Non–Contrast-Enhanced Computed Tomography of the Liver

The attenuation value of the normal liver typically varies between 54 and 60 Hounsfield units (HU), which is approximately 8 HU greater than that of the spleen, owing to glycogen and iron stores in the liver. Increased density may be seen in hemochromatosis, glycogen storage disease, Wilson disease, β-thalassemia, sickle cell disease, and with certain drugs (amiodarone, cisplatin). A false appearance of increased hepatic density may occur in anemia, in which the decreased attenuation of the blood pool gives the impression of increased hepatic density relative to the intrahepatic vessels. Decreased hepatic density most frequently is related to fatty infiltration of the liver or occasionally secondary to hepatic edema. Noncontrast CT is useful for detecting diffuse abnormalities, such as hemochromatosis or fatty infiltration (Figs. 16.11 and 16.12), in which the attenuation of the liver is increased (hemochromatosis) or decreased (fatty infiltration). Both of these processes may be obscured by the administration of intravascular contrast medium. Hemorrhage or faint calcifications also are better visualized on unenhanced CT (Fig. 16.13).

FIGURE 16.11 Nonenhanced computed tomography through the liver of a patient with hemochromatosis shows diffuse increased attenuation of the liver compared with the spleen.

FIGURE 16.12 Nonenhanced computed tomography through the liver of a patient with fatty infiltration shows low attenuation of the hepatic parenchyma compared with the hepatic blood vessels and liver capsule.

FIGURE 16.13 Unenhanced computed tomography reveals numerous calcifications in a patient with amyloid.

Hepatic neoplasms usually have a high water content, resulting in relative hypoattenuation compared with liver parenchyma. The portal veins and bile ducts also are of lower attenuation than liver parenchyma, and a vessel running vertically through a section may mimic a small tumor, leading to errors in diagnosis. On unenhanced studies, the attenuation difference between liver and tumor may be subtle and may require viewing at very narrow window widths to allow focal lesion detection, but much higher lesion-to-liver attenuation difference can be achieved by the administration of intravenous contrast medium (Tidebrant et al, 1990).

Contrast-Enhanced Computed Tomography of the Liver

The administration of an iodinated contrast agent serves many purposes in hepatic CT imaging, including improved lesion detection and characterization and better vascular mapping. Because a precise rate of injection is essential to image quality, a dedicated power injector is required. Different methods are commercially available to determine the time of maximal arterial enhancement for each patient, depending on factors such as cardiac function and state of hydration (Sica et al, 2000).

Lesion conspicuity is enhanced when there is maximal contrast between a lesion and the surrounding parenchyma. The liver receives 75% to 80% of its blood supply from the portal venous system and only 20% to 25% from the hepatic artery; however, the majority of liver tumors receive most of their blood supply from the hepatic arterial system (Honda et al, 1992). The noncirrhotic liver displays maximal contrast enhancement at approximately 70 seconds from the start of the intravenous administration of contrast medium. At this time, referred to as the portal venous phase of enhancement, maximal contrast between a liver lesion and the surrounding parenchyma is seen with clear delineation of the portal and hepatic veins. Routine evaluation of the liver should be performed using portal venous phase imaging.

The pattern of contrast enhancement also is important for lesion characterization. Certain lesions, such as focal nodular hyperplasia (FNH) and hemangiomata (discussed in greater detail later in this chapter), have specific patterns of enhancement on arterial phase and portal venous phase images. Hypervascular malignant neoplasms, such as HCC and metastatic neuroendocrine carcinoma, display prominent contrast enhancement and increased lesion conspicuity on the arterial phase images, but these lesions may become isodense to the remaining liver and and may be invisible on the portal venous phase images (Fig. 16.14). When HCC or neuroendocrine mestastases are suspected, arterial phase images should be acquired in addition to the routine portal venous phase images.

FIGURE 16.14 Arterial and portal venous phase images as part of a triphasic examination in a patient with metastatic renal cell carcinoma. A, Late arterial phase image reveals multiple hypervascular enhancing foci of metastatic renal cell carcinoma (arrows). B, Portal venous phase image at the same level does not reveal the numerous masses. The low-attenuation lesion represents a partially treated hypoattenuating metastasis.

Computed Tomographic Angiographic of the Liver

MDCT scanners can acquire high-resolution images (<1-mm slice thickness) of the aorta and hepatic arterial anatomy, referred to as early arterial phase images. The intravenous administration of contrast material is performed using a high injection rate of 4 to 5 mL/s to provide maximal contrast enhancement of the arteries, before opacification of the veins or abdominal organs. The same volume of intravenous contrast material is administered as that for routine abdominal CT. Water is administered as a negative contrast agent to facilitate three-dimensional postprocessing. Additional late arterial phase images can be obtained through the hepatic parenchyma in the same breath hold in patients with suspected hypervascular lesions. A major attribute of CT angiography is that it is performed as an adjunct to a routine CT scan. CT of the chest, abdomen, and pelvis can be performed during the same examination to allow for a staging examination in addition to vascular mapping.

Gross Morphology

Three scissurae interrupt the surface of the liver and help define its segmentation (see Chapter 1B). The interlobar fissure is an incomplete structure that defines the inferior separation between the right and the left liver; the scissura here is generally difficult to identify on axial CT, but its position may be estimated, because it is orientated in a vertical plane defined by the gallbladder fossa inferiorly (Fig. 16.16) and the middle hepatic vein superiorly. The gallbladder lies in the main interlobar scissura on the inferior surface of the liver. Three-dimensional reformatting of axial CT data provides a clear depiction of the interlobar scissura and its relationship to the hepatic segments (see Fig. 16.6).

FIGURE 16.16 Normal hepatic segmental and vascular anatomy on computed tomography. A, On cephalad sections, the three hepatic veins are seen to enter the inferior vena cava (ivc). B, The lines of the hepatic veins divide the liver into sectors. The right hepatic vein divides the right liver into anterior and posterior sectors; the middle hepatic vein separates the right from the left liver and represents the line of the interlobar scissura; the left hepatic vein separates segments II and III of the left lobe. C, Approaching the midpoint of the liver, the left portal vein (pvl) is seen. The fissure for the ligamentum venosum (arrows) divides the caudate lobe (c) from the left lateral segments. D, The next section shows the horizontal portion of the right portal vein (pvr). The fissure for the ligamentum teres is now seen (large arrows); this structure divides the lateral segments of the left liver from the caudate lobe (c), segment IV. E, On the last section, the gallbladder (GB) has come into view; a line drawn along the axis of the gallbladder to the IVC represents the inferior extent of the interlobar scissura. R, right hepatic vein; M, middle hepatic vein; L, left hepatic vein.

Slightly to the right of midline, toward the patient’s left side, the anteroinferior portion of the diaphragmatic surface of the liver is notched by the fissure for the ligamentum teres, or umbilical fissure, which defines the inferior border between the medial and lateral segments of the left liver. The ligamentum teres passes through this fissure and usually is surrounded by a small amount of fat. When the ligamentum teres passes out of the liver ventrally, it is located in the free edge of the falciform ligament. The third fissure is present at the point of contact between the lateral segments of the left hepatic lobe and the caudate lobe. This is the fissure for the ligamentum venosum, which is in continuity with the umbilical fissure.

Segmental Anatomy

The segmental anatomy of the liver is based on both the hepatic venous outflow and the inflow pedicles. A functional scheme that corresponds to the liver anatomy and is useful surgically has been described (Bismuth, 1982). The three main hepatic veins divide the liver into four sectors, each of which is independent in that it receives a separate portal venous and hepatic arterial supply and is drained by a separate bile duct. The middle hepatic vein divides the liver into a right and left liver. The right liver is divided into two sectors by the right hepatic vein, and the left liver is divided similarly by the left hepatic vein. Because axial CT readily shows the course of all three major hepatic veins on contrast-enhanced scans obtained near the diaphragm, the major hepatic sectors are easy to identify at this level. The inferior boundary between the anterior and posterior sectors of the right lobe has to be estimated by extrapolating the line of the right hepatic vein onto lower sections. An imaginary line drawn between the IVC and the gallbladder divides the right and left liver on caudal sections and corresponds to the line of the middle hepatic vein. Three-dimensional reformatting can assist in localization of the hepatic segments (see Fig. 16.6). The fissure for the ligamentum teres divides the medial and lateral segments of the left liver and corresponds to the line of the left hepatic vein. The anterior and posterior sectors of the right lobe are subdivided into inferior (V and VI) and superior (VIII and VII) segments. The right portal vein runs horizontally as it enters the right liver, and this level demarcates the anterior and posterior sectors.

Vascular Anatomy

In classic arterial anatomy (see Chapter 1B), the celiac axis gives rise to the common hepatic artery, which bifurcates into the proper hepatic artery and the gastroduodenal artery (see Fig. 16.3). The proper hepatic artery divides into the right and left branches before entering the liver, but the point at which the proper hepatic artery gives rise to the left and right hepatic arteries varies. Although classic arterial anatomy is the most common pattern seen, variant hepatic and celiac arterial anatomy has been reported in 55% of patients based on initial cadaveric dissections by Michels (1955). Many of these variants have significance for preoperative planning and surgical management. Preoperative knowledge of variant anatomy can assist in selection of treatment options and in surgical planning, and it facilitates surgical dissection and may help avoid iatrogenic injury (Figs. 16.17 and 16.18).

FIGURE 16.17 Three-dimensional volume-rendered computed tomographic angiogram reveals a replaced right hepatic artery (arrows) originating from the superior mesenteric artery. The right hepatic artery courses posterior to a stent in the common bile duct (arrowheads).

FIGURE 16.18 Three-dimensional volume-rendered computed tomographic angiogram reveals the right hepatic artery (solid arrow) originates from the celiac axis and courses posterior to the gastroduodenal artery (open arrow).

The portal vein originates at the junction of the splenic vein (SV) and superior mesenteric vein (SMV), immediately posterior to the neck of the pancreas. It courses toward the right and cephalad, as it enters the hepatoduodenal ligament. Within this ligament, the portal vein courses parallel to the proper hepatic artery, which lies on its anteromedial surface, and the common bile duct, which lies on its anterolateral surface. After entering the hepatic parenchyma, the portal vein branches to supply each portal sector (see Fig. 16.1A) and subsequently each segment. A spectrum of portal venous variants has been described, many of which have major implications for safe and efficacious hepatic resection and percutaneous hepatobiliary intervention. Covey and colleagues (2004) reported the presence of variant portal venous anatomy in 35% of a group of 200 patients studied. CT is ideally suited to display these variants, an awareness of which may help avoid iatrogenic injury (Fig. 16.19).

FIGURE 16.19 Variant portal venous anatomy. Thick-slab maximum intensity projection reveals that the portal venous branch perfusing the anterior sector of the right hepatic lobe (arrow) shares a common trunk with the left portal vein (arrowhead).

The hepatic veins course between the hepatic sectors and have a short extrahepatic course before joining the IVC (Blumgart et al, 2001). The right hepatic vein drains directly into the IVC, and the middle hepatic vein and left hepatic vein usually join before draining into the IVC. A variable number of retrohepatic veins drain from the posterior aspect of the liver into the IVC, and a large inferior right hepatic vein, referred to as an accessory right hepatic vein, may be present in some patients (see Fig. 16.1B).

Biliary Anatomy

The intrahepatic biliary tree branches in a fashion nearly identical to the portal system (Fig. 16.20; see Chapter 1B). The left and right hepatic ducts form the common hepatic duct, near the lateral margin of the main portal vein, near its junction with the right portal vein. The common hepatic duct continues inferiorly toward the left and posteriorly, and it maintains its anterolateral position with respect to the portal vein throughout its course within the hepatoduodenal ligament. It becomes retroperitoneal at the level of the head of the pancreas and occupies a position on the posterolateral surface of the pancreas, until it joins the pancreatic duct immediately before entering the ampulla of Vater. The confluence of the right and left hepatic ducts is often seen lying anterior to the portal venous confluence.

FIGURE 16.20 Contrast-enhanced computed tomography in a patient with a minimally dilated biliary system. A, The intrahepatic bile ducts are seen as branching, low-attenuation structures adjacent to the portal veins. At the porta hepatis, the hepatic artery (arrow) is seen to pass between the main portal vein (pv) and the common hepatic duct. B, A scan caudal to the porta hepatis shows the common hepatic duct and the cystic duct running adjacent to each other in the hepatoduodenal ligament (arrows). The hepatic artery (ha) is in a more medial position.

Visualization of the intrahepatic bile ducts with CT originally was considered to be evidence of biliary obstruction; but with newer scanners and thin collimation, peripheral bile ducts measuring 1 to 3 mm may be seen in normal subjects (Liddell et al, 1990). The common duct, which measures 3 to 6 mm in cross-sectional diameter, is seen as a circular structure of near-water density posterolateral to the head of the pancreas on a postcontrast scan. The CT diagnosis of biliary obstruction is based on the demonstration of dilated intrahepatic or extrahepatic bile ducts. Dilated intrahepatic ducts appear on CT as linear branching or circular structures of near-water density that enlarge as they approach the junction of the left and right hepatic ducts in the porta hepatis. The extrahepatic bile duct is considered unequivocally dilated if it is 9 mm or more in diameter; less than 7 mm is considered normal. High-resolution images and reformatting techniques allow for depiction of the biliary tree on CT that was once impossible (Fig. 16.21).

FIGURE 16.21 Coronal reformatted image of the confluence of the right (solid arrow) and left (open arrow) hepatic ducts reveals soft tissue thickening and enhancement along the common bile duct (arrowheads), reflecting recurrent gallbladder carcinoma in a patient after cholecystectomy. Note the bilobar intrahepatic biliary ductal dilation.

Although CT has proved to be accurate in establishing a diagnosis of biliary obstruction, a direct correlation between the caliber of the biliary tree and the presence of clinically significant obstruction has not been found. In patients with significant dilation of the biliary tree, in whom the obstruction is later relieved surgically or by spontaneous passage of a calculus, the bile duct may remain more dilated than normal for the remainder of the patient’s life. In such patients, the CT findings may falsely suggest the presence of biliary obstruction. Likewise, a normal-caliber bile duct can be observed in the presence of a surgically correctable cause of jaundice. Intermittently obstructing calculi and subtle strictures of the extrahepatic duct may be present when the overall duct caliber is normal. When a discrepancy exists between clinical or biochemical evidence and the CT findings, magnetic resonance cholangiopancreatography (MRCP) or direct cholangiography by the percutaneous or endoscopic route should be performed to resolve the problem.

CT can also help ascertain the cause of obstruction in many cases. Although abrupt termination of the extrahepatic duct suggests a malignant process, smooth and gradual tapering of bile ducts favors benign disease. The use of water as a negative oral contrast agent aids in identification of small distal bile duct calculi.

Cyst (See Chapter 69A, Chapter 69B, Chapter 79A, Chapter 79B )

Hepatic cysts are common and occurr in 2% to 7% of the population (Horton et al, 1999). Hepatic cysts may be either congenital or acquired. Congenital cysts are more common and are thought to be caused by a malformation of a bile duct that has lost its communication with the remainder of the biliary tree. Lined by a single layer of cuboidal or columnar epithelium that secretes fluid, the cyst fills with serous fluid (Blumgart et al, 2001). The acquired type of hepatic cyst is usually secondary to inflammation, trauma, or parasitic disease. Hepatic cysts typically are discovered incidentally and have no malignant potential.

At CT, a hepatic cyst is round or ovoid and sharply defined with an imperceptible wall; it shows water attenuation and does not enhance after administration of an intravenous contrast agent. Although small cysts do not affect the adjacent hepatic parenchyma, very large cysts may result in lobar atrophy with contralateral compensatory hypertrophy (Blumgart et al, 2001).

Multiple hepatic cysts may be associated with polycystic renal disease (Fig. 16.22) but may occur in the absence of renal cysts. Occasionally, patients may present with discomfort or biliary obstruction secondary to a large cyst (Fig. 16.23). In such cases, therapeutic intervention may be indicated.

FIGURE 16.22 Multiple simple hepatic cysts in a patient with polycystic kidneys.

FIGURE 16.23 Giant simple cyst arising in right lobe of liver. It is well circumscribed and has homogeneous, near-water attenuation.

Hemangioma

Hemangiomas (see Chapter 79A, Chapter 79B ) are the most benign solid tumors of the liver (Blumgart et al, 2001). The incidence of cavernous hemangiomata has been reported as 7% in an autopsy series (Karhunen, 1986). Cavernous hemangiomata may range in size from less than 1 cm to greater than 40 cm, referred to as giant hemangiomata (Blumgart et al, 2001). Hemangiomata usually are incidentally detected lesions seen in women (Horton et al, 1999).

Hemangiomata are composed of endothelium-lined vascular spaces separated by fibrous septa, and they derive their blood supply from the hepatic artery (Horton et al, 1999). On unenhanced CT, a hemangioma has low attenuation compared with the adjacent hepatic parenchyma. After the intravenous administration of contrast material, peripheral globular enhancement is seen on the arterial phase images. The attenuation of the peripheral nodules equals that of the aorta (Quinn & Benjamin, 1992), and venous phase images reveal centripetal enhancement to the center of the lesion (Leslie et al, 1995; Nelson & Chezmar, 1990). Because the peripheral, nodular, clumplike enhancement is seen best on arterial phase images, it is important to acquire images during this phase (Fig. 16.24).

FIGURE 16.24 Cavernous hemangioma of the right liver showing typical enhancement starting at the periphery of the lesion (A to C) and finally showing complete opacification (D).

Giant hemangiomata (>6 to 10 cm; Bouras et al, 1996; Mitsudo et al, 1995; Ros et al, 1987) have a heterogeneous appearance with a low-attenuation central scar on unenhanced CT. The low attenuation is attributed to thrombosis, hyalinization, and fibrosis (Ros et al, 1987). The typical early, peripheral, nodular, clumplike enhancement is observed on the arterial phase images, but giant hemangiomata often do not completely fill in with contrast material on delayed images (Fig. 16.25; Vilgrain et al, 2000).

FIGURE 16.25 A, Volume-rendered three-dimensional image of a giant hemangioma. The image is oriented such that the patient is facing forward, with the observer looking down from above. Note the peripheral nodular, clumplike enhancement (black arrow) and the central low-attenuation scar (white arrow). The hemangioma is in contact with the left hepatic vein (arrowhead) and with the inferior vena cava (IVC). B, Volume-rendered coronal image of the same patient. The giant hemangioma exerts mass effect on a long segment of the IVC (arrows), which is displaced to the left of midline. The right kidney (arrowhead) is displaced inferomedially by the mass. Resection was performed with a good result. (Courtesy L.H. Blumgart, MD.)

Most hemangiomata do not cause clinical symptoms. However, larger tumors are more likely to cause symptoms such as abdominal pain, increasing abdominal girth, early satiety, and nausea and vomiting (Blumgart et al, 2001). These symptoms are attributed to the rapid expansion of the tumor or thrombosis and infarction resulting in stretching or inflammation of the Glisson capsule (Blumgart et al, 2001). Large hemangiomata can lead to complications such as an inflammatory process manifested by low-grade fever, weight loss, abdominal pain, and elevated erythrocyte sedimentation rate (Takayasu et al, 1990). Other complications include Kasabach-Merritt syndrome, a coagulopathy with systemic fibrinolysis and thrombocytopenia (Maceyko & Camisa, 1991), intratumoral hemorrhage, spontaneous rupture resulting in hemoperitoneum (Vilgrain et al, 2000), and volvulus of a pedunculated hemangioma (Tran-Minh et al, 1991). Pain or secondary complications may necessitate surgical intervention. CT angiography can play an important role in delineating the arterial supply to these tumors, facilitating surgical enucleation or hepatic resection.

Focal Nodular Hyperplasia

FNH (see Chapter 79A, Chapter 79B ) is the second most common benign liver tumor, with a reported prevalence ranging from 0.9% (Nguyen et al, 1999) to 3% (Karhunen, 1986). FNH usually is incidentally detected when patients are scanned for other reasons (Carlson et al, 2000). With the increased use of CT and faster scan protocols, FNH is being detected more frequently (Carlson et al, 2000). FNH is more commonly seen in women, and it occurs in relatively young patients (Nguyen et al, 1999). At histopathologic analysis, classic FNH contains nodular hyperplastic parenchyma that is at least partially surrounded by fibrous septa and a central scar. The central scar contains fibrous connective tissue, cholangiolar proliferation with surrounding inflammatory infiltrates, and malformed vessels (Nguyen et al, 1999; Wanless et al, 1985).

On unenhanced CT, FNH has the same or slightly lower attenuation than the liver. When FNH has the same attenuation as the liver, the lesion may be invisible or may be detectable only because of the central, low-attenuation scar or mass effect on the adjacent structures (Carlson et al, 2000). The value of unenhanced images is to ensure the absence of intralesional hemorrhage, intratumoral fat, and calcifications, findings atypical of FNH (Carlson et al, 2000). During the early phases (arterial, early portal venous), the typical pattern of FNH is diffuse, immediate, homogeneous, hyperdense contrast enhancement. The prompt, diffuse arterial enhancement is due to the rich arterial supply. Rapid washout of contrast material is seen in the late portal venous phase and on delayed images, as lesions tend to become isodense to the liver on these views (Figs. 16.26 and 16.27; Carlson et al, 2000).

FIGURE 16.26 Focal nodular hyperplasia. A, Arterial phase image shows a well-circumscribed, brightly enhancing lesion in segment IV/V. B, During the portal phase, the lesion is isodense with liver parenchyma and cannot be identified.

FIGURE 16.27 Focal nodular hyperplasia. A, Contrast-enhanced computed tomographic image acquired in the late arterial phase reveals the arterial supply to a well-circumscribed hypervascular mass in the right hepatic lobe. B, Oblique coronal, volume-rendered three-dimensional reformatted image of the same patient reveals early venous drainage from the mass via a large vein (arrow) into the inferior vena cava (arrowhead). The major hepatic veins have not yet opacified with contrast material.

A central scar is thought to be present at histopathology in almost all cases of FNH, but on CT, scars are less frequently visualized, seen in approximately one third of patients (Shamsi et al, 1993; Welch et al, 1985). The central scar is usually hypodense to the liver on unenhanced and early contrast-enhanced images, and it displays gradual fill-in on the portal venous phase and delayed images owing to diffusion of contrast material into the myxomatous stroma.

Adenoma

Hepatic adenoma (see Chapter 79A, Chapter 79B ) is an uncommon benign neoplasm usually discovered in women. A causative link has been described between the use of oral contraceptives and the development of hepatic adenomas (Blumgart et al, 2001). Other risk factors for the development of this neoplasm are androgen-containing steroids (Soe et al, 1992) and type I glycogen storage disease (Labrune et al, 1997). Adenomas are usually solitary but may be multiple in 30% of patients (Foster & Berman, 1977). A distinct entity referred to as liver adenomatosis, a term coined in 1985, refers to multiple (>10) adenomas in a patient without other known risk factors (Flejou et al, 1985).

Adenomas contain large plates of hepatocytes separated by dilated sinusoids perfused solely by peripheral arterial feeding vessels (adenomas lack a portal venous supply) under arterial pressure. Adenomas have poor connective tissue support, and the combination of poor connective tissue support and arterial pressure predisposes to hemorrhage. Multiple and large adenomas are more prone to spontaneous hemorrhage (Leese et al, 1988). Intracellular and intercellular lipids manifest as macroscopic fat within the tumor (Ichikawa et al, 2000).

The imaging appearance of adenomas parallels the histopathologic appearance. Unenhanced CT may be valuable in detecting the presence of intralesional hemorrhage or fat. Calcifications have been reported in 10% of lesions (Grazioli et al, 2000, 2001). Adenomas tend to be isoattenuating relative to normal liver on unenhanced CT and on portal venous phase images. Small adenomas usually enhance homogeneously in the arterial phase and are hyperattenuating to the liver (Grazioli et al, 2001). Larger adenomas are more heterogeneous in appearance than smaller lesions (Grazioli et al, 2001), presumably because of the presence of acute or prior hemorrhage. Peripheral enhancement reflects the presence of large subcapsular feeding vessels, with a resultant centripetal pattern of enhancement.

Biliary Hamartoma

Bile duct hamartoma (see Chapter 79A, Chapter 79B ), also known as von Meyenburg complex, is a common benign tumor composed of disorganized bile ducts and ductules with a fibrocollagenous stroma (Horton et al, 1999). The tumors usually range from 1 to 15 mm, do not communicate with the biliary tree, and are scattered throughout the liver (Wei et al, 1997). Bile duct hamartomas may be single, although they are often multiple (Blumgart et al, 2001), and they have a nonspecific imaging appearance such that they may be mistaken for metastases or microabscesses (Eisenberg et al, 1986; Lev-Toaff et al, 1995; Sada & Ramakrishna, 1994).

Bile Duct Adenoma

Bile duct adenomas are usually incidentally detected, benign, asymptomatic lesions (Welch et al, 1985). Bile duct adenomas are usually solitary and subcapsular, ranging in size from 1 mm to 1 cm. On unenhanced CT, a bile duct adenoma appears as a well-defined hypoattenuating or isoattenuating mass. Usually, little or no enhancement is seen after contrast administration. There is no specific imaging finding, however, and definitive diagnosis can be made only at histologic analysis (Horton et al, 1999).

Pyogenic Abscess

Recent surgery, biliary disease, diverticulitis, Crohn disease, and alcoholism all predispose to pyogenic hepatic abscess (see Chapter 66), commonly caused by Clostridium species and gram-negative bacteria such as Escherichia coli and Bacteroides, which enter the liver via the biliary tree or portal venous system (Mergo & Ros, 1997). Ascending cholangitis and portal phlebitis are the most common causes of pyogenic hepatic abscesses (Murphy et al, 1989).

As a result of the widespread use of broad-spectrum antibiotics, the clinical presentation and CT appearance vary widely (Halvorsen et al, 1984). Pyogenic hepatic abscesses may be classified as either microabscesses (<2 cm) or macroabscesses, larger confluent lesions. Microabscesses appear as small, well-defined, hypodense lesions on contrast-enhanced CT. They may be widely scattered or clustered with a tendency to coalesce (Jeffrey et al, 1988). Larger pyogenic abscesses range in appearance from unilocular cavities with smooth outer margins to highly complex and septated structures with internal debris and irregular contours. Most large pyogenic abscesses appear as a well-defined mass of low attenuation on unenhanced CT. The attenuation value of the abscess cavity depends on the age of the abscess; it becomes lower as the abscess matures. Gas bubbles may be seen if anaerobic bacteria are present, and the periphery and internal septa may enhance after contrast agent administration. Abscesses often have a thick wall, which enhances with contrast administration (Fig. 16.28). In addition, there may be hepatic enhancement peripheral to the enhancing wall, secondary to increased capillary permeability. This is referred to as the double-target sign (Mendez et al, 1994; Murphy et al, 1989).

FIGURE 16.28 Contrast-enhanced computed tomography of a pyogenic liver abscess shows enhancement of the walls and internal septa. A sympathetic right-sided pleural effusion is seen.

Fungal Abscesses

Fungal hepatic abscesses generally are disseminated microabscesses that occur in immunosuppressed patients. The most common fungal organism implicated is Candida albicans. Other fungal infections that cause microabscesses include cryptococcus, histoplasmosis, and mucormycosis. With contrast-enhanced CT, hepatic microabscesses appear as small, hypodense lesions ranging from several millimeters to 1.5 cm in size. A bull’s-eye appearance may be identified, with a small, high-attenuation focus centrally surrounded by a low-attenuation zone. Authors have reported significant increase in the sensitivity and lesion conspicuity using arterial phase CT, compared with portal venous phase CT, when evaluating liver lesions in immunocompromised patients suspected to have hepatosplenic fungal infections (Metser et al, 2005).

Echinococcus

In endemic areas, involvement of the liver by hydatid disease is a common finding. Echinococcus granulosus (see Chapter 68) presents with a large solitary mass or multiple well-defined cystic lesions, which often contain internal “daughter” cysts (Fig. 16.29). Coarse calcifications of the wall are present in 50% of patients (Fig. 16.30), and daughter cysts are identified in approximately 75% (de Diego Choliz et al, 1982; Murphy et al, 1989). Communication between the cysts and the biliary tree is found in approximately 25% of patients (de Diego Choliz et al, 1982), and frank rupture of cyst contents into the bile ducts occurs in 5% to 10%, accompanied by clinical features of cholangitis. In contrast, Echinococcus alveolaris infection resembles an infiltrating hepatic tumor clinically and radiographically with its irregular margins and heterogeneous density (Didier et al, 1985).

FIGURE 16.29 Contrast-enhanced axial computed tomography reveals a multiseptated echinococcal cyst in the right hepatic lobe. Note eccentric calcifications along the wall of one of the cysts (arrow).

FIGURE 16.30 Unenhanced computed tomography reveals a calcified rim of echinococcal cyst (arrow). Air within the cyst was from recent instrumentation.

Amebic Abscess (See Chapter 67)

The protozoan Entamoeba histolytica infects 10% of the world’s population. Hepatic abscess is the most common extraintestinal complication of amebiasis and occurs in approximately 8.5% of all patients with amebic infection (Ralls, 1998). On CT, amebic abscesses appear as well-defined masses of near-water attenuation with a thick enhancing rim. One or more internal septations may be present. A feature of amebic liver abscess that may aid in distinguishing it from other focal hepatic lesions is its tendency to extend beyond the surface of the liver (Radin et al, 1988). The CT findings are not specific, however, and serologic tests are necessary to confirm the diagnosis.

Fatty Infiltration

Fatty infiltration (see Chapter 65), as seen in patients on chemotherapy or in patients with systemic disorders, such as diabetes mellitus, cystic fibrosis, or malnourishment, results in a decrease in hepatic density. Mild degrees of fatty change may be subtle, unless liver density is compared carefully with the density of the spleen. The liver is normally 6 to 12 HU higher in attenuation than the spleen, and reversal of this relationship is the earliest CT indication of fatty infiltration. With more advanced changes, the hepatic parenchyma becomes less dense than the intrahepatic vessels. In most instances, fatty infiltration is diffuse and uniform (see Fig. 16.12), but a nonuniform, focal distribution also can occur and occasionally may mimic a mass (Fig. 16.31). Fatty infiltration should be suspected if blood vessels can be seen passing through the focal area in a normal pattern (Fig. 16.32).

FIGURE 16.31 Numerous foci of fatty infiltration. Contrast-enhanced computed tomography reveals numerous low-attenuation lesions in a patient with breast cancer. Note lack of mass effect or distortion of the hepatic vessels. Lesions were stable over time and were shown to represent focal fatty deposition on magnetic resonance imaging.

FIGURE 16.32 Focal fatty infiltration. A wedge-shaped area of low attenuation is visible in the right liver. The hepatic vessels pass through the area normally with no deviation.

An awareness of the common locations of focal fatty infiltration and focal fatty sparing is important, so as not to mistake these for tumor. Common locations for focal fatty infiltration include segment IV adjacent to the falciform ligament (Ohashi et al, 1995; Paulson et al, 1993) and around the gallbladder (Yoshimitsu et al, 1997). A common location for focal fatty sparing is in the posterior aspect of segment IV (Matsui et al, 1995; White et al, 1987) or along the gallbladder fossa. It has been suggested that areas of focal fatty sparing are due to aberrant venous drainage to the liver, because these areas do not receive portal venous flow from the main portal trunk (Gabata et al, 1997; Marchal et al, 1986; Matsui et al, 1995).

It has been shown that focal fatty sparing in a fatty infiltrated liver may occur secondary to a mass. This occurrence is presumably due to regionally decreased portal blood flow caused by compression of the adjacent portal venous branch distal to a mass. This fatty sparing can appear as wedge shaped, peripheral, segmental, or lobar, depending on the site of the portal venous compression (Grossholz et al, 1998).

Assessment for fatty infiltration is better performed with unenhanced CT than with contrast-enhanced CT, because factors such as the rate of contrast injection and timing of measurements significantly influence the optimal liver-to-spleen ratio threshold for diagnosing fatty liver. The required ratios are protocol specific, which limits the clinical usefulness of such measurements (Jacobs et al, 1998; Johnston et al, 1998). If it is unclear based on the CT findings whether an area of focal low attenuation represents a mass, magnetic resonance imaging (MRI) using opposed-phase gradient echo images may make a definitive diagnosis.

Cirrhosis (See Chapter 70A, Chapter 70B )

CT is capable of showing morphologic changes associated with advanced hepatic cirrhosis. Typical CT features are a nodular hepatic outline (in macronodular cirrhosis) caused by regenerative nodules of variable size, bands or regions of confluent fibrosis, relative atrophy of the right hepatic and quadrate lobes, and hypertrophy of the left lateral segment and caudate lobe (Fig. 16.33; Torres et al, 1986). Measurement of the transverse dimension of the caudate lobe compared with the adjacent right lobe provides an index of right hepatic lobe shrinkage and a relatively specific morphologic measurement of hepatic cirrhosis (Harbin et al, 1980). A caudate/right lobe ratio greater than 0.65, using the bifurcation of the main portal vein to divide the lobes provides 96% confidence in the diagnosis of cirrhosis. An MRI study suggested that using the right portal vein to set the lateral boundary of the caudate lobe when assessing the caudate/right lobe ratio was more accurate for diagnosing cirrhosis than using the main portal vein (Awaya et al, 2002). Evidence of coexistent portal hypertension is found with ascites, splenomegaly, and portal-systemic varices. MDCT combined with three-dimensional reformatting can help determine the extent of portosystemic collateral vessels, such as the left gastric vein, short gastric vein, esophageal and paraesophageal varices, splenorenal and gastrorenal shunts, and paraumbilical and abdominal wall veins (Kang et al, 2002).

FIGURE 16.33 Cirrhosis. A, The liver has an irregular outline. B, The interlobar fissure, delineated by the gallbladder, is deviated toward the right as a result of atrophy of the right liver with hypertrophy of the left liver and the caudate lobe.

Budd-Chiari Syndrome

Budd-Chiari syndrome (see Chapter 77) is caused by chronic hepatic venous congestion secondary to obstruction to hepatic venous outflow. The CT appearance is characterized by hepatomegaly and ascites; the hepatic veins are either obliterated and not seen, or they contain thrombus (Fig. 16.34). Precontrast scans show decreased attenuation of hepatic parenchyma because of congestion; postcontrast scans show normal enhancement of the caudate lobe, which is hypertrophied in chronic cases, and patchy enhancement of the remainder of the liver (Vogelzang et al, 1987). Concomitant portal vein thrombosis is present in 20% of patients with Budd-Chiari syndrome. A similar CT appearance of the liver, with patchy enhancement, is seen in patients with congestive heart failure; in contrast to patients with true Budd-Chiari syndrome, these patients have patent and enlarged hepatic veins (Moulton et al, 1988).

FIGURE 16.34 A, Contrast-enhanced computed tomography (CT) in a patient with acute hepatic venous thrombosis leading to Budd-Chiari syndrome shows nonenhancement of the thrombosed hepatic veins. There also is patchy peripheral parenchymal enhancement. B,

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