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Fig. 15.1a Fig. 15.2a Fig. 15.3a

Before turning to the material of the following section, the following questions should be answered to test whether the goal of the first lesson has been achieved. The answers to questions 1 to 6 can be found on the preceding pages. The an swers to the figure of question 7 can be looked up on page 76 after the individual questions listed in the text have been addressed.

II Which side of the body corresponds to the left side of the image? Superior or inferior? Where is anterior in the image, and where are the posterior structures?

H What is the luminal diameter of the inferior vena cava and abdominal aorta (upper limits of normal) in cm? How is aortic ectasia defined and from what luminal width in cm is it called an aneurysm?

9 What procedure can be added when the luminal diameter of the inferior vena cava is borderline and a right cardiac insufficiency must be excluded?

Q What vessel crosses between the aorta and SMA to the contralateral side on the sagittal image and can mimic a hypoechoic lymphoma? At what level is this vascular crossing?

9 What is the maximum longitudinal diameter of retroperitoneal lymph nodes that can still be called normal? What is the value of follow-up examinations for the evaluation of visualized lymph nodes?

9 Look at the three transducers shown. Which transducer is used for which body region? What is the rationale? What frequency (in MHz) belongs to each transducer? Write the answer below each transducer.

Fig. 16.1

Q Review this image step by step. What is the imaging plane? Which organs are shown? Name all structures, if possible. How does the image differ from a normal image? Try to give a differential diagnosis.

Working through the following pages should be preceded by a review of the sonographic sections obtained in the transverse plane. Where is the liver on a correctly oriented sonographic transverse section? Right or left? If you cannot answer this with certainty you should consult page 4 and recapitulate the intricate anatomic relationship of the organs as seen on transverse images by means of a cone coffee filter (the solution is found on p. 78).

The transducer is turned 90 and placed horizontally on the upper abdomen. With the patient taking a deep breath and holding it, the upper abdomen is systematically reviewed while the transducer is moved slowly and steadily in cranio-caudal direction (Fig. 17.1). By following the course of the vessels, they can be easily identified.

On these transverse sections, the examiner is confronted with a multitude of arteries, veins, biliary ducts, and lymph nodes, all confined to a small space and demanding differentiation from each other (all vessels are hypoechoic, but so are lymph nodes). Do you remember where the left renal vein crosses to the contralateral right side, or whether the right renal artery is anterior or posterior to the inferior vena cava to the right kidney? Refresh your basic anatomic knowledge

Fig. 17.1

by writing the names of all the numbered structures in Figure 17.2 and 17.3 below both figures and thereafter unfold the back cover page to compare your list with the key. Review again the topography of pancreas, duodenum, and spleen in relation to the major abdominal vessels as illustrated in Figure 17.3. To make the review easy, the three most important transverse sections of the upper abdomen are described and illustrated on the next page.


First, the patient has to take a deep breath and hold it, so that the inferiorly displaced liver can serve as an acoustic window for the pancreas and lesser sac, including the major vessels traversing it (see p. 79). Skin (1), subcutaneous fat (2), and both rectus muscles (3) are directly beneath the transducer. The ligamentum teres (7) with the obliterated umbilical vein can be delineated posterior to the linea alba (6), particularly in obese patients. The lesser sac is seen as a small cleft posterior to the liver (9) and, further posterior to it, the pancreas (33). The tail of the pancreas is often obscured by air shadows (45) arising from the stomach (26). The splenic vein (20) always runs directly along the posterior border of the pancreas. The renal vein (25), however, is more posterior between the SMA (17) and aorta (15), and is only imaged on more caudal sections (Fig. 18.3). A more cranial transverse section (Fig. 18.1) visualizes the celiac axis (32) together with the hepatic (18) and splenic (19) arteries. The gastric artery is generally not visualized. The origin of the SMA (17) is more caudal by about 1-2 cm (Fig. 18.2), as clearly illustrated on the sagittal images (Fig. 11.2). It should be noted that the display inverts the position of the organs (which are shown as if viewed from the patient's feet). The inferior vena cava (16), seen as an ovoid structure, is on the left side of the image, and the aorta (15), seen as a round structure, is on the right side anterior to the spine (35). The head of.the pancreas (33) characteristically surrounds the confluens (12) of the portal vein (11), which is frequently obscured by duodenal air (46) in the region of the lesser omentum.

Fig. 18.1c

Fig. 18.1b

Fig. 18.1c

Fig. 18.2c

Fig. 18.2a

Fig. 18.2b

Fig. 18.2c

The echogenicity of the pancreas changes with increasing age. In young and slim patients, the parenchyma is hypo-echoic in comparison with the surrounding tissue, including the hepatic parenchyma. The deposition of fat in the pancreas (pancreatic lipomatosis) can be found in older or obese patients and causes the parenchyma to increase its echogenicity, leading to a hyperechoic, i.e., brighter, appearance of the pancreas. The normal anteroposterior diameters of the pancreas are somewhat variable and should be less than 3 cm for its head and less than 2.5 cm for its body and tail. The causes of pancreatitis include biliary obstruction (cholestasis) secondary to a stone lodged in the distal common bile duct (biliary pancreatitis), increased viscosity of the bile secondary to parenteral nutrition and, above all, alcoholism (alcohol pancreatitis), which is, among others, related to protein plugs obstructing the small pancreatic duct.

Acute pancreatitis of the first degree can initially be devoid of any sonomorphology changes. The edema found in more advanced stages causes marked hypoechogenicity, increased thickness, and indistinctness of the pancreas (33).

Chronic pancreatitis is characterized by a heterogeneous fibrosis (Fig. 19.1), calcific deposits (53), and an undulated, irregular outline of the pancreas (Figs. 19.1,19.2). Moreover, a beaded or irregular dilatation of the pancreatic duct (75) can occur (Fig. 19.2). The normal pancreatic duct is smoothly outlined and measures up to 2 mm in diameter. Inflammatory lymph nodes (Fig. 19.3) in the vicinity of the pan creas, for instance anterior to the portal vein (11), can accompany pancreatitis.

The real contribution of sonography is not the early diagnosis of acute pancreatitis. This can be better achieved by laboratory tests or CT, particularly in view of the markedly increased bowel gas encountered with an acutely inflamed pancreas and interfering with sonographic imaging. Sonography has the role of excluding other diagnostic possibilities, such as cholecystitis, choledocholithiasis, and aortic aneurysm. Furthermore, sonography can be used to follow the pancreatitis and to detect its complications, such as inflammatory infiltration of the neighboring duodenal or gastric wall (46, 26) and thrombophlebitis of the adjacent splenic vein (20). It might be necessary to add color Doppler sonography of the splenic vein if the conventional sonographic evaluation of the spleen is normal. Moreover, necrotic paths in the retroperitoneum (grade II acute pancreatitis) and the development of pseudocysts should be discovered early, so that surgical intervention or puncture under sonographic or CT guidance can be carried out, if indicated, without undue delay. The inflammation does not always involve the entire pancreas, and segmental and "channel" pancreatitis confined to certain segments of the pancreas or along its duodenal surface can be encountered. These manifestations cannot always be reliably differentiated from other localized space-occupying processes, such as a carcinoma.

Fig. 19.1a

Fig. 19.2a

Fig. 19.1a

Fig. 19.2a

Fig. 19.3a

Fig. 19.3a

Looking at the normal echogenicity of the pancreas (33) on longitudinal (Fig. 11.2) or transverse sections (Fig. 18.3) reveals no appreciable difference in comparison with the echogenicity of the liver. With increasing age or obesity, the echogenicity increases as a manifestation of pancreatic lipomatosis (Fig. 20.1). This accentuates the contrast between pancreas and hypoechoic splenic vein (20).

Tumors of the pancreas (54) are generally more hypo-echoic than the remaining pancreas and are sometimes not easily differentiated from adjacent bowel loops (by peristalsis) or space-occupying lesions arising from peripancreatic lymph nodes (see p. 21). Pancreatic carcinomas have a poor prognosis and remain clinically silent for a long time. They are often only detected after they have metastasized, when they compress the common bile duct, or after they have led to an otherwise unexplained weight loss. Early retroperitoneal extension, nodal or hepatic metastases, and/or peri toneal carcinomatosis are responsible for the poor 5-year survival rate, which is far below 10%.

Endocrine pancreatic tumors are generally small at the time of diagnosis because of their systemic hormonal effects and, as all small pancreatic tumors, are best visualized by endosonography (Fig. 20.3). An annular transducer at the tip of an endoscope is positioned into the stomach or through the pylorus into the duodenum, surrounded by a water-filled balloon for acoustic coupling with the gastric or duodenal wall.

Because of the short penetration needed to reach the target structure, a high frequency (5-10 MHz) can be selected, resulting in improved resolution. The same principle is used in transesophageal echocardiography that also has, because of the use of high-frequency transducers, a markedly improved image quality in comparison with transthoracic echocardiography.

Fig. 20.1a Fig. 20.2 a Fig. 20.3 a

The criteria distinguishing inflammatory lymph nodes from metastatic and lymphomatous lymph nodes were already discussed on page 14. Depending on the incidence angle, the upper abdominal vessels (15, 16) can be visualized as ovoid structures on transverse sections and must be distinguished from pathologic lymph nodes (Figs. 21.1, 21.2). Familiarity with the normal vascular anatomy is therefore fundamental. Very hypoechoic lymph nodes that lack an echogenic hilus and displace, but do not invade, adjacent veins are suggestive of the presence of a lymphoma, such as chronic lymphatic leukemia (Fig. 21.2). The pathologic lymph node shown here is situated directly anterior and to the right of the bifurcation of the celiac axis (32) into the common hepatic artery (18) and splenic artery (19). The resultant space-occupying effect obliterates the characteristic fluke-like configuration of the celiac axis.

Occasionally, large nodal aggregates (Fig. 21.1) can be seen around and virtually "encasing ' the retroperitoneal or mesenteric vessels. In such cases, representative lymph nodes are identified and measured to assess any interval growth on subsequent studies. If intra-abdominal or retroperitoneal lymph nodes are encountered, the examination should proceed to measuring the size of the liver and spleen. Both organs must also be searched for heterogeneous infiltrations. Diffuse lymphomatous involvement of the splenic parenchyma does not always translate into sonomorphology changes, and the infiltrated spleen can appear normal or show only diffuse enlargement (Fig. 48.1). Additional lym-phadenopathy must be searched for in the inguinal, axillary and cervical regions. Paralytic fluid-filled intestinal loops are rarely mistaken for lymph nodes. An intestinal diverticulum (54) can mimic a tumor or enlarged lymph node, as shown in Fig. 21.3. Eliciting peristaltic activity from a paralytic intestinal loop by applying graded compression can clarify the differential diagnosis.

Fig. 21.1 a
Fig. 21.2a
Fig. 21.3a

After this session the standard sagittal and transverse sections are supplemented by oblique sections, clarifying the spatial orientation of individual structures. Answering the subsequent questions correctly is a prerequisite for the next session. The answer to question 4 is found on page 76.

H Draw the approximate course of the relevant upper abdominal vessels on a piece of paper, naturally just from memory without the help of this workbook. This drawing should include the biliary ducts. Test your knowledge by comparing your drawing with the one shown in Figure 17.2 and with the key on the unfolded back cover. Repeat this exercise until you succeed without making any mistakes.

9 How does the echogenicity of the pancreas parenchyma increase with advancing age? How is acute pancreatitis recognized? What other imaging modalities are available if sonography fails to delineate the pancreas because of increased bowel gas?

9 Try, without consulting this workbook and entirely from memory, to draw the three standard planes of the upper abdomen. Pay attention to the correct depth dimension of the individual vessels and to accurate annotation! Do not forget the structures of the anterior abdominal wall. Compare your finished sketches with the drawings shown in Figures Repeat these exercises until you get them right—only then will you have mastered the topographic anatomy of the most important sonographic planes and have laid the foundation for understanding the subsequent oblique sections.

El On this image, name every vessel and all other structures. Which vessel appears distended/congested? What can be the cause? Is this finding pathologic?

Porta Hepatis Orientation
Fig. 22.1


This session leaves the transverse plane and moves to a sonographic plane that visualizes the major structures in the

. Again, the patient has to be asked to take a deep breath and hold it so that liver and porta hepatis move inferiorly from under the acoustic shadow of the lung and ribs. The transducer is turned from the previous transverse orientation until the sound beam is parallel to the portal vein (roughly parallel to left costal arch) (Fig. 23.1a). Sometimes, the transducer has to be angled craniad (Fig. 23.1 b) to follow the course of the portal vein (11) from the porta hepatis to the confluens of the splenic vein and superior mesenteric vein (12) (Fig. 23.2).

Three hypoechoic layers can be delineated in the minor omentum. The normal position of the portal vein (11) is immediately anterior to the obliquely sectioned inferior vena cava (16), with the common bile duct (not visualized in Fig. 23.2) and hepatic artery proper (18) situated more anterior. Good visualization without intervening duodenal air also allows delineation of the pancreatic head, aorta (15), and SMA (17) on the right side of the display (i.e., on the patient's left side).

The major branches of the hepatic artery (18) divide at the porta hepatis, with one branch seen in cross-section on the sonographic orientation under discussion here. This cross-section should not be mistaken for preaortic lymph-adenopathy (Fig. 23.2b).

The common bile duct can be so narrow that it might be barely visible along the adjacent artery. Its normal diameter should be less than 6 mm. After cholecystectomy it assumes some reservoir function and can dilate up to 9 mm without pathologic significance. A borderline dilated common bile duct (obstructive cholestasis) can no longer be differentiated from adjacent vessels by its luminal diameter but only by its location anterior to the portal vein. Visualizing the duct's entire length is important to exclude intraductal gallstones (see p. 35). By moving the transducer, an attempt should be made to follow all three tubular structures upward to the porta hepatis. Distally, the common bile duct should be followed to the duodenal ampulla at the pancreatic head, the hepatic artery to the celiac axis, and the portal vein to the porto-splenic confluence or the splenic vein.

The normal luminal width of the portal vein is less than 13 mm when its main branch is measured perpendicular to its longitudinal axis. Dilatation should only be suspected with measurements exceeding 15 mm. A dilated portal vein alone is an uncertain criterion for the presence of portal hypertension. The highest accuracy is achieved by the definitive demonstration of portocaval collaterals, which are described on the next page.

lesser omentum

Normal values:

Portal vein Common bile duct Common bile duct, S/P cholecystectomy

Fig. 23.1b

The most common cause of increased pressure in the portal vein is impaired drainage secondary to cirrhosis. Direct compression of the portal vein by adjacent tumor is found less frequently. A pancreatic tumor can involve the splenic vein or superior mesenteric vein, without affecting the portal vein.

(11) to more than 13 mm should be considered suspicious for portal hypertension (Fig. 24.1). The luminal diameter of the portal vein is measured perpendicular to the vessel's longitudinal axis, which is usually obliquely oriented in relation to the sonographic image. The vascular wall is not included in the measurement. It should be kept in mind that splenomegaly of any other cause can lead to an increased luminal diameter of the splenic vein or portal vein, without the presence of portal hypertension.

A dilated portal vein with a diameter of more than 13 mm is by itself no certain criterion for portal hypertension. Additional criteria are splenomegaly (Fig. 48.2), ascites (Fig. 31.1), and portocaval collaterals. With progressing cirrhosis, collateral channels develop to the superior or inferior vena cava. Blood can drain from the portal system via a dilated coronary vein of the stomach and a dilated esophageal venous complex into the (hemi-)azygos vein and from there into the superior vena cava. This can lead to the severe clinical complication of bleeding esophageal varicose veins.

Occasionally, small venous connections between the splenic hilum and left renal vein open up, with resultant portosystemic drainage directly into the inferior vena cava (spontaneous splenorenal shunt). Less frequently, the umbilical vein, which passes through the falciform ligament and ligamentum teres from the porta hepatis to the umbilical vein, recanalizes (Cruveilhier-Baumgarten syndrome). In its advanced stage, this collateral circulation (Fig. 24.2) can produce dilated and markedly tortuous subcutaneous periumbilical veins referred to as caput medusae. In questionable cases, color Doppler sonography can be used to detect a decreased or reversed (hepatofugal) portal blood flow.

Evaluation of the lesser omentum should not only assess the luminal diameter of the portal vein but also exclude enlarged periportal lymph nodes (55) (Fig. 24.3), which frequently accompany viral hepatitis, cholecystitis, or pancreatitis. They are caused by inflammatory changes and should be repeatedly checked for resolution and exclusion of malignant lymphoma.

Checklist Portal Hypertension:

Demonstration of portocaval collaterals at the porta

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