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Editura „Victor Babeş”

Timişoara, 2016




Piaţa Eftimie Murgu 2, cam. 316, 300041 Timişoara Tel./ Fax 0256 495 210

e-mail: [email protected] www.evb.umft.ro

Director general: Prof. univ. dr. Dan V. Poenaru Director: Prof. univ. dr. Andrei Motoc

© 2016 Toate drepturile asupra acestei ediţii sunt rezervate.

Reproducerea parţială sau integrală a textului, pe orice suport, fără acordul scris al autorului este interzisă şi se va sancţiona conform legilor în vigoare.

ISBN 978-606-8456-92-8



I have read with great interest and pleasure the manuscript “Course of Abdominal Ultrasound for students”, written by Roxana Şirli and Ioan Sporea, two well known authors in the gastroenterology and internal medicine school from Timisoara, recognized experts in diagnostic imaging evaluation but also in interventional procedures guided by the different methods applied in the gastroenterology clinic, clinic supervised by Professor Ioan Sporea. The manuscript has all the characteristics of a real monograph, by all the aspects taken into account, in the imaging related to anatomy, physiology and pathology of abdominal organs visualized by echocardiographic imaging technique, not just the ones evaluated in gastroenterology. By all the details, the relation of imaging technique to the clinical part and the therapy of abdominal organs disease, the book represents a real manual, useful not only in medical students formation (as the title suggests), but also for a large medical group – fellows and specialists in internal medicine, Imagistics and radiology, urology, general surgery, as well as general practicians, often practicing the technique following not quite accurate and actual standards. The presentation and the language are of great clarity and efficacy, with a clear teaching, with scientific value character but also directed towards practical experience, useful, without a doubt in such an attempt.

Of course, the quality of echocardiographic imaging is exquisite, not just given by the image resolution and details, but also by the specificity of presented aspects, all resulted after large volume personal experience and performance. Actual and relevant data as well as the experience presented is certified not just by a simple “belletristic” and scientific reading of the book, but by a well certified experience in formation of many generations of practicians in abdominal echocardiography, certified by Professor Ioan Sporea and the team of Gastroenterology Clinic, that he is coordinating, a team in which Dr. Roxana Sirli is recognized as a high quality expert in that field. There isn’t, under any circumstances, the case of a publishing opportunism, but an exquisite attempt in teaching valuable information of great quality and actuality, and most important, coming from the experts most authorized in a very specific field.

Taking all this into consideration, I propose to the “Victor Babes” publishing house, the publishing of the book in form submitted by the authors.




Chapter 1.

Introduction in ultrasound; Contrast enhanced Ultrasound ...5 Chapter 2.

Elements of ultrasound anatomy ...11 Chapter 3.

Abdominal ultrasound in the diagnosis of diffuse liver diseases ...25 Chapter 4.

Abdominal ultrasound in the diagnosis focal liver lesions – fluid lesions ...43 Chapter 5.

Abdominal ultrasound in the diagnosis of focal liver lesions – solid lesions ...59 Chapter 6.

Ultrasound of the gallbladder and biliary tree ...82 Chapter 7.

Pancreatic Ultrasound ... 102 Chapter 8.

Ultrasound of the spleen ... 114 Chapter 9.

Ultrasound of the kidneys ... 122

Selective references ... 138


Chapter 1.

Introduction in ultrasound;

Contrast enhanced Ultrasound

Abdominal ultrasound is one of the most accessible imaging methods used in daily practice. In modern medicine it should be considered an extension of the clinical examination, and is helpful in both emergency and for the initial evaluation and follow up of patients with various abdominal symptoms, in patients with chronic liver diseases, in oncology patients, in those with mild abdominal trauma etc.

In our opinion, abdominal ultrasound is the logical approach that should follow history and physical examination of patients with abdominal complaints. Imagine transducer as a flashlight that will light the way and that will allow you to view intraabdominal organs. It is a valuable method, it is accessible, non-invasive, non-irradiant, inexpensive, repetitive. But in addition it must be remembered that it is operator dependent and that the ultrasound window is not always what we want, that the examination can be difficult in obese patients, in those who cannot collaborate with a deep inspiration (that facilitates evaluation), in those who cannot be mobilized, or in patients with flatulence.

Ultrasound image is formed by the reflection of ultrasonic waves emitted by the transducer by tissues. Reflected waves are captured by the transducer and then processed electronically, the resulting ultrasound images are projected on the monitor. Reflection of ultrasound is dependent of the impedance of tissue (tissue resistance to the passage of the sound waves). The denser the tissue is, the stronger it will reflect the ultrasound at the interface between the constituent structures.

The echo-texture of the normal liver is considered to be normoechoic (gray, like a fine blend of salt and pepper). What is whiter than normal liver is considered to be hyperechoic, what is darker - hypoechoic. Fluid structures do not reflect ultrasound and appear completely black, being labeled as anechoic or transonic (gall bladder, urinary bladder, vessels, ascites, pleural effusion, etc.). Structures that reflect the majority of ultrasound waves will appear white and will generate posterior shadow (bones, stones, calcifications). Taking into account that ultrasound is almost completely reflected at the interface between air and other medium, air will appear as intense hyperechoic, similar to stones or bone.


After this technique preamble, it should be noted that to make a quality ultrasound examination we should ensure to have always optimal examination conditions: in a dark room, with sufficient time for examination, with access to complete clinical information about the patient. It is always useful to follow an examination protocol, focusing on the area of interest.

The sections (incidences) used for the ultrasound examination are: longitudinal, sagital or axial (parallel to the spine); transverse (perpendicular to the spine); and oblique sections.

The examination must be dynamic, by scanning the examined organs in multiple planes, changing the incidence so that we don’t “miss” lesions in areas difficult to visualize. When performing ultrasound examination we should always consider the representation of organs in space, their anatomical reports. For example, with a high transverse section through the epigastria, the following organs can be viewed (from front to back): abdominal wall, left hepatic lobe, gastric antrum, pancreas, spleno-portal axis, the large vessels (aorta and inferior vena cava), and spine.

Before one can establish a diagnosis by ultrasound one must know very well the normal aspect of various organs. Thus the first chapter of this course will address to the fundamentals of ultrasound anatomy. To visualize various organs, vessels are important anatomical landmarks. Figure 1 is meant to be a memory refresher, where 15=aorta; 32=celiac trunk;

18=hepatic artery, 19=splenic artery, ** = left gastric artery, 17=superior mesenteric artery, 24=renal arteries, 16=inferior cava vein, 10=hepatic veins, 25=renal vein, 20=splenic vein,

* = superior mesenteric vein, 12=portal vein, 11=portal bifurcation, 66=main biliary duct, 14=gallbladder.

Fig. 1. Anatomical vascular landmarks (Hofer M. – Ultrasound Teaching Manual, Thieme, 1999)



Abdominal ultrasound is an imaging method widespread in medical practice, but unfortunately it was "handicapped" by the fact that, unlike in other imaging methods, contrast could not be used. In the recent years ultrasound has undergone a real effervescency due to the appearance and more frequent use of ultrasound contrast agents (contrast-enhanced ultrasound: CEUS).

In CEUS the ultrasound signal is amplified with the help of microbubbles, an effect discovered by a cardiologist (Joyner Claude), who observed that the ultrasonic signal was amplified in M mode, after injecting an iodine contrast agent for angiographic studies of the heart. The first clinical application of microbubbles was also performed in cardiology, when, after the intravenous injection of a mixture of saline with air, right-left intracardiac shunts were evaluated.

Then the first generation of ultrasound contrast agents soon followed (Echovist, then Levovist) consisting of disaccharide coated microbubbles containing air, mainly used to evaluate cardiac and peripheral vessels. The examination was done with ultrasound waves with high mechanical index (intensity) level, which made the microbubbles to be rapidly destroyed, thus amplifying the ultrasound signal. Levovist is taken up by the reticulo-endothelial system in the spleen and liver amplifying the ultrasound image of these organs, which lasts a few minutes, so it can be used to highlight isoechoic liver metastases (that contain no Kupffer cells), that could not be detected by standard ultrasound.

The second generation of ultrasound contrast agents (SonoVue) do not amplify the ultrasonic signal through microbubble destruction, but through microbubble resonance in the ultrasound field. The examination is made with low mechanical index (<0.4), which makes the microbubbles oscillate, not destroyed. The amplification time of the ultrasound signal is up to 4-6 minutes. Characteristic for second generation contrast agents is the microbubbles’ elastic response to compression and relaxation. This oscillation will generate an asymmetric, non- linear signal. This response is different from the signal generated by the examined tissue, thus permitting its’ separation by the vascular structures.

The SonoVue microbubbles are formed of a phospholipid shell that includes hexafluoride sulfur, a biologically inert gas. The microbubbles’ diameter varies between 1 and 10 microns (with an average of 2.3 microns), comparable in size to red blood cells. The microbubbles cannot cross the vascular wall, thus SonoVue is strictly an intravascular contrast agent (as opposed to contrast agents in CT and MRI that diffuse into the interstitium). Five to six minutes after injection, the microbubbles are destroyed and the inert gas is released and is cleared through exhalation (not through the kidney as CT or MRI contrast agents), therefore it is not contraindicated in patients with renal failure.


SonoVue microbubbles have a specific behavior in the ultrasound field, which derives from their high compressibility, in contrast to the surrounding tissue, virtually non-compressible (molecules move with only a few Angstroms in the ultrasound field). During a normal examination, the microbubbles’ diameter may vary from half to twice the original diameter.

The microbubbles have a natural frequency of oscillation (resonance) dependent on their diameter, which shows the highest energy conversion efficiency of the ultrasound in reflected signals, useful for obtaining the ultrasound image. The resonance frequency of 3-5 microns microbubbles is in the frequency range usually used for ultrasound examination (3-5 MHz).

At low intensity ultrasound examination (low mechanical index) the microbubbles response is non-linear because their diameter changes asymmetrically as compared to the equilibrium size.

This is because the energy required to compress the microbubbles is greater than that consumed for their expansion (microbubbles are becoming harder the lower the volume). Consequently, the signal obtained through their oscillation will be a distorted version of the insonation wave, effect known as non-linear response which is manifested by harmonic oscillations of the insonation frequency, visible in the spectrum of signals received by the transducer.

But not only microbubbles cause the appearance of harmonics, but also the examined tissues, the effect being more obvious when the insonation signal strength (mechanical index) is higher. In conventional B mode examination, tissue harmonics are used to reduce artifacts caused by reverberations, but in contrast mode (with low mechanical index) they will only contaminate the image, appearing as "noise". Examination with lower mechanical index, used in second generation contrast ultrasound agents studies, in addition to the fact that they generate less tissue harmonics, it also has the advantage of slowly destroying microbubbles, allowing real-time examination.

The safety profile of CEUS

To be used in clinical practice, any medical product must have a good safety profile.

For SonoVue, the only ultrasound contrast product used in Europe at the moment, the most important data on the safety profile originates from an Italian multicenter retrospective study (29 centers), that included a total a number of 23188 patients during a three years period (2001-2004). In this study there were no deaths in connection with contrast ultrasound examination, and the number of reported adverse reactions was 27: 23 of them minor, three moderate and only one severe. In this study, the total rate of adverse events was 0.0086%. In the safety studies published since the marketing study, deaths have been reported after administration of SonoVue, but only in patients with severe heart disease, recent myocardial infarction, the demise probably being related to the heart disease and not to SonoVue.


Based on these data we conclude that SonoVue is a medical product with a good safety profile, which can be used in most patients requiring this investigation, except in patients with acute myocardial infarction, severe ischemic heart disease or other severe cardiac diseases.

Characterization of focal liver lesions in contrast ultrasound (CEUS)

The principle of contrast ultrasound examination in the liver is based on the double blood supply of the liver (venous – from the portal vein and arterial – from the hepatic artery).

The liver lesions should be examined after bolus injection of the contrast agent in all three vascular phases (arterial, portal, and late - parenchymal), thus allowing their characterization, increasing the method’s sensitivity for a correct diagnosis.

Thus, 10-20 seconds after the contrast injection into an antecubital vein, it reaches the liver via the hepatic artery, the arterial phase lasting until the start of the portal (venous) phase, 30-45 seconds after the contrast injection. In the portal phase, most of the contrast agent reaches the liver through the portal vein. The portal phase lasts up to approx. 2 minutes, when the late phase starts (the balance phase), which lasts until the disappearance of the microbubbles from the circulation, about 4-5, maximum 6 minutes (Table 1).

Table I. Vascular phases in CEUS


ARTERIAL PHASE 10-20 s 25-35 s

VENOUS PHASE 30-45 s 120 s

PARENCHYMAL PHASE 120s until the disappearance of

the microbubbles from the tissue

Depending on their nature, focal liver lesions have a typical behavior following contrast, so it is possible to characterize them. Most important is the differentiation between malignant and benign lesions, which CEUS does very well. Characteristic for malignant lesions is the fact that the contrast does not persist in the lesion during the late phase, and the wash-out phenomenon occurs (Fig. 1). The enhancement pattern of each type of hepatic focal lesion during CEUS will be detailed in the focal liver lesions chapters.


Fig. 1. The focal liver lesions enhancement pattern in CEUS


Chapter 2.

Elements of ultrasound anatomy

1. The Liver

The liver is a parenchymal organ with typical appearance, crossed by vascular structures.

The normal liver is considered to be normoechoic (as a fine blend of salt and pepper) (Fig. 2).

The examination begins with the patient in supine position and continues in left lateral decubitus. For a good ultrasound "window" we usually require the patient to perform a deep inspiration, to maintain it for a few seconds while the examiner scans the liver structure. A convex transducer with variable frequency of 2-5 MHz is generally used, the frequency is chosen according to the examined subject characteristics (lower frequency for better penetration). If one is interested in details of liver surface or in superficial areas of the liver, linear transducers with higher frequency (4-8 MHz) should be used.

Fig. 2. Normal liver

For the examination of the liver, sagital sections, transverse and oblique sections, right sub-costal and also intercostal sections are used. The homogeneity and texture of the liver structure, the presence or absence of circumscribed lesions, the aspect of liver surface, the vessels’ patency (portal vein and hepatic veins) should be noted. Liver echogenity is assessed by comparison with the right kidney cortex, to which it should be similar.

The left hepatic lobe is examined in recurrent oblique sub-costal sections, starting from the epigastria, by scanning from bottom to top, to cover all its volume. By moving the transducer to the right, by the same movements, the right hepatic lobe is examined.


Also by oblique sub-costal sections the portal bifurcation will be examined (the right and left branches of the portal vein) and, in a higher plane, the hepatic veins and their confluence with the inferior vena cava is seen.

The left hepatic lobe and the caudate lobe (located before the inferior vena cava) are examined in sagital section, starting from the epigastria. It is recommended to measure the antero-posterior diameter of caudate lobe, since it is increased in patients with cirrhosis (> 35 mm) (Fig. 3). Scanning from the epigastria to the right we evaluate the entire liver by sagital sections, finding along the way the gallbladder.

Fig. 3. Increased caudate lobe in a patient with liver cirrhosis

In addition to sub-costal oblique and sagital sections it is recommended to use intercostal incidences for the evaluation of the liver dome, especially in less cooperative patients who cannot perform a deep inspiration.

During the examination of the liver it is mandatory to evaluate the vascular structures, important elements as anatomical landmarks for segmentation of the liver, but may also present modifications suggestive for certain diseases.

The hepatic veins (HV) are anechoic structures with thin, hyperechoic wall. There are three hepatic veins: right HV, middle HV and left HV that converge to the inferior cava vein similar to the fingers that converge to the palm of the hand (Fig. 4). They are examined through high sub-costal oblique sections. When the lumen is occupied by echo-dense material without Doppler signal (intravascular thrombus), the appearance is characteristic for Budd-Chiari syndrome. When they are dilated to more than 10 mm (measurement performed at 2 cm from their convergence in the inferior vena cava), the appearance is suggestive for congestive heart failure (cardiac liver) (Fig. 5).


Fig. 4. Normal HV Fig. 5. Dilated HV in cardiac liver

The portal vein (PV) is examined by a perpendicular sub-costal section. It's a transonic structure with hyperechoic wall, thicker than the HV’s, located posteriorly to the main biliary duct (MBD) (Fig. 6). Its maximum normal diameter is 13-14 mm, higher values being suggestive for portal hypertension. When the lumen is occupied by echodense material without Doppler signal, the aspect is suggestive for portal thrombosis, whose etiology (benign or malignant) should be established. The portal bifurcation is examined through right oblique sub-costal sections, and is located in a plane below the HV. Similar to PV, the portal branches have thicker walls than the HV (Fig. 7).

Fig. 6. Common portal vein (PV) and Fig. 7. Portal bifurcation main biliary duct (MBD) in hepatic hilum

Starting from the liver vessels, a functional segmentation of the liver was imagined.

Anatomically, the liver is divided into two lobes, the right and the left lobe, separated by the hepato-duodenal ligament (Fig. 8).


Fig. 8. Liver segmentation. LLL=Left liver lobe; RLL=Right liver lobe;

PV=Portal vein; IVC= Inferior cava vein

The functional segmentation (imagined by Couinaud) allows the definition of eight liver segments considering three vertical planes passing through the three hepatic veins, and a horizontal plane passing through the portal bifurcation, which separates the upper segments of the liver form the lower ones (Fig. 9). The caudate lobe (segment I) is considered a separate structure from the two lobes, delimited posteriorly by the inferior vena cava and anteriorly by the venous ligament. The left liver lobe includes segment II (superiorly) and segment III (inferiorly) and is delimited by the right liver lobe by the plane passing through the left HV.

Segment IV is located between the left HV and the middle HV. Between the middle and the right HV are segments V (inferiorly) and VIII (superiorly). Lateral to the right HV are the posterior segments of RLL, VII superiorly and VI (inferiorly).

Some practical observations:

 in the RLL, segments VII and VIII are in contact with the diaphragm;

 segment VI comes into contact with the right kidney;

 the caudate lobe is examined in sagital section;

 by cross section through the gallbladder cervix, the gallbladder bed is surrounded by the segments IV, V and VI;

 by cross section in the upper epigastria, segments IV, VII and VIII converge to the inferior vena cava.


Fig. 9. Liver segmentation

The main biliary duct (MBD) is examined in a section perpendicular to the costal margin, and is located in front of the PV (Fig. 6). Its maximum normal diameter is 5-6 mm, while in patients with cholecistectomy a normal value up to 7-8 mm is accepted. MBD, PV and hepatic artery (HA) are the constitutive elements of the hepatic hilum. HA intersects at a point the MBD and the PV, passing between them. The MBD and PV have the same trajectory, appearing as a

"double-barreled shotgun", but the “barrels” are unequal, the thinner one, situated anteriorly, is the MBD. When the ratio between the diameter of the PV and the MBD is inverted, the aspect is diagnostic for obstructive jaundice.

The intrahepatic bile ducts normally aren’t seen in standard ultrasound, since they have a very fine caliber. They will become evident when there is an obstacle downstream, appearing as transonic structures parallel with the branches of the portal vein, realizing the appearance of

"double duct". If dilatations are important in the incidence that visualizes the portal bifurcation the aspect will be of a "spider" (Fig. 10).

Fig. 10. Dilatations of intrahepatic bile ducts –"spider" aspect


2. Gallbladder

The gall bladder is the source of many abdominal complaints, and is an organ which can easily be examined by ultrasound. Examination is done by right sub-costal recurrent oblique sections; through sagital right sub-costal or by intercostal sections; in supine and mandatory in left lateral decubitus position. The examination must be made carefully, with full view of gallbladder, with special attention to the infundiblar area, where gallstones can hide. By turning the patient in the left lateral decubitus, the infundiblar area will become more accessible and possible stones can mobilize, falling by gravity to the bottom of the gallbladder, where they are better visualized.

The normal appearance of the gallbladder is of a pear shaped, anechoic structure with well-defined hyperechoic wall (Fig. 11). The normal diameters are generally smaller than 8/3 cm, the maximum accepted ones are 10/4 cm, and higher values are suggestive for hydrops.

The normal gallbladder wall thickness is maximum 4 mm. Following food ingestion, the gallbladder wall appears duplicated, due to smooth muscle contraction (Fig. 12).

Fig. 11. Normal gallblader Fig. 12. Gallblader contracted postprandially

3. Pancreas

Pancreatic ultrasound is “the corner-stone” of ultrasound examination, especially for a beginner in ultrasound. But patience and perseverance will lead to increasingly easier visualization of this organ. The examination difficulties come from the fact that the pancreas is a retroperitoneal deeply located organ, partially masked by the bowel loops, the gas contained in the intestinal loops working as a screen that prevents the penetration of ultrasound.

Examination begins from the epigastria, with mild, progressive compression that can mobilize and remove of the intestinal content, thus optimizing the acoustic window.


Before the examination, the ultrasonographist must be well acquainted with the local anatomy, with the vascular landmarks that will help him delineate the pancreas. The examination is done mainly through epigastric sections. The 3.5 MHz convex transducer is preferred. Rarely, in thin (or cachectic) people, a 5 MHz linear transducer is needed.

It is mandatory to examine the pancreas in a fasting patient. The presence of food in the stomach may prevent a correct examination or may create false pancreatic tumor images. The fasting period is 7-8 hours. Liquid consumption is allowed, but carbonated drinks are contraindicated (air in the stomach will make pancreatic examination difficult).

The pancreas will be examined through the gastric antrum or, if the transducer is placed at a high level in the epigastria, using the ultrasound window of the liver, or more rarely, below the antrum (the position of the transducer is midway between the xiphoid appendix and the umbilicus). The best ultrasound window for pancreatic examination will be obtained by high sections (avoiding the colon), through the left hepatic lobe or trans-gastric. For trans-gastric pancreatic examination, the antrum should contain no air.

The presence of liquid in the stomach plays the role of an ultrasound window for the examination of the pancreas. Hence the practical approach used in cases of difficult visualization of the pancreas, when the patient will be administered 500-700 ml plain water or apple juice that will form an ultrasound window in the stomach. After ingestion, 10-15 minutes are required for the debubbling of the ingested liquid. If examination is performed immediately after water ingestion, a hypoechoic (not anechoic) appearance of the stomach will be seen, which might be a surprise. This appearance is the consequence of the bubbling air in the water during deglutition. After 10-15 minutes, the stomach will be filled with transonic liquid that will act as an acoustic window for a better visualization of the pancreas. Sometimes it is possible to find no water in the stomach if the patient is in dorsal decubitus. In this case, the patient will be placed in a sitting position, so that water accumulates in the antrum, which is the ideal anterior landmark of the pancreas.

In order to examine the pancreas through a transverse epigastric section, firstly the spleno-portal axis (the portal vein and the splenic vein) should be identified. It delimits the pancreas posteriorly and appears like a transonic image, comma-shaped, situated anteriorly of the spine, aorta and inferior vena cava. The pancreas is delimited anteriorly by the gastric antrum or the left hepatic lobe (depending on the level at which the transverse section is performed) (Fig 14). Another important vascular reference is the celiac trunk, specifically the pancreatic and hepatic arteries: at their emergence from the celiac trunk they lie on the top of the pancreas. For this reason, when you see the emergence of celiac trunk of the aorta (the appearance of "fountain") (Fig. 15), the transducer must be angled slightly down and the pancreas will appear in the examination plan.


Fig. 13. Normal pancreas Fig. 14. Normal pancreas, slightly hyperechoic

Fig. 15. The emergence of the celiac trunk (TC) from the aorta (AO), with the hepatic artery (HA) and splenic artery (SA)

Between the posterior landmark (the spleno-portal axis) and the anterior landmark (the gastric antrum and the left hepatic lobe) the parenchymal structure of the pancreas is found.

The echogenity of the normal pancreatic parenchyma is similar to that of the liver (possibly slightly hypoechoic). In obese patients (due to fatty infiltration) or in elderly patients (fibrosis), the pancreas can by hyperechoic. All these appearances are normal, provided that the structure of the pancreatic parenchyma is fine, homogeneous (Fig. 14). A normal Wirsung duct can be visualized particularly in young persons, with a diameter of up to 2 mm. It is usually seen only along a portion, rarely in its entire length (Fig. 16).


Fig. 16. Normal pancreas with visible, normal Wirsung duct (WD)

Pancreatic examination in transverse section will visualize most of the pancreas, but the entire pancreas is almost never seen in a single section due to its slightly ascending trajectory.

Pancreatic tail is harder to examine due to the interposition of the gastric body and is sometimes better visualized in left sub-costal oblique section (Fig. 17).

Fig. 17. Pancreatic tail

Regarding the normal size of the pancreas opinions are divided. We do not consider pancreatic size as very important because of its wide individual variability. The easiest to measure is the body of the pancreas, by antero-posterior measurement in transverse epigastric section. Usually, the antero-posterior diameter of the pancreatic body is 10-20 mm, the head of the pancreas is considered normal up to 30 mm and the tail of the pancreas up to 20-25 mm.


4. The Spleen

The spleen is an organ with a parenchymatous structure, with echogenity similar to that of the liver. The ultrasound evaluation of the spleen is performed through left intercostal sections or by oblique sections under the left costal margin in supine position or in right lateral decubitus. The normal spleen is shaped as a crescent, less than 12/6 cm in size (Fig. 18). The entire spleen is relatively difficult to visualize, especially by beginner ultrasonographists. The examination of the spleen will be conducted so as to include both splenic poles in the ultrasound plane, allowing an accurate measurement of the long axis (the most important), as well as of the short axis in globular spleen (more than 6 cm thick). In tall individuals (over 180- 190 cm), a larger size, up to 13/7 cm is acceptable. A spleen with larger diameters than those mentioned should raise the suspicion of a liver disease or a blood disorder, but ultrasound cannot differentiate between the two. Sometimes an accessory spleen may be seen. It appears as a round parenchymal structure, 1-2 cm in diameter, located near the splenic hilum (Fig. 19).

Fig. 18. Normal spleen Fig. 19. Accessory spleen

5. The Kidneys

The kidneys are retroperitoneal organs with diameters of 10-12/5-6/3 cm. Renal ultrasound examination is performed with standard 3.5 MHz, preferably convex transducers.

The renal ultrasound approach can be through the loins (with the patient in ventral decubitus), by lateral approach (right lateral decubitus for the examination of the left kidney, and scanning is performed through the left lateral abdominal region and left lateral decubitus for the right kidney), or through sagital sections in a patient in dorsal decubitus. Generally, the right kidney is easier to visualize in lateral sections or with the patient in dorsal decubitus, using the liver as an acoustic window. For the left kidney, examination is easier in lateral or dorsal sections.

Additional intercostal sections are often used for renal ultrasound examination. For better


visualization, kidneys must be scanned both by longitudinal and transverse sections, until the largest diameter is visualized, considered as the real size of the kidney, which may be suggestive of renal pathology: small kidneys are suggestive of chronic renal failure. In transverse section, approximately in the middle of the kidney, the renal hilum with the renal artery and vein can be seen. Knowing the anatomy of this region is required for the evaluation of vascular structures if a venous (tumor) thrombosis or a renal artery stenosis is suspected.

The ultrasound anatomy of the kidney includes a peripheral hypoechoic area – parenchyma;

and a central hyperechoic area - the renal sinus (Fig 20). The ultrasound differentiation between the cortex and the medulla is possible only in children and in thin persons. In current ultrasound practice, this distinction is not possible, so that the renal sinus and the parenchyma will be discussed in relation to the kidney. Normally, the thickness of parenchymal area is 15-20 mm. Its narrowing and poor differentiation between the parenchyma and the renal sinus are suggestive for chronic renal failure.

Fig. 20. Normal kidney

6. Large vessels

The large vessels, aorta (AO) and the inferior vena cava (IVC) are retroperitoneal organs that are examined in axial midline section. Scan with the transducer along their length to examine them as long as possible. Slight, progressive compression facilitates the examination by pushing aside the bowel gases that are interposed between the transducer and the vessels.

Doppler examination shows blood flow at this level and can expose areas of stenosis or thrombosis.

The ultrasound appearance of the aorta is of a pulsating anechoic formation with hyperechoic wall, located anteriorly to the spine. During the examination, from top to down, the following structures are visualized: the emergence of celiac trunk, the superior mesenteric artery, and sometimes the inferior mesenteric artery (Fig. 21). In transverse section, the aorta


appears as a round structure and we can detect the emergence of the celiac trunk with the hepatic and splenic artery which are "lying" on the upper margin of the pancreas.

Approximately 1.5 cm below the celiac truck, the superior mesenteric artery is seen in front of aorta and the spleno-portal axis. A little lower the emergence of renal arteries (right renal artery in front of the ICV) can be seen.

Fig. 21. Aorta (AO), celiac trunk (CT) and Fig. 22. Aorta (AO), celiac trunk (CT) with superior mesenteric artery (SMA) hepatic artery (HA) and splenic artery (SA)

IVC is located slightly right of the spine, its ultrasound appearance is of a transonic formation with hyperechoic wall, with slow pulsations, related to respiratory movements (if aorta is pulsating, ICV is fluttering) (Fig.23). Its maximum normal diameter is also 20 mm, higher values are suggestive for heart failure.

Fig. 23. Inferior vena cava (IVC), superior mesenteric vein (SMV), head of the pancreas (PA).


7. The pelvis

Pelvic organs are examined in transverse and longitudinal sections above the pubes with the transducer angled to the legs. The urinary bladder will be seen as a round anechoic structure with hyperechoic wall, the size is variable depending of the post-urinary time. Normal bladder wall thickness is maximum 4 mm. In elderly men with prostate adenoma, the bladder wall may be thicker - "fighting bladder."

In men, the urinary bladder neck is surrounded by the prostate - a parenchymal structure with the maximum normal diameter 3/4 cm. Larger diameters are suggestive for prostate adenoma (Fig. 24).

Fig. 24. Prostate adenoma

In women the uterus is visualized posteriorly of the urinary bladder, as an echoic structure, pear shaped in longitudinal section. In adult fertile woman its maximum size is 9/5 cm. Normally the uterus is bent forward, an angle of 60° is formed between the cervix and uterus (Fig. 25). When the uterine fundus is found in the Douglas space (the uterus is bent backwards), it defines the uterus in retroversion (Fig. 26). The myometrium appears as a thick, hypoechoic area located peripherally, which encloses the endometrium, a hyperechoic area whose size varies according to the phases of the menstrual cycle. In cross section the uterus appears like a round structure, located at the base of the urinary bladder (Fig. 27). By scanning to the left and to the right we can visualize the ovaries, slightly hypoechoic, round or oval structures, maximum 3/2 cm diameter.


Fig. 25. Uterus in anteversion – longitudinal section Fig. 26. Uterus in retroversion – longitudinal section

Fig. 27. Uterus – cross section


Chapter 3.

Abdominal ultrasound in the diagnosis of diffuse liver diseases

The liver is the organ in which ultrasound evaluation has maximum value. In experienced hands, standard ultrasound, especially with contrast, can establish difficult diagnoses, without requiring other expensive imaging investigations required. Liver ultrasound should only be done in a clinical context, after knowing the patients’ history, after a brief physical examination, during which palpation of the liver is mandatory. Thru palpation we can appreciate the size of the liver (more accurately than by means of imaging) and its consistency – a useful element for the diagnosis of chronic liver diseases.

In the following we will refer to the value of ultrasonography for the diagnosis of acute hepatitis, of chronic hepatitis, of liver steatosis (diffuse or focal), for the diagnosis of liver cirrhosis and cardiac cirrhosis.

1. Acute hepatitis

Acute hepatitis is an acute illness of the liver, characterized by the increase of aminotransferases, especially GPT, values typically more than 10 times the upper limit of normal. Acute viral hepatitis can be caused by some typical hepatotropic viruses (hepatitis A, B, C and E virus) or by other viruses (herpes virus, Epstein-Barr virus or cytomegalus virus), by alcohol abuse, or rare causes: toxic drugs (Paracetamol, Halotan, etc), acute autoimmune hepatitis.

The diagnosis of acute hepatitis is made in an epidemiological context (contact with a hepatitis virus infected person; with possible infected blood or blood products; hepatotoxic drugs intake; alcohol abuse, etc.); in a biological and clinical context (asthenia, dyspepsia, often fever, with or without jaundice). Among blood tests, high elevated transaminase values, with or without increased bilirubin, with or without positive markers for infection with hepatitis viruses: HAV - IgM antiHAV; HBV - HBsAg and IgM anti HBV; HCV - RNA PCR HCV viral load, are needed for a positive diagnosis.

The ultrasound appearance of acute hepatitis is not characteristic. Liver ultrasound is frequently completely normal. Sometimes, some ultrasonographic signs can suggest this diagnosis.


Thickened and doubled gallbladder wall occurs in up to 80% of acute hepatitis, particularly in viral hepatitis (Fig. 1). It is due to hypoalbuminemia that generates gallbladder wall edema, and it’s a suggestive sign for acute viral hepatitis in a young person with jaundice and dyspeptic syndrome.

Fig. 1. Thickened and doubled wall in acute hepatitis

Other ultrasonographic signs, but with poor specificity are: diffuse liver hypoechogenity (difficult to evidence by ultrasound in the absence of a landmark structure), due to the hepatic edema; and possibly mild splenomegaly (slightly enlarged spleen – considering a spleen < 12 cm in its long axis as normal).

In acute alcoholic hepatitis, the background can be of hepatic steatosis (“bright liver”

with posterior attenuation on ultrasound), consequence of prolonged alcohol abuse, not of acute hepatitis.

2. Chronic hepatitis

Chronic hepatitis is a chronic inflammatory disease of the liver, of various etiologies, with an evolution of minimum 6 months, without a tendency to healing, with necrotic and fibrotic lesions as a pathological substrate. The biological expression of chronic hepatitis is usually a moderate cytolysis syndrome. To state the diagnosis of chronic liver disease, the cytolysis syndrome must last at least six months, because in some cases the detection of the moderately increased transaminase levels could be in the context of a previously undiagnosed acute hepatitis, which will heal spontaneously in several weeks.


Chronic hepatitis is most frequently caused by hepatitis B, C or B+D viruses. Hepatitis A does not become chronic. A common cause of chronic hepatitis is alcohol abuse which causes fatty liver (alcoholic steatohepatitis). Other causes of chronic hepatitis are: nonalcoholic steatohepatitis, autoimmune hepatitis, toxic drug hepatitis, cholestatic hepatitis or abnormal storage of metals in the liver – hemochromatosis (iron) and Wilson disease (copper).

Ultrasound examination in chronic hepatitis does no evidence typical signs. Most frequently (in approx. 50% of cases), a mild splenomegaly is detected (up to 13-14 cm). The majority of authors consider as the upper limit of normal 12 cm as the length of the long axis of the spleen. The width and the thickness of the spleen are not equally important, but a globulous spleen can be a sign of activation of the reticuloendothelial system. Larger splenomegaly (>15 cm) suggests liver cirrhosis (Fig. 2) in a clinical context.

Fig. 2. Splenomegaly in a patient with chronic hepatitis C (longitudinal diameter 15 cm)

A frequent ultrasound sign, especially in chronic hepatitis C (up to 70% of the cases), but also in autoimmune hepatitis or chronic hepatitis B, is finding lymph nodes in the hepatic hilum (adenopathies of the hepato-duodenal ligament) (Fig. 3). The lymph nodes of the hepato- duodenal ligament are usually oval, 5-10/10-20 mm in size. They are best visualized along the hepatic artery or the portal vein. They must be differentiated from malignant adenopathies, which are generally round and hypoechoic.

Fig. 3. Hepatic hilar adenopathy Fig. 4. Moderate hepatic steatosis


In patients with alcoholic or nonalcoholic steatohepatitis, and in some of those with chronic hepatitis C, the ultrasound appearance will be of hepatic steatosis (bright hyperechoic liver, with posterior attenuation (Fig. 4).

Although abdominal ultrasound does not give decisive evidence for the diagnostic of chronic hepatitis, it can be a useful tool for diagnostic and for a correct evaluation. Specifically ultrasound is used to choose the place where liver biopsy will be performed (ultrasound guided or assisted hepatic biopsy) and for follow-up assessment (every 6 months) in patients with severe fibrosis and cirrhosis for HCC screening.

In conclusion, ultrasound examination in chronic hepatitis has a limited value, only splenomegaly and hepato-duodenal ligament adenopathies are relatively constant elements (good sensitivity, but lower specificity).

3. Hepatic steatosis

Hepatic steatosis is defined as fatty loading of the liver higher than 10%. The main causes of hepatic steatosis are: chronic alcohol intake (alcoholic steatohepatitis – ASH syndrome), obesity, diabetes, dyslipidemia (non-alcoholic steatohepatitis – NASH syndrome).

Another cause of fatty liver chronic infection with hepatitis C virus (up to half of the chronic C virus patients have mild fatty loading).

Before the development of modern imaging methods (CT, ultrasound) it was believed that hepatic steatosis is always diffuse. Later, in the early 80s, this imaging methods showed that hepatic steatosis can also affect the liver unequally, therefore areas that have less fat (fatty-free areas) can appear on o fatty liver, and fatty loaded areas (focal fatty infiltration) can appear in a normal liver. The reason for this different fat load is not clear, it is likely due to changes in the arterial-portal-venous vasculature, well vascularized areas being less fatty.

Hepatic steatosis can be simple (asymptomatic) or it can be associated with inflammation, manifested through cytolysis syndrome (steatohepatitis). Ultrasound cannot differentiate between the two, therefore, in patients with steatosis the cytolysis syndrome should always be evaluated (an increased De Rittis GOT/GPT ratio can be suggestive for ethanolic etiology), and also the presence of HCV antibodies (association of liver steatosis with chronic hepatitis C virus).

Hepatic steatosis is easily and precisely diagnosed by ultrasound (sensitivity 90 %). The ultrasound appearance is of a hyperechoic liver as compared with the renal parenchyma, "bright liver", often accompanied by "posterior attenuation" due to partial absorption of ultrasound waves by the fatty tissue. There is a direct correlation between liver fat load and the severity of posterior attenuation. Thus, depending on the intensity of posterior attenuation, a subjective and


semi-quantitative assessment of the steatosis can be made: mild steatosis (discrete attenuation - Fig.5, Fig. 6), moderate steatosis (obvious attenuation – Fig.7, Fig. 8), and severe steatosis (difficult or impossible to visualize posterior diaphragm – Fig.9, Fig.10) Special attention should be given to patients with severe steatosis, in whom deep lesions are difficult to visualize due to posterior attenuation. In these cases, CT is recommended for solving unclear cases.

Fig. 5; Fig. 6. Mild hepatic steatosis

Fig.7; Fig. 8. Moderate hepatic steatosis

Fig. 9; Fig. 10. Severe hepatic steatosis – the diaphragm cannot be visualized


Focal steatosis and fatty-free areas are particular situations quite frequently encountered. The ultrasound appearance is the juxtaposition of liver tissue with different echogenity: fatty-free areas are hypoechoic areas in a hyperechoic liver (Fig. 11, Fig. 12), focal steatosis are hyperechoic areas in a liver with normal echogenity (Fig.13). The delimitation of these areas is clear, they have often a geographical contour and variable size. They never alter the hepatic surface or infiltrate and invade vascular structures.

Fig. 11. Fatty-free area in the right lobe Fig. 12. Fatty-free are in the left lobe

Fig. 13. Focal steatosis, surrounding the gallbladder

A common case of focal hepatic steatosis is the fatty hilum. This involves excess fat storage in a typical hepatic area, which is situated at the portal bifurcation. It is an oval shaped area, usually 3-4/2-3 cm in size, situated at the bifurcation of the portal vein, between its right and left branch. Differential diagnosis should exclude a hemangioma or a hepatic tumor.

The differential diagnosis of fatty-free areas is difficult, we have to exclude primitive or secondary liver tumors that can appear in fatty liver. This cannot be done only by standard ultrasound, contrast imaging methods are necessary, CEUS, CT or MRI.


In conclusion to the chapter on hepatic steatosis, it can be said that ultrasound is a good method for assessing hepatic steatosis (a non-invasive technique), and also a method for the semi-quantitative evaluation of steatosis (relatively well correlated with the histological fat loading of the liver). In the case of focal hepatic steatosis or fatty free areas, the positive ultrasound diagnosis is easy, while differential diagnosis will require an experienced ultrasonographist and sometimes, evaluation by contrast-enhanced ultrasound (CEUS).

4. Liver cirrhosis

Liver cirrhosis is the final stage of the majority of chronic liver diseases, in which necrosis, regenerative phenomena and fibrous changes coexist, resulting in the nodular transformation of the liver.

The etiology of liver cirrhosis is multiple, but alcohol and hepatitis viruses B and C are responsible in 90% of the cases. Rare causes are autoimmune hepatitis, Wilson’s disease (ceruloplasmin deficiency), hemochromatosis, alpha-1-antitrypsin deficiency, primary biliary cirrhosis, drug-induced cirrhosis, and cryptogenic cirrhosis (a rare condition).

Though advanced cirrhosis has a typical ultrasound appearance: ascites, irregular hepatic surface, heterogeneous structure of the liver, splenomegaly (90% specificity for the diagnostic); in early cirrhosis the ultrasound aspect can be perfectly normal (up to 20% of the cases).

The typical elements that can be found in liver cirrhosis (which are not necessarily present) are: caudate lobe hypertrophy, heterogeneous liver structure, splenomegaly, ascites, signs of portal hypertension, and changes in the gallbladder wall.

a) Caudate lobe hypertrophy

The caudate lobe (segment 1 of the liver) undergoes hypertrophy during the evolution of liver cirrhosis, so that it will be frequently enlarged in this pathological condition. In practice we measure the anterior-posterior diameter of the caudate lobe. An antero-posterior diameter greater than 35 mm is suggestive for the diagnostic of liver cirrhosis (Fig. 14, Fig. 15), since in about 2/3 of the cases the caudate lobe is hypertrophied. The antero-posterior diameter of the caudate lobe will be measured in a sagital section at epigastric level. The inferior vena cava (IVC) is seen and anterior to it, the ovoid structure of the caudate lobe will appear.

Subsequently, the maximum antero-posterior diameter of the caudate lobe will be measured. Certain measurement problems may occur in the case of marked steatosis (ultrasound waves are strongly absorbed by fat tissue) or, more rarely, in case of ascites.


Fig. 14. Normal caudate lobe (31 mm) Fig. 15. Enlarged caudate lobe (39 mm)

in liver cirrhosis in liver cirrhosis

b) Heterogeneous hepatic structure

The aspect of hepatic heterogeneity occurs in approximately half of the liver cirrhosis cases, as the consequence of fibrous changes, and of regeneration nodules. Practically, instead of the appearance of fine mixed salt and pepper, like in normal liver (Fig. 17), in the case of heterogeneous liver structure "salt and pepper" will appear coarsely milled (Figure 18). Special attention should be paid in patients with known liver cirrhosis, in which the liver structure is highly heterogeneous, particularly if this aspect is limited to certain areas. In these conditions the presence of a diffuse HCC should be suspected. It is recommended to measure the alpha- fetoprotein and to perform a contrast imaging method (ultrasound, CT or MRI) to elucidate the diagnostic.

Fig. 16. Macroscopic appearance of micronodular cirrhotic liver section


Fig. 17. Normal liver echostructure Fig. 18. Heterogenous structure

in liver cirrhosis in liver cirrhosis

c) Irregular hepatic surface

Irregular liver surface is the consequence of histological micronodular liver (which cannot be demonstrated by ultrasound inside the liver parenchyma, although the term is incorrectly used in everyday practice). Micronodular liver is a histological reality in liver cirrhosis, but ultrasound cannot highlight these parenchymal nodules.

Irregular liver surface is easily evidenced in the presence of ascites (Fig.19). In its absence the liver surface is difficult to assess. The examination can be facilitated by using high frequency transducer (5-9 MHz) (Fig. 20).

Fig. 19. Irregular liver surface Fig. 20. Irregular liver surface (5MHz transducer) liver cirrhosis and ascites


We have to mention that when we find through ultrasound a heterogeneous liver structure and an irregular liver surface in an asymptomatic patient, without any history of liver pathology, we need to think of a possible chronic liver disease. Clinical examination, biological evaluation, FibroScan, and endoscopic evaluation in these cases can discover unknown liver cirrhosis.

d) Splenomegaly

An enlargement of the spleen exceeding 12 cm along its long axis is frequent in the case of liver cirrhosis, in approximately 80% of the cases (Fig. 21). In these patients splenomegaly is more severe than in chronic hepatitis, frequently exceeding 15 cm. Splenomegaly larger than 18 or even 20 cm is often accompanied by hematological hypersplenism (thrombocytopenia<100,000/mm3, and/or leucopenia < 3000/mm3, and/or anemia). In other situations, the increase in the long axis of the spleen is not necessarily very important, but the spleen has a globulous appearance, through the increase of its width and thickness.

Fig. 21. Splenomegaly

e) Ascites

Ultrasound is a very sensitive method to evidence ascites, frequently encountered in patients with decompensated cirrhosis. It is also useful for assessing the volume of ascites and its evolution during diuretic therapy. We subjectively appreciate the ascites volume (minimal, small, moderate and large), based on the amount of liquid in the Douglas space and in the perihepatic space. We consider that in a minimal ascites the amount of peritoneal liquid is about 1-2 kg (Fig. 22), in a mild ascites 3-4 kg (Fig. 23), in a moderate ascites about 7-8 kg (Fig. 24) and in a voluminous ascites 10-15 kg (Fig. 25, Fig. 26).


Fig. 22. Minimal perihepatic ascites Fig. 23. Small ascites in Douglas space (8 MHz transducer)

Fig. 24. Moderate perihepatic ascites Fig. 25. Large ascites in the Douglas space Intestinal loops “float” in the ascites

The ultrasound appearance of ascites is of an anechoic image that changes form with changes in the patient’s position. We search for ascites in Douglas space, in Morrison space (interhepatorenal), perihepatic and perisplenic. In a patient with old ascites, the ascites may not be completely anechoic, it can be slightly hypoechoic and contain small echogenic particles in Brownian motion, aspect of ”dense” ascites (Fig. 26, Fig. 27). Excepting the patient with old ascites, “dense” ascites can also occur if the ascites is infected (spontaneous bacterial peritonitis), in hemoperitoneum or chylous ascites. A diagnostic paracentesis is recommended if "dense" ascites is found in a patient with liver cirrhosis.


Fig. 26. Fig. 27. Large, „dense” perihepatic ascites

f) Signs of portal hypertension (PHT)

One of the consequences of fibrosis in liver cirrhosis is the increase of portal circulation resistance. The consequences of portal hypertension include collateral abdominal, peritoneal circulation, the opening of vascular shunts and the appearance of varices, most frequently located in the esophagus.

One of the first signs of PHT in ultrasound is the increased diameter of the portal vein in the hilum to 13-14 mm (Fig. 28), and its lack of variability in inhale/exhale (Bolondi sign).

Dilatation of intrahepatic portal system may also occur in case of PHT in liver cirrhosis (Fig.29), but its assessment is somewhat subjective, since an upper limit size was not defined as for the portal vein in the hilum.

Fig. 28. Dilatation of the portal vein in the hilum Fig. 29. Dilatation of the portal bifurcation


Measurement of the splenic vein in front of the aorta and in the splenic hilum can provide some elements of PHT. Thus, a splenic vein larger than 10 mm measured or in front of the aorta or larger than 8 mm measured in the hilum (Fig. 30) and (Fig. 31), respectively, can be a sign of portal hypertension.

Fig. 30 Dilatation of the splenic-portal axis Fig. 31. Splenomegaly and dilatation of the splenic vein in the hilum

Other signs of HTP are the dilation of visceral veins and the appearance of venous shunts. The detection of collateral epigastric circulation (dilation of the gastric coronary vein), of spontaneous splenic-renal shunts or of splenic varices (Fig. 32) are typical signs of portal hypertension. In ultrasound they appear as multiple anechoic images that communicate between them and the Doppler examination shows present flow (Fig. 33).

Fig. 32. Splenic varices Fig. 33. Splenic varices – Doppler examination

Repermeabilization of the umbilical vein is a severe sign of PHT that can be found in 10- 20% of advanced cirrhosis cases. The repermeabilization of the umbilical vein will be checked starting from the left branch of the portal vein (Fig. 34), where a vascular (venous) cord starts, continuing to the lower side of the liver and then, posteriorly to the abdominal wall, towards the umbilicus (Fig. 35).


Fig. 34. Repermeabilization of the Fig. 35. Repermeabilization of the umbilical vein intrahepatic aspect umbilical vein - abdominal wall

Portal thrombosis (the presence of echo dense material in the lumen of the portal bifurcation or the common PV) (Fig. 36) in a patient known with liver cirrhosis should raise the suspicion of HCC. In malignant PV thrombosis due to HCC, the portal thrombus is actually neoformation tissue, vascularized, which will enhance following contrast bolus in CEUS, CT or MRI with contrast. Portal thrombosis may also be benign, in this case the blood clots form as a result of slowdown of the portal blood flow in PHT. Since it is avascular, the benign portal thrombus will not enhance following contrast bolus in contrast imaging.

Fig. 36. Portal thrombosis (Common portal vein)


g) Changes in the gallbladder wall

A frequent aspect in liver cirrhosis is the thickening and duplication of the gallbladder wall due to edema secondary to hypoalbuminemia, portal hypertension and lymphatic stasis.

The diameter of the normal vesicular wall is less or equal to 4 mm. Given that in liver cirrhosis gallstones are found often enough, special attention must be paid to the differential diagnosis with acute cholecystitis, in which an ultrasound diagnostic criteria is also the thickening of the gallbladder wall. But acute cholecystitis is also accompanied by a suggestive clinical aspect and the ultrasound Murphy’s sign (intense pain at pressure with the transducer in the gallbladder area).

In liver cirrhosis, the gallbladder wall can be thickened, reaching 6-8 or even 10 mm (Fig.

37, Fig. 38), most frequently doubled (with a “sandwich” appearance). In ascites with unknown etiology, by measuring the gallbladder wall we can differentiate ascites due to peritoneal carcinomatosis and due to tuberculosis, in which the vesicular walls are normal, from of the one in liver cirrhosis were the gallbladder has thickened, doubled wall.

Fig. 37. Gallbladder with thickened, doubled Fig. 38. Gallbladder with thickened wall - liver cirrhosis wall, filled with sludge in liver cirrhosis


Approximately one third of the patients with liver cirrhosis have gallstones and/or biliary sludge (Fig.39), but most often they are asymptomatic gallstones, satellite to the background disease, and they do not require surgical intervention.

In PHT we can also notice varices near the gallbladder that appear as anechoic, confluent structures (Fig.39), with Doppler signal (Fig.40), in the immediate vicinity of the gallbladder.


Fig. 39. Gallstones and gallbladder varices Fig. 40. Gallbladder varices - Doppler

5. Cardiac liver

Cardiac liver includes changes due to vascular alterations and venous stasis, secondary to right heart failure. The ultrasound aspect of cardiac liver appears in a clinical context, with signs of right or global heart failure, in a patient with a known long history of cardiac disease or with an old broncho-pulmonary disease (cordus pulmonale), with dyspnoea, hard cyanotic edema of the inferior limbs and frequently ascites.

The ultrasound signs of cardiac liver are dilation of the hepatic veins and of the inferior vena cava (IVC). Dilation of the hepatic veins (SHV) is typical (Fig. 41) and can be quantified by measuring their diameter 2 cm from the junction with the inferior vena cava (IVC). In right or global heart failure SHV will appear larger than 10 mm, very well visible up to the periphery (Fig. 42). The normal respiratory variability of the hepatic veins disappears. Another ultrasound sign of heart failure is the dilation of the inferior vena cava, to more than 20 mm in diameter (Fig. 43), but especially the disappearance of the physiological inspiration/expiration variability.

Fig. 41. Dilation of SHV in cardiac liver Fig. 42. Right SHV visible in the periphery in cardiac liver


Fig. 43. Dilation of IVC in heart failure

In heart failure sometimes we can detect peritoneal effusion (ascites) in variable amount, particularly in the Douglas space or in the perihepatic area. The presence of pleural effusion is relatively frequent. It appears as an anechoic crescent situated outside the diaphragm (Fig. 44), which allows the differentiation from the peritoneal effusion (fluid bellow the diaphragm) (Fig. 45). The volume of pleural effusion (small or large) can also be correctly assessed by ultrasound. The diagnosis of pleural effusion is easier to make on the right side (where the ultrasound window of the liver is used) than on the left side. The pericardial effusion appears as an anechoic area surrounding the heart (Fig. 46) and has a variable volume. We recommend in all cases of suspected pericardial effusion to request echocardiographic examination, by which the cardiologist will confirm the diagnosis (there is a possibility of confusion between pericardial effusion and highly hypoechoic pericardial fat). Unlike pericardial fat, pericardial effusion changes with the movements of the patient.

Fig. 44. Fluid in the right pleura Fig. 45. Fluid in the right pleura and ascites


Fig. 46. Pericardial effusion

6. Budd-Chiari syndrome

Budd-Chiari syndrome is a clinical condition characterized by the thrombosis of the hepatic veins. It can be idiopathic, but it may a consequence of coagulopathies, myeloproliferative diseases, and neoplastic conditions. The diagnosis can be suspected in the presence of edema, ascites and hepatalgia with sudden onset.

In ultrasound the SHV cannot be viewed, partially or totally, due to the presence in their lumen of an echo dense material – thrombosis. In case of doubt we will use Doppler examination, which will show the absence of venous flow in the SHV.

More rarely, ultrasound will detect partial thrombosis, a solid like structure in the vascular lumen. of a hepatic vein. Also, the presence of thrombosis in the inferior vena cava can be detected by accident or in a clinical context. This thrombosis is more frequently found in renal or hepatic cancers.


Chapter 4.

Abdominal ultrasound in the diagnosis focal liver lesions – fluid lesions

Abdominal ultrasound is often the first imaging method performed in a patient for various complaints, whether about abdominal symptoms; or for the evaluation of a patient with a suspected or established chronic liver disease; for the follow-up of an oncology patient; or for the assessment of an individual with minimal abdominal trauma. In these circumstances often focal liver lesions are found, which we expect to find or not. Some of them have a typical aspect in standard ultrasound (biliary cysts, hydatid cysts, small hemangiomas), but more often the appearance of the lesion does not allow its definite diagnosis based only in gray scale ultrasound. In the latter case additional imaging investigations with contrast should be performed and when those are inconclusive, liver biopsy.

Below we will discuss the focal liver fluid lesions: simple hepatic cyst, polycystic liver, hydatid cyst, liver hematoma and liver abscess.

1. Simple liver cysts (or biliary cysts)

Liver simple cysts are non-parasitic, relatively common in clinical practice (1-3% of the ultrasound examinations performed). It is most frequently an incidental ultrasound finding, an

“incidentaloma”, its cause is the lack of communication of the bile ducts with the biliary tree.

The clinical signs in simple liver cysts are generally absent, very rarely they can generate symptoms, such as discomfort or pain in the right hypochondrium (large cysts or with intracystic hemorrhage).

The ultrasound appearance of hepatic cysts is usually typical, as an anechoic lesion with a very thin wall (sometimes not visualized by US), because they are lined by a single epithelial layer (Fig. 1, Fig. 2, Fig. 3, Fig. 4). The posterior enhancement is typical of all liquid structures and is due to the acceleration of ultrasound speed when passing from a solid environment (the liver) to the liquid environment of the cyst.



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