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Chapter11:Image-guided ablationofHCC
http://internalmedicinebook.com
60. Pilot study of irreversible electroporation (IPE) to treat earlystage primary liver cancer (HCC). http://clinicaltrials.gov/ct2/
show/NCT01078415 (accessed September2014).
61. Lencioni R, Cioni D, Della Pina MC, Crocetti L. New options
for image-guided ablation. J Hepatobiliary Pancreat Sci 2010; 17
(4):399–403.
62. Kingham TP, Karkar AM, D'Angelica MI, etal. Ablation
64. Shah SA, Cleary SP, Wei AC, etal. Recurrence aer liver
resection for hepatocellular carcinoma:risk factors, treatment,
and outcomes. Surgery 2007; 141 (3):330–339.
65. Rossi S, Ravetta V, Rosa L, etal. Repeated radiofrequency
ablation for management of patients with cirrhosis with small
hepatocellular carcinomas:a long-term cohort study. Hepatology
2011; 53 (1):136–147.
of perivascular hepatic malignant tumors with irreversible
electroporation. J Am Coll Surg 2012; 215 (3):379–387.
63. Silk MT, Wimmer T, Lee KS, etal. Percutaneous ablation of
peribiliary tumors with irreversible electroporation. J Vasc
Interv Radiol 2014; 25 (1):112–118.
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Chapter
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Embolization of liver tumors:Anatomy
12
Hyo-Cheol Kim and Jin WookChung
In transcatheter management of hepatic tumors, it is essential
to understand hepatic vascular anatomy in detail to enhance
therapeutic results and prevent complications due to non-target
treatment.
e purpose of this chapter is to review celiac trunk and hepatic
artery variations, non-hepatic arteries arising from hepatic arteries, and extrahepatic collateral supply to hepatic tumors.
two separate trunks from the aorta in combination of the CHA
and SMA (hepatomesenteric trunk) and that of the LGA and
splenic artery (gastrosplenic trunk) (Figure 12.3). e CHA
can also arise from the hepatogastric trunk, hepatosplenomesenteric trunk, and celiacomesenteric trunk, or directly from the
aorta. Rarely, the CHA can arise from the LGA in normal celiac
trunk anatomy.
Occasionally, there are situations in which it is dicult
Celiac trunk anatomy
Normal celiac trunk anatomy and variations
e celiac trunk is a wide branch from the front of the aorta just
below the aortic hiatus of the diaphragm. It passes nearly horizontally forward and slightly to the right above the pancreas
and the splenic vein, and divides into three major branches of
the le gastric artery (LGA), common hepatic artery (CHA),
and splenic artery. It may give o one or both inferior phrenic
arteries (IPAs), dorsal pancreatic artery, and, rarely, colic or
jejunal branches (Figure12.1).1 e superior mesenteric artery
(SMA) separately arises from the aorta inferior to the origin of
the celiac axis. Usually, the LGA is the rst major branch of the
celiac trunk. However, in about 4% of the population, the LGA
directly arises from the supraceliac or juxtaceliac aorta, which
represents the most common form of celiac trunk variation. If
IPAs arise from the celiac trunk, their origin is almost always
located proximal to the LGA (Figure12.1).
Celiac trunk variation is found in approximately 10% of the
general population.2 Celiac trunk variations can be considered
as the result of the origin of the CHA, LGA, splenic artery, and
SMA from the aorta in dierent combinations. Among 15 possible combinations of their origin (Figure12.2), we could nd
13 types in clinical practice.
3
In describing celiac trunk and hepatic artery variations, it is
extremely important to dene the terminology used. e CHA
should be dened as the common trunk of a hepatic artery
(regardless of its size or anatomical distribution) and the gastroduodenal artery (GDA). According to our experience, the
most common type of celiac trunk variation was the common
trunk of the CHA and splenic artery and the separate origins of
the LGA and the SMA from the aorta, which was followed by
to dene the celiac trunk anatomy because of embryological communicating channels (Figure 12.4) and absent CHA
(Figure12.5).
Celiac stenosis or occlusion
Celiac stenosis or occlusion is the initial obstacle in transcatheter management of hepatic tumors. For successful and uneventful placement of a catheter in the target hepatic arteries, it is
important to recognize celiac stenosis early and to understand
the anatomy and hemodynamic alteration related to celiac stenosis. If the celiac trunk is severely stenotic or occluded, particular skill is required to pass a catheter through it or along
alternative collateral pathways without causing arterial injury.
Reported causes of celiac trunk stenosis or occlusion are
atherosclerosis, dissection, injury from previous catheter
manipulation, surgical trauma, Takayasu arteritis, and extrinsic compression by the median arcuate ligament.5 Bron and
Redman5 noted an incidence of 12.5% among 713 patients
referred for abdominal aortography. ey found that the
most important etiology of celiac stenosis was atherosclerosis. In contrast to the general belief that atherosclerosis is the
major cause of the celiac stenosis, there are studies that report
extrinsic compression by the median arcuate ligament of the
diaphragm as the major cause of celiac stenosis in asymptomatic individuals and the Asian population.
6,7
According to a
series of David and Harold,6 12 of 50 asymptomatic individuals had celiac stenosis of 50% or more. On lateral aortography,
the proximal celiac trunk showed a U-shaped conguration
with compression along the superior aspect, a characteristic of
impingement by the median arcuate ligament of the diaphragm
(Figure12.6). us, most cases of celiac stenosis in that series
resulted from median arcuate ligament compression.
4
Interventional Oncology, Second Edition, ed. Jean-François H.Geschwind and Michael C.Soulen. Published by Cambridge University Press.
©Cambridge University Press2016
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AB
Figure 12.1 Normal celiac trunk with
an aberrant left hepatic artery, a jejunal
branch, and a long hepatic falciform
artery. (A) The first branches of the celiac
trunk are the inferior phrenic arteries
(open arrows). The left gastric artery gives
off the aberrant left hepatic artery (thick
arrow) supplying liver segments 2 and
3. Arrowheads indicate a jejunal branch
from the proximal splenic artery and
the thin arrow indicates the right gastric
artery from the segment 4 hepatic artery.
(B) Open arrows indicate the hepatic
falciform artery arising from the aberrant
left gastric artery.
Figure 12.2 Schematic diagrams of 15 possible types of celiac trunk variations. The last two types have not been observed. CH = common hepatic artery; CM =
celiacomesenteric; GM = gastromesenteric; GSp = gastrosplenic; GSpM = gastrosplenomesenteric; HG = hepatogastric; HGM = hepatogastromesenteric; HGSp =
hepatogastrosplenic; HM = hepatomesenteric; HSp = hepatosplenic; HSpM = hepatosplenomesenteric; LG = left gastric artery; SM = superior mesenteric artery;
Sp = splenic artery; SpM = splenomesenteric.
AB
Figure 12.3 Celiac trunk variation
in combination of gastrosplenic trunk
(A) and hepatomesenteric trunk (B).
Because of the associated celiac stenosis,
superior mesenteric arteriogram shows
hypertrophied collateral circulation via the
dorsal pancreatic artery from the superior
mesenteric artery (thick arrow) and an
anastomotic channel (thin arrows) between
the ascending part of the segment 2
hepatic artery and the fundic branch of the
left gastric artery (arrowheads). When there
is an accessory left gastric artery from the
left hepatic artery, the fundic branch from
the left gastric artery is usually replaced
by it. Note the early branching of the right
hepatic artery from the common hepatic
artery (open arrow).
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AB
Figure 12.4 (A, B) Ambiguous celiac trunk
anatomy due to persistent embryological
communicating channels (thick arrows).
Because they are widely patent and
almost equal in diameter, it is impossible
to determine the celiac trunk anatomy,
whether the common hepatic artery is
replaced from the left gastric artery or
replaced from the superior mesenteric
artery. The thin arrow indicates the origin of
the right gastroepiploic artery.
AB
Figure 12.5 Ambiguous celiac trunk
anatomy due to absent common hepatic
artery. (A) The entire left hepatic artery is
replaced from the left gastric artery. The
gastroduodenal artery arises from the celiac
trunk as usual with the right gastric artery
(arrow). (B) The entire right hepatic artery
AB
is replaced from the superior mesenteric
artery.
Figure 12.6 Severe celiac stenosis and
segmental chemoembolization via the
stenotic celiac trunk. (A) Celiac arteriogram
shows acute downward angulation of the
celiac trunk with poor opacification of the
common hepatic artery due to reversed
competitive flow from the gastroduodenal
artery. (B) Superior mesenteric arteriography
demonstrates excellent opacification of
hepatic arteries and the splenic artery via
hypertrophied pancreaticoduodenal arcade
and dorsal pancreatic artery. The common
hepatic artery is atrophic due to chronic
celiac stenosis. (C) Thin-section arterial
phase computed tomography scan reveals
severe compression of the proximal celiac
C
D
trunk by the median arcuate ligament of
the diaphragm (arrows). (D) Test injection
of the celiac axis in left anterior oblique
projection shows characteristic appearance
of the celiac stenosis due to median arcuate
ligament compression. (E) It was possible
to advance a microcatheter through the
severely stenotic celiac axis and select
the right anterior segment hepatic artery.
Segmental chemoembolization was
successfully performed.
E
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AB
AB
the intrahepatic collateral channel, selective segment 4 hepatic arteriography reveals tumor stain (open arrows). The tumor was successfully treated with
chemoembolization.
Figure 12.7 Accentuation of celiac
compression by the median arcuate
ligament of the diaphragm during expiration.
(A) Celiac arteriogram during inspiration
shows mild focal stenosis at the superior
aspect of the proximal celiac trunk (arrow).
(B) Deep expiration accentuates celiac trunk
compression and almost stops the blood
flow through the celiac trunk (arrow).
Figure 12.8 Celiac stenosis and
embolization of intrahepatic collateral
channels in a patient with celiac trunk
variation of hepatomesenteric trunk and
aberrant left hepatic artery from the left
gastric artery. (A) Superior mesenteric
arteriogram demonstrates hypertrophied
anastomotic channels between the right
gastric artery and the left gastric artery
(open arrows), and between the segment
4 hepatic artery and aberrant left hepatic
artery from the left gastric artery (arrows).
The flow of the left gastric artery is also
reversed. (B) After coil embolization of
In an Asian study using spiral computed tomography (CT)
scan and direct pressure measurement, the incidence of hemodynamically signicant celiac stenosis in an asymptomatic
population was 7.3%, and the most important etiology was
extrinsic compression by the median arcuate ligament of the
diaphragm.7 In that study, atherosclerosis was only a minor
cause of celiac stenosis. Deep expiration accentuates the compression of the celiac axis by the median arcuate ligament of the
diaphragm (Figure12.7).
Although celiac stenosis is frequently encountered, clinically signicant ischemia is rarely reported due to rich collateral circulation. e collateral circulation associated with
celiac stenosis develops via pathways of the pancreaticoduodenal arcades, dorsal pancreatic arteries, replaced or accessory
right hepatic arteries (RHAs), interlobar collaterals, or gastric
anastomosis (Figures15.6 and 15.8). Celiac trunk or hepatic
artery variations greatly aect the pattern of collateralization.8
According to the severity of celiac stenosis, the ow direction of
the GDA or CHA is reversed by retrograde ow from the SMA.
In severe celiac stenosis, celiac arteriography poorly visualizes
hepatic arterial territory due to competitive unopacied ow
from the SMA, and superior mesenteric arteriography better
opacies hepatic arterial territory through hypertrophied pancreaticoduodenal arcade or dorsal pancreatic artery pathways
(Figure12.6). Interlobar collaterals in celiac stenosis may cause
untoward embolization of non-target organ due to reversed
ow of hepatic arteries. On that occasion, it is necessary to
embolize interlobar collaterals for safe and eective treatment
(Figure12.8).
If possible, access through the occluded celiac trunk is
superior to that through the pancreaticoduodenal arcades in
microcatheter manipulation and superselective catheterization
of tumor-feeding arteries. In our experience, catheterization
through the pancreaticoduodenal arcade required longer procedure time and, sometimes, additional devices. erefore, we
suggest that catheterization through the occluded celiac trunk
should be the initial approach with an occluded celiac trunk.
For the inexperienced angiographer, there is increased risk of
arterial dissection as a result of repeated attempts at catheterization of the celiac trunk when the trunk is signicantly stenotic or occluded.
e pancreaticoduodenal arcade is the most common collateral pathway in cases of common hepatic or celiac arterial
occlusion. It can be an alternative route for hepatic chemoembolization in patients with celiac occlusion. e techniques to
catheterize the target hepatic arteries in celiac occlusion were
described in detail by Kwon etal.9 Even the le hepatic artery
(LHA) arising from the LGA can be catheterized in the retrograde fashion through the pancreaticoduodenal arcade. e
gastric anastomosis between the right gastric artery (RGA) and
LGA can be a route for successful catheterization of the LHA
arising from the occluded or severely stenotic LGA in patients
with celiac trunk variation.
With the recent advances in helical CT technology, it
became possible to detect celiac stenosis and predict its etiologies. in-section helical CT successfully demonstrates
the median arcuate ligament of the diaphragm obstructing
the celiac axis. e CT ndings of celiac compression by the
median arcuate ligament are eacement or narrowing of the
celiac axis by an anterior so-tissue band (Figure12.6), dilated
peripancreatic collateral vessels, and poststenotic dilation of
the distal celiac axis.7 In most patients with celiac occlusion
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A B
AB
Figure 12.9 Unusual anatomical course
of the common hepatic artery, which arises
from the celiac trunk and runs through the
portocaval space (arrows).
Figure 12.10 (A) The anomalous origin
of the common hepatic artery from the
left gastric artery. (B) It passes through the
fissure for the ligamentum venosum on
computed tomography scan (arrows).
due to median arcuate ligament compression, it is possible to
pass a microcatheter through the compressed potential lumen
(Figure 12.6). erefore, in selective catheterization of the
occluded celiac axis, it is quite useful to carefully review helical
CT scans. in-section helical CT in arterial phase may also
demonstrate major collateral vessels, including unusual ones,
and enable preprocedural evaluation of their anatomy for successful catheterization.
or below the pancreas head. Rarely, the CHA arising from the
celiac trunk passes through the portocaval space, when it looks
normal on celiac arteriography (Figure12.9). e CHA rarely
arises from the LGA through the ssure for the ligamentum
venosum (Figure12.10). When the CHA arises from the LGA,
it sequentially gives o the LHA, RHA, andGDA.
As a PHA variation, the PHA may arise from the LGA,
celiac trunk, GDA, SMA, or directly from the aorta, with the
GDA separately arising from the celiac trunk orSMA.
Hepatic artery anatomy
Normal hepatic artery anatomy and variations in
its origin and anatomiccourse
In normal celiac trunk anatomy, the CHA typically bifurcates
into the GDA and proper hepatic artery (PHA), and the PHA
bifurcates into the RHA and LHA. e classic CHA lies in the
hepatoduodenal ligament to the le of the common bile duct
and anterior to the portal vein. erefore, the hepatic artery
runs across the portal vein anteriorly. is standard hepatic
arterial anatomy has been reported in 50–65% of patients on
cadaveric and angiographic investigations.
2,10
ere is a wide spectrum of hepatic artery variations
encompassing the territory of variant hepatic arteries (from the
CHA to subsegmental hepatic arteries), their aberrant origin,
and their abnormal anatomical course.
As CHA variations, the CHA arises from the SMA in the
hepatomesenteric trunk as a celiac trunk variation. In the
hepatomesenteric trunk, the CHA could take various anatomical pathways in relation to the pancreas and the portal vein.
Most times, it runs through the portocaval space or across
the portal vein anteriorly. Occasionally, it may pass through
In hepatic artery variations, the vascular territory of variant hepatic arteries can vary from subsegmental to lobar distribution. In addition, hepatic artery variations can coexist
(Figure 12.11). e aberrant RHA can arise from the SMA,
celiac trunk, or directly from the aorta, with an incidence of
15–20%. e aberrant LHA arises from the LGA with a similar
incidence. e most common variants of the hepatic artery are
the aberrant LHA from the LGA and the aberrant RHA from
the SMA. e aberrant RHA from the SMA is usually the rst
major artery arising from the SMA. is vessel almost always
possesses the origin of the main cystic or accessory cystic
artery. Occasionally, it may arise from the pancreaticoduodenal trunk. e aberrant LHA from the LGA runs within the
ligamentum venosum with a characteristic appearance and frequently sends smaller branches to the stomach and esophagus
(Figure12.11). In aberrant LHA from the LGA, all of the side
branches before reaching the umbilical point are esophageal or
gastric branches.
Variant arteries running through the ssure for the ligamentum venosum include the CHA, PHA, and LHA from the LGA.
e accessory LGA from the LHA or PHA, the le IPA from
LHA, and aberrant le gastric venous drainage also can pass
through the ssure for ligamentum venosum. Variant arteries
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AB
CD
FE
Figure 12.11 Recognition of multiple
variant hepatic arteries in a patient.
(A) Arterial-phase computed tomography
(CT) scan shows a small enhancing
nodule in hepatic segment 4. (B, C) CT
scan also demonstrates the presence of
aberrant left hepatic artery in the fissure
for the ligamentum venosum (arrows in
B) and aberrant right hepatic artery in the
portocaval space (arrows in C). (D) There
is no tumor stain on common hepatic
arteriography. The missing right posterior
segmental artery (faintly opacified by
the reflux of the contrast material via the
pancreaticoduodenal arcade) and the left
hepatic artery supplying hepatic segment
2 and 4 should be recognized. (E) Selective
angiogram of the right posterior segmental
artery from the superior mesenteric
artery shows another tumor stain (arrow).
(F) Selective left hepatic arteriogram shows
the aberrant left hepatic artery supplying
hepatic segment 2 and 4 and tumor stain
in segment 4 (white arrow). All of the side
branches (arrowheads) before reaching the
umbilical point are gastric or esophageal
branches. Note the hepatic falciform artery
arising from the segment 4 hepatic artery
(black arrows).
running through the portocaval space include the RHA from
the CHA, the RHA and CHA from the celiac trunk, the RHA
and PHA and CHA from the SMA, and RHA from theaorta.
Aberrant origin of subsegmental or segmental hepatic arteries may not be easily recognized on celiac arteriography. Careful
interpretation of dynamic CT, tracing of individual segmental
hepatic arteries on celiac arteriography, adequate opacication
of the LGA on celiac angiography, and routine SMA arteriography can avoid missing them. Most of these variant hepatic
arteries can be accurately predicted with thin-section helical
dynamic CT (Figure12.10 and Figure12.11).
ere are also hepatic artery variations within the CHA in
about 10% of patients. Multiple hepatic arteries arise from the
CHA as separate trunks, as trifurcation, two or three hepatic
arterial trunks sequentially o the CHA, or aberrant origin
of the RHA, or LHA from the GDA or pancreaticoduodenal
artery(PDA).
All of these hepatic artery variations can coexist with celiac
trunk variations.
Intrahepatic variations in branching segmental hepatic arteries
ere are also diverse variations in intrahepatic branching of
segmental hepatic arteries. e RHA is one of the most constant vessels of the liver. e right hepatic lobe can be partly
supplied by an accessory RHA from SMA or celiac trunk in
fewer than 5% of the population.
arises from the LHA (Figure12.12). e anterior and posterior
section of the right hepatic lobe is commonly supplied by multiple arteries.
e le hepatic lobe is supplied by the one LHA (from the
PHA or LGA) only in less than half of the population.
aberrant LHA from the LGA can supply the whole le hepatic
11,12
Rarely, a segmental RHA
11,13
e
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conventional concept of the posterosuperior–anteroinferior
relationship of segments 2 and 3, the average orientation of
the intersegmental plane between segments 2 and 3 is slightly
slanted anteriorly from the vertical plane (Figure12.14).16 e
scissurae may curve, undulate, or even interdigitate within the
liver.15 Radiological determination of the segmental and subsegmental portal venous anatomy can be done by evaluation of
the overlapping transverse slices in an interactive cine mode or
by performing three-dimensional rendering.
15
Non-hepatic arteries arising from hepatic arteries
Figure 12.12 Intrahepatic variation. The right posterior segmental artery
(arrowheads) arises from the proper hepatic artery as the first branch with the
segment 3 hepatic artery (arrow).
lobe, segments 2 and 3 and a part of segment 4, segments 2 and
3, segments 2 and 4, or segment 2 alone. Segment 4 was usually
supplied by two or three hepatic arteries. Le medial arterial
branches arise from the LHA on the umbilical portion of the
portal vein, arise from the LHA before reaching the umbilical
portion of the portal vein, or arise from theRHA.
e caudate lobe is usually supplied by multiple arteries.2
According to our experience, almost all caudate arteries arise
from the proximal segment of hepatic arteries, including the
PHA, the ascending part of the main LHA or middle hepatic
artery, the main RHA and the proximal segment of the right
anterior and posterior segmental artery (Figure 12.13). e
caudate lobe is divided into three subsegments of the Spiegel
lobe, paracaval portion and caudate process. e paracaval portion and caudate process almost always are supplied by feeders
from the main RHA or the proximal segment of its branches.
In contrast, the hepatic artery supplying the Spiegel lobe is
evenly distributed to the proximal segment of hepatic arteries. Because the caudate lobe is supplied by multiple feeders
from the RHA and LHA, wedged injection of a caudate hepatic
artery frequently demonstrates anastomotic channels between
multiple feeders and between the RHA andLHA.
Segmental localization of livertumors
Accurate segmental localization is important for eective segmental transcatheter management of hepatic tumors.
Inaccurate segmentation in CT interpretation can lead to prolonged procedure time and erroneous treatment of innocent
hepatic segment. e conventional method dividing hepatic
segments according to Couinaud’s classication is based on the
concept of three vertical planes that divide the liver into four
segments and a transverse scissura that further subdivides the
segments into two subsegments each.14 Although convenient for
daily radiologic practice, clinical and extraclinical studies have
demonstrated that the shape and localization of the hepatic segments based on this conventional method do not always match
real situations.15 As an example, segment 8 extends posterior
to the right hepatic vein. In addition, in contrast to the vague
A non-hepatic artery is dened as an artery that arises from
the PHA or its distal branches and supplies organs and areas
other than hepatic parenchyma. Non-hepatic arteries include
the cystic artery, RGA, hepatic falciform artery (HFA), accessory LGA, PDA, and le IPA, in descending order of frequency. Some of these non-hepatic arteries can be detected
only on superselective angiography with the use of a microcatheter, especially HFAs and small accessory LGA and RGA.
erefore, to identify these arteries, careful analysis of celiac
axis arteriograms and superselective angiograms is required.
According to a recent investigation using a microcatheter and
superselective angiography,17 the most frequent site of origin
of non-hepatic arteries except the cystic artery was the LHA.
More than two-thirds of patients had one or more non-hepatic
arteries from the LHA and one-third of patients had gastric
arteries from the LHA. In contrast, only 3% of the non-hepatic
arteries except the cystic artery arose from the RHA. More than
40% of patients had multiple non-hepatic arteries.
Inadvertent infusion of therapeutic materials at a hepatic
artery proximal to the origin of a non-hepatic artery may
unavoidably induce diverse complications aer transcatheter
liver-directed therapies. ey include cholecystitis or gallbladder infarction, gastroduodenal mucosal lesions, pulmonary
oil embolism, and supraumbilical skin rash. erefore, the
preprocedural identication of non-hepatic arteries arising
from the hepatic arteries is important to reduce complications
related to various transcatheter therapies such as chemoembolization, intra-arterial infusion chemotherapy, and yttrium-90
radioembolization. Advances in microcatheters and digital
subtraction angiography systems enable identication of small
tumor-feeding vessels and permit selective insertion of microcatheters into small segmental or subsegmental arteries distal
to the non-hepatic arteries. is superselective procedure can
reduce not only hepatic parenchymal injury but also unintentional infusion of chemoembolic agent into the non-hepatic
arteries.
If superselective catheterization of tumor-feeding arteries is not possible, it is essential to use appropriate preventive
measures:embolization of a non-hepatic artery with adequate
embolic materials before the therapeutic infusion or infusion through an occlusion balloon catheter to redirect blood
ow in non-hepatic arteries toward the liver. Flow to the
non-target organ is maintained by distal collateral vessels. If the
non-hepatic artery acts as the tumor-feeding vessel, it should
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AB
CD
EF
Figure 12.13 Blood supply and territory
of the caudate lobe. (A) Arterial-phase
computed tomography (CT) scan shows
nodular enhancing tumor (arrow) at
the Spiegel lobe of the caudate lobe.
(B) Common hepatic arteriogram shows an
ill-defined tumor stain (arrows). (C) Delayed
parenchymal phase image shows the typical
outline of the caudate lobe (arrows) on
anteroposterior projection. (D) Selective
right hepatic arteriogram shows a feeding
artery from the proximal segment of
the right anterior segmental artery
(arrows). Iodized-oil CT scan was obtained
immediately after segmental Lipiodol
chemoembolization. (E) Iodized-oil CT scan
at the level of the middle hepatic vein (black
arrow) shows the cross-sectional anatomical
location of the paracaval portion (white
arrows). (F) Iodized-oil CT scan at the level
of the tumor (black arrow with compact
iodized oil uptake) shows the territory of the
caudate lobe. The caudate hepatic artery
supplies a far posterior aspect of the hepatic
segment 4 (white arrow). (G) Iodized-oil CT
scan at the level of the central bile duct (the
bifurcation area). There is iodized oil uptake
in the wall of the bile duct (arrows), which
implies the caudate hepatic artery can
supply the bile duct or anastomose with
a bile duct artery.
G
be treated superselectively by advancing a microcatheter to
a tumor feeder from the non-hepatic artery. If superselective
catheterization is not possible, other alternative therapeutic
methods, including surgery, ablation therapy, and injection
therapy, should be considered.
with the LGA. Occasionally, the RGA is larger than the LGA
or too small to identify on celiac or common hepatic arteriography as the RGA. In cases of aberrant anatomy and small
RGA, the LGA may be used to identify the origin of the RGA.
When cannulation of the RGA is dicult as a result of tortuosity or orientation of the origin, retrograde catheterization
Right gastricartery
e RGA usually arises from the hepatic artery, descends to the
pyloric end of the stomach, and passes from right to le along
the lesser curvature, supplying it with branches, and anastomosing with the LGA (Figure12.15).1 Usually, the RGA is the
minor contributor to the gastric perfusion when compared
through the anastomotic arcade between the LGA and RGA
can be a good alternative and has proved to be eective for
RGA embolization.
18
Regardless of the presence or absence of anatomic variations, the most common origin site of the RGA is the PHA
(40–59%), followed by the LHA (17–45%) (Figure 12.1). In
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A B
Figure 12.14 Segmental localization of
a tumor in the left lateral segment of the
liver. (A) Small nodular enhancing tumor
(arrow) is located at the posterior aspect
of the left lateral segment below the
level of the left portal vein. (B) On celiac
arteriography, the tumor (arrows) overlaps
with the segment 3 hepatic artery.
(C) Selective angiogram of the segment 3
hepatic artery shows no tumor stain. Note
the hepatic falciform artery arising from
the segment 3 hepatic artery (arrows).
(D) Segment 2 hepatic arteriogram shows
nodular tumor stain (arrows). Lipiodol
chemoembolization was performed
DC
exclusively at the segment 2 hepatic
artery. (E) Sagittal reformatted image of
the immediate iodized-oil computed
tomography demonstrates the orientation
of the intersegmental plane between
segments 2 and 3 (arrows), which is
slanted posteriorly at the superior aspect
and undulating in its contour.
E
AB
Figure 12.15 Recognition of gastric arteries.
(A) Celiac arteriogram shows trifurcation
of the common hepatic artery into the left
hepatic artery, right hepatic artery, and
gastroduodenal artery. The right gastric
artery arises from the trifurcation of the
common hepatic artery and anastomoses
with the left gastric artery (black arrows). The
artery indicated by white arrows arises from
the ascending segment of the left hepatic
artery before reaching the umbilical point,
which strongly suggests the possibility of the
about three-fourths of patients, the RGA arises from the PHA
or its distal branches. In the remaining patients, the RGA arises
from the bifurcation point of the CHA or GDA (Figure12.15).
e RGA rarely arises from the CHA or RHA.
2,17
Identication of the RGA is crucial for transcatheter management of hepatic tumors, as gastroduodenal necrosis, ulceration, and perforation have all been identied as complications
of inadvertent delivery of chemotherapeutic agent.18 In hepatic
arterial infusion chemotherapy, successful embolization of
the RGA was accomplished in more than 90% of patients and
sucient embolization of the RGA signicantly reduced the
incidence of endoscopically conrmed acute mucosal lesions.
Depending on the regional therapy being considered, the need
for prophylactic embolization of the gastric variants must be
taken into account.
Accessory left gastricartery
e accessory LGA runs from the liver to the stomach and
supplies the esophagus and the cardia and fundus of the stom-
2,19
ach.
In 1928, Adachi reported that accessory LGA was seen
accessory left gastric artery. (B) On selective
angiography, it supplies the distal esophagus
and the cardia of the stomach.
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