Disclosure
Background: Upper gastrointestinal (GI) 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 radiologist. The first decision point in managing GI bleeding is defining its location: Is it a UGIB or a lower GI bleed (LGIB)? 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. A coffee-grounds appearance occurs with precipitated 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. For excellent patient education resources, visit eMedicine's Esophagus, Stomach, and Intestine Center. Also, see eMedicine's patient education article Gastrointestinal Bleeding. Pathophysiology: UGIB occurs from a variety of etiologies. The pathophysiology of the bleeding is often mucosal erosion with subsequent hemorrhage. About 90% of the cases of UGIB arise from Mallory-Weiss tears, variceal hemorrhage due to portal hypertension, peptic ulcer disease, and gastritis. Prior to the emergence 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. 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 and a neoplasm may also cause UGIB. Frequency:
Mortality/Morbidity:
Race: No well-described racial predilection for UGIB exists. Sex: 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 is approximately 2:1 in both countries. The mortality rates are similar in both sexes. Age: The number of cases of UGIB increases with patient age. In a study performed in 1995 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. Anatomy: UGIB arises from branches of the celiac artery and superior mesenteric artery (SMA). 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 the SMA. The left gastric artery (LGA) 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 (40%) or proper hepatic arteries (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 gastroduodenal and SMAs, 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 the SMAs, 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. Clinical Details: In the vast majority (>75%) of cases, UGIB 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 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 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. Preferred Examination: Upper endoscopy is the initial procedure of choice for the evaluation of acute UGIB. 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. 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 LGA or the GDA 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 B condition and some with a Child C condition. Currently, upper GI barium examinations have no role in the diagnosis of acute UGIB. Limitations of Techniques: Endoscopy is often the first-line diagnostic examination and treatment option in UGIB. However, findings can be nondiagnostic in about 10% of cases. For example, in the setting of a 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 LGA or GDA. In these situations, prophylactic embolization is helpful. Prophylactic embolization of the LGA without prior documented bleeding is advocated because almost 90% of the patients with this condition survive if the bleeding is controlled. The left gastric artery is involved in 85% of the cases of UGIB.
Duodenum, Ulcers
Peptic ulcer disease
Findings: Plain radiographs of the abdomen are not usually helpful in the diagnosis of acute UGIB. 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 results in chronic, not acute, UGIB), aneurysms with calcifications, and ascites suggestive of portal hypertension, may be seen on radiographs. Degree of Confidence: 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 UGIB. |
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Findings: Usually, abdominal CT is not used in the evaluation of acute UGIB from arterial sources, although it has been helpful in some series. However, in the detection of UGIB from pseudoaneurysms of the mesenteric vessels 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. 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 TIPS procedure. Degree of Confidence: CT is currently not the study of choice in the evaluation of acute UGIB. 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 at CT. In the catastrophic situation of aortoenteric fistula, CT may be helpful in detecting an early leak. False Positives/Negatives: 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 UGIB. These include underopacification of bowel loops, suboptimal visualization of the biliary system and small visceral aneurysms, and difficulty in evaluating the esophagus.
Findings: MRI has a limited role in the evaluation of acute UGIB from arterial sources. In the setting of aneurysms and pseudoaneurysm, magnetic resonance angiography (MRA) may be helpful in depicting small 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. Degree of Confidence: Similar to CT, MRI has no real role in the assessment of acute UGIB. 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.
Findings: Ultrasonography has no role in the setting of acute UGIB. It may be helpful in establishing portal vein patency prior to TIPS placement in patients with variceal bleeding. Cross-sectional CT or MRI is used to detect occult sources of UGIB. Degree of Confidence: Ultrasonography has a limited role in the management of UGIB; uses are noted above.
Findings: Tagged-RBC and sulfur colloid studies are not generally used for the evaluation of UGIB. The diagnosis of UGIB is usually established with clinical parameters and endoscopic means. Nuclear medicine studies are usually reserved for the investigation of LGIB in areas that cannot be reached with endoscopy because of anatomical or technical (ie, brisk bleeding) reasons. 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. Degree of Confidence: Often, nuclear medicine studies are not helpful in determining the site or source of UGIB. Endoscopy is the preferred test.
Findings: Angiography is often the next step if medical management or endoscopy fails to control UGIB. 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. 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 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 GDA 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 SMA 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 is performed of the gastroduodenal, left gastric, and splenic arteries. 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 many as 50% occult UGIBs. Degree of Confidence: The degree of confidence in the angiographic diagnosis of UGIB is high. Arteriography can be used to accurately identify 90% of acute UGIBs. 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. False Positives/Negatives: 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.
Intervention: Selective arterial embolization is effective in arresting arterial bleeding from peptic ulcer disease, Dieulafoy disease, and Mallory-Weiss tear. 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 the control of variceal bleeding. TIPS 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. The angiographic appearance of an acute UGIB 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 LGIB, and it is infrequently used for UGIB. In general, active extravasation is required prior to embolotherapy in a case of upper GI arterial bleeding. 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 LGA is used for the treatment of hemorrhagic gastritis with a good success rate; embolization is ineffective because the bleeding is capillary or mucosal. 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, 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 SMAs. Thus, after embolization of the branches of the GDA, a superior mesenteric arteriogram should be obtained to evaluate reconstitution of the bleeding artery. Occasionally, both the branches from the celiac and SMAs may to have to be embolized to control duodenal bleeding. Concurrent correction of any underlying coagulopathy is important to aid in thrombosis. In 1986, 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. 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 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 feeding vessel may be effective in controlling hemorrhage. Medical/Legal Pitfalls:
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