Albumin

Albumin is synthesized in the liver and is a measure of hepatic synthetic function. Low levels of serum albumin can be caused by impaired hepatic synthesis, urinary or enteric losses, or extravascular distribution (e.g., in ascites). Because the half-life of serum albumin is approximately 20 days, serum albumin levels are often normal in patients with acute liver abnormalities.

Alkaline Phosphatase

An increased level of the liver isoenzyme alkaline phosphatase (ALP) implies the presence of cholestasis but does not indicate the level of obstruction. Hepatobiliary origin of ALP can be suggested when γ-glutamyl transpeptidase (GGT) level is also increased. Disproportionately increased ALP levels can be seen with infiltrative malignancy.

α-Fetoprotein

The α-fetoprotein (AFP) level is commonly used to screen for or confirm the presence of hepatocellular carcinoma (HCC). The normal serum level of AFP is less than 10 ng/ml. For screening purposes, a level greater than 20 ng/ml may be considered abnormal, but this cutoff has a low positive predictive value because minor increases of AFP are common in patients with chronic liver disease. Increasing AFP levels over time should be considered suspicious, and a level exceeding 400 ng/ml is often considered diagnostic of HCC when correlated with typical imaging findings. Unfortunately, many HCCs, particularly small tumors, are not associated with an AFP level this high, and as many as 20% to 40% of patients with HCC have a normal serum AFP level. AFP levels can also be increased in patients with germ cell tumors and rarely with some gastrointestinal (GI) malignancies.

Aminotransferases (ALT, AST)

Alaninaminotransferase (ALT) and aspartate aminotransferase (AST) are sensitive indicators of hepatocellular injury (necrosis or inflammation). Levels of 500 to 1500 IU are common in acute viral or drug-induced hepatitis. Mild increase of ALT and AST concentrations can be seen with alcoholic hepatitis and biliary obstruction. Passage of a common bile duct stone can result in a transient severe increase in aminotransferase levels. An AST/ALT ratio greater than 1.5 to 2 may suggest alcoholic liver disease.

Antismooth Muscle Antibody

An increased antismooth muscle antibody level can be present in the setting of autoimmune hepatitis.

Bilirubin

The serum bilirubin level is often increased in cases of hepatocellular disease and biliary obstruction. Contrary to popular belief, the ratio of conjugated to unconjugated bilirubin may be an unreliable indicator of biliary obstruction. It can be more helpful to correlate bilirubin levels with other indicators of cholestasis, such as ALP or 5′ nucleotidase, when biliary obstruction is suspected.

γ-Glutamyl Transpeptidase

GGT level is a nonspecific indicator of liver disease but is often increased in alcohol induced liver injury. Serum GGT levels often parallel ALP levels.

Immunoglobulins

Diffuse increase of immunoglobulin (Ig) levels can be seen in patients with chronic liver disease of various causes. Specific increase of IgG can be present in patients with autoimmune hepatitis. IgM levels may be increased in the setting of primary biliary cirrhosis, and IgA may be disproportionately increased in alcoholic liver disease.

5′ Nucleotidase

The enzyme 5′ nucleotidase is found in bile canalicular membranes and is a specific marker of cholestasis. However, it is a less sensitive screening test for cholestasis than is ALP.

Prothrombin Time

A measurement of prothrombin time represents an assessment of fibrinogen (factor I), prothrombin (factor II), and clotting factors V, VII, and X. These factors are produced by the liver and have a relatively short half-life. Therefore, acute hepatocellular injury can result in an increased prothrombin time, and prothrombin time correlates with the severity of liver damage. Vitamin K deficiency and coumarin-like medications also affect prothrombin time. An increased prothrombin time in association with a normal serum albumin level (another indicator of hepatic synthetic function with a significantly longer half-life) implies acute, rather than chronic, hepatic dysfunction.

Hepatic Veins

The right, middle, and left hepatic veins converge at the hepatic venous confluence and drain blood from the liver into the IVC just below the right atrium. The hepatic venous confluence has a variety of configurations, but most commonly, the middle and left hepatic veins share a common trunk before entering the IVC (Fig. 12-2). Segment I (caudate lobe) has a separate venous drainage directly to the IVC.

Figure 12-2 Typical hepatic venous anatomy shown on axial maximum intensity projection magnetic resonance image (balanced steady state free precession sequence).

The middle hepatic vein is of particular importance to hepatic surgeons. In patients undergoing right hepatic resection or right hemiliver donation, the surgeon typically bisects the liver approximately 1 cm to the right of the middle hepatic vein. When such surgery is contemplated, this line serves as a landmark for determining the relative volumes of the right and left lobes. When living liver donation is being considered, it is important to note large tributaries of the middle hepatic vein that drain the right lobe (e.g., segments V and VIII), because these will be transected in the case of right hemiliver transplantation and may require reimplantation in the recipient.

Many individuals have accessory hepatic veins that drain the inferior right hepatic lobe directly into the IVC. In some patients, more than one inferior accessory vein is present. These have a similar relevance to hepatic transplant surgery as large tributaries of the middle hepatic vein. In general, tributaries and accessory hepatic veins in the range of 5 to 10 mm in diameter that cross a transection plane are considered significant. Inferior accessory hepatic veins can also serve as a collateral pathway to circumvent intrahepatic vena cava obstruction (Fig. 12-3).

Figure 12-3 Coronal maximum intensity projection image from contrast-enhanced magnetic resonance imaging in a patient with a large mass (focal nodular hyperplasia) obstructing inferior vena cava (IVC). Arrows show direction of blood flow.

Portal Veins

The portal vein forms from the confluence of the splenic and superior mesenteric veins, and normally contributes a substantial portion of the hepatic blood flow (at least 75%). The main portal vein travels within the hepatoduodenal ligament as it enters the liver hilum. The portal vein typically bifurcates into right and left branches, each of which subsequently branches into anterior and posterior branches (right portal vein) or medial and lateral branches (left portal vein) (Fig. 12-4). These major branches further bifurcate to supply their respective hepatic segments. The portal vein branch to the caudate lobe can originate from either the left or the right portal vein.

Figure 12-4 Axial maximum intensity projection image from an enhanced computed tomographic scan shows standard portal vein branching pattern.

The branching pattern of the portal vein may have important implications for the liver surgeon. It is important to recognize portal vein branching variants in patients scheduled for liver resection or donor hemihepatectomy to prevent inadvertent interruption of the portal blood supply to the remaining liver. A variety of portal vein branching variations have been described. Portal trifurcation refers to simultaneous branching of the main portal vein into right posterior segment, right anterior segment, and left portal vein branches (Fig. 12-5). Additional variants are possible involving the lack of a common trunk for the right posterior and anterior segment branches, including origin of the right posterior segment branch from the main portal vein and origin of the right anterior segment branch from the left portal vein (Figs. 12-6 and 12-7). Other, less frequent anomalous portal branching patterns are possible. Some studies have demonstrated a somewhat weak concordance between anomalous portal vein branching and variant bile duct anatomy. However, bile duct anomalies can be present in the absence of variant portal venous branching, and the presence of a normal/classic portal vein branching pattern does not preclude anomalous biliary anatomy. Anomalous branching of the portal vein has also been associated with malposition of the gallbladder. Additional congenital variants of the portal vein include prepancreatic portal vein (often associated with situs inversus), double portal vein, and agenesis of the main portal vein or one of its major branches.

Figure 12-5 Contrast-enhanced axial computed tomographic scan of a patient with portal trifurcation.

Figure 12-6 Oblique axial maximum intensity projection reconstruction of a gadolinium-enhanced magnetic resonance scan of a patient with variant portal venous anatomy.

Figure 12-7 Common portal vein branching patterns. Variants are denoted by dashed lines; normal anatomy by solid lines.

Hepatic Artery

The hepatic artery travels in the hepatoduodenal ligament anterior to the portal vein and supplies the liver with oxygen-rich arterial blood and approximately 25% of the total hepatic blood flow. The common hepatic artery typically originates from the celiac axis together with the splenic and left gastric arteries. After giving off the gastroduodenal artery, the proper hepatic artery bifurcates into the right and left hepatic arteries, which further branch to supply the hepatic segments. The caudate lobe can receive its blood supply from branches of either the right or left hepatic artery.

Correctly mapping out the hepatic arterial anatomy is important before liver and biliary surgery, hepatic chemoembolization, or placement of a chemoinfusion pump. Hepatic artery variants are extremely common. The term replaced is used when the entire right hepatic artery, entire left hepatic artery, or entire common hepatic artery arises from an atypical location. The terms accessory or partially replaced are used when only part of the arterial blood supply to the right or left lobe arises from an atypical location.

Fortunately, most replaced or accessory arteries can be identified by looking in only two locations. The replaced or accessory left hepatic artery arising from the left gastric artery can be found traveling in the fissure for the ligamentum venosum (Fig. 12-8). The replaced or accessory right hepatic artery can usually be identified in the portocaval space (Fig. 12-9). The most common hepatic artery variants are the left hepatic artery (or a portion thereof) arising from the left gastric artery and the right hepatic artery (or a portion thereof) originating from the superior mesenteric artery. Other variants include origin of the hepatic artery directly from the aorta; origin of one of the hepatic arteries before the origin of the gastroduodenal artery; trifurcation of the hepatic artery into left, right, and gastroduodenal arteries; and origin of the left hepatic artery from the celiac axis.

Figure 12-8 Enhanced axial computed tomographic image through the liver of a patient with hereditary hemorrhagic telangiectasia demonstrating the typical location of an accessory or replaced left hepatic artery arising from the left gastric artery. The artery is enlarged because of intrahepatic arteriovenous shunting.

Figure 12-9 Oblique axial maximum intensity projection image of a replaced right hepatic artery arising from the superior mesenteric artery (SMA). IVC, Inferior vena cava.

The artery supplying segment IV of the liver is often overlooked but is important to identify in patients who may be undergoing hemihepatectomy (including living hemiliver donors) (Fig. 12-10). In particular, it is important to note whether the segment IV artery arises from the left or right hepatic artery. When arising from the right hepatic artery, additional steps are needed to preserve the segment IV artery during right hepatectomy. A segment IV artery arising from the right hepatic artery has occasionally been referred to as a middle hepatic artery. The posterior part of segment IV can also receive blood supply from caudate artery branches.

Figure 12-10 Oblique coronal maximum intensity projection image from a computed tomographic angiogram demonstrating the segment IV artery and a replaced right hepatic artery arising from the superior mesenteric artery (SMA).

Steatosis

More commonly referred to as fatty liver, hepatic steatosis is often dismissed as a clinically insignificant radiologic finding. However, diffuse fatty infiltration of the liver can be associated with increased liver function tests, and if left unchecked, some types of steatosis can progress to steatohepatitis (manifesting as diffuse fatty infiltration, abnormal liver function tests, and hepatomegaly) and cirrhosis. For this reason, steatosis is a finding worthy of reporting. Hepatic steatosis results from a variety of hepatic insults in addition to dietary indiscretion (Box 12-1).

Sonography is the least specific cross-sectional imaging modality for the diagnosis of hepatic steatosis. The diagnosis may be suggested when the hepatic parenchyma demonstrates increased echogenicity associated with sound attenuation, resulting in poor depth of penetration and poor visualization of the hepatic veins, portal triads, and diaphragm (Fig. 12-24).

Figure 12-24 Longitudinal right upper quadrant sonogram through the liver and right kidney of a patient with hepatic steatosis.

CT is more specific for the diagnosis of steatosis, which is suggested when the hepatic parenchyma is at least 10 HU lower in attenuation than the spleen on an unenhanced scan or 25 HU lower on a portal-phase contrast-enhanced CT scan. A liver attenuation of less than 40 HU on an unenhanced CT scan is also suggestive of steatosis. Steatosis can be subjectively diagnosed when hepatic vessels stand out as hyperdense against the low-attenuation background of fatty liver parenchyma (Fig. 12-25). This degree of steatosis may create the appearance of an enhanced scan.

Figure 12-25 Unenhanced axial computed tomographic scan of a patient with hepatic steatosis.

Chemical-shift MRI is highly specific for the diagnosis of hepatic steatosis. Areas of fatty infiltration will lose signal intensity on opposed-phase gradient-echo images relative to in-phase images (Fig. 12-26). Chemical-shift imaging is much more sensitive to the presence of steatosis than fat saturation or short tau inversion recovery MRI, because the latter techniques do not suppress the signal from water protons. MR spectroscopy has been used to further quantify the degree of fatty infiltration of the liver.

Figure 12-26 Axial in-phase (A) and opposed-phase (B) gradient-echo magnetic resonance images of the liver in a patient with diffuse hepatic steatosis.

Steatosis may manifest in a variety of patterns and distributions (Box 12-2) (Fig. 12-27). Regardless of the pattern or imaging modality used to image the patient with hepatic steatosis, areas of uncomplicated fatty infiltration should not cause mass effect or displace vessels. One additional feature of hepatic steatosis is its capacity to change or fluctuate significantly over a relatively short period (<1 month) given changes in patient behavior or exposure. Resolution can occur in response to correction of the underlying metabolic abnormality or removal of the responsible hepatic toxin, whereas progression can result from continued exposure.

Figure 12-27 A, Unenhanced axial computed tomographic and in-phase (B) and opposed-phase (C) magnetic resonance (MR) images through the liver of a patient with heterogeneously distributed hepatic steatosis. MR imaging was performed to ensure findings on computed tomography (CT) represented fatty infiltration rather than tumor. T1W, T1-weighted.

Diffusely infiltrating lymphoma can mimic hepatic steatosis but can be distinguished with chemical-shift MRI. Acute hepatitis from causes other than steatosis may cause a relatively low-attenuation liver on CT, but such a liver may be decreased or normal in echogenicity with sonography and often will be associated with periportal edema and gallbladder wall thickening. Table 12-5 summarizes imaging findings that suggest hepatic steatosis.

Table 12-5 Imaging Findings of Hepatic Steatosis

* Iron deposition may also cause signal loss on opposed-phase images if the out-of-phase echo time is longer than the in-phase echo time (common with 3.0-Tesla magnetic resonance scanners).

Iron Deposition

Iron may be deposited in the liver in two general ways. Deposition of iron directly into the hepatocytes occurs with primary or hereditary hemochromatosis, an autosomal recessive disorder resulting in abnormally increased intestinal absorption of iron. Hereditary hemochromatosis affects the liver, pancreas, heart, joints, endocrine glands, and skin. The spleen is typically unaffected by hereditary hemochromatosis. The presence of excess iron causes organ damage, resulting in cirrhosis, diabetes, heart failure, and arthralgias. These patients are also at increased risk for HCC (Fig. 12-28).

Figure 12-28 Axial portal-phase contrast-enhanced computed tomographic scan through the liver of a patient with cirrhosis and focus of hepatocellular carcinoma (HCC) secondary to primary hemochromatosis.

Iron may also be taken up by the reticuloendothelial system (RES). RES iron deposition is commonly seen in patients with hemolytic anemia or those who require multiple blood transfusions. Iron deposition related to anemia or blood transfusions typically affects the spleen and bone marrow in addition to the liver. Once the RES system becomes saturated with iron, iron can be deposited in the parenchymal cells of various organs as with primary hemochromatosis. Therefore, although the presence of iron within organs such as the pancreas is a helpful differentiating feature between hereditary hemochromatosis and other iron deposition disorders, it is not an entirely specific finding. Increased hepatic iron can also be present in patients with paroxysmal nocturnal hemoglobinuria (PNH) or hemolytic anemia (e.g., sickle cell disease, prosthetic heart valve). With these disorders, excessive iron may be detected within the renal cortex in addition to the RES of the spleen and liver. Patients with PNH are prone to vascular thrombosis; therefore, if PNH is suspected, one should be sure to look for evidence of hepatic vein or portal vein thrombosis.

Iron deposition within the liver is not easily detected with ultrasonography, although the secondary effects (cirrhosis, HCC) may be evident. Unenhanced CT of patients with increased hepatic iron may demonstrate a dense liver (>70 HU) (Fig. 12-29). However, increased liver attenuation on unenhanced CT is not specific for the presence of iron, because patients receiving amiodarone therapy, patients exposed to a prior intravenous iodine dose, and some patients with glycogen storage disease may also have increased attenuation of their liver on CT (see Fig. 12-16).

Figure 12-29 Unenhanced axial computed tomographic image in a patient with primary hemochromatosis. This patient also eventually developed hepatocellular carcinoma.

Figure 12-16 Unenhanced axial computed tomographic image through the abdomen of patient taking the drug amiodarone.

MRI is more specific for iron deposition, demonstrating signal loss on all pulse sequences because of the ferromagnetic properties of iron (Figs. 12-30 and 12-31). T2*-weighted images (gradient-echo images obtained with a relatively long TE) are highly sensitive to the presence of iron and may be used to quantify the amount of iron present. We frequently consult the in-phase and opposed-phase gradient-echo images routinely obtained as part of our liver protocol to confirm the presence of iron, because the liver will appear to lose signal on the longer TE images in such cases.

Figure 12-30 Axial T2-weighted magnetic resonance imaging through the upper abdomen of a patient with primary hemochromatosis.

Figure 12-31 Axial T2-weighted magnetic resonance image of a patient with hemosiderosis associated with end-stage renal disease.

MRI can also demonstrate excess iron within the pancreas and heart in patients with hereditary hemochromatosis (see Fig. 12-30). As with the liver, these organs will demonstrate a decrease in signal intensity on most imaging sequences, most noticeable on T2*-weighted images. Once the diagnosis of hereditary hemochromatosis has been established, it is important to assess the liver for evidence of organ damage (cirrhosis) and the presence of HCC (see Fig. 12-28). Nodules or masses within the liver that demonstrate increased signal intensity on T2-weighted images or nodular enhancement after administration of intravenous gadolinium chelate should be viewed with suspicion. Table 12-6 summarizes the imaging findings of hepatic iron deposition disorders.

Table 12-6 Imaging Findings of Hepatic Iron Deposition

Uncommon Deposition Disorders

A variety of disorders may result in abnormal deposition of substances other than fat or iron within the liver. However, most deposition disorders have nonspecific manifestations on imaging studies. Patients with hepatolenticular degeneration (Wilson disease) have abnormal accumulation of copper within the liver, as well as the brain and cornea. Because of the high atomic number of copper, patients with this disorder may demonstrate a hyperdense liver with CT, although this is uncommon. With all modalities, none of the imaging findings of Wilson disease is specific. More commonly, patients with Wilson disease manifest nonspecific evidence of chronic liver disease such as steatosis and cirrhosis.

Patients with amyloidosis have deposition of protein-mucopolysaccharide complexes in various organs, including the liver. Hepatic amyloidosis may manifest as hepatomegaly or areas of low attenuation on CT. However, no specific findings exist that allow a definitive imaging diagnosis of amyloidosis.

Although glycogen deposited within the liver as a result of glycogen storage disease may appear hyperattenuating on CT images, a low-density liver resulting from associated hepatic steatosis is more common. As with other storage diseases, hepatomegaly may be present. Patients with glycogen storage disease type I (von Gierke) or type III are at risk for development of hepatic adenomas.

Causes of Cirrhosis

Cirrhosis is a nonspecific diagnosis that is the end result of a variety of hepatic insults leading to hepatocellular injury. Most cases of cirrhosis apparent on imaging studies are due to alcohol abuse or viral hepatitis. Table 12-7 lists various categories of causes of cirrhosis.

Table 12-7 Causes of Cirrhosis

Cirrhosis is usually preceded by hepatitis. This inflammatory process of the liver may be caused by toxic, metabolic, immune, infectious, or other types of insult. In the acute phase, hepatitis may be characterized clinically by some combination of fever, right upper quadrant pain, malaise, jaundice, elevated liver function tests, and hepatomegaly. Acute hepatitis uncommonly manifests sonographically as hepatomegaly with decreased echogenicity of the hepatic parenchyma and relatively increased echogenicity of the portal vein walls (sometimes referred to as the “starry-sky” appearance), although some studies show this is a nonspecific finding. Periportal edema manifests as periportal sonolucency. Thickening (edema) of the gallbladder wall may be noted. With CT, the periportal edema appears as fluid attenuation tracking along the portal vessels in the place of periportal fat (Fig. 12-32). Alcoholic and nonalcoholic steatohepatitis may be associated with low-attenuation hepatic parenchyma caused by fatty infiltration. Chronic active (viral) hepatitis is frequently associated with lymphadenopathy in the hepatoduodenal ligament (Fig. 12-33). With MRI, the periportal edema present in acute hepatitis manifests as high periportal signal intensity on T2-weighted images. The liver may also demonstrate mildly increased signal intensity on T2-weighted and decreased signal intensity on T1-weighted images, although these changes are likely to be subtle. Associated steatosis will be most evident with in- and opposed-phase MRI.

Figure 12-32 Axial enhanced computed tomographic scan through the upper abdomen of a patient with periportal edema caused by acute viral hepatitis.

Figure 12-33 Axial T2-weighted magnetic resonance (MR) image shows hepatoduodenal ligament lymph nodes in a patient with hepatitis C. High signal intensity is normal for lymph nodes on fat-suppressed T2-weighted MR images.

Gross Morphologic Findings and Patterns of Cirrhosis

Figure 12-34 illustrates some typical morphologic changes of cirrhosis that may be present on imaging studies. Not all findings will be present in all cases of cirrhosis, and early in its course, morphologic changes of cirrhosis may be undetectable with imaging. It is also important to emphasize that not all cirrhotic livers will be reduced in volume. Some cirrhotic livers will appear normal in size or enlarged (Fig. 12-35). A quantitative approach to diagnosing cirrhosis has been advocated by some. In our experience, however, calculation of such ratios as the caudate-right lobe ratio is rarely necessary to suggest the diagnosis of cirrhosis because other morphologic findings are usually sufficient. For readers who prefer objective criteria, we include an illustration of the modified caudate-right lobe ratio (Fig. 12-36). A modified caudate-right lobe ratio of at least 0.9 has been shown to have an accuracy rate of almost 75% for the diagnosis of cirrhosis when applied to MR images and should be expected to work equally well for CT. Examination of the left lateral segment (lateral section) of the liver with a high-frequency linear US transducer may identify subtle nodularity of the liver or rounding of the contour of the left lateral segment that may aid in suggesting a diagnosis of cirrhosis (Fig. 12-37).

Figure 12-34 Typical morphologic changes of cirrhosis.

Figure 12-35 Coronal T2-weighted magnetic resonance imaging (MRI) in a patient with cirrhosis caused by alcohol abuse and hepatitis C.

Figure 12-36 The modified caudate-right lobe ratio for diagnosing cirrhosis.

Figure 12-37 Sonogram of left lateral segment (section) of the liver in a patient with cirrhosis performed with a high-frequency linear transducer.

A cirrhotic liver consists of regenerative nodules with intervening fibrosis, regardless of cause. As a result, significant overlap of imaging findings exists between the various causes of cirrhosis. Despite this overlap, certain imaging appearances are more commonly associated with a particular causative factor. For example, enlargement of the caudate lobe and a right posterior hepatic notch are more common with alcoholic cirrhosis than with viral-induced cirrhosis, although this combination of findings is not specific. Unfortunately, a specific imaging diagnosis is not possible in the majority of cases of cirrhosis, and multiple contributing causes may be present in any given patient (e.g., alcohol and viral hepatitis). Therefore, imaging findings should always be correlated with clinical data before rendering a specific diagnosis. Table 12-8 lists imaging findings that can suggest the cause of cirrhosis.

Table 12-8 Imaging Findings Suggestive of (But Not Specific for) Cause of Cirrhosis

* Low signal intensity surrounding the intrahepatic portal vein branches, most conspicuous on portal- and equilibrium-phase gadolinium-enhanced images.

† Liver iron deposition is not uncommon in cirrhosis of other causes; however, the pancreas is uninvolved in such cases.

Figure 12-38 Axial enhanced computed tomographic scan of a patient with primary sclerosing cholangitis. Note the round shape of the liver.

Figure 12-39 Axial, unenhanced, fat-suppressed, T1-weighted magnetic resonance image through the upper abdomen of a patient with primary biliary cirrhosis.

Extrahepatic Findings in Cirrhosis

When imaging findings suggest the diagnosis of cirrhosis, one should be sure to look for the host of extrahepatic findings that may be present. Stigmata of portal hypertension include splenomegaly, ascites, and varices (Fig. 12-40). Table 12-9 outlines some of the more common venous collateral pathways encountered in patients with portal hypertension. Enlarged lymph nodes are commonly seen in the hepatoduodenal ligament and elsewhere in the setting of cirrhosis. Siderotic deposits within the spleen (Gamna–Gandy bodies) may be noted on MRI (Fig. 12-41). These lesions are most conspicuous on long TE gradient-echo images and appear as small, very-low-signal intensity foci scattered throughout the spleen. Patients with advanced cirrhosis may manifest bowel wall thickening. Edematous thickening of the ascending colon is particularly characteristic, although other segments of large or small bowel may be involved. Colon thickening related to cirrhosis and portal hypertension should not be confused with inflammatory or neoplastic processes. Thickening related to cirrhosis can be seen along the dependent wall of the colon or involving the haustrations. Air-distended nondependent portions of the colon often maintain a thin wall in the setting of portal hypertension (Fig. 12-42).

Figure 12-40 Axial maximum intensity projection image of portal-phase gadolinium-enhanced magnetic resonance imaging through the upper abdomen of a patient with cirrhosis and portal hypertension resulting in large paraumbilical varices.

Table 12-9 Common Collaterals of Portal Hypertension

* In this table, supply and drainage refer to the abnormal (portal to systemic) pattern induced by portal hypertension.

Figure 12-41 Axial T1-weighted image of the abdomen in a patient with cirrhosis and portal hypertension demonstrating Gamna–Gandy bodies in the spleen.

Figure 12-42 Axial enhanced computed tomography through the abdomen of a patient with cirrhosis and portal hypertension demonstrating edema of colon.

Imaging Mimics of Cirrhosis

One should be aware of entities that may simulate some of the morphologic features of cirrhosis. Patients with liver metastases who have been treated with chemotherapy may occasionally develop morphologic changes in the liver that simulate cirrhosis (Fig. 12-43). This has most frequently been described with breast carcinoma, although other tumors may behave similarly. Some chemotherapy agents can also directly cause hepatotoxicity. Diffuse metastatic disease replacing normal hepatic parenchyma can simulate cirrhosis by creating a nodular architecture that may be associated with stigmata of portal hypertension. The liver contour may appear irregular in patients with pseudomyxoma peritonei, and mucin may simulate simple ascites in such patients, potentially creating confusion with cirrhosis (Fig. 12-44). An appearance of cirrhotic liver morphology may also be created after partial hepatectomy or in the setting of congenital segmental atrophy, although there should be no nodularity or fibrosis of such a liver in the absence of true cirrhosis. Areas of scarring and liver regeneration after fulminant hepatitis and nodular regenerative hyperplasia (regenerative nodules that occur in the absence of fibrosis) may likewise simulate cirrhosis. Granulomatous diseases such as sarcoidosis can mimic cirrhosis early in their course (because of innumerable nodules throughout the liver) or progress to cirrhosis over time (Fig. 12-45).

Figure 12-43 Axial enhanced computed tomographic images through the liver in a patient with breast cancer metastases before treatment (A) and several years after treatment (B). Note that the liver has developed a cirrhotic appearance after therapy (B).

Figure 12-44 Unenhanced axial computed tomographic scan through the upper abdomen of a patient with mucinous peritoneal metastatic disease.

Figure 12-45 Enhanced axial computed tomographic images through the upper abdomen of a patient with sarcoidosis performed at time of diagnosis (A) and 5 years later (B).

Parenchymal Findings Associated with Cirrhosis

The cirrhotic hepatic architecture is typically heterogeneous and hyperechoic with grayscale US. Unenhanced CT and MRI may show heterogeneity because of areas of fibrosis, fatty infiltration, or iron deposition (Fig. 12-46). Contrast-enhanced CT and MRI often reveal heterogeneous enhancement because of hemodynamic alterations, as well as differential enhancement of cirrhotic nodules and fibrosis.

Figure 12-46 Axial unenhanced computed tomographic image through the liver in a patient with cirrhosis and hepatic steatosis.

Regenerative nodules are present in all cirrhotic livers but are not always obvious with imaging. MRI is better than US or CT for demonstrating regenerative nodules throughout the liver (Fig. 12-47

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