Hepatobilary Flashcards
Arterial enhancing liver lesions
- HCC
- Haemangioma
- Focal Nodular Hyperplasia
- Hepatic Adenoma
- Primary Hepatic Carcinoid
- METs
- (RCC, Thyropid, NET, Leimyosarc, choricarcinoma, Melanoma, breast, colon, ovarian cystaadenocarcinoma)
Hypervascular liver lesions may be caused by primary liver pathology or metastatic disease.
Differential diagnosis
- Primary lesions
- hepatocellular carcinoma (HCC)
- most common hypervascular primary liver malignancy
- early arterial phase enhancement and then rapid wash out
- rim enhancement of capsule may persist
- haemangioma
- benign;
- most common liver tumour overall
- discontinuous, nodular, peripheral enhancement starting in arterial phase gradual central filling in enhancement must match blood pool in each phase, or not a haemangioma (i.e. similar to aorta in arterial, portal vein in portal phase, etc)
- small haemangiomas (<1.5 cm) may demonstrate “flash filling” - complete homogeneous enhancement in arterial phase (no gradual filling in)
- focal nodular hyperplasia (FNH)
- bright arterial phase enhancement except central scar
- isodense/isointense to liver on portal venous phase
- central scar enhancement on delayed phase
- hepatic adenoma
- arterial phase: transient homogeneous enhancement
- returns to near isodensity on portal venous and delayed phase image
- primary hepatic carcinoid
- background liver disease (cirrhosis)
- vascular shunts
- regenerative nodules
- dysplastic nodules
- hepatocellular carcinoma
- hepatocellular carcinoma (HCC)
What is Budd Chiari syndrome?
What is Budd-Chiari Syndrome?
Budd-Chiari syndrome is a condition in which the hepatic veins (veins that drain the liver) are blocked or narrowed by a clot (mass of blood cells). This blockage causes blood to back up into the liver, and as a result, the liver grows larger. The spleen (an organ located on the upper left side of the abdomen that helps fight infection by filtering the blood) may also grow larger.
Budd-Chiari Syndrome may also cause other conditions, including:
Portal hypertension (increased pressure in the portal vein, which carries blood from the intestines to the liver).
Esophageal varices (twisted veins in the esophagus, or “food tube”).
Ascites (a buildup of fluid in the abdomen).
Cirrhosis (scarring of the liver).
Varicose veins (abnormal, swollen blood vessels) in the abdomen and/or rectum.
What causes Budd-Chiari syndrome?
Budd-Chiari syndrome can be caused by conditions and situations that cause your blood to clot (form a blockage). These include:
Myeloproliferative diseases (those that affect the blood and bone marrow), including polycythemia (the body makes too many red blood cells), and thrombocythemia (the body produces too many platelets).
Sickle cell disease (a blood disease in which red blood cells change shape from round to sickle-shaped).
Inflammatory bowel disease (a group of disorders that cause irritation and swelling of the digestive tract).
Pregnancy.
What are the symptoms of Budd-Chiari syndrome?
The symptoms of Budd-Chiari syndrome include:
Pain in the upper abdomen.
Ascites (swelling in the abdomen caused by excess fluid).
Jaundice (skin, whites of the eyes and mucous membranes turn yellow).
Enlarged and tender liver.
Bleeding in the esophagus.
Edema (swelling) in the legs.
Liver failure.
Hepatic encephalopathy (reduced brain functioning caused by liver disease).
Vomiting.
Enlarged spleen.
Fatigue (extreme tiredness).
can A-1 Anti tryspin deficiency cause cirrhosis?
Alpha-1-antitrypsin deficiency
Assoc Prof Craig Hacking◉◈ and Radswiki◉ et al.
Alpha-1-antitrypsin (A1AT) deficiency is a hereditary metabolic disorder and is the most common genetic cause of emphysema and metabolic liver disease in children. It results in the unopposed action of neutrophil elastase and subsequent severe basal panlobular emphysema and respiratory symptoms. Accumulation of altered alpha-1-antitrypsin in hepatocytes incites an inflammatory response and chronic liver disease.
Epidemiology
Estimated prevalence is thought to be around 1 in 1,500 to 3,500 individuals with European ancestry. It reported to be uncommon in people of Asian descent.
Clinical presentation
The classic presentation of the disease is with dyspnea in the 4th to 5th decades of life. Two-thirds of individuals show clinical features but most carriers are asymptomatic.
Pathology
Alpha-1-antitrypsin (A1AT) is a protein that prevents enzymes such as elastase from degrading normal host tissue. Over 90% of the alpha-1-antitrypsin protein is produced in hepatocytes by codominant gene expression on chromosome 14. The alpha-1-antitrypsin protein inhibits neutrophil elastase. In patients with severe deficiency, the neutrophil elastase acts unopposed resulting in damage to the lower respiratory tract. This damage is predominantly basal because of the gravitational distribution of pulmonary blood flow.
Associations
asthma
pancreatitis
aneurysms, including intracranial aneurysms 18
Radiographic features
Thoracic manifestations
Plain radiograph and CT
panlobular emphysema
the emphysema pattern was traditionally thought to be panlobular, although more recent studies have also suggested a variable pattern to the emphysema
basal predominance, in contradistinction to centrilobular emphysema, which shows apical predominance; the two conditions can coexist in smokers
emphysema may develop in 75-85% of cases 12
bronchiectasis: up to 40% 9
frank bullae formation: non-specific feature 13
bronchial wall thickening: non-specific feature 13
hepatopulmonary syndrome
Nuclear medicine
Reduced perfusion and ventilation in the lower zones on a ventilation/perfusion (V/Q) study.
Abdominal manifestations
Hepatic manifestations of this disease are those of cirrhosis.
Treatment and prognosis
Emphysema and cirrhosis are usually considered the most common causes of death 8.
Survival is substantially worse in smokers, who have a 20-year decrease in longevity relative to non-smokers. According to one study, the overall median survival time was ~55 years 7.
Alpha-1-antitrypsin replacement therapy, most often by weekly intravenous infusions of alpha-1-antitrypsin purified from human plasma, has been used in some situations to partially correct the biochemical defect 14,15.
While randomized, placebo-controlled clinical trials have confirmed a reduction in the decline in lung density in patients receiving augmentation therapy 14, its efficacy in reducing mortality is uncertain 16. Other management strategies include avoidance of smoking and of other risk factors for cirrhosis.
Lung and liver transplant is generally reserved for those with end stage disease 24,25.
Complications
cirrhosis with increased risk of hepatocellular carcinoma 19
A1AT deficiency carriers are at 70-100% increased risk of lung cancer 20
Differential diagnosis
The differential will depend on the organ involved:
for thoracic manifestations: see differential for panlobular emphysema
near identical imaging appearances with ritalin lung
for hepatic manifestations: see differential for cirrhosis
Can Haemachromatosis cause Cirrhosis?
Hemochromatosis
Dr Vikas Shah◉ and Assoc Prof Frank Gaillard◉◈ et al.
Hemochromatosis is an iron overload disorder characterized by a progressive increase in total body iron stores and deposition of iron in some non-reticuloendothelial system (RES) body organs which results in some instances in organ dysfunction.
This article focus on the general principles of hemochromatosis, as well as effects of iron accumulation in the liver, the most frequently affected organ. Clinical and imaging changes in other organ systems are discussed separately:
hemochromatosis: cardiac manifestations
hemochromatosis: skeletal manifestations
hemochromatosis: pancreatic manifestations
hemochromatosis: CNS manifestations
Epidemiology
Hemochromatosis may be primary which is a genetic disorder or secondary which can result from a variety of diseases.
Primary hemochromatosis
Primary hemochromatosis is primarily (90%) due to an abnormal HFE gene, the protein product of which regulates iron absorption from the gastrointestinal tract. The two most common HFE gene mutations are C282Y and H63D. Homozygosity for the C282Y mutation and heterozygosity for C282Y/H63D mutations (also called compound heterozygosity) result in iron overload 7.
Approximately 2-5% of the population are heterozygous carriers (Caucasian population), resulting in a 0.2-0.5% prevalence of homozygous individuals 6. This makes hemochromatosis one of the most common genetic disorders in Caucasians of Northern European ancestry.
Although the genetic defect is distributed equally among men and women, the iron loss as a result of menstruation is protective, resulting in a clinical male predilection (M:F ~ 2:1).
In men, the diagnosis usually becomes evident in middle age (30-40 years of age) whereas, in women, clinical manifestation is delayed until the post-menopausal period.
Secondary hemochromatosis
Secondary hemochromatosis is rare and is usually seen in association with diseases that chiefly cause hemosiderosis. The distribution of iron in both RES and non-RES tissues can thus assist in the imaging differentiation between primary and secondary disease 6.
Etiology
- frequent transfusion
- mainly depositional siderosis in the reticuloendothelial system (RES)
- if > 40 units transfused: then may cause hemochromatosis (non-RES iron deposition)
- high erythrogenic requirements (hemolytic anemia, myelodysplasia)
- mainly depositional siderosis in RES from transfusion
- increased duodenal iron absorption may lead to hemochromatosis (non-RES iron deposition)
- bantau siderosis: rare cause in Africa due to iron-laden locally-brewed beer
Clinical presentation
As hemochromatosis may affect a number of organ systems, patients not surprisingly may present with a variety of signs and symptoms. These are most pronounced in primary hemochromatosis and include 4:
- hyperpigmented skin “bronze”: 90%
- hepatomegaly: 90%
- arthralgia: 50% (see skeletal manifestations of hemochromatosis)
- diabetes: 30% (see pancreatic manifestations of hemochromatosis)
- heart failure/arrhythmia: 15% (see cardiac manifestations of hemochromatosis)
- hypogonadotropic hypogonadism (see CNS manifestations of hemochromatosis)
Pathology
- The fundamental pathology that underlies hemochromatosis is the accumulation of iron and an increase in total body iron stores (as high as 50-60g) and abnormal non-reticuloendothelial deposition, which in turn leads to organ dysfunction.
- Hemochromatosis is distinct from, and should not be confused with, hemosiderosis which refers to the reticuloendothelial system (RES) iron deposition and does not cause organ damage.
- Eventual organ dysfunction is the final step in a cascading sequence of events 5:
- increased gastrointestinal absorption of iron
- increased cellular uptake of iron into non-RES
- liver is the primary organ of deposition
- pancreatic, cardiac, skeletal, and CNS deposition can occur once hepatic deposition is extensive
- iron gets deposited in periportal hepatocytes (ferritin and hemosiderin)
- perilobular fibrosis ensues with fibrous septa
- can progress to cirrhosis with broad fibrous septa surrounding large areas of relatively normal liver parenchyma
Radiographic features
- General visceral features of hemochromatosis are increased organ density (CT) and reduced organ signal intensity (MRI). Secondary imaging features include hepatomegaly, cirrhosis and signs of heart failure.
- The pattern of iron deposition is important. Predominant involvement of the liver, without deposition in spleen or bone marrow, is consistent with non-RES iron deposition and is characteristic of primary hemochromatosis. Iron deposition in the spleen and bone marrow, but to a lesser degree in the liver is consistent with RES deposition and is most likely due to hemosiderosis, which may or may not be associated with secondary hemochromatosis.
CT
- CT, although readily available, is not very sensitive for the diagnosis of hemochromatosis 6. In positive cases, marked homogeneous increase in liver density (75-130 HU) is demonstrated, making the portal vessels and hepatic veins appear of low attenuation relative to the liver on non-contrast CT.
- Dual-energy CT can be used to quantitate iron deposition.
- MRI
- See the sub-article on MRI liver iron quantification.
- MRI is not only the most sensitive imaging modality for the diagnosis of hemochromatosis but is also able to estimate iron concentration within the liver, thus forestalling the need for repeated biopsies 6.
Diagnosis
- Visceral iron results in susceptibility artefact which leads to T2* signal loss. The result is a low signal that is seen on all sequences, but particularly gradient echo and T2. It is useful to compare organ signal to that of skeletal muscle, with lower organ signal than muscle indicating the presence of iron.
- Gradient in-phase and out-of-phase sequences are particularly useful, demonstrating changes that are the opposite of those seen in hepatic steatosis. In hemochromatosis, the liver on in-phase sequence (which is usually obtained second, and thus more susceptible to T2* effects) demonstrates low signal, whereas the out-of-phase sequence demonstrates higher signal 6.
- In primary hemochromatosis, spleen and bone marrow signal is typically normal and low pancreatic signal is usually only seen if there is cirrhosis.
Quantification
- Quantitative MR techniques for measuring iron deposition have been developed, consisting of multiple gradient-echo sequences with progressively increasing TEs. The degree to which signal drops can then be plotted and an estimate of iron concentration generated. In cases with very high concentration, the method is unreliable as too little signal is returned from the liver 6.
- Treatment and prognosis
- Treatment in primary disease involves frequent phlebotomy which improves symptoms such as hepatomegaly, skin pigmentation, lethargy, and abdominal pain. However, arthritis is not affected by therapy. This also improves mild abnormalities of glucose metabolism. However, if type I diabetes mellitus has developed, insulin replacement will still be required. Some improvement in hepatic fibrosis and cardiac dysfunction can also be expected.
- Secondary hemochromatosis and hemosiderosis may require iron chelation therapy, depending on the underlying cause.
- Poor prognostic factors include the development of:
- cirrhosis
- hepatocellular carcinoma (HCC)
- diabetes
- cardiomyopathy
- Differential diagnosis
- General imaging differential considerations for hepatic appearances include:
- hemosiderosis, e.g. thalassemia with iron deposition mainly in spleen/bone marrow compared with primary hemochromatosis where iron is mainly in the liver
- other causes of a hyperdense liver on CT 6
- amiodarone
- Wilson disease
- colloidal gold treatment
can wilsons disease cause cirrhosis?
Wilson disease (hepatobiliary manifestations)
Dr Pablo Lorenzzoni◉ and Dr Yuranga Weerakkody◉ et al.
Hepatobiliary manifestations of Wilson disease vary largely from fatty changes to cirrhosis and occasionally fulminant hepatic necrosis. They result from accumulation of copper in the liver.
For a general discussion of the underlying condition, please refer to the article Wilson disease.
Epidemiology
Hepatic dysfunction is considered the most common manifestation of Wilson disease in childhood, usually presenting at age 10-13 years 5.
Radiographic features
General
The form of liver disease varies, depending on the severity of the disease at the time of diagnosis and pathological findings include fatty changes, acute hepatitis, chronic active hepatitis, cirrhosis and occasionally fulminant hepatic necrosis
The liver can later develop cirrhosis and has several unique radiological findings in comparison to other types of cirrhosis.
Specific features include 1:
multiple nodular lesions in the liver
presence of perihepatic fat layer and normal caudate lobe which is contrary to other types cirrhosis.
CT
Hepatic attenuation can be increased 7 or normal where the latter is thought to result from fatty infiltration and copper deposition canceling effects of each other. Evidence of cirrhosis may be seen in later stages.
Liver MRI
Copper is non-ferromagnetic and therefore cannot be seen on MR imaging.
MR imaging demonstrates the contour abnormalities and parenchymal nodules of the liver in more than half of the patients with Wilson disease, which is thought to correlate with the severity of hepatic dysfunction and clinical manifestations.
commonest finding is cirrhotic change 6
iron in regenerative nodules may result in numerous small nodular T2 hypointensities scattered throughout the liver which can be similar to those of deposits seen in patients with cirrhosis resulting from viral infection
Treatment and prognosis
Medical treatment is usually with copper chelators (D-penicillamine, trientine) or zinc and this can achieve symptomatic improvement and normal life expectancy. Orthotopic liver transplantation is indicated in advanced cases with hepatic decompensation or in patients with fulminant Wilson disease 4.
HCC has been reported in patients with Wilson disease. However, a recent report indicated that the risk of HCC was low in Wilson disease even in cases of cirrhosis8.
References
Can you get HCC in Steatohepatitis without cirrhosis?
yes
Hepatocellular carcinoma in non-alcoholic steatohepatitis: Current knowledge and implications for management
George Cholankeril, Ronak Patel, Sandeep Khurana, and Sanjaya K Satapathy
Author information Article notes Copyright and License information Disclaimer
This article has been cited by other articles in PMC.
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Abstract
With the prevalence of hepatitis C virus expected to decline, the proportion of hepatocellular carcinoma (HCC) related to non-alcoholic steatohepatitis (NASH) is anticipated to increase exponentially due to the growing epidemic of obesity and diabetes. The annual incidence rate of developing HCC in patients with NASH-related cirrhosis is not clearly understood with rates ranging from 2.6%-12.8%. While multiple new mechanisms have been implicated in the development of HCC in NASH; further prospective long-term studies are needed to validate these findings. Recent evidence has shown a significant proportion of patients with non-alcoholic fatty liver disease and NASH progress to HCC in the absence of cirrhosis. Liver resection and transplantation represent curative therapeutic options in select NASH-related HCC patients but have placed a significant burden to our healthcare resources and utilization. Currently NASH-related HCC is the fastest growing indication for liver transplant in HCC candidates. Increased efforts to implement effective screening and preventative strategies, particularly in non-cirrhotic NASH patients, are needed to reduce the future impact imposed by NASH-related HCC.
Can PBC cause HCC within 10 years?
yes - 4% risk of developing HCC in 10 years. More common in males, older pts, T2DM, and previous HBV.
https://aasldpubs.onlinelibrary.wiley.com/doi/full/10.1002/hep.26176
50% of Cholangioca’s Occur in the CBD.
T/F?
True.
Stat Dx
General Features
Best diagnostic clue
Klatskin tumor: Small hilar mass obstructing bile ducts on CT or ERCP
Location
Distribution in different segments of biliary tree
Distal common bile duct (CBD) (30-50%)
Common hepatic duct (14-37%)
Proximal CBD (15-30%)
Confluence of hepatic ducts (Klatskin tumor) (10-26%)
Isolated left or right hepatic duct (8-13%)
Cystic duct (6%)
Classified based on anatomy and radiographyPeripheral (10%)
Intrahepatic; proximal to secondary biliary radicles
Perihilar (50%)
Klatskin tumor: Hilar tumor involving the confluence of hepatic ducts
Distal (40%)
Extrahepatic; distal CBD
May arise as short stricture or small polypoid mass
Which has the better prognosis?
Intrahepatic vs klatskin tumour?
Intrahepatic 30% 5YS (Dahnert)
Klatskin 11% 5YS (https://www.ncbi.nlm.nih.gov/books/NBK6906/)
Percent of HCC found by USS in screening population?
At best 80% by the best operators in dedicated centres.
But in usual circumstances 65%.
Who are the screening population for HCC?
- Non-cirrhotic HBV
- HCV and Fibrosis
- NAFLD and Fibrosis
- Virtually all cirrhotics
6 monthly.
What is a postive Screening USS for HCC?
What are the Major Criteria for Dx HCC?
- Non- Rim Arterial Phase hyper-enhancement (Non-rim APHE)
- Size >10mm diameter (if less than 10mm -> 3 month screening)
- Enhancing Capsule
- non-peripheral wash out
- Threshold growth
Why can CT/MRI detect HCCs?
- Changes in Blood supply
- angiogenesis
- venous drainage evolution
- other features
- Fibrous capsule/septal formation and other morphological features
- changes in hepatocyte cell membrane transporter function
- increased cellularity (DWI)
why do HCCS have hyper enhancement?
- Marked angiogenesis. Increased unpaired arteries
- Late arterial phase enhancement.
- hall mark of progressed HCC
- not always seen in dysplastic nodules or early HCC.
- Not specific for HCC however.
- You must scan at the right time. Early art phase will not catch the enhancement.
- PIcture 2 is the same patient as picture 1, but done in the early arterial phase ie aortic/angiographic phase. THere hasn’t been enough time for the contrast to get into the lesion.
- Picture 3 shows late arterial phase
Which is most classic for HCC?
Nonrim APHE is. more classical for HCC.
Rim APHE is more classic for Colorectal Mets or intrahepatic Cholangio ca
Rim APHE = LR-M categorization in LI-Rads
What happens to the venous drainage of HCC?
- There are multiple venous changes.
- Change in vascular drainage from hepatic veins to portal veins, therefore predilection for PV invasion
- Rapid drainage of contrast material from lesion
- reduced intralesional portal vein supply
- increased cellularity in lesion, so reduced extracellular volume
- All these findings lead to the phenomenon of WASHOUT in HCC.
- This picture is taken in the LATE VENOUS PHASE (LVP) with the lesion appearing dark cf liver.
What is Wash out?
- here is a lesion showing wash out.
- either in the PV or delayed or late venous phase, the lesion becomes darker than background liver.
- COMPARE this to FADE,
- where the lesion demonstrates arterial phase Hyper Enhancement which then becomes less bright in the PV and Delayed phase,
- but it never gets darker than the adjacent liver.
- Wash out by itself is not specific for HCC.
- Can be seen in
- Cirrhotic/
- regenerative nodules and
- Dysplastic nodules
Is wash out specific for HCC?
Wash out by itself is not specific for HCC.
Can be seen in
- Cirrhotic/
- regenerative nodules and
- Dysplastic nodules
BUT when both of these things happen at the same time:
- Arterial Phase Hyper enhancement
- portal venous phase or late venous phase wash out
Then these features are highly specific for HCC.
- Roughtly 100% specific for HCC > 2cm
- Roughly 90% specific for 1-2cm HCC
Because HCC is supplied by lots of abnormal vessels supplied by hepatic artery branches and altered venous drainage.
If there is sufficient pre-test probability (ie patient with cirrhosis/CLD), with these imaging findings, then we can dx HCC without a liver Bx.
The findings of Non-rim APHE and washout are highly specific for HCC. But how sensitive are they?
- THe findings are unfortunately insensitive.
- up to 40% of small HCCs do not show arterial hyperenhancement
- Approx 50% of small HCCs don’t have typical wash out
- Biopsy still an important tool for lesion with non-diagnostic findings.
What is the ‘capsule’ re HCC?
- Develops as part of hepatocarcinogenesis
- seen in 70% of nodular progressed HCCs
- Not typically seen in cirrhotic nodules, dysplastic nodules or early HCC>
What is a capsule?
- Thin peripheral rim of enhancing tissue in the PV or LVP
What are the typical findings of HCC on CT??
What is Threshold growth RE HCC?
- Size increase of 50% or more in 6 months or less
- one diamter
- only apply if you’re sure its a mass.
- ie don’t apply to a THID or a THAD.
THAD:
Transient hepatic attenuation differences (THAD) lesions refer to areas of parenchymal enhancement visible during the hepatic artery phase on helical CT. They are thought to be a physiological phenomenon caused by the dual hepatic blood supply. Occasionally, they may be associated with hepatic tumours such as hepatocellular carcinoma.
THID:
Transient hepatic intensity differences (THIDs) are a phenomenon observed on MRI imaging of the liver. They are considered a direct equivalent to transient hepatic attenuation differences (THADs) noted on CT. They may be focal or nonfocal.
Does this Lesion meet Threshold growth criteria for HCC?
- No.
- there is an increase in diameter of just over 50% but in an 8 month period. so doesn’t reach threshold growth criteria.
What are the different types of HCC?
- Early
- progressed
- nodule in a nodule
- infiltrating
- angioinvasice
What is an Early HCC?
- First Stage of HCC
- the precursor to Progressed HCC
- <2cm diameter
- usually 10-15mm
- Vaguely nodular
- no capsule
- vascular invasion and intrahepatic mets are very rare
- blood supply changes not mature
- so unlikely to demonstrate typical HCC imaging features.
What is ‘Progressed HCC’?
- Overtly malignant and distinctly nodular
- usually, over 2cm diameter but may be < 2 cm
- vascular invasion
- intrahepatic mets
- established blood supply changes with angiogenesis and change to portal venous drainage (from HV)
- Typical imaging findings of HCC.
- Tumour capsule characteristic, with internal fibrous septa.
Image shows:
- NR APHE
- Wash out
- Capsule
What is the rate of Multifocal HCC?
- more than 30% of patients present with Multifocal disease
What is a Nodule in a Nodule?
- Small progressed HCC within a dysplastic Nodule
- Infrequent
- Important to look for a recognise
- In this picture we see:
- a T1 bright dysplastic nodule on the pre contrast
- then art phase can be
What is Infiltrating HCC?
- Difficult.
- non-mass forming malignancy
- Ill-defined margins
- typical arterial hyperenhancement and washout often not both present
- poor prognosis
- venous invasion common.
In the HBP image, the bright areas are normal hepatocytes which have taken up contrast. The rest (dark) is infiltrating HCC.
What are the Characteristics of angioinvasice HCC?
- Invades PV, HV and IVC
- Often extensive at dix
- V. Poor Prognosis
- usually seen as a contraindication to liver transplant
- LI-RADS ‘tumour in vein” TIV
what is this?
How do you tell the difference between thrombus and Tumour in PV/vessel?
- HCC tumour thrombus is usually grossly expansile
- where as bland clot is usually not expansile.
What are ancillary features of Progressed HCC?
- Mosaic Architecture + Sepat
- Corona enhancement
- Fat
What is corona enhancement?
- Progressed hypervascular HCC
- Enhancement of peritumoural venous drainage area
- early drainage of contrast from HCC into surrounding sinusoids
- late arterial phase to early PV phase
- fades out subsequently.
- There’s a higher risk of satellite nodules/mets within the area of the corona.
- include the corona in the treatment/resection volume.
Is fat common or uncommon in HCC?
- Fat is quite common in HCC.
- Good indicator of hepatocellular origin of a nodule in a cirrhotic patient.
- seen in dysplastic nodules as well.
Other liver lesions containing fat:
- HCC
- Dysplastic Nodules
- HNF 1-alaph inactivated hepatocellular adenoma (HNF 1a HCA)
- Hepatic angiomyolipoma in the non-cirrhotic liver.
- VERY RARE in FNH.
Picture shows:
- HCC with macroscopic fat within it on CT.
- This becomes more obvious on IP and OP imaging on MRI
- Markedly steatotoic HCC usually slightly better prognosis
- Large HCC with inhomogenous T1 IP imaging.
- large amounts of fat on OP
- Quite a lot of art phase enhancement with wash out on the PVP (portal venous phase)
- doesn’t look like FNH. and the presence of fat would certainly go against that as well.
- Fat containing HCC is best seen in OP MRI
*
Best modality to image fat containing HCC?
- Fat containing HCC is best seen in OP MRI
- high-grade dysplastic nodules and HCC may contain fat
The presence of fat tends not to be critical in HCC, as other typical features are usually present.
Fat-containing HCCs usually have a better prognosis.
What do HCCS look like on T2W imaging?
- HCC are usually T2 bring (mild to moderate)
- but small lesions may not be t2 bright.
- around 80% of progressed HCC are T2 bright. This may be homogenous or heterogenous
- LEARNING POINT
- a t2 bright nodule in a cirrhotic liver is highly suspicious for malignancy.
What do HCCs look like on DWI?
- HCCs have densely packed cells
- 80% poorly differentiated HCCs show true restriction. ie on ADC
- only 50% of well-differentiated HCCs demonstrate restricted diffusion.
- Things to note
- background liver is cirrhotic and fibrous and therefore diffusion restricted.
- therefore DWI is insensitive
- DWI restricting nodules are non-specific as diffusion restriction is seen in HCC and cholangiocarcinoma.
- LEARNING POINTS
- a diffusion restricted nodule in cirrhosis is highly sus for malignancy (not specific for HCC)
- The absence of diffusion restriction in a lesion fulfilling criteria for HCC or a lesion suspicious for HCC means nothing.
What are the Major Criteria for Dx of HCC (4)
and
what are the ancillary findings
(3)
- Primovist/gadoxetic acid/EOB = liver specific MRI contrast agents
- EOB/primovist-MRI doesn’t really help you with typical Progressed HCC.
- The hepatocyte uptake of EOB relies mainly on the expression of OATP transporters on the surface membrane.
What is the normal waveform of the Hepatic veins?
- Hepative veins
- triphasic flow pattern
- artial contraction (right atrium)
Normal hepatic vein Doppler
Dr Bahman Rasuli◉ and Dr Matt A. Morgan◉ et al.
The hepatic veins have a characteristic spectral Doppler waveform. Alterations in the normal hepatic vein waveform may reveal or confirm abnormalities in the heart or liver.
Terminology
The shape of the hepatic vein spectral Doppler waveform is primarily determined by pressure changes in the right atrium, or more exactly the blood flow resulting from the resultant pressure gradients. Multiple terms have been used to describe the hepatic vein waveform, including “phasic”, “triphasic”, “tetrainflectional”, and “periodic”. Some prefer the term “periodic” since the term “triphasic” already has a specific application in arterial spectral Doppler waveforms and since “periodic” suggests that the waveform is transmitted by cardiac motion rather than systolic flow.
Radiographic features
The normal periodic hepatic vein waveform is typically described in four parts:
a wave: atrial contraction
coinciding with the “p wave” on the electrocardiogram, contraction elevates pressure within the right atrium creating a gradient for late diastolic filling of the right ventricle
this also creates a pressure gradient favouring a lesser degree of retrograde flow into the IVC and hepatic veins
the small reversal of flow typically results in a small wave above the baseline, reversed from the overall net flow back to the heart
s wave: ventricular systole
as systole commences, right ventricle contraction results in longitudinal, apically orientated traction on the tricuspid annulus
the resultant “stretching” of the right atrium results in a drop in pressure, creating a gradient for anterograde flow from the inferior vena cava and hepatic veins, most pronounced at mid-systole
this typically forms the highest velocity deflection seen in the waveform
v wave: atrial overfilling
a transitional inflection point
as blood fills the right atrium, the flow from the hepatic veins and IVC slows, resulting in the s wave returning back to baseline
if the atrium fills to capacity then there may be a small amount of flow “recoil” backward, resulting in a v wave that rises above the baseline
d wave: tricuspid valve opening
as the tricuspid valve opens, blood flows from the right atrium into the right ventricle, resulting in a net flow of blood away from the liver and the waveform again dives back down below the baseline
this wave is almost always lower in magnitude than the s wave
Sometimes a c wave occurs as a second small inflection above the baseline, right after the a wave, reflecting the effect of the tricuspid valve bulging into the right atrium.
Differential diagnosis
Alterations in the normal hepatic venous Doppler waveform often indicate cardiac dysfunction, although it may also reflect disease of the hepatic parenchyma and/or vasculature. The consequent haemodynamic perturbations may manifest as:
- increased pulsatility (exaggeration of anterograde/retrograde velocities)tricuspid regurgitation
- abnormally high amplitude of the a and v waves
- diminished or reversed s wave
- congestive heart failure
- abnormally high amplitude of the a and v waves
- maintenance of a dominant anterograde S wave > D wave
- this presumes tricuspid valvular competence
- decrease in phasicity (diminution of anterograde/retrograde velocities)cirrhosis
- often associated with spectral broadening of the Doppler envelope and truncation of the a wave
- hepatic veno-occlusive disease (e.g. Budd-Chiari)
what does the normal doppler wave form of the portal vein look like?
- Low-velocity 10-20cm/s flow pattern
- respiratory vaiation present
- pulsation in PV flow is seen in tricuspid regurg and low BMI
- Portal Veins
In terms of complexity, the portal venous waveform is somewhere between those of the hepatic artery and hepatic veins. A model for understanding portal venous flow requires accepting two pieces of information. First, physiologic flow should always be antegrade, which is toward the transducer and therefore creates a waveform that is above the baseline. Second, hepatic venous pulsatility is partially transmitted to the portal veins through the hepatic sinusoids, which accounts for the cardiac variability seen in this waveform. It should also be kept in mind that the flow velocity in this vessel is relatively low (16–40 cm/sec) compared with that in the vessel coursing next to it, namely, the hepatic artery.
The normal portal venous waveform (Fig 23) should gently undulate and always remain above the baseline. The peak portal velocity (V1) corresponds to systole, and the trough velocity (V2) corresponds to end diastole. At first, one may incorrectly reason that systole should cause back pressure and create the trough; however, such is not the case. The primary influence on variation in portal venous pressure is atrial contraction, which occurs at end diastole. Atrial contraction, toward end diastole, transmits back pressure, first through the hepatic veins, then to the hepatic sinusoids, and ultimately to the portal circulation, where forward portal venous flow (velocity) is consequently decreased (the trough). In fact, prior studies of patients with increased portal venous pulsatility secondary to tricuspid regurgitation have noted that the portal venous waveform resembles an inverted hepatic venous waveform (1). Therefore, at end diastole, the atrium contracts and the portal venous waveform reaches a low point (trough). The degree of undulation is highly variable but may be quantified with a PI (Fig 24). It is important to note that the PI calculation for the portal vein is different from that for the hepatic arteries (arterial PI = (V1–V2)/Vmean). In the portal veins, the PI is calculated as V2/V1, with V1 normally being greater than 0.5.
What does the normal hepatic artery wave form look like?
- low impedance/resistance wave form
- artery flow pattern
- same flow direction as the portal vein
- https://pubs.rsna.org/doi/10.1148/rg.311105093 Radiographics article
What is the HU of the liver cf the spleen on NCCT?
How much do the HA and PV contribute to liver blood flow?
- The liver is 8-10HU higher than the spleen on non-contrast CT
- The HA contributes 25% of blood flow to the liver
- the PV contributes 75% of blood flow to the liver
- Most tumours have only arterial blood supply.
Where to where does the falciform ligament extend?
what land marks does it divide?
- extends from the umbilicus to the diaphragm
- divides the medial and lateral segments of the left lobe of the liver
- The falciform ligament is a broad and thin peritoneal ligament. It is sickle-shaped and a remnant of the ventral mesentery of the fetus.
It is situated in an anteroposterior plane but lies obliquely so that one surface faces forward and is in contact with the peritoneum behind the right rectus abdominis and the diaphragm, while the other is directed backward and is in contact with the left lobe of the liver.
It contains between its layers a small but variable amount of fat and its free edge contains the obliterated umbilical vein (ligamentum teres) and if present, the falciform artery, and paraumbilical veins. The falciform ligament divides the left and right subphrenic compartments but may still allow passage of fluid from one to the other.
Where is the ligamentum teres
- Round ligament/obliterated umbilical vein
- lies in the free edge of the falciform liagement
- hyperechoic structure in the left lobe of the liver
- LAND MARK
- gastroesophageal junction
where is the main lobar fissure of the liver? what is its landmark/what does it divide?
- extends from the GB to the porta hepatis
- divides the (American left and right lobes)
- ie divides segs 2/3 from the rest.
Where is the fissure of the the Liagementum venosum?
- Between the caudate lobe and the lateral segment of the left lobe
- contains the hepatogastric ligament.
LIVER MRI sequences
- SSFSE or fast gradient echo scout images
- Axial T1W gradient echo in and out phase
- axial FS T2 dual TE
- Axial DWI
- Axial 3D gradient echo T1 pre and post con (art, PV and equilibrium phases)
What is MR elastography?
- MR technique to noninvasively quantify the stiffness of the liver
- a mechanical driver is placed adjacent to the liver to generate shear waves within the abdomen at a predetermined frequency (40-120Hz)
- MR images are then aqcuried with a gradient echo sequence as the waves propagate thru theliver
- the velocity and wavelength of theawves propagating depend on the stiffness of the tissue.
- velocity and wavelength increase with greater tissue stiffness.
- used to assess liver fibrosis
Causes of Hepatitis
- viral
- hep A, B, NonA Non B, delta
- CMV
- EBV
- HSV
- Rubella
- Yellow fever
- Chemical Hepatitis
- Etoh
- Drucgs
- isoniazine
- halothane
- chlorpromazine
- phenytoin
- methyldopa
- panadol
- Toxins CCl4
US Imaging features of Hepatitis
- GB wall thickening may occur
- increased echogenicity of portal triads in acute hepatitis
- ddx cholangitis
- decreased echogencity in chronic hepatits
- echogenicity
- patterns are difficult to evaluate and there is interobserver variability
- only fatty liver substantially increases echogenicity of the eliver
- Acute hepatitis is a clinical and laboratory diagnosis. Starry sky appearance appears as bright echogenic dots throughout a background of decreased liver parenchymal echogenicity. It has poor sensitivity and specificity.
MRI appearances of hepatitis
- Increased T1 and T2 relaxation times in the liver
- high signal bands paralleling portal vessels on T2 (periportal oedema)
- There is severe gallbladder wall T2 hyperintensity in keeping with oedema, which compresses the mucosa of the gallbladder.
Cystic duct, CBD pancreatic duct are within normal limits with no obstructing lesions seen.
Marked high T2 signal is also demonstrated within the periportal spaces consistent with oedema.
Liver also appears slightly enlarged with recanalisation of the umbilical vein noted.
Overall findings suggestive of acute hepatitis and could account for the markedly deranged LFTs.
- Case Discussion
This case demonstrates markedly abnormal gallbladder wall and periportal oedema with a normal CBD. Appearances suggest an acute hepatitis. Full viral hepatitis screen was carried out and found to be negative. The patient then absconded from the ward.
US features of Liver Cirrhosis
what two things are rare in cirrhotic livers
USS features of Portal hypertension
What is in this picture?
- Small liver
- increased echogenicity
- coarse
- heterogenous
- nodular surface
- Hypoechoic regenerating nodules (image)
- Simple cysts and haemangiomas are rare in cirrhotic livers
- Unequal distribution of cirrhosis in different segments (ie sparring)
- left lobe appears larger than right
- lateral seg of left lob (II and III) enlarges
- IVa and IVb shrink
- the caudate lobe enlarges
- Portal hypertension
- hepatic wedge pressure >10mmhg
- collaterals
- left gastric
- paraoesophageal
- mesenteric
- retroperitoneal veins
- spleonreal
- Splenomegally ascites
Definition of cirrhosis
two types of cirrhosis.
which one has a big liver and which one has a small liver?
- hepatic fibrosis with the formation of nodules that lack a central vein
- Two types
-
Chronic sclerosing cirrhosis
- minimal regnerative activity of hepatocytes
- little nodule formation
- liver is hard and small
-
Nodular cirrhosis:
- regenerative activity with presence of many small nodules
- initially the liver may be enlarged.
-
Chronic sclerosing cirrhosis
Causes of Liver Cirrhosis.
- Etoh
- Hepatitis B
- Biliary cirrhosis
- Hemochromatosis
- Heart failture
- Wilson disease
- A-Antitrypsin
- Drugs
% of patients with cirrhoisis who develop HCC?
- 10% of patients develop cirrhosis
- haemangiomas are much less common 2%
Causes of Fatty Liver
8
- Obesity
- etoh
- hyperalimentation (IV nutrition)
- debilitation
- Chemo
- hepatitis
- steroids
- cushing syndrome
US imaging features of Fatty Liver
3
- renal cortex appears more hypointense relative to liver than normal
- intrahepatic vessel borders become indistinct or cannot be visualised
- nonvisualisation of diaphragm bc of increased beam attunuation
Features of focal fatty SPARING
- Focal fatty sparing typically has a geographic appearance and occurs in characteristic locations 1,3:
- adjacent to the porta hepatis (segment 4)
- gallbladder fossa (picture)
- adjacent to the falciform ligament
- subcapsular parenchyma
- MRI
Requires both in- and out-of-phase imaging and contrast to adequately assess 1.
Pseudolesions (focal sparing) are better seen on out-of-phase imaging, but otherwise, appear normal and similar to the rest of the liver on T2 and contrast-enhanced sequences 1. Hepatobiliary contrast agents such as gadoxetate disodium can show greater delayed uptake and biliary excretion when compared to the fatty liver due to a greater concentration of functioning hepatocytes 4.
The rest of the liver demonstrates:
T1: hyperintense
T2: mildly hyperintense
IP/OP: signal drop out on the out-of-phase sequence
imaging features of Fatty liver on CT
- Fatty areas are hypodense, while normal liver appears relatively hyperdense
- herpative veins and poeral veins appear dense relative to decreased parenchymal density
- common focal fatty deposit segment 4 near fissure for falciform lig.
- Most radiologists use a HU cut off of < 40.
- MRI in and out of phase imaging to verify the presence of fat
what is this?
-
Focal confluent fibrosis
- wedge shaped area of low attenuation on NCCT
- T1 hypo and T2 hyper on MRI
- Retraction of overlying liver capsule. 90%
- Total lobar or segmental involvement can be seen
- Located in medial segment of the left lobe +/- anterior segment of the right lobe
- may show delayed persistent enhancement
- https://radiopaedia.org/articles/confluent-hepatic-fibrosis
- Confluent hepatic fibrosis
Dr Mostafa El-Feky◉ and Dr Matt A. Morgan◉ et al.
Confluent hepatic fibrosis is a possible result of chronic injury to the liver, most commonly from cirrhosis or hepatic vascular injury.
Radiographic features
Confluent hepatic fibrosis is a cause of wedge-shaped or concave-marginated abnormalities in the cirrhotic liver: it occurs more frequently in the medial and anterior segments of the liver and tends to extend from the hilum to the periphery.
CT
wedge-shaped regions of hypoattenuation on non-contrast CT
hypoattenuating on the arterial and portal venous phases
the fibrosis may gradually enhance
MRI
wedge-shaped regions of moderate T2 hyperintensity
T1 hypointensity (possible increased T1 signal from cholestasis)
progressive postcontrast enhancement on the dynamic sequence but does not show enhancement on the delayed phase with hepatospecific contrast agents
lack fat signal intensity
Confluent hepatic fibrosis is categorised as LR1 or LR2 in the LI-RADS classification system. If findings are indeterminate between fibrosis and hepatocellular carcinoma, it should be graded LR3 or LR4.
Differential diagnosis
The main differential diagnoses are:
hepatocellular carcinoma
enhancement pattern allows differentiation
not associated with volume loss or capsular retraction
cholangiocarcinoma
peripheral cholangiocarcinoma may also show capsular retraction but generally is more masslike
dilated intrahepatic bile ducts are also more common in cholangiocarcinoma than with confluent hepatic fibrosis
hepatic epithelioid haemangioendothelioma
may show capsular retraction but otherwise has a different appearance and enhancement pattern
Practical points
For unknown reasons, confluent fibrosis is more common in primary sclerosing cholangitis and alcohol-related cirrhosis than with viral cirrhosis.
References
what is this?
- Gaucher disease is a rare genetic disorder passed down from parents to children (inherited). When you have Gaucher disease, you are missing an enzyme that breaks down certain types of fatty substances (lipids). These lipids can build up in organs such as your spleen and liver.
- Gaucher disease (GD) is the most common lysosomal storage disorder in humans. It is an autosomal recessive, multisystem disease arising from a deficiency of glucocerebrosidase or beta-glucosidase activity, resulting in the accumulation of a glycolipid (glucocerebroside) within the lysosomes of macrophages, particularity in the bone marrow, spleen and liver.
- Radiographic features
- Plain radiograph
- Skeletal involvement is seen in 70-100% of patients and primarily involves long bones (tibia, humerus, femur) as well as vertebrae. Ribs, hands and wrists, ankles and feet, and mandible may also be involved 6.
- Features of skeletal involvement include:
- osteopenia
- osteonecrosis
- pathological/crush fractures
- endosteal scalloping
- Erlenmeyer flask deformities
- H-shaped vertebrae
- paranasal sinus obliteration due to medullary expansion 9
- MRI
- spleen
- massive splenomegaly
- splenic nodules (30%) 1
- splenic infarcts (33%)
- liver
- hepatomegaly: less marked than the degree of splenomegaly
- T2: hyperintense stellate areas representing inflammation and fibrosis 3
- areas of hepatic ischaemia
- skeletal system
- long bones are most severely affected
- reduced T1 and T2 signal from involved bone marrow (due to infiltration of Gaucher cells)
- bone marrow burden (BMB) score may be obtained from MRI images 4
- may give a “salt and pepper pattern” due to scattered involvement
- features of superimposed osteonecrosis
- metaphyseal notching of humeri
- pathological fractures
- Erlenmeyer flask deformity
- spleen
what is this condition?
- Hemochromatosis
- iron overload
- The clinical finding is Bronze diabetes
- cirrhosis
- DM
- hyperpigmentation
- Types
- Primary
- AR
- defect in intestinal mucosa causing increased iron absorption
- iron excess in parenchymal cells, ie liver, pancreas, myocardium, pituitary, thyroid synovium
- leads to cellular damage, organ dysfunction and malignancy
- secondary
- non-genetic cause of iron accumulation
- Multiple transfusions
- iron is deposited in phagocytic cells in the spleen and liver (KUPFFER CELLS)
- less toxic
- Primary
- Radiographic features
General visceral features of haemochromatosis are increased organ density (CT) and reduced organ signal intensity (MRI). Secondary imaging features include hepatomegaly, cirrhosis and signs of heart failure.
The pattern of iron deposition is important. Predominant involvement of the liver, without deposition in spleen or bone marrow, is consistent with non-RES iron deposition and is characteristic of primary haemochromatosis. Iron deposition in the spleen and bone marrow, but to a lesser degree in the liver is consistent with RES deposition and is most likely due to haemosiderosis, which may or may not be associated with secondary haemochromatosis.
- Diagnosis
Visceral iron results in susceptibility artefact which leads to T2* signal loss. The result is a low signal that is seen on all sequences, but particularly gradient echo and T2. It is useful to compare organ signal to that of skeletal muscle, with lower organ signal than muscle indicating the presence of iron.
Gradient in-phase and out-of-phase sequences are particularly useful, demonstrating changes that are the opposite of those seen in hepatic steatosis. In haemochromatosis, the liver on in-phase sequence (which is usually obtained second, and thus more susceptible to T2* effects) demonstrates low signal, whereas the out-of-phase sequence demonstrates higher signal 6.
In primary haemochromatosis, spleen and bone marrow signal is typically normal and low pancreatic signal is usually only seen if there is cirrhosis.
Imaging features of Haemachromatosis US
- Hyperechoic liver
Imaging features of Haemachromatosis on CT
- Dense liver >75 HU
- much denser than spleen
- Intrahepatic vessels stand out as low density structures
Imaging features of primary and seconday Haemachromatosis on MRI
- Primary hemochromatosis
- The Liver pancreas and myocardium hypointense on T2W and T2* gradient echo sequence in primary hemochromatosis with sparing of the spleen and the bone marrow.
- In secondary hemochromatosis
- there is decreased signal intensity of the liver, spleen and bone marrow with sparing of the pancreas
- the amount of iron can be quantified using Gradient echo sequences with T2* weighting and progressively longer TEs. Free websites allow calc of estimated hepatic iron concentration
- iron deposition and decreased in signal intensity in the kidneys are only seen in intravascular hemolysis cause by mechanic stress in pts with heart valves, paroxysmal noctural hemoglobuinuria and in hemolytic crisis of sickle cell disease
- Signal changes in the liver are in keeping with iron deposition in haemochromatosis. A second cavernous haemangioma is shown in segment IV.
T2 BLADE fat-suppressed with an echo train of 116ms. The segment VIII mass is hyperintense, “lightbulb bright”’. There is a diffuse signal drop throughout the liver (susceptibility).
Low signal liver parenchyma on T1 in-phase. The mass is hyperintense relative to the liver.
Paradoxical increase in signal of the liver parenchyma on T1 out-of-phase, yet the mass is hyperintense relative to liver parenchyma.
40-minute post IV gadoxetate sodium (hepatocyte-specific contrast agent).
Case Discussion
There are several causes for increased hepatic attenuation on CT. In this case, the differentiating feature of primary haemochromatosis is the increased density of the liver only. In secondary haemochromatosis (e.g. frequent transfusions), the spleen would be expected to be hyperdense as well.
CT is not suitable for quantifying iron load in the liver, although this was practised in some institutions until the 1990s 1. However, MR quantification of iron content in the liver, using several gradient recalled echo sequences, is a non-invasive alternative to biopsy.
Cavernous haemangiomas of the liver are classically hypointense relative to liver parenchyma on T1-weighted imaging. In this case, the haemangiomas appear relatively hyperintense because of the diffuse signal drop in the liver parenchyma secondary to iron deposition; there is little, if any iron deposition in the haemangioma.
A hyperdense liver on non-contrast CT is an ‘old chestnut’ radiology exam case. Watch out for ancillary features that may point to the diagnosis such as pulmonary fibrosis and pacemaker (amiodarone), or increased density in the spleen and pancreas (secondary haemochromatosis).
what is this?
- amebic abscess
- entamoeba histolytica
- imaging features
- abscesses do not contain gas unless secondarily superinfected
- irregular shaggy borders
- internal sepations 30%
- multiple abscesses 25%
- Treatment
- conservative - metronidazole
- abscess drainage indicated if no response to rx or non-surgical candidate.
Imaging features of echinococcus granularis
what sign is this?
- well-delineated cysts (multilocular > unilocular)
- size of cyts usually very large
- daughter cysts within larger cysts is pathognomonic
- rim like cyst calcification in 30%
- double rim sign (pericyts endocyst)
-
Water lily sign
- The water-lily sign, also known as the camalote sign, is seen in hydatid infections when there is detachment of the endocyst membrane which results in floating membranes within the pericyst that mimic the appearance of a water lily.
It is classically described on plain radiographs (mainly chest X-ray) when the collapsed membranes are calcified but may be seen on ultrasound, CT, and MRI.
- enhancement of cyst wall.
Imaging features of Echinococcus multilocularis
- poorly marginated multiple hypodense liver lesions
- lesions infiltrative
- chronic granulomatous reaction with necrosis, cavitation
- calcification punctate and dystrophic, not rim like
- https://www.hindawi.com/journals/crira/2014/638375/
what is this? what other forms of this disease are there?
Fig. 3—34-year-old man with AIDS and bacillary peliosis. A, Transverse contrast-enhanced CT image shows large ill-defined, hypoattenuating lesion (white arrow) with heterogeneous peripheral enhancement within left liver lobe. Smaller subcapsular hypoattenuating lesion (black arrow) with ring enhancement can also be seen in right liver lobe. B, Transverse contrast-enhanced CT image (different scan level) shows multiple enlarged lymph nodes, feature typically seen in bacillary peliosis. C, Transverse contrast-enhanced CT image obtained after 9 months shows progression of disease with multiple hypoattenuating lesions disseminated within liver parenchyma with multiple small accumulations of contrast material in center of lesions (so-called target sign). D, After treatment with antibiotics, transverse contrast-enhanced CT image shows resolution of liver lesions and lymphadenopathy
https://www.ajronline.org/doi/pdf/10.2214/AJR.05.0167
- PEliosis Hepatitis
- rare benign disorder a/w steroid medication, sprue, diabetes, vasculitis, hematologic disorders
- bacillary peliosis hepatitis is caused by Bartonella species in HIV positive patients
- Multiple spherical lesions with centrifugal or centripetal enhancement.
- On angio lesions seen as multiple nodular vascular lesions on late arterial phase
*
hyperechoic lesions with a hypoechoic halo are ____ until proven other wise
What is this?
frequency
in what situation may this enlarge?
What types of this are there?
A homogeneous hyperechoic lesion is seen with well-defined borders and normal surrounding hepatic parenchyma, typical of hepatic haemangioma.
Case Discussion
A hepatic haemangioma is a relatively benign hypervascular liver lesion. It is the most common benign tumour of the liver. It is frequently diagnosed as an incidental finding on imaging and most patients are asymptomatic. A peripheral location within the liver is most common.
- Frequency:
- 4% of pop
- 80% in females
- may enlarge in preg or with Estrogen administration
- Two types:
- Typical Hemangioma (common)
- small
- asymptomatic
- discovered incidently
- Giant hemangioma
- >5cm
- uncommon
- may be symptomatic
- Hemorrhage
- thrombosisis
- Kasaback-Merritt syndrome:
- sequestration of thrombocytes in hemagnioma causing thrombocytopenia
- Typical Hemangioma (common)
Name that syndrome:
Giant hemangioma with sequestation of thrombocytes and thrombocytopenia
Kasabach-Merritt Syndrome
Kasabach-Merritt phenomenon (KMP), first described in 1940, is a rare but life-threatening coagulopathy of infancy which presents with thrombocytopenia, microangiopathic hemolytic anemia, and consumptive coagulopathy in the setting of a rapidly enlarging vascular tumor.
Typical Imaging characteristics of a Hemangioma on USS
- 80% Hyperechoic
- 10% hypoechoic which may have a hyperechoic rim
- espec in fatty liver (picture)
- Markedly echogenic liver due to hepatic steatosis makes the haemangioma appear hypoechoic. Note the absence of echogenic walls to vessels.
- https://radiopaedia.org/cases/hepatic-steatosis-and-haemangioma
- Giant hemangiomas are heterogenous
- Anechoic peripheral vessels may be demonstrated on USS DOppler
- Posterior acoustic enhancement is common (even in hypoechoic lesions)
Typical imaging features of Haemangiom on CT
- Hypodense, well circumscirbed lesion on precontrast scan
- Globular or nodule intense peripaherl enhancement during artphase
- Fill in occurs within minutes (longer for giant hemangiomas) (but also occurs for mets)
- Multiple giant liver haemangiomata demonstrating characteristic peripheral puddling enhancement with gradual central filling. The enhancing components follow aortic density. Central cleft due to cystic degeneration/liquefaction.
Incidental atrial septal defect noted on the delayed phase scans.
Typical imaging characteristics of Liver ____ on MRI
what sign is this?
- Liver hemangioma
- Hyperintense (similar to CSF) on heavily T2W seqeucnes (LIGHT BULB SIGN)
- Post gad peripheral nodular enhancement with pentripetal fill in
- imaging modality of choice
Imaging characteristics of Liver haemangioma on SPECT Tc99m RBCS
- decreased activity on early dynamic images
- increased activity on delayed 1-2 hour blood pool imagines
- only useful if lesion is > 3cm due to limited spatial resolution.
what is this?
At least five masses are seen at liver parenchyma with maximum diameters of 60×40mm. The masses show early homogenous enhancement and become isodense with surrounding parenchyma on delayed images.
Case Discussion
Path proven hepatic adenomas which are benign, generally hormone-induced, liver tumors.
Hepatic adenoma is traditionally considered the most frequent hepatic tumor in young women on the oral contraceptive pill.
https://radiopaedia.org/cases/hepatic-adenoma-multiple
CT features of HCC
- hypodense mass lesion
- may appear hyperdense in fatty liver
- enhancement
- early arterial enhancement
- prominent AV shunting causes early enhancement
- remains enhanced on PV phase
- Venous invasion 40%
- Calcs
- more commonly seen in fibrolamellar HCC
- 40%
- better prognosis
- younger pts
- normal afp
- central scar calcification
- more commonly seen in fibrolamellar HCC
USS features of HCC
- Most small HCCs are hypoechoic
- larger HCCs are heterogenous
- Fibrolamellar HCCs are Hyperechoic
- feeding tumour vessels may be seen on colour doppler
Angiography Features of HCC
what sign is this?
- Hypervascular
- AV shinting is typical
- Dilated arterial supply
- DSA: angiography
hypervascular tumour
threads and streaks pattern: sign of tumour thrombus in the portal vein
- https://pubs.rsna.org/doi/10.1148/radiol.2361030114
what is fibrolamellar HCC?
- malignant hepatocellular tumour with distinct clinical and pathological differences to HCC
- Lobulated heterogenous mass with a central scar in an otherwise normal liver
- It is uncommon to find evidence of cirrhosis, vascular invasion or multifocal disease in F-HCC.
- Hypointense (on all MR sequences) fibrous scar.
- this widely described imaging features has been used to discriminate btwn Firbolemella ca and FNH
- however in rare cases, Fibrolamella ca may demonstrate a hyperintense scar on T2, which simulates the hyperintense scar of FNH.
- Dense heterogenous enhancement in the artery and portal phases.
- the scar usually does not enhance and is best visulaied on delayed images
what is this sign and what does it mean?
Peripheral wash out sign is characteristic of mets
https://link.springer.com/article/10.1007/s00261-019-02034-y
What is the most common mesenchymal malignancy of the liver in adults?
AngioSarcoma
- Rare malignancy
- Tumour arises from endothelial cells
- Risk factors
- thorotrast 10%
- vinyl chloride
- arsenic
- hemochromatosis
- neurofibromatosis
- Multilocular mass with disseminated appearance and cystic areas
- Can mimic Haemangiomas on CT
- Primary hepatic angiosarcoma (PHA) is a rare hepatic tumor, originating from endothelial and fibroblastic tissue, primarily made up of vessels and composed of abundant vasculature. It represents only 0.1–2% of all primary liver malignancies [1]. PHA commonly occurs in ages from 60 to 70 years.
- Hepatic angiosarcoma is a rare malignancy but is still the third most common primary liver tumour. They have a variable appearance on both CT and MRI, reflecting the pleomorphic histological nature. Prognosis is very poor, with survival uncommon beyond one year from diagnosis.
what is this?
-
Epitheliod hemangioendothelioma
- female predominance
- middle age
- associated with OCP and vinyl chloride
- Predominant periphery of the liver,
- intratumorsal calcification,
- changes of the liver contour with
- capsular retraction and
- compensatory hypertrophy of the normal liver
- Invasion of the PVs and Hepatic veins
What are the indications of Alchohol ablation of liver tumors?
- HCC
- Ho extrahepatic spread
- <5cm single or multiple
- Child A or B Cirrhosis
- Mets
- <5cm, single lesion
- Vascular lesion
- carcinoid
- islet cell tumour
Describe the proceedure of RF ablation of liver tumuors.
- conscious sedaition
- localise lesion on CT or US
- single or multiple electrodes used
- the size of the coagulated area can be increased by use of multiple electrodes or by using a cluster probe (up to 9 separate electrode tips).
- can be done percut/laparoscopy or laparotmy
- Complicaitons
- more likely when tumour is superficial or close to hilar structures.
- prolonged ablation time
- several lesions treated simultaneously
- intraperitoneal hx
- liver abscess
- intestinal perf
- pain fever
What is arterioportal shunting in the liver?
- Direct commnication between branches of HA and PV.
- Appears as wedge shaped areas of hyperattenuation on late arterial phase CT
- Types
- Contribute arterial blood to the Portal venous blood supply of venous sinusoids
- Transsinusoidsal
- most commonly seen in hepatic cirrhosis but may also occur bc of focal infection or nodules of disease compromising portal circulation
- when they are seen in cancer pts, attention should be paid to the apex of the lesion where small mets may be evolving.
- Transtumoural:
- most common in the setting of HCC where a perinodular arteriolar plexus appears to cause a wedge of aterialised parenchyma
- both transsinusoidal and transtumor mechanisms contribute to this effect
- this pattern is also seen after RF Albation
- Transplexal
- the wall of the large bile ducts carry a vascular plexus that communicates with HA and drains to both hepatic sinusoids and the portal vein
- this type of shunting manifests from the perihilar level.
- they are encountered in cirrhosis PV thormosis or occlusion and in the setting of lobar infection
- Transsinusoidsal
- Contribute arterial blood to the Portal venous blood supply of venous sinusoids
- Aerterioportal communication via vasa vasorum of PV
- trans vasal
- occurs commonly in conjunction with transplexal shunting and is commonly seen in PV occlusion or HCC.
- trans vasal
what is this?
what are the causes?
- Thombosis of the main hepatic veins branches of hepatic veins or IVC with possible extension into the PV.
- Clinical
- ascites
- pain
- hepatosplenomegaly
- Causes
- idiopathic 50-75%
- Secondary
- coag anomalities
- clotting disorders
- polycythemia
- Tumours
- HCC, RCC
- Trauma
- OCP
- Chemo
- coag anomalities
- Mottled peripheral hypodensity to the right liver, mainly in the periphery of segments V, VI, VII and VIII. The right and middle hepatic veins do not opacify. The left and caudate lobes of the liver have a normal appearance with normal opacification of enlarged left hepatic veins. The portal veins opacify normally. As best as can be determined the peripheral right portal vein branches opacify normally. The hepatic artery is not well seen secondary to timing of the CT. Splenomegaly.
Cholecystectomy. Adrenal glands, kidney and pancreas have a normal appearance. No free fluid or free gas.
Bilateral pleural effusions, larger on the left. Minor bibasal atelectasis.
Conclusion:
Appearances are of right liver hypoperfusion, probably from venous congestion from complete right and middle hepatic vein thrombosis. This represents Budd-Chiari syndrome.
Hepatic Pseudoaneurysms may occur secondary to _____
pancreatitis
Things to look for on CT post Liver Transplant
- Atelectasis and Pleural effusions common
- increased periportal attenuation (periportal Collar 70%) (periportal oedema)
- ascites
- splenomegaly
- noninfected loculated intraperitoneal fluid collections
- abscesses
- hepatic, splenic
- perihepatic
- pancreatic
- Hepatic infarction 10%
- Hepatic hematoma
- Sludge
- inspissated thick bile 15%
- maybe extensive and cause biliary casts
- Splenic infarction
- hepatic calcification
- IVC thomrbosis
- Pseudoaneusym of HA
- Recurrent Hepatic Tumour.
Bile cast syndrome (BCS) is a complication of orthotopic liver transplantation (OLT). It is characterized by the presence of biliary casts and debris causing biliary obstruction. It occurs in 4 %-18 % of OLT recipients 1. It can present as cholangitis and graft damage or loss.
What is this?
- passive hepatic congestion
- COngested liver in cardiac disease
- stasis of blood in liver bc of impaired hepatic venous drainage
- Early enhancement of dilated IVC and hepatic veins on CT bc of contrast reflux from RA into IVC
- Heterogenous rerticulated mosaic parenchymal patten of liver
- Periportal edema
- enlarged liver and ascites
- cardiomegaly.
what is Boeck Disease?
- hepatic sarcoidosis
- non-caseating granulomas are evident in multiple organs.
- most common finding is non-specific hepatosplenomegaly
- diffuse parenchymal heterogeneity or multinodular pattern with low attenuating nodules in liver and spleen that gradually become isodense after contrast
- Advanced disease may simulate cirrhosis
- nodules hypointense on T1 and T2
- periportal adenopathy.
https://www.eurorad.org/case/15636
Non-enhanced abdominal CT (Fig. 1) showed cirrhotic changes of the liver, with increased size of the left and caudate lobe, contour irregularity, and parenchymal heterogeneity. Contrast-enhanced abdominal CT (Fig. 1) revealed a pattern of multiple hypodense macro-nodules. Signs of portal hypertension or involvement of the spleen were absent. Abdominal MRI (Fig. 2) was scheduled. T1-weighted MR-images showed large confluent hypointense nodules. Nodules appeared slightly hyperintense in T2-weighted MR-images, hypointense on T2-weighted fat-saturated MR-images, and demonstrated signal dropout on opposed-phase images. Abdominal lymph nodes were not enlarged. No foci of abnormal enhancement or restricted diffusion were detected. Vascular architecture and bile duct morphology were intact. A liver biopsy was performed, revealing non-caseating epithelioid granulomas, large regenerative nodules with fat deposition and fibrotic changes (Fig. 3). A subsequent chest CT (Fig. 4) revealed mild hilar and mediastinal lymphadenopathy. Intrapulmonary nodules were also seen. Resolution of chest imaging findings was noted after 6 months of treatment with corticosteroids and azatheioprine.
What is this condition?
- HELLP
- Haemolysis
- elevated liver enzymes
- Low platelets
- Variant of preeclampsia in primigravidas. rarely seen in multis
- intrahepatic or subcapsular fluid collection (hematoma) on US or CT
- Liver infarction with small or large peripheral wedge shaped hypoattenuating lesions
