Major advances in the percutaneous management of hepatoportal venous disease and portal hypertension have been introduced in the past decade. This article looks at many of these techniques.
is a fellow in Vascular and Interventional Radiology in the
Department of Radiology, University of Michigan Medical Center, Ann
Arbor, MI. He received his MD from American University of Beirut in
1994 and completed his residency at the University of Michigan
is the William Martel Professor of Radiology, at the University of
Michigan Medical School.
Major advances in the percutaneous management of
hepatoportal venous disease and portal hypertension have been
introduced in the past decade. These include catheter-directed
thrombolysis, mechanical thrombectomy, embolization,
recanalization, balloon angioplasty (percutaneous transluminal
angioplasty [PTA]), stent placement, and transjugular
intrahepatic portosystemic shunt (TIPS). TIPS has proved to be a
safe and effective interventional radiological procedure for the
treatment of acute variceal hemorrhage that is unresponsive to
sclerotherapy, intractable ascites, and Budd-Chiari syndrome. In
addition, it has largely replaced surgical shunt procedures.
Recanalization and stenting can relieve hepatic outflow
obstruction effectively in patients with Budd-Chiari syndrome.
The transhepatic or transjugular approach allows for a variety of
percutaneous radiologic interventions for occlusive portal vein
diseases, including acute and chronic portal vein thrombosis and
portal vein stenosis. The interventional radiologist has played a
major role in developing and advancing techniques that have the
potential to replace many of the traditional medical and surgical
treatments for a variety of occlusive disorders in the hepatic
and portal veins and inferior vena cava.
The interventional radiologist plays a major role in the
evaluation and management of the diseases involving the hepatic and
portal veins. Using a multitude of minimally invasive procedures,
the interventional radiologist is able to evaluate the hepatoportal
vasculature and better characterize the disease process. A variety
of radiologic interventional techniques has been introduced in the
management of the patients with hepatoportal venous diseases. The
basic methods in current use include embolization, thrombolysis,
mechanical thrombectomy, balloon angioplasty, recanalization,
stenting, and transjugular intrahepatic portosystemic shunt (TIPS).
Choosing an appropriate technique for lesions in the portal and
hepatic veins requires proper clinical evaluation, noninvasive
imaging studies, and diagnostic angiography. This paper reviews the
anatomy, angiography, and major advances in the percutaneous
management of patients with hepatoportal venous diseases.
The splenic vein commences with the 5 to 6 branches originating
from the spleen. As the splenic vein courses along the
posterosuperior part of the pancreas, it receives numerous short
tributaries and joins the superior mesenteric vein behind the neck
of the pancreas. The tributaries of the splenic vein are the short
gastric veins, the pancreatic veins, the left gastric vein, and the
inferior mesenteric vein. In the presence of portal hypertension,
portosystemic collaterals develop between the splenic vein and the
left renal vein. The inferior mesenteric vein drains blood from the
left colic, sigmoidal, and superior hemorrhoidal veins. The latter
anastomoses with the middle and inferior hemorrhoidal veins of the
Superior mesenteric vein
The superior mesenteric vein is second in size to the portal
vein. It drains blood from the veins of the small intestine, the
cecum, and the ascending and transverse colon. Its tributaries are
the jejunal veins, the ileal veins, the middle colic vein, the
ileocolic vein, the right colic vein, and the gastrocolic trunk
(GCT). The GCT enters the right side of the distal superior
mesenteric vein, carrying blood from the gastroepiploic vein, the
colic vein, and the pancreatic arcade veins.
The valveless portal vein is an afferent nutrient vessel of the
liver and, therefore, should be considered an arterial vessel. It
carries blood from the entire digestive tract (stomach, duodenum,
small intestines, and colon), the spleen, pancreas, omentum, and
gallbladder. The tributaries of the portal vein are the splenic
vein, the inferior mesenteric vein, the superior mesenteric vein,
the coronary vein, the pancreatic vein, the pyloric vein, and the
The portal vein commences with the junction of the splenic vein
and superior mesenteric vein behind the neck of the pancreas. It
courses in the hepatoduodenal ligament dorsal to the bile duct and
the hepatic artery. The main portal vein divides into the right and
left portal radicles. The right portal vein divides into the
posterior and anterior segmental branches; each subdivides into the
superior and inferior subsegmental branches. The left portal vein
divides into the caudate medial and lateral segmental branches.
Each hepatic segment receives its exclusive blood supply. There is
no communication between the large portal venous branches. Table 1
shows the measurement of the portal vein and its branches.
This information can be used as reference for proper balloon and
stent sizing in the treatment of occlusive lesions in the splenic,
superior mesenteric, and portal veins.
The central hepatic veins course posteromedially, and empty into
the inferior vena cava. The coronary ligament covers them. With
some variations, there are three main hepatic veins--the right
hepatic vein, the middle hepatic vein, and the left hepatic vein.
The left hepatic vein drains the left lobe, which is composed of
two major radicles. The middle hepatic vein carries blood from the
areas supplied by the right and left portal veins. It sometimes
joins the left hepatic vein before emptying into the inferior vena
cava. The right hepatic vein drains the right hepatic lobe. Several
smaller accessory hepatic veins empty into the vena cava below the
main hepatic veins. There are free anastomoses among the various
tributaries of the hepatic veins, providing collaterals in the
presence of localized hepatic vein occlusion.
Hepatic blood flow
A fifth of the cardiac output of blood passes through the liver
sinusoids each minute via the hepatic artery and portal vein. It
has been estimated that two-thirds of total hepatic blood flow
comes from the portal vein.
The role of hepatic arterial circulation has not been considered to
be vital to the function of the hepatic parenchyma. It supplies the
bile duct, connective tissue, and gallbladder, as well as the
hepatic sinusoids. The hepatic arterial and portal venous blood
mixes in the parenchyma and leaves the liver by way of the hepatic
veins. The hepatic artery and the portal vein have a reciprocal
interaction; the hepatic arterial flow increases in a variety of
conditions that result in reduced portal vein flow, including the
following: cirrhosis and portal hypertension, hemorrhage after a
side-to-side portacaval shunt, and creation of TIPS.
From a hemodynamic point of view, the common trait in
hepatoportal diseases is a progressive increase in resistance to
portal vein blood flow, resulting in portal hypertension. Diseases
can occur before blood enters the liver (presinusoidal), in the
liver itself (sinusoidal), and after it leaves the liver
(postsinusoidal) (Table 2). Obstruction at any level will lead to
the development of portosystemic collaterals and gastrointestinal
Normal portal vein pressure is 5 to 10 mm Hg. Portal
hypertension is defined as portal venous pressure >11 mm Hg or a
portosystemic gradient >6 mm Hg.
Usually, it becomes clinically significant when the gradient is
>11 mm Hg.
Clinically, patients may present with bleeding gastroesophageal
varices or recurrent ascites.
Prehepatic (presinusoidal) portal hypertension
Presinusoidal portal hypertension has multiple etiologies. It can
manifest by increased superior mesenteric and inferior mesenteric
vein pressures with normal intrahepatic portal pressure. In this
case, a transhepatic portal vein catheterization is preferred to
facilitate recanalization of a chronically occluded portal vein
using balloon angioplasty or stent placement.
Hepatic (sinusoidal) portal hypertension
--Sinusoidal portal hypertension is usually caused by liver
cirrhosis, which is the end stage of many forms of liver injury
characterized by fibrosis. In the United States, cirrhosis is a
major cause of death in people between the ages of 45 to 65 years.
Most cases of cirrhosis are due to alcohol abuse, but other
etiologies include viral infection, toxin, altered immune response,
biliary obstruction, as well as metabolic and congenital
Posthepatic portal hypertension
This group includes 3 main diseases: veno-occlusive disease (VOD)
of the liver, Budd-Chiari syndrome, and hepatic venous or vena
caval webs. In the early stage of VOD, microscopic changes include
subendothelial edema of the hepatic venules, endothelial cell
damage, and microthrombosis. Later features include sclerosis of
the venular walls and intense collagen deposition in the sinusoids
resulting in hepatocyte necrosis.
Portal hypertension caused by increased flow
Portal hypertension can develop when portal flow is increased (eg,
with arterioportal fistula, pancreatic arteriovenous malformations,
or massive splenomegaly). This entity is also known as hyperkinetic
portal hypertension. A cure can be achieved by eliminating the
source of increased portal flow by either surgical intervention or
Vessels of the liver may be involved by a variety of systemic or
primary diseases. In addition, intrahepatic vessels may be affected
in parenchymal liver disease, such as alcoholic liver disease,
viral hepatitis, and idiopathic portal hypertension. The effects of
hepatic or portal venous disease depend on the level of occlusion,
the type of vessel involved, and whether the occlusion is acute or
Lesions of the portal vein and its branches
Acute portal vein occlusion
--Portomesenteric venous thrombosis is an uncommon cause of
mesenteric ischemia. Conditions associated with mesenteric venous
thrombosis include hypercoagulable states, portal hypertension,
intra-abdominal inflammation, and postoperative state or trauma.
Unlike mesenteric ischemia caused by arterial occlusion, mesenteric
venous thrombosis causes less distinct demarcation. Sudden
occlusion of the portal vein or its branches can lead to true
infarction in the liver, so-called infarct of Zahn.
The natural history and outcome of portomesenteric venous
thrombosis are not well known. The clinical presentation depends on
the extent of thrombosis and the presence of collateral vessels; it
can be as devastating as ischemic intestinal necrosis or remain
unnoticed until cavernomatous transformation develops and bleeding
from portal hypertension brings the patient to clinical attention.
Portal vein occlusion occurs in a variety of conditions including
cirrhosis, shunt surgery for portal hypertension, trauma,
omphalitis, TIPS, coronary embolization, and involvement by primary
neoplasm (hepatoma, cholangiocarcinoma, or pancreatic
The inciting factors in trauma, stagnant circulation, and
malignancy are likely to be endothelial damage and blood
Chronic portal vein occlusion
When portal vein thrombosis becomes chronic, numerous collateral
channels develop. They originate from the superior mesenteric vein
and ascend along the hepatoduodenal ligament in the venous phase of
the superior mesenteric angiogram. This is known as
cavernomatous transformation of the portal vein
. This term was originally described as a pathologic condition of
the portal vein and lesser omentum that gives a sponge-like
This, in fact, is caused by numerous fine collateral blood channels
in the presence of portal vein occlusion, rather than representing
cavernomatous transformation of the portal vein.
Chronic mesenteric vein thrombosis
In chronic mesenteric vein thrombosis, numerous small collateral
veins appear throughout the mesentery without filling the superior
mesenteric vein in the venous phase of the superior mesenteric
angiogram. If the portal vein is occluded, the intrahepatic portal
branches may reconstitute by peribiliary venous collaterals.
Neoplastic portal vein occlusion
--Neoplasms shown to occlude the portal vein include hepatocellular
carcinoma, cholangiocarcinoma, and pancreatic tumors.
Angiographically, the involved veins show localized narrowing or
occlusion, and portal vein invasion by hepatocellular carcinoma
shows characteristic fine, linear abnormal vessels coursing the
portal vein radicles.
--Portal vein phlebitis may occur with or without associated
thrombosis, usually resulting from intra-abdominal suppuration,
such as intra-abdominal abscess, appendicitis, or colonic
diverticulitis. In newborn infants, it can result from acute
omphalitis or umbilical vein catheterization.
--Hepatoportal sclerosis is an important cause of noncirrhotic
(idiopathic) portal hypertension. It affects the intrahepatic
portal vein branches, resulting in periportal and lobular
Splenic vein occlusion
--The causes of splenic vein occlusion include pancreatitis,
pancreatic tumors, and peripancreatic or retroperitoneal neoplasm.
Splenic vein occlusion can cause hypersplenism and gastric bleeding
from gastric varices.
Imaging findings, which suggest splenic vein occlusion, are gastric
varices without esophageal varices and collateral veins in the left
upper abdomen. The diagnosis is confirmed by celiac or splenic
angiography, which shows the short gastric (left gastric, left
gastroepiploic), right gastroepiploic, and omental venous
Lesions of the hepatic outflow tract
Lesions of the hepatic venous outflow tract may involve the
intrahepatic or central hepatic veins, or the hepatic portion of
the inferior vena cava. Disease of the hepatic veins may be primary
or associated with a systemic disease, neoplasm, or surgical
--Veno-occlusive disease is a clinical syndrome seen in patients
who consume herbal teas and in 10% to 60% of patients receiving
bone marrow transplants.
Liver enlargement, pain, jaundice, and ascites characterize the
syndrome. Patients with mild to moderate disease usually recover
with medical therapy alone; in contrast, severe disease often
results in multiorgan failure and death.
The Budd-Chiari syndrome
--Hepatic vein occlusion (the Budd-Chiari syndrome) is an uncommon
cause of portal hypertension and hepatic failure. It is
characterized by hepatic venous and/or inferior vena cava outflow
obstruction. The most common etiology worldwide is membranous
obstruction of the hepatic veins or inferior vena cava. In the
United States, hepatic vein or inferior vena cava thrombosis is the
usual cause. Predisposing factors include polycythemia vera,
paroxysmal nocturnal hemoglobinuria, systemic lupus erythematosus,
idiopathic thrombocytopenia, oral contraceptive use, pregnancy,
myeloproliferative disease, Behçet's disease, hypercoagulable
state, and it can also occur idiopathically.
The majority of patients present with massive ascites as well as
tender and enlarged livers.
Ultrasound, computed tomography (CT), and magnetic resonance
imaging (MRI) have been used in patients with suspected Budd-Chiari
syndrome. MRI is an excellent imaging modality for evaluating these
patients and can offer vascular information necessary for
intervention. Like CT, MRI can depict hepatomegaly, inhomogeneous
liver enhancement, ascites, and occlusion of the hepatic segment of
the inferior vena cava by tumor, such as hepatoma or hypernephroma.
In addition, it can provide the important
vascular anatomy including the caliber of the hepatic veins and
inferior vena cava, and extent of the occlusive disease.
Angiographic studies (arteriography and venography) remain the
gold standard for the diagnosis of Budd-Chiari syndrome. Celiac
arteriography shows hepatomegaly with an inhomogeneous hepatogram
and can exclude neoplasms causing hepatic outflow obstruction. The
first angiographic study in a patient with suspected Budd-Chiari
syndrome should be an inferior venacavography. It may show
occlusion or stenosis of the vena cava at the hepatic level. If the
hepatic veins are occluded, no flow defect may be seen on a
venacavogram. The hepatic veins should then be catheterized
selectively and a wedged hepatic venogram should be performed. This
gives the typical appearance, called "spider-web," which represents
intrahepatic collateral channels between the hepatic venules and
systemic veins. If the main and all accessory hepatic veins are
blocked, a 22-gauge needle can be introduced into the liver
percutaneously from the right lateral approach, and 20 to 30 mL of
carbon dioxide should be injected to fill the hepatic and portal
veins as well as the collateral channels. Liver biopsy should be
obtained whenever possible because the result is useful in
determining treatment options. In the presence of ascites, the
liver biopsy can be performed relatively safely using the
Angiography is frequently used for the evaluation of patients
with hepatoportal diseases prior to a portosystemic shunt operation
and percutaneous hepatic-portal interventions. A number of
angiographic techniques are available to evaluate hepatoportal
blood flow, vascular anatomy, and underlying lesions. These fall
into three major groups: (1) arterial, (2) hepatic venous, and (3)
portal venous. Each of these groups gives important information
about the hepatoportal vascular anatomy and hemodynamics in
patients with cirrhosis, portal hypertension, and hepatoportal
venous disease. Selection of the angiographic methods should depend
on the underlying disease, intended interventions, and the
availability of veins for access.
The technique generally used for arterial studies is the
standard Seldinger technique. The femoral approach is the most
preferable. Celiac angiography in the evaluation of patients with
hepatoportal disease and portal hypertension is performed to do the
following: exclude causes of massive upper gastrointestinal
bleeding other than varices, to exclude hepatoma, and to show the
portal vein and portosystemic collateral veins. Superior mesenteric
and splenic angiography is performed to visualize the patency of
the splenic, superior mesenteric, and portal veins. Visualization
of the superior mesenteric and portal veins is accomplished by
injecting a large volume of contrast medium into the superior
mesenteric artery. An intra-arterial injection of a vasodilator,
such as tolazoline or nitroglycerine, just before contrast
injection enhances portal vein visualization.
Wedged hepatic venography
Wedged hepatic venography is used for the evaluation of
cirrhosis, portal hypertension, and other hepatoportal venous
diseases. Wedged hepatic venous pressure reflects portal pressure
in the absence of presinusoidal block. In cirrhosis, wedged hepatic
venous pressure minus right atrial pressure gives a portosystemic
gradient, which represents intrahepatic resistance to portal flow.
Normal wedged hepatic venous pressure in a patient with esophageal
varices indicates that presinusoidal block is the cause of portal
hypertension. If the portal blood flow is hepatopetal, the main
portal vein will not fill with the injection of contrast medium
into a wedge hepatic vein. Carbon dioxide wedged hepatic venography
is commonly used to visualize the portal vein since it fills the
portal vein even in the presence of hepatopetal portal flow. Wedged
hepatic venography can be performed with either the femoral or
jugular approach using an end-hole catheter or an occlusion balloon
catheter. If the portal vein cannot be visualized with the wedged
hepatic injection, carbon dioxide is injected into the liver
parenchyma, which usually fills the portal vein.
Transhepatic portal vein catheterization
The transhepatic approach is used for intervention in the portal
vein and its branches. The technique is similar to percutaneous
transhepatic cholangiography and employs a 22-gauge Chiba needle
introduced in the right midaxillary line at the 9th-10th or
10th-11th intercostal space. After dilating the tract, a 5F sheath
is placed for portography and pressure measurement. At the end of
the procedure, the percutaneous tract can be embolized with Gelfoam
(Pharmacia and Upjohn, Inc., Peapack, NJ) pledgets or coils to
prevent bleeding from the puncture site. The transhepatic approach
is also used for stent placement of the hepatic vein in patients
with Budd-Chiari syndrome.
Splenoportography was developed prior to arterial portography
and is not currently a popular procedure because of its potential
complications. An 18-gauge needle is placed in the spleen and
iodinated contrast is injected into the splenic pulp to visualize
the splenic and portal veins. If the portal flow is reversed, the
portal vein may not fill with the splenic injection.
Contraindications include coagulopathy and ascites.
Now splenoportography can be performed safely with the injection
of carbon dioxide using a 22- or 25-gauge needle introduced into
the spleen under ultrasound guidance. The transsplenic approach can
be used for catheterization of the splenic and portal veins when
the transhepatic or transjugular approach is not feasible. Splenic
arterial embolization prior to transsplenic portal vein
catheterization reduces bleeding from the spleen. At the end of the
procedure, the splenic tract should be occluded with gelatin
pledgets or coils.
A number of interventional methods have been developed by which
hepatoportal venous diseases can be treated percutaneously.
Commonly used techniques include the following: (1) embolization,
(2) thrombolysis, (3) mechanical thrombectomy, (4) venous
recanalization, (5) balloon angioplasty, (6) stenting, and (7)
TIPS. Selection of the appropriate angiographic and intervention
techniques for hepatic-portal interventions should begin with a
thorough clinical evaluation. Review of the available noninvasive
imaging studies prior to intervention is essential. In most
instances, no single angiographic technique is capable of providing
all the necessary intervention; a combination of several techniques
is usually required. A brief review of each technique and its
indications are discussed.
The most common site for bleeding varices is in the esophagus.
Endoscopic sclerotherapy remains the initial therapeutic treatment
for esophageal varices. Approximately 10% to 15% of patients have
gastric varices that may not be amenable to endoscopic therapy.
Rarely, the variceal bleeding may occur at unusual sites--including
the duodenum, ileum, colon, rectum, bladder, or enterostomy or
In 1974 Lunderquist and Vang
first described variceal percutaneous transhepatic embolization
(PTE) in patients with cirrhosis and portal hypertension.
Percutaneous transhepatic embolization remains a useful option when
variceal bleeding recurs following sclerotherapy, or varices in the
stomach or at the unusual sites cannot be treated by the endoscopic
approach. Variceal embolization is often used when varices continue
to fill following creation of TIPS.
Prior to a transhepatic procedure, celiac and superior
mesenteric angio-graphies should be performed to exclude a source
of upper gastrointestinal bleeding other than variceal bleeding.
The portal venous phase of celiac and superior mesenteric
angiographies should be evaluated for patency of the portal venous
system. A branch of the right portal vein is punctured from the
right lateral approach in the midaxillary line midway between the
costophrenic angle and inferior angle of the liver using a 22-gauge
needle. The needle is withdrawn with injections of small amounts of
contrast medium until a portal vein radicle is visualized. After
confirmation of the needle in the portal vein, a 0.018-in Cope
mandril wire (Cook Inc., Bloomington, IN) is advanced into the
portal vein. The needle is then removed, and the portal vein is
catheterized using a 3/4 coaxial dilator, a 6F Cope introducer, or
Neff percutaneous access set (each product from Cook Inc.).
After a 5F catheter has been introduced into the proximal
splenic vein, a splenoportogram is performed to obtain a road map.
A 5F Cobra catheter is introduced to embolize varices filled from
the splenic vein (Cook Inc., Bloomington, IN). Several embolic
materials or agents can be used to control variceal bleeding. These
include Gelfoam (Pharmacia & Upjohn, Co., Kalamazoo, MI),
absolute alcohol, coil, and glue. The feeding veins and varices
should be occluded throughout their course. Although the method is
relatively safe and effective in controlling acute variceal
bleeding, variceal bleeding usually recurs from new gastric and
esophageal varices. Therefore, a portal vein decompression
procedure, such as TIPS, is required for long-term control of
variceal bleeding. The potential complications of coronary vein
embolization include portal/splenic thrombosis, systemic
embolization, death, hemoperitoneum, pneumothorax, subcapsular
hematoma, and gallbladder puncture.
Balloon angioplasty has been used to treat focal stenosis of the
hepatoportal venous system, webs and membranes of the inferior vena
cava, and suprahepatic and infrahepatic stenosis of the inferior
vena cava in orthotopic liver transplants.
Balloon angioplasty should be a first-line treatment for
stenosis in the hepatic and portal veins as well as the inferior
vena cava. Stent placement is indicated in the following
conditions: (1) unsuccessful percutaneous transluminal angioplasty
(PTA), (2) restenosis following PTA, (3) hepatoportal occlusion,
(4) diffuse lesions, (5) extrinsic compression, and (6)
inflammation, such as pancreatitis. Stents can maintain patency of
large veins effectively, but restenosis ocurrs frequently in small
veins due to myointimal hyperplasia. The most commonly used stents
in the hepatoportal system are self-expandable stents such as
Wallstent (Boston Scientific Corporation, Natick, MA).
Large-diameter stents are available for inferior vena cava
stenosis, including Wallstent and Cook-Z Stent (Cook Inc.).
Mechanical thrombectomy has become a useful percutaneous method
in recanalizing acute thrombosis, particularly when thrombolysis is
contraindicated. There are 2 types of mechanical thrombectomy
devices available: (1) mechanical devices with external
motor-driven, rotating action for thrombofragmentation (products
include the Amplatz Thrombectomy/Clot Buster, Microvena, White Bear
Lake, MN; and the Arrow-Trerotola Percutaneous Thrombolytic Device,
Arrow International, Reading, PA) and (2) hydrodynamic devices that
remove clots by the Venturi effect (products include the Hydrolyser
catheter, Cordis Endovascular, Warren, NJ; AngioJet Rheolytic
Thrombectomy system, Possis Medical, Minneapolis, MN; and the Oasis
catheter, Boston Scientific Corp., Natick, MA). Clinical experience
with these devices in the portal venous system is limited, and
their safety and efficacy are unknown.
Thrombolytic agents can be used in the treatment of acute
thrombosis of the portal or hepatic veins.
They can be infused intravenously or directly into thrombus.
Catheter-directed thrombolysis is safer and more effective than
intravenous thrombolysis. Two basic techniques of the
catheter-directed lysis are the infusion method and pulse-spray
technique. Both methods are used for thrombolysis in the hepatic
and portal veins as well as their main branches. The thrombolytic
agents that are currently available in the United States are
alteplase (Activase, Genentech Inc., San Francisco, CA) and
reteplase (Retavase, Centocor, Inc., Malvern, PA). Urokinase
(Abbokinase, Abbott Laboratories, Abbott Park, IL) is not available
in the United States.
TIPS are shunts created percutaneously between the hepatic vein
and the portal vein using the jugular vein. TIPS have been shown to
be safe and effective in treating patients with esophageal variceal
hemorrhage unresponsive to endoscopic scelerotherapy, and
intractable ascites. The procedure involves catheterization of the
right or middle hepatic vein from the jugular vein. Once the
catheter has been wedged in a distal hepatic vein, a carbon dioxide
digital subtraction venogram is obtained to identify the location
of the portal vein radicle. Once the right portal vein radicle is
punctured from the hepatic vein using a Colapinto needle, a
guidewire is advanced into the splenic or superior mesenteric vein.
After portal vein pressure measurement, a direct portogram is
performed. The liver parenchymal tract is dilated to 8 mm using an
angioplasty balloon catheter. Then a metallic stent is deployed
from the main portal vein through the liver parenchyma to the
central hepatic vein. The stent is then dilated to 10 mm in
diameter. If the portosystemic gradient has been reduced to <12
mm Hg, the procedure is considered successful and is terminated.
The TIPS are then checked for patency using Duplex ultrasound at 24
hours and every 3 months.
Interventions in the portal vein and its branches
Acute portal and mesenteric vein thrombosis
The natural history and outcomes of portomesenteric venous
thrombosis are not well known. Its clinical presentation depends on
the extent of thrombosis and the presence of collateral
Current therapeutic methods for acute portomesenteric thrombosis
include anticoagulant therapy, systemic thrombolytic therapy,
catheter-directed thrombolysis, and mechanical thrombectomy. Early
recognition and treatment of the underlying causes may prevent the
development of portal hypertension.
Intravenous thrombolytic therapy has been used in patients with
portal vein thrombosis, resulting in symptomatic relief.
Now catheter-directed thrombolysis is the standard method of
treating both arterial and venous thrombosis. In the hepato-portal
venous system, a percutaneous transhepatic or transjugular approach
has been used for intrathrombic delivery of lytic agents in
patients with mesenteric and portal vein thrombosis.
When rapid removal of clots is needed, or when lytic agents cannot
be used because of contraindications, use of mechanical
thrombectomy devices is a viable option. AngioJet and Fogarty
(Edwards Lifesciences, Irvine, CA) catheters have been used for the
treatment of portomesenteric thrombosis. Others have also used
similar mechanical devices in the portal venous system.
Chronic portal vein thrombosis
--Chronic portal vein thrombosis with cavernomatous transformation
may cause portal hypertension and variceal bleeding. Portal vein
thrombosis accounts for about half of the cases of portal
hypertension in children. A percutaneous transhepatic or
transjugular approach can be used to recanalize chronic portal vein
occlusion in both adults and children (Figure 1). In children,
sclerotherapy has been effective with reported long-term success
Shunts are indicated in cases of sclerotherapy failures. Cwikiel et
described a case of an 8-year-old child in whom stent
recanalization of the chronically occluded portal vein with
cavernomatous transformation was performed successfully. This
technique, if successful, has the potential to replace surgical
shunts in children.
Stein and Link
have reported their experience with recanalization and
reconstruction with endovascular stents in 21 patients with
symptomatic spleno-mesenteric-portal venous thrombosis. Their
indications for the procedure were variceal bleeding, ascites,
hypersplenism, and enteropathy. TIPS procedures were performed in 5
cases. The technical success of portal vein reconstruction was
85.7%, and the 30-day mortality rate was 14.3% (mortality was not
procedure related). Stein and Link concluded that portal vein
reconstruction is safe and effective in treating symptomatic
chronic portal vein occlusion.
Transhepatic stent placement has also been used for the
treatment of proximal portal vein stenosis associated with
pancreatitis, causing recurrent bleeding from duodenopancreatic
and mesenteric vein occlusion, causing jejunal variceal bleeding.
In patients with cirrhosis complicated by chronic portal vein
occlusion with or without cavernomatous transformation, TIPS is
performed following portal vein recanalization.
Neoplastic portal vein occlusion
--Various tumors can cause portal vein narrowing, including
hepatocellular carcinoma, pancreatic adenocarcinoma,
cholangiocarcinoma, and metastatic neoplasm. If the portal vein
involvement causes portal hypertension and bleeding, intraportal
stent placement can restore portal blood flow and relieve portal
Stenosis of portal anastomosis complicating liver
--Stenosis of the portal vein at the site of anastomosis after
liver transplantation is rare, with an incidence of 0.5% to 6.5%.
Portal venoplasty is a safe and effective procedure for the
treatment of portal hypertension associated with portal vein
stenosis arising from complications from liver transplantation in
both adults and children.
The usual approach is percutaneous transhepatic, although some
prefer the transjugular intrahepatic access because of the
decreased risk of bleeding.
Access to the portal vein is gained by a standard percutaneous
transhepatic approach or transjugular approach. After the portal
vein has been catheterized, a 6F sheath is introduced into the
portal vein. The portal vein stenosis is crossed using a 0.035-in
hydrophilic-coated wire and a 5F end-hole catheter is introduced.
Once the lesion has been crossed, a 5F pigtail catheter is advanced
into the proximal splenic vein, and a pressure gradient across the
lesion is obtained. A splenoportogram is then obtained to delineate
the portal venous anastomotic stenosis prior to balloon
angioplasty. High technical success rates can be achieved,
resulting in resolution of portal hypertension. Before withdrawal
of the sheath, the liver parenchymal tract should be occluded with
gelatin sponge pledgets or coils to prevent bleeding from the
hepatic capsular puncture site. After portal venoplasty, follow-up
with imaging studies is needed to detect recurrent stenosis.
Recurrent stenosis can be treated successfully with repeated
balloon angioplasty. Although most portal vein stenosis responds to
balloon angioplasty, their long-term efficacy remains unknown.
Splenic vein occlusion
--Asymptomatic splenic vein occlusion requires no treatment. When
splenic vein occlusion causes gastric variceal bleeding or
hypersplenism, splenectomy is usually performed. Standard
sclerotherapy is ineffective in treating acute bleeding from
If the patient is not a surgical candidate, splenic vein
recanalization and stenting may be used as an alternative
treatment, but its long-term efficacy is not known.
Interventions in the hepatic veins and inferior vena
Therapeutic options for hepatic venous outflow obstruction
depend on the underlying pathologic process, extent of occlusive
lesions, and clinical course. Surgery has played the major role in
the treatment of Budd-Chiari syndrome.
Now percutaneous radiology-guided interventions play a significant
role in the treatment of hepatic venous outflow obstruction, and
they have replaced many of the surgical procedures, such as
surgical construction of portosystemic shunts and resection of
membranous webs from the inferior vena cava. Orthotopic liver
transplantation remains the preferred treatment when surgical or
percutaneous interventions are not feasible or have failed, or when
biopsy results show severe progressive hepatic fibrosis with
deteriorating liver function.
--Based on the pathologic findings of microthrombi and fibrin
deposition in VOD, treatments have been aimed at anticoagulation
and promoting fibrinolysis. This could be useful early in the
disease process. However, once multiorgan failure sets in, the risk
of bleeding increases significantly and there is no proven survival
TIPS has been used as a treatment for VOD. Fried et al
reported 6 cases of VOD managed with TIPS; 5 of the 6 patients
died, 1 patient with less advanced disease survived. Currently,
there is no proven beneficial role of TIPS except to manage
concomitant portal hypertension and variceal bleeding (Figure
The Budd-Chiari syndrome
--The prognosis of untreated patients with Budd-Chiari syndrome is
poor; 89% die within 3.5 years of the onset of symptoms.
Medical treatment with diuretics and anticoagulants may relieve
symptoms but appears to have no significant survival benefit.
Thrombolytic therapy is generally considered an effective
treatment. Surgery has played the major role in the management of
Budd-Chiari syndrome; it can help maintain hepatic function and
prevent variceal bleeding. Surgical treatments that have been used
include construction of portosystemic shunt, mesoatrial shunt,
portoatrial shunt, resection of membranous webs, and orthotopic
Because of their demonstrated safety and efficacy, percutaneous
interventions have been used with increasing frequency as the
preferred alternative to surgery for patients with Budd-Chiari
syndrome. These include percutaneous transluminal balloon
angioplasty, stent placement, and TIPS.
Liver transplantation is the only treatment option for patients
with progressive hepatic fibrosis with deteriorating liver
TIPS has been shown to improve hepatic synthetic dysfunction and
resolve ascites, providing an effective bridge to hepatic
transplantation for patients with Budd-Chiari syndrome.
PTA should be the first intervention for focal stenosis or webs
of the hepatic vein and inferior vena cava.
The reported mean patency of balloon angioplasty of this lesion is
For recurrent lesions and lesions unresponsive to angioplasty,
stent placement is required.
Recanalization and stent placement are usually required for
treatment of extensive hepatic vein occlusion
(Figure 4). Reports in the literature indicate that initial
technical success rate is high with 1-year patency rates of 80% to
Because frequent restenosis requires repeated PTA, Venbrux
used self-expandable Z-stents in the severely stenotic inferior
vena cava in patients with Budd-Chiari syndrome. Stents of
appropriate size should be used to prevent migration of the stent.
Self-expandable stents such as Wallstents (12 or 14 mm in diameter)
are commonly used for the treatment of central hepatic vein
stenosis. The stents should extend to the junction of the hepatic
vein and inferior vena cava. Stent protrusion into the suprahepatic
inferior vena cava should be avoided, as it may interfere with
future hepatic transplantation. The usual stent sizes for vena
caval stenosis or occlusion are 15 to 20 mm.
Hepatic venous outflow obstruction complicating liver
--Hepatic venous outflow obstruction can occur as a complication
following orthotopic liver transplantation. The level of
obstruction can be at the hepatic vein, suprahepatic caval
anastomosis, or both hepatic vein and hepatic portion of the
inferior vena cava. Stent placement of the right hepatic vein and
the inferior vena cava (if necessary) can relieve hepatic venous
obstruction effectively and restore donor liver function.
Suprahepatic caval anastomotic stenosis is a rare complication
of hepatic transplantation with reported incidences of 0.8% to
Caval stenosis may also occur at the infrahepatic anastomosis.
Clinical presentations of inferior vena cava stenosis depend on
their location and severity. Suprahepatic caval stenosis can cause
lower extremity edema, ascites, and hepatic failure. PTA and stent
placement have replaced the old surgical treatments such as
hepatopexy, thrombectomy, and retransplantation for cava stenosis.
PTA has been shown to be an effective treatment for suprahepatic
caval anastomotic stenoses.
(Figure 5). Recurrent stenosis usually responds favorably to
repeated PTA. In reported cases, the time interval between the
operation and the percutaneous intervention ranged from 3 weeks to
4.5 years. The balloon sizes used for PTA were 8 to 20 mm in
diameter. When obstruction is caused by kinking of the suprahepatic
inferior vena cava in the early postoperative period,
self-expandable stents should be used to avoid rupture of the
Several fundamental requirements are needed to be able to
accurately evaluate and successfully treat the diseases involving
the hepatic vasculature. First, understanding the extrahepatic and
intrahepatic vascular anatomy and its relationship to other
structures within or outside the liver is crucial. Second,
familiarity with the noninvasive imaging of the liver such as
ultrasound, CT, and MRI is important. Third, knowledge of the
pathophysiology and natural history of each disease can prevent
unnecessary interventions and make the interventional radiologist's
role clinically important. Choosing an appropriate interventional
method for hepatoportal occlusive disease should begin with proper
clinical evaluation. No single technique is capable of treating
complex hepatoportal lesions. Thoughtful selection of current
interventional techniques is essential for the safe and effective
performance of hepatic-portal interventions. These include
angiography, embolization, thrombolysis, mechanical thrombectomy,
recanalization, angioplasty, stenting, and TIPS.