Rare hepatic lesions and uncommon patterns of common hepatic

Transcription

Rare hepatic lesions and uncommon patterns of common hepatic
Rare hepatic lesions and uncommon patterns of common
hepatic lesions on dynamic multiphasic MDCT studies
Poster No.:
C-1324
Congress:
ECR 2011
Type:
Educational Exhibit
Authors:
C. Kakkar , P. Koteshwara , A. M. Polnaya , K. Rajagopal , N. M.
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Mulimani , V. R. K. Rao ; Manipal, Karnataka/IN, Mangalore,
Karnataka/IN
Keywords:
Abdomen, Liver, Biliary Tract / Gallbladder, CT, Diagnostic
procedure, Infection, Neoplasia, Tropical diseases
DOI:
10.1594/ecr2011/C-1324
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Learning objectives
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To illustrate the imaging patterns of uncommon hepatic lesions on dynamic
multiphasic studies.
To emphasize on uncommon patterns of common hepatic lesions leading to
diagnostic dilemma.
Background
Primary or secondary hepatic lesions have a varying patterns of enhancement on
multiphasic MDCT studies which are helpful in diagnosis however there are group of
lesions such as coexisting hepatocellular and cholangiocarcinoma , hepatic tuberculosis,
oriental cholangiohepatitis etc which may not be diagnosed on imaging due to
overlapping patterns and final result depends on histopathology.
Rupture of primary hepatic tumors is a rare but catastrophic entity and most patients
succumb to this emergency. We came across a few cases of "bloody liver" secondary to
a ruptured haemangioma and heptomas.
"Lumps and bumps" of the liver surface secondary to entities like cirrhosis is
quiet common however certain entities like pseudocirrhosis can also have a similar
appearance. Malignant lesions like haemangioendothelioma, peripherally placed
hepatoma can cause extreme degree of capsular retraction which can cause a bumpy
surface of liver.
Alpha fetoprotein is a marker of hepatoma however we in our experience observed a few
cases which did not show any elevation of this tumor marker and a retrospective analysis
showed that all these tumors were encapsulated hepatoma and histopathology showed
all these lesions to be well differentiated form of hepatocelullar carcinoma.
Imaging findings OR Procedure details
The imaging pattern are described based on either the gross morphological pattern of
the lesion like lumpy bumpy liver, rocks in liver, gas in liver , fat in liver.
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Enhancement pattern in the form of filling lesions showing overlapping patterns such as
hepatocholangiocarcinoma and metastases.Capsular enhancement pattern in hepatoma
which has served a very specific feature in our review.
Bloody liver secondary to ruptured neoplasms.
Images for this section:
Fig. 1
Fig. 2: Cirrhosis with Hepatocellular carcinoma and significant capsular retraction. A :
Plain CT image shows an ill defined hypodense lesion in the right lobe with marked
retraction of the hepatic capsule. B and C : There is intense enhancement in the
subcapsular location(arrow)with heterogeneous arterial enhancement more inferiorly.
Gross free fluid noted in perihepatic location.
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Fig. 3: D , E and F( contd.) : Portovenous phase images show infiltrative pattern of
the lesion which appears hypodense suggestive of washout. G )There is persistence of
contrast enhancement in region of capsular retraction which is relatively hyperdense to
the adjacent lesion and hepatic parenchyma. A close mimic of such an appearance in
cirrhosis can be confluent hepatic fibrosis.
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Fig. 4: Malignant Haemangioendolthelioma: A and B ) Plain CT image shows a
hypodense lesion (arrows)in the right lobe . The lesion is deriving blood supply from the
right hepatic artery (dotted arrow) and shows predominantly a peripheral enhancement
Fig. 5: C and D (contd.) Arterial phase image shows another homogenously enhancing
focus adjacent to the primary lesion.The primary lesion shows a focal area of capsular
retraction(arrowhead)which is better appreciated on magnified view.
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Fig. 6: E and F (contd.) : Portovenous phase the lesion is heterogeneous and largely
isodense to rest of hepatic parenchyma. Delayed phase the lesion is isodense to rest of
hepatic parenchyma.
Fig. 7: Pseudocirrhosis : Known case metastatic carcinoma breast post chemotherapy.
A and B) Axial portovenous phase images show surface nodularity (arrowhead) with
hypodense branching pattern involving the hepatic parenchyma diffusely.
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Fig. 8: C(contd.) Hepatomegaly with hypoattenuating branching pattern in the entire liver.
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Fig. 9
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Fig. 10: Ruptured Haemangioma: A and B ) Plain CT reveals a large hypodense lesion in
the right lobe of liver with fuzziness of hepatic margins inferiorly(arrowhead) and adjacent
fluid collection(arrow).
Fig. 11: C and D (contd.) : Post contrast arterial phase lesion shows peripheral
enhancement (black arrow)with suspicious site of rupture(arrowhead) and associated
perihepatic fluid (dotted arrow).
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Fig. 12: E and F (contd.): The lesion shows progressive centripetal filling in the
portovenous phase (arrows)associated fluid collection (arrowhead). The lesion is
isodense to the liver in delayed phase.
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Fig. 13: Ruptured Hepatoma: A) Well defined isodense lesion in the right lobe of liver
( arrows) with central hypodense area. Hyperdense collection noted in the lesser sac
(asterisk) suggestive of haemoperitoneum.
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Fig. 14: B and C (contd.) : Lesion shows arterial enhancement (arrows) with adjacent
haematoma extending inferiorly anterior to the pancreas in lesser sac.
Fig. 15: D and E (contd.) : Lesion shows some areas of washout in the periphery with
a sharply defined capsule showing delayed enhancement (arrowhead). Another lesion
hypodense lesion noted in the left lobe (arrow). Haematoma in the lesser sac (asterisk).
Fig. 16: F and G (contd.) : The primary lesion shows a significant blush on selective right
hepatic artery angiography (arrows) with multiple smaller lesions detected in the adjacent
parenchyma (arrowhead). Post embolisation there is significant reduction in the tumor
blush.
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Fig. 17: Hepatoma with rupture and atretic suprahepatic Inferior vena cava: A) Plain
CT shows hyperdense fluid in the left lumbar region suggestive of haemoperitoneum.
B :Arterial phase there is an ill defined lesion (arrows) deriving blood supply from the
branch of left hepatic artery. Lesion shows solid enhancement in the arterial phase.
Fig. 18: C and D (contd.) : Portovenous phase the liver shows nodular surface with
markedly enlarged caudate lobe(asterisk).The lesion is hypodense to the rest of hepatic
parenchyma suggestive of washout.
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Fig. 19: E and F (contd.): Portovenous phase there is abrupt change in the calibre of
inferior vena cava with non visualization of suprahepatic segment of infeiror vena cava.
The supradiaphragmatic segment was receiving the venous drainage through enlarged
collaterals.
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Fig. 20: G and H : Marked hypertrophy of the caudate lobe with main portal vein arching
across it.Dilated and enlarged azygous and hemiazygous veins due to atresia of inferior
vena cava. Multiple perisplenic collaterals noted secondary to portal hypertension.
Fig. 21
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Fig. 22: Hepatocellular carcinoma: A) Plain CT study shows a large lesion in the right lobe
with calcific focus(arrowhead). B,C and D) Arterial phase shows a prominent vascular
channel in periphery of lesion(arrow)with intensely enhancing areas in the centre of lesion
(dotted arrow). Lesion shows solid enhancement in the periphery on inferior sections.
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Fig. 23: C and D (contd.) : Lesion shows enhancing areas of contrast puddling in the
centre of lesion suggestive of arterioportal shunting (arrowhead).
Fig. 24: G (contd.) : Delayed phase lesion shows peripheral capsular enhancement
(arrowhead)with enhancing vascular channels in the centre.Serum AFP:Not elevated.
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Fig. 25: Encapsulated Hepatoma with normal AFP levels: A ) A large well defined
lesion with solid peripheral enhancement and central non enhancing area suggestive of
necrosis. B)Coronal portovenous phase there is appreciation of capsular enhancement
(arrowhead) .
Fig. 26: C and D (contd.) Lesion is largely hypodense to rest of the hepatic parenchyma
in portovenous and delayed phase (at 180 seconds) . The capsular enhancement and
delineation is best appreciated on delayed phase.
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Fig. 27
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Fig. 28: Well defined lesion in the right lobe of liver showing central (arrow) and peripheral
calcification(arrowhead).No enhancement in the arterial and portovenous phases. Final
Diagnosis :Hydatid disease.Close differential can be a chronic abscess.
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Fig. 29: Middle aged man with history of recurrent abdominal pain and jaundice. A
and B: Plain CT reveals multiple small hyperdensities in the right lobe suggestive of
calcification(arrow).Biliary radical dilatation in the left lobe (arrowheads)
Fig. 30: C and D (contd.) : Contrast sequences . Coronal CT reveals a branching pattern
of the calcifications suggestive of intraductal calculi. Curved reformatted image shows
soft tissue density within the CBD . Dilated biliary radicals in the left lobe. Possibility
of worm infestation (ascariasis) causing oriental cholangiohepatitis considered. Further
work up and follow up : No evidence of malignancy / progression of disease. Close mimic
can be an intraductal cholangiocarcinoma.
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Fig. 31: Tubercular Cholangitis : A and B)Unenhanced axial CT section shows linear
calcifications along the biliary radicals(arrow).Ill defined soft tissue density along the
biliary radicals (dotted arrow).
Fig. 32: C and D): Arterial and portovenous phase shows wall calcifications along the
dilated radicals (discontinuous arrow) and minimal enhancement of the soft tissue in the
periportal location (arrow).
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Fig. 33: E) Coronal CT section in portovenous phase shows minimal enhancing soft
tissue density along the walls of the common bile duct which appears mildly prominent.
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Fig. 34: F)Conglomerated low attenuation paraortic lymph nodal mass(arrow)with biliary
radical dilatation (dotted arrow).
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Fig. 35: Calcified Hydatid: Densely calcified lesion in the right lobe of liver in subcapsular
location.
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Fig. 36
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Fig. 37: Hepatoma with intratumoral pseudoaneurysm: A)A large well define
lesion(arrows)in the right lobe which is isodense to rest of hepatic parenchyma. The lesion
shows a well defined hyperdensity within (arrowhead).
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Fig. 38: B (contd.) : Arterial phase lesion is showing significant enhancement with intense
enhancement (similar to aorta noted in the region of hyperdensity (refer previous image)
suggestive of pseudoaneurysm. C)The lesion shows area of washout on portovenous
phase.
Fig. 39: D (contd.) : Coronal portovenous image shows fluid level in the region of
pseudoaneurysm . Non - enhancing area noted in the lesion (asterisk) suggestive of
necrosis. E: Delayed phase there is capsular enhancement. Final Diagnosis : Well
differentiated Hepatocellular carcinoma. AFP levels : Within normal limits.
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Fig. 40
Fig. 41: A and B : Plain and contrast enhanced CT shows a large well defined
encapsulated lesion in the right lobe showing multiple hypodense areas suggestive of
air pockets. Coronal sections reveals multiple small satellite lesions adjacent to the
larger lesion with associated stranding in the perihepatic space inferiorly. Final Diagnosis:
Hydatid disease. Other possibility can be a cholangitic abscesses.
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Fig. 42
Fig. 43: Hepatic Lipoma in patient with multiple renal angiomyolipomas: Well defined fat
density lesion in the right lobe of liver(arrowhead).
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Fig. 44
Fig. 45: Tubercular Abscess:A)Axial contrast enhanced CT study shows a well defined
lesion in the right lobe with thick enhancing rim (arrow) with central area of caseous
necrosis in a case of nodular isolated hepatic tuberculosis
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Fig. 46: Multiple microabscesses in the right lobe of the liver forming complex mass
lesion . (B) Arterial phase reveals a minimally enhancing lesion in the right lobe with
an artery traversing through the lesion. Area of necrosis noted in the periphery. C)
Portovenous phase reveals the mass to be well circumscribed composed of multiple tiny
abscesses
Fig. 47: Lymphoma with extensive necrosis: Middle aged male patient with fever
and upper abdominal pain.HIV status negative. A)Gray scale image shows a large
hypoechoic lesion in the right lobe mimicking an abscess. B)Arterial phase the lesion
shows peripheral solid and centrally liquefied ( asterisk)lesion in the right lobe.Geographic
hypodense area(arrows)in the spleen.
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Fig. 48: C and D (contd.):Portovenous phase the lesion shows a hepatic lesion with
peripheral solid enhancement (arrows) and central necrosis (asterisk).Splenomegaly
with a necrotic lesion(asterisk) involving large part of splenic parenchyma. Enlarged
enhancing lymph node in the left inguinal region(arrowhead).
Fig. 49
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Fig. 50: Amoebic Abscess : A)Plain CT image shows a well defined hypodense lesion
in the right lobe of liver. B)Arterial phase lesion shows minimal enhancement in the
periphery and in the centre.
Fig. 51: C (contd.): In portovenous phase the lesion is showing increasing enhancement
centripetally(asterisk.) Minimal perihepatic fluid noted posteriorly(arrowhead). D: Delayed
phase there is significant filling up of the lesion.
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Fig. 52: Multiple haemangiomas with a large exophytic lesion : Well defined hypodense
lesion in the right lobe (arrow) with a large hypodense lesion in the peritoneum (arrow).
There is a rim of hepatic tissue around the lesion(arrowhead). B and C: Arterial phase
the lesion shows a peripheral nodular enhancement(arrowhead).
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Fig. 53: E,F,G and H(contd.): Portovenous phase the lesion shows progressive
filling(arrowhead)with complete filling in the delayed phase.
Fig. 54: Hepatocholangiocarcinoma: A and B) The lesion shows intense enhancement
in the arterial phase an is hyperdense to hepatic parenchyma.
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Fig. 55: C and D (contd.): There is no washout in the portovenous phase with lesion
being hyperdense to the hepatic parenchyma on portovenous and delayed phase.
Fig. 56: Hepatocholangiocarcinoma : A)On plain scan the lesion is isodense to the rest
of parenchyma(arrowhead). B:Intense enhancement noted in the lesion on arterial phase
(arrowhead) with central non-enhancing area.
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Fig. 57: C and D(contd.): Coronal portovenous phase the lesion is hyperdense
(arrowhead) to the hepatic parenchyma. Delayed phase the lesion is hyperdense to the
rest of hepatic parenchyma (arrowhead).
Fig. 58: Colorectal Metastases: A ) Isodense lesion with central hypodensity in the right
lobe. B) Arterial phase lesions shows more enhancement relative to hepatic parenchyma
C and D) Portovenous and delayed phase there is increasing enhancement of the lesion
suggestive of progressive filling pattern.
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Fig. 59: E(contd.) :Coronal portovenous image shows sharply demarcated lesion in the
right lobe. F: A large proliferative growth noted in the region of rectum. Final Diagnosis :
Metastasis from adenocarcinoma.
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Conclusion
Multiphasic analysis permits diagnosis of a lot of hepatic lesions such as hepatomas,
haemangiomas , adenomas , metastases etc however we observed there are a few
lesions like hepatocholangiocarcinoma ,metastases, infective pathologies which can
cause a diagnostic dilemma and may mimic other pathologies.
Capsular retraction can be seen in multiple pathologies and is not specific for a single
entity.
Personal Information
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