Core Curriculum, The: Ultrasound
1st Edition

Abdomen Ultrasound
Imaging Technique
The abdomen is examined with sector or curved array transducers using frequencies of 5.0 to 2.25 MHz. The highest frequency that allows adequate penetration is used [1]. Routine examinations are conducted following a minimum fast of 4 hours to allow for filling of the gallbladder. Emergency examinations are conducted without patient preparation.
The liver is examined in transverse and longitudinal planes. The entire liver, porta hepatis, portal veins (PVs), hepatic veins, and intrahepatic inferior vena cava (IVC) are examined and documented on recorded images. Much of the liver is examined using an intercostal approach. Having the patient breathe in deeply will depress the liver for examination along the costal margin. An image that includes the liver and the right kidney should always be obtained to compare the relative echogenicity of the parenchyma of each organ. The right pleural space and right hemidiaphragm are included in the examination.
The intrahepatic bile ducts are examined along with the PVs and peripheral portal triads. Recorded images should include the right and left branches of the PVs and bile ducts. The common bile duct (CBD) is visualized in the porta hepatis and its diameter is measured (see Figs. 2.6, 2.7). Its course should be followed through the pancreatic head to its terminus in the descending duodenum.
The gallbladder (GB) is examined in its long and short axes with careful inspection for gallstones, luminal contents, wall thickness, and surrounding pathology. The examination is conducted with the patient in supine, left lateral decubitus, erect (sitting), and prone positions as needed to aid in the detection of gallstones and to document their mobility.
The pancreas is examined by transverse and sagittal imaging in the epigastrium. The left lobe of the liver serves as a sonographic window to the pancreas. Visualization of the pancreas is easy when the left lobe is large and is difficult when the left lobe is small. Air in the transverse colon and small bowel may obscure the pancreas and must be moved out of the way by graded transducer pressure. The patient is told that the examiner will “press hard” and is asked to tell the examiner if the maneuver becomes painful. In my experience other touted maneuvers, such as filling the stomach with water, seldom are worth the effort. Only graded compression works reliably to visualize the hidden pancreas. The

splenic vein (SV) serves as the major sonographic landmark for the neck, body, and tail of the pancreas. The tail region is often obscured by gas in overlying small bowel. Masses in the tail region may be seen by using a left lateral approach to image the tail in the splenic hilum region through the spleen. The pancreatic head is identified by finding the PV commencement at the junction of the SV and superior mesenteric vein (SMV). The head envelops this confluence and extends caudally to wrap under the SMV as the uncinate process. This caudal extension of the head and the uncinate process is best shown in transverse plane. This area is particularly important to examine because it includes the terminus of the CBD and the pancreatic duct into the duodenum. Many disease processes (tumors, obstructing stones) involve this area.
The spleen is best imaged with the patient supine utilizing a posterior intercostal approach in the left upper quadrant [2,3]. Unless the spleen is enlarged, placing the patient in a right lateral decubitus position may be counterproductive because hyperexpansion of the left lung obliterates the narrow intercostal window to the spleen.
The peritoneal cavity is carefully inspected for the presence of ascites, blood, abscess, or tumor. Examination should include the major peritoneal recesses including the subdiaphragmatic spaces on both sides, the hepatorenal fossa (Morison’s pouch), the paracolic gutters, and the pelvis and cul de sac.
US examination of the abdomen is commonly extended to include the retroperitoneum, kidneys, abdominal aorta, and IVC. These examinations are discussed in subsequent chapters.
Localization of tumors to segments of the liver is critical in the planning of surgical resection. The international Couinaud (pronounced “kwee-NO”) system of hepatic nomenclature is currently utilized [4,5,6]. This system is based on the distribution of portal and hepatic veins. The right and left lobes are divided by the main hepatic fissure defined by the middle hepatic vein in the superior portion of the liver and by a line connecting the GB with the IVC in the inferior portion of the liver. Each segment has a branch PV at its center and a hepatic vein at its periphery. Segments are numbered clockwise starting with the caudate lobe (segment 1), left lobe (segments 2-4), and right lobe (segments 5-8) (Table 2.1, Fig. 2.1). The caudate lobe is anatomically distinct, extending between the IVC and the left lobe and separated from the left lobe by the fissure of the ligamentum venosum (Fig. 2.2).
Blood supply to the liver is provided by both the PV (~70%) and the hepatic artery (~30%). This dual blood supply makes infarction rare in the liver. Both enter the liver at the porta hepatis and divide into right and left lobe branches. Doppler documents blood flow direction in both vessels as into the liver (hepatopetal). Spectral Doppler shows a low-resistance, arterial flow pattern for the hepatic artery with forward flow throughout the cardiac

cycle. Diastolic flow velocity increases and resistance index decreases after eating. The PV shows continuous antegrade venous flow with small pulsations that mirror the cardiac cycle. Mean velocity in the PV is 15-18 cm/sec.
Table 2.1: Couinard’s Liver Segments
American Name International Name
1 Caudate lobe Caudate lobe
2 Left lobe, lateral segment Left lateral superior subsegment
3 Left lobe, lateral segment Left lateral inferior subsegment
4 Left lobe, medial segment Left medial subsegment
5 Right lobe, anterior segment Right anterior inferior subsegment
6 Right lobe, anterior segment Right anterior superior subsegment
7 Right lobe, posterior segment Right posterior inferior subsegment
8 Right lobe, posterior segment Right posterior superior subsegment
Figure 2.1 Couinaud’s Liver Segments. Diagrammatic representation of Couinaud’s numerical liver segments. FLT, fissure of the ligamentum teres; IVC, inferior vena cava; LHV, left hepatic vein; MHV, middle hepatic vein; RHV, right hepatic vein. Adapted from Smith D, Downey D, Spouge A, et al. Sonographic demonstration of Couinard’s liver segments. J Ultrasound Med 1998;17:375-381.
Venous drainage of the liver is by three major hepatic veins that enter the IVC just below the diaphragm (Fig. 2.3). The right hepatic vein divides the anterior and posterior segments of the right lobe and enters the IVC separately. The middle and left hepatic veins may join just before entering the IVC. The middle hepatic vein separates the right and left lobe while the left hepatic vein divides the medial and lateral segments of the left lobe. Hepatic veins have no valves and their blood flow reflects the triphasic pulsatility of the IVC and right atrium. Spectral Doppler shows prominent antegrade flow toward the heart during systole reflecting movement of the tricuspid valve toward the cardiac apex. A second antegrade peak is produced in early diastole by opening of the tricuspid valve. In late diastole flow is reversed in the hepatic vein owing to atrial contraction. The caudate lobe drains directly into the IVC via small venous channels.
The liver parenchyma has homogeneous echogenicity equal to or slightly greater than the echogenicity of renal parenchyma (Fig. 2.4). Liver echogenicity is slightly less than that of the spleen. Portal triads are seen as echogenic foci well out into the periphery of the liver

(Fig. 2.4). Fissures and ligaments are usually invested in fat and are highly echogenic (Fig. 2.2). The fissure of the ligamentum teres in the left lobe must not be mistaken for an echogenic mass (Fig. 2.5).
Figure 2.2 Caudate Lobe. The caudate lobe (c) is between the inferior vena cava (I) and the fissure of the ligamentum venosum (long arrow). The inferior vena terminates in the right atrium (A). The curved arrow indicates the right hepatic vein. Also seen are the portal vein (p) and the hepatic artery (short arrow).
Figure 2.3 Normal Hepatic Veins. Transverse image through the liver obtained just below the diaphragm shows the right (R), middle (M), and left (L) hepatic veins converging to enter the inferior vena cava.
Biliary Tree
Intrahepatic bile ducts (IHBD) course in the portal triads with the PVs and hepatic arteries. In the portal triads the relationship of the three structures to each other is not constant. The bile ducts may be anterior to, posterior to, or wrap around the PV [7]. Small bile ducts progressively anastomose to form the right and left lobe bile ducts that join in the porta hepatis to form the common hepatic duct. The common hepatic duct becomes the CBD approximately 3 cm distally at the junction of the cystic duct. The common hepatic duct and CBD are approximately 10 cm in length (Figs. 2.6, 2.7). Since they course outside of the liver parenchyma both are considered extrahepatic bile ducts (EHBD). The CBD joins with the main PV and the proper hepatic artery to cross the foramen of Winslow in the hepatoduodenal ligament. In this region the three structures maintain a constant relationship with the larger PV posterior and the smaller CBD and hepatic artery anterior. In cross section the three structures resemble Mickey Mouse with the vein being his face, the CBD his right ear, and the hepatic artery his left ear (Fig. 2.8). Dilatation of the CBD enlarges Mickey’s right ear. The distal CBD passes behind the duodenum to run in a groove formed by the posterior pancreatic head and the medial aspect of the duodenum (see Fig. 2.14). The CBD enters the duodenum opposite the uncinate process of the pancreas.
Figure 2.4 Normal Liver and Kidney Echogenicity. The parenchyma of the liver and kidney are equal in echogenicity. The white arrow indicates the location of the hepatorenal fossa (Morison’s pouch). The portal triads (black arrows) are well visualized.
Figure 2.5 Normal Fat in Fissure of Ligamentum Teres. Transverse image through the left lobe of the liver demonstrates a focal echogenic area (arrow) that might be mistaken for an echogenic mass. This is the characteristic appearance and location of fat in the fissure of the ligamentum teres. Imaging in the longitudinal plane shows an elongated appearance to fat in the fissure. This patient also has a dilated bile duct (D) anterior to the portal vein (P).
Figure 2.6 Common Bile Duct. The common bile duct (arrow) anterior to the portal vein (p) is measured with cursors (+). Compare to appearance of the dilated common bile duct in Figure 2.5. The gallbladder (G) is also seen.
Figure 2.7 Porta Hepatis. The portal vein (p), common duct (short arrow), and hepatic artery (large arrow) course in the hilum of the liver, the porta hepatis. Note the oblique orientation of the hepatic artery as it courses between the common duct and the portal vein. Cursors (+) measure the diameter of the common bile duct.
Figure 2.8 Mickey Mouse. Transverse image of the portal triad as it crosses the hepatoduodenal ligament resembles Mickey Mouse with the face being the portal vein (curved arrow), the hepatic artery being the left ear (short arrow), and the common bile duct being the right ear (long arrow).


The GB is a pear-shaped, bile-filled sac nestled in a concave fossa on the visceral surface of the liver (Figs. 2.6, 2.9). The fundus usually projects beyond the edge of the liver while the body and neck extend dorsally toward the porta hepatis. The hepatic surface of the GB is attached to the liver by blood vessels and connective tissue whereas the inferior surface and fundus of the GB are covered by visceral peritoneum. Occasionally the GB is suspended on a mesentery and is not closely applied to the liver. The GB wall is made up of three layers of tissue. The inner mucosa is redundant and loosely connected to the fibromuscular layer. The mucosa is mucin-secreting columnar epithelium and is continuous with the epithelium of the cystic duct and biliary tree. The fibromuscular layer provides the framework of the sac with interlaced fibrous tissue and smooth muscle. The external coat is the covering peritoneum. The cystic duct is 4 cm long extending from the GB neck to the hepatic duct which it joins to form the CBD. The mucosal lining of the cystic duct forms 5-12 folds that constitute the spiral valve of Heister. These folds may cast acoustic shadows and mimic small stones lodged in the cystic dust. After a fast of 4 or more hours the normal GB is well distended and easily visualized by US as a gourd-shaped sac of fluid. Normal bile is echo-free. The normal GB does not exceed 5 cm in transverse diameter. In 4% of patients the fundus

folds back on itself forming a “Phrygian cap.” Additional normal folds may be seen near the neck of the GB. The GB wall is visualized as a thin echogenic line at the GB interface with the liver. Wall thickness is measured between the liver parenchyma and the GB lumen. This measurement, which includes the liver capsule, the entire GB wall, and intervening tissue, is normally less than 3 mm.
Figure 2.9 Normal Gallbladder. Image through the long axis of the gallbladder (G) demonstrates a tortuous gallbladder neck (arrow). Gallbladder wall thickness is measured between the gallbladder lumen and the hepatic parenchyma (cursors, +). This gallbladder wall measures a normal 2 mm.
Figure 2.10 Aortic Branch Arteries. Longitudinal image through the aorta (A) shows the origin of the celiac axis (fat arrow) and the superior mesenteric artery (skinny arrow). The splenic vein (open arrow) is seen in cross section.
The pancreas is identified on US by recognition of the blood vessels within and around the pancreatic parenchyma (Figs. 2.10, 2.11, 2.12, 2.13 and 2.14). The neck, body, and tail of the pancreas course anterior and parallel to the SV. The total length of the pancreas from head to tail is 12-15 cm. The neck of the pancreas is anterior to the confluence of the SV and the SMV that forms the PV. The SV is of uniform diameter (<10 mm) until its junction with the SMV where the combined veins form a teardrop-shaped dilatation (Figs. 2.12, 2.13 and 2.14). The SMV courses in sagittal plane just to the right and usually slightly anterior to the superior mesenteric artery (SMA). The uncinate process of the pancreas extends leftward beneath the SMV to form a

tapered projection. Blunting of the normally tapered uncinate process is a sensitive sign of pancreatic enlargement or tumor. The SMA arises anteriorly from the aorta at or near the level of the crossing SV (Fig. 2.10). The SMA is surrounded by a collar of echogenic fat and appears, on transverse section, as the hole in a doughnut (Figs. 2.12, 2.14). The left renal vein and the transverse portion of the duodenum course underneath the SMV and SMA caudal to the level of the pancreas. The celiac axis arises from the aorta just cephalad to the pancreas (Fig. 2.10). In transverse plane the bifurcation into the hepatic and splenic arteries resembles a seagull in flight. The left gastric artery origin off the celiac axis may be seen in longitudinal plane.
Figure 2.11 Inferior Vena Cava. Longitudinal image through the inferior vena cava (V) shows the right renal artery (arrow) crossing behind the cava. G, gallbladder.
Figure 2.12 Normal Pancreas–Transverse. The pancreas is recognized by identifying its adjacent vasculature: the splenic vein (small white arrow), the superior mesenteric artery (black arrowhead), the inferior vena cava (curved black arrow), and the aorta (fat black arrow). The junction of the splenic vein with the superior mesenteric vein marks the commencement of the portal vein and is recognized by its teardrop shape (large white arrow) at the right end of the splenic vein.
The CBD extends caudally in the posterior aspect of the pancreatic head where it is commonly visualized as a tubular structure that ends at the major papilla entering the descending duodenum (Fig. 2.14). The pancreatic duct courses centrally within the pancreatic parenchyma from the tail to the head (Fig. 2.15). It joins the CBD to drain into the major papilla in 80% of individuals. In the remaining 20% the pancreatic duct enters the duodenum separately at the minor papilla. The hypoechoic muscular wall of the stomach should not be mistaken for the pancreatic duct (Fig. 2.16). The gastroduodenal artery courses anterior and parallel to the CBD. Doppler US confirms its identification.
The normal echogenicity of the pancreatic parenchyma depends upon the amount of fatty infiltration. The pancreas has no distinct capsule and, with aging, fat infiltrates between the lobules of parenchyma and increases the echogenicity. In children and younger adults the pancreas resembles a slab of meat and has well-defined margins with echogenicity


approximately equal to liver parenchyma. In older patients the pancreas resembles a dust mop and has poorly defined margins with echogenicity just slightly less than fat.
Figure 2.13 Normal Pancreas–Sagittal. Longitudinal image demonstrates the superior mesenteric vein (long arrow) extending cranially to its junction with the splenic vein to form the portal vein (black curved arrow). The hepatic artery (white curved arrow) is seen in cross section. A portion of the neck of the pancreas (2 small arrows) is seen anterior to the superior mesenteric vein.
Figure 2.14 Normal Head of the Pancreas. Transverse view demonstrates the gastroduodenal artery (GDA) and the common bile duct (CBD) coursing adjacent to the head of the pancreas. The splenic vein (s) extends rightward to the commencement of the portal vein (p). Also seen are the superior mesenteric artery (a) and the aorta (A).
Figure 2.15 Normal Pancreatic Duct. A normal pancreatic duct (2 white arrows) courses in the substance of the pancreas anterior to a collapsed splenic vein (s). The portal vein origin (v) and superior mesenteric artery (a) are also seen on this transverse image.
Figure 2.16 Stomach Wall Mimics the Pancreatic Duct. The hypoechoic posterior wall of the stomach (white arrow) may be mistaken for the pancreatic duct. This error is avoided by recognizing that the stomach wall is anterior to, rather than within, the pancreas and by identifying the anterior wall of the stomach (black arrow). Also seen on this transverse image are the superior mesenteric vein (v) and artery (a) and the aorta (A).
The spleen is normally visualized in the left upper quadrant of the abdomen between the diaphragm and the fundus of the stomach (Fig. 2.17). The spleen is soft and pliable allowing it to conform to the shape of the structures around it. Its diaphragmatic surface is smooth and convex, matching the concavity of the diaphragm. Its visceral surface is rounded and smooth with concavities for the stomach, left kidney, and the splenic flexure of the colon. Usual dimensions in adults are 12 cm in length, 7 cm in breadth, and 3-4 cm in thickness.
The spleen parenchyma is a network of lymphatic follicles (the white pulp) surrounded by vascular lakes filled with blood (the red pulp). On US the splenic parenchyma is extremely homogeneous with mid-to-low-level echogenicity slightly greater than that of the liver. The SV runs a relatively straight course rightward from the splenic hilum to the commencement of the PV dorsal to the neck of the pancreas. The SV receives the small inferior mesenteric vein in the region of the distal body of the pancreas and joins with the larger SMV to form the PV. The splenic artery is tortuous as it courses from the celiac axis to the splenic hilum. As the splenic artery enters the hilum it divides into six or more branches which ramify throughout the parenchyma. The capsule of the spleen is covered by closely applied visceral peritoneum except at the hilum and a small “bare area” at the posterior dome of the diaphragm. The spleen is anchored by phrenicolienal, lienorenal, and gastrolienal ligaments that converge at the hilum.
Peritoneal Cavity
The peritoneal cavity is that portion of the abdominal cavity that is bounded by the parietal peritoneum. It consists of numerous recesses formed by organs, ligaments, and peritoneal reflections [8]. The lesser sac is the large potential space behind the stomach. It communicates with the remainder of the peritoneal cavity only by the small opening of the foramen of Winslow. Fluid in the lesser sac usually occurs only as a result of disease in structures bordering the lesser sac [9]. The major recesses of the greater peritoneal cavity are the right

and left subdiaphragmatic spaces, the hepatorenal recess (Morison’s pouch) (Fig. 2.18), the paracolic gutters, and the pelvic cul-de-sac. These recesses are most apparent when fluid is present in the peritoneal cavity.
Figure 2.17 Normal Spleen. Longitudinal image shows a normal spleen (S; between cursors, +, 1, 2) conforming to the smooth curve of the diaphragm (arrow).
Figure 2.18 Hepatorenal Recess. Transverse image shows the location of the hepatorenal recess (Morison’s pouch) (arrow) between the liver and the right kidney.
Diffuse Hepatic Disease
Hepatomegaly is a nonspecific finding in primary and systemic diseases of the liver. Causes include vascular congestion, infection, tumors and cysts, diffuse cellular infiltration (lymphoma, leukemia), storage diseases, and fatty infiltration.
  • Length of the right lobe >15.5 cm is 87% accurate in the diagnosis of hepatomegaly (Fig. 2.19) [10].
  • Extension of the right lobe beyond the lower pole of the right kidney suggests hepatomegaly (Fig. 2.19).
  • Rounding of the inferior edge of the liver suggests pathologic enlargement (Fig. 2.20).
  • Reidel’s lobe is an elongation of the right lobe of the liver that may extend to the iliac crest. It is commonly found as a normal variation in thin women and may be mistaken for hepatomegaly. Reidel’s lobe is recognized by noting an associated decreased volume of the left hepatic lobe.
Viral Hepatitis
Viral hepatitis is a common illness throughout the world. It is classified as hepatitis A (spread by fecal-oral contamination), hepatitis B (spread by blood products and sexual contact), and hepatitis C (spread by blood transfusion).
  • Acute hepatitis causes diffuse interstitial edema and infiltration of inflammatory cells. US examination is commonly normal but may show hepatomegaly, GB wall edema, and

    diffuse decrease in parenchymal echogenicity. The latter finding has been called the starry sky liver because the bright portal triads stand out as “stars” against a background of dark parenchyma (Fig. 2.21). Differential diagnosis of starry sky liver includes acute hepatitis, glycogen storage disease, leukemia, passive hepatic congestion, and toxic shock syndrome [11].
  • Chronic hepatitis implies continuing, usually low-grade, liver injury. US findings are usually normal until cirrhosis develops.
Figure 2.19 Hepatomegaly. The right lobe of the liver extends well below the lower pole of the right kidney (K) and measures 20 cm (between cursors, +), well exceeding the normal limit of 15.5 cm.
Fatty Liver
Infiltration of hepatocytes with lipid is a common and non-specific reaction to hepatocyte injury. This abnormality has a multitude of causes (Box 2.1).
Figure 2.20 Blunting of the Liver Edge. A. A high frequency linear array transducer shows blunting of the edge of the liver (arrows). This finding is a sign of hepatomegaly or diffuse hepatic disease. B. A normal sharp liver edge (arrows) is shown for comparison.
Figure 2.21 Acute Hepatitis. Transverse image at the level of the hepatic veins and inferior vena cava (i) shows the “starry sky” appearance of bright portal triads (arrows) on a background of edematous hypoechoic liver parenchyma.

  • Fatty infiltration increases the echogenicity of the liver parenchyma and causes increased attenuation of the US beam resulting in poor definition of the deep portions of the liver and the diaphragm (Fig. 2.22). The fatty liver significantly exceeds the echogenicity of normal renal parenchyma.
  • Diffuse fatty liver involves all of the liver parenchyma. Vessels course normally through the parenchyma without distortion, encasement, or mass effect.
  • Focal fatty liver usually occurs in a lobar or segmental distribution. Angulated geometric boundaries between involved and spared areas of liver parenchyma are characteristic.
  • Single or multiple nodular areas of focal fatty infiltration may occur and simulate tumors and metastatic disease [12]. A key finding is the absence of mass effect on vessels within and adjacent to the focal fatty nodules. Focal fatty nodules tend to occur in the same areas as focal fatty sparing [13].
  • An interdigitating pattern of fatty infiltrated and spared parenchyma is an uncommon but characteristic pattern of involvement.
  • Focal sparing in diffuse fatty liver simulates hypoechoic masses (Fig. 2.23). Recognizing that the liver parenchyma is diffusely echogenic and that the spared, more hypoechoic areas are in characteristic locations makes this diagnosis. Common areas for focal sparing (and for focal fat infiltration) are the medial segment of the left lobe (segment IV), anterior to the PV bifurcation, near the GB bed, and in subcapsular parenchyma.
  • P.38

  • Correlation with CT of the liver that shows low attenuation in areas of fatty infiltration and normal attenuation in areas of fatty sparing is diagnostic in problem cases.
  • The patterns of fatty infiltration are related to the relative blood flow distributions of the PV and hepatic artery either preferentially carrying toxins to, or preferentially sparing, portions of the liver [14].
Figure 2.22 Diffuse Fatty Liver. The liver is markedly echogenic and difficult to penetrate with US despite the use of a 2.5-MHz transducer. The diaphragm (arrow) and right kidney (K) are barely visualized. The liver parenchyma is markedly more echogenic than the renal parenchyma.
Cirrhosis is the final common pathway of chronic injury to the liver from many causes (Box 2.2). Parenchymal necrosis is followed by extensive fibrosis and nodular regeneration of hepatocytes with progressive distortion of lobar and vascular architecture [15].
  • Cirrhosis alters hepatic echotexture resulting in liver parenchyma that appears heterogeneous, nodular, grainy, or coarse, (Figs. 2.24, 2.25). Visualization of portal triads in the periphery of the liver is decreased. The echotexture of hepatic parenchyma does not correlate well with hepatic function or the severity of cirrhosis. In addition, this appearance is not specific and may be seen in other conditions such as diffuse metastatic disease (especially from breast cancer) or infiltrative hepatocellular carcinoma (HCC).
  • Increased echogenicity of the liver indicates fatty infiltration, which is commonly present in cirrhosis.
  • P.39


  • Scarring and nodular regeneration result in a nodular surface of the liver best seen with a linear array transducer (Fig. 2.26) or when ascites is present (Fig. 2.25) [16]. This finding is more specific for cirrhosis than is altered echotexture. The nodular contour varies from fine to coarse to grossly lobular [17].
  • Asymmetric shrinkage of the right lobe with relative hypertrophy of the left lobe and caudate lobe are common findings in alcoholic cirrhosis. Portal venous flow from the stomach, where most alcohol is absorbed, is preferential to the right lobe, relatively sparing the left and caudate lobes.
  • Nodules are a constant and problematic feature of cirrhosis.
  • Portal hypertension is evidenced by splenomegaly, ascites, enlargement of the PV and mesenteric veins, and the presence of portosystemic collaterals.
  • The hepatic artery is enlarged and tortuous in advanced cirrhosis.
  • Patients with cirrhosis are prone to PV thrombosis.
  • Cirrhosis decreases the compliance of the walls of hepatic veins resulting in spectral Doppler waveforms that are dampened and lack the normal pulsatility and flow reversal with atrial contraction that is characteristic of the hepatic veins [18]. This finding has been called portalization of the hepatic veins.
  • HCC develops in 5-12% of patients with cirrhosis.
Figure 2.23 Focal Sparring in Fatty Liver. A hypoechoic area (arrow) with angulated margins located near the gallbladder (G) is characteristic of focal sparring in a markedly echogenic fatty liver. Gallstones in the gallbladder cast an acoustic shadow (open arrow).
Figure 2.24 Cirrhosis. The fibrosis and altered architecture of cirrhosis cause a coarse appearance of the hepatic parenchyma with limited visualization of portal triads.
Figure 2.25 Cirrhosis and Ascites. The liver (L) appears shrunken and nodular as it is suspended in a sea of ascites (a). Note the echogenicity of the liver is nearly identical to the echogenicity of the right kidney (K) parenchyma. The “bare area” of the liver (arrow) is closely applied to the diaphragm and is not covered by ascites.
Figure 2.26 Nodular Liver Surface in Cirrhosis. Inspection of the liver surface with a high-frequency, linear array transducer demonstrates the surface nodularity (arrows) characteristic of cirrhosis.
Nodules in Cirrhosis
Patients with cirrhosis are at high risk of developing HCC. Detection of this tumor is markedly impaired by the scarring and nodule formation that is characteristic of cirrhosis. A variety of nodular masses are seen in cirrhosis [19].
  • Regenerative nodules are present in all cirrhotic livers; however, imaging studies demonstrate them in only 25-50% of patients. Each nodule consists of a group of regenerating hepatocytes surrounded by fibrous septa. Regenerating nodules are usually <10 mm in size. Most regenerating nodules are isoechoic and are poorly seen on US. When seen,

    the nodules are hypoechoic (Fig. 2.27). Nodularity is best appreciated by examining the surface of the liver with a high-frequency, linear array transducer (Fig. 2.26) [16].
  • Dysplastic regenerative nodules (adenomatous hyperplasia) contain areas of cellular atypia without distinct malignancy. These nodules are a precursor of HCC. Most exceed 10 mm in size. These nodules are best recognized as a solid hypoechoic dominant nodule surrounded by a group of smaller nodules [20].
  • Small HCCs (<3 cm) are difficult to differentiate from regenerative nodules. US detection rates of these small cancers are reported at 55-84%. Most small HCCs are hypoechoic solid tumors without necrosis. A thin peripheral hypoechoic halo, corresponding to a fibrous capsule, is a characteristic finding. Spectral Doppler shows high-velocity flow (70-90 cm/sec) in feeding arteries [21].
  • Focal confluent fibrosis may be seen as a mass replacing hepatic parenchyma. Focal fibrosis may occur in any form of cirrhosis but is most common in primary sclerosing cholangitis [20]. Confluent fibrosis may be wedge-shaped, peripheral, segmental, or lobar [22]. Associated parenchymal atrophy is prominent.
  • Hemangiomas and cysts are rare in cirrhotic livers, probably because they get obliterated by the cirrhotic process [20].
  • Metastatic disease from primary cancers outside of the liver is uncommon in cirrhotic livers, probably because cirrhosis creates an unfavorable environment for metastatic tumor growth [23].
Figure 2.27 Regenerative Nodules in Cirrhosis. Innumerable small hypoechoic nodules are seen throughout the liver in this patient with cirrhosis.
Portal Hypertension
US diagnosis of portal hypertension depends on indirect signs because non-invasive measurement of PV pressure is not currently possible.
  • PV diameter >13 mm and SV or SMV diameter >10 mm suggests portal hypertension (approximately 80% sensitivity and specificity) (Fig. 2.28) [24].
  • PV flow velocity < 21 cm/sec is 80% predictive [24].
  • Splenomegaly and ascites are usually present with significant portal hypertension.
  • Identification of porto-systemic collateral vessel enlargement (varices) is the most specific evidence of portal hypertension. A patent enlarged paraumbilical vein coursing through the fissure of the ligamentum teres (Fig. 2.29) and along the falciform ligament to the anterior abdominal wall and umbilicus is highly indicative. Additional enlarged collateral vessels may be seen along the lesser curve of the stomach (in the gastrohepatic ligament), in the hilum of the spleen (Fig. 2.30), and in the retroperitoneum especially near the renal hilum [25].
  • P.42


  • Retrograde flow in the PV (hepatofugal flow–away from the liver) (Fig. 2.31) is indicative of advanced portal hypertension.
  • Calcification may be seen in the wall of the portal, splenic, or mesenteric veins with long-standing portal hypertension [26].
Figure 2.28 Portal Hypertension–Dilated SMV. Longitudinal image shows dilatation of the superior mesenteric vein (large arrow) to 12 mm (between cursors, +). This finding is highly indicative of portal hypertension. Seen posterior to the enlarged superior mesenteric vein is the inferior vena cava (i) and right renal artery (small arrow). p, neck of pancreas.
Figure 2.29 Portal Hypertension–Enlarged Paraumbilical Vein. Transverse image shows a dilated paraumbilical vein (arrow) seen as a “hole” in the normally echogenic fissure of the ligamentum teres. Enlarged paraumbilical vein collaterals are definitive evidence of portal hypertension.
Figure 2.30 Portal Hypertension–Collaterals. The spleen (S) is massively enlarged, and a markedly dilated and tortuous porto-systemic collateral vein (arrow) is seen in the splenic hilum.
Figure 2.31 Portal Hypertension–Reversed Flow in Portal Vein. Spectral Doppler shows flow in the portal vein (fat black arrow) to be out of the liver (L). The spectral trace (short white arrow) is below the baseline (open white arrow), indicating flow away from the Doppler US pulse shown by the dotted line (open black arrow). When correlated with the anatomic position of the Doppler sample volume (small black arrow), this finding confirms reversed blood flow direction in the portal vein.
Portal Vein Thrombosis
PV thrombosis occurs in association with cirrhosis, HCC, portal hypertension, hypercoagulable states, pancreatitis, and cholecystitis. Clinical presentation is non-specific.
  • The PV is enlarged and filled with hypoechoic thrombus (Fig. 2.32) [27].
  • Color flow US shows complete absence of blood flow or blood flow around an intraluminal thrombus (Fig. 2.32).
  • P.44

  • Cavernous transformation of the PV refers to PV thrombosis with collateral flow in multiple tortuous collateral vessels that course in the bed of the PV (Fig. 2.33) [28].
  • Hepatic artery resistance index (RI) is lowered (RI <0.50) by PV thrombosis [29].
  • Normal color flow US examination excludes the diagnosis.
Figure 2.32 Thrombosed Portal Vein. A. Color Doppler image through the porta hepatis shows absence of blood flow in the dilated portal vein (fat arrow). High-velocity turbulent blood flow (mixed colors) is evident in the adjacent hepatic artery (open arrow). B. Transverse color Doppler image of the right lobe reveals extension of blood clot into intrahepatic branches (arrows) of the portal vein (see Color Figure 2.32A, B).
Figure 2.33 Cavernous Transformation of the Portal Vein. Transverse image through the porta hepatis shows multiple small collateral veins (arrow) in the bed of the occluded portal vein. Ascites (a) is present. The inferior vena cava (i) is dilated.
Passive Hepatic Congestion
Compromise of hepatic venous drainage by congestive heart failure or constrictive pericarditis causes stasis of blood in the liver parenchyma. Elevated central venous pressure is transmitted to the hepatic veins and the hepatic parenchyma. The liver becomes engorged and edematous [30].
  • The IVC and hepatic veins dilate with increasing central venous pressure. The hepatic veins are considered dilated when their diameter exceeds 9-10 mm [31].
  • The IVC and hepatic veins lose their normal triphasic pulsatility on spectral Doppler and show an abnormal pattern of continuous blood flow toward the heart [30].
  • Portal venous blood flow becomes pulsatile as elevated pressure from the right heart is transmitted to the PV [32].
  • Additional non-specific findings that are commonly present include cardiomegaly, pleural effusions, pericardial effusions, ascites, and hepatomegaly [30].
Budd-Chiari Syndrome
Budd-Chiari syndrome is characterized by obstruction or severe stenosis of hepatic venous outflow at the level of the hepatic veins or extrahepatic IVC. In Western countries Budd-Chiari syndrome is most often caused by thrombosis induced by systemic or malignant diseases. In Asian countries the cause is most often a membranous or segmental obstruction of the IVC. Patients present with abdominal pain, hepatomegaly, and ascites.
  • Color Doppler shows no flow in one or more of the hepatic veins or the IVC. Retrograde flow away from the IVC into intrahepatic venous collaterals may be seen [33].
  • Intrahepatic veno-venous collaterals are characteristic. These may appear as large tortuous intrahepatic veins or tiny “spider web” small vessel collaterals deep within the parenchyma or in the subcapsular area [34].
  • Occlusion of the hepatic veins may result in portal hypertension with reversed flow in the PV and enlarged porto-systemic collateral veins. These changes may reverse after therapy.
  • Webs appear as echogenic flap-like structures in the IVC near the junction with hepatic veins. IVC occlusion may be short segment (1 cm) or long segment (5 cm). The thrombosed IVC may be calcified [35].
  • P.45

  • When the syndrome is chronic, the caudate lobe is classically hypertrophied whereas the involved lobes are atrophic. The involved parenchyma is heterogeneous in echogenicity. The caudate lobe drains directly into the IVC via small veins and is typically spared by hepatic vein thrombosis.
Figure 2.34 Hepatocellular Carcinoma. A large hepatocellular carcinoma (small arrows) replaces the right hepatic lobe and bows the right hepatic vein (open arrow). The margins of the hepatoma are poorly defined. The liver parenchyma (L) is heterogeneous because of cirrhosis. i, inferior vena cava.
Liver Masses
Hepatocellular Carcinoma
HCC is the most common primary hepatic malignancy. It nearly always occurs in a setting of cirrhosis or chronic hepatitis. Serum alpha-fetoprotein is often elevated.
  • US findings are usually non-specific in HCC. Tumors occur as a solitary mass (Fig. 2.34), as a dominant mass with small satellite lesions, as multiple nodules, or as diffuse parenchymal infiltration.
  • Small HCCs (<3 cm) are usually homogeneous, solid, hypoechoic nodules that are difficult to differentiate from regenerative nodules in the cirrhotic liver. A thin peripheral hypoechoic halo corresponding to a fibrous capsule favors HCC [21]. Pulsatile blood flow shown by color Doppler or power Doppler US favors HCC [36].
  • Larger HCCs are more variable in appearance with heterogeneous solid areas and areas of hemorrhage and necrosis.
  • Intratumoral fat deposits cause diffuse or focal areas of increased echogenicity. Small HCCs with high fat content are echogenic masses that resemble hemangiomas. Because hemangiomas are uncommon in cirrhotic livers, HCC should always be considered the prime diagnosis.
  • Many tumors are hypervascular with arteriovenous shunting. Doppler demonstrates high-velocity pulsatile flow most conspicuous in the periphery of the tumor. Color and power Doppler show a fine network of blood vessels around the periphery of the tumor or a branching network of internal vascularity [37].
  • Tumor invasion of PVs (25-40%) and hepatic veins (16%) is characteristic of HCC. Tumor thrombus is visualized as a low-density plug within a dilated vein (Fig. 2.35). Doppler shows complete venous occlusion or flow around a partially obstructing thrombus. Extension of tumor into the IVC is a cause of Budd-Chiari syndrome.
Figure 2.35 Hepatocellular Carcinoma with Portal Vein Invasion. A. A hepatocellular carcinoma (arrow) is seen as an irregular heterogeneous hypodense mass in the inferior right lobe. B. The tumor (curved arrow) invades the portal vein, filling and expanding the vein with tumor thrombus (straight arrow).

Fibrolamellar Carcinoma
Fibrolamellar carcinoma is a distinct variant of HCC in its clinical, pathologic, and imaging features. It is characteristically found in adolescents and young adults who lack the risk factors for HCC. Hemorrhage and necrosis are characteristically absent from the tumor [38].
  • A large, lobulated, well-defined hepatic mass in a young person (mean age, 23) is characteristic (Fig. 2.36) [38].
  • A central stellate fibrous scar is common. The scar may include calcification that is also stellate in appearance.
  • Echotexture is variable and usually mixed with hyperechoic and isoechoic components [38].
  • Hemorrhage, necrosis, vascular invasion, and multifocal disease are usually conspicuously absent.
  • The major differential diagnosis is focal nodular hyperplasia (FNH).
Hepatic Cavernous Hemangioma
Cavernous hemangioma is the most common primary neoplasm of the liver. Fortunately, all are benign with no malignant potential. Most cause no symptoms and are discovered incidentally by US or CT. Hemangiomas consist of a mass of blood-filled vascular channels lined by endothelial cells. Thrombosis in the vascular channels leads to fibrosis, scarring, and calcification.
  • The characteristic US appearance is a well-defined, homogeneous, hyperechoic solid mass (Fig. 2.37). Accentuated through-transmission is often present. High echogenicity is produced by the numerous interfaces of the interlacing vascular spaces. Acoustic enhancement results from the fact that the lesion is mostly slow-flowing liquid blood.

    The demonstration of a liver mass with these classic features is considered sufficient to make a definite diagnosis of hemangioma by many radiologists, particularly if the patient has no history of malignant disease and if liver chemistries are normal [39].
  • When lesion size is >3 cm, thrombosis and scarring commonly result in an ill-defined central hypoechoic zone. Calcification may be present within the hypoechoic zone. Lesions with large hypoechoic areas have a characteristic thin hyperechoic border [40].
  • In 10% of patients, multiple hemangiomas are present, often raising concern for metastatic disease.
  • In a fatty-infiltrated liver, hemangiomas may appear hypoechoic compared to the abnormal liver parenchyma (Fig. 2.38).
  • Most cavernous hemangiomas remain stable in size over time [41]. However, lesions that double or triple in diameter have been reported [42].
  • Blood flow within hemangiomas is exceedingly slow. Typically, color and spectral Doppler will show no detectable signal within the lesion [43]. Power Doppler may show a diffuse color “blush” believed to be caused by the architecture of the lesion rather than

    by blood flow [44]. Doppler findings are not specific for hemangiomas, because metastatic lesions may also show the absence of internal vascularity [43].
  • A specific diagnosis of cavernous hemangioma can be made by radionuclide-labeled, red blood scintigraphy and by contrast-enhanced CT and MR [45].
  • Atypical appearance on imaging studies may lead to image-guided biopsy. Fine needle aspiration yields only blood and endothelial cells, results usually considered inadequate for a specific diagnosis. Core biopsy with an 18-gauge needle has been shown to be definitive and safe [46]. The needle path selected for biopsy should always pass through normal parenchyma before entering the lesion to prevent unimpaired bleeding into the peritoneal cavity.
Figure 2.36 Fibrolamellar Carcinoma. A heterogeneous but rather well-defined solid mass is measured between the cursors (+, x). The patient is a 37-year-old male with no clinical or imaging evidence of hepatitis or cirrhosis.
Figure 2.37 Classic Appearance of Cavernous Hemangioma. A solid, well-defined, uniformly echogenic mass is indicated by the cursors (+). Accentuated through-transmission (arrow) is seen distal to the mass. Color Doppler demonstrated no Doppler signal within the mass. Blood flow is usually too slow to be detected by Doppler.
Figure 2.38 Cavernous Hemangioma in Fatty Liver. The cavernous hemangioma (between cursors, +) is well defined and uniformly low in echogenicity compared to the diffusely fatty infiltrated liver. d, common bile duct; i, inferior vena cava; p, portal vein.
Focal Nodular Hyperplasia
FNH is the second most common benign tumor of the liver. The lesion is a proliferation of nonneoplastic hepatocytes held together in abnormal arrangement by a network of fibrous tissue with a dominant scar [47]. Abundant, thick-walled arteries and sinusoids lined by endothelial and Kupffer cells are present within the mass. FNH is more common in women and is usually discovered as an incidental finding.
Figure 2.39 Focal Nodular Hyperplasia. The mass is recognized by the focal bulge (arrows) it produces in the liver contour. Its echogenicity is isoechoic to liver parenchyma (l). Note the slightly altered echotexture and lack of portal triads in the mass.

  • The lesion is typically solitary (80-95%) and homogeneous. Because of its excellent blood supply necrosis and hemorrhage are rare. Most lesions are smaller than 5-cm diameter [47].
  • US shows a homogeneous solid mass that is isoechoic or slightly hypoechoic compared to normal liver parenchyma (Fig. 2.39) [47]. Only surface mass effect or displacement of vessels may identify the mass.
  • A central scar with fibrous septations extending from it is a characteristic finding often not shown well by US. When seen, the scar is echogenic and hypervascular. The central hypervascular nidus may be shown by color flow US even when the scar is not evident [47].
  • Radiocolloid scintigraphy is commonly diagnostic. Because of the presence of Kupffer cells in FNH, radionuclide activity within the lesion is equal to or greater than normal liver in 50-70% of lesions.
  • On follow-up, the lesions may decrease in size or disappear [48].
  • Calcifications are an atypical feature of FNH. When present the lesion is difficult to differentiate from fibrolamellar carcinoma [49].
Figure 2.40 Hepatic Adenoma. This hepatic adenoma (black arrow) is strikingly echogenic and causes marked attenuation of the US beam (white arrow). These findings are caused by high fat content of the tumor confirmed by its low density on computed tomography and on pathologic examination following surgical resection.
Hepatocellular Adenoma
Hepatocellular adenoma (HA) is a rare benign neoplasm of hepatocytes proliferating in an abnormal pattern that lacks portal triads, central veins, and Kupffer cells [47]. The tumor is seen most often in women and may be related to use of oral contraceptives. Multiple HAs are seen in association with glycogen storage disease, type I (von Gierke’s disease). Hemorrhage is common and malignant degeneration may occur. Surgical removal is recommended.
  • Lesions are typically solitary, solid, and may be hypoechoic (20-40%), hyperechoic (30%), or mixed (50%). Fat is sometimes present with the tumor causing focal or diffuse areas of increased echogenicity (Fig. 2.40).
  • HA tends to be larger than FNH at discovery with an average size of 10 cm [47]. HA lacks the central scar characteristic of FNH.
  • Color Doppler shows intratumoral veins usually 1-5-mm diameter with characteristic continuous flat venous flow [50].
  • Hemorrhage may occur into the tumor with rupture into the peritoneal cavity.
Figure 2.41 Multiple Metastases from Breast Carcinoma. The liver is riddled with numerous small echogenic nodules.

Metastases to the Liver
The liver is a common site of metastases from intestinal, pancreas, breast, and lung carcinoma.
  • Multiple lesions (Fig. 2.41) are a characteristic of metastatic disease, although solitary metastases are sometimes seen especially with colon carcinoma (Fig. 2.42).
  • Metastases may resemble any other hepatic lesion and must always be considered in the differential diagnosis.
  • A target or bull’s eye appearance is common with lesions being hypoechoic with an echogenic center.
  • A hypoechoic peripheral rim of parenchyma compressed by an expanding lesion is most often seen with a metastatic lesion [51].
  • Calcified lesions are seen most often with mucinous adenocarcinoma and sarcomas.
  • Cystic metastases usually occur with cystic primary lesions such as cystadenocarcinoma.
  • Homogeneous solid hypoechoic lesions are seen with lymphoma.
Figure 2.42 Solitary Metastases from Colon Carcinoma. A solitary metastasis is barely seen as a subtle hypoechoic solid mass (arrow).
Figure 2.43 Benign Hepatic Cyst. This lesion is sharply defined, completely lacking in internal echoes, has a thin wall, and shows accentuated through-transmission seen as bright echoes deep to the lesion.

Benign Hepatic Cysts
Benign hepatic cysts are seen in 2-5% of the population. Rarely, cysts may develop internal hemorrhage or infection.
  • Simple hepatic cysts are anechoic with thin walls and show posterior acoustic enhancement (Fig. 2.43). They are easily overlooked on US because of their similarity to blood vessels on initial inspection.
  • Many benign hepatic cysts have septations that are thin and avascular and most have lobulated contours. Size varies from tiny to huge.
  • Cysts are commonly multiple and occur in clusters of two or three.
  • Doppler confirms that the cysts are avascular and that no flow is present in the cyst wall or septa.
Pyogenic Liver Abscess
Pyogenic liver abscesses develop as complications of biliary tract infection, sepsis, or trauma. Often no precipitating cause is evident. Patients present with fever, pain, and jaundice.
  • Abscesses have a variable appearance. Most common is a cystic mass with irregular, thick, shaggy walls containing echogenic fluid with particulate matter (Fig. 2.44) and clumped debris that may layer [52].
  • P.52

  • Internal septa are common. Air may be present within the abscess.
  • Early, pre-abscess phlegmon may be seen as a subtle alteration of hepatic echotexture.
  • US is commonly used to guide aspiration and catheter drainage.
Figure 2.44 Pyogenic Abscess. The margins of this abscess (arrows) are ill defined. An irregular central fluid collection contains fluid with suspended particulate matter. k, right kidney.
Figure 2.45 Amebic Abscess. This amebic abscess is much better defined than are most pyogenic abscesses. A hypoechoic wall surrounds the lesion. Internal contents show hypoechoic echoes but no internal vascularity was detected with Doppler.
Amebic Liver Abscess
Amebic abscess is the most common form of liver abscess worldwide. PVs carry amebic organisms to the liver from infestations in the colon. Patients present with pain and malaise and are usually much less acutely ill than patients with pyogenic abscess.
  • The appearance of amebic abscess overlaps that of pyogenic abscess. Lesions are round or oval, hypoechoic or anechoic, and have echo-poor walls (Fig. 2.45) [52]. Lesions are multiple in 25% of cases and vary in size up to 20 cm.
  • Characteristic features are a pattern of fine homogeneous granular internal echoes (Fig. 2.45) and location in the right lobe near the liver capsule.
  • Complications include rupture of the abscess through the liver capsule and diaphragm into the right pleural space and free rupture into the peritoneal cavity.
  • Diagnosis is made by serology and evidence of intestinal amebiasis. Guided fluid aspiration is needed only if pyogenic abscess is a strong consideration. Treatment is medical with amebicides.
  • Lesions require 2 years or longer to resolve. Continued presence of cystic lesions does not imply that therapy has failed [53].
Hepatic Hydatid Cyst
Hydatid disease is caused by infestation with the parasite, Echinococcus granulosus. Hydatid cysts are most common in the liver, but may be seen in any organ. Patients present with low-grade fever and a tender liver [54].
  • The appearance of the cyst is variable and dependent upon the stage of disease.
  • Unilocular, anechoic cysts with walls of variable thickness characteristically contain hydatid sand, fine particulate parasitic debris that layers in the most dependent portion of the cyst. A second diagnostic finding is the visualization of two parallel echogenic

    lines in the cyst wall. The outer line represents the pericyst, a dense fibrous capsule, and the inner line represents the endocyst, a thin membranous wall.
  • The water lily sign refers to the presence of floating, undulating membranes within a cystic mass. The floating membrane is the detached endocyst that has ruptured.
  • Small cystic masses with walls of variable thickness are “daughter cysts” within the “mother cyst.” Visualization of daughter cysts is pathognomonic of hydatid disease (Fig. 2.46).
  • Hydatid fluid may evolve from being thin and anechoic to becoming echogenic viscous gel. This results in the cyst appearing more like a solid mass. Recognition of the folds of collapsed membranes is diagnostic [55].
  • Calcification in the walls and septa is common. Calcifications become thicker and denser with age.
  • Diagnosis is made by serologic testing. Effective treatment is often difficult and may be medical, surgical resection, or catheter drainage.
  • Complications include rupture into the peritoneal cavity reported to sometimes cause anaphylactic reaction, obstruction of the PV causing portal hypertension, obstruction of or rupture into the biliary tree causing jaundice or cholangitis, and rupture into the pleural space.
Figure 2.46 Hydatid Cyst. This cystic mass contains multiple daughter cysts (white arrow) characteristic of hydatid disease. Partially seen adjacent to this cyst is a large unilocular hydatid cyst (black arrow).
Microabscesses are usually the result of opportunistic infection in immunocompromised patients. Causative organisms include Candida and other fungi, Pneumocystis carinii, cytomegalovirus, Mycobacterium avium intracellulare, and M. tuberculosis.
  • Multiple small (<10 cm) target lesions with a central echogenic dot surrounded by a hypoechoic halo are typical of fungal infections. Lesions are found in both liver and spleen (see Fig. 2.97) [56].
  • Innumerable tiny echogenic lesions seen diffusely throughout the liver and spleen are characteristic of Pneumocystis.
  • Lesions may calcify with healing.
Bilomas are collections of bile leaked from the biliary system as a complication of trauma, surgery, or instrumentation.
  • Most bilomas are found within or adjacent to the liver, although they may be anywhere in the peritoneal cavity.
  • Collections are anechoic and well defined with acoustic enhancement. Within the liver, bilomas are rounded cystic masses (Fig. 2.47). Outside of the liver the fluid assumes the shape of the space available to it.
  • P.54

  • Internal septations, debris, and layering fluid within a biloma are caused by traumatic hemorrhage.
  • Diagnosis of a bile leak is made most easily by hepatobiliary scintigraphy.
Figure 2.47 Biloma. This biloma (arrows) occurred as a complication of partial hepatic resection. Internal echoes indicate that some blood is present within the lesion.
Hematomas also result from trauma or surgery. The appearance changes with time.
  • Fresh clot within a hematoma appears echogenic compared to hepatic parenchyma.
  • Within a few days the hematoma becomes progressively cystic and begins to shrink. Septations and internal debris are common (Fig. 2.48).
Hepatic Calcifications
Patterns of hepatic calcifications (Fig. 2.49) are listed in Table 2.2 [126].
Figure 2.48 Hematoma. This hematoma (between cursors, +, x) was discovered a few days after laparoscopic cholecystectomy. The hematoma is becoming cystic but still contains echogenic clot and debris.
Figure 2.49 Granuloma. Calcification from previous granulomatous disease is seen as a bright echogenic focus (fat arrow) that casts a dense acoustic shadow (small arrows).

Biliary Tree
Biliary Obstruction
US is approximately 90% accurate in differentiating obstructive from non-obstructive jaundice by depicting the presence of biliary dilatation. The 10% inaccuracy arises from the fact that biliary obstruction is not always accompanied by biliary dilatation and that biliary dilatation does not always mean biliary obstruction (Box 2.3). US accurately determines the

level of obstruction in 92-95% of cases and the cause of obstruction in 71-88% of cases (Table 2.3) [57].
Table 2.2: Patterns of Hepatic Calcifications
Lesion Pattern of Calcification
Granulomas Multiple, discrete calcifications with no associated mass.
Echinococcus cyst Peripheral, rim calcifications in wall of main cyst or daughter cysts. Old healed lesions show coarse calcification.
Hepatic cavernous hemangiomas Solitary, dense, coarse calcification in central hypoechoic zone within a solid echogenic mass.
Hepatocellular carcinoma Dystrophic coarse calcification in necrotic heterogeneous mass. Fine granular or punctate calcification also occurs.
Fibrolamellar carcinoma Calcification in central stellate fibrous scar with a well-defined solid mass without necrosis.
Metastatic disease Stippled, granular, amorphous calcification is common in mets from mucinous cystadenocarcinomas.
  Sarcoma mets may have chondroid or osteoid calcification.
Adapted from: Stoupis C, Taylor H, Paley M, et al. The rocky liver: radiologic-pathologic correlation of calcified hepatic masses. RadioGraphics 1998;18:675–685.
  • Enlargement of the intrahepatic biliary tree distorts the normal anatomy of the portal triads as the IHBD become tortuous and more prominent than the PVs. IHBD are dilated when their diameter exceeds 2 mm or exceeds 40% of the diameter of the adjacent PV. Color Doppler is used to confirm the absence of blood flow in the enlarged tubes (Fig. 2.50). Enlargement of the bile duct to the size of the adjacent PV has been called the parallel tube sign or the shotgun sig n (Fig. 2.5).
  • As IHBD enlarge they become tortuous and irregular like the gnarly branches of an oak tree (Fig. 2.50). Confluence of enlarged IHBD creates a stellate appearance of merging tubes.
  • Acoustic enhancement may be seen distal to dilated bile ducts but is not seen distal to intrahepatic veins or arteries (Fig. 2.51).
  • Debris in the bile ducts caused by blood, pus, or sludge may make dilated bile ducts isoechoic to liver parenchyma and difficult to visualize.
  • The common duct is considered dilated in adults when the internal diameter of the duct in porta hepatis exceeds 7 mm. The more distal common duct coursing adjacent to the pancreas is commonly larger especially in older adults. For patients older than 60 years of age, the distal common duct may be considered normal up to 10 mm in internal diameter.
  • P.57

  • In neonates and infants, 2 mm is the upper limit of normal size for the common duct. In children up to age 13, 3 mm is the upper limit of normal diameter [58].
  • The normal size of the common duct after cholecystectomy remains controversial, with a number of studies indicating that mild post-operative dilatation of the common duct is common [59]. A reasonable approach is to consider 10 mm to be the upper limit of normal diameter for asymptomatic patients and 7 mm to be the upper limit of normal in symptomatic patients following cholecystectomy.
Table 2.3: Causes of Biliary Obstruction
Level of Obstruction Most Common Causes
Porta hepatis Cholangiocarcinoma (Klatskin tumor)
  Enlarged metastatic lymph nodes in the hilum
Suprapancreatic Cholangiocarcinoma
(between porta hepatis and pancreas) Enlarged metastatic lymph nodes
  Impacted gallstone
  Benign stricture
Pancreatic Gallstone impacted at ampulla
(most common level of obstruction) Periampullary neoplasm
  Pancreatic carcinoma
  Duodenal carcinoma
  Benign stricture
  Chronic pancreatitis
  Iatrogenic (biliary surgery)
Figure 2.50 Dilated Bile Ducts. Dilated bile ducts (white arrows) are seen as tortuous tubular structures in the liver. Color Doppler (shown in black and white on this image) makes differentiation of bile ducts (white arrows) and blood vessels (black arrows) easy.
Figure 2.51 Dilated Bile Ducts. Dilated bile ducts are seen throughout the liver in this patient with long-standing jaundice. The larger bile duct shows accentuated through-transmission (between arrows). This finding may be seen with enlarged bile ducts but not with blood vessels.
Figure 2.52 Stone in the Common Bile Duct. Longitudinal, A, and transverse, B, images show a stone as an echogenic focus (white arrow) in the dilated distal common bile duct (d). Acoustic shadowing (black arrow) is clearly seen in the longitudinal image but not on the transverse image. Stone shadowing was subsequently demonstrated on the transverse image by centering the stone in the US beam. a, superior mesenteric artery; i, inferior vena cava; l, liver; p, pancreas; s, splenic vein.

Common duct stones are the most common cause of obstructive jaundice (36-50% of cases). Stones are found in the bile ducts in 12% of patients undergoing cholecystectomy. The fact that 4% of patients in autopsy series have biliary stones is evidence that biliary stones may be relatively asymptomatic and pass spontaneously. Sensitivity of US in the diagnosis of stones in the CBD is only approximately 55-75%. Careful scanning technique is required.
  • Biliary stones appear as shadowing echogenic foci within the duct (Fig. 2.52). The demonstration of shadowing is technique dependent.
  • False-positive US diagnosis of biliary stones may result from surgical clips, air in the biliary tree, hepatic artery calcification, calcified lymph nodes, or tumor within the duct.
  • The presence or absence of stones within the GB is not predictive of biliary stones as a cause of obstructive jaundice.
Air in the Biliary Tree
Pneumobilia is most often caused by sphincterotomy or surgical biliary-enteric anastomosis. Other causes include incompetence of the sphincter of Oddi or fistulas between the biliary tree and intestine. Air may be mistaken for stones in the biliary tree.
  • Air is seen as linear or punctate foci of high echogenicity (Fig. 2.53) associated with acoustic shadowing and ring-down artifact. Air bubbles will commonly move with changes in patient position. Shimmering ring-down artifact seen with real-time scanning is characteristic.
  • Air is preferentially seen in the non-dependent bile ducts.
  • P.59

  • Extensive atherosclerotic calcification of intrahepatic arteries may mimic air or stones in the biliary tree [60].
Figure 2.53 Air in the Biliary Tree. Air in the biliary tree appears as brightly echogenic branching structures (arrows). With patient movement, air will rise into non-dependent bile ducts. Reverberation artifact and acoustic shadowing are transiently visualized during real-time scanning. This patient’s pneumobilia was caused by choledochojejunostomy.
Ascaris in the Biliary Tree
Ascariasis is the most common parasitic infection worldwide. The roundworm usually lives in the intestine but may migrate through the ampulla of Vater and gain access to the biliary tree and pancreatic duct resulting in cholangitis, acute cholecystitis, or, often fatal pancreatitis.
  • The roundworm appears as an echogenic tubular structure within the bile duct (Fig. 2.54), the GB, or the pancreatic duct. Most striking is to observe a living worm moving within the bile duct. Adult worms are 15-50 cm in length and 3-6 mm thick. A central hypoechoic tube that extends the length of the worm is a characteristic finding. This tube is the worm’s digestive tract [61].
Figure 2.54 Ascaris in the Biliary Tree. The roundworm (arrow) is seen as a tubular echogenic structure within the common bile duct. i, inferior vena cava; p, portal vein.
Figure 2.55 Classification of Congenital Biliary Cysts. Type I choledochal cysts are focal, saccular or fusiform, dilatations of the common bile duct. Type II cysts are true diverticuli of the common bile duct. Type III, choledochoceles, are dilatations of the terminal intraduodenal portion of the common bile duct. Type IV cysts refers to multiple intrahepatic and extrahepatic bile duct cysts. Caroli’s disease is classified Type V. Reproduced with permission from Brant WE, Helms CA, Fundamentals of Diagnostic Radiology, Lippincott-Williams & Wilkins, Baltimore, 1999.

Choledochal Cysts
Choledochal cysts are uncommon congenital anomalies of the bile ducts characterized by cystic dilatation of portions of the intra- or extrahepatic biliary tree [62,63]. Choledochal cysts are usually discovered in infancy or childhood (60%). However, diagnosis may be delayed until adulthood. Patients are usually female (70-84%) and present with abdominal mass, jaundice, pain, or pancreatitis. Biliary stasis results in an increased incidence of gallstones and carcinoma of the bile ducts or GB. The Todani classification is commonly used (Fig. 2.55) [64].
  • US demonstrates cystic dilatation of portions of the biliary tree.
  • Type I choledochal cyst is most common (80-90%) and consists of dilatation of the CBD (Fig. 2.56). The dilatation may be focal or diffuse, saccular or fusiform. The GB commonly arises from the cyst. The IHBD are normal.
  • Type II (2%) is a true diverticulum of the CBD. The connection to the CBD is usually small and may be occluded.
  • Type III is a choledochocele (1.4-5.0%). Similar in appearance to a ureterocele, it involves dilatation of the distal CBD within the duodenum.
  • Type IV (19%) refers to multiple cystic dilatations of both IHBD and EHBD.
  • Type V is Caroli’s disease.
Caroli’s Disease
Caroli’s disease is a rare congenital malformation of the IHBD characterized by non-obstructing saccular or fusiform dilatation of the IHBD. The condition presents in childhood and has an autosomal recessive inheritance pattern. Complications include biliary stones, recurrent bacterial cholangitis, hepatic fibrosis, portal hypertension, and hepatic failure [65].
  • Segmental and saccular dilatation of the IHBD is characteristic. The EHBD are normal.
  • Additional findings include biliary calculi, hepatic abscesses, and evidence of cirrhosis and portal hypertension.
  • P.61

  • Caroli’s disease is found in association with autosomal recessive polycystic kidney disease and medullary sponge kidney.
Figure 2.56 Type I Choledochal Cyst. Marked focal dilatation of the common bile duct (C) to 18 mm is evident. The intrahepatic bile ducts and the remainder of the common bile duct were normal in size and appearance. Also evident are the portal vein (p), hepatic artery (arrow), and gallbladder (g).
Sclerosing Cholangitis
Sclerosing cholangitis is characterized by intra- and extrahepatic biliary fibrosis with progressive obliteration of the bile ducts. Primary sclerosing cholangitis is idiopathic but associated with ulcerative colitis, Crohn’s disease, and retroperitoneal fibrosis. It eventually leads to biliary cirrhosis and hepatic failure [66].
  • Bile ducts show focal areas of dilatation and focal areas of narrowing with wall thickening and irregularity. Both IHBD and EHBD may be affected. Bile duct dilatation that is focal and discontinuous is characteristic.
  • Debris representing sludge, pus, or desquamated epithelium is commonly present within the bile ducts. Biliary calculi are seen in approximately 8% of patients. Stones create a linear cast of the bile duct with variable acoustic shadowing, or appear as a discrete echogenic focus within a dilated duct [67].
  • The GB may show mild to marked wall thickening.
  • Some cases have extensive fibrosis with minimal ductal dilatation. These cases are difficult to recognize with US. Cholangiography is the preferred method of making this diagnosis [66].
Recurrent Pyogenic Cholangitis
Also called Oriental cholangiohepatitis in the literature, recurrent pyogenic cholangitis is related to infestation with Clonorchis sinensis and other parasites. Bacterial superinfection by Escherichia coli and other enteric pathogens is nearly always present. It is one of the most common diseases of the biliary tract in Southeast Asia and Hong Kong, and is seen in the United States primarily in Asian immigrants [68].
  • The major US features are diffuse dilatation of the intra- and extrahepatic bile ducts associated with numerous biliary calculi.
  • Fibrosis and inflammation thicken the walls of the bile ducts and cause increased echogenicity of the portal triads.
  • Gallstones are usually present in the GB.
Figure 2.57 AIDS-Related Cholangiopathy. A. View of the porta hepatis reveals marked irregular thickening of the wall of the common bile duct (arrow). B. Image of the gallbladder shows marked thickening of the gallbladder wall (between cursors, +) with a small gallbladder lumen (g).

Acquired Immunodeficiency Syndrome-Related Cholangiopathy
Acquired immunodeficiency syndrome (AIDS)-related cholangiopathy encompasses several types of biliary diseases encountered in patients with AIDS. Opportunistic infection plays a role in the illness with cytomegalovirus, Cryptosporidium species, and Enterocytozoon bieneusi organisms cultured from the bile. Patients present with abdominal pain and markedly elevated serum alkaline phosphatase [69].
  • The walls of the bile ducts and GB are thickened, often markedly, because of mucosal inflammation and edema (Fig. 2.57) [69].
  • IHBD and EHBD are usually dilated.
  • Edema of the ampulla causes an echogenic nodule and tapered narrowing at the termination of the CBD [70].
  • Findings may mimic sclerosing cholangitis with irregular narrowing of the IHBD and EHBD.
Peripheral Cholangiocarcinoma
Cholangiocarcinoma arising in small bile ducts in the periphery of the liver is the second most common primary hepatic malignancy. Approximately 10% of cholangiocarcinomas are peripheral. Intrahepatic cholelithiasis, Caroli’s disease, Clonorchis infestation, and Thorium exposure are predisposing factors. The tumor is an adenocarcinoma and is rare before age 40 [71,72].
  • Peripheral cholangiocarcinoma presents as an intrahepatic mass similar to HCC and must be considered in the differential diagnosis of intrahepatic neoplasms. Peripheral cholangiocarcinoma often occurs in the absence of cirrhosis.
  • The most common appearance is a solitary hyperechoic or hypoechoic mass (78%). Multiple nodules or a dominant mass with satellite nodules is less common (17%). A peripheral hypoechoic rim is frequently present (35%). Size ranges from 1-20 cm. Intrahepatic biliary dilatation may be seen peripheral to the mass [73].
  • P.63

  • An infiltrative tumor is occasionally seen (5%) and is recognized by heterogeneous echogenicity of the involved parenchyma [73].
  • Calcifications are occasionally present. Unlike HCC, peripheral cholangiocarcinoma rarely invades portal or hepatic veins.
Hilar Cholangiocarcinoma
Cholangiocarcinoma that arises in the hilum of the liver (the porta hepatis) is commonly called a Klatskin tumor. The tumor occurs at the confluence of the right and left bile ducts. Approximately 25% of cholangiocarcinomas are hilar [74].
  • The IHBD are diffusely dilated whereas the EHBD remain normal size [72]. The GB is not obstructed provided the tumor has not extended to the cystic duct.
  • The mass itself is usually small, scirrhous, echogenic, poorly defined, and difficult to visualize. The dilated ducts end abruptly at the hilum. The tumor mass itself is seen in 37-87% of cases [75,76].
  • Lobar parenchymal atrophy occurs proximal to obstructed ducts. The dilated ducts are crowded together and unusually close to the liver surface [72].
  • Metastases extend to regional lymph nodes, liver, and peritoneal cavity. The hilar tumor may invade the adjacent PV and hepatic artery [76].
Distal Cholangiocarcinoma
Distal cholangiocarcinoma occurs in the EHBD and presents early with biliary obstruction and jaundice. The prognosis is better than with peripheral or hilar cholangiocarcinoma because the tumors are small and more often resectable.
  • A polypoid, echogenic, or hypoechoic mass is seen within the lumen at the abrupt termination of a dilated CBD (Fig. 2.58).
  • If the mass is scirrhous, which is frequent, it is commonly not visible. The dilated common duct just ends abruptly. A similar appearance may be produced by benign strictures.
  • Sludge in the distal duct may mimic tumor (Fig. 2.59).
Figure 2.58 Cholangiocarcinoma. The dilated common bile duct (d) abruptly ends at a small soft tissue mass (arrow) that fills the duct. The hepatic artery (a) is visualized but the portal vein is not included in this anatomic plane.
Figure 2.59 Sludge in the Common Bile Duct. Long-term impaction of a gallstone in the distal common bile duct resulted in the more proximal duct (d; between cursors, +) filling with sludge (arrow) mimicking a polypoid mass in the dilated duct. Also seen in this image are the portal vein (p), hepatic artery (a), a portion of the neck of the gallbladder near the cystic duct (c), and a transiently distended portion of the duodenum (b).

Thickening of the Gallbladder Wall
Thickening of the GB wall is a non-specific finding caused by diseases of the GB as well as by extrinsic conditions (see Box 2.4 for differential diagnosis).
  • The standard measurement of GB wall thickness is made from the GB lumen to the liver parenchyma (Fig. 2.60). This measurement includes the GB mucosa, smooth muscle of its wall, liver capsule, and any tissue between the liver and GB. The normal measurement is 3 mm or less. Greater than 5 mm is unequivocally thickened. Between 3 and 5 mm is equivocal.
  • Thickening of the GB wall with striations and fluid pockets is evidence of acute gangrenous cholecystitis in the appropriate clinical setting [77].
Sludge refers to bile that appears echogenic due to the presence of calcium bilirubinate granules and cholesterol crystals mixed with mucus. Sludge is commonly an incidental finding that is related to the lack of bile turnover in patients who are fasting for prolonged periods of time. Sludge is especially common in hospitalized patients. However, sludge may also be seen in patients with obstruction of the cystic duct or more distal bile ducts. Sludge

requires 5-7 days to form and is not caused by routine overnight fasting requested in preparation for GB US. Sludge may fill the entire GB, layer below anechoic bile, or form into balls or masses (tumefactive sludge). Sludge may become viscous and thicken to the consistency of toothpaste (see Fig. 2.62).
Figure 2.60 Thickened Gallbladder Wall. The standard measurement of the gallbladder (g) wall is made between the gallbladder lumen and the parenchyma of the liver (between the arrows). This gallbladder wall is thickened to 8 mm and appears edematous with echolucent striations within the wall. This patient has acute acalculous cholecystitis.
  • Echogenic bile is commonly called sludge (Fig. 2.61) (see Table 2.4 for differential diagnosis).
  • Sludge layers dependently and does not cause acoustic shadowing (Fig. 2.61).
  • Tumefactive sludge is viscous and forms intraluminal masses that mimic GB carcinoma (Fig. 2.62).
  • Mobile “sludge balls” move within the GB but do not cast acoustic shadows.
Gallstones affect 10-15% of the population and are a major cause of GB morbidity (Box 2.5). Most gallstones are mixtures of cholesterol, calcium bilirubinate, and calcium carbonate. Key US findings are
  • Gallstones appear as rounded echodensities in the GB lumen that cast acoustic shadows and move with changes in patient position (Fig. 2.63). When all three features are


    present, the accuracy of US diagnosis is nearly 100%. Most gallstones are round in shape, although some appear angulated or faceted.
  • The acoustic shadow is usually dark and clean (Fig. 2.64). Stones with a rough surface may cause reverberation artifact that produces a dirty shadow. Shadowing is produced by sound absorption. Depiction of shadowing depends upon stone size and US technique. Stones smaller than 3 mm may not cause shadows. To improve visualization of an acoustic shadow use a higher-frequency transducer, insure that the stone is centered in the beam, and adjust the transmit zone or focal zone to depth of the stone (Table 2.5).
  • P.68

  • Movement of gallstones is called the rolling stone sign (Fig. 2.63). Move the patient into upright or lateral decubitus positions to demonstrate stone mobility. Stones typically layer dependently. However, stones may “float” following administration of contrast agents into the biliary system or when bile is highly concentrated.
  • All gallstones show similar US features. US cannot be used to detect stone calcification or determine stone composition.
  • Cholelithiasis is rare in infants and uncommon in children except for those with hemolytic anemia who are prone to develop calcium bilirubinate stones.
Figure 2.61 Layering Sludge in the Gallbladder. Sludge layers dependently within the gallbladder (g) to form a fluid-fluid layer (arrow) with echolucent bile.
Table 2.4: Echogenic Debris in Gallbladder Lumen
Diagnosis US Findings
Sludge Echogenic material layers but causes no shadowing. Found in patients with prolonged fasting or biliary obstruction.
Pus Particulate matter disperses throughout the GB lumen or layers without shadowing. Findings of acute cholecystitis are present.
Blood Particulate debris, no shadowing, in patient with hemobilia.
Pseudosludge Caused by volume averaging of the GB wall and adjacent liver into the GB lumen. Seen in longitudinal but usually not in transverse views of the GB. Disappears when higher frequency (narrower beam) transducer is used.
Layering tiny gallstones Echogenic layer causes acoustic shadow. Surface of the layer is often bumpy. Changing patient position may allow visualization of individual stones.
Sludge with gallstones Layering nonshadowing echogenic bile contains discrete stones that shadow.
Milk of calcium bile Echogenic bile with high calcium carbonate content layers and causes acoustic shadowing. May be indistinguishable from multiple tiny stones.
Cholesterol crystals Tiny 1–2-mm floating particles produce comet tail artifacts.
Gas bubbles Tiny echodensities cause comet tail or reverberation artifact and rise to the most nondependent portion of the GB.
Figure 2.62 Tumefactive Sludge in the Gallbladder. Toothpaste-like sludge forms an echogenic mass (s) filling the gallbladder. Doppler examination showed no vascularity within the mass excluding gallbladder carcinoma. Several small gallstones (arrow) are trapped within the sludge.
Figure 2.63 Rolling Stone. A. With the patient supine the gallstone (arrow) is in the neck of the gallbladder. B. With the patient in left lateral decubitus position the gallstone (arrow) rolls to the gallbladder fundus.
Figure 2.64 Gallstone. A large gallstone within the gallbladder produces a bright surface echo (white arrow) and causes a dark acoustic shadow (between black arrows).
Table 2.5: Differential Diagnosis of Gallstones in the Gallbladder
Diagnosis US Findings
Gallstones Echogenic balls in GB lumen
  Acoustic shadow
  Move within GB lumen
Sludge ball Nodule of medium echogenicity in GB lumen
  No acoustic shadow
  Moves slowly
Blood clot Hypoechoic nodule
  No acoustic shadow
Polyp Hypoechoic to echogenic nodule
  No acoustic shadow
  Fixed position
Gas bubbles Bright echoes
  Comet tail/reverberation artifacts
  Move to nondependent lumen
Parasites Elongated or oval shape
(Ascaris, Clonorchis) May shadow
  May move spontaneously if still alive
Gallbladder Filled with Gallstones
A GB filled with gallstones may be difficult to differentiate from a gas-filled bowel loop. Characteristic findings have been described as the wall-echo-shadow sign (WES triad) or the double-arc-shadow sign [78].
  • Two parallel echogenic lines represent the wall of the GB (proximal arc) and the surface of the packed gallstones (distal arc) separated by a thin anechoic space of residual bile (Fig. 2.65). A dense acoustic shadow emanates from the gallstones (see Table 2.6 for differential diagnosis) [79].
  • A normal GB is not visualized.
Acute Cholecystitis
Acute cholecystitis is most commonly caused by impaction of a gallstone in the GB neck obstructing the GB and resulting in inflammation of the GB wall. Ischemia and bacterial infection are contributing and inciting factors. Patients present with pain, right upper quadrant tenderness, and leukocytosis. The differential diagnosis of patients with this set of symptoms is extensive and US is usually the first imaging study performed. No US finding is pathognomonic. The more findings that are present, the greater the likelihood of the diagnosis. The obstructing stone may spontaneously disimpact resulting in resolution of symptoms.
  • Gallstones are present in 90-95% of cases. An immobile stone impacted in the GB neck is a key finding that is easily overlooked. Careful attention to the GB neck region is required for diagnosis.
  • P.69

  • A positive sonographic Murphy’s sign is strong evidence of acute cholecystitis. Transducer pressure is gently applied to multiple areas of the abdomen. When maximum tenderness is elicited directly over the visualized GB, the sonographic Murphy’s sign is considered positive. The sonographic Murphy’s sign is negative if no tenderness is present, if tenderness is diffuse, or if maximum tenderness is not clearly localized to the GB. An “equivocal” Murphy’s sign is a negative Murphy’s sign. Demonstration of Murphy’s sign is usually not possible in obtunded patients.
  • P.70

  • Thickening of the GB wall (>5 mm) with striated appearance of linear echolucencies is caused by edema and inflammation (Figs. 2.66, 2.67).
  • Pericholecystic fluid is seen as discrete fluid collections between the GB and liver.
  • Distended GB (GB hydrops) with diameter >5 cm is indicative of GB obstruction.
  • Echogenic debris in GB lumen may be sludge, pus, blood, or necrotic tissue (Figs. 2.66, 2.68).
  • Doppler findings are non-specific in acute cholecystitis with patients showing hypervascularity, normal flow, and no flow [80].
Figure 2.65 Gallbladder Filled with Gallstones. A. Transverse image through the gallbladder shows two arching echogenic lines (arrow) and a dense acoustic shadow (S), the WES sign or double-arc-shadow sign. B. In longitudinal plane the two echogenic lines (arrow) are more linear in configuration and the shadow (S) from the gallstones is elongated.
Table 2.6: Differential Diagnosis of Double-Arc-Shadow Appearance or Non-Visualization of the Gallbladder
Diagnosis US Findings
GB filled with gallstones The proximal arc, representing the GB wall, is smooth and uniform in thickness. The second arc, representing the gallstones packed within the GB, is commonly bumpy because many stones are present. The acoustic shadow is dark and “clean.”
Air in bowel loop The soft tissue-air interface is seen as a single, curving, very bright echo. The shadow is “dirty” due to reverberation and ring-down artifacts produced by gas.
Porcelain GB Calcification of the GB wall is often non-uniform in thickness and may be discontinuous. Acoustic shadowing is clean.
Air in the GB wall (emphysematous cholecystitis) The soft tissue-air interface is bright. Bright ring-down artifact emanates from air bubbles in the wall. Confirm with plain radiography or CT. Patient is usually seriously ill.
Adenomyomatosis with cholesterol crystals in Rokitansky-Aschoff sinuses GB wall is thickened and irregular. Cholesterol crystals in small intramural diverticuli (Rokitansky-Aschoff sinuses) produce echogenic foci with comet-tail artifacts. Patient is not seriously ill.
Agenesis of the GB This is a rare condition (0.04% of the population). It is usually associated with other congenital anomalies.
Figure 2.66 Acute Cholecystitis. The gallbladder (g) is filled with echogenic bile. A gallstone (small arrow) is impacted in the gallbladder neck. The gallbladder wall (large arrow) is markedly thickened with a striated appearance indicative of wall edema. Murphy’s sign was strikingly positive.
Atypical forms and complications of acute cholecystitis include the following:
Acalculous cholecystitis refers to acute cholecystitis developing in the absence of gallstones. In children, approximately one-half of the cases of acute cholecystitis are acalculous. Adults rarely develop acalculous cholecystitis unless they have a predisposing condition. Most cases occur in adult patients, who are hospitalized because of recent major surgery, trauma, burns, or debilitating diseases, are immunocompromised, or who are receiving intravenous hyperalimentation. Most cases are related to prolonged biliary stasis,

ischemia, and biliary infection. Outpatients who develop acalculous cholecystitis are usually elderly males with advanced arterial disease.
Figure 2.67 Acalculous Cholecystitis. Transverse image of the gallbladder (g) shows marked circumferential striated thickening of the gallbladder wall (arrow) in this post-operative patient with ascites (a).
Figure 2.68 Gangrenous Cholecystitis. The gallbladder (g) is markedly distended and so filled with echogenic debris, pus, and blood that it is difficult to recognize as the gallbladder. A stone casts an acoustic shadow (arrow).
  • Findings are identical to acute calculous cholecystitis (Figs. 2.60, 2.67), except that gallstones are absent and the cystic duct is often patent on biliary scintigraphy.
Gangrenous cholecystitis refers to necrosis, hemorrhage, ulceration, and microabscess formation in the GB wall. Gangrenous changes complicate 20-30% of cases of acute cholecystitis. Patients are at high risk for perforation and mortality is in the 5-10% range. Findings that suggest gangrene in acute cholecystitis include:
  • Linear echogenic membranes within the lumen represent sloughed mucosa.
  • Coarse echogenic material within the bile represents necrotic debris (Fig. 2.68).
  • A striated appearance of GB wall thickening is more common in gangrenous cholecystitis.
  • Murphy’s sign is absent in 70% of cases because the GB is denervated.
  • Perforation is a common sequela of gangrenous cholecystitis and occurs in approximately 10% of acute cholecystitis. Perforation occurs most commonly near the fundus and results in generalized peritonitis or a pericholecystic abscess.
Emphysematous cholecystitis is characterized by the presence of gas in the GB wall and lumen. It is associated with gangrene (75%), early GB perforation (20%), and high mortality (15%). Gas-producing bacteria are causative. Most patients are elderly and up to 50% have diabetes [81].
  • Intraluminal gas causes a dense band of bright echoes with prominent reverberation echoes [82].
  • Gas bubbles in bile appear similar to gas bubbles in a glass of champagne–the “effervescent GB sign”[81].
  • Intramural gas causes a string of bright, comet tail artifacts that emanate from the GB wall (Fig. 2.69) [82]. Similar echoes occur in association with adenomyomatosis of the GB, but patients with this condition are not acutely ill.
  • The presence of air in the GB wall is easily confirmed with CT and is often evident on plain radiographs.
  • Additional findings of acute cholecystitis are commonly present. Gallstones are absent in most cases.
Figure 2.69 Emphysematous Cholecystitis. US image shows a bright echogenic focus (large arrow) in the gallbladder wall that produces a reverberation artifact (small arrow) and acoustic shadow in an acutely ill elderly man. The importance of this finding was not immediately recognized. The diagnosis of emphysematous cholecystitis was delayed for 8 hours and the patient died during emergency surgery. In the acute setting US signs of air in the gallbladder or its wall must be immediately recognized and confirmed with radiographs or computed tomography. The gallbladder (g) contains echogenic bile that proved to be blood, pus, and cellular debris.

Chronic Cholecystitis
Chronic cholecystitis occurs as a result of continued irritation by gallstones. Patients have recurring symptoms of biliary colic. The cystic duct is usually chronically obstructed.
  • Gallstones are usually present.
  • Thickening of the GB wall reflects chronic inflammation but is not always present. The GB wall may remain normal on US examination but show the pathologic changes of chronic inflammation [83].
Porcelain Gallbladder
Calcification of the GB wall in chronic cholecystitis is referred to as porcelain GB. Porcelain GB is associated with an increased risk of GB carcinoma (11-22%) [84].
  • The calcified wall appears as a hyperechoic semilunar-shaped structure with posterior acoustic shadowing (Fig. 2.70). Calcifications may be thin and regular, clump-like, or discontinuous [84].
  • Reverberation and comet tail artifacts seen with emphysematous cholecystitis are absent.
Gallbladder Polyps
GB polyps are quite common being present in 4-6% of the population [85]. Most (90%) are cholesterol polyps, which are abnormal deposits of cholesterol in a polypoid mass. Cholesterol polyps have no neoplastic potential and are incidental findings. The remainder (10%) are adenomatous polyps that have potential for malignant transformation.
  • Polyps appear as echogenic nodules attached to the GB wall (Fig. 2.71). They do not cause acoustic shadowing. They do not move from their attachment site with changes in patient position.
  • P.73

  • Polyps <10 mm size are most likely incidental cholesterol polyps. Follow-up is not warranted because the incidence of malignant transformation is extremely low [85].
  • Polyps >10 mm are also most likely cholesterol polyps, but probably should be followed for evidence of growth because some are adenomas that could eventually becomes cancerous.
  • Cholesterolosis refers to the presence of deposits of cholesterol esters in the GB mucosa resulting in numerous tiny polypoid mucosal projections [86].
Figure 2.70 Porcelain Gallbladder. Calcification (arrow) in the wall of the gallbladder (g) produces a uniform arching echodense line with acoustic shadowing. The liver (l) is cirrhotic and ascites (a) is present.
Adenomyomatosis of the Gallbladder
Adenomyomatosis is a benign hyperplasia of the epithelium and smooth muscle of the GB wall with herniations of mucosa forming tiny pockets in the wall called Rokitansky-Aschoff sinuses [86]. The condition is entirely benign with no malignant potential, although the findings may mimic GB carcinoma [87].
Figure 2.71 Gallbladder Polyp. A small lobulated echogenic mass (arrow) is suspended from the non-dependent wall of the gallbladder (g). No acoustic shadowing is present.
Figure 2.72 Adenomyomatosis of the Gallbladder. A. Image through the body of the gallbladder (g) shows the characteristic comet tail artifacts (arrows) produced by cholesterol crystals within Rokitansky-Aschoff sinuses in the gallbladder wall. B. Image through the fundus of the gallbladder (g) shows irregular thickening (arrows) of the fundal wall characteristic of adenomyomatosis.

  • Adenomyomatosis may be diffuse, segmental, or focal. The GB fundus is nearly always involved (Fig. 2.72).
  • The GB wall is thickened diffusely or focally.
  • The most characteristic findings are comet tail artifacts that project from the thickened wall (Fig. 2.72). These are caused by the presence of cholesterol crystals that precipitate in the Rokitansky-Aschoff sinuses.
  • Gallstones are commonly present but are not related to the disease process.
Gallbladder Carcinoma
GB carcinoma affects primarily older individuals (>60 years). Pathologic types are adenocarcinoma (90%) and squamous cell carcinoma (10%). GB carcinoma has a variety of appearances [88].
  • An intraluminal polypoid soft tissue mass >2 cm size is likely carcinoma (Fig. 2.73). Polyps are often sessile and fungating. Color flow US shows vessels extending into the mass and differentiates tumor from tumefactive sludge.
  • The GB may be partially or entirely replaced by a soft tissue mass that extends into the liver.
  • Focal or diffuse, asymmetric, irregular thickening of the GB wall may be carcinoma.
  • High-velocity, arterial blood flow (mean peak velocity, 34 cm/sec) is characteristic of tumor masses [89].
  • Gallstones are present in 60-90% of cases. Gallstones may distort or obscure findings of GB carcinoma [90].
  • Porcelain GB is present in 4-20% of cases.
  • P.75

  • Tumor spread is commonly directed into the adjacent liver and may cause biliary obstruction.
  • Hematogenous metastases nearly always involve the liver.
  • Lymphatic spread involves nodes in the porta hepatitis, around the celiac axis or SMA, and in peripancreatic areas.
  • Fine granular or punctate calcification occurs with mucinous adenocarcinoma.
  • Metastases to the GB from other tumors have findings similar to GB carcinoma.
Figure 2.73 Gallbladder Carcinoma. A. An irregular solid polypoid mass (M) projects on a stalk (arrow) into the gallbladder lumen (g). B. Spectral Doppler shows an arterial waveform and confirms the presence of arteries within the mass and provides differentiation from tumefactive sludge. Compare to Figure 2.62.
Acute Pancreatitis
Acute pancreatitis is most commonly caused by alcohol abuse or a gallstone impacted in the distal CBD. Additional causes include trauma, surgery, endoscopic pancreatography, and drugs. Inflammatory changes vary from mild interstitial edema to extensive necrosis with hemorrhage. Contrast-enhanced CT is used for initial evaluation to detect necrosis [91]. US is utilized for follow-up, to detect complications, and to guide intervention.
  • US may be normal in mild pancreatitis.
  • Edema causes focal or diffuse enlargement of the pancreas with ill-defined margins and hypoechoic parenchyma in areas of fluid infiltration (Figs. 2.74, 2.75). Edematous peripancreatic fat is decreased in echogenicity with hypoechoic stranding densities.
  • Hemorrhage may cause hyperechoic masses of clot blood in association with the other findings described.
  • P.76

  • Unencapsulated pancreatic fluid collections containing high levels of amylase and lipase may be found anywhere, but are most common in the pancreatic bed (Fig. 2.76), lesser sac, perirenal areas, and small bowel mesentery. Fluid is usually anechoic unless complicated by hemorrhage or infection (Fig. 2.77). Thin fascial membranes limit the fluid collections. This fluid may resolve spontaneously or require drainage. US is commonly used to measure the fluid dimensions and follow changes in size and appearance. Fluid collections may extend into the mediastinum, groin, beneath the serosa of the intestinal tract, or beneath the capsule of the liver or spleen (see Fig. 2.94) [92].
  • Pancreatic pseudocysts are encapsulated by a distinct wall of granulation tissue and fibrosis. Pseudocysts complicate 10-20% of cases of acute pancreatitis. They are well defined with distinctly visualized walls of measurable thickness (Fig. 2.78). Unencapsulated fluid collections develop into pseudocysts when the fluid collection has been present for approximately 6 weeks. Small pseudocysts usually resolve spontaneously but large pseudocysts commonly require surgical or catheter drainage.
  • P.77


  • Pancreatic ascites is found in approximately 7% of cases and is associated with increased morbidity and a high rate of recurrence. Debris and septations may be seen within the ascites.
  • Infection may complicate an area of pancreatic necrosis, an unencapsulated fluid collection, or a pseudocyst. Progressive infection may evolve into a discrete abscess. Diagnosis commonly requires percutaneous aspiration with Gram’s stain and culture of the fluid. The US appearance alone cannot accurately diagnose the presence or absence of infection. Infected fluid collections may remain anechoic, but infection is more likely if a fluid collection contains gas bubbles or if the fluid is echogenic with debris and floating particulate matter. Surgical or catheter drainage of abscesses is required [93]. Mortality of an untreated pancreatic abscess exceeds 50% [94].
  • Pancreatic-intestinal fistula results in extraluminal gas collections with wall thickening or mass in the affected portion of the intestinal tract.
  • Biliary obstruction may be caused by impacted stones, inflammation, or fibrosis.
  • Pseudoaneurysms result from erosion of the pancreatic inflammation into an artery. Hemorrhage is contained by the adventitia and fibrosis. The splenic, gastroduodenal, left gastric, and pancreaticoduodenal arteries are commonly involved. The diagnosis is made by Doppler confirmation of pulsatile blood flow within a cystic mass. Prior to aspiration or catheter placement every pancreatic fluid collection should be examined with Doppler to diagnose the unrecognized pseudoaneurysm [95].
  • Venous thrombosis may also result from the inflammatory process. The SV is commonly affected and results in development of enlarged collateral vessels around the spleen, stomach, and left kidney. Thrombosis may extend into the PV. Splenomegaly and splenic infarction may result. Doppler should be utilized to confirm patency of all visualized veins in the pancreatic area.
Figure 2.74 Diffuse Acute Pancreatitis. The pancreas (P) is diffusely enlarged and diffusely decreased in echogenicity because of edema. A, aorta; a, superior mesenteric artery; i, inferior vena cava; l, liver; p, commencement of portal vein.
Figure 2.75 Focal Acute Pancreatitis. A. Transverse scan. B. Longitudinal scan. The head of the pancreas (H) is enlarged and decreased in echogenicity because of edema. Cursors (+) measure the enlarged pancreatic head. A, aorta; a, superior mesenteric artery; D, duodenum; i, inferior vena cava; l, liver; S, stomach; v, superior mesenteric vein.
Figure 2.76 Pancreatic Fluid Collection in Lesser Sac. Transverse image shows a huge fluid collection (F) surrounding a portion of the pancreas (p) and extending anteriorly through the peritoneum into the lesser sac.
Figure 2.77 Necrotizing Pancreatitis. A complex echogenic fluid collection (F) replaces the pancreatic parenchyma. The fluid appears echogenic and septated because of tissue necrosis and hemorrhage.
Figure 2.78 Pancreatic Pseudocyst. A well-defined fluid collection (F) in the pancreatic tail region has a measurably thick wall (arrow). It was proven to be a pancreatic pseudocyst by its high amylase content. The lesion was initially mistaken for a left renal cyst.
Chronic Pancreatitis
Chronic pancreatitis is a chronic inflammatory disease of the pancreas characterized by progressive pancreatic damage with irreversible fibrosis. This process results in major structural abnormalities in varying combination including parenchymal atrophy, calcifications, stricture and dilatation of the pancreatic duct, fluid collections, pseudomass formation, and alteration of peripancreatic fat [94,96]. Although many patients with chronic pancreatitis have recurrent episodes of acute pancreatitis, chronic pancreatitis appears to be a separate entity. Patients with chronic pancreatitis average 13 years younger than those with acute pancreatitis. Acute pancreatitis seldom results in the development of chronic pancreatitis. Causes of chronic pancreatitis include alcoholism (70%), autoimmune disease, tropical pancreatitis [97], and non-alcoholic duct-destructive pancreatitis [98].
  • Punctate echodensities, with or without acoustic shadowing, are commonly present (50%) and represent ductal calculi or parenchymal calcifications (Fig. 2.79) [99].
  • The gland is focally or diffusely atrophic (54%) [99]. The parenchyma is heterogeneous, coarsened, and increased in echogenicity with irregular contours. Atrophy may result in exocrine insufficiency and diabetes.
  • The pancreatic duct has focal strictures and dilated segments (68%) [99]. This “beaded” dilatation is characteristic.
  • Focal areas of pancreatic enlargement (Fig. 2.80) caused by focal inflammation are common (30%) and must be distinguished from tumors [96]. The presence of calcifications within the mass strongly favors pancreatitis over tumor. Percutaneous biopsy, guided by US or CT, is commonly needed to make an accurate diagnosis.
  • Bile ducts may be dilated because of inflammatory stricture of the CBD.
  • Fluid collections are caused by superimposed acute pancreatitis (30%).
  • Pancreatic pseudocysts are found in 25-40% of patients.
  • P.79

  • Peripancreatic tissues show inflammatory change with fascial thickening and stranding densities in peripancreatic fat. These changes result in poor definition of the pancreatic margins.
Figure 2.79 Chronic Pancreatitis. Transverse image of the pancreas demonstrates numerous calcifications in the pancreatic parenchyma seen as punctate echodensities (arrows). a, superior mesenteric artery; s, splenic vein.
Adenocarcinoma of the Pancreas
Pancreatic carcinoma is an aggressive and usually fatal tumor. The only realistic hope for cure is early detection and aggressive surgery (Whipple procedure). US is highly accurate in the detection of the pancreatic carcinoma with reported sensitivity of 88-94% [100]. Color Doppler is used to assess vascular involvement by tumor [101]. Approximately 70% of tumors occur in the pancreatic head.
Figure 2.80 Chronic Pancreatitis. Chronic inflammation was the biopsy-proven cause of enlargement of the pancreatic head (M; between cursors, +) seen in A and the massive dilatation of the pancreatic duct (d; between cursors, +) to 21 mm seen in B. This mass is indistinguishable from pancreatic carcinoma and must be biopsied for diagnosis. Both A and B are transverse images through portions of the pancreas. s, splenic vein; S, stomach.

  • Small pancreatic carcinomas (2-3 cm) are homogeneous, solid, hypoechoic, and ill defined (Fig. 2.81) [100].
  • Larger tumors (>3-4 cm) are more heterogeneous with well-defined, irregular, or lobulated margins (Fig. 2.82) [100].
  • Dilatation of the bile ducts and/or pancreatic ducts is commonly caused by the tumor, but is rarely the only sign of tumor.
  • Calcifications are not a feature of pancreatic adenocarcinoma.
  • Tumors may cause proximal acute pancreatitis or pancreatic atrophy due to obstruction.
  • Tumor invasion of the PV, SMA, SMV, hepatic artery, or celiac trunk makes the tumor non-resectable. Involvement of the SV or artery does not preclude surgical resection. Absence of vessel involvement is indicated by clear visualization of the hyperechoic vessel wall or demonstration of unaffected pancreatic parenchyma between the hypoechoic tumor and the vessel wall [101]. Vascular encasement is considered to be present when hypoechoic tumor surrounds 50% or more of the vessel wall. Reduction in size or change in shape of the vessel lumen indicates vascular compression. Thrombosis is visualized as soft tissue density in the vessel lumen with diversion of blood flow around the intraluminal mass or absence of blood flow with the vessel.
  • The tumor metastasizes to the liver, regional nodes, and peritoneal cavity. These areas should always be carefully inspected for metastatic disease.
Figure 2.81 Adenocarcinoma of Pancreas. A mass (M; between cursors, +, x) in the pancreatic tail region is homogeneous, solid, and hypoechoic. This tumor proved to be resectable. P, pancreas; a, superior mesenteric artery; s, splenic vein.
Figure 2.82 Adenocarcinoma of Pancreas. This large mass (M; between cursors, +, x) in the pancreatic head was initially missed because of failure to examine in detail the pancreatic head. Although the superior mesenteric vein (v) is compressed, the bile and pancreatic ducts were not yet affected. This is a sagittal plane image.

Islet Cell Tumors
Islet cell tumors may function and secrete hormones (insulin, gastrin, glucagon), or be non-functional and grow to large size prior to detection. Tumors may be benign or malignant but are characteristically slow growing.
Figure 2.83 Insulinoma. A small functioning islet cell tumor (between arrowheads) is poorly visualized in the pancreatic tail. Careful examination is required to detect these small, often isoechoic, tumors. l, liver; s, splenic vein.
  • Small functioning tumors are often not detected by transabdominal US (Fig. 2.83). Intraoperative US is commonly used to improve detection and limit surgery even when the tumor location has been previously shown by other imaging methods. Tumor localization by palpation and intraoperative US approaches 100%.
  • Small tumors are solid, homogeneous, and may be isoechoic or hypoechoic and relatively well defined (Fig. 2.84). Functioning tumors are hypervascular.
  • Larger tumors are heterogeneous with areas of necrosis and hemorrhage commonly present. Calcifications are found in 20% of large lesions.
  • Tumors may invade adjacent organs or metastasize to lymph nodes and liver.
Mucinous Cystic Neoplasm of the Pancreas
Mucinous cystic neoplasm (macrocystic tumor) occurs as a malignant tumor (mucinous cystadenocarcinoma) or as a benign tumor with malignant potential (mucinous cystadenoma).

Tumors are characterized by copious mucin production that may result in multicystic masses, striking dilatation of the pancreatic duct, or diffuse multicystic enlargement of the pancreas [102,103,104]. Tumors that arise in peripheral pancreatic ducts are mucinous cystadenomas/carcinomas. Tumors that arise in the main pancreatic duct are called intraductal papillary mucinous tumors [103].
Figure 2.84 Malignant Islet Cell Neoplasm. A round homogeneous solid mass occupies the pancreatic tail in the hilum of the spleen (S). Although the mass appears well defined, surgery demonstrated invasion of the spleen, left kidney, and stomach.
Figure 2.85 Mucinous Cystadenocarcinoma of the Pancreas. A well-defined multiloculated cystic mass (arrow) is seen in the tail of the pancreas. a, superior mesenteric artery; i, inferior vena cava; l, liver; r, left renal vein; s, splenic vein.
  • Multilocular cystic mass with six or fewer cysts of 2-cm diameter or larger is highly characteristic of mucinous cystic neoplasm (93% of cases) (Fig. 2.85) [104]. Mucin within the cysts is commonly echogenic. Mural nodules and solid components may be present.
  • Calcifications may be seen in the cyst walls or septa.
  • Intraductal papillary tumors dilate the main pancreatic duct by massive mucin secretion. Because the mucin is echogenic, the dilated duct may be difficult to visualize [102,103]. Ductal dilatation may be segmental or diffuse. Filling defects within the dilated duct may represent papillary tumor or globs of mucin. Ectasia of branch pancreatic ducts results in multicystic change throughout the pancreas. Endoscopic pancreatography confirms the diagnostic findings.
  • Metastases to the liver are usually cystic.
Serous Cystadenoma of the Pancreas
Serous cystadenoma (microcystic tumor) is a benign cystic neoplasm without malignant potential. The tumor grows slowly and is commonly large at presentation.
  • Cysts are commonly so small that the mass appears solid and highly echogenic because of the numerous reflective surfaces. Occasionally cysts 5-10 mm in size are visible.
  • A central stellate echogenic scar is sometimes present.
True Pancreatic Cysts
True pancreatic cysts are rare and are seen far less frequently than pancreatic pseudocysts. Congenital epithelial lined cysts are usually solitary. Multiple pancreatic cysts are seen with von Hippel-Lindau syndrome and autosomal dominant polycystic disease.
  • Cysts are well-defined, spherical anechoic masses with thin walls (Fig. 2.86).

Pancreatic Lymphoma
Pancreatic or peripancreatic lymphoma may be difficult to differentiate from primary pancreatic malignancy.
Figure 2.86 Multiple Pancreatic Cysts in von Hippel-Lindau Syndrome. Multiple, well-defined small cysts (arrows) occupy the pancreatic head as seen on this transverse image. v, superior mesenteric vein.
  • Lymphoma appears as single or multiple homogeneous hypoechoic masses within or around the pancreas.
  • Lymphadenopathy may be prominent elsewhere in the abdomen.
Metastases to the Pancreas
Metastases to the pancreas are uncommon; they are reported in autopsy series in only 3-11% of patients with known malignancy. Common primary tumors are melanoma, breast, lung, and renal carcinoma [106].
  • Metastases appear as single or multiple hypoechoic masses (Fig. 2.87).
  • Renal cell carcinoma metastases may be cystic and appear many years after the primary lesion [106].
Cystic Fibrosis
Cystic fibrosis is a genetic disease characterized by increased volume of abnormally viscous mucous secretions from exocrine glands. The pancreas is a major site of involvement. Secretions precipitate within the pancreatic ducts and result in obstruction, dilatation, and creation of small cysts. Patients develop exocrine pancreatic insufficiency and malabsorption [107].
Figure 2.87 Colon Carcinoma Metastases to Pancreas. The metastases are seen as multiple hypoechoic nodules (arrows) in the pancreas. v, superior mesenteric vein.

  • The affected pancreas is decreased in size and increased in echogenicity because of diffuse atrophy and fatty infiltration (70-100% of patients) [107].
  • Cysts of varying size (1 mm to several cm) and calcifications are uncommonly seen throughout the pancreatic parenchyma.
  • The GB is small and sclerotic and occasionally is not visualized. Sludge and gallstones are common.
  • The bile ducts have thick walls and contain viscous echogenic bile.
  • The liver may show the diffuse increased echogenicity of fatty infiltration and changes of cirrhosis.
Accessory Spleens (Splenules)
Isolated nodules of functioning splenic tissue are found separated from the spleen in 10% of the population. They vary in size from a few millimeters up to several centimeters. They must be recognized as normal splenic tissue to avoid mistaking them for pathological masses [108].
  • Round or oval solid masses with echogenicity identical to parent spleen are characteristic (Fig. 2.88).
  • Splenules are found most often near the splenic hilum.
  • Blood supply is from the splenic artery and SV.
  • Accessory spleens are multiple in 10% of patients.
Splenosis refers to the implantation of ectopic splenic tissue on peritoneal surfaces resulting from trauma with fragmentation of the spleen. Severe traumatic injury to the spleen commonly results in splenectomy. The residual implanted splenic tissue then hypertrophies and assumes the function of the parent spleen. A clinical clue to this condition is the absence of Howell-Jolly bodies in the peripheral blood in a patient with a history of splenectomy. Howell-Jolly bodies are fragments of nuclear material within red blood cells. When functioning splenic tissue is present, these red blood cells are filtered from the blood.
Figure 2.88 Accessory Spleen. A round nodule (a) identical in echogenicity to the parent spleen (S) is seen in the splenic hilum. This is the characteristic appearance and location of an accessory spleen. Note how the spleen conforms to the shape of the left hemidiaphragm (arrow).
Figure 2.89 Splenosis. A round nodule (between arrows) of uniform echogenicity similar to spleen is seen in the left upper quadrant anterior to the left kidney (LK) in a patient with a history of previous splenectomy. Technetium-99m sulfur colloid radionuclide imaging confirmed functioning splenic tissue. Reproduced with permission from Brant WE, Jain KA. Current imaging of the spleen. Radiologist 1996;3:185-192.

  • Rounded nodules of solid tissue of varying size are seen in the left upper quadrant. Nodules have the homogeneous echotexture of splenic tissue. Most are less than 5 cm in size (Fig. 2.89).
  • Functioning splenic tissue may be confirmed with a radionuclide sulfur colloid scan.
US measurement of the maximum splenic dimension shows good correlation with the volume and weight of the spleen [109]. Splenomegaly may be the only sign of disease. The causes of splenomegaly are many. Unfortunately, US is unable to differentiate the various etiologies in the majority of cases because the echotexture of the spleen remains normal despite the presence of disease. Causes of splenomegaly include portal hypertension, lymphoproliferative disorders (lymphoma, leukemia, polycythemia vera, hereditary spherocytosis, etc.), infiltrative disorders (Gaucher’s disease, amyloidosis), infections (malaria, infectious mononucleosis, AIDS), and vascular disorders (acute SV thrombosis) [110].
  • Longest splenic dimension greater than 14 cm is diagnostic of splenomegaly (Fig. 2.90).
  • The spleen tip commonly extends over the lower pole of the left kidney.
  • The presence of focal defects, other pathological findings in the abdomen, and clinical history provide clues to the etiology of splenomegaly.
Figure 2.90 Splenomegaly. This enlarged spleen measures over 18 cm in length (between cursors, +). The tip of the spleen overlies the lower pole of the left kidney (K). These findings are signs of splenomegaly.

Wandering Spleen
In rare cases the spleen lacks its normal attachments and has a long vascular pedicle that allows the spleen to move freely within the abdomen. The misplaced spleen may present as an abdominal mass or may cause abdominal pain because of torsion.
  • Solid abdominal mass has the characteristic homogeneous echotexture and shape of the spleen.
  • The spleen is absent from the left upper quadrant of the abdomen.
  • The wandering spleen is supplied by the splenic artery and SV.
  • Findings of torsion include rapid enlargement of the spleen, splenic infarction, and dilatation of the SV near the spleen with no dilatation of the SV near the PV [111].
Wraparound Liver
In some individuals the left lobe of the liver is exceptionally elongated and partially envelops the spleen simulating a subcapsular splenic hematoma or fluid collection. This wraparound portion of the liver is often thin and not obviously part of the liver on initial inspection.
  • The normal liver is slightly hypoechoic compared to the normal spleen. Envelopment of the spleen may suggest a pathological condition such as subcapsular hematoma (Fig. 2.91).
  • Careful examination confirms that the tissue partially enveloping the spleen is contiguous with the parenchyma and vascularity of the liver. The liver is observed to move separately from the spleen during respiration.
Focal Calcifications
Calcifications reflect previous granulomatous disease, most commonly histoplasmosis or tuberculosis. Splenic artery calcifications are a common manifestation of atherosclerotic disease. Splenic artery aneurysm is the most common visceral artery aneurysm.
  • Granulomatous calcifications appear as focal bright echodensities with or without acoustic shadowing. No associated mass is evident (Fig. 2.92).
  • P.87

  • Splenic artery calcifications are linear and within the wall of the tubular artery. Doppler confirms arterial flow.
  • Splenic artery aneurysms commonly occur near the splenic hilum. Two-thirds are calcified. Aneurysms larger than 2 cm require treatment because of increased risk of rupture.
Figure 2.91 Wraparound Liver. A. Transverse US image. B. Axial CT scan in the same anatomic plane. An elongated left lobe of the liver (L) wraps around the spleen (S) and simulates a subcapsular splenic fluid collection or mass. Demonstrating continuity of the elongated left lobe with the rest of the liver as clearly seen on the CT scan confirms this anatomic variant.
Figure 2.92 Splenic Granulomas. Multiple punctate echodensities (arrows) represent calcified granulomas in the spleen.
Posttraumatic Splenic Cyst
Posttraumatic cysts are the most common cystic lesion of the spleen [112]. They occur as the end result of an intrasplenic hematoma.
  • Cystic lesion has a thick fibrous wall.
  • Calcification of the wall is very common (Fig. 2.93).
  • Floating and layering internal echodensities are caused by hemorrhagic debris.
Figure 2.93 Posttraumatic Splenic Cyst. This posttraumatic cyst within the spleen (S) has a thick calcified wall (fat arrow) that casts an acoustic shadow that obscures the cyst contents and its far wall (long arrow).
Figure 2.94 Pancreatic Fluid Collection in the Spleen. Pancreatic juices released during episodes of acute pancreatitis may gain access to the spleen by migrating along the splenic artery or vein as these vessels pass through pancreatic parenchyma. Digestive enzymes necrose splenic tissue (S) and result in complex fluid collections (F). Reproduced with permission from Brant WE, Jain KA. Current imaging of the spleen. Radiologist 1996;3:185-192.

Pancreatic Pseudocyst in the Spleen
Fluid associated with acute pancreatitis may dissect along the splenic vessels to the splenic hilum and subcapsular locations in the spleen.
  • Subcapsular fluid collection is found in association with pancreatitis (Fig. 2.94) [92].
True Splenic Cyst
True splenic cysts are congenital lesions that are lined by epithelium. These are often discovered in utero or in early childhood.
  • The well-defined anechoic mass has smooth thin walls (Fig. 2.95).
  • The cyst may have fine septations or low levels of internal echoes caused by floating cholesterol crystals.
Figure 2.95 Congenital Spleen Cyst. A well-defined cyst in the spleen (S) of a young child contains anechoic fluid and has thin walls. Reproduced with permission from Brant WE, Jain KA. Current imaging of the spleen. Radiologist 1996;3:185-192.
Figure 2.96 Pyogenic Splenic Abscess. A large portion of the spleen is replaced by a fluid collection (F) that contains numerous gas bubbles that are seen as floating echodensities (arrow). US-guided aspiration confirmed pyogenic abscess. Reproduced with permission from Brant WE, Jain KA. Current imaging of the spleen. Radiologist 1996;3:185-192.

Pyogenic Splenic Abscess
Pyogenic splenic abscesses are caused by hematogenous infection (75%), penetrating trauma (15%), or as a complication of splenic infarction (10%) [112]. Fever, chills, and pain may be pronounced, or the patient may be relatively asymptomatic.
  • Single or multiple, poorly defined hypoechoic or anechoic masses in a septic patient suggest splenic abscess.
  • Gas within the abscess produces focal echodensities with shadowing and ring-down artifact (Fig. 2.96).
  • Debris within the abscess layers and moves with changes in patient position.
  • Aspiration and catheter drainage may be guided by US.
Splenic Microabscesses
Microabscesses occur in the setting of an immunocompromised patient with an opportunistic infection [113]. Common causative organisms include Mycobacterium tuberculosis and M. avium-intracellulare, Pneumocystis carinii, candidiasis, and other fungal infections. Kaposi’s sarcoma may produce similar lesions. Tiny lesions are best visualized with higher-frequency transducers (5 MHz).
  • Multiple echolucencies 1-10 mm in size (Fig. 2.97).
  • Multiple echodensities 1-10 mm in size.
  • Both the liver and spleen are commonly affected.
Hydatid Disease of the Spleen
Involvement of the spleen is seen in only 2% of human infestations with Echinococcus [114].
  • Cystic lesions are solitary and anechoic in most cases.
  • Intracystic daughter cysts are highly characteristic when present. They have a cyst within a cyst appearance (Fig. 2.46).
  • Layering debris within the cyst is hydatid sand, a mixture of parasite fragments and debris.
  • P.90

  • Some lesions appear more solid with infolded membranes and hydatid sand filling the fluid spaces.
  • The wall of the lesion calcifies in chronic cases.
Figure 2.97 Splenic Microabscesses. Numerous small echolucencies throughout the splenic parenchyma (S) were caused by Mycobacterium tuberculosis in a patient with AIDS.
As the major organ of the lymphatic system the spleen is commonly affected by lymphoma and leukemia [115]. Patterns of disease involvement include infiltrative without discrete masses, miliary with numerous tiny lesions (<2 cm), and massive with extensive replacement of spleen parenchyma [112].
  • Splenic enlargement is a frequent finding when the spleen is diffusely infiltrated. A normal-sized spleen does not, however, exclude involvement.
  • Focal lesions are hypoechoic. Lesions may be multiple and small, or large and confluent replacing most of the parenchyma. Most lesions are strikingly homogeneous.
  • Occasionally, lesions are cystic because of massive necrosis.
Metastases to the Spleen
Metastases to the spleen are usually a late manifestation of disseminated malignancy in terminal patients. The most common primary tumors are melanoma and breast, lung, or ovary carcinoma. Isolated metastases (without mets seen elsewhere) are rare but are reported with colon and renal carcinomas and gynecologic malignancies [116].
  • Intrasplenic masses of variable and non-specific appearance. Lesions may be solitary or multiple and appear hypoechoic, hyperechoic, mixed, or partially cystic.
Splenic Infarction
Infarction occurs as a result of occlusion of branches of the splenic artery, or of thrombosis of venous sinusoids when the spleen is massively enlarged [112]. Arterial occlusion is associated with hemolytic anemias, endocarditis, arteritis, and pancreatic carcinoma. Most patients present with pain, but up to 40% are asymptomatic [117].
  • In the first 24 hours, infarctions are well defined, wedge shaped, and hypoechoic (Fig. 2.98). Extension to the splenic capsule is characteristic. Some lesions are round or oval rather than classic wedge shaped.
  • P.91

  • With time, echogenicity increases and the size of the lesion decreases. Liquefaction may occur. The parenchyma may eventually return to normal appearance or show a vague area of heterogeneous echogenicity.
  • Complications include subcapsular hemorrhage and rupture with free bleeding into the peritoneal cavity.
Figure 2.98 Infarction of the Spleen. Several areas of acute infarction are seen as irregular or wedge-shaped areas of mixed hypoechogenicity (arrows) in the spleen (S). A left pleural effusion (E) is also evident. Reproduced with permission from Brant WE, Jain KA. Current imaging of the spleen. Radiologist 1996;3:185-192.
Splenic Hemangioma
Hemangiomas are found much less commonly in the spleen than in the liver. Although scarce, hemangiomas are the most common primary neoplasm of the spleen. Multiple splenic hemangiomas are seen with Klippel-Trenaunay-Weber syndrome [118].
  • Most appear as well-defined, homogeneous, echogenic masses, identical to the typical appearance of hemangioma in the liver.
  • Some have cystic spaces of varying size.
  • Lesions may contain areas of fibrosis and focal calcification.
  • Doppler usually shows no signal because blood flow is very slow. High-sensitivity settings on high-grade modern equipment may demonstrate slow flow in some areas of the lesion.
Splenic Lymphangioma
Lymphangiomas are similar to hemangiomas except that the vascular spaces are filled with lymph rather than blood [112]. The lesions may be solitary or multiple.
  • A well-defined cystic appearing mass is typical. Internal septations are common. Echogenic debris may be present within the locules.
Angiosarcomas of the spleen are rare lesions, accounting for less than 2% of all soft tissue sarcomas [119]. Exposure to thorium dioxide (Thorotrast), vinyl chloride, and arsenic are predisposing factors.
  • Splenic parenchyma is nodular and heterogeneous.
  • Prominent tortuous vessels with turbulent flow on Doppler are seen in and near the lesion.
  • P.92

  • Pulsatile, high-velocity flow is present in the splenic and, occasionally, the portal veins.
  • The splenic artery is enlarged with high-flow velocities.
Figure 2.99 Splenic Hematoma. An intraparenchymal hematoma (H) is seen as a solid-appearing mass with variable echogenicity within the spleen (S).
Splenic Peliosis
Splenic peliosis is a rare cause of spontaneous splenic rupture [120]. Peliosis refers to the presence of multiple blood-filled cystic spaces (1-10-mm size) in the spleen or liver parenchyma. Both organs are usually affected. The etiology is unknown. Most patients are asymptomatic and the lesion is discovered incidentally.
  • Multiple hypoechoic or hyperechoic lesions with ill-defined margins.
  • Doppler characteristics have not been described. On CT enhancement is delayed and from the periphery similar to enhancement of hemangiomas.
Subcapsular/Intraparenchymal Splenic Hematoma
The spleen parenchyma is injured and bleeding occurs, but the splenic capsule remains intact.
  • The blood of a subcapsular hematoma appears hypoechoic and flattens or indents the spleen parenchyma. The splenic capsule is seen as a bright crescentic line providing the outer boundary of the hematoma.
  • Intraparenchymal hematomas appear as intraparenchymal masses of varying echogenicity (Fig. 2.99).
  • Beware the wraparound liver described previously.
Splenic Rupture
Injury lacerates the splenic parenchyma and the splenic capsule resulting in fragmentation of the spleen and blood in the peritoneal cavity.
  • Fluid seen in the peritoneal cavity is indicative of hemoperitoneum. The fluid may be anechoic or contain particulate matter or clots.
  • Immediately after injury, liquid blood defines splenic lacerations as irregular jagged lines (Fig. 2.100).
  • With clotting of blood 24-48 hours after injury the laceration may not be identifiable because the blood is isoechoic with splenic parenchyma.
  • When the clotted blood liquefies, lacerations are again easily seen.
Figure 2.100 Splenic Laceration. A splenic laceration appears as a slightly hypoechoic jagged line (arrows) extending through the spleen (S). The patient had a hemoperitoneum.

Peritoneal Cavity
Ascites is an accumulation of fluid within the peritoneal cavity. Ascites may be a transudate or exudate, blood, pus, bile, urine, pancreatic juice, or lymphatic fluid. US is highly sensitive in detecting intraperitoneal fluid and demonstrates as little as a few mL of fluid.
  • Gravity and peritoneal reflections determine the location of fluid in the peritoneal cavity (Fig. 2.101). Fluid in the subdiaphragmatic spaces separates the liver and spleen from the diaphragm. Fluid in the hepatorenal fossa (Morison’s pouch) is seen as an echolucent band between the liver and right kidney. Fluid in the pelvis fills the cul-de-sac and outlines pelvic organs. Loops of bowel float freely within copious ascites.
  • Transudative ascites is always anechoic. Exudative ascites may also be anechoic; however, the presence of floating particulate matter or septations is definitive evidence of exudate (Fig. 2.102).
US is currently frequently used to detect the presence of hemoperitoneum in the setting of abdominal trauma [121]. Detection of even a tiny amount of fluid is used to triage patients urgently to CT or laparotomy. Fluid in the abdominal cavity in this setting is considered evidence of organ injury. US detection of solid organ injury is insensitive and clearly inferior to contrast-enhanced CT [122,123]. In addition, hemoperitoneum is absent in 17-34% of patients with abdominal visceral injuries, most commonly in patients with bowel and mesenteric injury [124,125].
  • Acute intraperitoneal hemorrhage is anechoic to hypoechoic. Floating particulate matter may be seen and may produce fluid-fluid levels.
  • Blood clots appear as echogenic masses within the intraperitoneal fluid. The clot evolves with time to become more hypoechoic.
Pseudomyxoma Peritonei
Implants of mucin-producing cells on peritoneal surfaces results in a gelatinous form of ascites that tends to loculate and produce cystic pseudomasses. Causes include mucinous cystadenomas and cystadenocarcinomas of the appendix, colon, and ovary.
Figure 2.101 Ascites. Free intraperitoneal fluid occupies the recesses of the peritoneal cavity preferentially filling gravity-dependent spaces. A. Fluid in seen in Morison’s pouch (arrow) between the right kidney and the liver. B. Loops of small bowel (arrows) float freely in copious ascites (a). C. Fluid in the pelvis (FL) outlines the uterus (large arrow) and the broad ligament (small arrow). Fluid distends the cul-de-sac posterior to the uterus.

  • Fluid is loculated and usually multiseptated. Internal fluid shows low-level echogenicity caused by mucinous debris (Fig. 2.103).
Peritoneal Metastases
Peritoneal implantation of metastatic tumor nodules occurs most commonly with ovarian, gastric, colon, and pancreas carcinomas.
  • Peritoneal implants are seen as soft tissue nodules that extend from peritoneal surfaces (Fig. 2.104). They are best visualized when ascites is present. Tiny tumor implants, most common with ovarian carcinoma, may not be visualized with US.
  • The normal flow of peritoneal fluid determines the pattern of intraperitoneal seeding. Peritoneal tumor is commonly seen in the cul-de-sac and hepatorenal fossa. Tumor implants are most easily recognized on the peritoneal surface of the diaphragm and on the liver.
  • P.95

  • Tumor implantation on the greater omentum causes irregular nodular thickening of the omentum seen between the bowel and the anterior abdominal wall. This flattened mass of tumor has been called omental cake.
Figure 2.102 Malignant Ascites. Fluid pockets in the peritoneal cavity are spanned by fine septations (arrow) in this patient with widespread malignant melanoma.
Intraperitoneal Abscess
US is an excellent screening method for the detection of intraperitoneal abscesses; however, abdominal wounds, surgical dressings, drainage tubes, and bowel gas limit its use to a small subset of patients. Interloop abscesses, between loops of small bowel, are better demonstrated by CT. Abscesses are caused by spillage of contaminated fluid into the peritoneal cavity as a result of trauma, surgery, pancreatitis, bowel perforation, or by infection elsewhere.
  • Any loculated fluid collection in the peritoneal cavity is suspicious for abscess in a high-risk patient. The presence of mass effect with the fluid collection making its own space and displacing adjacent structures is strong evidence of loculation.
  • P.96

  • Internal debris, fluid levels, and septations are commonly present (Fig. 2.105). A large amount of conglomerated internal debris may suggest a solid mass.
  • Air within the fluid collection is strong evidence of abscess. Air bubbles within fluid are seen as bright floating foci with comet tail artifacts. Pockets of air are seen as bright interfaces with acoustic shadowing and reverberation artifacts. This appearance is difficult to differentiate from air within bowel. A fixed position and unusual shape are suggestive.
Figure 2.103 Pseudomyxoma Peritonei. Mucinous fluid is echogenic and gelatinous filling loculated recesses in the peritoneal cavity.
Figure 2.104 Peritoneal Metastases. Tumor implants (arrows) project from the diaphragm into ascites (a) in this patient with peritoneal spread of colon carcinoma. l, liver.
Lymphoceles are cystic collections of lymphatic fluid that occur as a result of surgical or traumatic disruption of lymphatic vessels. They are seen commonly after lymphadenectomy in the retroperitoneum or pelvis and following renal transplantation.
Figure 2.105 Intraperitoneal Abscess. An abscess appears as an echogenic fluid collection (between arrows) with septations in the gallbladder fossa complicating a cholecystectomy.

  • Lymphoceles are typically anechoic loculated fluid collections located in or near an area of previous surgery. Size varies from a few cm to huge.
  • Internal septations and debris occur with complicating hemorrhage or infection.
  • Diagnosis is confirmed by image-guided percutaneous aspiration.
1. American Institute of Ultrasound in Medicine. Guidelines for performance of the abdominal and retroperitoneal ultrasound examination. Rockville, MD: AIUM, 1991.
2. Brant WE, Jain KA. Current imaging of the spleen. Radiologist 1996;3:185-192.
3. Goerg C, Schwerk WB, Goerg K. Sonography of focal lesions of the spleen. AJR Am J Roentgenol 1991;156:949-953.
4. Smith D, Downey D, Spouge A, et al. Sonographic demonstration of Couinaud’s liver segments. J Ultrasound Med 1998;17:375-381.
5. Lafortune M, Madore F, Patriquin H, et al. Segmental anatomy of the liver: a sonographic approach to the Couinard nomenclature. Radiology 1991;181:443-448.
6. Dodd GD. An American’s guide to Couinaud’s numbering system. AJR Am J Roentgenol 1993;161:574-575.
7. Lim J, Ryu K, Ko Y, et al. Anatomic relationship of intrahepatic bile ducts to portal veins. J Ultrasound Med 1990;9:137-143.
8. Meyers MA. Dynamic radiology of the abdomen: normal and pathological anatomy. (3rd ed.) New York: Springer Verlag, 1988.
9. Dodds WJ, Foley WD, Lawson TL, et al. Anatomy and imaging of the lesser peritoneal sac. AJR Am J Roentgenol 1985;141:567-575.
10. Gosink B, Leymaster C. Ultrasonic determination of hepatomegaly. J Clin Ultrasound 1981;9:37-42.
11. Cazier PR, Sponaugle DW. “Starry sky” liver with fasting: variations in glycogen stores? J Ultrasound Med 1996;15:405-407.
12. Wang S-S, Chiang J-H, Tsai Y-T, et al. Focal hepatic fatty infiltration as a cause of pseudotumors: ultrasonographic patterns and clinical differentiation. J Clin Ultrasound 1990;18:401-409.
13. Rubaltelli L, Savastano S, Cellini L, et al. Hyperechoic pseudotumors in segment IV of the liver. J Ultrasound Med 1997;16:569-572.
14. Itai Y, Matsui O. Blood flow and liver imaging. Radiology 1997;202:306-314.
15. Brown JJ, Naylor MJ, Yagan N. Imaging of hepatic cirrhosis. Radiology 1997;202:1-16.
16. Di Lelio A, Cestari C, Lomazzi A, et al. Cirrhosis: diagnosis with sonographic study of the liver surface. Radiology 1989;172:389-392.
17. Dodd GI, Baron R, Oliver JI, et al. Spectrum of imaging findings of the liver in end-stage cirrhosis: part I, gross morphology and diffuse abnormalities. AJR Am J Roentgenol 1999;173:1031-1036.
18. Colli A, Cocciolo M, Riva C, et al. Abnormalities of Doppler waveform of the hepatic veins in patients with chronic liver disease: correlation with histologic findings. AJR Am J Roentgenol 1994;162:833-837.
19. Taylor AJ, Carmody TJ, Quiroz FA, et al. Focal masses in cirrhotic liver: CT and MR imaging features. AJR Am J Roentgenol 1994;163:857-862.
20. Dodd GI, Baron R, Oliver JI, et al. Spectrum of imaging findings of the liver in end-stage cirrhosis: part II, focal abnormalities. AJR Am J Roentgenol 1999;173:1185-1192.
21. Choi BI, Takayasu K, Han MC. Small hepatocellular carcinomas and associated nodular lesions of the liver: pathology, pathogenesis, and imaging findings. AJR Am J Roentgenol 1993;160:1177-1187.
22. Ohtomo K, Baron RL, Dodd GD, III, et al. Confluent hepatic fibrosis in advanced cirrhosis: appearance at CT. Radiology 1993;188:31-35.
23. Mergo PJ, Ros PR, Buetow PC, et al. Diffuse disease of the liver: radiologic-pathologic correlation. Radiographics 1994;14:1291-1307.
24. Haag K, Rössle M, Ochs A. Correlation of duplex sonography findings and portal pressure in 375 patients with portal hypertension. AJR Am J Roentgenol 1999;172:631-635.
25. Subramanyam BR, Balthazar EJ, Madamba MR, et al. Sonography of portosystemic venous collaterals in portal hypertension. Radiology 1983;146:161-166.

26. Ayuso C, Luburich P, Vilana R, et al. Calcifications in the portal venous system: comparison of plain films, sonography, and CT. AJR Am J Roentgenol 1992;159:321-323.
27. Parvey HR, Raval B, Sandler CM. Portal vein thrombosis: imaging findings. AJR Am J Roentgenol 1994;162:77-81.
28. De Gaetano A, Lafortune M, Patriquin H, et al. Cavernous transformation of the portal vein: patterns of intrahepatic and splanchnic collateral circulation detected with Doppler sonography. AJR Am J Roentgenol 1995;165:1151-1155.
29. Platt J, Rubin J, Ellis J. Hepatic artery resistance changes in portal vein thrombosis. Radiology 1995;196:95-98.
30. Gore RM, Mathieu DG, White EM, et al. Passive hepatic congestion: cross-sectional imaging features. AJR Am J Roentgenol 1994;162:71-75.
31. Henriksson L, Hedman A, Johansson R, et al. Ultrasound assessment of liver veins in congestive heart failure. Acta Radiol 1982;23:361-363.
32. Hosoki T, Arisawa J, Marukawa T, et al. Portal blood flow in congestive heart failure: pulsed duplex sonographic findings. Radiology 1990;174:733-736.
33. Millener P, Grant E, Rose S, et al. Color Doppler imaging findings in patients with Budd-Chiari syndrome: correlation with venographic findings. AJR Am J Roentgenol 1993;161:307-312.
34. Kane R, Eustace S. Diagnosis of Budd-Chiari syndrome: comparison between sonography and MR angiography. Radiology 1995;195:117-121.
35. Chou Y-H, Tiu C-M, Hwang J-I, et al. Primary Budd-Chiari syndrome: duplex ultrasonic diagnosis. J Med Ultrasound (Taiwan) 1993;2:78-83.
36. Koito K, Namieno T, Morita K. Differential diagnosis of small hepatocellular carcinoma and adenomatous hyperplasia with power Doppler sonography. AJR Am J Roentgenol 1998;170:157-161.
37. Tanaka S, Kitamra T, Fuijita M, et al. Value of contrast-enhanced color Doppler sonography in diagnosing hepatocellular carcinoma with special attention to the “color-filled pattern.” J Clin Ultrasound 1998;26:207-212.
38. McLarney J, Rucker P, Bender G, et al. Fibrolamellar carcinoma of the liver: radiologic-pathologic correlation. RadioGraphics 1999;19:453-471.
39. Leifer D, Middleton W, Teefey S, et al. Follow-up of patients at low risk for hepatic malignancy with a characteristic hemangioma at US. Radiology 2000;214:167-172.
40. Moody A, Wilson S. Atypical hepatic hemangioma: a suggestive sonographic morphology. Radiology 1993;188:413-417.
41. Mungovan JA, Cronan JJ, Vacarro J. Hepatic cavernous hemangiomas: lack of enlargement over time. Radiology 1994;191:111-113.
42. Nghiem HV, Bogost GA, Ryan JA, et al. Cavernous hemangiomas of the liver: enlargement over time. AJR Am J Roentgenol 1997;169:137-140.
43. Perkins A, Imam K, Smith W, et al. Color and power Doppler sonography of liver hemangiomas: a dream unfulfilled? J Clin Ultrasound 2000;28:159-165.
44. Young L, Yang W, Chan K, et al. Hepatic hemangioma: quantitative color power US angiography–facts and fallacies. Radiology 1998;207:51-57.
45. Brant WE, Floyd JL, Jackson DE, et al. The radiological evaluation of hepatic cavernous hemangioma. JAMA 1987;257:2471-2474.
46. Heilo A, Stenwig A. Liver hemangioma: US-guided 18-gauge core-needle biopsy. Radiology 1997;204:719-722.
47. Beutow PC, Pantongrag-Brown L, Buck JL, et al. Focal nodular hyperplasia of the liver: radiologic pathologic correlation. Radiographics 1996;16:369-388.
48. Di Stasi M, Caturelli E, De Sio I, et al. Natural history of focal nodular hyperplasia of the liver: an ultrasound study. J Clin Ultrasound 1996;24:345-350.
49. Caseiro-Alves F, Zins M, Mahfouz A-E, et al. Calcification in focal nodular hyperplasia: a new problem for differentiation for fibrolamellar hepatocellular carcinoma. Radiology 1996;198: 889-892.
50. Golli M, Tran Van Nhieu J, Mathieu D, et al. Hepatocellular adenoma: color Doppler US and pathologic correlations. Radiology 1994;190:741-744.
51. Wernecke K, Vassallo P, Bick U, et al. The distinction between benign and malignant liver tumors on sonography: value of a hypoechoic halo. AJR Am J Roentgenol 1992;159:1005-1009.
52. Ralls P, Barnes P, Radin D, et al. Sonographic features of amebic and pyogenic abscesses: a blinded comparison. AJR Am J Roentgenol 1987;149:499-501.
53. Ralls P, Quinn M, Boswell WJ, et al. Patterns of resolution in successfully treated hepatic amebic abscess. Radiology 1983;149:541-543.

54. Beggs I. The radiology of hydatid disease. AJR Am J Roentgenol 1985;145:639-648.
55. Durr-E-Sabih, Sabih Z, Khan A. “Congealed waterlily” sign: a new sonographic sign of liver hydatid cyst. J Clin Ultrasound 1996;24:297-303.
56. Görg C, Weide R, Schwerk W, et al. Ultrasound evaluation of hepatic and splenic microabscesses in the immunocompromised patient: sonographic patterns, differential diagnosis, and follow-up. J Clin Ultrasound 1994;22:525-529.
57. Laing F, Jeffrey RJ, Wing V. Biliary dilatation: defining the level and cause by real-time ultrasound. Radiology 1986;160:39-42.
58. Hernanz-Schulman M, Ambrosino M, Freeman P, et al. Common bile duct in children: sonographic dimensions. Radiology 1995;195:193-195.
59. Graham M, Cooperberg P, Cohen M, et al. The size of the normal common hepatic duct following cholecystectomy: an ultrasonographic study. Radiology 1980;135:137-140.
60. White L, Wilson S. Hepatic arterial calcification: a potential pitfall in the sonographic diagnosis of intrahepatic biliary calculi. J Ultrasound Med 1994;13:141-144.
61. Kubaska S, Chew F. Biliary ascariasis. AJR Am J Roentgenol 1997;169:492.
62. Kim OH, Chung HJ, Choi BG. Imaging of choledochal cyst. RadioGraphics 1995;15:69-88.
63. Savader SJ, Benenati JF, Venbrux AC, et al. Choledochal cysts: classification and cholangiographic appearance. AJR Am J Roentgenol 1991;156:327-331.
64. Todani T, Watanabe Y, Narusue M, et al. Congenital bile duct cysts: classification, operative procedure, and review of 37 cases, including cancer arising from choledochal cyst. Am J Surg 1977;134:263-269.
65. Miller WJ, Sechtin AG, Campbell WL, et al. Imaging findings in Caroli’s disease. AJR Am J Roentgenol 1995;165:333-337.
66. Majoie CMLM, Reeders JWAJ, Sanders JB, et al. Primary sclerosing cholangitis: a modified classification of cholangiographic findings. AJR Am J Roentgenol 1991;157:495-497.
67. Dodd GI, Niedzwiecki G, Campbell W, et al. Bile duct calculi in patients with primary sclerosing cholangitis. Radiology 1997;203:443-447.
68. Lim JH. Oriental cholangiohepatitis: pathologic, clinical, and radiologic features. AJR Am J Roentgenol 1991;157:1-8.
69. Miller FH, Gore RM, Nemcek AA, Jr, et al. Pancreaticobiliary manifestations of AIDS. AJR Am J Roentgenol 1996;166:1269-1274.
70. Da Silva F, Boudghene F, Lecomte I, et al. Sonography in AIDS-related cholangitis: prevalence and cause of an echogenic nodule in the distal end of the common bile duct. AJR Am J Roentgenol 1993; 160:1205-1207.
71. Soyer P, Bluemke DA, Reichle R, et al. Imaging of intrahepatic cholangiocarcinoma: 1. peripheral cholangiocarcinoma. AJR Am J Roentgenol 1995;165:1427-1431.
72. Bloom C, Langer B, Wilson S. Role of US in the detection, characterization, and staging of cholangiocarcinoma. RadioGraphics 1999;19:1199-1218.
73. Wibulpolprasert B, Dhiensiri T. Peripheral cholangiocarcinoma: sonographic evaluation. J Clin Ultrasound 1992;20:303-314.
74. Soyer P, Bluemke DA, Reichle R, et al. Imaging of intrahepatic cholangiocarcinoma: 2. hilar cholangiocarcinoma. AJR Am J Roentgenol 1995;165:1433-1436.
75. Hann LE, Greatrex KV, Bach AM, et al. Cholangiocarcinoma at the hepatic hilus: sonographic findings. AJR Am J Roentgenol 1997;168:985-989.
76. Neumaier C, Bertolotto M, Perrone R, et al. Staging of hilar cholangiocarcinoma with ultrasound. J Clin Ultrasound 1995;23:173-178.
77. Teefey SA, Baron RL, Bigler SA. Sonography of the gallbladder: significance of striated (layered) thickening of the gallbladder wall. AJR Am J Roentgenol 1991;156:945-947.
78. Rybicki F. The WES sign. Radiology 2000;214:881-882.
79. Hammond D. Unusual causes of sonographic nonvisualization or nonrecognition of the gallbladder: a review. J Clin Ultrasound 1988;16:77-85.
80. Paulson E, Kliewer M, Hertzberg B, et al. Diagnosis of acute cholecystitis with color Doppler sonography: significance of arterial flow in thickened gallbladder wall. AJR Am J Roentgenol 1994;162:1105-1108.
81. Wu C-S, Yao W-J, Hsiao C-H. Effervescent gallbladder: sonographic findings in emphysematous cholecystitis. J Clin Ultrasound 1998;26:272-275.
82. Bloom RA, Libson E, Lebensart PD, et al. The ultrasound spectrum of emphysematous cholecystitis. J Clin Ultrasound 1989;17:251-256.
83. Teefey S, Kimmey M, Bigler S, et al. Gallbladder wall thickening: an in vitro sonographic study with histologic correlation. Acad Radiol 1994;1:121-127.

84. Kane R, Jacobs R, Katz J, et al. Porcelain gallbladder: ultrasound and CT appearance. Radiology 1984;152:137-141.
85. Collett J, Allan R, Chisholm R, et al. Gallbladder polyps: prospective study. J Ultrasound Med 1998;17:207-211.
86. Berk R, van der Vegt J, Lichtenstein J. The hyperplastic cholecystoses: cholesterolosis and adenomyomatosis. Radiology 1983;146:593-601.
87. Raghavendra B, Subramanyam B, Balthazar E, et al. Sonography of adenomyomatosis of the gallbladder: radiologic-pathologic correlation. Radiology 1983;146:747-752.
88. Rooholamini SA, Tehrani NS, Razavi MK, et al. Imaging of gallbladder carcinoma. Radiographics 1994;14:291-306.
89. Li D, Dong B-W, Wu Y, et al. Image-directed and color Doppler studies of gallbladder tumors. J Clin Ultrasound 1994;22:551-555.
90. Wibbenmeyer L, Sharfuddin M, Wolverson M, et al. Sonographic diagnosis of unsuspected gallbladder cancer: imaging findings in comparison with benign gallbladder conditions. AJR Am J Roentgenol 1995;165:1169-1174.
91. Paulson E, Vitellas K, Keogan M, et al. Acute pancreatitis complicated by gland necrosis: spectrum of findings on contrast-enhanced CT. AJR Am J Roentgenol 1999;172:609-613.
92. Fishman EK, Soyer P, Bliss DF, et al. Splenic involvement in pancreatitis: spectrum of CT findings. AJR Am J Roentgenol 1995;164:631-635.
93. vanSonnenberg E, Wittich G, Chon K, et al. Percutaneous radiologic drainage of pancreatic abscesses. AJR Am J Roentgenol 1997;168:979-984.
94. Patel B, Chenoweth J, Parvey H, et al. Complications of chronic pancreatitis: imaging findings. Radiologist 1998;5:227-236.
95. Lee M, Wittich G, Mueller P. Percutaneous intervention in acute pancreatitis. RadioGraphics 1998;18:711-724.
96. Patel B, Chenoweth J, Garvin P, et al. Role of imaging in the diagnosis of chronic pancreatitis and differentiation from carcinoma of the pancreas. Radiologist 1998;5:245-255.
97. Moorthy T, Nalini N, Narendranathan M. Ultrasound imaging in tropical pancreatitis. J Clin Ultrasound 1991;20:389-393.
98. Van Hoe L, Gryspeerdt S, Ectors N, et al. Nonalcoholic duct-destructive chronic pancreatitis: imaging findings. AJR Am J Roentgenol 1998;170:643-647.
99. Luetmer PH, Stephens DH, Ward EM. Chronic pancreatitis: reassessment with current CT. Radiology 1989;171:353-357.
100. Karlson B-M, Ekbom A, Lindgren P, et al. Abdominal US for diagnosis of pancreatic tumor: prospective cohort analysis. Radiology 1999;213:107-111.
101. Angeli E, Venturine M, Vanzulli A, et al. Color Doppler imaging in the assessment of vascular involvement by pancreatic carcinoma. AJR Am J Roentgenol 1997;168:193-197.
102. Procacci C, Graziani R, Bicego E, et al. Intraductal mucin-producing tumors of the pancreas: imaging findings. Radiology 1996;198:249-257.
103. Procacci C, Megibow A, Carbognin G, et al. Intraductal papillary mucinous tumor of the pancreas: a pictorial essay. RadioGraphics 1999;19:1447-1463.
104. de Lima JJ, Javitt M, Mathur S. Mucinous cystic neoplasm of the pancreas. RadioGraphics 1999;19:807-811.
105. Hough DM, Stephens DH, Johnson CD, et al. Pancreatic lesions in von Hippel-Lindau disease: prevalence, clinical significance, and CT findings. AJR Am J Roentgenol 1994;162:1091-1094.
106. Ng C, Loyer E, Iyer R, et al. Metastases to the pancreas from renal cell carcinoma: findings on three-phase contrast-enhanced helical CT. AJR Am J Roentgenol 1999;172:1555-1559.
107. Agrons G, Corse W, Markowitz R, et al. Gastrointestinal manifestations of cystic fibrosis: radiologic-pathologic correlation. RadioGraphics 1996;16:871-893.
108. Subramanyam B, Balthazar E, Horii S. Sonography of the accessory spleen. AJR Am J Roentgenol 1984;143:47-49.
109. Loftus W, Chow L, Metreweli C. Sonographic measurement of splenic length: correlation with measurement at autopsy. J Clin Ultrasound 1999;27:71-74.
110. Paterson A, Frush D, Donnelly L, et al. A pattern-oriented approach to splenic imaging in infants and children. RadioGraphics 1999;19:1465-1485.
111. Masmune A, Okano T, Satake K, et al. Ultrasonic diagnosis of torsion of the wandering spleen. J Clin Ultrasound 1994;22:126-128.
112. Urritia M, Mergo P, Ros L, et al. Cystic lesions of the spleen: radiologic-pathologic correlation. RadioGraphics 1996;16:107-129.

113. Murray JG, Patel MD, Lee S, et al. Microabscesses of the liver and spleen in AIDS: detection with 5-MHz sonography. Radiology 1995;197:723-727.
114. Franquet T, Montes M, Lecumberri FJ, et al. Hydatid disease of the spleen: imaging findings in nine patients. AJR Am J Roentgenol 1990;154:525-528.
115. Goerg C, Schwerk W, Goerg K, et al. Sonographic patterns of the affected spleen in malignant lymphoma. J Clin Ultrasound 1990;18:569-574.
116. Ishida H, Konno K, Ishida J, et al. Isolated splenic metastases. J Ultrasound Med 1997;16:743-749.
117. Goerg C, Schwerk WB. Splenic infarction: sonographic patterns, diagnosis, follow-up, and complications. Radiology 1990;174:803-807.
118. Ros PR, Moser RP, Jr., Dachman AH, et al. Hemangioma of the spleen: radiologic-pathologic correlation in ten cases. Radiology 1987:481-485.
119. Aytac S, Fitoz S, Atasoy C, et al. Multimodality demonstration of primary splenic angiosarcoma. J Clin Ultrasound 1999;27:92-95.
120. Kohr R, Haendiges M, Taube R. Peliosis of the spleen: a rare cause of spontaneous splenic rupture with surgical implications. Am Surgeon 1993;59:197-199.
121. Goletti G, Ghiselli G, Lippolis P, et al. The role of ultrasonography in blunt abdominal trauma: results in 250 consecutive cases. J Trauma 1994;36:178-181.
122. McKenney K. Role of US in the diagnosis of intraabdominal catastrophes. RadioGraphics 1999;19:1332-1339.
123. McGahan JP, Richards J. Blunt abdominal trauma: the role of emergent sonography and a review of the literature. AJR Am J Roentgenol 1999;172:897-903.
124. Shanmuganathan K, Mirvis S, Sherbourne C, et al. Hemoperitoneum as the sole indicator of abdominal visceral injuries: a potential limitation of screening abdominal US for trauma. Radiology 1999;212:423-430.
125. Richards J, McGahan J, Simpson J, et al. Bowel and mesenteric injury: evaluation with emergency abdominal US. Radiology 1999;211:399-403.
126. Stoupis C, Taylor H, Paley M, et al. The rocky liver: radiologic-pathologic correlation of calcified hepatic masses. RadioGraphics 1998;18:675-685.