19 Liver

10.1055/b-0034-75812

19 Liver

Herzog\, Christopher

With an average volume of 1400 to 1700 mL and a maximum craniocaudal expansion of 12 cm, the liver represents the largest parenchymatous organ of the body. Although liver size distinctly varies with body size and gender, a liver volume of ≥ 2000 mL and a craniocaudal stretch of ≥ 15 cm is equivalent to hepatomegaly. The normal proportion between the right and left liver lobe is 3:2. If there is gas in the biliary tree, it tends to be located centrally (see Fig. 20.11 , p. 707), whereas gas in the portal branches (seen in intestinal ischemia) collects peripherally (see Fig. 24.21 , p. 753). On computed tomography (CT) scans, gas usually is more prominent in the right than the left liver lobe (due to scanning in a supine position).

Overall density (attenuation) of normal adult liver on post-contrast CT scans amounts to 60 to 70 HU but may range between 38 and 80 HU on non–contrast-enhanced images. All lobes have approximately the same attenuation; thus, geographic variation of attenuation within an individual is usually < 10 HU. On non–contrast-enhanced scans, CT attenuation should be 8 to 10 HU greater than that of spleen or muscle. Portal as well as hepatic veins are seen as lower-attenuation branching structures within the parenchyma, whereas near-water-attenuating bile ducts are difficult to delineate. Abnormally decreased density usually is a sign of fatty infiltration (steatosis), but it may also be due to drug toxicity, infection (e.g., viral hepatitis), or diffuse tumor infiltration (e.g., lymphoma). In case of steatosis, CT attenuation decreases by ~15 HU per 10% increase in fat; > 15% fat infiltration on non–contrast-enhanced scans leads to masking of intrahepatic vessels (see Fig. 19.33 , p. 695). Higher levels of fat infiltration cause an inversion of contrast, where liver vessels appear hyperdense as compared with liver parenchyma.

Abnormally increased liver density usually is observed in the presence of iron overload (hemochromatosis/hemosiderosis), but it may also be induced by other metals, such as copper (Wilson disease), iodine (amiodarone), gold (antirheumatic base treatment), and thallium. Rare causes are acute massive protein overload and glycogen storage diseases. CT attenuation increases proportionally with metal overload, but increase in attenuation strongly depends on effective beam energy and thus varies depending on tube voltage, type of scanner, and patient size. After proper intravenous contrast administration, the blood vessels are highly attenuating and help in delineating the lobular and segmental anatomy of the liver. The portal vein, formed by the confluence of the superior mesenteric vein and splenic vein, ascends through the hepatoduodenal ligament at the anterior margin of the inferior vena cava into the porta hepatis, where it bifurcates into the right and left portal vein. The hepatic artery lies anterior to the portal vein. The left portal vein extends over the anterior surface of the caudate lobe into the left lobe. The right portal vein bifurcates into anterior and posterior branches, which run through the central portions of the anterior and posterior segments. The segmental classification (S1–S8) of the liver is due to the anatomy of the portal vein branches (P1–P8), while hepatic vein anatomy is the landmark for the segmentation (Fig. 19.1).

**Fig. 19.1 Diagram of hepatic segmental anatomy.** The hepatic venous anatomy provides landmarks for the fissures dividing the liver into lobes and segments.


CL	caudate lobe
FLV	fissure of the ligamentum venosum
IVC	inferior vena cava
LHV	left hepatic vein
LLS	lateral segment of the left lobe
LMS	medial segment of the left lobe
MHV	middle hepatic vein
PV	portal vein
RAS	anterior segment of the right lobe
RHV	right hepatic vein
RPS	posterior segment of the right lobe (Modified after Webb.)

At the higher level, the left hepatic vein and at the lower level, the left intersegmental fissure, which contains fat and the ligamentum teres, separate the medial and lateral segments of the left hepatic lobe. Similarly, the middle hepatic vein and interlobular fissure, which contains the gallbladder recess, separate the left and right hepatic lobes (Fig. 19.2). The right hepatic vein bisects the right lobe into the anterior and posterior segments, but the right intersegmental fissure cannot be visualized directly by CT. Sometimes an accessory right hepatic vein is present.

Some anatomical variants may resemble an abnormality. An unusually prominent lateral segment may extend laterally to the spleen (see Fig. 19.13 , p. 681). The rare congenital absence of the right or left lobe results in hypertrophy of the contralateral lobe. Children who have received a left lateral segment liver transplant develop an unusually shaped liver for obvious reasons. The papillary process of the caudate lobe may sometimes appear separate from the liver and simulate an extrinsic mass. Scalloping of the diaphragm in the elderly may create an accessory fissure of the right hepatic lobe. This is a normal variant (Fig. 19.3).

**Fig. 19.2 Hepatic veins on contrast-enhanced CT.**


LHV	left hepatic vein
MHV	middle hepatic vein
RHV	right hepatic vein

**Fig. 19.3 Accessory “fissure” in an 83-year-old woman.** Fissure caused by scalloping of the diaphragm is seen in the right lobe of the liver (arrow).

The bare area of the liver refers to the posterior surface of the liver, which is in direct contact with the diaphragm. It helps in differentiating pleural fluid collections, which are seen throughout the entire posterior aspect of the posterior perihepatic space, whereas peritoneal fluid stops medially at the bare area of the liver, except for patients with a liver transplant and consequently absent bare area (Fig. 19.5 , p. 677).

CT images of the liver should be acquired in a helical scanning mode, with a slice collimation of at least 5 mm and a gantry rotation time ≤ 0.5s. On current multidetector-row CT scanners, slice collimation ranges from 1.2 to 0.6 mm and continuous volume data sets can be acquired within 2 to 8 seconds. These technical parameters give way for full liver coverage during one breath hold, as well as (near) isometric voxel size and thus artifact-free image reformation in any spatial orientation (coronal, sagittal, etc.). Best results for multiplanar image reformation can be obtained by reconstructing overlapping axial thin slices (≤ 3 mm) at 50% increment. Raw data should be acquired during inspiratory breath hold and with the patient lying in a supine position. The scan range usually extends from the lower parts of the lung to the lower margin of the liver. However, if liver imaging is performed in the course of an abdominal scan, scans may extend caudally to the symphysis. Optimal image contrast is achieved by applying window/level settings of 250/40 in native and delayed CT scans and 350/60 in postcontrast scans.

Proper timing of bolus injection of contrast material is key to sufficient liver visualization and thus requires adequate volume and rate of delivery. In patients with a normal body mass index (BMI), 100 to 120 mL of contrast material with an iodine concentration ≥ 320 mg I/mL are injected at a rate of 5 mL/s.

Four phases of liver parenchyma attenuation can be distinguished after contrast material injection (Fig. 19.17 , p. 683): hepatic arterial phase (~18–25 sp.i.), portal venous phase (~30–40 sp.i.), parenchymal phase (~70–80 sp.i.), and delayed or equilibrium phase (2–5 min p.i.). The hepatic arterial phase (HAP) is suited for hepatic arterial angiography, the portal venous phase (PVP) for detection and characterization of hypervascular tumors. The parenchymal phase (PP) is a standard procedure in abdominal CT imaging, and the delayed phase (DP) may be added to further characterize hepatic masses (particularly useful for identification of cholangiocarcinomas and hemangiomas). A proper HAP shows densely opacified arteries, moderately enhanced portal veins, and only minimally enhanced liver parenchyma. During the PVP, portal and hepatic veins are densely opacified and hyperdense as compared with liver parenchyma, which also is maximally enhanced. In the PP, liver parenchyma, vessels, and most masses appear isodense. Nonenhanced CT scans of the liver can distinguish benign lesions such as fatty infiltration, calcifications, or cysts and thus may be used in the course of baseline scans in oncological staging but not for follow-up examinations.

Blood supply of normal liver parenchyma constitutes 75% of portal venous and 25% of arterial blood; that of liver tumors, 80% and 95%, respectively.

Highest diagnostic accuracy in detecting the number and determining the extent of liver lesions still is obtained by using CT arterial portography (CTAP). However, with the introduction of helical CT scanners and power injectors for continuous delivery of contrast material, this technique has largely been abandoned. Proper CTAP imaging requires injection of up to 150 mL of dilute iodine (150 mg I/mL) injected at a rate of 3 mL/s into a catheter placed in the superior mesenteric artery or splenic artery. Helical CT of the liver is then performed during the PVP and late venous phase. With this approach, lesions ≥ 1 cm are detected with up to 100% sensitivity and 91% specificity.

For multidetector-row CT, sensitivity and specificity range from 86% to 92% and 71% to 91%, respectively, depending not only on the type and vascularity of the lesion but also on the number of the contrast phase applied. Thus, for initial oncological staging, a triphasic protocol is recommended: scanning before contrast administration and during the late HAP and PVP. Any follow-up examination can be restricted to late arterial and venous scans in the presence of hypervascular lesions (hepato-cellular carcinoma, metastases, carcinoids, etc.).

The differential diagnostic aspects of focal liver abnormalities as seen on CT are discussed in Table 19.1. Table 19.2 discusses diffuse liver abnormalities.

**Table 19.1 Focal liver lesions**
Disease	CT Findings	Comments
Vascular
Hepatic venous outflow obstruction (Budd–Chiari syndrome) Fig. 19.4	Segmental or global venous outflow obstruction. Often accompanied by large regenerative nodules. Hepatic veins usually not visualized or even clotted with thrombotic material (hypodense). Scan recommendation: Multiphasic CT (nonenhanced CT, portal venous phase [PVP], parenchymal phase [PP]). Nonenhanced CT: Typically, peripheral low attenuation of the liver parenchyma, with higher attenuation in central portions of the left lobe and the caudate lobe. PVP: Patchy enhancement on early contrast images. PP: Reverse of this pattern or persistent patchy central enhancement. Diagnostic pearls: Despite appropriate enhancement of the inferior vena cava (IVC), aorta, and hemiazygos vein, there is a lack of contrast in the hepatic veins. Characteristics include collateral gastric veins “flip-flop” pattern of central portions of the left liver lobe and caudate lobe on PVP (enhancement) and PP images (decreased enhancement).	Rare clinical entity of obstruction of hepatic venous outflow. Causing agents may be pregnancy, hyper-coagulopathy states, oral contraceptives, invading tumors, and congenital webs. Occlusion may occur at the level of intrahepatic venules, hepatic veins, or the IVC. Associated findings include narrowing of the IVC and dilated collateral veins (azygos, hemiazygos, or subcutaneous), ascites, and portal thrombosis. Hepatomegaly, regional intrahepatic attenuation differences, and large regenerative nodules are characteristic.
Liver infarction Fig. 19.5	A wedge-shaped, low-attenuation lesion due to local vascular obstruction. Initially, infarcts are poorly marginated but become more discernible in a subacute/chronic situation. Scan recommendation: Biphasic CT (nonenhanced CT, PP). Nonenhanced CT: Wedge-shaped, low-attenuation lesion with poor delineation to surrounding liver tissue. The more subacute/chronic the infarction, the better demarcated the margins. PP: Distribution segmental or diffuse, non- or patchy heterogeneous enhancement, depending on degree and extent of occlusion. Diagnostic pearls: Wedge-shaped, low-attenuation lesions with segmental distribution on pre- and postcontrast scans.	Histologic feature of acute hepatic infarction is centrilobular necrosis with local hemorrhage. Chronic findings include focal atrophy of the involved segment and hypodense or cystic changes. The portal venous system accounts for 75% of the blood supply of the liver. Thus, hepatic infarction usually is caused by the superimposition of portal vein occlusion on preexisting hepatic artery stenosis. Etiology for hepatic artery stenosis includes atherosclerosis, embolism, thrombosis, vasculitis, and hypotension/shock. Portal vein occlusion/thrombosis may be (1) caused by pregnancy or oral contraceptives, (2) iatrogenic (during intra-abdominal surgery, surgery of thrombogenic organs (prostate, uterus, etc.), or (3) paraneoplastic (pancreas).
Infection
Pyogenic abscess Fig. 19.6	Small abscesses are sharply defined lesions, often surrounded by a capsule and septated. They may aggregate into a single large cavity. Scan recommendation: Biphasic CT (nonenhanced CT, PP). Nonenhanced CT: Well-defined, round lesions, denser than water but less dense than liver. PP: Distinct enhancement of capsule and septa. No enhancement of central portion (necrosis). Diagnostic pearls: “Cluster of grapes” sign: cluster of multilocular collections of pus coalescing into larger centrally located septated cavities.	Destruction of hepatic parenchyma with localized collection of pus due to a bacterial infection. Twenty to 30% contain gas, but gas–fluid levels are rare. Immature abscesses may not be cystic. Usually occur in immunocompromised or older patients with predisposing conditions, such as biliary/pancreatic diseases, diverticulitis, colitis, appendicitis, trauma, and septicemia. Necrotic metastases (from sarcoma or ovarian carcinoma) may look alike and even become infected.
Opportunistic abscess Fig. 19.7	Multiple round hypodense hepatic lesions. Micronodular abscesses may even make liver appear almost normal or slightly heterogeneous. Scan recommendation: Biphasic CT (nonenhanced CT, PP). Nonenhanced CT: Multiple small hypodense lesions. PP: Lesions remain hypodense without any attenuation. Diagnostic pearls: Multiple ill-defined micronodular hypodense lesions seen on pre- and postcontrast scans.	Microabscesses typically are observed in immuno-compromised patients and are caused by Candida, less commonly by Aspergillus, Pneumocystis carinii, or atypical mycobacteria. Because needle biopsy may be false-negative, open wedge biopsy is usually required for final diagnosis. Differential diagnosis: rule out biliary hamartomas, Caroli disease, and metastases. Typically, similar nodules are also found in the spleen and/or lung (septicemia).
Amebic abscess Fig. 19.8	Peripherally located, well-defined, round, hypodense cystic lesion with enhancing capsule. Scan recommendation: Biphasic CT (nonenhanced CT, PP). Nonenhanced CT: Hypodense as compared with normal liver parenchyma. PP: Nonenhancing center, enhancing inner rim, and hypodense outer rim. Diagnostic pearls: Well-defined, round, targetlike lesions with preference for the right liver lobe.	Underlying infection is amebiasis of the cecum and ascending colon. In ~8% of cases, amebas invade liver through the portal venous system. Common in developing countries (~10% of the world population). May be complicated by rupture into the peritoneum, through the diaphragm, subphrenic abscess, biliary obstruction, or septic emboli. Do not touch lesions; antimicrobial therapy and cytotoxic drugs are treatment of choice. Differential diagnosis: rule out hepatic pyogenic abscess, hepatic hydatid cyst, and biliary cystadeno-carcinoma.
Echinococcal (hydatid) cyst Fig. 19.9	Large, well-defined, cystic liver mass surrounded by several peripheral satellite (daughter) cysts. Scan recommendation: Biphasic CT (nonenhanced CT, PP). Nonenhanced CT: Cysts appear hypodense to normal liver parenchyma. PP: Enhancement of cysts’ walls and septations. Diagnostic pearls: Large well-defined, hypodense, cystic liver mass with intracystic septations, irregular wall calcifications surrounded by numerous (less hypodense) daughter cysts.	Caused by Echinococcus granulosus or Echinococcus multilocularis: parasitic eggs are ingested after contact with dogs or foxes/contaminated food or water. E. granulosus infiltrates liver within days, develops into typical hydatid cysts, and grows up to 3 cm per year in diameter. E. multilocularis effects a diffuse tissue infiltration, induces a granulomatous hepatic tissue reaction followed by necrosis, cavitation, and calcifications. Air–fluid levels typically represent cyst rupture and not infection. Rupture into the biliary tree is the most common complication, causing biliary dilation and cyst wall discontinuity. Clinical symptoms of biliary rupture are pain, fever, and jaundice. Treatment of choice is surgical resection; alternatively, percutaneous aspiration/injection and albendazole may be used.
Congenital
Caroli disease Fig. 19.10a, b	Multiple low-attenuating cystic masses in the liver associated with a dilated biliary tree. Scan recommendation: Biphasic CT (nonenhanced CT, PVP, PP). Nonenhanced CT: Multiple round to saccular hypodense cysts. PP: Cysts may contain a hyperdense central “dot” representing enhancing portal radicles. Diagnostic pearls: Multiple well-delineated, round to saccular hypodense cysts with a hyperdense central “dot” during the PVP.	Rare condition characterized by multiple saccular dilations of the intrahepatic bile ducts throughout the liver. Medullary sponge kidney is associated in 80% of cases.
Trauma
Biloma (bile pseudocyst) Fig. 19.11	Water-density, usually crescent or ovoid mass within or immediately adjacent to the liver. Scan recommendation: Biphasic CT (nonenhanced CT, PP). Nonenhanced CT: Near-water density. PP: No contrast enhancement of the wall or contents. Diagnostic pearls: Well-delineated, homogeneous, round, near-water- density lesions without enhancement after contrast application.	Intra- or extrahepatic collection of bile after traumatic rupture or surgery of the biliary tree.
Laceration Fig. 19.12	Irregular cleft or low-attenuation area that often extends to the periphery of the liver. A solitary (simple) or branching (stellate/radiating pattern may be seen. Often accompanied by intra- and perihepatic hemorrhage. Scan recommendation: Biphasic CT (nonenhanced CT, PP). Nonenhanced CT: Lacerations show near-water density. Hemorrhage may be acute (unclotted) or subacute (clotted). Unclotted blood (> 50 HU) and clotted blood (< 90 HU) typically are hyperdense to lacerations and liver parenchyma. PP: Active hemorrhage seen as contrast extravasation (Caveat: Injection rate must be ≥ 5 mL/s).	Small hyperdense blood clots may be detected within the laceration. Lacerations evolve from sharply marginated low-attenuation lesions into indistinguishable areas after several weeks.
Intrahepatic hematoma Fig. 19.13a, b	Round, oval, changing density patterns depending on acuteness of hemorrhage. Scan recommendation: Biphasic CT (nonenhanced CT, PP). Nonenhanced CT: Subacute hematoma usually hyperdense (< 90 HU), chronic hematoma (10–30 d after onset of bleeding) usually hypodense (20–25 HU). PP: Subacute hematoma may become isodense after CM. Diagnostic pearls: Hyperdense intrahepatic round, oval, or irregular lesions on nonenhanced CT scans.	Usually secondary to penetrating or blunt trauma, rarely due to adenoma, metastasis, or arteriovenous malformation (AVM). Differential diagnosis: bilioma: remains hypodense on all scans.
Subcapsular hematoma	Well-marginated, crescentic or lenticular fluid collection beneath the hepatic capsule. High-attenuation lesion in the beginning and diminishing gradually over several weeks to become a low-attenuation lesion. Scan recommendation: Biphasic CT (nonenhanced CT, PP). Nonenhanced CT: Subacute hematoma usually hyperdense (< 90 HU), chronic hematoma (10–30 d after onset of bleeding) usually hypodense (20–25 HU). PP: Subacute hematoma may appear isodense after CM. Diagnostic pearls: Well-marginated, crescentic fluid collection beneath the hepatic capsule.	May result from trauma, surgery, or percutaneous interventions (cholangiography, biopsy, portography, or biliary drainage procedures). Patients usually report right chest pain during breathing or pain radiating into the right shoulder. Pain usually diminishes within a few days, but it may continue. Keep patients on strong medication as needed.
Inflammation
Hepatic sarcoidosis Fig. 19.14	Presence of diffuse small noncaseating granulomas in the liver of patients with known Boeck disease (sarcoidosis). Scan recommendation: Biphasic CT (nonenhanced CT, PP). Nonenhanced CT/PVP: Multiple ill-defined, hypodense hepatic noduli or heterogeneous appearance of liver parenchyma, often accompanied by hepatosplenomegaly. PP: Hepatic noduli become isodense to normal liver parenchyma. Diagnostic pearls: Always consider in patients with lymphadenopathy and hepatosplenomegaly. Often also found in the spleen.	Histologically, noncaseating epithelioid granulomas with multinucleated giant cells of Langerhans type. Causing agent of granulomas unknown. Two thirds of patients are women 20 to 40 y old. Up to 80% of all patients with sarcoidosis present with involvement of abdominal organs, particularly of the liver and spleen. Treatment through corticosteroids, antiinflammatory agents, and cytotoxic drugs. May not be discernible from liver hamartoma, opportunistic abscesses, metastases.
Focal fatty infiltration Fig. 19.15	Varies from a small oval focus, typically adjacent to the intersegmental fissure, to segmental, lobar, or geographic distribution. No mass effect, contour change, or vascular displacement. Scan recommendation: Biphasic CT (nonenhanced CT, PP). Nonenhanced CT: Poor delineation to normal liver parenchyma (iso-/slightly hypodense). PP: Slightly hypodense as compared with normal liver parenchyma; noncompromised intralesional vessels. Diagnostic pearls: Poorly delineated lesion often adjacent to the intersegmental fissure slightly hypodense to normal liver parenchyma on all phases and noncompromising hepatic vessels.	Histologically regional reversible accumulation of triglycerides within hepatocytes that can simulate neoplasia. Typically associated with obesity, alcoholism, small bowel bypass surgery, diabetes, chemotherapy, hyperalimentation, blunt abdominal trauma, cystic fibrosis, congestive heart failure, Reye syndrome, steroid therapy, and Cushing syndrome. Lesion may occur and disappear within weeks.
Periportal edema Fig. 19.16	Nonenhancing low-density collection encasing the branches of the portal vein (see also Fig. 24.3 , p. 741).	Common postoperative finding in liver transplants. Does not indicate rejection. May also occur in combination with significant edema of other abdominal organs.
Radiation hepatitis	Sharply defined band of diminished density in the liver corresponding to the radiation port.	May develop within days/months after radiation therapy (radiation dose ≥ 35 Gy). May show evidence of recovery.
Benign neoplasms
Hepatic hemangioma Fig. 19.17a–d	Benign neoplasm of thin, fibrous stroma that surrounds multiple vascular channels lined by a single layer of endothelial cells. Scan recommendation: Multiphasic CT (nonenhanced CT, hepatic arterial phase [HAP], PP, delayed phase [DP]). Nonenhanced CT: Small hemangiomas are usually well-circumscribed masses isodense to blood. Large hemangiomas appear more heterogeneous and may contain central fibrotic cleft of low density. HAP: Early peripheral global or nodular enhancement. PP: Progressive centripetal filling usually isodense to blood. DP: Persistent global enhancement that stays isodense with blood. Diagnostic pearls: < 10 cm lesion commonly in subcapsular location (right > left liver lobe) with peripheral globular enhancements on HAP scans and progressive centripetal enhancement following contrast phases (flash filling). Hemangiomas usually are isodense to blood and thus show a similar enhancement pattern as the aorta.	The most common hepatic neoplasm, seen in 7% or more of the normal population. A significant proportion of hemangiomas does not present a characteristic pattern of contrast enhancement and may thus simulate metastasis. Metastases from breast carcinoma and gastrointestinal stromal tumor (GIST) may not be discernible from typical hemangiomas (see Fig. 24.13 , p. 747). Hemangiomas grow slowly from childhood to adulthood, more rapidly during pregnancy. May spontaneously regress.
Focal nodular hyperplasia (FNH) Fig. 19.18a–c Fig. 19.19a, b	Well-circumscribed benign hamartomatous liver lesion with subcapsular preference. Majority of FNH appear solitary and < 5 cm in diameter (80% of cases). Scan recommendation: Multiphasic CT (nonenhanced CT, HAP, PP, DP). Nonenhanced CT: Hypo- or isodense to normal liver parenchyma. Any central scar appears even more hypodense. HAP: Bright homogeneous enhancement. PP: Hypo-/isodense to normal liver parenchyma. DP: Isodense to normal liver parenchyma. If there is a scar, it is hyperdense. Diagnostic pearls: Well-differentiated mass with distinct homogeneous enhancement on HAP and continuously becoming isodense to liver parenchyma; on delayed images, often showing a hyperdense central scar. May resemble a cross section of a grapefruit.	Rare benign liver tumor most often seen in women between age 20 and 50 y. Histologically, a hyperplastic stroma response to local abnormal vasculature. Oral contraceptives have stimulating effect on FNH growth but are not responsible for existence per se. Usually incidentally detected, multiple in 7% to 20% of cases. Central scars are visible in ~70% of large and 30% of small FNHs. Central scar also seen in atypical HCCs, fibrolamellar hepatomas, hepatic adenomas, and giant hemangiomas. Absence of intratumoral calcifications, necrosis, and hemorrhage may help to differentiate from these lesions. Any definitive diagnosis requires hepatic biopsy.
Hepatic adenoma Fig. 19.19a, b	Heterogeneous subcapsular hypervascular lesion, on average 8 to 15 cm in diameter, with a preference for the right lobe of the liver and surrounded by a pseudocapsule. Scan recommendation: Multiphasic CT (nonenhanced CT, HAP, PVP, DP). Nonenhanced CT: Well-defined mass with intratu-moral presence of hypodense (fat) and/or hyperdense (calcifications, hemorrhage) areas. HAP: Heterogeneous hyperdense enhancement. PVP: Hypo-/iso-/hyperdense to normal liver parenchyma. DP: Homogeneous isodense (to liver) enhancement. Pseudocapsule appears hyperdense as compared with normal liver parenchyma and adenoma. Diagnostic pearls: Well-defined, heterogeneous (intratumoral fat/hemorrhage), hypervascular lesion with pseudocapsule on DP images in a noncirrhotic liver.	Usually unilocular large lesions, typically in young women taking oral contraceptives. May also occur in men who use androgens or anabolic steroids. Multilocular adenomas (hepatic adenomatosis) seen in patients with glycogen storage disease or diabetes mellitus. Internal hemorrhage or necrosis is common (36%). Histologically, adenomas lack bile ducts and portal/central veins but contain hepatocytes that are arranged in cords/sheets. May contain malignant foci. Forming of a pseudocapsule due to compression of adjacent liver tissue. On CT scans, often indistinguishable from HCC, but presence of a pseudocapsule and absence of cirrhosis are suggestive.
Nodular regenerative hyperplasia Fig. 19.20	Either multiple micronodular or solitary macronodular, preferably hypervascular liver lesions. Size varies from < 1 mm (micronodular) to 4 cm (macronodular). Scan recommendation: Multiphasic CT (nonenhanced CT, HAP, PVP). Nonenhanced CT: Lesions isoattenuating to normal liver parenchyma. HAP/PVP: Homogeneously hyperdense lesions sometimes with hypodense peripheral “halo.” Diagnostic pearls: Multiple micronodular liver lesions with hyperattenuation on both HAP and PVP images.	Histologically, regenerative nodules consist of hyper-plastic hepatocytes surrounding dilated, atypically formed, large sinusoids. Peripheral halo, if present, evoked by enlarged surrounding sinuses (peliosis). May mimic metastases. Larger nodules may have central scar and thus be indistinguishable from FNH.
Mesenchymal (biliary) hamartoma Fig. 19.14 , p. 681	Multiple micronodular (< 15 mm), low-density cystic or solid lesions. Scan recommendation: Multiphasic CT (nonenhanced CT, PVP, PP). Nonenhanced CT: Cystic lesions with near-water density. Solid lesions have low density compared with normal liver parenchyma. PVP: Cystic lesions isodense to water; solid lesions enhance strongly. PP: Cystic lesions remain isodense; solid lesions become isodense to normal liver parenchyma. Diagnostic pearls: Multiple small lesions with identical near-water attenuation on pre- and postcontrast scans.	Rare. Histologically, proliferated bile ducts embedded in mesenchymal tissue. May be associated with polycystic liver disease. Solid lesions may mimic hemangioma. Cystic lesions have similar CT features as sarcoidosis but without coexistent lesions in the spleen.
Hepatic cyst Fig. 19.21	Sharply delineated, round or oval lesion of near-water attenuation. Scan recommendation: Biphasic CT (nonenhanced CT, PP). Nonenhanced CT: Near-water density. PP: No contrast enhancement of the wall or contents. Diagnostic pearls: Well-delineated, homogeneous, round, near-water density lesions without enhancement after contrast application.	May be multiple. Incidence is ~2.5% in the Western population, higher in Asian women. Associated with von Hippel–Lindau disease, polycystic kidney disease, and autosomal dominant polycystic liver disease. In case of septations, irregular inner margins, intracystic components, and contrast attenuation rule out cystic neoplasm. Nonenhanced CT helps to distinguish intracystic hemorrhage (hyperdense) from neoplasm (hypodense).
Hepatic angiomyolipoma Fig. 19.22a, b	Sharply delineated hepatic mass of variable shape and diameter (0.5–30 cm) containing intralesional fat. Scan recommendation: Multiphasic CT (nonenhanced CT, PVP, PP). Nonenhanced CT: Heterogeneous attenuation depending on predominant tissue component. PVP: Strong attenuation (angioid components). PP: Delayed enhancement. Diagnostic pearls: Well-delineated hepatic mass with hyperattenuation on PVP scans and presence of intralesional fat and vessels.	Rare. Seen predominantly in patients with renal angiomyolipomas. Histologically, composed of fat, smooth muscle cells, and proliferating blood vessels.
Biliary cystadenoma	Cystic mass in the liver parenchyma with septated, multilocular appearance.	Rare lesion, primarily in middle-aged women. May recur and develop into a malignant cystadenocarcinoma. Distinction not important as surgical resection is treatment of choice for both. Differential diagnosis: liver abscess/hydatid cysts.
Hepatic lipoma	Distinct area of intrahepatic fat. Sometimes fine septa of soft tissue density are present. Identical low-attenuation values on pre- and postcontrast scans.	Rare. May be distinguished from focal steatosis (poorly discernible, blood vessels crossing through lesions) and metastases from liposarcoma (heterogeneous lesions with distinct attenuation on postcontrast scans).
Intrahepatic extension of a pancreatic pseudocyst	Round intrahepatic cystic mass or tubular lucencies simulating dilated bile ducts (see also Fig. 20.11 , p. 707).	Complication of pancreatitis.
Malignant neoplasms
Hepatocellular carcinoma (HCC) Fig. 19.23	CT appearance is variable: focal, multinodular, or diffuse. May contain fatty tissue, necrosis, and, occasionally, calcifications. Portal vein invasion in 25% to 40%, hepatic vein invasion in up to 15%. Scan recommendation: Triphasic CT (nonenhanced CT, HAP, PVP). Nonenhanced CT: Hypodense mass with or without necrosis, calcification, fat. HAP: Heterogeneous wedge-shaped enhancement (perfusion abnormalities due to portal vein occlusion). PVP: Hypo isodense to liver parenchyma with local contrast accumulation. Diagnostic pearls: Large heterogeneous, hypervascular mass invading portal vein suspicious for HCC. Smaller HCC may mimic metastasis/hemangioma in cirrhotic liver.	The most common primary liver tumor. Predisposing conditions: cirrhosis due to ethanol or virus hepatitis, hemochromatosis, Wilson disease, Gaucher disease, glycogen storage disease (type 1), tyrosinosis, and biliary atresia. The total number and location of lesions are often difficult to estimate.
Fibrolamellar hepatocellular carcinoma (HCC) Fig. 19.24	Well-defined, large, solitary heterogeneous mass; often hypodense central scar and radial septa. Necrosis and calcification are common (30% of patients). Scan recommendation: Multiphasic CT (nonenhanced CT, HAP, PVP, DP). Nonenhanced CT: Well-defined hypodense mass. Necrosis and calcification are common. HAP: Hyperattenuating and heterogeneous. PVP: Hypo-/isodense to liver parenchyma. DP: Hyperdense scar/septa/capsule.	Rather uncommon form of HCC. Involves younger population and is unrelated to cirrhosis. Less malignant than standard HCC. Lymph node/lung metastases and biliary/vessel infiltration are signs of malignancy. May mimic FNH/HCC. Central scar on T2-weighted MRIs hyperintense in FNH versus hypointense in fibrolamellar HCC. HCC lacks scar and often comes with underlying cirrhosis.
Hepatic metastases Fig. 19.25a–f	Either hypo- (common) or hyperdense (less common) lesions with random distribution pattern within normal-enhancing liver tissue. Variable in size (few millimeters to several centimeters). Scan recommendation: Triphasic CT (nonenhanced CT, HAP, PP) necessary only for initial oncological staging. Nonenhanced CT: Iso-/hypoattenuating to normal liver parenchyma. HAP: Hypervascular metastases appear hyperdense. PP: Hypodense, sometimes hypodense center (central necrosis) with peripheral rim enhancement (viable tumor or compressed normal parenchyma). Diagnostic pearls: Hepatic cysts, hemangiomas, abscesses, sepsis, sarcoidosis, peliosis hepatis, and biliary hamartoma may mimic metastases. Vascular rim enhancement typical for epithelial metastases. Metastases of ovarian cystadenocarcinoma typically infiltrate liver from outside and thus may be found primarily in a subcapsular location. Breast cancer metastases may be indistinguishable from hemangiomas.	Most common liver malignancy (~20 times more common than all primary liver neoplasms combined). Common sites of origin are the colon, stomach, pancreas, breast, and lung. Usually multiple and involving both lobes. Right or left lobe involvement occurs in 20% and 3%, respectively. New appearance of a liver lesion in a patient with a known malignancy most indicative of a metastatic lesion. Pre- and early postcontrast scans are recommended to depict the maximum number of metastases. CT features lack histologic specificity except for vascularity. Pancreatic islet cell, carcinoid, renal cell carcinoma, sarcoma, pheochromocytoma, and germ cell tumors often are hypervascular. Cystadenocarcinoma and sarcoma (pancreas, GI, ovarian) often cystic (hypoattenuating). Mucinous carcinomas (colon, rectum, and stomach), treated breast, medullary thyroid, osteosarcoma, carcinoid, and leiomyosarcoma metastases frequently calcify.
Hepatic lymphoma Fig. 19.26	Primary hepatic lymphomas (rare) or secondary involvement in Hodgkin disease or non–Hodgkin lymphoma. Scan recommendation: Biphasic CT (nonenhanced CT, PP). Nonenhanced CT necessary only for initial oncological staging. Diagnostic pearls: Primary liver lymphoma is a solitary mass with no distinguishing CT features. Secondary infiltrating lymphoma is usually impossible to differentiate from normal liver parenchyma. Nodular or mixed forms are often low attenuating and distinguishable on CT but less common.	Due to a high content of lymphatic tissue, lymphomas are often found in the periportal area. Primary lymphoma of the liver is rare, but secondary lymphomatous involvement is found in 60% of Hodgkin disease and in 50% of non–Hodgkin lymphomas. May complicate liver transplant.
Hepatic sarcomas (angiosarcoma, hemangiosarcoma, and hemangioendothelial sarcoma)	Hemorrhagic, hypervascular, heterogeneous tumor: multifocal or diffusely infiltrating. Size ranging from micronodular to large. Vascular channels within lesion may be capillary or cavernous. Scan recommendation: Triphasic CT (nonenhanced CT, PVP, DP) shows progressive enhancement over time. Nonenhanced CT: Single/multiple hypodense masses. Central hyperdensity represents fresh hemorrhage. PVP: Usually hypodense mass with heterogeneous nodular enhancement. Rarely peripheral nodular enhancement with centripetal progression. DP: Persistence of contrast material in central vessels. Diagnostic pearls: Multiphasic CT shows progression of contrast enhancement over time. Consider hemangiomas as differential diagnosis that usually enhance relative to blood vessels (aorta, vena cava).	Most common mesenchymal liver tumor (~2%) often associated with liver cirrhosis, hemochromatosis, or von Recklinghausen disease. Histologically, a malignant spindle cell tumor of endothelial origin, forming poorly organized vessels and growing along predefined vascular structures. Typically also involves skin, soft tissue, breast, liver, and spleen. Environmental carcinogens (such as thorotrast, polyvinyl chloride, etc.) and radiation exposure may trigger tumor growth.
Epithelioid hemangioendothelioma Fig. 19.27a, b	Well-defined, peripheral (often confluent), typically targetlike nodules. Calcifications rare. Scan recommendation: Multiphasic CT (nonenhanced CT, PVP, DP). Nonenhanced CT: Nodules of decreased attenuation as compared with normal liver. PVP/PP: Targetlike appearance: Hypodense center (myxoid stroma); hyperdense inner peripheral rim (highly vascularized); hypodense outer peripheral rim (edema). Diagnostic pearls: Targetlike appearance of peripherally located and partly coalescing lesions. Capsular retraction due to fibrosis and ischemia.	Low-malignant, slowly progressing, highly vascularized liver tumor of unknown etiology. Epithelioid cells stain positive for factor VIII–related antigen. Tumor affects women more than men (association with contraceptives?). Typical age group: 28 to 58 y. Eighty percent of patients survive 5 to 10 y after diagnosis. Nodule resection and liver transplantation are treatment of choice.
Peripheral (intrahepatic) cholangiocarcinoma (PCC) Fig. 19.28a, b	Heterogeneous large hepatic mass with dilated bile ducts and capsular retraction. Can be mass forming (well circumscribed), periductal infiltrating (i.e., branchlike growth along bile ducts with local obstruction of bile ducts), or intraductal growing (segmental/focal bile duct dilation). Scan recommendation: Multiphasic CT (nonenhanced CT, HAP, PP, DP). Nonenhanced CT: Well-defined, lobulated, hypodense mass often with punctuated calcifications and intrahepatic bile duct dilation. HAP: Rimlike enhancement. PP: Progressive centripetal filling usually not isodense to blood. DP: Distinct delayed enhancement (due to fibrotic stroma of tumors) Diagnostic pearls: Tumor often visible only on delayed images. Tumor margins often best depicted on DP/PP images.	PCC and intraductal growing cholangiocarcinoma often missed due to ill-defined margins and low attenuation. Five to 10 minutes after contrast injection is optimal for delayed imaging. Accounts for ~15% of liver cancers, but only 10% of all cholangiocarcinomas are intrahepatic. Associated with repeated cholangitis, hepatolithiasis, congenital cystic liver disease, and primary sclerosing cholangitis (PSC). Age peak: 50 to 60 y. Treatment of choice is surgical resection. Five-year survival rate is 30%.
Hepatoblastoma	Low-attenuation hepatic tumor with peripheral rim enhancement. Scan recommendation: Consider MRI instead of CT (radiation issues with children).	Most frequent hepatic malignancy in children, usually affecting the right lobe.
Embryonal sarcoma	Large liver tumor with numerous cystic regions. Scan recommendation: Consider MRI instead of CT (radiation issues with children).	Rare tumor found exclusively in pediatric patients; 75% occur in the right lobe.
Biliary cystadenocarcinoma Fig. 19.29	Large, well-defined, complex cystic mass with macroscopic nodules, septations, and, rarely, calcifications.	Eighty-five percent of tumors arise from intrahepatic bile ducts, 14% from extrahepatic bile ducts, and < 1% from the gallbladder. Distinction between (benign) cystadenoma and cyst-adenocarcinoma not important as surgical resection is treatment of choice for both.
Extrahepatic tumors	Tumors of adrenal, kidney, stomach, and gallbladder can invade or displace the liver and thus have an appearance similar to that of primary liver tumors.	Multiplanar reformations allow for better delineation of anatomical structures/pathology.

**Fig. 19.4 Budd–Chiari syndrome.** Despite appropriate enhancement of the inferior vena cava (IVC), aorta, and hemiazygos vein, there is a lack of contrast in the hepatic veins. Note the collateral gastric veins ventrally to the hemiazygos vein and medially to the cardia.

**Fig. 19.5 Right liver lobe with decreased attenuation due to infarction after liver transplantation.** The hyperdense stripe posterior to the right liver lobe represents the diaphragm (arrow). There is fluid on both sides of the diaphragm in the absence of a bare area.

**Fig. 19.6 Liver abscess with typical “cluster of grapes” sign.** Cluster of multilocular pus collections coalesce into a larger centrally located septated cavity.

**Fig. 19.7 Opportunistic abscesses.** Multiple ill-defined, micronodular, hypodense lesions.

**Fig. 19.8 Amebic abscesses.** Well-defined, round, targetlike lesions with nonenhancing center, enhancing inner rim, and hypodense outer rim (edema).

**Fig. 19.9 Echinococcal (hydatid) cyst.** Large well-defined cystic liver mass surrounded by several peripheral satellite (daughter) cysts.

**Fig. 19.10a, b Caroli disease.** Multiple well-delineated round cysts. Hyperdense central dots (i.e., portal radicles) are not yet visible on the axial image during the hepatic arterial phase (HAP) (a), but they are seen on the coronal multiplanar reconstruction (MPR) during the portal venous phase (PVP) (b).

**Fig. 19.11 Giant biloma.** The biloma within the left liver lobe is secondary to biliary tree damage.

**Fig. 19.12 Liver laceration due to blunt trauma.** Hypodense irregular cleft is seen through the right liver lobe. Note the adjacent perihepatic fluid and nonattenuation of the right kidney.

**Fig. 19.13a, b Intrahepatic hematoma.** Precontrast image (a) shows a slightly hyperdense intrahepatic lesion surrounded by hypodense edema. Postcontrast image (b) shows normal attenuation of liver parenchyma but not hematoma. Note an unusually prominent lateral segment of the liver.

**Fig. 19.14 Sarcoidosis of the liver.** Multiple ill-defined, hypodense hepatic noduli. Signs of cirrhosis are evident in the nodular liver margin, marked ascites, and inhomogeneous parenchymal contrast, which is most likely also due to sarcoidosis. No involvement of the spleen is seen. Micrometastases or cystic liver hamartomas may have similar CT features.

**Fig. 19.15 Focal fatty infiltration.** Large ill-defined hypodense lesion in the right liver lobe, with noncompromising hepatic vessels.

**Fig. 19.16 Periportal edema.** Low-density band (arrow) within the porta hepatis surrounding the branches of the portal vein.

**Fig. 19.17a–d Hemangioma.** Hypodense lesions in liver segments 2 and 8 on noncontrast scans (a). After contrast material injection, early peripheral nodular enhancement is seen during the HAP (b), progressive centripetal filling during the PP (c), and persistent global enhancement that stays isodense with blood during the DP (d).

**Fig. 19.18a–c Focal nodular hyperplasia (FNH).** On precontrast scans, a hypodense lesion (a) is visible ventrally in the left liver lobe (liver segment 2) with distinct homogeneous enhancement during the HAP (b) and becoming isodense to liver parenchyma during the PP (c). Note the hypodense central scar on all scans.

**Fig. 19.19a, b Hepatic adenoma.** Large well-defined mass in the left liver lobe with a fatty center and hyperdense attenuation during the HAP (a). The lobe becomes isodense to normal liver parenchyma during the PP (b). Note also the small FNH in the right liver lobe (liver segment 6 dorsally) with similar attenuation features but a hypodense central scar that becomes slightly hyperdense during the PP.

**Fig. 19.20 Nodular regenerative hyperplasia.** Multiple hepatic macronoduli with strong attenuation during the HAP are seen in a patient with underlying severe liver cirrhosis.

**Fig. 19.21 Liver cysts in the left liver lobe.** Sharply delineated, round or oval lesion of near-water attenuation without contrast enhancement of the cyst wall.

**Fig. 19.22a, b Large hepatic angiomyolipoma.** Sharply delineated hepatic mass with strong attenuation during the PVP (a) and delayed enhancement during the PP (b). Note intralesional vessels and fat.

**Fig. 19.23 Multifocal hepatocellular carcinoma (HCC).** Visible is HCC with distinct enhancement during the HAP. Note also marked liver cirrhosis and perihepatic ascites.

**Fig. 19.24 Fibrolamellar HCC.** Large well-defined, heterogeneous mass with hypodense central scars, radiating septa, areas of necrosis, and calcifications.

**Fig. 19.25a–f Hepatic metastases.** Vessel infiltration (a) and local cholestasis (b) are typical signs of malignancy. CT appearance depends on primary neoplasm: vascular rim enhancement in colon carcinoma (c); subcapsular location in ovarian cystadenocarcinoma (d); mainly cystic in pancreatic cystadenocarcinoma (e); slightly hypervascular in pancreatic islet cell (i.e., neuroendocrine) tumor (f).

**Fig. 19.26 Secondary hepatic and splenic involvement of a patient with non–Hodgkin lymphoma.** Low-attenuating lesion in the liver and spleen. Local cholestasis in the liver is highly suspicious for a malignancy.

**Fig. 19.27a, b Epithelioid hemangioendothelioma.** Well-defined hypodense nodules on nonenhanced CT and targetlike appearance during the PVP.

**Fig. 19.28a, b Peripheral cholangiocarcinoma (PCC).** Comparison of well-defined periductal-infiltrating (a) and mass-forming (b) type. Note the rimlike enhancement during the PVP.

**Table 19.2 Diffuse liver disease**
Disease	CT Findings	Comments
Peliosis hepatis Fig. 19.30	Cystic dilation of the central vein of the hepatic lobule leading to blood filled endothelial-lined sinusoidal cavities. Scan recommendation: Multiphasic CT (nonenhanced CT, AP, PVP, DP). Nonenhanced CT: Depending on size of lesions liver may appear normal (lesions < 10 mm) or show multiple low-attenuation lesions. AP: Typically, ringlike high attenuation (although some lesions may show central attenuation). PVP: Centripetal contrast enhancement. DP: Lesions remain hyperdense as compared with normal liver parenchyma. Diagnostic pearls: Multiple hypodense nodular lesions on nonenhanced CT restricted to the liver with ringlike enhancement on early and late global enhancement on delayed postcontrast scans.	Two subtypes, histologically can be distinguished: parenchymal and phlebectatic. Only the phlebectatic type is lined by endothelium. Peliosis is a rare disorder of unknown etiology. There is an association with exposure to cytotoxic agents, long-term steroid use, chronic diseases (AIDS, TB, etc.), and immuno suppression. Differential diagnosis includes hypervascular metastases and hepatic hemangioma. Metastases appear hypodense on delayed images (wash-out phenomenon). Hemangiomas show similar centripetal progression of contrast attenuation, but enhancement pattern is more patchy/nodular.
Portal vein thrombosis Fig. 19.31a, b	Segmental to global hypoperfusion of the liver depending on extent and localization of the thrombus. Portal vein may be enlarged (acute) or normal (chronic) in size. Scan recommendation: Multiphasic CT (nonenhanced CT, PVP, DP). Nonenhanced CT: Segmental (wedge-shaped) or global hypodensity of liver parenchyma. PVP: Segmental to global hypoattenuation of the liver parenchyma. In acute thrombosis, walls of the portal vein may enhance, the thrombus not. In chronic thrombosis, usually enlarged collaterals termed cavernous malformations. DP: Necrotic areas hypodense; nonnecrotic areas hypo- to isodense to normal liver parenchyma. Diagnostic pearls: Clotted portal vein with segmental/global hepatic hypoperfusion on all scans.	May be caused by neoplasms, infections, cirrhosis, trauma, hypercoagulable states, or hepatic venous obstruction.
Passive hepatic congestion Fig. 19.32	Backflow of venous blood into liver veins due to insufficient hepatic venous outflow. Scan recommendation: Contrast-enhanced CT. PVP/DP: Retrograde backflow of contrast into dilated IVC and hepatic veins. Often by formation of a contrast/noncontrast (blood) level in the IVC. Contrast in liver veins often higher than in the aorta. Often periportal hypodensity (due to perivascular lymphedema).	Typically caused by cardiac failure such as constrictive pericarditis, cardiomyopathy, right-side valvular disease, or congestive heart failure. Thus, typically accompanied by pericardial and pleural effusion, hepatomegaly, and ascites.
Inflammation
Fatty liver (hepatic steatosis) Fig. 19.33	Fatty degeneration of hepatocytes due to a variety of infectious, toxic, and ischemic agents. Scan recommendation: Multiphasic CT (nonenhanced CT, PVP, DP). Nonenhanced CT: Diffuse/lobular/segmental hepatic hypoattenuation compared with spleen (normal liver parenchyma 10 HU > spleen). Inversion of contrast between vessel (hyperdense) and liver parenchyma (hypodense). PVP/DP: Often not visible on postcontrast scans. Diagnostic pearls: Liver hypodense compared with spleen. Contrast inversion between vessels and parenchyma on nonenhanced CT. Uncompromised course of hepatic vessels through fatty infiltrations.	Causative agents may be alcohol, cytotoxic drugs, obesity, diabetes mellitus, hepatitis, steroid treatment, hyperalimentation, or liver transplantation. Typically accompanied by hepatomegaly (75%). Hypodense lesions may be masked on noncontrast scans. May mimic diffuse hepatic infiltration from neoplasms or lymphoma. Contrast inversion between vessel and liver parenchyma indicates > 10% to 15% intrahepatic fat.
Cirrhosis Fig. 19.34	Nonreversible parenchymal destruction accompanied by fibrosis, nodular regeneration, and abnormal reconstruction of normal lobar architecture. Scan recommendation: Multiphasic CT (nonenhanced CT, PVP, DP). Nonenhanced CT: Nodular hyperdensity (> 70–140 HU) of liver parenchyma due to increased iron storage of regenerative nodules. PVP/PP: Nodular hyperdensity becomes isodense to liver parenchyma. DP: Late enhancement of fibrotic areas. Diagnostic pearls: Nodular liver contour with multiple hyperdense (> 70–140 HU) intrahepatic nodules on nonenhanced CT scans, accompanied by left lobular hypertrophy and right lobular atrophy.	Heterogeneous appearance of liver parenchyma with presence of regenerative nodules causing a nodular liver contour, enlargement of the caudate lobe and lateral segment of left lobe, and atrophy of the right lobe and medial segment of the left lobe. Three subtypes of cirrhosis depending on the type of nodular regeneration: micronodular (< 0.5 cm), due to alcohol abuse; macronodular (0.5 cm to several cm), due to viral hepatitis; mixed type, due to chronic bile duct obstruction. Splenomegaly, ascites, collateral veins, colonic interposition, and small bowel edema are associated findings.
Primary biliary cirrhosis (PBC)	Idiopathic liver cirrhosis of unknown etiology due to chronic destruction of intrahepatic bile ducts. Scan recommendation: Multiphasic CT (nonenhanced CT, PVP, DP). Nonenhanced CT: Nodular hyperdensity (> 70–140 HU) of liver parenchyma due to multiple regenerative nodules. PVP/PP: Regenerative nodules become isodense to liver parenchyma. DP: Late enhancement of fibrotic areas. Diagnostic pearls: nodular liver contour with multiple hyperdense intrahepatic nodules on nonenhanced CT scans, lobular hypertrophy, and atrophy.	PBC almost exclusively affects women between age 30 and 60 y. The etiology of the disease is unknown, but it is typically associated with other autoimmune diseases (scleroderma, Sjögren syndrome, and rheumatoid arthritis). Histologic features are damaged epithelial cells, necrotic bile ducts, and fibrosis of portal triads. Typical clinical symptoms include tiredness, pruritus (bilirubin), intermittent abdominal pain, and jaundice, but in 50% of cases, asymptomatic hepatomegaly is the first sign of PBC. Liver transplantation is the sole treatment option, but the risk of PBC recurrence in the transplant is slightly increased.
Hemochromatosis Fig. 19.35a, b	Iron overload disorder with functional impairment of hepatocytes. Scan recommendation: Multiphasic CT (nonenhanced CT, PVP, DP). Nonenhanced CT: Homogeneous hyperattenuation (> 70–140 HU) of liver parenchyma due to increased iron storage. Hepatic and portal veins appear hypodense. PVP/PP: Difference in attenuation between liver parenchyma and vessels diminishes. Diagnostic pearls: Clear differentiation on nonenhanced CT between hyperdense liver parenchyma and hypodense vessels that diminishes on postcontrast scans.	Two subtypes of hemochromatosis: primary hemochromatosis, an autosomal recessive disorder of iron metabolism, with excessive deposition of iron in the liver, pancreas, myocardium, endocrine glands, joints, and skin; and secondary hemochromatosis, with iron deposition in the reticuloendothelial cells due to either increased iron intake (multiple transfusions, nutritive), or alcohol-induced toxic liver disease. Iron concentration directly proportional to the difference between actual and normal HU value (60 HU). Contrast only necessary to rule out/in HCC.
Wilson disease	Inflammatory periportal reaction followed by nodular liver cirrhosis due to sinusoidal and periportal copper deposition. Scan recommendation: Nonenhanced CT: Multiple hyperdense regenerating nodules and typical cirrhotic changes.	Autosomal recessive disease of copper metabolism usually diagnosed in childhood. Toxic levels of copper accumulate in the liver, brain, and cornea secondary to impaired biliary excretion.
Sarcoidosis	Nonspecific hepatosplenomegaly with diffuse small noncaseating granulomas in the liver of patients with known Boeck disease (sarcoidosis). Scan recommendation: Biphasic CT (nonenhanced CT, PP). Nonenhanced CT: Multiple hypodense hepatic noduli or simply heterogeneous appearance of liver parenchyma, often accompanied by hepatosplenomegaly. PVP/PP: Isodensity of hepatic noduli compared with normal liver parenchyma. Diagnostic pearls: Always consider in patients with lymphadenopathy and hepatosplenomegaly. Nodular pattern often seen in both liver and spleen.	Histologically, noncaseating epithelioid granulomas with multinucleated giant cells of Langerhans type. Granulomas usually more apparent in the portal triad regions than in the liver parenchyma. Causing agent unknown. Two thirds of patients are women between 20 and 40 y of age. Up to 80% of all patients with sarcoidosis present with involvement of abdominal organs, particularly of the liver and spleen. Treatment with corticosteroids, antiinflammatory agents, and cytotoxic drugs. Unusually concomitant involvement of the spleen and thus similar findings in Fig. 21.10 , p. 715 .
Amyloidosis	Nonspecific hepatomegaly and lymphadenopathy. Scan recommendation: Multiphasic CT (nonenhanced CT, PP, DP). Nonenhanced CT: Global or focal hypoattenuation of liver parenchyma. PP: Global or focal hypoattenuation of liver parenchyma. DP: Delayed contrast enhancement may be present. Diagnostic pearls: Global or focal hypoattenuation of liver parenchyma on pre- and postcontrast scans.	Deposition of fibrils of light-chain immunoglobulins in a perivascular location within the spaces of Disse.
Infection
Tuberculosis (TB) Fig. 21.12 , p. 717	Multiple round, hypodense hepatic lesions. Scan recommendation: Multiphasic CT (nonenhanced CT, PP). Nonenhanced CT: Multiple small, hypodense lesions. PP: Lesions remain hypodense—attenuation. Diagnostic pearls: Multiple micronodular hypodense lesions seen on pre- and post-contrast scans. In presence of miliar lesions, the liver may appear almost normal.	Occurs in patients after primary TB infection as a result of subsequent hematogenous spreading of the disease (miliary TB). Typically, also involves other parenchymatous organs, such as the kidneys, spleen, brain, and lung. Differential diagnosis: rule out biliary hamartomas, Caroli disease, and metastases. Concomitant involvement of the spleen as visible is typical.
Schistosomiasis	Multiple high-attenuating hepatic lesions ranging in size from a few millimeters to several centimeters. Scan recommendation: Multiphasic CT (nonenhanced CT, PP). Nonenhanced CT: Either a “tortoise shell” appearance of the liver with multiple hypodense, partly calcified lesions (Schistosoma japonicum) or low-density peri-portal changes combined with multiple hypodense, noncalcified lesions (S. mansoni). PP: Center of lesions hypodense, marked peripheral contrast enhancement.	Schistosomiasis is a parasitic disease caused by Schistosoma japonicum and S. mansoni. The disease is endemic in tropical countries (Africa, the Caribbean, eastern South America, southeast Asia, and the Middle East). Schistosomes live and mature in the portal veins, inciting a granulomatous reaction with central necrosis and eventually periportal fibrosis.
Neoplasms
Diffuse hepatocellular carcinoma (HCC) Fig. 19.23 , p. 689	Diffuse irregular, low-density changes, variable degree of contrast enhancement. Scan recommendation: Triphasic CT (nonenhanced CT, HAP, PVP). Nonenhanced CT: Hypodense mass with necrosis, calcification, fat. HAP: Heterogeneous enhancement (perfusion abnormalities due to portal vein occlusion). PVP: Hypo-/isodense to liver parenchyma with local contrast accumulation. Diagnostic pearls: Large heterogeneous, hypervascular mass invading the portal vein.	The most common primary liver tumor. Predisposing conditions: cirrhosis due to ethanol or virus hepatitis, hemochromatosis, Wilson disease, Gaucher disease, glycogen storage disease (type 1), tyrosinosis, and biliary atresia. The total number and location of lesions are often difficult to estimate. Treatment options include resection, chemoembolization, and liver transplantation depending on extent and cause of disease. Liver cirrhosis is often an overlying finding.
Diffuse metastatic disease Fig. 19.25 , p. 689	Liver may be normal in size or show diffuse hepatomegaly due to multiple low-contrast lesions. Contrast enhancement usually shows subtle displacement of normal liver parenchyma with diffuse metastatic spreading. Scan recommendation: Triphasic CT (nonenhanced CT, HAP, PP) necessary only for initial oncological staging. Nonenhanced CT: Iso-/hypoattenuating to normal liver parenchyma. HAP: Hypervascular metastases appear hyperdense. PP: Hypodense, sometimes hypodense center (central necrosis) with peripheral rim enhancement (viable tumor or compressed normal parenchyma). Diagnostic pearls: Hepatic cysts, hemangiomas, abscesses, sepsis, sarcoidosis, peliosis hepatis, and biliary hamartoma may mimic metastases.	Most common liver malignancy. Common sites of origin are the colon, stomach, pancreas, breast, and lung. Usually involving both liver lobes. Pre- and early postcontrast scans are recommended to depict the maximum number of metastases. CT features lack histologic specificity except for vascularity. Pancreatic islet cell, carcinoid, renal cell carcinoma, sarcoma, pheochromocytoma, and germ cell tumors often are hypervascular. Cystadenocarcinoma and sarcoma (pancreas, GI, and ovarian) are often cystic (hypoattenuating). Mucinous carcinomas (colon, rectum, and stomach), treated breast, medullary thyroid, osteosarcoma, carcinoid, and leiomyosarcoma metastases frequently calcify.
Diffuse lymphoma	Multiple hypodense, poorly delineated lesions or diffuse infiltrating mass that is usually more clearly delineated on postcontrast scans. Scan recommendation: Biphasic CT (nonenhanced CT, PP): Nonenhanced CT only at initial oncological staging. PP: Micronoduli/diffuse mass remains hypodense as compared with normal liver parenchyma.	Commonly accompanied by lymphadenopathy and splenomegaly. Primary liver lymphoma is a solitary mass with no distinguishing features. Secondary infiltrating lymphoma is usually difficult to differentiate from normal liver parenchyma. Nodular or mixed forms are less common, low attenuating, and thus more distinguishable from normal liver parenchyma.