Normal echogenicity Renal medulla < R enal cortex < L iver Liver < S pleen Liver < P ancreas . Pancreas < R enal sinus
Sonographically the vessels seen visible within the liver parenchyma are hepatic and portal veins. Hepatic arteries and bile ducts not seen unless abnormally dilated but seen in porta hepatis.
Portal veins Echogenic (bright) walls - used for evaluation of evaluation of liver parenchyma. Enter the liver through porta hepatis. Main portal vein divide in the middle of liver. More horizontally oriented. Pass within lobes and segments. Flow towards liver ( hepatopetal ) .
Main portal vein: normal doppler Continuous, forward flow. Low velocity (15-28 cm/sec.) Hepatopetal flow. Undulating pattern -Respiratory variation -Increase flow on inspiration. May reflect cardiac variation. Slightly turbulent.
Hepatic veins Imperceptible margins. Enlarge toward the IVC. More vertically oriented. Umbrella configuration. Runs between lobes and segments. Used as anatomic divider of the liver. Flow away from the liver ( hepatofugal ).
Cirrhosis Three major pathologic mechanisms combine to create cirrhosis: cell death, fibrosis , and regeneration. Cirrhosis has been classified as Micronodular , nodules are 0.1 to 1 cm in diameter (Alcohol) Macronodular , nodules of varying size, up to 5 cm in diameter (Chronic viral hepatitis)
Clinical Presentation The classic clinical presentation of cirrhosis is Hepatomegaly. Jaundice. Ascites. However, serious liver injury may be present without any clinical clues.
USG The sonographic patterns associated with cirrhosis include the following. Volume redistribution Early stages of cirrhosis the liver may be enlarged. Advanced stages the liver is often small, with relative enlargement of the caudate lobe, left lobe, or both, compared with the right lobe. Ratio of the caudate lobe width to the right lobe width (C/RL) is an indicator of cirrhosis. A C/RL value of > 0.65 is considered indicative of cirrhosis.
Lobar redistribution. A, Sagittal image showing an enormous caudate lobe. B, Transverse sonogram shows the right lobe is small, with enlargement of the left lateral segment. C, Subcostal oblique view showing a tiny right lobe of the liver, which is separated from the large left lobe by the main lobar fissure (arrows) A right/left lobe ratio of sagittal diameters in midclavicular line and midline respectively of 1. 3 or less can differentiate cirrhosis from normal liver.
Coarse echotexture Increased echogenicity and coarse echotexture are frequent observations in diffuse liver disease. Liver attenuation is correlated with the presence of fat, not fibrosis. Cirrhotic livers without fatty infiltration had attenuation values similar to those of controls.
Parenchymal changes. A, Coarse parenchyma and innumerable tiny, hyperechoic nodules. B, Coarse parenchyma and innumerable tiny, hypoechoic nodules. C, Coarse parenchyma and surface nodularity.
Nodular surface Irregularity of the liver surface during routine scanning has been appreciated as a sign of cirrhosis when the appearance is gross or when ascites is present. The nodularity corresponds to the presence of regenerating nodules and fibrosis. Regenerating nodules (RNs) These regenerating hepatocytes are surrounded by fibrotic septae . RNs tend to be isoechoic or hypoechoic with a thin, echogenic border that corresponds to fibrofatty connective tissue.
Dysplastic nodules. AKA adenomatous hyperplastic nodules They are larger than RNs (diameter of 10 mm) and are considered premalignant. They contain well-differentiated hepatocytes, a portal venous blood supply, and atypical or frankly malignant cells. The portal venous blood supply can be detected with color Doppler flow imaging and distinguished from the hepatic artery–supplied HCC
Contour abnormality . A and B, Small, end-stage livers with surface nodularity, best appreciated in patients with ascites, as shown here.
Portal Hypertension Normal portal vein pressure is 5 to 10 mm Hg (14 cm H2O). Portal hypertension is defined by (1) Wedge hepatic vein pressure or direct portal vein pressure more than 5 mm Hg greater than IVC pressure, (2) Splenic vein pressure greater than 15 mm Hg, or (3) Portal vein pressure (measured surgically) greater than 30 cm H2O.
Pathophysiologically , portal hypertension can be divided into presinusoidal and intrahepatic groups, depending on whether the hepatic vein wedge pressure is normal ( presinusoidal ) or elevated (intrahepatic). Cirrhosis is the most common cause of intrahepatic portal hypertension. Sonographic findings of portal hypertension include the secondary signs of Splenomegaly. Ascites. Portosystemic venous collaterals.
PORTOSYSTEMIC VENOUS COLLATERALS: MAJOR SITES IDENTIFIED ON ULTRASOUND 1. Gastroesophageal junction 2. Paraumbilical vein in falciform ligament 3. Splenorenal and gastrorenal veins 4. Intestinal-retroperitoneal anastomoses 5. Hemorrhoidal veins
Duplex Doppler sonography Dilated portal vein (>13 mm). Low Portal venous velocity (<16 cm/sec). Less than 20% increase in the diameter of the portal vein with deep inspiration. Portal vein loses its undulatory flow pattern and becomes monophasic. As the severity of portal hypertension increases, flow becomes biphasic and finally hepatofugal (away from the liver). Chronic liver disease is also associated with increased splanchnic blood flow (superior mesenteric arteries and splenic arteries).
A, Sagittal image of recanalized paraumbilical vein in patient with gross ascites. B, Sagittal image shows enlarged coronary vein running cephalad from the splenic vein (SV).
C, Gray -scale image, and D, color Doppler image, show extensive varices in the distribution of the coronary vein.
E, Gray -scale image, and F, color Doppler image, show splenic hilar varices.
Portal hypertension with reversal of portal venous flow. Spectral and color Doppler image of the main portal vein shows hepatofugal flow. Spectral Doppler waveform is below the baseline, confirming that the flow is away from the liver