Fatty Liver Remedy

Curing Your Fatty Liver Forever

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Normal Variants, Fatty Liver

In athletic persons, hyperechoic structures (I) that appear to arise from the concave diaphragmatic surface (13) can indent the hepatic dome (9) (Fig. 27.1). These structures are only a few millimeters in width and are im prints caused by thickened muscular bundles that run from the central tendon to the costal insertion of the diaphragm. They have no clinical significance and should not be mistaken for pathologic processes. A similar diaphragmatic muscular bundle can also be seen as a mirror artifact along the pulmonary side of the diaphragm (Fig. 27.2).

Fig. 27.2a

Fig. 27.1b

Fig. 27.1b

A fatty liver or hepatic steatosis produces a diffuse increase in echogenicity of the liver (Fig. 27.3). This increased echogenicity is best appreciated in comparison with the renal echogenicity (29). In normal patients, liver and kidney exhibit about the same echogenicity (Fig. 37.3). The reflection caused by severe hepatic fatty infiltration results in sound attenuation (Fig. 27.4) that increases in the liver commensurate with the distance from the transducer. The resultant decreased echogenicity in the more posterior regions of the liver might not be adequate for evaluation. Do you remember why the hepatic parenchyma appears more echogenic behind the gallbladder (70)? If not, look it up on page 9.

Fig. 27.4a

Fig. 27.4a

Fatty infiltration is not only diffuse throughout the liver, but may also be confined and regional. These focal fatty changes (63) predominantly occur around the gallbladder fossa or anterior to the portal vein (11). The areas of increased fat content are sharply demarcated and more echo-genic than the surrounding hepatic parenchyma (9). They can assume a geographic configuration (Fig. 28.1) and have no space-occupying effect. Adjacent hepatic veins (10) or the branches of the portal veins (11) are not displaced.

The falciform ligament (8), which is composed of connective tissue and surrounded by fat, is seen as a similar echogenic structure that sharply interrupts the adjacent normal hepatic parenchyma (Fig. 28.2). It must be distinguished from focal fatty infiltration.

Diffuse fatty infiltration might not involve the entire liver, resulting in focal fatty sparing (62). These regions of relatively reduced fatty content are primarily found in the immediate vicinity of the portal vein or gallbladder (14) (Fig. 28.4). Again, this finding lacks a space-occupying component. Adjacent vessels are not displaced (Fig. 28.3); peripherally located areas of increased or relatively reduced fatty infiltration show no bulging hepatic border and do not project into the gallbladder, as is sometimes the case with tumors or metastases.

The branches of the portal vein (11) can be distinguished from hepatic veins by their hyperechoic outline. This appearance is caused by the density difference between the portal vein wall, periportal connective tissue, and accompanying biliary duct and hepatic artery. This hyperreflectivity of the portal vein wall (5) becomes accentuated in the vicinity of the porta hepatis (Fig. 28.2) where it should not be mistaken for focal fatty infiltration. Since the hepatic veins (10) traverse the parenchyma without concomitant vessels, they lack a density difference and do not show any wall hyperecho-genicity. Only a large hepatic vein perpendicular to the sound beam can exhibit a hyperechogenic wall.

Fig. 28.1a

Fig. 28.1a

Fig. 28.4a

d 36.5mm 38.5hm

Hepatic cysts (64) can be congenital (dysontogenetic) or acquired. In contrast to congenital biliary dilatations (Caroli syndrome), the congenital cysts contain no bile but serous fluid (Fig. 29.1). They are of no clinical consequence unless associated with polycystic kidneys (Fig. 38.3) (risk of renal failure).

The criteria to distinguish a cyst from a lesion of low echogenicity are as follows: echo-free content, spherical shape, smooth outline, distal acoustic enhancement (70), and edge effect (see p. 9). Congenital cysts can exhibit indentations or delicate septa, and parasitic hepatic cysts must then be excluded (Fig. 30.3). Diagnostic difficulties can arise when internal echoes are found secondary to intracystic hemorrhage.

Hepatic hemangiomas (61) are homogeneously echogenic (bright) in comparison to the remaining hepatic tissue (9), have a smooth outline, and lack an echogenic rim. A draining, but not dilated, hepatic vein (10) can be characteristically found in their immediate vicinity (Fig. 29.3). Most hemangiomas are small (Fig. 29.2), but they can reach considerable size and are then generally of rather heterogeneous echogenicity, making it difficult to establish a definitive diagnosis. The lesion (54) shown in (Fig. 29.4) can represent a large hemangioma or malignant tumor, but actually is a focal nodular hyperplasia (FNH), which is not always iso-echoic in relation to the surrounding hepatic parenchyma. Unclear cases can be further evaluated by a dynamic CT with serial images after bolus injection of contrast medium. A hemangioma exhibits a characteristic enhancement and delayed washout. How would you interpret the echo-free areas (68, 69) seen in Figure 29.3 b? The answer can be found in the key at the end of this workbook.

Fig. 29.1a

Fig. 29.1b

Fig. 29.4a

Fig. 29.4a


Another important group of focal hepatic changes comprises inflammatory and parasitic changes. The primary causes of a focal inflammation are cholangitis, fungal disease, and hematogenous seeding, particularly in immunosuppressed patients.

Hepatic abscesses (58) can produce a rather variable sonomorphology, including an anechoic center due to liquefaction (Fig. 30.2), heterogeneous foci surrounded by a rim of decreased echogenicity, and echogenic lesions (Fig. 30.1). The effectiveness of inserted drainage catheters (59) can be easily monitored by follow-up sonographic examinations (Fig. 30.1). If compression of adjacent biliary ducts has led to obstruction (cholestasis), bile can be drained by internal stents into the duodenum or percutaneous transhepatic catheters into a collection bag.

Occasionally, an infectious process can introduce air bubbles (60) into the biliary ducts (Fig. 30.2). Intraductal air without implying a hepatic (9) infection can be seen after endoscopic retrograde cholangiopancreatography (ERCP) as well as in patients with a papillotomy or biliary-enteric anastomosis.

The most common parasitic involvement of the liver is cystic echinococcal disease (Echinococcus cysticus), which characteristically produces several daughter cysts within a large cyst. Such hydatid cysts should not be aspirated since this might lead to peritoneal seeding of the larvae. Echinococcal disease can be treated medically with mebendazole or surgically by excision. Alveolar echinococcal disease (Echinococcus alveolaris) poses more sonographic difficulties. A lesion with a mixed solid, liquid, and cystic pattern, traversed by several septa, is typically found (54) (Fig. 30.3). Differentiating this finding from a primary hepatocellular carcinoma, metastasis (compare Fig. 32.3), abscess, or old hematoma is virtually impossible.

Checklist of Criteria for Establishing a Cyst:

• Spherical configuration

• Echo-free interior

• Smooth outline

• Distal acoustic enhancement

• Sharply defined distal wall

• Edge shadowing due to critical angle phenomenon

Fig. 30.1 a Fig. 30.2a Fig. 30.3a


In addition to chronic alcoholism, the possible causes of cirrhosis include viral hepatitis, metabolic disorders, and exposure to toxic environmental substances. Latent cirrhosis with hepatic decompensation can be present without sono-graphically detectable changes, and sonography is not suitable for excluding a cirrhosis. More advanced stages produce several sonographic changes that can serve as criteria for the presence of a cirrhosis.

While the normal liver (9) exhibits a thin echogenic capsule along its border (Fig. 26.3), the cirrhotic liver has an irregular surface (small undulations and bumps), which causes increased sound scattering with loss of the normal capsular reflection. This results in absent or only patchy capsular visualization. The absence of a capsular line is best appreciated when the liver is surrounded by ascites (68) (Fig. 31.1). Furthermore the peripheral vasculature becomes rarefied in cirrhosis (Fig. 31.1), with the remaining visualized vessels showing a variable diameter and an increased angle, at their confluence (> 45°). Normal hepatic veins (10) have a straight course, join each other at an acute angle and are visible to the hepatic periphery (Fig. 25.2). In cirrhosis, the portal vein branches close to the porta hepatis show thickening of their hyperreflective walls and sudden changes in caliber ("pruned portal tree"). Regenerating nodules are of normal echogenicity and recognized only indirectly by displaced adjacent vessels. Finally, a deformed and biconvex hepatic configuration, decreased pliability (as revealed when pressing down the transducer over the liver), and an enlarged and rounded left lobe or caudate lobe suggest cirrhosis.

The complications of cirrhosis include portal hypertension and its sequelae (see p. 24), ascites (68), and hepatocellular carcinomas (54) that arise from long standing cirrhosis (Fig. 31.2). Therefore, a cirrhotic liver must be carefully and thoroughly (!) scrutinized for pathologic lesions. Only the late stage of cirrhosis produces a shrunken liver (Fig. 31.2). The hepatocellular carcinomas (54) can be iso-echoic in relation to the remaining hepatic parenchyma (9) and might only be detectable by the convex displacement of adjacent hepatic veins (9) (Fig. 31.3).

Checklist of Criteria for Establishing Hepatic Cirrhosis:

• Absence of thin, hyperechoic capsular line

• Paucity of peripheral hepatic vessels

• Obtuse angulation of the hepatic veins > 45

• Accentuated echogenic wall of the portal vein

• Abrupt caliber changes of the branches of the portal vein

• Regenerating nodules with displacement of adjacent vessels

• Nodular liver contour (advanced stage only)

• Contracted liver (advanced stage only)

• Signs of portal hypertension

Fig. 31.2a

Fig. 31.3a

Fig. 31.2a

Fig. 31.3a


Secondary neoplastic lesions (metastases) in the liver do not only arise from primary tumors of the intestinal tract, but also from primary tumors in the breast and lung. The sonographic findings are polymorphic. Hepatic metastases (Fig. 32.2) from colorectal carcinomas are often echogenic (56), presumably related to neovascularity secondary to their relatively slow growth. The more rapidly growing metastases from bronchogenic or mammary carcinomas consist almost exclusively of tumor cells and have the tendency to be more hypoechoic. In view of their multifarious presentation, metastases cannot be reliably assigned to any particular primary tumor.

Characteristically, metastases (56) exhibit a hypoechoic halo or rim as seen in Figures 32.1 and 32.2. This hypoechoic zone could represent proliferating tumor or perifocal edema. Central necrosis (57) can frequently be seen as cystic areas caused by liquefaction (Fig. 32.3). Large metastases generally exhibit a space-occupying feature as evidenced by displacement of adjacent vessels. They can compress biliary ducts, possibly leading to regional intrahepatic cholestasis (Fig. 34.2). If located peripherally, they frequently (but not necessarily) expand the hepatic contour that is seen as a localized convexity.

After chemotherapy, various signs of tumor regression can be encountered, such as heterogeneous scars, calcifications, or partial cystic liquefaction, depending on the therapeutic effect. Such regressively altered metastases or small metastatic nodules cannot be easily separated from areas of cirrhotic transformation. It is crucial to follow these findings sonographically to assess their growth potential. Alternatively, a percutaneous needle biopsy under sonographic or CT guidance can be obtained. Multiple metastases that vary in size and echogenicity suggest several episodes of hematogenous spreads.

Do you remember why the hypoechoic bands (45) seen in Figure 32.1 appear in the liver and why the region in between (70) is more echogenic (brighter) than the remaining hepatic parenchyma (9)? Just keep in mind that the gallbladder (14) lies between both findings and the transducer, with the gallbladder wall (80) hit tangentially by the sound beam. If you are still puzzled, you should go back to page 9.

Fig. 32.2a

Fig. 32.2a

Before you proceed from the sonographic examination of the liver to the evaluation of the gallbladder, you should try to work through the following questions. The required drawings should be done on a piece of paper. The answers to the questions 6a-c can be found on page 76, but check the answers only after all the questions have been answered so that the suspense does not disappear too early! (You would otherwise inadvertently read the answers to the second and third image questions, that are listed next to each other on page 76.)

O Fry to draw from memory the body marker that shows the section of the porta hepatis. Then make a drawing in the shape of a cone coffee filter and systematically enter from front to back all lines, organs, and vessels that can be expected to appear in this sonographic section. Compare your drawing (but only after completion) with the findings in Figures 23.2 b and c. Did you place all major structures in the lesser omentum at the correct depth? If not, repeat this exercise until you succeed without making any mistakes.

9 What is the name of the sonographic section for measuring the luminal diameter of the hepatic vein? Name this section, draw the appropriate body marker, and then proceed as in question 1.

9 What sonographic section is used to measure the liver? What are the maximum diameter values and what are the terms given to them? Can you draw such an image from memory? You already know how to proceed (see above).

Q Write down the three characteristic findings of portal hypertension and the five characteristic findings of cirrhosis. Compare your answers with the material on pages 24 and

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