Pediatric Focal Nodular Hyperplasia

  • Etiology: benign vascular tumor composed of functioning hepatocytes
  • Imaging: enhances to level of inferior vena cava and does not enhance to level of aorta, feeding vessel goes to center of lesion, central scar often vascular on arterial phase but isodense on later phases, lesion becomes isodense in late venous phase, no hemorrhage or necrosis
  • CT: isodense or hyperdense on non contrast, hypervascular with homogenous enhancement with large feeding artery on arterial phase, isodense to liver on venous phase
  • MRI: classically completely fills in with gadoxetate disodium, central scar is myxoid making it hyperintense on T2 and having delayed enhancement
  • Treatment: rarely surgically resected
  • Clinical: normal AFP, < 20% of patients are symptomatic, female preponderance, three populations: solitary lesion in 2-5 years old and adolescents / multiple lesions as late complication post chemotherapy (regenerating hepatic nodules)

Radiology Cases of Focal Nodular Hyperplasia

Axial and coronal CT with contrast of the abdomen arterial phase imaging (left) shows an enhancing round lesion in the dome of the liver that has a central scar which fills in on the portal venous phase imaging and becomes isodense with the surrounding liver parenchyma (center). Axial T1 MRI with Eovist (hepatocyte specific) contrast of the abdomen in the arterial phase (right upper) again shows the enhancing round lesion with a central scar that fills in the portal venous phase imaging (right center) and then retains its contrast on the delayed phase imaging (right lower).