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The majority are found incidentally however they can present with pain or mass effects if large (>4cm). Complications are rare and the risk of rupture is small therefore resection is not justified.
A relatively common benign tumour of hepatocytes that almost always occurs in non-cirrhotic livers.
A hyperplastic tumour-like malformation of hepatocytes that resembles cirrhosis except fibrosis is absent. There are nodules of replicating hepatocytes without fibrous septae that compress adjacent cells.
It can be diagnosed with a combination of imaging modalities: hyperechoic on USS, hypodense on CT and increased signal on T1-weighted MRI (the gold-standard). Despite being the 18th most frequent cancer in the UK, HCC is the 6th most common cancer world-wide due to a high prevalence in Asia. Usually a solitary tumour, though it may be multi-centric or with satellite lesions around a central mass. Histologically, there are large dysplastic hepatocytes with round nuclei and clear cytoplasm. Trabecular (over half of all), mixed, compact, pseudo-glandular, fibrolamellar and scirrhous.
Abdominal pain (due to liver capsule stretch), anorexia, malaise, persistent fever and weight loss are the most common symptoms. Biopsy is generally avoided due to the risk (<2%) of seeding along the needle track, however in smaller lesions with moderately raised AFP and equivocal imaging fine-needle aspiration may be needed (given that clotting is normal). Liver function tests may show a raised AST:ALT ratio and increased alkaline phosphatase (ALP).
If surgery is possible then outcome for small (T1) tumours is good with 70% 5-year survival.
For non-resectable tumours TACE (transcatheter chemoembolization) can be used to induce ischaemia and deliver high dose chemotherapy, which is then repeated 2-3 times. Other local therapies include percutaneous ethanol injection and radiofrequency ablation, which can be as effective as surgery for small tumours.
A primary malignant tumour of biliary epithelial cells, which is 10 times less common than HCC.
Spread is initially to lymph nodes, and then later there is direct invasion of surrounding structures and peritoneal carcinomatosis. The most common presentation is with painless jaundice, weight loss and abdominal discomfort; therefore an important differential diagnosis is pancreatic cancer. ALT and AST mildly raised, however they may be up to 5x above upper limit of normal if cholangitis is present.
Positron emission tomography (PET) scanning has a role in increasing the sensitivity of diagnosis. Endoscopic retrograde cholangiopancreatography (ERCP) also shows the presence of strictures and allows intervention with stenting and allows brushings or biopsies to be taken. Surgery forms the mainstay of CC treatment however resection is only possible in 10-15% of cases. Palliative biliary stenting is needed to maintain liver function and prevent progressive cholangitis. Distant metastases are 40 times more common as a malignant cause of hepatic mass than a primary liver tumour. Leukaemia, lymphoma and carcinoid tumours are also associated with disseminated disease in the liver.
The most common masses in a well patient without previous liver disease are haemangioma, adenoma or a simple cyst. Malignant metastases are much more common that primary hepatic malignancies, often arising from the GIT, or other sites via haematogenous spread. Transabdominal coronal plane US images  shows a heterogenous complex mass like lesion in the right lobe of the liver.
CT scan demonstrates a large heterogenous mass mainly  in the anterior segments of the liver.On pre contrast CT scan the mass apears slightly hyperdense.
The patient underwent surgery and histopathology confirmed the diagnosis of a ruptured liver adenoma.
July 15, 2006This article is based on a presentation given by Richard Baron and adapted for the Radiology Assistant by Robin Smithuis.
Richard Baron is Chair of Radiology at the University of Chicago and well known for his work on hepatobiliary diseases.
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 beginning at the periphery as one or more nodular areas of enhancement. This means that in the arterial phase the areas of enhancement must have almost the density of the aorta, while in 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.
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. These lesions need to be differentiated from other lesions with a scar like FLC, FNH and Cholangiocarcinoma. Notice that the enhancing parts of the lesion follow the bloodpool in every phase, but centrally there is scar tissue that does not enhance. The lesion definitely has some features of a hemangioma like nodular enhancement in the arterial phase and progressive fill in in the portal venous and equilibrium phase. 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. If you had to pick one word to characterize a hemangioma on US, you would probably say 'hyperechoic'.
You have to realize however, that this simply means that the lesion is hyperechoic to normal liver. If the liver is hyperechoic due to steatosis, the hemangioma can appear hypoechoic (figure).
Hemangiomas must be differentiated from other lesions that are hypervascular or lesions that show peripheral enhancement and progressive fill in.
HCC is the most frequent abdominal malignancy worldwide and is especially common in Asia and mediterrean countries. If you take a cohort of patients with hepatitis C and you follow them for 10 years, 50% of them will have end stage liver disease and 25% will have HCC.
Always look how they present in the other phases and compare with the bloodpool and remember that rim enhancement is never hemangioma. These early HCC's are very different from the large ones that we see in the non-cirrhotic patients. HCC is a silent tumor, so if patients do not have cirrhosis or hepatitis C, you will discover them in a late stage.
They 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. Many patients with cirrhosis have portal venous thrombosis and many patients with HCC have thrombosis. First, if you have a malignant thrombus in the portal vein, it will always enhance and you'll see it best in arterial phase. Secondly, if you have a malignant thrombus in the portal vein, it will increase the diameter of the vessel. Early HCC needs to be differentiated from other hypervascular lesions, that will be hyperdense in the arterial phase. NECT, arterial and portal venous phase in a patient with Hepatitis C with two lesions in the liver (arrows). In the portal venous phase the lesion is again isodense to the surrounding liver parenchyma and you can't see it.
However if you look at the bloodpool, you will notice that on all phases it is as dense as the bloodpool. So we have a HCC in the right lobe on the upper images and a hemangioma in the left lobe on the lower images.
In the arterial phase we see a hyperdense structure in the lateral segment of the left lobe of the liver. However if we look at the NECT on the right, we'll notice, that it is not enhancement that we're looking at.
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 later phases.
Unfortunately, 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 later phases. The finding of hemorrhage as an area of high attenuation can be seen in as many as 40% of adenomas. Fat deposition within adenomas is identified on CT in only approximately 7% of patients and is better depicted on MRI. Chemical-shift imaging showing loss of signal on out-of-phase images can confirm the presence of fat.
HCC is known to contain fat in as many as 40% of lesions, therefore the presence of fat does not help differentiate the lesions.
Although adenomas are benign lesions, they can undergo malignant transformation to hepatocellular carcinoma (HCC). Although malignant transformation is rare, for this reason, surgical resection is advocated in most patients with presumed adenomas. Significant overlap is noted between the CT appearances of adenoma, HCC, FNH, and hypervascular metastases, making a definitive diagnosis based on CT imaging criteria alone difficult and often not possible. Patients with glycogen storage disease, hemochromatosis, acromegaly, or males on anabolic steroids also are more prone to developing hepatic adenomas. As a result of the risk of intraperitoneal hemorrhage and the rare occurrence of malignant transformation to HCC, surgical resection has been advocated in most patients with presumed HA. Some advocate surgical resection only when tumors are larger than 5 cm or when AFP levels are elevated, since these two findings are associated with higher risk of malignancy. The value of percutaneous fine needle biopsy for the diagnosis of HA is controversial for two reasons.
In addition, a considerable risk of hemorrhage exists when biopsy is performed on these hypervascular tumors.
Adenomas may diminish after oral contraceptives are discontinued, but this does not lower the risk of malignant transformation.
When a definitive diagnosis of FNH can be made using imaging studies, surgery can be avoided and lesions can be observed safely using radiologic studies. All the normal constituents of the liver are present but in an abnormally organized pattern. The central scar may be detected as a hyperechoic area, but often cannot be differentiated.
CT will show FNH as a vascular tumor, that will be hyperdens in the arterial phase, except for the central scar. On the left a typical FNH with a central scar that is hypodens in the portal venous phase and hyperdens in the equilibrium phase.
On T2-weighted images the scar appears as hyperintense in 80% of patients, which is very typical. FNH seen as hypervascular lesion in the late arterial phase and isodense to normal liver in the portal venous phase.
The diagnosis of FNH is based on the demonstration of a central scar and a homogeneous enhancement. Moreover a central scar may be found in some patients with fibrolamellar hepatocellular carcinoma, hepatic adenoma and intrahepatic cholangiocarcinoma.
The key to the diagnosis in the lesion on the left is the fact that it is isoattenuating to normal liver in the portal venous phase and stays that way without a wash out on the delayed phase (not shown).
This could also be an adenoma, but HCC would be unlikely because they show a fast wash out.
If you look at the images on the left and just would consider the T2W-images, what could be the cause of the central area of high signal? Fibrolamellar carcinoma (FLC) has a dark scar on T2WI and FNH has a brigth scar on T2WI in 80% of the cases. FLC characteristically manifests as a 10-20 cm large hepatic mass in adolescents or young adults.
The typical risk factors for HCC such as cirrhosis, elevated alphafetoprotein, viral hepatitis, alcohol abuse are absent. FLC characteristically appears as a lobulated heterogeneous mass with a central scar in an otherwise normal liver. 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. In contrast to FNH the central scar in FLC will usually be hypointense on T2WI and will less often show delayed enhancement. While FNH is always very homogeneous, FLC is usually heterogeneous following contrast administration. However when you look carefully you will notice the lamellar and heterogenous structure of FLC compared to the homogeneous appearance of FNH. The diagnosis of a cholangiocarcinoma is often difficult to make for a radiologist and even a pathologist. It can be a constricting or an expanding lesion, because it can have a fibrous or a glandular stroma. First look at the images on the left and try to find good descriptive terms for what you see. The lesion is hypodens in the arterial and portal venous phase with some peripheral enhancement. 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. Another cause of local retraction is atrophy due to biliary obstruction or chronic portal venous obstruction. The case on the left demonstrates how difficult the detection of ta cholangiocarcinoma can be. Only on the delayed images at 8-10 minutes after contrast injection a relative hyperdense lesion is seen.
Most liver metastases are multiple, involving both lobes in 77% of patients and only in 10% of cases there is a solitary metastasis. 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 (figure).
Hypervascular metastases are less common and are seen in renal cell carcinoma, insulinomas, carcinoid, sarcomas, melanoma and breast cancer. Although breast cancer metastases can be hypervascular, it was shown that routine use of adding arterial phase imaging, did not show any advantage.
When calcified liver metastases are revealed by CT in a patient with unknown primary tumor, colon cancer will be the most likely cause. Cystic liver metastases are seen in mucinous ovarian ca, colon ca, sarcoma, melanoma, lung ca and carcinoid tumor. Peritumoral edema makes lesions appear larger on T2WI and is very suggestive of a malignant mass.
On dynamic contrast-enhanced MRi the characteristics of metastases are the same as for CECT. This pattern suggests aggressive behavior and is seen in bronchogenic, breast and colon carcinoma, . However, this pattern is not specific for metastases as it can also be seen in primary malignant liver neoplasms (eg, HCC) and benign liver neoplasms (eg, adenoma in glycogen storage disease). A similar appearance has been described with liver abscesses.Calcified metastases may shadow when they are densely echogenic (figure). Focal fatty sparing in a diffusely fatty 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 a contrast enhanced CT hypovascular lesions can be obscured if the liver itself is lower in density due to fat deposition. If a patient is known to have a fatty liver, it is better to do an MRI or ultrasound for the detection of livermetastases. No metastases were seen, but on an ultrasound of the same region multiple metastases were detected.
The presentation of liver abcesses is very much dependend on the way the bacteria have entered the liver.
The bacteria enter through the slow flow portal system and they are layered within the vessel. 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. Finally there is a direct route as in penetrating injury or direct spread of cholecystitis into the liver.
Only when you have a population with livertransplants, bilomas in an infarcted area would look the same. It is very important to make the diagnosis of liver absces because it is a benign disease that kills and the radiologist may be the first to raise the suspicion.

Whenever you see a small cyst-like lesion in a patient who recently underwent an ERCP, be very carefull to assume it is just a simple cyst. So any cystic structure near the biliary tract in a patient, who recently has undergone a biliary procedure, is suspicious of a liver abces. Minsung Choi,Byung Ha Choi,Hyoung-Joong Kim Korean Journal of Legal Medicine. This article will concentrate on the most common forms: for a full review, including rare lesions, see Assy's review (World J Gastro, 2009).
The best imaging modality is technetium-99m labelled red blood cell scintigraphy, however it is not always available. However if they are large and increasing in size rapidly, or there is uncertainty over the diagnosis they may be resected (misdiagnosis of malignancy as haemangiomas is reported).
Patients tend to present with a mass or pain, which may be due to liver capsule stretch or rupture. It is most frequently found in women (4 times compared to in men) and at 20-50 years of age. Many can be diagnosed on contrast enhanced CT, the typical appearance of FNH is a mass <5cm in diameter with a central hypodense scar.
It is associated with portal vein thrombosis; it is thought that reduction in blood supply causes hepatocyte atrophy and a reactive hyperplasia that is manifest as NRH. Due to this, NRH can cause portal hypertension and in the West it is the most common cause of raised portal pressure in the absence of cirrhosis.
Fat accumulates as macrovesicular steatosis within hepatocytes (see image "Hepatic steatosis").
90% of all HCC arise in cirrhotic livers with 4% of people with cirrhosis developing HCC per year. In cirrhosis it is common to have multiple dysplastic nodules synchronously of which some will progress to HCC, so there may be more than one primary HCC present. This subtype does not have the same risk factors and most commonly presents as a single painful mass in an otherwise normal liver. In a patient with known cirrhosis, development of HCC may trigger decompensation and hepatic encephalopathy and ascities (in 30-60%). Non-cirrhotic patients with chronic HBV and haemochromatosis patients should also be screened. This is useful to debulk large tumours however it is contraindicated in multi-centric tumours and decompensated cirrhosis due to the risk of acute liver failure.
Sorafenib, a multi-target tyrosine kinase inhibitor, gives modest survival benefit in advanced disease. However those patients suitable for liver transplantation have a much better prognosis because the underlying cirrhosis is also cured.
There may also be itching and episodes of cholangitis due to strictures causing cholestasis. This occurs because no bile salts can enter the gut, impairing absorption of fat-soluble vitamins.
CT and magnetic resonance cholangio-pancreatography (MRCP) will demonstrate the anatomy of the lesion. If there are no distant metastases and invasion of the porta hepatis vessels then major surgery can be attempted e.g. The liver is the most common site for distant metastases and is involved in 40% of all metastatic disease. On postcontrast CT the hyperdense structures are not well enhanced suggestive hematoma but the middle part of the mass show faint enhancement. It is believed to represent a hyperplastic response to increased blood flow in an intrahepatic arteriovenous malformation.
In these metastases the halo is most probably related to a combination of compressed normal hepatic parenchyma around the mass and a zone of cancer cell proliferation. Hypervascular metastases have to be differentiated from other hypervascular tumors that can be multifocal like hemangiomas, FNH, adenoma and HCC.
Helical CT screening for HCC in patients with Cirrhosis: Frequency and causes of False-Positive interpretation. Intraperitoneal metastasis of hepatocellular carcinoma after spontaneous rupture: A case report.
Haemoperitoneum secondary to spontaneous rupture of hepatocellular carcinoma: CT diagnosis. Spontaneous rupture of hepatocellular carcinoma: Conservative management and selective intervention.
The differential diagnosis can be divided into two categories: those masses which are more likely to affect a cirrhotic liver and those that usually arise in an otherwise healthy liver. Haemangiomas can normally be diagnosed using a combination of ultrasound scan (USS) and contrast-enhanced computerised tomography (CT).
The presence of symptoms, history of OCP use and imaging with USS and contrast-enhanced CT normally can give the diagnosis without need for a liver biopsy. It can normally be diagnosed using vascular studies and excluding portal vein thrombosis as the cause for portal hypertensison.
It is thought to arise due to aberrant venous drainage from the pancreas that causes an area of hyperinsulinaemia, which drives the steatosis. Some patients (10%) may present with variceal bleeding, which may be associated with thrombosis of the portal vein from vascular invasion. However in some diseases the underlying pathology may not be cured despite transplant due to relapse (e.g. On examination, the gall bladder may be palpable and in association with jaundice this suggests that gallstones are not the cause of the jaundice, according to Courvoisier’s law. 80% of all metastases are multiple but colorectal cancer and renal cell carcinoma often cause solitary metastatic deposits. Hypovascular metastases have to be differentiated from focal fatty infiltration, abscesses, atypical hypovascular HCC and cholangiocarcinoma. For example, hepatic adenomas can occur in cirrhotic livers but only very rarely, contrary to non-cirrhotic livers where they are relatively common. On biopsy, there are proliferating hepatocytes in an area around a central scar, which contains a central artery.
The complication rate is low and resection is not suggested unless there is doubt over the diagnosis. The combination of aflatoxin and HBV is the most common aetiology in North Africa and parts of China.
50-60% are perihilar (also known as Klatskin tumours) and 20-25% involve the distal bile duct. 5-year survival following resection is 10-30% (better for more distal tumours) due to 75% recurrence. Prognosis is associated with poor liver reserve, advanced disease and severity of haemorrhage. Conversely, hepatocellular carcinomas may occur in previously normal livers but it is very rare. Liver masses in otherwise healthy people are often found incidentally; for example when having an ultrasound scan (USS) for a different reason. Patients with cirrhosis will be under regular follow-up with USS to screen for development of malignant masses.
He was admitted to the surgery department and submitted to abdominal ultrasonography, which revealed free peritoneal fluid and left liver haematoma was suspected. Computerised tomography (CT) scan showed a tumour on the left side of the liver and free peritoneal fluid [Figure 1].
After transfusion of two units of red cell concentrate and haemodynamic stabilisation, emergency laparotomy was performed. It revealed a 1-l haemoperitoneum and a 5-cm diameter left liver tumour which was ulcerated and haemorrhagic. Often, HCC is associated with known hepatic viral infection or cirrhosis, and while it can take decades for malignancy to develop, occasionally cases are seen in very young children. CT depicts solid organ injuries and has been used to classify injuries to the liver and eliminate patients with pathological liver, who are excluded from the conservative treatment.
It may be related to venous congestion, haemorrhage, trauma, or central necrosis [10] and therefore prone to intraperitoneal rupture. Factors that contribute to bleeding may include increased intravascular pressure secondary to tumour embolus, [10] causing intra-hepatic venous obstruction with shunting of blood, [11] and a hyperaemic liver circulation [11] caused by proximity of vessels to metastatic nodules or primary tumours. However, direct pressure of the tumour against the capsular surface of the liver seems the most plausible explanation. A sudden increase in intra-abdominal pressure resulting from sneezing, coughing or vomiting may cause rupture of tumours that are necrotic or hypervascular. Large tumour size, peripheral location and protruding contour are all associated with an increased risk for rupture of HCC.
It was reported that various surgical procedures, including perihepatic packing, suture plication of bleeding tumours, injection of alcohol, hepatic artery ligation, and hepatic wedge resection or lobectomy are effective against haemostasis. Unfortunately, only a few patients are suited for this procedure, owing to the presence of cirrhosis or extensive replacement of liver tissue by tumour.
The outcome is determined by the stage of both the neoplastic and the underlying liver disease, the rapidity of diagnosis, the degree of haemorrhage and the type of therapy.

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