Update on Portal Vein Embolization: Evidence-based
Outcomes, Controversies, and Novel Strategies
Benjamin J. May, MD, Adam D. Talenfeld, MD, and David C. Madoff, MD
Portal vein embolization (PVE) is an established therapy used to redirect portal blood flow away from the tumor-bearing liver to the
anticipated future liver remnant (FLR) and usually results in FLR hypertrophy. PVE is indicated when the FLR is considered too
small before surgery to support essential function after surgery. When appropriately applied, PVE reduces postoperative morbidity
and increases the number of patients eligible for curative hepatic resection. PVE also has been combined with other therapies to
improve patient outcomes. This article assesses more recent outcomes data regarding PVE, reviews the existing controversies, and
reports on novel strategies currently being investigated.
BSA = body surface area, FLR = future liver remnant, HCC = hepatocellular carcinoma, HVE = hepatic vein embolization, PVE =
portal vein embolization, PVL = portal vein ligation, TAE = transarterial embolization, TELV = total estimated liver volume
Rates of primary liver cancer have continued to increase
dramatically over the past decade in the United States, and
the liver remains a common site of metastases (1). Surgical
resection of primary tumors and metastases confined to the
liver is the mainstay of curative therapy. Owing to the
liver’s unique ability to regenerate, most of the organ can
be resected if indicated. However, major hepatic resection
places patients at risk for developing complications related
to liver insufficiency, particularly in the perioperative
period, before the liver has had time to regenerate.
Although causes of postoperative liver insufficiency are
multifactorial, the anticipated volume of liver that remains
after surgery, termed the future liver remnant (FLR), has
been shown to be a strong independent predictor of
postoperative complications (2,3).
Portal vein embolization (PVE) is an established image-
guided procedure that has been adopted worldwide (4).
Embolization of portal branches feeding tumor-bearing
segments leads to concomitant atrophy of these segments
and hypertrophy of the FLR (5). This procedure has been
shown to reduce postoperative complications and increase
the number of patients able to undergo surgery with
curative intent (6,7). Since the last review published in
this journal (8), additional experience and outcomes data
have further delineated the role of PVE. In addition, PVE
has been combined with other therapies to improve
hypertrophy and expand the treatment options available
to patients. This article reviews the most recent data
regarding PVE and presents novel combination therapies
currently being investigated.
PATHOPHYSIOLOGY AND MECHANISM
considerations of PVE have been previously described
(8,9). However, it is worthwhile to review the key
concepts because they provide a basis for more recent
After hepatic injury or partial resection, changes in both
hemodynamics and metabolic pathways stimulate regen-
eration of noninjured segments, with the portal vein
playing a central role in transporting trophic factors (10–
12). Regeneration on a cellular level begins within hours,
and most patients achieve adequate regeneration within a
few weeks (13,14). However, patients with underlying liver
damage, particularly cirrhosis, can demonstrate attenuated
rates and degrees of hypertrophy (15). Regeneration after
PVE typically occurs at a slower rate compared with
hepatectomy (ie, greater stimulus for FLR growth when
pathophysiology,rationale,and basic technical
& SIR, 2013
J Vasc Interv Radiol 2013; 24:241–254
None of the authors have identified a conflict of interest.
From the Department of Radiology, Division of Interventional Radiology, New
York–Presbyterian Hospital/Weill Cornell Medical Center, 525 East 68th
Street, P-518, New York, NY 10065. Received August 9, 2012; final revision
received October 8, 2012; accepted October 9, 2012. Address correspon-
dence to D.C.M.; E-mail: email@example.com
liver parenchyma is removed rather than subjected to
embolization) (Fig 1). In contrast to the postembolization
syndrome common with transarterial therapy, which results
from necrosis, the apoptosis-mediated cell death resulting
from PVE is known to cause minimal pain and fever (16).
Makuuchi et al (17) were the first to describe the use of
PVE as a means of improving surgical outcomes by
preventing perioperative liver insufficiency. Subsequent
studies have shown that increased FLR volume is
associated with improved biliary excretion, albumin
uptake, and postoperative liver function (18–20).
PVE has traditionally been performed via one of three
approaches, termed transileocolic, contralateral, and ipsi-
lateral approaches. The oldest, the transileocolic approach,
is a surgical procedure performed in the operating room
under general anesthesia. After performing a right lower
quadrant incision, a major ileocolic venous branch is
accessed via direct puncture allowing for catheter manip-
ulation to the portal vein. This approach has the advantage
of avoiding puncture through the liver. However, this
surgical procedure has generally been replaced by the less
invasive percutaneous contralateral and ipsilateral techni-
ques, which are performed using ultrasound-guided trans-
hepatic puncture. The contralateral approach accesses
the portal system via the FLR. This technique allows
for easier catheter manipulation to the tumor-bearing
liver because of fewer acute angles between access and
target portal branches. However, the contralateral approach
risks damage to the FLR during access and catheter
The ipsilateral approach involves percutaneous access
through the tumor-bearing liver, avoiding potential damage
to the FLR during instrumentation. The acute angles
necessary for embolization of adjacent liver segments can
be overcome using reverse curve catheters. Care must be
taken to avoid access through tumor to prevent peritoneal
seeding. If a safe route is not visualized, the contralateral
approach remains a reasonable alternative.
EVALUATION OF PATIENTS
CONSIDERED FOR HEPATECTOMY
PVE is indicated when the FLR is either too small or
borderline in size to support essential hepatic function. How-
ever, the absolute size of the FLR does not accurately predict
which patients are at risk for liver insufficiency because larger
patients require larger volumes of liver to support function. A
standardized FLR, expressed as a percentage of FLR in relation
to total functioning liver volume, allows for a more accurate
assessment of FLR and comparison of outcomes data between
patients of varying sizes (2).
To calculate the standardized FLR, volumes of the FLR
and total functioning liver volume must be obtained.
Typically, FLR volume is measured directly using cross-
sectional volumetric software. Computed tomography
(CT) volumetry can also be used to measure total liver;
however, this requires exclusion of tumor volume from the
overall liver volume. Measuring tumor volume can be
tedious and imprecise, particularly when tumor burden is
Alternatively, the total estimated liver volume (TELV) can
be calculated based on the close relationship between body
surface area (BSA) and liver volume. Vauthey et al (21)
derived the following formula for estimating liver volume by
analyzing liver size and BSA in 292 Western adults.
TELV ¼ ?794.41 þ 1,267.28 (BSA)
A third method of calculating standardized FLR uses
body weight, rather than BSA, to determine the TELV.
Although multiple similar formulas exist in the literature, a
meta-analysis published in 2005 determined the Vauthey
formula to be least biased and most accurate for adults
(22). Although Chun et al (23) later found the body weight
method to be equally as predictive as BSA, a more recent
study comparing direct volumetric liver measurement and
estimated liver volume based on BSA found the TELV
method to be superior (P o .005) (24).
interquartile ranges) degree of hypertrophy after PVE. The shaded zone (days 22–56 after PVE) identifies the ‘‘plateau’’ period during
which the degree of hypertrophy did not change significantly between measurement points. (Used with permission from Ribero D,
Abdalla EK, Madoff DC, Donadon M, Loyer EM, Vauthey J-N. Portal vein embolization before major hepatectomy and its effects on
regeneration, resectability and outcome. Br J Surg 2007; 94:1386–1394.)
Degree of hypertrophy of the standardized FLR over time after PVE with kinetics of FLR growth, plotted as median (with
May et al ’ JVIR
242 ’ Update on Portal Vein Embolization
Multiple factors are considered when deciding which patients
would benefit from PVE, including baseline liver function,
standardized FLR, and complexity of the planned surgery. In
recent years, substantial outcomes data have been reported
allowing for better defined indications for PVE. In patients
with normal liver function, a standardized FLR of 10% can
support essential hepatic function; however, standardized
FLR o 20% is associated with increased postoperative
complications (25). Kishi et al (7) published a series of 301
hepatectomy. They found that patients with a preoperative
standardized FLR o 20% had significantly higher rates of
postoperative liver insufficiency and death from liver failure
compared with patients with standardized FLR Z 20%
(P o .05) (Fig 2a and b). In addition, patients who
underwentPVE before surgery
standardized FLR from o 20% to 4 20% had statistically
equivalent rates of liver insufficiency as patients with 4 20%
at baseline. Ribero et al (3) found that both standardized
FLR o 20% and degree of standardized FLR hypertrophy
after PVE o 5% predicted outcome after resection (Fig 3).
Based on these results and other supporting publications
(25,26), a Consensus Conference on the Multidisciplinary
Treatment of Hepatocellular Cancer in 2010 recommended
PVE for standardized FLR o 20% in patients with preserved
liver function (27).
Higher standardized FLR cutoffs are considered for
patients with additional risk factors such as hepatic steatosis,
hepatotoxic chemotherapy exposure, and compensated
to increase their
from Kishi Y, Abdalla EK, Chun YS, et al. Three hundred and one consecutive extended right hepatectomies: evaluation of outcome
based on systematic liver volumetry. Ann Surg 2009; 250:540–548.) (Available in color online at www.jvir.org.)
Rates of (a) hepatic insufficiency and (b) death by preoperative standardized FLR (sFLR) volume. (Adapted with permission
(sFLR) volume and degree of hypertrophy. (Used with permis-
sion from Ribero D, Abdalla EK, Madoff DC, Donadon M, Loyer
EM, Vauthey J-N. Portal vein embolization before major hepa-
tectomy and its effects on regeneration, resectability and out-
come. Br J Surg 2007; 94:1386–1394.)
Presence of hepatic dysfunction by standardized FLR
Volume 24 ’ Number 2 ’ February ’ 2013243
cirrhosis. Multiple studies have shown an increased risk of
postoperative complications in patients with hepatic stea-
tosis (28–30). In a meta-analysis of four studies involving
1,000 patients, de Meijer et al (31) found that patients
with 4 30% steatosis had significantly higher risk of
compared with patients without steatosis (relative risk
and 95% confidence interval 2.01 and 1.66–2.44 vs 2.79
and 1.19–6.51). Similarly, patients who have been exposed
to hepatotoxic chemotherapy have been shown to be at
increased risk for postoperative complications. Pawlik et al
(32) reviewed the outcomes of 212 patients who underwent
resection for colorectal metastases; 173 of the patients
received preoperative chemotherapy.
associated with grade 3 sinusoidal dilation (P ¼ .017), and
irinotecan was associated with steatohepatitis. Vauthey et al
(33) found the same associations of oxaliplatin with
sinusoidaldilation(P o .001)
associated with an increased 90-day mortality (P ¼ .001).
Based on these results, many authors consider PVE when
standardized FLR is o 30% in patients with either hepatic
steatosis or significant exposure to hepatotoxic chemotherapy.
Cirrhosis is another risk factor that is given serious
consideration before hepatic resection. Patients with
advanced cirrhosis are not considered for hepatic resection.
For patients with well-compensated cirrhosis (ie, Child-
Pugh class A) who are considered for resection, a standar-
dized FLR 4 40% is recommended. This recommendation
is supported by a prospective alternative allocation trial in
which 28 patients with chronic liver disease were allocated
to PVE or no PVE before resection (34). The mean
standardized FLR size in the PVE group was 35%. The
PVE group had a significantly lower incidence of
pulmonary complications, ascites, and liver failure.
Although the above-discussed recommendations are
useful when considering patients for PVE, additional
factors such as patient age, comorbidities, and complexity
of planned surgery are also considered. Until additional
evidence-based criteria are defined further, the decision to
perform PVE is made on a case-by-case basis. Optimally,
an interdisciplinary team should be involved in deciding
when PVE is appropriate.
Complications of PVE are similar to other image-guided
transhepatic procedures. Complications include subscapu-
lar hematoma, bile duct damage, hemoperitoneum, and
include nontarget embolization, recanalization of segments
that received embolization, and complete portal vein
thrombosis. In 2010, the Society of Interventional Radi-
ology established quality improvement guidelines for
transcatheter embolization, including a suggested threshold
for PVE-related major complications of 6% and threshold
for PVE-related morbidity of 11% (35).
Most published complication rates are well below this
range. A meta-analysis published in 2008 pooled data from
37 studies from 1990–2005 involving 1,088 patients (36).
Percutaneous PVE was performed in most cases (72%), with
Table 1. Complication Rates for Portal Vein Embolization Reviewed in Literature
Number of Patients;
Complication Rate Complication TypeNumber
Kodama et al (2002) (38) 47 patients; 7 (15%)
Portal vein thrombus
Migration of embolic material to FLR
Transient liver failure
Occlusion of portal vein
Rupture of gallbladder metastasis
Left or main portal vein thrombus
Di Stefano et al (2005)
188 patients; 24 (12.8%)
Abulkhir et al (2008) (36)Meta-analysis of 37 studies
involving 1,088 patients;
reported morbidity 2.2%
FLR ¼ future liver remnant.
May et al ’ JVIR
244 ’ Update on Portal Vein Embolization
the transileocolic technique used in the remaining cases. The
overall pooled morbidity was 2.2% with 0% procedure-
related mortality. Di Stefano et al (37) reviewed the records
of 188 patients who underwent PVE via the contralateral
approach resulting in 24 (12.8%) adverse events without
mortality. Transient liver failure occurred at a significantly
higher rate in patients with cirrhosis (5 of 30; P o .001).
Kodama et al (38) reviewed 47 percutaneous PVE procedures
in 46 patients (11 via contralateral approach). Complications
occurred more frequently in the punctured lobe leading the
authors to recommend the ipsilateral approach. The specific
complications reported in these studies are listed in Table 1.
PVE TECHNIQUE MODIFICATIONS AND
Sequential Arterial and Portal
Transcatheter arterial chemoembolization is an established
therapy used to provide locoregional control of unresect-
able hepatocellular carcinoma (HCC) and as a bridge to
transplant (39). In addition, this therapy has been applied
in sequence with PVE before hepatectomy for HCC
(Fig 4a–g ). There are several theoretical benefits to this
combined approach. HCC typically arises in a background
of advanced liver disease presenting challenges for resec-
tion. Because of increased postoperative complication
rates, patients with cirrhosis require a relatively robust
FLR to be considered amenable to resection; if standar-
dized FLR is o 40%, PVE is indicated. Additionally, as
previously discussed, cirrhotic livers often demonstrate
decreased propensity to regenerate and require prolonged
time intervals to achieve satisfactory hypertrophy. Trans-
catheter arterial chemoembolization performed before PVE
results in a greater inflammatory response, which is known
to contribute to liver regeneration (40). In addition, HCC
preferentially derives its blood supply from the hepatic
artery. After PVE, there is a compensatory increase in
hepatic artery flow, termed the hepatic artery buffer
response, which can lead to accelerated tumor growth
(41). Locoregional control offered by transcatheter arterial
chemoembolization may prevent progression of disease
during the interval between PVE and resection. Finally,
HCC is associated with the development of arterioportal
shunts, which can mitigate the effects of PVE (32).
Embolization of these arterioportal shunts is performed
during transcatheter arterial chemoembolization.
Aoki et al (42) published a retrospective review of 17
patients who underwent sequential transcatheter arterial
chemoembolization and PVE, 16 of whom subsequently
underwent resection. PVE was performed a median of 9
days after transcatheter arterial chemoembolization (range,
4–44 days). Transient increases in liver enzyme and
bilirubin levels returned to baseline after several days
following both transcatheter arterial chemoembolization
and PVE. There was no procedural mortality and a 25%
minor complication rate. The standardized FLR increased
significantly after PVE to a median of 51% (range, 39%–
68%; P o .01). One patient did not undergo resection
because of an increase of the percent of indocyanine green
retained by the liver at 15 minutes from 17% to 28%. The
5-year overall survival after curative intent resection was
55.6%, and 5-year disease-free survival after resection was
In 2006, Ogata et al (43) published a retrospective
analysis of 36 patients with HCC and cirrhosis who
underwent resection after PVE; 18 of the patients had
transcatheter arterial chemoembolization 3 weeks before
PVE. The transcatheter arterial chemoembolization plus
PVE group demonstrated a greater mean increase in FLR
volume compared with the PVE alone group (12.5% vs
8.4%; P ¼ .022). The transcatheter arterial chemo-
embolization plus PVE group also demonstrated an
increased incidence of complete tumor necrosis (15 of 18
vs 1 of 18; P o .001) and a higher 5-year disease-free
survival (37% vs 19%; P ¼ .041).
More recently, Yoo et al (44) reported their results of
135 patientswith HCC;
transcatheter arterial chemoembolization plus PVE, and
64 underwent PVE only before right hepatectomy. PVE
was performed an average of 1.2 months after transcatheter
arterial chemoembolization. Liver function tests transiently
worsened before returning to baseline in most patients;
however, one patient (1 of 71; 1.4%) developed persistently
elevated transaminase levels and did not undergo resection.
The remaining patients had successful resections. Compared
with the PVE only group, the transcatheter arterial
chemoembolization plus PVE group demonstrated a higher
mean increase in FLR (7.3% vs 5.8%; P ¼ .035) and
improved overall (P ¼ .028) and recurrence-free (P ¼
.001) survival (comparison using the log-rank test). The 1-
year, 3-year, 5-year, and 10-year cumulative survival rates for
the transcatheter arterial chemoembolization plus PVE group
were 97%, 83%, 72%, and 58% compared with 89%, 73%,
56%, and 31% for the PVE only group. The 1-year, 3-year, 5-
year, and 10-year recurrence-free survival rates for the
transcatheter arterial chemoembolization plus PVE group
were 83%, 70%, 61%, and 56% compared with 62%, 51%,
38%, and 24% for the PVE only group. The authors
concluded that sequential transcatheter arterial chemoembo-
lization and PVE is a safe and effective therapy for increasing
the rate of hypertrophy of the FLR and is associated with
longer recurrence-free survival.
Combination Therapy after Inadequate
Although PVE typically leads to reliable rates of hyper-
trophy, liver regeneration can be variable, especially when
comorbidities such as underlying hepatic dysfunction or
diabetes are present. When FLR hypertrophy is inadequate
after PVE, adjunct therapies such as arterial embolization
or hepatic vein embolization (HVE) can be performed.
Volume 24 ’ Number 2 ’ February ’ 2013245
coils in a 56-year-old man with a history of human immunodeficiency virus, hepatitis C, and HCC. (a) Contrast-enhanced axial CT
image shows a large mass in the right hepatic lobe (arrows). (b) Contrast-enhanced axial CT image shows marginal FLR (FLR/TELV ¼
30%) (arrows). (c) Anteroposterior subtracted angiographic image from the celiac axis shows a large hypervascular mass (arrows). (d)
Arteriography performed immediately after bland embolization with 40-mm microspheres shows complete stasis of the tumor
vascularity. (e) Anteroposterior flush portogram obtained 4 weeks later shows a 6-F vascular sheath in a right portal vein branch and a
5-F flush catheter within the main portal vein. (f) Final portal venogram shows occlusion of the portal vein branches to segments 5–8
(arrowheads) with continued patency of the veins supplying the left liver (arrows). (g) Contrast-enhanced CT image obtained 1 month
after right PVE shows substantial atrophy of the right liver, complete necrosis of the tumor, and FLR hypertrophy (FLR/TELV ¼ 54%).
The FLR is depicted by the arrows. The degree of hypertrophy is 24%. The patient successfully underwent a right hepatectomy.
Combined transcatheter arterial hepatic embolization and transhepatic ipsilateral right PVE using tris-acryl particles and
May et al ’ JVIR
246 ’ Update on Portal Vein Embolization
Transarterial embolization (TAE), or bland embolization,
has been used in the setting of inadequate FLR hypertrophy
following PVE. This therapy adds a component of inflam-
mation and necrosis, both of which are known to stimulate
liver hypertrophy. Arterial embolization alone has been
shown to induce hypertrophy of the FLR, although to a
lesser degree compared with PVE (45).
In 2000, Nagino et al (46) first described the use
of TAE to improve FLR volume in two patients with
hypertrophy after PVE. In both patients, PVE in the
setting of underlying liver disease led to negligible
hypertrophy of the FLR at 58 days (patient 1) and 14
days (patient 2). TAE with ethanol was performed on 50%
of the liver intended to be resected. The FLR volume
increased from 470 mL to 685 mL (46%) 2 weeks after
TAE (patient 1) and from 649 mL to 789 mL (22%) 3
weeks after TAE (patient 2). Both patients experienced
postembolization syndrome with fever and abdominal pain.
TAE after PVE was complicated by prolonged abnormal
liver function tests (patient 1), which returned to baseline
after 2 weeks, and liver abscess (patient 2), which required
necrosis in the segments targeted by TAE.
In 2006, Gruttadauria et al (47) reported on the use of
TAE to improve FLR hypertrophy after PVE for colorectal
metastasis. In this report, TAE was performed with
microparticles and absorbable gelatin sponge (Gelfoam)
(patient 1) and microparticles and coils (patient 2) after
FLR hypertrophy was deemed inadequate 6 weeks
following PVE. In patient 1, FLR increased from 379
cm3to 505 cm3after PVE, with subsequent increase to 916
cm33 weeks after TAE. In patient 2, FLR increased from
302 cm3to 344 cm3after PVE, with a subsequent increase
to 521 cm33 weeks after TAE. Complications were not
reported. TAE resulted in improved hypertrophy allowing
for subsequent hepatic resection.
Selective HVE has also been used to provide additional
stimulus for regeneration when FLR hypertrophy is inade-
quate.Hwanget al (48)
trial postulating that occlusion of the hepatic veins draining
the tumor-bearing liver could lead to increased hypertrophy of
the FLR. Patients were included for selective HVE if FLR
hypertrophy was deemed inadequate by volumetric CT
analysis 2 weeks after PVE. Coil embolization of the right
hepatic vein was performed with either an inferior vena cava
filter or vascular plug placed proximally to prevent coil
migration. Of the 12 patients who were treated with HVE,
two patients failed to demonstrate adequate FLR hypertrophy
for resection. One patient had inadvertent embolization of the
hepatic vein draining the FLR and ultimately did not undergo
Two-stage Hepatectomy and PVE
Surgical resection of colorectal liver metastasis is asso-
ciated with long-term survival and is potentially curative
when complete resection is feasible. However, only 20%–
30% of patients are considered resectable, most often
because of bilobar pattern of disease. Two-stage hepatect-
omy, using hypertrophy of PVE, has been developed to
increase the number of patients with bilobar colorectal liver
metastasis amenable to resection (49). During the first stage
of treatment, tumor within the projected FLR is resected or
in some cases ablated. When the FLR is cleared of tumor,
PVE can be performed to increase the FLR volume. PVE is
typically performed between hepatic resections to improve
FLR volume, particularly because these patients have
usually been exposed to hepatotoxic neoadjuvant chemo-
therapy. In some cases, surgical portal vein ligation (PVL)
during the first-stage surgery is performed rather than PVE;
however, this practice is controversial, as discussed later.
When adequate FLR hypertrophy is achieved, the second-
stage hepatectomy targets the remainder of liver metas-
tases, typically requiring a right or extended right
Narita et al (50) reported on the outcome of 80 patients
with colorectal liver metastasis scheduled for two-stage
hepatectomy; 61 patients completed second-stage resec-
tion. The main reason for not completing the second-stage
surgery was tumor progression (16 of 80; 20%). Of the 61
patients who completed therapy, all but 3 incorporated
PVE (n ¼ 55) or surgical PVL (n ¼ 3). For patients
completing two-stage hepatectomy, 5-year overall survival
was 32%, and overall median survival was 39.6 months.
Brouquet et al (51) reported on the outcome of 65
patients with colorectal metastases who underwent first-
stage hepatectomy; 47 completed the second-stage resec-
tion. This study also compared these outcomes with
nonsurgical patients with disease confined to the liver
who also demonstrated an objective response to systemic
chemotherapy. This analysis was intended to eliminate
potential selection bias because two-stage resection was
offered only to patients who showed a response to modern
chemotherapeutic regimens. The overall 5-year survival
rate of the surgical group was 51% compared with 15% for
the medical group (P ¼ .005). For the 47 patients who
completed the second-stage resection, 5-year survival was
improved to 64%. Most of two-stage hepatectomy proce-
dures included PVE. The authors concluded that although
the surgical group benefited from improvements in sys-
temic chemotherapy, resection conferred a clear additional
Combined Right and Segment 4 PVE
Before extended right hepatectomy, some authors have
argued for extending right PVE to include segment 4 as a
means of improving hypertrophy of segments 2 and 3
(Fig 5a–f) (46). However, catheter manipulation into
demanding, and inadvertent reflux of embolic material to
4 ismore technically
Volume 24 ’ Number 2 ’ February ’ 2013247
the FLR has been reported (52,53). Capussotti et al (52)
evaluated 26 patients who underwent right PVE (n ¼ 13)
and combined right and segment 4 PVE (n ¼ 13). The
authors found no difference in the volume increase (P ¼
.20) or rate of increase (P ¼ .40) of segments 2 and 3 for
right PVE and combined right and segment 4 PVE leading
them to recommend against extended
However, more recent studies comparing right PVE and
combined right and segment 4 PVE have reported
improved hypertrophy of segments 2 and 3 when
embolization of segment 4 is also performed (54) without
increased incidence of complications (3,54). Kishi et al
(54) compared 15 patients who underwent right PVE with
58 patients who underwent combined right and segment 4
PVE. Compared with right PVE alone, the combined right
and segment 4 PVE group demonstrated a greater absolute
increase in volume in segments 2 and 3 (median, 106 mL
vs 141 mL; P ¼ .044) and a higher hypertrophy rate for
segments 2 and 3 (median, 26% vs 54%; P ¼ .021). The
complication rates were similar for right PVE and
combined right and segment 4 PVE groups (7% vs 10%;
P 4 .99), and no PVE complication precluded resection. It
has been suggested that the disparate outcomes between
these studies may reflect a difference in technical
experience and sample size.
Adjuvant Chemotherapy after PVE
Progression of disease is a primary concern after PVE
because it may preclude curative intent surgery. More
woman with intrahepatic cholangiocarcinoma. (a) Contrast-enhanced CT image of the liver shows a mass (arrows) involving segments
1, 4, 7, and 8 and abutting the inferior vena cava. (b) CT image obtained before PVE shows marginal FLR (FLR/TELV ¼ 17%). The FLR is
depicted by the arrows. (c) Anteroposterior flush portogram shows a 6-F vascular sheath in a right portal vein branch (arrowheads)
and a 5-F flush catheter within the main portal vein (arrow). (d) Final portogram shows occlusion of the portal vein branches to
segments 4–8 with continued patency of the veins supplying the left lateral liver (arrows). Note coils in the segment 4 branches
(arrowheads). (e) CT image obtained 1 month after right PVE shows substantial FLR hypertrophy (FLR/TELV ¼ 29%). The FLR is
depicted by the arrows with newly seen convexity of the left lateral margin (arrowheads). The degree of hypertrophy is 12%. (f) CT
image obtained after uncomplicated extended right hepatectomy shows massive hypertrophy of the remnant liver.
Transhepatic ipsilateral right PVE extended to segment 4 using tris-acryl particles and coils performed in a 74-year-old
May et al ’ JVIR
248 ’ Update on Portal Vein Embolization
recent series on two-stage hepatectomy have reported a
20% dropout rate after first-stage resection because of
progression of disease (51,55). In addition, accelerated
tumor growth after PVE has been reported for both primary
and metastatic liver tumors (56–59). Neoadjuvant che-
motherapy can be administered in an attempt to provide
tumor control in the interim between PVE and resection;
however, concerns have been raised about its potentially
deleterious effect on liver hypertrophy and lack of efficacy
in preventing progression of disease.
The effects of systemic neoadjuvant chemotherapy on
liver hypertrophy after PVE have been addressed by
hypertrophy after PVE in patients with colorectal liver
metastases who underwent PVE either with concomitant
neoadjuvant chemotherapy (n ¼ 43) or without chemo-
therapy (n ¼ 22) before resection. At 4 weeks, the
chemotherapy group, which included 26 patients treated
in part with the vascular endothelial growth factor receptor
blocker bevacizumab, demonstrated
hypertrophy compared with the no chemotherapy group.
Similarly, Covey et al (61) reported on patients with
colorectal liver metastases who underwent PVE either with
neoadjuvant chemotherapy (n ¼ 47) or without chemo-
therapy (n ¼ 53). These groups showed no significant
difference in median contralateral liver growth after PVE.
However, a smaller series looking at patients with
colorectal metastasis found that patients treated with
neoadjuvant chemotherapy after PVE (n ¼ 10) had
significantly decreased FLR hypertrophy (median 89 mL
vs 135 mL; P ¼ .016) compared with patients who did not
receive chemotherapy after PVE (n ¼ 5) (62).
Chemotherapy has not been proven to prevent progres-
sion of disease between PVE and resection. A more recent
study examined the effect of chemotherapy on disease
progression between the first and second stages of a
two-stage hepatectomy (63). Of the initial 47 patients
who underwent first-stage resection, 25 patients (53.2%)
were treated with subsequent chemotherapy compared
with 22 (46.8%) patients who did not receive interval
chemotherapy. Portal vein occlusion was performed in
80.9% of patients (PVE in 27 and PVL in 11), but
the relative number of patients in each group treated with
PVE or PVL was not reported. Second-stage hepatectomy
was not completed in 11 patients (23.4%), all owing
to progression of disease. There was no statistically
significant difference in either the number of patients
with progression of disease or the dropout rates between
the groups treated or not treated with interval chemother-
apy (progression of disease, 12 vs 13; P ¼ .561 and
dropout, 16% vs 31.8%; P ¼ .303). Conclusions based
on these results are tempered by the fact that the decision
to treat with interval chemotherapy was made by a
disease management team with no randomization. The
authors concluded that chemotherapy after first-stage
PVL versus PVE
Intraoperative right PVL has been performed during the
initial stage of two-stage hepatectomy or other surgical
intervention as a means of inducing FLR hypertrophy
without necessitating an additional PVE procedure (64–
66). Comparative studies between PVE and PVL have
shown mixed results. Aussilhou et al (67) retrospectively
compared patients who underwent PVE (n ¼ 18) with
patients who underwent PVL during the first stage of a
two-stage hepatectomy (n ¼ 17). They found the increase
in left liver volume to be similar between the two groups
(35% ? 38 vs 28% ? 26; P ¼ .7) and no difference in
morbidity (58% for PVE vs 36% for PVL; P ¼ .6).
Similarly, Capussotti et al (68) retrospectively compared
patients with colorectal liver metastases who underwent
PVL (n ¼ 17) with patients who underwent PVE (n ¼ 31)
at their institution. These authors found similar volumetric
increases of segments 2 and 3 for PVE versus PVL
(53.4% vs 43.1%; P ¼ .39). However, the PVL group
had a significantly longer interval between occlusion and
CT evaluation compared with the PVE group (median, 40
days vs 29 days; range, 13–135 days vs 18–42 days;
P ¼ .01).
Other studies found inferior FLR hypertrophy after PVL
compared with PVE. Broering et al (69) compared PVL
(n ¼ 17) and PVE (n ¼ 17) before extended right
hepatectomy for both primary and metastatic disease.
Increase in left lateral liver volume was significantly
higher for the PVE group compared with the PVL group
(188 mL ? 81 vs 123 mL ? 58; P ¼ .012). In addition,
hospital stay was significantly shorter for PVE compared
with PVL (4 days ? 2.9 vs 8.1 days ? 5.1; P o .01).
More recently, Robles et al (70) compared left lobe
hypertrophy in patients undergoing two-stage hepatectomy
who had PVL (n ¼ 23) versus PVE (n ¼ 18). This group
found that PVE resulted in improved median percent
increase of the FLR compared with PVL (40% vs 30%;
P o .05). The inferior hypertrophy after PVL may be
explained by portal-portal shunts, which can lead to
recanalization of the ligated right portal vein (71).
Laparoscopic PVL, although a less morbid procedure
than open surgical PVL, has been associated with a 22%
rate of inadequate FLR hypertrophy (72).
In an attempt to improve on the technical aspects of PVE
(eg, better FLR hypertrophy rates, reduced complications),
many novel approaches have been developed including
transarterial, transsinusoidal, and reversible PVE as well as
the addition of stem cell infusion to the FLR after PVE.
These approaches are described in this section.
Madoff et al (73) described a technique in pigs of
transarterial PVE in which a 3:1 mixture of iodinated oil
Volume 24 ’ Number 2 ’ February ’ 2013 249
and absolute ethanol was infused slowly through a 3-F
microcatheter via lobar hepatic artery branches and
allowed to pass into the portal system via the peribiliary
plexus (Fig 6a–f ). The investigators performed the
procedure in five pigs and compared degree of hypertrophy
in five pigs receiving traditional percutaneous transhepatic
common trunk (straight arrow) supplies arteries to the left lobe and left middle lobe. The arteries supplying the right lobe (white
arrowheads) and the right middle lobe (black arrowheads) are seen. The common hepatic artery (HA), the gastroduodenal artery (GDA),
and the right gastric artery (curved arrow) are also shown. (b) Abdominal radiograph shows a 3-F microcatheter (arrow) within the targeted
arteries to the left lobe and left middle lobe early within the transarterial PVE procedure. (c) Abdominal radiograph obtained in a later phase
of the procedure shows ethiodized oil (Ethiodol)–ethanol mixture within the common arterial trunk (arrowhead) and the dense filling of the
mixture within the left lobe and left middle lobe territory (arrows). (d) Abdominal radiograph obtained at completion of the procedure
shows filling of many of the small portal branches (arrow). (e) Close-up image from (d) shows the Ethiodol-ethanol mixture within the small
portal branches (arrowheads). (f) Photograph taken immediately after liver explantation shows massive enlargement of the right (R) and
right middle (RM) lobes with severe atrophy of the left middle (LM) and left (L) lobes and part of the right middle lobe that received
embolization. The right and right middle lobes have rounded margins, whereas the left and left middle lobes have sharp margins. (Used
with permission from Madoff DC, Gupta S, Pillsbury EP, et al. Transarterial versus transhepatic portal vein embolization to induce selective
hepatic hypertrophy: a comparative study in swine. J Vasc Interv Radiol 2007; 18:79–93.) (Available in color online at www.jvir.org.)
Transarterial PVE procedure. (a) Hepatic anteroposterior arteriogram shows normal hepatic arterial anatomy in a pig. A
May et al ’ JVIR
250 ’ Update on Portal Vein Embolization
PVE. All procedures were technically successful. They
found pigs receiving transarterial PVE sustained FLR
hypertrophy increases that were nearly double FLR hyper-
trophy increases sustained by pigs receiving traditional
percutaneous PVE. There were no adverse clinical sequelae
in the experimental group, and liver function tests were at
or near baseline after several days in all animals.
included a better safety profile than traditional percuta-
neous transhepatic PVE, which requires direct hepatic
puncture. Reported disadvantages of transarterial PVE
included longer duration of transarterial PVE procedures
necessitated by slow embolic infusion and potential non-
target embolization by virtue of the relatively high inci-
dence of variant hepatic arterial and portal anatomy.
Finally, 4 19 mL of embolic infusion was required in all
transarterial PVE cases, whereas a maximum of 15–20 mL
of ethiodized oil has been reported as the upper limit
allowable to prevent overt pulmonary complications. The
investigators report a limitation of their study being that all
animals had normal livers, rather than cirrhotic livers
containing tumors. It is uncertain how these factors might
alter the flow and effect of the embolic mixture.
described bythe authors
Smits et al (74) described a technique in pigs of
transjugular or transfemoral retrograde PVE they termed
transsinusoidal PVE in which ethylene vinyl alcohol
copolymer mixed with tantalum powder in dimethyl
sulfoxide (Onyx; ev3, Irvine, California) is injected via a
hepatic vein. Because of the low viscosity of Onyx, these
investigators were able to reflux the embolic material via
the sinusoids into the target portal vein branches by
wedging a microcatheter in the selected hepatic vein. The
authors correlated transsinusoidal embolization findings
with anatomy seen by indirect portography. Potential
disadvantages highlighted by the authors included a need
to monitor for reflux of the agent toward the base catheter
or from venovenous shunting into other hepatic vein
branches. In three of eight pigs, embolization of one of
two hepatic lobes could not be performed because the
investigators could not find a hepatic vein that allowed
anatomically appropriate embolization. There was one case
of nonocclusive nontarget embolization of the main portal
vein secondary to extension of refluxed Onyx from the
target portal vein branch. The authors did not measure
degree of FLR hypertrophy in this feasibility study.
Patients who undergo traditional PVE but do not ultimately
undergo resection are typically left with permanently
occluded portal veins, which can limit the use of alternative
therapies. For this reason, Lainas et al (75) were the first to
describe intentional reversible PVE, whereby they found
significantFLR volume increases
(Curaspon; Curamedical, Zwanenburg, The Netherlands)
dissolved in a 4:1 mixture of iodinated contrast medium
and saline, the authors reported an average 43% FLR volume
increase in nine monkeys at 1 month after PVE, with
complete revascularization seen by follow-up direct porto-
graphy at 12–16 days after the procedure. However, a
subsequent rabbit model study found that absorbable gelatin
sponge (Gelfoam) resulted in significantly decreased FLR
hypertrophy compared with permanent embolic agents (76).
Reversible PVE has also been proposed as a method to
improve engraftment of transplanted hepatocytes in the
treatment of metabolic liver disease. Dagher et al (77)
reported on the results of genetically modified hepatocytes
that were autotransplanted into the FLR during reversible
partial right PVE in seven monkeys. They documented a
44% mean increase in FLR volume. Biopsies performed 14
days, 8 weeks, and 16 weeks after PVE revealed
engraftment of 7.4%, 2.6%, and 1.8% of transplanted
cells. These authors concluded that reversible PVE could
improve engraftment of transplanted liver cells in the
treatment of metabolic liver disease.
PVE with Adjuvant Stem Cell
Bone marrow–derived stem cells are known to play a role
in liver regeneration and can repopulate damaged hepato-
cytes (78,79). In 2004, Gehling et al (80) demonstrated
that partial hepatectomy induces mobilization of a
distinct population of progenitor cells from the bone
marrow, identified as CD133þ, which are capable of
differentiation into hepatocytes. Based on these findings,
researchers have investigated the intraportal infusion of
stem cells in conjunction with PVE to improve rapidity of
Esch et al (81) initially described the use of bone
marrow stem cells to improve FLR hypertrophy in 2005;
the same group performed a prospective investigation in
2007 (82). In both reports, CD133þstem cells were
harvested from the iliac crest at the time of PVE and
infused into the FLR shortly after multisegment PVE. The
prospective study compared six patients who underwent
PVE plus stem cell infusion with seven patients treated
with PVE alone. Patients in the PVE plus stem cell group
were selected based on clinical concern for inadequate FLR
growth. Despite this concern, the PVE plus stem cell group
demonstrated a significantly greater increase in mean FLR
volume (P ¼ .049), greater percent increase of FLR size (P
¼ .039), and higher daily growth rates (P ¼ .03).
In a follow-up study published in 2012, this same group
of investigators reviewed the outcomes of 11 patient
treated with PVE plus stem cell with 11 patients treated
with PVE alone (83). Both absolute and relative increases
in FLR volumes 14 days after PVE were significantly
greater in patients receiving PVE plus stem cell than in
patients receiving PVE alone. Patients receiving the
combined procedure had mean FLR volume growth of
Volume 24 ’ Number 2 ’ February ’ 2013 251
139 mL ? 66 compared with 63 mL ? 40 in the PVE only
group (P ¼ .004). The relative FLR volume increase was
also greater for the PVE plus stem cell group compared
with PVE alone (10.2% ? 5.2 vs 4.4% ? 3.0; P ¼ .006).
There were no significant differences between groups
regarding major complications or 30-day mortality after
the procedure. The authors concluded that there is faster
FLR growth after PVE combined with stem cell transplan-
tation compared with PVE alone.
Since the previous review published in this journal, PVE
has continued to gain acceptance worldwide as an estab-
lished procedure to reduce postoperative complications and
increase the number of patients able to undergo curative
intent surgery. A wealth of outcomes data has proven PVE
to be a safe procedure with acceptably low procedure-
related morbidity and negligible procedure-related mortal-
ity. PVE has also been combined with additional therapies
in novel ways to improve its efficacy further. The
investigational technique of reversible PVE with transpor-
tal stem cell transplant raises hope of transforming tradi-
tional PVE for malignant disease into a new, minimally
invasive therapy for chronic hepatic insufficiency. Addi-
tional research is required to delineate better outcomes-
based indications for PVE and to address controversies that
continue to arise in the application of this highly successful
1. Simard EP, Ward EM, Siegel R, Jemal A.
incidence trends in the United States: 1999 through 2008. CA Cancer J
Clin 2012; 62:118–128.
2. Shoup M, Gonen M, D’Angelica M, et al.
hepatic dysfunction in patients undergoing major liver resection.
J Gastrointest Surg 2003; 7:325–330.
3. Ribero D, Abdalla EK, Madoff DC, Donadon M, Loyer EM, Vauthey
JN. Portal vein embolization before major hepatectomy and its effects
on regeneration, resectability and outcome. Br J Surg 2007; 94:
4. Breitenstein S, Apestegui C, Petrowsky H, Clavien PA.
art’’ in liver resection and living donor liver transplantation: a worldwide
survey of 100 liver centers. World J Surg 2009; 33:797–803.
5. Correa D, Schwartz L, Jarnagin WR, et al.
changes in the first year after portal vein embolization. Arch Surg 2010;
6. Azoulay D, Castaing D, Smail A, et al.
metastases from colorectal cancer after percutaneous portal vein
embolization. Ann Surg 2000; 231:480–486.
7. Kishi Y, Abdalla EK, Chun YS, et al.
extended right hepatectomies: evaluation of outcome based on sys-
tematic liver volumetry. Ann Surg 2009; 250:540–548.
8. Madoff DC, Abdalla EK, Vauthey JN.
preparation for major hepatic resection: evolution of a new standard of
care. J Vasc Interv Radiol 2005; 16:779–790.
9. Avritscher R, Duke E, Madoff DC.
outcomes, controversies and future directions. Expert Rev Gastroenterol
Hepatol 2010; 4:489–501.
10. Fausto N, Campbell JS, Riehle KJ.
11. Schweizer W, Duda P, Tanner S, et al.
phy complex (AHC) of the liver: portal vein, but not bile duct obstruction,
Cancers with increasing
Volumetric analysis predicts
‘‘State of the
Kinetics of liver volume
Resection of nonresectable liver
Three hundred and one consecutive
Portal vein embolization in
Portal vein embolization: rationale,
Liver regeneration. Hepatology
is the main driving force for the development of AHC in the rat. J Hepatol
12. Goto Y, Nagino M, Nimura Y. Doppler estimation of portal blood flow
after percutaneous transhepatic portal vein embolization. Ann Surg 1998;
13. Nagino M, Nimura Y, Kamiya J, et al.
biliary tract cancer patients after right portal vein embolization. Hepatol-
ogy 1995; 21:434–439.
14. Taub R.Liver regeneration: from myth to mechanism. Nat Rev Mol Cell
Biol 2004; 5:836–847.
15. Yamanaka N, Okamoto E, Kawamura E, et al.
injured human liver regeneration after hepatectomy as assessed on the
basis of computed tomography and liver function. Hepatology 1993; 18:
16. Ikeda K, Kinoshita H, Hirohashi K, Kubo S, Kaneda K.
kinetics and intralobular distribution of apoptotic hepatocytes after portal
branch ligation with special reference to their relationship to necrotic
hepatocytes. Arch Histol Cytol 1995; 58:171–184.
17. Makuuchi M, Thai BL, Takayasu K, et al.
tion to increase safety of major hepatectomy for hilar bile duct
carcinoma: a preliminary report. Surgery 1990; 107:521–527.
18. Hirai I, Kimura W, Fuse A, Suto K, Urayama M.
preoperative portal embolization for safe hepatectomy, with special
reference to assessment of nonembolized lobe function with 99mTc-
GSA SPECT scintigraphy. Surgery 2003; 133:495–506.
19. Uesaka K, Nimura Y, Nagino M.
right portal vein embolization: an appraisal by biliary indocyanine green
excretion. Ann Surg 1996; 223:77–83.
20. Ijichi M, Makuuchi M, Imamura H, Takayama T.
relieves persistent jaundice after complete biliary drainage. Surgery
21. Vauthey JN, Abdalla EK, Doherty DA, et al.
weight predict total liver volume in Western adults. Liver Transpl 2002; 8:
22. Johnson TN, Tucker GT, Tanner MS, Rostami-Hodjegan A.
liver volume from birth to adulthood: a meta-analysis. Liver Transpl 2005;
23. Chun YS, Ribero D, Abdalla EK, et al.
future liver remnant volume measurement. J Gastrointest Surg 2008; 12:
24. Shah A, Goffette P, Hubert C, et al.
to quantify future liver remnants after preoperative portal vein emboliza-
tion to predict postoperative liver failure. Hepatogastroenterology 2011;
25. Abdalla EK, Barnett CC, Doherty D, Curley SA, Vauthey JN.
hepatectomy in patients with hepatobiliary malignancies with and with-
out preoperative portal vein embolization. Arch Surg 2002; 137:
675–680, discussion 680–681.
26. Vauthey JN, Pawlik TM, Abdalla EK, et al.
722–730, discussion 730–732
27. Dixon E, Abdalla E, Schwarz RE, Vauthey JN. AHPBA/SSO/SSAT
sponsored consensus conference on multidisciplinary treatment of
hepatocellular carcinoma. HPB 2010; 12:287–288.
28. Kooby DA, Fong Y, Suriawinata A, et al.
perioperative outcome following hepatic resection. J Gastrointest Surg
29. Gomez D, Malik HZ, Bonney GK, et al.
morbidity following hepatic resection for colorectal metastasis. Br J Surg
30. McCormack L, Petrowsky H, Jochum W, Furrer K, Clavien PA.
steatosis is a risk factor for postoperative complications after major
hepatectomy: a matched case-control study. Ann Surg 2007; 245:
31. de Meijer VE, Kalish BT, Puder M, Ijzermans JN.
and meta-analysis of steatosis as a risk factor in major hepatic resection.
Br J Surg 2010; 97:1331–1339.
32. Pawlik TM, Olino K, Gleisner AL, Torbenson M, Schulick R, Choti
MA. Preoperative chemotherapy for colorectal liver metastases: impact
on hepatic histology and postoperative outcome. J Gastrointest Surg
33. Vauthey JN, Pawlik TM, Ribero D, et al.
predicts steatohepatitis and an increase in 90-day mortality after surgery
for hepatic colorectal metastases. J Clin Oncol 2006; 24:2065–2072.
Changes in hepatic lobe volume in
Dynamics of normal and
Preoperative portal emboliza-
Changes in hepatic lobar function after
Body surface area and body
Comparison of two methods of
Comparison of different methods
Is extended hepatectomy for
AnnSurg 2004; 239:
Impact of steatosis on
Steatosis predicts postoperative
May et al ’ JVIR
252 ’ Update on Portal Vein Embolization
34. Farges O, Belghiti J, Kianmanesh R, et al.
before right hepatectomy: prospective clinical trial. Ann Surg 2003; 237:
35. Angle JF, Siddiqi NH, Wallace MJ, et al.
lines for percutaneous transcatheter embolization: Society of Interven-
tional Radiology Standards of Practice Committee. J Vasc Interv Radiol
36. Abulkhir A, Limongelli P, Healey AJ, et al.
embolization for major liver resection: a meta-analysis. Ann Surg 2008;
37. Di Stefano DR, de Baere T, Denys A, et al.
portal vein embolization: evaluation of adverse events in 188 patients.
Radiology 2005; 234:625–630.
38. Kodama Y, Shimizu T, Endo H, Miyamoto N, Miyasaka K.
tions of percutaneous transhepatic portal vein embolization. J Vasc Interv
Radiol 2002; 13:1233–1237.
39. Lewandowski RJ, Geschwind JF, Liapi E, Salem R.
intraarterial therapies: rationale and overview. Radiology 2011; 259:
40. Michalopoulos GK. Liver regeneration. J Cell Physiol 2007; 213:
41. Nagino M, Nimura Y, Kamiya J, Kanai M, Hayakawa N, Yamamoto
H. Immediate increase in arterial blood flow in embolized hepatic
segments after portal vein embolization: CT demonstration. AJR Am J
Roentgenol 1998; 171:1037–1039.
42. Aoki T, Imamura H, Hasegawa K, et al.
and portal venous embolizations in patients with hepatocellular carci-
noma. Arch Surg 2004; 139:766–774.
43. Ogata S, Belghiti J, Farges O, Varma D, Sibert A, Vilgrain V.
arterial and portal vein embolizations before right hepatectomy in
patients with cirrhosis and hepatocellular carcinoma. Br J Surg 2006; 93:
44. Yoo H, Kim JH, Ko GY, et al.
moembolization and portal vein embolization versus portal vein emboli-
zation only before major hepatectomy for patients with hepatocellular
carcinoma. Ann Surg Oncol 2011; 18:1251–1257.
45. Denecke T, Seehofer D, Steffen IG, et al.
embolization for induction of hepatic hypertrophy before extended right
hemihepatectomy in hilar cholangiocarcinomas: a prospective rando-
mized study. J Vasc Interv Radiol 2011; 22:1254–1262.
46. Nagino M, Kanai M, Morioka A, et al.
before extensive liver resection in patients with markedly poor functional
reserve. J Vasc Interv Radiol 2000; 11:1063–1068.
47. Gruttadauria S, Luca A. Mandala L, Miraglia R, Gridelli B. Sequential
preoperative ipsilateral portal and arterial embolization in patients with
colorectal liver metastases. World J Surg 2006; 30:576–578.
48. Hwang S, Lee SG, Ko GY, et al.
hepatic vein embolization after portal vein embolization to induce further
liver regeneration in patients with hepatobiliary malignancy. Ann Surg
49. Jaeck D, Oussoultzoglou E, Rosso E, Greget M, Weber JC, Bachellier
P. A two-stage hepatectomy procedure combined with portal vein
embolization to achieve curative resection for initially unresectable
multiple and bilobar colorectal liver metastases. Ann Surg 2004; 240:
50. Narita M, Oussoultzoglou E, Bachellier P, Rosso E, Pessaux P, Jaeck
D. Two-stage hepatectomy procedure to treat initially unresectable
multiple bilobar colorectal liver metastases: technical aspects. Dig Surg
51. Brouquet A, Abdalla EK, Kopetz S, et al.
stage resection of advanced colorectal liver metastases: response-based
selection and complete resection define outcome. J Clin Oncol 2011; 29:
52. Capussotti L, Muratore A, Ferrero A, Anselmetti GC, Corgnier A, Regge
D.Extension of right portal vein embolization to segment IV portal
branches. Arch Surg 2005; 140:1100–1103.
53. van Gulik TM, van den Esschert JW, de Graaf W, et al.
the use of portal vein embolization. Dig Surg 2008; 25:436–444.
54. Kishi Y, Madoff DC, Abdalla EK, et al.
portal veins before extended right hepatectomy justified? Surgery 2008;
55. Narita M, Oussoultzoglou E, Jaeck D, et al.
multiple bilobar colorectal liver metastases. Br J Surg 2011; 98:
Portal vein embolization
Quality improvement guide-
Preoperative portal vein
Sequential preoperative arterial
Sequential transcatheter arterial che-
Arterial versus portal venous
Portal and arterial embolization
Sequential preoperative ipsilateral
High survival rate after two-
Is embolization of segment 4
Two-stage hepatectomy for
56. Elias D, De Baere T, Roche A, Mducreux Leclere J, Lasser P.
liver regeneration following right portal embolization the growth rate of
liver metastases is more rapid than that of the liver parenchyma. Br J
Surg 1999; 86:784–788.
57. Kokudo N, Tada K, Seki M, et al.
colorectal metastases after preoperative hemihepatic portal vein embo-
lization. Hepatology 2001; 34:267–272.
58. Hayashi S, Baba Y, Ueno K, et al.
growth rate in embolized hepatic lobe after portal vein embolization. Acta
Radiol 2007; 48:721–727.
59. Simoneau E, Aljiffry M, Salman A, et al.
stimulates tumour growth in patients with colorectal cancer liver
metastases. HPB 2012; 14:461–468.
60. Zorzi D, Chun YS, Madoff DC, Abdalla EK, Vauthey JN.
with bevacizumab does not affect liver regeneration after portal vein
embolization in the treatment of colorectal liver metastases. Ann Surg
Oncol 2008; 15:2765–2772.
61. Covey AM, Brown KT, Jarnagin WR, et al.
embolization and neoadjuvant chemotherapy as a treatment strategy
for resectable hepatic colorectal metastases. Ann Surg 2008; 247:
62. Beal IK, Anthony S, Papadopoulou A, et al.
prior to hepatic resection for colorectal liver metastases and the effects
of periprocedure chemotherapy. Br J Radiol 2006; 79:473–478.
63. Muratore A, Zimmitti G, Ribero D, Mellano A, Vigano L, Capussotti
L.Chemotherapy between the first and second stages of a two-stage
hepatectomy for colorectal liver metastases: should we routinely recom-
mend it? Ann Surg Oncol 2012; 19:1310–1315
64. Kianmanesh R, Farges O, Abdalla EK, Sauvanet A, Ruszniewski P,
Belghiti J.Right portal vein ligation: a new planned two-step all-surgical
approach for complete resection of primary gastrointestinal tumors
with multiple bilateral liver metastases. J Am Coll Surg 2003; 197:
65. Schnitzbauer AA, Lang SA, Goessmann H, et al.
ligation combined with in situ splitting induces rapid left lateral liver lobe
hypertrophy enabling 2-staged extended right hepatic resection in small-
for-size settings. Ann Surg 2012; 255:405–414.
66. Homayounfar K, Liersch T, Schuetze G, et al.
(R0) with portal vein ligation—towards curing patients with extended
bilobular colorectal liver metastases. Int J Colorectal Dis 2009; 24:
67. Aussilhou B, Lesurtel M, Sauvanet A, et al.
as efficient as portal vein embolization to induce hypertrophy of the left
liver remnant. J Gastrointest Surg 2008; 12:297–303.
68. Capussotti L, Muratore A, Baracchi F, et al.
efficient method of increasing the future liver remnant volume in the
surgical treatment of colorectal metastases. Arch Surg 2008; 143:
69. Broering DC, Hillert C, Krupski G, et al.
portal vein ligation for induction of hypertrophy of the future liver
remnant. J Gastrointest Surg 2002; 6:905–913.
70. Robles R, Marin C, Lopez-Conesa A, Capel A, Perez-Flores D, Parrilla
P. Comparative study of right portal vein ligation versus embolisation
for induction of hypertrophy in two-stage hepatectomy for multiple
bilateral colorectal liver metastases. Eur J Surg Oncol 2012; 38:586–593.
71. Denys AL, Abehsera M, Sauvanet A, Sibert A, Belghiti J, Menu
Y. Failure of right portal vein ligation to induce left lobe hypertrophy
due to intrahepatic portoportal collaterals: successful treatment with
portal vein embolization. AJR Am J Roentgenol 1999; 173:633–635.
72. Are C, Iacovitti S, Prete F, Crafa FM.
vein ligation prior to major hepatectomy. HPB 2008; 10:229–233.
73. Madoff DC, Gupta S, Pillsbury EP, et al.
patic portal vein embolization to induce selective hepatic hypertrophy: a
comparative study in swine. J Vasc Interv Radiol 2007; 18:79–93.
74. Smits ML, Vanlangenhove P, Sturm EJ, et al.
vein embolization with ethylene vinyl alcohol copolymer (Onyx): a
feasibility study in pigs. Cardiovasc Intervent Radiol 2012; 35:1172–1180.
75. Lainas P, Boudechiche L, Osorio A, et al.
recanalization time course following reversible portal vein embolization.
J Hepatol 2008; 49:354–362.
76. van den Esschert JW, van Lienden KP, Alles LK, et al.
tion after portal vein embolization using absorbable and permanent
embolization materials in a rabbit model. Ann Surg 2012; 255:311–318.
Proliferative activity of intrahepatic
Acceleration of primary liver tumor
Portal vein embolization
Combined portal vein
Portal vein embolisation
Right portal vein
Right portal vein ligation is
Portal vein ligation as an
Portal vein embolization vs
Feasibility of laparoscopic portal
Transarterial versus transhe-
Liver regeneration and
Volume 24 ’ Number 2 ’ February ’ 2013253
77. Dagher I, Nguyen TH, Groyer-Picard MT, et al.
engraftment and long-term transgene expression after reversible portal
embolization in nonhuman primates. Hepatology 2009; 49:950–959.
78. Theise ND, Nimmakayalu M, Gardner R, et al.
in humans. Hepatology 2000; 32:11–16.
79. Korbling M, Katz RL, Khanna A, et al.
donor origin in recipients of peripheral-blood stem cells. N Engl J Med
80. Gehling UM, Willems M, Dandri M, et al.
mobilization of a unique population of haematopoietic progenitor cells in
human healthy liver donors. J Hepatol 2005; 43:845–853.
Liver from bone marrow
Hepatocytes and epithelial cells of
Partial hepatectomy induces
81. Esch JS, Knoefel WT, Klein M, et al.
CD133þ bone marrow cells to the liver: a novel concept to support
hepatic regeneration. Stem Cells 2005; 23:463–470.
82. Furst G, Esch JS, Poll LW, et al.
autologous CD133þ bone marrow stem cells for liver regeneration:
initial experience. Radiology 2007; 243:171–179.
83. Esch JS, Schmelzle M, Furst G, et al.
marrow-derivedstem cells after
tion enhances functional hepatic reserves after extended right hepa-
tectomy: a retrospective single-center study. Ann Surg 2012; 255:
Portal application of autologous
Portal vein embolization and
Infusion of CD133þ bone
selective portalvein emboliza-
May et al ’ JVIR
254 ’ Update on Portal Vein Embolization