T1 fat suppressed images before and after intravenous gadolinium demonstrate an area of relatively low precontrast T1 signal adjacent the falciform ligament. This area remains relatively hypointense compared to the background hepatic parenchyma on postcontrast imaging. This is a common site of differential focal fatty infiltration or sparing, likely due to differential perfusion in this region, often by branches of the left gastric artery or venous drainage into systemic veins.
The T1 in phase images demonstrate that there is high signal in this region and the paired out of phase images demonstrate that this region significantly loses signal, consistent with focal fatty infiltration.
Is this all?
The background hepatic parenchymal signal remainder of the liver is higher on the out of phase imaging than the in-phase imaging. This is unusual. Typically in a normal liver signal remains constant. In diffuse fatty infiltration, signal loss would be expected in areas of fatty infiltration. In this instance, however, the inverse is demonstrated for the bulk of the hepatic parenchyma.
Why does this occur? This is due to hepatic haemosiderosis in the remainder of the liver. In phase imaging has a longer TE(time to echo) than out of phase imaging. As a result there is more time for Iron atoms to result in local dephasing on in phase imaging. In turn this manifests as loss of signal compared to out of phase imaging.
So think of hepatic haemosiderosis as the inverse of hepatic steatosis with regards to liver in and out of phase imaging. In this case they can be to differentiated as they are occuring in distinct areas. If they are occurring in the same area of hepatic parenchyma combined defects can be difficult to differentiate and will depend on the extent of either present.
The T1 in phase images demonstrate that there is high signal in this region and the paired out of phase images demonstrate that this region significantly loses signal, consistent with focal fatty infiltration.
Is this all?
The background hepatic parenchymal signal remainder of the liver is higher on the out of phase imaging than the in-phase imaging. This is unusual. Typically in a normal liver signal remains constant. In diffuse fatty infiltration, signal loss would be expected in areas of fatty infiltration. In this instance, however, the inverse is demonstrated for the bulk of the hepatic parenchyma.
Why does this occur? This is due to hepatic haemosiderosis in the remainder of the liver. In phase imaging has a longer TE(time to echo) than out of phase imaging. As a result there is more time for Iron atoms to result in local dephasing on in phase imaging. In turn this manifests as loss of signal compared to out of phase imaging.
So think of hepatic haemosiderosis as the inverse of hepatic steatosis with regards to liver in and out of phase imaging. In this case they can be to differentiated as they are occuring in distinct areas. If they are occurring in the same area of hepatic parenchyma combined defects can be difficult to differentiate and will depend on the extent of either present.
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