focal liver lesion and tumors hepatology.pptx

hcc, hepatic adenoma, hemangioma

1. FOCAL LIVER LESIONS PRESENTED BY DR.SAMBIT KUMAR PATEL DM RESIDENT HEPATOLOGY SCBMCH

2. For surgery

3. PV anatomy and flow

4. ULTRASONOGRAPHY PROS Availability/ low cost Parenchyma assessment Detection of liver lesion and characterise Into solid/cystic Doppler to detect complications of phtn Hcc surveillance and FNAC CONS Operator dependent technical limitations

5. MULTIPHASIC CT SCAN For detection, characterization & differentiation of benign and malignant liver lesions. Non contrast CT- Calcification, fat, hemorrhage. Contrast CT- Arterial phase(early 15-20 sec p.i ./late 35-40 sec p.i .) Portal venous phase(70-80 sec p.i .) Delayed phase(6 min p.i .)

6. Understanding the phases Liver has dual blood supply. Normal parenchyma is supplied for 80% by portal vein & only for 20% by hepatic artery. All liver tumors get their blood supply from hepatic artery.

7. Arterial phase Hypervascular tumors enhance via the hepatic artery, when normal liver parenchyma does not yet enhance, because contrast is not yet in the portal venous system. Hypervascular tumors enhance optimally at 35 sec after contrast injection. Hypervascular lesions Benign: Hemangioma Adenoma FNH Malignant: HCC Metastases( RCC,carcinoid,thyroid ca,NET,sarcoma )

8. Portal venous phase Normal liver parenchyma enhances in this phase. To detect hypovascular tumors(more common, majorities are metastases ). Scanning is done at about 75 seconds . Delayed/equilibrium/washout phase Begins at about 3-4minutes after contrast injection &imaging is best done at 10 minutes. Valuable for washout of contrast (HCC), retention of contrast in blood pool ( hemangioma ) & retention of contrast in fibrous tissue ( capsule of HCC, central scar of FNH ).

9. MRI LIVER SPECIFIC AGENTS act like non-specific extracellular gadolinium chelates post bolus injection and show three primary phases of vascular and tissue enhancement. However, in the delayed ( hepatobiliary ) phase, they are taken up by the liver as their excretion is not only through the renal but the hepatic route as well.

10. CE-MRI TIMING

11. Focal liver lesions Benign Hemangioma Focal nodular hyperplasia(FNH) Adenoma Cyst Abscess Malignant Hepatocellular carcinoma(HCC) Fibrolamellar carcinoma(FLC) Intrahepatic cholangiocarcinoma (ICCA) Metastases Hepatoblastoma Lymphoma Angiosarcoma Epithelial hemangioendothelioma

12. HEMANGIOMA Commonest benign hyper vascular liver tumor. female predominant Size varies , > 10 cm (giant hemangioma ). Calcification is rare & seen in <10%, usually in the central scar of giant hemangioma .

13. USG Typically well defined, homogeneous & hyper- echoic lesions(67%-79%). May be hypoechoic , within background of fatty liver . Large lesion-heterogeneous with central hypo -echoic foci.

14. CT SCAN NECT: Well defined low density mass. CECT: Diagnostic triad Discontinuous, nodular, peripheral enhancement starting at arterial phase & gradual central filling in. Retention of contrast in delayed phase.

15. MRI T1WI: Hypo-intense relative to liver parenchyma. T2WI: Significantly hyperintense –producing light bulb appearance. GD: Similar to CECT.

16. FOCAL NODULAR HYPERPLASIA 2 nd most common benign tumor Characterized by a central fibrous scar surrounded by nodules of hyperplasic hepatocytes & small bile ductules. More prevalent in women of reproductive age & associated with OCP use. Usually solitary(95%). No capsule. Asymptomatic.

17. USG in FNH Subtle iso -echoic mass with contour abnormality. Central scar- hypo/hyper-echoic linear or stellate area. Doppler study: well developed peripheral & central blood vessels are seen.

18. CT SCAN NECT: Homogeneous low density mass, often with a central low density (central scar). CECT: lesion enhance markedly & uniformly in arterial phase with exception of central scar. Isodense to normal liver parenchyma in PVP. Contrast accumulates within the central scar in delayed phase.

19. FNH conti .

20. HEPATIC ADENOMA Consists of hepatocytes arranged in cords. Lacks of portal tracts, hepatic vein, kupffer cell & biliary canaliculi . Fat & glycogen rich hepatocytes are often present. Most common in women, with H/O OCP or anabolic steroid. Usually solitary. Central hemorrhage/necrosis. Thin capsule. Association: type 1 glycogen storage disease. Complication: potential for rupture & may result hemoperitonium , risk of malignant transformation .

21. USG : Well demarcated with variable echogenecity .

22. CT SCAN: NECT: low attenuation mass (fat, glycogen), high density if hemorrhage present. CECT: early peripheral with centripetal enhancement, no retention of contrast in later phases because of AV shunting .

23. MRI T1WI: mildly increased signal intensity( fat & hemorrhage). T2WI: heterogeneous with iso , hypo & hyperintense areas. Capsule- hypointense rim. T1C+(GD) : similar to CECT.

24. HEPATOCELLULAR CARCINOMA(HCC) Commonest primary malignant neoplasm of liver. Consists of abnormal hepatocytes arranged in a typical trabecular pattern. May be solitary, multiple nodules or diffusely infiltrating. Alpha- fetoprotein levels are elevated. 80% of HCC occur in cirrhotic liver. There is propensity toward venous invasion(PV>HV).

25. USG Variable in appearance. Small <5 cm usually hypoechoic , can uniformly hyperechoic indistinguisable from focal fat / hemangioma . A thin ,peripheral hypoechoic halo( fibrous capsule). Larger tumors often are heterogeneous ( necrosis,hge & fibrosis). May invade the portal & hepatic veins. Most tumor will show central vascularity on Doppler study.

26. CT SCAN NECT: large hypodense mass, often with central area of low attenuation(necrosis). May be isodense to liver. CECT: non necrotic area enhances strongly in arterial phase & early washout in subsequent phases . Peripheral rim enhancement in delayed phage. Detection of venous invasion ( portal,hepatic veins,IVC ).

27. MRI T1WI : variable (fatty change, internal fibrosis,hemorrhage ) T2WI : hyperintense CEMR : similar to CECT

28. Regenerative nodules

29. FIBROLAMELLAR CARCINOMA Histologic subtype of HCC. young adults & adolescents. No coexisting liver disease. The serum AFP levels are usually normal. The prognosis is better compared with HCC. Hemorrhage & necrosis –rare. A fibrous central scar may present. Calcification is common(within the scar in stellate pattern).

30. USG Echogenecity of FLC is variable. Puncate calcification & central echogenic scar. CT SCAN: NECT: well defined ,low density mass with a more low attenuating central scar. CECT: moderate enhancement of the lesion with delayed enhancement of scar.

31. CT SCAN: NECT: well defined ,low density mass with a more low attenuating central scar. CECT: moderate enhancement of the lesion with delayed enhancement of scar

32. HCC FLC Risk factor Occur in cirrhotic liver Normal liver Age Old Age Young adult S.AFP Elevated Normal Central scar Less common More common Hemorrhage, necrosis more less Calcification Portal vein thrombus Less common More common More common Less common

33. INTRAHEPATIC CHOLANGIOCARCINOMA 10 % of all cholangiocarcinoma . Usually large, firm masses with abundant fibrous tissue. Desmoplastic reaction is prominent. Age: 7 th decade. M>F. Increased incidence- carolis disease, sclerosing cholangitis , IH calculi & IBD. A normal Serum AFP may be helpful in suggesting ICCA rather than HCC.

34. CT SCAN NECT: well defined round to oval hypo dense mass. CECT : typically shows early peripheral enhancement. Centre of the tumor remains no enhanced (abundant fibrous stroma ). In delayed phase centre of the tumor is enhanced . Capsule retraction and biliary dilatation adjacent to mass is highly suggestive of ICCA.

35. early peripheral enhancement. Centre of the tumor remains no enhanced In delayed phase centre of the tumor is enhanced

36. MRI The tumour is hypointense on T1WI & hyperintense on T2WI with an irregular contour . CEMRI is similar to CECT.

37. HCC IHCC Pathology Soft tumor(lack of stroma ) Hard mass(abundant fibrous tissue) Risk factor Cirrhosis, alcoholism Sclerosing cholangitis carolies disease,IBD Hge & necrosis Common rare Capsular retraction Less common Common(fibrosis) Vascular invasion common Less common NECT Hypodense Homogenous hypodense CECT Early enhancement(Arterial phase), early washout( later phases). Heterogeneous minor peripheral enhancement with gradual enhancement centrally.

38. hemangioma ICCA metastasis age Any age Older age(7 th decade) Older(but can occur any age) sex F M M=F MRI(T2WI) Iight bulb appearance Hyperintense Variable Cystic—light bulb Post contrast Nodular peripheral enhancement Mild heterogenious peripheral enhancement,except central scar Peripheral r im like enhancement Bile duct invasion no common Less common Capsular retraction No common No

39. Metastases Liver is the most common site of metastasis. Usually multiple. Majorities are hypovascular (GI tract,lung breast& head,neck tumour , lymphoma). Hypervascular metastasis are less ( NET, RCC, carcinoid , sarcoma, melanoma). Calcified metastases are uncommon( colon, stomach, breast,melanoma ). Cystic meatstases occur from mucinous ca of ovary, colon, sarcoma, melanoma

40. USG Sonographic appreance is variable( iso , hypo, hyperechoic , calcified or cystic).

41. CT SCAN NECT: Typically hypodense , may be iso or hyperdense , cystic, mixed,calcified . CECT: Enhancement is typically peripheral in arterial phase & washout in delayed phase.

42. MRI Variable but usually most metastatic nodules are hypointense on T1W & hyperintense on T2WI. High signal intensity in T1WI- mets from melanoma, ca colon. Higher signal on T2WI- mets with liquifective necrosis. CEMRI: variable .

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