Lange Review Ultrasonography Examination, 4th Edition
Chapter 4. Abdominal Sonography
Charles S. Odwin and Arthur C. Fleischer*
Major Vessel Landmarks. Major vessels are used as landmarks to identify normal anatomy and pathology. All vessels are anechoic and are tubular shaped when imaged along their long axis and round or oval shaped in their short axis. It is important to know the location of the organ to help determine the long axis of the vessel. Fig. 4–1 illustrates the major vessels of the abdomen.
FIGURE 4–1. The abdominal viscera with major vessels.
Aorta. The aorta is the largest artery in the body, which enters into the abdominal cavity through the hiatus of the diaphragm at the level of the twelve thoracic vertebra (T12). At this level, it is called the abdominal aorta. It follows a vertical course anterior to the spine and slightly to the left of midline. The aorta distributes oxygenated blood to all parts of the body through systemic circulation. An increased distance between the aorta and spine may indicate retroperitoneal pathology such as adenopathy, fibrosis, or a hematoma.
The abdominal aorta bifurcates at the level of the fourth lumbar vertebra (L4) into the right and left common iliac arteries. The common iliac arteries bifurcate into the internal iliac arteries (hypogastrics), which supply blood to the internal organs in the pelvis and to the external iliac arteries, which supplies blood to the lower extremities.
Measurements. The abdominal aorta decreases in caliper as it courses inferiorly. The normal anteroposterior dimension of the aorta lumen should be <3 cm at the diaphragm narrowing to approximately 1.5 cm at bifurcation.
Branches Of the Aorta. Superior to inferior
Celiac. The celiac axis or trunk is the first visceral branch of the abdominal aorta. It is approximately 2–3 cm long and trifurcates into common hepatic artery, left gastric artery, and splenic artery.
1. The common hepatic artery, which follows a horizontal course to the right. The gastroduodenal artery is a branch of the common hepatic artery and follows a vertical course and is used as the landmark for the anterior lateral aspect of the head of the pancreas. After the gastroduodenal artery branch, the common hepatic artery becomes the proper hepatic artery and enters the liver at the level of the porta hepatis. The hepatic artery courses anteriorly to the portal vein and adjacent to the common bile duct. Once the hepatic artery is intrahepatic, it branches into the right, left, and middle hepatic arteries.
2. The left gastric artery is sometimes visualized on ultrasound.1
3. The splenic artery follows a tortuous horizontal course along the posterosuperior margin of the pancreatic body. It enters the spleen at the splenic helium.
Superior mesenteric artery (SMA) arises from the anterior border of the abdominal aorta about 1 cm inferior from the celiac trunk and follows a vertical and parallel course with the aorta. The SMA is posterior to the body of the pancreas.
Renal arteries branch from the posterior-lateral border of the aorta and course horizontally to the hilum of the kidneys. The right renal artery courses posteriorly to the inferior vena cava. The left renal artery courses directly into the renal hilum.
Gonadal arteries are small vessels that arise off the anterior border of the aorta and inferior to the renal arteries. They are not routinely visualized by ultrasound.
The inferior mesenteric artery is a small artery that arises off the anterior aspect of the abdominal aorta. It follows a vertical course and is slightly to the left of midline. It is not routinely imaged on an ultrasound examination.
PATHOLOGY OF ARTERIES
Arteriosclerosis is primarily an arterial disease in which the vessel wall loses its elasticity and becomes hardened. Atherosclerosis is the most common form in which lipid deposits occur in the inner lining of the artery wall (tunica intima). These deposits may lead to fibrosis and calcifications.
Aneurysm is the dilatation of a segment of a vessel wall caused by a weakness of all three layers of the vessel wall. They are more common in arteries than veins. The most common cause of aneurysms is arteriosclerosis and associated hypertension. Other causes include congenital weakness of a vessel wall, trauma, untreated syphilis, or infections, especially those resulting from bacterial endocarditis. Marfan syndrome is associated with aneurysms in the ascending portion of the aorta extending up to the aortic valve.
Aortic abdominal aneurysm (AAA) is diagnosed when a focal or generalized dilatation is depicted with the aortic anteroposterior diameter >3 cm. The aorta is measured from outer border to outer border. In addition, the size of the lumen is also measured when plaque or calcifications are present. Any aneurysm >7 cm is at a great risk of rupturing. A ruptured aortic aneurysm is a surgical emergency with the majority of rupture from the lateral wall below the level of the renal arteries. Untreated aortic aneurysm has a mortality rate of almost 100%. Aneurysms are classified as true, dissecting, or pseudo (false).
True aneurysm has dilatation of all three layers of the vessel wall (tunica intima, tunica media, tunica adventitia). Clinical findings include palpable pulsatile abdominal mass of physical examination and back or leg pain. The following lists the types of true aneurysms:
1. Fusiform: the most common type of aortic aneurysms characterized by an elongated spindle-shaped dilatation of the artery
2. Saccular: characterized by a focal outpouching of the vessel wall; primarily caused by trauma or infection
3. Berry: small round outpouchings 1–1.5 cm in diameter, typically found within the cerebral vascular system; rupture usually causes death
Dissecting aneurysm (not a true aneurysm) occurs when there is a tear of the intima layer of the vessel wall causing blood to collect between the intima layer and media layer. The artery will have two lumens, a true lumen and a false lumen. Dissecting aneurysms most frequently involve the ascending aorta and more commonly seen in people with hypertension or Marfan syndrome. Clinical findings include severe pain over the site of the aneurysm, and in cases where the dissection is at the level of the ascending aorta, the pain may mimic myocardial infarction (MI). Sonographic appearance may include the demonstration of two lumens with a pulsating intimal flap.
Pseudoaneurysm (false aneurysm) results from a tear in the vessel wall that permits blood to escape into the surrounding tissue. The blood becomes walled off from the vessel and presents as a mass adjacent to the vessel wall. Color Doppler is used to diagnose a pseudoaneurysm; the site of communication between the true lumen and false lumen may be demonstrated, and the blood flow in the false lumen is turbulent. The major causes are from either an arterial catheterization or trauma.
Inferior Vena Cava. The inferior vena cava (IVC) is a large vein formed at the confluence of the right and left common iliac veins at the level of the fourth lumbar (L4). The IVC lies slightly to the right of midline and courses anteriorly as it carries deoxygenated blood into the right atrium of the heart. The IVC varies in size with respiration, increases with exhalation and held inspiration, and decreases with a Valsalva maneuver.
Major Branches into the IVC
Hepatic Veins. See section under liver.
Renal Veins. The right renal vein is located anterior to the right renal artery and follows a short course from the hilum of the right kidney into the IVC. The left renal vein follows a course anterior to the aorta and posterior to the superior mesenteric artery (SMA) before entering into the IVC.5
Gonadal Veins. The right gonadal vein empties directly into the IVC. The left gonadal vein empties into the left renal vein, which drains into the IVC.
Pathology that Affects the Size of the IVC
The IVC is dilated with hepatomegaly, pulmonary hypertension, congestive heart failure (CHF), constrictive pericarditis, right atria myxoma, atherosclerotic heart disease, and right ventricular failure.
The most common tumor that involves the IVC is renal cell carcinoma. Renal cell carcinoma may invade the renal vein and the IVC. This is more common with the right kidney because of the short distance the right renal vein has to travel to enter into the IVC. Thrombus may also be identified as low-level echoes within the IVC. Thrombus in the IVC may cause Budd–Chiari disease.
Causes of IVC Displacement
Mass in posterior, caudate, or right hepatic lobe of the liver
Right renal mass
Right adrenal mass
Retroperitoneal tumors: retroperitoneal liposarcoma, leiomyosarcoma, osteosarcoma, rhabdomyosarcoma
Portal System. See liver section below.
Gross Anatomy of the Liver
The liver is the second largest organ in the body. The right lobe is five to six times larger than the left lobe. The normal sonographic longitudinal measurement of the liver is <15 cm, >15.5 cm is considered hepatomegaly.1 The mean anterior to posterior measurement taken at the midclavicular line is approximately 10.5 cm. A Riedel’s lobe is a normal variant of the right lobe of the liver, which is more common in women than men. Riedel’s lobe is a tongue-like projection extending downward from the right lobe of the liver. This can sometimes be mistaken for a hepatomegaly or a tumor.
The liver is completely covered by connective tissue known as Glisson’s capsule. It is mostly an intraperitoneal organ except for the bare area posterior to the dome of the liver, porta hepatis region, and the gallbladder fossa region.
Standards for Describing Liver Anatomy: Lobes, Ligaments, and Fissures
A number of different standards are used for liver division: hepatic veins, fissures, ligaments, and portal veins. Ligaments and fissures are used as landmarks in the more caudad liver sections. (See Fig. 4–2.) Couinaud segment anatomy (used for hepatic lesion localization) divides the liver into eight segments and uses both hepatic veins and portal veins as landmarks.5
FIGURE 4–2. (A) Graphic representation. IVC = inferior vena cava; RPS, RAS = right lobe posterior and anterior segments; LMS, LLS = medial and lateral segments of left lobe; FLV = fissure of ligamentum venosum; RPV = right vein branch; RHV, MHV = right and middle hepatic veins; BD = bile duct. (B) LMS, LLS = medial and lateral segments of left lobe; FL = falciform ligament; LT = ligamentum teres. (Reprinted with permission from Sexton CC, Zeman RK: Correlation of computed tomography, sonography and gross anatomy of the liver, AJR 1983; Oct;141(4):711–718.)
Traditional Anatomy of the Liver
Traditionally the liver is anatomically subdivided into four lobes: right, left, quadrate, and caudate lobes, which are based on external landmarks. (See Fig. 4–3.)
FIGURE 4–3. (A) Lobes, ligaments, and fissures. (B) Anterior projection of the liver. (C) Posterior view of the diaphragmatic surface of the liver. The caudate lobe is located on the posterosuperior surface of the right lobe, opposite the tenth and eleventh thoracic vertebrae.
Couinaud Standard for Describing Liver Segments
This method of anatomy is widely used in Europe and now becoming the universal nomenclature for location of hepatic lesions.1 Each segment has its own blood supply with a branch of the portal vein in the center bounded by a hepatic vein. The liver is divided into eight functionally segments with each segment having its own blood supply. (See Fig. 4–4.)
FIGURE 4–4. Couinaud’s anatomy.
Functional Anatomy of the Liver
Functionally, the liver is divided into three lobes: right, left, and caudate, which is based on vascular supply.
The normal liver parenchyma is homogeneous in texture, and its echogenicity may be compared with other abdominal organs.
The following is going from the most echogenic to the least echogenic:
renal sinus > pancreas > liver > spleen > renal cortex > renal medullary pyramids
Middle Hepatic Vein. Divides the liver into right and left lobes (Fig. 4–3A).
Right Hepatic Vein. Divides the right lobe of the liver into anterior and posterior segments (Fig. 4–3A).
Left Hepatic Vein. Divides the left lobe of the liver into medial and lateral segments (Fig. 4–3A).
Both the right and left hepatic veins drain blood from the caudate lobe.
Ligamentum Venosum. The ligamentum venosum is a remnant of the fetal ductus venosus. It divides the caudate lobe from the left lobe. It may be visualized sonographically on either a longitudinal or a transverse scan as an echogenic line extending transversely from the porta hepatis.
Ligamentum Teres (Round Ligament). (Fig. 4–3C). The ligamentum of teres is contained in the falciform ligament. It is a remnant of the fetal umbilical vein. It courses within the left intersegmental fissure, dividing the left lobe into medial and lateral segments. Sonographically, it is best visualized on a transverse view as a round echogenic structure just to the left of midline.
Falciform Ligament. (Fig. 4–3B). The falciform ligament is a fold of peritoneum, which contains the ligamentum of teres. It extends from the umbilicus to the diaphragm and attaches the liver to the anterior abdominal wall and diaphragm. It divides the right and left lobe of the liver on the diaphragmatic surface. Sonographically it is seen as a round, hyperechoic area in the left lobe of the liver.
Coronary Ligament. The coronary ligament is contiguous with the falciform ligament. It connects the posterior surface of the liver to the diaphragm.
Main Lobar Fissure (Middle Intersegmental Fissure). The main lobar fissure separates the right and left lobes of the liver. It is visualized sonographically as an echogenic linear line extending from the portal vein to the neck of the gallbladder. Table 4–1 is a guide to the anatomic structures useful in defining segmental anatomy
TABLE 4–1 • Intersegmental Fissures
Liver Vessels—Hepatic Veins, Portal Vein, Hepatic Artery
The liver has a dual blood supply system. It receives blood from both the hepatic artery and the portal vein. The main portal vein blood carries nutrients from the gastrointestinal tract, gallbladder, pancreas, and spleen. The majority of the total blood supplied to the liver is from the main portal vein.
Hepatic Veins. There are three hepatic veins: right, middle, and left. They follow a superior posterior course and drain deoxygenated blood into the inferior vena cava. Hepatic veins are nonpulsatile, increase in size as they course superiorly toward the inferior vena cava, and the walls are less echogenic than the portal veins (Table 4–2) (Table 4–3).
TABLE 4–2 • Couinaud’s Anatomy
TABLE 4–3 • Differentiation between the Portal Vein and Hepatic Veins
Portal Vein. The portal vein is formed posterior to the pancreatic neck by the confluence of the splenic vein and superior mesenteric vein. It follows a cephalic right oblique course and enters into the liver at the porta hepatis also known as the portal triad. The portal triad contains (1) portal vein, (2) hepatic artery, and (3) bile duct. The main portal vein lies anterior to the inferior vena cava, cephalic to the head of the pancreas, and caudal to the caudate lobe. The main portal vein bifurcates in the liver into the right and left portal veins.
Right Portal Vein. The right portal vein is larger than the left portal vein. It follows a posterior caudad course and further divides into anterior and posterior branches.
Left Portal Vein. The left portal vein follows a cephalic anterior course to supply blood to the left lobe of the liver. It is the umbilical portion of the portal vein.
Hepatic Artery. The hepatic artery originates from the celiac axis and courses transversely. The hepatic artery and the common bile duct are anterior to the portal vein as they enter the liver at the portal hepatis, with the common bile duct slightly more lateral. The hepatic artery is at the same level as the hepatoduodenal ligament and is superior to the head of the pancreas.
Common Bile Duct. The common bile duct is formed by the confluence of the common hepatic duct and the cystic duct. The superior portion of the biliary duct, which is anterior to the right portal vein is the common hepatic duct. The common bile duct follows an oblique postero-caudal course and travels along the dorsal aspect of the pancreatic head before it joins with the main pancreatic duct, and together they enter into the second portion of the duodenum.
Liver Function Tests
1. Aspartate aminotransferase (AST), formerly known as serum glutamic-oxaloacetic transaminase (SGOT): This is increased with hepatocellular disease and is useful in detecting acute hepatitis before jaundice occurs and following in the course of hepatitis. It is not increased in cases of such chronic liver disease as cirrhosis or obstructive jaundice. It is increased in liver cell necrosis due to viral hepatitis, toxic hepatitis, and other forms of acute hepatitis.
2. Alanine aminotransferase (ALT), formerly known as serum glutamic pyruvic transaminase (SGPT): This enzyme is increased with hepatocellular disease and is used to assess jaundice. It rises higher than AST in cases of hepatitis and takes 2–3 months to return a normal level.
3. Alkaline phosphatase (ALP): Normally found in serum. Its level rises in liver and biliary tract disorders when bile excretion is impaired. Obstruction of bile can be caused by either a biliary or liver disorder such as; obstructive jaundice, biliary cirrhosis, acute hepatitis, and granulomatous liver disease.
4. Ammonia: Normally metabolizes in the liver and is excreted as urea; increased in hepatocellular disease.
5. Alpha-fetal protein (α-AFP): A protein normally produced by the fetal liver and yolk sac, GI tract, scrotal and hepatocellular (hepatomas) germ cell neoplasms, and other cancers in adults. AFP level is used to monitor chemotherapy treatment and prenatal diagnosis neural tube defects in the fetus, rarely in other cases.
6. Bilirubin: Derived from the breakdown of red blood cells into hemoglobin. Excreted by the liver in bile (main pigment). When destruction of red blood cells increases greatly or when the liver is unable to excrete normal amounts, the bilirubin concentration in the serum increases. If it is increased too high, jaundice may occur. Levels of indirect and direct bilirubin may determine intrahepatic and extrahepatic obstruction.
Direct bilirubin (conjugated bilirubin): It is elevated when there is an obstruction of the biliary system. obstructive jaundice.
Indirect bilirubin (unconjugated bilirubin): Excessive destruction of red blood cells/hemolysis associated with anemias and liver disease; elevation of the total bilirubin occurs with hepatitis, hepatic metastasis.
7. Hematocrit: Volume percentage of erythrocytes in the whole body; a drop in hematocrit can indicate a hematoma due to liver trauma or bleeding elsewhere in the body.
8. Leukocytosis: A substantial increase in white blood cells above the normal range indicates an inflammatory process or abscess.
9. Prothrombin time (PT): Prothrombin is converted to thrombin in the clotting process by action of vitamin K that is absorbed in the intestines and stored in the liver. When liver function is compromised by liver disease, prothrombin is decreased and can cause uncontrolled hemorrhage.
10. Urinary bile and bilirubin: Bile and bilirubin are not normally found in the urine. There may be spillover into the blood when there is obstructive liver disease and excessive red cell destruction. Bile pigments are found in the blood when there is a biliary obstruction. Bilirubin is found alone when there is an excessive amount of red blood cell destruction.
11. Urinary urobilinogen: This test is used to differentiate between a complete obstruction of the biliary tract versus an incomplete obstruction of the biliary tract.
Urobilinogen is a product of hemoglobin breakdown and can be elevated in cases of liver disease, hemolytic disease, or severe infections. Urobilinogen does not increase or there is no excess amount found in urine in cases of complete biliary obstruction.
12. Fecal urobilinogen: Traces of urobilinogen are normally found in fecal matter, but an increase or decrease in normal amounts may indicate hepatic digestive abnormalities. An increase may suggest an increase in hemolysis. A decrease is seen with complete obstruction of the biliary system.
Diffuse Hepatocellular Disease. There is a decrease in liver function with an increase in the liver enzymes; the increase in the liver enzymes is directly related to the amount of hepa-tocytic necrosis. Total bilirubin levels may be elevated with increase prothrombin time (blood clotting factor). Diffuse liver disease has a varied sonographic appearance depending on whether it is acute or chronic (Tables 4–4 and 4–5).
TABLE 4–4 • Diffuse Liver Disease
TABLE 4–5 • Focal Disease of the Liver
Causes of Jaundice
Medical Jaundice (Nonobstructive)
Hepatocellular Diseases—Disturbances within the liver cells that interfere with excretion of bilirubin:
Fatty liver (most common cause ETOH abuse)
Hemolytic Disease—An increase in red blood cell destruction that results in the increase of indirect bilirubin (nonobstructive jaundice):
Surgical Jaundice (Obstructive)—Interference with the flow of bile caused by obstruction of the biliary tract. There are many causes of obstruction, some of the causes are:
Mass in the head of the pancreas
Mass in the porta hepatis
Enlarged lymph nodes at the level of the porta hepatis
Vascular Abnormalities Within the Liver
Intrahepatic—Most common cause is cirrhosis, Budd–Chiari syndrome
Extrahepatic—thrombosis, occlusion and compression of portal or splenic veins, congestive heart failure
Formation of collateral venous channels
Gastrointestinal tract bleeding caused by opening of low pressure vascular channels
Dilatation of the portal vein (>13 mm)
Dilatation of SMV and splenic vein (>10 mm)
Formation of collaterals (portal vein, splenic vein, SMV can be normal size)
Varices—esophageal, splenorenal, gastrorenal, intestinal
Portafugal (reversal) blood flow
Recanalization of the umbilical vein >3 mm
Portal Vein Obstruction
Thrombosis, invasion of the portal vein by tumor
Hepatocellular carcinoma, pancreatic or GI cancer or lymphoma
Nonvisualization of the portal vein
Echoes within the portal vein
Dilatation of the splenic and superior mesenteric vein (proximal to the level of obstruction)
Obstruction of the hepatic veins caused by thrombosis or compression from a liver mass
Abnormal liver function tests
Reduced or nonvisualization of the hepatic veins
Hepatic veins proximal to the obstruction may be dilated
Large and hypoechoic caudate lobe
Abnormal Doppler blood flow
Sonography of Transjugular Intrahepatic Portosystemic Shunt (TIPS)
Transjugular intrahepatic portosystemic shunt (TIPS) is a procedure performed on patients with portal hypertension or cirrhosis. The procedure consists of placement of a metallic shunt with fluoroscopic guidance using the internal jugular vein as an access site. Once the catheter with the preloaded shunt is directed into a major hepatic vein, usually the right, the catheter is directed toward the main portal vein and pushed through the liver. Once the shunt is deployed, there is flow from the portal vein directly into a hepatic vein.
Duplex color Doppler sonography is used to confirm patency of the TIPS and determines the relative velocity in the proximal, mid, and distal portion of the TIPS. In general, velocities within the TIPS can range from 90 to 190 cm/s. Intimal hyperplasia or thrombus can obstruct the shunt.
Sonography of Liver Transplant
Sonography has an important role in assessing the flow within liver transplants. It is also used for guided biopsy/aspiration of intrahepatic lesions or perihepatic collections. Sonography is also used for preoperative assessment of candidates for liver transplants to ensure patency of the main portal vein and to determine whether there are any intrahepatic masses.
Duplex color Doppler sonography of a patient with a liver transplant includes assessment of flow (spectral and color Doppler) of the main portal vein, right and left portal veins, main hepatic artery, right and left hepatic artery, right, middle, and left hepatic veins, inferior vena cava, and splenic artery and vein. Spectral waveforms obtained from these vessels determine direction and relative velocity of flow. Waveforms obtained from the hepatic veins correlate with “liver compliance,” which is diminished in cirrhosis and passive liver congestion or rejection. Normal values for velocities of the blood flow in these vessels have been reported.
In addition, the shape of the waveforms suggests “downstream” resistance. For example, the waveform from the main hepatic artery can demonstrate a “spikey” appearance early after transplantation only to become less resistant as the anastomosis matures. The interested reader should consult the reference suggested in this study guide for further information regarding this topic.
The gallbladder is mostly intraperitoneal and is located in the gallbladder fossa, which is on the visceral surface of the liver. It lies between the right and left lobes of the liver and posterior and caudal to the main lobar fissure. The gallbladder is a pear-shaped structure with a thin wall that is <3 mm. It is approximately 8 cm in length, with a transverse diameter <5 cm. The gallbladder is divided into three main segments: fundus, body, and neck. The fundus is the most anterior segment, while the neck has a fixed anatomic relationship to the right portal vein and main lobar fissure. The neck tapers to form the cystic duct. The spiral valves of Heister are located in the cystic duct, and stones may collect here.
The right and left hepatic ducts join to form the common hepatic duct whose function is to transport bile to the gallbladder. Bile enters and exits the gallbladder via the cystic duct. The cystic duct unites with the common bile duct to transport concentrated bile to the second portion of the duodenum.
The three main functions of the gallbladder are to concentrate bile, store the concentrated bile, and transport the bile to the duodenum. The release of the hormone cholecystokinin is stimulated when food enters into the stomach, especially fatty foods and dairy products. Cholecystokinin stimulates the gallbladder to contract and the sphincter of Oddi to relax and open. The intraductal pressure decreases with the contraction of the gallbladder and the opening of the sphincter of Oddi. The bile flows to the small intestine, which aids in the digestion of food by breaking down fatty foods and dairy products.
Gallbladder Variants and Anomalies
Junctional Fold. Is the most common variant, which is a fold or kinking located on the posterior gallbladder wall between the body and neck.
Phrygian Cap. A fold located in the fundal portion of the gallbladder (Fig. 4–5).
FIGURE 4–5. Gallbladder with variants.
Hartmann’s Pouch. A small sac located between the junctional fold and the neck of the gallbladder. It is an area where stones may collect (Fig. 4–5)
Septation. A thin wall or partition into the lumen of the gallbladder. This is seen as a thin linear hyperechoic structure within the gallbladder.
Congenital anomalies are rare; the gallbladder can have an ectopic location and be found intrahepatic.
Laboratory Values of Biliary Tract Disease
White Blood Count (WBC). Increases in cases of infection, acute cholecystitis, chronic cholecystitis, cholangitis
Serum Bilirubin. Increases in cases where the biliary system becomes obstructed, gallbladder carcinoma
Abnormal Liver Function Tests
Serum Alkaline Phosphatase (ALP). Increases in cases of posthepatic jaundice
Prothrombin Time (PT). The clotting time is longer in patients with acute cholecystitis, carcinoma of the gallbladder, and prolonged common bile duct obstruction.
Aspartate aminotransferase (AST) and alanine aminotransferase (AST) are abnormal in cases of cholecystitis, choledocholithiasis, and any injury to the bile ducts.
Sonographic Nonvisualization of the Gallbladder. The most common reason for not visualizing the gallbladder on a sonogram is normal physiological contraction of the gallbladder caused by the patient not being NPO. The gallbladder may not be identified in patients who have had a cholecystectomy, ectopic gallbladder, chronic cholecystitis with the gallbladder lumen filled with gallstones, solid mass obliterating the gallbladder, intrahepatic obstruction, or a porcelain gallbladder. Agenesis of the gallbladder is very rare. When the gallbladder in not identified on ultrasound, the gallbladder fossa should be documented. This can be accomplished by locating the right portal vein and following the main lobar fissure from the right portal vein to the gallbladder fossa region.
Causes of a Large Gallbladder (Hydrops). A large gallbladder can be caused by prolonged fasting, intravenous hyperalimentation, a cystic obstruction, or obstruction of the common bile duct. A Courvoisier gallbladder is a large gallbladder caused by an obstruction at the distal portion of the common bile duct. The patient has “painless” jaundice, elevated serum bilirubin, and abnormal liver function tests. The obstruction is usually caused by a malignancy in the area of the distal CBD (pancreatic head carcinoma, common duct carcinoma, duodenal carcinoma, ampulla of Vater carcinoma) or diabetes and postvagotomy.
Causes of a Small Gallbladder. A common cause of a small gallbladder is that the patient has eaten. Other causes include: intrahepatic biliary obstruction (bile is unable to enter into the gallbladder) chronic cholecystitis; liver disease that destroys the liver parenchyma and, therefore, decreases the production of bile; and in extremely rare cases, congenital hypoplasia of the gallbladder.
Causes of Low Level Echoes in the Gallbladder Lumen/with Mobility
Biliary Sludge. The most common cause of sludge is stasis of bile attributable to cholecystitis, extrahepatic obstruction, hyperalimentation, or in patients who have been NPO for a long period of time. Sludge is a common precursor to gallstones. Sludge appears as low-level nonshadowing echoes in the dependent portion of the gallbladder that moves with a change in the patient position. Other causes of mobile low level echoes within the gallbladder lumen include; blood, pus and viscous bile. Intraluminal echoes that do not shadow or are nonmobile include: polyps, cholesterosis, artifacts, septi (junctional fold), and gallbladder carcinoma.
Pathology of the Gallbladder
Reasons for Gallbladder Wall Thickening >3 mm (Table 4–6)
TABLE 4–6 • Reasons for Gallbladder Wall Thickening >3 mm
Cholelithiasis (Gallstones). Patients may present asymptomatic or with right upper quadrant (RUQ) pain and a history of nausea and vomiting after eating. Cholecystitis is sometimes present. The following sonographic characteristics need to be present in order to diagnose gallstones:
1. Echogenic foci—Echogenic due to the acoustic mismatch between the stones and bile
2. Posterior acoustic shadowing—Most of the sound is absorbed (attenuated), producing a shadow.
3. Gravity dependent—Stones are gravity dependent and move to the most dependent portion of the GB when the patient position is changed.
Structures That Can Mimic Gallstones
• Gas in the duodenum
• Surgical clips from post-cholecystectomy
• Valves of Heister and folds in gallbladder
Shadowing from the spiral valves of Heister—refraction artifact from the cystic duct
Bowel—usually not a clean shadow
Air in the biliary tree—from previous surgery or GB fistula
Low-level echoes in the gallbladder lumen—no shadowing
Polyps. Polyps are not gravity dependent and do not move with changing patient position.
Adenomyomatosis. Hyperplastic change in the gallbladder wall (Table 4–6).
Causes of gallstones in children include hemolysis; for example, sickle cell disease, cystic fibrosis, malabsorption syndrome (Crohn’s disease), hepatitis, and congenital biliary anomalies (choledochal cyst, biliary atresia).
Mirizzi Syndrome. Refers to a common hepatic duct obstruction caused by a stone in the cystic duct with a normal common bile duct. Most patients present with clinical findings of RUQ pain, jaundice and fever.
Acute Cholecystitis. Acute cholecystitis is inflammation of the gallbladder wall with decreased gallbladder function. Acute cholecystitis is usually caused by an obstruction at the level of the cystic duct, bacterial infection in the biliary system, or pancreatic enzyme reflux. Clinically, the patient may present with acute RUQ pain that may radiate to the right scapular area. Patient may have a sonographic Murphy’s sign which is a focal pain over the gallbladder when compressed by the transducer, this should not be confused with clinical Murphy’s sign in which tenderness occur with a sudden stop in inspiratory effort when pressure is applied to the RUQ. Sonographic findings may include diffuse gallbladder wall thickening >3 mm; gallstones; “halo” sign suggestive of subserosal edema; cystic artery along the anterior gallbladder wall; transverse diameter >5 cm; sludge; and pericholecystic fluid. The laboratory findings in acute cholecystitis may include elevated serum bilirubin and abnormal liver function test results.
Complications of Acute Cholecystitis
Empyema—Pus in the Gallbladder. Clinically, the patient presents sicker than with acute cholecystitis, and sonographically, there will be low-level echoes in the gallbladder lumen with thickening gallbladder wall.
Emphysematous Cholecystitis—Rare occurrence caused by gas forming bacteria in the wall of the gallbladder
Gangrene of the Gallbladder—Caused by absence of blood supply to the gallbladder
Perforation of the Gallbladder—Caused by infection and gallstones
Pericholecystic Abscess—Usually caused by perforation of the gallbladder
Ascending Cholangitis—Caused by spreading of the inflammation of the gallbladder
Acalculous Cholecystitis—Less than 5% of patients with cholecystitis will not have gallstones. The cause of acalculous cholecystitis is a combination of bile stasis and direct vascular changes. The etiology of this combination: trauma, patients who are NPO for long period of time
Chronic Cholecystitis—Caused by recurrent or chronic inflammatory changes of the gallbladder. It is the most common cause of symptomatic gallbladder disease and is associated with gallstones in 90% of the cases. Clinically, the patient presents with intermittent RUQ pain and intolerance to fatty and fried foods. Laboratory findings can include elevated AST, ALT, alkaline phosphatase, and increase of direct serum bilirubin. The sonographic appearance includes small or normal size gallbladder, gallstones, sludge, and thicken echogenic gallbladder wall. A positive WES sign may be imaged: the double arc and shadowing are caused by W-echo from the gallbladder wall, E-echo from the gallstone, S-shadowing from gallstones.
Fistula between the gallbladder and duodenum
Causes of pericholecystic fluid include acute cholecystitis, pericholecystic abscess, ascites, pancreatitis, peritonitis, and acquired immunodeficiency syndrome (AIDS).
Porcelain Gallbladder—Porcelain gallbladder is defined as an intramural calcification of the gallbladder wall, which occurs in association with chronic cholecystitis in most cases. The etiology is unknown and has an increased incidence of gallbladder carcinoma. The sonographic appearance of porcelain gallbladder includes the following:
• Curvilinear echogenic structure in the gallbladder fossa with posterior acoustic shadowing. The gallbladder wall of porcelain gallbladder can be so calcific that the distal acoustic shadow obscures the visualization of the posterior wall.
• Hyperechoic anterior and posterior gallbladder wall with distal acoustical shadowing
• Convex or Irregular gallbladder wall with areas of echo densities and shadowing
Benign Tumors of the Gallbladder—Benign tumors of the gallbladder are rare. They represent overgrowth of the epithelial lining. Patients are usually asymptomatic.
Adenoma—The most common of the benign gallbladder tumors. They are frequently located in the fundus portion of the gallbladder and <1 cm in size. Sonographically, they appear as low-level echo masses that do not shadow or move to the dependent portion of the gallbladder.
Adenomyomatosis (a form of hyperplastic cholecystosis)—
• Hyperplasia of the epithelial and muscular surfaces of the gallbladder wall
• Epithelial and intramural diverticula (Rokitansky-Aschoff sinuses)
There are various types and the most common type is usually located at the fundus. They may also be annular or they can be either diffuse or segmental
Diffuse or segmental wall thickening
Intraluminal diverticula (RS sinuses) may be filled with bile, sludge or stones and appear either as anechoic or echogenic with distal shadowing or comet tail artifact. The reverberations are the sonographic appearance that differentiates this disease from an adenoma.
Cholesterolosis (strawberry gallbladder)—A form of hyperplastic cholecystosis. The gallbladder usually appears normal on ultrasound.
Polyps—Small echo-densities attached to the gallbladder wall by a stalk; they do not shadow or move to the dependent portion of the gallbladder.
Carcinoma of the Gallbladder—The most common biliary malignancy. Pancreatic cancer is the most common malignant cause to obstruct the biliary tree. Most carcinomas of the gallbladder are adenomas. They usually do not occur until the sixth or seventh decade and are more common in women than men. Previous gallbladder disease; for example, inflammatory disease or gallstones are often precursors. Gallstones are usually present. Most patients have direct extension into the liver and surrounding structures (lymphatic). Signs and symptoms are similar to chronic cholecystitis (may be asymptomatic, loss of appetite, nausea, vomiting, intolerance to fatty foods and dairy products.) Sonographic appearance usually includes gallstones in addition to:
Solid mass filling the gallbladder lumen (most common type)
Localized thickened gallbladder wall with a small gallbladder lumen
Fungating mass projecting from the gallbladder wall into the lumen
The intrahepatic radicles converge to form the main right and left hepatic ducts at the porta hepatis. The right and left hepatic ducts unite to form the common hepatic duct.
The common hepatic duct joins the cystic duct to form the common bile duct. The common bile duct courses along the hepatoduodenal ligament (ligament that attaches the liver to the duodenum), behind the duodenal bulb and posterior aspect of the pancreatic head to enter the second portion of the duodenum. The common bile duct joins with the main pancreatic duct at the ampulla of Vater (see Fig. 4–6).
FIGURE 4–6. Gallbladder and biliary ducts anatomy.
The common hepatic duct is always anterior the right portal vein, except in cases normal variant or congenital anomalies. The normal common bile duct lumen measures ≤6 mm; the walls are not included in the measurement. The normal diameter of the common bile duct may increase 1 mm per decade starting at the sixth decade. This is due to the common bile duct becoming ecstatic with age. An enlarged common bile duct after a cholecystectomy is normal; if a patient is symptomatic (jaundiced or RUQ pain), a retained stone or a postoperative stricture must be ruled out.
Bile Duct Measurements in a Fasting Patient
Common Hepatic Duct ≤ 4 or 5 mm
Common Bile Duct ≤ 6 mm
Sonographic Appearance of the Biliary System. The cystic duct and intrahepatic ducts (right and left hepatic ducts) are not usually visualized on ultrasound unless they are dilated. The extrahepatic ducts (common hepatic duct and common bile duct, which are also known as the common ducts) are routinely visualized on ultrasound.
Sonographic Criteria for Intrahepatic Dilatation
The bile duct courses anterior to the portal veins. When dilated, a “parallel channel sign” or “double-barrel shotgun sign” is imaged.
Increased numbers of tubular structures are imaged in the periphery of the liver.
Stellate formation of the tubes near the porta hepatis.
Posterior acoustic enhancement distal to the ducts.
The sonographic appearance of the biliary system varies depending on the level of obstruction. Ducts dilate proximal to the level of obstruction. Intrahepatic dilatation may be the only sonographic indication of an obstruction (Table 4–7). There may be intrahepatic dilatation with common bile duct dilatation with a normal gallbladder or intrahepatic and common bile duct dilatation with a small gallbladder (Table 4–8). The cause of the latter is chronic cholecystitis.
TABLE 4–7 • Types of Biliary Obstruction
TABLE 4–8 • Level of Obstruction Causing Intrahepatic Dilatation
Biliary Atresia—The most common fatal liver disorder in children in the United States. There are two forms. In atresia of the intrahepatic radicles, there is nonvisualization of the biliary radicles and gallbladder. In atresia of the extrahepatic radicles, there is an anastomosis of the biliary tree to the jejunum (second part of the small intestine), there will be dilatation of the intrahepatic radicles, and occasionally, the gallbladder will also be imaged. It is difficult to differentiate between biliary atresia and neonatal hepatitis. A nuclear medicine scan and hepatic biopsy may be needed to make a definite diagnosis.
Caroli’s Disease—Caroli’s disease is a genetic trait characterized by a segmental saccular dilatation of the intrahepatic ducts. Caroli’s disease leads to bile stasis, bacterial growth, abscesses, cholangitis, formation of stones, and decreased liver function caused by the compression of the hepatocytes.
Sonographically, the liver will have multiple cystic structures that communicate with the intrahepatic ducts. Stones and echoes may appear within the bile ducts.
Choledochal Cyst—Choledochal cyst is characterized as a cystic dilatation and outpouching of the common duct wall. The signs and symptoms are intermittent jaundice, RUQ pain, RUQ mass, and failure to thrive. Sonographically, the dilated common bile duct is imaged entering into the cystic mass, and the gallbladder is imaged as a separate cystic structure. The intrahepatic radicles may be dilated.
Biliary System Pathology
Cholangitis—Inflammation of the biliary tract caused by bacterial infection of the biliary tract. Cholangitis is associated with biliary stasis caused by obstruction; for example, choledocholithiasis, biliary stricture, and neoplasm. The signs and symptoms are fever, jaundice, and upper abdominal pain. Abnormal laboratory tests include leukocytosis, increased serum bilirubin, and increased serum alkaline phosphatase. Sonographic appearance may include air in the biliary system, dilatation of the extrahepatic ducts, and the gallbladder may be enlarged.
Sclerosing cholangitis—Inflammation and fibrosis of bile duct commonly associated with intrahepatic calculi complications
Choledocholiths—Stones in the common bile duct, which may cause common bile duct obstruction. The stones usually originate in the gallbladder. The signs and symptoms are biliary colic and jaundice. Patients may also present with gallstones and cholangitis. Laboratory tests show an increased serum bilirubin, increased alkaline phosphatase, and bacteremia. Sonographically, stones in the common bile duct are difficult to image because of the deep position of the duct, overlying bowel gas and a very small amount of fluid surrounding the stone. A stone may be positioned more posterior than the focal zone of the transducer. The common bile duct may be dilated with an echogenic focus and posterior acoustic shadowing.
Primary Malignant Tumors of the Biliary Tree
Adenocarcinoma and Squamous Cell Carcinoma—All branches of the biliary tree may be affected, with the common bile duct being the most common site. Predisposing factors associated with carcinoma of the biliary tree are inflammation, cholelithiasis, and chronic ulcerative colitis. Signs and symptoms are anorexia, weight loss, RUQ pain, and jaundice. Sonographically, intraluminal soft tissue echoes mark dilatation with a normal pancreatic head, focal biliary stricture, or abrupt termination of the duct.
Klatskin Tumor—A Klatskin tumor is a carcinoma that arises at the union of the right and left hepatic ducts. This type of tumor has the worst prognosis because the patient typically does not have any symptoms and, therefore, does not get diagnosed until the liver is involved. Sonographically, it presents as a solid mass at the junction of the right and left hepatic ducts. There is intrahepatic duct dilatation without extrahepatic duct dilatation.
The pancreas lies transversely in the retroperitoneal cavity. It extends from the C-loop of the duodenum to the splenic helium and is divided into four parts: head, neck (sometimes included with the head), body, and tail. The size and shape of the pancreas may vary in size depending on the age and body habitus of the patient. The anteroposterior measurements of the pancreas are approximately: head 3 cm, body 2 cm, and tail 2 cm. The pancreas has no capsule and is generally dumbbell or sausage shaped. Fig. 4–7 demonstrates the pancreas and its related landmarks.
FIGURE 4–7. Anatomy of the pancreas.
The pancreas can sometimes be difficult to visualize on ultrasound, and vascular landmarks are used to identify the pancreas and the pancreatic region. The head of the pancreas is anterior to the inferior vena cava and right renal vein. The common bile duct can be seen at the posterior lateral margin of the pancreatic head. The gastroduodenal artery may be visualized at the anterior lateral margin. Both structures are imaged as anechoic round structures that appear to be within the head of the pancreas.
The uncinate process is a tongue-like extension of the pancreatic neck. A prominent uncinate process will displace the superior mesenteric artery and vein anterior to the pancreas.
The body of the pancreas is the largest portion of the gland. The splenic vein is the most reliable landmark used to visualize the pancreas. The splenic vein courses along the posterior margin of the pancreas and joins with the superior mesenteric vein to form the portal vein. The portal confluence is posterior to the neck of the pancreas. The body is anterior to the superior mesenteric artery, superior mesenteric vein, splenic vein, left renal vein, and aorta. The left renal vein is imaged posterior to the superior mesenteric artery and anterior to the aorta.
The tail of the pancreas lies anterior to the left kidney and medial to the splenic helium. The splenic artery courses along the superior anterior border, and the splenic vein courses along the posterior border.
The main pancreatic duct, also called the Wirsung’s duct, courses the entire length of the pancreas. It extends from the tail of the pancreas and joins with the common bile duct at the ampulla of Vater before entering into the second portion of the duodenum. The accessory duct, or Santorini duct, courses diagonally through the head of the pancreas and enters into the duodenum separately.
Table 4–9 lists the landmarks used for visualizing the pancreas on a sonographic examination.
TABLE 4–9 • Landmarks for Visualizing the Pancreas
Sonographic Appearance. The pancreas is a homogeneous organ with either the same echogenicity as the liver or slightly more echogenic than the normal liver. In children, the pancreas is less echogenic and relatively larger than in the adult. The pancreas is more difficult to visualized with advance age. The pancreas, which has no true capsule and becomes more echogenic, tends to blend in with the surrounding retroperitoneal fat. The main pancreatic duct may be seen as a tubular structure coursing from the tail of the pancreas to the head. The normal caliber varies from 2 to 3 mm, the largest diameter being in the head of the pancreas.
Functions. The pancreas has endocrine and exocrine functions. The islets cells of Langerhans has three different types of cells, and each cell secretes a different type of hormone. The alpha cells secrete glucagon; beta cells secrete insulin; and delta cells secrete somatostatin.
The exocrine function of the pancreas secretes amylase, lipase, and trypsin. These enzymes aid in digestion and are produced in the pancreas and travel to the duodenum through the pancreatic duct.
Pancreatic Diseases (Table 4–10)
TABLE 4–10 • Diseases of the Pancreas
Pancreatitis. Pancreatitis is a diffuse inflammatory process of the pancreas in which the pancreatic enzymes autodigest the pancreatic tissue. There are a number of mechanisms that cause the pancreatic enzymes to become activated within the pancreas. The most common causes in older adults include alcohol, biliary tract disease, trauma, surgery, perforated peptic ulcer disease, and drugs.
Causes of pancreatitis in younger patients include infectious agents—mumps and mononucleosis. Hereditary causes include cystic fibrosis and congenital pancreatitis (rare). Pancreatitis can be classified as either acute with or without complications or chronic.
Acute Pancreatitis. Patients present with abdominal pain characteristically in the epigastrium or periumbilical region with nausea and vomiting. The pain usually radiates to the back and commonly occurs following a large meal or alcohol binge. There is abdominal distention attributable to the decrease in gastric and intestinal motility and chemical peritonitis. The entire gland is usually affected, and sonographically, the pancreas may appear normal or is less echogenic.
Laboratory Values. Serum amylase will increase within the first 24 hours and remain elevated for 48–72 hours. Serum lipase will remain elevated for 5–14 days. There will also be an elevated white count, and if biliary obstruction occurs, an elevation in serum bilirubin will also be present. Complications of pancreatitis may include: pseudocyst, abscess, hemorrhage, phlegmon, and biliary and duodenal obstruction.
Edematous form occurs when the pancreas goes through inflammatory changes and interstitial edema. The gland becomes enlarged and is less echogenic on ultrasound. Acute pancreatitis may also be associated with intraperitoneal or retroperitoneal fluid.
Hemorrhagic pancreatitis occurs when there is a rapid progression of the disease caused by autodigestion of the pancreatic tissue, which causes areas of fat necrosis. This leads to rupture of the vessels in the pancreas and hemorrhage. Sonographically, the appearance will vary depending on when the bleeding occurred. A mass may appear as homogeneous, cystic with debris, or heterogeneous. The pancreatic duct may be dilated.
Phlegmonous pancreatitis is a severe form of acute pancreatitis where the inflammation may extend to outside the pancreas. Sonographically, the pancreas is hypoechoic.
Pancreatic pseudocyst is the most common complication associated with acute pancreatitis. They are not true cysts because they do not have an epithelial covering. Pancreatic enzymes and blood escape from the pancreatic tissue and become encapsulated form pseudocysts. They are most commonly found in the lesser sac (anterior to the pancreas and posterior to the stomach) and may also be found in the pararenal space and transverse mesocolon. Sonographically, they are round, smooth thin-walled, and primarily anechoic and may be either singular or multiple. The fluid usually reabsorbs into the body; a small percentage may rupture.
Chronic pancreatitis occurs from continued destruction of the pancreatic parenchyma usually from repeated bouts of acute pancreatitis. Sonographically, the pancreas is either normal or small in size, with an irregular contour. The parenchyma is heterogeneous with increased echogenicity, and in 50% of cases, patients with malabsorption syndromes will have calcifications. With dilation of the pancreatic duct, stones may be imaged within the dilated duct. The common bile duct may also be dilated.
Benign neoplasms may originate from endocrine or exocrine tissue. These focal lesions include: islet cell tumors, cystadenoma, and papilloma of the duct. Pancreatic cysts, abscesses, metastatic diseases to the pancreas, and lymphomas have the same sonographic appearances as when they are visualized in other areas of the body (Table 4–11).
TABLE 4–11 • Focal Lesions of the Pancreas
Malignant Tumors. Pancreatic carcinoma can be subdivided into adenocarcinoma, cystadenocarcinoma, and such endocrine tumors as islet cell carcinoma. Adenocarcinoma is the most common, and it is usually located within the head. Sonographically, the pancreas is enlarged with irregular borders, the parenchymal pattern changes and becomes less echogenic. Dilation of the pancreatic duct. Associated findings include: dilatation of the common bile duct secondary to enlargement of the pancreatic head; liver metastases; nodal metastases; portal vein involvement; compression on the inferior vena cava; and Courvoisier’s sign (Table 4–11).
Cystadenocarcinoma is visualized sonographically as an irregular cystic lobulated mass with thick walls. It is more commonly seen in the body or tail.
Islet Cell Carcinomas are usually small and well circumscribed and found in the body and tail. One-third of all islet cell tumors are nonfunctioning tumors, and 92% of these are malignant.
With any type of pancreatic carcinoma, clinically, they are associated with an increase in alkaline phosphatase and bilirubin secondary to biliary obstruction. Metastasis to the liver, portal vein, and lymphadenopathy may also be seen.
The spleen is the largest mass of reticuloendothelial tissue in the body. It normally measures approximately 12–14 cm in length, 7 cm in width, and 3 cm in anteroposterior dimension. It is located in the left upper quadrant, left hypochondriac region, inferior to the diaphragm, and posterolateral to the stomach. The tail of the pancreas is medial to the splenic hilum. The left kidney is medial and posterior to the spleen; the stomach and left colic flexure are both medial to the spleen.
The spleen is an intraperitoneal organ except for the hilum area. The capsule is fibroelastic and is composed of small fibrous bands that give the spleen its framework and permit it to expand in size. The splenic artery, which is a branch of the celiac axis, courses along the anterior superior border of the pancreas and enters into the spleen at the splenic hilum. The splenic artery divides into six branches once it enters into the spleen. The splenic vein exits at the splenic hilum and courses transversely across along the posterior aspect of the pancreas and joins with the superior mesenteric vein to form the portal vein.
The spleen is not essential to life, but it has important functions, especially during the fetal period. It is the main component of the reticuloendothelial system and its functions include the breakdown of hemoglobin and the formation of bile pigment; formation of antibodies, production of lymphocytes and plasma cells; a reservoir for blood; and blood formation in the fetus (erythrocytes) or when there is severe anemia.
The spleen is a homogeneous organ and is either slightly less echogenic or isoechoic to the normal liver. The spleen is crescent shaped with a convex superior lateral border and concave medially. The inferior portion is tapered.
Congenital Anomalies. The most common congenital anomaly is the accessory spleen. Splenic tissue separate from the spleen is usually found near the splenic hilum or adjacent to the tail of the pancreas. Accessory spleens are typically small and round and have the same echogenicity as the spleen. They are difficult to demonstrate on ultrasound and must be differentiated from lymphadenopathy.
A wandering spleen is a spleen in an ectopic location usually found in the pelvis. The patient usually presents with an abdominal or pelvic mass and intermittent pain. Splenic torsion may occur and color Doppler is used to document the vascularity.
Asplenia is rare and often associated with congenital heart disease and other anomalies.
Aplasia is failure of the spleen to develop.
Neoplasms of the Spleen
The spleen is seldom the site for primary disease but often the site for secondary disease. Benign and malignant tumors are rare.
Benign Neoplasms of the Spleen. These include congenital cysts, cysts associated with polycystic disease, hemangiomas (most common primary tumor of the spleen), and lymphangioma (Table 4–12).
TABLE 4–12 • Focal and Diffuse Pathology of the Spleen
Trauma. Blunt trauma (motor vehicle accident, sports injury) to the spleen is a common cause for trauma to the spleen. A subcapsular hematoma may form, grow, and cause the spleen to rupture. Spontaneous rupture of the spleen may also occur in certain disease states (i.e., leukemia), when the spleen is massively enlarged and soft.
Malignant Tumors of the Spleen
Primary malignant tumors arise from the capsule (sarcoma) the most common one being angiosarcoma or they may come from the splenic tissue (lymph), lymphoma. Secondary malignant tumors of the spleen are metastatic from the breast, malignant melanoma, or the ovaries (Table 4–12).
Pathologies of the Spleen
The pathological sonographic appearance of the spleen can be divided into two categories: focal and diffuse. Diffuse splenomegaly can be caused by congestive splenomegaly (i.e., cirrhosis, portal hypertension, and heart failure); infections (i.e., hepatitis, HIV/AIDS, tuberculosis); storage disease (i.e., Gaucher’s disease, diabetes mellitus, and Niemann–Pick disease); and hemodialysis. It is important to remember that diseases go through different stages and the sonographic appearance will vary depending upon the stage of the disease (Table 4–13).
TABLE 4–13 • Causes of Splenomegaly
Some disease processes that affect the spleen will not produce any focal lesions or changes in the echogenicity of the spleen. They will affect the splenic size by either causing atrophy or enlargement of the spleen (Table 4–13).
Atrophy of the spleen is seen less commonly than splenomegaly. Myelofibrosis and sickle cell disease cause destruction of the splenic parenchyma. The spleen decreases in size and sonographically becomes echogenic. In many cases, an atrophic spleen is not visualized on ultrasound.
Splenic Size. The size of the spleen varies with energy and nutritional state of the person. It also varies at different states in life—at birth, it has the same proportion to the total body weight as in the adult. The relationship of the spleen to body size and nutritional state of the individual is important.
The paired kidneys and ureters are retroperitoneal, lying anterior to the deep muscles of the back (psoas major muscle). The kidneys have three layers for protection and support. The true capsule or fibrous capsule is the most inner layer and is imaged sonographically as an echogenic reflector surrounding the renal cortex. Surrounding the true capsule is a layer of fat (adipose) called the perirenal fat. The adrenal gland is located anterior, superior, and medial to the each kidney and is separated from the kidney by the layer of perirenal fat. Gerota’s fascia is a fibrous sheath that encloses both the adrenal gland and the kidney.
The kidney is divided into two regions, the renal sinus and the parenchyma. The renal parenchyma is measured from the margin of the renal sinus to the border of the kidney. The average adult kidney size is 11.5 cm in length, 6 cm in width, and 3.5 cm in thickness. In children, renal size varies with age.
Sonographically, the kidney parenchyma has two distinct areas: the outer cortex and the inner medullary pyramids, which surround the renal sinus. The cortex is homogeneous with relativity low-level echoes that are slightly less echogenic than the normal liver. The medullary pyramids are relatively hypoechoic round or triangular areas between the cortex and the renal sinus. These are separated from each other by bands of cortical tissue, called columns of Bertin, which also extend inward to the renal sinus. The intense specular echoes at the corticomedullary junction are from the arcuate arteries.
The inner echogenic portion of the kidney consists of the renal sinus. The renal sinus contains fat, calyces, infundibula, renal pelvis, connective tissue, renal vessels, and lymphatics. The renal hilum is where blood vessels, nerves, lymphatic vessels, and the ureter enter or exit the renal sinus.
The superior end of the ureter is expanded and forms a funnel-shaped sac called the renal pelvis, which is located within the renal sinus. The renal pelvis is divided into two or three tubes called major calyces, and they are divided into 8 or 18 minor calyces. The apex of the medullary pyramid, called the renal papilla, indents each minor calyx.
The infundibula (funnel portion of the calyces) are collapsed and not seen within the echogenic renal sinus in a subject that has restricted fluid intake. During diuresis, the narrow channels traversing the sinus can be identified. In patients with an extrarenal pelvis, a fluid-filled structure extending medially to the kidney can be identified. Placing the patient in a prone position will compress the extrarenal pelvis and assist in making the diagnosis.
Maternal pyelocaliectasis without mechanical obstruction is commonly observed during pregnancy and seen more frequently in the right kidney. Fetal pyelectasis is also common in utero, and there are measurements used to distinguish it from hydronephrosis. Structures adjacent to the kidneys (Table 4–14).
TABLE 4–14 • Structures Adjacent to the Kidneys
Functions of the Kidneys
The kidneys serve in the excretion of inorganic compounds; for example Na+, K+, Ca++; excretion of organic compounds; for example, creatinine; blood pressure regulation; erythrocyte volume regulation; and vitamin D and Ca++metabolism.
The ultimate goals of the kidney functions are to
1. Maintain salt and water balance
2. Regulate the fluid volume
3. Maintain acid and base balance
Blood and urine tests are performed to determine renal dysfunction. Renal function cannot be estimated by the use of ultrasound.
1. Serum creatinine is elevated with renal dysfunction. Renal dysfunction occurs when the functioning unit of the kidney (nephron) is destroyed.
2. Blood urea nitrogen (BUN) is elevated when there is acute or chronic renal disease or urinary obstruction. A decrease in BUN may occur with overhydration, liver failure, or pregnancy.
Renal Congenital Anomalies
Renal congenital anomalies include incorrect position, number, and shape. One of the most common anomalies is a duplex collecting system. There may be duplication of the ureters, which may enter into the bladder separately, or more commonly, they will join together and enter into the bladder as one ureter.
Position. Embryologically, the kidneys form in the pelvis in an anteroposterior orientation. They ascend and rotate to the adult position, so that the upper pole of each kidney is more medial than the lower pole. Kidneys located outside of the renal fossa are called ectopic kidneys.
Pelvic kidney occurs when the kidney fails to ascend out of the pelvis.
Horseshoe kidney is the most common form of fusion anomaly. The kidneys lie in an oblique transverse position in the lower abdomen. The kidneys are more commonly fused together at lower poles than at the middle or upper poles.
Number. Anomalies of kidney number would include a solitary kidney (single functioning kidney with the ipsilateral atrophied kidney), unilateral renal agenesis (absence of one kidney and ureter), and a supernumary kidney (duplication of the kidney, pelvis, and ureter).
Unilateral renal agenesis is frequently associated with other genital anomalies; for example, bicornuate uterus, unicornuate uterus, and uterine and vaginal septations.
Bilateral renal agenesis is fatal.
Shape. Congenital variations include hypertrophied columns of Bertin (prominent cortical tissue in the medulla <3 cm), fetal lobulation (lobulated renal surface), dromedary (splenic) hump (bulge of cortical tissue on the lateral aspect of the left kidney), renunculus, and fusion of the kidney (horseshoe kidney, cake kidney). All of the above, except the latter, may mimic a mass on ultrasound. Congenital cystic diseases that distort the reniform shape are also included in this category, infantile polycystic kidney disease, adult polycystic kidney disease and multicystic kidney disease.
Polycystic Disease. Polycystic disease may be present at birth or may not manifest until adulthood.
Infantile Polycystic Kidney Disease (IPKD) or autosomal recessive polycystic disease (ARPKD) or (Potter type I). This is the least common and most fatal of the three cystic diseases. It is an autosomal recessive trait and is more common in females (2:1). Sonographically, it presents as bilateral echogenic, enlarged kidneys with cysts (the cysts classically are too small to be resolved). If survival past infancy occurs, hepatic fibrosis becomes a complication, with death resulting from hepatic failure and/or bleeding from esophageal varices.
Adult Polycystic Kidney Disease (APKD) or autosomal dominant polycystic kidney disease (ADPKD) or Potter type III. This is an autosomal dominant disease and occurs relatively frequently. The disease may be latent for many years and not manifest itself until the fourth decade. Patients present with decreasing renal function, hypertension, and may have flank pain. Sonographically, APKD presents as bilateral large kidneys with randomly distributed cortical cysts of various sizes, and in the advanced stages, the kidneys loose the reniform shape. Associated finding include cysts in the liver, pancreas, and spleen. Destruction of the residual renal tissue in advance stages leads to renal failure.
Medullary Cystic Disease. It can be either dominant or recessive. Juvenile onset is autosomal recessive and adult onset is autosomal dominant. Clinically, patients present with renal failure. Sonographically, there are small cysts in the medullary portion of both kidneys with a decreased definition between the cortical/medulla junctions. Hydronephrosis is caused by an obstruction of the outflow of urine. The renal pelvis and calyces become dilated and compress the renal parenchyma causing renal insufficiency. The dilatation may be unilateral or bilateral depending upon the level of the obstruction. The amount of dilation determines whether it is mild (Grade 1), moderate (Grade 2), or severe (Grade 3). The absence of a renal jet and an RI of less than 0.70 will substantiate the diagnosis of renal obstruction.
Hydronephrosis. There are two major classifications of hydronephrosis: intrinsic and extrinsic.
Intrinsic Hydronephrosis. This may be the result of
Bleeding or blood clot
Extrinsic Hydronephrosis. This may be the result of Pregnancy (usually involves the right kidney)
Pelvic masses (e.g., ovarian or fibroids)
Bladder neck obstruction
Inflammatory lesions—pelvis, gastrointestinal, retroperitoneal
Congenital Hydronephrosis. This is present and existing from the time of birth. This may present as
Ureteropelvic junction (UPJ) obstruction
Ectopic ureterocele usually caused by a duplex collecting system
Posterior urethral valve (PUV)
False-Positive Hydronephrosis. This denotes a test result positive for hydronephrosis when there is no hydronephrosis present. Sonographically, the following may mimic hydronephrosis (dilatation of the collecting system).
Renal sinus lipomatosis
False-Negative Hydronephrosis. This denotes a test result that wrongly excludes the diagnosis of hydronephrosis. Patients suffering from severe dehydration or intermittent obstruction may have hydronephrosis without dilatation of the collecting system.
Nephrolithiasis with intermittent obstruction
Tables 4–15 and 4–16 outline the clinical and sonographic findings associated with cystic and solid renal masses.
TABLE 4–15 • Renal Cystic Masses
TABLE 4–16 • Solid Renal Masses
Nephrolithiasis (Renal Calculi)
Nephrolithiasis are more commonly found in men than women and typically in people who have urinary stasis. Nephrolithiasis may be composed of uric acid, cystine, or calcium. Sonographically, renal calculi appear as highly reflective echogenic foci. A high-frequency transducer with proper settings of the focal zones is necessary to document posterior shadowing. Using tissue harmonics can also assist in seeing posterior acoustic shadowing. The “twinkle sign” is a color artifact that has been seen with urinary stones. The “twinkle sign” is described as rapidly changing colors that are seen posterior to an echogenic reflector, that is, stones). A Staghorn calculus is large stones located in the central portion of the kidney, the collecting system, and takes the shape of the calyces. Renal obstruction may be secondary to stones located in the collecting system.
Laboratory Values. In cases of chronic obstruction, there is an increase in serum creatinine and BUN levels. In acute obstruction, there are no specific lab values. Urine may show hematuria and/or bacteria.
Signs and Symptoms. Renal colic, flank pain, nausea, and vomiting.
Renal failure is the kidneys’ inability to filter metabolites from the blood resulting in decreased renal function, which may be either acute or chronic. Laboratory findings are increased serum BUN and serum creatinine levels.
Prerenal Causes. Renal hypoperfusion secondary to a systemic cause can occur as a result of vascular disorders leading to renal failure and includes the following conditions.
Nephrosclerosis. Arteriosclerosis of the renal arteries, resulting in ischemia of the kidney. Nephrosclerosis develops rapidly in patients with severe hypertension.
Infarction. This may result from occlusion or stenosis of the renal artery.
Renal Artery Stenosis. Any narrowing of the renal artery will affect the blood flow to the kidney, resulting in atrophy of the kidney and decreased renal function.
Congestive Heart Failure. This may cause renal hypoperfusion secondary to heart failure.
Thrombosis. Thrombosis of the renal vein will increase the intravascular pressure and, thus, decrease blood flow to the kidney.
Sonography Doppler of the renal artery is employed to detect arterial blood flow patterns either directly from the renal artery or indirectly from parenchyma flow patterns.
Renal Parenchymal Disease—Infection and Inflammatory Disease
Acute Tubular Necrosis. Of the acute renal medical diseases, this is the most common cause of acute renal failure. The destruction of the tubular epithelial cells of the proximal and distal convoluted tubules may occur as a result of ingestion or inhalation of toxic agents, ischemia caused by trauma, hemorrhage, acute interstitial nephritis, cortical necrosis, and diseases of the glomeruli.
Pyelonephritis. Infection is the most common disease of the urinary tract, and the combination of parenchymal, caliceal, and pelvic inflammation constitutes pyelonephritis. Bacteria ascending from the urinary bladder or adjacent lymph nodes to the kidney usually cause infection of the kidney.
Glomerulonephritis. Etiology is unknown, but it frequently follows other infections.
Metabolic Disorders. Diabetes mellitus, amyloidosis, gout, and nephrocalcinosis (deposit of calcium in the renal parenchyma) are metabolic disorders associated with renal failure.
Chronic Nephrotoxicity This is caused by exposure to radiation, heavy metals, industrial solvents, and drugs.
Sonography. In acute renal failure, the kidney may be normal sized or enlarged. There may be decreased definition between the medullary/cortical junctions. As the case progresses from acute to chronic, the echogenicity will increase. There is no definite correlation between the echogenicity of the kidney, the kidney size, and degree of decreased renal function. Patients in end-stage renal failure will have small echogenic kidneys that are difficult to image sonographically.
Postrenal Causes. These include urinary tract obstruction, which cause hydronephrosis, and may be congenital or acquired intrinsically and extrinsically.
Sonography. There are varying degrees of the dilation of the renal sinus, calyces, infundibulum, and pelvis.
Renal Medical Diseases (Table 4–17)
TABLE 4–17 • Renal Medical Diseases
Type I. There is increased cortical echogenicity with a decrease in corticomedullary differentiation. Type I diseases are those caused by glomerular infiltrate, such as acute and chronic glomerulonephritis, acute lupus nephritis, nephrosclerosis, any type of nephritis, and renal transplant rejection. All these disorders can cause the echogenicity of the renal cortex to be greater than the liver and spleen. As the disease progresses to the chronic state, the kidney becomes smaller, the cortex becomes more echogenic, and eventually the medulla will become equally echogenic.
Type II. There is distortion of normal anatomy involving cortex and medullary pyramids; sonographically, there is a decrease in the corticomedullary differentiation in either a focal or diffuse manner. The type II pattern is seen with such focal lesions as cysts, abscesses, hematomas, bacterial nephritis (lobar nephronia), infantile polycystic disease, adult polycystic disease, chronic pyelonephritis, and chronic glomerulonephritis.
The transplanted kidney is placed within the iliac fossa. A baseline sonogram is performed within 48 hours postoperatively to document the exact location, size, and sonographic appearance of the transplanted kidney. The most serious sign of transplant rejection is renal failure. Clinical signs of renal rejection include, fever, pain, and decreased urine output. The laboratory results are the same as renal failure, elevated BUN, and serum creatinine.
Acute rejection of the transplanted kidney may be caused by acute tubular necrosis or arterial obstruction. Differentiating between the different causes of renal failure is important to ensure proper treatment is administered.
In cases of acute rejection, the kidney appears sonographically as an enlarged kidney with increased cortical echogenicity, decreased renal sinus echogenicity, irregular sonolucent areas in the cortex, enlarged and decreased echogenicity of the pyramids, distortion of the renal outline, and indistinct corticomedullary junction.
Rejection caused by acute tubular necrosis usually results in a normal sonogram. In rejection caused by acute renal arterial occlusion, the sonographic appearance seems grossly normal. However, duplex Doppler studies may reveal an absence of or decreased diastolic flow.
Perinephric fluid collections, commonly associated with the transplanted kidneys, are lymphocele, urinoma, abscess, and hematoma (Table 4–18).
TABLE 4–18 • Perinephric Fluid Collections
The ureters are located in the retroperitoneal cavity and course along the anterior surface of the psoas muscle along the medial side. The ureters are approximately 6 mm in diameter. The three most common places for obstruction to occur are: at the ureteropelvic junction (UPJ); as they cross over the pelvic brim; and at the junction into the bladder. In the pelvis, the ureters are anterior to the iliac vessels.
Urine can be imaged entering into the urinary bladder with the use of color Doppler. Color Doppler is used because the ureteral jet will cause a Doppler shift because of the continued changes in the turbulent flow in the urine. If the bladder has recently been overly distended, ureteral jets may not be imaged because of the specific gravity of the urine in the ureters and in the bladder being similar, thus causing no Doppler shift. Ureteral jets occur at regular intervals, approximately every 2–3 seconds. They appear as bursts of color entering from the base of the bladder flowing toward the center of the bladder and lasting for a fraction of a second. The absence or decrease of a ureteral jet indicates the presence of an obstruction.
Congenital Anomalies of the Ureters
These include double or bifid ureter, narrowing, strictures, diverticuli, and hydroureter caused by a congenital defect, as in a polycystic kidney, or acquired, as in a low ureteral obstruction.
Megaureter in Childhood (Primary-Nonobstructive, Nonrefluxing Megaureter)
This includes prune belly syndrome (Eagle-Barrett syndrome), deficiency of the abdominal musculature, and urinary tract abnormalities (large hypotonic bladder, undescended testes, hydroureter), and retroperitoneal fibrosis, which fixes the ureter and prevents peristalsis, leading to functional obstruction.
This is caused by reflux of urine or obstruction. Ureteral abnormalities are viewed in Table 4–19.
TABLE 4–19 • Ureteral Abnormalities
The urinary bladder is a thin-walled triangular structure that is located directly posterior to the pubic bone. The apex of the bladder points anteriorly and is connected to the umbilicus by the median umbilical ligament, the remains of the fetal urachus. The ureters enter at a posteroinferior angle, and the urethra extends from the bladder neck to the exterior of the body. The trigone is the area of the bladder between the neck and apex. It contains three orifices: two for the ureters and one for the urethra.
A normal distended urinary bladder on ultrasound is imaged as a midline symmetrical anechoic structure. The bladder wall is imaged as a thin, smooth, echogenic line that measures between 3 and 6 mm in thickness. The normal bladder volume varies and can usually reach 500 mL without any major discomfort.
Bladder stones can develop in the bladder or form in the kidney. Patients passing a urinary tract stone present with renal colic, flank pain, and hematuria. Sonographically, the bladder stone appears as an echogenic focus with posterior acoustic shadowing. Calculi are gravity dependent (calculi moves to the dependent portion of the bladder when the patient is placed in a decubitus position). Ureteral jets are usually normal; rarely do the calculi obstruct the ureter.
During a pelvic ultrasound examination, the bladder wall thickness, irregularities of the wall, bladder shape, and lumen should be evaluated. There may be an extrinsic mass; for example, a fibroid or enlarged prostate, compressing the bladder and causing bladder distortion. Table 4–20 reviews abnormalities that will distort the wall and shape of the bladder.
TABLE 4–20 • Urinary Bladder Abnormalities
The adrenal glands are part of the endocrine system and consist of two distinct regions: the medulla, which is surrounded by the cortex. The adrenal glands are triangle-shaped structures located superior and anteromedial to the upper pole of the kidney. They measure 5 × 5 × 1 cm but at birth are proportionately much larger. Gerota’s fascia encloses the kidneys, adrenals, and perinephric fat.
The right adrenal gland lies posterior and lateral to the inferior vena cava, lateral to the right crus of the diaphragm, and medial to the right lobe of the liver. To image the right adrenal gland the patient is typically placed in a left lateral decubitus position (right side up). The right adrenal gland is located between the right lobe of liver, inferior vena cava, and right kidney.
The left adrenal gland lies medial to the spleen, lateral to the aorta, and posterior to the tail of the pancreas. Sonographically, the normal adrenal glands in adults are difficult to visualize because of their small size and the echo texture being similar to the surrounding retroperitoneal fat. To image the left adrenal gland, the patient lies in a right lateral decubitus position (left side up) the transducer is placed in a coronal position. The left adrenal glands liebetween the spleen, aorta, and left kidney, and these structures are used as sonographic landmarks. Computed tomography (CT) is the imaging modality of choice. Adrenal tumors may be identified on a sonogram usually by their displacement and/or compression of adjacent structures. See Table 4–21 for adrenal gland malfunctions.
TABLE 4–21 • Adrenal Gland Malfunctions
Right Adrenal Pathology Will Displace
Left Adrenal Pathology Will Displace
The adrenal cortex, which produces steroid hormones, is subdivided into three zones listed from outer to inner: (1) the zona glomerulosa, which produces mineralocorticoids (for the regulation of aldosterone to regulate electrolyte metabolism); (2) the zona fasciculata, which produces glucocorticoids (for the regulation of cortisol, which is an antistress and antiinflammatory hormone); and (3) the zona reticularis, which produces gonadocorticoids (for regulation of the secretion of androgens and estrogens, which are the sex hormones of an individual).
The adrenal cortical hormones are regulated by the adreno-corticotropic hormones (ACTH) of the anterior pituitary gland. A decrease in adrenal cortical function leads to an increased ACTH, which then stimulates the adrenal cortex. An increase in concentration of adrenal hormones leads to a drop in ACTH secretion, which leads to a drop in the activity of adrenal cortex.
The adrenal cortex may be affected either by lesions that produce an excess of steroid hormones or by lesions that produce a deficiency. The adrenocortical hormone levels may be abnormal (increased or decreased production) as a result of a pituitary tumor, which can cause the overproduction or underproduction of ACTH.
The adrenal medulla produces epinephrine (adrenalin) and norepinephrine. These hormones have a wide range of effects.
Epinephrine dilates the coronary vessels and constricts the skin and kidney vessels. It increases coronary output, raises oxygen consumption, and causes hyperglycemia.
Norepinephrine constricts all arterial vessels except the coronary arteries (which dilate). It is the essential regulator of blood pressure.
Epinephrine, in particular, is responsible for the fight or-flight reaction. It stimulates the metabolic rate, allowing energy that is more available.
Sonography is not routinely used to image the gastrointestinal tract because of the air within the bowel lumen. Normal bowel patterns can be imaged and recognize bowel peristalsis on abdominal sonographic examination. Knowledge of the gastrointestinal (GI) tract is essential for identifying the location of the pathology.
The GI tract is composed of the esophagus, the stomach, the small intestine, and the colon.
The esophagus is a tubular structure that extends from the pharynx to the stomach. Its main function is to bring food and water to the stomach. The gastroesophageal junction (GEJ) can be identified slightly to the left of midline on a sagittal scan. Sonographically, it appears round with an echogenic center with a hypoechoic rim also referred to as a “target sign” or “bull’s eye” located posterior to the left lobe of the liver and anterior to the aorta.
The stomach lies between the esophagus and the duodenum. The opening between the stomach and the duodenum is called the pyloric orifice. The main function of the stomach is to break down food to chyme, which then passes through to the duodenum. Sonographically, the fluid-filled stomach is imaged as an anechoic structure with echogenic foci and thin walls. The small intestine lies between the stomach and the colon and is divided into three parts: duodenum, jejunum, and the ileum. The main function of the small intestine is to absorb food.
The ileocecal valve connects the distal portion of the ileum to the first section of the colon, the cecum. The appendix is located in the right lower quadrant as a tubular structure that extends from the cecum. The ascending colon ascends from the cecum along the right side of the body to the posterior inferior surface of the liver. The ascending colon bends to the left and forms the hepatic flexure. The transverse colon extends across the body from the hepatic flexure to the splenic flexure. The splenic flexure is located posterior and inferior to the spleen and bends inferiorly forming the descending colon, which courses along the left side to the body and terminates at the sigmoid colon.
The sigmoid is the narrowest portion of the colon, and the distal end forms the rectum. The anal canal is the distal end of the rectum, which expels solid waste products (feces) from the body.
The diaphragm is a dome-shaped muscle separating the thorax from the abdominal cavity. The diaphragm covers the superior and lateral border of the liver on the right side and the spleen on the left side. Sonographically, the diaphragm is identified as a thin, echogenic, curvilinear interface between the lungs and liver (spleen).
The subphrenic space is between the liver (or spleen) and the diaphragm and is a common site for abscess.
CRURA OF THE DIAPHRAGM
The diaphragmatic crura are right and left fibromuscular bundles that attach to the lumbar vertebra at the level of L3 on the right and L1 on the left. They act as anchors to the diaphragm.
The left crus can be visualized anterior to the aorta above the level of the celiac artery. Below the celiac artery, the crura extend along the lateral aspects of the vertebral columns. The right crus is visualized posterior to the caudate lobe and the inferior vena cava.
Ascites is an abnormal accumulation of serous fluid in the peritoneum. The most common cause for ascites in the United States is cirrhosis and accounts for about 80 percent of causes.3 Ascites are catogrized into:
• Transudative—anechoic/freely mobile usually benign, free-floating bowel in the abdomen
• Exudative—internal echoes/loculated—associated with infection and malignancy
• Bowel matted or fixed to posterior abdominal wall—associated with malignancy
• Nonmobile fluid associated with coagulated hematoma (trauma)
Pathology Associated with Ascites
• Congestive heart failure
• Infection (inflammatory process)
• Kidney failure
• Liver failure/disease—end-stage fatty liver, cirrhosis
• Ruptured aneurysm
• Pyogenic peritonitis
• Portal venous system obstruction
• Obstruction of lymph nodes
• Obstruction of vessels—Budd–Chiari syndrome
• Acute cholecystitis
• Ectopic pregnancy
The clinical presentation of ascites is a distended abdomen. In cases of massive ascites, respiratory distress will also be present.
Accumulations occur (supine position) in the following order:
1. Inferior tip—right lobe liver
2. Superior portion—right flank
3. Pelvic cul de sac
4. Right and Left paracolic gutter
5. Morison’s pouch
• Ascites is found inferior to the diaphragm
• Gross (massive) ascites—extrahepatic portion falciform ligament seen attaching the liver to anterior abdominal wall
• Ascites may cause a downward displacement of the liver
• May cause gallbladder wall to appear to thicken
• Liver may appear more echogenic
• May see patent umbilical vein
• Changing patient’s position to observe fluid movement may be useful
• Disproportional accumulation in lesser sac suggestive of adjacent organ pathology (i.e., acute pancreatitis, pancreatic CA)
An abscess is an encased collection of pus (acute/chronic). A cavity formed by liquefactive necrosis within solid tissue.
Pathology Associated with Abscesses
• Penetrating trauma (wounds)
• Postsurgical procedures
• Retained products of conception
• Pelvic inflammatory disease
• Chronic bladder disease
• Sepsis—blood-borne bacterial infection
• Long-standing hematomas
• Postcholecystectomy—site of the gallbladder fossa
• GI tract—peptic ulcer perforation; bowel spill during surgery (peritonitis)
• Urinary tract infection
• Infected ascites with septa/debris
• Amebic abscess—may be densely echogenic
Clinical Presentation. Pain, spiking fever, chills, elevated white blood cell count, solitary or multiple sites, tenderness
Hepatic Abscess Intrahepatic
Abscesses are most often associated in the Western hemisphere with cholangitis; also seen with sepsis and penetrating trauma to liver.
• Location: within liver parenchyma
• Differential diagnosis: solid tumor, usually round lesion with scattered internal echoes, variable through transmission
Abscess associated with cholecystectomy
• Location: inferior to liver; fluid collection anterior to right kidney (Morison’s pouch); gallbladder fossa (postcholecystectomy)
Abscess associated with bacterial spill into peritoneum during surgical procedure; bowel rupture; peptic ulcer perforation; trauma
• Location: fluid collection superior to the liver, inferior to diaphragm; transmission variable; gas (dirty shadowing)
General Sonographic Findings. A variable, complex, solid, cystic lesion with septa, debris, and scattered echoes; through transmission may be good; mass/cyst with shaggy/thick irregular walls; mass displacing surrounding structures; complex mass with dirty shadowing from within. Presence of gas within a mass suggests an abscess (may also be attributable to fistulous communication with bowel or airway or outside air).
General Differential Diagnosis. Necrosing tumor with fluid center (these usually have thicker walls and no gas).
Ascites Versus Abscess
A localized area of ascites may be mistaken for an abscess. Place the patient in the erect or Trendelenburg position; ascites will shift to the dependent portion, but an abscess will not, unless it contains air; the air/fluid level will shift.
Pleural effusions are nonspecific reactions to an underlying pulmonary or systemic disease such as cirrhosis. Obtaining fluid for analysis may allow a more specific diagnosis.
Sonographic appearance shows a pleural effusion usually as an echo-free (anechoic), wedge-shaped area that lies posteromedial to the liver and posterior to the diaphragm. Occasionally, pleural effusions contain internal echoes, sometimes indicating the presence of a neoplasm. These echoes may be caused by blood or pus (empyema), especially when the collection is loculated. Loculated effusions do not always lie adjacent to the diaphragm and may be loculated anywhere on the chest wall. Sometimes effusions lie between the lung and the diaphragm and are known as subpulmonic. Right-sided pleural effusions can be assessed easily on a view demonstrating the diaphragm and the liver. Effusions on the left side are more difficult to see in the supine position but can be seen more readily with the patient in an oblique position and imaging through the spleen.
The retroperitoneum is the area between the posterior portion of the parietal peritoneum and the posterior abdominal wall, extending from the diaphragm to the pelvis.
The retroperitoneum is divided into three areas by the renal fossa (Gerota’s fascia). Fig. 4–8 demonstrates the division of the retroperitoneum into anterior perirenal and posterior perirenal spaces.
FIGURE 4–8. Cross-sectional anatomy of the retroperitoneal compartments.
1. The anterior perirenal space contains the retroperitoneal portion of the intestines and the pancreas.
2. The perirenal space contains the kidneys, ureters, adrenal glands, aorta, IVC, and retroperitoneal nodes.
3. The posterior perirenal space contains the posterior abdominal wall, iliopsoas muscle, and quadratus muscle.
The retroperitoneal area is subject to infection, bleeding, inflammation, and tumors.
Anterior Perirenal Space. Pancreatic pathology, carcinoma of the duodenum, ascending and descending colon causing bowel thickening or infiltration resulting in a “bull’s eye.”
Perirenal Space. Kidney diseases, adrenal diseases, invasion or displacement of inferior vena cava, aortic aneurysms, ureteral abnormalities, sarcoma, liposarcoma, aortic, and retroperitoneal adenopathy
Posterior Perirenal Space. Renal transplant is usually performed in this extraperitoneal space within the iliac fossa, using the iliac vessels for anastomosis.
Primary Retroperitoneal Tumors
Primary retroperitoneal tumors are mostly malignant; rapidly growing; and larger tumors are more likely to show evidence of necrosis and hemorrhage. Concurrence of mass with ascites indicates invasion of peritoneal surfaces.
Liposarcoma. Originates from fat. Liposarcoma has a complex echogenic pattern with thick walls.
Fibrosarcoma. Originates from connective tissue. Fibrosarcoma has a complex mostly sonolucent pattern, invading surrounding tissues.
Rhabdomyosarcoma. Originates from muscle. It occurs as a solid, complex, or homogeneous echogenic mass, invading surrounding tissue.
Leiomyosarcoma. Originates from smooth muscle. It occurs as a complex echo-dense mass that may have areas of necrosis and cystic degeneration.
Teratoma. Originates from all three germ cell layers. Most teratomas occur in the area of the upper pole of the left kidney. Ninety percent are benign. They are complex with echogenic and cystic areas. Fifty percent occur in children.
Neurogenic Tumors. Originate from nerve tissue and occur mostly in the paravertebral region. They are heterogeneous and echogenic.
Secondary Retroperitoneal Tumors
Secondary retroperitoneal tumors are primary recurrences from previously resected tumors or recurrent masses from previous renal carcinoma.
Ascitic fluid along with a retroperitoneal tumor usually indicates seeding or invasion of the peritoneal surface. Evaluation of the para-aortic region should be made for extension to the lymph nodes. The liver should also be evaluated for metastatic involvement.
Retroperitoneal fibrosis is the formation of thick sheets of connective tissue extending from the perirenal space to the dome of the bladder. It encases, rather than displaces, the great vessels, ureters, and lymph channels, causing obstruction. Severe uropathy may ensue. The etiology of retroperitoneal fibrosis is usually idiopathic, but it may sometimes be associated with aortic aneurysm.
Clinical Findings. The clinical findings in retroperitoneal fibrosis include hydronephrosis, hypertension, anuria, fever, leukocytosis, anemia, nausea and vomiting, weight loss, malaise, palpable abdominal or rectal mass, and abdominal, back, or flank pain. It is more frequent in males than females, and it most common at age 50 through the 60s.
Sonographic Findings. Retroperitoneal fibrosis appears as thick masses anterior and lateral to the aorta and inferior vena cava, extending from renal vessels to the sacral promontory. The anterior to hypoechoic sheets have smooth, well-defined anterior margins and irregular, poorly defined posterior margins. The differential diagnosis includes lymphoma, nodal metastases, and retroperitoneal sarcoma or hematoma.
Retroperitoneal Fluid Collections. Collections of fluids in the retroperitoneum include abscesses, hematomas, urinomas, lymphoceles, and cysts.
The lymphatic system arises from veins in the developing embryo and is closely associated with veins throughout most parts of the body. Lymphatic vessels assist veins in their function by draining many of the body tissues and, thus, increasing the amount of fluid returning to the heart. The lymph vascular network does not form a closed-looped system such as the blood vascular system. Lymph vessels begin as tiny, colorless, unconnected capillaries in the connective tissues. These merge to form progressively larger vessels that are interrupted at various sites by small filtering stations called lymph nodes. The lymph fluid from the entire body ultimately drains into the inferior vena cava.
This lymphatic network has tremendous clinical significance. Interruption of lymph drainage in an area generally creates considerable swelling (edema) owing to the accumulation of fluids. In addition, the lymph vessels offer a variety of routes for cancer cells to move from one site to another (metastasis).
Lymph nodes contain lymphocytes and reticulum cells, their function being one of filtration and production of lymphocytes and antibodies. All the lymph passes through nodes, which act as filters not only for bacteria but also for cancer cells. Enlargement of lymph nodes is a usual sign of an ongoing bacterial or carcinogenic process. Normal lymph nodes measure <1 cm in size. The parietal nodes follow the same course as the prevertebral vessels, while the visceral nodes are more superficial and generally follow the same course that the organ-specific vessels follow. Sonographically, we can evaluate lymph nodes in the pelvis, retroperitoneum, portahepatis, perirenal, and prevertebral vasculature.
Function. The functions of the lymph nodes are: (1) the formation of lymphocytes, (2) the production of antibodies, and (3) the filtration of lymph.
Sonographic Appearance. To visualize lymph nodes, they must be at least 2 cm in size. They are very homogeneous. Lymph nodes are typically hypoechoic, but there is no through transmission. Lymphomas have a nonspecific appearance but in general the following are true:
• Adenopathy secondary to lymphoma is usually sonolucent.
• Adenopathy secondary to metastatic disease is usually complex.
• Posttherapy enlarged nodes are usually very echogenic but may develop cystic areas secondary to necrosis.
Periaortic nodes have specific characteristics: They may drape the great vessels anteriorly (obscuring sharp anterior vascular border); may have a lobular, smooth, or scalloped appearance; and with mesenteric involvement, they may fill most of the abdomen in an irregular complex necrosis.
Para-aortic nodes may displace the celiac axis and superior mesenteric artery anteriorly. Enlarged nodes posterior to the aorta will displace the great vessels away from the spine; this is referred to as the floating aorta sign. The “sandwich” sign occurs when nodes surround the mesenteric vessels.
Sonographic Technique. Concentrates on prevertebral vessels, aorta, inferior vena cava; portahepatic (can produce biliary obstruction); spleen size; iliopsoas muscles; urinary bladder contour; perirenal; retroperitoneum; and pelvis.
Para-aortic lymph nodes are involved with lymphoma in 25% of cases and 40% with Hodgkin’s disease. The sonographic appearance of these lymphomatous nodes varies from hypoechoic to anechoic with no increased through transmission. Occasionally, anechoic nodal masses may resemble cystic structures. Nodal enlargement secondary to other neoplasms or inflammatory processes, such as retroperitoneal fibrosis, may be indistinguishable from lymphomatous lymphadenopathy. Para-aortic or paracaval nodes frequently obscure the sharp anterior vascular border or compress the aorta or inferior vena cava. Placing a patient in a decubitus position demonstrating the aorta and inferior vena cava facilitates sonographic imaging of the retroperitoneal area down to the aortic bifurcation.
Tumors of Lymphoid Tissue
Lymphomas (Tumors of Lymphoid Tissue). Hodgkin’s disease (40%) is a malignant condition characterized by generalized lymphoid tissue enlargement (e.g., enlarged lymph nodes and spleen). Twice as many males as females are affected. It usually occurs between the ages of 15 and 34, or after 50. Histopathologic classification: Reed–Sternberg (RS) cells and multinucleated cells are present.
Non-Hodgkin’s disease (60%) is further subdivided into nodular and diffuse histopathologies. It is a heterogeneous group of diseases that consists of neoplastic proliferation of lymphoid cells that usually disseminate throughout the body. It occurs in all age groups with the incidence increasing with age.
Mesenteric nodal involvement in <4% in patients with Hodgkin’s disease but >50% in non-Hodgkin’s patients. Lymphomatous cellular infiltration of the greater omentum may be seen as a uniformly thick, hypoechoic band-shaped structure. The appearance of mesenteric nodes can resemble that of retroperitoneal nodes.
Mesenteric masses may also appear as multiple cystic or separated masses that may resemble fluid-filled bowel loops. Perihepatic nodes, celiac axis nodes, splenic-hilar, and renal-hilar nodes may also be demonstrated sonographically. Although most are hypoechoic to anechoic, inhomogeneous areas of increased echogenicity can be found in areas of focal necrosis within large nodes. Nodes can encase or invade adjacent organs and produce significant organ displacement, whereas portal nodes produce biliary obstruction.
Extranodal Lymphoma. The liver, kidneys, GI tract, pancreas, and thyroid may show lymphomatous involvement.
Hepatic Lymphoma. Hepatic lymphomatous involvement presents as multiple hypoechoic or anechoic focal parenchymal defects. Although these anechoic lesions may resemble cystic structures, they rarely demonstrate enhanced posterior acoustic transmission or peripheral refractory shadowing. Hepatic abscesses, metastases from sarcomas or melanomas, focal areas of cholangitis, radiation fibrosis, and extensive hemosiderosis have presented with findings sonographically indistinguishable from hepatic lymphoma.
Renal Lymphomas. Less than 3% of all non-Hodgkin’s lymphomas present with renal involvement, mainly Burkitt’s lymphoma or diffuse histiocystic lymphomas.
Gastrointestinal Lymphoma. Fifteen percent of non-Hodgkin’s lymphomas may present with gastrointestinal involvement. Sonographic features include a relatively hypoechoic mass with central echogenic foci. The sonographic appearance is nonspecific for lymphomatous involvement; gastric carcinoma or gastric wall edema may have the same sonographic appearance.
Pancreatic Lymphoma. Ten percent of non-Hodgkin’s patients present with pancreatic involvement—portions of tissue represented by focal hypoechoic or anechoic masses.
Thyroid Lymphoma. Lymphomatous thyroid masses also present in the same manner.
There are three inflammatory conditions of the lymphatic system: acute and chronic lymphadenitis and infectious mononucleosis.
Common primary tumors with metastases to lymph are those of the breast, lung, melanoma, prostate, cervix, and uterus.
1. Enlarged nodes can mimic aortic aneurysm at lower gain settings on longitudinal scans; transverse scans are needed to differentiate.
2. Aneurysms enlarge fairly symmetrically, whereas enlarged nodes tend to drape over prevertebral vessels.
3. Bowel can mimic enlarged nodes so check for peristalsis; nodes are reproducible, whereas bowel is not.
RETROPERITONEAL VERSUS INTRAPERITONEAL MASSES
The retroperitoneal location of a mass is confirmed when there is any of the following:
• Anterior renal displacement
• Anterior displacement of dilated ureters
• Anterior displacement of the retroperitoneal fat ventrally and often cranially, whereas hepatic and subhepatic lesions produce inferior and posterior displacement. The direction of displacement may permit diagnosis of the anatomical origin of right upper quadrant masses.
• Anterior vascular displacement—aorta, inferior vena cava, splenic vein, superior mesenteric vein
1. Crossin JD, Mauradali D, Wilson SR. US of Liver Transplants: Normal and Abnormal 1. RadioGraphics. 2003:1093-1114.
2. Kanterman RY, Darcy MD, Middleton WD, et al. Doppler sonography findings associated with transjugular intrahepatic portosystemic shunt malfunction. AJR. 1997; 168:467-472.
3. Runyon BA. Care of Patients with Ascitis. N. Engl J Med 1994; 330:337.
4. Rumack CM, Wilson SR, Charboneau JW. Diagnostic Ultrasound. 3rd ed. Elsevier Mosby. St. Louis. Missouri; 2005
5. Tortora GJ. Derrickson B. Principles of Anatomy and Physiology 11th ed. John Wiley & Sons Inc. Hoboken, NJ; 2006