DOI:10.2214/AJR.05.1367
AJR 2007; 188:160-166
© American Roentgen Ray Society
Transient Hepatic Intensity Differences: Part 2, Those Not Associated with Focal Lesions
Stefano Colagrande1,
Nicoletta Centi1,
Roberta Galdiero2 and
Alfonso Ragozzino2
1 Department of Clinical Physiopathology, Section of Radiodiagnostics,
University of Florence, Viale Morgagni 85, Florence 50134, Italy.
2 Section of Radiodiagnostics, Ospedale SM Grazie Pozzuoli, Naples, Italy.
Received August 8, 2005;
accepted after revision October 21, 2005.
Address correspondence to S. Colagrande
(stefano.colagrande{at}unifi.it)
Abstract
OBJECTIVE. The purpose of our study was to evaluate and to show the
range of appearance of transient hepatic signal intensity differences when not
associated with focal lesions, and to correlate morphology, cause, and
pathogenesis.
CONCLUSION. Hepatic arterial phenomena, visualized on MRI and CT,
must be considered important signs of underlying liver disorders, which these
phenomena contribute to evaluate. Accordingly, the hepatic arterial phase must
always be performed on MRI as well as on CT, even if no focal lesion is
expected.
Keywords: arterial phenomena • dynamic MRI • hemodynamics • liver • liver disease • liver perfusion abnormalities • MRI • THID • transient hepatic intensity differences
Introduction
As stated in part 1 of this article
[1], transient hepatic signal
intensity differences can also not be associated with focal lesions. The aim
of this second part of our article is to show their wide range of appearance
and to rule out a possible diagnostic value. Transient hepatic intensity
difference, in this case, can be induced by three pathogenetic mechanisms:
portal hypoperfusion due to portal branch compression or thrombosis, flow
diversion caused by arterioportal shunt or by an anomalous blood supply, and
inflammation of the biliary vessels or adjacent organs
[2,
3].
Transient hepatic intensity differences without a focal lesion may have
three appearances: sectorial, which is triangular areas with a straight border
that follows portal dichotomy; polymorphous, having various shapes and
extension, usually without a straight border that does not follow portal
dichotomy; and diffuse, having a varied appearance, which is the generalized
equivalent of the sectorial transient hepatic intensity difference.
Accordingly, we have organized our article into three groups.
Sectorial Differences
This type of transient hepatic intensity difference is usually caused by
portal hypoperfusion due to portal (Fig.
1) or hepatic vein thrombosis, long-standing biliary obstruction,
or an arterioportal shunt, which may be congenital (Figs.
2A and
2B) or, more frequently, due to
liver cirrhosis or trauma [2,
4,
5]
(Fig. 3). In an arterioportal
shunt, mixing of venous low-pressure and arterial high-pressure blood leads to
an arterial reaction with a similar mechanism to that of an aberrant venous
supply or drainage or of shunts produced by a focal lesion (see part 1
[1]).
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Fig. 1 —58-year-old man with liver cirrhosis and sectorial transient
hepatic intensity differences due to portal thrombosis secondary to
hepatocellular carcinoma radiofrequency ablation. Axial gradient-echo
T1-weighted gadolinium-enhanced arterial phase image (TR/TE, 146/2) shows
wedge-shaped arterial phenomenon (arrowhead) caused by portal branch
thrombosis (arrow). Note also another hypointense treated nodule in
anterior portion of liver segment V, with peripheral enhanced area due to
arterial reaction.
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Fig. 2A —63-year-old man with sectorial transient hepatic intensity
difference in right hepatic lobe caused by congenital arterioportal shunt.
Axial gradient-echo T1-weighted gadolinium-enhanced arterial phase MR images
(TR/TE, 146/2) show arterial phenomenon (arrowheads) caused by
arterioportal shunt (arrow, A).
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Fig. 2B —63-year-old man with sectorial transient hepatic intensity
difference in right hepatic lobe caused by congenital arterioportal shunt.
Axial gradient-echo T1-weighted gadolinium-enhanced arterial phase MR images
(TR/TE, 146/2) show arterial phenomenon (arrowheads) caused by
arterioportal shunt (arrow, A).
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Fig. 3 —42-year-old woman with sectorial transient hepatic intensity
differences in right hepatic lobe caused by posttraumatic arterioportal shunt.
Axial gradient-echo T1-weighted gadolinium-enhanced arterial phase MR image
(TR/TE, 146/2) shows wedge-shaped arterial phenomenon (arrowheads)
caused by arterioportal shunt (arrow) due to percutaneous hepatic
biopsy performed 1 month earlier.
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Sometimes transient hepatic intensity differences without a focal lesion
may appear round because of a blockade in a portal or hepatic vein that does
not reach the hepatic capsule (blind vessel). Moreover, sectorial transient
hepatic intensity differences, especially when next to a Glisson's capsule,
can show a pseudoglobular shape
[2] that is due to the
relationship between the position of arterialization in the liver and the MRI
slice direction and orientation.
Pseudoglobular arterializations in the cirrhotic liver can create several
differential diagnostic problems in hepatocellular carcinoma. However, unlike
arterializations, hepatocellular carcinomas greater than 15 mm present T1 and
T2 signal alterations on baseline scanning, show a washout phenomenon in the
portal phase, and do not take up the hepatobiliary contrast agent on
late-phase MRI [6].
Nevertheless, diagnostic problems may persist in small, highly differentiated
hepatocellular carcinomas (T1 and T2 isointensity, no washout, late
concentration of hepatobiliary contrast agent).
In cases of cholangitis, sectorial transient hepatic intensity differences
(Fig. 4) may be caused by
peribiliary plexus impairment that leads to a decrease in portal blood flow to
the sinusoids and arterial compensation. Moreover, arterializations caused by
cholangitis may also assume other patterns (nodular, lobar, or diffuse) as a
result of the wide range of presentation and extension of cholangitis
[7] (Figs.
5A,
5B, and
5C).
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Fig. 4 —61-year-old man with postbiopsy focal cholangitis and
sectorial transient hepatic intensity differences. Axial gradient-echo
T1-weighted gadolinium-enhanced arterial phase MR image (TR/TE, 146/2) shows
wedge-shaped arterial phenomenon (arrowhead) caused by peribiliary
plexus impairment secondary to dilation of inflamed subsegmental biliary
vessels (arrow).
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Fig. 5A —57-year-old woman with cholangitis and nonsectorial transient
hepatic intensity differences in hepatic dome. Axial T2-weighted MR image
(TR/TE, 12,000/82) shows localized dilation of bile ducts (arrow).
Note small perihepatic effusion.
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Fig. 5B —57-year-old woman with cholangitis and nonsectorial transient
hepatic intensity differences in hepatic dome. Axial gradient-echo T1-weighted
gadolinium-enhanced arterial phase MR images (146/2) show further appearance
of arterializations with biliary vessel disease: peribiliary (arrows,
B), distributed along dilated biliary vessels, and pseudoglobular,
mimicking a focal lesion (arrowhead, C).
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Fig. 5C —57-year-old woman with cholangitis and nonsectorial transient
hepatic intensity differences in hepatic dome. Axial gradient-echo T1-weighted
gadolinium-enhanced arterial phase MR images (146/2) show further appearance
of arterializations with biliary vessel disease: peribiliary (arrows,
B), distributed along dilated biliary vessels, and pseudoglobular,
mimicking a focal lesion (arrowhead, C).
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Polymorphous Differences
Polymorphous arterial phenomena have four main causes.
The first cause is extrinsic compression of the liver surface exerted by
ribs or stretched diaphragmatic pillars during deep inspiration or by
subcapsular collections (Figs.
6A and
6B). Such compression causes
an increase of tissue pressure in the subcapsular region, which results in
decreased portal perfusion and then in a usually slight arterial reaction
[8].
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Fig. 6A —69-year-old man with postsurgical subcapsular collection and
polymorphous transient hepatic intensity differences. Axial T2-weighted MR
image (TR/TE, 12,000/84) reveals hyperintense collection (arrow)
beneath Glisson's capsule, causing compression on adjacent marginal liver
parenchyma.
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Fig. 6B —69-year-old man with postsurgical subcapsular collection and
polymorphous transient hepatic intensity differences. Axial gradient-echo
T1-weighted gadolinium-enhanced arterial phase MR image (146/2) shows
polymorphous arterial phenomenon (arrowheads) laterally positioned to
hypointense collection and caused by extrinsic compression of liver
surface.
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Second, an anomalous blood supply may result from atypical arteries
[9], collateral venous vessels,
or accessory veins [8] (Figs.
7A and
7B). The latter may act,
accordingly to the pressure gradient, as anomalous supply or drainage vessels
and are known as the "third hepatic inflow," which supplies small
areas of the liver parenchyma, especially segment IV. These anomalous
accessory veins enter the liver separately from the portal venous system.
Nevertheless, they communicate with the intrahepatic portal branches to
various extents, causing localized portal hypoperfusion and hepatic arterial
perfusion reaction. These hemodynamic changes, if persistent, can also
determine focal metabolic alterations that result in focal sparing in fatty
liver or nodular fat accumulation in the normal liver
[2,
8] (Figs.
8A,
8B, and
8C).
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Fig. 7A —40-year-old man with polymorphous transient hepatic intensity
differences due to anomalous venous supply and drainage by right gastric vein.
Axial gradient-echo T1-weighted gadolinium-enhanced arterial phase MR images
(TR/TE, 146/2) show polygonal arterial phenomenon in segment IV
(arrowheads).
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Fig. 7B —40-year-old man with polymorphous transient hepatic intensity
differences due to anomalous venous supply and drainage by right gastric vein.
Axial gradient-echo T1-weighted gadolinium-enhanced arterial phase MR images
(TR/TE, 146/2) show polygonal arterial phenomenon in segment IV
(arrowheads).
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Fig. 8A —56-year-old woman with segmental localized steatosis in liver
segment IV due to persistent polymorphous perfusion alterations. Axial
gradient-echo T1-weighted (TR/TE, 216/1.5) (A) and axial T2-weighted
(872/210) (B) MR images show signal intensity variation of segment IV
(arrows) with respect to surrounding liver parenchyma.
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Fig. 8B —56-year-old woman with segmental localized steatosis in liver
segment IV due to persistent polymorphous perfusion alterations. Axial
gradient-echo T1-weighted (TR/TE, 216/1.5) (A) and axial T2-weighted
(872/210) (B) MR images show signal intensity variation of segment IV
(arrows) with respect to surrounding liver parenchyma.
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Fig. 8C —56-year-old woman with segmental localized steatosis in liver
segment IV due to persistent polymorphous perfusion alterations. Axial
iodinated contrast-enhanced arterial phase helical CT image better shows
relative hypodensity in segment IV (arrow) caused by segmental fat
accumulation secondary to persistent hemodynamic changes.
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Third, in cases of inflammation of adjacent organs (cholecystitis,
pancreatic abscesses) (Figs.
9A and
9B), the morphogenesis of
transient hepatic intensity differences is related to the spread of
inflammatory mediators by contiguity. Increased arterial flow can also be
secondary to portal inflow reduction due to interstitial edema
[9].
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Fig. 9A —63-year-old woman with gallstone causing inflammatory
changes, main biliary duct compression (Mirizzi syndrome), and related
polymorphous transient hepatic intensity differences. Axial T2-weighted MR
image (TR/TE, 12,000/84) reveals large calculus lodged in gallbladder
(arrow), wall thickening, and slight parenchymal hyperintensity due
to inflammation.
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Fig. 9B —63-year-old woman with gallstone causing inflammatory
changes, main biliary duct compression (Mirizzi syndrome), and related
polymorphous transient hepatic intensity differences. Axial gradient-echo
T1-weighted gadolinium-enhanced arterial phase MR image (146/2) shows wide
arterial phenomenon caused by spread of inflammatory mediators
(arrowheads).
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Percutaneous hepatic biopsy and the outcome of interventional treatment of
liver neoplasms, by physical or chemical agents, are the fourth cause of
polymorphous transient hepatic intensity differences, whose peculiarity is
their variety: direct trauma, induced inflammation, thrombosis, or
arterioportal shunt. These transient hepatic intensity differences may appear
either irregular, positioned around or lateral to injury (Figs.
10A and
10B), or regular and sectorial
with regard to the characteristics of portal vessel damage or injury, as in
case of a postbiopsy arterioportal shunt
(Fig. 3) or portal thrombosis
after radiofrequency ablation (Fig.
1). Hemodynamic changes occurring after interventional procedures
are often stable, so that a biopsy outcome may be identified as a sectorial
area, fatty in normal liver or spare in fatty liver
[2,
8] (Figs.
11A,
11B,
11C, and
11D).
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Fig. 10A —60-year-old woman with previous hepatocellular carcinoma
treated with radiofrequency ablation and polymorphous transient intensity
difference in right hepatic lobe. Axial gradient-echo T1-weighted
gadolinium-enhanced arterial phase MR images (TR/TE, 146/2) show irregularly
shaped arterial phenomenon (arrowhead, B) positioned laterally
to large hypointense lesion that is outcome of radiofrequency ablation
(arrow).
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Fig. 10B —60-year-old woman with previous hepatocellular carcinoma
treated with radiofrequency ablation and polymorphous transient intensity
difference in right hepatic lobe. Axial gradient-echo T1-weighted
gadolinium-enhanced arterial phase MR images (TR/TE, 146/2) show irregularly
shaped arterial phenomenon (arrowhead, B) positioned laterally
to large hypointense lesion that is outcome of radiofrequency ablation
(arrow).
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Fig. 11A —65-year-old woman with focal triangular steatosis in liver
segment VIII that represents end stage of previous persistent sectorial
perfusion alterations caused by hepatic biopsy. Steatosis represents the final
outcome of a persistent arterial phenomenon: It may appear to be either
irregular (Figs. 10A and
10B) or regular and sectorial,
depending on characteristics of portal vessel damage or injury. Axial
gradient-echo T1-weighted (TR/TE, 216/1.5) unenhanced (A) and axial
T1-weighted (216/1.5) gadolinium-enhanced (B) arterial phase MR images
show slightly wedge-shaped hyperintensity compared with surrounding parenchyma
and relatively wedge-shaped hypoenhancing area, respectively
(arrows).
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Fig. 11B —65-year-old woman with focal triangular steatosis in liver
segment VIII that represents end stage of previous persistent sectorial
perfusion alterations caused by hepatic biopsy. Steatosis represents the final
outcome of a persistent arterial phenomenon: It may appear to be either
irregular (Figs. 10A and
10B) or regular and sectorial,
depending on characteristics of portal vessel damage or injury. Axial
gradient-echo T1-weighted (TR/TE, 216/1.5) unenhanced (A) and axial
T1-weighted (216/1.5) gadolinium-enhanced (B) arterial phase MR images
show slightly wedge-shaped hyperintensity compared with surrounding parenchyma
and relatively wedge-shaped hypoenhancing area, respectively
(arrows).
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Fig. 11C —65-year-old woman with focal triangular steatosis in liver
segment VIII that represents end stage of previous persistent sectorial
perfusion alterations caused by hepatic biopsy. Steatosis represents the final
outcome of a persistent arterial phenomenon: It may appear to be either
irregular (Figs. 10A and
10B) or regular and sectorial,
depending on characteristics of portal vessel damage or injury. Axial helical
CT image confirms triangular hypodense area (arrow) in segment
VIII.
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Fig. 11D —65-year-old woman with focal triangular steatosis in liver
segment VIII that represents end stage of previous persistent sectorial
perfusion alterations caused by hepatic biopsy. Steatosis represents the final
outcome of a persistent arterial phenomenon: It may appear to be either
irregular (Figs. 10A and
10B) or regular and sectorial,
depending on characteristics of portal vessel damage or injury. Axial sonogram
(convex, obtained with 3.5-MHz probe) shows sectorial triangular area that is
hyperechoic with respect to surrounding liver parenchyma (arrow).
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Fig. 12 —23-year-old man with hepatic vein obstruction (Budd-Chiari
syndrome) associated with a diffuse patchy pattern of transient hepatic
intensity differences. Axial gradient-echo T1-weighted gadolinium-enhanced
arterial phase MR image (TR/TE, 216/1.5) reveals diffuse marble aspect of
liver parenchyma caused by sinusoidal obstruction and consequent
transsinusoidal plexus activation. Hypointense oval structure in caudate lobe
is due to obstructed transjugular intrahepatic portosystemic stent-shunt.
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Diffuse Differences
Transient hepatic signal intensity differences that are diffuse have
various patterns depending on the obstacle location and on related
compensatory shunts [2,
3]. These intensity differences
are secondary to portal hypoperfusion due to blood flow obstruction before,
after, or at the level of the sinusoids.
In postsinusoidal obstruction (Budd-Chiari syndrome, right heart failure,
and venous occlusive disease), hepatic parenchyma may assume a marbled aspect,
defined as a "patchy" pattern
(Fig. 12), due to increased IV
pressure, consequent transsinusoidal plexus activation, arterial compensation,
and general centrolobular enhancement during the arterial phase. In this case,
the portal system becomes the only means of drainage for the liver.
When blockade occurs at the level of the portal trunk (before the
sinusoids), as in thrombosis, or before the centrolobular vein (into
sinusoids), as in cirrhosis, portal flow is adequate for central parenchymal
areas but not for the peripheral zones. The arterial response produces
enhancement of subcapsular liver regions with relative hypodensity in the
central and perihilar areas. This pattern of enhancement, based on peribiliary
plexus activation, is called "central-peripheral"
[2,
3] (Figs.
13A,
13B, and
13C).
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Fig. 13A —44-year-old woman with portal trunk and right portal branch
obstruction due to central cholangiocellular carcinoma and related diffuse
central-peripheral pattern of transient hepatic intensity difference. Axial
T2-weighted MR image (TR/TE, 12,000/84) reveals hyperintense mass
(arrow) causing portal blood flow obstruction before sinusoids.
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Fig. 13B —44-year-old woman with portal trunk and right portal branch
obstruction due to central cholangiocellular carcinoma and related diffuse
central-peripheral pattern of transient hepatic intensity difference. Axial
gradient-echo T1-weighted gadolinium-enhanced arterial phase MR image (146/2)
shows diffuse peripheral enhancement of liver parenchyma (arrowheads)
and relative hypoperfusion of central areas (arrows).
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Fig. 13C —44-year-old woman with portal trunk and right portal branch
obstruction due to central cholangiocellular carcinoma and related diffuse
central-peripheral pattern of transient hepatic intensity difference. Axial
gradient-echo T1-weighted gadolinium-enhanced portal venous phase MR image
(146/2) confirms enhanced mass (arrow) and shows central-peripheral
pattern is visible but fading (not so evident as on arterial phase image).
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Fig. 14A —51-year-old man with obstruction of main bile duct due to
pancreatic head carcinoma (not shown), dilation of entire biliary tree, and
diffuse peribiliary pattern of transient hepatic intensity difference. Axial
T2-weighted MR image (TR/TE, 12,000/84) shows hyperintense dilated biliary
vessels (long-standing biliary obstruction) (arrow) determining
impairment of peribiliary plexus.
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Fig. 14B —51-year-old man with obstruction of main bile duct due to
pancreatic head carcinoma (not shown), dilation of entire biliary tree, and
diffuse peribiliary pattern of transient hepatic intensity difference. Axial
gradient-echo T1-weighted gadolinium-enhanced arterial phase MR images (146/2)
reveal diffuse cylindric enhancement of liver parenchyma spread along dilated
bile ducts (arrowheads).
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Fig. 14C —51-year-old man with obstruction of main bile duct due to
pancreatic head carcinoma (not shown), dilation of entire biliary tree, and
diffuse peribiliary pattern of transient hepatic intensity difference. Axial
gradient-echo T1-weighted gadolinium-enhanced arterial phase MR images (146/2)
reveal diffuse cylindric enhancement of liver parenchyma spread along dilated
bile ducts (arrowheads).
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Finally, in biliary tree dilation (choledocholithiasis, cholangiocellular
carcinoma, pancreas head carcinoma), the peribiliary plexus may become
obstructed, with a consequent decrease in portal blood flow to the sinusoids
and arterial compensation. Such long-standing biliary obstruction
[2,
3] determines a cylindric
arterialization along the dilated biliary vessels, called a
"peribiliary" pattern
[3] (Figs.
14A,
14B, and
14C). Transient hepatic
intensity differences associated with biliary disease may have two other
appearances: sectorial high intensity, caused by malignant involvement of the
portal branches and peribiliary sites, even without any biliary vessel
dilation (see Figs. 9A and
9B in part 1
[1]); and polymorphous
variable-intensity (Figs. 4,
5A,
5B, and
5C) localized arterial
phenomena proximal to the inflammation site and attributable to edema
involving the peribiliary plexus
[7].
Conclusion
Transient hepatic intensity differences are the exact MRI equivalent of
transient hepatic attenuation differences on helical CT, so that even on MRI
they must be considered important signs of underlying liver disorders, which
they help to assess. As a consequence, the hepatic arterial phase must always
be performed on MRI as well as on CT, even if no focal lesion is expected to
be found.
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Top
Abstract
Introduction
