Regionally Inhomogeneous Texture

Liver

Diffuse Changes in Hepatic

Parenchyma

Enlarged Liver

Small Liver

Homogeneous Hypoechoic Texture

Homogeneous Hyperechoic Texture

Regionally Inhomogeneous

Texture

Diffuse Inhomogeneous Texture

Localized Changes in Hepatic

Parenchyma

Differential Diagnosis of Focal Lesions

Focal Fatty Infiltration

Necrosis

Portal Venous Gas Embolism

The sonographic texture of the hepatic parenchyma is determined by the size, density, brightness, and distribution/arrangement of the individual echoes. In other words, irregular ultrasound texture is the sequel to changes in one or more of these echo characteristics. These changes may pertain uniformly to the entire organ or just to a segment, region, or zone.

In parenchyma with limited segmental, regional or zonal irregularities (parenchyma with circumscribed “splotches”) one has to differentiate between changes found in one or more segments (Fig. 2.35), or those developing in typical perivenous fashion or along the portal structures ( 2.2 g and h), and those whose distribution appears without any semblance of order. In the latter case, in B-mode ultrasonography it becomes rather difficult to distinguish these changes from infiltrating metastatic changes (Fig. 2.36).

Fig. 2.35 Segmental inhomogeneity: varying degree of fatty infiltration of the liver (segment II): varying degree of fatty infiltration and/or heterogenetic fatty infiltration of the parenchyma, the segmental limits are respected; the portal branch runs unrestrained within this segment.

Fig. 2.36 Example of periportal inhomogeneity: periportal infiltration in metastatic pancreatic cancer.

Focal FattyInfiltration

Focal fatty infiltration of the liver (FFI) appears as a mass within the classic findings of fatty liver ( 2.6, Figs. 2.35, 2.37, 2.38, 2.39) (see above). It is a rather common finding, characterized by the juxtaposition of two different areas of the parenchyma with echoes of the same size/brightness, which may be densely (hyperechoic) packed as a sign of high fat content or more loosely (hypoechoic) packed when fat content is low, but always displaying a homogeneous arrangement. The underlying pathologic etiology of this difference in density of the fatty infiltration is caused by an organic (aberrant vessels) or a functional failure of perfusion. These regional differences in density of the fatty infiltration can be seen more often in certain situations, such as nutritionally related or after narcosis fatty infiltration.

There are a number of prime locations for focal fatty infiltration (posteriorly in segment IV, at the gallbladder fossa, around the veins, left > right). Quite often they exhibit a smooth map-like delineation toward the neighboring

Fig. 2.37 Focal fatty infiltration. Inhomogeneous splotches of hyperechoic/hypoechoic parenchyma in the left hepatic lobe without involvement of the vessels.

Fig. 2.38 Segmental fatty infiltration. Hyperechoic parenchyma with fatty infiltration along segment II of the left hepatic lobe; tongue-like delineation of the fatty infiltration without any changes in the surface or the course of the vessels.

parenchyma but still fit in harmoniously with the hepatic architecture, i. e., they do not deform any boundaries, or change the surface, or alter the course of any vessels. Focal fatty infiltration seems to take place more frequently in certain situations, such as severe nutritional steatosis or after anesthesia. If B-mode ultrasonography is the only diagnostic modality used, it is sometimes impossible to differentiate between focal infiltration and diffuse metastasis, in which case abdominal CT or hepatobiliary scintiscanning would have to be employed. However, the difference can be easily detected if the homogeneous isoechogenic contrasting of the parenchyma of both densities can be seen in the portal phase of CEUS after the introduction of the contrast agent.

Fig. 2.39 Segmental fatty infiltration. Pseudotumorous pseudonodular hyperechoic areas respecting the boundaries and surfaces of vessels and segments.

Necrosis

Portal VenousGasEmbolism

Necrotizing intra-abdominal disease (e. g., acute mesenteric ischemia, pancreatitis), diseases with a breakdown in the barrier between the intestinal lumen and the portal venous system (e. g., penetrating gastrointestinal ulcer, diverticulitis, ileus), and septic conditions with gas-producing pathogens from the portal catchment areas (e. g., toxic colon, necrotizing enterocolitis) may sweep gas bubbles into the liver via the portal vein. In ultrasonography, these bubbles appear as coarse turbulent echoes within the portal vein; in the hepatic parenchyma they are deposited first in the periportal regions and present there as coarse echoes (Fig. 2.40). Eventually, these coarse echoes spread across the entire parenchyma, and within just a few hours portal venous gas embolism can develop into life-threatening acidosis (Kussmaul respiration) and fatal hepatic failure.

texture, with an irregular arrangement of echoes of varying coarse graininess and brightness.

Fig. 2.40 Portal venous gas embolism. Small particles (gas bubbles) are detectable within the portal branches. Initial periportal deposits of gas bubbles (abundant gas leads to hyperechoic echoes within the whole liver).

Liver

Diffuse Changes in Hepatic

Parenchyma

Enlarged Liver

Small Liver

Homogeneous Hypoechoic Texture

Homogeneous Hyperechoic Texture

Regionally Inhomogeneous

Texture

Diffuse Inhomogeneous Texture

Localized Changes in Hepatic

Parenchyma

Differential Diagnosis of Focal Lesions

Chronic Hepatitis

Cirrhosis

Disseminated Tumor Growth

Diffuse Tumor Growth

During the course of hepatitis there will be periportal and parenchymal inflammation, accompanied by edema and necrosis. As a result size, density, brightness, and distribution of the individual echoes within all of the hepatic parenchyma will exhibit coarse inhomogeneity of varying degree. The surface becomes increasingly irregular and displays fibrotic dimpling, which also will be found along the hepatic veins where it leads to irregular margins (“nibbling away”). Eventually the veins will become tortuous and increasingly rarefied in the periphery. The branches of the portal veins present with multiple periportal echoes, while

the consistency of the liver becomes increasingly firm and in the end hard (Fig. 2.41). The extent of the sonographic changes depends not so much on the possible etiology of chronic hepatitis but rather on its duration and severity. Any pathologically enlarged lymph nodes at the porta hepatis will correlate with the severity and activity of chronic hepatitis caused by autoimmune or chronic viral infections. There is a fluid transition between the sonographic findings of chronic hepatitis and cirrhosis of the liver.

Fig. 2.41 Chronic hepatitis. Irregular surface, inhomogeneous parenchyma, irregular corkscrew-like hepatic vein with so-called “nibbling away.” Other criteria: firmer consistency.

In a liver with cirrhotic changes, the diffuse irregular parenchymal echotexture by itself is a rather poor criterion for the presence or absence of any cirrhosis. Irregular surface, typical changes in the shape, firm/hard consistency of the organ, rarefied hepatic veins, splenomegaly, and collateralization in portal hypertension are much more reliable indicators of any cirrhotic transformation (Figs. 2.42, 2.43, 2.44, 2.45, 2.46, 2.47, 2.2 l, 2.4f–h, 2.7). The types of parenchymal disturbance may differ: a relatively homogeneous hyperechoic texture is more typical of fatty cirrhosis, while a parenchymal change characterized by large nodules is most probably due to autoimmune or chronic viral inflammation. The vascular architecture could also provide clues about the possible etiology: rarefied vessels are typical of autoimmune or chronic viral inflammation, whereas in toxic cirrhosis quite often the vessels can still be imaged, and in cardiac cirrhosis the hepatic veins will always be easy to visualize.

Fig. 2.42 Chronic autoimmune hepatitis. Irregular surface, inhomogeneous and coarse parenchyma. Hepatic veins already rarefied. Other criteria: firmer consistency, splenomegaly; in this case ascites.

Fig. 2.43 Cirrhosis of the liver. Irregular surface, ascites, coarse inhomogeneous parenchyma, rarefied hepatic veins. Other criteria: firmer consistency at one-finger palpation.

a Cardiac cirrhosis with engorged hepatic vein visible far into the periphery; homogeneous dense parenchyma with subtly irregular surface, ascites.

d In the longitudinal view at the midline, typical beak-like/dolphin-nosed appearance, large caudate lobe.

b Atrophic posthepatitic liver cirrhosis with coarse, irregular surface, inhomogeneous surface and coarser parenchyma, rarefied liver veins, ascites. Accessory finding: gallbladder stone.

e Plug-like parenchymal hump beside the gallbladder (echogenic wall thickening) in liver cirrhosis; ascites.

c Primary biliary cirrhosis: irregular surface, inhomogeneous coarsened parenchyma, rarefied liver veins.

f Rigid inferior right lobe with coarsely irregular surface, ascites.

Liver veins and portal veins in liver cirrhosis

g Inhomogeneous coarse parenchyma, subtly irregular surface, the rarefied hepatic veins cannot be visualized.

j Parenchyma of a liver cirrhosis with rarefied hepatic veins (same scan as in k, grayscale image).

h Necrotizing liver cirrhosis with inhomogeneous coarse parenchyma, irregular surface, rarefied hepatic veins, “amputated” portal vein.

k Rarefied hepatic veins, visible in CDS.

i Differential diagnosis of irregular parenchymal echotexture; in this case, hepatocellular carcinoma (HCC) in underlying cirrhosis.

l Normal hepatic flow in the portal vein.

Diffuse TumorGrowth

Diffuse infiltration of the liver by a tumor is an infrequent finding; in rare cases, it may simply lead to increased liver size and coarse hypoechoic parenchyma (e. g., in chronic lymphocytic leukemia), but more often it is seen as an irregular region within the liver (e. g., breast

cancer) (Figs. 2.48, 2.49, 2.50). The decisive diagnostic aspect is the presence of criteria for malignancy (see below). On the other hand, diffuse tumor growth is rather the rule in hepatocellular carcinoma (HCC) and cannot be clearly differentiated from the cirrhotic tis-

sue. Secondary signs of malignancy (see above) and the use of CEUS can be an option for locating tumor tissue.

●Size. For solitary masses it is quite useful to specify the size, particularly in follow-up studies. The size is defined by two orthogonal diameters and given in centimeters or millimeters; it is better to measure a mass in all three planes (longitudinal, transverse, sagittal). To compare the findings for future reference, reproducible reference structures should be included in the image. Multiple masses are characterized by descriptive terms (e. g., small nodular, large nodular).

●Shape. A mass may be round, oval, bizarre, or map-like; only the shape of solitary masses should be described.

●Margin. This term specifies how the mass is delineated against the surrounding tissue; the margin may be sharp, smooth, and easily detectable, or blurred and irregular, or even undetectable.

●Center/edge. Masses may possess a capsule, a hypoechoic ring of parenchyma (“halo”), and peripheral vasculature. Others present with an anechoic, hypoechoic, or hyper-

vascularization (arterial, venous, shunting), especially the range of frequencies of the arteries. The use of contrast agents in CEUS allows better detection of small isoechogenic and hidden lesions in addition to B- mode criteria.1 Using the additional assessment criteria of dynamics and density of vascularization in lesions, it is often possible to characterize these lesions and determine their pathogenesis (see below).

●Extrahepatic factors. Proper assessment of a mass has to include any changes in other organs (primary tumor? lymphadenop-

athy?) and clinical parameters (e. g., fever, night sweat).

●Change in or activity of the mass. In fol- low-up studies the sonographer can track any changes taking place spontaneously, under an antibiotic regimen, or with chemotherapy (Figs. 2.53, 2.54, 2.55). Structural changes due to age and size of focal masses, especially in fast-growing tumors, can cause completely different appearances at the time of assessment even if they arise from the same tumor (Fig. 2.56).