The normal CT attenuation of the liver in non-enhanced imaging studies varies from 55 to 65 Hounsfield units (HU). The normal liver usually appears homogeneous on CT, and its attenuation exceeds that of the spleen in healthy subjects, by about 10 HU. The relatively large inter-individual range in attenuation values is due to the varying fat and glycogen content of the organ. Increased diffuse deposition of fat leads to a reduction in attenuation, while increased glycogen is reflected as an increase in CT measured density.
Blood circulation in the liver comprises two major components: the hepatic artery and the portal vein. Because of this dual source blood supply, the pattern of extracellular parenchymal contrast uptake and the associated changes in tissue attenuation over time follow a complex multicompartmental perfusion model. The overall hepatic perfusion cycle can be differentiated into three idealized phases:
Because of individual variations in cardiac output, blood volume, and visceral perfusion, the use of bolus tracking techniques to determine the arrival time of the contrast agent is mandatory. Bolus tracking relies on sequential low dose scans obtained at the level of the upper abdominal aorta; aortic enhancement values are immediatley displated and when aortic enhancement reaches a predefined threshold of about 150 HU, hepatic scanning begins. The delay between adequate bolus detection in the upper abdominal aorta and initiation of scanning is as little as 4 seconds with current MDCT images.
Approximately 10 seconds after the initiation of scanning, during the early arterial phase contrast enhancement of the abdominal aorta and the hepatic artery is observed, without admixture of enhanced portal venous blood. The late arterial phase, at approximately 20 seconds after scanning initiation leads to a clear depiction of the hepatic artery and its branches, owing to distinctive contrast enhancement. However, a minimal admixture of enhanced portal venous blood may already have occurred.
The Redistribution or Portal venous Phase imaged about 30 seconds after scan initiation allows early visualization of the portal vein and its intrahepatic branches, while the hepatic veins are still nonenhanced. Maximal contrast enhancement of the portal vein and its intrahepatic branches is reached after approximately 40 seconds. If monoslice CT scanners are used to perform biphasic liver scanning, all the contrast enhanced phase previously described are combined in one hepatic areterial-portal venous phase.
The hepatic benous phase can be acquired 60 seconds after scan initiation. Simultaneous enhancement of hepatic and portal veins is seen.
Because of retained contrast agent, focal liver lesions such as cholangiocarcinoma benefit from further delayed hepatic imaging, after most of the parenchymal contrast agent has been drained from the liver.
DETECTION OF LIVER MASSES:
The conspicuity of a liver lesion depends on the attenuation difference between the lesion and the normal liver. On a non enhanced CT scan, liver tumors are usually not visible, because the inherent contrast between tumor tissue and the surrounding liver parenchyma is too low. Only a minority of tumors contain calcifications, cystic components, fat or hemorrhage and will be detected on a NECT. So, IV contrast is needed to increase the conspicuity of lesions.
In the arterial phase, hypervascular tumors will enhance via the hepatic artery, when normal liver parenchyma does not yet enhances, because contrast is not yet in the portal venous system. These hypervascular tumors will be visible as hyperdense lesions in a relatively hypodense liver. However when the surrounding liver parenchyma starts to enhance in the portal venous phase, these hypervascular lesion may become obscured.
In the portal venous phase, hypovascular tumors are detected, when the normal liver parenchyma enhances maximally. These hypovascular tumors will be visible as hypodense lesions in a relatively hyperdense liver.
In the equilibrium phase at about 10 minutes after contrast injection, tumors become visible, that either lose their contrast slower than normal liver. These lesions will become either relatively hyperdense or hypodense to the normal liver.
In the equilibrium phase at about 10 minutes after contrast injection, tumors become visible, that either lose their contrast slower than normal liver, or wash out their contrast faster than normal liver parenchyma.
The optimal timing and speed of contrast injection are very important for good arterial phase imaging. Hypervascular tumors will enhance optimally at 35 sec after contrast injection (late arterial phase). This time is needed for the contrast to get from the peripheral vein to the hepatic artery to diffuse into the liver tumor.
Timing of scanning is important, but almost as important is speed of contrast injection. For arterial phase imaging, the best results are with an injection rate of 5ml/sec. There are two reasons for this better enhancement: at 5ml/sec there will be more contrast delivered to the liver when we start scanning and this contrast arrives in a higher concentration.
Portal venous phase imaging works on the opposite idea. The best moment to start scanning is at about 75 sec, so this is a late portal venous phase, because enhancement of the portal vein already starts at 35 sec in the late arterial phase. This late portal venous phase is also called the hepatic phase because there already must be enhancement of the hepatic veins.
The equilibrium phase is when contrast is moving away from the liver and the liver starts to decrease in density. This phase begins at about 3-4 minutes after contrast injection and imaging is best done at 10 minutes after contrast injection.
Relative hyperdense lesions in the delayed phase
Fibrous tissue that's well organized and dense is very slow to let iodine or gadolinium ion. Once contrast gets in however, it is equally slow to get back out in the equilibrium phase. So, when the normal liver parenchyma washes out, the fibrous components of a tumor will look brighter than the background liver tissue. Cholangiocarcinoma may have a fibrous stroma and in the delayed phase it may be the only time when you see the tumor.
Relative hypodense lesions in the delayed phase
Now the issue at hand is in small enhancing lesions in a cirrhotic liver whether it is a benign lesion like a regenerating nodule or a HCC. In the delayed phase we see that the tumor is washed out more than the surrounding liver parenchyma. Benign lesions typically will not show this kind of wash out. For instance a FNH or adenoma will show fast enhancement in the arterial phase, become isodense in the portal venous phase, but it will stay isodense with liver in the equilibrium phase. These benign tumors do not have enough neoplastic neovascularity to have a fast wash out. Especially in cirrhotic patients, we have to rely heavily on delayed phase to differentiate benign little enhancing lesions from small HCCs.
Normal Blood Pool and Hemangioma
Normally we compare the density of lesions filling with contrast to the density of the liver parenchyma. In hemangiomas however we should not compare the densty of the lesion to the liver, but to the blood pool. This means that the areas of enhancement in a hemangioma sould match the attenuation of the appropriate vessels (bloodpool) at all times. So in the arterial phase the enhancing parts of the lesion must have almost the same attenuation value as the enhancing aorta, while in the portal venous phase it must match the enhancement of the portal vein. In the equilibrium phase it has the same enhancement as the vessels. Eventually the lesion will become iso-attenuating to the liver, but only because the vessels become iso-attenuating with the liver. In NECT also, the density of the tumor is the same as the density of vessels.
Use arterial phase imaging in the following situations:
Hemangioma Imaging:
Hemangiomas, the most common benign solid tumors of the liver occur in two variants, capillary and cavernous. Capillary hemangiomas are far more common but are clinically insignificant. They tend to be small hypervascular lesions (> 2cm) encountered at the time of laparoscopy and may be the source of considerable diagnostic uncertainty. Cavernous hemangiomas are more relevant clinically because of the potential for complications and associated symptoms. Cavernous hemangiomas may vary in size from less than 1 cm to 30-40 cm or more ("giant hemangiomas"). The size of the lesion appears to correlate with symptoms, and it is the large pedunculated tumors that are most commonly symptomatic and that are encountered at operation. These tumors are usually sharply demarcated from surrounding liver tissue and may be partly necrotic or fibrotic. In some instances, infarct of the hemangioma may cause fibrosis or calcification, making it difficult to distinguish from other benign or malignant tumors. The acute nature of some symptoms related to hemangiomas may not be related to increase in size but rather to thrombosis and infarction of part of the tumor.
Hemangiomas are typically well demarcated and distinct from the surrounding hepatic parenchyma. The sharp interface between the tumor and the normal liver parenchyma permits surgical enucleation in most cases. However, not all of these tumors can be enucleated, and it is the histologic features of the tumor liver interface that defines how easily a parenchymal sparing technique may be utilized.
Histologically, four variants of the interface between the hemangioma and normal liver have been described. A fibrolamellar interface, characterized by a capsule like fibrous ring of variable thickness, is most common. In this situation, blood vessels either transverse the fibrous lamella or parallel the periphery of the hemangioma. The normal hepatic parenchyma may be atrophic, and a plane betwen the hemangioma and the normal liver tissue can be well defined. A second variant, the "interdigiting" pattern, is marked by the lack of a fibrous lamella surrounding the hemangioma, the lamella being replaced by an ill-defined plane between the normal liver tissue and the vascular channels of the hemangioma. The other two histologica variants of the hemangioma liver interface are a compression interface, in which the periphery of the tumor is well demarcated in the absence of a fibrous lamella and in which the surrounding liver parenchyma demonstrates marked atrophy and an irregular or spongy interface characterized by an ill defined margin. The latter variant may appear to be intercalated into the surrounding liver parenchyma at various points, making enucleation difficult.
Hemangiomas are usually solitary but are multiple in approximately 10% of cases. Their borders are clear, but they are not encapsulated. The cut surface is sponge like and typically dark reddish. Histologically, it is made up of variously sized vascular spaces lined by flat endothelial cells and interspersed with fibrous tissue. As the hemangioma grows, various degenerative changes are seen in its center, including old and new thrombus formation, necrosis, scarring, hemorrhage, and calcification. When degeneration and fibrous changes become more prominent, the lesion is refered to as a sclerosed hemangioma.
On non-enhanced CT, hemangioma is depicted as a well demarcated hypodense area with the same density as the aorta. It is sometimes round but more often oval or irregular. Large lesions sometimes have a geographic (irregular) shape. In the arterial phase of dynamic CT, peripheral enhancement is seen first, followed by gradual filling toward the center (filling in) and prolonged enhancement on the equilibrium phase- a pattern characteristic of hemangioma. The density of hemangiomas reflects the vascular spaces, and on precontrast, arterial and equilibrium phase dynamic CT, the fact that the tumor's density is similar to that of the aorta is useful diagnostic proof. In the type of small hemangioma containing small sinusoids, dynamic CT may show the entire tumor to be enhanced from the early phase. In hemangiomas exceeding 4 cm, a more irregular, hypodense area in the center or a septum-like structure may be found because of thrombus, necrosis, and scar formation. Calcification and cystic degeneration are also found in some cases. Rarely, fluid-fluid formation is seen.
Hemangioma is the most common benign liver tumor. It is composed of multiple vascular channels lined by endothelial cells. In 60% of case more than one hemangioma is present. The size varies from a few millimeters to more than 10 cm (giant hemangiomas). Calcification is rare and seen in less than 10% usually in the central scar of giant hemangioma.
CT will show hemangiomas as sharply defined masses with the same density as the vessels on NECT and CECT. The enhancement pattern is characterized by sequential contrast opacification begining at the periphery as one or more nodular areas of enhancement. All these areas of enhancement must have the same density as the bloodpool. This means that in the arterial phase the areas of enhancement must have almost the density of the aorta while the portal venous phase the enhancement must be of the same density as the portal vein. Even on delayed images the density of a hemangioma must be of the same density as the vessels. Finally most hemangiomas show complete fill in with contrast.
Small hemangiomas may show fast homogeneous enhancement ("flash filling"). Small HCC and hypervascular metastases may mimic small hemangiomas because they all show homogeneous enhancement in the arterial phase. By looking at the other phases to see if the enhancing areas match the bloodpool, it is usually possible to differentiate these lesions.
Large hemangiomas can have an atypical appearance. Complete fill in is sometimes prevented by central fibrous scarring. These lesions need to be differentiated from other lesions with a scar like FLC, FNH and Cholangiocarcinoma. The enhancing parts of the lesion follow the bloodpool in every phase, but centrally there is scar tissue that does not enhance.
Peripheral enhancement
The enhancement of a hemangioma starts peripheral. It is nodular or globular and discontinuous. Rim enhancement is continuous peripheral enhancement and is never hemangioma. Rim enhancement is a feature of malignant lesions, especially metastases.
Progressive fill in
In the portal venous phase however, the enhancement is not as bright as the enhancement of the portal vein. The conclusion must be, that this lesion does not match bloodpool in all phases, so it cannot be a hemangioma. So progressive fill in is a non specific feature, that can be seen in many other lesions like metastases or primary liver tumors like cholangiocarcinoma. The delayed enhancement in this lesion is due to fibrotic tissue in a cholangiocarcinoma and is a specific feature of these tumors.
Hepatocellular Carcinoma (HCC)
HCC may be solitary, multifocal or diffusely infiltrating. HCC consists of abnormal hepatocytes arranged in a typical trabecular pattern. Larger HCC lesions typically have a mosaic appearance due to hemorrhage and fibrosis. Early HCC appear as small lesions that transiently enhance homogeneously. Late HCC tend to be very large with a mozaic pattern, a capsule, hemorrhage, necrosis and fat evolution. HCC becomes isodense or hypodense to liver in the portal venous phase due to fast wash out. On delayed images, the capsule and sometimes septa demonstrate prolonged enhancement. It is very important to make the distinction between just thrombus and tumor thrombus. If it is a malignant thrombus in the portal vein, it will best enhance in arterial phase and it will increase the diameter of the vessel. Sometimes a tumor thrombus may present with neovascularity within the thrombus. Early HCC needs to be differentiated from other hypervascular lesions, that will be hyperdense in the arterial phase.
Hepatic Adenoma
Hepatocellular adenomas are large, well circumscribed encapsulated tumors. They consist of sheets of hepatocytes without bile ducts or portal areas. 80% of adenomas are solitary and 20% are multiple. Adenomas typically measure 8-15 cm and consist of sheets of well differentiated hepatocytes. Adenomas are prone to central necrosis and hemorrhage because the vascular supply is limited to the surface of the tumor. The pathogenesis is believed to be related to a generalized vascular ectasia that develops due to exposure of the liver to oral contraceptives and related synthetic steroids.
CT will show most adenomas as a lesion with homogeneous enhancement in the late arterial phase, that will stay isodense to the liver in late phases. Unofortunately this homogeneous enhancement in the late arterial phase is not specific to adenomas, since small HCC's and hemangiomas as well as hypervascular metastases and FNH can demonstrate similar enhancement in the arterial phase. Malignant lesions however have a tendency to loose their contrast faster than the surrounding liver, so they may become relatively hypodense in late phases. The findings of hemorrhage as an area of high attenuation can be seen in as many as 40% of adenomas. This is however also a feature of HCC and large hemangiomas.
Fat deposition within adenomas is identified on CT in only approximately 7% of patients and is better depicted on MRI. Typically adenomas have well defined borders and do not have lobulated contours. A low attenuation pseudocapsule can be seen in as many as 30% of patients. This capsule will only show enhancement on delayed scans. Coarse calcifications are seen in only 5% of patients. On the left an adenoma with fat deposition and a capsule.
Adenomas may rupture and bleed, causing right upper quadrant pain. The two most common liver lesiond causing hepatic hemorrhage are HA and HCC. Although adenomas are benign lesions, they can undergo malignant transformation to hepatocellular carcinoma (HCC).
Significant overlap is noted between the CT appearance of adenoma, HCC, FNH, and hypervascular metastases, making a definitive diagnosis based on CT imaging criteria alone difficult and often not possible.
Focal Nodular Hyperplasia (FNH)
FNH is the second most common tumor of the liver. FNH is not a true neoplasm. It is believed to represent a hyperplastic response to increased blood flow in an intrahepatic arteriovenous malformation. All the normal consitutuents of the liver are present but in an abnormally organized pattern.
CT will show FNH as a vascular tumor, that will be hyperdense in the arterial phase, except for the central scar. The diagnosis of FNH is based on the demonstration of a central scar and a homogeneous enhancement. However, a typical central scar may not be visible in as many as 20% of patients. Moreover a central scar may be found in some patients with fibrolamellar hepatocellular carcinoma, hepatic adenoma and intrahepatic cholangiocarcinoma, It is isoattenuating to normal liver in the portal venous phase and stays that way without a wash out on the delayed phase. This could also be an adenoma, but HCC would be unlikely because they show a fast wash out.
Fibrolamellar carcinoma (FLC)
FLC is an uncommon malignant hepatocellular tumor, but less aggressive than HCC. FLC characteristically manifests as a 10-20 cm large hepatic mass in adolescents or young adults. FLC characteristically appears as lobulated heterogenous mass with a central scar in an otherwise normal liver. Calcifications occur in 30-60% of fibrolamellar tumors. Imaging features of FLC overlap with those of other scar producing lesions including FNH, HCC, Hemangioma and Cholangiocarcinoma. FNH, in particular, may simulate FLC, since both have similar demographic and clinical characteristics. While FNH is always very homogeneous, FLC is usually heterogeneous following contrast administration. On NECT, a FLC usually presents as a big mass with central calcifications.
Cholangiocarcinoma
Cholangiocarcinoma usually presents as a mass of 5-20 cm. In 65% there are satellite nodules and in some cases punctate calcifications are seen. The diagnosis of a cholangiocarcinoma is often difficult due to varying morphology and histology. It can be a constricting or an expanding lesion, because it can have a fibrous or a glandular stroma. It can be located anywhere in the intrahepatic bile ducts or common bile duct. The lesion may have following characteristics:
Blood circulation in the liver comprises two major components: the hepatic artery and the portal vein. Because of this dual source blood supply, the pattern of extracellular parenchymal contrast uptake and the associated changes in tissue attenuation over time follow a complex multicompartmental perfusion model. The overall hepatic perfusion cycle can be differentiated into three idealized phases:
- Arterial Phase
- Portal venous Phase or Redistribution Phase
- Hepatic venous Phase or Equilibrium Pase
Because of individual variations in cardiac output, blood volume, and visceral perfusion, the use of bolus tracking techniques to determine the arrival time of the contrast agent is mandatory. Bolus tracking relies on sequential low dose scans obtained at the level of the upper abdominal aorta; aortic enhancement values are immediatley displated and when aortic enhancement reaches a predefined threshold of about 150 HU, hepatic scanning begins. The delay between adequate bolus detection in the upper abdominal aorta and initiation of scanning is as little as 4 seconds with current MDCT images.
Approximately 10 seconds after the initiation of scanning, during the early arterial phase contrast enhancement of the abdominal aorta and the hepatic artery is observed, without admixture of enhanced portal venous blood. The late arterial phase, at approximately 20 seconds after scanning initiation leads to a clear depiction of the hepatic artery and its branches, owing to distinctive contrast enhancement. However, a minimal admixture of enhanced portal venous blood may already have occurred.
The Redistribution or Portal venous Phase imaged about 30 seconds after scan initiation allows early visualization of the portal vein and its intrahepatic branches, while the hepatic veins are still nonenhanced. Maximal contrast enhancement of the portal vein and its intrahepatic branches is reached after approximately 40 seconds. If monoslice CT scanners are used to perform biphasic liver scanning, all the contrast enhanced phase previously described are combined in one hepatic areterial-portal venous phase.
The hepatic benous phase can be acquired 60 seconds after scan initiation. Simultaneous enhancement of hepatic and portal veins is seen.
Because of retained contrast agent, focal liver lesions such as cholangiocarcinoma benefit from further delayed hepatic imaging, after most of the parenchymal contrast agent has been drained from the liver.
DETECTION OF LIVER MASSES:
The conspicuity of a liver lesion depends on the attenuation difference between the lesion and the normal liver. On a non enhanced CT scan, liver tumors are usually not visible, because the inherent contrast between tumor tissue and the surrounding liver parenchyma is too low. Only a minority of tumors contain calcifications, cystic components, fat or hemorrhage and will be detected on a NECT. So, IV contrast is needed to increase the conspicuity of lesions.
In the arterial phase, hypervascular tumors will enhance via the hepatic artery, when normal liver parenchyma does not yet enhances, because contrast is not yet in the portal venous system. These hypervascular tumors will be visible as hyperdense lesions in a relatively hypodense liver. However when the surrounding liver parenchyma starts to enhance in the portal venous phase, these hypervascular lesion may become obscured.
In the portal venous phase, hypovascular tumors are detected, when the normal liver parenchyma enhances maximally. These hypovascular tumors will be visible as hypodense lesions in a relatively hyperdense liver.
In the equilibrium phase at about 10 minutes after contrast injection, tumors become visible, that either lose their contrast slower than normal liver. These lesions will become either relatively hyperdense or hypodense to the normal liver.
In the equilibrium phase at about 10 minutes after contrast injection, tumors become visible, that either lose their contrast slower than normal liver, or wash out their contrast faster than normal liver parenchyma.
The optimal timing and speed of contrast injection are very important for good arterial phase imaging. Hypervascular tumors will enhance optimally at 35 sec after contrast injection (late arterial phase). This time is needed for the contrast to get from the peripheral vein to the hepatic artery to diffuse into the liver tumor.
Timing of scanning is important, but almost as important is speed of contrast injection. For arterial phase imaging, the best results are with an injection rate of 5ml/sec. There are two reasons for this better enhancement: at 5ml/sec there will be more contrast delivered to the liver when we start scanning and this contrast arrives in a higher concentration.
Portal venous phase imaging works on the opposite idea. The best moment to start scanning is at about 75 sec, so this is a late portal venous phase, because enhancement of the portal vein already starts at 35 sec in the late arterial phase. This late portal venous phase is also called the hepatic phase because there already must be enhancement of the hepatic veins.
The equilibrium phase is when contrast is moving away from the liver and the liver starts to decrease in density. This phase begins at about 3-4 minutes after contrast injection and imaging is best done at 10 minutes after contrast injection.
Relative hyperdense lesions in the delayed phase
Fibrous tissue that's well organized and dense is very slow to let iodine or gadolinium ion. Once contrast gets in however, it is equally slow to get back out in the equilibrium phase. So, when the normal liver parenchyma washes out, the fibrous components of a tumor will look brighter than the background liver tissue. Cholangiocarcinoma may have a fibrous stroma and in the delayed phase it may be the only time when you see the tumor.
Relative hypodense lesions in the delayed phase
Now the issue at hand is in small enhancing lesions in a cirrhotic liver whether it is a benign lesion like a regenerating nodule or a HCC. In the delayed phase we see that the tumor is washed out more than the surrounding liver parenchyma. Benign lesions typically will not show this kind of wash out. For instance a FNH or adenoma will show fast enhancement in the arterial phase, become isodense in the portal venous phase, but it will stay isodense with liver in the equilibrium phase. These benign tumors do not have enough neoplastic neovascularity to have a fast wash out. Especially in cirrhotic patients, we have to rely heavily on delayed phase to differentiate benign little enhancing lesions from small HCCs.
Normal Blood Pool and Hemangioma
Normally we compare the density of lesions filling with contrast to the density of the liver parenchyma. In hemangiomas however we should not compare the densty of the lesion to the liver, but to the blood pool. This means that the areas of enhancement in a hemangioma sould match the attenuation of the appropriate vessels (bloodpool) at all times. So in the arterial phase the enhancing parts of the lesion must have almost the same attenuation value as the enhancing aorta, while in the portal venous phase it must match the enhancement of the portal vein. In the equilibrium phase it has the same enhancement as the vessels. Eventually the lesion will become iso-attenuating to the liver, but only because the vessels become iso-attenuating with the liver. In NECT also, the density of the tumor is the same as the density of vessels.
Use arterial phase imaging in the following situations:
- Characterisation of a liver lesion of unknown origin
- Detection of HCC in patients with a high alpha 1 fetoprotein
- Screening of cirrhotic patients for HCC
- Detection of metastases in patients with hypervascular tumors
Hemangioma Imaging:
Hemangiomas, the most common benign solid tumors of the liver occur in two variants, capillary and cavernous. Capillary hemangiomas are far more common but are clinically insignificant. They tend to be small hypervascular lesions (> 2cm) encountered at the time of laparoscopy and may be the source of considerable diagnostic uncertainty. Cavernous hemangiomas are more relevant clinically because of the potential for complications and associated symptoms. Cavernous hemangiomas may vary in size from less than 1 cm to 30-40 cm or more ("giant hemangiomas"). The size of the lesion appears to correlate with symptoms, and it is the large pedunculated tumors that are most commonly symptomatic and that are encountered at operation. These tumors are usually sharply demarcated from surrounding liver tissue and may be partly necrotic or fibrotic. In some instances, infarct of the hemangioma may cause fibrosis or calcification, making it difficult to distinguish from other benign or malignant tumors. The acute nature of some symptoms related to hemangiomas may not be related to increase in size but rather to thrombosis and infarction of part of the tumor.
Hemangiomas are typically well demarcated and distinct from the surrounding hepatic parenchyma. The sharp interface between the tumor and the normal liver parenchyma permits surgical enucleation in most cases. However, not all of these tumors can be enucleated, and it is the histologic features of the tumor liver interface that defines how easily a parenchymal sparing technique may be utilized.
Histologically, four variants of the interface between the hemangioma and normal liver have been described. A fibrolamellar interface, characterized by a capsule like fibrous ring of variable thickness, is most common. In this situation, blood vessels either transverse the fibrous lamella or parallel the periphery of the hemangioma. The normal hepatic parenchyma may be atrophic, and a plane betwen the hemangioma and the normal liver tissue can be well defined. A second variant, the "interdigiting" pattern, is marked by the lack of a fibrous lamella surrounding the hemangioma, the lamella being replaced by an ill-defined plane between the normal liver tissue and the vascular channels of the hemangioma. The other two histologica variants of the hemangioma liver interface are a compression interface, in which the periphery of the tumor is well demarcated in the absence of a fibrous lamella and in which the surrounding liver parenchyma demonstrates marked atrophy and an irregular or spongy interface characterized by an ill defined margin. The latter variant may appear to be intercalated into the surrounding liver parenchyma at various points, making enucleation difficult.
Hemangiomas are usually solitary but are multiple in approximately 10% of cases. Their borders are clear, but they are not encapsulated. The cut surface is sponge like and typically dark reddish. Histologically, it is made up of variously sized vascular spaces lined by flat endothelial cells and interspersed with fibrous tissue. As the hemangioma grows, various degenerative changes are seen in its center, including old and new thrombus formation, necrosis, scarring, hemorrhage, and calcification. When degeneration and fibrous changes become more prominent, the lesion is refered to as a sclerosed hemangioma.
On non-enhanced CT, hemangioma is depicted as a well demarcated hypodense area with the same density as the aorta. It is sometimes round but more often oval or irregular. Large lesions sometimes have a geographic (irregular) shape. In the arterial phase of dynamic CT, peripheral enhancement is seen first, followed by gradual filling toward the center (filling in) and prolonged enhancement on the equilibrium phase- a pattern characteristic of hemangioma. The density of hemangiomas reflects the vascular spaces, and on precontrast, arterial and equilibrium phase dynamic CT, the fact that the tumor's density is similar to that of the aorta is useful diagnostic proof. In the type of small hemangioma containing small sinusoids, dynamic CT may show the entire tumor to be enhanced from the early phase. In hemangiomas exceeding 4 cm, a more irregular, hypodense area in the center or a septum-like structure may be found because of thrombus, necrosis, and scar formation. Calcification and cystic degeneration are also found in some cases. Rarely, fluid-fluid formation is seen.
Hemangioma is the most common benign liver tumor. It is composed of multiple vascular channels lined by endothelial cells. In 60% of case more than one hemangioma is present. The size varies from a few millimeters to more than 10 cm (giant hemangiomas). Calcification is rare and seen in less than 10% usually in the central scar of giant hemangioma.
CT will show hemangiomas as sharply defined masses with the same density as the vessels on NECT and CECT. The enhancement pattern is characterized by sequential contrast opacification begining at the periphery as one or more nodular areas of enhancement. All these areas of enhancement must have the same density as the bloodpool. This means that in the arterial phase the areas of enhancement must have almost the density of the aorta while the portal venous phase the enhancement must be of the same density as the portal vein. Even on delayed images the density of a hemangioma must be of the same density as the vessels. Finally most hemangiomas show complete fill in with contrast.
Small hemangiomas may show fast homogeneous enhancement ("flash filling"). Small HCC and hypervascular metastases may mimic small hemangiomas because they all show homogeneous enhancement in the arterial phase. By looking at the other phases to see if the enhancing areas match the bloodpool, it is usually possible to differentiate these lesions.
Large hemangiomas can have an atypical appearance. Complete fill in is sometimes prevented by central fibrous scarring. These lesions need to be differentiated from other lesions with a scar like FLC, FNH and Cholangiocarcinoma. The enhancing parts of the lesion follow the bloodpool in every phase, but centrally there is scar tissue that does not enhance.
Peripheral enhancement
The enhancement of a hemangioma starts peripheral. It is nodular or globular and discontinuous. Rim enhancement is continuous peripheral enhancement and is never hemangioma. Rim enhancement is a feature of malignant lesions, especially metastases.
Progressive fill in
In the portal venous phase however, the enhancement is not as bright as the enhancement of the portal vein. The conclusion must be, that this lesion does not match bloodpool in all phases, so it cannot be a hemangioma. So progressive fill in is a non specific feature, that can be seen in many other lesions like metastases or primary liver tumors like cholangiocarcinoma. The delayed enhancement in this lesion is due to fibrotic tissue in a cholangiocarcinoma and is a specific feature of these tumors.
Hepatocellular Carcinoma (HCC)
HCC may be solitary, multifocal or diffusely infiltrating. HCC consists of abnormal hepatocytes arranged in a typical trabecular pattern. Larger HCC lesions typically have a mosaic appearance due to hemorrhage and fibrosis. Early HCC appear as small lesions that transiently enhance homogeneously. Late HCC tend to be very large with a mozaic pattern, a capsule, hemorrhage, necrosis and fat evolution. HCC becomes isodense or hypodense to liver in the portal venous phase due to fast wash out. On delayed images, the capsule and sometimes septa demonstrate prolonged enhancement. It is very important to make the distinction between just thrombus and tumor thrombus. If it is a malignant thrombus in the portal vein, it will best enhance in arterial phase and it will increase the diameter of the vessel. Sometimes a tumor thrombus may present with neovascularity within the thrombus. Early HCC needs to be differentiated from other hypervascular lesions, that will be hyperdense in the arterial phase.
Hepatic Adenoma
Hepatocellular adenomas are large, well circumscribed encapsulated tumors. They consist of sheets of hepatocytes without bile ducts or portal areas. 80% of adenomas are solitary and 20% are multiple. Adenomas typically measure 8-15 cm and consist of sheets of well differentiated hepatocytes. Adenomas are prone to central necrosis and hemorrhage because the vascular supply is limited to the surface of the tumor. The pathogenesis is believed to be related to a generalized vascular ectasia that develops due to exposure of the liver to oral contraceptives and related synthetic steroids.
CT will show most adenomas as a lesion with homogeneous enhancement in the late arterial phase, that will stay isodense to the liver in late phases. Unofortunately this homogeneous enhancement in the late arterial phase is not specific to adenomas, since small HCC's and hemangiomas as well as hypervascular metastases and FNH can demonstrate similar enhancement in the arterial phase. Malignant lesions however have a tendency to loose their contrast faster than the surrounding liver, so they may become relatively hypodense in late phases. The findings of hemorrhage as an area of high attenuation can be seen in as many as 40% of adenomas. This is however also a feature of HCC and large hemangiomas.
Fat deposition within adenomas is identified on CT in only approximately 7% of patients and is better depicted on MRI. Typically adenomas have well defined borders and do not have lobulated contours. A low attenuation pseudocapsule can be seen in as many as 30% of patients. This capsule will only show enhancement on delayed scans. Coarse calcifications are seen in only 5% of patients. On the left an adenoma with fat deposition and a capsule.
Adenomas may rupture and bleed, causing right upper quadrant pain. The two most common liver lesiond causing hepatic hemorrhage are HA and HCC. Although adenomas are benign lesions, they can undergo malignant transformation to hepatocellular carcinoma (HCC).
Significant overlap is noted between the CT appearance of adenoma, HCC, FNH, and hypervascular metastases, making a definitive diagnosis based on CT imaging criteria alone difficult and often not possible.
Focal Nodular Hyperplasia (FNH)
FNH is the second most common tumor of the liver. FNH is not a true neoplasm. It is believed to represent a hyperplastic response to increased blood flow in an intrahepatic arteriovenous malformation. All the normal consitutuents of the liver are present but in an abnormally organized pattern.
CT will show FNH as a vascular tumor, that will be hyperdense in the arterial phase, except for the central scar. The diagnosis of FNH is based on the demonstration of a central scar and a homogeneous enhancement. However, a typical central scar may not be visible in as many as 20% of patients. Moreover a central scar may be found in some patients with fibrolamellar hepatocellular carcinoma, hepatic adenoma and intrahepatic cholangiocarcinoma, It is isoattenuating to normal liver in the portal venous phase and stays that way without a wash out on the delayed phase. This could also be an adenoma, but HCC would be unlikely because they show a fast wash out.
Fibrolamellar carcinoma (FLC)
FLC is an uncommon malignant hepatocellular tumor, but less aggressive than HCC. FLC characteristically manifests as a 10-20 cm large hepatic mass in adolescents or young adults. FLC characteristically appears as lobulated heterogenous mass with a central scar in an otherwise normal liver. Calcifications occur in 30-60% of fibrolamellar tumors. Imaging features of FLC overlap with those of other scar producing lesions including FNH, HCC, Hemangioma and Cholangiocarcinoma. FNH, in particular, may simulate FLC, since both have similar demographic and clinical characteristics. While FNH is always very homogeneous, FLC is usually heterogeneous following contrast administration. On NECT, a FLC usually presents as a big mass with central calcifications.
Cholangiocarcinoma
Cholangiocarcinoma usually presents as a mass of 5-20 cm. In 65% there are satellite nodules and in some cases punctate calcifications are seen. The diagnosis of a cholangiocarcinoma is often difficult due to varying morphology and histology. It can be a constricting or an expanding lesion, because it can have a fibrous or a glandular stroma. It can be located anywhere in the intrahepatic bile ducts or common bile duct. The lesion may have following characteristics:
- The lesion is hypodense in the arterial and portal venous phase with some peripheral enhancement.
- The lesion is hyperdense in the equilibrium phase indicating dens fibrous tissue.
- The lesion causes retraction of the liver capsule.
The finding of an infiltrating mass with capsular retraction and delayed persistent enhancement is very typical for a cholangiocarcinoma.
Infiltrative cholangiocarcinoma does not cause mass effect, because when the stroma matures, the fibrous tissue will contract and cause retraction of the liver capsule. There are not many tumors that cause retraction of the liver capsule, since most tumors will bulge. The most common tumor that causes retraction besides cholangiocarcinoma is metastatic breast cancer. This will give a pseudo-cirrhosis appearance. Another cause of local retraction is atrophy due to biliary obstruction or chronic portal venous obstruction. Only on the delayed images, a relative hyperdense lesion is seen. This is the fibrous component of the tumor. Some cholangiocarcinomas have a glandular stroma.
Hepatic metastases
The liver is the most common site of metastases. The most common organs of origin are colon, stomach, pancreas, breast and lung. Most liver metastases are multiple, involving both lobes in 77% of patients and only in 10% of cases there is a solitary metastases.
Hypovascular metastases are the most common and occur in GI tract, lung, breast, and head/neck tumors. They are detected as hypodense lesions in the late portal venous phase. In this phase, the attenuation of the normal liver parenchyma increases, revealing the relatively hypoattenuating metastases, sometimes with peripheral enhancement. The rim enhancement that occurs represents viable tumor peripherally, which appears against a less viable or necrotic center.
Hypervascular metastases are less common and are seen in renal cell carcinoma, insulinomas, carcinoid, sarcomas, melanoma, and breast cancer. They are best seen in the late arterial phase at 35 sec after contrast injection. Although breast cancer metastases can be hypervascular, it was shown that routine use of adding arterial phase imaging did not show any advantage.
Calcified liver metastases are uncommon. Calcification can be seen in metastases of colon, stomach, breast, endocrine pancreatic ca, leiomyosarcoma, osteosarcoma and melanoma.
Cystic liver metastases are seen in mucinous ovarian ca, colon ca, sarcoma, melanoma, lung ca and carcinoid tumor.
Metastases in fatty liver
Focal fatty sparing in a diffusely farry liver or foci of focal fatty infiltration can simulate metastases. However on nonenhanced scans these regions of fat variation tend to be nonspherical and geographic with no mass effect or distortion of the local vessels.
On the other hand a fatty liver can also obscure metastases.
On a CECT hypovascular lesions can be obscured if the liver itself is lower in density due to fat deposition.
Liver Abscess
The presentation of liver abscess is very much dependent on the way the bacteria have entered the liver. There are four routes for bacteria to get into the liver. The common route is through the portal vein as a result of abdominal infection. The bacteria enter through the slow flow portal system and they are layered within the vessel. The bacteria will fall down into the dependent portion of the right lobe. In sepsis the spread will be via the arterial system as in patients with endocarditis and there will be multiple abscesses spread out through the periphery of the liver. The biliary route is often the result of biliary manipulation as in ERCP. It is usually central in location and then spreads out. Finally there is a direct route as in penetrating injury or direct spread of cholecystitis into the liver.
Characteristic appearance:
- Hypovascular lesions.
- Low density, so it may be cystic, i.e. fluid containing.
- Clustered or satellite lesions. These lesions are multiple but not spread out through the liver.
- Associated portal venous thrombosis.
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