imaging hepatic tumours
DESCRIPTION
my seminar presentatoin... long live radiodiagnosisTRANSCRIPT
IMAGING OF HEPATIC TUMOURS
Speaker: Dr Sharma (PG)Moderator: Dr Jatishwor Singh
(HOD)
INTRODUCTION Liver tumors can be divided into
nonneoplastic and neoplastic. They can be either hepatocellular,
cholangiocellular, Mesenchynal or other miscellenous catogory.
The aim of this seminar is to have a overview of hepatic tumours , imaging features and to highlight recent advances in this field.
Embryology of liver The liver primordium (third week)- appear
as outgrowth of the endodermal epithelium at the distal end of the foregut.
The hepatic diverticulum or liver bud, consists of rapidly proliferating cells that penetrate the septum transversum, which forms Hematopoietic cells, Kupffer cells, and connective tissue cells.
Epithelial liver cords intermingle with the vitelline and umbilical veins, which form hepatic sinusoids,parenchyma (liver cells) and lining of the biliary ducts.
FUNCTIONAL SEGMENTAL LIVER ANATOMY
GOLDSMITH &WIIDBURNE
COUINAUD & BISMUTH
CAUDATE CAUDATE 1
LEFT LOBE LEFT LATERALSEGMENT
SUP SUBSEGMENT 2
INF SUBSEGMENT 3
LEFT MEDIALSEGMENT
MED SUP SUBSEGMENT 4A
MED INF SUBSEGMENT 4B
RIGHT LOBE RIGHT ANTERIORSEGMENT
ANT INF SUBSEGMENT 5
ANT SUP SUBSEGMENT 8
RIGHT POSTERIORSEGMENT
POST INF SUBSEGMENT 6
POST SUP SUBSEGMENT 7
Vascular Distribution
Imaging Techniques X-RAYS ULTRASOUND Plain, Contrast , Doppler. COMPUTED TOMOGRAPHY SCAN (MDCT) PLAIN, CONTRAST MR IMAGING- PLAIN,CONTRAST,MRA, MRCP. RADIONUCLEIDE IMAGING. Miscellenous- Angiography , Contrast oil injection etc
Ultrasonography Ultrasound - Commonest, safest and
most widely used. Introduction of microbubbles contrast like
Livovist & perflurocarbon increased both sensitivity and specificity of detecting focal liver tumors.
Microbubble persist in liver within kupffer cells, producing bright enhancement.
Liver metastasis lacking kupffer cell will not enhance.
Overall lesion detection for USG equivalent to CT/MRI.
NCCT Not routinely done. May be used for identification of
calcification, hemorrhage, iron deposition, or determination of precontrast attenuation.
Also used for some neoplasm which become isoattenuated on postcontrast study.
Single phase contrast CT Bolus contrast enhanced CT, with
imaging in peak hepatic parenchymal enhancement (PV Phase).
Injection 125-150 ml 350mgI/ml contrast, followed by saline flush 20-50ml @ 3ml/sec is adequate.
Most useful for routine depection of liver abnormalities like focal lesions.
Multiphase CT Useful in detection of hypervascular
mass, characterization of liver mass, and preoperative planning.
Best performed on MDCT. Image acquisation- Early arterial phase
(25 sec) , Late hepatic arterial phase(35-40 s), and Portal venous phase (60-75 sec)
125-150ml contrast @5ml/sec.
In Arterial phase hypervascular tumors enhances via HA ,in a relatively hypodense liver.
In Portal venous phase , hypovascular tumors are detected, when the normal liver parenchyma enhances maximally and tumors will be hypodense lesions.
In Equilibrium phase, at about 10 minutes after contrast injection, tumors either lose their contrast slower than normal liver(hyperdense), or wash out their contrast faster than normal liver parenchyma(hypodense).
Cholangiocarcinoma – AP, PVP & EP. Delayed/prolonged Enhancement.
Tailored CT protocolsingle slice scanner-take about 20 seconds to scan the liver. 64-slice scanner-examine the whole liver in 4 seconds
Angiography assisted CT CT hepatic angiography-With catheter in
hepatic artery or celiac axis. CT arterial portography- catheter in SMA
or splenic artery. They are Replaced by newer advances
in MDCT and MRI. CT 1-4 wk after iodized oil inj. into HA is
used to detect small HCC. Oil is rapidly cleared by normal hepatic RE system within 1wk, but retained in vascular hepatic neoplasm, as hyperdense mass.
MRI- Plain T1,T2 and GRE sequences. Most tumours are SI in T1 w seq
(except for fat containing lesion and MM)
On T2 most masses are hyperintense. Other sequences used- Fat supressed,
STIR, HASTE etc.
Contrast MRI GD chelates- shorten t1 and t2 relxn. So
cause enhancement of t1. SPIO contrast-taken selectively by RES,
causes profound t2 shortening and normal hepatic signal loss. Tumour uptake depends on presence of kupffer cells.
Double contrast GD + SPIO has increased sensitivity for HCC in cirrhosis.
Mn-DPDP-T1 shortening agents taken up by hepatocytes. Better for metastasis.
Benign Liver tumorsNonneoplastic Neoplastic Potential
Hepatocellular origin
Necrotic noduleFocal nodular hyperplasiaNodular regenerative hyperplasiaRegenerative nodule.
Hepatocellular adenoma
Cholangiocellular origin
Simple cystPolycystic liver diseaseIntrahepatic choledochal cyst
AdenomaCystadenoma
Mesenchymal origin
Inflammatory tumor Hemangioendothelioma
Hemangioma Lymphangioma,LipomaAngiomyolipomaFibromaNeuroendocrine tumors
Other Hamartoma, TeratomaExtramedullary hematopoiesis
Malignant Neoplasms Hepatocellular Carcinoma Fibrolamellar Hepatocellular
Carcinoma Hepatocellular Carcinoma with
Sarcomatous Changes Cholangiocarcinomas Adenosquamous/Squamous Carcinoma Lymphoma Hepatoblastoma Sarcoma Metastases
Neoplasm in infants Benign Adenoma Hemangioendothelioma Malignant Hepatoblastoma Hepatocellular carcinoma Metastases Neuroblastoma Lymphoma Leukemia Sarcoma Rhabdomyosarcoma Teratocarcinoma
Simple Cysts Developmental cysts accounts for 5-14%. solitary or multiple with single epithelial lining.
Polycystic liver disease- assd with PCKD. D/T ductal plate malformation. Varying sizes. Imaging-
cystic lesions.
USG-anechoic, well-defined smooth capsule and exhibits posterior enhancement
CT- circumscribed near water attenuation. No enhancement. MRI- T1 T2 Non enhancing.
Complication-rare. Hemorrhage, Rupture
Simple cyst.
Complex cysts May have solid nodules,
thickened walls, hemorrhages,
Septations, Internal echo, Calcification etc
M Nodule
Biliary Hamartoma(von Meyenburg complex)
Dilated biliary duct with variable amount of fibrous stroma.
Arise from embryonic bile duct that fail to involute.
CT- small hypoattenuating cyst like structures with little or no enhancement.
MRI- multiple small lesions of cystic SI. Most do not enhance, but some show internal enhancement d/t compressed hepatic parenchyma.
Biliary Hamartoma
Peribiliary cyst. Cystic dilatation of obstructed periductal
gland adjacent to large I/H or E/H bile duct.
If extensive, a string-of-beads appearance is evident.
Usually asymptomatic. Imaging- discrete, clustered, cystic
structure with thin septa paralleling bile duct & central portal vein.
Peribiliary cyst- along bile ducts.
Adult Cavernous Hemangioma
Most common liver tumor in adults. Occurs at all ages. Typically <3cm.
Predominate in the posterior segment of the right lobe. Occasional patient develops multiple hemangiomas. Diffuse hemangiomatosis is rare.
Most hemangiomas are asymptomatic and discovered incidentally.
Giant hemangiomas (>4cm)can have unusual findings, like portal vein obstruction & tend to contain central scar.
Ultrasonography- Homogeneous, well marginated, and
hyperechoic tumor(70%). Less often- hyperechoic rim of varying thickness
with isoechoic or even hypoechoic center , post. acoustic enhancement , nonhomogenous centre, or scalloped margins may be seen.
Blood flow velocity is usually slow & Doppler US is noncontributory.
Microbubble-enhanced US- In AP, bright peripheral puddles and pools seen. With time centripetal progression with sustained enhancement in PVP. Delayed washout is common.
Hemangioma- hyperechoic tumor, AP( rim enhancement),delayed 142 sec (central fill-in).
CT- Hypodense to liver and isodense to blood. A
fibrotic component or thrombosis lowers CT density.
Postcontrast- irregular, nodular peripheral enhancement pattern during the arterial phase. Enhancement from the periphery toward the center, a prolonged tumor blush, vascular lakes, and delayed contrast washout.
Smaller ones are round diffusely enhancing while larger ones tend toward an oval or lobular shape.
Central scarring- Causes incomplete central opacification.
Hemangioma NECT, late arterial, late portal venous and equilibrium phase.
MRI
Most hemangiomas - Hypointense on precontrast T1, Hyperintense in T2.
Small hemangiomas-uniform enhancement, and larger ones usually show peripheral nodular enhancement progressing to uniform centripetal enhancement.
Large tumors tend to maintain a persistent central hypointensity.
Most hemangiomas increase lesion to- liver contrast on ferumoxides-enhanced T2-weighted MR images.
Hemangioma.T2-w ( hyperintense ) & T1-w FSE MRI(hypointense)
Scintigraphy
Both planar and SPECT Tc-99m–red blood cell imaging have high sensitivity and specificity in differentiating cavernous hemangiomas from other liver tumors.
Early perfusion phase Tc-99m–red blood cell scintigraphy shows a focal photopenic defect that gradually fills-in in a centripetal manner. A perfusion/ blood-pool mismatch is the hallmark.
Technetium-99m–sulfur colloid and hepatobiliary scintigraphy-- filling defect.
Infantile Hemangioma Especially assd with Kasabach-Merritt
syndrome. More common in girl and tends to be
multiple. With age, these tumors tend to involute with few sequelae.
Large hemangiomas in T2-weighted MRI appear hyperintense nodules containing fast flow flow voids and hyperintense tumors on GRE images.
Early rim enhancement after gadolinium, with progressive fill-in on delayed imaging
Regress after interferon-a-2a therapy.
FOCAL NODULAR HYPERPLASIA 2nd MC hepatic benign tumour. Mostly in young women. Majority < 5cm. Solitary in 75-80%. Typically
subcapsular. Usually nonencapsulated. Along with hepatocyte, BV, BD, and
kupffer cell, they contain central or eccentric fibrous scar with spoke-wheel radiating fibrous bands.
USG Subtle contour abnormality(stealth lesion)
and displacement of vascular structure. Echogenicity may vary from hypo to hyperechoic rarely.
Central scar- hypoechoic linear or stellate area.
Doppler- blood vessels can be seen coursing within central scar.
Microbubble contrast- AP-hypervascular with stellate lesional vessels
and tortuous feeding artery. PVP- Sustained enhancement with unenhanced
central scar.
FNH- Isoechoic, microbubble contrast ‘spoked-wheel’ pattern & central scar.
CT Homogenous iso/slight hypoattenuating. 1/3rd cases,well def. hypoattenuating scar. Prominent vasc supply marked
enhancement in AP (homogenous except for scar and septa).
Hepatic parenchymal phase– Iso attn. Delayed image- pseudocapsule
enhancement( compressed hepatic tissue). Fibrous scar- Hypo attn (AP), Enhance on
delayed images. 50% FNH takes up sulfur colloid in sulfur
scanning and 10% becomes “hot”.
FNH with central scar-NECT, PVP and Equilibrium phase
MRI
Unenhanced - similar to hepatic tissue. Iso/sl. hypo t1, Iso/sl. Hyper t2.
Central scar ½-¾ cases- hypo t1,hyper t2. Contrast-hyper (AP), Iso(PVP), scar
enhancement in delayed phases. Mn/t1 shortening Gd contrast- enhancement
in delayed image. SPIO- show signal loss.(lack specificity) Scintigraphy- rarely for confirmation of
diagnosis. FNH show sulfur colloic concentration.
Atypical features in 10-20%.
FNH- hypointense on T1and hyperintense on T2. Enhances with contrast.
99 mTc-HIDA --prolonged retention of tracer in the area of FNH.
Hepatocellular adenoma Uncommon benign primary neoplasm. Encapsulated. Usually solitary. 8-15 cm. F>M, increase in OCP users. Regress or
disappear after OCP withdrawl. Can have spontanous hemorrhage.
Adenomatosis- rare charecterised by numerous hepatic adenomas. F>M. Do not appear to be steroid dependent, and do not regress on steroid withdrawl. Show high risk of HCC.
USG Nonspecific. Echogenicity hypo/hyper/iso/mixed. Paucity of central vascular structure. Microbubble contrast has limited utility.
Majority are ‘cold’ on Tc-sulfur colloid imaging.
Adenomas are assd with glycogen storage disease in childrens.
Adenoma
CT-- variable
Unenhanced- Hypo attn (lipid, old hrge, necrosis) Hyper attn ( hrge, glycogen).
Contrast- Moderate enhancement (AP & early PVP). Homogenous enhancement if uncomplicated.
25% thin capsule seen- hypo attn (AP), hyper attn (PVP).
Adenoma
MRI Heterogeneous SI. Majority- hyper t1(lipid/hrge), iso/hyper
t2. Capsule – low SI.
Contrast GE seq- Usually hyperintense. May be iso/hypo.
SPIO- some show signal loss.
Hepatic adenoma - hypointense on T1, hyperintense on T2 &inhomogeneouscontrast enhancement
Angiomyolipoma Benign, unencapsulated mesenchymal
tumour. Contain SM,BV and adipose tissue. Vary in size. Solitary or multiple. USG-Well defined echogenic mass. CT- low attn lesion (<-20 HU) MRI– hyper T1, Hypo fat supression. Non fat component show early and
prolonged enhancement.
Hepatocellular carcinoma 90% primary hepatic malignancy. 5th MC cancer worldwide. AFP raised. M>F, solitary/multifocal/diffuse. 3 patterns- Nodular (mc) Massive pattern. Diffuse pattern. Expansive or invasive. Abnormal hepatocyte arranged in trabecular
sinusoidal pattern. Vascular tumour supplied by hepatic A.
Arterioportal shunting, spontanous hrge and rupture may occur rarely.
USG Variable. May be hypo/hyper or complex
echogenicity. Small<5cm-solid &hypoechoic. Thin
peripheral hypoechoic halo seen. Larger tumour becomes complex &
inhomogenous. Calcification rare. Doppler- High velocity flow &
neovascularity. Microbubble contrast- Hypervascular tmr
enhance in AP, ‘washout’ in PVP.
A) Exophytic HCC. (B) Multifocal HCC. ©nodular liver with suspicion of a lesion (D) contrast in the same patient as ©
CT Variable appearance. Mostly hypoattenuating. Some are
isoattenuating with hypo attng. capsule. Hyper attn- d/t hemorrhage. Hypo attn- d/t necrosis , fatty changes. Calcification- 5-10%. Contrast– Transiently hyper attn. in HAP.
But 20% appear hypo attn. in HAP. Fibrous capsule remain unenhanced.
Small HCC are homogenous and larger lesions are heterogenous.
PV(parenchymal)Phase- Isoattenuating. Rarely hypoattng. Tumour capsule/septa- enhances. Delayed images(3-6mt) Small percentage appear hypoattng. Fibrosis, capsule or septa show
prolonged enhancement. CECT can demonstrate vascular
invasion, A-P shunting, tumour thrombus etc.
NECT and Arterial phase image showing hypodense capsule of HCC
Multifocal hepatocellular carcinoma (postcontrast)
MRI Variable. T1- hypo/iso/hyper SI T2-hyperintense(70-90%). >3cm lesions
usually show hyperintensity. Capsule- appear hypointense rim in T1,
and in T2w. Either single hypointense rim or double
layer peripheral band( inner low signal fibrous tissue and outer high signal zone of vessels and ducts).
Internal Features: Intratumoural septa- thin. Hypointense in t1
and t2 w seq.Central scar – Low SI in T1. Low or high SI
in T2w. Contrast MRI Peak enhancement from 10s to 2 min., with
absent or minimal delayed enhancement. Most become isointense in PV Phase and
iso/hypo SI in equilibrium phase. Delayed Phase- washout of HCC(hypo SI)
and enhancement of capsule.
HCC-T1, T2 and Early contrast
CT 1-4wk after i/a injection of iodized oil, is capable of demonstrating small HCC missed by noninvasive technique.
CT arterial portography- sensitive for small HCC. But With 50% failure for setallite nodules.
Double contrast MRI study- SPIO followed
by Gd contrast study improve detection of HCC in cirrhosis Pt.
TNM staging of liver cancerPrimary tumor:Tx Cannot be assessed.T0 No evidence of primary tumor.T1 Solitary tumor without vascular invasion.T2 Solitary tumor with vascular invasion or multiple tumors, none >5cm.T3 Multiple tumors >5 cm or tumors involving major portal or hepatic branch.T4 Direct invasion of adjacent organs.
Lymph node involvement:
Nx Regional nodes cannot be assessed
N0 No regional nodes involved
N1 Regional nodes involved
Distant metastasis:
Mx Distant metastasis cannot be assessed
M0 No distant metastasis
M1 Distant metastasis
C/C Liver diseaseRegenerative nodule(Siderotic Nodule)
Dysplastic nodule Small HCC
Well defined enlarged parenchymal nodule
Hypo/iso/hyper T1Iso/Hypo T2(hypo SI d/t iron content- siderotic nodule)
X enhance HAP
GE Image- nodule within nodule app. Or Hyper I focus within hypo I nodule.
Nodule>1mm with dysplasia
Hypo/Hyper T1Iso/hypo T2
X enhance HAP
Enhance on CT & not on SPIO
HCC < 2cm.
Hypo/Hyper T1Iso/hyper T2Rarely hypo T2
Enhance in HAP.
Hypo attn on all CT phases & enhance on SPIO
Fibrolamellar HCC Histologic subtype of HCC. Occur in younger pt without underlying
liver disease. M>F. AFP Normal. Better prognosis. Malignant hepatocyte saperated into
cords by thin multilamellated fibrous strands.
Usually very large, aggressive local invasion, nodal or distant metastasis.
USG- variable echo. Punctate calcification and central echogenic scar.
CT: Large well defined lobulated mass showing heterogenous enhancement.
Central scar (50%).. Often show calcification. Delayed enhancement.
MRI: Hypo on T1, heterogenous hyper SI T2. Mass show heterogenous
enhancement, with no enhancement of central scar.
Central scar- Hypo SI in T1 and T2. Lack of delayed enhancement.
Fibrolamellar carcinoma with central calcifications-NECT, AP & PVP (radiating septa).
FS T2 and T1 GRE in AP and PVP (peripheral capsule and necrotic nodule)
Central scar
FNH Fibrolemellar HCC
USG
CT
T2 MRI
Enhancement
+++(hypoechoic)
Calcification rare.
Hyperintense on T2
delayed enhancement.
+++(echogenic)
Calcification Common
Hypointense on T2,
no delayed enhancement.
IH cholangiocarcinoma Adeno Ca from small intrahepatic bile
ducts. 2nd MC primary hepatic neoplasm(10%).
Firm hypovascular tumour with predominant fibrous stroma. Large amount of interstitial space in fibrous stroma causes slow diffusion of contrast.
Features- peripheral biliary ductal dilatation, PV encasement, segmental atrophy etc.
CT: Hypoattng mass with lobular margins,
showing mild early peripheral enhancement, gradual centripetal enhancement & delayed contrast pooling(10-20 min). Satellite nodules are frequent.
MRI: Hypo on T1, Hyper/Iso T2. Enhancement similar to CT.
Central Scar(50% Cases)- Hypo on T1 & hypo/iso/hyper T2.Delayed enhancement.
Hepatic and delayed phase in a patient with multifocal cholangiocarcinoma causing retraction of liver capsule
Metastases Liver is 2nd MC site of metastasis. Variable clinical and imaging
presentations. Precontrast images are important to
show calcification, and hemorrhage. Some Met like breast, colon, lung, and
carcinoid show retraction of adjacent liver capsule.
MDCT has advantage with thin section capability.
Hypovascular Metastasis
Hypervascular metastasis
Calcifying Metastasis
Colon adenocarcinomaPancreatic adenocarcinomaGastric adenocarcinomaTransitional cell carcinoma
Renal cell carcinomaNeuroendocrineIslet cell carcinomaCarcinoidMalignant pheochromocytomaThyroid carcinomaSome sarcomasMalignant melanoma
Mucin-producing adenocarcinomaOsteogenic or chondrosarcomaSome neuroendocrine tumors
USG Multiple solid lesion with hypoechoic halo(may
be d/t compressed nornal tissue, proliferating cells, fibrosis or vascularization).
Microbubble Contrast- AP-Hypervascular metastasis show
enhancement in HAP. Hypovasc. Met. Show enhancement less than liver.
PVP- Virtually all metastasis will be unenhanced relative to Liver in PVP(lack kipffer cells)..
USG- various features
ECHOGENIC MET. (hypervasc)
Hypoechoic met. (hypovasc)
Cystic met. Target lesion
Diffuse Disorganised(infiltrative)
GITRCCCarinoidChorio ca.Islet cell ca
BreastLungGastricPancreasLymphoma
Cystadeno caMucinous caSarcoma
Bronchogenic ca.
BreastLungMM
(a) Large necrotic metastasis. (b) Miliary metastases (c) Following microbubble contrast agent(d) Calcified metastases from breast carcinoma
CT-Hypovascular metastasis Most metastasis are hypovascular. CT- In Arterial Phase, most common
pattern is continuous ring like enhancement at periphery.
Hypoattenuating on PV Phase. Hypervascular metastasis: They are hyperattenuating in AP.
Becomes isoattenuating in PVP, so difficult to detect in PVP.
CT PVP-Multiple cystic liver metastases from a cystic pancreatic acinar carcinoma
Metastatic islet cell carcinoma. Precontrast and contrast- rim-enhancing nodules.
MRI Usually Hypo T1, Hyper T2. Hyper SI in T1- hemorrhagic, MM. 15-27% have central more hyperintense area in
T2(necrosis)– Target sign. 50% colorectal met. Show central area of low SI
relative to high SI tumour edge in T2- Halo sign. D/T Central desmoplasia and coagulative Necrosis.
Contrast: Hypovasc met.-Hypointense in HAP with
perilesional enhancement. Hypervasc met.- Hyperintense in HAP. Isointense in PVP.
Delayed images(5-10 min)- 1/4th of met. Show hypointense rim compared to centre of lesion(peripheral washout sign). Seen in hypervasc met > hypovasc met.
MRI and contrast CT are comparable- 80-90% sensitivity. MRI more sensitive for solitary metastasis.
CT remains the screening procedure of choice.
Pre op staging- CT,MRI &MDCT+Angio used. CTAP is being replaced by non-invasive Techniques.
Improvement of lesion detection with liver-specific agent-T1-weighted GRE image and Mangafodipir-enhanced MR
Hepatocyte-specific contrast agents- Early ring-like enhancement with delayed
washout.
Biliary Cystadenocarcimoma Uncommon biliary neoplasm. F>M, middle age patients. Unilocular or septated large cystic mass
containing mucinous or serous fluid. CT- Intrahepatic mass with non-enhancing
cystic spaces with high attenuating wall/septa. Mural or septal nodule when present enhances. Calcification may be seen.
MRI- Cystic locules with hypointense septa. T1-SI depend on fluid content. Serous- hypo, Mucinous-iso/hyper, Hrgic-hyper SI.
Epithelioid hemangioendothelioma
Rare neoplasm of vascular origin. Adults. F>M. Peripheral solid nodules composed of
myxoid stroma with relatively hypocellular center.
Usually multiple larger peripheral lesion coalescing to form confluent mass.
CT- Hypoattenuating mass showing peripheral enhancement.
MRI- Hypointense in T1, hyperintense in T2. Peripheral Enhancement Seen.
Epithelioid hemangioendothelioma – Contrast-CT -large heterogeneous, lobulated tumor involving both right and left lobes.
Primary hepatic Angiosarcoma
Rare,primary mesenchymal liver tumor. In Elderly men and have poor prognosis. Metastasis is common.
Association exists with prior exposure to certain chemical carcinogens.
Multifocal but well-marginated nodules throughout the liver.
USG- Large mass of mixed echogenicity. CT -Hypodense mass. Hetrog. enhancement. Hypointense on T1- and markedly
hyperintense on T2-w images, with hypointense septa in T2-weighted.
Angiosarcoma- T2W and AP CT and MRI showing non-enhancing lesionswith feeding artery
Primary Lymphoma Primary hepatic lymphomas are rare. Most of these tumors are Non-Hodgkin’s T-
cell lymphomas. Usually present as a discrete tumor. USG-Homogeneous lesions anechoic or
hypoechoic and mimic a cyst, although unlike a cyst they lack through transmission. Some are surrounded by a halo.
Most primary liver lymphomas are hypointense on T1- and hyperintense on T2-weighted images. They show heterogeneous postcontrast enhancement.
Secondary Lymphoma Non-Hodgkin’s lymphoma is more often
focal. Calcifications seen rarely. Portal and periportal intrahepatic
infiltrates causes jaundice. MRI-Hypointense on T1- and hypo- to
hyperintense on T2-weighted images. Postcontrast enhancement varies.
Use of phosphorus MR spectra from P-31 MR spectroscopy appears potentially useful.
NHL-contrast CT-Several focal hypodense tumors & intrahepatic tumor tracking along portal vessels.
Hepatoblastoma Most common primary liver neoplasm in
children under 3 years. Rarely seen in adults. M>F. Elevated AFP seen.
Prevalence is increased in Beckwith- Wiedemann syndrome and in hemihypertrophy.
Originates from embryonal hepatic tissue and usually consists of epithelial cells or mixture of epithelial and mesenchymal cells.
Readily metastasize. Vascular displacement or amputation may occur.
Imaging features similar to HCC. May have local invasion, cystic changes, necrosis or irregular shaped calcification.
US- Mixed echogenic large lesion with poorly defined margins.
CT- Hypodense mass. Variable enhancement.
MRI-Hypointense on T1- and hyperintense on T2. Heterogeneity is often evident.
Hepatoblastoma shows uptake of sulfur colloid; however, does not have uptake of both Tc-99m–sulfur colloid and HIDA.
Hepatoblastoma –Contrast CT- large slightly enhancing tumor containing central necrosis and calcifications
TSTC (too small to characterize)LesionsJones (1992), Schwartz (1999), Khalil (2005)
For lesions which, due to their small size and atypical imaging features, cannot be confidently categorized, the term TSTC lesions has been coined. Usually for lesion <15mm in CT/MRI.
Accounts abt.12% of liver lesions with a known Pt. with malignancy. (80% are benign).
Patient without a known malignancy –usually considered as benign.
Patient with a known malignancy-- a single TSTC lesion can be assumed as benign.
Even multiple TSTCs- mostly benign, esp. when they are small, sharply defined and hypodense.
Avoid 'we can't rule out metastases'
Chemoembolization Intraarterial embolization techniques used
to treat hepatocellular carcinomas consist of inert particle embolization, chemotoxic agents(chemoembolization), and injection of radioactive particles (radioembolization).
Transcatheter chemoembolization is commonly used using Ethiodol (Lipiodol).
Later, after injecting a chemotherapeutic agent, if needed, embolization of the vessel in question is performed using particulate matter.
CT shows residual Ethiodol retained in a multifocal hepatocellular carcinoma
Radioembolization Intrahepatic artery Tc-99m-MAA injection
estimates the relative tumor-to–normal parenchyma uptake of various size microspheres, including those containing therapeutic radiopharmaceutical agent
Hepatocellular carcinomas have also been embolized with iodine-131 iodized oil (Lipiodol) and gelatin sponges through a superselectively placed arterial catheter.
Provided long-term palliation without complications.
Percutaneous Techniques Hepatocellular carcinomas can be treated
using a direct percutaneous approach.injection of chemical agents such as
ethanol, acetic acid, and hot saline to induce tumor coagulation necrosis.
thermally mediated techniques such as radiofrequency (RF) ablation, laser photocoagulation, microwave therapy, and cryotherapy result in similar tumor cell death.
Imaging provides needle and catheter insertion guidance.
Most percutaneous ablation is performed using US guidance, although for tumors not visualized by US, MRI guidance in an open magnet is an option.
Either CT, contrast-enhanced US, or MR are used to detect residual tumors shortly after ablation.
Radiofrequency ablation of hepatocellular carcinoma. A: Pretherapy B: hyperdense center immediate post-therapy C: Residual changes are present 2 months.
Cryoablation Destroys tumor tissue by freezing. Liquid
nitrogen is the freezing Medium. Either a percutaneous or an open surgical
approach is used for cryoablation.US/MRI used.
Magnetic resonance guidance- identifies the tumor nodule in question and the size of the surrounding frozen liver tissue. An open MR unit reveals resultant ice balls as sharply defined expanding regions of signal loss encasing tumors S/O resultant necrosis.
REFERENCES: Lee/Sagel : CT With MRI Corr. 4th ed. Grainger/Allison : Diag.Radiology 5th ed. Skucas : Advanced Imaging Abd. 2006. Rumack : Diag. Ultrasonography 3rd ed. Margulis: GI Imaging AJR, Radiology.
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