Presentation
Elevated AFP more than 400 ng/mL, suspected HCC.
Patient Data
There is a large encapsulated heterogenous solitary lesion with necrotic areas devoid of calcifications. This mass shows a continuous enhancing peripheral rim occupying the left lobe of the liver mainly segment two and four. It measures around 11 cm in diameter. It appears pushing the middle hepatic vein.
It appears compressing the inferior vena cava but not infiltrating it.
No evidence of portal vein thrombosis.
The volume of the right lobe of the liver measures more than 1200 mL. However, CT of the chest is advised to rule out metastases.
No evidence of retroperitoneal lymph node enlargement could be seen.
The spleen, pancreas, adrenal glands, and kidneys appear normal.
Case Discussion
Hepatomas, present an encapsulated hypervascular tumor. Charestrictsic early vivid enhancement (mainly during late arterial phase) and early washout (portal and later phases) to become indistinct or hypodense relative to adjacent hepatic parenchyma. Multiphase CT with a late arterial phase is essential as many lesions are only visible during the arterial phase.
Some lesions may show a ‘mosaic’ pattern of enhancement on CT with an enhancing grid-like pattern as well as later rim enhancement.
Any enhancing lesion in a cirrhotic background of the liver is considered hepatoma until proven otherwise.
Large lesions may demonstrate vascular invasive features, undergo hemorrhage, and contain areas of fat, thrombosis, and necrosis.
Any new solid lesion on US hyperechoic/hypoechoic in relation to adjacent parenchyma in a high-risk patient is considered a potential HCC. Large lesions may show internal heterogeneity, due to hemorrhage, necrosis, or fat and often cause portal vein thrombosis or tumor thrombus, which can expand the vein. High-velocity Doppler signals from within the lesion occur in the majority of cases as a result of arterioportal shunting.
The patient underwent resection of the left lobe and gallbladder. Tissue specimen of the lesion confirmed moderately differentiated HCC with lymphovascular invasion. No pathological changes of gallbladder.