Hypervascular Liver Lesions

__________________________________________________________
Aya Kamaya, MD, Error: Reference source not found, Error: Reference source not found, Katherine E. Maturen, MD, Grace A. Tye, MD, Yueyi I. Liu, MD, PhD, Naveen N. Parti, MD, Terry S. Desser, MD Stanford University Medical Center, Stanford, CA University of Michigan Health Systems, Ann Arbor, MI Stanford University, Stanford, CA Greenville Radiology, Greenville, SC

http://dx.doi.org/10.1053/j.sult.2009.06.001, How to Cite or Link Using DOI http://www.sciencedirect.com/science/article/pii/S0887217109000547

Hypervascular hepatocellular lesions include both benign and malignant etiologies. In the benign category, focal nodular hyperplasia and adenoma are typically hypervascular. In addition, some regenerative nodules in cirrhosis may be hypervascular. Malignant hypervascular primary hepatocellular lesions include hepatocellular carcinoma, fibrolamellar carcinoma, and peripheral cholangiocarcinoma. Vascular liver lesions often appear hypervascular because they tend to follow the enhancement of the blood pool; these include hemangiomas, arteriovenous malformations, angiosarcomas, and peliosis. While most gastrointestinal malignancies that metastasize to the liver will appear hypovascular on arterial and portal-venous phase imaging, certain cancers such as metastatic neuroendocrine tumors (including pancreatic neuroendocrine tumors, carcinoid, and gastrointestinal stromal tumors) tend to produce hypervascular metastases due to the greater recruitment of arterial blood supply. Finally, rare hepatic lesions such as glomus tumor and inflammatory pseudotumor may have a hypervascular appearance.

Figure 1. Focal nodular hyperplasia. (A) Grayscale sonogram of large FNH in caudate lobe of liver (demarcated by calipers) is isoechoic to rest of liver. No internal portal triads seen in mass. (B) Power Doppler sonogram of same liver mass demonstrates spokewheel vascularity (arrows). (C) Same mass on arterial-phase CT is homogeneously hypervascular (arrow). (D) On portal-venous phase CT, mass (arrow) is isodense to remainder of liver. (E) On delayed-phase image, mass (arrow) is isodense to liver. No central scar is evident in this FNH. (Color version of figure is available online.)

Figure 2. Patient with focal nodular hyperplasia in right lobe of liver. (A) Lesion is hypervascular on arterial phase with hypodense central scar (arrow). (B) Lesion is isodense on portal-venous phase.

Figure 3. Patient with Budd-Chiari syndrome and hypervascular large regenerative nodules (arrows) seen on CT.

Figure 4. Forty-three-year-old female with Budd-Chiari syndrome with numerous hypervascular large regenerative nodules (arrows) on arterial-phase MRI (A and B), which become isointense on portal venous phase images (C).

Figure 5. Adenoma. (A) T2-weighted fat-saturated image shows heterogeneously bright lesion. (B) Lesion is hypointense (arrow) on T1-weighted in-phase imaging, compared to adjacent liver. (C) Dropout of signal on T1weighted, out-of-phase image (arrow) confirms intracellular lipid. (D) Lesion is heterogeneously hypervascular on T1 arterial-phase image (arrow). (E) T1 portal-venous phase. Lesion remains hypervascular (arrow). (F) CT arterial-phase. Lesion is hypervascular (arrow). (G) CT portal-venous phase. Periphery of lesion slightly washes out while center enhances (arrow).

Figure 6. Bleeding adenoma. (A) Noncontrast CT shows high-density area corresponding to area of hemorrhage. (B)

Postcontrast CT shows enhancing adenoma surrounding area of hemorrhage (arrowheads). Other smaller adenomas are more evident through rest of liver (arrows).

Figure 7. Bleeding adenoma. Forty-year-old female with hypervascular adenoma (arrow) and acute subcapsular bleed (arrowheads).

Figure 8. Small hepatocellular carcinoma. (A) Lesion is hypervascular on arterial-phase image (arrow). (B) Central washout seen on portal-venous phase; capsule is slightly hyperdense (arrow). (C) On delayed phase, lesion further washes out (arrow) compared to background liver.

Figure 9. Hepatocellular carcinoma. (A) Arterial-phase image shows hypervascular hepatocellular carcinoma (arrows) with areas of neovascularity (arrowheads). (B) On delayed phase, hepatocellular carcinoma masses wash out compared to normal liver (arrows), and lower attenuation areas of fat are more evident (arrowheads).

Figure 10. Forty-eight-year-old female with large heterogeneous partially exophytic hepatocellular carcinoma that has ruptured, with sentinel clot sign (higher density clotted blood) layering next to liver in left upper quadrant consistent with active bleeding.

Figure 11. (A) Fibrolamellar carcinoma in 21-year-old female, with visible low-density central scar (arrow). (B) Fibrolamellar carcinoma in a 16-year-old female. Lesion is hypervascular on arterial phase with large avidly enhancing tumor vessels. (C) Calcifications in the scar (arrow) are more evident on portal venous phase as portions of the tumor wash out in comparison to the background liver

Figure 12. Thirty-eight-year-old male with hepatitis B and peripheral cholangiocarcinoma. (A) Mass is hypervascular (arrow) on arterial-phase CT. (B) On portal-venous phase, lesion is hyperdense (arrow) but slightly less dense than blood pool. (C) On delayed-phase images, lesion (arrow) is hyperdense compared to adjacent liver but not as dense as blood pool of aorta.

Figure 13. Peripheral cholangiocarcinoma in 44-year-old male. (A) Arterial-phase image shows mild rim hyperenhancement (arrow). (B) Mass is hypodense on portal-venous phase. (C) Area of increased density (arrow) on delayed-phase image; biliary ductal dilatation is also evident.

Figure 14. Hereditary hemorrhagic telangiectasia with large vascular malformation in liver (arrow), which led to heart failure.

Figure 15. Small hemangioma. (A) Lesion (arrow) brightly enhances similar to blood pool on arterial-phase image; associated small transient hepatic attenuation differences seen peripheral to lesion. (B) Enhancement of lesion (arrow) persists on delayed phase, similar to aorta

Figure 16. Forty-nine-year-old female with hemangioma. (A) Early postcontrast MRI shows peripheral nodular enhancement (arrow). (B) Two minutes delayed image shows progressive peripheral enhancement (arrow). (C) Four minutes delayed image shows further progressive enhancement (arrow) similar in intensity to blood pool. (D) Lesion is light-bulb bright on T2-weighted image, with hyperintense central scar. (E) Lesion is dark (arrow) on in-phase T1weighted image. (F) Out-of-phase T1-weighted image shows fatty background liver with signal dropout; lesion (arrow) does not change in signal intensity.

Figure 17. Hepatic angiosarcoma. (A) Arterial-phase images show irregular bizarrely shaped areas of enhancement (arrows) in liver. (B) Irregular areas of enhancement in liver (arrows) appear to fill in on portal-venous phase.

Figure 18. Twenty-three-year-old male post bone marrow transplant with hepatic peliosis. Periphery of lesion (arrow) is hypervascular in continuous ring, forming target sign.

Figure 19. Glomus tumor of liver. (A) Arterial phase shows hypervascular peripheral nodule (arrow) and hypervascular rim. (B) Portal-venous phase image with nodule (arrow) still avidly enhancing, similar to aorta. (C) Delayed-phase image with nodule (arrow) again similar to blood pool

Figure 20. Inflammatory pseudotumor in liver. (A) Hyperdense tumor rim (arrow) on arterial phase. (B) Portions of tumor washout on portal-venous phase (arrow). (C) Lesion continues to appear hypodense on delayed phase with rim of hyperdense adjacent liver (arrow).

Figure 21. Seventy-six-year-old male with metastatic carcinoid. (A) Partially calcified spiculated mesenteric mass (arrow) with desmoplastic reaction. (B) Hypervascular liver metastases (arrow) enhance brightly on arterial-phase images. (C) Hyperdense capsule (arrow) on portal-venous phase with washout of the hepatic mass. (D) Lesion washes out (arrow) on delayed-phase image

Figure 22. Forty-seven-year-old male with metastatic neuroendocrine tumor. (A) Metastatic lesions most evident when hypervascular on arterial-phase images. Some lesions associated with adjacent transient hepatic attenuation differences; some have central area of low attenuation, likely reflecting necrosis. On portal venous (B) and delayed images (C), lesions are less conspicuous.

Figure 23. Unusual case of breast cancer metastases to liver with hyperdense/hypervascular appearance. (A) Arterialphase images show numerous metastatic lesions with variable enhancement, although majority are hypervascular. (B) Many lesions remain hyperdense on portal-venous phase at same level. (C) Some lesions have become isodense, while other lesions remain hyperdense on delayed phase.