Updated: Sep 10, 2008
Upper gastrointestinal bleeding (UGIB) is defined as hemorrhage that emanates proximal to the ligament of Treitz. It is a common and potentially life-threatening condition. More than 350,000 hospital admissions are attributable to UGIB, which has an overall mortality rate of 10%. Although more than 75% of cases of bleeding cease with supportive measures, a significant percentage of patients require further intervention, which often involves the combined efforts of gastroenterologists, surgeons, and interventional radiologists.1,2,3,4
The first decision point in managing GI bleeding is defining the site and cause of bleeding: is it an upper GI or a lower GI hemorrhage?5,6
Clinically, UGIB often causes hematemesis (vomiting of blood) or melena (passage of stools rendered black and tarry by the presence of altered blood). The color of the vomitus depends on its contact time with the hydrochloric acid of the stomach. If vomiting occurs early after the onset of bleeding, it appears red; with delayed vomiting, it is dark red, brown, or black. Coffee-ground emesis results from precipitation of blood clots in the vomitus. Hematochezia (red blood per rectum) usually indicates bleeding distal to the ligament of Treitz. Occasionally, rapid bleeding from an upper GI source may result in hematochezia.
The rate and extent of hemorrhage, coupled with the patient's comorbidities, determine the clinical presentation of UGIB. Endoscopy is a critical early intervention that can be used to establish the source of bleeding, and it also offers therapeutic options. If bleeding cannot be controlled by means of endoscopy, further interventions with catheter-directed embolotherapy or surgery may be warranted.7
For excellent patient education resources, visit eMedicine's Esophagus, Stomach, and Intestine Center. Also, see eMedicine's patient education article Gastrointestinal Bleeding.
Related eMedicine topics:
Upper Gastrointestinal Bleeding: Surgical Perspective
Lower Gastrointestinal Bleeding: Surgical Perspective
Pediatrics, Gastrointestinal Bleeding
Related Medscape topics:
Resource Center Minimally Invasive Gastrointestinal Surgery
Specialty Site Gastroenterology
Specialty Site Radiology
CME Gastrointestinal Bleeding in the Elderly
CME SSRIs and Venlafaxine Linked to Greater Risk for Gastrointestinal Tract Bleeding
Upper gastrointestinal bleeding occurs from a variety of etiologies. The pathophysiology of the bleeding is often mucosal erosion with subsequent hemorrhage. About 90% of cases of UGIB arise from Mallory-Weiss tears, variceal hemorrhage due to portal hypertension, peptic ulcer disease, and gastritis.8
Prior to the introduction of H2-blockers, UGIB was mostly caused by peptic ulcer disease. Most of these ulcers occur in the duodenum. Gastritis, with subsequent gastric erosions and bleeding, is associated with recent alcohol ingestion, portal hypertension, or the use of anti-inflammatory drugs such as aspirin or ibuprofen (Motrin). Patients with severe underlying systemic disease, such as burns and trauma, and those who have undergone surgery may also have gastric erosions. Esophagogastric mucosal tears (Mallory-Weiss syndrome) are often preceded by retching or non-bloody vomiting that is followed by hematemesis.
Neoplasms from the esophagus, stomach, duodenum, or pancreas may result in UGIB because of mucosal erosion, neovascularity, and/or pseudoaneurysm formation. Arteriosclerotic aortic aneurysms may also rupture into the small intestine, often with fatal results.
Similarly, mucosal erosion is the etiology of Dieulafoy lesion. A Dieulafoy erosion is an abnormal cirsoid aneurysmal artery that protrudes through a tiny mucosal defect, usually within 6 cm of the gastroesophageal junction on the lesser curve of the stomach.
Angiodysplasia is an uncommon cause of UGIB. It may occur in the stomach or duodenum, often in young individuals, in whom the cause of the vascular malformation is developmental. In older individuals, the lesions are thought to develop as a result of chronic intermittent obstruction of the mucosal veins, which results in dilatation of the submucosal and mucosal veins.
Variceal bleeding from the esophagus or stomach is usually the result of portal hypertension secondary to cirrhosis. Although the precise etiology of variceal rupture is unknown, factors contributing to hemorrhage include erosion of the overlying mucosa by acid-peptic reflux, varix wall and esophageal mucosal thickness, and varix wall tension. Splenic vein occlusion is frequently caused by pancreatitis or pancreatic carcinoma. The blood from the spleen bypasses the obstruction through the left and right gastroepiploic veins, the short gastric and left gastric veins, and the arc of Barkow. The collaterals from the short gastric vein form gastric varices, which can cause gastric bleeding.
Trauma can result in direct hemorrhage from an upper GI source or subsequent pseudoaneurysm formation, which, by comparison, has an increased propensity to bleed. Hemobilia from iatrogenic causes, such as percutaneous biliary drainage and blunt or penetrating trauma, and a neoplasm may also cause UGIB.
Hemosuccus pancreaticus, bleeding into the pancreatic duct, is a rare cause of upper gastrointestinal bleeding. It is usually associated with chronic pancreatitis, pancreatic pseudocyst, and peripancreatic aneurysm, and is rarely seen in patients with a history of traumatic injury, familial pancreatitis, and neoplasia. Endoscopic retrograde cholangiopancreatography will demonstrate bleeding into the pancreatic duct. Treatment of the associated vascular lesion with selective embolization is usually successful.
Related Medscape topic:
Resource Center Peptic Ulcer Disease
More than 350,000 annual hospital admissions, or approximately 100 cases per 100,000 per year, occur because of upper gastrointestinal bleeding.
In the United Kingdom, the overall incidence of acute upper gastrointestinal hemorrhage is 103 cases per 100,000 adults per year.9 The findings of further studies from different countries are difficult to ascertain because of a paucity of large, retrospective studies and because of the use of indirect methods for calculation and estimation.
No well-described racial predilection for upper gastrointestinal bleeding exists.
Studies from the United States and the United Kingdom have revealed a male-to-female ratio that is greater than that of other studies. The male-to-female ratio for upper gastrointestinal bleeding is approximately 2:1 in both countries. The mortality rates are similar in males and females.
The number of cases of upper gastrointestinal bleeding increases with patient age. In a study performed in the United States, about 44.5% of all patients were aged 60 years or older. Morbidity and mortality rates also increased with age; 73.2% of deaths occurred in patients older than 60 years.10
Upper gastrointestinal bleeding arises from branches of the celiac artery and superior mesenteric artery (SMA), and rarely from aortointestinal fistula. Embolization and surgical procedures are relatively safe in terms of ischemic risk in this region because of the rich collateral network between the celiac artery and SMA, as well as between the branches of the celiac artery.
The left gastric artery arises from the celiac artery in 90% of individuals and supplies the stomach and distal esophagus. It is usually the first major branch of the celiac artery. It courses along the lesser curvature of the stomach and forms an anastomosis with the right gastric artery, which arises from the left hepatic artery (40%) or proper hepatic artery (40%). The right gastric artery supplies the pylorus and distal posterior surface of the stomach. The short gastric arteries (from the splenic artery) and the right and left gastroepiploic arteries (from the gastroduodenal artery [GDA] and splenic arteries, respectively) supply the greater curvature of the stomach.
The duodenum is supplied by the branches of the GDA and SMA, and occasionally from the hepatic arteries. A rich arterial communication exists between the GDA and SMA via the pancreatic arcade arteries and inferior pancreaticoduodenal artery. Thus, the angiographic evaluation of pyloroduodenal bleeding requires contrast material injections in both the celiac artery and SMA, as well as their branches.
Variceal bleeding often arises from esophageal or gastric varices from the coronary vein or short gastric veins in portal hypertension. Rarely, bleeding from varices in the small bowel may cause UGIB.
In the vast majority of cases (>75%), upper gastrointestinal bleeding ceases with conservative measures. The first step in managing GI bleeding is determining the location: is the upper or lower tract involved? Clinically, the presence of hematemesis and melena are suggestive of bleeding proximal to the ligament of Treitz. Hematochezia often suggests bleeding from a lower GI source. However, a contact time of blood in the gut for 8 hours is required for melena and patients with rapid bleeding from an upper GI source pass bright red blood rectally because of rapid GI transit. Therefore, nasogastric (NG) tube aspiration and endoscopy is necessary if there is any question regarding the location of GI bleeding.
The clinical presentation of UGIB depends on the rate and duration of the bleed and the patient's underlying comorbidities. Blood loss of 500 mL is often required before systemic abnormalities appear. Greater blood loss can result in shock, with peripheral vasoconstriction and orthostatic hypotension (which implies significant volume depletion of >15%). Clinical symptoms include syncope, lightheadedness, nausea, sweating, tachycardia, and hypotension.
In the setting of acute blood loss, several laboratory values changes are observed. Obviously, the hematocrit level should decrease; however, the value may not be correlated with real blood loss because of hemodilution and equilibration with extravascular fluid. Mild leukocytosis and thrombocytosis often develop within 6 hours after the onset of bleeding. The blood urea nitrogen level may also be elevated in UGIB. This occurs because of the breakdown of blood proteins to urea by intestinal bacteria, coupled with a reduction in the glomerular filtration rate.
If an upper GI source is suspected, an NG tube is passed into the stomach. If red blood or a coffee-grounds appearance is found, saline irrigation is performed; this procedure allows estimation of the amount of bleeding and clears the stomach for subsequent endoscopy. If the initial lavage fluid is clear, the tube is kept in place for several hours, because duodenal bleeding may initially result in a clear NG aspirate. Resuscitative measures, including the placement of large-bore intravenous lines for volume repletion, are concurrently begun.
Upper endoscopy is the initial procedure of choice for the evaluation of acute upper gastrointestinal bleeding. Early endoscopy allows estimation of the rate of recurrent bleeding and enables various therapeutic options. It is also helpful in diagnosing and treating variceal bleeding. Recent studies have shown that early endoscopy is associated with lower healthcare costs and improved medical outcomes, compared with other procedures. However, upper GI endoscopic findings are nondiagnostic in about 10% of cases.11,12,13,14
If endoscopy has failed to reveal a bleeding source or if the bleeding cannot be controlled, angiography is used for diagnosis and therapy. Angiography has been shown to depict the source with bleeding rates as low as 0.5 mL/min. If no active bleeding is identified angiographically in a patient with documented recurrent bleeding by endoscopy, prophylactic embolization of the left gastric artery or the gastroduodenal artery may be performed to control gastric or pyloroduodenal bleeding, respectively.
With advances in both endoscopic and angiographic techniques, surgical options are often limited in acute UGIB because of its morbidity and mortality rates. In the setting of recurrent variceal bleeding that is refractory to endoscopic control, the use of transjugular intrahepatic portosystemic shunts (TIPS) is preferred in the management of patients with a Child class B condition and in some with a Child class C condition. Currently, upper GI barium examinations have no role in the diagnosis of acute UGIB.
Endoscopy is often the first-line diagnostic examination and treatment option for upper gastrointestinal bleeding. However, findings can be nondiagnostic in about 10% of cases. For example, in the setting of massive UGIB, endoscopy may not be helpful because intraluminal blood cannot be adequately cleared. Angiography is limited by the rate of bleeding, which usually must be at least 0.5 mL/min before it is detected. Its accuracy in the detection of acute UGIB is 90%, and it is helpful in assessing occult UGIB.
A positive angiographic finding of bleeding is needed to initiate embolization, except in cases in which bleeding has been localized before — for example, in the left gastric artery (LGA) or gastroduodenal artery. In these situations, prophylactic embolization is helpful. Prophylactic embolization of the LGA without prior documented bleeding is advocated because almost 90% of patients with this condition survive if the bleeding is controlled. The left gastric artery is involved in 85% of cases of UGIB.
Duodenum, Ulcers
Esophagus, Tear
Gastric Carcinoma
Gastric Ulcer
Portal Hypertension
Peptic ulcer disease
Mallory-Weiss tears
Hemorrhagic gastritis
Esophageal varices
Aortoenteric fistula
Pseudoaneurysms
Dieulafoy vascular malformations
Hemobilia
Hemosuccus pancreaticus
Esophageal, gastric, duodenal, and pancreatic neoplasms
Angiodysplasia
Plain radiographs of the abdomen are not usually helpful in the diagnosis of acute upper gastrointestinal bleeding. The pathophysiology of acute UGIB is often mucosal erosion with subsequent hemorrhage, which is not detected with plain radiographs. Occasionally, free air under the diaphragm is seen in cases of perforated viscous, and this may be accompanied by UGIB. Other etiologies, such as upper GI masses (which usually result in chronic, not acute, UGIB), aneurysms with calcifications, and ascites suggestive of portal hypertension, may be seen on radiographs.15
The radiographic findings, as outlined above, are usually nonspecific. Calcifications associated with aneurysms, in the aorta or branch vessels, are reliable but rare findings regarding a source of upper gastrointestinal bleeding.
Usually, abdominal CT is not used in the evaluation of acute upper gastrointestinal bleeding from arterial sources, although it has been helpful in some series. However, in the detection of UGIB from pseudoaneurysms of the mesenteric vessels, branches of the celiac axis, or aortoenteric fistulas, it is the study of choice. In addition, in the evaluation of masses of the upper GI system or liver tumors that may be contributing to hemobilia, CT is an excellent modality. Occasionally, hemorrhage into the peritoneum can be detected on CT scans.16
In the setting of portal hypertension, the presence of varices and the patency of the portal and splenic veins can be evaluated prior to a transjugular intrahepatic portosystemic shunt (TIPS) procedure or splenic artery embolization.
CT is currently not the study of choice in the evaluation of acute upper gastrointestinal bleeding. If occult bleeding from masses or aneurysms is suspected, CT may be helpful. However, small pseudoaneurysms, small bowel tumors, and small biliary tumors can easily be missed by CT. In the catastrophic situation of aortoenteric fistula, CT may be helpful in detecting an early leak.
The usual drawbacks of upper abdominal CT for the evaluation of subtle lesions also apply to the use of this modality in the evaluation of upper gastrointestinal bleeding. These include underopacification of bowel loops, suboptimal visualization of the biliary system and small visceral aneurysms, and difficulty in evaluating the esophagus.
MRI has a limited role in the evaluation of acute upper gastrointestinal bleeding from arterial sources. In the setting of aneurysms and pseudoaneurysm, magnetic resonance angiography may be helpful in depicting the vascular abnormalities. With magnetic resonance cholangiography, the depiction of subtle biliary abnormalities may be helpful in cases of hemobilia. MRI is comparable to CT in the evaluation of masses that cause UGIB.
Similar to CT, MRI has no real role in the assessment of acute upper gastrointestinal bleeding. It may be helpful in depicting small visceral pseudoaneurysms or masses, but a normal MRI finding is often only a starting point for further investigation.
Ultrasonography has no role in the setting of acute upper gastrointestinal bleeding. It may be helpful in establishing portal vein patency prior to transjugular intrahepatic portosystemic shunt (TIPS) placement in patients with variceal bleeding. Cross-sectional CT or MRI is used to detect occult sources of UGIB.
Ultrasonography has a limited role in the management of upper gastrointestinal bleeding; uses are noted above.
Tagged-RBC and sulfur colloid studies are not generally used for the evaluation of upper gastrointestinal bleeding. The diagnosis of UGIB is usually established with clinical parameters and endoscopic means. Nuclear medicine studies are usually reserved for the investigation of lower gastrointestinal bleeding in areas that cannot be reached with endoscopy because of anatomical or technical reasons (ie, brisk bleeding).16
In addition, significant artifacts associated with nuclear medicine bleeding scanning can be present in the upper abdomen; these are caused by cardiac and vascular activity and breathing motion. Blood from UGIB often pools in the cecum, and the exact site of bleeding is often difficult to ascertain.
Often, nuclear medicine studies are not helpful in determining the site or source of upper gastrointestinal bleeding. Endoscopy is the preferred test.
Angiography is often the next step if medical management or endoscopy fails to control upper gastrointestinal bleeding. Angiography is minimally invasive; it often allows precise localization of bleeding; and it enables the use of therapeutic options, which include embolization or vasopressin infusion. A hemorrhage rate of 0.5-1.0 mL/min is required before it can be visualized with angiography. The detection of bleeding may be enhanced with carbon dioxide as an arterial contrast agent because of the low viscosity of the gas.17,18,19
Endoscopic evaluation is critical in providing information for subsequent angiography. For example, if variceal bleeding is suspected instead of arterial bleeding, endoscopy can be used to guide subsequent therapy in favor of a transjugular intrahepatic portosystemic shunt (TIPS) procedure. In cases such as hemorrhagic gastritis, which is an important cause of UGIB caused by physiologic stress, the endoscopic diagnosis can guide subsequent vasopressin infusion. If a mass or recurrent bleeding from a suspected ulcer in the duodenum is present, the gastroduodenal artery can be embolized.
Angiographic evaluation of UGIB is usually performed via common femoral artery access achieved with the Seldinger technique. A catheter is directed into the celiac artery and superior mesenteric artery for angiography. Prior diagnostic examinations such as endoscopy or CT can be used to guide subsequent catheterization.
Acute arterial bleeding is seen as the extravasation of contrast medium of arterial opacity at the bleeding site. The extravasating contrast agent frequently flows toward the dependent part of the viscous, creating the pseudovein appearance. If the bleeding is demonstrated on the celiac or superior mesenteric angiogram, a more selective injection of the extravasating artery (superselective catheterization) is performed for confirmation of the bleeding and embolization. If contrast agent extravasation is not seen with the selective injections, superselective catheterization of the gastroduodenal, left gastric, and splenic arteries is performed.
Angiography is insensitive in the detection of venous bleeding, such as variceal hemorrhage from portal hypertension. Clinical suspicion and endoscopic findings are helpful in evaluating variceal bleeds. However, angiography can be helpful in the detection of as much as 50% of occult UGIB.
The degree of confidence in the angiographic diagnosis of upper gastrointestinal bleeding is high. Arteriography can be used to accurately identify 90% of acute UGIB. It is also useful in depicting occult bleeding in 50% of patients. However, a bleeding rate of 0.5-1.0 mL/min is required for the angiographic depiction of hemorrhage. Venous bleeding (eg, from variceal bleeding) is difficult to detect with angiography.
Bowel motion, prior barium examinations, and abnormal staining from inflammation or breathing artifact can hinder angiographic depiction of bleeding. Multiple superselective injections may be required for a confident diagnosis. A bleeding rate of 0.5-1.0 mL/min is required to visualize angiographic hemorrhage. Otherwise, a false-negative angiogram results. Alternatively, if the bleeding has stopped at the time of study, the clinical parameters may be helpful in this distinction. Venous hemorrhage from portal hypertension might be another cause of false-negative findings.
Selective arterial embolization is effective in arresting arterial bleeding from peptic ulcer disease, Dieulafoy disease, Mallory-Weiss tear, hemobilia, and hemosuccus pancreaticus. Intra-arterial vasopressin infusion is an ineffective treatment for bleeding from ulcer disease, but it is effective in controlling bleeding from hemorrhagic gastritis. Vasopressin is infused intravenously for control of variceal bleeding. Transjugular intrahepatic portosystemic shunt (TIPS) placement is an effective means of controlling variceal bleeding unresponsive to endoscopic sclerotherapy or banding. When gastroesophageal varices continue to fill after placement of a TIPS in the patient with massive variceal bleeding, variceal embolization is performed.20,21,22
The angiographic appearance of an acute upper gastrointestinal bleeding is extravasation of contrast medium during the arterial phase, which runs toward the dependent part of the viscus and may persist as an opaque pooling of contrast medium during the capillary and venous phase. Carbon dioxide is more frequently used as an arterial contrast agent for the diagnosis of both upper and lower GI hemorrhage.
In general, active extravasation should be demonstrated prior to embolotherapy in a case of upper GI arterial bleeding. The bleeding from Mallory-Weiss tears is usually self-limiting, and if no bleeding is seen during angiography, embolotherapy is not initiated. Vasopressin infusion into the left gastric artery is used for treatment of hemorrhagic gastritis with a good success rate; embolization is ineffective because the bleeding is capillary or mucosal in nature. Endoscopic therapy is the first and safest choice of treatment, but the presence of multiple bleeding sites precludes the use of endoscopic therapy in hemorrhagic gastritis.
Vasopressin causes constriction of the arterioles and capillaries. It is infused at a rate of 0.2 U/min once the catheter is placed in the appropriate vessel. After 20 minutes of the infusion, a repeat angiogram is obtained to check for recurrent bleeding or the degree of vasoconstriction. If hemostasis is not achieved, the infusion rate is increased to 0.4 U/min. The maximal dose is 0.6 U/min, because higher rates lead to myocardial or intestinal ischemia. The optimal result is cessation of hemorrhage with pruning, but patent, vessels extending to the area of interest. The infusion is continued for 24 hours and adjusted as necessary. The initial success rate for gastric bleeding is approximately 70%, but recurrent bleeding frequently occurs. Vasopressin infusion is contraindicated in patients with coronary artery disease.
Embolotherapy with Gelfoam pledgets, polyvinyl alcohol, or (less often) coils, can be used to effectively control UGIB. If a 3F coaxial catheter can be placed in the bleeding artery at or close to the site of extravasation, microcoils (platinum coils) may be used. Placing a coil proximal to the bleeding site may result in recurrent bleeding via collaterals. Because of the rich collateral circulation in this region, ischemia is rarely a problem in the absence of prior GI surgery. However, combined therapy with vasopressin infusion and embolization should be avoided because of the potential risk of ischemia to the embolized viscus.
The duodenum has a dual blood supply from the branches of the celiac and superior mesenteric arteries. Thus, after embolization of the branches of the gastroduodenal artery, a superior mesenteric arteriogram should be obtained to evaluate reconstitution of the bleeding artery. Occasionally, both branches from the celiac and superior mesenteric arteries may have to be embolized to control bleeding from the duodenum. Concurrent correction of any underlying coagulopathy is important to aid in thrombosis.
Gomes et al reported an 88% success rate with embolization, compared with a 52% success rate with vasopressin. Major complications occurred in 12.5% of patients treated with embolization and in 8.7% of patients treated with vasopressin.23
In esophageal variceal bleeding that is refractory to banding or sclerosis, TIPS placement is the procedure of choice in patients with a Child class B condition and in some with a Child class C condition. Subsequent embolization of large varices during the procedure is controversial. As a rule, if large varices fill despite the presence of a satisfactory portosystemic gradient (<12 mm Hg) after a TIPS procedure, selective embolization is performed. In variceal bleeding secondary to hepatoma, embolization of the hepatic feeding vessel may be effective in controlling hemorrhage.
Balloon-occluded retrograde transvenous obliteration (BRTO) through the left renal-inferior phrenic vein from a femoral vein approach is an effective method of treatment for gastric variceal bleeding that cannot be treated by endoscopic method.
Fallah MA, Prakash C, Edmundowicz S. Acute gastrointestinal bleeding. Med Clin North Am. Sep 2000;84(5):1183-208. [Medline].
Kandarpa K, Aruny JE. Acute gastrointestinal bleeding. In: Handbook of Interventional Radiologic Procedures. 2nd ed. 1996: 130-8.
Reuter SR, Redman HC, Cho KC. Gastrointestinal bleeding. In: Gastrointestinal Angiography. 1986: 282-338.
Richter JM, Isselbacher KJ. Gastrointestinal bleeding. In: Harrison's Principles of Internal Medicine. 12th ed. 1991: 261-4.
Cappell MS, Friedel D. Initial management of acute upper gastrointestinal bleeding: from initial evaluation up to gastrointestinal endoscopy. Med Clin North Am. May 2008;92(3):491-509, xi. [Medline].
Eisen GM, Dominitz JA, Faigel DO. An annotated algorithmic approach to upper gastrointestinal bleeding. Gastrointest Endosc. Jun 2001;53(7):1-6. [Medline].
Tammaro L, Di Paolo MC, Zullo A, Hassan C, Morini S, Caliendo S, et al. Endoscopic findings in patients with upper gastrointestinal bleeding clinically classified into three risk groups prior to endoscopy. World J Gastroenterol. Aug 28 2008;14(32):5046-50. [Medline].
Venbrux AC. Upper gastrointestinal bleeding: diagnostic evaluation and management. In: SCVIR Syllabus: Thoracic and Visceral Vascular Interventions. 1996: 235-46.
Rockall TA, Logan RF, Devlin HB. Incidence of and mortality from acute upper gastrointestinal haemorrhage in the United Kingdom. Steering Committee and members of the National Audit of Acute Upper Gastrointestinal Haemorrhage. BMJ. Jul 22 1995;311(6999):222-6. [Medline].
Yavorski RT, Wong RK, Maydonovitch C. Analysis of 3,294 cases of upper gastrointestinal bleeding in military medical facilities. Am J Gastroenterol. Apr 1995;90(4):568-73. [Medline].
da Silveira EB, Lam E, Martel M, Bensoussan K, Barkun AN. The importance of process issues as predictors of time to endoscopy in patients with acute upper-GI bleeding using the RUGBE data. Gastrointest Endosc. Sep 2006;64(3):299-309. [Medline].
Spiegel BM, Vakil NB, Ofman JJ. Endoscopy for acute nonvariceal upper gastrointestinal tract hemorrhage: is sooner better? A systematic review. Arch Intern Med. Jun 11 2001;161(11):1393-404. [Medline].
Lee JG, Turnipseed S, Romano PS, Vigil H, Azari R, Melnikoff N, et al. Endoscopy-based triage significantly reduces hospitalization rates and costs of treating upper GI bleeding: a randomized controlled trial. Gastrointest Endosc. Dec 1999;50(6):755-61. [Medline].
Axon AT, Bell GD, Jones RH, Quine MA, McCloy RF. Guidelines on appropriate indications for upper gastrointestinal endoscopy. Working Party of the Joint Committee of the Royal College of Physicians of London, Royal College of Surgeons of England, Royal College of Anaesthetists, Association of Surgeons, the British Society of Gastroenterology, and the Thoracic Society of Great Britain. BMJ. Apr 1 1995;310(6983):853-6. [Medline].
Lefkovitz Z, Cappell MS, Kaplan M. Radiology in the diagnosis and therapy of gastrointestinal bleeding. Gastroenterol Clin North Am. Jun 2000;29(2):489-512. [Medline].
Schillaci O, Spanu A, Tagliabue L, Filippi L, Danieli R, Palumbo B, et al. SPECT/CT with a hybrid imaging system in the study of lower gastrointestinal bleeding with technetium-99m red blood cells. Q J Nucl Med Mol Imaging. Jul 3 2008;[Medline].
Ettorre GC, Francioso G, Garribba AP. Helical CT angiography in gastrointestinal bleeding of obscure origin. AJR Am J Roentgenol. Mar 1997;168(3):727-31. [Medline].
Hawkins IF, Caridi JG, LeVeen RF. Use of carbon dioxide for the detection of gastrointestinal bleeding. In: Techniques in Vascular and Interventional Radiology. 2000: 130-8.
Laing CJ, Tobias T, Rosenblum DI, Banker WL, Tseng L, Tamarkin SW. Acute gastrointestinal bleeding: emerging role of multidetector CT angiography and review of current imaging techniques. Radiographics. Jul-Aug 2007;27(4):1055-70. [Medline].
Coldwell DM. Embolotherapy of miscellaneous lesions. In: Radiologic Interventions: Embolotherapy. 1997: 93-103.
Patel TH, Cordts PR, Abcarian P. Will transcatheter embolotherapy replace surgery in the treatment of gastrointestinal bleeding?. Curr Surg. May 2001;58(3):323-7. [Medline].
Weintraub JL, Haskal ZJ. Embolotherapy of upper gastrointestinal hemorrhage. In: Techniques in Vascular and Interventional Radiology. 2000: 162-70.
Gomes AS, Lois JF, McCoy RD. Angiographic treatment of gastrointestinal hemorrhage: comparison of vasopressin infusion and embolization. AJR Am J Roentgenol. May 1986;146(5):1031-7. [Medline].
Stuber T, Hoffmann MH, Stuber G, Klass O, Feuerlein S, Aschoff AJ. Pitfalls in detection of acute gastrointestinal bleeding with multi-detector row helical CT. Abdom Imaging. Jul 3 2008;[Medline].
upper gastrointestinal bleeding, upper GI bleeding, UGIB, gastrointestinal bleeding, GI bleeding, hematemesis, variceal bleeding, upper GI hemorrhage, lower GI bleeding, LGIB, hemorrhage
Manish K Varma, MD, Chief of Interventional Radiology, Department of Radiology, Tripler Army Medical Center
Manish K Varma, MD is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, and Radiological Society of North America
Disclosure: Nothing to disclose.
Anthony W Allen, MD, Chief, Interventional Radiology, Brooke Army Medical Center; Associate Professor of Radiology, Uniformed Services University of the Health Sciences
Anthony W Allen, MD is a member of the following medical societies: American College of Radiology
Disclosure: Nothing to disclose.
Michael AJ Sawyer, MD, Director, Videoendoscopic Surgical Institute of Oklahoma, Consulting Staff, Department of Surgery, Comanche County Memorial Hospital; Consulting Staff, Great Plains Surgical Clinic, Lawton, Oklahoma
Michael AJ Sawyer, MD is a member of the following medical societies: American College of Surgeons, Society for Surgery of the Alimentary Tract, Society of American Gastrointestinal and Endoscopic Surgeons, and Society of Laparoendoscopic Surgeons
Disclosure: Nothing to disclose.
Robert A Koenigsberg, DO, MSc, FAOCR, Professor, Director of Neuroradiology, Program Director, Diagnostic Radiology and Neuroradiology Training Programs, Department of Radiology, Hahnemann University Hospital, Drexel University College of Medicine
Robert A Koenigsberg, DO, MSc, FAOCR is a member of the following medical societies: American Osteopathic Association, American Society of Neuroradiology, Radiological Society of North America, and Society of NeuroInterventional Surgery
Disclosure: Nothing to disclose.
Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.
George Hartnell, MB, Professor of Radiology, Tufts University School of Medicine, Director of Cardiovascular and Interventional Radiology, Department of Radiology, Baystate Medical Center
George Hartnell, MB is a member of the following medical societies: American College of Cardiology, American College of Radiology, American Heart Association, Association of University Radiologists, British Institute of Radiology, British Medical Association, Massachusetts Medical Society, Radiological Society of North America, Royal College of Physicians, Royal College of Radiologists, and Society of Cardiovascular and Interventional Radiology
Disclosure: Nothing to disclose.
Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Disclosure: Nothing to disclose.
Kyung J Cho, MD, FACR, William Martel Professor of Radiology, Interventional Radiology Fellowship Director, University of Michigan Health System
Kyung J Cho, MD, FACR is a member of the following medical societies: American College of Radiology, American Heart Association, American Medical Association, American Roentgen Ray Society, Association of University Radiologists, and Radiological Society of North America
Disclosure: Nothing to disclose.
Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis. American Association for the Study of Liver Diseases - Private Nonprofit Research Organization
American College of Gastroenterology - Medical Specialty Society. 1997 (revised 2007 Sep). 17 pages. NGC:005907
Preparation of patients for GI endoscopy.
American Society for Gastrointestinal Endoscopy - Medical Specialty Society. 2003 Apr. 5 pages. NGC:003818
The role of transjugular intrahepatic portosystemic shunt in the management of portal hypertension. American Association for the Study of Liver Diseases - Private Nonprofit Research Organization. 2005 Feb. 15 pages. NGC:004222
ASGE guideline: the role of endoscopy in the patient with lower-GI bleeding.
American Society for Gastrointestinal Endoscopy - Medical Specialty Society. 2005 Nov. 5 pages. NGC:004584
ASGE guideline: the role of endoscopy in acute non-variceal upper-GI hemorrhage.
American Society for Gastrointestinal Endoscopy - Medical Specialty Society. 2004 Oct. 8 pages. NGC:004062
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