STDA variceal

7/30/2019 STDA variceal

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By Melissa M. Smith, PhD, RN,ACNS-BC

Learn how to recognize and treat

this life-threatening complication.

Variceal HemorrhagefromEsophagealVaricesAssociated

withAlcoholic LiverDisease

Overview: Esophageal varices occur in about half of all

people with alcoholic cirrhosis. About one-third of these

will experience variceal hemorrhage,a life-threatening event.

This article describes alcoholic cirrhosis and its complica-

tions, discusses the etiology of esophageal varices and the

risk factors for hemorrhage,and addresses emergent treat-

ment. Further treatment options,including endoscopic vari-ceal ligation, endoscopic injection sclerotherapy, balloon

tamponade, and transjugular intrahepatic portosystemic

shunt placement, are also discussed.

32 AJN M February 2010 M Vol. 110, No. 2 ajnonline.com

Two days after admission the patient was alertand oriented, and her ammonia level was within the

normal range. But while being prepared for transferto the medicalsurgical unit, Ms. Barth vomited alarge amount of bright red blood and blood clots.Because of this patients history of alcohol abuse,the team suspected bleeding esophageal varices asthe likely cause of her hematemesis (see Figure 1).

The nurse immediately turned the patient onto herside and raised the head of the bed to a high Fowlerposition to protect her airway. Vital signs were as fol-lows: heart rate, 124 beats per minute; respiration,28 breaths per minute; blood pressure, 90/52 mmHg.The cardiac monitor revealed sinus tachycardia. Pulseoximetry revealed an oxygen saturation level of 86%on room air. The physician ordered an immediatetransfusion of two units of packed red blood cells. Anurse initiated oxygen through a nonrebreather maskto help correct the hypoxemia. Once the patient wasstable and the oxygen saturation level reached 94%,low-flow oxygen was administered via nasal cannula,with an order to adjust the flow as necessary to main-tain oxygen saturation at 94%. A Yankauer suctioncatheter was readily available in case interventionwas needed to prevent aspiration. In an effort tocontrol the bleeding, an initial bolus of octreotide(Sandostatin) 50 micrograms IV was administered,

followed by a continuous infusion of 50 microgramsper hour.

Marie Barth, a 63-year-old woman, wasadmitted to the ICU from the EDwith hepatic encephalopathy causedby alcoholic cirrhosis. (This case is a

composite based on my experience.) She was con-fused and disoriented, and a review of her medicalrecords indicated long-term alcohol abuse. Her vitalsigns on admission were as follows: heart rate, 80beats per minute; respiration, 24 breaths per min-ute; blood pressure, 116/64 mmHg. Physical as-sessment revealed cachexia, jaundice, jugular veindistension, and a distended, tender abdomen withshifting dullness. Laboratory results indicated anelevated serum ammonia level of 230 microgramsper deciliter. Paracentesis of the abdomen revealedcloudy ascitic fluid suggestive of spontaneous bacte-rial peritonitis, and a specimen was sent for laboratorytesting. A lactulose (Chronulac and others) enema

was ordered to quickly lower her serum ammonialevel.

2.6 HOURSContinuing Education


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Figure1. EsophagealVarices

Normally, the hepatic portal vein

brings blood from the spleen and thegastrointestinal tract, and its associ-

ated organs, to the liver. As cirrho-

sis progresses, portal hypertension

is induced by an increased resist-

ance to blood flow through the

damaged liver. Limited blood flow

through the liver causes an increase

in splanchnic ar terial flow. Together,

these two factors can overload the

portal system.The increased pres-

sure stimulates the development of

collateral channelsvarices(seen

in the close up), which attempt tobypass the portal vein flow into the

liver. Portal hypertension causes

splenomegaly (enlargement of the

spleen), ascites (fluid retention in

the abdomen), blood clotting defi-

ciencies, and hepatic encephalopa-

thy (mental confusion).

[email protected] AJN M February 2010 M Vol. 110, No. 2 33

Normal blood

flow to liver

Portal vein

Esophageal and

gastric varices


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The consulting gastroenterologist recommendedendoscopic treatment as soon as hemostasis wasachieved. Orders were also given for immediate andthen daily liver function tests, as well as for a com-plete blood count and prothrombin time test. Initiallaboratory results revealed a hemoglobin level of

7.3 g/dL and a hematocrit value of 23%. The physi-cian ordered a transfusion of three more units ofpacked red blood cells. Prothrombin time was ele-vated at 25 seconds.

ALCOHOLIC CIRRHOSIS: AN OVERVIEW

The pathogenesis of alcoholic liver disease isnt fullyunderstood. But its known that in the liver ethanoloxidizes into acetaldehyde, which appears to be theprincipal agent for various toxic effects. As acetalde-hyde and its metabolite acetate accumulate, numer-ous metabolic processes are disrupted; one result isthe development of fatty livera condition in whichlipid vacuoles form inside the liver cells, resulting incell degeneration and death. If the patient abstainsfrom alcohol, fatty liver damage is often, though

not always, reversible. But if alcohol consumptioncontinues, liver damage can progress to alcoholic

hepatitis or cirrhosis or both. Alcoholic hepatitis ischaracterized by fibrosis and inflammation; necro-sis (often focal) may also occur. Alcoholic cirrhosisis characterized by extensive fibrosis associated withthe formation of nodules that disrupt liver structure(see Figure 2). (For more on alcoholic liver disease,see Gender, Level of Alcohol Intake, and RelativeRisk of Liver Disease.1-3)

Cirrhosis leads to several severe complications.The extensive fibrosis compromises blood flow with-in the liver, inhibiting perfusion and resulting inportal hypertension. Blood backs up into the veinsof the stomach and esophagus, resulting in gas-trointestinal and esophageal varices. Other com-plications contribute to the likelihood of varicealbleeding. Portal hypertension contributes to ascites,the accumulation of fluid in the peritoneal cavity. Insome patients with cirrhosis and ascites, the renin-

angiotensin-aldosterone system is activated, resultingin sodium and total body water retention.4 Patientswith cirrhosis and ascites are at higher risk for bac-terial infections, including spontaneous bacterialperitonitis (bacterial peritonitis in the absence of anabscess or other intraabdominal source of infec-tion).5, 6 The cirrhotic livers inability to process tox-ins causes them to build up in the bloodstream,leading to hepatic encephalopathy; the buildup oftoxins can also increase portal pressure, makingvariceal hemorrhage more likely.7 In some patients

liver failure leads to renal failure (hepatorenal syn-drome). Theres evidence that this is a relativelyfrequent event in patients with cirrhosis and upper-gastrointestinal hemorrhage.8

Signs and symptoms of alcoholic liver disease.Presentation will depend on disease severity. In apatient still able to compensate, signs and symptomscan be vague and might include intermittent mildfever, unexplained epistaxis (nosebleed), morning in-digestion, spider angiomas, palmar erythema, ankleedema, abdominal pain, hepatomegaly, and spleno-megaly.6 As the disease progresses, the patient can nolonger compensate. Signs and symptoms result fromboth impaired liver function and portal hyperten-sion. Those associated with impaired liver functioninclude jaundice, muscle wasting, weight loss, weak-

ness, spontaneous bruising, epistaxis, and purpura(the last three are indications of coagulopathy). Those

Gender,Level of Alcohol Intake,and Relative Riskof LiverDisease

A

large prospective study in Denmark investigatedthe relationship between self-reported alcohol

intake and the risk of developing liver disease, survey-

ing more than 13,000 adults and following them for

12 years.1 The researchers found that, at an intake of

28 to 41 alcoholic beverages weekly, the relative risk

of developing cirrhosis was 7% for men and 17% for

women, and that, at any level of intake, women had

a significantly higher risk of developing cirrhosis than

men.The reasons for this arent fully understood. Ely

and colleagues point out that women generally havea lower volume of body water than men, resulting in

a higher blood alcohol level per amount consumed;

gender differences in how alcohol is metabolized are

also thought to play a role.2

Others have hypothesizedthat estrogens increase gut permeability and portal

endotoxin levels, leading to greater injury to the liver.3

The cirrhotic livers inability to process toxins causes them to build

up in the bloodstream, which can increase portal pressure,

making variceal hemorrhage more likely.


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associated with portal hypertension include varicealhemorrhage, ascites, hepatic atrophy, hepatic enceph-alopathy, and hypotension. Continuous mild fever,white nails, clubbing of fingers, sparse body hair, andgonadal atrophy may also be present.6, 9

ESOPHAGEAL VARICES: PREVALENCE AND RISK FACTORS

Esophageal varices occur in about half of peoplewith cirrhosis; indeed, one comprehensive reviewstates that if followed long enough, most cirrhoticseventually develop the condition.10 Hemorrhage oc-curs in about one-third of people with varices andis life threatening. Each bleeding event carries a20% to 30% risk of death; up to 70% of patients

who arent treated die within one year of the initialevent.10

Factors associated with an increased risk of initialvariceal hemorrhage include larger variceal size (diam-eter greater than 5 mm); the presence of red spotsor wales on the varices; more severe portal hyper-tension, with risk increasing at hepatic venous pres-sures above 12 mmHg; and more severe cirrhosis,with or without ascites.10, 11 (Cirrhosis is sometimesevaluated according to the Child-Pugh scoring sys-tem, which incorporates factors such as serum al-bumin and bilirubin levels, prothrombin time, andthe presence or absence of ascites and encephalopa-thy. Patients with Child-Pugh Class C cirrhosisthe

Figure2. LiverChangeswith CirrhosisA. Normal liver. B. Cirrhosis. Note the small size of the cirrhotic liver.

A

B


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poorest prognosisare at higher risk for varicealbleeding than are those with less severe disease.12)

Factors associated with increased risk of rebleed-ing include those above plus more severe initial hem-orrhage, being older than 60 years of age, the presenceof bacterial infection, and renal failure.10 (See FactorsAssociated with Increased Risk of Variceal Hemor-rhage.10-12)

EMERGENT TREATMENT

Immediate treatment of variceal hemorrhage includesprotecting the airways to prevent aspiration, pro-viding hemodynamic support, treating coagulopa-thy, and reducing portal pressure.13, 14

Protect the airway. To prevent aspiration, pa-tients should be turned to one side and the head of

the bed raised to a high Fowler position. Patientswith massive hemorrhage should be intubated.15 AYankauer suction catheter should be readily avail-able in the event that intervention is needed to pre-

vent aspiration.Provide hemodynamic support. Both normal sa-

line and blood components are typically given. Cur-rent guidelines for treating acute variceal hemorrhagestate that one goal of blood transfusions is to main-tain the hemoglobin level at about 8 g/dL.11 (Alter-natively, the goal can be to maintain hematocrit at24% to 30%.16, 17) Its important to remember that,in patients with portal hypertension, excessive trans-fusion can increase portal pressure and lead to fur-ther bleeding.

Patients who receive significant transfusions areat risk for hypocalcemia and hyperkalemia.15 Andnormal saline infusion increases the risk of hyperna-tremia. Thus serum potassium, calcium, and sodiumlevels must be closely monitored.

Treat coagulopathy. A cirrhotic liver is incapableof synthesizing vitamin K, which is necessary forcoagulation; thus if coagulopathy is present, par-enteral vitamin K and fresh frozen plasma may beordered.13 The goals of treatment are not only tocontrol the initial bleed but also to prevent rebleed-ing, which occurs within hours to days or weeks inabout 50% of patients.18,19 However, one review cau-tioned that the safety and efficacy of vitamin K

administration in this population hasnt been dem-onstrated.20

Reduce portal pressure. Octreotide is the drug ofchoice in the management of acute variceal bleeding.An analogue of the peptide somatostatin, it worksby inhibiting the release of vasodilatory hormonessuch as glucagon, which indirectly causes vasocon-striction of the viscera and decreased portal veinflow. Although regimens vary, one review found thatan initial bolus of 50 micrograms IV achieved themaximum hemodynamic effect, followed by a con-tinuous infusion of 25 to 50 micrograms hourly forup to five days to control bleeding.21 Possible adverseeffects of this regimen include dizziness, orthostatichypotension, palpitations, nausea, and hypoglycemia.

Vasopressin (Pitressin) is also effective, but itsused less often because its extremely potent andcan have serious adverse effects.14, 21 Typically an ini-

tial dose of 0.2 units per minute IV is given, with thedosage increasing by 0.2 to 0.4 units every hour (toa maximum of 0.9 units per minute) until the bleed-ing is controlled; the dosage is then lowered by 0.1

to 0.2 units per minute every 12 hours. Vasopressinconstricts mesenteric arterioles and decreases portalflow, thereby lowering portal pressure. One large re-view concluded that hemostasis was achieved in 70%to 85% of cases; however, early rebleeding occurredin 30% to 50%.10 Some experts think vasopressinmay actually increase mortality because of its vaso-constrictive effects on other organs such as the heartand intestines.15 But studies have shown that con-comitant administration of nitroglycerin (Nitro-Bidand others) reduces this effect.10 Shah and Kamathrecommend administering nitroglycerin through apatch, with doses adjusted to blood pressure read-ings.14 Unfortunately, neither octreotide nor vasopres-sin increases survival rate.15

Once hemostasis has been achieved, definitivetreatment by endoscopy can be performed.

ENDOSCOPIC TREATMENT

Therapeutic endoscopy is considered the definitivetreatment for active variceal hemorrhage. Endoscop-ic variceal ligation (EVL) is the preferred therapy,with endoscopic injection sclerotherapy (EIS) an al-ternative if ligation proves technically difficult.16 Thetechnique is performed using an endoscope with a

banding device mounted at its tip. The varix isdrawn into the suction chamber of the endoscope

Treatment of variceal hemorrhage includes protecting the

airways, providing hemodynamic support, treating

coagulopathy, and reducing portal pressure.



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and an elastic band is applied at or just distal to thebleeding point. This causes vessel thrombosis, ne-crosis, and fibrosis, destroying the varix. Its recom-mended that a multiband ligator be used to minimizethe need for reintubation.22 Repeat procedures arerequired every one to two weeks, until all varices havebeen eliminated.11 Complications include bleeding ul-cers and esophageal perforation; systemic complica-tions are rare.10, 11 (To see a video of this procedure,go to http://bit.ly/31jSB5.)

In EIS, a catheter with a retractable needle ispassed through the endoscope. The needle is insert-ed directly into the varix and a sclerosant such assodium morrhuate or sodium tetradecyl is injected.The sclerosant and edema serve to stop the acutehemorrhage. The procedure is typically repeated oneweek later and then at three-week intervals, until theresulting thrombosis and fibrosis destroy the varix.10

Complications include bleeding ulcers, esophagealperforation, stricture formation, and pleural effu-sions; systemic complications such as aspirationpneumonia and spontaneous bacterial peritonitishave also been reported.10, 15

One large review concluded that, compared withEIS, EVL resulted in faster variceal elimination, fewercomplications, and fewer rebleeding episodes.10 ButEVL also had a higher rate of variceal recurrence. Itsunclear whether the concomitant administration ofoctreotide with EVL or EIS improves patient out-comes.10

Both EVL and EIS are performed using moderate

(conscious) sedation. During either procedure, twonurses should be present: one to monitor the patientsvital signs (including oxygen saturation level) andprotect the patients airway, another to assist the gas-troenterologist. Because sclerosants are quite caus-tic, during an EIS procedure its also important toprotect the patients and clinicians eyes.

BALLOON TAMPONADE

When endoscopy isnt available to treat varicealhemorrhage, balloon tamponade can be used. It canalso be used as an adjunct to pharmacotherapy andEVL or EIS, especially when bleeding is difficult tocontrol.23, 24 The device used most often is theSengstakenBlakemore tube (SBT), which has bothesophageal and gastric balloons; when inflated, thesecompress the varices and decrease esophageal bloodflow. To reduce the patients risk for aspiration, thestomach might be lavaged with sterile saline to re-move blood before insertion25; however, theres anincreased risk of additional bleeding due to traumafrom the nasogastric tube. Although balloon tam-ponade controls acute hemorrhage in more than80% of cases, rebleeding upon deflation is com-mon.12 Complications include esophageal ulceration

and perforation, aspiration pneumonia, and air-way obstruction caused by SBT migration into the

larynx; mortality rates of up to 20% have been re-ported.

Before SBT insertion, the nurse should inspectand inflate all balloons to check for leaks, then de-flate them and label each port. Because insertioncan induce projectile vomiting and further deterio-ration of the patients condition, clinicians should beprepared to clear the patients airway and to resusci-tate if necessary. Following insertion, the esophagealballoon is inflated to the specified pressure and tubeplacement is radiographically confirmed. To main-tain correct position, the tube is then securely tapedto the side of the face. If the applied force, knownas skin traction, isnt adequate to stop the bleeding,a weighted traction apparatus can be applied; how-ever, this may increase the risk of tube migration.26

Because of the risk of airway obstruction fromtube migration, the tubes position should be clearly

marked so that any displacement can be quickly rec-ognized27; scissors should be readily available to cutthe tube if the airway becomes compromised. Be-cause of the risk to the esophageal mucosa of pres-sure necrosis, the physician might order balloondeflation for 30 to 60 minutes every eight hours.25

Upon deflation, rebleeding occurs in as many as50% of cases, and clinicians must be prepared withcontingency measures.28

SALVAGE THERAPY: TIPS PLACEMENT

Salvage therapy refers to final available treatmentfor a given condition, when prognosis is poor and the

patient hasnt responded to or cant tolerate othertreatments. The goal is to effect cure or improve thepatients quality of life.

Factors Associatedwith IncreasedRiskofVariceal Hemorrhage10-12

Initial hemorrhageRisk increases with the following:

larger variceal size (diameter > 5 mm)

presence of red spots or wales on the varices

more severe portal hypertension (hepatic

venous pressure > 12 mmHg)

more severe cirr hosis, with or without ascites

(Child-Pugh Class C cirrhosis)

Recurrent hemorrhageRisk increases with all of the above, and with the

following:

severity of initial bleed

age > 60 years

bacterial infection

renal failure

active alcoholism

http://bit.ly/31jSB5http://bit.ly/31jSB5


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Resuscitate: Airwaymaintain airwayBreathingadminister high-flow oxygen

Circulationestablish IV access, then transfuse

with PRBCs; to correct coagulopathy, transfuse

platelets or fresh frozen plasma

Initiate

pharmacotherapy

Definitive treatment: Endoscopic treatment (EVL or EIS)

within 12 hours of bleeding event

If endoscopy unavailable, or in the event of massive or uncontrolled

hemorrhage: Balloon tamponade

Rebleeding: Repeat endoscopic

treatment; if unsuccessful, place TIPS

For variceal hemorrhage associated with alcoholicliver disease, salvage therapy usually involves place-ment of a transjugular intrahepatic portosystemicshunt (TIPS).14 The procedure is performed by aninterventional radiologist. Angiography is used tocreate a shunt between the hepatic and portal veins,which is then maintained by placement of a fenes-trated metal stent. Although patients who undergoTIPS placement are less likely to bleed than arethose undergoing endoscopic therapy, their chancesof survival arent improved and may be worse.15

Procedure-related complications include hematomas,liver capsule rupture, and pulmonary edema; long-term complications include encephalopathy, liver fail-ure, hemolysis, and TIPS stenosis. Another option iscreation of a surgical shunt through an anastomosisbetween the portal vein and the vena cava. How-ever, surgical shunts carry a significantly increasedrisk of death compared with endoscopic therapy.15

Following either procedure, the patients vital signsmust be closely monitored to ensure that bleedinghas been effectively controlled; serum ammonia level


Figure3. TreatmentofVaricealHemorrhage

EIS = endoscopic injection sclerotherapy; EVL = endoscopic variceal ligation;

PRBC = packed red blood cell;TIPS = transjugular intrahepatic portosystemic shunt

o

o

o


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and level of consciousness should also be periodi-cally reassessed.

For a quick guide to treatment for variceal hem-orrhage, see Figure 3.

CASE REVISITED

Over the next two days, two EVL procedures wereperformed and octreotide continued to be infused.In addition to the five units of packed red bloodcells already given to Ms. Barth, she also receivedtwo units of fresh frozen plasma. But 44 hours afterthe first variceal hemorrhage, rebleeding occurred;the patient again vomited blood and her conditiondeteriorated.

A polymorphonuclear leukocyte count of 310cm2 was indicative of spontaneous bacterial peri-tonitis, and Ms. Barth was started on a five-daycourse of cefotaxime (Claforan) 6 g IV per day. Be-

cause antibiotic treatment failure isnt unusual withthis complication, she required close monitoring.(Indications of such failure include rapid deteriora-tion with developing shock within the first hour ofinitiating therapy, or less than a 25% reduction inpolymorphonuclear leukocyte count on follow-upparacentesis two days after initiating therapy.) Lac-tulose enemas were repeated to quickly lower herserum ammonia level. But on her fifth day in theICU, Ms. Barth again became encephalopathic andher kidneys began to fail. Despite salvage therapy,her condition continued to deteriorate and, a weeklater, she died. M

Melissa M. Smith is the director of and assistant professor inthe Division of Nursing at Aultman College of Nursing andHealth Sciences in Canton, OH. Contact author: [email protected]. The author of this article has no significant ties,financial or otherwise, to any company that might have aninterest in the publication of this educational activity. Emergencyis coordinated by Polly Gerber Zimmermann, MS, MBA, RN,CEN: [email protected].

REFERENCES

1. Becker U, et al. Prediction of risk of liver disease by alcoholintake, sex, and age: a prospective population study.Hepatology 1996;23(5):1025-9.

2. Ely M, et al. Gender differences in the relationship betweenalcohol consumption and drink problems are largelyaccounted for by body water. Alcohol Alcohol1999;34(6):894-902.

3. Enomoto N, et al. Role of Kupffer cells and gut-derivedendotoxins in alcoholic liver injury. J Gastroenterol Hepatol2000;15 Suppl:D20-D25.

4. Moore KP, Aithal GP. Guidelines on the management ofascites in cirrhosis. Gut2006;55 Suppl 6:vi1-vi12.

5. Fasolato S, et al. Renal failure and bacterial infections in

patients with cirrhosis: epidemiology and clinical features.Hepatology 2007;45(1):223-9.

6. Fitzpatrick E. Assessment and management of patients withhepatic disorders. In: Smeltzer SC, et al., editors. Brunnerand Suddarths textbook of medicalsurgical nursing. 11thed. Philadelphia: Lippincott Williams and Wilkins; 2008.vol. 2. p. 1284-343.

7. Goulis J, et al. Bacterial infection in the pathogenesis ofvariceal bleeding. Lancet1999;353(9147):139-42.

8. Crdenas A, et al. Renal failure after upper gastrointestinalbleeding in cirrhosis: incidence, clinical course, predictivefactors, and short-term prognosis. Hepatology 2001;34(4 Pt1):671-6.

9. Sargent S. The aetiology, management and complications ofalcoholic hepatitis. Br J Nurs 2005;14(10):556-62.

10. Luketic VA, Sanyal AJ. Esophageal varices. I. Clinical pres-entation, medical therapy, and endoscopic therapy.Gastroenterol Clin North Am 2000;29(2):337-85.

11. Garcia-Tsao G, et al. Prevention and management of gas-troesophageal varices and variceal hemorrhage in cirrhosis.Hepatology 2007;46(3):922-38.

12. Garcia-Tsao G, Lim JK. Management and treatment ofpatients with cirrhosis and portal hypertension: recommen-dations from the Department of Veterans Affairs HepatitisC Resource Center Program and the National Hepatitis CProgram. Am J Gastroenterol2009;104(7):1802-29.

13. Sartin JS. Liver diseases. In: Copstead LE, Banasik JL, edi-tors. Pathophysiology. 4th ed. St. Louis: Saunders/Elsevier;2010. p. 868-901.

14. Shah VH, Kamath P. Management of portal hypertension.Postgrad Med2006;119(3):14-8.

15. Hegab AM, Luketic VA. Bleeding esophageal varices. Howto treat this dreaded complication of portal hypertension.Postgrad Med2001;109(2):75-89.

16. Berry PA, Wendon JA. The management of severe alcoholicliver disease and variceal bleeding in the intensive care unit.Curr Opin Crit Care 2006;12(2):171-7.

17. de Franchis R. Evolving consensus in portal hypertension.Report of the Baveno IV Consensus Workshop on method-ology of diagnosis and therapy in portal hypertension.J Hepatol2005;43(1):167-76.

18. de Franchis R, Primignani M. Why do varices bleed?Gastroenterol Clin North Am 1992;21(1):85-101.

19. McCormick PA, et al. Why portal hypertensive varicesbleed and bleed: a hypothesis. Gut1995;36(1):100-3.

20. Mart-Carvajal AJ, et al. Vitamin K for upper gastrointesti-nal bleeding in patients with liver diseases. CochraneDatabase Syst Rev 2008(3):CD004792.

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22. McAvoy NC, Hayes PC. The use of transjugular intrahep-atic portosystemic stent shunt in the management of acuteoesophageal variceal haemorrhage. Eur J GastroenterolHepatol2006;18(11):1135-41.

23. Jalan R, Hayes PC. UK guidelines on the management ofvariceal haemorrhage in cirrhotic patients. British Society ofGastroenterology. Gut2000;46 Suppl 3-4:III1-III15.

24. Pasquale MD, Cerra FB. SengstakenBlakemore tube place-ment. Use of balloon tamponade to control bleeding varices.Crit Care Clin 1992;8(4):743-53.

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26. Christensen T, Christensen M. The implementation of aguideline of care for patients with a SengstakenBlakemoretube in situ in a general intensive care unit using transitionalchange theory. Intensive Crit Care Nurs 2007;23(4):234-42.

27. Collyer TC, et al. Acute upper airway obstruction due todisplacement of a SengstakenBlakemore tube. Eur JAnaesthesiol2008;25(4):341-2.

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