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IOAN SPOREA CRISTINA CIJEVSCHI PRELIPCEAN

A A A B B B D D D O O O M M M I I I N N N A A A L L L U U U L L L T T T R R R A A A S S S O O O U U U N N N D D D

I I I N N N

C C C L L L I I I N NI N I IC C CA A AL L L

P PR P R RA A AC C C T T T I I I C CE C E E

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"VICTOR BABEŞ" UNIVERSITY OF MEDICINE AND PHARMACY TIMIȘOARA

IOAN SPOREA CRISTINA CIJEVSCHI PRELIPCEAN

ABDOMINAL ULTRASOUND IN

CLINICAL PRACTICE

„Victor Babeş” Publishing

Timişoara, 2017

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TEXTBOOK collection

VICTOR BABEŞ PUBLISHING

2 Eftimie Murgu Sq., Room. 316, 300041 Timişoara Tel./ Fax 0256 495 210

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

General director: Prof. univ. dr. Dan V. Poenaru Director: Prof. univ. dr. Andrei Motoc

Scientific referent: Prof. univ. dr. Lucian Petrescu CNCSIS code: 324

© 2017

All rights reserved. Partial or in whole reproduction of this book, on any media, is strictly forbidden without the written approval of the authors and will be sanctioned in accordance to current copyright laws

ISBN 978-606-786-051-1

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4 Professor IOAN SPOREA, MD PhD

Consultant in Gastroenterology and Internal Medicine

HEAD OF THE DEPARTMENT OF GASTROENTEROLOGY AND HEPATOLOGY

"VICTOR BABEŞ" UNIVERSITY OF MEDICINE AND PHARMACY TIMIȘOARA

Professor CRISTINA CIJEVSCHI PRELIPCEAN, MD PhD Consultant in Gastroenterology and Internal Medicine

INSTITUTE OF GASTROENTEROLOGY IAŞI

“GR. T. POPA” UNIVERSITY OF MEDICINE AND PHARMACY IAŞI

In collaboration with:

Professor Lucas Greiner, MD, PhD Director of ISCUS

Wuppertal, Germany

Associate Professor Roxana Șirli, MD, PhD

Consultant in Gastroenterology and Internal Medicine

DEPARTMENT OF GASTROENTEROLOGY AND HEPATOLOGY

"VICTOR BABEŞ" UNIVERSITY OF MEDICINE AND PHARMACY TIMIȘOARA

Lecturer Mirela Dănilă, MD, PhD Consultant in Gastroenterology

DEPARTMENT OF GASTROENTEROLOGY AND HEPATOLOGY

"VICTOR BABEŞ" UNIVERSITY OF MEDICINE AND PHARMACY TIMIȘOARA

Associate Professor Alina Popescu, MD, PhD Consultant in Gastroenterology and Internal Medicine

DEPARTMENT OF GASTROENTEROLOGY AND HEPATOLOGY

"VICTOR BABEŞ" UNIVERSITY OF MEDICINE AND PHARMACY TIMIȘOARA

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CONTENTS:

Foreword ... 6

1. THE LIVER ... 8

2. THE GALLBLADDER ... 70

3. THE PANCREAS ... 92

4. THE SPLEEN ... 118

5. THE DIGESTIVE TRACT ... 126

6. THE KIDNEYS ... 143

7. THE RETROPERITONEUM (LYMPH NODES, INFERIOR VENA CAVA, AORTA) ... 158

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Foreword

What is the aim of this book? Starting from the concept of clinical ultrasound we promote, our aim is to integrate imaging data in a clinical context, considering the patient as a whole. Based on medical history, clinical examination, biologic and paraclinic investigations, we will obtain a diagnosis as accurate as possible, followed by a treatment adequate for the disease and its stage.

Usually imaging books focus on images, and do not include clinical data that lead to a specific imaging appearance. This approach can be found in imaging treatises, but for the young clinician (fellow in training or young specialist), as well as for an experienced doctor, the stream of thought and the approach should go from symptoms and syndromes, to investigations and diagnosis. At the same time, the high rate of new information regarding etiopathogenesis, assessment techniques and treatment in some diseases frequently makes the doctor lag behind the information flow. This happens more rarely in the main field of activity and more frequently regarding related specialties (e.g. for a gastroenterologist, information in the field of hematology, nephrology, etc.).

To whom is this book addressed? To all clinicians regardless of their specialty, as well as to imaging specialists, who need to have clinical information on a disease not only to treat the disease, but also to understand the strategy of diagnosis and staging of the disease.

This book is intended for internists (and specialties derived from internal medicine such as gastroenterology, nephrology, hematology, metabolic and nutritional diseases), surgeons, emergency doctors or family physicians. This last category has perhaps one of the most difficult tasks, of being an interface between the patient and the specialist. The position of the family physician, having to decide whether to refer a patient to a specialist, or to continue the investigation of an illness himself/herself, is often extremely difficult. Both approaches involve certain risks: the frequent referral of a patient to a specialist will lead to the patient’s refusal to see

”one more specialist”, while the delay in asking for specialized advice might postpone diagnosis and consequently, the initiation of adequate treatment. Hence, the responsibility of the family doctor to stay as accurately informed as possible in many areas, for an adequate judgment of the clinical case, in order to seek the specialist’s advice at the right time.

A particular category of doctors that we had in mind while writing this book is that of fellows in training. The beginning of residency is a time of success (at the residency examination), but also of responsibility and stress in front of the complexity of mostly new material. This is why we aim at providing fellows in training with useful material for their training in the field of ultrasound.

Last, but not least this book is intended for radiologists. The process of their training is mainly devoted to learning how to work with images (in ultrasound, computed tomography or magnetic resonance imaging). However, the relationship with the clinical information, with novelties in clinical specialties is most frequently absent. This is why the results formulated by radiologists are often descriptive and rarely have a clinical conclusion. Training the imaging

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specialist in clinical ultrasound will help him/her to integrate the result of the examination with the clinical judgment of the case.

We hope that the combined ultrasound and clinical information, along with images that we considered the most conclusive, will allow newcomers to this field to understand ultrasound accurately, and experienced practitioners to verify and consolidate their knowledge. The book presents the point of view of the authors, based on a long ultrasound experience and teaching practice.

The authors

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CHAPTER 1

THE LIVER

The ultrasound (US) of the liver is an area in which the optimum use of this technique along with the experience of the examining doctor can establish a difficult diagnosis and can frequently prevent other, possibly more expensive examinations.

The US of the liver must be carried out based on a previously made clinical diagnosis (the patient referred for US should be accompanied by a form indicating the clinical diagnosis, or better, the ultrasonographist will examine a patient he already knowns from the clinic). For ambulatory patients, the US examination will start with a short medical history and with the clinical examination, in which the inspection and palpation of the abdomen and liver can be extremely useful. The easiest and perhaps the most accurate diagnosis of hepatomegaly is made by palpation (which is more accurate than any imaging method). The consistency of the liver can also be very precisely evaluated by palpation. The daily practice of liver palpation of an experienced clinician will certainly lead to better results compared to the limited experience of a young doctor.

Clinical thinking will be different if the liver is soft as compared to a hard liver. Thus, if the liver is enlarged and hard on palpation, signs of liver cirrhosis or tumoral liver (either primary tumor or metastases) will be sought by ultrasound. Although liver cirrhosis most frequently has obvious imaging signs, approximately 20-30% of cirrhotic patients will have a normal hepatic US appearance. However, knowing the clinical characteristics of the liver, even if the US appearance is normal, additional examinations will be performed (elastography techniques: transient elastography - FibroScan, VTQ by ARFI - Siemens elastography; upper digestive endoscopy for possible esophageal varices; biologic tests; liver biopsy or laparoscopy for histological staging).

Many times, the ultrasonographist, who often knows the clinical diagnosis of liver cirrhosis, cannot resist the impulse to correlate his/her knowledge on the disease with the imaging appearance. Thus, although in a number of cirrhosis cases the liver structure is homogeneous (without major architectural alterations), knowing the clinical diagnosis the doctor describes it as heterogeneous or even with micronodular structure. The objectivity of the imaging description should prevail even in a known clinical context.

Liver US can be divided into:

A) Diagnosis of diffuse liver diseases;

B) Diagnosis of focal liver lesions - cystic

- solid: a) benign

b) malignant

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A) DIAGNOSIS OF DIFFUSE LIVER DISEASES

1. ACUTE HEPATITIS

Definition: acute hepatitis is a humoral and biochemical syndrome characterized by increased aminotransferases. It is classically considered that a more than 10 fold increase in aminotransferases level (particularly ALT) is a typical sign for acute hepatitis. In Romania, acute hepatitis is most frequently caused by viral infections and rarely by other causes (drugs, acute alcoholic hepatitis, acute autoimmune hepatitis, etc.).

Acute viral hepatitis can be caused by hepatotropic viruses (hepatitis A, B, C and E) or by other viruses such as Herpes virus, Epstein-Barr or Cytomegalovirus.

Acute viral hepatitis can evolve with or without jaundice. It should be mentioned that a high percentage of acute viral hepatitis (regardless of the causative virus, but particularly those caused by B or C virus) are anicteric. This is why in an adult population, particularly in endemic areas for hepatitis such as Romania, signs of previous infection, such as anti-HAV or anti-HBs antibodies are frequently positive (although many patients do not remember having a jaundice episode).

The health care policy to vaccinate newborns against hepatitis B virus aims at diminishing the incidence of acute and chronic hepatitis. In the endemic area of Romania, it is also recommended to vaccinate children against hepatitis A virus. The solution of the bivalent A+B vaccination is a correct alternative (Twinrix).

The clinical signs of acute hepatitis are fatigue, dyspeptic syndrome, fever and jaundice that often occur at the onset hence the frequent clinical situation in which abdominal ultrasound is performed for the assessment of an icteric syndrome.

The liver ultrasound findings in acute hepatitis are nonspecific, frequently completely normal, although sometimes, suggestive ultrasonographic signs can be present.

Gallbladder wall thickening is found in up to 80% of cases of acute hepatitis, particularly in viral hepatitis (Fig. 1.1). It is caused by hypoalbuminemia that generates gallbladder wall edema. Finding a thickened gallbladder wall in a young or middle aged person with dyspeptic syndrome and particularly with jaundice can be a useful diagnostic element for acute hepatitis.

Fig. 1.1 Gallbladder wall thickening in acute hepatitis

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Other less specific ultrasonographic signs are diffuse hepatic hypoechogenicity (difficult to demonstrate in the absence of a landmark structure) due to liver edema and possibly mild splenomegaly (slightly enlarged spleen – considering a spleen < 12 cm long as normal). Most frequently, splenomegaly is a sign of background chronic liver disease, on which an acute episode can occur. A particular situation is a background chronic liver disease, on which acute viral hepatitis with a different virus develops (for example, chronic hepatitis B, complicated with acute viral hepatitis D or A, or more rarely C). If an acute cytolysis syndrome (aminotransferases more than 10 times higher than the normal range) occurs in a patient with chronic viral hepatitis, an acute viral hepatitis with a different virus should be suspected.

In acute alcoholic hepatitis, the background can be that of liver steatosis (ultrasound aspect of hyperechoic, “bright”, liver with posterior attenuation). Also, in acute alcoholic hepatitis, a small amount of transient ascites can sometimes be found.

Therefore, in the diagnosis of acute hepatitis, ultrasound has a limited value, the thickening of the gallbladder wall (doubled appearance) being the most frequent sign. Ultrasound is much more useful in the differential diagnosis of the etiology of an icteric syndrome, in which case it can differentiate parenchymal jaundice (non-dilated bile ducts) from obstructive jaundice (dilated bile ducts).

Medical history can play an important role in establishing the etiology of an acute hepatitis (recent consumption of a large amount of alcohol, hepatotoxic drugs or contact with hepatotoxic agents). Viral markers can be useful (Ag HBs), but irrelevant in the initial phases of hepatitis C (in which case PCR RNA HCV should be performed).

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CHRONIC HEPATITIS

Definition: chronic liver inflammatory disease of various etiologies, with an evolution of at least 6 months, without a tendency to healing, with necrotic and fibrotic lesions as a histopathological substrate. Thus, after accidental detection of moderate cytolysis, its chronic character should be declared only after at least 6 months, since moderately increased aminotransferases levels can be a sign of a previously undiagnosed acute hepatitis, which will heal spontaneously in several weeks.

Chronic hepatitis is most frequently caused by hepatitis B, C or D viruses. Hepatitis A does not evolve to chronic hepatitis. Approximately 5-10% of the cases of acute hepatitis B will become chronic, while in acute hepatitis C, chronicity rate reaches up to 80% of cases (hepatitis C is most frequently anicteric in the acute phase). Other causes of chronic hepatitis are autoimmune hepatitis, drug induced liver disease, cholestatic hepatitis or abnormal metals storage in the liver – hemochromatosis (iron) and Wilson disease (copper). In patients with chronic hepatitis, etiology (for therapy) and histological staging (for prognosis and therapy) must be established.

The clinical signs of chronic hepatitis can be absent, discrete or more rarely noticeable.

Chronic hepatitis (both B and C) are to a large extent completely asymptomatic and detected accidentally (most frequently by high aminotransferases levels found during a routine examination).

This is why we consider that any patient with increased aminotransferases levels (minimally or slightly increased; even in the event that they return to normal values on a subsequent examination) should be investigated. In Romania, the most frequent cause of increased aminotransferases levels in asymptomatic patients seems to be the infection with the hepatitis C virus (approx. 3.5% of the Romanian population is anti-HCV positive). Other frequent causes are chronic hepatitis B and liver steatosis (alcoholic or non-alcoholic steatohepatitis - NASH).

A frequent sign of chronic hepatitis is fatigue, often intense. The lack of correlation between the intensity of the physical and intellectual activity and fatigue severity can be a sign suggesting chronic liver disease. Other symptoms in chronic hepatitis are dyspeptic syndrome, exercise or rest hepatalgia, mild jaundice, bleeding gums, purpura, etc.

Which tests should be performed when chronic hepatitis is suspected? A minimum of biological tests: aminotransferases (GOT/AST, GPT/ALT), gamma-glutamyl transpeptidase, alkaline phosphatase, HBs Ag, and anti-HCV antibodies should be determined.

Aminotransferases, the expression of hepatocyte lesion, may increase in all liver disease (however, 1/3 of chronic hepatopathies can evolve with normal aminotransferases). Gamma- glutamyl transpeptidase (GGT) is a reliable marker of cholestasis (if alkaline phosphatase is also increased) or of chronic alcohol consumption (if only GGT is increased). The markers of viral hepatitis are HBs Ag for chronic hepatitis B and anti-HCV antibodies for chronic hepatitis C.

Chronic hepatitis D is not possible in the absence of hepatitis B.

Ultrasound examination in chronic hepatitis does not reveal typical signs. Most frequently (in approx. 50% of cases), splenomegaly is detected. Most authors consider a spleen smaller than 12 cm long as normal. The width or thickness of the spleen is not equally important, but a globulous

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spleen can be a sign of activation of the reticuloendothelial system. Usually, in chronic hepatitis, the spleen is slightly enlarged (13-14 cm) (Fig. 1.2). Larger splenomegaly (more than 15 cm) suggests, in a clinical context, liver cirrhosis. It should be emphasized that a normal spleen does not exclude a chronic hepatitis.

In a personal study, we aimed to correlate the size of the spleen with the histological activity of chronic hepatitis, but we found only a weak direct correlation (the correlation between the spleen size and Knodell histological score was 0.47).

Ultrasound evidence of hilar adenopathies (lymph nodes of the hepatoduodenal ligament) is relatively common. They can occur in chronic hepatitis B or autoimmune hepatitis, but are extremely frequent in chronic hepatitis C (Fig. 1.3). Italian studies have reported the presence of adenopathies in the hepatoduodenal ligament in approximately 70% of chronic hepatitis C cases and have monitored the evolution of lymph node size for the evaluation of therapeutic response to interferon.

Fig. 1.2 Splenomegaly Fig. 1.3 Hilar oval adenopathy in chronic hepatitis C

In the current ultrasound practice, when hilar adenopathy is identified, one should further investigate for the presence of hepatitis C virus (anti-HCV antibodies) and hepatitis B virus (HBs Ag), or for chronic autoimmune or cholestatic hepatitis.

- Fig 1.4. Hilar oval adenopathy in chronic hepatitis C

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The lymph nodes of the hepatoduodenal ligament are usually oval, 5-10/10-20 mm in size (Fig. 1.4). They are best visualized along the hepatic artery or along the portal vein.

Other ultrasonographic signs for chronic hepatitis are non-specific and inconsistent. A discrete hepatic heterogeneity (inhomogeneity) rather suggests liver cirrhosis than chronic hepatitis.

The signs of hepatomegaly (particularly the “rounding” of the caudo-ventral liver margin) are non- specific. Liver steatosis can be identified in chronic alcoholic hepatitis or in NASH (increased hepatic echogenicity with or without acoustic shadowing [posterior attenuation]). The thickening or irregular trajectory of the bile ducts are both suggestive signs for cholestatic liver disease (sclerosing cholangitis).

The clinical examination is particularly useful in chronic liver disease. Palpation of the liver by an experienced doctor can bring relevant data on the liver size (hepatomegaly) and its consistence. The diagnosis of splenomegaly is made by ultrasound (much more objective than assessment by palpation).

The temporal diagnosis (evolution longer than 6 months), and the clinical and biological diagnosis of chronic hepatitis are followed by staging, mandatory both for prognosis and therapy.

The staging can be performed using non-invasive methods or by liver biopsy.

The non-invasive methods for liver fibrosis assessment are:

- biological tests (such as FibroTest-ActiTest);

- ultrasound-based elastographic tests: Transient Elastography (FibroScan), point shear- waves Elastography (Siemens: VTQ - ARFI) and 2D-SWE (Aixplorer system), strain elastography (Hitachi);

- MRI elastography.

Ultrasound guided or ultrasound assisted liver biopsy (LB) is still widely used in the clinical setting. We prefer to perform LB under sedation with Midazolam (Dormicum), 2.5-5 mg/i.v., which induces conscious sedation, with retrograde amnesia. The biopsy site is localized using ultrasound (avoiding large vascular structures, cysts or hemangiomas), and is usually at the level of the middle axillary line, in the hepatic parenchyma. Subsequently, the biopsy will be performed without ultrasound guidance (ultrasound assisted LB). Some authors use the ultrasound guided technique, in which the needle attached to a ”pistol” is guided into the liver in real time.

Ultrasound can be useful for assessing potential complications that can occur during biopsy:

hemoperitoneum - anechoic or slightly hypoechoic image in the perihepatic space or in the Douglas pouch; subcapsular or intraparenchymal hematoma (anechoic/hypoechoic image under the liver capsule or within the parenchyma). The risk of complications after LB is relatively low and consists of a vagal response to puncture, hemoperitoneum, intrahepatic or subcapsular hematoma, transient subscapular pain.

In conclusion, ultrasound examination in chronic hepatitis has a limited value, only splenomegaly and hepatoduodenal ligament adenopathies being relatively constant elements (good sensitivity, but lower specificity). The other ultrasound signs are inconsistent.

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The new methods used for the non-invasive evaluation of fibrosis (elastography or biologic tests) will probably be widely used in daily practice (as it currently happens in countries such as France).

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15 3.

LIVER STEATOSIS

Definition: fat buildup in the liver, which affects more than 10% of the organ. The main causes of liver steatosis are chronic alcohol abuse (alcoholic steato-hepatitis – ASH syndrome) and steatosis occurring in obese, diabetic patients and in dyslipidemic syndromes (non-alcoholic steato- hepatitis – NASH syndrome). Another etiology is chronic hepatitis C (up to half of the cases have mild steatosis).

From a clinical point of view, steatosis most frequently has no subjective symptoms. Exercise hepatalgia, rest hepatalgia, and moderate fatigue rarely occur.

Clinical examination reveals hepatomegaly, most frequently moderate, of increased consistency. The firm consistency of the liver on palpation suggests the possibility of steato-fibrosis (or even steato-cirrhosis). Evaluation using FibroScan or ARFI can be useful in these cases.

From an imaging point of view, steatosis can be divided into diffuse liver steatosis and focal liver steatosis.

Ultrasound examination is very reliable in the diagnosis of diffuse liver steatosis, in which a fatty loading of the liver higher than 10% will translate into an increased hepatic echogenicity -

”bright liver” (Fig.1.5), frequently accompanied by acoustic shadowing (posterior beam attenuation), due to the partial absorption of ultrasounds by the fatty tissue. There is a direct correlation between the severity of fatty loading of the liver and the degree of acoustic shadowing.

Thus, depending on the intensity of posterior beam attenuation, steatosis is subjectively categorized as mild (discrete attenuation), moderate (obvious attenuation), and severe steatosis (difficult or impossible to visualize the diaphragm).

Fig. 1.5 Diffuse liver steatosis

The sensitivity of ultrasound in the diagnosis of liver steatosis is approximately 70-80%.

Another imaging technique that can accurately assess steatosis is computed tomography (CT). This technique will allow the detection of increased liver density (the fat content of the liver can be evaluated). CT is a costly technique and also irradiant and thus not used for the sole assessment of liver steatosis.

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Other ultrasound signs that can be observed in liver steatosis are hepatomegaly (”rounded”

hepatic contours), increased liver diameters, reduced filling of the hepatic veins (due to compression by fatty liver tissue).

In daily practice, the examination will begin with liver palpation. After assessing the size (hepatomegaly) and consistency of the liver, an abdominal ultrasound will be performed, which allows assessment of both hepatomegaly and liver steatosis severity (based on ultrasound brightness and the intensity of posterior attenuation). After evaluating the body mass index (BMI) in order to assess the presence of obesity, other causes of steatosis should be investigated, using the data collected through anamnesis: alcohol consumption, association of diabetes mellitus or known dyslipidemia. Other relevant information can be obtained from biological data: gamma-glutamyl transpeptidase, blood glucose level (possibly glucose tolerance test) and lipids profile (particularly triglyceride values).

Liver steatosis can be simple (asymptomatic) or it can be accompanied by secondary hepatic injury (cytolysis). This is why, in case of steatosis, the clinician will investigate a possible increase in aminotransferases levels (possibly with an increased De Rittis ratio - GOT/GPT - if the etiology is alcohol abuse) and also the presence of anti-HCV antibodies (steatosis that can occur in chronic hepatitis C).

After assessing the severity of steatosis by ultrasound and after establishing its etiology, the patient should be informed regarding the available therapeutic measures (alcohol withdrawal, balancing diabetes, treatment of dyslipidemia, weight loss to achieve a normal BMI, moderate physical activity). A quarterly reevaluation of the ultrasound appearance of the liver should be performed, until the liver aspect returns to normal.

Focal hepatic steatosis is a particular case of fatty loading of the liver, characterized by lipid accumulation within the hepatocytes restricted to a certain area. Another possible explanation for focal steatosis is the fact that in a certain hepatic area, intrahepatocytic fat droplets have different sizes compared to lipid accumulations in other parts of the liver (resulting in a different ultrasound appearance). However, the explanation of excess lipid accumulation restricted to certain areas is currently not very clear.

The ultrasound appearance of focal hepatic steatosis is somewhat typical; it translates into a hyperechoic area of variable size in the liver. The background is also defined by steatosis, but in some cases, the rest of liver may present as normal on ultrasound examination. The area affected by focal steatosis generally is not clearly delimited (unlike delimitation in the case of hemangiomas).

Focal steatosis may occur without any objective cause, or it can be the consequence of long- term corticosteroid therapy. A particular case of focal liver steatosis is the focal fat accumulation in the hepatic hilum. It involves excess fat storage in a typical hepatic area, 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 branches. It has a hyperechoic appearance and is relatively well circumscribed. For an experienced ultrasonographist, the diagnosis is relatively easy, but differential diagnosis should be performed in order to exclude a hemangioma or a hepatic tumor of the hilum.

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A particular version of steatosis is the presence of fatty free areas in a liver with steatosis. The US appearance is of a bright liver with posterior attenuation, which includes one or more hypoechoic areas (Figs. 1.6, 1.7) that actually are areas with normal echogenicity on the background of global steatosis. The etiology of fatty free areas is so far unknown.

Fig. 1.6 Hypoechoic area – fatty free area Fig. 1.7 Fatty free area Fatty free areas may have various shapes and sizes, and in some cases they can affect an entire lobe. The hypoechoic hepatic area is sometimes less clearly delimited, while in other cases there is a clear delimitation between these areas and the normal hepatic parenchyma, through one of the hepatic veins.

The ultrasound differential diagnosis of fatty free areas is often difficult, because one must suspect a hypoechoic primary or secondary hepatic tumor occurring in a liver affected by hepatic steatosis. The ultrasound characteristics that can differentiate between the two diagnoses are not always clear and they usually require second line contrast imaging methods, such as contrast- enhanced ultrasound (CEUS). This technique will reveal the same enhancement pattern following contrast bolus in the focal steatosis, fatty free areas and in the adjacent hepatic parenchyma in all vascular phases (arterial, portal and late phase).

In cases of difficult differential diagnosis of focal steatosis or fatty free areas, when contrast- enhanced ultrasound has not answered the question (extremely rare cases), computed tomography can be used, which will easily differentiate areas with or without fatty loading.

Sometimes, focal steatosis areas (less commonly fatty free areas) can be spread into the liver parenchyma, causing hepatic inhomogeneity. Differential diagnosis in these situations is made with hepatocarcinoma and the multicentric form of metastatic liver. In these cases, the ultrasonographist’s experience is the most important factor in diagnosis, possibly complemented by CEUS.

In conclusion, we can state that ultrasound is a good, non-invasive technique for assessing liver steatosis, as well as for the quantitative evaluation of steatosis (relatively well correlated with the histological fat loading of the liver). In cases with focal liver steatosis or fatty free areas, positive ultrasound diagnosis is easy, while differential diagnosis will require an experienced ultrasonographist, and sometimes, evaluation by CEUS.

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18 4.

LIVER CIRRHOSIS

Definition: liver cirrhosis is the final stage of most chronic liver diseases, in which fibrous changes occur in the liver alongside with necrosis and regenerative phenomena. Liver cirrhosis is considered to be an irreversible state of nodular transformation of the liver parenchyma.

The etiology of liver cirrhosis is varied, but alcohol abuse and hepatitis viruses B and C are the most frequently incriminated. Thus, in a study carried out for 3 years in the Department of Gastroenterology Timişoara regarding the etiology of liver cirrhosis, hepatitis C virus was the most frequent (33.4%), followed by alcohol abuse (30%) and hepatitis B virus (25.5%). It goes without saying that in some situations the etiology is multifactorial, the combination of a viral infection with alcohol abuse being extremely common. Liver cirrhosis is frequently found in alcoholics, and subsequently, the search for hepatitis viruses markers (HBs Ag, anti-HCV Ab and anti-HDV Ab) will sometimes lead to the identification of chronic hepatitis virus infection.

In addition to the major etiologies of liver cirrhosis (alcohol or hepatitis viruses), 5-10% of cases have rare causes, being secondary to: autoimmune cirrhosis, Wilson cirrhosis (ceruloplasmin deficiency), hemochromatosis, alpha-1-antitrypsin deficiency cirrhosis, primary biliary cirrhosis, drug-induced cirrhosis, and cryptogenic cirrhosis (a rare condition). Thus, in a group of 1200 liver transplants performed in Dallas, almost 10% were performed for cryptogenic cirrhosis. In our group (in an endemic hepatitis virus area), the frequency of cryptogenic cirrhosis is much lower, but this might be due to the fact that cirrhosis is too easily labeled as alcoholic when no other etiological factor can be determined (without taking into account the need for alcohol consumption in a toxic dose for a long enough time).

The diagnosis of liver cirrhosis starts with the clinical examination.

The inspection of the abdomen and chest can reveal collateral abdominal circulation (not a very specific sign) or the presence of spider angiomas (spider naevi) on the chest. "Spider naevi"

are frequent in liver cirrhosis, so if they are correctly diagnosed (recognized), they represent a solid argument for the diagnosis. One should always inspect the chest for this sign in any chronic liver disease. Applying pressure makes them disappear, while if the pressure stops they will subsequently reappear, this being a criterion for differentiation of various vascular angiectasis.

Liver palpation provides significant clinical information. The patient in dorsal decubitus, with the knees slightly bent for the relaxation of the abdominal muscles, will be asked to perform deep inspiration-expiration movements, which will allow for an accurate liver palpation in order to assess the consistency of the liver. During deep inspiration, the liver will descend (pushed by the diaphragm) and will be easily accessible. Palpation will continue during expiration, when the clinician’s hand will follow the margin of the withdrawing liver. After several inspiration/expiration movements, based on palpation, a doctor with good clinical experience will be able to assess if hepatomegaly is present or not, as well as the liver consistency (clinical elastography). We insist on the adequate and correct palpation of the liver, for this method is superior to certain imaging methods used in order to evaluate liver size.

Ultrasound examination in liver cirrhosis may reveal multiple changes, but in some cases it can be normal (in up to 20% of cases).

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The typical elements that can be found in liver cirrhosis, but which are not necessarily present, are:

– caudate lobe hypertrophy;

– heterogeneous liver echotexture;

– splenomegaly;

– ascites;

– signs of portal hypertension;

– changes in the gallbladder wall.

Caudate lobe hypertrophy

The caudate lobe or the first hepatic segment suffers from hypertrophy in the evolution of liver cirrhosis; therefore it will be frequently enlarged in patients suffering from this condition.

Several ways of evaluating the caudate lobe have been described; for example, the calculation of its volume or its relation with the size of the right hepatic lobe. Both methods are laborious and provide no additional diagnostic elements.

In current practice, the easiest method is to measure the anteroposterior diameter of the caudate lobe by means of ultrasound. In order to differentiate the anteroposterior diameter of the caudate lobe in healthy and cirrhotic subjects, we performed a prospective study which included 200 healthy subjects (126 women and 74 men). We aimed at correlating the size of the caudate lobe with the patients’ gender, height, age and body mass index (BMI). The mean anteroposterior diameter in this group was 21.4 mm and we found that it was not influenced by patients’ gender, age, height or weight.

Fig.1.8. Normal caudate lobe Fig. 1.9. Enlarged caudate lobe

By comparing these results with a group of 24 cases of known liver cirrhosis, we found that the mean diameter of the caudate lobe in cirrhosis was 47 mm (p<0.01). These data led us to use the

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caudate lobe hypertrophy as a sign of liver cirrhosis (Fig. 1.9). But which is the normal range?

Based on a long ultrasound experience and personal studies, we consider the upper normal limit for the anteroposterior diameter of the caudate lobe to be 35 mm. However, there is an overlapping of normal and cirrhosis cases, so that we generally consider a size of the caudate lobe greater than 40 mm as relevant for cirrhosis (Figs.1.10, 1.11).

In current ultrasound practice, approximately 2/3 of cirrhosis cases have a hypertrophic caudate lobe; sometimes with a typical ultrasound appearance (a large, globulous appearance being particularly useful for diagnosis). The caudate lobe size will be used for the diagnosis of liver cirrhosis only in a well known clinical context.

Fig. 1.10 Caudate lobe larger than 35 mm Fig. 1.11 Caudate lobe larger than 35 mm

The anteroposterior diameter of the caudate lobe should be measured in a sagittal section at epigastric level. The inferior vena cava (IVC) should be identified and the ovoid structure situated anteriorly is the caudate lobe. Subsequently, the maximum anteroposterior diameter of the caudate lobe should be measured. Measurement of the caudate lobe can be difficult in cases of marked steatosis (ultrasounds are strongly absorbed by fatty tissue) or, more rarely, in the case of ascites.

Heterogeneous liver echotexture

Liver echotexture changes, particularly hepatic heterogeneity occur in approximately half of cirrhotic cases (Fig. 1.12). Hepatic heterogeneity is the consequence of fibrous changes that lead to the formation of regenerative nodules. However, there are liver cirrhosis cases without imaging changes of the hepatic echotexture.

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Fig. 1.12 Hepatic heterogeneity and irregular liver surface in ascites

We wish to insist on the use of “liver micronodulation” term in ultrasound description. Liver micronodulation is a histological reality in cirrhosis, but ultrasound cannot evidence these small nodules. The way to accurately diagnose hepatic nodules by ultrasound is to evaluate the liver surface in cases with ascites (Figs. 1.12, 1.13, 1.14). The anterior and, to a smaller extent, the posterior liver surface are easy to examine if ascites is present. Thus, nodules with a size of less than 5 mm in micronodular cirrhosis and more than 5 mm in macronodular cirrhosis can be seen.

The examination of the liver surface in ascites is easier by using high frequency transducers (5-9 MHz) (Fig. 1.19). In ascites-free cirrhosis, it is almost impossible to notice liver surface changes.

Fig. 1.13. Liver surface in ascites Fig. 1.14. Liver surface in ascites using high frequency transducers (5-9 MHz)

A particular situation in the ultrasonographic practice is that of routine ultrasound performed in a patient without a history of liver disease and without a particular clinical illness. If a change in the liver architecture (heterogeneity) is found, a possible cirrhogenic liver disease should be suspected. Clinical, biological, and endoscopic examination, as well as elastography (FibroScan) can diagnose cirrhosis that was completely unknown before the ultrasound examination.

In cases with marked liver heterogeneity (which occurs particularly in advanced viral cirrhosis), differential diagnosis with diffuse hepatocellular carcinoma (HCC) is required. In these

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cases, alpha-fetoprotein should be determined; values higher than 400 ng/ml are diagnostic for HCC.

Assessment of liver structure by ultrasound will carefully investigate the presence of hepatic areas with a rosette or hypoechoic appearance, suggestive of HCC (Fig. 1.15). The possible development of HCC on a background of cirrhosis will be dealt with later in this book.

Fig. 1.15 Hypoechoic area in a case of liver cirrhosis - HCC

The role of ultrasound in the evaluation of significant liver fibrosis should be emphasized.

Transient elastography (FibroScan) and subsequently, other elastography techniques (2D-SWE, VTQ-ARFI or Hi RT-E) are methods that non-invasively assess liver fibrosis. Studies have shown that these methods are sensitive and specific for diagnosing chronic hepatitis with significant fibrosis (F≥2) or cirrhosis.

Splenomegaly

An enlargement of the spleen (over 12 cm long) is frequent in cases of liver cirrhosis (Figs. 1.16, 1.17). The spleen of a cirrhotic patient is larger than in chronic hepatitis, so that approximately 80%

of cirrhosis cases are accompanied by splenomegaly, which frequently exceeds 15 cm. Sometimes, splenomegaly larger than 18 or even 20 cm can be found, which is often accompanied by hematological hypersplenism (thrombocytopenia < 100,000/mm3 and/or leukopenia < 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. We must emphasize the importance of a correct measurement of the spleen along the long axis, especially for beginners in ultrasound.

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Fig. 1.16 Splenomegaly Fig. 1.17 Splenomegaly

We will present the clinico-biological correlations that we suggest using when splenomegaly is accidentally detected by routine ultrasound. Thus, splenomegaly is diagnosed if the long axis of the spleen is larger than 12 cm. Considering the statistical frequency of diseases with splenomegaly, the following clinico-biological approach to hepatic pathology should be initiated. One should search for a history of liver disease followed by clinical examination where liver palpation is essential (it will possibly demonstrate hepatomegaly and will assess liver consistency). Then, the patient will be evaluated using FibroScan, a method with a sensitivity of more than 90% for the diagnosis of cirrhosis. Biologic tests will include relevant targeted tests for the clinical suspicion.

These are blood count and platelet count (for a possible hematological disease), aminotransferases (GOT and GPT as a specific sign of liver disease), and the markers of a chronic viral liver disease (HBs Ag and anti-HCV antibodies). If clinical hepatomegaly is absent, the aminotransferases are normal, the viral markers are normal, and the FibroScan values are less than 7 kPa, the hepatic etiology of splenomegaly can almost be excluded. In this case, hemolytic anemia, lymphoma, chronic myeloid leukemia and other hematologic causes of splenomegaly should be suspected and investigated.

Ascites

The presence of ascites is frequent in decompensated cirrhosis. Ultrasound is the ideal method for diagnosing ascites and evaluating its volume.

Considering that in Romania ultrasound is an inexpensive and repetitive method available to the clinician, it should always be used for assessing the presence and volume of ascites. The palpation and percussion of the abdomen for the evaluation of ascites is already of historical value, because we probably all had cases in which ascites was suspected following the clinical exam, but abdominal ultrasound showed no ascites (severe obesity, tumors or abdominal cysts).

Ascites should be investigated using ultrasound in the pouch of Douglas, in Morrison’s pouch (inter-hepato-renal space), in the perihepatic (Figs. 1.18, 1.19) and perisplenic spaces. Ascites can be detected practically in any recess. It appears as an anechoic image that changes in form with the change of the patient's position.

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Ascites may have two different ultrasound appearances: completely anechoic (Fig. 1.20, 1.21), and ”dense” ascites. The latter can signify old ascites, protein-rich ascites, superinfected ascites, chylous or hemorrhagic ascites. ”Dense” ascites does not have a completely anechoic appearance, but it is slightly hypoechoic and usually contains small echogenic particles (Fig. 1.22), subject to Brownian motion.

Fig. 1.18. Perihepatic ascites Fig. 1.19. Perihepatic ascites

Fig. 1.20. Ascites Fig. 1.21. Ascites

Fig. 1.22.”Dense” ascites

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When ”dense” ascites is identified, exploratory paracentesis is compulsory. It can assess the macroscopic aspect of the fluid (hemorrhagic or chylous), also allowing the evaluation of proteins concentration, and particularly of the number of leukocytes and polymorphonuclear cells/ml. It is considered that more than 500 leukocytes/ml or more than 250 polymorphonuclear cells/ml in the ascites fluid are signs of infected ascites (spontaneous bacterial peritonitis), even if the culture of the ascites fluid is sterile.

Exploratory paracentesis should be performed on the first evaluation of a patient with vascular decompensated cirrhosis or if the patient’s general condition worsens. It can be performed in the classical manner, without ultrasound control, or, in the case of small ascites, with a thick abdominal wall, under ultrasound guidance. Protein content (exudate or transudate) and other pathological biological elements should be analyzed from the fluid extracted. In unexplained worsening of the clinical status of a patient with vascular decompensated cirrhosis, paracentesis is mandatory to diagnose a possible spontaneous bacterial peritonitis.

Ascites can be a sign of cirrhosis, but it is not always necessarily present.

In cases of cirrhosis with ascites, the subjective ultrasound evaluation of the ascites volume (minimal, small, moderate and large) is performed based on the amount of fluid in the Douglas pouch and in the perihepatic area. This evaluation, even if subjective, is useful from a therapeutic point of view, in order to establish the diuretic treatment doses and the general therapeutic approach. We consider that in minimal ascites, the amount of peritoneal fluid is approximately 1-2 l, in small ascites 3-4 l, in moderate ascites 7-8 l, and in large ascites more than 10-15 l.

Signs of portal hypertension (PHT)

One of the consequences of fibrosis in liver cirrhosis is the increased resistance to portal blood flow. The consequences of portal hypertension include collateral abdominal circulation, the opening of vascular shunts and the formation of varices most frequently located in the esophagus.

Portal hypertension (PHT) is the rule in liver cirrhosis, but it does not appear from the beginning and is not always easy to prove. If liver cirrhosis is suspected based on clinical signs, the abdomen should be inspected for collateral circulation (special attention should be paid to the possible confusion between collateral circulation and abdominal blood vessels that might be visible through the transparency of the skin). The next step is ultrasound assessment for portal hypertension signs. It starts with the assessment of the portal vein, by measuring its size in the hilum, considered to be normal up to a diameter of 13 mm. A diameter of the portal vein greater than 13 mm is a sign of portal hypertension.

However, based on a long ultrasound experience and personal studies, we demonstrated that there is always a correlation between the diameter of the portal vein and the severity of portal hypertension. Thus, in a group of liver cirrhosis cases without esophageal varices (the easiest way to assess portal hypertension), the mean diameter of the portal vein was 12.29±2.12 mm. In patients with grade I esophageal varices, the mean diameter of the portal vein in the hilum was 13.63±3.20 mm, in patients with grade II varices it was 14.42±2.05 mm, while in patients with grade III varices, the mean diameter of the portal vein decreased to 12.80±1.81 mm. This study showed that in the initial phases of portal hypertension, there is a linear correlation between the diameter of portal vein

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and the endoscopic size of esophageal varices, but later, as portal hypertension worsens and the collateral esophageal veins (esophageal varices) open, the diameter of the portal vein decreases.

Hence the practical finding that an increased diameter of the portal vein is a sign of portal hypertension, but the evaluation and quantification of PHT by upper digestive endoscopy is compulsory in any case of cirrhosis.

There is a small number of patients, particularly taller and heavier men, who may have normal anatomical portal vein variants with a diameter of up to 15 or even 16 mm. In these cases, the signs of chronic liver disease and PHT should be excluded.

An important sign of PHT is the absence of inspiration/expiration variability of portal vein diameter (Bolondi sign).

Another sign of PHT in liver cirrhosis is the dilation of the intrahepatic portal system. Its assessment is somewhat subjective, as there are no normal limits for its size.

Measurement of the preaortic diameter of the splenic vein and in the splenic hilum can provide additional elements for the diagnosis of PHT. Thus, splenic vein preaortic diameter greater than 10 mm and a hilum diameter greater than 8 mm are both signs of portal hypertension.

Other signs of PHT are dilation of visceral veins and the development of venous shunts. The detection of collateral epigastric circulation (dilatation of the gastric coronary vein) (Fig. 1.30), of spontaneous spleno-renal shunts or of splenic varices are typical signs of portal hypertension. An experienced ultrasonographist will find many signs of PHT in patients with liver cirrhosis that will contribute to the accurate diagnosis and staging of the disease.

Repermeabilization of the umbilical vein (Figs. 1.23, 1.24) is a severe sign of PHT and can be found in 10-20% of advanced cirrhosis cases.

Fig. 1.23 Repermeabilisation of the Fig. 1.24 Repermeabilisation of the umbilical vein umbilical vein

The repermeabilisation of the umbilical vein should be searched for starting from the left branch of the portal vein, where a vascular (venous) cord starts, continuing to the lower margin of the liver and then on the posterior face of the abdomen towards the umbilicus. The umbilical vein

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with a diameter greater than 5 mm has a diagnostic value for PHT. Sometimes, the repermeabilized venous cord has a 10-12 mm diameter. It is an internal correspondent of collateral abdominal circulation. In case of a doubtful diagnosis of permeabilized umbilical vein, a 5-9 MHz (surface) transducer and power Doppler can be used, which will facilitate the visualization of the venous flow.

Regarding PHT, we must mention the role of Doppler ultrasound for the assessment of cirrhosis. Thus, the evaluation of the flow direction in the splenic and portal veins proved to be useful for prognosis. Using pulsed Doppler, Bolondi demonstrated that in approximately 8% of cirrhosis cases, a reversed flow occurs in the portal and splenic veins due to opening of spontaneous venous shunts. At the same time, Bolondi has proven that flow reversals have a protective role, decreasing the risk of variceal bleeding.

Regarding the value of pulsed Doppler in the evaluation of portal pressures and flows, the results were disappointing (due to non-reproducibility of results). After years of studies in search of the best parameters to evaluate, current clinical practice no longer uses Doppler parameters for the evaluation of portal hypertension or of the risk of variceal bleeding.

Color Doppler or power Doppler are also useful for demonstrating the vascular character of some anechoic structures (e.g. extremely tortuous splenic varices) (Figs. 1.25, 1.26, 1.27) or for evidencing portal hypertension in patients with ascites. Combining power Doppler with pulsed Doppler will allow differentiating between a dilated tortuous hepatic artery (as is frequently the case in liver cirrhosis) and the portal vein or the common bile duct.

Power Doppler is also useful for the evaluation of the portal system in order to detect potential portal thrombosis (Fig. 1.28), which is less common in uncomplicated cirrhosis, but rather frequent in cases of hepatocellular carcinoma which complicates cirrhosis.

Fig. 1.25 Splenic varices using Power Doppler Fig. 1.26 Tortuous splenic varices

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Fig. 1.27 Evidencing portal hypertension Fig. 1.28 Portal thrombosis using Power Doppler

It should also be mentioned that some studies have proven a relationship between the values of hepatic elasticity measured by FibroScan and the occurrence of complications in liver cirrhosis.

Thus, liver stiffness values lower than 20 kPa are rarely associated with esophageal varices, while values higher than 40 kPa suggest an increased risk of variceal rupture. The annual monitoring of patients with cirrhosis using FibroScan allows the assessment of the relative risk of complications (PHT, ascites).

Changes in the gallbladder wall

Assessment of the gallbladder wall by ultrasound is part of the diagnosis in cases suspected to have liver cirrhosis. The normal size of the gallbladder wall is less than or equal to 4 mm, measured at the level of the anterior wall. There are two major situations in which the thickening and most frequently also doubling of the gallbladder wall occur: acute cholecystitis and liver cirrhosis. Acute cholecystitis is most frequently calculous and is accompanied by sonographic Murphy’s sign (intense pain caused by pressing the ultrasound probe over the visualized gallbladder). In liver cirrhosis, the gallbladder wall can be thickened, reaching 6-8 or even 10 mm (Figs. 1.29, 1.30), most frequently doubled (with a “sandwich” appearance). Doubled gallbladder wall in cirrhosis is caused mainly by hypoalbuminemia (which is why it can also occur in nephrotic syndrome), and also by portal hypertension and lymphatic stasis.

Fig. 1.29 Thickened gallbladder wall Fig. 1.30 Thickened gallbladder wall and biliary in a case of liver cirrhosis sludge in a case of liver cirrhosis

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In ascites of unknown etiology, the measurement of the gallbladder wall can differentiate between malignant or bacterial ascites, with normal gallbladder walls, from ascites due to liver cirrhosis, with a thickened, doubled gallbladder wall.

In one of our studies that included 62 patients with known liver cirrhosis who were compared to 12 patients with peritoneal carcinomatosis, we found that 52/62 (83.9%) patients with cirrhosis had a thickened gallbladder wall (5 - 15 mm, mean 6.45±2.57 mm). Only 10 of the 62 cirrhosis cases (16.1%) had a normal gallbladder wall. In the 12 cases with peritoneal carcinomatosis (diagnosed by laparoscopy and morphology), the mean diameter of the gallbladder wall was 3.83±1.27 mm (within normal limits). Based on this study and on published data, we may consider that the aspect and thickness of the gallbladder wall are the first ultrasonographic signs suggestive of etiology in ascites of unknown etiology.

Another practical aspect that should be known is the association of liver cirrhosis with gallstones in approximately 1/3 of cases. They have a complex etiology, but their main cause is the impairment of conjugation of indirect bilirubin, which precipitates excessively. Detection of gallstones in cirrhosis is frequent, but most times they are asymptomatic, without requiring surgery.

The clinical decision is complicated in cases of gallstones in patients with cirrhosis and thickened gallbladder wall. Is it due to cirrhosis or is it an acute calculous cholecystitis? The answer is given by the clinical signs with intense colicky pain and possibly fever, and particularly by the positive ultrasound Murphy’s sign (the pressure of the ultrasound probe on the gallbladder will cause intense pain), which all support the diagnosis of acute cholecystitis.

Another practical aspect related to the gallbladder and liver cirrhosis is the possibility to detect biliary sludge by ultrasound (Figs. 1.31, 1.32). Biliary sludge appears as a solid structure in the gallbladder, changing its position and shape with the patient’s position. The cause of biliary sludge is most frequently biliary stasis. The causes, the ultrasound appearance, the evolution of biliary sludge will be discussed in the chapter on the ”Ultrasound of the gallbladder” of this book.

Figs. 1.31 Biliary sludge Figs. 1.32 Biliary sludge

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We have reviewed the ultrasound changes that may occur in liver cirrhosis. In advanced cirrhosis all the described signs may be present, while in other cases only one them or none at all can be found, and in those cases the diagnostic value of ultrasound is extremely low.

What should we do if the clinical suspicion of cirrhosis is not confirmed by ultrasound?

FibroScan (values higher than 14 kPa) or other types of elastography can be useful.

Considering the past difficulties in the diagnosis of liver cirrhosis in certain situations, we wish to discuss the results of a retrospective necropsy study performed in Timişoara County Hospital. Thus, over a 22 year period (1974-1995), of 6153 necropsy cases, 632 (10.3%) had macroscopic cirrhosis. 1/3 of cirrhosis cases were women and 2/3 were men. Of the 632 cirrhosis cases, 283 (44.8%) had the diagnosis of liver cirrhosis mentioned on the observation sheet before death, but 349 cases (55.2%) had unknown liver cirrhosis. These findings confirm the difficulties for encountered to accurately diagnose cirrhosis (before introduction of elastography techniques). In the group of patients who died of cirrhosis, the complications found on necropsy were the following: esophageal varices in 48.2% cases; upper digestive hemorrhage in 24.5% cases; ascites in 36.4% cases; jaundice in 10.9% cases.

Currently, FibroScan and other elastography techniques (VTQ-ARFI and 2D-SWE) as well as biological tests such as FibroTest are used for an accurate diagnosis. In unclear cases, liver biopsy or diagnostic laparoscopy should be used for a precise diagnosis.

We conclude the chapter on ultrasound examination of liver cirrhosis by stating that ultrasound is a good method for evaluating liver cirrhosis, both for confirming the diagnosis (with a sensitivity close to 80%) and for the assessment of complications (ascites, PHT or hepatocellular carcinoma).

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5. HEPATIC VASCULAR DISEASES

In this chapter, two clinical entities will be discussed:

– cardiac liver (cardiac cirrhosis, congestive hepatopathy – part of congestive heart failure);

– Budd-Chiari syndrome.

Cardiac liver

Definition: liver changes due to vascular alterations and venous stasis in right-sided heart failure.

The clinical signs in this condition are somewhat typical: signs of right or global cardiac failure (hepatalgia, ascites, edema in right cardiac failure, and also dyspnea in global cardiac failure). The most frequent clinical situation will be that of a patient with firm, cyanotic peripheral edema, painful on palpation, and often with ascites. Usually, this is a patient with a known long history of cardiac or bronchopulmonary disease (chronic pulmonary heart disease).

Ultrasound examination in case of congestive hepatopathy reveals the following signs:

– dilation of the hepatic veins (Fig. 1.33) is typical in right or global heart failure. The hepatic veins become visible up to the periphery, and their branches are also visible on ultrasound (Fig.

1.34). This dilation can be quantified, a diameter of the hepatic veins larger than 10 mm, 2 cm from the junction with the inferior vena cava (IVC), being considered as pathological. The (normal) respiratory variability of the hepatic veins’ diameter also disappears;

– dilation of the inferior vena cava, usually more than 20 mm in diameter (Fig. 1.35), but especially the absence of the normal inspiration/expiration variability.

– detection of peritoneal effusion is common, particularly in the Douglas space or in the perihepatic area;

– presence of pleural effusion is relatively frequent. It occurs as an anechoic crescent situated above the diaphragm (Fig. 1.36), which allows the differentiation from peritoneal effusion (fluid bellow the diaphragm). The volume of pleural effusion (small or large) can also be correctly assessed by an experienced ultrasonographist. The diagnosis of pleural effusion is easier to make on the right side (where the ultrasound window of the liver is used) (Fig. 1.36), than on the left side. At the same time, ultrasound can be successfully used for evaluating basal chest percussion dullness, allowing for differential diagnosis between pleural effusion (anechoic extra-diaphragmatic image) and pneumonia block. The value of ultrasound in the assessment of pleural effusion should not be overlooked, and this method should be used promptly in case of suspected pleural effusion.

– pericardial effusion appears as a anechoic area surrounding the heart (Fig. 1.37) and is variable in volume. We recommend in all cases of suspected pericardial effusion an 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 patient’s movements.

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Fig. 1.33 Dilation of hepatic veins Fig. 1.34 Dilation of hepatic veins

Fig. 1.35 Dilation of the inferior vena cava Fig. 1.36 Pleural effusion

Fig. 1.37 Pericardial effusion

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Pulsed Doppler examination may reveal relatively typical changes in patients with cardiac liver (high positive retrograde waves in the hepatic veins). Also, the examination of the portal vein using this technique will show a portal vein with pronounced undulations.

In current ultrasound practice, the cardiac disease is most frequently known and ultrasound only confirms the signs of cardiac liver. More rarely, ultrasonographic signs of cardiac liver are detected in a patient without known cardiac disease, who will be referred to the cardiologist for evaluation.

Budd-Chiari syndrome

Definition: a clinical condition characterized by thrombosis of hepatic veins (Fig. 1.38). It can be idiopathic, but it may occur in other situations as well: coagulopathies, myeloproliferative diseases, neoplastic conditions. Clinical diagnosis can be suspected in the presence of edematous syndrome and hepatalgia with sudden onset (sometimes in a young person).

Ultrasound diagnosis is made by absence of partial or total visualization of the hepatic veins.

Thus, visualization of the hepatic veins excludes the diagnosis of Budd-Chiari syndrome. In case of doubt regarding hepatic veins, Power Doppler or color Doppler should be used, which will show or not the venous flow. In uncertain cases, a contrast agent (SonoVue) can be injected to better visualize vascular structures and reveal the presence or absence of flow in hepatic veins.

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

Another rare condition is hepatic veno-occlusive disease, which is the consequence of the occlusion of the small hepatic veins with secondary hypoxic liver injury. It may occur after chemotherapy with high doses of cytostatics, after radiation therapy, after liver or bone marrow transplantation. Ultrasound does not show typical changes, only signs of portal hypertension, portal thrombosis (possibly with the subsequent appearance of portal cavernoma), thickening and doubling of the gallbladder wall may be found.

If venous thrombosis (hepatic veins, inferior vena cava) is suspected, CEUS is useful for diagnosis.

Fig. 1.38 Budd-Chiari syndrome

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B) DIAGNOSIS OF FOCAL LIVER LESIONS

1. CYSTIC (LIQUID) LESIONS

This chapter will deal with the following: simple liver cysts, biloma, polycystic liver and hydatid cyst.

Simple liver cysts (or biliary cysts)

Definition: simple liver cysts are non-parasitic, benign entities, relatively common in clinical practice (1-3% of the ultrasounds performed). They are most frequently incidental ultrasound findings (incidentalomas). Their cause is the lack of communication of the bile ducts with the biliary tree.

The clinical signs in simple liver cyst are generally completely absent. Detection is usually incidental. Very rarely, large cysts with intracystic hemorrhage can generate symptoms, such as discomfort or pain in the right hypochondrium. However, once diagnosed, liver cysts may cause symptoms, particularly in patients with cenestopathic neurosis, who, knowing the diagnosis of liver cyst, will hold it responsible for some dyspeptic symptoms or functional pain in the right hypochondrium or flank (irritable colon-like). In this case, the patient must be assured of the benign character of the liver cyst, of the lack of danger and complications, which will usually lead to symptoms relief.

Liver palpation generally reveals a normal liver, but hepatomegaly may be found in some cases. Rarely, large cysts, close to the liver surface, can be palpated.

The ultrasound appearance of simple liver cysts is relatively typical, as anechoic structures with a very thin wall (Figs. 1.39, 1.40, 1.41). The cysts have a round or oval shape, generally 1-5 cm in size. Their size can exceed 5 cm (Figs 1.43, 1.44), reaching up to 15 cm. The outline of the cyst may be clear-cut or irregular (generating a ”geographical” aspect of the outline) (Fig. 1.42). In general, the cyst is completely anechoic and displays ”posterior enhancement”(Figs. 1.45, 1.46).

This 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. It appears as a discretely echogenic band behind the cyst.

Fig. 1.39; Fig. 1.40 Anechoic structure with thin wall and posterior enhancement – simple liver cyst

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Fig. 1.41 Anechoic structure with thin wall, Fig. 1.42 Anechoic mass with thin wall simple liver cyst and ”geographical” aspect of the outline,

simple liver cyst

Fig. 1.43 Anechoic structure with thin wall, Fig. 1.44 Anechoic structure with thin wall simple liver cyst larger than 5cm and posterior enhancement, - simple liver cyst

76 mm in diameter

Fig. 1.45 Posterior enhancement - liver cyst Fig. 1.46 Posterior enhancement - liver cyst

More rarely, simple liver cysts can have fine septa inside. When inner septa are present, particularly if the cyst has a thick wall, differential diagnosis with a hydatid cyst should be made.

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