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60 ULTRASOUND: THE REQUISITES

Box 3-2 Hepatic Target Lesions

are not nearly as common as the malignant lesions just mentioned. Hemangioma is a very common lesion but only rarely produces a target appearance. It is important to realize that target lesions are much more likely to be malignant than benign (Box 3-2).

In addition to target lesions, metastases can have a variety of sonographic appearances, as illustrated in Figure 3-14. Although it is not possible to predict the primary tumor based on the sonographic appearance of the liver metastases, some trends are useful. Hyperechoic metastases tend to arise from the gastrointestinal tract, most commonly from the colon. Neuroendocrine tumors are another relatively common cause of hyperechoic metastases. The colon is also the most common source for calcified metastases, although mucinous primary tumors of the ovary, breast, and stomach can also calcify (Box 3-3). Cystic hepatic metastases are unusual but do occur. They generally have thick walls, thick septations, or obvious solid components and therefore do not mimic simple hepatic cysts. Cystic

Box 3-3 Calcified Hepatic Masses

spaces in metastases may result from a cystic primary tumor (ovary) or from necrosis, such as squamous cell carcinomas, sarcomas, and large lesions from any primary tumor.

With widespread hepatic metastases the liver may appear diffusely heterogeneous and it may be difficult to identify individual lesions. High-resolution views focused on the superficial aspect of the liver increase the chance of identifying individual lesions (Fig. 3-15). This pattern is particularly typical for breast cancer. The differential diagnosis for this appearance includes cirrhosis, hepatic fibrosis, hepatic lymphoma, fatty infiltration, and diffuse hepatocellular carcinoma (Box 3-4).

In many clinical situations when metastatic disease is suspected, definite tissue confirmation is required before therapy can be initiated. With experience, liver lesions can be sampled with ultrasound guidance with a high degree of success. Even lesions less than 1 cm can be sampled with 90% success rates (Fig. 3-16). Because the course of the needle can be followed in real time, ultrasound-guided biopsies can be performed much more rapidly than CT-guided biopsies. When there is a known extrahepatic primary malignancy, it is usually

Liver 61

Box 3-4 Diffuse Hepatic Inhomogeneity

adequate to perform fine-needle aspirations (using 22to 25-gauge needles) for cytologic analysis. When there is no known primary tumor, suspected liver metastases should be sampled with core needles (using 18to 20-gauge needles). This allows immunohistochemical studies to be done so that the primary tumor can be identified with more certainty.

Hepatocellular Carcinoma

Hepatocellular carcinoma (HCC) is the most common primary malignancy of the liver. It is sometimes referred to as hepatoma. Although HCC can occur in normal livers, it is strongly associated with chronic liver disease, especially hepatitis B and C infection and cirrhosis. HCC is a major health problem in Asia and sub-Saharan Africa, owing to the high prevalence of hepatitis and aflatoxin ingestion. In non-Asian populations, alcoholic cirrhosis is the most important condition predisposing to HCC. Other predisposing factors include hemochromatosis, Wilson’s disease, and type I glycogen storage disease.

Cirrhotic livers pathologically display a spectrum of nodular lesions. Regenerating nodules form because of

replication of hepatocytes and resulting compression and distortion of adjacent stroma and fibrous tissue. Adenomatous hyperplasia (also known as nodular hyperplasia, adenomatous hyperplastic nodules, and microregenerative nodules) is defined as a nodule that is significantly larger than the other regenerative nodules in a cirrhotic liver. They are usually larger than 1 cm and may contain atypical cells or actual malignant foci. In the latter case they are considered early HCC. It is believed that many HCCs develop from the following sequence: regenerative nodule to adenomatous hyperplasia to atypical adenomatous hyperplasia to HCC.

The growth pattern of HCC is quite variable: it may be solitary, multifocal, or diffuse and infiltrating. One pattern that is typical is a large dominant lesion with scattered smaller satellite lesions. Echogenicity is also variable, and in general the sonographic appearance is nonspecific. Figure 3-17 shows a variety of appearances of HCC. Calcification and cystic changes can occur but are very unusual. Most HCCs are hypervascular with chaotic-appearing internal vessels. Post-contrast scans are reported to show enhancement to a greater degree than adjacent liver parenchyma.

HCC has a strong tendency to invade the hepatic vasculature. Estimates of venous invasion range as high as 30% to 60% for the portal veins and 15% for the hepatic veins. These figures tend to apply to extensive tumors that are typically seen in non-screened populations. The incidence of venous invasion is much lower for small tumors that are typically seen in high-risk populations that are being screened for HCC. Regardless of the rate of vascular invasion, detection of intravenous soft tissue in a patient with a hepatic mass or masses strongly suggests HCC. Tumor thrombus tends to expand the lumen of the vein to a greater extent than bland thrombus. In

many patients, arterial flow is detectable within tumor thrombus on Doppler analysis. This is a reliable sign that distinguishes tumor thrombus from bland thrombus. Because the tumor thrombus and its arterial supply invades peripheral portal veins and then grows into the more central portal veins, the arterial flow in tumor thrombus is hepatofugal in direction.

Fibrolamellar HCC is an unusual variant that occurs in younger patients without coexistent liver disease and has a much better prognosis than typical HCC. It is usually solitary and is more likely to contain calcification than typical HCC (Fig. 3-18). The central scar that is often present histologically is only occasionally seen sonographically.

Sonography is widely used in Asia to screen patients at risk for HCC, with a reported sensitivity of up to 95%. In North America, sensitivity is lower owing to the larger body habitus of the patient population. Nevertheless, ultrasound is frequently used in North America in the surveillance schemes of patients with hepatitis. In advanced cirrhosis, the diffuse hepatic inhomogeneity and nodularity reduces sensitivity as low as 50%. Interestingly, large tumors that involve liver segments diffusely are often harder to detect with sonography than are smaller tumors. Given this, it is likely that sonographic sensitivity is higher when patients are screened earlier in their disease, before the development of HCC. Any solid mass detected on an initial sonogram in a patient with cirrhosis should be considered malignant until proved otherwise. Even masses that have a typical appearance of hemangioma have a 50% chance of being HCC. In screened high-risk populations, new masses that develop over the course of surveillance have a risk of being HCC approaching 100%, regardless of the appearance.

64 ULTRASOUND: THE REQUISITES

Figure 3-18 Fibrolamellar hepatocellular carcinoma. Transverse view of the left lobe of the liver shows a solid mass (cursors) with a focal region of calcification (arrowhead). The patient was a 23-year-old man with no history of previous liver disease.

Lymphoma

Hepatic lymphoma usually presents in the setting of advanced disease elsewhere and is of the non-Hodgkin variety. Primary hepatic lymphoma occurs most often in the setting of an immunocompromised state such as AIDS or post transplantation. On sonography, it usually simulates metastatic disease, typically appearing as target lesions or as homogeneous hypoechoic masses

A

(Fig. 3-19). Unlike metastatic disease, it is very unusual for lymphoma to appear hyperechoic, to contain cystic spaces, or to contain calcification. Because lymphoma is a very homogeneous tumor, it may generate very few internal reflections. This is why it is typically hypoechoic. In rare instances, it can appear anechoic and simulate a cyst. It may also have some detectable posterior enhancement, although this is less than expected for a cyst of similar size.

INFECTIONS

Pyogenic Abscess

Pyogenic liver abscesses are most often a secondary development of seeding from intestinal sources, such as appendicitis or diverticulitis; as a direct extension from cholecystitis or cholangitis; or from endocarditis. Like abscesses elsewhere in the body, hepatic abscesses typically appear as complex fluid collections with a mixed echogenicity (Fig. 3-20). However, it is important to realize that abscesses in the liver may mimic solid hepatic masses. The presence of through transmission will often provide a clue to the liquefied nature of the mass. Contrast medium–enhanced CT usually shows findings characteristic of an abscess even when the ultrasound evaluation shows an apparently solid lesion. Abscesses

B

may also appear as thick-walled cystic lesions or as cysts with fluid-fluid levels. Gas may result in highly reflective regions with shadowing or ring-down artifacts. Abscesses may calcify with healing. The differential diagnosis for these various appearances primarily includes hematoma, hemorrhagic cyst, and necrotic or hemorrhagic tumor.

sonographic appearance is a target lesion with a central echogenic region and a peripheral hypoechoic halo. Early lesions may have a hypoechoic focus centrally, caused by necrosis and fungal elements. This appearance has been called a “wheel within a wheel.” With healing, candidal abscesses become uniformly hyperechoic and ultimately may calcify.

Fungal infections of the liver usually occur in immunocompromised patients; the most common organism is Candida. Although it usually causes very small lesions (referred to as microabscesses), larger lesions occasionally occur (Fig. 3-21). The typical

Pneumocystis carinii infection of the liver is becoming increasingly common in patients with AIDS. Aerosolized pentamidine controls the infection in the lungs but does not achieve the sufficient systemic concentration necessary to prevent dissemination to other

C

organs, including the liver, spleen, pancreas, and kidneys. Pathologically, the lesions in these various organs are granulomas that may or may not show calcification. Sonographically, the appearance is very characteristic and consists of multiple echogenic foci scattered throughout the liver (Fig. 3-22). The same appearance has been reported in a very limited number of cases

Figure 3-22 Pneumocystis carinii infection of the liver. Longitudinal view demonstrates multiple diffuse non-shadowing small hyperechoic foci throughout the liver. Similar foci were seen in the kidneys bilaterally.

Figure 3-21 Fungal microabscesses in different patients. A, Conventional gray-scale image showing multiple tiny (<1 cm) hypoechoic lesions. B, Magnified image showing an approximately 1-cm hypoechoic lesion with a small central echogenic focus. C, Magnified image showing multiple 1 cm or smaller lesions with a “wheel within a wheel” pattern.

of Mycobacterium avium-intracellulare and cytomegalovirus infection of the liver. Small punctate calcified granulomas are very common in areas where histoplasmosis is endemic.

Parasitic Infection

Echinococcal disease is usually caused by a tapeworm, Echinococcus granulosus. Humans are a secondary host who get infected by ingesting egg-infested vegetables. The liver is the most commonly affected organ, although the lungs, spleen, bones, kidneys, and central nervous system can also be affected. Echinococcal cysts in the liver have an external membrane called the ectocyst and an internal germinal layer called the endocyst. In addition, the host forms a fibrous capsule around the cyst that is called the pericyst. Sonographically, hydatid cysts may appear as relatively simple cysts, cysts with multiple internal daughter cysts, cysts with detached floating endocystic membranes, cysts with internal debris, and cysts with internal or peripheral calcification (Fig. 3-23).

Other parasitic infections of the liver include amebic abscesses and schistosomiasis. Amebic abscesses result from primary colonic involvement with hepatic seeding through the portal vein and are indistinguishable from pyogenic abscesses. Schistosomiasis is rare in the United States but quite common worldwide. Ova reach the

peripheral portal triads and cause a granulomatous reaction. The resulting periportal fibrosis appears as thickened echogenic portal triads.

TRAUMA

In the setting of blunt abdominal trauma, sonography is now being used to evaluate for potential hemoperitoneum. However, acute hepatic lacerations are difficult to detect with sonography. This is because acute hematomas are often isoechoic to liver parenchyma and produce only subtle alterations in hepatic echogenicity (Fig. 3-24). Like hematomas elsewhere, hepatic hematomas become progressively more liquefied over a

matter of days to weeks. Because of this limitation, CT is the modality of choice for detecting and quantifying liver hematoma. Sonography is a useful problem-solving tool when questions concerning the biliary tract or hepatic vasculature arise.

DIFFUSE PARENCHYMAL DISEASE

Hepatitis

Hepatitis usually results in no detectable sonographic abnormality. In a limited number of patients it can cause increased echogenicity of the portal triads, which appear as small bright areas on views of the liver periphery (Fig. 3-25). This appearance has been referred to as

the “starry sky” sign. Unfortunately, it can be seen in the absence of hepatitis, and, when present, it is often subtle. Hepatitis can also produce marked thickening of the gallbladder wall, contraction of the gallbladder lumen, and periportal lymphadenopathy.

Fatty Infiltration

Fatty infiltration of the liver is characterized pathologically by intracellular deposition of triglycerides within hepatocytes. It is extremely common in North America and is usually due to obesity. Other common causes include alcohol abuse, cholesterol-lowering medications, and certain chemotherapy agents. In addition, corticosteroids, diabetes, malnutrition, total parenteral nutrition, and toxins (such as carbon tetrachloride) are potential causes.

Fatty infiltration of the liver causes a variety of fairly characteristic abnormalities on sonography. These are illustrated in Figure 3-26. Fatty infiltration most often manifests in a diffuse distribution and results in uniform increased echogenicity of the liver. Because the normal liver is only slightly more echogenic than the kidney, the diagnosis of fatty infiltration is best made by noting a marked discrepancy between the hyperechoic liver and the less echogenic kidney. In addition, because the normal pancreas is more echogenic than the liver, fatty infiltration should be considered whenever the liver appears hyperechoic compared with the pancreas. More advanced fatty infiltration will cause significant sound beam attenuation and will make the hepatic vessels, and in some cases the diaphragm, difficult to visualize. Another characteristic of fatty infiltration is an increased concentration of tiny reflections from the liver parenchyma that result in a finer echotexture than

normal liver. With experience, this echotexture can be recognized with reasonable accuracy.

In many cases of otherwise diffuse fatty infiltration, there will be focal areas of spared normal liver parenchyma that appear hypoechoic with respect to the fatty infiltrated parenchyma. If the fatty infiltration is not recognized, the spared areas of normal parenchyma may be mistaken as focal hypoechoic lesions. Fortunately, the spared parenchyma is usually located in front of the right portal vein or portal bifurcation or around the gallbladder. The combination of these typical locations and the fact that focal sparing is usually not spherical generally allows for a confident diagnosis of focal fatty sparring. In fact, when the presence or absence of fatty infiltration in the liver is uncertain, it is often possible to detect the characteristic areas of focal sparing, which allows for a more confident diagnosis of fatty infiltration in the remainder of the liver.

In cases in which fatty infiltration of the liver is patchy, the geographic margins of the abnormally echogenic fatty liver and the lack of mass effect on hepatic vessels serve as clues to the diagnosis. Occasionally, fatty infiltration will be focal and nodular. This frequently occurs in the anterior aspect of the left lobe (especially the medial segment) immediately adjacent to the falciform ligament. Another typical location for focal fatty infiltration is anterior to the portal vein bifurcation, which is exactly where focal fatty sparing also typically occurs. The paradoxical deposition and lack of deposition of fat in this location is not well understood but may be related to relative differences in perfusion to this area. Regardless of the cause, if an elongated hyperechoic lesion is seen in these typical locations in patients with no known primary malignancy, the diagnosis of focal fatty infiltration is almost