Benign Tumors Of The Liver
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BENIGN TUMORS OF THE LIVER MARIA THERESA M. NAVARRO, MD 4th Year Radiology Resident Department of Medical Imaging Quirino Memorial Medical Center
Hepatic Hemangioma s
HEPATIC HEMANGIOMAS
CAVERNOUS HEMANGIOMA – most common benign neoplasm of the liver second most common hepatic tumor, exceeded only by metastases affects all age groups women > men within the right lobe of the liver few millimeters to greater than 20 cm diameter
HEPATIC HEMANGIOMAS
mesodermal in origin histologically : blood-filled cavernous vascular spaces of variable size and shape lined single layer of flat endothelium stable lesions, rarely increase or decrease in size
IMAGING FEATURES OF CAVERNOUS HEMANGIOMAS
PLAIN FILMS mostly,
too small to be identified on plain films of the abdomen very large lesions, nonspecific findings : hepatomegaly or a large upper abdominal mass
IMAGING FEATURES OF CAVERNOUS HEMANGIOMAS
CHARACTERISTIC (but rarely seen) presence
of multiple calcified phleboliths numerous calcified “trabeculations and spicules” that arise from a central point and radiate out toward the periphery of the lesion
IMAGING FEATURES OF CAVERNOUS HEMANGIOMAS
ULTRASOUND well-circumscribed,
homogenous, densely echogenic masses with posterior acoustic enhancement differential diagnosis: hepatocellular ca metastatic disease hepatic adenoma focal nodular hyperplasia
IMAGING FEATURES OF CAVERNOUS HEMANGIOMAS
ULTRASOUND demonstrate
varying internal complexity, depending on the degree of thrombosis, fibrosis, hemorrhagic necrosis, or calcification sonographic heterogeneity – more common in larger lesions. hyperechoic pattern (67% to 70%) – presence of multiple vascular interfaces between the walls of the cavernous sinuses and the blood within them
IMAGING FEATURES OF CAVERNOUS HEMANGIOMAS
COMPUTED TOMOGRAPHY CT
diagnosis is based on the understanding of the neoplasm’s vascular hemodynamics blood typically circulates slowly within the the dilated cavernous spaces of this tumor and tends to flow from peripherally located sinusoids toward those at the lesion center.
IMAGING FEATURES OF CAVERNOUS HEMANGIOMAS
COMPUTED TOMOGRAPHY
series of noncontrast-enhanced CT scans to localize suspected hemangioma rapid-sequence, single-level dynamic CT scan are obtained to the largest segment of the lesion during an IV bolus injection of 150 ml of 60% contrast agent (42g of iodine) sequential delayed scans acquired for up to 30 minutes after injection or until lesion is isodense with normal hepatic parenchyma so that the lesion’s contrast enhancement profile can be evaluated.
IMAGING FEATURES OF CAVERNOUS HEMANGIOMAS
DYNAMIC PHASE OF BOLUS CONTRAST INJECTION
show peripheral enhancement at the margins of the hemangioma initial enhancement need not encircle the entire lesion but may appear as : well defined focal regions of intense nodular enhancement at or near the lesion periphery during the arterial phase of hepatic enhancement (10 to 30 seconds after bolus initiation) - mural nodules represent as feeding vascular nidus
IMAGING FEATURES OF CAVERNOUS HEMANGIOMAS
DYNAMIC PHASE OF BOLUS CONTRAST INJECTION centripetal
pattern of hemangioma with fill-in occuring from the periphery toward the lesion center the most intense enhancement is seen early and involves those vascular spaces that received the iodinated contrast first the degree of lesion enhancement then gradually decreases as the concentration of iodine in the bloodstream falls
(Left) Axial NECT shows large mass in lateral segment, most of which is isodense to blood except for hypodense foci of scar. (Right) Axial CECTin venous parenchymal phase shows cloud-like peripheral enhancement that is isodense to vessels
(Left) Sagittal sonogram shows uniformly hyperechoic lesion in peripheral right lobe. (Right) Axial CECT in venous phase shows typical large hemangioma with nodular peripheral enhancement and nonenhancing scar (arrow). Capillary hemangioma (curved arrow) isodense to vessels in all phases.
“Even though CT is highly accurate in the diagnosis of hemangiomas, it does not consistently yield characteristic enhancement patterns, thus limiting is clinical usefulness.”
IMAGING FEATURES OF CAVERNOUS HEMANGIOMAS
MAGNETIC RESONANCE IMAGING Most
sensitive modality for detecting hepatic cavernous hemangioma high signal characterics similar to those of fluids Hypointense on T1 images and significantly hyperintense on T2 images Retain their marked signal intensity on heavily T2-weighted multiecho images (“light bulb sign”)
IMAGING FEATURES OF CAVERNOUS HEMANGIOMAS
MAGNETIC RESONANCE IMAGING Well-circumscribed,
smoothly marginated lesions and appear spheroid, ovoid, or lobulated Low-signal-intensity clefts and septation – larger hemangiomas and correspond to hypodense regions on dynamic bolus CT studies
IMAGING FEATURES OF CAVERNOUS HEMANGIOMAS
MAGNETIC RESONANCE IMAGING HEMANGIOMAS
METASTASES
Homogenous hyperintense pattern
Heterogenous amorphous appearance
Well-circumscribed
Ringed morphology
Smoothly marginated
Indistinct margination Surrounding peritumoral edema
IMAGING FEATURES OF CAVERNOUS HEMANGIOMAS
RED BLOOD CELL SCINTIGRAPHY typically display a “hot spot” appearance on delayed labeled-RBC scans, reflecting the circulatory characteristics of these neoplasms
IMAGING FEATURES OF CAVERNOUS HEMANGIOMAS
ANGIOGRAPHY Has long been considered gold standard in the diagnosis of hepatic hemagioma Classic Finding : normal main and feeding hepatic artery early contrast accumulation within the lesion during the late arterial phase Prolonged, delayed stain that persists throughout the capillary phase and well into the late venous phase
IMAGING FEATURES OF CAVERNOUS HEMANGIOMAS
ANGIOGRAPHY Atypical angiographic features: Hypovascular
mass Or a dense, homogeneous hypervascular mass Arterial-portal venous shunting
Identification of a persistent pool of contrast puddling within such lesions may be the only means of diagnosing these complicated hemangiomas short of performing a biopsy or surgical resection
APPROACH TO IMAGING OF SUSPECTED HEMANGIOMAS
(Modification scheme by Freeny) GROUP I Patients who have well-circumscribed, homogeneous, hyperechoic lesions No clinical symptoms referable to the liver Normal liver function results No known primary neoplasm Patients who have lesions with atypical sonographic patterns Abnormal clinical findings Known primary neoplasm
Group I Patients
Labeled-RBC scintigraphy with SPECT tomographic imaging is the preferred procedure of definitive lesion characterization due to its relative low cost and near 100% specificity and positive predictive value. (1.5 cm to 2.0 cm lesions)
Group I Patients
Magnetic Resonance Imaging reserved for lesions smaller than1.5 to 2.0 cm lesions 2.5 cm or smaller located adjacent to the heart or major intrahepatic vessels Both modalities – useful in patients with multiple suspected hemangiomas
Group I Patients
MRI is not advocated if the patient has a known primary hypervascular endocrine neoplasm If these studies yield undeterminate findings for hemangioma
angiography or percutaneous needle
APPROACH TO IMAGING OF SUSPECTED HEMANGIOMAS
(Modification scheme by Freeny) GROUP II Patients who have focal hepatic lesions detected on routine dynamic-incremental bolus CT studies
HEMANGIOM A
Peripheral contrast enhancemen t
Delayed Images Show Isodense Fill-
APPROACH TO IMAGING OF SUSPECTED HEMANGIOMAS
GROUP II
ATYPICAL CT FEATURES ADDITIONAL IMAGING WITH LABELED-RBC SPECT
KNOWN PRIMARY TUMOR
ABNORMAL LIVER FINDINGS
MRI using the size and specific criteria already outlined
APPROACH TO IMAGING OF SUSPECTED HEMANGIOMAS
GROUP III
Whose hepatic lesions are first detected on MRI
MRI APPEARANCE IS CLASSIC NO KNOWN PRIMARY NEOPLAS
HEMANGIOM A
APPROACH TO IMAGING OF SUSPECTED HEMANGIOMAS
GROUP III ATYPICAL MRI APPEARANCE KNOWN PRIMARY NEOPLASM (hypervascular endocrine tumor) ADDITIONAL SPECT CTAngiography or IMAGING WITH FINDINGS Percutaneous LABELED-RBC NEGATIVENeedle Biopsy SPECT LESIONS TOO SMALL
APPROACH TO IMAGING OF SUSPECTED HEMANGIOMAS
Lesions less than 1 cm are difficult to consistently characterize using any noninvasive modality Follow-up ultrasound or MRI at 6 unchanged inmonthschanged in size size and and morphology morphology no further evaluation
percutaneous biopsy
Hepatocellular Adenoma, Focal Nodular Hyperplasia, and Others
Hepatocellular Adenoma,
Uncommon solid primary liver tumor Related to the use of oral contraceptives in women and anabolic steroids in men Pathology : large (usually > 10 cm) solitary lesions with a thin tumor capsule
maybe rich in fat or glycogen
Ultrasound : well-delineated heterogenous but primarily echogenic hepatic mass
Hyperechogenicity – attributed to the presence of intratumoral fat and glycogen
Hepatocellular Adenoma,
Non-contrast-enhanced CT Predominantly isodense with liver but may appear either uniformly hypodense due to extensive steatosis Or heterogeneous with foci of hypodensity caused by tumor necrosis and areas of hyperdensity secondary to recent intratumoral hemorrhage
Hepatocellular Adenoma,
Distinctive perfusion characteristic of HA arterial phase of contrast infusion (15 to 25 seconds after bolus injection of contrast media) - consists of dense enhancement maybe homogenous in small tumors or heterogeneous in a larger mass The lesion become hyperdense relative to normal liver, which has enhanced minimally at this time.
Hepatocellular Adenoma,
portal venous phase (45 to 180 seconds after the injection of contrast media)
tumoral enhancement diminishes rapidly and the tumors become isodense to normal liver during the
Radionuclide Scintigraphy Most HAs are devoid of Kupffer cells, they appear cold on sulfur colloid scintigraphy Show uptake of the tracer Because of the lack of bile ductules, the tracer is not excreted, and delayed scans therefore depict HAs as areas of markedly increased
Hepatocellular Adenoma,
Hepatocellular Adenoma,
Magnetic Resonance Imaging Mimic malignant liver tumors, with the non-necrotic, nonhemorrhagic solid component showing Hypointense appearance on T1 images and slight hyperintense on T2 images However, the high fat or glycogen content, or both, of these tumors can render them isointense or even hyperintense on T1 images Hypointense tumor capsule best seen on T1 images Intratumoral bleeding – hyperintense on T1 images and hypointense on T2 images
(Left) Axial T1WI MR shows hypointense encapsulated mass with hyperintense foci (hemorrhage or fat). (Right) Axial T2WI MR shows mass nearly isointense to liver with central focus of hyperintensity (hemorrhage).
Hepatocellular Adenoma,
Angiograms Hypervascular tumors with large peripheral vessels Centripetal flow Usually there is no arteriovenous shunting or vascular invasion, as is often seen in hepatocellular carcinoma No specific diagnostic specificity can be gained
Hepatocellular Adenoma,
CONCLUSION Hypervascular tumors with large peripheral vessels Centripetal flow Usually there is no arteriovenous shunting or vascular invasion, as is often seen in hepatocellular carcinoma No specific diagnostic specificity can be gained
FOCAL NODULAR HYPERPLASIA
Clinical Background most common solid benign tumor of the liver usually found incidentally etiology unknown, but postulated that a congenital vascular malformation may trigger the development of hepatocyte hyperplasia hormonal influence more common in women on their 3rd to 5th decades controversy regarding its association with the use of oral contraceptives
FOCAL NODULAR HYPERPLASIA
Pathology well-circumscribed, usually solitary mass, no capsule with centrally located scar tissue surrounded by nodules of hyperplastic hepatocytes nodules divided by thin septae that radiate from the central scar, when there is one no normal portal venous structures usually located at the liver surface bulge in the liver contour or pedunculated mass 1 cm to > 15 cm hemorrhage, necrosis, and calcification are rare
FOCAL NODULAR HYPERPLASIA
Radiology
Diagnostic : presence of hepatocellular reticuloendothelial function in liver tumors that possess a cental scar containing vessels and bile ducts
FOCAL NODULAR HYPERPLASIA
Ultrasound as much as 2/3 appear homogenous and isoechoic to normal liver and may be visible only because of the mass effect they exert on adjacent hepatic vessels some cases, FNH appear as inhomogenous mass central scar maybe detected as hyperechoic area but often cannot be differentiated from other hypoechoic or isoechoic areas
FOCAL NODULAR HYPERPLASIA
Color-coded Doppler Ultrasound the hypervascular nature of FNH take on the appearance of numerous scattered arterial and venous Doppler signals exhibiting a “comet tail” appearance throughout the tumor
FOCAL NODULAR HYPERPLASIA
Computed Tomography with the exception of a central scar, the appearance of FNH on CT scans is usually indistinguishable from that of HA generally isodense to normal liver on noncontrast-enhanced CT studies can be identified only if they deform the liver contours or possess a prominent stellateshaped central scar
FOCAL NODULAR HYPERPLASIA
Dynamic CT scan arterial phase (approximately the first 30 seconds) - rapid enhancement, appearing hyperdense relative to liver portal phase – steady decrease in attenuation, so they appear relatively isodense or hypodense to uninvolved liver tissue delayed CT scan – vascular scar tissue appear hyperdense perfusion profile also seen in both hepatocellular carcinoma and adenoma
(Left) Axial CECTin arterial phase shows intense homogeneous enhancement of mass with central scar with thin radiating septa. Typical FNH appearance resembles cross section of an orange. (Right) Axial CECT in venous phase shows mass (arrow) isodense to liver with delayed enhancement of central scar.
FOCAL NODULAR HYPERPLASIA
Nuclear Scintigraphy technetium sulfur colloid scans, which portray reticuloendothelial cellular function, the uptake of tracer is normal approximately 50% of FNHs and uptake is increased in approximately 10% as many of 40% of the FNHs do not possess reticuloendothelial cellular function, the presence of a “cold lesion” does not exclude the possibility of FNH.
FOCAL NODULAR HYPERPLASIA
MRI Scan suggested if the liver tumor appears isointense on both T1 and T2 images and has a central scar some cases, detected only by their mass effect on normal hepatic vasculature plus the presence of central scar (hypointense on T1 and hyperintense on T2 images) uncommonly FNH may mimic other solid tumors by being hypointense on T1 and hyperintense on T2 images.
(Left) Axial T1 C+ MR in arterial phase shows intense homogeneous enhancement of mass with central hypointense scar. (Right) Axial T2WI MR shows mass is minimally hyperintense, scar (arrow) is hyperintense.
FOCAL NODULAR HYPERPLASIA
Hepatic scars are also not specific for FNH
“Thus differentiation of FNH from other malignant or benign (solid) tumors is frequently not possible with MRI”
FOCAL NODULAR HYPERPLASIA
Dynamic T1 MRI studies arterial phase (first 30 seconds) – dense enhancement 60 seconds after injection – rapid washout of the agent leading to isointensity of the FNH to normal liver similar tumoral enhancement in differentiated hepatocellular carcinoma
FOCAL NODULAR HYPERPLASIA
Angiography seldom performed for the tissue characterization of focal liver tumors hypervascular mass possessing a centrifugal or “spoke wheel” pattern of vascular supply
MACROREGENERATIVE NODULE AND NODULE REGENERATIVE HYPERPLASIA
Clinical Background MACROREGENERATIVE NODULE (MRN) 10%-14% of the patients with chronic liver disease, such as advanced cirrhosis Severe hepatic injury such as aftermath of massive hepatic necrosis
MACROREGENERATIVE NODULE AND NODULE REGENERATIVE HYPERPLASIA
Clinical Background NODULAR REGENERATIVE HYPERPLASIA (NRH) much rarer condition arises without any hepatic injury or fibrosis but is associated with a variety of systemic diseases such as rheumatoid arthritis and polyarteritis nodosa.
MACROREGENERATIVE NODULE (MRNs)
Pathology Well-circumscribed nodules composed of hepatocytes that are arranged in normal cords and contain portal areas Fibrosis is absent or slight Multiple 1 to 6 cm in diameter Necrosis and hemorrhage (rare)
NODULAR REGENERATIVE HYPERPLASIA (NRH)
Pathology Not known May stem from occlusion of the intrahepatic branches of the portal vein Few millimeter to 1 cm Scattered diffusely throughout the liver
MACROREGENERATIVE NODULE AND NODULE REGENERATIVE HYPERPLASIA
Cross sectional imaging – difficult because of the small size of NRH altered gross hepatic morphology that accompanies cirrhosis and MRNs alteration in the echogenicity and MR signal intensity of uninvolved hepatic tissue can interfere with lesion detection No specific features on UTZ and CT, except for round liver lesions up to several centimeters in diameter in the setting of MRNs
MACROREGENERATIVE NODULE AND NODULE REGENERATIVE HYPERPLASIA
however on T2 MR images, MRNs may appear as low-signal-intensity nodules
(Left) Axial CECT shows dysmorphic liver with collateral blood vessels on the surface of the liver. Hypervascular lesion with hypodense ring (arrow) represents a focus of nodular regenerative hyperplasia (Right) Axial CECTshows dysmorphic liver; intra and extrahepatic collaterals bypassing occluded portal vein.
(Left) Axial T7 C+ MR shows numerous 2 cm hyperintense lesions in a patient with Budd-Chiari syndrome. (Right) Axial T2WI MR demonstrates inconspicuous hypointense foci of nodular regenerative hyperplasia (arrow) in the right hepatic lobe.
HEPATIC CYSTS
Clinical Background and Pathology
maybe classified as: Developmental Infectious Traumatic
arise from the bile duct epithelium (cholangiocellular) unilocular solitary or multiple
HEPATIC CYSTS
Clinical Background and Pathology
Cyst wall – 1mm or less in thickness lined
by a simple layer of cuboidal epithelium less commonly by squamous or columnar epithelium
adjacent liver tissue is normal and free of fibrosis or inflammation 5 to 14% of the population slightly more prevalent in women
HEPATIC CYSTS
Ultrasound
anechoic posterior wall is well seen enhanced through transmission
HEPATIC CYSTS
Computed Tomography
thin-walled sharply marginated lesions water density ( 0 + 15 HU) non-enhancing versus HYDATID CYSTS possess septations, mural calcifications and daughter cysts within the parent cyst
HYDATID CYST
HEPATIC CYSTS
Magnetic Resonance Imaging
long T1 and T2 relaxation hypointense on T1 and markedly hyperintense on T2 homogenous, sharply marginated signal intensity is indistinguishable from hepatic hemangioma comparable to signal intensity of bile and CSF
POLYCYSTIC LIVER DISEASE
Clinical Background and Pathology
numerous simple hepatic cysts adjacent liver tissue contains fibrotic areas (von Meyenberg complexes)
POLYCYSTIC LIVER DISEASE
Radiology
multiple cysts of variable size and different internal composition often in combination with PKD appearance of the cysts on ultrasound, CT, and MRI studies can vary broadly as a consequence of multiple episodes of intracystic hemorrhage comparable to the cysts of PKD
MESENCHYMAL TUMORS AND HETEROTOPIC RESTS
Clinical Background and Pathology Hemangioma – most common prevalence of remaining mesenchymal benign liver tumor is low no unique radiographic features exception are tumors that contain fat
lipomas, angiomyolipomas, myelolipomas
no malignant potential
MESENCHYMAL TUMORS AND HETEROTOPIC RESTS
Ultrasound fat-containing tumors are echogenic posterior acoustic enhancement in homogenous appearing tumors (specifically lipomas) Computed Tomography low density = > 20 HU pure lipomas show no enhancement partial and inhomogenous contrast enhancement should suggest angiomatous (angiomyolipoma) or myeloid (myelolipoma)
MESENCHYMAL TUMORS AND HETEROTOPIC RESTS
combined use of ultrasound and CT may permit the diagnosis and exclude other lipomatous tumors of the liver Magnetic Resonance Imaging fat-containing tumors high signal intensity on T1 and T2 images comparable to the subcutaneous or retroperitoneal fat
HEPATIC HEMANGIOMA
FOCAL NODULAR HYPERPLASIA
FOCAL NODULAR HYPERPLASIA
Hepatic Hemangioma s
HEPATIC HEMANGIOMAS
CAVERNOUS HEMANGIOMA – most common benign neoplasm of the liver second most common hepatic tumor, exceeded only by metastases affects all age groups women > men within the right lobe of the liver few millimeters to greater than 20 cm diameter
HEPATIC HEMANGIOMAS
mesodermal in origin histologically : blood-filled cavernous vascular spaces of variable size and shape lined single layer of flat endothelium stable lesions, rarely increase or decrease in size
IMAGING FEATURES OF CAVERNOUS HEMANGIOMAS
PLAIN FILMS mostly,
too small to be identified on plain films of the abdomen very large lesions, nonspecific findings : hepatomegaly or a large upper abdominal mass
IMAGING FEATURES OF CAVERNOUS HEMANGIOMAS
CHARACTERISTIC (but rarely seen) presence
of multiple calcified phleboliths numerous calcified “trabeculations and spicules” that arise from a central point and radiate out toward the periphery of the lesion
IMAGING FEATURES OF CAVERNOUS HEMANGIOMAS
ULTRASOUND well-circumscribed,
homogenous, densely echogenic masses with posterior acoustic enhancement differential diagnosis: hepatocellular ca metastatic disease hepatic adenoma focal nodular hyperplasia
IMAGING FEATURES OF CAVERNOUS HEMANGIOMAS
ULTRASOUND demonstrate
varying internal complexity, depending on the degree of thrombosis, fibrosis, hemorrhagic necrosis, or calcification sonographic heterogeneity – more common in larger lesions. hyperechoic pattern (67% to 70%) – presence of multiple vascular interfaces between the walls of the cavernous sinuses and the blood within them
IMAGING FEATURES OF CAVERNOUS HEMANGIOMAS
COMPUTED TOMOGRAPHY CT
diagnosis is based on the understanding of the neoplasm’s vascular hemodynamics blood typically circulates slowly within the the dilated cavernous spaces of this tumor and tends to flow from peripherally located sinusoids toward those at the lesion center.
IMAGING FEATURES OF CAVERNOUS HEMANGIOMAS
COMPUTED TOMOGRAPHY
series of noncontrast-enhanced CT scans to localize suspected hemangioma rapid-sequence, single-level dynamic CT scan are obtained to the largest segment of the lesion during an IV bolus injection of 150 ml of 60% contrast agent (42g of iodine) sequential delayed scans acquired for up to 30 minutes after injection or until lesion is isodense with normal hepatic parenchyma so that the lesion’s contrast enhancement profile can be evaluated.
IMAGING FEATURES OF CAVERNOUS HEMANGIOMAS
DYNAMIC PHASE OF BOLUS CONTRAST INJECTION
show peripheral enhancement at the margins of the hemangioma initial enhancement need not encircle the entire lesion but may appear as : well defined focal regions of intense nodular enhancement at or near the lesion periphery during the arterial phase of hepatic enhancement (10 to 30 seconds after bolus initiation) - mural nodules represent as feeding vascular nidus
IMAGING FEATURES OF CAVERNOUS HEMANGIOMAS
DYNAMIC PHASE OF BOLUS CONTRAST INJECTION centripetal
pattern of hemangioma with fill-in occuring from the periphery toward the lesion center the most intense enhancement is seen early and involves those vascular spaces that received the iodinated contrast first the degree of lesion enhancement then gradually decreases as the concentration of iodine in the bloodstream falls
(Left) Axial NECT shows large mass in lateral segment, most of which is isodense to blood except for hypodense foci of scar. (Right) Axial CECTin venous parenchymal phase shows cloud-like peripheral enhancement that is isodense to vessels
(Left) Sagittal sonogram shows uniformly hyperechoic lesion in peripheral right lobe. (Right) Axial CECT in venous phase shows typical large hemangioma with nodular peripheral enhancement and nonenhancing scar (arrow). Capillary hemangioma (curved arrow) isodense to vessels in all phases.
“Even though CT is highly accurate in the diagnosis of hemangiomas, it does not consistently yield characteristic enhancement patterns, thus limiting is clinical usefulness.”
IMAGING FEATURES OF CAVERNOUS HEMANGIOMAS
MAGNETIC RESONANCE IMAGING Most
sensitive modality for detecting hepatic cavernous hemangioma high signal characterics similar to those of fluids Hypointense on T1 images and significantly hyperintense on T2 images Retain their marked signal intensity on heavily T2-weighted multiecho images (“light bulb sign”)
IMAGING FEATURES OF CAVERNOUS HEMANGIOMAS
MAGNETIC RESONANCE IMAGING Well-circumscribed,
smoothly marginated lesions and appear spheroid, ovoid, or lobulated Low-signal-intensity clefts and septation – larger hemangiomas and correspond to hypodense regions on dynamic bolus CT studies
IMAGING FEATURES OF CAVERNOUS HEMANGIOMAS
MAGNETIC RESONANCE IMAGING HEMANGIOMAS
METASTASES
Homogenous hyperintense pattern
Heterogenous amorphous appearance
Well-circumscribed
Ringed morphology
Smoothly marginated
Indistinct margination Surrounding peritumoral edema
IMAGING FEATURES OF CAVERNOUS HEMANGIOMAS
RED BLOOD CELL SCINTIGRAPHY typically display a “hot spot” appearance on delayed labeled-RBC scans, reflecting the circulatory characteristics of these neoplasms
IMAGING FEATURES OF CAVERNOUS HEMANGIOMAS
ANGIOGRAPHY Has long been considered gold standard in the diagnosis of hepatic hemagioma Classic Finding : normal main and feeding hepatic artery early contrast accumulation within the lesion during the late arterial phase Prolonged, delayed stain that persists throughout the capillary phase and well into the late venous phase
IMAGING FEATURES OF CAVERNOUS HEMANGIOMAS
ANGIOGRAPHY Atypical angiographic features: Hypovascular
mass Or a dense, homogeneous hypervascular mass Arterial-portal venous shunting
Identification of a persistent pool of contrast puddling within such lesions may be the only means of diagnosing these complicated hemangiomas short of performing a biopsy or surgical resection
APPROACH TO IMAGING OF SUSPECTED HEMANGIOMAS
(Modification scheme by Freeny) GROUP I Patients who have well-circumscribed, homogeneous, hyperechoic lesions No clinical symptoms referable to the liver Normal liver function results No known primary neoplasm Patients who have lesions with atypical sonographic patterns Abnormal clinical findings Known primary neoplasm
Group I Patients
Labeled-RBC scintigraphy with SPECT tomographic imaging is the preferred procedure of definitive lesion characterization due to its relative low cost and near 100% specificity and positive predictive value. (1.5 cm to 2.0 cm lesions)
Group I Patients
Magnetic Resonance Imaging reserved for lesions smaller than1.5 to 2.0 cm lesions 2.5 cm or smaller located adjacent to the heart or major intrahepatic vessels Both modalities – useful in patients with multiple suspected hemangiomas
Group I Patients
MRI is not advocated if the patient has a known primary hypervascular endocrine neoplasm If these studies yield undeterminate findings for hemangioma
angiography or percutaneous needle
APPROACH TO IMAGING OF SUSPECTED HEMANGIOMAS
(Modification scheme by Freeny) GROUP II Patients who have focal hepatic lesions detected on routine dynamic-incremental bolus CT studies
HEMANGIOM A
Peripheral contrast enhancemen t
Delayed Images Show Isodense Fill-
APPROACH TO IMAGING OF SUSPECTED HEMANGIOMAS
GROUP II
ATYPICAL CT FEATURES ADDITIONAL IMAGING WITH LABELED-RBC SPECT
KNOWN PRIMARY TUMOR
ABNORMAL LIVER FINDINGS
MRI using the size and specific criteria already outlined
APPROACH TO IMAGING OF SUSPECTED HEMANGIOMAS
GROUP III
Whose hepatic lesions are first detected on MRI
MRI APPEARANCE IS CLASSIC NO KNOWN PRIMARY NEOPLAS
HEMANGIOM A
APPROACH TO IMAGING OF SUSPECTED HEMANGIOMAS
GROUP III ATYPICAL MRI APPEARANCE KNOWN PRIMARY NEOPLASM (hypervascular endocrine tumor) ADDITIONAL SPECT CTAngiography or IMAGING WITH FINDINGS Percutaneous LABELED-RBC NEGATIVENeedle Biopsy SPECT LESIONS TOO SMALL
APPROACH TO IMAGING OF SUSPECTED HEMANGIOMAS
Lesions less than 1 cm are difficult to consistently characterize using any noninvasive modality Follow-up ultrasound or MRI at 6 unchanged inmonthschanged in size size and and morphology morphology no further evaluation
percutaneous biopsy
Hepatocellular Adenoma, Focal Nodular Hyperplasia, and Others
Hepatocellular Adenoma,
Uncommon solid primary liver tumor Related to the use of oral contraceptives in women and anabolic steroids in men Pathology : large (usually > 10 cm) solitary lesions with a thin tumor capsule
maybe rich in fat or glycogen
Ultrasound : well-delineated heterogenous but primarily echogenic hepatic mass
Hyperechogenicity – attributed to the presence of intratumoral fat and glycogen
Hepatocellular Adenoma,
Non-contrast-enhanced CT Predominantly isodense with liver but may appear either uniformly hypodense due to extensive steatosis Or heterogeneous with foci of hypodensity caused by tumor necrosis and areas of hyperdensity secondary to recent intratumoral hemorrhage
Hepatocellular Adenoma,
Distinctive perfusion characteristic of HA arterial phase of contrast infusion (15 to 25 seconds after bolus injection of contrast media) - consists of dense enhancement maybe homogenous in small tumors or heterogeneous in a larger mass The lesion become hyperdense relative to normal liver, which has enhanced minimally at this time.
Hepatocellular Adenoma,
portal venous phase (45 to 180 seconds after the injection of contrast media)
tumoral enhancement diminishes rapidly and the tumors become isodense to normal liver during the
Radionuclide Scintigraphy Most HAs are devoid of Kupffer cells, they appear cold on sulfur colloid scintigraphy Show uptake of the tracer Because of the lack of bile ductules, the tracer is not excreted, and delayed scans therefore depict HAs as areas of markedly increased
Hepatocellular Adenoma,
Hepatocellular Adenoma,
Magnetic Resonance Imaging Mimic malignant liver tumors, with the non-necrotic, nonhemorrhagic solid component showing Hypointense appearance on T1 images and slight hyperintense on T2 images However, the high fat or glycogen content, or both, of these tumors can render them isointense or even hyperintense on T1 images Hypointense tumor capsule best seen on T1 images Intratumoral bleeding – hyperintense on T1 images and hypointense on T2 images
(Left) Axial T1WI MR shows hypointense encapsulated mass with hyperintense foci (hemorrhage or fat). (Right) Axial T2WI MR shows mass nearly isointense to liver with central focus of hyperintensity (hemorrhage).
Hepatocellular Adenoma,
Angiograms Hypervascular tumors with large peripheral vessels Centripetal flow Usually there is no arteriovenous shunting or vascular invasion, as is often seen in hepatocellular carcinoma No specific diagnostic specificity can be gained
Hepatocellular Adenoma,
CONCLUSION Hypervascular tumors with large peripheral vessels Centripetal flow Usually there is no arteriovenous shunting or vascular invasion, as is often seen in hepatocellular carcinoma No specific diagnostic specificity can be gained
FOCAL NODULAR HYPERPLASIA
Clinical Background most common solid benign tumor of the liver usually found incidentally etiology unknown, but postulated that a congenital vascular malformation may trigger the development of hepatocyte hyperplasia hormonal influence more common in women on their 3rd to 5th decades controversy regarding its association with the use of oral contraceptives
FOCAL NODULAR HYPERPLASIA
Pathology well-circumscribed, usually solitary mass, no capsule with centrally located scar tissue surrounded by nodules of hyperplastic hepatocytes nodules divided by thin septae that radiate from the central scar, when there is one no normal portal venous structures usually located at the liver surface bulge in the liver contour or pedunculated mass 1 cm to > 15 cm hemorrhage, necrosis, and calcification are rare
FOCAL NODULAR HYPERPLASIA
Radiology
Diagnostic : presence of hepatocellular reticuloendothelial function in liver tumors that possess a cental scar containing vessels and bile ducts
FOCAL NODULAR HYPERPLASIA
Ultrasound as much as 2/3 appear homogenous and isoechoic to normal liver and may be visible only because of the mass effect they exert on adjacent hepatic vessels some cases, FNH appear as inhomogenous mass central scar maybe detected as hyperechoic area but often cannot be differentiated from other hypoechoic or isoechoic areas
FOCAL NODULAR HYPERPLASIA
Color-coded Doppler Ultrasound the hypervascular nature of FNH take on the appearance of numerous scattered arterial and venous Doppler signals exhibiting a “comet tail” appearance throughout the tumor
FOCAL NODULAR HYPERPLASIA
Computed Tomography with the exception of a central scar, the appearance of FNH on CT scans is usually indistinguishable from that of HA generally isodense to normal liver on noncontrast-enhanced CT studies can be identified only if they deform the liver contours or possess a prominent stellateshaped central scar
FOCAL NODULAR HYPERPLASIA
Dynamic CT scan arterial phase (approximately the first 30 seconds) - rapid enhancement, appearing hyperdense relative to liver portal phase – steady decrease in attenuation, so they appear relatively isodense or hypodense to uninvolved liver tissue delayed CT scan – vascular scar tissue appear hyperdense perfusion profile also seen in both hepatocellular carcinoma and adenoma
(Left) Axial CECTin arterial phase shows intense homogeneous enhancement of mass with central scar with thin radiating septa. Typical FNH appearance resembles cross section of an orange. (Right) Axial CECT in venous phase shows mass (arrow) isodense to liver with delayed enhancement of central scar.
FOCAL NODULAR HYPERPLASIA
Nuclear Scintigraphy technetium sulfur colloid scans, which portray reticuloendothelial cellular function, the uptake of tracer is normal approximately 50% of FNHs and uptake is increased in approximately 10% as many of 40% of the FNHs do not possess reticuloendothelial cellular function, the presence of a “cold lesion” does not exclude the possibility of FNH.
FOCAL NODULAR HYPERPLASIA
MRI Scan suggested if the liver tumor appears isointense on both T1 and T2 images and has a central scar some cases, detected only by their mass effect on normal hepatic vasculature plus the presence of central scar (hypointense on T1 and hyperintense on T2 images) uncommonly FNH may mimic other solid tumors by being hypointense on T1 and hyperintense on T2 images.
(Left) Axial T1 C+ MR in arterial phase shows intense homogeneous enhancement of mass with central hypointense scar. (Right) Axial T2WI MR shows mass is minimally hyperintense, scar (arrow) is hyperintense.
FOCAL NODULAR HYPERPLASIA
Hepatic scars are also not specific for FNH
“Thus differentiation of FNH from other malignant or benign (solid) tumors is frequently not possible with MRI”
FOCAL NODULAR HYPERPLASIA
Dynamic T1 MRI studies arterial phase (first 30 seconds) – dense enhancement 60 seconds after injection – rapid washout of the agent leading to isointensity of the FNH to normal liver similar tumoral enhancement in differentiated hepatocellular carcinoma
FOCAL NODULAR HYPERPLASIA
Angiography seldom performed for the tissue characterization of focal liver tumors hypervascular mass possessing a centrifugal or “spoke wheel” pattern of vascular supply
MACROREGENERATIVE NODULE AND NODULE REGENERATIVE HYPERPLASIA
Clinical Background MACROREGENERATIVE NODULE (MRN) 10%-14% of the patients with chronic liver disease, such as advanced cirrhosis Severe hepatic injury such as aftermath of massive hepatic necrosis
MACROREGENERATIVE NODULE AND NODULE REGENERATIVE HYPERPLASIA
Clinical Background NODULAR REGENERATIVE HYPERPLASIA (NRH) much rarer condition arises without any hepatic injury or fibrosis but is associated with a variety of systemic diseases such as rheumatoid arthritis and polyarteritis nodosa.
MACROREGENERATIVE NODULE (MRNs)
Pathology Well-circumscribed nodules composed of hepatocytes that are arranged in normal cords and contain portal areas Fibrosis is absent or slight Multiple 1 to 6 cm in diameter Necrosis and hemorrhage (rare)
NODULAR REGENERATIVE HYPERPLASIA (NRH)
Pathology Not known May stem from occlusion of the intrahepatic branches of the portal vein Few millimeter to 1 cm Scattered diffusely throughout the liver
MACROREGENERATIVE NODULE AND NODULE REGENERATIVE HYPERPLASIA
Cross sectional imaging – difficult because of the small size of NRH altered gross hepatic morphology that accompanies cirrhosis and MRNs alteration in the echogenicity and MR signal intensity of uninvolved hepatic tissue can interfere with lesion detection No specific features on UTZ and CT, except for round liver lesions up to several centimeters in diameter in the setting of MRNs
MACROREGENERATIVE NODULE AND NODULE REGENERATIVE HYPERPLASIA
however on T2 MR images, MRNs may appear as low-signal-intensity nodules
(Left) Axial CECT shows dysmorphic liver with collateral blood vessels on the surface of the liver. Hypervascular lesion with hypodense ring (arrow) represents a focus of nodular regenerative hyperplasia (Right) Axial CECTshows dysmorphic liver; intra and extrahepatic collaterals bypassing occluded portal vein.
(Left) Axial T7 C+ MR shows numerous 2 cm hyperintense lesions in a patient with Budd-Chiari syndrome. (Right) Axial T2WI MR demonstrates inconspicuous hypointense foci of nodular regenerative hyperplasia (arrow) in the right hepatic lobe.
HEPATIC CYSTS
Clinical Background and Pathology
maybe classified as: Developmental Infectious Traumatic
arise from the bile duct epithelium (cholangiocellular) unilocular solitary or multiple
HEPATIC CYSTS
Clinical Background and Pathology
Cyst wall – 1mm or less in thickness lined
by a simple layer of cuboidal epithelium less commonly by squamous or columnar epithelium
adjacent liver tissue is normal and free of fibrosis or inflammation 5 to 14% of the population slightly more prevalent in women
HEPATIC CYSTS
Ultrasound
anechoic posterior wall is well seen enhanced through transmission
HEPATIC CYSTS
Computed Tomography
thin-walled sharply marginated lesions water density ( 0 + 15 HU) non-enhancing versus HYDATID CYSTS possess septations, mural calcifications and daughter cysts within the parent cyst
HYDATID CYST
HEPATIC CYSTS
Magnetic Resonance Imaging
long T1 and T2 relaxation hypointense on T1 and markedly hyperintense on T2 homogenous, sharply marginated signal intensity is indistinguishable from hepatic hemangioma comparable to signal intensity of bile and CSF
POLYCYSTIC LIVER DISEASE
Clinical Background and Pathology
numerous simple hepatic cysts adjacent liver tissue contains fibrotic areas (von Meyenberg complexes)
POLYCYSTIC LIVER DISEASE
Radiology
multiple cysts of variable size and different internal composition often in combination with PKD appearance of the cysts on ultrasound, CT, and MRI studies can vary broadly as a consequence of multiple episodes of intracystic hemorrhage comparable to the cysts of PKD
MESENCHYMAL TUMORS AND HETEROTOPIC RESTS
Clinical Background and Pathology Hemangioma – most common prevalence of remaining mesenchymal benign liver tumor is low no unique radiographic features exception are tumors that contain fat
lipomas, angiomyolipomas, myelolipomas
no malignant potential
MESENCHYMAL TUMORS AND HETEROTOPIC RESTS
Ultrasound fat-containing tumors are echogenic posterior acoustic enhancement in homogenous appearing tumors (specifically lipomas) Computed Tomography low density = > 20 HU pure lipomas show no enhancement partial and inhomogenous contrast enhancement should suggest angiomatous (angiomyolipoma) or myeloid (myelolipoma)
MESENCHYMAL TUMORS AND HETEROTOPIC RESTS
combined use of ultrasound and CT may permit the diagnosis and exclude other lipomatous tumors of the liver Magnetic Resonance Imaging fat-containing tumors high signal intensity on T1 and T2 images comparable to the subcutaneous or retroperitoneal fat
HEPATIC HEMANGIOMA
FOCAL NODULAR HYPERPLASIA
FOCAL NODULAR HYPERPLASIA
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