REVIEW ARTICLE THORNBURG ET AL.

Interventional Radiology
in the Management of the Liver
Transplant Patient
Bartley Thornburg,1 Nitin Katariya,2 Ahsun Riaz,1 Kush Desai,1 Ryan Hickey,1
Robert Lewandowski,1 and Riad Salem 1,2
1
Department of Radiology, Section of Interventional Radiology, Northwestern Memorial Hospital, Robert H. Lurie Comprehen-
sive Cancer Center, Chicago, IL; and 2Department of Surgery, Division of Transplantation, Comprehensive Transplant Center,
Northwestern University, Chicago, IL

Liver transplantation (LT) is commonly used to treat patients with end-stage liver disease. The evolution of surgical tech-
niques, endovascular methods, and medical care has led to a progressive decrease in posttransplant morbidity and mortal-
ity. Despite these improvements, a multidisciplinary approach to each patient remains essential as the early diagnosis and
treatment of the complications of transplantation influence graft and patient survival. The critical role of interventional
radiology in the collaborative approach to the care of the LT patient will be reviewed.

Liver Transplantation 23 1328–1341 2017 AASLD.

Received April 14, 2017; accepted July 3, 2017.

Liver transplantation (LT) is the definitive therapy for
patients with end-stage liver disease. Since the incep-
tion of LT, progressive improvement in medical care,
surgical methods, and endovascular techniques have
significantly decreased the morbidity and mortality of
Abbreviations: APF, arterioportal fistula; AS, anastomotic strictures;
CC, choledochocholedochostomy; CDT, catheter-directed thrombolysis;
CJ, choledochojejunostomy; DDLT, deceased donor liver transplanta-
tion; DUS, Doppler ultrasound; ERCP, endoscopic retrograde chol-
angiopancreatography; HABR, hepatic artery buffer response; HAS,
hepatic artery stenosis; HAT, hepatic artery thrombosis; HCC, hepa-
tocellular carcinoma; HV, hepatic vein; IR, interventional radiology;
IVC, inferior vena cava; LDLT, living donor liver transplantation;
LFT, liver function test; LT, liver transplantation; MELD, Model
for End-Stage Liver Disease; MRCP, magnetic resonance cholangio-
pancreatography; NAS, nonanastomotic strictures; PHP, portal
hyperperfusion; PTA, percutaneous transluminal angioplasty; PV,
portal vein; PVR, portal vein recanalization; PVS, portal vein ste-
nosis; PVT, portal vein thrombosis; RI, resistive index; TACE,
transarterial chemoembolization; TIPS, transjugular intrahepatic
portosystemic shunt.
Address reprint requests to Riad Salem, M.D., M.B.A., Department
of Radiology, Section of Interventional Radiology, Northwestern
Memorial Hospital, Robert H. Lurie Comprehensive Cancer Center,
676 North St. Clair, Suite 800, Chicago, IL 60611. Telephone:
312-695-6371; E-mail: r-salem@northwestern.edu
Additional supporting information may be found in the online ver-
sion of this article.
1328 | REVIEW ARTICLE
this lifesaving procedure. On the basis of OPTN data
as of March 24, 2017, the 1- and 3-year patient sur-
vival after primary LT are 92% and 84%. Advance-
ments within the field of interventional radiology (IR)
have allowed many of the complications and sequelae
of transplantation to be treated in a minimally invasive
fashion. The role of IR in the management of the LT
patient will be discussed, including the treatment of
vascular and biliary complications, the applicability of
transjugular intrahepatic portosystemic shunts (TIPSs)
after LT, and the use of portal vein recanalization and
TIPS (PVR-TIPS) prior to LT.
Hepatic Artery Stenosis
Hepatic artery stenosis (HAS) occurs in 4%-11% of
LTs, mostly at the site of an arterial anastomosis
(Supporting Fig. 1).(1-4) The development of HAS is
associated with allograft rejection, microvascular injury
from cold preservation of the liver, disruption of the
vasa vasorum, clamp injury, caliber size mismatch, prior
transarterial chemoembolization (TACE), extrinsic
compression, and technical issues.(5) Patients with HAS
typically present with graft dysfunction or biliary com-
plications, but a stenosis may be subclinical in up to
20% of patients, which emphasizes the importance of
close laboratory and imaging surveillance.(6,7) Addition-
ally, early diagnosis of HAS is critical because delay has
LIVER TRANSPLANTATION, Vol. 23, No. 10, 2017
been shown to increase the severity of biliary complica-
tions and the chance of graft loss.(7,8)
HAS is generally diagnosed with Doppler ultra-
sound (DUS). Ultrasound findings include increased
velocity at the stenosis (peak systolic velocity >400-
450 cm/second), decrease in the resistive index (RI)
beyond the stenosis (<0.5), and a tardus parvus wave-
form. These findings are highly suggestive of a high-
grade (>70%) stenosis. Additionally, gradual decrease
of the RI on serial ultrasounds has been suggested as
an indicator of imminent thrombosis.(9,10)
Treatment of HAS has evolved over the last several
decades. Initially, options were primarily surgical,
including resection of the stenotic segment with re-
anastomosis, the use of an interposition graft, or the
creation of an aortic conduit. Over time, the advance-
ment of endovascular techniques and devices has
allowed most patients with HAS to be treated with
minimally invasive endovascular procedures rather
than surgical revision.
Endovascular management of HAS includes both
percutaneous transluminal angioplasty (PTA) and
stent placement (Fig. 1). PTA and stent placement
both have a high technical success rate (80%-93%) and
a procedural complication rate of 7%-10%, including
access site complications, arterial dissection, and less
frequently, arterial rupture.(6,11,12) A recent meta-
analysis of 26 studies compared the efficacy of PTA
versus stent placement for the treatment of HAS.
These studies showed no difference in procedural suc-
cess, complications, return to normal liver function,
arterial patency, survival, or requirement for re-
intervention or retransplantation between PTA and
stent placement.(13) There was a trend in the more
recent studies included in the meta-analysis of a lower
retransplantation rate, likely reflecting progressive
improvement in surgical and endovascular techniques,
medical care, and imaging detection.
Other studies have similarly found no difference in
primary patency or assisted patency between PTA and
primary stent placement.(14,15) However, Le et al.
demonstrated a strong trend toward longer time to
Copyright V
C 2017 by the American Association for the Study of Liver
Diseases.
View this article online at wileyonlinelibrary.com.
DOI 10.1002/lt.24828
Potential conflict of interest: Nothing to report.
THORNBURG ET AL.
re-intervention in the stent group (105.8 days) com-
pared with the PTA group (51.0 days).(14) In this
study, the 1-year primary patency rate of the entire
cohort was 63.6%, but the assisted patency rate was
95%. These results reinforce the importance of con-
tinued clinical and imaging follow-up of transplant
patients who are treated for HAS. Ultimately, due to
the relative equivalence in outcomes, the decision to
place a stent depends on operator preference and the
anatomy of the lesion, or stenting may be reserved for
lesions that fail to respond to angioplasty.
There is some controversy as to whether all patients
with HAS require endovascular treatment. Pulitano
et al. questions whether patients who develop HAS
later in their postoperative course receive any clinical
benefit compared with those with earlier HAS devel-
opment.(16) This analysis of 54 patients found that
HAS intervention was associated with improved biliary
stricture–free survival, but only in patients with steno-
sis detected within the first 6 months of transplant.
For patients who developed HAS later than 6 months
after transplant, there was no difference in biliary stric-
ture–free survival, which is thought to be due to the
development of arterial collaterals. Additionally, no
patients with asymptomatic HAS and normal liver
function tests (LFTs) developed biliary strictures.
These results suggest that patients developing HAS
more than 6 months postoperatively may be managed
conservatively. However, patients who undergo watch-
ful waiting need to be selected carefully because previ-
ous studies have shown that the rate of thrombosis is
significantly higher in patients who do not undergo
endovascular therapy (65% versus 19%).(11) Addition-
ally, other studies have shown that patients with HAS
who do not receive endovascular management are
twice as likely to develop biliary complications and to
have decreased overall survival when compared with
those who undergo endovascular therapy.(1,17)
Hepatic Artery Thrombosis
Hepatic artery thrombosis (HAT) is a potentially dev-
astating complication that carries a mortality rate of
27%-58% and is the most common cause of graft
loss.(18-21) HAT occurs in up to 4%-11% of adult LTs
and 11%-26% of pediatric LTs.(2,3,18,19,22) However, a
recent retrospective review of 1560 patients from 1991
to 2009 demonstrates a progressive decline in the inci-
dence of HAT over the interval years of the study with
a current rate of 2%-3%.(23) Risk factors for HAT
REVIEW ARTICLE | 1329
THORNBURG ET AL. LIVER TRANSPLANTATION, October 2017



FIG. 1. A 59-year-old male

with hepatitis B cirrhosis and
HCC who underwent LT. (A)
Two weeks after transplant,
ultrasound was performed for
increased LFTs showing signifi-
cantly decreased RI and severe
dampening of the spectral
Doppler waveform. (B) Angiog-
raphy demonstrated a long seg-
ment severe stenosis, which was
felt to be caused by retrograde
dissection from the anastomosis
into the recipient common
hepatic artery with subintimal
thrombus. (C) After 6 mm 3
40 mm self-expanding bare
metal stent placement, there was
brisk hepatic arterial flow. (D)
Follow-up ultrasound showed
normal spectral waveform and
RI.


include small arteries (pediatric transplants), back-table
reconstruction involving multiple anastomoses, celiac
stenosis, aortic conduits, and prior TACE.(19)
Clinically, HAT may present with nonspecific signs
such as fever, leukocytosis, increased LFTs, pain, or
fatigue. Graft dysfunction is more commonly seen in
early HAT (1 month after transplant), whereas bili-
ary complications are more common in late HAT.
Imaging findings of HAT include characteristic abnor-
malities on DUS. Loss of arterial signal is highly sensi-
tive (>90%) and is the most common DUS finding of
HAT (Supporting Fig. 2). Additionally, increased RI
of the artery proximal to the thrombosis may be
observed.(9,10)
Treatment options for HAT include retransplanta-
tion, surgical revascularization, and endovascular revas-
cularization. Ultimately, retransplantation is necessary in
at least half of the patients with HAT, but with the rela-
tive scarcity of organ availability, surgical or endovascu-
lar revascularization is often attempted as a definitive
treatment or bridge to retransplantation.(19,24)
Surgical revascularization has been shown to be suc-
cessful in cases of early thrombosis with the majority of
patients not requiring retransplantation, which empha-
sizes the need for routine, frequent screening with
DUS.(25) However, surgical revascularization cannot
relieve extensive thrombosis involving the intrahepatic
arterial system, in which case, catheter-directed thera-
pies may be of value. In 1989, Hidalgo et al. first
reported the use of catheter-directed thrombolysis
(CDT) for HAT.(26) Since then, most reports of CDT
for HAT are small series with conflicting results.
Singhal et al. reviewed 16 studies in 2010, including a
total of 69 patients who were treated with CDT for
HAT.(21) Most patients (47/69, 68%) in this analysis
had successful revascularization. If CDT is performed,
Saad et al. suggested a clinical therapeutic window of
1-3 weeks after transplantation until 1-3 months after
transplant.(20) CDT in the very early posttransplant
period is associated with a high risk of bleeding com-
plications, and patients who develop late HAT often
have mature collaterals, which decrease the need to

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LIVER TRANSPLANTATION, Vol. 23, No. 10, 2017
subject the patient to the risk of thrombolysis. How-
ever, despite these recommendations, most studies
have focused on immediate technical success rather
than longterm clinical outcomes, and therefore, the
effect of CDT for HAT on graft survival, patient sur-
vival, and incidence of biliary complications is difficult
to determine.
Recently, Kogut et al. published a review of 26
patients who underwent CDT for HAT.(27) The
hepatic artery was successfully recanalized in 46% of
patients, but 30% developed major bleeding complica-
tions (access site and intra-abdominal) requiring either
transfusion or surgical intervention. Furthermore,
between patients with successful and unsuccessful
recanalization, there was no difference in survival, need
for surgical revascularization, retransplantation rate,
development of ischemic biliary complication, or pro-
cedural complications.
Despite the lack of data regarding longterm clinical
outcomes, CDT is often performed in a salvage set-
ting, knowing that surgical revascularization or retrans-
plantation may be performed if endovascular means
fail. In addition to its utility as a salvage or temporizing
procedure, angiography obtained after revascularization
provides important information regarding underlying
arterial stenoses, as well as the complexity of the arte-
rial anatomy and surrounding vasculature that may be
valuable if subsequent surgical revascularization or
retransplantation is necessary. These studies and the
variability in the results underscore the need to individ-
ualize treatment of HAT based on the clinical presen-
tation, availability of organs for retransplantation, and
local expertise with endovascular therapies.
Arterioportal Fistula
Arterioportal fistula (APF) is an uncommon complica-
tion after LT and is associated with prior biopsy or
percutaneous cholangiography.(3,28) Most APFs are
asymptomatic, discovered incidentally on surveillance
imaging, and regress spontaneously.(28,29) They may
also present with hemobilia or with sequelae of graft
ischemia including dysfunction, infarction, or necro-
sis.(30,31) DUS often fails to detect small, asymptom-
atic APF but is useful in detecting larger, symptomatic
fistulae. Findings on DUS include decreased hepatic
RIs and arterialization of the involved portal vein (PV)
branches.
APFs were previously treated primarily with surgical
ligation, but advancements in endovascular methods
THORNBURG ET AL.
allow most to be definitively managed with coil embo-
lization (Supporting Fig. 3). However, several factors
dictate whether endovascular treatment should be pur-
sued. In small and asymptomatic APF, the risk of
hepatic artery dissection or thrombosis from endovas-
cular manipulation may outweigh the clinical benefit of
closing the fistula. If watchful waiting of an APF is
pursued, close imaging follow-up is critical to ensure
that embolization is performed before the APF
becomes hemodynamically significant or involves
larger hepatic artery branches. If these occur, the risk
of biliary ischemia increases following embolization.
For these reasons, the risks and benefits in each case
must be weighed prior to APF embolization.
Portal Vein Stenosis
and Thrombosis
Portal vein stenosis (PVS) is a rare complication of
adult and pediatric whole liver grafts, with a reported
incidence of 1%-2%.(32-34) The complication is more
common in adult split grafts (4%) and pediatric split
grafts (7%-27%). The increased incidence is due to
size mismatch of the donor PV, short donor PV
requiring interposition grafts, and the need for more
complex PV reconstructions.(32-36) Nearly all PVSs
occur at the anastomosis, and most occur more than 6
months after transplantation.(37,38) Patients with PVS
may present with symptoms of portal hypertension
(ascites or varices), increased LFTs, or portal vein
thrombosis (PVT). The imaging diagnosis of PVS is
usually obtained with DUS, which demonstrates an
elevated peak PV velocity of >125 cm/second or a 3-
4–fold increase in PV velocity at the stenosis (Support-
ing Fig. 4).
PTA of posttransplant PVS was first described
by Olcott et al. in 1990 and now is the treatment
of choice.(39) PVS intervention is often performed
using a right-sided transhepatic route, which pro-
vides a direct path to the stenosis, but some opera-
tors will use a transjugular (TIPS) route or
transsplenic access (Supporting Fig. 5). The severity
of the stenosis is determined by the venographic
appearance and pressure gradient across this steno-
sis. The 2 largest series of posttransplant PV
angioplasty have used 3 and 5 mm Hg to indicate
a stenosis, but the exact gradient which indicates
hemodynamic significance is debatable.(37,40) There
is also no consensus regarding the need for
periprocedural anticoagulation or postprocedural
REVIEW ARTICLE | 1331
THORNBURG ET AL.
antiplatelet therapy. The use of these medications
will depend on center protocols or operator
preference.
In a series of 30 children and adolescents with PVS,
Funaki et al. showed that at the time of initial treat-
ment, one-third of patients had elastic recoil requiring
bare metal stent placement.(37) In the remaining
patients, half developed recurrent stenosis requiring
stent placement. In patients who underwent stent
placement, either initially or upon recurrence, patency
was achieved in 100% of the patients with a mean
follow-up of 46 months. Other series also showed
100% patency in cases of bare metal stent placement
with a follow-up of 10-67 months.(41,42) Despite the
very high patency of bare metal stents, stent placement
is often reserved for cases of intraprocedural elastic
recoil or early restenosis (within 6 months). This hesi-
tation is due to potential complications, including
interference with the utilization of the PV for potential
retransplantation, as well as progressive stenosis in
pediatric patients as they grow.
Like PVS, PVT is an uncommon complication of
LT. Most cases of PVT occur early (1 month from
transplant), and the vast majority of these are associ-
ated with eventual graft loss.(32) Patients with post-
transplant PVT present similarly to those with PVS.
They may be asymptomatic, present with abnormal
LFTs, or with symptoms of portal hypertension. DUS
will demonstrate a lack of Doppler color flow and
echogenic thrombus within the PV.
PVT is typically treated with endovascular meth-
ods. Most interventional radiologists will use either a
transjugular intrahepatic or a direct transhepatic
approach to manage posttransplant PVTs (Fig. 2). If
prolonged CDT is necessary, a transjugular approach
may have a lower risk of bleeding compared with a
direct transhepatic route. Additionally, if the PVT
extends into the intrahepatic PV, the placement of a
TIPS will provide the outflow necessary to maintain
PV patency after thrombectomy. However, the
approach will depend on the clinical situation and
operator preference.
Because of the low incidence of PVT following LT,
there are little data regarding the efficacy of CDT in
these patients, particularly regarding longterm graft
salvage and patient survival. Most of the literature is
case reports or small case series using various throm-
bectomy devices and techniques. Ultimately, the treat-
ment of posttransplant PVT will vary center to center
depending on operator expertise and organ availability
for retransplant.
1332 | REVIEW ARTICLE
LIVER TRANSPLANTATION, October 2017
Hepatic Vein and Inferior
Vena Cava Complications
Hepatic vein (HV) and inferior vena cava (IVC) steno-
sis occur in <2% of LT patients.(34,43) In the early
postoperative period, HV/IVC stenosis may be due to
size mismatch, twisting, dissection, or technical issues.
Late stenosis is more common and is most often due
to perivascular fibrosis or intimal hyperplasia, but it
may also be caused by compression or twisting of a
growing split graft. Caval reconstruction and piggy-
back anastomoses have similar incidences of vascular
outflow stenosis.(44,45)
HV stenosis causes venous outflow obstruction of
the graft which can lead to edema, portal hypertension,
and subsequent cirrhosis. Often, patients have pre-
served liver function without LFT abnormalities, but
they may present with ascites, varices, and hydrotho-
rax.(46) Additionally, HV stenosis may lead to
decreased clearance of immunosuppressive agents lead-
ing to elevated tacrolimus trough levels.(47) The symp-
tomatology of IVC stenosis depends on the location:
stenosis above the HV anastomosis will present simi-
larly to HV stenosis, whereas stenosis below the HV
anastomosis may present with lower extremity edema
or ascites.
Imaging diagnosis of HV stenosis begins with
DUS, which will reveal decreased velocity in the PV
and HV, dampening of the normal biphasic or tripha-
sic waveform in the HV, and aliasing at the HV
anastomosis.
When HV stenosis is suspected, venography is per-
formed to assess the angiographic appearance and to
obtain pressure measurements (Fig. 3). The veno-
graphic approach to the HV is typically through the
internal jugular vein. In cases of HV occlusion or high-
grade stenosis limiting access via a transjugular
method, direct transhepatic access to the HV may be
necessary to aid in catheterization. A gradient >10
mm Hg is most commonly used to define a hemody-
namically significant stenosis.(48,49) However, some
authors have found clinical improvement after treating
patients with a gradient as low as 3 mm Hg.(50) Most
operators will begin treatment of the stenosis with pro-
longed plain balloon angioplasty, which has a very low
complication rate and a high technical success rate
(approaching 100%).(51,52) However, plain balloon
angioplasty often requires multiple treatments to
achieve longterm patency.(47,51) Kubo et al. showed
that primary patency of HV angioplasty was 60% at
LIVER TRANSPLANTATION, Vol. 23, No. 10, 2017 THORNBURG ET AL.



FIG. 2. A 64-year-old female with nonalcoholic steatohepatitis (NASH) cirrhosis who had LT. At the time of transplant, splenec-
tomy was performed due to intraoperative bleeding. (A) One week following LT, ultrasound was performed for increasing LFTs dem-
onstrating no detectable color flow in the extrahepatic or intrahepatic PVs. (B) Percutaneous transhepatic portal venography was
performed showing patency of the superior mesenteric vein (arrow), but near complete thrombosis of the main PV (arrowhead). There
was very little flow into the intrahepatic PV branches. Catheter-directed thrombolysis was initiated. After 48 hours of thrombolysis,
there was a persistent thrombus in the main PV, but there was significantly improved intrahepatic portal flow. Rheolytic thrombec-
tomy with an AngioJet catheter (Boston Scientific, Marlborough, MA) was performed after which (C) there was near complete clear-
ance of the PVT with only a small amount of mural thrombus in the main PV (arrow) and nonocclusive thrombus in the right PV
(arrowhead). (D) Coronal contrast-enhanced MRI performed 1 year after thrombolysis showed a maintained patency of the PV.


1 year, but due to the ease of repeat intervention, the
assisted primary patency rate during follow-up was
100%.(53) The use of cutting balloon angioplasty to
decrease the incidence of elastic recoil and recurrent
stenosis has been described and is used by many opera-
tors if there is initial failure of plain balloon
angioplasty.(54)
Treatment of IVC stenosis also begins with plain
balloon angioplasty, but recurrence rates are as high as
50%.(55,56) Ultimately, many patients with IVC steno-
sis will require stent placement, which has been shown
to have very high longterm patency rates (Supporting
Fig. 6).(50,56,57) Because of the frequent need for even-
tual stenting, some authors suggest that stent
placement should be considered as a first-line ther-
apy.(58) However, due to the theoretical risk of IVC
stent migration, malposition, or occlusion of the HV
ostium, others recommend that serial angioplasty
should be considered in reliable patients.(59)
Splenic Steal/Portal
Hyperperfusion Syndrome
Splenic steal syndrome is a cause of graft ischemia and
occurs in approximately 4% of LTs.(60) This syndrome
was previously thought to represent siphoning, or
“stealing,” of hepatic blood flow by a splenic artery

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THORNBURG ET AL. LIVER TRANSPLANTATION, October 2017



FIG. 3. A 12-year-old female who had LT at the age of 11 years old for autoimmune hepatitis and liver failure. She presented with
increased LFTs and splenomegaly 9 months after transplant and a biopsy raised concern for venous outflow obstruction. She under-
went 8-mm HV angioplasty (not shown). (A) Follow-up sagittal contrast-enhanced CT showed a recurrent band-like stenosis at the
HV ostium (arrow). (B) Venography confirmed severe stenosis at the HV ostium (arrow) with reflux of contrast into hepatic paren-
chyma (arrowhead) due to outflow obstruction. (C) Cutting balloon angioplasty was performed, but follow-up venography demon-
strated persistent stenosis (not shown). (D) Therefore, self-expanding bare metal stents were placed to fully resolve the stenosis (a
second stent was placed to ensure adequate coverage of the ostium). The LFTs normalized and the spleen decreased in size on
follow-up imaging (not shown).


previously hypertrophied by portal hypertension and
splenomegaly. A more recent theory posits a mecha-
nism of increased portal venous flow (portal hyperper-
fusion [PHP]) causing a concomitant decrease in
hepatic arterial flow rather than direct siphoning of
blood flow. This decreased hepatic arterial flow occurs
both by direct compression of the sinusoids, as well as
through the hepatic artery buffer response (HABR), a
regulatory mechanism of arterial vasoconstriction
mediated by adenosine.(61,62) The most common pre-
sentation of splenic steal or PHP is graft dysfunction
(increased LFTs), but in severe cases, patients may
manifest symptoms of portal hypertension, including
ascites and hydrothorax, which are often resistant to
medical therapies. Longterm effects of the arterial
vasoconstriction include biliary strictures, reperfusion
injury, and small-for-size syndrome.(61,63)
DUS demonstrates a high-resistance graft, includ-
ing elevated RIs (>0.8), lack of arterial diastolic flow,
or even reversal of diastolic flow. These sonographic
findings may also be seen in graft edema, rejection, or
infection, and these entities must be excluded before
PHP can be diagnosed. Angiography will demonstrate
brisk splenic arterial flow and slow flow through an

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LIVER TRANSPLANTATION, Vol. 23, No. 10, 2017
otherwise patent hepatic artery. The angiography find-
ings are subjective, and although no objective angio-
graphic criteria currently exist, these findings in
conjunction with clinical suspicion and a corroborating
DUS can establish the diagnosis of PHP with
confidence.
If necessary, splenic artery ligation, splenectomy, or
mesocaval shunts can be performed to modulate portal
venous flow if PHP is suspected at the time of trans-
plant.(64,65) However, in the postoperative period, the
endovascular treatment for PHP is primarily proximal
splenic artery embolization, which can be performed
with coils or vascular plugs. This procedure decreases
splenic arterial flow and therefore decreases portal
venous flow to the liver, which via the HABR, sig-
nificantly improves hepatic arterial flow and hepatic
arterial RIs with a low complication rate.(61,66) Com-
plications include splenic infarction, which can lead to
abscess and sepsis. However, proximal embolization is
generally preferred to distal or parenchymal emboliza-
tion in order to maintain distal collaterals, which mini-
mizes these risks.
Biliary Complications
Biliary complications of LT include strictures, bile leaks,
stones, debris, and sphincter of Oddi dysfunction.
Although the incidence of biliary complications has
been decreasing due to improvements in surgical techni-
ques, these complications continue to be a source of
morbidity and mortality in LT patients. Risk factors for
biliary strictures include the use of T tubes, Roux-en-Y
anastomoses, ischemia/reperfusion injury, HAT, CMV
infection, and primary sclerosing cholangitis.(67,68)
Whether a choledochocholedochostomy (CC, duct-to-
duct) or choledochojejunostomy (CJ, duct-to-jejunum
with a Roux-en-Y) is performed will depend on surgeon
preference, underlying liver pathology, size of the donor
and recipient bile ducts, history of prior transplant, and
history of biliary surgery. Of the 2 types of anastomoses,
CC is most common, is technically easier, and has the
advantage of preserving sphincter function.
Biliary strictures occur in 5%-15% of deceased
donor liver transplantations (DDLTs) and up to 28%-
32% of living donor liver transplantations (LDLT)
and present on average 5-8 months after transplant.(69)
They are classified as anastomotic strictures (AS) or
nonanastomotic strictures (NAS). AS, which are more
common in CJ anastomoses, are thought to be related
to inadequate mucosa to mucosa anastomosis, local
THORNBURG ET AL.
tissue ischemia, and the fibrotic nature of the healing
process. Patients with AS present with the stigmata of
biliary obstruction, including jaundice, abdominal
pain, increased LFTs, and fever in the setting of chol-
angitis. NAS are frequently located at the hilum but
may also be diffusely intrahepatic. Predisposing factors
for NAS include ischemia and immunologic factors.
Ischemic strictures usually present within 1 year of
transplant whereas immunologic strictures often pre-
sent after 1 year.(70)
Management of biliary strictures is most commonly
accomplished using endoscopic retrograde cholangio-
pancreatography (ERCP), particularly in patients with
CC anastomoses and native small bowel anatomy. Pro-
tocols will vary at each center, but typically involve rou-
tine stent exchange and upsize every several months for
1 year. Endoscopic management is successful in 80%-
90% of AS anastomoses in DDLTs, compared with
60%-75% of AS in LDLT and 25%-33% of NAS in
LDLT.(69,71,72) If patients have had prior Roux-en-Y
bypass surgery or received a CJ anastomosis at the time
of transplant, endoscopic therapy of biliary strictures
may be challenging; therefore, percutaneous therapies
are often performed.
Percutaneous cholangiography is performed to define
the location and severity of the biliary stricture, followed
by biliary drain placement. Cholangiography and drain
placement can be performed via left- or right-sided
ducts depending on patient anatomy and operator pref-
erence. Multiple sessions of prolonged inflation cholan-
gioplasty are performed over a period of several weeks to
months. At each dilation, a sheath cholangiogram is
performed to assess the size of the native duct and the
durability of the prior intervention. To combat the
fibrotic nature of biliary stenoses, cutting balloon chol-
angioplasty is often performed, either in response to an
elastic or recurrent stenosis, or by routine at every chol-
angioplasty session.(73,74) In contrast to ERCP protocols
that often continue for a year after transplant, percuta-
neous cholangioplasty is usually performed for weeks to
months with the goal of removing the external drainage
catheter for patient comfort. Because of variability of
protocols and follow-up, longterm success has been
reported to range from 33%-74% for percutaneously
treated AS.(75-77) Future studies should investigate the
use of drug-eluting balloons in the setting of biliary AS
to determine their effect on the fibrotic healing response
and longterm patency (Fig. 4).
The use of covered metallic stents has been evalu-
ated in the treatment of benign biliary strictures and
was found to be noninferior to multiple plastic
REVIEW ARTICLE | 1335
THORNBURG ET AL. LIVER TRANSPLANTATION, October 2017



FIG. 4. A 65-year-old male

with hepatitis C cirrhosis who
had LT with Roux-en-Y biliary
anastomosis. Four years after
transplantation, he presented
with increased LFTs. (A)
MRCP demonstrated mild bili-
ary dilatation. The biliary anas-
tomosis could not be reached
endoscopically due to tortuosity
and bowel adhesions. A percu-
taneous transhepatic biliary
drain was placed, followed by 3
sessions of plain and cutting
balloon angioplasty (not shown).
(B) Despite these measures,
cholangiography still showed
moderate irregular stenosis at
the CJ anastomosis (arrow). (C)
Cholangioplasty was then per-
formed with a 7-mm paclitaxel-
coated angioplasty balloon. (D)
Cholangiogram 4 weeks after a
drug-coated balloon cholangio-
plasty showed no recurrent ste-
nosis. The biliary drain was
removed, and the patient has
remained asymptomatic during
follow-up.


stents.(78) Covered metallic stents require significantly
less subsequent endoscopic therapies, and the resolu-
tion rate for posttransplant strictures was >90%. In
cases of endoscopic failure or inability to reach the
stricture due to small bowel anatomy, covered stents
may also be deployed via a percutaneous route. Addi-
tionally, if patients have Roux-en-Y anastomosis at the
time of transplant, the creation of a Hudson loop (sur-
gical fixation of the afferent roux limb to the anterior
abdominal wall) allows for percutaneous retrograde
access to the biliary tree (Fig. 5).(79) If a Hudson loop
is created, patients may undergo cholangioplasty and
plastic stent placement with protocols similar to endo-
scopic therapy, avoiding the risks associated with per-
cutaneous transhepatic access.
When a patient is found to have a biliary stricture, it
is vital to evaluate the hepatic artery, as 67%-80% of
AS are associated with HAS or HAT.(6,77,80) Treating
the underlying hepatic arterial pathology makes a
patient more likely to respond to percutaneous or
endoscopic treatment of the biliary stricture.(81)
Posttransplant TIPS
TIPS is performed on 1%-4% of LT recipients.(82-84)
Portal hypertension in a transplant liver may be due to
recurrence of the original liver disease or from graft com-
plications including HV outflow obstruction, IVC steno-
sis, chronic rejection, and small donor liver size. The
clinical presentation is similar to that of portal hyperten-
sion in a native liver, including ascites, varices, and hydro-
thorax. However, the pharmacologic treatment of these
conditions may be more complicated in the transplant
patient due to chronic immunosuppression.
When considering TIPS on a transplant liver, sev-
eral technical factors must be considered. A piggyback
cavocaval anastomosis may lead to caudal angulation of

1336 | REVIEW ARTICLE

LIVER TRANSPLANTATION, Vol. 23, No. 10, 2017 THORNBURG ET AL.



FIG. 5. A 63-year-old male

with hepatitis C cirrhosis who
underwent LT complicated by
multiple biliary infections was
treated with Roux-en-Y biliary
reconstruction with a Hudson
loop formation. Three years
after reconstruction, he pre-
sented with fever, jaundice, and
increased bilirubin. MRCP
showed mild intrahepatic biliary
dilatation. (A) After percutane-
ous access into the Hudson
loop, a directional catheter was
advanced through the afferent
loop to the hepaticojejunostomy
(arrow). (B) The catheter was
advanced, and cholangiography
demonstrated a severe biliary
stricture near the hilum. (C)
Cholangioplasty was performed
with a 6-mm balloon. (D)
Three 8.5-Fr plastic biliary
stents were placed with immedi-
ate near-complete resolution of
the biliary dilatation.


the HV ostium. Additionally, in split graft transplants,
the liver often rotates as it grows, which can distort the
orientation of the HV and PV. These anatomic factors
may complicate both access to the HV as well the
transhepatic parenchymal puncture. In these cases,
ancillary techniques may be helpful, including the use
of a gun-sight method and intravascular ultrasound
guidance for assistance in the PV puncture (Supporting
Fig. 7).(85) Despite these potentially complicating fac-
tors, technical success of TIPS on transplant livers is as
high as 97%-98%.(84,86)
Overall, clinical response and survival following
TIPS is lower in transplanted compared with native
livers. A review of 13 retrospective studies demon-
strated a 57% clinical response rate for the treatment of
posttransplant ascites, compared with historical aver-
ages of 70%-90%.(86) This disparity may in part be due
to the decrease in renal function caused by calcineurin
use, as well as the longterm effect of hepatitis on renal
function.(86) A case-controlled study by King et al.
showed a statistically lower clinical success rate of 77%
for TIPS in transplanted livers compared with 93% in
native patients.(87) Post-TIPS survival is also decreased
in transplant patients compared with patients with
native livers, with 1-year survival rates of 54% for
transplanted patients undergoing TIPS for ascites and
44% for those with varices.(86)
The Model for End-Stage Liver Disease (MELD)
score threshold for pursuing an elective TIPS should
be lower for posttransplant patients. King et al. showed
that in patients with MELD  15, there was a signifi-
cantly higher mortality in posttransplant patients com-
pared with native livers, whereas the mortality of
patients undergoing TIPS with a MELD < 15 was
not statistically different.(87) Similarly, a multivariate
analysis showed that MELD score was an independent
predictor of survival in posttransplant patients under-
going TIPS, with a significant mortality increase in

REVIEW ARTICLE | 1337

THORNBURG ET AL.
patients with MELD  15.(82) These studies demon-
strate that TIPS plays an important role in posttrans-
plant patients with recurrent portal hypertension but
should be used judiciously in patients with MELD
scores  15.
Pretransplant PVR
Combined With TIPS
PVT occurs in 10%-25% of patients with cirrhosis prior
to LT and is an independent risk factor for increased
posttransplant morbidity and mortality.(88-90) Because
of this association with worsened outcomes, it is a rela-
tive contraindication to LT at many centers, particularly
in cases of chronic PVT with cavernous transformation.
Although patients with PVT can undergo transplanta-
tion, it is not uncommon that they require either jump
grafts or nonphysiologic PV anastomoses, including
cavoportal hemitransposition, renoportal anastomoses,
and portal vein arterialization, which increase postopera-
tive morbidity and mortality.(91-94)
Techniques have been described that allow for per-
cutaneous recanalization of chronically thrombosed
PVs in conjunction with TIPS placement (Supporting
Fig. 8).(95,96) The TIPS provides outflow and alleviates
venous stasis, allowing for a high rate of longterm PV
patency, which can then be used at the time of trans-
plant. In a recently published series of patients, 23
underwent transplantation after PVR-TIPS. All
patients received a physiologic PV anastomosis, and all
but 1 received an end-to-end anastomosis (22/23,
96%). In this series, complications specific to PVR-
TIPS included bleeding at the splenic access site (2/
20, 10%), which did not require embolization or sple-
nectomy. None of the patients who underwent PVR-
TIPS followed by LT developed posttransplant PV
stenosis or recurrent PVT during follow-up.
An additional advantage of preoperative PVR-TIPS
is the ability to identify and embolize spontaneous por-
tosystemic shunts (eg, splenorenal shunts) that may
cause posttransplant portal steal syndrome and com-
promise the graft. It has been suggested that shunts
larger than 10 mm in diameter should be closed prior
to, or at the time of transplant.(97-99) After PVR-TIPS
is performed, these spontaneous shunts can be readily
embolized via an endovascular approach using coils or
vascular plugs. Not only does this decrease the inci-
dence of posttransplant portal steal syndrome, but it
also promotes hepatopetal flow through the recanalized
PV which helps maintain patency prior to transplant.
1338 | REVIEW ARTICLE
LIVER TRANSPLANTATION, October 2017
The applicability of PVR-TIPS will depend on local
practice patterns and expertise, but it should be consid-
ered in patients with PVT who are awaiting LT to
allow for a physiologic end-to-end anastomosis.
In conclusion, LT is the definitive therapy for
patients with end-stage liver disease. Because of
advancements in medical care, surgical methods, and
endovascular techniques, posttransplant morbidity and
mortality have decreased significantly. IR plays a vital
role in the management of LT patients, and moving
forward, outcomes will continue to improve with ongo-
ing multidisciplinary collaboration between transplant
surgeons, hepatologists, and interventional radiologists.
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