2. Dr.K.Vinayachandran Nair MD,DM.
Encouraging us and asking right questions.
Dr.Jagdeesh MRCPCH ,FRCR. Passion about
liver nodules. Also lending many slides.
Few slides taken from google images.
3. I have to tell stories of
3 heroes… !
• Appropriate use of USG,CT and
MRI in liver imaging.
4. Ultrasound of liver what we can diagnose and
what we can not.
Primary liver lesions in cirrhotic liver.
CT versus MRI in liver lesions.
6. 65 year old male with dyspepsia , bloating ,
not alcoholic.
10. Caudate to right lobe
ratio more than 0.65
specific for cirrhosis.
11. Portal vein diameter is
not sensitive in
detecting portal
hypertension.
Color doppler is to
confirm direction of
flow , reversal
indicates portal
hypertension.
13. Increase of less than
20% in diameter of
portal vein with deep
inspiration indicates
portal hypertension.
Very difficult criteria
…!
14. Sensitivity and specificity varies from 60-
100% according to different studies.
World journal gastroenterology..2010.
15. Other criteria include
Cork screw / enlarged hepatic artery.
Loss of phasicity and pronounced cardiac
periodicity.
Reduced portal vein velocity.
Congestion index (ratio of area to flow velocity)
16. Is controversial. May not be beneficial
USG is not useful in detecting small (1-2 cm)
HCCs (sensitivity of 13 %).
More sensitive in detecting larger ( more than 4
cm) HCCs(sensitivity of 75%)
Can not differentiate between dysplastic nodule
and HCC.
AJR July 2002
20. Agents such as
perflubutane microbubble
cause contrast related
enhancement of focal liver
lesions.
Enhancement pattern is
used to assess cellular
differentiation of HCCs.
This can be repeated
realtime.
AJR
22. A technique to assess
fibrosis of liver.
Employs modified
ultrasound probe which
assesses velocity of a shear
wave created by a
vibratory source.
Values of above 12.5kPa
are indicative of cirrhosis.
23. 50 year old male with
Progressive abdominal
distension.
? Mass in right upper
quadrant
24. Lack of visualization of
hepatic veins and
narrowing of caliber of IVC
indicating Budd Chairi
syndrome. A difficult
diagnosis on USG needs
IVCgram for confirmation.
25. 20 year old nursing student studying in
Karnataka has come to emergency with right
upper quadrant pain , not jaundiced --?
cholecystitis
27. LFT showed elevated transaminases.
Hepatitis A IgM marker positive.
Final diagnosis – anicteric viral hepatitis.
29. Reason for showing this case is that there are
no specific sonographic findings for hepatitis.
Reduced echotexture of liver , gall bladder
wall thickening , hepatomegaly , starry sky
appearance of liver due to periportal edema
are described findings.
30. 27 years old male working as executive in a
company comes with elevated liver
transaminases.
Claims to be teetotaller.
33. Liver echogenicity exceeds that
of right kidney and spleen.
And
There is beam attenuation.
34. Most often subjective..!!
Grade 1– increased texture with good
visualization of diaphragm and intrahepatic
vessels.
Grade 2- mild impairment of visualization.
Grade 3– severe impairment of visualization.
35. Here there is fatty infiltration , hepatomegaly
and elevated liver enzymes. (AST and ALT).
Histologically, there is inflammation and
fibrosis.
Radiologically it is not possible to separate
NASH from ordinary fatty liver.
Fatty liver involves about 15% of population.
NASH involves about 2-5% of population.
37. 25 year old healthy male for employment
health checkup.
39. When USG shows hemangioma typical
features in a nononcology patient this
modality alone is considered sufficient.
42. Not sensitive in detecting small HCCs.
Can not differentiate between HCC and
dysplastic nodule.
Entire liver can not be assessed , few USG
blind areas in liver.
Moderate sensitivity in detecting cirrhosis.
43. Hemangioma in a nononcology patient , cyst
and to certain extent abscesses can be
confidently diagnosed with USG, for other
focal lesions one needs to assess further.
45. Varying signals; varying sizes, varying enhancement
Siphon out the dysplastic nodules & HCC!!
How!
Lesions MRI features:-post contrast behaviour
Intermediate/vague features/cross over features
Varying signals; varying sizes, varying enhancement
Siphon out the dysplastic nodules & HCC!!
How!
Lesions MRI features:-post contrast behaviour
Intermediate/vague features/cross over features
Varying signals; varying sizes, varying enhancement
Siphon out the dysplastic nodules & HCC!!
How!
Lesions MRI features:-post contrast behaviour
Intermediate/vague features/cross over features
51. Size
- diameter of less than 2 cm are more likely to be benign than
malignant
Vascularity
- shift from predominantly venous perfusion to predominantly
arterial perfusion
- dedifferentiated nodules - markedly enhanced on
early arterial phase
Hepatocellular Function
- hepatocellular contrast agents
52. most common cirrhosis-associated hepatocellular nodules
T2 : Isointense to liver; hypointense ( iron)
T1: Variable
Postcontrast:
- No arterial enhancement
- isointense enhancement to the liver
- washout isointense to liver
54. Low grade and high grade
T2 : hypointense or isointense to liver,
T1: Variable
Postcontrast:
- Patchy ill defined nodular arterial
enhancement
- isointense enhancement to the liver
- hypointense to liver in the later phases, no
definite tumor capsule
56. T2 : Hyperintense ( 94%) – isointense to spleen
T1: Variable
Postcontrast:
- Intense arterial enhancement
- isointense on the portal venous phase
- wash out on the later phase with persistent
tumor capsule
59. T1- and T2-weighted MR images, the mosaic pattern appears
as areas of variable signal intensities
lesions enhance in a heterogeneous fashion during the
arterial and later phases
61. Diffuse type HCC a
permeative tumor often with portal vein
thrombus.
62. LESION T2 T1 ART DEL
Reg N Low-iso Int - High No enhancement No wash out
Dys N Low-iso Int - High Heterogenenous
moderate
enhancement
Irregular wash
out with no
capsule
HCC Int - High Low - Int Intense
enhancement
Wash out with
enhancing
capsule
63. CT versus MRI mosaic pattern- 88%
T1- and T2-weighted MR
images, the mosaic pattern
appears as areas of variable
signal intensities
lesions enhance in a
heterogeneous fashion during
the arterial and later phases
64. When doing survey for metastasis , CT is
better as it can assess extra hepatic lesions
better than MRI.
65. In patient with chronic liver disease , for
characterization of regenerative ,dysplastic
nodules and HCC , MRI is better than CT.
66. There are several arterial phase enhancing
lesions.
TAHD – transient hepatic attenuation
difference.
Confluent hepatic fibrosis.
67. Contrast MR has sensitivity of near 81% and
specificity of near 85%.
CT has sensitivity of near 73% and sensitivity
of near 93%.
Imaging not sensitive for lesions less than 20
mm and diffuse lesions.
69. USG is the first line modality in liver imaging.
Used to rule out liver disease and diagnose
with confidence common lesions like cysts
and hemangiomas.
70. Multiphasic CT is the standard reference
study in liver disease. Standard in assessing
and follow up of oncology patients. When
high resolution MRI is not available can be
used to image cirrhosis.
71. MRI is modality of choice in assessing
cirrhosis liver . It is increasingly preferred in
follow up of patients and in children where
radiation is an issue.
Tissue specific contrast agents are being
available and are helpful.
72. Biopsy or follow up is advised in doubtful
lesions or histopathological confirmation is
necessary for management.
Decisions should be patient specific.
Good evening! Thank you for having me here to talk to you on Primary .....
Size
As lesions grow, the likelihood of high-grade dysplasia or frank malignancy increases. As a general rule, lesions with a diameter of less than 2 cm are more likely to be benign than malignant and, if malignant, are usually well differentiated (16,17). By comparison, lesions with a diameter of more than 2 cm are more likely to be malignant than benign and tend to be characterized by moderate to poor differentiation.
Vascularity
Regenerative nodules and low-grade dysplastic nodules are predominantly portally perfused and, after gadolinium administration, show enhancement similar to that of the surrounding liver (18,19). As dedifferentiation progresses within these nodules, angiogenic pathways are activated that induce new vessel formation, which manifests as an increased density of unpaired arteries and capillary units (16,18,20). This development leads to an increasing shift from predominantly venous perfusion to predominantly arterial perfusion as low-grade dysplastic nodules and hepatocellular carcinomas become high-grade lesions (18). The increasingly dedifferentiated nodules appear more markedly enhanced on early arterial phase images obtained after the intravenous injection of a contrast agent, with more pronounced washout on venous phase images and equilibrium phase images (21,22). The major shift in angiogenesis typically occurs during the transition from low-grade to high-grade dysplasia (18).
Hepatocellular Function
Regenerative nodules generally have normal hepatocellular function and therefore demonstrate avid uptake of hepatocellular contrast agents. As dedifferentiation proceeds, the number of expressed organic ion transporters decreases, with a resultant progressive reduction in the uptake of hepatocellular agents (22–25).
Kupffer Cell Density
The density of Kupffer cells within regenerative lesions is similar to that in the surrounding nonneoplastic hepatic parenchyma. The cell density is visible at contrast-enhanced imaging because Kupffer cells avidly accumulate particulate agents through phagocytic mechanisms. With dedifferentiation, the Kupffer cell density changes; however, such changes are unpredictable during the early stages of carcinogenesis. According to empirically derived values reported in the literature, dysplastic nodules and well-differentiated hepatocellular carcinomas have variable Kupffer cell densities, ranging from diminished to elevated levels (26–28). Moderately and poorly differentiated hepatocellular carcinomas tend to have a diminished Kupffer cell density (26,27).
form in response to necrosis, altered circulation, or other stimuli (
most have a diameter of less than 2 cm,
Steatotic regenerative nodules tend to occur in multiples (Fig 2). A single fatty nodule is suggestive of a dysplastic or malignant process (Fig 3).
Lesions with dysplastic features that do not satisfy the histologic criteria for malignancy or invasion are described as either(a) dysplastic foci (<1 mm in diameter) or (b) dysplastic nodules (≥1 mm in diameter). Dysplastic nodules usually occur in the setting of cirrhosis and may be classified as low or high grade, according to the degree of dysplasia.
Fig. 37.2. Dysplastic nodules, cirrhotic liver, MRI findings. A Coronal SSTSE image
(SSTSE): Multiple low signal intensity nodules are present with a cirrhotic
liver with splenomegaly and ascites (*). B Axial fat-suppressed TSE
image (TSE fatsat): All nodules show low signal intensity. C Axial arterial
phase image (ART): The largest nodule shows increased enhancement
(arrow); other lesions show variable enhancement. D Axial delayed phase
image (DEL): The largest nodule (arrow) does not show any enhancing tumor
capsule. E Axial opposed-phase image (T1 opposed-phase): Most hepatic
nodules are bright. F Axial in-phase image (T1 in-phase): Several nodules
lose their signal due to iron accumulation, i.e. siderotic nodules
(arrows); note also the dark Gamna-Gandy bodies in the spleen. G Detailed
view of the arterial phase (ART): The largest nodule clearly shows enhancement
(arrow). H Detailed view of the delayed phase (DEL): The largest nodule
does not show a tumor capsule (arrow)
Fig. 37.3. Dysplastic nodules, histopathology, drawings. A Photomicrograph
shows a large nodule surrounded by fibrous septa. H&E stain, ×20. B A detailed
photomicrograph shows increased cellularity with variable size of the
nuclei indicating at least dysplastic changes. H&E stain, ×100. C Situation I
shows the presence of several dysplastic (DN) and regenerative (RN) nodules
in a cirrhotic liver. D Situation II shows the presence of a focus of HCC
with the largest DN (arrow)
37 Cirrhosis III – Dysplastic Nodules 81
Only 52% have these classic features
Fig. 46.2. HCC, cirrhotic liver, large, mosaic pattern, typical MRI findings. A Axial
SSTSE image (SSTSE): HCC is predominantly hyperintense to the liver. The
tumor capsule is hypointense and not visible. B Axial in-phase image (T1 inphase):
HCC is predominantly hyperintense to the cirrhotic liver with a
darker tumor capsule. C Axial arterial phase image (ART): HCC shows intense
enhancement in some areas, indicating themosaic pattern. D Axial delayed
phase image (DEL): HCC shows washout with enhanced thick tumor
capsule. E A detailed view of the SSTSE image (SSTSE): HCC shows areas
with high and low signal indicating the mosaic pattern. F Axial opposedphase
T1-w GRE image (T1 opposed-phase): HCC as well as the cirrhotic
liver show no signs of fatty infiltration. G Axial portal phase image (POR):
HCC shows washout with enhanced thick tumor capsule. H A detailed view
of the axial delayed phase 2D T1-w GRE image (DEL): HCC is surrounded by
an enhanced thick tumor capsule (arrow)
Not sensitive for lesions less than 20 mm and carcinomatosis.