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22 Interventions oftheHepatic Veins, Inferior Vena Cava, andPortal Vein
255
22.2.3 Post-Procedural Care
The patients are observed in the daycare unit for 4–6hours to
rule out hepatic bleeding.
22.2.4 Complications
Most of the complications are minor, including puncture site
hematoma and abdominal pain related to small subcapsular
hematoma. Major complications are infrequent, including
cardiac arrhythmia, transcapsular puncture causing hemoperitoneum, and perforation of the hepatic artery. Others
include hemobilia, pseudoaneurysm, or arteriovenous stula
[1, 2, 6].
Persistent or new-onset severe abdominal pain and signs
of hypovolemia should prompt further workup to rule out
subcapsular or intraperitoneal hemorrhage [1, 2]. If a postprocedural hepatic venogram shows active bleeding, the tract
can be embolized by gel foam or glue. Bleeding from hepatic
arterial branches necessitates selective transarterial embolization. RHV branches may be empirically embolized when
no obvious bleeding source is identied [7].
Transcaval Liver Biopsy
Transcaval liver biopsy (transjugular/transfemoral route)
remains an alternative option where hepatic vein cannulation
is technically not feasible (unsuitable hepatic venous anatomy, Budd–Chiari syndrome, or markedly shrunken liver).
Under real-time USG guidance, the biopsy is taken after
wedging the TJLB stiff cannula against the wall of the intrahepatic segment of IVC [8]. The transfemoral approach is
associated with fewer complications and procedure time than
the transjugular route [9].
– Preemptive TIPS: It refers to the early preventive
insertion of TIPS (within 24 hours or 72 hours of
admission) in patients at high risk of uncontrolled variceal bleeding and bleeding-related mortality (Child B
with active bleeding on endoscopy, Child C with 10–13
point and, HVPG >20mm Hg)
– Secondary prophylaxis of variceal bleeding*
– Rescue/salvage TIPS: for failure to control bleeding on
endoscopy
– Other types of portal hypertension-related bleeding:
Recurrent bleeding from ectopic/stomal varices
(failed NSBB and/or endoscopic therapy)
Severe transfusion-dependent portal hypertensive
gastropathy.
• Refractory hydrothorax
• Hepatorenal syndrome
• Portal vein thrombosis
• Budd–Chiari syndrome
• Hepatic veno-occlusive disease
• Pre-operative TIPS: to decrease the risk of intraoperative
bleeding and improve surgical outcomes in patients with
portal hypertension
*The two most common indications in clinical practice
are refractory ascites and secondary prophylaxis of variceal
bleeding.
22.3.2 Contraindications ofTIPS [12–14]
Absolute and relative contraindications are listed in
Table22.1.
22.3.3 Pre-Procedural Evaluation [12–14]
22.3 Transjugular Intrahepatic Portosystemic Shunt (TIPS)
The transjugular intrahepatic portosystemic shunt (TIPS) is
an articial channel created between the portal vein (PV) and
IVC to treat the complications of portal hypertension.
Without any realizable hepatic vein (Budd–Chiari syndrome), the shunt is created directly between the PV and
IVC, also called DIPS (direct IVC to PV shunt). Due to its
low invasiveness, TIPS has a better safety prole than surgery in cirrhotic patients.
22.3.1 Indications ofTIPS [10, 11]
• Refractory ascites*
• Variceal bleeding
Patients are selected through a multidisciplinary
approach, considering the risks versus benefits. The two
most important pre-procedural considerations include
baseline liver and cardiac function. Pre-procedural evaluations include:
• Basic laboratory investigations: Liver (LFT) and renal
function tests (KFT), serum electrolytes, and complete
blood count (CBC).
• Screening tests for covert and overt encephalopathy
before elective TIPS.
• Cardiac evaluation: A cardiac history, examination,
12-lead ECG, N-Terminal pro-B-type natriuretic peptide
(NT-proBNP), and echocardiogram.
• Cross-sectional imaging: CECT or CE-MRI (preferably
CECT) helps evaluate vascular anatomy and patency
before elective TIPS.Imaging may also reveal other sig-
256
Table 22.1 Contraindications of TIPS [12–14]
Absolute Relative
Severe congestive heart failure or tricuspid
regurgitation
Severe liver failure
Severe pulmonary hypertension (mPAP>45mmHg)
Unrelieved biliary obstruction or Caroli’s disease
Uncontrolled systemic infection/sepsis
Multiple hepatic cysts
CTP≥14 points, bilirubin>5mg/dL, MELD>18*
mPAP Mean pulmonary arterial pressure, CTP Child-Pugh score, MELD Model for end-stage liver diseases, HE Hepatic encephalopathy
Severe organic renal failure (serum creatinine>3mg/dL)
Extensive or central hepatocellular carcinoma
Moderate pulmonary hypertension (mPAP within 35–45mm hg)
Serum total bilirubin>3mg/dl
Persistent or recurrent HE (especially if not precipitated by modiable factors)
grade≥2 (west-heaven scale) despite adequate treatment
Deranged coagulation
R. K. Patel and A. Mukund
nicant ndings, such as intrahepatic mass, portosystemic
collaterals, and hernia, which could complicate the procedure and affect TIPS outcomes.
TIPS creation involves puncturing hepatic parenchyma
and PV, thus considered a high bleeding risk procedure [5].
Coagulopathy, if present, should be corrected to as near normal as possible. The Society of Interventional Radiology
(SIR) suggests an INR <2.5, platelet counts >30,000/mm3,
and brinogen levels >100mg/dl for TIPS [5]. Pre-procedural
antibiotic coverage is optional.
22.3.4 Technique
TIPS is performed as an in-patient procedure. General anesthesia is the best option for TIPS; however, it may be performed under conscious sedation with adequate analgesia.
After obtaining jugular access, right atrial, IVC, and pulmonary artery pressure (PAP) are measured. HV, preferably
RHV, is cannulated using a 5F MPA catheter and 0.035′ softtipped hydrophilic guidewire (Fig.22.2a). A 10F introducer
sheath (Flexor Check Flo Introducer with dilator) is advanced
into the HV over a stiff guidewire. 10F catheter with stiffening cannula (RUPS-100, Cook Inc., Bloomington, IN) is
wedged against the HV wall, and the catheter/trocar stylet
assembly of RUPS-100 is punctured forward through the
liver parenchyma and toward the PV.The optimal site of PV
puncture is the right PV within 2cm from the main PV bifurcation, avoiding extrahepatic PV puncture. Free backow of
blood indicates that the catheter tip is within the PV.A small
amount of contrast run further conrms this. A soft-tipped
hydrophilic guidewire is manipulated into the superior mesenteric vein or splenic vein, and a 5F MPA catheter is
advanced (Fig. 22.2b). Direct portal venography and PV
pressure measurement are taken. Over an exchange length
stiff guidewire, the parenchymal tract is dilated using a balloon catheter (6–10mm balloon). Sites of waist formation on
the balloon are good indicators of the PV/HV ends of the
tract (Fig.22.2c). 10F sheath is advanced into the PV, and a
calibrated pigtail is placed within the PV.The 10F sheath is
retracted to IVC while a calibrated pigtail is left within the
PV. The stent-graft length is measured using simultaneous
venography through a calibrated pigtail and 10F introducer
sheath (Fig. 22.2d). 10F sheath is again advanced into the
PV. An expanded polytetrauoroethylene (ePTFE) stentgraft of appropriate size is deployed, extending from the PV
entry site to the HV-IVC junction. A bare metallic stent is
placed overlappingly with its distal half within the PV to
smoothen the shunt conguration (Fig.22.2e). Alternatively,
Viator TIPS Endoprosthesis (W.L.Gore & Associates), specially designed for TIPS (having a 2cm uncovered segment
for PV and the remaining covered part), can be used instead
of two separate stents. After stent deployment, balloon
angioplasty is performed using a 6–10mm balloon. Finally,
the post-TIPS pressure gradient is measured. Jugular site
venous hemostasis is obtained with manual compression.
The most critical step in TIPS creation is PV access [13].
The traditional technique of PV localization includes wedge
or balloon-occluded hepatic venography using contrast or
CO2. In the authors’ institute, transabdominal USG is an
adjunct to uoroscopy while attempting PV puncture. Other
methods of PV localization include intravascular USG
(IVUS probe placed in IVC through femoral approach), percutaneous wire placement within PV, and gun-sight technique (percutaneous through and through puncture of HV/
IVC and PV under USG guidance followed by shunt creation
after snaring the wire through transjugular approach). A
transsplenic approach has also been described for portal vein
recanalization and TIPS creation in patients with portal vein
thrombosis. A wire-loop snare is placed through the transsplenic route, and the snare loop is targeted from the transjugular route to establish the PV access and completion of
TIPS [13, 15, 16].
22.3.5 Post-Procedural Care
The patient is monitored in the ICU or HDU for 24hours
following TIPS.CBC, INR, and LFT are repeated within
cd
22 Interventions oftheHepatic Veins, Inferior Vena Cava, andPortal Vein
Fig. 22.2 Steps of TIPS. (a)
Right hepatic vein
catheterization through
transjugular route; (b) Right
PV puncture using RUPS-100
cannula, followed by
portogram through a 5F
angiographic catheter; (c)
Dilatation of parenchyma
tract using an 8-mm balloon;
(d) Measurement of
parenchymal tract using
simultaneous portogram via
calibrated pigtail and IVC
venogram through 10F long
sheath placed at HV-IVC
junction; (e) Placing an 8-mm
covered stent across the
parenchymal tract and an
8-mm bare metallic stent in
an overlapping manner to
complete TIPS creation. RHV
Right hepatic vein, PV Portal
vein
257
a
b
72 hours or sooner if a complication such as acute liver
failure is suspected. Shunt patency is assessed using color
doppler at regular intervals (at 1, 3, and 6months, and then
at 6months intervals). Anticoagulant is started to maintain
a target INR of 2–3 in patients with Budd–Chiari syndrome [17].
22.3.6 Complications ofTIPS
Myriads of complications may occur at every step during
TIPS creation. A detailed discussion of the complications
and their management is beyond the scope of this chapter.
The major complications include:
22.3.6.1 Extrahepatic Portal Vein Puncture [18, 19]
Inadvertent extrahepatic PV puncture leads to devastating
intraperitoneal hemorrhage due to a lack of parenchymal
tamponade. Thus, PV puncture should be performed under
real-time USG guidance. If this complication occurs, the rst
e
rescue step is to inate a balloon catheter across the puncture
site, followed by immediate deployment of a stent-graft.
22.3.6.2 Hepatic Artery Injury [18–20]
Although uncommon, hepatic artery injury may lead to intraperitoneal hemorrhage, pseudoaneurysm, arterial occlusion,
arterio-portal shunting, and arterio-biliary stula formation.
Hepatic arterial bleeding requires super-selective transarterial embolization using coils or a vascular plug. Stenting
may be required in some cases to avoid the potential risk of
hepatic infarction with embolization.
22.3.6.3 Post-TIPS Hepatic Encephalopathy [21,
22]
Hepatic encephalopathy (HE) is the most common postTIPS complication, seen in 25–45% of cases. Careful patient
selection is crucial to prevent this complication. Risk factors
include age >65 yrs, diabetes mellitus, previous HE, CTP
score >10, and sarcopenia. Patients not responding to medical therapy may require embolization of a large spontaneous
portosystemic shunt (if any) and/or TIPS reduction.
258
R. K. Patel and A. Mukund
22.3.6.4 Post-TIPS Hepatic Failure (PTLF) [18,
21–23]
TIPS reduces portal perfusion that may precipitate liver failure in patients with poor hepatic reserve. A reduction of postTIPS- PPG to <5m Hg is associated with an increased risk of
liver failure and thus should be avoided by choosing the
appropriate stent size. Furthermore, various technical factors, such as occlusion of the hepatic artery, hepatic vein(s)
by the covered stent in case of common origins, and
thrombosis/occlusion of a major branch of PV, can cause
hepatic infarction and PTLF.Thus, precise stent placement is
of utmost importance in avoiding such complications. While
most cases of PTLF are treated conservatively, progressive
hepatic failure, despite medical treatment, may require shunt
reduction. Ultimately patients need liver transplantation.
22.3.6.5 TIPS Dysfunction Resulting
inRecurrent Symptoms ofPortal
Hypertension [18, 19, 21]
Given a higher patency rate, a PTFE stent-graft is recommended for TIPS. This is because the PTFE stent-graft
excludes biliary contamination of TIPS which otherwise
causes pseudo-intimal hyperplasia and TIPS stenosis.
Presently, most shunt malfunction occurs due to various
technical errors and mechanical causes. A stent short of the
HV-IVC junction (>1cm) results in HV stenosis secondary
to intimal hyperplasia; thus, the stent should be extended to
the HV-IVC junction. Abnormal conguration of the stent
may also result in shunt stenosis and subsequent thrombosis.
The presence of competing varices or SPSS diverts the ow
away from the TIPS, resulting in sluggish ow and secondary stent thrombosis within the TIPS.Rarely, hepatocellular
carcinoma invades the vein or TIPS, causing shunt
occlusion.
TIPS Revision [19, 21, 24, 25]
Shunt dysfunction leads to the recurrence of symptoms, such
as variceal bleed and ascites. USG is an important screening
tool for the early detection of suspicious shunt dysfunction.
USG ndings of shunt dysfunction include absent ow,
aliasing, and velocity >190cm/sec at the stenotic site, velocity <90cm/sec in the non-stenotic segment, change in shunt
velocity >50 cm/sec compared to previous Doppler, antegrade intrahepatic portal ow, and portal vein velocity
<30cm/sec in the pre-stent segment [24]. The gold standard
of diagnosis is venography with pressure measurement, performed only in patients with inconclusive or suspicious
Doppler ndings. Absent ow, >50% reduction in caliber or
portosystemic gradient >12–15mm Hg on venography indicates shunt dysfunction [21, 24, 25]. At times, intra-stent or
HV outow stenosis is only detected based on a high portosystemic gradient [19].
Stent dysfunction is managed with mechanical thrombectomy, angioplasty, and thrombolysis (Fig.22.3). Few cases
require additional stent placement within the TIPS.Abnormal
shunt conguration may require a TIPS extension with an
additional stent. Ultimately, a new parallel TIPS may be created when all methods of shunt revision fail [21, 24].
ab c
Fig. 22.3 DIPS recanalization: (a) Coronal CECT showing intra-stent
thrombosis (white arrow A) with recurrence of ascites. (b) Balloon
maceration (black arrow B) through transjugular route with local
thrombolysis with urokinase performed. (c) Post-thrombolysis venogram showing recanalized shunt with good run-off. DIPS Direct IVC to
PV shunt
22 Interventions oftheHepatic Veins, Inferior Vena Cava, andPortal Vein
259
22.3.7 Discussion
As the risks outweigh the benets, TIPS is not indicated to
prevent primary variceal bleeding. However, no further prophylactic measure of variceal hemorrhage is required if TIPS
is performed for another indication, such as refractory ascites [10].
Results from three RCTs have demonstrated the survival
benets of early preventive insertion of TIPS within 24hrs or
within 72hrs of admission, also called “preemptive TIPS” in
patients at high risk of uncontrolled bleeding and bleedingrelated mortality [26–28]. The denition of high-risk criteria
varies from study to study. A European multicenter RCT
applied highly selected criteria for preemptive TIPS: Child
class B with active bleeding on endoscopy or Child class C
with 10–13 scores. TIPS group showed a signicant reduction in the 1-year probability of failure to control bleeding or
rebleeding (ARR-47%) and, most importantly, 1-year mortality (ARR-25%) [27]. Another recent Chinese single- center
RCT also demonstrated a signicant reduction in bleedingrelated mortality and 1-year transplant-free mortality following preemptive TIPS, however with a lower ARR (13%) than
the European RCT.This was due to the inclusion of patients
with a lower risk of failure to control bleeding or rebleeding:
Child class B without active bleeding and patients with hepatitis B on antiviral therapy [28].
TIPS controls ascites better than large volume paracentesis (LVP) [10]. Nevertheless, the data regarding the survival
benets of TIPS are conicting. Notably, most of the previous RCTs (6 out of 7) used bare stents; thus, a higher rate of
shunt dysfunction could be expected [10]. However, the most
randomized control trial (RCT) comparing PTFE-TIPS with
LVP in patients with recurrent ascites has demonstrated
improved 1-year survival without any increased incidence of
hepatic encephalopathy [29]. In addition, TIPS has also been
shown to improve the quality of life and nutritional status in
patients with refractory ascites [30, 31].
8mm vs. 10mm Shunt
Recent meta-analyses, including RCTs and non-RCTs, have
demonstrated that an 8-mm shunt is associated with a lower
risk of hepatic encephalopathy compared to a 10-mm stent.
Liu etal. showed a 32% decreased risk of HE in 8-mm vs.
10-mm shunt (HR: 0.68, 95% CI: 0.51~0.92, p < 0.0001)
while a 76% increased risk of rebleeding/paracentesis.
However, no overall survival (OS) difference was noted [32].
Another recent meta-analysis by Huang etal. did not show
any signicant differences in variceal rebleeding between 8and 10-mm shunt, however with a lower shunt dysfunction in
the 10-mm stent group [33]. Data regarding survival differences (8 vs. 10mm) are conicting, and further studies are
required.
22.4 Balloon-Occluded Retrograde Transvenous Obliteration (BRTO)
Although less common, gastric variceal bleeding in cirrhosis
is associated with higher morbidity and mortality. Endoscopic
therapy is also difcult and less effective in gastric varices
[34]. TIPS seems to be less effective in gastric variceal bleeding, as gastric varices may bleed despite adequate portal
pressure reduction [35]. Balloon-occluded retrograde transvenous obliteration of gastric varices (BRTO) was initially
developed in Japan as an alternative strategy. BRTO results
in direct obliteration of gastric varices after occlusion of the
dominant efferent shunt. Unlike TIPS, BRTO can be performed in patients with poor hepatic reserve. Furthermore,
BRTO improves hepatic synthetic function [36–38].
22.4.1 Indications andContraindications
ofBRTO
Table 22.2 summarizes the various indications and contraindications of BRTO.
22.4.2 Pre-Procedural Evaluation
Pre-procedural assessments include clinical, laboratory,
endoscopic, and imaging evaluations. Actively bleeding
patients need stabilization before the procedure. The patient
should be evaluated for hepatic encephalopathy. Laboratory
investigations include liver and renal function tests, complete blood count, INR, and arterial ammonia.
Shunt occlusion increases the portal pressure and may
worsen the esophageal varices, increasing the esophageal
bleeding risk. A UGI endoscopy must be considered before
BRTO to evaluate the esophageal varices, and high-risk
esophageal varices, if found, should be treated
endoscopically.
Table 22.2 Indications and contraindications of BRTO
Indications:
Recurrent gastric variceal bleeding patients with failed medical and
endoscopic therapies
Prophylaxis against rebleeding after primary endoscopic therapy
Active gastric variceal bleeding as an alternative to TIPS
Management of recurrent shunt-related hepatic encephalopathy
Contraindications:
Severe uncorrected coagulopathy
Gross ascites
Portal vein thrombosis (gastrorenal shunt is the only outow vein)
High-risk esophageal varices
Absence of any catheterizable gastrorenal shunt
260
ab
Fig. 22.4 BRTO for hepatic
encephalopathy. (a) Coronal
MIP CT portogram showing a
dilated and tortuous lienorenal
shunt. (b) Shunt embolization
with a sclerosant mixture after
occlusion of the efferent vein
using a balloon catheter
placed via jugular route. PV
Portal vein, LRV Left renal
vein
R. K. Patel and A. Mukund
Prior imaging, especially triple-phase CT or MRI, plays a
crucial role in patient selection and procedural planning.
Multiplanar imaging, especially the coronal reformat images,
is essential to evaluate the shunt morphology (Fig.22.4a).
Assessment of shunt diameter and narrowest site are critical
in choosing the appropriate occlusion balloon or plug size.
Another important imaging parameter is portal vein patency.
In patients with complete portal vein, closure of only the outow shunt can lead to mesenteric venous hypertension,
mesenteric ischemia, and possibly entire splanchnic portal
venous thrombosis. Other relevant imaging features include
ascites. The presence of ascites is a sign of relative decompensation and would be expected to increase after shunt
closure.
22.4.3 Requirements
• 5F angiographic catheter (MPA/C2/SIM1/Picard)
• 0.035″ angled glide wire and stiff wire
• 6-12F Flexor Check-Flow Introducer sheath
• A compliant balloon catheter (balloon size 1–2mm larger
than the diameter of the shunt).
• Sclerosant, gel foam, lipiodol
22.4.4 Sclerosants
Sodium tetradecyl sulfate (3% STS) is the most commonly used sclerosant. The average STS required for
BRTO is around 10ml. However, some cases require up to
20 ml. Alternatively, 3% polidocanol can also be used
(avg. volume- 10 ml). Nowadays, ethanolamine oleate is
preferred owing to its hemolytic nature, causing acute
renal failure [39].
22.4.5 Relevant Anatomy
A clear understanding of gastric variceal anatomy is crucial
for technical success and for avoiding complications. The
gastric variceal system consists of three components: (1)
afferent vein (portal venous inow), (2) central variceal
part, and (3) efferent vein (systemic outow vein). Afferent
supply is from the left gastric/posterior/short gastric vein or
a combination of these. The most frequent efferent includes
the inferior phrenic vein, which joins with the left adrenal
vein and drains into the left renal vein to form a gastrorenal
shunt (85% of cases). Less common efferents include gastrocaval (10%) shunt or rarely into other systemic veins
[40]. Drainage patterns vary (Kiyosue classication), and
their recognition is crucial for successful variceal obliteration [41].
22.4.6 Techniques
Balloon Retrograde Transvenous Obliteration
The procedure is performed under local anesthesia with conscious sedation.
1. Vascular access: Right femoral or internal jugular access
and placement of a 6-12F vascular sheath. A preprocedural CT or MRI review helps decide the approach
that provides the best angle for shunt catheterization.
2. Shunt catheterization: The sheath is advanced into the
left renal vein, followed by catheterization of the gastrorenal shunt using a selective catheter (SIM1/Cobra/MPA
catheter). A compliant balloon is advanced into the shunt
over the guidewire.
3. Shunt occlusion: Preferably, the gastrorenal shunt is
occluded with the compliant balloon at the narrow point.
22 Interventions oftheHepatic Veins, Inferior Vena Cava, andPortal Vein
261
4. Retrograde venography: Balloon-occluded venography
is performed to evaluate the shunt anatomy and identify
the signicant efferent draining veins. If found, additional
signicant efferent channels are embolized with coils or
gel foam and sclerosant through the microcatheter.
5. Sclerosant injection: A mixture of 3% sodium tetradecyl
sulfate mixed with lipiodol and air (2: 1: 3 ratio) is
injected deep into the gastric variceal system through a
microcatheter after balloon occlusion (Fig. 22.4b).
Iodinated contrast has also been used instead of lipiodol
in some previous studies. Embolization should be stopped
when there is minimal lling of the afferent vasculature.
Care should be taken to avoid the spilling of sclerosant
into the spleno-portal axis.
6. Sclerosant dwelling time: Occlusion balloon catheter is
inated for 4–24hours and removed only after the stagnation of the sclerosant is conrmed on a follow-up
X-ray.
Modications of BRTO [39, 42]
Plug-Assisted Retrograde Transvenous Obliteration
(PARTO)
PARTO is a modication of BRTO where a vascular plug
is used in place of a balloon to occlude the efferent shunt.
Usage of the vascular plug obviates the risk of balloon rupture and decreases the procedure time.
Technique
1. Vascular access and shunt catheterization step is the same
as that of BRTO.
2. Advancement of the vascular sheath into the shunt: This
is the most challenging step required for plug deployment
within the shunt. Stiff wire support is required to advance
the sheath into the shunt.
3. A venogram is taken through the sheath to evaluate the
shunt anatomy and to conrm the sheath position before
plug deployment.
4. A vascular plug is deployed at the narrowest part keeping
a microcatheter distal to the site of the plug. The plug size
should be 30–50% more than the narrowest diameter. A
mixture of thick gel foam slurry made with contrast is
administered through the microcatheter to clog the crevices of the mesh. A contrast venogram is taken through
the microcatheter to conrm the shunt occlusion by the
plug. If found, any other signicant efferent veins should
be embolized using coils/gel foam slurry.
5. Finally, 3% sodium tetradecyl sulfate mixed with lipiodol
and air (2: 1: 3 ratio) is injected through the microcatheter
to ll the shunt and varices. CBCT can be used to ensure
the complete embolization (Fig.22.5).
6. In the end, the vascular plug is detached to complete the
procedure.
7. A non-contrast CT abdomen is taken after 24–48hours to
ensure complete variceal embolization and to rule out
complications if any.
If available, cone-beam CT (CBCT) can be used to delineate the gastric variceal system better during the procedure.
It is also very helpful to ensure the adequate embolization of
the shunt.
Other Modications of BRTO
One of the modications is CARTO which uses coils and gel
foam/sclerosant instead of vascular plugs or indwelling balloons. CARTO is possible even when shunt size, angle, or
vascular tortuosity precludes BRTO/PARTO.A larger shunt
(even up to 25–30mm) can also be occluded using this technique. Multiple coils are placed through a 4F glidecath/
microcatheter at the narrowest portion of the shunt until
there is complete occlusion, followed by injection of gel
foam slurry/sclerosant solution (CARTO-I). CARTO-II
includes an initial standard BRTO approach, followed by the
deployment of multiple coils to occlude the gastrorenal
shunt. Upon complete occlusion of the shunt, the occlusion
balloon is deated and removed.
Another modication includes BATO (balloon-occluded
antegrade transvenous obliteration), in which variceal embolization is performed through the afferent vein through percutaneous transhepatic or an existing TIPS (trans-TIPS)
route. Both BRTO/PARTO and BATO may be combined to
achieve variceal obliteration in exceptional circumstances.
The advantages and disadvantages of different shunt
occlusion techniques are summarized in Table22.3 [39, 42].
22.4.7 Complications ofShunt Occlusion
Procedures [39, 42, 43]
1. Transient and self-limited epigastric/low backache, fever,
and nausea
2. Worsening of esophageal varices leading to increased risk
of bleeding
3. Worsening of ascites or hydrothorax
4. Pulmonary embolism either through collateral veins or
due to balloon rupture
5. Portal vein thrombosis
6. Renal vein thrombosis
22.4.8 Discussion
The technical success rate of BRTO ranges from 79 to 100%,
with a rebleeding rate of 0 to 20% [44–46]. A meta-analysis
by Park etal. reported a clinical success rate of 97.3% in
treating gastric varices, while major complications were
262
cd
Fig. 22.5 PARTO for gastric
varices. (a) Coronal CT
portogram (inset axial image)
showing dilated and tortuous
gastric varices (black arrow
A) with a large gastrorenal
shunt (open white arrow A).
(b) Placement of a 7F
vascular sheath through the
transfemoral route into the
gastrorenal shunt and
advancing a microcatheter
(black arrow B) through the
sheath deep into the shunt. (c)
Shunt occlusion by a vascular
plug (open black arrow C),
followed by embolization of
gastric varices using a
lipiodol, 3% STS, and air
mixture (1:2;3) (dotted black
area C). (d) Follow-up CT
after 2months showing
resolution of varices (white
circle D). IVC Inferior vena
cava, LRV Left renal vein,
AVP Amplatzer vascular plug
R. K. Patel and A. Mukund
a
b
Table 22.3 Advantages and disadvantages of different shunt occlusion techniques [39, 42]
Advantages Disadvantages
BRTO Proven outcomes in GV bleeding
PARTO
CARTO No balloon or vascular plug size limitation
BAT O Useful in patients with TIPS
GV Gastric varices, GR Gastrorenal
May be feasible when anatomy precludes advancement of a
sheath into the shunt that is required for plug deployment
No indwelling balloon→ short procedure time
No risks of balloon rupture
May not require coil embolization of smaller efferent veins
Feasible even for larger shunts up to 25–30mm
Feasible in difcult shunt anatomy when BRTO/PARTO is
not possible
Useful even in the absence of GR shunt
Longer procedure time
Toxicity-related sclerosing agents
Balloon rupture
Higher-level monitoring even after the procedure till the
indwelling balloon is kept
Shunt anatomy may preclude the advancement of a sheath
into the shunt
Limited by the shunt size up to 18mm (as the largest available
plug size is 22mm)
More procedural time than PARTO
Most costly due to the usage of multiple coils
Longer procedure time to embolism afferent veins
Need for percutaneous transhepatic or TIPS access
distal SMV
I
II
22 Interventions oftheHepatic Veins, Inferior Vena Cava, andPortal Vein
263
noted only in 2.6% of cases. Importantly, BRTO led to the
recurrence of the esophageal varices in 33.3% of patients
[47].
BRTO/PARTO in a setting of portal vein thrombosis can
be potentially life-threatening owing to the risk of mesenteric venous congestion and bowel ischemia [40]. However,
a small series of two non-cirrhotic cases showed satisfactory
resolution of gastric varices after BRTO in subacute portal
vein thrombosis without any signicant complications [48].
Shunt occlusion increases the portal ow, thereby causing
hepatic perfusion and improving hepatic synthetic function.
Patients experience improvement in CTP and MELD scores
as well. However, not all patients experience improved
hepatic synthetic function (serum albumin, bilirubin, and
prothrombin time) following shunt occlusion. Improvement
in liver function depends on baseline liver stiffness, shunt
diameter, and change in HVPG [36–38]. In a study of 50
patients with more than 3months of follow-up after shunt
occlusion, a lower baseline LSM was a predictive factor for
improved serum albumin (sensitivity-78.4% and specicity-
69.2% with a cut-off of 22.9kPa) [38]. Baseline liver, splenic
stiffness, and HVPG are also predictors of esophageal variceal exacerbation following shunt occlusion. A recent study
by Furuichi et al. demonstrated that LSM at 6 months of
>19.9kPa and SSM at day 7 of >21.7kPa were predictors of
the occurrence of EGV [49].
22.5 Portal Vein Thrombosis (PVT)
22.5.1 Cirrhosis withPVT
Patients with liver cirrhosis have a higher risk of portal vein
thrombosis (PVT). The pathogenesis of PVT is multifactorial; however, portal vein stasis and alteration in hemostasis
play the most important role. Prevalence of PVT increases
with increased severity of cirrhosis: 10% in compensated cirrhosis, 17% in child B/C cirrhosis, and up to 26% in liver
transplant candidates. PVT causes the worsening of portal
hypertension and its related complications [53, 54].
Color Doppler USG is the rst-line imaging modality
used to diagnose PVT. CT or MR portography is recommended to conrm PVT and complete staging of
PVT.Various classication systems exist for PVT in cirrhotics; however, the Yerdel classication is the most widely
used (Fig.22.6) [55].
Management
In asymptomatic patients with PVT, regular follow-up is
recommended. Potentially LT candidates, patients with
>50% occlusion/progressive PVT of the trunk or both main
branches, and extension of thrombus into the SMV are indi-
BRTO vs. TIPS in Gastric Variceal Bleeding
GOV-1 varices are treated similarly to esophageal varices,
where TIPS plays an important role. In patients with bleeding from GOV-2 and IGV-1 who have a gastrorenal shunt,
BRTO/PARTO is an alternative considering the fact that
these varices even bleed at a lower pressure (<12 mm Hg).
TIPS decreases hepatic portal perfusion, which leads to
worsening liver function and hepatic encephalopathy. BRTO/
PARTO does the opposite of TIPS. Several recent metaanalyses comparing TIPS vs. BRTO in gastric variceal bleeding have concluded that BRTO is associated with a lower rate
of rebleeding and post-procedural hepatic encephalopathy as
well as better survival than TIPS [50–52].
Treatment should be individualized (TIPS vs. BRTO)
depending on the vascular anatomy, associated comorbidities, availability, and local expertise. TIPS may be a
better option in patients with associated ascites and/or portal
vein thrombosis without any other contraindications. In contrast, BRTO may be a good option for patients having a high
risk of post-TIPS hepatic encephalopathy or heart failure
[10, 50–52].
PV
SMV
<50% luminal thrombosis of
PV +/-minimal extension into
SMV
III
Complete thrombosis of
PV and proximal SMV
Fig. 22.6 Yerdel classication of non-malignant portal vein thrombosis (PVT)
>50% luminal thrombosis of
PV +/-minimal extension into
SMV
IV
Complete thrombosis of PV
and proximal as well as
264
R. K. Patel and A. Mukund
cations of treatment. Systemic anticoagulation is the initial
treatment of choice, and the patients should be screened
every 3 to 6months [53]. Portal vein recanalization with
TIPS (PVR-TIPS) re-establishes the portal ow and can
also facilitate liver transplantation. Indications of PVRTIPS in patients of cirrhosis with PVT include (1) no
response to 6 months of anticoagulation, (2) presence of
signicant complications of portal hypertension, (3) old
thrombus >6months, less likely to respond to anticoagulation, and (4) contraindication to anticoagulation.
Embolization of varices or splenorenal shunt may also be
performed simultaneously with TIPS to enhance PV ow
and patency [53, 56].
TIPS in PVT is technically more challenging as intrahepatic PV branches are either occluded or narrowed. Thus,
USG guidance is imperative for targeting PV during TIPS
creation. Pre-procedural CT portography and intraprocedural indirect venography may help target PV in patients
with PVT.Once PV access is obtained, a guidewire is negotiated through the thrombus into SMV or splenic vein. The
remaining steps of PVR-TIPS are similar to conventional
TIPS. PV recanalization may not be successful in patients
with chronic PVT and cavernoma. In such cases, TIPS is created between HV and a dominant periportal collateral vein
[57, 58].
If PV puncture through the transjugular route fails, a
transsplenic or transhepatic approach may be considered.
Transsplenic access seems to be technically easier than the
transhepatic approach during PVR-TIPS.Using a 21G needle, transsplenic or transhepatic access is obtained, followed
by catheterization of the right or left portal vein using different guidewire/catheter combinations. A GooseNeck snare is
then placed at the intended site of PV puncture, and the snare
loop is targeted through a transjugular intrahepatic approach
to obtain a through and through access. The remaining procedure is accomplished through the jugular route. After TIPS
creation, PV recanalization is attempted by mechanical
thrombectomy, angioplasty, thrombolysis, or a combination
of these. A combination of mechanical and pharmacological
thrombolysis achieves a superior recanalization rate than
mechanical thrombolysis alone. In the end, the transsplenic/
transhepatic tract is embolized using coils/glue/plug to minimize bleeding. The transhepatic/transsplenic approach may
be inappropriate in patients with ascites and coagulopathy
due to the higher bleeding risk [56–60].
22.5.2 Non-cirrhotics withPVT
In non-cirrhotics, PVT has one or more identiable risk factors in about 70% of patients, while it remains idiopathic in
Table 22.4 Differences in imaging features between acute and chronic
portal vein thrombosis (PVT) [61, 62]
Acute PVT Chronic PVT
High-density thrombus on
non-contrast CT
Lack of signicant
Porto-portal collaterals
Normal spleen size
H/o recent surgery
Cavernoma/portosystemic collaterals
Splenomegaly
Portal biliopathy
Alteration in hepatic echotexture and
morphology secondary to longstanding portal hypoperfusion
30% of cases [61]. In addition to systemic prothrombotic
conditions, local factors also play an essential role in its
pathogenesis (e.g., acute pancreatitis and umbilical sepsis).
Acute PVT remains asymptomatic or may present with
abdominal pain. Some patients may develop mesenteric
venous ischemia and bowel infarction. Chronic PVT leads to
portal hypertension and presents with complications due to
portal hypertension similar to cirrhosis.
Imaging is helpful in the diagnosis and evaluation of the
extent of PVT and provides clues to differentiate acute
from chronic PVT.Table22.4 summarizes the differentiating imaging features between acute and chronic PVT [61,
62].
Management
Acute PVT necessitates prompt initiation of anticoagulation
therapy (at least for six months) as the recanalization rate
decreases with a delay in anticoagulation therapy [61, 63].
Various radiological interventions, such as catheter-directed
thrombolysis [tissue plasminogen activator (t-PA) or urokinase] via transjugular or transhepatic route, mechanical
thrombolysis, or combined pharmaco-mechanical thrombolysis, and catheter-directed transarterial infusion of thrombolytics (infusion via SMA), have been tried in different
settings [61, 64]. However, the data regarding the safety and
efcacy of these interventions in the setting of acute PVT are
scarce [62, 64].
Chronic PVT is managed similarly to PVT in patients
with cirrhosis.
22.6 HV andIVC Angioplasty
Budd–Chiari syndrome (BCS) refers to hepatic venous outow tract obstruction (HVOTO) anywhere from the level of
the small hepatic veins to the IVC-RA junction, which leads
to venous congestion, hypoxic injury, and necrosis of hepatocytes. Clinical presentation may vary, including an acute,
subacute, chronic, or fulminant form. The chronic form simulates cirrhosis and presents with complications of portal
hypertension, while the fulminant form presents with acute
liver failure.