Embolotherapy of upper gastrointestinal

Embolotherapy of Upper Gastrointestinal Hemorrhage Joshua L. Weintraub, MD and Ziv J. Haskal, MD

Angiography is indicated for nonvariceal upper gastrointestinal hemorrhage that does not respond to medical or endoscopic therapy. Therapeutic options include vasopressin infusion and embolotherapy. Although initial studies showed a high early success rate with intra-arterial infusions of vasopressin, there is a high rate of recurrent hemorrhage. Embolotherapy, however, occludes the bleeding vessel and is less prone to rebleeding. The stomach is richly vascularized, allowing for the safe and appropriate use of embolic agents with a low risk of ischemia. This article outlines the techniques and results for controlling various causes of upper gastrointestinal hemorrhage. Copyright © 2000 by W.B. Saunders Company

efore the advent of H2-blockers, upper gastrointestinal

B (UGI) hemorrhage was mostly caused by peptic ulcer disease. The prophylactic use of these agents and antacids has lessened the incidence of stress ulcers, gastritis, and bleeding peptic ulcers that warrant endovascular intervention or surgery. In addition to peptic disease, the differential diagnosis of UGI hemorrhage includes Mallory-Weiss tears, gastroesophageal varices, portal gastropathy, arteriovenous malformations, aortoenteric fistulae, hematobilia, visceral pseudoaneurysms, Dieulafoy's disease, hemorrhagic and drug-induced gastritides, and benign and malignant tumors. This article focuses on management of nonvariceal sources of UGI hemorrhage.

cular anastamoses are present, including those provided by the short gastric arteries. The duodenum is supplied by the GDA, which arises from the common hepatic artery and from branches of the pancreaticoduodenal arcade, which is a rich vasculature network formed by both celiac and superior mesenteric artery (SMA) branches. Accordingly, angiographic study of the SMA is imperative in cases of duodenal bleeding.

Diagnostic Workup Patients presenting with massive UGI bleeding initially require fluid resuscitation and stabilization. A nasogastric tube should be placed in nearly all patients with UGI bleeding to minimize the risk of aspiration. Gastric lavage can be performed through the nasogastric tube, and the amount of bleeding can be evaluated. Performing an immediate endoscopy is important for identification of the cause and the site of bleeding. For example, peptic disease coexists in approximately 30% of patients with portal hypertension; therefore, endoscopic confirmation of peptic versus variceal bleeding is required at nearly every episode of acute bleeding. Furthermore, temporary or curative therapy may be achieved under endoscopic guidance. Bleeding scans have little role in patients with UGI hemorrhage and should be reserved for hidden, repeated bleeds.

Anatomic Considerations The stomach is very richly vascularized, allowing the safe and appropriate use of embolotherapy with low risk of ischemia (Fig 1). The left gastric artery (LGA), which typically arises from the celiac artery (90%), primarily supplies the stomach and the distal esophagus. The LGA may also originate directly from the aorta (3%), from splenogastric (4%) or hepatogastric trunks (2%), which arise directly from the aorta. The LGA follows the lesser curvature of the stomach and anastamoses with the right gastric artery, a small branch of the left hepatic (40%), or proper hepatic arteries (40%). Less commonly, the right gastric artery may arise from the right hepatic artery (10%) or gastroduodenal artery (GDA) (8%). The gastroepiploic artery forms an arcade between the splenic and GDA and supplies the greater curvature of the stomach. Multiple intervas-

From the Department of Radiology, MHB 4-100, Columbia College of Physicians and Surgeons, New York, NY. Address reprint requests to Joshua L. Weintraub, MD, New York Presbyterian Hospital/Columbia, 177 Fort Washington Ave, MHB 4-100, New York, NY 10032. Copyright © 2000 by W.B. Saunders Company 1089-2516/00/0303-0008510.00/0 doi: 10.1053/tvir.2000.9733 1 6 ~)

Endoscopic and Surgical Therapy Endoscopic techniques are capable of controlling UGI bleeding in most patients for whom bleeding does not cease spontaneously) Whenever possible, endoscopy should be the first line of diagnosis and treatment in patients with UGI hemorrhage. Methods for controlling bleeding include electrocoagulation, epinephrine or sclerosant injection, and variceal banding. If the bleeding cannot be controlled, determination of the site of bleeding will direct the interventional radiologist to the appropriate vascular territory, should the bleeding arrest in the interim and active extravasation no longer be demonstrable. Because empiric embolization is generally safe, appropriate, and effective within the stomach and duodenum, this guidance is essential. Surgical therapy provides definitive treatment for the patient with massive UGI bleeding; however, operative mortality rates of 20% are daunting. These rates are higher in high-risk populations and emergency situations. 2 Because many conditions may heal with medical therapy once the bleeding is controlled (eg, benign ulcers, Mallory-Weiss tears, and so on), the role of surgery in UGI bleeding has decreased substantially.

Techniques in Vascular and Interventional Radiology, Vol 3, No 3 (September), 2000: pp 162-170

catheters and easier manipulation. If the patient has a coagulopathy, the sheath can be left in place at the end of the examination, providing secure access for fluid resuscitation or monitoring. A selective diagnostic celiac angiogram is initially performed. We usually use a 5F C2 catheter or, if necessary, a 5F Simmons 1 catheter. Hydrophilic-coated 4F or 5F C2 catheters may be used to provide more subselective studies of the celiac artery and may obviate coaxial microcatheters. The ROsch left gastric catheter (Cook Inc, Bloomington, IN) or a Wahman loop is useful for selecting the LGA. Occasionally, we have used 3F coaxial microcatheters. The Tracker 325 microcatheter (Boston Scientific, Natick, MA) is useful for embolization because of its comparatively larger inner lumen, although many effective microcatheters are available. The results of the upper endoscopy examination guide the selective catheterizations and therapeutic options. If a bleeding site has not been identified before angiography, we perform celiac angiography, followed by subselective LGA, GDA, and splenic artery injections to attempt to identify the bleeding source. In addition, the SMA and inferior mesenteric artery are catheterized if necessary.

Fig 1, Conventional arterial supply to the stomach and proximal duodenum: a, left gastric artery (LGA); b, fundal branches of LGA; c, esophageal branches of LGA; d, short gastric arteries; e, left gastroepiploic arteries; f, right gastroepiploic arteries; g, gastroduodenal artery (GDA); h, inferior pancreaticoduodenal artery; i, right gastric artery,

Endovascular Techniques Angiography is indicated for nonvariceal UGI bleeds that do not respond to medical or endoscopic therapy, The therapeutic options include vasopressin infusion and embolotherapy. Although early studies showed a high early success rate with intra-arterial infusions of vasopressin to control hemorrhage, more than 20% of patients have recurrent hemorrhage. 3,4 In one report, Gomes compared patients treated with vasopressin to those treated with embolization. 3 Although initial control of hemorrhage was similar in the 2 groups, several patients in the vasopressin group experienced rebleeding, reducing the overall success rate to 52%, versus 88% in the embolization groups. 3 Both techniques are intended to locally reduce prograde perfusion to the affected site. In the case of vasopressin, the local reduction in blood pressure is intended to allow the patient's intrinsic clotting abilities to provide hemostasis, hence the treatment failures in patients with coagulopathies. In contrast, embolotherapy can allow ablation of the bleeding vessel by temporary or permanent occlusion of the specific bleeding site with the use of embolic materials. As such, the embolized site is less prone to rebleeding. In other cases, embolization can be used in a manner similar to vasopressin. When the bleeding site is generalized, as in patients with hemorrhagic or other gastritides, large-particle embolization (eg, Gelfoam slurry or pledgets; Pharmacia & Upjohn, Kalamazoo, MI) effectively reduces local tissue blood flow to allow the patient to heal the affected sites. Therefore, correction of coagulopathies is equally important for patients undergoing embolization or vasopressin infusion. In general, local vasopressin infusion for control of UGI bleeding is reserved for cases in which embolization cannot be achieved. We routinely start our embolizations with placement of a 5F or 6F vascular sheath. This allows for expeditious exchange of EMBOLOTHERAPY OF UGI HEMORRHAGE

Choice of Embolic Agents Because most of the causes of UGI bleeding are benign, Gelfoam is the most common emholic agent we use. It can be cut into thin pledgers and delivered through a catheter with a 3-mL syringe (called "torpedoes"). Alternatively, slurry can be created, mixing the cut pieces of Gelfoam, saline, and contrast through 2 syringes that are connected by a 3-way stopcock. This slurry can be delivered through a microcatheter as well. Gelfoam is considered a temporary occlusive agent, and the vessel may recanalize in 2 to 4 weeks. Embolization coils can permanently occlude the treated vessel. When chosen appropriately, their advantages include precise placement, control over nontarget embolization, and obviation of the risk of tissue level embolization leading to tissue necrosis. There are several types of coils available, including stainless steel Gianturco coils (Cook Inc), 0.035-in platinum Nester coils (Cook Inc), microcoils with and without fibers, and Guglielmi detachable coils (GDC) (Boston Scientific/ Target, Fremont, CA). Gianturco coils and Nester coils require placement of a 0.035-in inner lumen catheter for deployment. Microcoils are available in a variety of shapes, ranging from straight to complex helical varieties of differing lengths and diameters. The addition of polyester fibers to microcoils has greatly increased their embolic efficiency and allowed the use of fewer coils. GDC coils can be partially deployed through microcatheters; they can be removed and repositioned if not in the desired location or configuration. Because of their cost, these coils are rarely used to embolize UGI bleeds. Food and Drug Administration-(FDA)-approved detachable balloons are available and can provide similar angiographic control. They are more complicated to use, however. Polyvinyl alcohol particles (PVA) are available in various sizes, ranging from 50 to 1,000 l~m. They are mixed into a suspension and delivered in a manner similar to Gelfoam. The exact threshold for the size of particle that will cause mucosal ischemia or tissue infarction is unknown; therefore, we use particles larger than 350 tam. We reserve PVA for embolization of tumors in which more distal embolization is needed.

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Recently, Embosphere Microspheres (BioSphere Medical, Rockland, MA) have been approved by the FDA and may have a role in embolotherapy of gastrointestinal hemorrhage. Other embolic agents include autologous blood clot, alcohol, sodium tetradecol, Gelfoam powder, and tissue adhesives (ie, glue). Autologous blood clots are largely of historical importance and are rarely used. Gelfoam powder provides a tissue level occlusion that, although theoretically temporary, can cause ischemia or infarction; this agent is no longer available for use in the United States. Dehydrated alcohol and sodium tetradecol are inappropriate for UGI embolotherapy because of the likelihood of producing tissue infarction and necrosis. Tissue adhesives are not currently approved by the FDA. Once available, they may be a useful alternative if they are formulated to avoid undesired distal tissue infarction.

Sites of Hemorrhage Treatment of hemorrhage that does not respond to medical or endoscopic therapies can be approached with arteriography directed at identifying an actively bleeding site or empiric embolization. If possible, angiography and embolization are guided by the endoscopic findings.

Mallory-Weiss Tears, Gastric Ulcers, and Dieulafoy's Erosions The LGA supplies the lower esophagus, which is the site of most Mallory-Weiss tears (Fig 2), gastric ulcers, and Dieula-

roy's lesions. A Dieulafoy's erosion consists of 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. 5 The LGA can usually be catheterized with either a 4F or 5F C2 catheter, a ROsch left gastric catheter, or a Wahman loop. When an accessory or replaced left hepatic artery is present, the LGA should be selectively catheterized (ie, distal to the origin of the shared left gastric-left hepatic artery common trunk). Gastric arteries can be distinguished from left hepatic arteries because of the characteristic curved appearance of the former, as they travel in and around the mucosal folds of the stomach. Given the dual blood supply of the liver, if the LGA cannot be catheterized distal to a left hepatic artery, larger particulate agents can still be used for embolization. Both Gelfoam pledgets (1- to 3-mm pieces) and Gianturco 0.035-in or 0.038-in coils or microcoils (2 to 3 mm) are used for embolization. In the past, autologous blood clot and other agents have been used. Gelfoam powder (not currently available) and small PVA particles are inappropriate because of the risk of infarction. Embolization should be continued until there is complete stasis of blood flow. If no active extravasation is identified, selective arteriography of alternative source vessels should be performed, including the splenic, inferior phrenic, cholecystic, right gastric, and left hepatic artery. Empiric embolization of the LGA should be performed if no active bleeding is seen and yet the bleeding site lies in the vascular territory of this artery (Fig 3).

Fig 2. Mallory-Weiss tear embolized with Gelfoam pledgets. An 18-year-old college freshman presented with massive hematemesis. No bleeding was seen on endoscopy, (A) Left gastric arteriogram shows extravasation from a Mallory-Weiss tear. (B) Successful embolization with Gelfoam pledgets,

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to achieve from a prograde GDA approach, distal embolization can be attempted through the SMA and pancreaticoduodenal arcade arteries. Diffuse hyperemia of the gastric mucosa can be treated with intra-arterial infusion of vasopressin or empiric embolization of the LGA or GDA. With vasopressin infusion, we infuse 0.2 U/min for 20 minutes into the LGA. A repeat arteriogram is performed after 20 minutes. If there is ongoing bleeding, the dose is doubled to 0.4 U/min for an additional 20 minutes. If bleeding still continues, we discontinue the vasopressin for 20 minutes and empirically embolize the LGA. If bleeding ceases after the vasopressin infusion, the patient is transferred to the intensive care unit and continued on infusion for 24 hours. The dose is then decreased by 0.1 U/min every 12 hours, and then 0.9 normal saline is infused at 30 mIJh for 12 hours. The catheter is subsequently removed at the bedside. 6 Empiric embolization has largely replaced vasopressin infusion because of its safety.

Duodenal Ulcer Branches of the GDA supply the duodenum and duodenal ulcers. The duodenum has a rich collateral blood supply, and careful subselective angiography is necessary to ensure adequate treatment. Initially, celiac angiography should be performed, followed by selective angiography of the GDA (Fig 4). If a bleeding site is identified, the catheter should be advanced slightly distal to the site of hemorrhage. A 4F or 5F Cobra hydrophilic catheter and a 0.035-in hydrophilic guidewire often enable one to catheterize the distal branches without resorting to a coaxial microcatheter system. This makes delivery of Gelfoam slurry, pledgets, and coils significantly easier because of the larger catheter lumen. If extravasation continues despite Gelfoam embolization, coils may be used to ablate the target vessel, ie, entirely pack its lumen. SMA arteriography must be performed to evaluate collateral supply to the embolized bleeding site. If extravasation is identified, the inferior pancreaticoduodenal arteries can be catheterized for additional embolization. Fig 3. Empiric embolization of the LGA. A 41-year-old man with restrictive cardiomyopathy was placed on a left ventricular assist device. He developed a brisk UGI bleed whose site could not be located by endoscopy. His blood pressure was 60•40 mm Hg at time of angiography. (A) The branches of the celiac artery are small in caliber because of the patient's hypotension. Contrast extravasation may not be demonstrable in patients with hypovolemic shock. (B) The LGA has been empirically embolized, the patient's blood pressure improved, and the bleeding was arrested.

Pseudoaneurysms Pancreatitis and trauma, both accidental and iatrogenic, can result in pseudoaneurysms of all branches of the celiac artery or proximal SMA. These pseudoaneurysms can rupture into the gastrointestinal tract or peritoneal cavity and should be treated with coil embolization (Fig 5). Both GDC and Gianturco coils are useful in this setting. It is important to either occlude the neck of the aneurysm or to densely pack it with coils to decrease the risk of rupture (Fig 6).

Diffuse Gastritis Despite an endoscopic diagnosis of diffuse gastritis, often an actively bleeding artery can be identified on angiography. Similar to our approach for gastric ulceration, we start with a celiac injection and proceed to subselective injections of the LGA, GDA, splenic, and right and left gastroepiploic arteries. In addition, the SMA is injected. If an active site of bleeding is identified, embolization is performed with either Gelfoam or coils, as previously described. If the bleeding site is from the GDA, it is important to embolize both sides of the bleeding site to provide proximal and distal control. When this is impossible

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Hemobilia Hemobilia can have many causes, including neoplasms, blunt or penetrating trauma, and iatrogenic injuries (Fig 7). Tumors often erode into the biliary tree or directly into the gastrointestinal tract. When treating bleeding malignancies, we often use PVA particles to obtain more distal embolization of the tumor. This must be done selectively so as not to infarct portions of normal gastrointestinal tract. Iatrogenic trauma can result from erosions of metallic biliary endoprostheses into the duodenum, endoscopic sphincteroto-

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Fig 4. Embolotherapy of a duodenal ulcer, A 60-year-old man receiving chronic corticosteroid therapy presented with hematemesis. The bleeding duodenal ulcer could not be controlled by endoscopy. (A) Angiography of a celiac/SMA common arterial trunk injection shows a gastroduodenal artery bleed. (B) A selective common hepatic artery injection shows duodenal bleeding with contrast and filling defects (presumably blood) within the common bile duct. (C) A later image shows contrast opacifiying the duodenum and common bile duct. The bleeding was successfully embolized with Gelfoam pledgets.

mies, liver biopsies, transjugular intrahepatic portosystemic shunts, and transhepatic biliary procedures. Branches of the hepatic artery can be safely embolized in nearly all patients, except those with significant impairment of liver function. Selective focal embolization of the lesion is the objective, which should be achieved with proximal and distal embolization. Initial celiac angiography is performed to attempt to identify the bleeding vessel and to confirm patency of the portal vein. Selective hepatic artery catheterization must be performed in multiple projections and magnifications if the bleeding site is not readily seen. When there is bleeding after transhepatic biliary or portal interventions, the indwelling

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catheter may have to be removed over a guidewire during hepatic angiography to aid in the visualization of a subtle pseudoaneurysm or extravasation along the transhepatic catheter tract. Microcoils are typically used for these procedures.

Results Angiography was first used to identify gastrointestinal bleeding in the mid-1960s. 7 Intra-arterial vasopressin infusion was first studied in the late 1960s, 8 followed closely by arterial embolization. 9 One of the first studies to evaluate angiography to control massive nonvariceal UGI bleeding was performed by

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Fig 5. Aneurysm of the inferior pancreaticoduodenal arcade. To permanently ablate the abnormal arterial segment, it is densely packed with coils. The Patient is a 54-year-old surgeon with no history of pancreatitis, who presented with sudden abdominal pain. (A) Computed tomography (CT) with contrast shows peripancreatic hemorrhage. (B) SMA angiography shows retrograde filling of the celiac artery and its branches. The celiac artery origin is occluded. (C) An aneurysmal abnormal segment of the inferior pancreaticoduodenal arcade is identified during SMA angiography (arrows). (D) The inferior pancreaticoduodenal arcade was catheterized from an SMA approach with the use of a microcatheter and was densely packed with 25 platinum microcoils. There was no further bleeding, It is important to occlude the entire aneurysmal segment to prevent collateral filling through the many vessels supplying this territory, The correlation between celiac artery stenosis or occlusion and pancreaticoduodenal aneurysms is controversial.

Dempsey et al. 1° In his study, 39% of patients (25/64) had contrast extravasation identified at the time of angiography. Embolization when the bleeding site was identified caused surgery to be avoided in 50% of the patients. This was associated with a 45% reduction in mortality (83% versus 38%). These results strongly support the use of embolization in patients with ongoing hemorrhage. 10 Lang et al performed one of the first studies to evaluate empiric embolization for UGI bleeding. 11 Twenty percent of their patients had normal arteriograms. The authors showed that prophylactic embolization of the LGA territory significantly reduced the risk of recurrent hemorrhage. Other investigators have substantiated these results. 12 While at the Hospital of the University of Pennsylvania, we evaluated laboratory and clinical factors that contribute to success in the treatment of UGI hemorrhage with embolization. I3 Embolization was successfully performed in 97% of the

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89 patients who underwent 94 embolizations. Clinical success, defined as hemodynamic stabilization, cessation of clinically detectable bleeding, and hematocrit stabilization, occurred in 59% of patients, with a hospital mortality rate of 37%. More than 50% of the failures occurred within the first 24 hours after embolization. Targeted empiric embolization proved as successful as embolization of an angiographically identified source of extravasation. The age of the patient, presence of underlying malignancy, and the duration of bleeding did not significantly affect success. Similarly, neither the target vessels nor the embolic agent had an impact on the clinical outcome. An ongoing coagulopathy reduced success by 40%. Mortality was significantly increased by the presence of coagulopathy, anglographic extravasation, and immediate technical failure to control the hemorrhage. These results have been substantiated by other authors. 14 Embolization can decrease the arterial inflow and perfusion pressure by occluding the primary inflow

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Fig 6. Pseudoaneurysm arising at the common hepatic artery bifurcation. A 72-year-old woman complained of vague right upper quadrant pain, prompting CT evaluation. (A) CT angiography shows a pseudoaneurysm at the junction of the hepatic artery and the GDA. A replaced right hepatic artery is present. (B) Celiac arteriography confirms that the pseudoaneurysm arises at the common hepatic artery bifurcation. (C) Rather than densely packing the aneurysm with coils, both the ingress and egress were occluded, isolating the aneurysm (arrows). The GDA origin was embolized, followed by the left hepatic and common hepatic arteries. (D) Celiac angiography shows the aneurysm to be completely excluded from blood flow. (Courtesy of Scott O. Trerotola, MD. Reprinted with permission from the SCVIR Case Club.)

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Fig 7. Embolization of a bleeding pancreatic malignancy. A recently bleeding site was intentionally recanalized to allow permanent embolization with the use of coils. A 52-yearwoman underwent biliary metallic stent placement for biliary obstruction that was caused by a large pancreatic tumor. On day 5, she developed a massive UGI hemorrhage with a systolic blood pressure of 70 mm Hg. She was vigorously resuscitated. On arrival in the interventional radiology suite, she was stable, and the bleeding had arrested spontaneously. Initial celiac angiography showed irregular and occluded right hepatic and GDA (not shown). There was no extravasation. (A) Cholangiography, performed at an outside facility before admission, shows obstruction at the liver hilum, despite Wallstent (Boston Scientific, Watertown, MA) placement. (B) The stump of the occluded hepatic artery was probed with the use of a cobra-shaped catheter and hydrophilic guidewire until the clot at the bleeding site was dislodged. (C) Angiography, which was performed after the occlusion was recanalized, shows rapid extravasation into the small bowel. (D) Coil embolization of the occluded hepatic artery. (E) Final SMA angiography was performed to exclude retrograde filling of the bleeding site. The patient remained free of gastrointestinal bleeding at 5-month follow-up.

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vessels; however, the patient's intrinsic coagulation factors may be necessary to ensure durable thrombosis. Thus, all efforts to correct coagulopathies should be made.

Conclusions Embolization has mostly replaced vasopressin in the treatment of UGI hemorrhage. Patient care must be individualized and based on several factors, including the patient's vascular anatomy, site of bleeding, stability, and underlying cardiovascular disease, as well as the skill and experience of the interventional radiologist. The mode of therapy should be the most expeditious one to safely treat the patient.

References 1. Petrini JL, Jr: Endoscopic therapy for gastrointestinal bleeding: Postgrad Med 84:239-245, 1988 2. Kim B, Wright HK, Bordan D, et al: Risks of surgery for upper gastrointestinal hemorrhage: 1972 versus 1982. Am J Surg 149:474476, 1985 3. GomesAS, Lois JF, McCoy RD:Angiographictreatment of gastrointestinal hemorrhage: Comparison of vasopressin infusion and embolization. AJR Am J Roentgeno1146:1031-1037, 1986 4. Chang YC, Tsang YM, Kung KL, et al: Transcatheter control of intractible gastrointestinal bleeding. J Formos Med Assoc 90:81-87, 1991

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5. Reilly HFd, aI-Kawas FH: Dieulafoy's lesion. Diagnosis and management. Dig Dis Sci 36:1702-1707, 1991 6. Kadir S, Ernst CB: Current concepts in angiographic management of gastrointestinal bleeding. Curr Probl Surg 20:281-343, 1983 7. Baum S, Nusbaum M, Blakemore WS, et al: The preoperative radiographic demonstration of intra-abdominal bleeding from undetermined sites by percutaneous selective celiac and superior mesenteric arteriography. Surgery 58:797-805, 1965 8. Nusbaum M, Baum S, Blakemore WS: Clinical experience with the diagnosis and management of gastrointestinal hemorrhage by selective mesenteric catheterization. Ann Surg 170:506-514, 1969 9. Rosch J, Dotter CT, Brown MJ: Selective arterial embolization. A new method for control of acute gastrointestinal bleeding. Radiology 102:303-306, 1972 10. Dempsey DT, Burke DR, Reilly RS, et al: Angiography in poor-risk patients with massive nonvariceal upper gastrointestinal bleeding. Am J Surg 159:282-286, 1990 11. Lang EV, Picus D, Marx MV, et al: Massive upper gastrointestinal hemorrhage with normal findings on arteriography: Value of prophylactic embolization of the left gastric artery. AJR Am J Roentgenol 158:547-549, 1992 12. Carreira JM, Reyes R, Pulido-Duque JM, et al: Diagnosis and percutaneous treatment of gastrointestinal hemorrhage. Long-term experience. Rev Esp Enferm Dig 91:684-692, 1999 13. Duszak RL, Shlansky-Goldberg RD, Cope C, et al: Transcatheter embolization in the management of upper gastrointestinal hemorrhage: Laboratory and clinical factors contributing to success. J Vasc Intervent Radiol 6:14, 1995 (abstr) 14. Encarnacion CE, Kadir S, Beam CA, et al: Gastrointestinal bleeding: Treatment with gastrointestinal arterial embolization. Radiology 183: 505-508, 1992

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