AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

The portal vein carries approximately 1500 mL/min of blood from the small and large bowel, the spleen, and the stomach to the liver. Obstruction of portal venous flow, whatever the etiology, results in a rise in portal venous pressure. The response to increased venous pressure is the development of a collateral circulation diverting the obstructed blood flow to the systemic veins. These portosystemic collaterals form by the opening and dilatation of preexisting vascular channels connecting the portal venous system and the superior and inferior vena cava. High portal pressure is the main cause of the development of portosystemic collaterals; however, other factors such as active angiogenesis also may be involved. The most important portosystemic anastomoses are the gastroesophageal collaterals. Draining into the azygos vein, these collaterals include esophageal varices, which are responsible for the main complication of portal hypertension—massive upper GI hemorrhage.

The most common causes of upper GI bleeding are duodenal and gastric ulcers, responsible for 35% and 20% of cases, respectively. Bleeding from esophageal varices is responsible for only 5-11% upper GI bleeding (incidence varies depending on geographic location). Other causes for upper GI bleeding are acute gastric erosions/hemorrhagic gastritis (18%), Mallory-Weiss tears (10%), gastric carcinoma (6%), and other causes (6%).

Pathophysiology

Obstruction of the portal venous system at any level leads to increased portal pressure. Normal pressure in the portal vein is 5-10 mm Hg because the vascular resistance in the hepatic sinusoids is low. An elevated portal venous pressure (>10 mm Hg) distends the veins proximal to the site of the block and increases capillary pressure in organs drained by the obstructed veins. Because the portal venous system lacks valves, resistance at any level between the right side of the heart and the splanchnic vessels results in retrograde flow of blood and transmission of elevated pressure. The anastomoses connecting the portal and systemic circulation may enlarge to allow blood to bypass the obstruction and pass directly into the systemic circulation.

Recent studies have demonstrated the role of endothelin-1 (ET-1) and nitric oxide (NO) in the pathogenesis of portal hypertension and esophageal varices. ET-1 is a powerful vasoconstrictor synthesized by sinusoidal endothelial cells that has been implicated in the increased hepatic vascular resistance of cirrhosis and in the development of liver fibrosis. NO is a vasodilator substance that is synthesized by sinusoidal endothelial cells. In the cirrhotic liver, the production of NO is decreased, and endothelial nitric oxide synthase (eNOS) activity and nitrite production by sinusoidal endothelial cells are reduced.

Obstruction and increased resistance can occur at 3 levels in relation to hepatic sinusoids, as follows:

• Presinusoidal venous block (eg, portal vein thrombosis, schistosomiasis, primary biliary cirrhosis): These lesions are characterized by elevated portal venous pressure but a normal wedged hepatic venous pressure (WHVP).
• Postsinusoidal obstruction (eg, Budd-Chiari syndrome, venoocclusive disease, in which the central hepatic venules are the primary site of injury): WHVP characteristically is elevated.
• Sinusoidal obstruction (eg, cirrhosis) is characterized by increased hepatic venous pressure gradient (HVPG), with WHVP being equal to portal venous pressure.

Gastroesophageal varices have 2 main inflows, the first is the left gastric or coronary vein. The other major route of inflow is the splenic hilus, through the short gastric veins. The gastroesophageal varices are important because of their propensity to bleed.

Studies of hepatic microcirculation have identified several mechanisms that may explain the increased intrahepatic vascular resistance. These mechanisms may be summarized as follows:

• A reduction of sinusoidal caliber due to hepatocyte enlargement
• An alteration in the elastic properties of the sinusoidal wall due to collagen deposition in the space of Disse
• Compression of hepatic venules by regeneration nodules
• Central vein lesions caused by perivenous fibrosis
• Venoocclusive changes
• Perisinusoidal block by portal inflammation, portal fibrosis, and piecemeal necrosis

The following are risk factors for variceal hemorrhage:

• Variceal size: The larger the varix, the higher the risk of rupture and bleeding. However, patients may bleed from small varices too.
• The presence of endoscopic red color signs (eg, red whale markings, cherry red spots)
• The Child classification, especially the presence of ascites, increases the risk of hemorrhage.
• Active alcohol intake in patients with chronic alcohol-related liver diseases
• Local changes in the distal esophagus (eg, gastroesophageal reflux) have been postulated to increase the risk of variceal hemorrhage. However, evidence to support this view is weak. Recent studies indicate that gastroesophageal reflux does not initiate or play a role in esophageal hemorrhage.

A well-documented association exists between variceal hemorrhage and bacterial infections, and this may represent a causal relationship. Infection could trigger variceal bleeding by a number of mechanisms, including the following:

• The release of endotoxin into the systemic circulation
• Worsening of hemostasis
• Vasoconstriction induced by contraction of stellate cells

Frequency

United States

In Western countries, alcoholic and viral cirrhosis are the leading causes of portal hypertension and esophageal varices.

Thirty percent of patients with compensated cirrhosis and 60-70% of patients with decompensated cirrhosis have gastroesophageal varices at presentation.

The de novo rate of development of esophageal varices in patients with chronic liver diseases is approximately 8% per year for the first 2 years and 30% by the sixth year.

The risk of bleeding from esophageal varices is 30% in the first year after identification.

Bleeding from esophageal varices accounts for approximately 10% of episodes of upper GI bleeding.

International

Hepatitis B is endemic in the Far East and Southeast Asia, particularly, and South America, North Africa, Egypt, and other countries in the Middle East. Schistosomiasis is an important cause of portal hypertension in Egypt, Sudan, and other African countries. Hepatitis C is becoming a major cause of liver cirrhosis worldwide.

Mortality/Morbidity

Patients who have bled once from esophageal varices have a 70% chance of rebleeding, and approximately one third of further bleeding episodes are fatal. The risk of death is maximal during the first few days after the bleeding episode and decreases slowly over the first 6 weeks. Mortality rates in the setting of surgical intervention for acute variceal bleeding are high.

Associated abnormalities in the renal, pulmonary, cardiovascular, and immune systems in patients with esophageal varices contribute to 20-65% of mortality.

Sex

• In females, alcoholic liver disease, viral hepatitis, venoocclusive disease, and primary biliary cirrhosis usually are responsible.
• In males, alcoholic liver disease and viral hepatitis usually are responsible.

Age

• Portal vein thrombosis and secondary biliary cirrhosis are the most common causes of varices in children.
• Cirrhosis is the most common cause of esophageal varices in adults.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

• Symptoms of liver disease
• • Weakness, tiredness, and malaise
  • Anorexia
  • Sudden and massive bleeding with shock on presentation
  • Nausea and vomiting
  • Weight loss - Common with acute and chronic liver disease, mainly due to anorexia and reduced food intake, and regularly accompanies end-stage liver disease, when a loss of muscle mass and adipose tissue often is a striking feature
  • Abdominal discomfort and pain - Usually felt in the right hypochondrium or under the right lower ribs (front, side, or back) and in the epigastrium or the left hypochondrium
  • Jaundice or dark urine
  • Edema and abdominal swelling
  • Pruritus - Usually associated with cholestatic conditions, such as extrahepatic biliary obstruction, primary biliary cirrhosis, sclerosing cholangitis, cholestasis of pregnancy, and benign recurrent cholestasis
  • Spontaneous bleeding and easy bruising
  • Encephalopathic symptoms - Disturbance of the sleep-wake cycle, deterioration in intellectual function, memory loss and, finally, inability to communicate effectively at any level, personality changes, and, possibly, display of inappropriate or bizarre behavior
  • Impotence and sexual dysfunction
  • Muscle cramps - Common in patients with cirrhosis
• Past medical history
• • Previous jaundice suggests the possibility of a previous acute hepatitis, hepatobiliary disorder, or drug-induced liver disease.
  • Recurrence of jaundice suggests the possibility of reactivation, infection with another virus, or the onset of hepatic decompensation.
  • Patients may have a history of blood transfusion or administration of various blood products.
  • A history of schistosomiasis in childhood may be obtained from patients in whom infection is endemic.
  • Intravenous drug abuse
• Family history of hereditary liver disease such as Wilson disease
• Risk factors for upper GI bleeding
• • Bleeding diathesis
  • Peptic ulcer disease
  • Use of alcohol or nonsteroidal anti-inflammatory drugs (NSAIDs)
  • Documented cirrhosis
  • Documented episodes of GI tract bleeding
  • History of recent vigorous retching or emesis before an attack of hematemesis or melena

Physical

• Pallor may suggest active internal bleeding.
• Low blood pressure, increased pulse rate, and postural drop of blood pressure may suggest blood loss.
• Parotid enlargement may be related to alcohol abuse and/or malnutrition.
• Cyanosis of the tongue, lips, and peripheries due to low oxygen saturation may be observed.
• Patients may experience dyspnea and tachypnea.
• A hyperdynamic circulation with flow murmur over the pericardium may be present.
• Jaundice may be present because of impairment of liver function.
• Look for telangiectasis of the skin, lips, and digits.
• Gynecomastia in males results from failure of the liver to metabolize estrogen, resulting in a sex hormone imbalance.
• Fetor hepaticus occurs in portosystemic encephalopathy of any cause (eg, cirrhosis).
• Palmar erythema and leuconychia may be present in patients with cirrhosis.
• Ascites, abdominal distention due to accumulation of fluid, may be present. Ascites may be associated with peripheral edema and may involve the abdominal wall and genitalia.
• Numerous dilated veins radiating out of the umbilicus may be observed. Distended abdominal wall veins may be present, with the direction of venous flow away from the umbilicus.
• The liver may be small.
• Splenomegaly occurs in portal hypertension.
• Testicular atrophy is common in males with cirrhosis, particularly those with alcoholic liver disease or hemachromatosis.
• Venous hums, continuous noises audible in patients with portal hypertension, may be present as a result of rapid turbulent flow in collateral veins.
• During the rectal examination, obtain a stool sample for visual inspection. A black, soft, tarry stool on the gloved examining finger suggests upper GI bleeding.

Causes

Diseases interfering with portal blood flow can result in portal hypertension and the formation of esophageal varices. Causes of portal hypertension usually are classified as prehepatic, intrahepatic, and posthepatic.

• Prehepatic
• • Splenic vein thrombosis
  • Portal vein thrombosis
  • Extrinsic compression of the portal vein
• Intrahepatic
• • Congenital hepatic fibrosis
  • Hepatic peliosis
  • Idiopathic portal hypertension
  • Sclerosing cholangitis
  • Tuberculosis
  • Schistosomiasis
  • Primary biliary cirrhosis
  • Alcoholic cirrhosis
  • Hepatitis B virus–related and hepatitis C virus–related cirrhosis
  • Wilson disease
  • Hemachromatosis
  • Alpha-1 antitrypsin deficiency
  • Chronic active hepatitis
  • Fulminant hepatitis
• Posthepatic
• • Budd-Chiari syndrome
  • Thrombosis of the inferior vena cava
  • Constrictive pericarditis
  • Venoocclusive disease of the liver

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

Acute gastric erosions
Portal vein thrombosis
Splenic vein thrombosis
Venoocclusive disease
Alcoholic cirrhosis
Hepatoportal arteriovenous fistula

Gastric varices: These are the source of bleeding in 5-10% of patients with variceal hemorrhage. Higher rates are reported in patients with left-sided portal hypertension due to thrombosis of the splenic vein.

Portal hypertensive gastropathy: This is a common complication of cirrhosis and portal hypertension, but significant bleeding from this source is relatively uncommon.

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• Complete blood count: Results may show anemia, leucopenia, and thrombocytopenia in patients with cirrhosis. Anemia may be secondary to bleeding, nutritional deficiencies, or bone marrow suppression secondary to alcoholism. Many patients with portal hypertension have some degree of hypersplenism. The hematocrit value may be low in patients with upper abdominal bleeding.
• Type and crossmatch blood and order 6 units of packed red blood cells.
• Prothrombin time: Because the coagulation factors involved in this test are synthesized by the liver, impairment of the liver function may result in a prolonged prothrombin time.
• Liver function tests: A mild elevation of the plasma activity of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) may occur in cirrhosis, although activity may be normal.
• Blood urea, creatinine, and electrolytes: Blood urea and creatinine levels may be elevated in patients with esophageal bleeding. Drug treatment, cirrhosis, ascites, and blood loss may contribute to changes in the serum electrolytes of these patients.
• Arterial blood gas and pH measurements
• Hepatic serology helps in the assessment of the cause of cirrhosis.

Imaging Studies

• Ultrasound of the upper abdomen may be indicated, especially if biliary obstruction or liver cancer is suspected.

Other Tests

• Rectal examination: Obtain a stool sample for visual inspection. A black, soft, tarry stool on the gloved examining finger suggests upper GI bleeding.

Procedures

• Endoscopy is required at an early stage to formulate the management plan. If active variceal bleeding or an adherent clot is observed, variceal hemorrhage can be diagnosed confidently. The presence of variceal red color signs (eg, cherry red spots, red whale markings, blue varices) indicates an increased risk of further bleeding.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

• Esophageal varices with no history of bleeding
• • Patients with esophageal varices and no prior history of variceal hemorrhage should be treated with nonselective beta-adrenergic blockers (eg, propranolol, nadolol, timolol), provided that the use of beta-blockers is not contraindicated (eg, because of insulin-dependent diabetes mellitus, severe chronic obstructive lung disease, congestive heart failure).
  • The dose of nonselective beta-blockers is determined by a 25% decrease in resting heart rate or a decrease in heart rate to 55 beats per minute or the development of adverse effects.
  • The use of beta-blockers decreases the risk of initial variceal bleeding by approximately 45%.
  • If contraindications to using beta-blockers exist, long-acting nitrates (eg, isosorbide 5-mononitrate) are alternatives.
  • Treatment with beta-blockers should be continued indefinitely.
  • The role of endoscopic sclerotherapy or variceal ligation for prevention of esophageal variceal hemorrhage is still controversial.
  • Combined sclerotherapy and treatment with nonselective beta-blockers offer no advantages over the use of beta-blockers alone for prevention of esophageal varices hemorrhage.
• Bleeding esophageal varices
• • Assess the rate and volume of bleeding. Check blood pressure and pulse with the patient in the supine position and with the patient in a sitting position.
  • Gain venous access and obtain blood for immediate hematocrit. Obtain a type and crossmatch. Measure the platelet count and prothrombin time. Send blood for renal and liver function tests and measure serum electrolytes.
  • Provide emergency treatment as outlined below.
• Emergency treatment
• • Promptly resuscitate and restore circulating blood volume of patients with suspected cirrhosis and variceal hemorrhage
  • Establish intravenous access for blood transfusion. While the blood is being crossmatched, start rapid infusion of 5% dextrose and colloid solution until blood pressure is restored and urine output is adequate.
  • Establish airway protection in patients with massive upper GI tract bleeding, especially if the patient is not fully conscious.
  • If indicated, correct clotting factor deficiencies with fresh frozen plasma, fresh blood, and vitamin K-1.
  • Insert a nasogastric tube to assess the severity of bleeding and to lavage gastric contents before endoscopy.
  • Consider pharmacologic therapy (octreotide or somatostatin) and endoscopy as soon as the patient has been resuscitated. The aim is to establish the cause and to control the bleeding.
  • Endoscopic therapy probably has replaced balloon tamponade as the initial therapy for variceal bleeding. Balloon tamponade now rarely is necessary, and, when it is used, it must be performed by experienced personnel because it is potentially dangerous.
• Endoscopic therapy
• • Endoscopic sclerotherapy
  • • Endoscopic sclerotherapy is successful in controlling acute esophageal variceal bleeding in up to 90% of patients. Control should be obtained with 1-2 sessions. Patients continuing to bleed after 2 sessions should be considered for alternative methods to control their bleeding.
    • In the United States, sodium tetradecyl sulfate or sodium morrhuate generally has been used as a sclerosant, while polidocanol or ethanolamine has been more popular in Europe. Variations in the technique or the sclerosant used have not been shown to influence the outcome.
    • Serious complications related to sclerotherapy have been reported in 15-20% of patients, with an associated mortality rate of 2%.
    • Complications of sclerotherapy may include mucosal ulceration, bleeding, esophageal perforation, mediastinitis, and pulmonary complications. Long-term complications, such as esophageal stricture formation, also may occur.
  • Endoscopic variceal ligation (banding)
  • • Endoscopic variceal ligation is based on the widely used technique of rubber-band ligation of hemorrhoids. The esophageal mucosa and the submucosa containing varices are ensnared, causing subsequent strangulation, sloughing, and eventual fibrosis, resulting in obliteration of the varices.
    • Rebleeding occurs less frequently with endoscopic variceal ligation than with endoscopic sclerotherapy (26% vs 45%).
    • Endoscopic ligation requires placement of an opaque cylinder over the end of the endoscope. This decreases the endoscopic field of view and may allow pooling of blood. Thus, in patients with active bleeding, visualization may be impaired more with ligation than with sclerotherapy.
    • Recent trials have demonstrated that ligation and sclerotherapy achieved similar rates of initial hemostasis in patients whose varices were actively bleeding at the time of treatment.
    • Local complications are less common with ligation compared to sclerotherapy. For example, esophageal strictures were found to be less common with ligation compared to sclerotherapy. Systemic complications, such as pulmonary infections and bacterial peritonitis, were not significantly different in the 2 groups. However, a trend was observed toward a decrease in these 2 complications in patients treated with ligation.

Surgical Care

Surgical care and therapeutic radiologic procedures for variceal hemorrhage

Approximately 5-10% of patients with esophageal variceal hemorrhage have conditions that cannot be controlled by endoscopic and/or pharmacologic treatment. Balloon tamponade (eg, Minnesota tube, Sengstaken-Blakemore tube, Linton-Nachlas tube) may be used as a temporary option in their management. Definitive salvage options may include the following:

• Surgical interventions include the following:
• • Portosystemic shunt
  • Devascularization (transabdominal devascularization of the lower 5 cm of the esophagus and the upper two thirds of the stomach, with staple gun transection of the lower esophagus) rarely is performed but may have a role in patients with portal and splenic vein thrombosis who are not suitable candidates for shunt procedures and who continue to have variceal bleeding despite endoscopic and pharmacologic treatment.
  • Orthotopic liver transplantation is the treatment of choice in patients with advanced liver disease.
• Therapeutic radiologic procedures include the following:
• • Percutaneous transhepatic embolization (PTE) of gastroesophageal varices involves catheterization of the gastric collaterals that supply blood to varices via the transhepatic route. A variety of agents had been used, with varying degrees of success in controlling acute bleeding. Generally, this procedure is less effective than endoscopic sclerotherapy for treatment of variceal hemorrhage and is much less effective compared to medical and surgical options. Thus, it should be reserved for situations in which acute variceal bleeding is not controlled by pharmaceutical treatment, endoscopic sclerotherapy, or endoscopic variceal ligation and in which contraindications for surgical management are present.
  • Transjugular intrahepatic portosystemic shunts (TIPS) are an effective salvage procedure for stopping acute variceal hemorrhage after failure of medical and endoscopic treatment. However, this procedure is associated with a number of complications; 20% of patients develop encephalopathy, and 50% may occlude their shunt in 1 year. Thus, it should be considered as a bridge to subsequent liver transplantation.

Consultations

Consider early consultation with a gastroenterologist and a surgeon, particularly for patients with active bleeding from esophageal varices.

Diet

In patients with hemodynamically significant upper GI tract bleeding, a nasogastric tube should be in place for 24 hours to assist in identifying any rebleeding. Gastric lavage may be performed frequently through the nasogastric tube, and the volume and appearance of material aspirated from the stomach should be recorded. Do not allow any food by mouth.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Two major categories of drugs (vasoconstrictors and vasodilators) are used to treat acute bleeding related to portal hypertension.

The main advantages to using vasoactive agents include the ability to treat variceal bleeding in the emergency department, lowering of the portal pressure, and offering the endoscopist a clearer view of varices because of less active bleeding. They represent an ideal treatment for sources of portal hypertensive bleeding other than esophageal varices (eg, gastric varices > 2 cm below the gastroesophageal junction or portal hypertensive gastropathy).

In the treatment of acute variceal bleeding, somatostatin, terlipressin, or octreotide is now the preferred therapy prior to endoscopy. Intravenous infusions of octreotide will lower portal blood pressure and can prevent rebleeding during the initial hospitalization.

Drug Category: Vasoconstrictors

Reduce portal blood flow and/or increase resistance to variceal blood flow inside the varices. Therefore, these drugs reduce blood flow in the gastroesophageal collaterals because of their vasoactive effects on the splanchnic vascular system.

Drug Category: Antisecretory agents

Used as adjunct to nonoperative management of secreting cutaneous fistulas of the stomach, duodenum, small intestine (jejunum and ileum), or pancreas.

Drug Category: Beta-adrenergic blockers

May block effect of vasodilators, decrease platelet adhesiveness and aggregation, and increase release of oxygen to tissues.

Drug Category: Vasodilators

Reduce the intrahepatic vascular resistance without decreasing peripheral or portal-collateral resistance.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Because of the frequency and severity of recurrent variceal bleeding, effective preventive treatment is mandatory in patients surviving an episode of acute variceal bleeding. This may include one of the following options:
• • Elective portocaval shunt
  • Distal splenorenal shunt
  • Devascularization procedures
  • Sclerotherapy
  • Endoscopic variceal banding ligation
  • TIPS may be indicated if medical treatment or endoscopic therapy is ineffective.

Further Outpatient Care

• The administration of propranolol and other nonselective beta-blockers in patients with cirrhosis reduces the portal pressure by reducing the portal collateral flow. This results from splanchnic vasoconstriction promoted by the blockade of vasodilating beta2-adrenoceptors in the splanchnic circulation and by decreasing heart rate and cardiac output due to blockade of cardiac beta1-adrenoceptors.
• Beta-blocker therapy is indicated in patients with esophageal varices and in patients treated for variceal hemorrhage with sclerotherapy or banding. Patients selected for beta-blocker therapy should have no contraindications to beta-blockers.

In/Out Patient Meds

• Adjust the dose of beta-blockers.
• If therapy with beta-blockers is not successful, addition of a second drug (eg, nitroglycerin, a long-acting nitrate) should be considered in an attempt to further decrease HVPG.

Transfer

• Patients with acute esophageal bleeding require urgent treatment in a hospital setting.

Complications

• Severe and persistent upper GI hemorrhage (ie, requiring >5-U transfusion)
• High morbidity and mortality (30-40% of the group with severe persistent GI hemorrhage) - Factors such as underlying liver disease and associated abnormalities of the renal, cardiovascular, and immune systems contribute to the high morbidity and mortality.
• Complications associated with GI bleeding - Vascular collapse; the sequelae of hypotension, cardiomyopathy, arrhythmias, aspiration pneumonia, sepsis, spontaneous bacterial peritonitis, overtransfusion, and rebound rebleeding of varices; and encephalopathy
• Complications related to blood transfusion
• Complications related to therapeutic procedures used in management of bleeding esophageal varices
• • Balloon tamponade - Aspiration pneumonia, esophageal perforation, superficial lesions of the gastric mucosa, pressure necrosis to the nasal passages, mouth, or lips
  • Sclerotherapy - Perforation of the esophagus (2-6%), esophageal ulceration and bleeding (2-13%), pleural effusion (16-48%), fever (30%), chest pain (40%), and esophageal stricture (7%)
  • Variceal banding - Rebleeding during the course of banding
  • Surgical procedures - For example, distal splenorenal shunt surgery is associated with an increased incidence of hepatic encephalopathy.
  • Liver transplantation - Rejection, infection, sepsis, and complications related to immunosuppressive drugs used postoperatively.
  • Complications related to pharmacotherapy

Prognosis

• Patients with HVPG of 20 mm Hg measured 48 hours after esophageal varices bleeding have a higher 1-year mortality rate.
• Other factors that can affect prognosis of patients with esophageal varices include the following:
• • Rebleeding
  • Child classification, especially the presence of ascites
  • Active alcohol intake in patients with chronic alcohol-related liver diseases
  • Occurrence of complications (eg, bacteremia and/or endotoxemia, spontaneous bacterial peritonitis, portosystemic encephalopathy, hepatorenal syndrome)
• Several factors are known to influence the prognosis of esophageal bleeding. These include the following:
• • The natural course of the disease causing portal hypertension
  • The severity of portal hypertension
  • The location and number of the bleeding varices
  • The functional status of the liver and the severity of liver disease (early rebleeding, within 5 d of admission, occurred in 21% of patients classified as Child-Pugh grade A, 40% of patients classified as grade B, and 63% of patients classified as grade C)
  • Presence of associated systemic disorders
  • Continued alcohol abuse
  • Response to emergency treatment

Patient Education

• All patients with esophageal varices should take beta-blockers to reduce the risk of bleeding unless beta-blockers are contraindicated by coexisting medical conditions. Patients also should be educated about the adverse effects of beta-blockers and the possible risks of their abrupt discontinuation.
• Educate patients about the benefits and disadvantages of available treatment options.
• For excellent patient education resources, visit eMedicine's Esophagus, Stomach, and Intestine Center, Liver, Gallbladder, and Pancreas Center, and Heartburn/GERD/Reflux Center. Also, see eMedicine's patient education articles Gastrointestinal Bleeding, Cirrhosis, and Gastritis.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Vasopressin should not be administered via a central line, especially in elderly patients.
• Initiating therapy to prevent recurrent bleeding as soon as the acute bleeding episode is controlled adequately is critical.
• Liver transplantation should be considered for patients with end-stage liver disease. The selection of candidates is dictated by the patient's clinical status, etiology of cirrhosis, abstinence from alcohol, and availability of a donor organ.

Special Concerns

• Patients with massive acute bleeding from esophageal varices who refuse blood transfusions because of their religious beliefs may constitute a challenge to the treating team.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

• Bosch J, Abraldes JG, Groszmann R. Current management of portal hypertension. J Hepatol. 2003;38 Suppl 1:S54-68. [Medline].
• D''Amico G, Pagliaro L, Bosch J. Pharmacological treatment of portal hypertension: an evidence-based approach. Semin Liver Dis. 1999;19(4):475-505. [Medline].
• Garcia-Tsao G. Portal hypertension. Curr Opin Gastroenterol. 2000;16:282-289.
• Garcia-Tsao G. Angiotensin II receptor antagonists in the pharmacological therapy of portal hypertension: a caution. Gastroenterology. Sep 1999;117(3):740-2. [Medline].
• Gotzsche PC, Gjorup I, Bonnen H, et al. Somatostatin v placebo in bleeding oesophageal varices: randomised trial and meta-analysis. BMJ. Jun 10 1995;310(6993):1495-8. [Medline].
• Goulis J, Patch D, Burroughs AK. Bacterial infection in the pathogenesis of variceal bleeding. Lancet. Jan 9 1999;353(9147):139-42. [Medline].
• Groszmann RJ, Garcia-Tsao G, Bosch J. Beta-blockers to prevent gastroesophageal varices in patients with cirrhosis. N Engl J Med. Nov 24 2005;353(21):2254-61. [Medline].
• Gupta TK, Toruner M, Chung MK, Groszmann RJ. Endothelial dysfunction and decreased production of nitric oxide in the intrahepatic microcirculation of cirrhotic rats. Hepatology. Oct 1998;28(4):926-31. [Medline].
• Hanisch E, Doertenbach J, Usadel KH. Somatostatin in acute bleeding oesophageal varices. Pharmacology and rationale for use. Drugs. 1992;44 Suppl 2:24-35; discussion 70-2. [Medline].
• Lubel JS, Angus PW. Modern management of portal hypertension. Intern Med J. Jan 2005;35(1):45-9. [Medline].
• Nevens F. Review article: a critical comparison of drug therapies in currently used therapeutic strategies for variceal haemorrhage. Aliment Pharmacol Ther. Sep 2004;20 Suppl 3:18-22; discussion 23. [Medline].
• Patch D, Armonis A, Sabin C, et al. Single portal pressure measurement predicts survival in cirrhotic patients with recent bleeding. Gut. Feb 1999;44(2):264-9. [Medline].
• Poo JL, Jimenez W, Maria Munoz R, et al. Chronic blockade of endothelin receptors in cirrhotic rats: hepatic and hemodynamic effects. Gastroenterology. Jan 1999;116(1):161-7. [Medline].
• Samonakis DN, Triantos CK, Thalheimer U. Management of portal hypertension. Postgrad Med J. Nov 2004;80(949):634-41. [Medline].
• Shulkes A, Wilson JS. Somatostatin in gastroenterology. BMJ. May 28 1994;308(6941):1381-2. [Medline].
• Williams SG, Westaby D. Management of variceal haemorrhage. BMJ. May 7 1994;308(6938):1213-7. [Medline].

Article Last Updated: Apr 12, 2006