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.[1, 2, 3]
High portal pressure is the main cause of the development of portosystemic collaterals; however, other factors such as active angiogenesis may also 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 gastrointestinal (GI) hemorrhage.
The most common causes of upper GI bleeding are duodenal (35%) and gastric ulcers (20%). 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%).
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.
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.
Studies have demonstrated the role of endothelin-1 (ET-1) and nitric oxide (NO) in the pathogenesis of portal hypertension and esophageal varices.[2, 4] 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 is characteristically 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. 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
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, as well as 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 with esophageal varices, alcoholic liver disease, viral hepatitis, venoocclusive disease, and primary biliary cirrhosis are usually responsible.
In males with esophageal varices, alcoholic liver disease and viral hepatitis are usually responsible.
Age
Portal vein thrombosis and secondary biliary cirrhosis are the most common causes of esophageal varices in children.
Cirrhosis is the most common cause of esophageal varices in adults.
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 is often 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
Lifestyle and history of diseases, such as nonalcoholic steatohepatitis (NASH), diabetes mellitus, and hyperlipidemia
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
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.
Diseases that interfere 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
Complete blood cell (CBC) 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 cross-match blood and order 6 units of packed red blood cells.
Prothrombin time (PT): 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 (ABG) and pH measurements
Hepatic serology helps in the assessment of the cause of cirrhosis.
Ultrasonography of the upper abdomen may be indicated in those with esophageal varices, especially if biliary obstruction or liver cancer is suspected.
Endoscopy is required at an early stage to formulate the management plan for those with esophageal varices. 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.
Patients with esophageal varices and no previous 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).[1, 5, 6, 7, 8]
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 as effective as treatment with propranolol in decreasing the incidence of first variceal bleeding and death in cirrhotic patients with higher-risks of bleeding from esophageal varices.
Kumar et al investigated whether endoscopic variceal ligation alone or a combination of endoscopic variceal ligation plus propranolol and isosorbide mononitrate was more effective for secondary prophylaxis in patients with previous variceal bleeding.[9] Patients were randomly assigned to receive endoscopic variceal ligation alone (n = 89) or the combination therapy (n = 88). No difference between the groups was observed for rebleeding 2 years after initial therapy (P = 0.822).[9] The authors concluded that endoscopic variceal ligation alone is sufficient to prevent variceal rebleeding, whereas addition of propranolol and isosorbide mononitrate to endoscopic variceal ligation may increase risk for adverse effects.
Combined sclerotherapy and treatment with nonselective beta-blockers offer no advantages over the use of beta-blockers alone for prevention of esophageal varices hemorrhage.
Approximately 50% of patients with NASH with severe fibrosis had esophageal varices. NASH patients with esophagogastric varices need to be followed up carefully like patients with other chronic liver disorders.
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 measurement. Obtain a type and cross-match. 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 the circulating blood volume of patients with suspected cirrhosis and variceal hemorrhage.
Establish intravenous access for blood transfusion. While the blood is being cross-matched, start rapid infusion of 5% dextrose and colloid solution until the 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 the bleeding and to lavage gastric contents before performing endoscopy.
Consider pharmacologic therapy (octreotide or somatostatin) and endoscopy as soon as the patient has been resuscitated. The aim is to establish the cause of and to control the bleeding.
Endoscopic therapy probably has replaced balloon tamponade as the initial therapy for variceal bleeding. Balloon tamponade is now rarely necessary, and, when it is used, it must be performed by experienced personnel because the procedure is potentially dangerous.
D'Amico et al reviewed studies that compared emergency sclerotherapy to vasoconstrictive drugs for variceal bleeding in patients with cirrhosis and concluded that vasoactive drugs are safe and effective whenever endoscopic ligation (banding) therapy is not promptly available.[10] In addition, the pharmacotherapy seemed to create less adverse events than emergency sclerotherapy. The meta-analysis included 17 trials representing 1817 patients. Vasoactive drugs varied between trials (ie, vasopressin, 1 trial; terlipressin, 1 trial; somatostatin, 5 trials; octreotide 10 trials). No significant differences were found comparing sclerotherapy with each vasoactive drug for any outcome regarding efficacy; however, adverse events were significantly more frequent with sclerotherapy.[10]
Endoscopic sclerotherapy
Endoscopic sclerotherapy is successful in controlling acute esophageal variceal bleeding in up to 90% of patients. Hemorrhagic 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 has generally been used as a sclerosant, whereas 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, may also occur.
Endoscopic variceal ligation (banding)[11, 12]
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 (26%) than with endoscopic sclerotherapy (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.
Clinical 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 with sclerotherapy. For example, esophageal strictures were found to be less common with ligation compared with sclerotherapy. Systemic complications, such as pulmonary infections and bacterial peritonitis, were not significantly different between the 2 groups. However, a trend was observed toward a decrease in these 2 complications in patients treated with ligation.
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 the management of these patients. 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) is rarely 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, PTE is less effective than endoscopic sclerotherapy for treatment of variceal hemorrhage, and it is much less effective compared with 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 shunt (TIPS) placement is 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 within 1 year. Thus, TIPS placement should be considered as a bridge to subsequent liver transplantation.
Role of liver transplantation
Liver transplantation is indicated for patients with end-stage liver disease resulting in cirrhosis (viral hepatitis, alcoholic, nonalcoholic steatohepatitis, cholestatic liver disease), fulminate liver failure, and early stage hepatocellular carcinoma. Careful assessment of patients for liver transplantation is required. However, this procedure has revolutionalized the management of patients with end-stage liver disorders.
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.
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. Vasoactive agents 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 before performing endoscopy. Intravenous infusions of octreotide will lower portal blood pressure and can prevent rebleeding during the patient's initial hospitalization.
Clinical Context:
Has vasopressor and antidiuretic hormone (ADH) activity. Increases water resorption at the distal renal tubular epithelium (ADH effect) and promotes smooth muscle contraction throughout the vascular bed of the renal tubular epithelium (vasopressor effects). However, vasoconstriction is also increased in splanchnic, portal, coronary, cerebral, peripheral, pulmonary, and intrahepatic vessels. Decreases portal pressure in portal hypertension.
Notable adverse effect is coronary artery constriction that may dispose patients with coronary artery disease to cardiac ischemia. This can be prevented with concurrent use of nitrates. Rarely used.
Clinical Context:
Synthetic analogue of vasopressin. Only pharmacologic agent shown to reduce mortality from variceal bleeding.
Widely used in Europe. In the United States, has orphan drug status to treat bleeding esophageal varices.
Has longer biologic activity compared with vasopressin.
Significantly reduces portal and variceal pressure and azygos flow. Beneficial when combined with sclerotherapy. Also has advantage of preserving renal function (particularly important in patients with cirrhosis).
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.
Clinical Context:
Naturally occurring tetradecapeptide isolated from the hypothalamus and pancreatic and enteric epithelial cells. Diminishes blood flow to portal system due to vasoconstriction, thus decreasing variceal bleeding. Has similar effects as vasopressin but does not cause coronary vasoconstriction. Rapidly cleared from the circulation, with an initial half-life of 1-3 min.
Clinical Context:
Synthetic octapeptide. Compared with somatostatin, has similar pharmacologic actions with greater potency and longer duration of action.
Antisecretory agents are used as adjuncts to nonoperative management of secreting cutaneous fistulas of the stomach, duodenum, small intestine (jejunum and ileum), or pancreas.
Clinical Context:
Competitive nonselective beta-adrenergic receptor antagonist without intrinsic sympathomimetic activity. Competes with adrenergic neurotransmitters (eg, catecholamines) for binding at sympathetic receptor sites. Similar to atenolol and metoprolol, propranolol blocks sympathetic stimulation mediated by beta1-adrenergic receptors in the heart and vascular smooth muscles.
Beta-adrenergic blockers may block the effect of vasodilators, decrease platelet adhesiveness and aggregation, and increase the release of oxygen to tissues.
Clinical Context:
Causes relaxation of vascular smooth muscle by stimulating intracellular cyclic guanosine monophosphate production. Result is a decrease in blood pressure.
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.
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.
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.
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 of those with esophageal varices.
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 the 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
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)
Samy A Azer, MD, PhD, MPH, Professor of Medical Education and Head of Curriculum Development Unit, King Saud University, Riyadh, Saudi Arabia; Visiting Professor of Medical Education, Faculty of Medicine, University of Toyama, Japan; former Professor of Medical Education, Chair of Medical Education Research and Development Unit, Faculty of Medicine, Universiti Teknologi MARA, Malaysia; former Consultant to the Victorian Postgraduate Medical Foundation, Melbourne, Australia; former Senior Lecturer in Medical Education, Faculty Education Unit, Faculty of Medicine, Dentistry and Health Sciences, University of Melbourne and University of Sydney, Australia
Disclosure: Nothing to disclose.
Specialty Editors
Waqar A Qureshi, MD, Associate Professor of Medicine, Chief of Endoscopy, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine and Veterans Affairs Medical Center
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Simmy Bank, MD, Chair, Professor, Department of Internal Medicine, Division of Gastroenterology, Long Island Jewish Hospital, Albert Einstein College of Medicine
Disclosure: Nothing to disclose.
Alex J Mechaber, MD, FACP, Senior Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Disclosure: Nothing to disclose.
Chief Editor
Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
