Lipid-poor hepatic adenoma
Deranged liver function tests. Lesion seen on ultrasound.
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A 5.4 x 4.0 cm lesion in hepatic segment 7/6 and is slightly hyperintense to liver on T2 and isointense on T1. Signal intensity does not decrease on out of phase T1 imaging (unlike the rest of the background liver, due to mild steatosis). The lesion shows arterial enhancement with washout through the portal venous and delayed phases and a thin pseudocapsule. No contrast uptake in the hepatocellular phase.
A 1 cm T2 hyperintense lesion is seen at the periphery of segment 5. This shows arterial enhancement that becomes isointense to liver of subsequent phases, including the hepatocellular phase.
An 8 mm T2 hyperintense lesion in segment 7 shows apparent progressive peripheral enhancement, and no uptake on on hepatocellular phase.
The common hepatic and common bile ducts measure up to 7 mm in diameter, which may reflect the patient is post cystectomy starts. No choledocholithiasis is identified. The pancreas has a normal appearance.
A 1.8 x 0.9 cm lesion is seen in the posterior to segment 6 within Morrison's pouch. This lesion is hyperintense on T2, with possible peripheral enhancement. A small residual collection is likely. Further likely collections around the anterior and lateral liver surface, and around the head of the pancreas.
In the right abdominal wall musculature, between obturator internus and transversus abdominis there is a complex 9 x 4 cm T2 hyperintense region, likely a collection. This is only well seen on the coronal images, but the superior component is seen on the axial post contrast images and there appears to be peripheral enhancement. This is similar to when was seen on CT dated 7 June, 2014.
Large lesion in segments 7/6 is favoured to represent a lipid poor hepatic adenoma, on a background of hepatic steatosis. The small segment 5 lesion is likely focal nodular hyperplasia (FNH).
Persistent collections in Morrison's pouch, around the pancreas head and in the right abdominal wall.
This case shows the importance of identifying any background liver parenchyma changes before characterising lesions. With lipid-rich adenomas we expect the lesion to become hypointense to liver on out-of-phase T1 imaging. In this case the lesion became slightly hyperintense because the background fatty liver lost signal, while the lipid-poor adenoma maintained it's signal.
The enhancement pattern - arterial enhancement, washout and lack of hepatocellular uptake differentiates it from focal nodule hyperplasia.
The lesion is incidental to the patient's deranged LFTs.