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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1209_Библиотеки_им_академика_М_И_Перельмана.pdf
361
search were “portal/thrombosis/anticoagulation,” “portal/thrombosis/revascularization,” “portal/thrombosis/transplant,” “portal/thrombosis/thrombolysis,” and “portal/thrombosis/thrombectomy.” The data was classifi ed using the GRADE system.
Seven retrospective cohort studies and one prospective pilot study were included
(Table 32.2 ).
Results
Clinical Relevance of PVT After Liver Transplantation
PVT occurs in less than 4 % [ 2 – 4 ] of liver transplant recipients, but it typically
occurs within 30 days of transplantation, resulting in a high risk of graft loss. The
relevance of PVT is increasing as transplantation in the setting of pre-transplant
PVT has gained support in the published literature [ 7 , 8 ]. Liver transplantation is
performed in patients with pre-existing PVT in 2–26 % of cases, and rethrombosis
occurs in 6.2–28.6 % of those patients [ 9 ]. Improving surgical options for patients
with pre-transplant PVT [ 10 ] may result in an increased incidence of post-transplant
PVT. Thus, the relevance of the best application of surgical and endovascular therapies is likely to increase. To date, no studies specifi cally quantify the impact of
post-transplant PVT on cost, hospital stay, morbidity and mortality .
Treatment Strategies
The existing published literature regards surgical revascularization as a fi rst-line
intervention to salvage the liver graft after early, post-transplant PVT. Since publications addressing treatment options for post-transplant PVT are limited to a few
case reports and a short case series, this analysis was expanded to review endovascular treatment options that have been applied to PVT when it occurs in the general
population. In such cases, nonsurgical options include anticoagulation alone or in
combination with endovascular techniques such as catheter-directed thrombolysis,
mechanical thrombectomy, balloon angioplasty, and stent placement – often in
combination. The success rates of these therapies in patients with native livers, and
their relevance to liver transplant recipients are addressed.
Treatment choices vary with factors such as operator preference, the time
interval since major surgery , symptom duration and progression, and the extent
of thrombosis. At minimum, the published literature supports the feasibility of
endovascular revascularization of acute to subacute PVT not complicated by
bowel infarction or peritonitis, and suggests that 30-day mortality rates, complication rates, and long-term patency rates are at least comparable to surgical
alternatives.
32 Management of Early Post-transplant Portal Vein Thrombosis: Results…
362
Table 32.2 Management of PVT or PMVT
Author (year) N
Mean
age Method
Technical
success (%)
Clinical
success (%)
Recurrence
(%)
Major
complications (%)
Study type ( quality of
evidence)
Jensen (2013) [
1 ] 15 NR Surgery 60 60 NR NR Retrospective cohort
(low)
Duffy (2009) [
18 ] 84 21 Variable Variable Variable NR NR Retrospective cohort
(low)
Hollingshead
(2005) [
19 ]
20 37.6 Thrombolysis 75 85 NR 60 Retrospective cohort
(low)
Liu (2009) [
20 ] 46 48 Thrombolysis 74 98 9 % at 4 m 0 Retrospective cohort
(low)
De Santis (2010)
[
21 ]
9 59 Thrombolysis 89 89 NR 0 Prospective pilot
(low)
Luo (2013) [
22 ] 18 NR Mechanical device,
thrombolysis, TIPS
a
100 94.4 28 % at mean
19 m
11 Retrospective cohort
(low)
Kim (2005) [
23 ] 11 44.3 Mechanical device,
thrombolysis
91 91 0 % at mean
42 m
9.1 % Retrospective cohort
(low)
Cao (2013) [
24 ] 14 61.2 Angioplasty
+/− stent
100 100 43 % at mean
16 m
0 Retrospective cohort
(low)
a
TIPS transjugular intrahepatic portosystemic shunt
J.M. Lorenz and M.V. Patel
363
Anticoagulation
Early initiation of anticoagulation has been standard practice for acute PVT for
decades, and this approach is endorsed by the American Association for the Study
of Liver Diseases (AASLD) guidelines [ 11 ]. In patients with native livers, antico-
agulation is the most commonly employed sole treatment strategy, and in any
patient, anticoagulation limits the risk of clot progression. Senzolo et al. performed
a prospective study of 56 cirrhotic patients with PVT in native livers demonstrating
that anticoagulation alone achieved a rate of recanalization, either partial or complete, of 63 %, whereas failure to treat with anticoagulation achieved a rate of only
5 % [ 12 ]. In addition, with anticoagulation, only 15 % progressed compared to 71 %
of patients without anticoagulation. In the general population, anticoagulation to
treat PVT has been shown to increase survival and increase symptom-free survival
[ 13 , 14 ], and durable results can be expected as long as patients pass the hurdle of
increased morbidity and mortality associated with PVT that presents within 1 month
[ 13 ].
In patients with native livers, PVT results in late complications in 83.3 % if
recanalization is not achieved and in 27.3 % after successful recanalization [ 15 ]. At
minimum, these results support the use of endovascular techniques for revascularization in cases likely to persist or progress despite anticoagulation. Such cases
include liver transplant recipients, cirrhotics, Budd-Chiari patients, and any patient
with poor or diminishing liver function. Intrahepatic PVT occurring early after liver
transplantation severely limits the application of anticoagulation as a sole treatment
option since such cases are associated with biliary stricture formation [ 16 ], hepatic
infarction [ 17 ] and death [ 18 ] in published series and case reports. PVT after trans-
plantation causes reduced 5-year survival [ 6 ] and a high risk of graft loss, particu-
larly when it presents early [ 3 ]. Therefore, early post-transplant PVT is more likely
to prompt fi rst-line treatment with invasive revascularization techniques in conjunction with the limited role of anticoagulation as an adjunctive therapy to prevent
progression or recurrence. Duffy et al. [ 18 ] reported a graft salvage rate of 46 % for
48 patients with post-transplant PVT treated only with anticoagulation, but the
interval between transplant and PVT was not specifi ed. In any patient with clinical
signs of bowel ischemia, endovascular or surgical management is warranted since
mortality rates over 50 % have been described [ 5 , 18 ].
Surgical Revascularization
Literature supporting surgical over endovascular revascularization for early PVT is
limited. Jensen et al. performed a case-control study of pediatric liver transplant
recipients. In 15 patients out of 415 recipients, early portal vein thrombosis (occurring in less than 30 days) was noted [ 1 ]. Operative restoration of portal fl ow was
achieved in 60 %. The authors noted that patients with early portal vein thrombosis
had preserved allograft function and no increase in mortality ; they recommended
multi-institutional studies. Duffy et al. [
18 ] reported a graft salvage rate of 32 % for
32 Management of Early Post-transplant Portal Vein Thrombosis: Results…
364
22 patients that underwent surgical revision with thrombectomy for post-transplant
PVT, and retransplantation in 20 of 84 cases of post-transplant PVT. Again, for all
cases, the interval to PVT was not specifi ed.
Thrombolysis Without Mechanical Methods
Thrombolysis without mechanical thrombectomy has been applied to PVT and
PMVT for decades in patients with native livers. Hollingshead et al. retrospectively
reviewed 20 acute or subacute cases; thrombolysis alone resulted in partial to complete resolution of thrombus by imaging in 75 %, symptom resolution in 85 %, and
a 60 % major complication rate [ 19 ]. The route of delivery of thrombolytic agent
varied and included cases of catheter-directed venous infusion, mesenteric arterial
infusion, or a combination.
Liu et al. retrospectively reviewed 46 patients with acute or subacute PVT or
PMVT treated with thrombolysis and reported partial to complete resolution in 74
%, but in this study, no major complications were encountered [ 20 ]. For 32 patients
(70 %), catheter-directed venous thrombolysis was the sole route of delivery of
thrombolytic agent rather than combined mesenteric arterial and venous infusion, a
possible explanation for the low complication rate. The majority exhibited both
SMV and portal venous thrombosis. Partial or complete clearance of thrombus was
observed in 100 %, and the 4-month recurrence rate was only 10 %. This study
lends support for the application of venous catheter-directed thrombolysis as a better fi rst-line option than the combination of venous and arterial thrombolytic delivery in the majority of cases. When complete clearance of thrombus fails to establish
hepatopetal portomesenteric fl ow, mesenteric arterial infusion of thrombolytic
agents may become an option.
De Santis et al. performed a short prospective pilot study using catheter-directed
portal venous thrombolysis to treat PMVT in nine patients with cirrhosis [ 21 ].
They achieved partial to complete clearance in eight of nine patients and noted one
recurrence. As expected, variceal pressure dropped from 30.7 ± 4.5 mmHg to
21.2 ± 6.6 mmHg (p = 0.012).
Mechanical Methods with Thrombolysis
Luo et al. retrospectively reviewed 18 patients that presented with subacute, symptomatic PMVT and were treated with balloon dilatation, sheath-directed thrombus
aspiration, and thrombolysis with creation of an intrahepatic portosystemic shunt
for access and treatment [ 22 ]. Thrombolysis was performed over a mean duration of
65.3 ± 29.5 h. The mean portosystemic gradient dropped from 33.8 ± 4.9 mmHg to
15.4 ± 2.1 mmHg (p < 0.001) as a result of treatment. Clinical success rate was 94.4 %.
Complications included one death, one patient with mild hepatic encephalopathy,
and one patient with hemothorax, the latter two cases managed conservatively.
J.M. Lorenz and M.V. Patel
365
During a mean follow-up duration of 18.6 ± 17.5 months, fi ve patients experienced
symptomatic TIPS malfunction and all others experienced no further recurrence.
While quality data is lacking, mechanical thrombectomy devices promise to
improve clot clearance and shorten the interval required for thrombolysis, thereby
improving technical success, patency rates, and complication rates in a manner similar to results seen for their application to deep venous thrombosis. Kim et al. performed a small, retrospective cohort study of 11 patients with acute to subacute
thrombosis variably involving the portal and superior mesenteric veins [ 23 ]. In all
patients, the strategy applied was initial therapeutic heparinization followed by
percutaneous , transhepatic thrombectomy using an endovascular mechanical
device. In 10 of 11 patients, catheter-directed thrombolysis followed via the transhepatic access sheath. Balloon dilatation was used to treat underlying stenoses, and
all patients were transitioned from post-procedure heparinization to long-term
Warfarin. The authors report immediate restoration of fl ow in 90.9 % of patients, all
of whom experienced rapid symptom relief. One case was complicated by hemothorax requiring a chest tube, and one patient died after unsuccessful restoration of
fl ow. This patient was a poor surgical candidate for whom endovascular recanalization was attempted despite presentation with peritonitis and sepsis. For the remaining nine patients, no recurrent signs or symptoms of PMVT were noted during a
mean follow-up period of 42 months ± 22.5. These preliminary results suggest that
durable results can be achieved with revascularization followed by long-term
anticoagulation.
Mechanical Methods Without Thrombolysis
For patients that require revascularization for acute to subacute PVT or PMVT but
for whom thrombolysis may be contraindicated due to factors such as very recent
transplantation or ongoing bleeding, some endovascular options may still apply.
Cao et al evaluated balloon angioplasty with or without stent placement in 14
patients with PMVT of variable underlying causes and achieved partial to nearcomplete clearance with brisk hepatopetal fl ow in all patients and a persistent 50 %
residual narrowing in only one patient [ 24 ]. Initial clinical success was 93 %. One
patient experienced acute rethrombosis in 8 days, and over a mean follow-up period
of 16.3 months, rethrombosis occurred in 43 %. Despite the high rethrombosis rate,
this small study shows the feasibility of treating some cases of PVT and PMVT
without thrombolytic agents.
Recommendations
• Anticoagulation is an option for a sole treatment strategy when subacute PVT or
PMVT occurs in patients with native livers, but is rarely an option for early PVT
after liver transplant ation . Anticoagulation typically augments surgical or
32 Management of Early Post-transplant Portal Vein Thrombosis: Results…
366
endovascular revascularization in liver transplant recipients (evidence quality
low, weak recommendation).
• Choice of intervention for revascularization should be made based on local
expertise, the timing of symptom progression, the status of the patient as a surgi-
cal candidate, and treatment-specifi c contraindications. Little precedent exists in
the published literature for establishing an algorithm for the application of surgi-
cal and endovascular therapies for PVT and PMVT, although the success of both
options has been established in limited retrospective cohort studies and case
reports (evidence quality low, weak recommendation).
A Personal View of the Data
Large, prospective cohort studies that directly address PVT and PMVT in the early
period after liver transplant ation are unlikely to be forthcoming, given the low incidence of this complication in an already limited cohort of liver transplant recipients.
Such studies would require multi-institutional cooperation. As a result, local opinion and expertise tends to trump evidence-based practice when managing this condition. While complication rates vary from 0 to 60 % for endovascular techniques,
most morbidity is managed conservatively and tolerated well, especially when compared with the morbidity associated with re-do surgery . At a minimum, in liver
transplant patients, PVT threatens graft and patient survival and all therapeutic
options should be available in transplant centers.
References
1. Jensen MK, Campbell KM, Alonso MH, et al. Management and long-term consequences of
portal vein thrombosis after liver transplantation in children. Liver Transpl.
2013;19(3):315–21.
2. Wozney P, Zajko AB, Bron KM, et al. Vascular complications after liver transplantation: a
5-year experience. Am J Roentgenol. 1986;147(4):657–63.
3. Khalef H. Vascular complications after deceased and living donor liver transplantation: a
single- center experience. Transplant Pro. 2010;42:865–70.
4. Buell JF, Funaki B, Cronin DC, et al. Long-term venous complication after full-size and seg-
mental pediatric liver transplantation. Ann Surg. 2002;236(5):658–66.
5. Kumar S. Mesenteric venous thrombosis. N Engl J Med. 2001;345:1683–8.
6. Millis JM, Seaman DS, Piper JB, et al. Portal vein thrombosis and stenosis in pediatric liver
transplantation. Transplantation. 1996;62(6):748–54.
7. Hibi T, Nishida S, Levi DM, et al. When and why portal vein thrombosis matters in liver trans-
plantation: a critical audit of 174 cases. Ann Surg. 2014;259(4):760–6.
8. Saidi RF, Jabbour N, Li YF, et al. Liver transplantation in patients with portal vein thrombosis:
comparing pre-MELD and MELD era. Int J Organ Transplant Med. 2012;3(3):105–10.
9. Sobhonslidsuk A, Reddy KR. Portal vein thrombosis: a concise review. Am J Gastroenterol.
2002;97:535–41.
J.M. Lorenz and M.V. Patel
367
10. Paskonis M, et al. Surgical strategies for liver transplantation in the case of portal vein throm-
bosis – current role of cavoportal hemitransposition and renoportal anastomosis. Clin
Transplant. 2006;20(5):551–62.
11. DeLeve LD, Valla DC, Garcia-Tsao G, et al. Vascular disorders of the liver. Hepatology.
2009;49(5):1729–64.
12. Senzolo M, Sartori TM, Rossetto V, et al. Anticoagulation and TIPS for portal vein thrombosis
in cirrhosis. Liver Int. 2012;32(6):919–23.
13. Rhee RY, et al. Mesenteric venous thrombosis: still a lethal disease in the 1990s. J Vasc Surg.
1994;20:688–97.
14. Abdu RA, Zakhour BJ, Dallis DJ. Mesenteric venous thrombosis – 1911 to 1984. Surgery.
1987;101:383–8.
15. Hall TC, Garcea G, Metcalfe M, et al. Impact of anticoagulation on outcomes in acute non-
cirrhotic and non-malignant portal vein thrombosis: a retrospective observational study.
Hepatogastroenterology. 2013;60(122):311–7.
16. Jeng KS, Huang CC, Lin CK, et al. Intrahepatic segmental portal vein thrombosis after living-
related donor liver transplantation. Transplant Proc. 2014;46(3):841–4.
17. Gladysz-Polak A, Polak WG, Jazwiec P, et al. Favorable resolution of hepatic infarctions in
transplanted liver after portal vein thrombosis treated by surgical thrombectomy: a case report.
Transplant Proc. 2006;38(9):3135–7.
18. Duffy JP, Hong JC, Farmer DG, et al. Vascular complications of orthotopic liver transplanta-
tion: experience in more than 4200 patients. J Am Coll Surg. 2009;208(5):896–903.
19. Hollingshead M, Burke CT, Mauro MA, et al. Transcatheter thrombolytic therapy for acute
mesenteric and portal vein thrombosis. J Vasc Interv Radiol. 2005;16(5):651–61.
20. Liu FY, Wang MQ, Fan QS, et al. Interventional treatment for symptomatic acute-subacute
portal and superior mesenteric vein thrombosis. World J Gastroenterol.
2009;15(40):5028–34.
21. De Santis A, Moscatelli R, Catalano C, et al. Systemic thrombolysis of portal vein thrombosis
in cirrhotic patients: a pilot study. Dig Liver Dis. 2010;42:451–5.
22. Luo JJ, Yan ZP, Wang JH, et al. Intrahepatic portosystemic shunt assisted by percutaneous
transhepatic approach for treatment of portal vein thrombosis. Zhonghua Gan Zang Bing Za
Zhi. 2013;21(11):855–9.
23. Kim HS, Patra A, Khan J, et al. Transhepatic catheter-directed thrombectomy and thromboly-
sis of acute superior mesenteric venous thrombosis. J Vasc Interv Radiol. 2005;16:1685–91.
24. Cao G, Ko GY, Sung KB, et al. Treatment of postoperative main portal vein and superior mes-
enteric vein thrombosis with balloon angioplasty and/or stent placement. Acta Radiol.
2013;54(5):526–32.
32 Management of Early Post-transplant Portal Vein Thrombosis: Results…
369© Springer International Publishing Switzerland 2016
J.M. Millis, J.B. Matthews (eds.), Diffi cult Decisions in Hepatobiliary
and Pancreatic Surgery, Diffi cult Decisions in Surgery: An Evidence-Based
Approach, DOI 10.1007/978-3-319-27365-5_33
Chapter 33
When Should Patients with Bleeding
Esophageal Varices Undergo TIPS Versus
Endoscopic Therapy?
John N. Gaetano and K. Gautham Reddy
Abstract Acute variceal bleeding is a serious sequela of cirrhosis and portal hyper-
tension, which carries signifi cant morbidity and mortality. Advances in therapeutic
techniques as well as accessibility and overall safety of esophagogastroduodenoscopy (EGD) allowed for endoscopic management to emerge as fi rst line therapy two
decades ago, and remain fi rst-line therapy today. Transjugular intrahepatic portosystemic shunt (TIPS) is a critical rescue therapy for those that fail endoscopic management, while rescue TIPS carries signifi cant morbidity and mortality, efforts to
identify patients that are likely to fail endoscopy and benefi t from early TIPS are
ongoing. Surgical portosystemic shunts, particularly distal splenorenal shunt, can
be considered for refractory bleeding in ideal patients with minimal comorbidities,
where surgeon experience is adequate and TIPS cannot be performed.
Keywords Acute variceal bleeding • Esophageal varices • TIPS • Endoscopic band
ligation • Splenorenal shunt
Introduction
Acute hemorrhage of esophageal varices continues to cause signifi cant morbidity
and mortality among those with portal hypertension. Primary and secondary prophylaxis, antibiotic and vasoactive drug administration, and improvements in endoscopic therapy have led to a decrease in the rates of hospitalization and decreased
rates of mortality over the last two decades [ 1 , 2 ]. However, the in-hospital mortality
of acute variceal bleeding remains strikingly high: up to 32 % in those with
J. N. Gaetano • K. G. Reddy (*)
Department of Gastroenterology, Section of Gastroenterology, Hepatology and Nutrition ,
The University of Chicago Medicine and Biological Sciences ,
5841 S. Maryland Ave, MC 7120 , Chicago , IL 60637 , USA
e-mail:
greddy@medicine.bsd.uchicago.edu
370
Child-Turcotte-Pugh (hereafter referred to as ‘Child-Pugh’) class C cirrhosis , making the management of acute variceal bleeding a diffi cult challenge [ 2 ].
The backbone of therapy of acute variceal hemorrhage requires prompt attention
to airway management , initiation of volume resuscitation, vasoactive therapy, antibiotic prophylaxis, and endoscopic therapy. Endoscopic band ligation, and previously endoscopic sclerotherapy, is the cornerstone of therapy. There remains a need
for rescue therapies and alternatives to endoscopy , namely transjugular intrahepatic
portosystemic shunt ( TIPS ) placement, balloon tamponade, and surgical portosystemic shunt formation. Timing and indications of rescue therapies lacks a standardized approach, and is the topic of this chapter.
Search Strategy
A literature search of English language publications from 1990 to present was used
to identify published data on surgical shunt, endoscopic therapy and transjugular
intrahepatic portosystemic shunt ( TIPS ) for the management of acute variceal
bleeding. Database searched was PubMed. Terms used in the search were “acute
variceal hemorrhage/bleeding” AND “endoscopic therapy” OR “TIPS” OR
“Surgical portosystemic shunt.” The PICO model was used for literature search
stratifi cation (Table 33.1 ).
Results
First Line Therapy
Endoscopic therapy as fi rst-line therapy for acute variceal hemorrhage became
consensus in the early 1990s. It was universally accepted in guidelines in 1995
[ 3 ], when endoscopic band ligation (EBL) was established as an alternative to
endoscopic sclerotherapy (ES). While EBL and ES have almost equal rates of
immediate hemostasis (89% and 88 %, respectively), in a meta-analysis of seven
randomized trials, ES is associated with higher rates of re-bleeding (31 % vs.
47 %), higher mortality (24 % vs. 32 %), and stricture formation (0 % vs. 11 %) [ 4 ].
Furthermore, multiple studies have reported that complications as a result of
therapy with EBL are signifi cantly less frequent when compared with ES, 11 %
vs. 25 % [ 5 – 7 ].
Table 33.1 Stratifi cation of
the literature search using the
PICO model
Patients Acute esophageal variceal hemorrhage
Intervention Endoscopic band ligation or sclerotherapy
Comparator TIPS or surgical shunt
Outcomes Mortality, morbidity
J.N. Gaetano and K.G. Reddy
371
Initial endoscopic therapy fails to control bleeding in 10–20 % of those who
present with acute variceal bleeding. Of those that are initially controlled with endoscopic therapy, rebleeding occurs in up to 30 % [ 8 ]. Failed therapy is been defi ned
as a failure to control bleeding, if the patient dies, or any one of the following are
met: (1) Fresh hematemesis or nasogastric aspiration of ≥100 mL of fresh blood >2
h after the start of a specifi c therapy, (2) development of hypovolemic shock, or (3)
a 3-g hemoglobin drop within any 24 h period if no transfusions are administered.
Rebleeding is defi ned as any bleeding that occurs more than 48 h after the initial
admission for variceal hemorrhage, provided there has been at least a 24-h period
without bleeding. “Early rebleeding” is defi ned as rebleeding within 6 weeks of the
onset of the initial bleed, while “late rebleeding” is defi ned as rebleeding after 6
weeks [ 9 ].
Rescue Therapies
Patient’s at high risk of early rebleeding (within 6 weeks) have the following characteristics: age >60, alcoholic cirrhosis , initial hemoglobin <8, thrombocytopenia,
encephalopathy, ascites , bleeding seen at endoscopy , red color signs (red wale signs)
on varices , large varices, high hepatic-venous pressure gradient (HVPG), and renal
failure. Risk factors associated with late rebleeding include: Liver failure, ascites,
hepatocellular carcinoma, active alcohol drinking, and red wale signs [ 10 ].
For patients who fail endoscopic therapy or in whom early rebleeding occurs, the
next therapeutic option is a critical decision point. In patients with rebleeding following initially successful endoscopic therapy, a second attempt at endoscopic therapy is reasonable, although data is limited in support of this approach [ 9 ]. In the
event of failure of initial endoscopic therapy or if a second rebleeding event occurs,
consensus guidelines from the American Association for the Study of Liver Disease
(AASLD), suggest an alternative modality should be considered.
Balloon Tamponade
Balloon tamponade is a temporary measure of achieving hemostasis by direct compression of bleeding varices and should be considered a bridge to a more defi nitive
treatment. Two types of oral-gastric tubes exist, the Sengstaken-Blakemore tube and
the Minnesota tube. Both tubes contain a gastric balloon and an esophageal balloon
with an aspiration port between the two. The Minnesota tube has an aspiration port
proximal to the esophageal balloon as well. The defl ated tube is placed with the
distal end into the stomach, then, the gastric balloon is infl ated and pulled upward
until secure at the GE junction. When the gastric balloon alone is insuffi cient to
control bleeding the esophageal balloon is infl ated. Esophageal balloon infl ation
increases the risk of necrosis at the GE junction. The gastric balloon tube should not
be infl ated for more than 48 h in order to prevent necrosis, and the esophageal
33 When Should Patients with Bleeding Esophageal Varices Undergo TIPS Versus…