7. • On a non enhanced CT-scan (NECT) liver tumors usually are not visible
• Only a minority of tumors contain calcifications, cystic components, fat or
hemorrhage and will be detected on a NECT.
• I/V contrast is needed to increase the conspicuity of lesions.
• Normal parenchyma is supplied for 80% by the portal vein and only for 20%
by the hepatic artery, so it will enhance in the portal venous phase.
• All liver tumors however get 100% of their blood supply from the hepatic
artery, so when they enhance it will be in the arterial phase.
• This difference in blood supply results in different enhancement patterns
between liver tumors and normal liver parenchyma in the various phases of
contrast enhancement.
THE CONTRAST PHASES OF
LIVER
9. • Optimal timing and speed of contrast injection are very important for good
arterial phase imaging.
• Hypervascular tumors will enhance optimally at 35 sec after contrast
injection.
• This time is needed for the contrast to get from the peripheral vein to the
hepatic artery and to diffuse into the liver tumor
• For arterial phase imaging the best results are with an injection rate of
5ml/sec.
THE ARTERIAL PHASE
10. • Portal venous phase imaging works on the opposite idea.
We image the liver when it is loaded with contrast through the portal vein to
detect hypo vascular tumors.
The best moment to start scanning is at about 75 seconds.
• This late portal venous phase is also called the hepatic phase because there
already must be enhancement of the hepatic veins.
• If you only do portal venous imaging, for instance if you are only looking for
hypo vascular metastases in colorectal cancer, fast contrast injection is not
needed, because in this phase the total amount of contrast is more important
and 3ml/sec will be sufficient.
THE PORTAL VENOUS PHASE
11. • The equilibrium phase is when contrast is moving away from the liver and the
liver starts to decrease in density.
• This phase begins at about 3-4 minutes after contrast injection and imaging is
best done at 10 minutes after contrast injection.
THE DELAYED/EQUILIBRIUM
STAGE
16. Hepatic Hemangiomas
• Benign vascular lesions of liver.
• The commonest liver tumor
• Autopsy studies : 0.4-20 percent
• 3-5 decades
• Thought to arise from congenital hamartomas
(abnormal growth of normal tissue), it can also develop
from dilatation of blood vessels in a normal tissue
• Usually asymptomatic
• Incidental discovery: US++
18. Hepatic Hemangiomas
US: well-defined, uniformly hyperechoic liver mass with peripheral feeder
vessels that are characteristic of a hemangioma.
Cavernous
angiomas
20. Hepatic Hemangiomas
CT: The pathognomic features of caverneous hemangioma: peripheral
nodular and discontinuous enhancement and progressive centripetal fill-
in
IV-
HAP
PVP
DP
21. The pattern of a peripheral,
discontinuous, intense
nodular enhancementnodular enhancement
during the arterial-dominant
phase with progressive
centripetal fill-incentripetal fill-in is
considered pathognomic
for hemangiomas
CT Findings:
Contrast-enhanced CT scans
reveal the pathognomic features
of a hemangioma, namely,
peripheral nodular
enhancement and progressive
centripetal fill-in (arrow).
0’’
15’1’
30’’
Cavernous HemangiomaCavernous Hemangioma
24. Hepatic Hemangiomas
Diagnosis
MRI:
. Hypointense and well defined in T1
. Marked hyperintensity that increases with echo time on T2
. The same caracteristic pattern of enhacement as is seen at CT
25. MRI Findings:
• MRI is more sensitive and specific than other imaging modalities in the diagnosis of
hemangiomas.
• Hemangiomas appear as smooth, lobulated, homogeneous, hypointense lesions on T1-
weighted images.
• On T2-weighted images, they appear hyperintense relative to liver. The high signal
intensity on T2-weighted images is due to the extremely long T2 relaxation time of the free
fluid (slowly moving blood)
Cavernous HemangiomaCavernous Hemangioma
27. Focal Nodular Hyperplasia (FNH)
. Benign nodule formation of normal liver tissue
. 2nd most common benign hepatic lesion
. More common in young and middle age women
. Male to female :5-17
. Usually asymptomatic
. A small minority (10-15%) may present with vague abdominal
symptoms from mass effect, a palpable mass, or hepatomegaly.
. Response of parenchyma to a vascular malformation or portal duct injury.
28. Focal nodular hyperplasia (FNH) is the second most commonFocal nodular hyperplasia (FNH) is the second most common
tumor of the liver and constitutes 8% of all liver tumorstumor of the liver and constitutes 8% of all liver tumors
• FNH occurs predominantly in women
(80 - 90%) during the third to fifth
decade.
• FNH is not a true neoplasm, and it is
believed to represent a hyperplastic
response to increased blood flow in an
intrahepatic arteriovenous
malformation.
• Kupffer cells are usually present in the
lesion
• Most cases of FNH occur as a solitary
lesion (80-95%)
FOCAL NODULAR HYPERPLASIA (FNH)
29. Focal Nodular Hyperplasia (FNH)
Rarely- encapsulated and pedunculated.
usually less than 5 cm in diameter
located in the subcapsular areas
A classic focal nodular hyperplasia,
paler than the surrounding liver, and
with a distinct central stellate scar.
30. Although FNH usually has no clinical significance, recognition ofAlthough FNH usually has no clinical significance, recognition of
the radiological characteristics of FNH is important to avoidthe radiological characteristics of FNH is important to avoid
unnecessary surgery, biopsy, and follow-up imaging.unnecessary surgery, biopsy, and follow-up imaging.
31. Focal Nodular Hyperplasia (FNH)
Diagnosis:
US: Nodule with varying echogenicity
Color Doppler imaging may show central vessels
32. Ultrasound
Doppler ultrasound shows centrifugal arterial flowcentrifugal arterial flow originating from the
central portion of the lesion or sometimes from a central vessel with a
stellate configuration.
Focal Nodular HyperplasiaFocal Nodular Hyperplasia
33. Focal Nodular Hyperplasia (FNH)
Diagnosis: CT
. Central scar
. Brisk homogeneous enhancement
. Well defined
. Early homogenesation
. Hypodense fibrous bands and septa that arise from the scar
. On delayed phase images the central scar may remain
hyperattenuating
. Without capsule
36. CT Findings: Typical CT finding of a FNH:
• In the native scan this benign
tumor appears to be almost
isodense to the surrounding liver
tissue; in its center a "scar" of
lower density can be seen
distinctly (top left image).
• 25 secs after contrast agent
application, enhancement starts
(top middle image), reaching its
maximum after 30-40 secs (top
right image). Note the typical
delicate structure of the
hypodense septae, which
appear in a radial order.
• After 45-60 secs, homogenous
contrasting is reached (bottom
left image); this is followed by a
gradual decay in contrasting.
Focal Nodular HyperplasiaFocal Nodular Hyperplasia
37. Focal Nodular Hyperplasia (FNH)
Diagnosis:MRI typical finding
. Isointense to hypointense on T1-weighted images
. Slightly hyperintense to isointense on T2-weighted images
. Brisk homogeneous enhancement
. Delayed enhancement of the central scar
38. Focal Nodular HyperplasiaFocal Nodular Hyperplasia
MRI Findings:
T1-weighted sequence.
A focal lesion (arrow) with a
diameter of 2.5 cm is hypointense
relative to the liver parenchyma.
T2-weighted sequence.
The lesion is slightly and
inhomogeneously hyperintense.
39. Hepatic Adenoma
. Rare hepatic tumor
. Women aged 20 to 40 years
. Association with oral contraceptive use
. Solitary (70%–80%)
. Can be associated with right upper-quadrant pain
. Risk of rupture, hemorrhage, or malignant transformation
. 5-10cm
. Benign neoplasm composed of normal hepatocytes no
portal tract, central veins, or bile ducts
. Surrounded by a capsule
. Surgical resection is generally advised
40. Hepatocellular AdenomaHepatocellular Adenoma
Ultrasound
• On US, HAs demonstrate variable echogenicity.
• The most adenomas are not specifically diagnosed at US and are usually further
evaluated with CT or other imaging modalities.
From: Luigi Grazioli et al. Hepatic Adenomas: Imaging and Pathologic Findings Radiographics. 2001;21:877-892.
Transverse US scan of the liver shows a
hypoechoic lesion (cursors) with a hyperechoic
center (arrow) due to recent hemorrhage.
Sagittal US scan of the liver shows a well-
defined, homogeneous, hyperechoic lesion in
the right lobe (arrow).
41. •Well circumscribed without lobulation
•Heterogeneous because of their mixed components of fat, hemorrhage,
and necrosis
•Diffuse heterogeneous arterial enhancement and iso attenuated on
delayed scan
•MRI:
CT SCAN
42. Hepatocellular AdenomaHepatocellular Adenoma
CT Findings:
Arterial-phase CT scan shows multiple
hypervascular lesions (arrows).
On a portal venous-phase CT scan, the
adenomas are isoattenuating relative to
the surrounding parenchyma.
From: Luigi Grazioli et al. Hepatic Adenomas: Imaging and Pathologic Findings Radiographics. 2001;21:877-892.
43. Hepatic Adenoma
• Hyper to isointense on T1
(hemorrhage) and slightly
hyperintense on T2 weighted
images
44. Liver cysts:
. May be single or multiple
. May be part of polycystic kidney disease
. Patients often asymptomatic
. No specific management required
47. Liver cysts: HYDATID CYST
• Hyper to isointense on T1 (hemorrhage) and
slightly hyperintense on T2 weighted images
• Same appearance on contrast-enhanced
image as CT scan
48. a typical case of a echinococcus cyst with 'daughter cysts' within the large cyst.
Most cases of echinococcus cysts however are not that typical.
LIVER CYSTS
51. Hepatocellular Carcinoma (HCC)
•The fifth most common tumor
•Rarely occurs before age of 40 and peaks at 70 years
•Male to female: 4/1
•Cirrhosis is the strongest predisposing factor for HCC
•80% of cases of HCC developing in a cirrhotic liver
•Causes of cirrhosis: hepatitis (B and C virus infection), alcohol,
Hemochromatosis and biliary cirrhosis
Most HCCs develop by means of a multistep progression: from a low-grade
dysplastic nodule to a high-grade dysplastic nodule, to a dysplastic nodule with a
focus of HCC, and finally to overt carcinoma.
Willatt et al Radiology: Volume 247: Number 2—May 2008
52. Several morphological forms
Massive(>3cms)
Nodular (<3cms)
Diffuse
Hepatocellular Carcinoma (HCC)
AFP (Alfa feto protein)
Is an HCC tumor marker
Values more than 100ng/ml are highly suggestive of HCC
Elevation seen in more than 70%
53. Hepatocellular Carcinoma (HCC)
US : hyperechoic, smaller tumors are hypoechoic.
Heterogeneous, hypervascular
US sensitivity about 75%.
54. Arterial Phase:
liver(30-35 sec)
HCC as supplied by arterial branch/neovascularization
Hepatocellular Carcinoma (HCC)
Venous Phase:
HCC which is enhanced during arterial phase has lost its contrast,
hence no enhancement of the tumor but rest of the liver enhances.
Contrast in brightness of the lesion with respect to surrounding liver.
Enhancement
Wash out phenomenan
CT or MR
55. Hepatocellular Carcinoma (HCC)
Delayed Phase :
Wash -out phenomenan persists and often exaggerated in smaller
lesions.
The tumor capsule
IV-
HAP
PVP
DP
capsule
57. • MRI
• Variable intensity of HCC on T1
• 35% hyper, 25% iso-, 40 % hypo
• Hyperintense (T1) often well-differentiated, contain fat,
copper, glycogen
• Almost always hyperintense on T2 MR
• The tumor capsule is hypointense on both T1- and T2-
weighted images in most cases
Hepatocellular Carcinoma (HCC)
60. Metastatic disease
• Most common malignant hepatic tumor
• Presence of extrahepatic malignancy should be sought in patients with
characteristic liver lesions per imaging studies.
• Common primaries : colon, breast, lung, stomach, pancreases, and
melanoma
• Mild cholestatic picture (ALP, LDH) with preserved liver function
• CT or US guided biopsy provides definitive diagnosis but not always
required.
61. Metastatic disease
Variable US features+++
Iso, hyper or hypo echoic++
Contrast-enhanced US (CEUS) (84%
accuracy)
Intraoperative US (IOUS) (96% accuracy)
Typical feature
62. Metastatic disease
• Most liver metastases are hypovascular and are best imaged during the
portal venous phase (colon, stomach and pancreas)
• Hypervascular metastases enhancing on the arterial phase
(neuroendocrine tumors, renal cell, breast, melanoma, thyroid)
• Calcification may be present with metastases from mucinous
gastrointestinal tract tumors and from primary ovarian, breast, lung, renal,
and thyroid cancer
• Other features : Hemorrhagic or cystic metastases
63. Metastatic disease
. On MRI, metastases are variable but are usually hypo- to isointense on T WI and
iso- to hyperintense on T2 WI
. Metastatic tumors with liquefactive necrosis or cystic neoplasms show higher
signal intensity on T2 WI
. Metastases may show central hypointensity on T2WI (coagulative necrosis, fibrin,
and mucin)
. High T1 signal intensity can be seen with metastases from melanoma, colonic
adenocarcinoma, ovarian adenocarcinoma, multiple myeloma and pancreatic
mucinous cystic tumor
. Comparing T2-weighted (TE 90) and T2-weighted (TE 160) sequences, metastases
become less intense Characterization
. T1-weighted 3D dynamic contrast-enhanced MRI Detection
68. •Green arrow: oval shaped hypodense area
consistent with hematoma
•Yellow arrow: linear shaped hypodense area
consistent with laceration
•Blue arrow: vague ill defined hypodense area
consistent with contusion
•Fluid around the liver
•There is almost a transsection of the liver,
but both lobes do enhance so there is still
normal vascular supply.
69. • Complete devascularization of the
right lobe (i.e. grade 4) .
• Contrast blush within the
intraparenchymal region, but also
extention beyond the lateral
margin of the liver.
• Hemoperitoneum.
• A second contrast blush at a lower
level
70. • Subcapsular hematoma greater
than 10 cm (i.e. grade 4 injury)
• Contrast blush
• No associated hemoperitoneum
71. Lacerations can be stellate, like the
example on the left or branching like
the one on the right.
http://www.schaffnerfamily.com/Slide%20shows/Liver,%20Mass%20Lesions/
http://www.emedicine.com/radio/topic286.htm
It is now accepted that there is no aetiological role of contraceptives, although the use of contraceptives may stimulate the growth of the tumour.
http://www.pruenergang.de/cases/ct2_e.html
On nonenhanced CT scans, FNH may appear as an isoattenuating or slightly hypoattenuating mass. Nonenhanced images are important because FNH may be missed without a precontrast study.
For the optimal evaluation of FNH, a helical CT scan with a 4-phase study should be performed. This evaluation should include nonenhanced and hepatic arterial, portal venous, and delayed–phase examinations.
After the administration of contrast material, the lesion becomes hyperattenuating relative to the surrounding liver in the arterial phase; this occurs approximately 20-30 seconds after the bolus of contrast agent is administered. In the portal venous phase, 70-90 seconds after the bolus injection, FNH is less conspicuous and becomes isoattenuating to the rest of the liver. During the delayed phase, approximately 5-10 minutes after the bolus injection, FNH is isoattenuating with normal liver.
In 15-33% of patients, conventional CT scans show the hypoattenuating stellate central scar.