Wo-Hypervascular Liver Lesions

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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, foc

nodular hyperplasia and adenoma are typically hypervascular. In addition, some regenerative nodules

cirrhosis may be hypervascular. Malignant hypervascular primary hepatocellular lesions include hepatocellulacarcinoma, fibrolamellar carcinoma, and peripheral cholangiocarcinoma. Vascular liver lesions often appea

hypervascular because they tend to follow the enhancement of the blood pool; these include hemangioma

arteriovenous malformations, angiosarcomas, and peliosis. While most gastrointestinal malignancies th

metastasize to the liver will appear hypovascular on arterial and portal-venous phase imaging, certain cancesuch as metastatic neuroendocrine tumors (including pancreatic neuroendocrine tumors, carcinoid, an

gastrointestinal stromal tumors) tend to produce hypervascular metastases due to the greater recruitment oarterial blood supply. Finally, rare hepatic lesions such as glomus tumor and inflammatory pseudotumor mahave a hypervascular appearance.
http://dx.doi.org/10.1053/j.sult.2009.06.001http://www.sciencedirect.com/science/help/doi.htmhttp://www.sciencedirect.com/science/help/doi.htmhttp://www.sciencedirect.com/science/article/pii/S0887217109000547http://dx.doi.org/10.1053/j.sult.2009.06.001http://www.sciencedirect.com/science/help/doi.htmhttp://www.sciencedirect.com/science/article/pii/S0887217109000547


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Figure 1. Focal nodular hyperplasia. (A) Grayscale sonogram of large FNH in caudate lobe of liver (demarcate

by calipers) is isoechoic to rest of liver. No internal portal triads seen in mass. (B) Power Doppler sonogram osame liver mass demonstrates spokewheel vascularity (arrows). (C) Same mass on arterial-phase CT

homogeneously hypervascular (arrow). (D) On portal-venous phase CT, mass (arrow) is isodense to remaind

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 arteria

phase with hypodense central scar (arrow). (B) Lesion is isodense on portal-venous phase.


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

CT.

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

phase images (C).


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

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


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

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

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

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


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

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

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


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

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

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


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Figure 16. Forty-nine-year-old female with hemangioma. (A) Early postcontrast MRI shows peripheral nodulenhancement (arrow). (B) Two minutes delayed image shows progressive peripheral enhancement (arrow). (C) Fouminutes delayed image shows further progressive enhancement (arrow) similar in intensity to blood pool. (D) Lesion 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 (arrowdoes not change in signal intensity.

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


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

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

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

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


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

Figure 23. Unusual case of breast cancer metastases to liver with hyperdense/hypervascular appearance. (A) Arteriaphase images show numerous metastatic lesions with variable enhancement, although majority are hypervascular. (

Many lesions remain hyperdense on portal-venous phase at same level. (C) Some lesions have become isodense, whiother lesions remain hyperdense on delayed phase.

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Wo-Hypervascular Liver Lesions