Transcatheter Arterial Chemoembolization for Hepatocellular

EDUCATION EXHIBIT
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Transcatheter Arterial
Chemoembolization for
Hepatocellular Carcinoma: Anatomic and
Hemodynamic Considerations in the Hepatic
Artery and Portal Vein1
Kwang-Hun Lee, MD ● Kyu-Bo Sung, MD ● Do-Yun Lee, MD
Sang Joon Park, MD ● Ki Whang Kim, MD ● Jeong-Sik Yu, MD
Hepatocellular carcinoma (HCC) is the most common malignant tumor of the liver. Although several therapeutic options have been advocated, transcatheter arterial chemoembolization (TACE) in particular
has been widely performed in the treatment of HCC. Still, hepatic arteriography and portography are mandatory for evaluation of (a) the
resectability and multiplicity of HCCs and (b) the hemodynamic status
of the portal vein. Thereafter, TACE can be considered as the initial
therapeutic modality. The possibility of nontarget organ complications
during TACE (eg, ischemic cholecystitis, splenic infarction, gastrointestinal mucosal lesions, pulmonary embolism and infarction, spinal
cord injury, ischemic skin lesions) should be taken seriously. A thorough understanding of the anatomic variants and hemodynamic features of the hepatic artery and portal vein is the first step in performing
effective and safe TACE for HCC.
©
RSNA, 2002
Abbreviations: CHA ⫽ common hepatic artery, HCC ⫽ hepatocellular carcinoma, LGA ⫽ left gastric artery, LGV ⫽ left gastric vein, LHA ⫽ left
hepatic artery, LPV ⫽ left portal vein, RHA ⫽ right hepatic artery, SMA ⫽ superior mesenteric artery, TACE ⫽ transcatheter arterial chemoembolization
Index terms: Hepatic arteries, chemotherapeutic embolization, 952.1264, 952.1266 ● Liver neoplasms, 761.323 ● Liver neoplasms, chemotherapeutic
embolization, 761.1264, 761.1266 ● Portal vein, therapeutic embolization, 957.1264, 957.1266 ● Shunts, arterioportal
RadioGraphics 2002; 22:1077–1091
1From
the Department of Diagnostic Radiology and Research Institute of Radiological Science, Yonsei University College of Medicine, Seoul, South
Korea (K.H.L., D.Y.L., S.J.P, K.W.K., J.S.Y.); and the Department of Radiology, Asan Medical Center, Ulsan University College of Medicine,
Seoul, South Korea (K.B.S.). Presented as an education exhibit at the 2001 RSNA scientific assembly. Received February 18, 2002; revision requested
April 1 and received May 8; accepted May 9. Address correspondence to K.H.L., Department of Diagnostic Radiology, YongDong Severance Hospital, 146-92 Dokok-Dong, Kangnam-Ku, Seoul 135-270, South Korea (e-mail: doctorlkh@yumc.yonsei.ac.kr).
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Figure 1. Anatomic variants of the hepatic arteries as
seen at digital subtraction angiography. (a) Replaced
posterior segmental artery from the SMA. Massive hypervascular tumor staining with a transtumoral arterioportal shunt is seen. (b) Anterior segmental artery from
the common hepatic artery (CHA). Multiple intrahepatic metastatic nodules are seen. (c) Replaced LHA
from the LGA. The replaced LHA supplies several
small, intrahepatic metastatic nodules. The LGA originates directly from the aorta. Note the regurgitation of
contrast material into the aorta (arrows) with no visualization of the celiac axis.
Introduction
Transcatheter arterial chemoembolization
(TACE) is widely used in the treatment of malignant liver tumors (1– 6). By interrupting the arterial supply, chemoembolization deprives the tumor of its major nutrient source, which results in
ischemic tumor necrosis.
Hepatocellular carcinoma (HCC) is the most
common malignant tumor of the liver. Although
several therapeutic options have been advocated,
transcatheter arterial chemoembolization (TACE)
in particular has been widely performed in the
treatment of HCC. In the past, surgical resection
was considered to be the only curative treatment
for HCC, but only a small number of patients
were able to undergo such treatment because
70%–90% of patients with HCC have underlying
liver cirrhosis and many HCCs consist of multiple
diffuse angioinvasive lesions. Moreover, in patients with severely impaired hepatic functional
reserve, surgical treatment can lead to catastrophic outcome (7,8). Recently, radio-frequency thermal ablation has been introduced as a
therapeutic modality, but this method has many
limitations in terms of the size and number of
HCCs that can be treated. In addition, some locations in the liver might be difficult to approach
even with imaging guidance. Nevertheless, hepatic arteriography and portography are mandatory for evaluation of the resectability and multiplicity of HCCs and of the hemodynamic status
of the portal vein. Thereafter, TACE can be considered as the initial therapeutic modality. A thorough understanding of the anatomic variants and
hemodynamic features of the hepatic artery and
portal vein is the first step in performing effective
and safe TACE for HCC.
In this article, we discuss and illustrate the anatomic variants and hemodynamic features of the
hepatic artery as well as extrahepatic collateral
routes, nontarget arteries, and hemodynamic
changes in the portal vein and how they influence
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Figure 2. Hepatic artery in the portocaval space. (a) On a celiac angiogram, the RHA arises from the celiac axis
(arrows). (b) CT scan shows that the RHA (arrows) branches early along the celiac axis and courses through the portocaval space. Although the most common artery that passes through the portocaval space is a replaced or accessory
RHA from the SMA, an RHA from different origins (eg, celiac axis, aorta, hepaticomesenteric trunk, celiacomesenteric trunk) also traverses the portocaval space.
TACE. We also discuss the correlation between
angiographic findings and dynamic computed
tomographic (CT) findings.
Anatomic Variants and Hemodynamic
Features of the Hepatic Artery
Common variants of the hepatic artery are the
replaced left hepatic artery (LHA) from the left
gastric artery (LGA) and the replaced right hepatic artery (RHA) from the superior mesenteric
artery (SMA) (9,10). These variants can coexist,
or the segmental artery may be replaced (Fig 1).
A replaced or accessory LHA courses along the
fissure for the ligamentum venosum, whereas a
replaced or accessory RHA passes through the
portocaval space. These findings can be predicted
at dynamic CT (11).
A replaced or accessory RHA can arise from
the SMA, originate early from the celiac trunk, or
originate directly from the aorta, hepaticomesenteric trunk, or celiacomesenteric trunk (Fig 2). In
the portocaval space, variants of the hepatic artery
as well as the posterior superior pancreaticoduodenal vessels and cavernous transformation of the
portal vein transect this space, but it is not difficult to differentiate these arteries by tracing these
vascular structures at CT (11).
The classic CHA lies in the hepatoduodenal
ligament to the left of the common bile duct and
anterior to the portal vein (10). The rarest variant
of the CHA is the replaced CHA from the LGA
(10,12). In such cases, the CHA courses through
the fissure for the ligamentum venosum (Fig 3b).
The accessory LGA that arises from the LHA or
proper hepatic artery, the left inferior phrenic artery that arises from the LHA, and the aberrant
left gastric vein (LGV) also course along the fissure for the ligamentum venosum. In general, the
gastroduodenal artery branches from the CHA
and has the right gastroepiploic artery as its terminal branch. Rarely, the entire hepatic artery arises
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Figure 3. Replaced proper hepatic artery from the LGA. (a) Gastroduodenal arteriogram demonstrates not only
the SMA due to the regurgitation of contrast material, but also the hepatic arteries, LGA, celiac axis, and splenic
artery due to flow through the connecting channel between the gastroduodenal artery from the SMA and the
RHA. The gastroduodenal artery actually arises from the SMA because the right gastroepiploic artery (arrowheads)
branches from the gastroduodenal artery near the SMA. Arteries that originate from the celiac axis are visualized
without complete opacification of the celiac orifice at superior mesenteric arteriography, which suggests partial stenosis of the celiac orifice. The tumors were supplied by the RHA, and chemoembolization was performed via the
SMA– gastroduodenal artery–RHA route because there was an obtuse angle between the RHA and gastroduodenal
artery. If a tumor is supplied by the LHA, it may be more desirable to perform chemoembolization via the LGA–
proper hepatic artery–LHA route due to the obtuse angle between the LHA and proper hepatic artery. (b) Arterialphase dynamic CT scan shows the replaced proper hepatic artery as it courses along the fissure for the ligamentum
venosum (arrow).
Figure 4. Aberrant RHA that arises directly from the aorta. (a) Digital subtraction angiogram shows a replaced
RHA (arrow) that arises from the aorta. Both inferior phrenic arteries arise together. Nodular hypervascular tumor
staining supplied by the anterior segmental artery is also seen. (b) On a CT scan, the replaced RHA arises from the
aorta and courses through the portocaval space (arrow).
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Figure 5. Stenosis of the celiac axis. (a) Superior
mesenteric arteriogram shows retrograde filling of the
CHA (arrow) via the pancreaticoduodenal arcade (arrowheads). (b) Common hepatic arteriogram shows a
prominent pancreaticoduodenal arcade (arrowheads).
(c) Sequential common hepatic arteriogram shows
contrast material washout in the pancreaticoduodenal
arcade due to unopacified flow from the SMA.
from the LGA, and the gastroduodenal artery
arises from the SMA (Fig 3a). In such cases, the
entire hepatic artery is considered to be the replaced proper hepatic artery from the LGA.
In the majority of cases, the aberrant RHA
arises from either the SMA or the gastroduodenal
artery. In less than 2% of cases, it arises from the
aorta (Fig 4).
Stenosis or occlusion of the celiac axis is commonly associated with enlargement of the arteries
of the pancreaticoduodenal arcade, which supply
the distribution of the celiac axis by means of retrograde flow from the SMA (Fig 5) (13,14). Stenosis or occlusion of the celiac axis is easily seen
at superior mesenteric arteriography as unopacified flow from the celiac axis. In nearly all cases of
celiac axis stenosis and in some cases of celiac axis
occlusion, chemoembolization or chemoinfusion
can be performed via the CHA; if this is not possible, these procedures can be performed via the
hypertrophic pancreaticoduodenal arcade. For
the unwary angiographer, there is an increased
risk of arterial dissection due to repeated attempts
at catheterization of the celiac axis when it is severely stenotic or occluded.
Several reports have described a nontumorous
arterioportal shunt that mimics hypervascular
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Figure 6. Nodular arterioportal shunt. (a) Dynamic arterial-phase CT scan demonstrates nodular attenuation (arrow). (b) On a dynamic equilibrium-phase CT scan, the nodule is isoattenuating. (c, d) Sequential hepatic angiograms show the typical branching portal vein in the central portion (arrow in c) and surrounding triangular staining
(arrow in d), findings that suggest a focal arterioportal shunt. (e) Spot image obtained after superselective subsegmental injection of iodized oil shows stippled accumulation of the oil in the portal branches (arrowheads).
tumor at dynamic CT, magnetic resonance (MR)
imaging, and hepatic angiography (15–17). An
arterioportal shunt is typically wedge-shaped at
dynamic CT or MR imaging and is contrast material– enhanced on arterial-phase images but becomes isoattenuating or isointense on portalphase images. However, an arterioportal shunt
may be nodular rather than wedge-shaped on
cross-sectional images; in fact, it has been reported to be nodular in 7%–31% of cases (16,17).
Therefore, it is imperative to correlate these findings with hepatic arteriographic findings. At hepatic arteriography, a typical arterioportal shunt
manifests as branching or dotlike vascular structures early in the arterial phase and, subsequently,
as wedge-shaped focal parenchymal staining (Fig
6). Its presence can be verified with selective injection of iodized oil and with follow-up imaging
including iodized oil– enhanced CT.
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Figure 7. Right-to-left gastric artery route. (a, b) Initial angiograms show the hepaticomesenteric trunk with a replaced lateral segmental artery from the LGA. Diffuse, multinodular tumor staining was seen in the entire liver.
TACE was performed via the hepaticomesenteric trunk and LGA. Initially, the right gastric artery was not visualized.
(c) Common hepatic arteriogram obtained during the second session of TACE shows that a right-to-left gastric artery route (arrowheads) has developed due to stenosis at the orifice of the LGA from previous catheterization. Some
residual tumor staining is also seen. The sharp demarcation at the junction between the right and left gastric arteries
(arrow) and the absence of unopacified flow from the LGA suggest occlusion of the LGA orifice. It was possible to
perform TACE via the proper hepatic artery and right-to-left gastric artery route with a 3-F coaxial microcatheter.
Extrahepatic Collateral Routes
TACE via the extrahepatic collateral routes is a
well-known procedure to interventional radiologists (9,14,18,19). There are numerous extrahepatic collateral routes, including periportal collateral vessels that arise from the gastroduodenal
artery or pancreaticoduodenal arcade, right and
left inferior phrenic arteries, right and left gastric
arteries, pancreaticoduodenal arcade (which supplies the gastroduodenal and proper hepatic arteries), right and left internal mammary arteries and
superior epigastric artery, intercostal artery, lumbar artery, adrenal arteries, capsular branches of
the right renal artery, branches of the middle or
right colic artery, and omental branches. There
are two mechanisms for the development of extra-
hepatic collateral routes. The first is deprivation
of the native hepatic artery due to repeated TACE
or chemoinfusion, dissection due to catheterization, or occlusion of the hepatic artery due to surgical ligation or chemoport catheterization. The
second is parasitization of the extrahepatic arteries without native hepatic artery injury in cases of
subcapsularly located HCC or exophytic growth
of HCC. Previous reports indicated that the survival rate for patients who underwent TACE via
collateral routes was comparable to that for patients who underwent conventional TACE via the
hepatic artery (20,21).
The anastomosis between the right and left
gastric arteries can serve as a collateral pathway to
the liver after occlusion of the hepatic artery
(13,14). In anatomic variants in which the replaced LHA or lateral segmental artery arises
from the LGA, when the LGA is occluded and
HCC is supplied by these arteries, the route created by the right and left gastric arteries can serve
as an important pathway for TACE (Fig 7).
In the majority of cirrhotic patients, atrophy of
the liver affects the right lobe, and the medial segment of the left lobe is greatly enlarged. The lateral segment of the left lobe and the caudate lobe
often become hypertrophic (22). In such cases,
the dome and anterior aspect of the shrunken
liver are surrounded by the omentum, which increases the chances that HCC on the surface or
with exophytic growth is supplied by the omental
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Figure 8. Omental HCC nodule fed by a single omental branch. (a) Equilibrium-phase CT scan shows diffuse
contraction of the liver due to cirrhosis and omental fat at the anterior surface of the liver. A single omental nodule
(arrow) is surrounded by omental fat. (b) On a common hepatic arteriogram, only faint nodular staining is seen (arrows). A mildly hypertrophic omental branch (arrowheads) is suspected to be the feeding vessel. However, staining of
the nodule is not definitely visualized because most of the contrast material injected into the CHA filled the hepatic
artery, the pancreaticoduodenal arcade of the gastroduodenal artery, and the right gastroepiploic artery. Superselective TACE was performed with a 3-F coaxial microcatheter and injection of a mixture of chemotherapeutic agent and
iodized oil. (c) Single spot image obtained after injection clearly depicts the draining omental vein (arrowheads). Embolization with absorbable gelatin sponge particles was subsequently performed. (d) Follow-up CT scan obtained 1
year later shows good uptake of the iodized oil without marginal tumor recurrence.
branches (Fig 8). These branches arise from the
right and left gastroepiploic arteries (10). The
right gastroepiploic artery is the terminal branch
of the gastroduodenal artery. The left gastroepiploic artery is usually the largest branch that originates from the distal splenic artery. TACE that is
performed with superselective embolization of an
omental branch might be more effective if it continues until filling of the omental vein is visualized, similar to performing TACE of a subsegmental hepatic artery until the surrounding portal
branches are seen.
Considerations
in Nontarget Arteries
The possibility of nontarget organ complications
during TACE should be taken seriously. Reported nontarget organ complications include
ischemic cholecystitis, splenic infarction, gastrointestinal mucosal lesions, pulmonary embolism
and infarction, spinal cord injury, and ischemic
skin lesions (23–29). There are two important
considerations regarding nonhepatic arteries during TACE depending on whether the nonhepatic
artery is acting as the feeding vessel for HCC. If it
is not acting as the feeding vessel, superselective
embolization should be performed to avoid nontarget organ injury after making certain that there
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Figure 9. Accessory LGA. (a) Common hepatic arteriogram shows diffuse tumor staining supplied by the LHA
and the thread and streak sign of tumor thrombus in the LPV (arrowheads). An accessory LGA arises proximal to the
umbilical point of the LHA. The distal branches of the accessory LGA demonstrate the typical coiled appearance (arrows). TACE of the LHA was performed after coil embolization of the accessory LGA to prevent inadvertent damage
to the gastric mucosa due to regurgitation of the embolic agents. (b) On a follow-up CT scan, the coils are located at
the fissure for the ligamentum venosum, through which the accessory LGA traverses (arrow). The patient had no gastric symptoms after undergoing TACE.
is no reflux of embolic material into the nontarget
artery. If that is not possible, the nontarget artery
should be embolized with a coil to maintain flow
to the hepatic artery while flow to the nontarget
organ is maintained by distal collateral vessels. If
the nonhepatic artery acts as the feeding vessel, it
should be embolized superselectively. If superselective embolization is not possible, other alternative therapeutic methods including surgery, ablation therapy, and injection therapy should be considered.
The most commonly encountered nontarget
arteries are the gastroduodenal artery, cystic artery, accessory LGA, and hepatic falciform artery.
The gastroduodenal artery is not considered to be
a nontarget artery in general TACE; however, in
chemoinfusion therapy by means of a percutaneously implanted catheter-port system, unwanted
chemotherapeutic agent can flow into the gastroduodenal artery. Therefore, the gastroduodenal artery is considered to be the nontarget artery,
and subsequent coil embolization is needed.
Coil embolization is not usually needed for the
cystic artery if the previously mentioned considerations are taken into account.
It may be more convenient to embolize an accessory LGA with coils for repeated procedures
including chemoembolization and chemoinfusion
(Fig 9). It is important to differentiate between
collapsed gastric fundal staining supplied by an
accessory LGA and hypervascular tumor staining
supplied by the LHA. It is possible to identify an
accessory LGA by visualizing the point of branching, the course of the artery, and the characteristic
tortuousness of the peripheral branches (30).
Branching occurs just before the point at which
the LHA kinks at the umbilical point. The umbilical point of the LHA is the point at which the
dorsolateral and ventrolateral branches of the
LHA divide in the umbilical fossa. In the anteroposterior projection, the LHA courses approximately parallel to the two lateral segmental hepatic arteries in the fissure for the ligamentum
venosum. Peripheral arterial branches have a
characteristic coiled appearance. Draining veins
can also have a characteristic tortuous appearance, but they can easily be differentiated from
the portal vein in patients with HCC due to the
presence of a transtumoral arterioportal shunt.
When this coiled appearance cannot be distinguished from neovasculature in the hypervascular
tumor, distention of the stomach with gas is helpful because it causes the arteries to separate and
stretch along the gastric wall.
The hepatic falciform artery arises as a small
terminal branch of the left or middle hepatic artery, runs through the hepatic falciform ligament,
distributes itself around the umbilicus, and communicates with branches of the superior and inferior
epigastric arteries (31). Prophylactic coil embolization of the hepatic falciform artery is controversial
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Figure 11. Unusual laminar flow mimicking portal
vein thrombus. (a) SMA portogram shows central filling defects in the main portal vein that mimic thrombus
(arrows). However, this finding actually represents unopacified laminar flow from the splenic vein. Portography of the celiac and splenic arteries showed central
filling with contrast material. (b) Dynamic arterialphase CT scan shows low attenuation centrally in the
main portal vein (arrowheads). (c) Dynamic equilibrium-phase CT scan shows full attenuation of the contrast material in the main portal vein.
(Fig 10). Some reports have recommended prophylactic embolization of the hepatic falciform
artery before TACE to prevent supraumbilical
skin and fat necrosis (31,32). Recently, however,
Kim et al (33) found no need for prophylactic
embolization of the hepatic falciform artery before
short-term hepatic arterial chemoinfusion with or
without subsequent embolization.
Hemodynamic
Features of the Portal Vein
Liver cirrhosis and portal vein invasion are frequently associated with HCC (34,35). Okuda et
al (36) reported a portal vein invasion rate of
63.5%, a finding that was confirmed at autopsy,
whereas Albacete et al (35) reported a portal vein
thrombosis rate of 26%–34%. Knowledge of portal vein hemodynamic features can be important
in determining the type of therapy to be used.
At portography of the SMA or of the celiac and
splenic arteries, a filling defect of the main portal
vein due to unopacified laminar flow is a common
finding. The typical finding consists of layering of
Figure 10. Hepatic falciform artery. Common hepatic arteriogram shows the thread and streak sign of
tumor thrombus in the LPV with an arterioportal shunt
and parenchymal tumor staining supplied by the hypertrophic middle hepatic artery and LHA. The RHA
arises from the gastroduodenal artery, and the hepatic
falciform artery arises from the middle hepatic artery
(arrows). Chemoinfusion was performed without prophylactic coil embolization of the hepatic falciform artery. The patient had no complications.
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Figure 12. Control of transtumoral arterioportal shunt and hepatofugal flow with repeated TACE. (a) Initial SMA
portogram shows an absence of right portal perfusion and poor left portal perfusion. (b) Initial replaced right hepatic
angiogram shows extensive hypervascular tumor staining in the liver dome with a transtumoral arterioportal shunt
and hepatofugal flow with coronary and paraumbilical varices. The patient underwent three sessions of TACE.
(c) SMA portogram obtained during the fourth session of TACE shows improved hepatopetal portal flow. (d) Replaced right hepatic angiogram shows neither definitive tumor staining nor a transtumoral hepatofugal shunt. Comparison of findings at initial portography (a) and arteriography (b) with those at portography (c) and arteriography
(d) performed after the third session of TACE demonstrates the disappearance of the transtumoral arterioportal
shunt following successful tumor management and improved hepatopetal portal flow. The accessory splenic artery is
seen to arise from the proximal SMA (arrow).
SMA flow to the right side and splenic flow to the
left side. However, although it is rare, turbulent
laminar flow in the central portion of the main
portal vein can mimic thrombus (Fig 11). Moreover, this finding can also be seen during dynamic
arterial-phase CT; therefore, it is imperative to
correlate this finding with dynamic portal-venousphase CT findings.
In patients with tumor thrombus in the portal
vein trunk or hepatofugal blood flow, TACE has
been considered to be contraindicated because of
the increased risk of liver failure due to hepatic
ischemia (1). However, recent reports by several
investigators have documented that TACE is effective and safe for the palliation of HCC and major portal vein invasion if tumor extent is limited,
hepatic function is preserved, and there is adequate collateral circulation around the main portal vein (34 –39). TACE has been reported to be
more effective in the treatment of nodular HCC
than of diffuse infiltrating HCC. If repeated
TACE is successful in tumor control, hepatofugal
portal flow due to a transtumoral arterioportal
shunt can be reversed to the normal hepatopetal
flow (Fig 12).
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Figure 14. Balanced hepatofugal portal flow. (a) SMA
portogram shows preserved hepatopetal portal flow
but a decrease in the size of the portal vein. Note the
marked development of a gastrorenal shunt. (b) Common hepatic arteriogram shows compensatory hypertrophic change in the hepatic arteries due to decreased
portal flow and size, as well as a diffuse parenchymal
arterioportal shunt. (c) Sequential common hepatic
arteriogram shows hepatofugal arterioportal and gastrorenal shunts.
Hepatofugal flow resulting from cirrhosis can
be categorized as segmental, lobar, balanced, or
total depending on its severity (Figs 13–15). As
cirrhosis becomes more advanced, the pressure
within the main portal vein is increased by hepatofugal flow. Subsequently, flow within the superior mesenteric vein and splenic vein forms extraportal systemic collateral vessels, resulting in
decreased size of the functionally blocked portal
vein and compensatory hypertrophy of the hepatic artery. This is different from hepatofugal
flow caused by tumor thrombus. In functional
hepatofugal portal flow, there is absence of cavernous transformation and of the “thread and
streak” sign (indicating tumor thrombus) and no
change in cirrhotic hepatofugal flow even after the
control of hepatic parenchymal tumor. In the absence of hepatopetal portal flow, TACE is quite
risky in the treatment of diffuse multisegmental
infiltrating tumor, whereas superselective embolization is safe and effective in the treatment of
nodular tumor (Fig 15).
Figure 13. Right lobar hepatofugal portal flow.
Common hepatic arteriogram shows right lobar hepatofugal portal flow (arrow) and unopacified laminar
flow into the LPV (arrowheads). The catheter tip is
positioned in the CHA, and when contrast material is
injected into the CHA, the right portal vein demonstrates homogeneous opacification because the opacified flow now moves in a hepatofugal direction due to
right lobar portal hypertension. Meanwhile, unopacified laminar flow from the LPV is caused by splanchnic
portal flow moving toward the LPV due to absence of
left lobar portal hypertension.
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Figure 15. Total hepatofugal portal flow. (a) SMA
portogram shows the absence of hepatopetal portal flow
and retroperitoneal varices of the veins of Retzius (white
arrows) with extension from the inferior mesenteric vein
(black arrow) to the inferior vena cava (arrowheads).
(b) Common hepatic arteriogram shows compensatory
hypertrophic hepatic arteries and nodular tumor staining. Superselective subsegmental chemoembolization
was performed. (c) Single spot image demonstrates
nodular uptake of iodized oil in the tumor and surrounding portal veins. Despite the fact that there was no
functionally hepatopetal flow, superselective chemoembolization could be performed safely because the tumor
was subsegmentally located.
Figure 16. Aberrant LGV. (a) SMA portogram shows unusual hepatofugal flow from the LPV to an aberrant LGV
and gastrorenal route (arrows). (b) Equilibrium-phase dynamic CT scan shows the aberrant LGV (arrows) as it
courses in the fissure for the ligamentum venosum. Arrowhead indicates the gastrorenal route.
Portosystemic collateral vessels that originate
from the left portal vein (LPV) are typically recanalized umbilical and paraumbilical veins located in and around the falciform ligament.
Rarely, an aberrant LGV may be seen (Fig 16)
(40 – 42). Such an aberrant LGV may represent a
persistent LPV and may have derived from the
left omphalomesenteric vein or from the subintestinal vein as an LPV independent of the usual right
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portal vein (40). It courses through the fissure for
the ligamentum venosum and is directly connected to the LPV branch. An aberrant LGV may
be clinically significant as (a) a potential source of
bleeding during surgery if this anatomic variant is
not appreciated, (b) a portosystemic collateral
route and the focus of gastric variceal bleeding in
cases of portal hypertension, (c) a hematogenous
metastatic route in cases of hepatic malignancy,
or (d) the cause of a possible pseudolesion of focal fat sparing or deposition.
Conclusion
An understanding of (a) the anatomic variants
and hemodynamic features of the hepatic artery,
(b) extrahepatic collateral routes, (c) nontarget
arteries, and (d) the hemodynamic features of the
portal vein is mandatory for performing effective
curative and palliative TACE for HCC.
Acknowledgments: We appreciate the thoughtful
comments provided by the reviewers of our manuscript. In addition, Dr Kwang-Hun Lee would like to
express his special thanks to his mentor and teacher,
Professor Kyu-Bo Sung.
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