Liver imaging snapshots role of CT USG MRI in liver imaging.
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presentation showing role of modalities in liver imaging. Role of USG,CT and MRI
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Liver imaging snapshots role of CT USG MRI in liver imaging.
- 1. Appropriate use of USG,CT and MRI in liver imaging.
- 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.
- 8. Coarse texture , multiple tiny nodules. Nodularity of liver contour. Cirrhosis of liver.
- 9. Surface nodularity with high frequency probe.
- 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.
- 12. Splenomegaly and collaterals are indicative of 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
- 17. Small HCC Large HCC
- 18. Diffuse type HCC , no mass detected on USG. Liver transplantation surgery showed diffuse HCC. Slide taken from AJR
- 19. IT CAN DIFFERENTIATE TUMOR FROM BLAND THROMBUS. Portal vein
- 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
- 21. Enhancement and washout in a poorly differentiated HCC 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.
- 32. Increased liver texture indicating fatty liver.
- 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.
- 36. Focal fatty infiltration can simulate mass. Focal fatty sparing can also mimic mass.
- 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
- 46. T2, T2FS T1
- 47. T1 in and opposed phase
- 48. Dynamic post contrastT1FS(fat saturation) with subtracted images
- 50. Regenerative Nodules ; Siderotic nodules Dysplastic Nodules HCC
- 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.
- 73. Diffusion weighted imaging Mixed extracellular and hepatocellular contrast agents -gadoxetic acid disodium MR spectroscopy Liver perfusion
- 74. Diffusion imaging liver.
Editor's Notes
- 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.