AJR 2004; 183:459-464
© American Roentgen Ray Society
Transient Hepatic Attenuation Differences
Stefano Colagrande1,
Nicoletta Centi1,
Giorgio La Villa2 and
Natale Villari1
1 Dipartimento di Fisiopatologia Clinica, Sezione di Radiodiagnostica,
Università degli Studi di Firenze, Policlinico di Careggi, Viale
Morgagni 85, Florence I-50134, Italy.
2 Dipartimento di Medicina Interna, Sezione di Epatologia, Università
degli Studi di Firenze, Florence I-50134, Italy.
Received September 26, 2003;
accepted after revision November 20, 2003.
Address correspondence to S. Colagrande
(s.colagrande{at}dfc.unifi.it).
Introduction
The liver has a dual blood supply (70% portal vein, 30% hepatic artery)
with compensatory relationships between the two inflows: arterial flow
increases when portal flow decreases. This flow occurs as a result of
communications among main vessels, sinusoids, and peribiliary venules that
open in response to nervous and humoral factors. Transient hepatic attenuation
differences are areas of parenchymal enhancement visible during the hepatic
arterial phase on helical CT
[1,
2]. Because of the wide
diffusion of hepatic arterial phase evaluation, transient hepatic attenuation
differences are now rather frequent. In a previous study from our group, the
differences were identified on 130 (13%) of 988 helical CT scans of the liver
[3]. Transient hepatic
attenuation differences have been associated with a large variety of liver
disorders
[1-3].
Our article aims to show the range of these arterial phenomena in a
comprehensive diagnostic organization correlating morphology with etiology and
pathogenesis.
Transient hepatic attenuation differences can be classified according to
morphology, etiology, pathogenesis, and association with focal lesions
[3]. According to morphology,
they can be organized into four groups: lobar multisegmental, sectorial,
polymorphous, and diffuse.
Lobar multisegmental differences involve all or almost all segments of one
hepatic lobe and are usually caused by a primary increase in arterial inflow
and therefore follow arterial distribution.
Sectorial differences follow the portal dichotomy, appearing as triangular
wedge- or fan-shaped areas with at least one "straight border"
sign (a clear separation line from the normally attenuating parenchyma) that
occurs because of the strict connection between the territory downstream
portal obstruction and the arterial reaction.
Polymorphous differences usually do not follow the portal dichotomy and
show various shapes and sizes without a straight border sign.
Diffuse differences involve the entire hepatic parenchyma and may assume a
patchy, central peripheral, or peribiliary pattern on the basis of the
location of the portal blockade.
According to etiopathogenesis, arterialization can be secondary or primary.
Secondary increases in arterial inflow may be caused by a decrease in the
portal flow—which is caused by portal or hepatic vein thrombosis,
compression by focal lesions, abscesses, long-standing biliary obstruction, or
parenchymal trauma—or by mixing of venous and arterial blood by an
arterioportal shunt, leading to a diversion of portal flow with relative
hypoperfusion of the contiguous parenchyma and arterial reaction. A similar
mechanism explains transient hepatic attenuation differences that develop in
cases of aberrant venous supply and drainage or shunts produced by
hepatocellular carcinoma or peripheral hemangioma.
Primary increases in arterial inflow are caused by focal hypervascular
lesions that lead to increased arterial supply (the so-called sump effect),
inflammation of adjacent organs (gallbladder, pancreas), or an aberrant
hepatic arterial supply.
Ideally, transient hepatic attenuation differences should be classified
according to their etiopathogenesis. However, this approach is impractical
because the most appreciable characteristics of these arterial phenomena are
morphology and association with focal lesions. We have organized our article
accordingly.
Lobar Multisegmental, with a Hypervascular Focal Lesion
Lobar multisegmental transient hepatic attenuation differences usually
occur when a hypervascular focal lesion leads to primary arterial inflow with
hyperperfusion of the surrounding parenchyma ("siphoning effect")
in the absence of portal hypoperfusion. They do not show a triangular shape or
a straight border sign. In this case, mediators most likely work on the right
or left hepatic artery, producing enhancement of the hepatic lobe containing
the lesion [1,
2] (Fig.
1A,
1B). Less frequently, the tumor
acts on the primary branch of the right or left hepatic artery and
"steals" blood flow from the ipsilobar contralateral segment,
which appears hypoattenuating with respect to the segment containing the tumor
[1].
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Fig. 1A. —61-year-old man with focal lesions (hemangiomas) causing homolateral
lobar transient hepatic attenuation difference ("siphoning
effect"). Arterial phase helical CT scan reveals transient hepatic
attenuation difference in left lobe (segments II, III, IV) (arrows)
surrounding two hemangiomas that are not yet enhanced. Relative hypertrophy of
left hepatic artery (arrowhead) is also present.
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Fig. 1B. —61-year-old man with focal lesions (hemangiomas) causing homolateral
lobar transient hepatic attenuation difference ("siphoning
effect"). T2-weighted image shows two hemangiomas (arrows) in
left liver lobe and cyst (arrowhead) in upper pole of right
kidney.
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Sectorial, With or Without a Focal Lesion
When a sectorial transient hepatic attenuation difference is associated
with a focal lesion, it could be malignant and induce portal hypoperfusion by
compression or infiltration of a portal branch. This type of arterialization
may be also seen in the case of liver abscesses caused by portal hypoperfusion
and probably by the spread of inflammatory mediators
[4]. When the focal lesion is
benign, it is usually small and located near the hepatic capsule. Sectorial
transient hepatic attenuation differences can be either wedge- or fan-shaped
[1,
5], depending on whether the
associated focal lesion is centrally or laterally positioned and inducing
arterioportal shunt (Fig. 2A,
2B,
2C,
2D) or portal thrombosis (Fig.
3A,
3B), or at its apex and causing
portal compression (Fig. 4).
When not associated with focal lesions, sectorial transient hepatic
attenuation differences can be caused by portal (Fig.
5A,
5B) or hepatic vein
thrombosis, long-standing biliary obstruction, or an arterioportal shunt. In
turn, an arterioportal shunt may be congenital or, more often, caused by liver
cirrhosis (Fig. 6A,
6B) or trauma
[6]. In such cases, transient
hepatic attenuation differences are always wedge-shaped, with the straight
border sign. Arterialization caused by cholangitis can be sectorial, but it
may also assume other patterns (nodular, lobar, or diffuse) because of its
wide range of presentation [7].
Finally, a sectorial transient hepatic attenuation difference may sometimes be
the only warning sign of a hidden nodular lesion (e.g., a nodule not
detectable for dimensional or contrast reasons) but determining portal
compression. The subsequent arterialization may herald abnormality, preceding
its clear CT detection as a nodular lesion. The latter possibility must be
considered whenever a sectorial transient hepatic attenuation difference has
no other explanation [8].
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Fig. 2A. —50-year-old man with sectorial wedge-shaped transient hepatic
attenuation difference caused by arterioportal shunt and associated with focal
lesion (hemangioma). Arterial phase helical CT scan reveals triangular
transient hepatic attenuation difference (arrows) in right lobe.
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Fig. 2B. —50-year-old man with sectorial wedge-shaped transient hepatic
attenuation difference caused by arterioportal shunt and associated with focal
lesion (hemangioma). Caudal CT scan shows small hemangioma
(arrowhead) located in lateral side of transient hepatic attenuation
difference (arrow).
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Fig. 2C. —50-year-old man with sectorial wedge-shaped transient hepatic
attenuation difference caused by arterioportal shunt and associated with focal
lesion (hemangioma). Color Doppler axial sonogram shows arterioportal shunt
(arrow) in hemangioma.
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Fig. 2D. —50-year-old man with sectorial wedge-shaped transient hepatic
attenuation difference caused by arterioportal shunt and associated with focal
lesion (hemangioma). Pulsed-wave Doppler sonogram confirms arteriovenous
flow.
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Fig. 3A. —52-year-old man with sectorial wedge transient hepatic attenuation
difference caused by portal thrombosis and associated with focal lesion
(hepatocellular carcinoma). Arterial phase helical CT scan shows triangular
transient hepatic attenuation difference (arrow) in right lobe and
large hepatocellular carcinoma (arrowhead) located at its side.
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Fig. 3B. —52-year-old man with sectorial wedge transient hepatic attenuation
difference caused by portal thrombosis and associated with focal lesion
(hepatocellular carcinoma). Portal phase cranial helical CT scan shows
thrombus (arrowhead) in portal branch of segments V and VI.
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Fig. 4. —Arterial phase helical CT scan in 68-year-old man shows sectorial
fan-shaped transient hepatic attenuation difference (arrow) caused by
portal compression by focal lesion (metastatic colon cancer)
(arrowhead) at its medial apex.
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Fig. 5A. —62-year-old man with sectorial wedge-shaped transient hepatic
attenuation difference caused by portal thrombosis without focal lesion in
cirrhotic liver. Arterial phase helical CT scan shows triangular transient
hepatic attenuation difference (arrow) in right lobe.
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Fig. 5B. —62-year-old man with sectorial wedge-shaped transient hepatic
attenuation difference caused by portal thrombosis without focal lesion in
cirrhotic liver. Portal phase caudal helical CT scan shows thrombotic
occlusion of major portal branch (arrowhead).
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Fig. 6A. —59-year-old woman with sectorial wedge-shaped transient hepatic
attenuation difference caused by arterioportal shunt without focal lesion in
cirrhotic liver. Arterial phase helical CT scan shows triangular transient
hepatic attenuation difference with straight border sign (arrow) in
right lobe and early opacification of portal vessel (arrowhead)
caused by arterioportal shunt.
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Fig. 6B. —59-year-old woman with sectorial wedge-shaped transient hepatic
attenuation difference caused by arterioportal shunt without focal lesion in
cirrhotic liver. Portal phase helical CT scan obtained at same level as
A confirms that early opacified vessel (arrowhead) is portal
branch.
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Polymorphous, Without a Focal Lesion
Polymorphous transient hepatic attenuation differences may be caused by an
aberrant blood supply; inflammation or parenchymal injuries from physical or
chemical agents, including contusion (Fig.
7A,
7B), extrinsic compression by
ribs, or stretched diaphragmatic pillars
(Fig. 8); percutaneous biopsy
(Fig. 9); or treatment of a
liver neoplasm (ethanol injection, radiofrequency ablation)
(Fig. 10). Polymorphous
transient hepatic attenuation differences usually appear as areas of irregular
enhancement around (Fig. 11) or lateral to (Fig. 10) an
injury; however, they have many different forms, sometimes even regular or
sectorial, according to the characteristics of portal vessel damage, as in the
case of an arterioportal shunt after biopsy
(Fig. 9).
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Fig. 7A. —62-year-old man with polymorphous transient hepatic attenuation
difference caused by liver contusion from accidental fall. Arterial phase
helical CT scan shows transient hepatic attenuation difference with irregular
margin (arrows) in right lobe. Parenchymal edema causes portal vessel
compression with consequent arterial reaction.
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Fig. 7B. —62-year-old man with polymorphous transient hepatic attenuation
difference caused by liver contusion from accidental fall. Arterial phase
helical CT scan obtained 1 month later shows arterial phenomenon has changed
into low-attenuation area (arrow) representing healing of injury and
renewal of portal flow.
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Fig. 8. —Arterial phase helical CT scan in 86-year-old woman with
polymorphous transient hepatic attenuation difference caused by liver
compression due to stretched diaphragmatic pillar shows irregular enhancement
(arrow) in subglissonian area.
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Fig. 9. —Arterial phase helical CT scan in 32-year-old man shows polymorphous
transient hepatic attenuation difference (arrow) in right lobe caused
by percutaneous liver biopsy. Biopsy-induced arterial phenomena may have wide
range of appearance. In this patient, regular (triangular) shape is probably
caused by occurrence of arterioportal shunt. Note hypertrophic artery branch
(arrowhead).
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Fig. 10. —Arterial phase helical CT scan in 74-year-old woman with
polymorphous transient hepatic attenuation difference caused by radiofrequency
ablation of hepatocellular carcinoma shows area of irregular enhancement
(arrow) in segment IV distal to injured parenchyma
(arrowhead). In this patient, arterialization was caused by
hypoperfusion resulting from portal vessel disruption.
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Fig. 11. —Arterial phase helical CT scan in 67-year-old man with polymorphous
transient hepatic attenuation difference caused by posttraumatic biloma shows
area of irregular enhancement (arrow) around large bile collection
(arrowhead). In this patient, arterialization is caused by
hypoperfusion resulting from portal vessel compression.
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An aberrant blood supply may result from anomalous arteries
[5]
(Fig. 12); collateral venous
vessels, as in superior vena cava obstruction; or accessory veins (capsular,
paraumbilical veins of Sappey, or an accessory cystic vein)
[1,
5] that may act, according to
the pressure gradient, as an anomalous supply or as drainage vessels. In
inflammation of adjacent organs (cholecystitis, pancreatic abscesses) (Fig.
13A,
13B), morphogenesis is related
to inflammatory mediators spreading by contiguity.
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Fig. 12. —Arterial phase helical CT scan in 62-year-old man shows polymorphous
transient hepatic attenuation difference (arrow) involving left lobe
and caused by aberrant blood supply. No other abnormalities were detected on
images obtained during either arterial or portal phase. In this patient,
enhancement is probably caused by aberrant left hepatic arterial branch
(arrowhead) originating from left gastric artery.
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Fig. 13A. —59-year-old woman with polymorphous transient hepatic attenuation
difference caused by acute calculus cholecystitis. Arterial phase helical CT
scan shows area of irregular enhancement (arrows) involving right
lobe (segment V). This transient hepatic attenuation difference was caused by
primary increase in arterial flow due to spreading of inflammatory mediators.
In general, increased arterial flow could also be caused by reduction of
portal inflow because of interstitial edema. Biliary tree (arrowhead)
is slightly dilated.
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Fig. 13B. —59-year-old woman with polymorphous transient hepatic attenuation
difference caused by acute calculus cholecystitis. Portal phase caudal helical
CT scan shows enlarged gallbladder with endoluminal stone
(arrowhead), wall thickening, and slight pericholecystic collection
(arrow).
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Diffuse, Various Patterns
Diffuse transient hepatic attenuation differences are associated with
diseases causing blood flow obstruction before, after, or at the level of
sinusoids, with resultant portal hypoperfusion. The arterial response shows
different patterns according to the location of the obstacle and the related
compensatory shunt [3]. These
types of arterialization are the generalized equivalent of the previously
mentioned sectorial transient hepatic attenuation differences not associated
with focal lesions. In fact, arterial phenomena triggered by portal or hepatic
vein obstruction or compression may range from small and marginal to large and
sectorial (Fig. 5A,
5B) to diffuse, depending on
the position of the venous branch in the portal or hepatic venous tree.
In obstruction after the sinusoid (Budd Chiari syndrome, right heart
failure), the increased venous pressure determines arterial compensation by
activation of the transsinusoidal plexus, and the portal system may be the
only drainage system of the liver. This arrangement results in a generalized
central lobular enhancement during the arterial phase of helical CT. The
hepatic parenchyma assumes a marbled aspect called a "patchy"
pattern (Fig. 14).
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Fig. 14. —Arterial phase helical CT scan in 17-year-old girl with diffuse
patchy transient hepatic attenuation difference caused by Budd-Chiari syndrome
shows marbled aspect of liver parenchyma (arrows) caused by opening
of transsinusoidal plexus.
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When blockade takes place at the level of the portal trunk (before the
sinusoids), as in portal vein thrombosis, or before the central lobular vein
(into sinusoids), as in cirrhosis, portal flow remains adequate for the
central zones of the liver, but not for the peripheral ones. The arterial
response, based on the activation of the peribiliary plexus, produces
enhancement of the peripheral subcapsular hepatic parenchyma with relative
hypodensity of the central perihilar area. The consequent CT pattern is called
a "central-peripheral" phenomenon (Fig.
15A,
15B).
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Fig. 15A. —45-year-old woman with diffuse central-peripheral transient hepatic
attenuation difference caused by complete thrombosis of portal trunk. Arterial
phase helical CT scan shows enhancement of peripheral hepatic parenchyma
(thin arrows) with relative hypodensity of central area
(arrowhead) and portal thrombosis (thick arrow).
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Fig. 15B. —45-year-old woman with diffuse central-peripheral transient hepatic
attenuation difference caused by complete thrombosis of portal trunk. Cranial
scan better defines central-peripheral pattern caused by opening of
peribiliary plexus.
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Finally, in dilatation of the biliary tree, as in choledocholithiasis or
pancreatic cancer, the peribiliary plexus may become obstructed, with a
consequent decrease in portal blood flow to the sinusoids and arterial
compensation. The effect of such long-standing biliary obstruction is a
peribiliary transient hepatic attenuation difference
(Fig. 16) characterized by a
cylindric ramified pathway along the dilated biliary tree.
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Fig. 16. —Arterial phase helical CT scan in 89-year-old woman with diffuse
peribiliary transient hepatic attenuation difference caused by long-standing
biliary obstruction (pancreatic cancer) shows enhancing areas (arrow)
adjacent to dilated biliary tree (arrowhead). Dilatation of bile
ducts results in compression of peribiliary plexus with decreased portal flow
and consequent arterialization.
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In conclusion, transient hepatic attenuation differences must be considered
neither pitfalls nor nodular lesions. Instead, they are important signs of an
underlying liver disorder and for this reason they are useful to detect and
characterize a large variety of liver diseases. Therefore, the hepatic
arterial phase must always be performed, even if no focal lesion is
expected.
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Introduction
Lobar Multisegmental, with a...
