LIVER PATHOLOGY DIFUSE DISEASES(1) PDF

LIVER PATHOLOGY ✓Parenchymal disease ✓Focal and diffuse abnormalities ✓Acute and chronic process Parenchyma: is the functional tissue of an organ as distinguished from the connective and supporting tissue. Focal: An abnormal condition of a part of an organ. A localized lesion. Diffuse: not defi...

LIVER PATHOLOGY ✓Parenchymal disease ✓Focal and diffuse abnormalities ✓Acute and chronic process Parenchyma: is the functional tissue of an organ as distinguished from the connective and supporting tissue. Focal: An abnormal condition of a part of an organ. A localized lesion. Diffuse: not definitely limited or localized. The whole organ results affected Acute: an acute disease is a disease of a short course Chronic: A disease that persists for a long time. A chronic disease is one lasting 3 months or more. Diffuse Disease Diffuse hepatocellular disease affects the hepatocytes and interferes with liver function. The hepatocyte is a parenchymal liver cell that performs all the functions of the liver. Signs and Symptoms Jaundice Easy Bruising Ascites Hepatomegaly: Is a common manifestation of diffuse liver disease. It is difficult to diagnose accurately with sonography. The normal length of the adult liver is 15 to 16 cm. The most reliably measurement is possibly the sagittal dimension from the dome to the tip of the right lobe. If this exceeds 15.5 cm, the liver is probably enlarged. Hepatomegaly can be definitely diagnosed when the liver extends beyond the inferior pole of the right kidney. The use of this method may be mistaken in the patient with a Riedel lobe. Normal liver Hepatomegaly  HEPATITIS Hepatitis: The term hepatitis describes inflammation of the liver. Hepatitis may be caused by alcohol, drugs, autoimmune diseases, metabolic diseases, and viruses. Types A, B, C, D, and E account for 95% of all acute hepatitis cases. Viral infection accounts for more than half the cases of acute hepatitis in the United States. These include hepatitis A, hepatitis B, and C, D, E and G. The three most common are A, B and C. In the United States about 60% of acute hepatitis is type B, 20 % type A and about 20 % is other types Hepatitis A: It is transmitted throughout fecal-oral route and is a common infection in parts of the world where sanitation is poor. Rarely become chronic. Usually (99%) is a short-term infection and usually clears in up two months. Vaccination can help prevent hepatitis A Hepatitis B: May go on to chronic hepatitis and progress to cirrhosis. Most adults infected fully recover and develop life- long immunity. Some patients will become chronic infected. It is very common worldwide and the spread is frequently passed on through the exchange of body fluids with an infected person. (Is estimated to a lot more infectious than HIV), also can be spread by unprotected sex, contaminated needles, from infected mother to her baby or through a blood transfusion. Vaccination can prevent hepatitis B Hepatitis C: Most of the patients will develop chronic liver disease and eventually develop cirrhosis, but it is more likely to cause chronic hepatitis and cirrhosis than the hepatitis B. It can spread by contact with infested blood (contaminated needles, blood transfusions, mother to child transfer at birth, hemodialysis, sexual contact). The hepatitis C virus can live on surfaces for several weeks. Many people do not have symptoms when they become infected with hepatitis C. No vaccination for hepatitis C has been created. Patients with hepatitis may present initially with flulike and gastrointestinal symptoms, including loss of appetite, nausea, vomiting, and fatigue. Jaundice may occur in severe cases of hepatitis. Laboratory values show abnormal liver function test results, with an increase in the ASP, AST, and bilirubin. Acute Hepatitis In acute hepatitis, damage to the liver may range from a mild disease to massive necrosis and liver failure. Rarely become chronic. Usually (99%) is a short-term infection and usually clears in up two months. Vaccination can help prevent hepatitis A. Sonographic findings include Normal liver appearance and echogenicity or Hepatomegaly Hypoechoic liver with accentuated brightness of the vessels and ducts walls (“starry night”) the gallbladder wall could be thick.  B A A. Sagittal image through liver and right kidney demonstrating decreased liver echogenicity and increased delineation of portal triad echoes secondary to edematous changes from acute hepatitis. This is “starry night” sign. B. Same patient as in figure A, with the overall gain increased to fill in the liver parenchyma. Right kidney is normal and appears more echogenic than liver due to decreased echogenicity of the liver. Copyright © 2018 Wolters Kluwer All Rights Reserved Chronic Hepatitis Chronic hepatitis exists when there is clinical or biochemical evidence of hepatic inflammation for at least 3 to 6 months. Chronic persistent hepatitis is a benign process. Chronic active hepatitis usually progresses to cirrhosis and liver failure. On ultrasound examination, The liver parenchyma is coarse, with decreased brightness of the portal triads; however, the degree of attenuation is not as great as that seen in fatty infiltration. The liver does not increase in size with chronic hepatitis. Following inflammation, dense fibrous tissue septa form, separates liver lobules, parenchymal cells will degenerate, followed by formation of regenerative nodules. Fibrosis may be evident and may produce soft shadowing posteriorly. Hepatitis. On ultrasound examination, the liver parenchyma is coarse with decreased brightness of the portal triad. Fatty Infiltration or hepatic steatosis Gross appearance of the fatty liver. Fatty Infiltration Fatty liver disease is now the most common cause for elevated liver function tests in the United States and affects approximately 25-35% of the general population Fatty infiltration of hepatocytes by itself usually does not disrupt physiologic processes. In more recent studies, 50% of patients are females. Fatty liver occurs in all age groups. Fatty liver is an acquired reversible disorder resulting in an accumulation of triglycerides within the hepatocytes.  With time, accumulation of fatty triglycerides within liver cells may cause liver lobules to separate and organ’s weight increases. Alcohol abuse and obesity are the two main leading causes Other factors influencing fat deposition include: Diabetes, severe hepatitis, corticosteroid use, chemotherapy, parenteral hyperalimentation, protein malnutrition, metabolic disorders, pregnancy, cystic fibrosis, tuberculosis and hyperlipidemia Fatty liver A fatty liver is enlarged and has a greasy, pale yellow look.  Common causes of fatty liver include: Alcoholic liver disease Diabetes mellitus Obesity Severe hepatitis Steroids Most patients with fatty liver are asymptomatic. However, if questioned, more than 50% of patients with fatty liver or NASH (non-alcoholic steatohepatitis) report persistent fatigue, malaise, or upper abdominal discomfort Moderate to severe fatty infiltration shows: 1. Increased echogenicity on ultrasound examination. 2. Enlargement of the lobe affected by the fatty infiltration is evident. 3. Portal veins may be difficult to see because of the increased attenuation of the ultrasound. 4. More difficult to see the outline of the portal vein and hepatic vein borders.  Eliminating process causing fatty metamorphosis may reverse infiltration. Sonographic features depend on the severity of fatty change and range from mild to severe. Key markers of fatty infiltration are diffuse increased echogenicity of liver parenchyma and decreased acoustic penetration due to increased attenuation of the sound beam. Hepatomegaly may be present. As fat and fibrous tissue ratio increases, reflectivity and granularity of liver parenchyma increase. Grade 1: There is a slight diffuse increase in fine echoes in the hepatic parenchyma, with normal visualization of the diaphragm and intrahepatic vessel borders. Grade 2: There is a moderate diffuse increase in fine echoes with slightly visualization of the intrahepatic vessels and diaphragm. Grade 3: There is a marked increase in fine echoes with poor or no visualization of the intrahepatic vessel borders, diaphragm, and posterior portion of the right lobe of the liver.  B A A. Sagittal image using curved linear array through right lobe and kidney demonstrates classic signs of fatty liver: heterogeneity, lack of visualization of internal vessels, marked difference in echogenicity between liver and kidney, and decreased sound penetration limiting visualization of diaphragm. B. Same patient: Lower frequency sector, liver is identified to diaphragm and renal parenchyma echoes are seen. Copyright © 2018 Wolters Kluwer All Rights Reserved Fatty infiltration. A, Grade I. slight diffuse increase in fine echoes in the hepatic parenchyma Grade II moderate diffuse increase in fine echoes with slightly visualization of the intrahepatic vessels. C, Grade III. marked increase in fine echoes with poor or no visualization of the intrahepatic vessel borders and posterior portion of the right lobe of the liver. Fatty infiltration is not always uniform throughout the liver parenchyma. It is not uncommon to see a patchy distribution of fat, especially in the right lobe of the liver. The fat does not displace normal vascular architecture.  Focal hepatic steatosis. Axial US scan of the liver shows an ovoid, uniformly hyperechoic focus (arrow), a finding consistent with focal fat. Copyright © 2018 Wolters Kluwer All Rights Reserved US scan shows patchy, diffuse hepatic steatosis (arrow), which simulates an infiltrative tumor. The other characteristic of fatty infiltration is focal sparing. This condition should be suspected in patients who have masslike hypoechoic areas in typical locations in a liver that is otherwise increased in echogenicity. The most common areas of focal sparing are anterior to the gallbladder or the portal vein, and the posterior portion of the left lobe of the liver. No mass effect!!!! Focal sparing of the caudate lobe.  Glycogen Storage Disease Glycogen storage disease Autosomal recessive genetic disorder. Is the result of defects in the processing of glycogen synthesis or breakdown within muscles, liver, and other cell types. The most common glycogen storage disease is Type I or von Gierke’s disease, that typically affect the liver Von Gierke disease is an inherited disorder caused by the buildup of a complex sugar called glycogen in the body’s cell, especially the liver, kidneys and small intestines, impairs their ability to function normally  Glycogen is stored in tissues, but body is unable to synthesize it. May cause hypoglycemia, abdominal distension, fatigue, and irritability Clinical and sonographic findings: 1. Age: infancy. 2.Hepatomegaly 3.Hypoglycemia 4.Impaired growth 5. Increased echogenicity with increased attenuation 6. Associated liver cell adenomas. 7.Prognosis: fatal disease with demise in the first year of life in type II patients. Type I may live into young adulthood.  Glycogen Storage Disease with Liver Cell Adenoma Transverse image in a man with known glycogen storage disease demonstrates fatty infiltration of the liver and hypoechoic liver lesions consistent with liver cell adenomas (cursors). Copyright © 2018 Wolters Kluwer All Rights Reserved Glycogen storage disease is associated frequently with adenoma (benign liver tumor) CIRRHOSIS Cirrhosis is a chronic degenerative disease of the liver in which the lobes are covered with fibrous tissue, the parenchyma degenerates and are infiltrated with fat In cirrhosis of the liver, scar tissue replaces normal, healthy tissue, blocking the flow of blood through the organ The characteristic of this disease is a chain of events consisting of cell death followed by regeneration and fibrosis. This sequence of events leads to a progressive and irreversible scarring that ends in liver failure and portal hypertension. The disease process is chronic and progressive, with liver cell failure and portal hypertension as the end stage.  Liver is the only body organ that can regenerate new healthy tissue if hostile environment is removed. Initial changes cause liver enlargement but continued insult results in atrophy. Parenchymal distortion may alter or compress biliary and vascular channels leading to jaundice and portal hypertension. New vascular channels can form collateral shunts, causing portal venous blood to bypass the liver. Vascular changes compromise liver function, producing hypoxia, necrosis, and atrophy that ultimately lead to liver failure. Copyright © 2018 Wolters Kluwer All Rights Reserved Cirrhosis is most commonly the result of chronic alcohol abuse but can be the result of nutritional deprivation, hepatitis, or other infection. “In USA the hepatitis C is now the most common cause of cirrhosis” Symptoms : oPatients with cirrhosis may seen asymptomatic, when is acute: oNausea oAnorexia oWeight loss oJaundice oDark urine oWeakness oAbdominal pain oVaricosities oChronic cirrhosis may progress to liver failure and portal hypertension The diagnosis of cirrhosis by ultrasound examination may be difficult. Early stage: Specific findings may show coarsening of the liver parenchyma secondary to fibrosis and nodularity. 1. Increased attenuation may be present, with decreased vascular markings. 1. Hepatosplenomegaly may be present, with ascites surrounding the liver. 1. Chronic cirrhosis may show nodularity of the liver edge, especially if ascites is present. 4. The hepatic fissures may be accentuated. 5. The isoechoic regenerating nodules may be seen throughout the liver parenchyma. 6. Portal hypertension may be present with or without abnormal Doppler flow patterns. Late stage: Smaller heterogeneous right and left lobes of the liver The caudate lobe may appear relatively enlarged, due to a independent drainage of the caudate lobe through the emissaries veins which drain directly in the IVC Possible IVC compression due to CL enlargement  More specific sonographic features are seen with late disease and can include: 1. Liver atrophy, especially right lobe 2. Caudate lobe hypertrophy 3. Surface nodularity 4. Internal textural changes ranging from fine to coarse and from hypoechoic to hyperechoic 5. Loss of delineation of intrahepatic vasculature 6. Possible findings related to portal hypertension A, Gross pathology of alcoholic cirrhosis with high degree of fat content. Biliary cirrhosis (liver is nodular). Micronodular cirrhosis (nodules are small with uniform size). Macronodular cirrhosis  Secondary findings of cirrhosis should be documented and can include: Portal hypertension Splenomegaly Varices Collaterals Ascites Common collaterals or varices include: Recanalization of the paraumbilical vein off of the left portal vein Esophageal varices Splenic varices Splenorenal shunt Copyright © 2018 Wolters Kluwer All Rights Reserved  B C B. Transverse scan demonstrates a cirrhotic liver with increased echogenicity. Ascites allows visualization of falciform ligament (arrow). C. On different patient with cirrhosis and ascites (A). Note nodularity of liver surface. Copyright © 2018 Wolters Kluwer All Rights Reserved Transverse: patient with end-stage alcoholic liver disease. Ascites outlines liver margins which show considerable lobulation. Liver is also decreased in size. Copyright © 2018 Wolters Kluwer All Rights Reserved Female patient with cirrhosis showing "coarsened" echo texture and enlarged left lobe of liver B, Early stages cirrhosis: hepatomegaly, decreased vasculature C, Cirrhotic liver with ascites. D, Advanced cirrhosis with attenuation. E, Late-stage cirrhosis with shrunken liver, ascites F, Late-stage cirrhosis with thick gallbladder wall, ascites, shrunken liver. Patients who have cirrhosis have an increased incidence of developing hepatoma tumors within the liver parenchyma. E F E. Sagittal: Level of IVC, enlarged caudate lobe (CL) associated with advanced cirrhosis. Caudate lobe enlargement is thought to be from alterations in portal blood flow to liver secondary to venous compression by fibrosis and regenerative nodules. Ascites (A). F. Sagittal: Image of cirrhotic liver demonstrates multiple hypoechoic areas that are compatible with regenerating nodules. Copyright © 2018 Wolters Kluwer All Rights Reserved  G H G. Patient presents with elevated AFP and cirrhosis. Arrow is pointing to a biopsy-proven HCC. H. Sonogram on another patient with a biopsy-proven HCC (double arrows) visualizes a regenerating nodule (single arrow). Copyright © 2018 Wolters Kluwer All Rights Reserved  Sonogram obtained with high frequency linear array on a patient with cirrhosis and ascites; one should notice the irregularity of the liver capsule (arrows) and heterogeneity of liver parenchyma. K Copyright © 2018 Wolters Kluwer All Rights Reserved Color Doppler image demonstrates corkscrew appearance of the hepatic artery (HA) that can occur because of decreased portal vein flow, increased arterial flow, and shrinkage of liver tissue. Increasing pulse repetition frequency (PRF) to reduce aliasing inside the artery caused flow in the portal vein not to be displayed which could lead to a false impression of portal vein thrombosis. Copyright © 2018 Wolters Kluwer All Rights Reserved As part of the sonographic appearance of the cirrhosis we have to include vascular signs of portal hypertension which is produce because portal flow cannot get through the liver to the hepatic veins and it must be reroute through collateral path ways or porto- systemic shunts. The distended collateral veins in the abdominal wall can be observe and are called “caput medusa sign” The increased pressure within the portal venous system produces Changes in portal vein direction and velocity Flattened spectral trace Monophasic hepatic venous flow on spectral Doppler Splenomegaly. Recanalization of the ligamentum teres and ligamentum venosum Ascites In an oblique plane through the right upper quadrant a shunt tube is identified within the previously seen venous channel. The round structure at the bottom of the image is the distended gallbladder floating in ascitic fluid. Color Doppler indicates flow within the shunt. Bidirectional flow within the main portal vein.  N M M. Color Doppler image demonstrates reversed flow (hepatofugal) in main portal vein and hepatopetal flow of the hepatic artery. N. Image of spectral Doppler of main portal vein demonstrates hepatofugal flow. Copyright © 2018 Wolters Kluwer All Rights Reserved  O P O. In patient with cirrhosis, transverse image of spleen demonstrates splenomegaly and portal hypertension. P. A sagittal image demonstrating multiple cystic areas superior to aorta compatible with esophageal varices. These areas are filled in with color Doppler.Copyright © 2018 Wolters Kluwer All Rights Reserved  Cirrhosis Sonogram obtained with high frequency linear array on a patient with cirrhosis and ascites; one should notice the irregularity of the liver capsule (arrows) and heterogeneity of liver parenchyma.  S Q R Q. Sagittal image of left upper quadrant showing a recanalized umbilical vein (arrows). R. Color Doppler image of same image as in Q showing flow toward the skin surface. S. Same image locations as in R now with a spectral Doppler signal showing that flow is venous. Copyright © 2018 Wolters Kluwer All Rights Reserved  T A color Doppler image following the recanalized umbilical vein under skin to level of umbilicus. Copyright © 2018 Wolters Kluwer All Rights Reserved Distended collateral veins visualized on the abdominal wall have been referred to as the “Caput Medusal” sign Photograph shows a caput medusae accentuated by a large amount of ascites in a patient being prepared for liver transplantation. An extensive plexus of veins is seen emanating from the umbilical region and radiating across the anterior abdominal wall. Note the large vein coursing inferiorly along the right flank (arrows). This is the superficial epigastric vein, which drains into the external iliac vein. A 43-year-old man known to have hepatitis C infection and a long history of alcohol abuse was admitted to the hospital with ascites and edema. For the previous year he had noticed painless enlarged veins on his abdomen. Examination revealed spider angiomas, palmar erythema, enlarged parotid glands, edema, hepatosplenomegaly, ascites, and an unusually large caput medusae Paracentesis yielded fluid that appeared to be a transudate. Abdominal ultrasonography revealed cirrhosis, hepatosplenomegaly, ascites, a recanalized umbilical vein, and patent hepatic veins.  B A Normal Hepatic Vascular Flow A. Color Doppler image of normal main portal vein (darker orange) and normal hepatic artery (brighter orange). B. Low resistive spectral tracing of hepatic artery. Sometimes zooming up image aids in better seeing Copyright © 2018 Wolters Kluwer All Rights Reserved small hepatic artery.  C D Normal Hepatic Vascular Flow C. Spectral Doppler tracing of the main portal vein showing continuous forward flow (hepatopetal). D. Spectral Doppler tracing of the middle hepatic vein showing normal hepatofugal triphasic, flow. Copyright © 2018 Wolters Kluwer All Rights Reserved  Cirrhosis L. Color Doppler image demonstrates corkscrew appearance of the hepatic artery (HA) that can occur because of decreased portal vein flow, increased arterial flow, and shrinkage of liver tissue. Increasing pulse repetition frequency (PRF) to reduce aliasing inside the artery caused flow in the portal vein not to be displayed which could lead to a false impression of portal vein thrombosis. Main portal L vein (MPV); hepatic vein (HV). Duplex criteria used in portal hypertension: Portal vein diameter of > 16 mm in quiet inspiration Hepatofugal portal vein flow with mean flow velocity < 10 cm/sec (normal velocity: 15 – 20 cm/sec) Dilated splenic vein Spleen > 13 cm Management of portal hypertension: The management depends on the causes and the patient condition. Management involves: Endoscopic techniques to control bleeding Paracentesis (a procedure in which a needle or catheter is inserted into the peritoneal cavity to obtain ascitic fluid for diagnostic or therapeutic purposes) Transjugular intrahepatic portosystemic shunt (TIPS). All these methods are transitory, and can relieve pressure in the portal venous system, improving the patient condition until the transplant. Transjugular Intrahepatic Portosystemic Shunt !! Portosystemic means between portal vein system and systemic circulation (IVC). Remember the blood from the intestines and spleen flow into the PV to reach the liver, where is processed and then go to the systemic circulation via hepatic vein to IVC and that pathway is interrupted, therefore the blood have to find a “detour” to finally arrive at the systemic circulation Five major sites of portosystemic venous collaterals visualized by ultrasound are: 1. Gastroesophageal junction: Between the coronary vein and the esophageal veins. 2. Paraumbilical vein in falciform ligament: Between the left portal vein to the systemic epigastric veins near the umbilicus 3. Splenorenal and gastrorenal veins: between the splenic, coronary, and short gastric veins and the left adrenal or renal veins. (Tortuous veins may be seen in the region of the splenic and hilum of the left kidney) 4. Intestinal-retroperitoneal anastomoses between intestine, liver and renal veins. 5. Hemorrhoidal veins: Between veins from the inferior mesenteric veins and systemic rectal veins which drain into the IVC. TIPS is a shunt inserted, within the liver to establishes communication between the portal vein and the systemic circulation. A transjugular puncture needle is passed under X-ray control into the jugular vein to reach the IVC and them the hepatic vein to the portal vein and a shunt is created. The tract is dilated to an approximate diameter of 10 mm and the stent is inserted. Once the shunt is established portal venous blood bypasses the liver through the new via, flowing straight into the hepatic vein. There are three types of shunts: Portocaval (between PV and hepatic vein to IVC) Mesocaval (between SMV and IVC) Splenorenal (between splenic vein and renal vein to IVC). All of them have the same purpose: to skip the damage liver and establish the flow directly from the portal vein or any of its tributaries directly to the IVC.  PORTACAVAL MESOCAVAL 93 119 SPL EN OR ENA L 94 120 Ultrasound is a useful tool to monitor stent patency. Shunt stenosis or occlusion can occur, and this can be detected with ultrasound. The most common site for a stenosis is at the junction of the stent with the PV. Stein appears as a parallel echogenic line inside the liver. The velocity of blood flow in the shunt should be consistent throughout the stent. Shunt stenosis should be considered when the flow velocity within the shunt is less than 50-60 cm/sec. Budd-Chiari syndrome Is an uncommon condition of the hepatic veins or IVC obstruction Could be congenital, because tumor extension (hepatic carcinoma or renal carcinoma) or due to hematologic disorders (polycytemia vera or coagulopathies) Can occur at any level: small hepatic veins, main hepatic veins, or junction of IVC and right atrium.  Clinical presentation: RUQ pain, hepatomegaly especially caudate lobe, ascites, hematemesis and splenomegaly Classic acute presentation: clinical triad of ascites, hepatomegaly, and abdominal pain, although these findings are nonspecific  Sonographic findings depend on degree of venous obstruction and underlying cause. Hepatic veins: not visible, narrow, or reversed flow. Gray-scale imaging may show hypertrophy of caudate lobe as liver directs its venous blood to caudate lobe due to direct venous drainage into IVC. Color Doppler may demonstrate enlarged caudate veins draining into IVC. Passive Liver Congestion Passive liver edema secondary to vascular congestion is a complication related to heart failure. Large volume of blood exiting liver must pass through hepatic veins, to IVC, and enter right side of heart. Resistance to flow into right side of heart from cardiac or pulmonary disorders will cause secondary dilatation of these vessels. Acute phase: liver enlarges, causing RUQ discomfort. Copyright © 2018 Wolters Kluwer All Rights Reserved  Sonography: Liver is easily penetrated, and dilated veins are readily visible. IVC is dilated and caliber may not change much with respiratory maneuvers. Pulsed Doppler waveforms of hepatic vein demonstrate highly pulsatile W-type pattern showing flow reversal during systole secondary to tricuspid regurgitation. Doppler tracings in portal vein are also more pulsatile than normal with minimal or slight flow reversal during diastole. Usually, all veins in body will dilate and be pulsatile. Copyright © 2018 Wolters Kluwer All Rights Reserved Transverse scan of IVC and hepatic veins showing dilatation from right heart failure. The image visualizes the Canadian Moose sign. A Copyright © 2018 Wolters Kluwer All Rights Reserved Transverse and sagittal scans of a patient in right ventricular heart failure show a dilated inferior vena cava (IVC) and hepatic veins (HV). Review How is Hepatitis A contracted? a. Infected needles b. Hereditary c. Fecal-oral contact d. Blood transfusions What does fatty infiltration look like on ultrasound? a. Hypoechoic and homogenous b. Hyperechoic/echogenic c. Isoechoic to the closest kidney Which statement best describes Budd-Chiari Syndrome? a. When scar tissue replaces normal liver tissue b. Fatty liver infiltration c. Liver cancer d. Thrombosis of the hepatic veins and/or IVC Normal Hep veins Thrombosed Hep veins Quiz What term defines blood flow toward the liver? A. Recanalized B. Postpetal C. Hepatopetal D. Hepatofugal Quiz Which sign describes the sonographic appearance associated with dilatation of the inferior vena cava and hepatic veins from right heart failure? A. Canadian Moose B. Double bubble C. Starry sky D. California Seagull Quiz Which sonographic feature is a classic sign of fatty liver infiltration? A. Homogeneity B. Hyperechoic internal echoes C. Decreased sound penetration D. Echogenic diaphragm Quiz Which sign describes the sonographic finding when the portal vein walls appear more hyperechoic against hypoechoic background of edematous liver parenchyma? A. Double bubble B. Eclipse C. Starry sky D. Seagull