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Major causes of upper gastrointestinal bleeding in adults Authors :Rome Jutabha, MD, Dennis M Jensen, MD Section Editor : Mark Feldman

, MD Deputy Editor, Anne C Travis, MD, MSc, FACG Last literature review version 18.2: May 2010 | This topic last updated: August 17, 2009 (More) INTRODUCTION Upper gastrointestinal (UGI) bleeding is a common medical condition that results in high patient morbidity and medical care costs. In a study from one large health maintenance organization, the annual incidence of hospitalization for acute UGI bleeding was 102 per 100,000; the incidence was twice as common in males as in females, and increased with age [1]. UGI bleeding commonly presents with hematemesis (vomiting of blood or coffeeground like material) and/or melena (black, tarry stools) (table 1). A nasogastric tube lavage which yields blood or coffee-ground like material confirms this clinical diagnosis. However, lavage may not be positive if bleeding has ceased or arises beyond a closed pylorus. The presence of bilious fluid suggests that the pylorus is open and, if lavage is negative, that there is no active upper GI bleeding distal to the pylorus. In comparison, hematochezia (bright red or maroon colored blood or fresh clots per rectum) is usually a sign of a lower GI source (defined as distal to the ligament of Treitz). Although helpful, the distinctions based upon stool color are not absolute since melena can be seen with proximal lower GI bleeding, and hematochezia can be seen with massive upper GI bleeding [2-4]. (See "Approach to the adult patient with lower gastrointestinal bleeding".) This topic review will summarize issues related to bleeding from peptic ulcers and esophageal varices. Other causes of bleeding are presented on their corresponding topic reviews. An overall approach to the patient with an upper GI bleed, the treatment of

bleeding peptic ulcers, and the less common causes of UGI bleeding are discussed separately. (See "Approach to upper gastrointestinal bleeding in adults" and "Treatment of bleeding peptic ulcers" and "Uncommon causes of upper gastrointestinal bleeding".) CATEGORIES UGI bleeding can be classified into several broad categories based upon anatomic and pathophysiologic factors (table 1). Several endoscopic studies have described the most common causes [5-7]. Results have varied, possibly reflecting trends over time or differences in study design, populations, and definitions: • A prospective series of 1000 cases of severe UGI bleeding at the UCLA and West Los Angeles Veterans Administration Medical Centers published in 1996 found the following distribution of causes [5]: • Peptic ulcer disease — 55 percent • Esophagogastric varices — 14 percent • Arteriovenous malformations — 6 percent • Mallory-Weiss tears — 5 percent • Tumors and erosions — 4 percent each • Dieulafoy's lesion — 1 percent • Other — 11 percent • More recent data suggest that the proportion of cases caused by peptic ulcer disease has declined [6,8]. Peptic ulcers were responsible for only 21 percent of episodes of upper gastrointestinal bleeding among 7822 patients included in a national, United States database between 1999 and 2001 [6]. The most common cause was nonspecific mucosal abnormalities (42 percent), while esophageal inflammation accounted for about 15 percent,

it renders the underlying mucosa more vulnerable to acid peptic damage by disrupting the mucous layer.and varices about 12 percent. liberating enzymes and toxins. Mallory-Weiss tears. and adhering to the gastric epithelium. Among ulcer cases. Helicobacter pylori — Helicobacter pylori is a spiral bacterium that infects the superficial gastric mucosa and appears to be transmitted by the fecal-oral route. the host . There are four major risk factors for bleeding peptic ulcers [9. The most common endoscopic findings in patients with upper gastrointestinal bleeding were an ulcer (33 percent) followed by an erosion (19 percent). In addition. Gastric ulcers were more common than duodenal ulcers (55 versus 37 percent).428 upper endoscopies performed between 2000 and 2004 in a practice setting (rather than in tertiary care) [7].10]: • Helicobacter pylori infection • Nonsteroidal antiinflammatory drugs (NSAIDs) • Stress • Gastric acid Reduction or elimination of these risk factors reduces ulcer recurrence and rebleeding rates [11-14]. • A large database study focused on 243. PEPTIC ULCER DISEASE Gastroduodenal ulcer disease remains a common cause of UGI bleeding (picture 1) [5]. The bacterium generally does not invade gastroduodenal tissue. and tumors) each accounted for less than 5 percent of cases. gastric ulcers were more common than duodenal ulcers representing about 55 percent of all ulcers. Instead. Patients with variceal bleeding were excluded from the analysis. Other causes (arteriovenous malformations.

is asymptomatic and does not progress. due to persistent immune stimulation of gastric lymphoid tissue.) H. pylori incites an inflammatory reaction which further perpetuates tissue injury. gastric lymphoma [15-18]. which usually combine one or two antibiotics plus an antisecretory agent. (See "Treatment regimens for Helicobacter pylori". and 4 versus 59 percent for gastric ulcer [20]. altered gastric secretion coupled with tissue injury leads to peptic ulcer disease. In one report of 19 published studies. the recurrence rates in cured versus noncured H. intestinal metaplasia. (See "Association between Helicobacter pylori infection and gastrointestinal malignancy". (See "Pathophysiology of and immune response to Helicobacter pylori infection". Patients . pylori infection was 6 versus 67 percent for duodenal ulcer. and eventually to gastric carcinoma or rarely. (See "NSAIDs (including aspirin): Pathogenesis of gastroduodenal toxicity". The majority of these ulcers are asymptomatic and uncomplicated. Various multidrug regimens.) Stress — Stress related ulcers are a common cause of acute UGI bleeding in patients who are hospitalized for life-threatening non-bleeding illnesses [30]. for example. gastritis progresses to atrophy. are a common cause of gastrointestinal ulceration [22-25]. However.) The chronic inflammation induced by H.) Nonsteroidal antiinflammatory drugs — NSAIDs. in most individuals. pylori upsets gastric secretory physiology to varying degrees and leads to chronic gastritis which. however.immune response to H. NSAIDs also have been implicated as an important factor for non-healing ulcers [29]. elderly patients with a prior history of bleeding ulcer disease are at increased risk for recurrent ulcer and complications [26-28]. pylori eradication should be attempted for all patients who are diagnosed with the infection and who have peptic ulcer disease to prevent ulcer recurrence and rebleeding [19. while in other cases. including aspirin. In some cases. NSAID-induced injury results from both local effects and systemic prostaglandin inhibition. have eradication rates in the range of 80 to 90 percent [21].20].

NSAIDs.) Control of gastric acidity is considered an essential therapeutic maneuver in patients with active UGI bleeding.with these secondary episodes of bleeding have a higher mortality than those admitted to the hospital with primary UGI bleeding [31]. Esophagogastric varices develop as a consequence of systemic or segmental portal hypertension. pylori. or physiologic stress leads to increased cell membrane permeability to back diffusion of hydrogen ions. (See "Approach to upper gastrointestinal bleeding in adults". as in patients with the Zollinger-Ellison syndrome.) Gastric acid — Gastric acid and pepsin are essential cofactors in the pathogenesis of peptic ulcers [36]. Rarely. hyperacidity is the sole cause of peptic ulceration. and ulceration [36]. The most common causes of systemic portal hypertension in . (See "Treatment of bleeding peptic ulcers". resulting in intramural acidosis.) ESOPHAGOGASTRIC VARICES The prospective series of 1000 patients at the UCLA and West Los Angeles Veterans Administration Medical Centers found that esophagogastric varices were the second most common cause of UGI bleeding. (See "Clinical manifestations and diagnosis of Zollinger-Ellison syndrome (gastrinoma)".) Treatment — A variety of endoscopic methods have been described to control active bleeding from peptic ulcers. The risk of stress ulcer-related bleeding is increased in patients with respiratory failure and those with a coagulopathy [32]. (See "Stress ulcer prophylaxis in the intensive care unit". Impairment of mucosal integrity by factors such as H. The most commonly used are injection and cautery/thermal techniques. accounting for 14 percent of episodes (picture 2A-B) [5]. cell death. Primary ulcer prophylaxis with antisecretory agents such as H2 receptor antagonists or proton pump inhibitors decreases the risk of stress related mucosal damage and UGI bleeding in high-risk patients [33-35].

. one of the following tests should be considered to confirm the clinical suspicion: • Endoscopic ultrasound may be useful for differentiating gastric varices from gastric folds. In addition.) Prognosis — Variceal bleeding stops spontaneously in over 50 percent of patients. If endoscopy is inconclusive and gastric variceal bleeding is suspected.) Isolated gastric varices can result from segmental portal hypertension due to obstruction of the splenic vein from pancreatic carcinoma or chronic pancreatitis (picture 3). but the mortality rate approaches 70 to 80 percent in those with continued bleeding. • Portal vein angiography or an abdominal CT scan may show venous collaterals and recanalization of the umbilical vein (picture 4). The risk factors for bleeding from gastric varices are similar to the risk factors for bleeding from esophageal varices [37]. (See "Prediction of variceal hemorrhage in patients with cirrhosis". (See "Wireless video capsule endoscopy". • Capsule endoscopy of the esophagus (PillCam ESO) may represent a minimally invasive alternative to endoscopy for the detection of esophageal varices and portal hypertensive gastropathy. • Barium X-rays may image large esophageal varices or large gastric folds suggestive of gastric varices (picture 5).the United States are alcoholic liver disease and chronic active hepatitis. The risk of rebleeding is high (60 to 70 percent) until gastroesophageal varices are obliterated. (See "Prediction of variceal hemorrhage in patients with cirrhosis". secondary gastric varices may develop after obliteration of esophageal varices with endoscopic therapies.) Diagnosis — Endoscopy is the diagnostic modality of choice for esophagogastric varices [5]. Each episode of variceal hemorrhage is associated with a 30 percent risk of mortality [38].

uptodate.) We encourage you to print or e-mail these topic reviews. However. prophylactic endoscopic sclerotherapy is not indicated due to the risks and complications of this procedure [39. (See "Prevention of recurrent variceal hemorrhage in patients with cirrhosis". Prophylactic propranolol or nadolol therapy is the only cost-effective therapy in this setting [39]. The administration of a nonselective beta blocker such as propranolol can also decrease the risk of rebleeding.The risk of rebleeding can be substantially reduced by follow-up endoscopic therapy to obliterate residual varices. Endoscopic variceal ligation also may be beneficial for high-risk patients [40.41].42. . long-term survival depends upon the severity of liver disease and may not be improved following successful variceal obliteration.) INFORMATION FOR PATIENTS — Educational materials on this topic are available for patients. In contrast.) Various treatments are available for acute hemostasis. (See "Primary prophylaxis against variceal hemorrhage in patients with cirrhosis". Treatment — Primary prophylaxis against variceal hemorrhage is desirable in view of the relatively high rate of bleeding from esophageal varices and the high mortality associated with this complication. Endoscopic band ligation and sclerotherapy continue to be the most commonly used. Liver transplantation is the only treatment that significantly improves the long-term prognosis in these patients.) The onset of massive UGI bleeding from gastroesophageal varices usually signifies advanced liver disease (Child class B or C). which includes these and other]. (See "General principles of the management of variceal hemorrhage". or to refer patients to our public web site. www. (See "Patient information: Upper endoscopy" and "Patient information: Peptic ulcer disease" and "Patient information: Gastroesophageal reflux disease in adults".

Zuckerman. Fleischer. et al. Epidemiology of hospitalization for acute upper gastrointestinal hemorrhage: A population-based study. An objective measure of stool color for differentiating upper from lower gastrointestinal bleeding. Mattek. Gastroenterology 1988. S. P. Yeomans. The frequency of peptic ulcer as a cause of upper-GI bleeding is exaggerated. Changing trends in acute upper-GI bleeding: a population-based study. GA. V. Jensen. DM. 5. 80:1035. S. et al. Trellis. RE. 95:1569. 3. 40:1614. G. 7. Pezzullo. Piovesana. Am J Gastroenterol 1997. RH. GR. Gastrointest Endosc 2008. . Diagnosis and treatment of severe hematochezia. Baldo. Loperfido. JC. Gralnek. R. Dig Dis Sci 1995. Machicado. 67:422. An evaluation of endoscopic indications and findings related to nonvariceal upper-GI hemorrhage in a large multicenter consortium. 8. Alexander. Sherman. DE. 2. et al. et al. 6. A prospective characterization of upper gastrointestinal hemorrhage presenting with hematochezia. Jutabha. 90:206. Clouse. Am J Gastroenterol 1995. Med Clin North Am 1996. Eur J Gastroenterol Hepatol 1995. 9. Gastrointest Endosc 2004. DR. Wilcox. 70:212. Boonpongmanee. GF. Cotsonis. 7:685. ND.REFERENCES 1. Critical issues in the pathophysiology and management of peptic ulcer disease. 4. CM. Gastrointest Endosc 2009. LN. 92:231. The role of urgent colonoscopy after purge. Hunt. Jensen. 59:788. N. IM. Longstreth. BK. E. Malfertheiner. DM. Management of severe upper gastrointestinal bleeding in the patient with liver disease. TM. Enestvedt.

MALT Lymphoma Study Group.10. Eradication of Helicobacter pylori reduces the possibility of rebleeding in peptic ulcer disease. H. 42:827. Helicobacter pylori infection and gastric lymphoma. 12. E. et al. Hepatogastroenterology 1995. Ramirez. Shibata. JM. Lauritsen. Treatment of H. A. 345:1591. 41:1. Rokkas. JAMA 1996. Gastrointest Endosc 1995. 19. Cancer 1996. I. et al. Nakamura. Hepps. et al. 15. J. GN. Bayerdorffer. Hansen. FC. Lancet 1995. Medical treatment of peptic ulcer disease. AH. 79:3. Karameris. KS. Parsonnet. 210:70. Helicobacter pylori and primary gastric lymphoma. Soll. Peptic ulcer and Helicobacter pylori: Eradication and relapse. Graham. Neubauer. Scand J Gastroenterol Suppl 1995. identifying high-risk groups by excess risk estimates. Imoto. T. Villadsen. Rudolph. et al. A histopathologic and immunohistochemical analysis of 237 patients. Yao. Helicobacter pylori infection in patients with gastric carcinoma in biopsy and surgical resection. Mavrogeorgis. HD. Pajares. L. et al. 28:939. 275:622. T. pylori infection: Its role in chronic gastritis. Hallas. Y. et al. et al. Aoyagi. J. S. Regression of primary gastric lymphoma of mucosa-associated lymphoid tissue type after cure of Helicobacter pylori infection. T. Scand J Gastroenterol 1995. 77:1044. . B. A. 330:1267. DY. 13. carcinoma and peptic ulcer. Rodriguez. Nonsteroidal anti-inflammatory drugs and upper gastrointestinal bleeding. 11. 18. S. pylori reduced the rate of rebleeding in peptic ulcer disease. Cancer 1997. 17. K. Ohuchi. 30:438. J. Scand J Gastroenterol 1993. A. Tytgat. N Engl J Med 1994. 14. 16.

J. Capurso. Hallas. Daugherty. 13:119. WE. Hansen. DJ. JL. Arch Intern Med 1996. JM. Smalley. The treatment of Helicobacter pylori infection in the management of peptic ulcer disease. RJ. 141:539. F. A meta-analysis of randomized controlled clinical trials. 27. F. 22. 156:2321. Feu. 100:1685. Raoul. 23. Ferrario. 13 Suppl 1:89. et al. Scand J Gastroenterol 1996. 24. NSAID-induced peptic ulcer disease: A critical review of pathogenesis and management. JH. Am J Epidemiol 1995. Turney. Relationship between H. Gastroenterology 1996. 31:126. Koch. WL. JR. Dig Dis 1995. Dig Dis 1994. et al. MB. N Engl J Med 1995. WA. Ray. Dezi. Scheiman. Lauritsen. Nonsteroidal anti-inflammatory drugs and the incidence of hospitalizations for peptic ulcer disease in elderly persons. JM. . Walsh. Am J Gastroenterol 2005. Girardi. 110:1244. LS. Non-steroidal anti-inflammatory drugs and ulcer complications: A risk factor analysis for clinical decision-making. A. JM. Nonsteroidal anti-inflammatory drugs and gastrointestinal disease: Pathophysiology. Kimmey. 28. MA. Perez-Aisa. I. Prevention of nonsteroidal anti- inflammatory drug-induced gastrointestinal mucosal injury. 26. Peterson. 333:984. 21. pylori eradication and reduced duodenal and gastric ulcer recurrence: A review. Lanas. treatment and prevention. EA. Dig Dis 1995. M. 12:210. JF. et al. A. Bjorkman. Hopkins. Management of nonsteroidal anti-inflammatory drug-induced upper gastrointestinal bleeding and perforation. Bretagne. 25.20. A nationwide study of mortality associated with hospital admission due to severe gastrointestinal events and those associated with nonsteroidal antiinflammatory drug use.

F. Hepatology 1997. AI. Nasogastric omeprazole: Effects on gastric pH in critically ill patients. Gastroenterology 1997. 37. DJ. JAMA 1996. 31. Guyatt. Balaban. BK. 90:708. Aliment Pharmacol Ther 1995. 36. T. Steingrub. H. Variceal hemorrhage. Kuusela. KD. Gastroenterology 1982. The role of acid in upper gastrointestinal haemorrhage due to ulcer and stress-related mucosal damage. N Engl J Med 1994. et al. 25:307. controlled study of prophylactic ranitidine in preventing stress-induced gastric mucosal lesions in neonatal intensive care unit patients. HD. GH. WL. Crit Care Med 1997. Risk factors associated with refractory peptic ulcers. Zimmerman. 92:79. 33. 112:473. 38. H. Risk factors for hemorrhage from gastric fundal varices. J. 30. Mullen. Navab. 9(Suppl 1):43. et al. Am J Gastroenterol 1995. Duckworth. Cook. Gastroenterology 1995. Fuller. 82:968. Esteva. JL. 35. Karikoski. Peterson. Lanas. AL. A randomized. GH. Y. 109:1124. J. Kokawa. Guyatt. CW. Cook. A critical evaluation of survival analysis. Risk factors for gastrointestinal bleeding in critically ill patients. 275:308. B. TF. . 29:795. Peura. Reeve. Shijo. DA. Smith. Kim. DJ. et al. Resolving discordant meta-analyses. DY. 34. et al. Ruuska. Upper gastrointestinal hemorrhage. Comparison of the causes and prognosis in primary and secondary bleeders. Teran. Graham. 330:377. DH. Meroz. J. T.29. et al. 25:346. et al. Remacha. JC. Siguencia. R. Scand J Gastroenterol 1994. Imperiale. Primary prophylaxis of variceal bleeding in cirrhosis: A cost-effectiveness analysis. 32. Stress ulcer: is routine prophylaxis necessary?. F. Am J Gastroenterol 1997. et al. 39. Stress ulcer prophylaxis in critically ill patients.

Tsai. The Veterans Affairs Cooperative Variceal Sclerotherapy Group. Randomized study comparing banding and propranolol to prevent initial variceal hemorrhage in cirrhotics with high-risk esophageal varices. 25:1346. Jutabha R. et al. . CS. 43. M. A randomized. 340:988. Gastroenterology 2005. Kumar. Lamba. N Engl J Med 1991. CY. YT. Sarin. 128:870. Martin P. 324:1779.40. 42. 41. single-blind. SK. Prophylactic sclerotherapy for esophageal varices in men with alcoholic liver disease. Gornbein J. Hepatology 1997. Savides T. Lay. et al. N Engl J Med 1999. GS. Teg. Comparison of endoscopic ligation and propranolol for the primary prevention of variceal bleeding. Endoscopic variceal ligation in prophylaxis of first variceal bleeding in cirrhotic patients with high-risk esophageal varices. multicenter clinical trial. Han SH. Jensen DM.

and is responsible for over one million days of work loss and 32.) Accurate identification of patients at highest risk of bleeding permits stratification in an attempt to avoid potentially harmful preventive treatments in the 60 to 75 percent of patients who will never have variceal bleeding. survivors of an episode of active bleeding have a 70 percent risk of recurrent hemorrhage within one year of the bleeding episode [3]. MD Section Editor : Bruce A Runyon.6 out of every 1000 adults in North America. Anne C Travis. The formation and progression of varices and the predictive factors and risk classification for bleeding will be reviewed here.000 deaths annually. MSc. Each episode of active variceal hemorrhage is associated with a 30 percent mortality [1. FACG Last literature review version 18. While several modalities are available for primary prophylaxis of variceal bleeding. . MD Deputy Editor.2]. a direct consequence of portal hypertension. 2010 (More) INTRODUCTION Cirrhosis affects 3.2: May 2010 | This topic last updated: April 5. In addition. Variceal hemorrhage occurs in 25 to 40 percent of patients with cirrhosis [4]. A major cause of cirrhosis-related morbidity and mortality is the development of variceal hemorrhage. many are associated with significant adverse effects. (See "Primary prophylaxis against variceal hemorrhage in patients with cirrhosis". MD.Prediction of variceal hemorrhage in patients with cirrhosis Author : Arun J Sanyal.

FORMATION OF VARICES Portal pressure is determined by the product of portal flow volume and resistance to outflow from the portal vein. An illustrative study evaluated the relation between the hepatic vein pressure gradient and the formation of and bleeding from varices [6]. in these patients. Varices develop in order to decompress the hypertensive portal vein and return blood to the systemic circulation. . with measurement of the difference between the wedged hepatic venous pressure (which approximates the sinusoidal and portal pressures in cirrhosis) and the free hepatic venous pressure. patients with lower values neither form varices nor bleed. elevated portal pressure results from both increased resistance to outflow through distorted hepatic sinusoids. This procedure is routinely performed in many European centers but only rarely in the United States. Cirrhosis is the most common cause of portal hypertension. Budd Chiari syndrome) level. sinusoidal (cirrhosis). Obstruction may occur at a presinusoidal (portal vein thrombosis. A systematic review of 12 studies found that a reduction of the hepatic vein pressure gradient to ≤12 was associated with a significant reduction in the risk of variceal bleeding and mortality [5]. and enhanced portal inflow due to splanchnic arteriolar vasodilation. They are seen when the pressure gradient between the portal and hepatic veins rises above 12 mmHg. The following observations were noted: • All 72 patients with varices by endoscopy had a gradient above 12 mmHg. Although it does not predict the size of varices. it may be useful for monitoring the success of therapy aimed at lowering portal pressures. portal fibrosis. or postsinusoidal (veno-occlusive disease. The portal-hepatic venous pressure gradient is obtained by hepatic venous catheterization. or infiltrative lesions). Portal hypertension (defined as hydrostatic pressure >5 mmHg) results initially from obstruction to portal venous outflow. such as beta blockers.

These include: • Location of varices • Size of varices • Appearance of varices . PREDICTIVE FACTORS Numerous clinical and physiologic factors are useful in predicting the risk of variceal hemorrhage in patients with cirrhosis. • The gradient did not predict the size of varices. • The two-year risk of bleeding was significantly higher in patients with small varices at enrollment compared with those without varices (12 versus 2 percent). and an alcoholic cause of cirrhosis. • Small varices progressed in size at a rate of 12 percent in year one. An endoscopy was performed annually. • New varices developed in 5 percent at year one. One of the largest prospective studies included 206 cirrhotic patients (113 without varices and 93 with small esophageal varices at baseline) who were followed prospectively for an average of 37 months [7]. being similar in those with large and small varices. The following findings were noted.4 mmHg. the presence of red wale marks on the first examination. and 28 percent at year three. none of these patients had a gradient below 12 mmHg. • Progression was predicted by the Child-Pugh score. PROGRESSION OF VARICES The rate of development and progression of esophageal varices in patients with cirrhosis has not been extensively evaluated.• The mean gradient in 49 patients with bleeding varices was 20. and 31 percent at year three.

Thus.9 units per patient). Gastric varices are often classified according to their location.The explanation for the relationship between variceal size and bleeding risk is derived from Laplace's law. 393 of whom were bleeding [8]. • Isolated gastric varices in the fundus (IGV1) occur less frequently than GOVs (10 versus 90 percent) [8]. The relationship between the site of the varices and clinical risk was illustrated in a prospective study of 568 consecutive patients with varices. small increments in the vessel radius result in a large increase in wall tension (which is the force tending to cause variceal rupture). The mean transfusion requirement in patients with bleeding gastric varices was higher than in those with esophageal varices (4.8 versus 2. but become progressively more superficial (nearer the mucosa) in the distal esophagus. Varices develop deep within the submucosa in the mid-esophagus. Varices in the gastric fundus also bleed frequently. Size of varices — The risk of variceal bleeding correlates independently with the diameter (size) of the varix. Bleeding from isolated gastric varices in the fundus (IGV1) occurred much more frequently than either GOVs or isolated gastric varices at other loci in the stomach (IGV2) (figure 1). and rectum. . esophageal varices at the gastroesophageal junction have the thinnest coat of supporting tissue and are most likely to rupture and bleed. which correlates with their risk of hemorrhage: • Varices in direct continuity with the esophagus along the lesser and greater curves of the stomach are called gastroesophageal varices (GOV) types 1 and 2 respectively. although theoretically varices may develop at any level of the gastrointestinal (GI) tract below the esophagus.• Clinical features of the patient • Variceal pressure Location of varices The most common sites for development of varices are the distal esophagus. stomach.

" • Diffuse erythema denotes a diffuse red color of the varix. several morphologic features of varices observed at endoscopy have been correlated with an increased risk of hemorrhage [7. none are exact and all involve subjective evaluation. Clinical features Several clinical features of the patient are related to the risk of variceal hemorrhage [12]: .8. or "red signs": • Red wale marks are longitudinal red streaks on varices that resemble red corduroy wales (picture 2). A commonly employed system of classification includes the following (picture 1) [9. Appearance of varices In addition to size.10]: • F1: Small straight varices • F2: Enlarged tortuous varices that occupy less than one-third of the lumen • F3: Large coil-shaped varices that occupy more than one-third of the lumen It is important to insufflate the esophagus while estimating variceal size.11]. • Cherry red spots are discrete red cherry-colored spots that are flat and overlie varices.There are several ways in which esophageal variceal size is quantified. Among these features include a number relating to a red appearance. failure to do so leads to overestimation. • Hematocystic spots are raised discrete red spots overlying varices that resemble "blood blisters.

• History of a previous variceal bleed predicts a high likelihood of a subsequent bleeding episode. variceal size. Variceal hemorrhage developed in 28 patients (32 percent). A higher score in this classification scheme is associated with a higher likelihood of variceal bleeding. In one study. These bleeding episodes may be considered as "early" or "late" with respect to their temporal relationship to the index bleed. over 70 percent experience further episodes of variceal bleeding after an index bleed. Variables predictive of a first bleed included: the level of variceal pressure. risk classification using the Child class. Risk factors for early and late rebleeding are listed in the table (table 2) [10. The risk of early rebleeding is greatest in the first 48 hours after admission and declines subsequently. The variceal pressure may be an important predictor for variceal hemorrhage. bilirubin level. The Child classification is an index of liver dysfunction based upon serum albumin concentration.• The degree of liver dysfunction is an important predictor of variceal hemorrhage. Specifically. and endoscopic appearance of varices (see below). while only one-third of all patients with cirrhosis experience variceal hemorrhage. The risk of early rebleeding is greatest immediately after cessation of active hemorrhage (50 percent of such episodes occur within 48 hours) and subsides over time.12.13]. and the interval between diagnosis of varices and the start of the study. As an example. 87 patients with cirrhosis and large esophageal varices who had never had variceal bleeding were followed for 12 months [15]. one-third of patients with an index bleed will rebleed within six weeks. and the presence of ascites and encephalopathy (table 1). the incidence of variceal bleeding with different levels of variceal pressure was as follows: . for example. Variceal pressure — Variceal pressure may be measured accurately and relatively noninvasively with a pressure-sensitive endoscopic gauge [14]. and one-third will rebleed after six weeks [3]. prothrombin time.

RISK CLASSIFICATION The Child class. Such a patient is clearly a candidate for prophylactic therapy to prevent bleeding. and presence of red wale markings can be used to calculate a prognostic index that numerically quantifies the risk of variceal hemorrhage in an individual patient (table 3) [9].• ≤13 mmHg .) One study evaluated variables that predicted the presence of high risk varices (ie medium to large varices) in 1000 patients with HCV who had advanced fibrosis but compensated liver function [16]. a patient with Child class C cirrhosis and tense ascites who has large varices with red signs has an approximately 76 percent likelihood of developing variceal hemorrhage within one year.1/11 (9 percent) • >14 and ≤15 mmHg . (See "Primary prophylaxis against variceal hemorrhage in patients with cirrhosis". Whether these data can be generalized to other forms of liver disease is unclear.18/25 (72 percent) Adding variceal pressure (categorized as > or ≤15.7/14 (50 percent) • >16 mmHg .000 (negative predictive value of 99 percent).0/25 (0 percent)\ • >13 and ≤14 mmHg . Such varices were vanishingly rare in those with a platelet count over 150. . The calculated risk is greatest in the first one to two years from the time of identification of these risk factors. As an example.2 mmHg) to the risk classification discussed below significantly improved the predictive value of this classification.2/12 (17 percent) • >15 and ≤16 mmHg . variceal size.

SE. Gastroenterology 1981. 82:968. Gastroenterol Clin North Am 1992. Clarke. DY. 2. SUMMARY • Variceal hemorrhage occurs in 25 to 40 percent of patients with cirrhosis. 80:800.) We encourage you to print or e-mail this topic. Smith. Prevention of initial variceal hemorrhage. 18:6s. et al. JL. JL. Clamp. JR. 21:149.) • These factors can be considered together to help predict the risk of hemorrhage in an individual patient (table 3). (See 'Predictive factors' above. 4.uptodate. Gastroenterology 1982. . These include. size and appearance of varices. DeDombal. (See "Patient information: Screening for esophageal varices". ND. A critical evaluation of survival analysis.) REFERENCES Graham. Variceal hemorrhage. their pressure and clinical features of the patient.INFORMATION FOR PATIENTS Educational materials on this topic are available for patients. FT. Grace. Graham. Smith. Prognostic factors in upper GI bleeding. (See 'Risk classification' above. DY. or to refer patients to our public web site www. Accurate identification of patients at highest risk of bleeding permits targeted use of preventive measures. 3. which includes this and other topics. The course of patients after variceal hemorrhage. the location. Endoscopy 1986. • Numerous clinical and physiologic factors are useful in predicting the risk of variceal hemorrhage in patients with cirrhosis.

et al. K. H. Sarin. Lahoti. A. The North Italian Endoscopic Club for the Study and Treatment of Esophageal Varices. 6:667. Incidence and natural history of small esophageal varices in cirrhotic patients. 27:213. Hepatic vein pressure gradient reduction and prevention of variceal bleeding in cirrhosis: a systematic review. T. Prediction of variceal hemorrhage by esophageal endoscopy. Groszman. Risk factors for hemorrhage from gastric fundal varices. et al. 8. Koyanagi. Hepatology 1992. Luca. N Engl J Med 1988. Beppu. . Rigau. Hepatology 1985. de Franchis. 6. et al. Morabito. classification and natural history of gastric varices: A long-term follow-up study in 568 portal hypertension patients. Primignani. 5:419. Saxena. J Hepatol 2003. Why do varices bleed? Gastroenterol Clin North Am 1992. Portal pressure. G. Noninvasive measurement of the pressure of esophageal varices using an endoscopic gauge: Comparison with measurements by variceal puncture in patients undergoing endoscopic sclerotherapy. J. Gastroenterology 2006. et al. D'Amico. 16:1343. Front Gastrointest Res 1986. JC. A prospective multicenter study. 9. M. S. J. et al. K. 11. Fisher. J. Garcia-Pagan. 9:247. Kokawa. Merli. 21:85. 12. G. JM. Gastrointest Endosc 1981. 7. Nicolini. RJ. G. D. Inokuchi. 38:266. Angeloni. R. M. Bordas. 14. Hepatology 1997. presence of gastroesophageal varices and variceal bleeding. 25:307. D'Amico. SP. Shijo. Pagliaro. L. 13. SK. Prediction of the first variceal hemorrhage in patients with cirrhosis of the liver and esophageal varices. Hepatology 1986.5. Kim. H. 10. N. Bosch. A. Prevalence. Bosch. 319:983. Six week prognostic indicators in upper gastrointestinal hemorrhage in cirrhotics. 131:1611. et al. G. Garcia-Tsao. RL.

RJ. . 27:15. Fontana. Hepatology 1998. Variceal pressure is a factor predicting the risk of a first variceal bleeding: A prospective cohort study in cirrhotic patients. 16. Gastrointest Endosc 2006.15. et al. Bustami. The prevalence and risk factors associated with esophageal varices in subjects with hepatitis C and advanced fibrosis. F. et al. Scheys. R. Di Bisceglie. AM. Nevens. Sanyal. 64:855. I. AJ.