congenital metabolic diseases, such as Wilson's disease. FAP typically affects patients between the third and sixth decade, suggesting that a relatively long period is required for the deposition of amyloid. Because of the increasingly long waiting list for hepatic transplantation, the explanted livers of FAP patients are currently accepted as donors for patients with terminal cirrhosis whose life expectation is inferior to the latency period of FAP. The term domino transplantation is applied in these situations because the explanted liver from a patient with FAP is in turn transplanted to another

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patient. In these patients, it is important to perform preoperative vascular examination to exclude anatomic variants of the hepatic artery that may change the surgical technique (Fig 2). Classically, invasive procedures such as conventional angiography have been used in that setting. More recently, the advent of new, noninvasive techniques, such as CT and MR angiography, have made it possible to study the vascular structures of the liver without the risk for angiography-related complications. In our hospital, the preoperative assessment in domino transplantation candidates is performed with CT angiography. This is a noninvasive and fast technique that readily characterizes arterial and portal variants, and also thoroughly studies the liver parenchyma and abdominal cavity.

Split and Living-Related Hepatic Transplantation Split-liver transplantation. Briefly, the split liver transplantation technique consists in splitting the liver in two and placing each portion in 2 different patients. This transplantation method was used for the first time at the end of the 1980s with poor results, and was abandoned by the majority of transplantation programs. More recently, the shortage of cadaveric donors and improvements of splitting techniques have convinced some surgical teams to pursue this option. Recent reports suggest that if good quality organs are selected, the incidence of severe complications with split transplantation is similar to standard hepatic transplantation. From the perspective of radiologists, split transplantation is of limited interest because preoperative imaging is usually not performed. Adult living-related liver transplantation. One of the most important issues in hepatic transplantation is the lack of sufficient donor organs. Over the past 10 years, the number of patients enrolled in the waiting list for transplantation has increased more than 15-fold, while the number of donors has increased only 3-fold. 53 Because of the shortage of cadaveric donors, some groups have presented living-related liver transplantation (LRLT) as an optional technique. The transplant should be performed by using the right hepatic lobe of the donor because, in contradistinction to pediatric patients, left lobe transplantation does not completely supply the metabolic demand of an adult. This complex transplantation procedure needs thorough preoperative vascular assessment before surgery is planned. Basically, the objectives of the presurgi-

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cal assessment are the following: (1) to assess the state of the hepatic vessels, and detect possible vascular abnormalities; (2) to evaluate the size, morphology, degree of steatosis, and presence o f incidental lesions in the donor liver; and (3) to perform hepatic volumetry. Imaging findings that can be considered reasons for exclusion from surgery are usually related to anatomic variants. Recently, Kamel et al54 reported the results of multidetector CT assessment of potential donors for LRLT. These investigators studied 40 potential liver donors. In 57% of the cases, there were no anatomic exclusions, whereas 37.5% were excluded from the program based on CT findings. In most cases, exclusions were related to variations in portal venous anatomy, and, specifically, early portal trifurcation with absence of the fight portal vein trunk (found in 8 of 40 patients). One of the most difficult issues in the preoperative assessment for fiver transplantation is to evaluate the origin of the artery of segment IV. The results of Kamel et al54 suggest that angiographic, multidetector, helical CT techniques are useful for this purpose. Helical CT depicted the origin and course of the artery to segment IV in 97% (39 of 40) of patients. The artery to segment IV arose from the right hepatic

artery in 62% of the cases and from the left hepatic artery in the remaining 37.5%. Another important aspect of pretransplantation evaluation is the presence o f portal variants because the absence of the right portal vein (early trifurcation of the portal vein) is a contraindication for right hepatectomy in L R L T (Fig 3B). Other common anatomic variants, such as anomalous origin of the left portal vein from the right anterior portal vein or an aberrant right hepatic duct, m a y also be contraindications to surgery (Fig 3A). The best mode for pretransplantation evaluation of the biliary tract is controversial. Most centers use intraoperative cholangiography, but recent reports suggest that M R cholangiography can be useful in this setting. In a recent report by Lee et al, 55 M R cholangiography detected anatomic variants in 16% (4 of 25) of adult liver donor candidates. However, 2 anatomic biliary variants that precluded surgery were not detected preoperatively. Despite this failure, we believe that multidetector helical CT or a comprehensive M R examination with M R angiography and cholangiography will probably be the only imaging procedures needed to evaluate potential adult liver donor candidates in the near future.

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