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Pictorial Essay
Transient Hepatic Attenuation Differences
Stefano Colagrande1, Nicoletta Centi1, Giorgio La Villa2, Natale Villari1

T
he liver has a dual blood supply usually caused by a primary increase in arterial in- Polymorphous differences usually do not
(70% portal vein, 30% hepatic ar- flow and therefore follow arterial distribution. follow the portal dichotomy and show various
tery) with compensatory relation- Sectorial differences follow the portal dichot- shapes and sizes without a straight border sign.
ships between the two inflows: arterial flow omy, appearing as triangular wedge- or fan- Diffuse differences involve the entire he-
increases when portal flow decreases. This shaped areas with at least one “straight border” patic parenchyma and may assume a patchy,
flow occurs as a result of communications sign (a clear separation line from the normally at- central peripheral, or peribiliary pattern on the
among main vessels, sinusoids, and peribiliary tenuating parenchyma) that occurs because of the basis of the location of the portal blockade.
venules that open in response to nervous and strict connection between the territory down- According to etiopathogenesis, arterializa-
humoral factors. Transient hepatic attenuation stream portal obstruction and the arterial reaction. tion can be secondary or primary. Secondary
differences are areas of parenchymal enhance-
ment visible during the hepatic arterial phase
on helical CT [1, 2]. Because of the wide diffu-
sion of hepatic arterial phase evaluation, tran-
sient 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 compre-
hensive diagnostic organization correlating
morphology with etiology and pathogenesis.
Transient hepatic attenuation differences
can be classified according to morphology, eti-
A B
ology, pathogenesis, and association with focal
lesions [3]. According to morphology, they can Fig. 1.—61-year-old man with focal lesions (hemangiomas) causing homolateral lobar transient hepatic attenu-
be organized into four groups: lobar multiseg- ation difference (“siphoning effect”).
mental, sectorial, polymorphous, and diffuse. A, 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
Lobar multisegmental differences involve all (arrowhead) is also present.
or almost all segments of one hepatic lobe and are B, T2-weighted image shows two hemangiomas (arrows) in left liver lobe and cyst (arrowhead) in upper pole of right kidney.

Received September 26, 2003; accepted after revision November 20, 2003.
1
Dipartimento di Fisiopatologia Clinica, Sezione di Radiodiagnostica, Università degli Studi di Firenze, Policlinico di Careggi, Viale Morgagni 85, Florence I-50134, Italy. Address
correspondence to S. Colagrande (s.colagrande@dfc.unifi.it).
2
Dipartimento di Medicina Interna, Sezione di Epatologia, Università degli Studi di Firenze, Florence I-50134, Italy.
AJR 2004;183:459–464 0361–803X/04/1832–459 © American Roentgen Ray Society

AJR:183, August 2004 459

 Colagrande et al.
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A B C

Fig. 2.—50-year-old man with sectorial wedge-shaped transient hepatic attenuation difference caused by arte-
rioportal shunt and associated with focal lesion (hemangioma).
A, Arterial phase helical CT scan reveals triangular transient hepatic attenuation difference (arrows) in right lobe.
B, Caudal CT scan shows small hemangioma (arrowhead) located in lateral side of transient hepatic attenuation
difference (arrow).
C, Color Doppler axial sonogram shows arterioportal shunt (arrow) in hemangioma.
D, Pulsed-wave Doppler sonogram confirms arteriovenous flow.

A B
Fig. 3.—52-year-old man with sectorial wedge transient hepatic attenuation difference caused by portal throm- Fig. 4.—Arterial phase helical CT scan in 68-year-old
bosis and associated with focal lesion (hepatocellular carcinoma). man shows sectorial fan-shaped transient hepatic at-
A, Arterial phase helical CT scan shows triangular transient hepatic attenuation difference (arrow) in right lobe tenuation difference (arrow) caused by portal com-
and large hepatocellular carcinoma (arrowhead) located at its side. pression by focal lesion (metastatic colon cancer)
B, Portal phase cranial helical CT scan shows thrombus (arrowhead) in portal branch of segments V and VI. (arrowhead) at its medial apex.

460 AJR:183, August 2004

 Hepatic Attenuation Differences

Fig. 5.—62-year-old man with sectorial wedge-

shaped transient hepatic attenuation difference
caused by portal thrombosis without focal lesion in
cirrhotic liver.
A, Arterial phase helical CT scan shows triangular
transient hepatic attenuation difference (arrow) in
right lobe.
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B, Portal phase caudal helical CT scan shows throm-

botic occlusion of major portal branch (arrowhead).

A B

Fig. 6.—59-year-old woman with sectorial wedge-

shaped transient hepatic attenuation difference
caused by arterioportal shunt without focal lesion in
cirrhotic liver.
A, Arterial phase helical CT scan shows triangular tran-
sient hepatic attenuation difference with straight border
sign (arrow) in right lobe and early opacification of portal
vessel (arrowhead) caused by arterioportal shunt.
B, Portal phase helical CT scan obtained at same level
as A confirms that early opacified vessel (arrowhead)
is portal branch.

A B

A B

Fig. 7.—62-year-old man with polymorphous transient hepatic attenuation difference caused by liver contusion from accidental fall.
A, 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.
B, 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.

AJR:183, August 2004 461


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Fig. 8.—Arterial phase helical CT scan in 86-year-old
woman with polymorphous transient hepatic attenua-
tion difference caused by liver compression due to
stretched diaphragmatic pillar shows irregular en-
hancement (arrow) in subglissonian area.
increases in arterial inflow may be caused by a
decrease in the portal flow—which is caused
by portal or hepatic vein thrombosis, compres-
sion 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 he-
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, arterializa-
tion is caused by hypoperfusion resulting from portal
vessel compression.
462
Colagrande et al.
Fig. 9.—Arterial phase helical CT scan in 32-year-old man
shows polymorphous transient hepatic attenuation differ-
ence (arrow) in right lobe caused by percutaneous liver bi-
opsy. 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).
patic attenuation differences that develop in
cases of aberrant venous supply and drainage
or shunts produced by hepatocellular carci-
noma 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 or-
gans (gallbladder, pancreas), or an aberrant
hepatic arterial supply.
Fig. 12.—Arterial phase helical CT scan in 62-year-old
man shows polymorphous transient hepatic attenua-
tion difference (arrow) involving left lobe and caused by
aberrant blood supply. No other abnormalities were de-
tected on images obtained during either arterial or por-
tal phase. In this patient, enhancement is probably
caused by aberrant left hepatic arterial branch (arrow-
head) originating from left gastric artery.
Fig. 10.—Arterial phase helical CT scan in 74-year-old
woman with polymorphous transient hepatic attenuation
difference caused by radiofrequency ablation of hepato-
cellular carcinoma shows area of irregular enhancement
(arrow) in segment IV distal to injured parenchyma (ar-
rowhead). In this patient, arterialization was caused by
hypoperfusion resulting from portal vessel disruption.
Ideally, transient hepatic attenuation differ-
ences should be classified according to their
etiopathogenesis. However, this approach is im-
practical because the most appreciable charac-
teristics 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 at-
tenuation differences usually occur when a hy-
pervascular focal lesion leads to primary
arterial inflow with hyperperfusion of the sur-
rounding 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. 1). 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].
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 hypoperfu-
sion by compression or infiltration of a portal
branch. This type of arterialization may be also
seen in the case of liver abscesses caused by por-
AJR:183, August 2004
 Hepatic Attenuation Differences

tal hypoperfusion and probably by the spread of
inflammatory mediators [4]. When the focal le-
sion is benign, it is usually small and located
near the hepatic capsule. Sectorial transient he-
patic attenuation differences can be either
wedge- or fan-shaped [1, 5], depending on
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laterally positioned and inducing arterioportal
shunt (Fig. 2) or portal thrombosis (Fig. 3), 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. 5) or hepatic vein throm-
terioportal shunt. In turn, an arterioportal shunt
may be congenital or, more often, caused by
liver cirrhosis (Fig. 6) or trauma [6]. In such
cases, transient hepatic attenuation differences
are always wedge-shaped, with the straight bor-
der sign. Arterialization caused by cholangitis

whether the associated focal lesion is centrally or bosis, long-standing biliary obstruction, or an ar- can be sectorial, but it may also assume other

Fig. 13.—59-year-old woman with polymorphous tran-

sient hepatic attenuation difference caused by acute
calculus cholecystitis.
A, Arterial phase helical CT scan shows area of irreg-
ular enhancement (arrows) involving right lobe (seg-
ment V). This transient hepatic attenuation difference
was caused by primary increase in arterial flow due to
spreading of inflammatory mediators. In general, in-
creased arterial flow could also be caused by reduc-
tion of portal inflow because of interstitial edema.
Biliary tree (arrowhead) is slightly dilated.
B, Portal phase caudal helical CT scan shows en-
larged gallbladder with endoluminal stone (arrow-
head), wall thickening, and slight pericholecystic
collection (arrow).

A B

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 paren-
chyma (arrows) caused by opening of transsinusoidal plexus.

Fig. 15.—45-year-old woman with diffuse central–pe-

ripheral transient hepatic attenuation difference
caused by complete thrombosis of portal trunk.
A, 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).
B, Cranial scan better defines central–peripheral pat-
tern caused by opening of peribiliary plexus.
A B

AJR:183, August 2004 463


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Fig. 16.—Arterial phase helical CT scan in 89-year-old
woman with diffuse peribiliary transient hepatic attenua-
tion difference caused by long-standing biliary obstruction
(pancreatic cancer) shows enhancing areas (arrow) adja-
cent to dilated biliary tree (arrowhead). Dilatation of bile
ducts results in compression of peribiliary plexus with de-
creased portal flow and consequent arterialization.
patterns (nodular, lobar, or diffuse) because of its
wide range of presentation [7]. Finally, a secto-
rial 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 arterializa-
tion may herald abnormality, preceding its clear
CT detection as a nodular lesion. The latter pos-
sibility must be considered whenever a sectorial
transient hepatic attenuation difference has no
other explanation [8].
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 con-
tusion (Fig. 7), extrinsic compression by ribs, or
stretched diaphragmatic pillars (Fig. 8); percu-
taneous biopsy (Fig. 9); or treatment of a liver
neoplasm (ethanol injection, radiofrequency ab-
lation) (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 sec-
464
Colagrande et al.
torial, according to the characteristics of portal
vessel damage, as in the case of an arterioportal
shunt after biopsy (Fig. 9).
An aberrant blood supply may result from
anomalous arteries [5] (Fig. 12); collateral
venous vessels, as in superior vena cava ob-
struction; or accessory veins (capsular, paraum-
bilical veins of Sappey, or an accessory cystic
vein) [1, 5] that may act, according to the pres-
sure gradient, as an anomalous supply or as
drainage vessels. In inflammation of adjacent
organs (cholecystitis, pancreatic abscesses)
(Fig. 13), morphogenesis is related to inflam-
matory mediators spreading by contiguity.
Diffuse,Various Patterns
Diffuse transient hepatic attenuation differ-
ences 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 he-
patic attenuation differences not associated with
focal lesions. In fact, arterial phenomena trig-
gered by portal or hepatic vein obstruction or
compression may range from small and mar-
ginal to large and sectorial (Fig. 5) to diffuse, de-
pending 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 compensa-
tion 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 pa-
renchyma assumes a marbled aspect called a
“patchy” pattern (Fig. 14).
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 acti-
vation of the peribiliary plexus, produces en-
hancement 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. 15).
Finally, in dilatation of the biliary tree, as
in choledocholithiasis or pancreatic cancer,
the peribiliary plexus may become ob-
structed, with a consequent decrease in por-
tal blood flow to the sinusoids and arterial
compensation. The effect of such long-stand-
ing biliary obstruction is a peribiliary tran-
sient hepatic attenuation difference (Fig. 16)
characterized by a cylindric ramified path-
way along the dilated biliary tree.
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 char-
acterize a large variety of liver diseases. There-
fore, the hepatic arterial phase must always be
performed, even if no focal lesion is expected.
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