USG evaluation of Liver Cirrhosis

1. USG Liver Cirrhosis
Dr. Yash Kumar Achantani
OSR

2. Normal echogenicity
Renal medulla < Renal cortex < Liver
Liver < Spleen
Liver < Pancreas.
Pancreas < Renal sinus

3. 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.

4. 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).

5. 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.

6. 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).

7. 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)

8. Etiology
 Alcohol: 60-70%
 Viral hepatitis: 10%
 Cryptogenic/nonalcoholic steatohepatitis (NASH): 10-15%
 Biliary disease, e.g. primary sclerosing cholangitis (PSC), primary biliary
cirrhosis (PBC): 5-10%
 Metabolic disease, e.g. hereditary haemochromatosis, Wilson disease,
alpha-1-antitrypsin deficiency: 5%
 Autoimmune hepatitis
 Vascular disease, e.g. congestive hepatopathy (right heart failure), Budd-
Chiari syndrome, Hepatic veno-occlusive disease: rare
 Cystic fibrosis
 Medications (e.g. methotrexate)

9. Clinical Presentation
The classic clinical presentation of cirrhosis is
Hepatomegaly.
Jaundice.
Ascites.
However, serious liver injury may be present without any
clinical clues.

10. 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.

11. 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.

12. 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.

13. Parenchymal changes. A, Coarse parenchyma and innumerable tiny, hyperechoic
nodules.
B, Coarse parenchyma and innumerable tiny, hypoechoic nodules.
C, Coarse parenchyma and surface nodularity.

14. 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.

15. 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

16. Contour abnormality. A and B, Small, end-stage livers with surface nodularity, best
appreciated in patients with ascites, as shown here.

17. 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.

18. 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.

19. 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

20. 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).

21. 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).

22. C, Gray-scale image, and D, color Doppler image, show extensive varices
in the distribution of the coronary vein.

23. E, Gray-scale image, and F, color Doppler image, show splenic hilar varices.

24. 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