The settings of the equipment used will have a profound impact on the sonographer’s ability to recognize and assess diffuse changes in the hepatic parenchyma. Apart from a careful analysis of the actual shape, texture, echogenicity, and distribution of the individual echoes representing the parenchyma, a successful overall assessment of the liver has to include as many additional criteria as possible (Table 2.6). Only by putting together the various criteria like pieces of a puzzle will a reliable assessment of this organ be achieved. One possibility, although to be used with caution, is a comparison of the hepatic parenchyma with that of other organs (kidney, spleen, pancreas, psoas muscle) (2.2a). This caveat has to do with the fact that apart from disease one has to take into

Parametric Ultrasonography

Parametric ultrasonography generates numbers, not images. This is supposed to neutralize any subjective bias on the part of the sonographer as well as any possible objective bias due to the presettings and/ or equipment used. Not only can tissues be detected and described objectively, but it is also possible to quantify and document the

account that aging will alter the characteristics of the different parenchymas differently (Table 2.7).

Thus, assessment of diffuse changes in the hepatic parenchyma is still influenced by any

brightness and homogeneity. These digital signals are then processed and compared by various statistical computer programs, and the result opens up the possibility of noninvasive classification of diffuse tissue changes in ultrasonography, objective quality control in ultrasound equipment, and improved imaging.

number of subjective aspects, and to a large extent depends on the sonographer’s experience.

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

Congested Liver

Fatty Liver

Fatty Liver Hepatitis

Fatty Cirrhosis

Diffuse Infiltration

Determining the Size of the Liver

Sonographic assessment of the size of the liver is fraught with problems.

Volumetric measurements yield a value of around 1/40 of the body weight (2.3–3%); for the average adult male this would mean 1500–1800 mL and for the adult female 1200–1500 mL.

Organ measurements yield a width (right– left) of 25–30 cm, a length (cephalocaudad) of 12–20 cm, and a sagittal depth (anteroposterior) of 6–10 cm. Different shapes are encountered depending on the build: in asthenic persons the liver expands mostly in the longitudinal direction, while in thick-set persons the largest dimension is in the sagittal plane. Therefore, the build alone will account for different normal values of size.

In ultrasonography the size of the liver is determined in the right midclavicular line (MCL), a normal value being 12 cm (9 cm in pyknics, up to 15 cm in asthenics). Assessment of the superior diaphragmatic aspect is critical, since ultrasound may not be able to clearly delineate the boundary because of superposition of the phrenicocostal sinus, and percussion is rather imprecise.

One option would be assessment of the inferior border at the costal margin; however, this value also varies widely depending on the build of the patient (normal: inferior edge at the costal margin), and cannot be relied on because of the respiratory motion of the liver or abnormal position of the diaphragm (emphysema, phrenic nerve palsy). Sagittal measurements also display a rather wide margin of error since there are no fixed markers to be used in reconstruction.

Determining the size of the caudate lobe, either in absolute terms or in relation to the right hepatic lobe, may aid in the presumed diagnosis of cirrhosis or Budd–- Chiari syndrome.

When assessing the size of the liver, the intersegmental comparison and the relation between right and left hepatic lobe (normal: left < right) have to be considered as well. If the left hepatic lobe slides in between the spleen and the diaphragm, displacing the spleen inferiorly, this is a firm sign of an enlarged left hepatic lobe (Fig. 2.16).

Fig. 2.16 Hepatomegaly should be documented by measurement. An enlargement of the left liver lobe may be identified by its position between the diaphragm and the spleen (“kissing phenomenon”): cranial, the hyperechoic liver (fatty liver); caudal, the normal spleen.

Fig. 2.18 Junction of the hepatic veins in acute failure of preexisting chronic hepatic congestion. Homogeneous parenchyma with an increased number of diffusely dispersed, finely grained echoes; rigid engorged hepatic veins and vena cava.

sis”) may result in the organ becoming smaller and would explain the distinct increase in consistency as well as the increasing echogenicity. The hepatic surface is smooth, possibly slightly irregular because of the ongoing fibrosis, the inferior margin is blunt or sharply angled. Sometimes an expansive hepatic pulse may be palpated. Capsular tension with concomitant pain would be unusual for chronic hepatic congestion, as it is more characteristic of acute

decompensation of the underlying congestion of the vena cava. As is also the case in acute hepatic congestion, the engorged hepatic veins can be visualized far into the periphery of the liver, and the junction of the hepatic veins at the vena cava is enlarged too.

Just as in acute congestion of the liver, duplex and color-flow duplex scanning demonstrate the impressive flow changes. The cardiac modulation may affect the duplex curve of the portal system. Sometimes there may be additional findings, such as ascites, pleural effusion, rigid enlarged lumen of the vena cava, and congestion-induced changes in other organs (kidneys, spleen, stomach). Table 2.8 is a summary of the criteria relevant in acute and chronic congestion of the liver.

Fig. 2.19 The same congestive liver seen in Fig. 2.18; the congested liver veins are reaching into the peripheral regions of the liver parenchyma.

Fig. 2.20 Cardiac cirrhosis. Irregular surface and homogeneous parenchyma; the engorged hepatic vein is visible far into the periphery. Signs of ascites and right pleural effusion (not seen here).

Fatty Liver(2.6)

Extrinsic and dynamic criteria. Fatty infiltration of the hepatic parenchyma is a frequent but nonspecific finding, increasing the volume of the liver and thus its size. Initially, this increase in total organ volume manifests itself by a change in the shape; the increased size of the liver as such becomes evident and can be quantified only in the more advanced stages. But even then the organ will still have a smooth surface and exhibit a normal soft consistency.

Fatty Changes of the Liver

Definition. Fatty liver or steatosis hepatis is present if the moist mass of the liver contains >10% fat, or if more than 50% of the hepatic cells display medium-sized or large lipid vacuoles and there is a diffuse pattern of distribution.

Pathogenesis. The causes of underlying fatty change may be exogenous:

●Increased fat transport

●Increased carbohydrate intake

or endogenous:

●Increased peripheral mobilization of fat

●Inhibited intracellular utilization of fat in the hepatic cells

●Increased fat synthesis in the hepatic cells

●Decreased removal of fat

Morphology. Morphology differentiates between small, medium, and large lipid vacuoles with low (5% of the moist mass

of the liver), moderate (6–8%), and marked (8–9%) involvement of the liver. The distribution pattern of the fatty change can be classified as peripheral, centroacinar, zonal, or diffuse.

Etiology. In terms of etiology, fatty liver is encountered as a nonspecific reaction in numerous diseases and conditions; these include:

●Overweight

●Metabolic disorders

●Alcohol

●Medication

●Chemical substances

●Phytotoxins and mycotoxins

●Infection

●Hypoxia

●Endocrine disorders

●Pregnancy

Fig. 2.21 Fatty liver/fatty liver hepatitis. Large right hepatic lobe with a diffuse increase in the delicate to moderate echotexture, which appears more densely packed, and signals fatty infiltration; the beginning inflammation is characterized by the irregular contour of the hepatic veins.

This increase in boundaries is also the reason for the typical increased echogenicity and degraded ultrasound conduction (i. e., attenuation). The degree of fatty infiltration, the type of fatty deposits in the hepatocytes (large vesicles = few additional boundaries; or small vesicles = numerous additional boundaries), the type of fat, and additional factors (severity of any concomitant inflammation, degree of fibrosis) will define any changes in the echotexture, in particular any changes in the num-

ber, size, and density of the echoes as well as in the degree of attenuation (Figs. 2.22, 2.23, 2.24). The homogeneous distribution of the echoes may vary between segments or regions but still remains one of the basic characteristics of fatty liver.

Causes. By itself, the sonographic finding of fatty liver cannot tell us anything about the underlying cause. Nutrition may be assumed as probable cause if there are also fatty changes

in other organs (abdominal wall, pancreas, body mass index (BMI) > 24), in which case the fatty changes in the liver could be regarded as “normal” findings. However, if a slim patient with a thin abdominal wall (BMI < 24) exhibits fatty liver whose consistency is significantly softer or harder than normal, this finding would have to be assessed as pathological and would mandate further work-up.

Fatty Cirrhosis

In fatty cirrhosis (Fig. 2.25) the liver has turned into a densely firm organ. In many cases there is a distinct shift in the mass relation of the lobes from right to left, with a more significant increase in the mass of the left lobe, and the right hepatic lobe even appearing smaller than normal. The caudate lobe may become quite prominent. The fine nodular surface in fatty cirrhosis can only be visualized by high-reso- lution probes; during routine studies the liver presents with a smooth surface. The individual echoes of the hepatic parenchyma are coarse, hyperechoic, and arranged as a homogeneous texture. A marked degradation in ultrasound

conduction can be detected. One typical finding is the hepatic veins beginning to rarify; however, in contrast to posthepatitic cirrhosis, they are still easily recognized. The portovenous system is prominent and exhibits distinct so-called periportal reinforcement, a scabby knotted bifurcation of the portal vein, enlarged central aspect of the vascular tree, and distinct caliber changes at the more peripheral segments. Other criteria of cirrhosis may also be evident: e. g., ascites, splenomegaly, thickening of the gallbladder wall, and collaterals in portal hypertension.

Fig. 2.25 Fatty cirrhosis. Liver with marked diffuse increase in moderately and coarsely textured echoes, which display irregular graininess and are more densely packed; the junction of the hepatic veins appears stunted, and the peripheral segments of the hepatic veins seem rarefied.

Diffuse Infiltration

Diffuse infiltration with an increased liver size may be the result of extracellular or intracellular substrate deposits.

Intracellular deposits. Apart from fatty infiltration as discussed above, these deposits are also encountered in other storage diseases such as hemochromatosis (Fig. 2.26) and the glycogen storage diseases. Just as in fatty liver, not only the echogenicity of the parenchyma increase but so also does sclerosis of the liver. The vascular architecture, particularly that of the hepatic veins, remains unchanged for a long time.

Extracellular infiltrations. These may be caused by fluid (edema) or cellular mechanisms (e. g., chronic lymphocytic leukemia) and lead to increased size and sclerosis of the

organ, with a typical decrease in parenchymal echogenicity but improved conduction. In many cases the echoes display a homogeneous/diffuse distribution, though regional differences (perivenous) or segmental patterns are also quite common.

Hepatomegaly can be caused by a diffuse infiltration of the liver by clusters of tumor cells or metastasis. These might not be distinguishable from the surrounding liver tissue due to low echogenic differentiation and missing indirect tumor signs (see below) or be only slightly detectable as a parenchymal inhomogeneity (e. g., diffuse liver metastasis in breast cancer or hepatomegaly in CASH seen during ultrasound monitoring in tumors with known liver metastasis; in these cases CEUS is a possibility for further assessment (see below)).

Fig. 2.26 Hemochromatosis. Early stage with diffuse induration of the parenchyma with normal vascular structure. In contrast to the fatty liver, sharp and smooth-margined vessels.