CT SCAN Non contrast study: Contrast study: arterial phase: 20-40secs Portal phase : 60-80secs Early delayed: > 180 sec , best at 4 mins Late delayed : 4-6hrs
Understanding the phases Liver -dual blood supply Normal parenchyma - 80% portal vein 20 % -hepatic artery All liver tumors blood supply from hepatic artery
Arterial phase 20- 40 sec Hypervascular tumors enhance via the hepatic artery Normal liver parenchyma not yet enhanced Hypervascular tumors enhance optimally at 35 sec
Delayed Phase Begins at about > 180 sec Best done at 10 minutes
Characterisation of liver masses Density: Enhancement: hypervascular tumors may look similar in arterial phase. Other phases can differentiates the lesions.
Hypovascular lesions : Hypovascular liver tumors are more common than hypervascular tumors. Most hypovascular lesions are malignant and metastases are by far the most common. Although primary liver tumors are mostly hypervascular , there are exceptions. 10% of HCC is hypovascular . Cholangioca is hypovascular , but may show delayed enhancement Scar :
SCAR T1W T2W FLC HYPO HYPO FNH HYPO HYPER
Central scar in all lesions are hypointense in both T1 and T2, except FNH is hyperintense due to edema. T2WI is better to differentiate FNH from FLC Capsule : Adenoma HCC Cystadenoma Cholangiocarcinoma Capsule in Adenoma not seen in portal venous phase and well appreciated in delayed phase NECT and Arterial phase image showing hypodense capsule of HCC Bright enhancing capsule of HCC in equilibrium phase
Retraction of the liver capsule : C holangiocarcinoma Metastasis from breast Peripheral enhancement and progressive fill in Peripheral rim enhancement is a typical feature of malignant lesions and only discontinuous nodular peripheral enhancement that matches bloodpool is a typical feature of hemangioma .
Pre contrast Arterial Phase Portal venous phase Delayed Hepatocelluar Ca Low attenuation Homogenous enhancement Washout of lesion I sodense Adenoma Low attenuation Homogenous enhancement 85% Iso or hypodense Iso or hypodense Haemangioma Low attenuation Peripheral puddles Partial Fill in Complete fill in FNH Iso /Low attenuation Homogenous enhancement Hypodense Isodense Hypervascular Mets Low attenuation Homogenous enhancement Hypodense Metastasis Low attenuation Hypodense Hypodense Cyst Low attenuation No enhancement Abscess Low attenuation may have irregular margins Transient regional enhancement Ring enhancement Multiphasic CT of Liver
Benign vascular lesions of liver. The commonest liver tumor 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 discovry : US++ hemangiomas
Sonographically : hemangiomas are typically hyperechoic and well demarcated and exhibit faint acoustic enhancement but may vary depending upon necrosis and hemorrhage. Color Doppler ultrasound demonstrates fi lling vessels in the periphery of the tumor but no signifi cant color Doppler fl ow deep within the hemangioma itself.
CT : The pathognomonic features of hemangioma : peripheral nodular and discontinuous enhancement and progressive centripetal fill-in IV- HAP PVP DP
Diagnosis CT : venous enhancement from periphery to center
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
Diagnosis MRI :
Pre contrast Arterial Phase Portal venous phase Delayed Hepatocelluar Ca Low attenuation Homogenous enhancement Washout of lesion Isodense Adenoma Low attenuation Homogenous enhancement 85% Iso or hypodense Iso or hypodense Haemangioma Low attenuation Peripheral puddles Partial Fill in Complete fill in FNH Iso /Low attenuation Homogenous enhancement Hypodense Isodense Hypervascular Mets Low attenuation Homogenous enhancement Hypodense Metastasis Low attenuation Hypodense Hypodense Cyst Low attenuation No enhancement Abscess Low attenuation may have irregular margins Transient regional enhancement Ring enhancement Multiphasic CT of Liver
CYSTS AND CYSTIC TUMORS S imple Cyst: A simple hepatic (bile duct) cyst isa single, unilocular cyst lined by a single layer of cuboidal , bile duct epithelium. wall is a thin layer of fi brous tissue, 1 mm or less in thickness. number fewer than 10. When more than 10 cysts are seen, one of the fi bropolycystic diseases should be considered. .
Bile Duct Hamartomas (von Meyenberg Complexes) focal disorderly collection of bile ducts that is due to failure of involution of embryonic bile ducts. lesions are 1 to 5 mm. On CT, innumerable cystic lesions less than 5 mm in diameter are present. They show no contrast enhancement
CYSTADENOMA AND CYSTADENOCARCINOMA Biliary cystadenoma and cystadenocarcinoma are currently considered forms of the same disease, with cystadenocarcinoma being overtly malignant and cystadenoma having malignant potential. commonly mucinous,rarely serous type Polypoid projections and papillary areas are frequently present usually solitary and may become up to 30 cm in size. ERCP studies can show communication of the tumor with the bile duct .
Cystadenoma or cystadenocarcinoma of the liver usually appears as a large, unilocular or multilocular mass on cross-sectional imaging. Ultrasound: Demonstrates the septa, as well as the mural nodules in the wall of these tumors. CT: Large, unilocular or multilocular low-attenuation intra hepatic masses with well defined thick fibrous capsules, mural nodules, and internal septa. Calcification may be seen within the wall and septa in a minority of cases.
multiseptated and have predominantly high signal on T2WI and mixed or low signal on T1WI. A low signal rim on T2-weighted images may be due to hemorrhage in the wall of the lesion.
Radiologically , it is impossible to distinguish cystadenomas from cystadenocarcinomas , However, the combination of septation and nodularity is suggestive of cystadenocarcinoma .
Focal nodular hyperplasia Asymptomatic/incidental Etiology- unkn / ? Cong vascular malformation Female -20-50 yrs. Typical central stellate fibrovascular scar - 50 % Hyper vascular Normal liver elements Hepatocytes Non communicating bile ducts, Kupffer cells Fibrous septa
USG: Well defined isoechoic mass Homogenous echotexture Central hypo scar Calcification seen in 1.4 % . DOPPLER : stellate flow pattern central A with centrifugal filling
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
NECT : Well defined with mass effect Attenuation same as that of liver parenchyma/ less - fat Central scar common. Arterial phase : Lesion enhance markedly and uniformly with the exception of central scar. Portal phase : Isodense with liver parenchyma Scar- low. Delayed imaging : iso dense Scar may show enhancement.
Diagnosis : CT HAP PVP DP IV-
Diagnosis : CT
MRI T1 : Isointense T2 : Slightly hyperintense to isointense . central scar is hypointense on T1 and hyperintense on T2. Early homogenous enhancement of FNH , late enhancement of the central scar.
T2 WITH SPIO : FNH shows loss of signal due to uptake of iron oxide particles by kupffer cells within the lesion. The degree of signal loss is greater than normal liver T1 WITH Mn DPDP / BOPTA FNH contains hepatocytes that take up these agents resulting in hyperintensity of the lesion relative to the liver.
Diagnosis :MRI typical finding
Pre contrast Arterial Phase Portal venous phase Delayed Hepatocelluar Ca Low attenuation Homogenous enhancement Washout of lesion Isodense Adenoma Low attenuation Homogenous enhancement 85% Iso or hypodense Iso or hypodense Haemangioma Low attenuation Peripheral puddles Partial Fill in Complete fill in FNH Iso /Low attenuation Homogenous enhancement Hypodense Isodense Hypervascular Mets Low attenuation Homogenous enhancement Hypodense Metastasis Low attenuation Hypodense Hypodense Cyst Low attenuation No enhancement Abscess Low attenuation may have irregular margins Transient regional enhancement Ring enhancement Multiphasic CT of Liver
. 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 . Benign neoplasm composed of normal hepatocytes no portal tract, central veins, or bile ducts . Surrounded by a capsule . Surgical resection is generally advised HEPATIC ADENOMA
USG : Large hyperechoic lesion- glycogen / fat
PLAIN CT : Low density lesion (fat) High density lesion ( hge ) CECT : Hypervascular lesion , rapid washout Calcification +/- 5 %
MRI Heterogenous Increased T1 signal Fat/ glycogen Low signal – hemorrhage/ necrosis/ scar Hypointense capsule T1 and T2 - 1/3 rd
Radionuclide Scintigraphy the absence of Kupffer cells, most (80%) of HA appear cold on sulphur colloid scintigraphy . On hepatobiliary scintigrams , HAs usually show uptake of the tracer. Because of the lack of bile ductules , the tracer is not excreted and delayed scans therefore depict HAs as areas of markedly increased activity
Pre contrast Arterial Phase Portal venous phase Delayed Hepatocelluar Ca Low attenuation Homogenous enhancement Washout of lesion Isodense Adenoma Low attenuation Homogenous enhancement 85% Iso or hypodense Iso or hypodense Haemangioma Low attenuation Peripheral puddles Partial Fill in Complete fill in FNH Iso /Low attenuation Homogenous enhancement Hypodense Isodense Hypervascular Mets Low attenuation Homogenous enhancement Hypodense Metastasis Low attenuation Hypodense Hypodense Cyst Low attenuation No enhancement Abscess Low attenuation may have irregular margins Transient regional enhancement Ring enhancement Multiphasic CT of Liver
Significant overlap is noted between the CT appearances of adenoma, HCC, FNH, and hypervascular metastases, making a definitive diagnosis based on CT imaging criteria alone difficult and often not possible. young women using oral contraceptives, Patients with glycogen storage disease, hemochromatosis , acromegaly , or males on anabolic steroids adenomas. A history of cirrhosis and high AFP levels favor HCC. A history of a primary hypervascular tumor favors metastases.
Hepatobiliary Gadolinium Enhanced MRI Hepatobiliary contrast agents can be used to detect metastases , characterize liver lesions (with or without hepatocyte function/uptake) and to evaluate biliary excretion. There are two different hepatobiliary paramagnetic gadolinium chelates , gadobenate dimeglumine ( Gd -BOPTA; Multi- Hance ®, Bracco Imaging, Milan, Italy) and gadoxetic acid (Gd-EOB; Primovist®, Bayer Schering Pharma AG, Berlin,
Hepatic Adenoma and Focal Nodular Hyperplasia: MR Findings with Superparamagnetic Iron Oxide Enhanced MRI (SPIO) SPIO is a contrast agent that undergoes phagocytosis by the reticuloendothelial system ( Kupffer cells). Hepatic adenoma FNH T1 HYPER ISO T2 HETEROGENOUS ISO TO HYPER SPIO POOR UPTAKE WELL UPTAKE
Fibrolamellar Carcinoma Age group: 5 - 35yrs Spontaneous No predisposing factor Solitary lobulated well defined tumor containing a central fibrous scar . Punctate calcification- in scar >50% cases
Moderate enhancement. Delayed enhancement of scar Prognosis - good .
USG: Large hyperechoic homogenous mass CT: Hypodense mass Well defined contour Central scar - Calc Marked enhancement because of its hypervascularity . MRI : Hypo/ iso on T1 Iso /slightly hyperintense on T2 Scar -hypointense on both T1 and T2.
FNH v/s FLC Central scar of FNH -hyperintense on T2. FNH rarely has calcification within the scar. FNH - usually asymptomatic. Biopsy normal hepatocytes with bile ductules in FNH Malignant, eosinophilic hepatocytes in FLC
Hepatocellular Carcinoma Most common primary malignancy of the liver Rising incidence, attributed to a rise in hepatitis B and C infection
Risk factors: hepatitis B (HBV) infection hepatitis C (HCV) infection alcoholism biliary cirrhosis food toxins e.g. aflatoxins congenital biliary atresia inborn errors of metabolism haemochromatosis alpha-1 antitrypsin deficiency type 1 glycogen storage disease Wilson disease
Usually too small to detect by imaging May be surrounded by fibrotic septa May contain iron , copper Siderotic regenerating Nodules Hyperdense on NCCT , disappear on HAP & PVP Variable on T1, Hypointense on T2 MR, “bloom” on GRE Regenerating Nodules
Dysplastic Nodules Rarely diagnosed by US or CT Iso to hyperintense on T1 (copper) Iso to Hypo on T2 ( opposite of HCC ) Should not enhance much on HAP
USG Small HCC’s (<3cms) hypoechoic with posterior acoustic enhancement >3cms- mosaic or mixed pattern
(1) single or massive HCC-(better prognosis) (2) nodular or multifocal HCC (3) diffuse or cirrhotomimetic HCC Frequently undergoes necroses and hemorrhages because of lack of stroma . Vascular invasion of perihepatic vessels is common. Conversely, biliary invasion is uncommon
Arterial Phase : liver(30-35 sec) HCC as supplied by arterial branch/ neovascularization 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
Delayed Phase : Wash -out phenomenan persists and often exaggerated in smaller lesions. The tumor capsule IV- HAP PVP DP capsule
Hepatocellular Carcinoma (HCC)
MRI . Variable intensity of HCC on T1 . 35% hyper, 25% iso-, 40 % hypo . Hyperintense (T1) often well - differentiated , contain fat, copper , glycogene . Almost always hyperintense on T2 MR . The tumor capsule is hypointense on both T1- and T2-weighted images in most cases . Other Features : Focal fat
Regenerative nodules Dysplastic nodules HCC T1 ISO HYPER ISO TO HYPO T2 ISO HYPO HYPER BOPTA INCREAS UPTAKE
SPIO increases the sensitivity of MR MnDPDP / BOPTA - hepatobiliary agent taken up by lesions that contain hepatocytes resulting in increased signal on T1.
MRI Small HCC’s v/s regenerative Cirrhotic nodule: hyper on T1 , iso / hypo on T2 HCC : hyperintense on T2 HCC arising in a siderotic nodule: “nodule within a nodule” appearance HCC - a small focus of high signal intensity within the low signal intensity nodule .
MRI
Portal venous invasion by hepatocellular carcinoma. portal phase-expanded low attenuation focus in right portal vein.
Hepatocellular carcinoma and regenerative nodule. T1w MRI (A) and T2w MRI (B) demonstrating a hepatocellular carcinoma (white arrowhead) and an adjacent atypical regenerative nodule (black arrowhead). Majority of hepatomas have decreased signal intensity on T1WI -increased signal -fat or glycogen content
Liver nodule < 1 cm > 1 cm Reapeat US at 3 months Growing/changing character Stable Investigate according to size 4 – phase MDCT/dynamic Contrast enhanced MRI Arterial hypervascularity AND venous or delayed phase washout Other contrast enhanced Study (CT or MRI) Arterial hypervascularity AND venous or delayed phase washout Yes No Yes No HCC Biopsy 2010 AASLD Algorithm for Investigation of Small Nodules Found On Screening in Patients with Cirrhosis Bruix J and Sherman M. AASLD Practice Guidelines , Management of Hepatocellular Carcinoma Hepatology November 2011 DIAGNOSIS : patients with cirrhosis or chronic hepatitis (even without cirrhosis)
Cholangiocarcinoma Cholangiocarcinoma usually presents as a mass of 5-20cm. In 65% there are satellite nodules and in some cases punctate calcifications are seen. Because cholangiocarcinoma has a varied morphology and histology, it is difficult to diagnose. It can be a constricting or an expanding lesion, because it can have a fibrous or a glandular stroma . It can be located anywhere in the intrahepatic bile ducts or common bile duct. The lesion is hypodens in the arterial and portal venous phase with some peripheral enhancement. The lesion is hyperdense in the equilibrium phase indicating dens fibrous tissue. The lesion causes retraction of the liver capsule
The finding of an infiltrating mass with capsular retraction and delayed persistent enhancement is very typical for a cholangiocarcinoma .
Pre contrast Arterial Phase Portal venous phase Delayed Hepatocelluar Ca Low attenuation Homogenous enhancement Washout of lesion Isodense Adenoma Low attenuation Homogenous enhancement 85% Iso or hypodense Iso or hypodense Haemangioma Low attenuation Peripheral puddles Partial Fill in Complete fill in FNH Iso /Low attenuation Homogenous enhancement Hypodense Isodense Hypervascular Mets Low attenuation Homogenous enhancement Hypodense Metastasis Low attenuation Hypodense Hypodense Cyst Low attenuation No enhancement Abscess Low attenuation may have irregular margins Transient regional enhancement Ring enhancement Multiphasic CT of Liver
METASTASES
Metastatic disease . Most common malignant hepatic tumor . Presence of extrahepatic malignancy should be sought in patients with characteristic liver lesions per imaging studies. Physical exam and history is very helpful. . 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.
Metastatic disease . MDCT are the most commonly used imaging modalities for detection and characterization of hepatic metastases . 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
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 n ecrosis 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 .
Pre contrast Arterial Phase Portal venous phase Delayed Hepatocelluar Ca Low attenuation Homogenous enhancement Washout of lesion Isodense Adenoma Low attenuation Homogenous enhancement 85% Iso or hypodense Iso or hypodense Haemangioma Low attenuation Peripheral puddles Partial Fill in Complete fill in FNH Iso /Low attenuation Homogenous enhancement Hypodense Isodense Hypervascular Mets Low attenuation Homogenous enhancement Hypodense Metastasis Low attenuation Hypodense Hypodense Cyst Low attenuation No enhancement Abscess Low attenuation may have irregular margins Transient regional enhancement Ring enhancement Multiphasic CT of Liver