Fatty liver (steatosis hepatis)

Concerning the liver in the oncologic field, PET/CT technique plays a very important role in the detection of metastases.

14.1.2. Diffuse liver diseases

The concept of diffuse liver disease is an ultrasound-morphologic appearence indicating a sort of disease. However, this is non specific, the sort of the illness can only be certified by biopsy.

Diffuse liver disease alters the reflection, reduction, homogenicity and vessel structure of the parenchyma. In addition, it can modify the liver's size and shape.

The reflection change indicates the modification of the acoustic echo amplitudes in the liver parenchyma, usually the amplitude increases. The diffuse decrease of the reflectivity can also happen rarely (acute hepatitis, leukemia, lymphoma, toxic shock, acut right heart failure).

In case of increased beam absorption or distal acoustic weakening, the far liver areas can only be imaged minimally or not at all if the usual amplification is applied. This can be usually corrected partly by the adjustment of the depth amplification.

Shape abnormalities include the rounded liver margin, surface incongruences (cirrhosis) and the hypertrophy of the left lobe or caudate lobe as well.

Most frequent reasons of diffuse liver diseases:

 fatty liver

 cirrhosis

 chronic hepatitis

 circulation disturbances

 metabolic and storage diseases

 diffuse miliary metastasis

 leukemia, lymphoma

14.1.2.1. Fatty liver (steatosis hepatis)

The triglicerides accumulate in the hepatocytes. The parenchyma reflectivity and the beam absorption increases (Figure 12). The increase of the reflectivity is usually homogeneous, rarely inhomogeneous.

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Figure 12: Fatty liver, small HCC, distal attenuation

Possible forms of fatty liver: diffuse steatosis or focal steatosis (focal deposition)

The focal forms develop due to the different perfusion statuses. It is characterized by no space occupying effect (no vessel displacement), and their appearence can change significantly during the check-up examinations. In the areas of decreased portal circulation (eg., ventral to the portal vein, next to the gallbladder) less fat is deposited, this area appears focally

hypoechoic - focal sparing (Figure 13). In case of focal deposition, round, nodular or girland (chart-like) hyperechoic infiltration areas develop in the intact liver.

Figure 13: Focal sparing next to the gallbladder

MR is rarely performed as imaging the diffuse fatty liver. Preferably in case of an imaging of other reason can come to that the diffuse steatosis of the liver, which was shown to be fatty by conventional techniques, (higher T1 signal intensity, less T2 signal intensity as usual) will be imaged by fat suppression.

In addition, differentiation of focal deposits / focal sparings (next to the gallbladder bed, portal branches, lig.teres hepatis) is available, too. Essential to note that there is no mass effect. (The exact extent of steatosis can be shown by proton spectroscopic imaging.) 14.1.2.2. Liver cirrhosis (cirrhosis hepatis)

No direct association among the extent of fibrosis, the degree of the dysfunction and the ultrasound morphology was detected, normal liver structure can be observed in case of an extended encephalopathy as well. The right lobe size can decrease, left lobe and caudate lobe hypertrophy develops. Lateral segment of the left lobe can increase besides the decrease of the medial segment's size. The fibrosis itself does not change the parenchyma reflectivity.

179 Increased reflection can be observed if it accompanies with fat deposition as well. On the other hand, rough echostructure, inhomogenecity can be observed in the parenchyma due to the miliary (4-5 mm or smaller) regenerative nodules. Bigger nodules result extensive surface incongruences (Figure 14).

Figure 14: Liver chirrosis, nodular surface, ascites

The regenerative nodules can appear as moderately hypoechoic lesions, mimicing

hepatocellular carcinoma which develops more frequently based on cirrhosis related to B and C viral hepatitis. The nature of the developing nodule can only be clarified by biopsy in some cases. Small amount of free abdominal fluid (ascites) can be imaged well by US. Signs of portal hypertension can be also recognised very well, however, the exact determination of the circulation statuses goes over the possibilities of the rutine US examination obviously. In this case, an accessory color duplex US examination using an appropriate top category device is necessary.

US features of portal hypertension:

 portosystemic collaterals can be seen (umbilical vein recanalisation, caput Medusae, splenorenal shunts, gastric veins)

 hepatofugal flow

 pulsatile portal Doppler spectrum

 dilation of the splenoportal veins

 disappearence of caliber change of the splenic vein

 compressed intrahepatic veins

 pathologic Doppler curve of the hepatic vein

 decreased portal flow speed

 decreased portal flow blood volume

 in postprandial situation, loss of portal flow increase

 in postprandial situation, loss of RI increase during the examination of the hepatic artery

MR respects:

The fibrotic conversion weaves around the portal venous sinusoids in cirrhosis, leading to blood redistribution in the liver and in the abdomen by the incapacitation of the flow. The hepatic surface is often irregular, bumpy and characteristically the right lobe is more frequently affected as the left one and the caudate lobe, which ones respond by reactive hyperplasia to the reduction of the right lobar parenchyma.

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Because of the fibrosis, the signal intensity is commonly moderately decreased on the T1-weighted images, but not on a constant way.

More importantly we can rely on the evaluation of the morphological lesions such as the nodular appearence of the liver parenchyma with the distorted vessels, enlarged caudate lobe and the secondary signs such as: dilatated collateral vessels (which can be imaged exquisitely by MR with signal void), splenomegaly and ascites.

MR angiography images the collateral and portal vessels replacing the invasive DSA. MRI is also suitable for the control of the surgically prepared portocaval shunts. Extension and

degree of the ascites can be clearly imaged by MRI (T2-weighted images).

As a complication of the long-standing portal hypertension or in case of a definitive liver tumor by the formation of a direct tumor thrombus in the portal vein, portal vein thrombosis can develop. Accordingly, further cumulative portal hypertension, ascites and varices of various extent evolves. The thrombotic portal vein can be fairly demonstrated by MR.