• When you see multiple hypodense lesions that cannot be diagnosed w certainty

  • Cysts: water density, sharp demarcation

  • Hemangiomas: slowly progressive peripheral nodular enhancement of arterial density.

  • Malignant lesion: inhomogeneous, irregular demarcation, peripheral enhancement less than arterial density. 

• When seen in patients w/o known malignancy = benign

• When seen in patients w/ known malignancy = 12% are malignant

  • Percentage of malignancy depended on the known primary tumor.

  • Most mets are breast CA which typically present as multiple small lesions

  • Liver mets from colorectal cancer and lymphoma are usually solitary or few larger masses.

• Stable features: small size and sharp edge. Heterogeneity and ST attenuation were associated w unstable behavior over time.

• Is it a hemangioma?

• If not, is it a FNH? 

  • Assess enhancement pattern and morphologic features (Inhomogeneity, capsule, scar, calcification or fat)

    • Homogeneous enhancement in arterial phase, hypodense central scars in arterial and venous phase, enhancement on equilibrium phase.

• If not, is it a lesion that needs further management (HCC, adenoma, FLC, hypervascular mets)? 

• Differentiate b/n touch and dont touch lesions

  • Benign dont touch: hemangioma, FNH and small adenomas

  • Touch: large adenomas >5 cm and malignant tumors like HCC, FLC and mets.

  • Differentiate enhancing solid lesions from vascular lesions (hepatic aneurysm, aortaportal shunt, pseudoaneurysm)

General features:

• Not true neoplasm but believed to represent a hyperplastic response to increased blood flow in a congenital intrahepatic AVM.

• All the normal constituents of the liver are present but in an abnormally organized pattern. 

• Second most common tumor of the liver.

  • 8% of all primary liver tumors, estimated prevalence b/n 0.3% - 3.0%.

• Demo: women 20-50 yo; 10:1 female to male ratio. 

• 80% are solitary; 20% coexist w hemangiomas

  • Both involve focal abnormalities in hepatic blood supply.

• Features:

  • 15% can grow when followed longitudinally though this is of no concern as there is NO MALIGNANT TRANSFORMATION.

  • Can RARELY have intralesional fat, but if they do they probably also have a central scar.

  • No calcification, inhomogeneity or capsule should be seen.

• Associated with:

  • Hepatic hemangiomas

  • Intracranial aneurysms

  • Dysplastic systemic arteries

Approach to FNH in 2 parts:

• Part 1: vascular nidus / central scar

  • Consists of biliary ductules and venules w/o fibrotic tissue. Can sometimes see a large feeding artery. Scar visible in ⅔ of large (>3 cm) and ⅓ of small FNH.

  • Central scars can also be found in FLHCC, hepatic adenoma and intrahepatic cholangiocarcinoma.

    • FNH has T2 bright scar in 80% of cases

    • FLHCC has T2 dark scar 

    • Sometimes differentiating between FLHCC and FNH is not possible.

  • MR features

    • In/out phase: hypointense to liver

    • T2: hyperintense to liver (possibly 2/2 slow flow w/n vessels)

      • Scar in hemangioma is hypointense to liver

    • EC C+: hyperintense on delayed phase

    • HBP C+: negative

• Part 2: Surrounding parenchymal hyperplastic response

  • MR features

    • In/out phase: iso/slightly hypointense to liver; rarely contain lipid

    • T2: isointense to minimally hyperintense relative to liver

    • EC C+: 

      • Art: marked homogeneous enhancement; lobulated w/o capsule

      • PV: isointense to liver

      • Delayed: isointense 

    • HBP C+: 

      • Isointense to hyperintense components relative to liver

        • Indicating functioning tho disordered hepatocytes and bile ducts

      • Central scar may not enhance 2/2 more rapid removal of contrast from circulation compared to other gad.

      • Most definitive way to distinguish from HCA

      • Not iso to hyperintense to liver

• US FINDINGS

  • Nonspecific ill-defined lesion

  • Central scar may be detected as a hyperechoic area but cannot be differentiated.

  • Vessels are sometimes seen within the scar on color doppler.

• CT FINDINGS

  • NECT: isodense or slightly hypodense to normal liver

  • CECT: homo-hypervascularity on arterial phase, isodense others

    • Hepatic arterial phase: transient, intense, homogeneous hyperdensity (cloud like) enhancement w/ hypodense central scar +/- large artery feeding central scar

    • Enhancement is less intense than the aorta

    • PV phase: blends in imperceptibly w normal liver; large draining veins -> hepatic veins

    • Delayed: Mass is isodense to normal liver, central scar is hyperdense 2/2 fibrous tissue

General features

• Large well-circumscribed encapsulated tumors that consist of sheets of well-differentiated hepatocytes and scattered Kupffer cells w/o bile ducts or portal areas

  • 80% of adenomas are solitary, 20% are multiple.

  • Typically measure 8-15 cm; considered large >5 cm

• Pathogenesis is related to a generalized vascular ectasia that develops 2/2 exposure of the liver to OCPs and related synthetic steroids. 

• Findings overlap with HCC, FNH, hypervascular mets making definitive dx often not possible. Clinical correlation in such cases is most helpful:

  • RF for HCA: young females on OCPs, anabolic steroids, metabolic syndrome, glycogen storage diseases, hemochromatosis, acromegaly.

  • Hx of cirrhosis and high AFP levels favor HCC.

  • Hx of primary hypervascular tumor favors mets.

• Associations: OCP, Androgenic steroids, Hepatic vascular disorders (Budd-chiari), Glycogen storage dz 1

• Appearance:

  • 40% have hemorrhage (also HCC and large hemangiomas)

    • Hepatic adenomas are prone to central necrosis and hemorrhage bc the vascular supply is limited to the surface of the tumor.

    • FNH and hemangiomas are not prone to spontaneous hemorrhage. 

    • HCC can spontaneously hemorrhage but typically occurs in cirrhotic livers and shows washout on venous phase

  • 7% have fat deposition 

  • 30% have low attenuation delayed enhancing pseudocapsule

  • 5% have coarse calcifications

• Histologic subtypes:

  • Each subtype has slightly different imaging features, making confident imaging diagnosis somewhat difficult and often requiring tissue sampling for confirmation.

  • Independent of subtype, adenomas >4 cm are at risk of developing intralesional hemorrhage and are usually treated w surgical resection or nonsurgical radiofrequency ablation or  bland embolization. Smaller lesions can be managed conservatively followed by images.

  • Shared by all subtypes:

    • Associated w obesity and metabolic syndrome

    • If >10 HCAs = hepatic adenomatosis; more likely to have steatosis

    • Can have intralesional or peritumoral hemorrhage

      • >5 cm tumor at risk of developing intralesional hemorrhage

      • Tx: surgical resection, nonsurgical RFA or bland embolization.

INFLAMMATORY SUBTYPE

• Most common (40-50%), has the highest bleeding risk (30%).

• Association: young women on OCPs, obesity and EtOH use

• Presentation: incidental, hemorrhage, systemic inflammatory syndrome

• Histology: sinusoidal prominence, inflammatory cell infiltration, tortuous and thickened arteries

• Appearance:

  • IHCA have significantly less intralesional steatosis than HNF1-a

  • Up to 30% have evidence of hemorrhage

  • 10% risk of malignant degeneration

  • T1: usually isointense - slightly hyperintense to surrounding liver.

  • OOP: liver more likely to lose SI bc of steatosis than IHCA itself.

  • T2WI: homogeneously or in peripheral distribution (Atoll sign; 40% of cases 2/2 dilated sinusoids and increased vascularity)

  • Enhancement: persistent hypervascularity through arterial/venous phases 2/2 sinusoidal dilation, peliotic areas and abnormal vessels.

    • Fading throughout phases; hyperintense to background

    • EC C+: persistent enhancement art -> venous

    • HBP C+: No central scar; almost never have isointense to hyperintense components of delayed phase.

HNF-ALPHA 1 SUBTYPE

• Second most common (30-35%), characterized by multiple adenomas; lowest risk of bleeding. 

• HNF1A gene promotes lipid deposition w/n HAs

• Association: familial hepatic adenomatosis, FAP, Exclusively in women w hx of OCPs

• T1WI: Hyper to isointense

• T2WI: Iso to slightly hyperintense

• In/out of phase: signal dropout on opposed phase images 2/2 homogeneous intralesional fat, background steatotic liver; nodules containing homogeneous low level intravoxel fat

• Enhancement: 

• Mild to moderate on arterial phase, though less than with inflammatory adenomas. 

• No persistent enhancement on venous and delayed phases

• No uptake on Primovist

BETA-CATENIN SUBTYPE

• Least common (10-15%), highest risk of malignant transformation.

• Association: seen in men on anabolic steroids and Von Gierke’s.

• Enhancement: often arterially enhancing without washout. 

• May take up primovist

UNCLASSIFIED SUBTYPE

• Including sonic hedghog which has propensity to bleed

• No specific imaging appearance

BILIARY HAMARTOMA