A brief theoretical overview of the most frequently clinically encountered benign and malignant hepatic mass lesions in day to day practise. The X-Ray, USG, CT, MRI images and videos in the presentation may help in reaching the diagnosis of the lesion. The presentation also includes nuclear medicine and angiographic findings of the lesions.

1. z
HEPATIC MASS LESIONS
DR. V RUCHIKA (JR-3) , DEPT. OF RADIOLOGY, PMCH.
GUIDED BY- DR.SANJEEV SUMAN (ASST. PROFESSOR)
DR. SANTOSH KUMAR PRASAD (SR)

2. z
HEPATIC MASS LESIONS
BENIGN
 LIVER CYSTS
 CYSTADENOMA
 BILIARY HAMARTOMA
 HEMANGIOMA
 FNH
 HEPATIC ADENOMA
 ABSCESS
 REGENERATIVE NODULE
 ATYPICAL REGENERATIVE
NODULES
MALIGNANT
 HCC
 FIBROLAMELLAR CARCINOMA
 METASTASIS
 INTRAHEPATIC
CHOLANGIOCARCINOMA
 HEPATOBLASTOMA
 INFANTILE
HEMANGIOENDOTHELIOMA
 BILIARY CYSTADENOCARCINOMA
 ANGIOSARCOMA
 EPITHELIOID
HEMANGIOENDOTHELIOMA
 LYMPHOMA

3. z
HYPERVASCULAR
LESIONS
BENIGN
• HEMANGIOMA
• FNH
• ADENOMA
MALIGNANT
• HCC
• FLC
METASTATIC
• RCC
• MELANOMA

4. z
IMAGING TECHNIQUES
 PLAIN RADIOGRAPHY: GROSS HEPATOMEGALY
CALCIFICATION
 USG/CEUS
 CT
 MRI
 ANGIOGRAPHY
 SCINTIGRAPHY: SULPHUR COLLOID, Tc99m LABELLED RBC
 PET

5. z
TRIPHASIC CT
 EARLY ARTERIAL PHASE
 LATE ARTERIAL PHASE
 PORTAL VENOUS PHASE
 DELAYED PHASE

6. z

7. z

8. z

9. z

10. z
VALUE OF DELAYED PHASE
 TUMOUR WASHOUT- VASCULAR TUMOUR
 RETENTION OF CONTRAST IN BLOOD POOL-
HEMANGIOMA
 RETENTION OF CONTRAST IN FIBROUS TISSUE:
CAPSULE AROUND HCC,
CHOLANGIOCARCINOMA WHEN FIBROUS,
FNH

11. z
LIVER CYSTS
 K/A BILE DUCT CYST BUT SHOW NO COMMUNICATION
WITH BILIARY SYSTEM.
 LINED BY SINGLE LAYER OF CUBOIDAL EPITHELIUM WITH
THIN (1mm) FIBROUS WALL.
 OLDER ADULTS; M>F
 ASYMPTOMATIC; COMPRESSIVE SYMPTOMS IF LARGE.
 >10 IN NO- ADPKD

12. z
z
USG
ANECHOIC
POST-ACOUSTIC
ENHANCEMENT
IMPERCEPTIBLE WALL
NO FLOW ON CDS

13. z
z
CT
HYPODENSE WITH CT
VALUE NEAR 0.
IF H/G OCCURS THEN CT
VALUE INCREASES.
CECT: NO ENHANCEMENT

14. z
z
MRI
T1WI: HYPOINTENSE
T2WI: EXTREMELY
HYPERINTENSE
CEMRI: NON-
ENHANCEMENT.
RADIONUCLIDE
UPTAKE: COLD
ANGIO: AVASCULAR

15. z
BILIARY
CYSTADENOMA
 SOLITARY
 MULTILOCULATED-
LOCULES MAY CONTAIN
TURBID, PURULRNT OR
BLOODY MUCIN.
 LARGE
 SLOW GROWING
 F>M
 PREMALIGNANT
 AVASCULAR
 SELDOM COMMUNICATES
WITH BILIARY TREE, IF SO
THEN BILIARY TREE MAY BE
DILATED WITH MUCIN.

16. z
z
USG
ANECHOIC TO LOW LEVEL
ECHOES DEPENDING ON
CONTENT
WELL DEFINED
MURAL NODULES AND
PAPILLARY PROJECTIONS
SEPTAL/ WALL
CALCIFICATIONS CAUSING
POST-ACOUSTIC
SHADOWING.

17. z
z
CT
HYPODENSE
DENSER CONTENTS THAN
THAT OF SIMPLE CYSTS OF
LIVER OR KIDNEY
CALCIFICATION OF WALLS
CECT: WALL, SEPTA,
PAPILLARY PROJECTIONS
ENHANCE

18. z
z
MRI
T1WI: HYPOINTENSE
T2WI: HYPERINTENSE
DEPENDING ON NATURE OF
FLUID
SEPTA: T1WI T2WI
HYPOINTENSE

19. z
CYSTADENOCARCINOMA
 PAPILLARY PROJECTIONS
MORE COMMON
 COARSE CALCIFICATION
 RAISED Ca 19-9, CEA
D/D: BENIGN CYST
HYDATID CYST
ABSCESS
HEMATOMA
HAMARTOMA
CYSTIC METS
EMBRYONAL SARCOMA

20. z
BILIARY HAMARTOMA ( VON
MEYERBURG COMPLEX)
 SMALL, FOCAL DEVELOPMENTAL LESIONS COMPOSED OF
DILATED INTRAHEPATIC BILE DUCTS SURROUNDED BY
FIBROUS INTERSTITIUM.
 SINGLE/MULTIPLE/INNUMERABLE
 <1cm

21. z
USG
HYPOECHOIC( (LESS
FREQUENTLY HYPERECHOIC)
BRIGHT ECHOGENIC FOCI
WITH COMET TAIL

23. z
CT
 NCCT: IRREGULAR WALL
HYPODENSE
 CECT: NO ENHANCEMENT
MRI
 T1WI: HYPOINTENSE
 T2WI/MRCP:
HYPERINTENSE

25. z
D/D
HYPOVASCULAR SOLID MASS:
 MULTIPLE MICROABSCESSES
 IRREGULAR FATTY INFILTRATION
 METASTATIC LIVER CANCER

26. z
HEMANGIOMA
 M/C BENIGN TUMOUR.
 F:M= 5:1
 HORMONE DEPENDENT: ENLARGE DURING PREGNANCY OR ESTROGEN
ADMINISTRATION.
 ASYMPTOMATIC;
>4cm : abdominal pain, discomfort, palpable mass.
 >10cm – CAVERNOUS HEMANGIOMA
 THROMBOCTOPENIA CAUSED BY SEQUESTRATION AND DESTRUCTION OF
PLATELETS WITHIN A CAVERNOUS HEMANGIOMA K/A KASABACH-MERRITT
SYNDROME.

27. z
HISTOLOGY
MULTIPLE VASCULAR CHANNELS
THAT ARE LINED. BY A SINGLE LAYER
OF ENDOTHELIUM AND SEPARATED
BY FIBROUS SEPTA.
DEGENERATIVE CHANGES ARE SEEN
IN CETER LIKE THROMBUS
FORMATION, NECROSIS, SCARRING,
HAEMORRHAGE AND CALCIFICATION.
SCLEROSED HEMANGIOMA-
DENEGERATED HEMANGIOMAS WITH
FIBROTIC CHANGES.

28. z
z
X-RAY
HEPATOMEGALY
PHLEBOLITHS
CALCIFIED
TRABECULATIONS/SPICULE
S THAT RADIATE FROM A
CENTRAL POINT
CENTRAL CALCIFIC SCAR.

29. z
USG
TYPICAL:
 WELL DEFINED
 HOMOGENOUS
 POST ACOUSTIC
ENHANCEMENT (>2.5cm
LESIONS)
ATYPICAL
 NON-HOMOGENOUS
 CENTRAL SCAR
 HYPOECHOIC;
ECHOGENIC BORDER
 LARGE LESIONS APPEAR
HETEROGENOUS WITH
CENTRAL HYPOECHOIC
SCAR.

31. z
 CDS: EXTREMELY SLOW
BLOOD FLOW NOT
ROUTINELY DETECTED.
 CEUS: DISCONTINUOUS
PERIPHERAL PUDDLE OF
ENHANCEMENT WITH
CENTRIPETAL FILLING.
 COMPLETE FILL IN ON
DELAYED IMAGES.
 SUSTAINED
ENHANCEMENT.

32. z
z
CT
NCCT: WELL DEMARCATED
 HYPODENSE
 ROUND, OVAL OR
IRREGULAR (GEOGRAPHICAL
)
CECT:
AP- PERIPHERAL
ENHANCEMENT WITH CENTER
FILLING IN.
EQUILIBRIUM PHASE-
PROLONGED ENHANCEMENT (
CHARACTERISTIC PATTERN OF
HEMANGIOMA)

34. z
MRI
T1WI: HOMOGENOUS HYPOINTENSE.
T2WI: HOMOGENOUS HYPERINTENSE
( LIGHT BULB SIGN )
CEMRI: SAME AS CECT.
• RBC SCINTIGRAPHY- HOT SPOT
ON DELAYED SCAN.
T1
T2
CS CS

36. z
SCLEROSED
HEMANGIOMA- MAY
MIMIC A MALIGNANT
MASS;
CT: HYPODENSE
T2WI: HYPOINTENSE
THAN CSF
PORTAL VENOUS
WASHOUT.
 FLASH HEMANGIOMA:
SMALL HEMANGIOMA
SHOWING FAST
HOMOGENOUS
ENHANCEMENT(
FLASH FILLING).
 D/D: METS
 HCC
 T/T: TAE

37. z
HEPATIC ADENOMA
 SOLITARY
 >10cm
 M/C IN FEMALES ( 20-40 YRS)
 A/W- H/O OCP
H/O ANABOLIC STEROID IN MEN
TYPE 1 GSD (VON GIERKE DISEASE)

38. z
TYPES
HNF 1 ⍺-
INACTIVATED
ADENOMA
INFLAMMATOR
Y (FORMERLY
TELANGIECTATI
C FNH)
β-CATENIN
ACTIVATED
ADENOMA
UNCLASSIFIED
FEMALE
PREDOMINANT
INTRATUMOUR
AL FAT
DEPOSITION.
F>M
MALIGNANT
TRANSFORMATI
ON IN THE
BACKGROUND
OF FATTY
LIVER.
M>F
MALIGNANT
TRANSFORMATI
ON
VAGUE SCAR
SEEN WITHIN
THE TUMOUR

39. z
PATHOLOGY
 NORMAL OR ATYPICAL HEPATOCYTE.
 NO BILE DUCTS OR KUPFFER CELLS.
 30% HAVE THIN CAPSULE
 INTERNAL H/G , NECROSIS, SCAR TISSUE, CALCIFICATION
OR FAT.

40. z
USG
 HNF 1 ⍺- INACTIVATED:
 ECHOGENIC;
 CEUS- AP: HYPERVASCULAR
 PV: NO WASHOUT.
 INFLAMMATORY:
 HYPO/ISO/HYPERECHOIC;
 CEUS- AP: ENHANCEMENT
WITH CENTRIPETAL FILLING
AND LATE WEAK WASHOUT.

42. z
CT
 NCCT: HYPODENSE (FAT)
 HYPERDENSE ( H/G)
 CECT: HYPERVASCULAR;
 RAPID WASHOUT.

44. z
z
MRI
HETEROGENOUS
T1WI: HYPER/INTERMEDIATE
T2WI: HYPERINTENSE.
CHEMICAL SHIFT SEQUENCE: SIGNAL
DROPOUT (FAT)
ATOLL SIGN: T2WI SHOWS BRIGHT RIM (
DILATED SINUSOIDS IN PERIPHERY) ,
SEEN IN INFLAMMATORY TYPE.
CEMRI: SAME AS USG.
RADIONUCLIDE: S COLLOID- COLD DUE
TO ABSENCE OF KUPFFER CELLS.
ANGIO: HYPERVASCULAR TUMOUR
WITH LARGE PERIPHERAL VESSELS.

45. ATOLL SIGN - T2WI SHOWS
BRIGHT RIM ( DILATED
SINUSOIDS IN PERIPHERY) ,
SEEN IN INFLAMMATORY TYPE.
This Photo by Unknown Author is
licensed under CC BY-SA
ATOLL- A ring shaped coral reef, island
or series of islets surrounding a water
body (lagoon).

46. z
FNH
 F>M (8:1) ; 20-50 YRS.
 SOLITARY, WELL CIRCUMSCRIBED MASS WITH CENTRAL SCAR.
 DEVELOPMENTAL HYPERPLASTIC LESION RELATED TO AN AREA OF CONGENITAL
VASCULAR MALFORMATION, PROBABLY PRE-EXISTING ARTERIAL SPIDER LIKE
MALFORMATION.
 THE EXCELLENT BLOOD SUPPLY MAKES H/G, NECROSIS AND CALCIFICATION RARE.
 HISTO: NORMAL HEPATOCYTES,
KUPFFER CELLS,
BILIARY DUCTS,
FIBROUS SEPTA.

47. z
z
USG
 SUBTLE MASS WITH CONTOUR
ABNORMALITIES.
 ISO/HYPOECHOIC WITH
HYPOECHOIC SCAR.
 DOPPLER: STELLATE FLOW
PATTERN.
 CEUS: AP- HYPERVASCULAR
WITH CENTRIFUGAL FILLING.
 NON-ENHANCING SCAR.

48. EARLY AP SHOWING
STELLATE VESSELS

49. z
z
CT
NCCT: HOMOGENOUS
HYPODENSE MASS WITH
MORE HYPODENSE
CENTRAL SCAR.
CECT: AP- HOMOGENOUS
ENHANCEMENT
 PV- ISODENSE
 DELAYED- SCAR
ENHANCES.

50. NCCT
AP DP
AP

51. z
z
MRI T1WI- HYPO/ISO
T2WI- HYPER/ISO
CENTRAL SCAR- T1: HYPO
 T2: HYPER.
CEMRI: SAME AS CT.
 T2 WITH SPIO- LOSS OF SIGNAL DUE
TO UPTAKE OF IRON OXIDE
PARTICLES BY KUPFFER CELLS .
 ANGIO: HYPERVASCULAR WITH
CENTRIFUGAL SPOKE WHEEL/STELLATE
PATTERN.
RADIONUCLIDE: S COLLOID + TBIDA (
TRIMETHYL BROMO IMINODIACETIC
ACID)
UPTAKE DUE TO KUPFFER CELLS.

52. z
ABSCESS
 BACTERIA CAN REACH THE LIVER VIA PV, HA, BILE DUCT
OR DIRECT INFECTION FROM ADJACENT STRUCTURES.
 TYPES: PYOGENIC,
AMOEBIC,
FUNGAL.

53. z
z
USG
 WELL DEFINED/ IRREGULAR
 THICK WALLED
 EARLY- HYPO/ALTERED
ECHOGENICITY.
 MATURE- CYSTIC WITH
ECHOFREE TO ECHOGENIC
CONTENT.
 AIR PRODUCING BACTERIA-
CAUSE POSTERIOR
REVERBERATION ARTIFACT.

54. z
CT  NCCT: HYPO
 CLUSTER SIGN- COALESCING
SMALL ABSCESSES.
 CECT: AP- DOUBLE TARGET SIGN=
 AREA AROUND NON-ENHANCING
CENTER ENHANCES ( MEDIAL ) WITH
SURROUNDING HYPODENSE
OUTERMOST LAYER.
 PV TO DELAYED- THICK RINGLIKE
ENHANCEMENT OF MEDIAL AND
OUTERMOST LAYER.
 WEDGE SHAPED ENHANCEMENT IN THE
SURROUNDING INDICATING INFLAMMED
PORTAL TRACTS DUE TO NARROWING/
OBSTRUCTION OF PV BRANCHES.

55. z
MRI
 T1WI- HYPO
 T2WI- HYPER
 DWI: RESTRICTION.
 CEMRI- AP: WEDGE ENHANCEMENT.

56. z
AMOEBIC ABSCESS
 USG: ROUND/OVAL
 HYPO
 ABSENCE OF
ABSCESS WALL
 FINE LOW LEVEL
INTERNAL ECHOES.

57. CT/MRI
 SAME AS PYOGENIC
ABSCESS

58. z
FUNGAL
 IMMUNOCOMPROMISED INDIVIDUALS.
 M/C CANDIDA.
 USG:
 WHEEL WITHIN A WHEEL- PERIPHERAL HYPO ZONE WITH INNER
ECHOGENIC WHEEL AND CENTRAL HYPO NIDUS CONTAINING NECROSED
TISSUE AND FUNGAL ELEMENTS.
 BULL’S EYE- 1-4cm; HYPER CENTER WITH HYPO RIM.
 M/C UNIFORMLY HYPO DUE TO FIBROSIS.
 ECHOGENIC

60. z
CT/MRI
CECT: AP- MICROABSCESSES WITH
FAINT RINGLIKE ENHANCEMENT.
DP- HYPO
MRI: T1WI- HYPO
T2WI- HYPER
CEMRI- PERIPHERAL RIM
ENHANCEMENT.

61. z
HCC
 M/C PRIMARY MALIGNANCY OF LIVER.
 ETIO: HBV,HCV
CHRONIC ALCOHOLISM
AFLATOXIN
NON-ALCOHOLIC STEATOHEPATITIS
CONG. BILIARY ATRESIA
INBORN ERRORS OF METABOLISM- HEMOCHROMATOSIS
⍺-1 ANTITRYPSIN DEFICIENCY
GSD TYPE 1
WILSON DISEASE.

62. z
CLINICAL FEATURES
 DELAYED SYMPTOMS
 RUQ PAIN
 WEIGHT LOSS
 ABDOMINAL SWELLING.

63. Most HCC develop by means of a multistep progression:
LOW -GRADE DYSPLASTIC NODULE
⬇
HIGH-GRADE DYSPLASTIC NODULE
⬇
DYSPLASTIC NODULE WITH A FOCUS OF HCC
⬇
OVERT CARCINOMA(HCC)

64. z
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 NODULE

65. z
DYSPLASTIC NODULE
 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

66. z
USG
 HYPO/HYPER.
 PERPHERAL HYPO HALO
DUE TO FIBROUS
CAPSULE.
 MIXED/MOSAIC PATTERN.

67. z
DOPPLER: DETECTS
VASCULARITY IN TUMOUR,
THROMBI IN PV.
CEUS:
AP- HYPERVASCULAR
PV- WASHOUT
HOWEVER, THERE ARE
VARIATIONS TO THIS.

69. z
CT
 3 PATTERNS: SOLITARY
 MULTICENTRIC
 DIFFUSE.
 LARGE HYPODENSE MASS
 CENTRAL LOW
ATTENUATION DUE TO
NECROSIS.
 FOCAL CALCIFICATION.(
7.5%)
 CECT:
 AP- HYPERVASCULAR
 PV-WASHOIUT
 DELAYED- HYPO WITH
ENHANCEMENT OF
CAPSULE.

70. NCCT AP PV

71. z
MRI
 T1WI- ISO/HYPER
 T2WI- HYPER
 DWI- INTRATUMOURAL HYPER
 CAPSULE- HYPO ON T1WI T2WI
 SCAR/CALCIFICATIN- HYPO ON T1WI T2WI
 SPIO- HYPER ON T2WI.
 CEMRI-
 AP: HYPERENHANCEMENT
 PV: WASHOUT.

72. 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)

73. z
HCC VARIANTS
FIBROLAMELLAR CLEAR CELL SARCOMATOID SCLEROSING
• YOUNG ADULTS (5-
35YRS)
• SPONTANEOUS.
• SOLITARY,
LOBULATED WELL
DEFINED
CONTAINING A
CENTRAL FIBROUS
SCAR.
• PUNCTATE
CALCIFICATION IN
SCAR IN >50%
CASES
• INHOMOGENOUS
AP
ENHANCEMENT,
INTRACYTOPLASMIC
FAT: SIGNAL DROP
ON OPPOSED PHASE
• CENTRAL
NECROSIS OR H/G.
• POOR
PROGNOSIS.
• INTENSE FIBROSIS
• PROGRESSIVE
AND PROLONGED
ENHANCEMENT.

75. z

76. z

77. z
METASTASIS
 M/C METASTATIC SITE AFTER NODES.
 MULTIPLE LESIONS IS COMMON.

78. z
TYPES
HYPERVASCULAR CALCIFIED CYSTIC
RCC, THYROID,
CARCINOID, MELANOMA,
ISLET CELL TUMOUR,
CHORIOCARCINOMA.
D/D:
HEMANGIOMA
FNH
ADEMOA
HCC
MUCINOUS CA OF GIT
(COLON, STOMACH,
RECTUM),
MELANOMA,
OVARIAN CA
MUCINOUS OVARIAN CA,
COLONIC CA, GIST.

80.  Conclusion :
 MDCT and MRI are the most commonly used imaging
modalities for detection and characterization of focal
hepatic lesion .
 Imaging modalities can make diagnosis for: Hepatic cyst
Caverneous hemangioma Typical FNH HCC .
 For others lesions biopsy will be often necessary

81. z
z
THANK YOU