TX STD Variceal. Clinic Liver Disease 2014

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Management of Acute VaricealBleeding

Jorge L. Herrera, MD

Endoscopic Band Ligation (EBL) of esophageal varices accompanies the article

at http://www.liver.theclinics.com/

INTRODUCTION

Acute variceal bleeding (AVB) remains one of the most dangerous complications of

portal hypertension. Advances in the management of AVB have resulted in a decline

in the rate of hospitalization in recent years,1 and mortality has decreased from

50%2 to between 15% and 20%3,4 over the last 3 decades. Despite these advances,

in-hospital mortality remains high and is related to the severity of the underlying

cirrhosis, ranging from 0% in Child A to 32% in Child C disease.5

A prompt and standardized approach to patients with variceal bleeding is required

to minimize the risk of bleeding-related mortality. This integrated and multidisciplinary

approach consists of airway protection, judicious volume resuscitation, vasoactive

therapy, antibiotic prophylaxis, and endoscopic intervention (Box 1).

Financial Disclosure: The author has no financial relationships in the subject matter or materials

discussed in this article.Division of Gastroenterology, University of South Alabama College of Medicine, Gastroenter-ology Academic Offices, 6000 University Commons, 75 University Boulevard S., Mobile, AL36688-0002, USAE-mail address: [email protected]

KEYWORDS

Portal hypertension Acute variceal bleeding Cirrhosis Endoscopic band ligation Endoscopy Vasoactive therapy

KEY POINTS

Recent changes in the management of acute variceal bleeding (AVB) have resulted indecreased mortality.

A structured approach incorporating airway safety, volume resuscitation, vasoactive and

antimicrobial pharmacotherapy, and early endoscopy minimizes morbidity and mortality

in patients presenting with AVB.

Presenting features that indicate a high risk of failing standard vasoactive and endoscopic

therapy include Child C cirrhosis, active bleeding on index endoscopy, presence of infec-tion, or a hepatic vein pressure gradient greater than 20 mm Hg.

Patients at high risk of failing standard therapy for AVB may benefit from more aggressive

approaches such as early TIPS placement following the index endoscopy.

Clin Liver Dis 18 (2014) 347357http://dx.doi.org/10.1016/j.cld.2014.01.001 liver.theclinics.com1089-3261/14/$ see front matter 2014 Elsevier Inc. All rights reserved.
mailto:[email protected]://dx.doi.org/10.1016/j.cld.2014.01.001http://liver.theclinics.com/http://liver.theclinics.com/http://dx.doi.org/10.1016/j.cld.2014.01.001mailto:[email protected]


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AIRWAY MANAGEMENT

Most patients presenting with AVB are alert, not massively bleeding, and have an intact

gag reflex. In this situation, no special precautions are needed to protect the airway.6

Patients presenting with altered mental status, often caused by hepatic encephalopa-

thy or intoxication, are at risk of aspiration and a decision to protect the airway via

endotracheal intubation should be made early in the course. Patients with massive

gastrointestinal bleeding not responding to initial interventions and in need of emergent

endoscopic therapy are at high risk for aspiration and should undergo endotracheal

intubation before sedation and endoscopy regardless of their mental status.7

VOLUME RESUSCITATION

At least 2 large-bore (1418 gauge) venous accesses should be placed on admission

for rapid administration of fluids and blood products. Excessive volume replacement

may lead to increased portal pressure and increases the risk for early rebleeding from

Box 1

Approach to variceal bleeding

Airway management

Consider endotracheal intubation if:

Altered mental status

Massive hemorrhage requiring emergent endoscopy

Volume resuscitation

Place 2 large-bore intravenous access catheters

Avoid excessive volume replacement

Maximum hemoglobin target of 7 to 8 g/dL

Use of FFP or platelets to correct coagulopathy may not be beneficial

Vasoactive therapy Reduce portal pressure by using one of the following:

Octreotide: 50 mg IV bolus followed by 50 mg/h infusion

Terlipressina: 2 mg every 4 h IV for 24 to 48 h, then 1 mg every 4 h

Somatostatina: 250 mg IV bolus followed by 250 to 500 mg/h infusion

Vasopressin: 0.4 units/min IV plus IV or transdermal nitroglycerin

Vapreotidea: IV bolus of 50 mg followed by 50 mg/h infusion

Antibiotic prophylaxis

Initiate antibiotics to reduce rebleeding risk; choose either:

Ceftriaxone 1 g IV every day for up to 7 days

Norfloxacin 400 mg orally once a day for up to 7 days

Endoscopic therapy

Obliterate varices using band ligation

Abbreviations:FFP, fresh frozen plasma; IV, intravenous.a Not currently available in the United States.

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varices; judicious use of volume expanders is recommended. In general, fluids should

be administered to keep systolic blood pressure at 100 mm Hg and maintain renal

perfusion. Saline use should be minimized because it may aggravate or precipitate

the formation of ascites and edema. Red blood cell transfusions should be adminis-

tered to achieve a hemoglobin no greater than 8 g/dL; higher levels have been asso-

ciated with increased portal pressure, more frequent complications, and worse

outcomes, particularly among patients with Child A or B cirrhosis.8

The routine use of platelet transfusions or fresh frozen plasma (FFP) to correct a low

platelet count or prolonged international normalized ratio (INR) is not supported by data

and may further contribute to volume overload and increased portal pressure. In partic-

ular, the use of FFP to normalize a prolonged INR may not result in improved coagula-

tion, because INR results have poor correlation with bleeding risk in cirrhosis.9 Recent

studies indicate that, despite a prolonged INR, some patients with cirrhosis show a hy-

percoagulable state caused by a deficiency of anticoagulant factors and a relative

excess of procoagulant factors,10 a balance that is not reflected by the INR results.

Likewise, increased levels of von Willebrand factor, often present in cirrhosis, enhance

platelet function and may compensate for the thrombocytopenia that is commonly pre-

sent in portal hypertension.11 For these reasons, the use of blood products to correct

coagulation abnormalities should be individualized on a case-by-case basis. Recom-

binant activated factor VII failed to achieve superiority compared with placebo in pa-

tients with variceal bleeding,12 and should not be routinely administered, although

selected patients with more severe bleeding may benefit from its use.

VASOACTIVE THERAPY

Interventions designed to decrease portal pressure should be instituted early in the

management of variceal bleeding. The use of vasoactive agents has been associated

with a significantly lower risk of acute all-cause mortality and transfusion require-

ments, improved control of bleeding, and shorter hospital stay.13 In most cases a var-

iceal source of bleeding can be suspected based on the patients history, physical

examination findings, or laboratory results. In this situation, empiric use of vasoactive

therapy to decrease portal pressure is recommended even before the source of

bleeding is confirmed.

Vasoactive drugs reduce portal pressure mainly by causing splanchnic vasocon-

striction and reducing portal blood flow. Two main classes of drugs are used: (1) vaso-pressin or its analogue terlipressin, and (2) somatostatin or its analogues octreotide or

vapreotide (see Box 1). In the United States, only vasopressin and octreotide are avail-

able. Vasopressin is generally not recommended because of its side effect profile and

its minimal effects on decreasing rebleeding and improving survival.14 Vasopressin

infusion is associated with significant ischemic side effects including coronary artery

vasoconstriction and mesenteric ischemia. To minimize side effects, it should be

used in combination with intravenous or transdermal nitroglycerine15 and only if other,

safer vasoactive drugs are not available.

Terlipressin is a vasopressin analogue with an improved side effect profile. It is a se-

lective vasoconstrictor of the splanchnic bed and does not need to be used as acontinuous infusion. Terlipressin provides a 34% relative risk reduction in mortality

in acute variceal hemorrhage,16 with an improved side effect profile compared with

vasopressin. At present, terlipressin is not approved by the US Food and Drug Admin-

istration for use in the United States.

The somatostatin analogue octreotide is the most commonly used vasoactive ther-

apy to control AVB in the United States. A Cochrane Review found that administration

Acute Variceal Bleeding 349


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of octreotide in AVB reduces the number of patients failing initial hemostasis, reduces

the need for blood transfusion, but does not improve mortality.17 Octreotide causes

rapid splanchnic vasoconstriction, presumably by inhibiting the release of glucagon,

a vasodilator hormone. Octreotide bolus injection results in a sharp decrease in portal

pressure and azygous vein blood flow18; however, this effect is short-lived,19 suggest-

ing that octreotides main benefit takes place in the first few minutes after initiating the

bolus injection. Because octreotide has effects on other neurohumoral systems, pro-

longed intravenous infusion as is currently recommended may provide other beneficial

effects such as blunting the postprandial increase in portal pressure once oral intake is

resumed after an episode of variceal bleeding.20

Octreotide is administered intravenously; following a 50-mg bolus, an infusion of

50mg/h is administered for a minimum of 48 hours and up to 5 days. Octreotide infu-

sion is typically stopped after therapy with nonselective b-blockers is initiated once the

patient is hemodynamically stable. Although octreotide has minimal side effects, its

efficacy is inconclusive and controversial, but some have found it to be superior to

vasopressin and an important adjunct in decreasing rebleeding.21

ANTIBIOTIC PROPHYLAXIS

Bacterial infection is independently associated with failure to control bleeding in

cirrhotic patients.22 The most common infections are spontaneous bacterial perito-

nitis, urinary tract infection, and pneumonia; up to 66% of cirrhotics admitted with var-

iceal bleeding develop an infection soon after admission.23 Infection and endotoxemia

in cirrhosis further worsen the peripheral and splanchnic vasodilatation present in por-

tal hypertension leading to increased portal blood flow and portal pressure. Infection

favors variceal bleeding by increasing sinusoidal pressure, interfering with platelet ag-gregation, and increasing the release of heparinlike substances by endothelial cells,

resulting in impaired coagulation.24

After an episode of variceal bleeding, the use of prophylactic antibiotics increases

the probability of remaining free of rebleeding and is superior to using on-demand an-

tibiotics in response to signs and symptoms of infection.25 Oral norfloxacin 400 mg

every 12 hours has been effective in decreasing infections in cirrhotics with gastroin-

testinal hemorrhage.26 More recently, 1 g of intravenous ceftriaxone administered

once a day for up to 7 days was more effective than norfloxacin inthe prophylaxis

of bacterial infections in patients with cirrhosis and hemorrhage.27 On multivariate

analysis, antibiotic prophylaxis has been an independent predictor of survival in pa-

tients with AVB.5 A meta-analysis concluded that antibiotic prophylaxis for inpatients

with cirrhosis is efficacious in reducing the number of deaths and bacterial infections

regardless of the underlying risk factors.28 Therefore, all patients with cirrhosis and

AVB should be started on prophylactic antibiotics soon after arrival at the hospital

and continued while hospitalized for up to 7 days.

ENDOSCOPIC THERAPY

Endoscopy allows confirmation of the source of bleeding and of the best therapeutic

intervention. Endoscopic therapy is effective in controlling bleeding and preventingearly rebleeding. Although endoscopy is considered one of the cornerstones of man-

agement of AVB, the timing of the endoscopic procedure is controversial. In general,

urgent endoscopy should be performed within 12 to 24 hours of arrival, after the pa-

tient is hemodynamically stabilized and antibiotic and vasoactive therapies have been

initiated.29 Immediate endoscopy on arrival is generally discouraged because the pa-

tient is usually unstable and sufficient time has not been allowed for vasoactive

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therapy to take effect. In addition, a large amount of blood in the stomach increases

the risk of aspiration and limits the ability to complete a diagnostic examination. If

emergent endoscopy is necessary, the use of intravenous erythromycin significantly

improves endoscopic visibility and shortens the duration of the index endoscopy.30

Endoscopic therapy for varices is designed to obliterate the varices and stop

bleeding. Two commonly used endoscopic methods are sclerotherapy and endo-

scopic band ligation (EBL). Endoscopic sclerotherapy controls acute bleeding in

80% to 95% of cases, but sclerotherapy is associated with a significant risk of com-

plications; its effect on early rebleeding rates is uncertain and it has no effect on sur-

vival. A meta-analysis of 10 randomized controlled trials showed an almost significant

benefit of EBL compared with sclerotherapy.31 Others studies have found that,

compared with sclerotherapy, EBL has fewer complications, lower rates of rebleeding,

and lower mortality.32As a result, EBL has largely replaced sclerotherapy as the main

endoscopic therapy tool for the management of variceal hemorrhage. EBL consists of

placing elastic bands at the base of the varices using commercially available banding

devices that are attached to the end of the endoscope (Video 1). After the bands are

placed, the varix is occluded and becomes thrombosed (Fig. 1). The bands subse-

quently fall off leaving a superficial ulcer that eventually heals, disrupting the flow of

blood in the varix. Sessions are repeated every 2 to 4 weeks until all varices are erad-

icated. Most patients undergo a single banding session during the index hospitaliza-

tion and return as outpatients for subsequent sessions.

EBL is highly effective in stopping variceal bleeding and decreasing the risk of early

rebleeding. Complications are not common and include transient difficulty swallowing;

chest pain, which occasionally may be severe and last hours or days; and develop-

ment of strictures after healing. Five to 10 days after banding, shallow ulcers form inthe esophagus that may cause bleeding. Post-EBL ulcer bleeding is more common

in Child C patients, but cannot be predicted based on results of INR or platelet

count.33 The use of pantoprazole limits the size of the ulcers but has not been shown

to be effective in decreasing the risk of bleeding.34

RESCUE THERAPIES

Most patients respond to the therapeutic maneuvers outlined earlier with cessation of

bleeding soon after admission to the hospital. Approximately 20% of patients either

Fig. 1. Esophageal varix after ligation.



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fail to respond to initial therapy or experience early rebleeding within the first 3 to

5 days.35,36 By consensus, treatment failure is defined as failure to control AVB within

24 hours or failure to prevent clinically significant rebleeding within 5 days after treat-

ment initiation.29 Following the traditional approach to variceal bleeding (Fig. 2),

rescue therapy is offered to patients who fail to stop bleeding or who rebleed soon af-

ter banding. Balloon tamponade, surgery, or placement of a transjugular intrahepatic

portosystemic shunt (TIPS) are potential rescue therapies. The choice of therapy de-

pends on the available local expertise and the magnitude of the bleeding.

Balloon tamponade is considered a temporizing option to stabilize the patient

before a more definitive intervention. Two types of tubes for balloon tamponade are

commercially available: the Sengstaken-Blakemore tube (SBT) and the Minnesota

tube. Both tubes consist of an esophageal balloon and a gastric balloon as well as

a gastric aspiration port. Compared with SBT, the Minnesota tube has a larger gastric

balloon and an additional aspiration port above the esophageal balloon. In most

cases, only the gastric balloon is initially inflated to provide pressure at the gastro-

esophageal (GE) junction, preventing blood flow to the esophageal varices. Inflation

of the esophageal balloon is associated with increased risk of complications; for

this reason the esophageal balloon is usually inflated only when bleeding persists

despite inflation of the gastric balloon. To reduce the risk of necrosis of the GE junc-

tion, the gastric balloon should not remain continuously inflated for more than 48 hours.

If the esophageal balloon is inflated, periodic deflation every 12 hours is recommen-

ded to reduce the risk of esophageal necrosis. In experienced hands, balloon tampo-

nade is highly effective in controlling bleeding but recurrence is common after balloon

deflation.37 Complications associated with balloon tamponade occur in 20% to 30%

of patients and include aspiration pneumonia and esophageal tears or rupture.38

Despite the associated risks, balloon tamponade can be lifesaving for a patient with

uncontrolled bleeding while preparations are made for more definitive therapies

such as placement of a TIPS or surgery.

Surgical approaches to AVB include the creation of portosystemic shunts to

decrease portal pressure or esophageal transection to disrupt blood flow into the

esophageal varices. Surgery should be the last resort in the management of AVB,

Variceal bleeding

Vasoactive therapy to reduce portalpressure

Endoscopic band ligation of varices

Bleeding controlled?

Continued pharmacologic andendoscopic therapy

Rescue therapies:TIPS

Balloon tamponadeEsophageal stents

Surgery

Yes No

Fig. 2. Traditional approach to variceal bleeding. TIPS, transjugular intrahepatic portosyste-mic shunt.

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because mortality is as high as 75%.39 Surgery should be reserved for the stable pa-

tient who has recovered from an episode of massive AVB in a setting in which EBL and

TIPS are not available. With the development of TIPS, the need to use emergent sur-

gery as a rescue modality in the management of AVB has virtually disappeared. TIPS

functions as a side-to-side portocaval shunt, effectively decreasing portal pressure

and leading to cessation of bleeding. TIPS is a radiologic procedure that can be per-

formed under moderate or deep sedation, avoiding the complications of general anes-

thesia. More details on the TIPS procedure, its indications, and complications are

given elsewhere in this issue by Richard Parker.

In the acute setting, TIPS is typically considered for patients who fail to stop

bleeding after initial endoscopic attempts, or who rebleed within the first 3 to 5 days

after successful EBL has been performed. In this situation TIPS is highly effective; it

controls bleeding in 94% of cases, with a low early rebleeding rate. However, when

used as rescue therapy, hospital mortality at 6 weeks was 36%.40 This high mortality

likely reflects the severity of the bleeding and underlying liver disease in patients who

are refractory to standard therapy for AVB; the urgency of TIPS is an independent pre-

dictor of early mortality.41

The use of a removable, covered, self-expanding esophageal stent to control var-

iceal bleeding has been explored.42 This specialized stent is supplied with an inser-

tion system that includes a gastric balloon that is inflated to anchor the stent at the

GE junction. Esophageal stent placement may be useful as rescue therapy in those

patients for whom balloon tamponade is being considered. Covered esophageal

stents were successfully placed in all subjects in a small study of 20 patients who

failed pharmacologic and endoscopic therapy to arrest bleeding. After stent place-

ment, bleeding stopped in all patients and the stents were removed in 5 to 7 daysafter other therapeutic interventions were completed. No significant stent-related

complications or rebleeding were observed during a 30-day observation period.37

Despite this encouraging report, the use of esophageal stents to treat refractory

AVB remains experimental.

RISK STRATIFICATION TO TAILOR THERAPY

Patients presenting with variceal bleeding and Child A cirrhosis usually respond to stan-

dard pharmacologic and endoscopic therapy without rebleeding or the need for rescue

therapy, and mortality in this group is typically low. In contrast, there is a high failure rateof standard therapy for AVB in Child C patients, those presenting with bacterial infec-

tion, those with evidence of renal insufficiency,43 or in patients with high portal pres-

sures.4 These patients often require rescue therapy. Rescue therapy with TIPS is

associated with a 30-day mortality of 29% and 60-day mortality of 35%.44 The delay

between the index bleed and TIPS placement, the number of endoscopic attempts

to stop bleeding, and the need to use balloon tamponade predict increased mortality

when using TIPS as a rescue modality.38 These data suggest that a more aggressive

approach may be needed for high-risk patients presenting with AVB.

The strongest predictor of a negative outcome in patients presenting with AVB is a

hepatic vein portal gradient pressure (HVPG) greater than 20 mm Hg. These patientsare 4 to 5.1 times more likely to fail standard therapy using vasoactive drugs and endo-

scopic therapy,3,45 require more blood transfusions, are more likely to experience

early rebleeding, and have longer hospitalizations. The value of a high HVPG predict-

ing poor outcome has been prospectively validated.46 HVPG is not commonly

measured in clinical practice; however, patients presenting with HVPG greater than

20 mm Hg are more likely to be Child C, present with a systolic blood pressure less



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than 100 mm Hg, have a nonalcoholic cause of liver cirrhosis,3 or show active bleeding

on the initial endoscopy despite ongoing vasoactive therapy.40 These clinical charac-

teristics can be used to identify a group of patients at presentation who are likely to

have high HVPG and a high risk of not responding to standard therapy and who

may benefit from more aggressive management such as early placement of TIPS.

The efficacy of an aggressive approach to high-risk patients was shown by Garcia-

Pagan and colleagues.47 Sixty-two patients presenting with variceal bleeding, who

were Child C (13 points) or Child B with bleeding at the initial endoscopy, were ran-

domized to standard medical therapy with EBL and vasoactive drugs or to early TIPS

after the initial endoscopic banding session. During a median follow-up of 16 months,

rebleeding or failure to control bleeding occurred in 14 (45%) patients managed with

EBL and vasoactive drugs compared with only 1 (3%) randomized to TIPS; 6-week

mortality was reduced from 33% in the standard care group to 4% in the early TIPS

group.46 Seven of the patients in the conventional arm required rescue TIPS, but

4 died, confirming the poor prognosis of patients who fail initial attempts at hemostasis

and require rescue TIPS. A retrospective review of cases admitted for AVB also found

that, among Child C or Child B patients with active bleeding on the index endoscopy,

early TIPS placement had superior outcomes compared with standard therapy and

rescue TIPS for nonresponders.48 The use of the recently developed covered stents

for TIPS likely contributed to the positive outcomes of these trials because the risk

of early thrombosis and TIPS dysfunction is lower.49

These preliminary data suggest that the approach to AVB should be stratified based

on clinical characteristics at presentation, as shown in Fig. 3. All Child A and Child B pa-

tients who show no active bleeding on the index endoscopy can be managed with EBL

and vasoactive drugs. In contrast, Child B patients who have active bleeding on the in-dex endoscopy despite vasoactive therapy and Child C patients with less than or equal

to 13 points may benefit from early intervention with TIPS placement using a covered

stent rather than allowing them to fail initial therapy and then considering rescue TIPS.

An aggressive approach or rescue therapy may not be appropriate for all patients.

Child C patients with 14 or 15 points are too ill to undergo TIPS and are unlikely to

benefit from this therapy. Likewise, patients presenting with AVB in association with

Variceal bleeding

Vasoactive therapy to reduce portalpressure

Endoscopic band ligation of varices

Child A, orChild B with no bleeding on

endoscopy, or

Child C >13 points

Child B with active bleeding onendoscopy

Child C 13 points

HVPG>20 mmHg

Endoscopic therapy andpharmacologic control of portal

pressure

Early TIPS using covered stent

Fig. 3. Approach to variceal bleeding based on risk stratification.

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hepatocellular carcinoma, serum creatinine greater than 3 mg/dL, portal thrombosis,

or evidence of sepsis are not likely to benefit from rescue therapy33 unless they are

being considered for urgent liver transplantation.

SUMMARY

The approach to AVB has changed in the last few years. Newer, safer vasoactive

drugs have been developed, some resulting in measurable reduction in mortality.

The value of prophylactic antibiotics to decrease early rebleeding has become

apparent and these are now standard of care. Endoscopic band ligation has replaced

variceal sclerotherapy as the endoscopic therapy of choice to obliterate varices. Using

readily available clinical parameters, a subset of high-risk patients can be identified at

presentation who are less likely to respond to the traditional approach to variceal

bleeding and may benefit from early TIPS placement to improve outcomes.

SUPPLEMENTARY DATA

Supplementary data related to this article can be found online at http://dx.doi.org/10.

1016/j.cld.2014.01.001.

REFERENCES

1. Jamal MM, Samarasena JB, Hashemzadeh M, et al. Declining hospitalization rate

of esophageal variceal bleeding in the United States. Clin Gastroenterol Hepatol

2008;6:68995.2. Graham DY, Smith JL. The course of patients after variceal hemorrhage. Gastro-

enterology 1981;80:8009.

3. Villanueva C, Piqueras M, Aracil C, et al. A randomized controlled trial comparing

ligation and sclerotherapy as emergency endoscopic treatment added to so-

matostatin in acute variceal bleeding. J Hepatol 2006;45:5607.

4. Abraldes JG, Villanueva C, Banares R, et al. Hepatic venous pressure gradient

and prognosis in patients with acute variceal bleeding treated with pharmaco-

logic and endoscopic therapy. J Hepatol 2008;48:22936.

5. Carbonell N, Pauwels A, Serfaty L, et al. Improved survival after variceal

bleeding in patients with cirrhosis over the past two decades. Hepatology 2004;40:6529.

6. Koch DG, Arguedas MR, Fallon MB. Risk of aspiration pneumonia in suspected

variceal hemorrhage: the value of prophylactic endotracheal intubation prior to

endoscopy. Dig Dis Sci 2007;52:22258.

7. Rudolph SJ, Landsverk BK, Freeman ML. Endotracheal intubation for airway pro-

tection during endoscopy for severe GI hemorrhage. Gastrointest Endosc 2003;

57:5861.

8. Villanueva C, Colomo A, Bosch A, et al. Transfusion strategies for acute gastroin-

testinal bleeding. N Engl J Med 2013;368:1121.

9. Tripodi A, Mannucci M. The coagulopathy of chronic liver disease. N Engl J Med2011;365:14756.

10. Tripodi A, Primignani M, Chantarangkul V, et al. An imbalance of pro- vs. anti-

coagulation factors in plasma from patients with cirrhosis. Gastroenterology

2008;38:137883.

11. Hugenholtz GG, Porte RJ, Lisman T. The platelet and platelet function testing in

liver disease. Clin Liver Dis 2009;13:1120.

http://dx.doi.org/10.1016/j.cld.2014.01.001http://dx.doi.org/10.1016/j.cld.2014.01.001http://refhub.elsevier.com/S1089-3261(14)00002-6/sref1http://refhub.elsevier.com/S1089-3261(14)00002-6/sref1http://refhub.elsevier.com/S1089-3261(14)00002-6/sref1http://refhub.elsevier.com/S1089-3261(14)00002-6/sref2http://refhub.elsevier.com/S1089-3261(14)00002-6/sref2http://refhub.elsevier.com/S1089-3261(14)00002-6/sref3http://refhub.elsevier.com/S1089-3261(14)00002-6/sref3http://refhub.elsevier.com/S1089-3261(14)00002-6/sref3http://refhub.elsevier.com/S1089-3261(14)00002-6/sref4http://refhub.elsevier.com/S1089-3261(14)00002-6/sref4http://refhub.elsevier.com/S1089-3261(14)00002-6/sref4http://refhub.elsevier.com/S1089-3261(14)00002-6/sref4http://refhub.elsevier.com/S1089-3261(14)00002-6/sref4http://refhub.elsevier.com/S1089-3261(14)00002-6/sref5http://refhub.elsevier.com/S1089-3261(14)00002-6/sref5http://refhub.elsevier.com/S1089-3261(14)00002-6/sref5http://refhub.elsevier.com/S1089-3261(14)00002-6/sref6http://refhub.elsevier.com/S1089-3261(14)00002-6/sref6http://refhub.elsevier.com/S1089-3261(14)00002-6/sref6http://refhub.elsevier.com/S1089-3261(14)00002-6/sref7http://refhub.elsevier.com/S1089-3261(14)00002-6/sref7http://refhub.elsevier.com/S1089-3261(14)00002-6/sref7http://refhub.elsevier.com/S1089-3261(14)00002-6/sref8http://refhub.elsevier.com/S1089-3261(14)00002-6/sref8http://refhub.elsevier.com/S1089-3261(14)00002-6/sref9http://refhub.elsevier.com/S1089-3261(14)00002-6/sref9http://refhub.elsevier.com/S1089-3261(14)00002-6/sref10http://refhub.elsevier.com/S1089-3261(14)00002-6/sref10http://refhub.elsevier.com/S1089-3261(14)00002-6/sref10http://refhub.elsevier.com/S1089-3261(14)00002-6/sref11http://refhub.elsevier.com/S1089-3261(14)00002-6/sref11http://refhub.elsevier.com/S1089-3261(14)00002-6/sref11http://refhub.elsevier.com/S1089-3261(14)00002-6/sref11http://refhub.elsevier.com/S1089-3261(14)00002-6/sref10http://refhub.elsevier.com/S1089-3261(14)00002-6/sref10http://refhub.elsevier.com/S1089-3261(14)00002-6/sref10http://refhub.elsevier.com/S1089-3261(14)00002-6/sref9http://refhub.elsevier.com/S1089-3261(14)00002-6/sref9http://refhub.elsevier.com/S1089-3261(14)00002-6/sref8http://refhub.elsevier.com/S1089-3261(14)00002-6/sref8http://refhub.elsevier.com/S1089-3261(14)00002-6/sref7http://refhub.elsevier.com/S1089-3261(14)00002-6/sref7http://refhub.elsevier.com/S1089-3261(14)00002-6/sref7http://refhub.elsevier.com/S1089-3261(14)00002-6/sref6http://refhub.elsevier.com/S1089-3261(14)00002-6/sref6http://refhub.elsevier.com/S1089-3261(14)00002-6/sref6http://refhub.elsevier.com/S1089-3261(14)00002-6/sref5http://refhub.elsevier.com/S1089-3261(14)00002-6/sref5http://refhub.elsevier.com/S1089-3261(14)00002-6/sref5http://refhub.elsevier.com/S1089-3261(14)00002-6/sref4http://refhub.elsevier.com/S1089-3261(14)00002-6/sref4http://refhub.elsevier.com/S1089-3261(14)00002-6/sref4http://refhub.elsevier.com/S1089-3261(14)00002-6/sref3http://refhub.elsevier.com/S1089-3261(14)00002-6/sref3http://refhub.elsevier.com/S1089-3261(14)00002-6/sref3http://refhub.elsevier.com/S1089-3261(14)00002-6/sref2http://refhub.elsevier.com/S1089-3261(14)00002-6/sref2http://refhub.elsevier.com/S1089-3261(14)00002-6/sref1http://refhub.elsevier.com/S1089-3261(14)00002-6/sref1http://refhub.elsevier.com/S1089-3261(14)00002-6/sref1http://dx.doi.org/10.1016/j.cld.2014.01.001http://dx.doi.org/10.1016/j.cld.2014.01.001


10/11

12. Bosch J, Thabut D, Albillos A, et al. Recombinant factor VIIa for variceal bleeding

in patients with advanced cirrhosis: a randomized controlled trial. Hepatology

2008;47:160414.

13. Wells M, Adams CP, Beaton M, et al. Meta-analysis: vasoactive medications for the

management of acute variceal bleeds. Aliment Pharmacol Ther 2012;35:126778.

14. Imperiale TF, Teran JC, McCullough AJ. A meta-analysis of somatostatin versus

vasopressin in the management of acute esophageal variceal hemorrhage.

Gastroenterology 1995;109:128994.

15. Groszman RJ, Kravetz D, Bosch J, et al. Nitroglycerin improves the hemodynamic

response to vasopressin in portal hypertension. Hepatology 1982;2:75762.

16. Ioannou G, Doust J, Rockey D. Terlipressin for acute esophageal variceal hemor-

rhage. Cochrane Database Syst Rev 2003;(1):CD002147.

17. Gotzsche PC, Hrobjartsson A. Somatostatin analogues for acute bleeding oeso-

phageal varices. Cochrane Database Syst Rev 2005;(1):CD000193.http://dx.doi.

org/10.1002/14651858.CD000193.pub2.

18. Zironi G, Rossi C, Siringo S, et al. Short- and long-term hemodynamic response to

octreotide in portal hypertensive patients: a double-blind, controlled study. Liver

1996;16:22534.

19. Escorsell A, Bandi JC, Andreu V, et al. Desensitization to the effects of intrave-

nous octreotide in cirrhotic patients with portal hypertension. Gastroenterology

2000;120:1619.

20. Vorobioff JD, Gamen M, Kravetz D, et al. Effects of long-term propranolol and oc-

treotide on postprandial hemodynamics in cirrhosis: a randomized controlled

trial. Gastroenterology 2002;122:91622.

21. Corley DA, Cello JP, Adkisson W. Octreotide for acute esophageal varicealbleeding: a meta-analysis. Gastroenterology 2001;120:94654.

22. Goulis J, Armonis A, Patch D. Bacterial infection is independently associated with

failure to control bleeding in cirrhotic patients with gastrointestinal hemorrhage.

Hepatology 1998;27:120712.

23. Blaise M, Pateron D, Trinchet JC, et al. Systemic antibiotic therapy prevents bac-

terial infection in cirrhotic patients with gastrointestinal hemorrhage. Hepatology

1994;20:348.

24. Wong F, Bernardi M, Balk R, et al. Sepsis in cirrhosis: report on the 7th meeting of

the International Ascites Club. Gut 2005;54:71825.

25. Hou MC, Lin HC, Liu TT, et al. Antibiotic prophylaxis after endoscopic therapyprevents rebleeding in acute variceal hemorrhage: a randomized trial. Hepatol-

ogy 2004;39:74653.

26. Rimola A, Bory F, Teres J, et al. Oral, nonabsorbable antibiotics prevent infection

in cirrhotics with gastrointestinal hemorrhage. Hepatology 1985;5:4637.

27. Fernandez J, Ruiz del Arbol L, Gomez C, et al. Norfloxacin vs. ceftriaxone in the

prophylaxis of infections in patients with advanced cirrhosis and hemorrhage.


28. Soares-Weiser K, Brezis M, Tur-Kaspa R, et al. Antibiotic prophylaxis of bacterial

infections in cirrhotic inpatients: a meta-analysis of randomized controlled trials.

Scand J Gastroenterol 2003;38:193200.29. de Franchis R. Evolving consensus in portal hypertension. Report of the Baveno

IV consensus workshop on methodology of diagnosis and therapy in portal hy-

pertension. J Hepatol 2005;43:16776.

30. Altraif I, Handoo FA, Aljumah A, et al. Effect of erythromycin before endoscopy in

patients presenting with variceal bleeding: a prospective, randomized, double

blind placebo-controlled trial. Gastrointest Endosc 2011;73:24550.

Herrera356
http://refhub.elsevier.com/S1089-3261(14)00002-6/sref12http://refhub.elsevier.com/S1089-3261(14)00002-6/sref12http://refhub.elsevier.com/S1089-3261(14)00002-6/sref12http://refhub.elsevier.com/S1089-3261(14)00002-6/sref13http://refhub.elsevier.com/S1089-3261(14)00002-6/sref13http://refhub.elsevier.com/S1089-3261(14)00002-6/sref14http://refhub.elsevier.com/S1089-3261(14)00002-6/sref14http://refhub.elsevier.com/S1089-3261(14)00002-6/sref14http://refhub.elsevier.com/S1089-3261(14)00002-6/sref15http://refhub.elsevier.com/S1089-3261(14)00002-6/sref15http://refhub.elsevier.com/S1089-3261(14)00002-6/sref16http://refhub.elsevier.com/S1089-3261(14)00002-6/sref16http://dx.doi.org/10.1002/14651858.CD000193.pub2http://dx.doi.org/10.1002/14651858.CD000193.pub2http://refhub.elsevier.com/S1089-3261(14)00002-6/sref18http://refhub.elsevier.com/S1089-3261(14)00002-6/sref18http://refhub.elsevier.com/S1089-3261(14)00002-6/sref18http://refhub.elsevier.com/S1089-3261(14)00002-6/sref19http://refhub.elsevier.com/S1089-3261(14)00002-6/sref19http://refhub.elsevier.com/S1089-3261(14)00002-6/sref19http://refhub.elsevier.com/S1089-3261(14)00002-6/sref20http://refhub.elsevier.com/S1089-3261(14)00002-6/sref20http://refhub.elsevier.com/S1089-3261(14)00002-6/sref20http://refhub.elsevier.com/S1089-3261(14)00002-6/sref21http://refhub.elsevier.com/S1089-3261(14)00002-6/sref21http://refhub.elsevier.com/S1089-3261(14)00002-6/sref22http://refhub.elsevier.com/S1089-3261(14)00002-6/sref22http://refhub.elsevier.com/S1089-3261(14)00002-6/sref22http://refhub.elsevier.com/S1089-3261(14)00002-6/sref23http://refhub.elsevier.com/S1089-3261(14)00002-6/sref23http://refhub.elsevier.com/S1089-3261(14)00002-6/sref23http://refhub.elsevier.com/S1089-3261(14)00002-6/sref24http://refhub.elsevier.com/S1089-3261(14)00002-6/sref24http://refhub.elsevier.com/S1089-3261(14)00002-6/sref25http://refhub.elsevier.com/S1089-3261(14)00002-6/sref25http://refhub.elsevier.com/S1089-3261(14)00002-6/sref25http://refhub.elsevier.com/S1089-3261(14)00002-6/sref26http://refhub.elsevier.com/S1089-3261(14)00002-6/sref26http://refhub.elsevier.com/S1089-3261(14)00002-6/sref27http://refhub.elsevier.com/S1089-3261(14)00002-6/sref27http://refhub.elsevier.com/S1089-3261(14)00002-6/sref27http://refhub.elsevier.com/S1089-3261(14)00002-6/sref28http://refhub.elsevier.com/S1089-3261(14)00002-6/sref28http://refhub.elsevier.com/S1089-3261(14)00002-6/sref28http://refhub.elsevier.com/S1089-3261(14)00002-6/sref29http://refhub.elsevier.com/S1089-3261(14)00002-6/sref29http://refhub.elsevier.com/S1089-3261(14)00002-6/sref29http://refhub.elsevier.com/S1089-3261(14)00002-6/sref30http://refhub.elsevier.com/S1089-3261(14)00002-6/sref30http://refhub.elsevier.com/S1089-3261(14)00002-6/sref30http://refhub.elsevier.com/S1089-3261(14)00002-6/sref30http://refhub.elsevier.com/S1089-3261(14)00002-6/sref30http://refhub.elsevier.com/S1089-3261(14)00002-6/sref30http://refhub.elsevier.com/S1089-3261(14)00002-6/sref29http://refhub.elsevier.com/S1089-3261(14)00002-6/sref29http://refhub.elsevier.com/S1089-3261(14)00002-6/sref29http://refhub.elsevier.com/S1089-3261(14)00002-6/sref28http://refhub.elsevier.com/S1089-3261(14)00002-6/sref28http://refhub.elsevier.com/S1089-3261(14)00002-6/sref28http://refhub.elsevier.com/S1089-3261(14)00002-6/sref27http://refhub.elsevier.com/S1089-3261(14)00002-6/sref27http://refhub.elsevier.com/S1089-3261(14)00002-6/sref27http://refhub.elsevier.com/S1089-3261(14)00002-6/sref26http://refhub.elsevier.com/S1089-3261(14)00002-6/sref26http://refhub.elsevier.com/S1089-3261(14)00002-6/sref25http://refhub.elsevier.com/S1089-3261(14)00002-6/sref25http://refhub.elsevier.com/S1089-3261(14)00002-6/sref25http://refhub.elsevier.com/S1089-3261(14)00002-6/sref24http://refhub.elsevier.com/S1089-3261(14)00002-6/sref24http://refhub.elsevier.com/S1089-3261(14)00002-6/sref23http://refhub.elsevier.com/S1089-3261(14)00002-6/sref23http://refhub.elsevier.com/S1089-3261(14)00002-6/sref23http://refhub.elsevier.com/S1089-3261(14)00002-6/sref22http://refhub.elsevier.com/S1089-3261(14)00002-6/sref22http://refhub.elsevier.com/S1089-3261(14)00002-6/sref22http://refhub.elsevier.com/S1089-3261(14)00002-6/sref21http://refhub.elsevier.com/S1089-3261(14)00002-6/sref21http://refhub.elsevier.com/S1089-3261(14)00002-6/sref20http://refhub.elsevier.com/S1089-3261(14)00002-6/sref20http://refhub.elsevier.com/S1089-3261(14)00002-6/sref20http://refhub.elsevier.com/S1089-3261(14)00002-6/sref19http://refhub.elsevier.com/S1089-3261(14)00002-6/sref19http://refhub.elsevier.com/S1089-3261(14)00002-6/sref19http://refhub.elsevier.com/S1089-3261(14)00002-6/sref18http://refhub.elsevier.com/S1089-3261(14)00002-6/sref18http://refhub.elsevier.com/S1089-3261(14)00002-6/sref18http://dx.doi.org/10.1002/14651858.CD000193.pub2http://dx.doi.org/10.1002/14651858.CD000193.pub2http://refhub.elsevier.com/S1089-3261(14)00002-6/sref16http://refhub.elsevier.com/S1089-3261(14)00002-6/sref16http://refhub.elsevier.com/S1089-3261(14)00002-6/sref15http://refhub.elsevier.com/S1089-3261(14)00002-6/sref15http://refhub.elsevier.com/S1089-3261(14)00002-6/sref14http://refhub.elsevier.com/S1089-3261(14)00002-6/sref14http://refhub.elsevier.com/S1089-3261(14)00002-6/sref14http://refhub.elsevier.com/S1089-3261(14)00002-6/sref13http://refhub.elsevier.com/S1089-3261(14)00002-6/sref13http://refhub.elsevier.com/S1089-3261(14)00002-6/sref12http://refhub.elsevier.com/S1089-3261(14)00002-6/sref12http://refhub.elsevier.com/S1089-3261(14)00002-6/sref12


11/11

31. Garcia-Pagan JC, Bosch J. Endoscopic band ligation in the treatment of portal

hypertension. Nat Clin Pract Gastroenterol Hepatol 2005;2:52635.

32. Lo GH, Lai KH, Cheng JS, et al. Emergency banding ligation versus sclerotherapyfor

the control of active bleedingfrom esophageal varices. Hepatology 1997;25:11014.

33. Vieira EC, DAmico EA, Caldwell SH, et al. A prospective study of conventional

and expanded coagulation indices in predicting ulcer bleeding after variceal

band ligation. Clin Gastroenterol Hepatol 2009;7:98893.

34. Shaheen NJ, Stuart E, Schmitz SM, et al. Pantoprazole reduces the size of post-

banding ulcers after variceal band ligation: a randomized controlled trial. Hepa-

tology 2005;41:58894.

35. Banares R, Albillos A, Rincon D, et al. Endoscopic treatment versus endoscopic

plus pharmacologic treatment for acute variceal bleeding: a meta-analysis. Hep-

atology 2002;35:60915.

36. Amitrano L, Guardascione MA, Manguso F, et al. The effectiveness of current

acute variceal bleed treatments in unselected cirrhotic patients: refining short-

term prognosis and risk factors. Am J Gastroenterol 2012;107:18728.

37. Pitcher JL. Safety and effectiveness of the modified Sengstaken-Blakemore tube:

a prospective study. Gastroenterology 1971;61:2918.

38. Gossat D, Bolin TD. An unusual complication of balloon tamponade in the treat-

ment of esophageal varices: a case report and brief review of the literature. Am J

Gastroenterol 1985;80:6001.

39. Jalan R, John TG, Redhead DN, et al. A comparative study of emergency trans-

jugular intrahepatic portosystemic stent shunt and esophageal transection in the

management of uncontrolled variceal hemorrhage. Am J Gastroenterol 1995;90:

19327.40. Vangeli M, Patch D, Burroughs AK. Salvage TIPS for uncontrolled variceal

bleeding. J Hepatol 2003;37:7034.

41. Chalasani N, Clark WS, Martin LG, et al. Determinants of mortality in patients with

advanced cirrhosis after transjugular intrahepatic portosystemic shunting.


42. Hubmann R, Bodlaj G, Czompo M, et al. The use of self-expanding metal stents

to treat acute esophageal variceal bleeding. Endoscopy 2006;38:896901.

43. Augustin S, Muntaner L, Altamirano JT. Predicting early mortality after acute

variceal hemorrhage based on classification and regression tree analysis. Clin

Gastroenterol Hepatol 2009;7:134754.44. Azoulay D, Castaing D, Majno P, et al. Salvage transjugular intrahepatic portosys-

temic shunt for uncontrolled variceal bleeding in patients with decompensated

cirrhosis. J Hepatol 2001;35:5907.

45. Moitinho E, Escrosell A, Bandi JC, et al. Prognostic value of early measurements

of portal pressure in acute variceal bleeding. Gastroenterology 1999;117:62631.

46. Monescillo A, Martinez-Lagares F, Ruiz del Arbol L, et al. Influence of portal hy-

pertension and its early decompression by TIPS placement on the outcome of

variceal bleeding. Hepatology 2004;40:793801.

47. Garcia-Pagan JC, Caca K, Bureau C, et al. Early use of TIPS in patients with

cirrhosis and variceal bleeding. N Engl J Med 2010;362:23709.48. Garcia-Pagan JC, Di Pascoli M, Caca K, et al. Use of early TIPS for high risk var-

iceal bleeding: results of a post-RCT surveillance study. J Hepatol 2013;58:4550.

49. Bureau C, Garcia Pagan JC, Layrargues GP, et al. Patency of stents covered with

polytetrafluoroethylene in patients treated by transjugular intrahepatic portosyste-

mic shunts: long-term results of a randomized multicenter study. Liver Int 2007;

27:7427.

http://refhub.elsevier.com/S1089-3261(14)00002-6/sref31http://refhub.elsevier.com/S1089-3261(14)00002-6/sref31http://refhub.elsevier.com/S1089-3261(14)00002-6/sref32http://refhub.elsevier.com/S1089-3261(14)00002-6/sref32http://refhub.elsevier.com/S1089-3261(14)00002-6/sref33http://refhub.elsevier.com/S1089-3261(14)00002-6/sref33http://refhub.elsevier.com/S1089-3261(14)00002-6/sref33http://refhub.elsevier.com/S1089-3261(14)00002-6/sref34http://refhub.elsevier.com/S1089-3261(14)00002-6/sref34http://refhub.elsevier.com/S1089-3261(14)00002-6/sref34http://refhub.elsevier.com/S1089-3261(14)00002-6/sref35http://refhub.elsevier.com/S1089-3261(14)00002-6/sref35http://refhub.elsevier.com/S1089-3261(14)00002-6/sref35http://refhub.elsevier.com/S1089-3261(14)00002-6/sref36http://refhub.elsevier.com/S1089-3261(14)00002-6/sref36http://refhub.elsevier.com/S1089-3261(14)00002-6/sref36http://refhub.elsevier.com/S1089-3261(14)00002-6/sref37http://refhub.elsevier.com/S1089-3261(14)00002-6/sref37http://refhub.elsevier.com/S1089-3261(14)00002-6/sref38http://refhub.elsevier.com/S1089-3261(14)00002-6/sref38http://refhub.elsevier.com/S1089-3261(14)00002-6/sref38http://refhub.elsevier.com/S1089-3261(14)00002-6/sref39http://refhub.elsevier.com/S1089-3261(14)00002-6/sref39http://refhub.elsevier.com/S1089-3261(14)00002-6/sref39http://refhub.elsevier.com/S1089-3261(14)00002-6/sref39http://refhub.elsevier.com/S1089-3261(14)00002-6/sref40http://refhub.elsevier.com/S1089-3261(14)00002-6/sref40http://refhub.elsevier.com/S1089-3261(14)00002-6/sref41http://refhub.elsevier.com/S1089-3261(14)00002-6/sref41http://refhub.elsevier.com/S1089-3261(14)00002-6/sref41http://refhub.elsevier.com/S1089-3261(14)00002-6/sref42http://refhub.elsevier.com/S1089-3261(14)00002-6/sref42http://refhub.elsevier.com/S1089-3261(14)00002-6/sref43http://refhub.elsevier.com/S1089-3261(14)00002-6/sref43http://refhub.elsevier.com/S1089-3261(14)00002-6/sref43http://refhub.elsevier.com/S1089-3261(14)00002-6/sref44http://refhub.elsevier.com/S1089-3261(14)00002-6/sref44http://refhub.elsevier.com/S1089-3261(14)00002-6/sref44http://refhub.elsevier.com/S1089-3261(14)00002-6/sref45http://refhub.elsevier.com/S1089-3261(14)00002-6/sref45http://refhub.elsevier.com/S1089-3261(14)00002-6/sref46http://refhub.elsevier.com/S1089-3261(14)00002-6/sref46http://refhub.elsevier.com/S1089-3261(14)00002-6/sref46http://refhub.elsevier.com/S1089-3261(14)00002-6/sref47http://refhub.elsevier.com/S1089-3261(14)00002-6/sref47http://refhub.elsevier.com/S1089-3261(14)00002-6/sref48http://refhub.elsevier.com/S1089-3261(14)00002-6/sref48http://refhub.elsevier.com/S1089-3261(14)00002-6/sref49http://refhub.elsevier.com/S1089-3261(14)00002-6/sref49http://refhub.elsevier.com/S1089-3261(14)00002-6/sref49http://refhub.elsevier.com/S1089-3261(14)00002-6/sref49http://refhub.elsevier.com/S1089-3261(14)00002-6/sref49http://refhub.elsevier.com/S1089-3261(14)00002-6/sref49http://refhub.elsevier.com/S1089-3261(14)00002-6/sref49http://refhub.elsevier.com/S1089-3261(14)00002-6/sref49http://refhub.elsevier.com/S1089-3261(14)00002-6/sref48http://refhub.elsevier.com/S1089-3261(14)00002-6/sref48http://refhub.elsevier.com/S1089-3261(14)00002-6/sref47http://refhub.elsevier.com/S1089-3261(14)00002-6/sref47http://refhub.elsevier.com/S1089-3261(14)00002-6/sref46http://refhub.elsevier.com/S1089-3261(14)00002-6/sref46http://refhub.elsevier.com/S1089-3261(14)00002-6/sref46http://refhub.elsevier.com/S1089-3261(14)00002-6/sref45http://refhub.elsevier.com/S1089-3261(14)00002-6/sref45http://refhub.elsevier.com/S1089-3261(14)00002-6/sref44http://refhub.elsevier.com/S1089-3261(14)00002-6/sref44http://refhub.elsevier.com/S1089-3261(14)00002-6/sref44http://refhub.elsevier.com/S1089-3261(14)00002-6/sref43http://refhub.elsevier.com/S1089-3261(14)00002-6/sref43http://refhub.elsevier.com/S1089-3261(14)00002-6/sref43http://refhub.elsevier.com/S1089-3261(14)00002-6/sref42http://refhub.elsevier.com/S1089-3261(14)00002-6/sref42http://refhub.elsevier.com/S1089-3261(14)00002-6/sref41http://refhub.elsevier.com/S1089-3261(14)00002-6/sref41http://refhub.elsevier.com/S1089-3261(14)00002-6/sref41http://refhub.elsevier.com/S1089-3261(14)00002-6/sref40http://refhub.elsevier.com/S1089-3261(14)00002-6/sref40http://refhub.elsevier.com/S1089-3261(14)00002-6/sref39http://refhub.elsevier.com/S1089-3261(14)00002-6/sref39http://refhub.elsevier.com/S1089-3261(14)00002-6/sref39http://refhub.elsevier.com/S1089-3261(14)00002-6/sref39http://refhub.elsevier.com/S1089-3261(14)00002-6/sref38http://refhub.elsevier.com/S1089-3261(14)00002-6/sref38http://refhub.elsevier.com/S1089-3261(14)00002-6/sref38http://refhub.elsevier.com/S1089-3261(14)00002-6/sref37http://refhub.elsevier.com/S1089-3261(14)00002-6/sref37http://refhub.elsevier.com/S1089-3261(14)00002-6/sref36http://refhub.elsevier.com/S1089-3261(14)00002-6/sref36http://refhub.elsevier.com/S1089-3261(14)00002-6/sref36http://refhub.elsevier.com/S1089-3261(14)00002-6/sref35http://refhub.elsevier.com/S1089-3261(14)00002-6/sref35http://refhub.elsevier.com/S1089-3261(14)00002-6/sref35http://refhub.elsevier.com/S1089-3261(14)00002-6/sref34http://refhub.elsevier.com/S1089-3261(14)00002-6/sref34http://refhub.elsevier.com/S1089-3261(14)00002-6/sref34http://refhub.elsevier.com/S1089-3261(14)00002-6/sref33http://refhub.elsevier.com/S1089-3261(14)00002-6/sref33http://refhub.elsevier.com/S1089-3261(14)00002-6/sref33http://refhub.elsevier.com/S1089-3261(14)00002-6/sref32http://refhub.elsevier.com/S1089-3261(14)00002-6/sref32http://refhub.elsevier.com/S1089-3261(14)00002-6/sref31http://refhub.elsevier.com/S1089-3261(14)00002-6/sref31

TX STD Variceal. Clinic Liver Disease 2014

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