Vascular Abnormalities
Dynamic contrast-enhanced single-section liver CT provides data for aortic, hepatic, and portal vein time-density curves, which are used to calculate
liver perfusion, arterial fraction, distribution volume, and mean transit time. Hepatic perfusion parameters are significantly altered in cirrhosis and vary with the severity of disease.
Patients with advanced cirrhosis tend to develop portal and mesenteric vein calcification; some portal vein calcifications are associated with portal venous thrombosis.
Portal Vein
Portal vein flow, as determined by duplex US, varies with the degree of cirrhosis. Portal vein velocity also decreases with progression of cirrhosis and is a more sensitive indicator than splenic vein velocity. Little correlation exists
among portal vein flow, splenic vein flow, and extent of esophageal varices, explained, in part, by the presence of collateral circulation.The loss
of reversed flow in the hepatic veins is a common finding in established cirrhosis.
Shunting Arterioportal shunting is not uncommon in cirrhosis. These shunts vary in their CT arterial portography appearance, ranging from single to multiple and from irregular, wedge-shaped to round. The margins vary in sharpness, and contrast enhancement is apparent in some. Smaller ones undoubtedly are not identified by pre- and postcontrast imaging and blend into normal liver parenchyma.Also complicating the issue is that arterioportal fistulas develop not only in cirrhotic livers but also in superimposed hepatocellular carcinomas.
Color Doppler US is useful in indirect shunt detection; an intrahepatic arterioportal fistula should be suspected when the resistance index (RI) in one hepatic lobe is decrease at least 20% relative to the other lobe, the pulsatility index (PI) is decreased at least 30%, and portal blood flow in the lobe with decreased RI and PI is reversed (43). An actual fistula is confirmed by angiography.
More prominent arterioportal shunts are seen as hyperintense regions precontrast MR and after SPIO contrast on T2-weighted TSE images. These patients also develop hepatic arteriosystemic venous shunting. By infusing Dsorbitol into the hepatic artery, a substance whose first-pass hepatic extraction is normally high, any resultant systemic availability reflects arteriovenous shunting. Considerable shunt variability is evident in cirrhotic patients.
In a cirrhotic liver and aberrant gastric venous drainage, the focal liver region involved by aberrant drainage is hypodense on CT, hypoechoic with US, and hyperintense on T1- and hypointense on T2-weighted MRI; as expected, this region shows early enhancement with dynamic CT and MRI.
Hepatic Veins Abnormal hepatic vein Doppler waveforms are found in most patients with established cirrhosis, although little correlation exists between
degree of liver failure and flow alterations.
Hepatic venography in patients with cirrhosis shows patchy parenchymal opacification.
Visualized hepatic vein branches are distorted and compressed.
Hepatic Artery
The postprandial hepatic artery RI does not increase as much in patients with liver disease as in those with a normal liver. In particular, patients with Child-Pugh class C disease have an increase in resistance of <10% rather than
>40% as found in a normal liver. This change mirrors findings in portal blood flow discussed previously. Whether this finding in cirrhotics is due to vascular or parenchymal factors is unknown.
liver perfusion, arterial fraction, distribution volume, and mean transit time. Hepatic perfusion parameters are significantly altered in cirrhosis and vary with the severity of disease.
Patients with advanced cirrhosis tend to develop portal and mesenteric vein calcification; some portal vein calcifications are associated with portal venous thrombosis.
Portal Vein
Portal vein flow, as determined by duplex US, varies with the degree of cirrhosis. Portal vein velocity also decreases with progression of cirrhosis and is a more sensitive indicator than splenic vein velocity. Little correlation exists
among portal vein flow, splenic vein flow, and extent of esophageal varices, explained, in part, by the presence of collateral circulation.The loss
of reversed flow in the hepatic veins is a common finding in established cirrhosis.
Shunting Arterioportal shunting is not uncommon in cirrhosis. These shunts vary in their CT arterial portography appearance, ranging from single to multiple and from irregular, wedge-shaped to round. The margins vary in sharpness, and contrast enhancement is apparent in some. Smaller ones undoubtedly are not identified by pre- and postcontrast imaging and blend into normal liver parenchyma.Also complicating the issue is that arterioportal fistulas develop not only in cirrhotic livers but also in superimposed hepatocellular carcinomas.
Color Doppler US is useful in indirect shunt detection; an intrahepatic arterioportal fistula should be suspected when the resistance index (RI) in one hepatic lobe is decrease at least 20% relative to the other lobe, the pulsatility index (PI) is decreased at least 30%, and portal blood flow in the lobe with decreased RI and PI is reversed (43). An actual fistula is confirmed by angiography.
More prominent arterioportal shunts are seen as hyperintense regions precontrast MR and after SPIO contrast on T2-weighted TSE images. These patients also develop hepatic arteriosystemic venous shunting. By infusing Dsorbitol into the hepatic artery, a substance whose first-pass hepatic extraction is normally high, any resultant systemic availability reflects arteriovenous shunting. Considerable shunt variability is evident in cirrhotic patients.
In a cirrhotic liver and aberrant gastric venous drainage, the focal liver region involved by aberrant drainage is hypodense on CT, hypoechoic with US, and hyperintense on T1- and hypointense on T2-weighted MRI; as expected, this region shows early enhancement with dynamic CT and MRI.
Hepatic Veins Abnormal hepatic vein Doppler waveforms are found in most patients with established cirrhosis, although little correlation exists between
degree of liver failure and flow alterations.
Hepatic venography in patients with cirrhosis shows patchy parenchymal opacification.
Visualized hepatic vein branches are distorted and compressed.
Hepatic Artery
The postprandial hepatic artery RI does not increase as much in patients with liver disease as in those with a normal liver. In particular, patients with Child-Pugh class C disease have an increase in resistance of <10% rather than
>40% as found in a normal liver. This change mirrors findings in portal blood flow discussed previously. Whether this finding in cirrhotics is due to vascular or parenchymal factors is unknown.
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