imaging of benign hepatic masses
TRANSCRIPT
PRESENTOR : Dr Navni Garg MODERATOR : Dr Sonal Krishan
SEMINARSEMINAR JUNE 26,2014 JUNE 26,2014
IMAGING IN BENIGN HEPATIC MASSES
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 cystGranulomatous: Tuberculosis SarcoidosisNeoplastic
Benign neoplasms
Hepatocellular(hepatocyte) Cholangiocellular
(bile duct epithelium)Mesenchymal
Adenoma
FNH (2nd most common)
Hepatic cysts
Biliary cystadenoma
Hemangioma (most common)
Mesenchymal hamartoma
Infantile hemangio-Endothelioma
Lymphangioma/Lipoma/fibroma/Angiomyolipoma/Leiomyoma/
Malignant neoplasms
Hepatocellular Cholangiocellular Mesenchymal
Cholangiocarcinoma
Cystadenocarcinoma
Angiosarcoma
Epitheliod hemangio-Endothelioma
Leiomyosarcoma
Lymphoma
Hepatcellular Ca
Fibrolamellar carcinoma
Hepatoblastoma
HEPATIC METASTASIS
Imaging modalities
99Tc-sulphur colloid
PET CT
Nuclear Medicine
USCTMRI
CTAP
CE-USG
Nuclear scans
Conventional
Radiological
Newer methods
DWIElastography 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
5 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 15-30 % 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 procedureStep 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-150-200ms, TE- minimum,8x2+- fat sat
T2 weighted sequence- SE T2 , TR 4000, TE- 100, with respiratory trigger. FSE breath hold.Fat suppressionHalf Fourier acquisition single shot turbospin echoe.
Contrast enhanced sequences
MRI protocol
Radiographics 2000
MRI CONTRAST AGENTSIN 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 approvedIONIC 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
1. Liver specific2. Hepatobilliary agents3. GI contrast4. 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 10-15 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 17-20 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
1. Mangafodipir/Teslascan =Mn-DPDP(Mn dipyridoxal diphosphate)
UNDER CLINICAL TRIAL
1. Multihance = Gd-BOPTA (Benzyl oxy propionic tetra acetate)Gadobenate dimeglumine
2. 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
nodulesDiffuse nodular hyperplasia
(with fibrosis)Nodular regenerative
hyperplasia Multiacinar regenerative
nodules Large regenerative nodule (if
0.5 cm) Lobar or segmental
hyperplasiaFocal nodular hyperplaisa
•Dysplastic or neoplastic lesions Hepatocellular adenoma
Dysplastic noduleHepatocellular 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
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
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
• Arterial Phase- Homogenous enhancement• PV phase- Iso to liv with hypo enhancing central scar• Delayed Phase- Iso /hypo to liver with hyperenhancing
scar
CECT
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
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
Sulphur colloid scan : hot spot Angiography : hypervascular mass
possessing centrifugal or spoke wheel pattern with dense tumor blush in capillary ,portal venous phase
B. Op de Beeck et al. : European Journal of Radiology(1999)
• 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
HEPATOCELLULAR ADENOMA
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
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
Alvin C. Silva, MD et al .RadioGraphics 2009;c
b
HEPATIC SCINTIGRAPHY
Uptake seen which doesnot get excreted therefore delayed enhancement
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
Cystic focal liver lesions
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
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
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: 1.5-35 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)
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
Tommaso Vincenzo B et al,EJR 2007
• 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
e
Baseline
LVP
Baseline AP
PVPTommaso Vincenzo B et al,EJR 2007
Baseline PVPAP
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 0.1-1.5cm. Not communicating with the billiary system
• USG :Multiple,anechoic• CT : <1.5 cm,multiple
hypodense,no enhancement
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. 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;
Liver cyst Varible sized Regular outline May be associated
with ADPKD
Biliary hamartoma <1.5 cm Irregular outline No such
association
• 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
Lipomatous tumours
Angiomyolipoma
Focal inflammatory lesions
• Abscesses• Hydatid cysts
PYOGENIC LIVER ABSCESSMC – STAPH, others : aerobic, non aerobicSources 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 lobesPortal 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 %)
25sPyogenic abscesses
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- detachedlaminated membrane (water-lily sign)-
III Fluid collection with septa representing walls of daughter cysts (honeycomb sign)
IVHeterogeneous 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
Mortele KJ et al. RadioGraphics 2004;
• 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.
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;
RadioGraphics 2001;
Focal hepatic lesions
Solid hepaticlesions
Cystic hepatic lesions
Small hemangioma FNH Adenoma Metastasis
‘Washout’’Capsule +/- Fat
Post/delay T2
Post/delay – ‘fades’T2 iso
Central scarringGd
Ring Enhancement
T2Diffusion
Benign Malignant
Lymphoma
Prim/Sec attenuation
T1T2
Cystic hepaticlesions
Developmental Miscellaneous
Hepatic cysts
Bile ducthamartoma
Rim Enhancement
< 1.5cm
Biliary Cystadenoma/Ca
Hematoma
MultilocularMural nodules
Fib capsule, CalcVariable SI
Bilioma
Neoplastic Inflammatory
Abscess
Subcapsularpseudocyst
Hydatid cyst
Air, Enh wallDouble target sign
‘Cluster sign’Low Att/
No wall/ enhancement
T1 T2
CalcificationDaughter cysts
Pericyst (T1,T2 )Matrix (T1 T2 )
Lt. liver lobeSigns of pancThin capsule
Signs of traumaLow att at CT
Meth Hb at MRI
No capsuleNo septa
No calcification
Solitary, heteenh solid comp
T1 T2
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 Vasc channels lined by
endothelial cells supported by reticular fibres
TYPE 2 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
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.
DWI in liver cysts
b=100
b=600
b =1000Hemangioma
b0 b100
b500 b1000
HCC
ADC
Lesion detection
Taouli and Koh , Radiology 2010.
Lesion characterisation
Treatment assessmentTaouli 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