PRESENTOR : Dr Navni Garg MODERATOR : Dr Sonal Krishan

PRESENTOR : Dr Navni Garg MODERATOR : Dr Sonal Krishan
IMAGING IN BENIGN HEPATIC MASSES PRESENTOR : Dr Navni Garg MODERATOR : Dr Sonal Krishan SEMINAR JUNE 26,2014

Focal liver lesion is by definition a discrete abnormality arising within the liver
Features of intra hepatic lesion Most of the lesion within the liver with respiration Bulging of the liver capsule Displacement and distortion of the portal and hepatic vessels Post displacement of IVC

BENIGN HEPATIC MASSES Developmental Infective/Inflammatory :
Pyogenic abscess Amoebic abscess Fungal abscess Hydatid cyst Granulomatous: Tuberculosis Sarcoidosis Neoplastic

Benign neoplasms Cholangiocellular (bile duct epithelium) Hemangioma
Hepatocellular (hepatocyte) Cholangiocellular (bile duct epithelium) Mesenchymal Hemangioma (most common) Mesenchymal hamartoma Infantile hemangio- Endothelioma Lymphangioma/ Lipoma/fibroma/ Angiomyolipoma/ Leiomyoma/ Hepatic cysts Adenoma FNH (2nd most common) Biliary cystadenoma

Malignant neoplasms Hepatocellular Mesenchymal Cholangiocellular
Hepatcellular Ca Fibrolamellar carcinoma Hepatoblastoma Cholangiocarcinoma Cystadenocarcinoma Angiosarcoma Epitheliod hemangio- Endothelioma Leiomyosarcoma Lymphoma HEPATIC METASTASIS

Imaging modalities Radiological Nuclear Medicine Newer Conventional
PET CT Newer methods Nuclear scans US CT MRI CTAP CE-USG DWI 99Tc-sulphur colloid Elasto graphy 99Tc-RBC scan

MDCT protocol for hepatic imaging
Radiographics 2001

CT arterioportogapgy scan(CTAP)
Principle: tremendous enhancement of normal liver parenchyma following the SMA or splenic artery injection Technique-conventional angiogarphy. End hole catheter in splenic artery /SMA 150 ml iodinated contrast 150 to 300 I/ml at 3 to ml/s. Start scan at 30s. Limitations – nontumous perfusion defect- d/t to laminar flow in the PV, aberrant vascular supply defect RCNA 1998

CT arterioportogapgy scan(CTAP)
most sensitive technique for detection of focal hepatic neoplasm. Sensitivity 80-90% for metastasis and 70% for primary malignant neoplasm.higher sensitivity for smaller liver SOL. Disadvantage-low specificity, cost and need for the invasive procedure. Replacement with GD and ferumoxide enhanced MRI may be reasonable. RCNA 1998

CT hepatic angiography scan
Principle: all hepatic neoplasm are largely supplied by the hepatic artery. Technique: angiographic catheter is placed in common hepatic artery. Scan delay 3-5 s of contrast injection.70 ml of diluted iodinated % at 2ml/s. Applications. use full in combination with the CTAP scan for characterizing the lesions and for for characterization of portal perfusion defect. RCNA 1998

Iodized oil CT scan Principle: lipiodol -iodized ethyl ester of acids of poppy seed oil.Prolonged retention of lipiodol in highly vascular and abnormal tissue. Technique: two step procedure Step 1- complete angiographic study f/b injection of 5- 20ml of lipiodol in proper hepatic artery beyond GDA . Step 2- CT scan of liver in 7 to 28 days. Applications – highly sensitive method for diagnosing small foci of the HCC and intrahepatic metastatic nodule of HCC. Sensitivity 97%, specificity 76%, accuracy 88%. Can differentiate between dysplastic nodule and small HCC

MRI in liver tumors T1weighted breath hold spoiled gradient- entire liver scanned in single breath hold ,TR ms, TE- minimum,8x2+- fat sat T2 weighted sequence- SE T2 , TR 4000, TE- 100, with respiratory trigger. FSE breath hold. Fat suppression Half Fourier acquisition single shot turbospin echoe. Contrast enhanced sequences

MRI protocol Radiographics 2000

MRI CONTRAST AGENTS IN LIVER IMAGING

MRI CONTRAST AGENTS Mri contrast maximises the SI b/w two tissues by either increasing or decreasing the SI of tissue relative to another Should produce large effect at low conc., s/b biocompatible, low tolerable toxicity,stable invivo as well as invitro(shelf life), s/b excreted in reasonable time, s/b organ specific as far as possible.

TYPES OF MRI CONTRAST T1 agents
Transitional & lanthanide (Gd) metal ions Paramagnetic substances (unpaired e-)resultent fluctuating magnetic field affect proton relaxation Increases T1 relaxation Increases SI (+contrast) T2 agents Feromagnetic & super paramagnetic substances, have little effect on tissue relaxivity Induce dephasing d/t their net positive magnetization Protons undergo transverse relaxation/ T2 relaxation Decreased SI on T2 (-ve contrast)

T1 AGENTS FDA approved IONIC
Gd-DTPA (gadopantate dimeglumine)= Magnevist NONIONIC Gd-DTPA-BMA(gadopentate diamide)=Omniscan Gd-HP-DO3A(gadoteridol)=Prohance Approved in european countries Gd-DOTA(gadoterate meglumine)= Dotarem

T1 Agents Dose .1mmol/kg in adults & children> 2 yrs Mt sequence & higher doses up to .3 mmol/kg can further increase lesion conspicuity Gd chelates c/b used as T2 agents if used in sufficiently high conc. T1 effect predominant at low doses Gd chelates rapidly leave the vascular spaces& after about 3 min. reach the equlibrium through out ECF compartment.

T1 Agents Cross the BBB similar to iodinated contrast used in CT ,thus anything which enhances with CT also enhances with MR contrast, detection better with MR contrast d/t better inherent contrast of image. S/E seen in 3-5 % of pt. Nausea ,transient rise of s.bilirubin & iron Can be safely given in pt. With impaired renal function, however dialysis recommended in pt. With severe renal impairment.

ORGAN & TISSUE DIRECTED CONTRASTAGENTS
Liver specific Hepatobilliary agents GI contrast Blood pool agents

LIVER SPECIFIC AGENTS T2 agents/-ve contrast/RES agents
Coated iron oxide particles of various sizes. Phagocytosed by RES of liver, spleen, BM, LN. Normal liver looses SI on T2 agents, Focal liver lesions like mets which do not contain kupffer cell c/b better seen. More specific the accumulation of agent in target tissue better the result & lesion tissue contrast SPIO (Ferum oxide/AMI-25, Magnetite/ Resovist/ SHU-555) & USPIO(AMI-227).

SPIO (super Paramagnetic iron oxide) (50+\- 19 nm)
1.Ferum oxide (Feridex/ AMI-25) FDA approved RES clears it (T1/2=8min.) Liver t1/2=2-3 days Dose micro gm/kg Slow infusion over 30 min. (pre & post contrast imaging inconvenience) S/E back ache,hypo tension (skilled personnel & resuscitation equipment s/b available when ever ferum oxide is administered)

SPIO 2.Magnetite/resovit/SHU-555 Phase III cl. trial
Dose =40 microgram(comparable to AMI-25) Particle size 61 nm. Max.hepatic signal loss in 10 min.

USPIO(ultra small SPIO)
Particle size nm Rapid infusion c/b given Small volume required S/E- back ache,hypo tension,flushing Taken up by normal & cirrhotic liver,FNH & adenoma,but excluded from HCC Clinical trials have not been reported.

USPIO AMI-227 Blood t1/2 long=200 hrs=blood pool agent
T2 - liver looses SI, BV dark Has gr. T1 effect. T1 -bright blood effect-delineates IV thrombus better. Good balance ofT1 & T2 effect, by bolus administration dynamic imaging of liver c/b done.

HEPATO BILLIARY AGENTS (T1 agents)
Soluble paramagnetic molecule Substantial hepatic uptake & Prolonged hepatocyte retention, billiary ex. T1agent – preferential T1 enhancement,beginning with in min & lasting for 2 hrs, imaging performed during window after renal clearance from blood & ECF

HEPATO BILLIARY AGENTS (T1 agents)
FDA APPROVED Mangafodipir/Teslascan =Mn-DPDP(Mn dipyridoxal diphosphate) UNDER CLINICAL TRIAL Multihance = Gd-BOPTA (Benzyl oxy propionic tetra acetate)Gadobenate dimeglumine eovist = Gd-EOB-DTPA (gadoxitate)

Mangafodipir/Teslascan
Dose 5-10 micromol/kg Enhances max. in 10 min.Imaging window 10 min-4hr Not effected by obstructed billiary system Focal liver lesion seen as hypointense lesion Mets –have no hepatocytes ,seen as low SI with in enhanced normal liver,whenever enhanement present (8%) seen as rim enhancement attributed to c ompressed hepatic tissue.

Mangafodipir/Teslascan
HCC-show detectable enhancement in 100% cases,complex pattern-Uniform, heterogenous;thick/nodular/peripheral;septal, capsular sparing,well defferentiated HCC may become nearly isointense to liver. Regenerating nodules-often enhances & become more concipicuous on post contrast images b/c cirrhotic/fatty liver show decrease enhancement.

Classification of Hepatocellular Nodules
Regenerative or hyperplastic nodules Monoacinar regenerative nodules Diffuse nodular hyperplasia (with fibrosis) Nodular regenerative hyperplasia Multiacinar regenerative nodules Large regenerative nodule (if 0.5 cm) Lobar or segmental hyperplasia Focal nodular hyperplaisa Dysplastic or neoplastic lesions Hepatocellular adenoma Dysplastic nodule Hepatocellular carcinoma

Nodular regenerative hyperplasia
Diffuse regenerative nodule not associated with of fibrosis.hyperplasic hepatocytes. A/W connective tissue disease,various drugs like steroids and anti proliferative drugs Portal hypertension in 50 %. Imaging- multiple nodule similar imaging feature to normal liver parenchyma, may contain hemorrhage On Tc 99 sulphur colloid scan diffuse or patchy uptake.

USG : iso to liver with asso portal HTN findings
CT : non enhancing multiple hypo nodules. Hmg may occur MRI : hyper on T1 and hypo on T2

Regenerative nodule Localized proliferation of the hepatocytes and their supporting stroma. Siderotic /nonsiderotic Low signal on the T2 and variable signal T1, no enhancement on arterial phase. may not be differentiated from dysplastic nodule

Adenomatous hyperplastic nodule(dysplastic nodule).
Benign but premalignat, in cirrhotic liver. 10 –14% of cirrhosis, massive hepatic fibrosis Contains iron and supplied by portal vein NECT- may be hyperdense but mostly are isoattenuating. CECT isoattenuating or slightly low attenuating on arterial, portal and delayed phase images and thus are difficult to depict on CT. May show enhancement in minority of cases similar to HCC.

Adenomatous hyperplastic nodule(dysplastic nodule
MRI- hyperintense on T1 w and hypointense on T2, Nodule with in nodule on T2 s/o HCC CT arterioportography- to differentiat AHN& HCC HCC supplied by hepatic artery so enhances on CTAP whereas dysplastic nodule is supplied by portal vein

dysplastic nodule. nonenhancing

dysplastic nodule. enhancing

HCC within a dysplastic nodule with MR imaging–histologic correlation.

FNH Second MC benign lesion F>M , 3rd to 5th decade
2% primary tumors in children Congenital vascular malformation -> hyperplasia of hepatocytes Kupffer’s cell activity seen Well circumscribed , non encapsulated mass with central scar surrounded by nodules of hyperplastic hepatocytes and kupffer cells No hmg or necrosis Contains hepatocytes, bileduct elements, kupffer cells and fibrous tissue RadioGraphics 2010

May be present on liver surface, nodules due to AVM
May be pedunculated Rt lobe > lt lobe > 7 cm in children

USG Subtle liver masses homogeneous,iso - hypoechoic to normal liver
Contour deformity Doppler :prominent vasc in the central scar, hypervascular tumors Numerous scattered arterial and venous signals : comet tail appearance

CONTRAST ENHANCED USG Arterial filling of mass (centrifugal)
Portovenous phase : iso to liver with central non enhancing scar Delayed : accumulation of contrast in scar

Stellate/linear/plicated non enhancing central area
FNH Centrifugal filling Stellate/linear/plicated non enhancing central area Sustained portal phase enhancement HEPATIC ADENOMA Centripetal filling No scar

NCCT Iso – hypodense Central hypodense scar
Calcification rules out FNH Bulge deformity on liver surface

CECT Arterial Phase- Homogenous enhancement
PV phase- Iso to liv with hypo enhancing central scar Delayed Phase- Iso /hypo to liver with hyperenhancing scar

MRI T1 : Hypo/iso T2 : hyper
Central scar is hyper on T2 due to vascular and myxoid tissue

CEMRI Homogeneous enhancement with rapid washout to isointensity with surrounding liver tissue Scar shows delayed and persistent enhancement

Gadobenate dimeglumine (gd BOPTA) has vascular interstitial distribution in the first few minutes after injection. Therefore 2-4 % of administered dose is taken up by hepatocytes and contrast is excreted in bile while the remaining dose undergoes renal excretion. In FNH there is lack of canalicular syatem leading to prolonged and excessive accumulation of contrast

MRI FNH 60-70% decrease in signal intensity on T2W SPIO MRI ( kupffer cell containing ) Homogeneous T1WI : iso /hypo Central scar HEPATIC ADENOMA 20% decrease in signal intensity on T2W SPIO MRI Heterogenous T1WI : hyper SUPERPARAMAGNETIC IRON OXIDE MRI : UNDERGOES PHAGOCYTOSIS WITH KUPFFER CELLS.causes t2 shortening of lesions containing kupffer cells causing decreased signal intensity on T2.

Sulphur colloid scan : hot spot
Angiography : hypervascular mass possessing centrifugal or spoke wheel pattern with dense tumor blush in capillary ,portal venous phase

HEPATOCELLULAR ADENOMA
Rare Usually solitary, > 10 cm 30-50 y F> M Association with oral contraceptives,anabolic steroid intake and GSD type I & III Lacks portal tracts and terminal hepatic veins -> necrosis, hemorrhage, and rupture common in large tumors The tumor lacks portal tracts and terminal hepatic veins; consequently, necrosis, hemorrhage, and rupture commonly occur in large tumors. There is also a potential for transformation to HCA. Therefore, this lesion should be surgically resected. More recently, the entity of multiple HCAs or adenomatosis is considered separately from typical HCA but it shows the same signal characteristics (Fig. 6). Patients with glycogen storage disease are at risk for developing multiple adenomas as well as HCA . Adenomas and FNH may be distinguished by the following features: the presence of a pseudocapsule, internal hemorrhage, or fat, which are more typical for adenomas, and a central scar that shows delayed enhancement,which is more typical for FNH. In most cases, hepatocellular adenoma cannot be confidently distinguished from HCC, based on the MRI appearance. Therefore, in appropriate clinical setting, biopsy or even surgery is indicated. B. Op de Beeck et al. : European Journal of Radiology(1999)

USG Heterogeneous echogenic due to intratumoral fat and glycogen
Anechoic areas may be present due to hemorrage and scar tissue

CONTRAST ENHANCED USG intense rapid enhancement during arterial phase less rapid washout during portal / sinusoid at last becomes isoechoic to liver parenhyma

Discrete perilesional feeding arteries manifest as enhancement around the tumor capsule
Never seen in HCC

NCCT Iso-hypodense Hypodensity due to excessive steatosis
Hyperdense areas due to hemorrage

Rapid early and transient enhancement due to hepatic artery hypervascularity. Rapid washin and wash out of the contrast that renders the tumor isodense to liver during portal venous phase

TRIPHASIC STUDY ARTERIAL : HYPERDENSE PV : ISODENSE HV : HYPODENSE

Tc 99 sulphur colloid –cold spot in 80% as they lack kupffer cells
MRI-iso to hyper on T1and T2 due to fat and glycogen; capsule may be hypo on T1WI Enhancement similar to CT SPIO- variable signal loss

a b c Alvin C. Silva, MD et al .RadioGraphics 2009;
Hepatic adenoma. (a) Axial arterial phase T1-weighted MR image shows a hypervascular mass in the periphery of the right lobe (arrow). (b, c) In-phase (b) and opposed-phase (c) T1-weighted MR images show the mass (arrow) with relatively lower signal intensity on the latter image, a finding that indicates the presence of intralesional fat and helps identify the mass as an adenoma rather than FNH. b c Alvin C. Silva, MD et al .RadioGraphics 2009;

HEPATIC SCINTIGRAPHY Uptake seen which doesnot get excreted therefore delayed enhancement

Cystic focal liver lesions
Hepatic cyst Developmental benign, not communicating with billiary tree Solitary unilocular cyst lined bile duct epithelium. 5-14 % of general population F>M (5:2) USG- anechoic with imperceptible wall and post acoustic enhancement. CT scan- water density attenuation, no enhancement MRI : T1-hypo,T2-hyper no enhancement Simple hepatic cysts are benign developmental lesions that do not communicate with the biliary tree .The current theory regarding the origin of true hepatic cysts is that they originate from hamartomatous tissue.

D/D Abscess Hydatid cyst Necrotic mets Hepatic cystadenocarcinoma
Hematoma Intrahep GB

COMPLICATED CYST Because of hemorrage or infection in simple cyst
USG :Presence of internal echoes, debris,thick septations, mural calcification or nodules CT : septations,internal debris and wall enhancement MRI : Hyper on both T1,T2 due to mixed blood products

PERIBILIARY CYST Seen in pts with severe liver disease
Small in size 0.2 – 2.5 cm Usually located centrally within porta hepatis or at the junction of the main right and left hep ducts Generally asymptomatic May rarely cause biliary obstruction Due to obstructed small periductal glands Mall

USG : discrete clustered cysts or tubular appearing parastructures having thin septa which parallel the bile ducts and portal veins

POLYCYSTIC LIVER DISEASE
More than 10 simple hepatic cysts Surrounding parenchyma frequently contains von meyenburg’s complexes Associated with periductal fibrosis and bile duct proliferation – congenital fibropolycystic disease of liver Associated with autosomal dominant polycystic kidney disease in 70%

No corelation exists between severity of renal ds and extent of liver involvement
LFTs normal

Polycystic liver disease
Polycystic liver disease. (a) Arterial-phase gadolinium-enhanced T1-weighted MR image, obtained in a 23-year-old woman with autosomal dominant polycystic kidney and liver disease, shows renal cysts (arrows) and the typical MR imaging appearance of hepatic cysts: homogeneity, well-defined borders, and no enhancement of wall or content. (b) Coronal projection MR cholangiogram obtained in a 67-year-old patient shows numerous hyperintense cysts of varying size scattered throughout the liver. Note that the cystic lesions do not communicate with the biliary tree.

Biliary Cystadenoma Slow growing multilocular cystic tumors
85 % : intrahepatic ( 55% - right lobe, 29%- left lobe , 16% - both lobes) F>M May communicate with intrahepatic bile ducts and secrete mucinous material into the duct Premalignant Calcification rare Avascular

USG: cm, solitary cystic mass , well defined thick capsule, mural nodules seen in the anechoic mass CT : Thin septa show enhancement

MRI T1WI-hypo, T2WI-hyper, septations are seen as dark bands separating high signal intensity locules

↑ CA19-9 and CEA in intracystic fluid of cystadenoma/ cystadenocarcinoma
Polypoid, pedunculated excrescences with coarse calcification in septa seen in cystadenocarcinoma

HEMANGIOMA MC benign lesion of liver
2 MC hepatic tumor after metastasis Prevalence -- 1–2% to 20% (F:M= 2:1–5:1) More common in right lobe of liver More common in subcapsular location/around intrahepatic vessels Blood filled vascular channels separated by thin fibrous septa lined by flat endothelium No kupffer cells

XRAY ABDOMEN : multiple calcific phlebolith, numerous calcified trebaculations and spicules arising from central point and radiating towards periphery

USG Sharply defined High reflective due to multiple interfaces between vascular spaces Homogeneous Lobulated margins if > 2.5 cm Involuting : heterogeneous

CONTRAST ENHANCED USG Peripheral puddles of enhancement
Centripetal filling Complete fill in on delayed imaging Sustained enhancement But all the phases of enhancement must have the same density as the blood pool.

DYNAMIC CT IMAGING

FLASH HEMANGIOMAS Small hemangiomas may show fast homogeneous enhancement ( flash filling) D/D : Small HCC , Hypervascular metastasis So look at all phases to see if the enhancing areas match the blood pool.

Hemangiomas have peripheral nodular, globular enhancement
D/D : rim enhancement is continous peripheral enhancement seen in malignant lesions ( metastases)

MORPHOLOGY ON MRI Sharp geographic margins
Lack of peripheral halo on T2WI Lack of deformity of the liver surface Superficial location Lack of displacement of hepatic vessels

MRI : T1- HYPO , T2 -HYPER

DYNAMIC MRI IMAGING WITH GADOBENATE DIMEGLUMINE (MULTIHANCE)
PLAIN SEC SEC

Hemangioma with central fibrosis : hypointense on T2WI
HCC and metastasis : hyperintense necrotic area on T2WI Giant hemangioma : heterogeneous on T2WI due to thrombosis,myxoid tissue,fibrosis . May show irregular flame shaped peripheral and central enhancement

RBC SCINTIGRAPHY Hot spot on delayed Tc99 –RBC scan
Scans are taken 1-2 hours after injection of patient’s isotope labelled blood Progressive increase in ratio of blood pool activity within the hemangioma to that of surrounding liver because of retarded blood flow in vascular sinusoids Initial photopenia with hot nodule on delayed blood pool images

Angiography : Gold std Normal main and feeding vessels
Early contrast accumulation within the lesion during the late arterial phase Persists throughout the venous phase : diagnostic Feeding vessels show crowding around the lesion

Atypical hemangioma Only 55% cases show typical enhancement patterns
Atypical features : lesions >6-8cm Due to hemorrhage, necrosis, cystic change and hyalinization Centrifugal (inside-out) enhancement Only peripheral enhancement Only central Diffuse Tommaso Vincenzo B et al,EJR 2007

e AP Baseline Baseline PVP LVP Tommaso Vincenzo B et al,EJR 2007

Baseline PVP AP 10mins

CT finding useful in differentiating liver tumor with central scar

Bile duct hamartoma (Von Meyenburg complex)
Incidental finding Due to failed involution of embryonic bile duct Grayish white nodular cm. Not communicating with the billiary system USG :Multiple,anechoic CT : <1.5 cm,multiple hypodense,no enhancement PVP -CECT scan obtained in an asymptomatic 44-year-old woman shows numerous small cystic lesions scattered throughout the liver. No enhancement is seen. At pathologic analysis, they appear as grayish-white nodular lesions 0.1–1.5 cm in diameter that do not communicate with the biliary tree and are scattered throughout the liver parenchyma. Mortele KJ et al. RadioGraphics 2001;

On USG, bright echogenic foci with ring down artifacts occuring due to presence of cholesterol crystals withih dilated tubules

MRI : hypo on T1 and hyper on T2 Irregularly outlined
MRI : hypo on T1 and hyper on T2 Irregularly outlined. No enhancement/rim enhancement ( due to compressed liver parenchyma) MR CHOLANGIOGRAPHY : multiple,tiny,cystic lesions that donot communicate with biliary tree

Bile Duct Hamartoma Mortele KJ et al. RadioGraphics 2001;
Biliary hamartomas in a 32-year-old woman.(a) Fast spin-echo T2-weighted MR image shows multiple small (1.5-cm-diameter), hyperintense nodules consistent with biliary hamartomas. (b) Coronal projection MR cholangiogram shows that all of the lesions are smaller than 1.5 cm in diameter and do not communicate with the biliary tree. (c) Arterial-phase gadolinium-enhanced T1-weighted MR image shows that some of the lesions have rimlike peripheral enhancement (arrows) Bile Duct Hamartoma Mortele KJ et al. RadioGraphics 2001;

Liver cyst Varible sized Regular outline May be associated with ADPKD Biliary hamartoma <1.5 cm Irregular outline No such association

Lipomatous tumours Include lipoma, myelolipoma and angiomyolipoma
A/W renal AML & tuberous sclerosis(10%) USG- hyperechoic SOL. CT scan- radiolucent fat, enhancement MRI- hyper on T1 & T2 Chemical shift imaging to differentiate lipomas from AML,myelolipomas

Angiomyolipoma

Focal inflammatory lesions
Abscesses Hydatid cysts

PYOGENIC LIVER ABSCESS
MC – STAPH, others : aerobic, non aerobic Sources Ascending cholangitis from biliary tree Phlebitis secondary to diverticulitis, appendicitis, pancreatitis , GI infections Arterial septicemia as result of endocarditis,pneumonitis or osteomyelitis Direct extension from contigous organs such as perforated ulcer, pneumonia, pyelonephritis Iatrogenic causes

Pyogenic vs Amoebic Biliary origin : multiple, both lobes
Portal vein source : solitary, right lobe (65%), left lobe (12%), both (23%) CT: Round (60%)or irregularly hypoattenuating area with peripheral rim enhancement Cluster sign : small abscesses coalescing together Double target sign : perilesional edema USG : Well defined or irregular & thick walled lesion , hypoechoic (36%) Gas – echogenic foci , Fluid-fluid interface, internal septations , debris Solitary unilocular Right lobe of liver (posterosuperior segments) CT : hypoattenuating with peripheral rim enhancement USG : Round or oval(82%) Absence of prominent abscess wall Hypoechoic compared to normal liver with fine internal echoes (58 %)

Pyogenic abscesses 25s

Pyogenic abscesses

Amoebic liver abscess

Cystic Hydatid Disease Gharbi’s Classification of Cystic Hydatid Disease
Type Ultrasonographic features and patterns I Pure fluid collection - univesicular cyst II Fluid collection with a split wall- detached laminated membrane (water-lily sign)- III Fluid collection with septa representing walls of daughter cysts (honeycomb sign) IV Heterogeneous appearance - presence of matrix - mimics a solid mass V Reflecting thick walls - calcifications

TYPE I TYPE III TYPE IV TYPE V

CT Well defined, round or oval cystic mass
Hyperdense to normal liver normally

Detached laminated membranes : linear areas of increased attenuation

Multiloculated, daughter cysts
Calcification : +/-

MRI T1WI : hypo T2WI : hyper
Peri cyst has low signal on T1 and T2 due to high collagen

Alveolar Echinococcosis
E multilocularis is responsible parasite. Liver is MC (90%) site of E multilocularis , 70% rt. Lobe. Foxes - main host , rarely cats & dogs. Endemic in upper Midwest of USA, Alaska, Canada, Japan, Central Europe, and parts of Russia Hilar infiltration in 50% of pts – dilatation of intrahepatic bile ducts and invasion of the portal and hepatic veins, with subsequent atrophy of the affected liver segments due to hypoperfusion The liver is the most common site of E multilocularis infection, with over 90% of infected patients having liver involvement. It is endemic to much of the upper Midwest of the United States, Alaska, Canada, Japan, Central Europe, and parts of Russia. At US, these lesions usually manifest with the “hailstorm” pattern, characterized by multiple echogenic nodules with irregular and indistinct margins . Lesions with central liquefactive necrosis appear hypoechoic, with some internal echoes and an irregular hyperechoic border. CT and MR images typically display multiple irregular, ill-defined lesions scattered throughout the involved liver that are generally hypoattenuating at CT (Fig 14) and hyperintense at T2- weighted MR imaging. This radiologic pattern may mimic either metastases or pyogenic abscesses.However, there is little or no enhancement after bolus administration of contrast medium, a finding that emphasizes the poor vascularization of the parasitic lesion Hilar infiltration is observed in approximately 50% of patients and results in dilatation of the intrahepatic bile ducts and invasion of the portal and hepatic veins, with subsequent atrophy of the affected liver segments due to hypoperfusion Mortele KJ et al. RadioGraphics 2004;

CT and MR - multiple irregular, ill-defined lesions scattered
US - “hailstorm” pattern – multiple echogenic nodules with irregular and indistinct margins - Lesions with central liquefactive necrosis appear hypoechoic, with some internal echoes and an irregular hyperechoic border CT and MR - multiple irregular, ill-defined lesions scattered throughout the involved liver that are generally hypo at CT and hyperintense at T2WI. - This mimic either metastases or pyogenic abscesses. - little or no enhancement. D/D – Cystadenoma / Ca, peripheral cholangio Ca or metastasis with peripheral bile duct dilatation. Differential diagnoses of alveolar echinococcosis include the possibility of several hepatic tumors. Type 2 and 3 lesions in the present study may mimic cystadenoma, cystadenocarcinoma, and peripheral cholangiocarcinoma or metastasis with peripheral bile duct dilatation. Mortele KJ et al. RadioGraphics 2004;

FUNGAL ABSCESS – Candidiasis
Wheel within wheel appearance Bulls eye /Target lesion : hyper centre with hypo rim Echogenic foci : scar Uniformly hypoechoic – M.C.

RadioGraphics 2001;

Focal hepatic lesions Solid hepatic Cystic hepatic Small hemangioma FNH Adenoma Metastasis ‘Washout’’ Capsule +/- Fat Post/delay T2 Post/delay – ‘fades’ T2 iso Central scarring Gd Ring Enhancement Diffusion Benign Malignant Lymphoma Prim/Sec attenuation T1

Cystic hepatic lesions Developmental Miscellaneous Hepatic cysts Bile duct hamartoma Rim Enhancement < 1.5cm Biliary Cyst adenoma/Ca Hematoma Multilocular Mural nodules Fib capsule, Calc Variable SI Bilioma Neoplastic Inflammatory Abscess Subcapsular pseudocyst Hydatid cyst Air, Enh wall Double target sign ‘Cluster sign’ Low Att/ No wall/ enhancement T1 T2 Calcification Daughter cysts Pericyst (T1,T2 ) Matrix (T1 T2 ) Lt. liver lobe Signs of panc Thin capsule Signs of trauma Low att at CT Meth Hb at MRI No capsule No septa No calcification Solitary, hete enh solid comp

D/D : Malignant cystic lesions
Cystic metastasis Ovarian tumors Teratomas Squamous cell Ca

Pediatric liver masses
MC liver neoplasm in children, as in adults, is metastasis Most primary tumors are malignant,1/3rd benign MC benign tumors are IHE, FNH, mesenchymal hamartoma, NRH & hepatocellular adenoma Malignant – Metasasis, hepatoblastoma, HCC, Lymphoma Others - Abcesses, hematoma Ellen MC, et al. RadioGraphics 2010; 30:801–826

D/D of Pediatric liver tumors
Age < 5years-hepatoblastoma ,IHE,mesenchymal hamartoma, metastasis. Age> 5 years : HCC, adenoma and metastasis. AFP- HCC , hepatoblastoma Solitary vs multiple SOL- IHE, metastasis, abscess,lymphoproliferative disease, adenoma,

Infantile hemangioendothelioma
90% before 6 months,F>M Mesenchymal tumor , vascular channels formed by endothelial proliferation Usually presents as hepatomegaly/abdominal mass/congestive heart failure due to AV Shunting in the lesion/ thrombocytopenia due to platelet sequestration (kasabach meritt syndrome ) May be associated with cutaneous hemangiomas Ellen MC, et al. RadioGraphics 2010; 30:801–826

TYPE 1 TYPE 2 Vasc channels lined by endothelial cells supported by reticular fibres Large irregular branching spaces lined by immature pleomorphic cells

USG Variable, highly echogenic to hypoechoic /anechoic mass.
Celiac axis & CHA are dilated Abdominal aorta caliber below coeliac axis origin reduces Hepatic veins become prominent

CT Hypodense ,well defined , homogeneous nodule Calcification in 40%
Centripetal filling as in hemangioma.

MRI Hypointense on T1WI and hyperintense on T2W
Heterogeneous if necrosis, hemorrage and fibrosis Feeder vessel-flow void Centripetal fill in of contrast post gadolinium

Mesenchymal hamartoma
Benign cystic mesenchymal tumor < 2 years, M>F Abdominal distension Large mass(5-22cm),right lobe, encapsulated and pedunculated, gelatinous mesenchymal tissue with cyst At MR imaging, the appearance of mesenchymal hamartoma depends on the cystic versus stromal (mesenchymal) composition of the mass, as well as the protein content of the fluid in the cysts (21,39,40). Solid portions may appear hypointense to adjacent liver on both T1- and T2-weighted images owing to fibrosis (21,37,41). The cystic portions are generally close to water signal intensity on T2-weighted images and demonstrate variable signal intensity on T1-weighted images, depending on the protein content of the cyst fluid (Fig 7) (21,40,41). After intravenous administration of gadolinium contrast material, enhancement is mild and limited to the septa and stromal components Ellen MC, et al. RadioGraphics 2010; 30:801–826

USG Solid / cystic mass, multilocular with anechoic areas with echogenic septae and stroma .

CT Complex mass, low attenuation areas separated with enhancing septa and stroma.

MRI Cystic component is hyper on T2 and mesenchymal (stromal) tissue is hypo on both T1 &T2

DW MRI in focal liver lesions
With advances in hardware and coil systems, DW MRI – now be applied to liver imaging with improved image quality. Enables qualitative & quantitative assessment of tissue diffusivity (ADC) without Gd chelates, which makes it a highly attractive technique, particularly in patients with severe RF at risk for NSF. Detection and characterization with better results compared with T2-WI. Should be interpreted in conjunction with conventional sequences. Taouli and Koh , Radiology 2010.

Taouli and Koh , Radiology 2010.
Visual liver lesion characterization with DW MR imaging. This figure gives a simplified approach to lesion characterization by using visual assessment with b of 0 sec/mm 2 and a higher b value and ADC maps. A benign fl uid-containing lesion shows strong signal decrease with high ADC, whereas a cellular malignant lesion shows no or minimal signal decrease, with low ADC compared with the surrounding liver parenchyma. A lesion with long T2 can sometimes show a T2 shinethrough effect (see text for explanations ). Black circles 5 hypointense, white circles 5 hyperintense Taouli and Koh , Radiology 2010.

Transverse breath-hold ( BH ) versus respiratory-triggered ( RT ) fat-suppressed single-shot SE echo-planar diffusion acquisition in a 78-year old woman with liver cysts. Respiratory-triggered acquisition (using navigator echo, four signals acquired) shows better image quality at b of 0 and 500 sec/mm 2 (with better lesion delineation) and more homogeneous ADC maps compared with breath-hold acquisition (two signals acquired). There is strong signal decrease of liver cysts (arrows), with corresponding high ADC values (approximately 2.9–3 x mm 2 /sec). DWI in liver cysts

b=100 b=600 Hemangioma b =1000

b0 b100 b500 b1000 ADC HCC

Lesion detection Taouli and Koh , Radiology 2010.
Fig 1-Lesion detection with DW MR imaging versus T2-weighted imaging. Transverse fat-suppressed breath-hold T2-weighted image, single-shot SE echo-planar diffusion images ( b 5 0 and 50 sec/mm 2 ), and postcontrast T1 weighted image in a 65-year-old man with metastatic liver disease from pancreatic cancer. Two small lesions in the right posterior lobe (solid arrows) are identified on T2-weighted and DW MR images; however, an additional small lesion (dashed arrows) is more conspicuous on DW MR image and is confirmed on postcontrast image. There is also a vertebral metastasis (arrowheads). Fig 2- Lesion detection at DW MR imaging versus gadolinium-DTPA-enhanced T1-weighted imaging. Breath-hold transverse single-shot SE echo-planar DW MR images ( b 5 0, 50, and 500 sec/mm 2 ), postcontrast T1-weighted image, and PET scan in a 56-year-old man with lung cancer. There is a tiny metastatic lesion of segment 6 (arrows) not identified prospectively at contrast-enhanced T1-wegihted imaging and is more conspicuous at DW MR imaging. The lesion was confirmed at FDG PET performed immediately after MR imaging. Lesion detection Taouli and Koh , Radiology 2010.

Lesion characterisation
: Lesion characterization with DW MR imaging. Transverse breath-hold single-shot SE echoplanar DW MR images ( b 5 0, 500, and 1000 sec/mm 2 ), postcontrast T1-weighted images during arterial phase ( ART ) and equilibrium phase ( EQU ), and ADC map in a 44-year-old woman with hemangioma (arrows) of the right hepatic lobe. The lesion is bright at b of 0 sec/mm 2 and attenuates progressively with increasing b values, with corresponding high ADC ( mm 2 /sec). Postcontrast images show early and persistent enhancement. Lesion characterisation

Treatment assessment Taouli and Koh , Radiology 2010.
Assessment of treatment response with DW MR imaging. Perfusion-insensitive ADC ( ADC high , using b values > 200 sec/mm 2 ) maps show a metastasis in the left lobe of the liver (a) before and (b) after treatment with an antiangiogenic agent. (c) Voxelwise histogram analysis shows a clear increase in the median ADC high after treatment, with a shift of the histogram toward the right (red line) compared with the pretreatment distribution (blue line). Treatment assessment Taouli and Koh , Radiology 2010.

CONCLUSION Accurate clinical information needed to select the most appropriate imaging modality Ultrasound is the initial modality for hepatic imaging Helical CT/ MRI are able to characterize the hepatic lesions DW-MRI has the potential to help detect and characterize focal lesions in the liver. Knowledge of imaging features of liver lesions is essential to avoid unnecessary work-up and to minimize patient anxiety

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PRESENTOR : Dr Navni Garg MODERATOR : Dr Sonal Krishan

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PRESENTOR : Dr Navni Garg MODERATOR : Dr Sonal Krishan

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